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1-) Medical microbiology is both a branch of medicine and microbiology which deals

with the study of microorganisms including bacteria, viruses, fungi and parasites which are of medical importance and are capable of causing diseases in human beings. It includes the study of microbial pathogenesis and epidemiology and is related to the study of disease pathology and immunology. In the medical laboratory, these microbiologists also work in a subdepartment dedicated to parasitology. The discipline consists primarily of four major spheres of activity: The provision of clinical consultations on the investigation, diagnosis, and treatment of patients suffering from infectious diseases. The establishment and direction of infection control programs across the continuum of care. Public health and communicable disease prevention and epidemiology. The scientific and administrative direction of a diagnostic microbiology laboratory. In addition to these primary activities, medical microbiologists are also involved in teaching at all levels, and in research, both basic and applied. This branch of microbiology is amongst the most widely studied and followed branches due to its great importance to medicine. Along with providing a deep knowledge and understanding of the nature of pathogens this line of study has also been applied in several immunological innovations in the field of medical science. Through the development of vaccines against invading organisms, deadly and debilitating diseases such as small pox, polio, and tuberculosis have been either eradicated or are more 2-) BACTERIAL TAXONOMYClassification seeks to describe the diversity of bacterial species by naming and grouping organisms based on similarities. Bacteria can be classified on the basis of cell structure, cellular metabolism or on differences in cell components such as DNA, fatty acids, pigments, antigens and quinones.[96] While these schemes allowed the identification and classification of bacterial strains, it was unclear whether these differences represented variation between distinct species or between strains of the same species. This uncertainty was due to the lack of distinctive structures in most bacteria, as well as lateral gene transfer between unrelated species.[128] Due to lateral gene transfer, some closely related bacteria can have very different morphologies and metabolisms. To overcome this uncertainty, modern bacterial classification emphasizes molecular systematics, using genetic techniques such as guanine cytosine ratio determination, genome-genome hybridization, as well as sequencing genes that have not undergone extensive lateral gene transfer, such as the rRNA gene.[129] Classification of bacteria is determined by publication in the International Journal of Systematic Bacteriology,[130] and Bergey's Manual of Systematic Bacteriology. [131] The International Committee on Systematic Bacteriology (ICSB) maintains international rules for the naming of bacteria and taxonomic categories and for the ranking of them in the International Code of Nomenclature of Bacteria. The term "bacteria" was traditionally applied to all microscopic, single-celled prokaryotes. However, molecular systematics showed prokaryotic life to consist of two separate domains, originally called Eubacteria and Archaebacteria, but now called Bacteria and Archaea that evolved independently from an ancient common ancestor.[8] The archaea and eukaryotes are more closely related to each other than either is to the bacteria. These two domains, along with Eukarya, are the basis of the three-domain system, which is currently the most widely used classification system in microbiolology.[132] However, due to the relatively recent introduction of molecular systematics and a rapid increase in the number of genome

sequences that are available, bacterial classification remains a changing and expanding field.[4][133] For example, a few biologists argue that the Archaea and Eukaryotes evolved from Gram-positive bacteria.[134] Identification of bacteria in the laboratory is particularly relevant in medicine, where the correct treatment is determined by the bacterial species causing an infection. The Gram stain, developed in 1884 by Hans Christian Gram, characterises bacteria based on the structural characteristics of their cell walls.[66] The thick layers of peptidoglycan in the "Gram-positive" cell wall stain purple, while the thin "Gram-negative" cell wall appears pink. By combining morphology and Gram-staining, most bacteria can be classified as belonging to one of four groups Culture techniques are designed to promote the growth and identify particular bacteria, while restricting the growth of the other bacteria in the sample. Often these techniques are designed for specific specimens; for example, a sputum sample will be treated to identify organisms that cause pneumonia, while stool specimens are cultured on selective media to identify organisms that cause diarrhoea, while preventing growth of non-pathogenic bacteria. As with bacterial classification, identification of bacteria is increasingly using molecular methods. Diagnostics using such DNA-based tools, such as polymerase chain reaction, are increasingly popular due to their specificity and speed, compared to culture-based methods.[138] These methods also allow the detection and identification of "viable but nonculturable" cells that are metabolically active but non-dividing.[139] 3-) Bacteria display many cell morphologies and arrangements Bacteria display a wide diversity of shapes and sizes, called morphologies. Bacterial cells are about one tenth the size of eukaryotic cells and are typically 0.5. 5.0 micrometres in length. However, a few species.for example Thiomargarita namibiensis and Epulopiscium fishelsoni.are up to half a millimetre long and are visible to the unaided eye.[29] Among the smallest bacteria are members of the genus Mycoplasma, which measure only 0.3 micrometres, as small as the largest viruses Some bacteria may be even smaller, but these ultramicrobacteria are not wellstudied. Most bacterial species are either spherical, called cocci (sing. coccus, from Greek .-kokkos, grain, seed) or rod-shaped, called bacilli (sing. bacillus, from Latin baculus, stick). Elongation is associated with swimming.[32] Some rod-shaped bacteria, called vibrio, are slightly curved or comma-shaped; others, can be spiralshaped, called spirilla, or tightly coiled, called spirochaetes. A small number of species even have tetrahedral or cuboidal shapes.[33] More recently, bacteria were discovered deep under the Earth's crust that grow as long rods with a star-shaped cross-section. The large surface area to volume ratio of this morphology may give these bacteria an advantage in nutrient-poor environments.[34] This wide variety of shapes is determined by the bacterial cell wall and cytoskeleton, and is important because it can influence the ability of bacteria to acquire nutrients, attach to surfaces, swim through liquids and escape predators.[35][36] Many bacterial species exist simply as single cells, others associate in characteristic patterns: Neisseria form diploids (pairs), Streptococcus form chains, and Staphylococcus group together in "bunch of grapes" clusters. Bacteria can also be elongated to form filaments, for example the Actinobacteria. Filamentous bacteria are often surrounded by a sheath that contains many individual cells. Certain types, such as species of the genus Nocardia, even form complex, branched filaments, similar in appearance to fungal mycelia.[37]The range of sizes shown by prokaryotes, relative to those of other organisms and biomolecules

Bacteria often attach to surfaces and form dense aggregations called biofilms or bacterial mats. These films can range from a few micrometers in thickness to up to half a meter in depth, and may contain multiple species of bacteria, protists and archaea. Bacteria living in biofilms display a complex arrangement of cells and extracellular components, forming secondary structures such as microcolonies, through which there are networks of channels to enable better diffusion of nutrients.[38][39] In natural environments, such as soil or the surfaces of plants, the majority of bacteria are bound to surfaces in biofilms.[40] Biofilms are also important in medicine, as these structures are often present during chronic bacterial infections or in infections of implanted medical devices, and bacteria protected within biofilms are much harder to kill than individual isolated bacteria.[41] 4-) Prokaryotes The prokaryotes are a group of organisms that lack a cell nucleus (= karyon), or any other membrane-bound organelles. They differ from the eukaryotes, which have a cell nucleus. Most are unicellular, but a few prokaryotes such as myxobacteria have multicellular stages in their life cycles.[1] The word prokaryote comes from the Greek - (pro-) "before" + (karyon) "nut or kernel".[2]The prokaryotes are divided into two domains: the bacteria and the archaea. Relationship to eukaryotes A distinction between prokaryotes and eukaryotes (meaning true kernel, also spelled "eucaryotes") is that eukaryotes do have "true" nuclei containing their DNA, whereas the genetic material in prokaryotes is not membrane-bound. Eukaryotic organisms may be unicellular, as in amoebae, or multicellular, as in plants and animals. The difference between the structure of prokaryotes and eukaryotes is so great that it is sometimes considered to be the most important distinction among groups of organisms. However, a criticism of this classification is that the word "prokaryote" is based on what these organisms are not (they are not eukaryotic), rather than what they are (either archaea or bacteria).[3] In 1977, Carl Woese proposed dividing prokaryotes into the Bacteria and Archaea (originally Eubacteria and Archaebacteria) because of the major differences in the structure and genetics between the two groups of organisms. The cell structure of prokaryotes differs greatly from that of eukaryotes. The defining characteristic is the absence of a nucleus. Also the size of Ribosomes in prokaryotes are smaller than in eukaryotes, which is now where respiration takes place.The genomes of prokaryotes are held within an irregular DNA/protein complex in the cytosol called the nucleoid, which lacks a nuclear envelope.[5] Prokaryotes generally lack membrane-bound cell compartments: such as mitochondria and chloroplasts. Instead processes such as oxidative phosphorylation and photosynthesis take place across the prokaryotic plasma membrane.[6] However, prokaryotes do possess some internal structures, such as cytoskeletons,[7][8] and the bacterial order Planctomycetes have a membrane around their nucleoid and contain other membrane-bound cellular structures.[9] Both eukaryotes and prokaryotes contain large RNA/protein structures called ribosomes, which produce protein. Prokaryotes are usually much smaller than eukaryotic cells.Prokaryotes also differ from eukaryotes in that they contain only a single loop of stable chromosomal DNA stored in an area named the nucleoid, while eukaryote DNA is found on tightly bound and organized chromosomes. Although some eukaryotes have satellite DNA structures called plasmids, these are generally regarded as a prokaryote feature, and many important genes in prokaryotes are Reproduction Bacteria and archaea reproduce through asexual reproduction, usually by binary fission or budding. Genetic exchange and recombination still occur, but this is a form of horizontal gene transfer and is not a replicative process, simply involving DNA being transferred between two cells, as in bacterial conjugation.

5-) Bacterial Ultrastructure: cell wall, Around the outside of the cell membrane is the bacterial cell wall. Bacterial cell walls are made of peptidoglycan (also called murein), which is made from polysaccharide chains cross-linked by unusual peptides containing D-amino acids.[11] Bacterial cell walls are different from the cell walls of plants and fungi which are made of cellulose and chitin, respectively.[12] The cell wall of bacteria is also distinct from that of Archaea, which do not contain peptidoglycan. The cell wall is essential to the survival of many bacteria, although L-form bacteria can be produced in the laboratory that lack a cell wall.[13] The antibiotic penicillin is able to kill bacteria by preventing the cross-linking of peptidoglycan and this causes the cell wall to weaken and lyse.[12] The lysozyme enzyme can also damage bacterial cell walls. There are broadly speaking two different types of cell wall in bacteria, called Grampositive and Gram-negative. The names originate from the reaction of cells to the Gram stain, a test long-employed for the classification of bacterial species.[14] Gram-positive bacteria possess a thick cell wall containing many layers of peptidoglycan and teichoic acids. In contrast, Gram-negative bacteria have a relatively thin cell wall consisting of a few layers of peptidoglycan surrounded by a second lipid membrane containing lipopolysaccharides and lipoproteins. Most bacteria have the Gram-negative cell wall and only the Firmicutes and Actinobacteria (previously known as the low G+C and high G+C Gram-positive bacteria, respectively) have the alternative Gram-positive arrangement.[15] These differences in structure can produce differences in antibiotic susceptibility, for instance vancomycin can kill only Gram-positive bacteria and is ineffective against Gram-negative pathogens, such as Haemophilus influenzae or Pseudomonas aeruginosa.[16] 6-) Other bacterial surface structures Fimbrae are protein tubes that extend out from the outer membrane in many members of the Proteobacteria. They are generally short in length and present in high numbers about the entire bacterial cell surface. Fimbrae usually function to facilitate the attachment of a bacterium to a surface (e.g. to form a biofilm) or to other cells (e.g. animal cells during pathogenesis)). A few organisms (e.g. Myxococcus) use fimbrae for motility to facilitate the assembly of multicellular structures such as fruiting bodies. Pili are similar in structure to fimbrae but are much longer and present on the bacterial cell in low numbers. Pili are involved in the process of bacterial conjugation. Non-sex pili also aid S-layers An S-layer (surface layer) is a cell surface protein layer found in many different bacteria and in some archaea, where it serves as the cell wall. All S-layers are made up of a two-dimensional array of proteins and have a crystalline appearance, the symmetry of which differs between species. The exact function of S-layers is unknown, but it has been suggested that they act as a partial permeability barrier for large substrates. For example, an S-layer could conceivably keep extracellular proteins near the cell membrane by preventing their diffusion away from the cell. In some pathogenic species, an S-layer may help to facilitate survival within the host by conferring protection against host defence mechanisms. ] Capsules and Slime Layers Many bacteria secrete extracellular polymers outside of their cell walls. These polymers are usually composed of polysaccharides and sometimes protein. Capsules are relatively impermeable structures that cannot be stained with dyes such as India ink. They are structures that help protect bacteria from phagocytosis and desiccation.

Slime layer is involved in attachment of bacteria to other cells or inanimate surfaces to form biofilms. Slime layers can also be used as a food reserve for the cell. A-Monotrichous; B-Lophotrichous; C-Amphitrichous; D-Peritrichous; Flagella Perhaps the most recognizable extracellular bacterial cell structures are flagella. Flagella are whip-like structures protruding from the bacterial cell wall and are responsible for bacterial motility (i.e. movement). The arrangement of flagella about the bacterial cell is unique to the species observed. Common forms include: Peritrichous - Multiple flagella found at several locations about the cell Polar - Single flagellum found at one of the cell poles Lophotrichous - A tuft of flagella found at one cell pole Flagella are complex structures that are composed of many different proteins. These include flagellin, which makes up the whip-like tube and a protein complex that spans 7-) Bacterial ultrastructure: bacterial spores An endospore is a dormant, tough, and temporarily non-reproductive structure produced by certain bacteria from the Firmicute phylum. The name "endospore" is suggestive of a spore or seedlike form (endo means within), but it is not a true spore (i.e. not an offspring). It is a stripped-down, dormant form to which the bacterium can reduce itself. The endospore becomes important when the bacterium is experiencing an environment that is deleterious to the usual vegetative state of the bacterium, such as in desiccating conditions. Endospores enable bacterium to survive periods of environmental stress lasting at least several thousand years, and revival of spores many millions of years old has been claimed.[1] When the environment becomes more favorable, the endospore can reactivate itself to the vegetative state. Most types of bacteria cannot change to the endospore form, but examples include Bacillus and Clostridium.[2] The endospore consists of the bacterium's DNA and part of its cytoplasm, surrounded by a very tough outer coating. Endospores can survive without nutrients. They are resistant to ultraviolet radiation, desiccation, high temperature, extreme freezing and chemical disinfectants. Common antibacterial agents that work by destroying vegetative cell walls don't work on endospores. Endospores are commonly found in soil and water, where they may survive for long periods of time. Some classes of bacteria can turn into exospores, also known as microbial cysts, instead of endospores. Exospores and endospores are two kinds of "hibernating" or dormant stages seen in some classes of microorganisms. The position of the endospore differs among bacterial species and is useful in identification. The main types within the cell are terminal, subterminal, and centrally placed endospores. Terminal endospores are seen at the poles of cells, whereas central endospores are more or less in the middle. Subterminal endospores are those between these two extremes, usually seen far enough towards the poles but close enough to the center so as not to be considered either terminal or central. Lateral endospores are seen occasionally. Examples of bacteria having terminal endospores include Clostridium tetani, the pathogen that causes the disease tetanus. Bacteria having a centrally placed endospore include Bacillus cereus, and those having a subterminal endospore include Bacillus subtilis. Sometimes the endospore can be so large the cell can be distended around the endospore, this is typical of Clostridium tetani.

8-) Bacterial metabolism is the process which bacteria use to stay alive. Metabolic processes in bacteria are quite diverse and extremely fascinating, at least for people who are interested in this sort of thing. Bacteria have evolved an astounding number of ways to access energy available in the natural environment so that they can use it to stay alive and perform a variety of functions. Bacterial metabolism is also harnessed by other organisms; humans, for example, rely on bacteria in their gut to break down food into components which their bodies can access. One aspect of bacterial metabolism involves the collection of energy. One of the processes available to bacteria is familiar to humans: respiration. However, unlike humans, bacteria can use gases other than oxygen in their respiration processes, and some bacteria are even capable of surviving in anaerobic environments as well as environments which contain air. This is a rather remarkable adaptation which allows the bacteria to survive in harsh environments as circumstances change. Many bacteria are heterotrophs, using organic materials for energy just like humans do. The organisms can access the molecules inside the materials in a variety of ways. One technique they use is fermentation, in which materials are broken down into usable components. Some bacteria can also photosynthesize, using the sun for energy as long as they have access to nutrients, and others are capable of surviving on inorganic materials. Known as lithotrophs or autotrophs, these bacteria can survive in extremely harsh environments. The utilization of energy inside a bacterium can also vary, depending on the species. Bacteria use energy for movement, if they are motile, and for a variety of other tasks. Some bacteria have evolved interesting ways to use the energy they can access to maintain internal functions. Bacterial metabolism allows bacteria to stay alive so that they can reproduce, ensuring that the species survives through at least one more generation. The diversity of processes used by bacteria to metabolize illustrates the wide range of environments in which they can survive. Bacteria are capable of using almost anything for energy, as long as they happen to be the right species in the right environment. Some, known as extremophiles, like environments so harsh that people originally thought 9-) bacterial growth and cell division Unlike multicellular organisms, increases in the size of bacteria (cell growth) and their reproduction by cell division are tightly linked in unicellular organisms. Bacteria grow to a fixed size and then reproduce through binary fission, a form of asexual reproduction.[93] Under optimal conditions, bacteria can grow and divide extremely rapidly, and bacterial populations can double as quickly as every 9.8 minutes.[94] In cell division, two identical clone daughter cells are produced. Some bacteria, while still reproducing asexually, form more complex reproductive structures that help disperse the newly formed daughter cells. Examples include fruiting body formation by Myxobacteria and aerial hyphae formation by Streptomyces, or budding. Budding involves a cell forming a protrusion that breaks away and produces a daughter cell. In the laboratory, bacteria are usually grown using solid or liquid media. Solid growth media such as agar plates are used to isolate pure cultures of a bacterial strain. However, liquid growth media are used when measurement of growth or large volumes of cells are required. Growth in stirred liquid media occurs as an even cell suspension, making the cultures easy to divide and transfer, although isolating single bacteria from liquid media is difficult. The use of selective media (media with specific nutrients added or deficient, or with antibiotics added) can help identify specific organisms.[96]

Most laboratory techniques for growing bacteria use high levels of nutrients to produce large amounts of cells cheaply and quickly. However, in natural environments nutrients are limited, meaning that bacteria cannot continue to reproduce indefinitely. This nutrient limitation has led the evolution of different growth strategies (see r/K selection theory). Some organisms can grow extremely rapidly when nutrients become available, such as the formation of algal (and cyanobacterial) blooms that often occur in lakes during the summer.[97] Other organisms have adaptations to harsh environments, such as the production of multiple antibiotics by Streptomyces that inhibit the growth of competing microorganisms.[98] In nature, many organisms live in communities (e.g. biofilms) which may allow for increased supply of nutrients and protection from environmental stresses.[40] These relationships can be essential for growth of a particular organism or group of organisms (syntrophy).[99] Bacterial growth follows three phases. When a population of bacteria first enter a high-nutrient environment that allows growth, the cells need to adapt to their new environment. The first phase of growth is the lag phase, a period of slow growth when the cells are adapting to the high-nutrient environment and preparing for fast growth. The lag phase has high biosynthesis rates, as proteins necessary for rapid growth are produced.[100] The second phase of growth is the logarithmic phase (log phase), also known as the exponential phase.
10-) Bacterial Genetics: DNA The Genetic Material Structure, Replication and Function (Control)

Most bacteria have a single circular chromosome that can range in size from only 160,000 base pairs in the endosymbiotic bacteria Candidatus Carsonella ruddii,[102] to 12,200,000 base pairs in the soil-dwelling bacteria Sorangium cellulosum.[103] Spirochaetes of the genus Borrelia are a notable exception to this arrangement, with bacteria such as Borrelia burgdorferi, the cause of Lyme disease, containing a single linear chromosome. The genes in bacterial genomes are usually a single continuous stretch of DNA and although several different types of introns do exist in bacteria, these are much more rare than in eukaryotes. Bacteria may also contain plasmids, which are small extra-chromosomal DNAs that may contain genes for antibiotic resistance or virulence factors. Bacteria, as asexual organisms, inherit identical copies of their parent's genes (i.e., they are clonal). However, all bacteria can evolve by selection on changes to their genetic material DNA caused by genetic recombination or mutations. Mutations come from errors made during the replication of DNA or from exposure to mutagens. Mutation rates vary widely among different species of bacteria and even among different clones of a single species of bacteria.Genetic changes in bacterial genomes come from either random mutation during replication or "stress-directed mutation", where genes involved in a particular growth-limiting process have an increased mutation rate. Some bacteria also transfer genetic material between cells. This can occur in three main ways. Firstly, bacteria can take up exogenous DNA from their environment, in a process called transformation. Genes can also be transferred by the process of transduction, when the integration of a bacteriophage introduces foreign DNA into the chromosome. The third method of gene transfer is bacterial conjugation, where DNA is transferred through direct cell contact. This gene acquisition from other bacteria or the environment is called horizontal gene transfer and may be common under natural conditions.Gene transfer is particularly important in antibiotic resistance as it

allows the rapid transfer of resistance genes between different pathogens.Article: Bacteriophage Bacteriophages are viruses that infect bacteria. Many types of bacteriophage exist, some simply infect and lyse their host bacteria, while others insert into the bacterial chromosome. 11) Genetic Recombination in Bacteria Transformation Many bacteria can acquire new genes by taking up DNA molecules (e.g., a plasmid) from their surroundings .The ability to deliberately transform the bacterium E. coli (Escherichia coli ) (okunuuEeriiya koli) has made possible the cloning of many genes . including human genes . and the development of the biotechnology industry. However, Griffith found that when living R cells (which should have been harmless) and dead S cells (which also should have been harmless) were injected together, the mouse became ill and living S cells could be recovered from its body. Furthermore, the type of the cells recovered from the mouse's body was determined by the type of the dead S cells. In the experiment shown, injection of The S-II cells remained true to their new type. Something in the dead S-II cells had made a permanent change in the phenotype of the R-I cells. The process was named transformation. Conjugation: BRLESME Some bacteria, E. coli is an example, can transfer a portion of their chromosome to a recipient with which they are in direct contact. As the donor replicates its chromosome, the copy is injected into the recipient. At any time that the donor and recipient become separated, the transfer of genes stops. Those genes that successfully made the trip replace their equivalents in the recipient's chromosome. The DNA that makes it across finds the homologous region on the female chromosome and replaces it (by a double crossover). Transduction: letimi Bacteriophages are viruses that infect bacteria. In the process of assembling new virus particles, some host DNA may be incorporated in them. Significance of genetic recombination in bacteria. Transformation, conjugation, and transduction were discovered in the laboratory. How important are these mechanisms of genetic recombination in nature? We don't really know, but The completion of the sequence of the entire genome of a variety of different bacteria (and archaea) suggest that genes have in the past moved from one species to another. This phenomenon is called lateral gene transfer (LGT). The remarkable spread of resistance to multiple antibiotics may have been aided by the transfer of resistance genes within populations and even between species. Bacterial conjugation is the transfer of genetic material between bacterial cells by direct cell-to-cell contact or by a bridge-like connection between two cells.[1] Discovered in 1946 by Joshua Lederberg and Edward Tatum,[2] conjugation is a mechanism of

12) The Role of Microorganisms in Genetic Engineering 'Genetic engineering' or genetic manipulation as it should properly be called, relies essentially on the ability to manipulate molecules in vitro. Most biomolecules exist in low concentrations & as complex, mixed populations which it is not possible to work with effectively. This problem was solved in 1970 using the molecular biologist's favourite bug, Escherichia coli , a normally innocuous commensal occupant of the human gut. By inserting a piece of DNA of interest into a vector molecule, i.e. a molecule with a bacterial origin of replication, when the whole recombinant construction is introduced into a bacterial host cell, a large number of identical copies is produced. Together with the rapid growth of bacterial colonies all derived from a single original cell bearing the recombinant vector, in a short time (e.g. a few hours) a large amount of the DNA of interest is produced. This can be purified from contaminating bacterial DNA easily & the resulting product is said to have been 'cloned'. Most vector molecules were originally derived from one of two sources: Plasmids - small, autonomously replicating circular pieces of bacterial DNA, which often carry antibiotic-resistance genes. Bacteriophages (phages) - viruses which infect bacteria. Rapidly, the original vector molecules were greatly modified to improve their usefulness as vectors, e.g: Insertion of selectable marker genes to pick out recombinant molecules containing foreign inserts (antibiotic resistance genes & genes which produce a coloured product & therefore a coloured bacterial colony). Removal or creation of useful sites for cloning Insertion of sequences which not only allow but greatly increase the expression of cloned genes in bacterial, animal & plant cells. Vector molecules & cloning are not the only contribution which microorganisms have made to genetic manipulation. The actual task of altering the DNA at a molecular level is carried out by the use of naturally-occurring enzymes - most of which are derived from bacteria or viruses: Restriction endonucleases: bacteria in natural environments are continually exposed to a dilute 'soup' of foreign DNA released from other organisms which have died & lysed. They are also exposed to bacteriophage DNA. If unable to protect themselves, they would rapidly become infected & killed. The answer to this problem are the many different restriction-modification systems possessed by different groups of bacteria.

13) Viruses: Taxonomy, Structure, Replication, and Cultivation A virus is a small infectious agent that can replicate only inside the living cells of organisms. Most viruses are too small to be seen directly with a light microscope. Viruses infect all types of organisms, from animals and plants to bacteria and archaea.[1] Since the initial discovery of the tobacco mosaic virus by Martinus Beijerinck in 1898,[2] about 5,000 viruses have been described in detail, Virus particles (known as virions) consist of two or three parts: the genetic material made from either DNA or RNA, long molecules that carry genetic information; a protein coat that protects these genes; and in some cases an envelope of lipids that surrounds the protein coat when they are outside a cell. The shapes of viruses range from simple helical and icosahedral forms to more complex structures. The average virus is about one onehundredth the size of the average bacterium.Viruses spread in many ways; plant viruses are often transmitted from plant to plant by insects that feed on sap, such as aphids, while animal viruses can be carried by blood-sucking insects. These disease-bearing organisms are known as vectors. Influenza viruses are spread by coughing and sneezing. The norovirus and rotavirus, common causes of viral gastroenteritis, are transmitted by the faecal-oral route and are passed from person to person by contact, entering the body in food or water. HIV is one of several viruses transmitted through sexual contact and by exposure to infected blood. Viruses can infect only a limited range of host cells called the "host range". This can be narrow or, as when a virus is capable of infecting many species, broad Classification system bases classification on phylum, class, order, family, genus, and species. Viruses were grouped according to their shared properties (not those of their hosts) and the type of nucleic acid forming their genomes. Later the International Committee on Taxonomy of Viruses was formed. However, viruses are not classified on the basis of phylum or class, as their small genome size and high rate of mutation makes it difficult to determine their ancestry beyond Order. As such, the Baltimore Classification is used to supplement The Baltimore classification of viruses is based on the mechanism of mRNA production. Viruses must generate mRNAs from their genomes to produce proteins and replicate themselves, but different mechanisms are used to achieve this in each virus family. Viral genomes may be single-stranded (ss) or double-stranded (ds), RNA or DNA, and may or may not use reverse transcriptase (RT). Additionally, ssRNA viruses may be either sense (+) or antisense (.). This classification places viruses into seven groups: Replication cycle Viral populations do not grow through cell division, because they are acellular. Instead, they use the machinery and metabolism of a host cell to produce multiple copies of themselves, and they assemble in the cell undergo changes that results in the fusion of viral and cellular membranes, or changes of Viruses can be released from the host cell by lysis, a process that kills the cell by bursting its membrane and cell wall if present: this is a feature of many bacterial and some animal viruses. Some viruses undergo a lysogenic cycle where the viral genome is incorporated by genetic recombination into a specific place in the host's chromosome. DNA viruses The genome replication of most DNA viruses takes place in the cell's nucleus. If the cell has the appropriate receptor on its surface, RNA viruses

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14) Fungi: Classification, Structure, Replication and Cultivation A fungus (pronounced /.f....s/; pl. Fungi or funguses) is a member of a large group of eukaryotic organisms that includes microorganisms such as yeasts and molds (British English: moulds), as well as the more familiar mushrooms. These organisms are classified as a kingdom, Fungi, which is separate from plants, animals, and bacteria. One major difference is that fungal cells have cell walls that contain chitin, unlike the cell walls of plants, which contain cellulose. These and other differences show that the fungi form a single group of related organisms, named the Eumycota (true fungi or Eumycetes), that share a common ancestor (a monophyletic group). Abundant worldwide, most fungi are inconspicuous because of the small size of their structures, and their cryptic lifestyles in soil, on dead matter, and as symbionts of plants, animals, or other fungi. They may become noticeable when fruiting, either as mushrooms or molds. The major phyla (sometimes called divisions) of fungi have been classified mainly on the basis of characteristics of their sexual reproductive structures. Currently, seven phyla are proposed: Microsporidia, Chytridiomycota, Blastocladiomycota, Neocallimastigomycota, Glomeromycota, Ascomycota, and Basidiomycota. Phylogenetic analysis has demonstrated that the Microsporidia, unicellular parasites of animals and protists, are fairly recent and highly derived endobiotic fungi (living within the tissue of another species).[93][116] One 2006 study concludes that the Microsporidia are a sister group to the true fungi, that is, they are each other's closest evolutionary relative.[117] The Chytridiomycota are commonly known as chytrids. These fungi are distributed worldwide. Chytrids produce zoospores that are capable of active movement through aqueous phases with a single flagellum, leading early taxonomists to classify them as protists. The Blastocladiomycota were previously considered a taxonomic clade within the Chytridiomycota. Recent molecular data and ultrastructural characteristics, however, place the Blastocladiomycota as a sister clade to the Zygomycota, Glomeromycota, and Dikarya (Ascomycota and Basidiomycota). The blastocladiomycetes are saprotrophs, feeding on decomposing organic matter, and they are parasites of all eukaryotic groups. The Neocallimastigomycota were earlier placed in the phylum Chytridomycota. Members of this small phylum are anaerobic organisms, living in the digestive system of larger herbivorous mammals and possibly in other terrestrial and aquatic environments. Sexual reproduction with meiosis exists in all fungal phyla (with the exception of the Glomeromycota).[70] It differs in many aspects from sexual reproduction in animals or plants. Differences also exist between fungal groups and can be used to discriminate species by morphological differences in sexual structures and reproductive strategies. Most fungi have both an haploid and diploid stage in their life cycles. In sexually reproducing fungi, compatible individuals may combine by fusing their hyphae together into an interconnected network; this process, anastomosis, is required for the initiation of the sexual cycle. Sexual reproduction in basidiomycetes is similar to that of the ascomycetes. Compatible haploid hyphae fuse to produce a dikaryotic mycelium. However, the dikaryotic phase is

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15) Sterilization, Disinfection, and Antisepsis Sterilization (or sterilisation, see spelling differences) is a term referring to any process that eliminates (removes) or kills all forms of life, including transmissible agents (such as fungi, bacteria, viruses, spore forms, etc.) present on a surface, contained in a fluid, in medication, or in a compound such as biological culture media.[1][2] Sterilization can be achieved by applying the proper combinations of heat, chemicals, irradiation, high pressure, and filtration. The term has evolved to include the disabling or destruction of infectious proteins such as Prions related to Transmissible Spongiform Encephalopathies (TES).[3] Disinfectants are substances that are applied to non-living objects to destroy microorganisms that are living on the objects.[1] Disinfection does not necessarily kill all microorganisms, especially non resistant bacterial spores; it is less effective than sterilisation, which is an extreme physical and / or chemical process that kills all types of life.[1] Disinfectants are different from other antimicrobial agents such as antibiotics, which destroy microorganisms within the body, and antiseptics, which destroy microorganisms on living tissue. Disinfectants are also different from biocides . the latter are intended to destroy all forms of life, not just microorganisms. Sanitisers are substances that simultaneously clean and disinfect.[2] Bacterial endospores are most resistant to disinfectants, but some viruses and bacteria also possess some tolerance. Disinfectants are frequently used in hospitals, dental surgeries, kitchens, and bathrooms to kill infectious organisms. Antisepsis: Prevention of infection by inhibiting or arresting the growth and multiplication of germs (infectious agents). Antisepsis implies scrupulously clean and free of all living microorganisms. 16) Antimicrobial Chemotherapy: Antibactenal, Antiviral, and Antifungal Agents Groups
According Their Specter, Activity and Molecular Mechanisms

An antibacterial is a compound or substance that kills or slows down the growth of bacteria.[1] The term is often used synonymously with the term antibiotic(s); today, however, with increased knowledge of the causative agents of various infectious diseases, antibiotic(s) has come to denote a broader range of antimicrobial compounds, including anti-fungal and other compounds.by a microorganism that is antagonistic to the growth of other microorganisms in high dilution.This definition excluded substances that kill bacteria but are not produced by microorganisms (such as gastric juices and hydrogen peroxide).With advances in medicinal chemistry, most of today's antibacterials chemically are semisynthetic modifications of various natural compounds. These include, for example, the beta-lactam antibacterials, which include the penicillins (produced by fungi in the genus 'Penicillium'), the cephalosporins, and the carbapenems.. Another classification system is based on biological activity; in this classification antibacterials are divided into two broad groups according to their biological effect on microorganisms: bactericidal agents kill bacteria, and bacteriostatic agents slow down or stall bacterial growth. Antiviral drugs are a class of medication used specifically for treating viral infections.[1] Like antibiotics for bacteria, specific antivirals are used for specific viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit their development. Antiviral drugs are one class of antimicrobials, a larger group which also includes antibiotic, antifungal and antiparasitic drugs. They are relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from viricides, which are not medication but destroy virus particles.

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Most of the antivirals now available are designed to help deal with HIV, herpes viruses (best known for causing cold sores and genital herpes, but actually causing a wide range of diseases), the hepatitis B and C viruses, which can cause liver cancer, and influenza A and B viruses. Researchers are working to extend the range of antivirals to other families of pathogens. An antifungal drug is a medication used to treat fungal infections such as athlete's foot, ringworm, candidiasis (thrush), serious systemic infections such as cryptococcal meningitis, and others. Such drugs are usually obtained by a doctor's prescription or purchased overthecounter. 17) Antimicrobial Chemotherapy: Genetic and Biochemical Mechanisms of Bacterial
Resistance. Side Effects

Bacterial resistance is the capacity of bacteria to withstand the effects of antibiotics or biocides that are intended to kill or control them. The term "multiple resistance" (MR) or "multi-resistance" is used when a bacterial strain is resistant to several different antimicrobials or antimicrobial classes. For instance, multi-drug resistant tuberculosis is simultaneously resistant to a number of antibiotics belonging to different chemical classes. gCross-resistant h bacteria are those that have developed survival methods that are effective against different types of antimicrobial molecules with similar mechanism(s) of action. Bacteria can transfer bits of genetic material to other bacteria, and when genetic information coding for several unrelated resistance mechanisms is transferred in a single event and expressed in the new bacterial host it is referred to as gcoresistance h. Emergence of resistance The first step in the emergence of resistance is a genetic change in a bacterium. There are two ways that can happen. 1. Spontaneous mutation in the bacterium fs DNA. Many antibiotics work by inactivating an essential bacterial protein. Genetic change can remove that protein. Also, mutations in the target protein can prevent the antibiotic from binding or it if does bind, prevent it from inactivating the target protein. Genetic change can also lead to increased production of the antibiotic fs target enzyme so that there are too many of them and the antibiotics cannot inactivate them all. Alternatively, the bacterium may produce an antibiotic-inactivating enzyme. As well, the bacterium may alter the permeability of its cell membrane, or wall to the antibiotic. 2. Transfer of antibiotic-resistant genes The second way for a bacterium to gain resistance is for an existing antibioticresistant gene to transfer from one bacterium to another bacterium. Microbiologist, Doctor John Turnidge, says they literally borrow their resistance genes from neighbouring bugs. "They fre the original life forms almost, so for thousands of millions of years they fve had a chance to work out ways to survive and one of those is to borrow genes from other bacteria to survive."

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18) Infection and Infectious Disease. Patterns of Infection. The Spread of Infection
Epidemiology

An infection is the colonization of a host organism by parasite species. Infecting parasites seek to use the host's resources to reproduce, often resulting in disease. Colloquially, infections are usually considered to be caused by microscopic organisms or microparasites like viruses, prions, bacteria, and viroids, though larger organisms like macroparasites and fungi can also infect. Hosts normally fight infections themselves via their immune system. Mammalian hosts react to infections with an innate response, often involving inflammation, followed by an adaptive response. Pharmaceuticals can also help fight infections. The branch of medicine that focuses on infections and pathogens is infectious disease medicine. Diagnostic approach Diagnosis of infections can be difficult as specific signs and symptoms are rare. If an infection is suspected, blood, urine and sputum cultures are usually the first step. Chest xrays and stool analysis may also aid diagnosis. Spinal fluid can be tested to ensure that there is no brain infection. Symptoms Extreme fatigue which may be ongoing for more than 2.3 months Continued weight loss Low grade or spiking fever Night sweats and chills Vague body aches and pain Bacterial or viral Bacterial and viral infections can both cause symptoms such as malaise, fever, and chills. It can be difficult to distinguish which is the cause of a specific infection. It's important to distinguish, because viral infections cannot be cured by antibiotics. There is a general chain of events that applies to infections. For infections to occur a given chain of events must ocur.The chain of events involves several steps which include the infectious agent, reservoir, entering a susceptible host, exit and transmission to new hosts. Colonization Infection begins when an organism successfully colonizes by entering the body, growing and multiplying. Most humans are not easily infected. Those who are weak, sick, malnourished, have cancer or are diabetic have increased susceptibility to chronic or persistent infections. Individuals who have a suppressed immune system are particularly susceptible to opportunistic infections. Entrance to the host generally occurs through the mucosa in orifices like the oral cavity, nose, eyes, genitalia, anus, or open wounds. Wound colonization refers to nonreplicating microorganisms within the wound, while in infected wounds replicating organisms exist and tissue is injured. All multicellular organisms are colonized to some degree by extrinsic organisms, and the vast majority of these exist in

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19) Infection and Infectious Disease. Pathogenicity and Virulence. Pathogenic and Opportunistic bacteria. Mechanisms of Bacterial Pathogenesis. Virulence Factors. Pathogenicity is the ability of a pathogen to produce an infectious disease in an organism.It is often used interchangeably with the term "virulence", although some authors prefer to reserve the latter term for descriptions of the relative degree of damage done by a pathogen. Virulence is the ability of an organism to invade the bloodstream.The pathogencity of a pathogen is determined by the pathogen's ability to produce toxins, its ability to enter tissue and colonize and its ability to spread from host to host. Virulence is by MeSH definition the degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its virulence factors. That is, virulence is the degree of pathogenicity of an organism: the relative ability of a pathogen to cause disease. The ability of bacteria to cause disease is described in terms of the number of infecting bacteria, the route of entry into the body, the effects of host defense mechanisms, and intrinsic characteristics of the bacteria called virulence factors. Host-mediated pathogenesis is often important because the host can respond aggressively to infection with the result that host defense mechanisms do damage to host tissues while the infection is being countered. The virulence factors of bacteria are typically proteins or other molecules that are synthesized by protein enzymes. These proteins are coded for by genes in chromosomal DNA, bacteriophage DNA or plasmids. Bacteria use quorum sensing to synchronise release of the molecules. These are all proximate causes of morbidity in the host. [edit] Methods by which pathogens cause disease Adhesion. Many bacteria must first bind to host cell surfaces. Many bacterial and host molecules that are involved in the adhesion of bacteria to host cells have been identified. Often, the host cell receptors for bacteria are essential proteins for other functions. Colonization. Some virulent bacteria produce special proteins that allow them to colonize parts of the host body. Helicobacter pylori is able to survive in the acidic environment of the human stomach by producing the enzyme urease. Colonization of the stomach lining by this bacterium can lead to Gastric ulcer and cancer. The virulence of various strains of Helicobacter pylori tends to correlate with the level of production of urease. Invasion. Some virulent bacteria produce proteins that either disrupt host cell membranes or stimulate endocytosis into host cells. These virulence factors allow the bacteria to enter host cells and facilitate entry into the body across epithelial tissue layers at the body surface. Immune response inhibitors. Many bacteria produce virulence factors that inhibit the host's immune system defenses. For example, a common bacterial strategy is to produce proteins that bind host antibodies. The polysaccharide capsule of Streptococcus pneumoniae inhibits phagocytosis of the bacterium by host immune cells. Toxins. Many virulence factors are proteins made by bacteria that poison host cells and cause tissue damage. For example, there are many food poisoning toxins produced by bacteria that can contaminate human foods. Some of these can remain in "spoiled" food even after cooking and cause illness when the contaminated food is consumed. Some bacterial toxins are chemically altered and inactivated by the heat of cooking.

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20) Viral pathogenesis is the study of how biological viruses cause diseases in their target hosts, usually carried out at the cellular or molecular level. It is a specialized field of study in virology. One main motivation for the study of viruses is the fact that they cause many important infectious diseases, among them the common cold, influenza, rabies, measles, many forms of diarrhea, hepatitis, yellow fever, polio, smallpox and AIDS. Herpes simplex causes cold sores and genital herpes and is under investigation as a possible factor in Alzheimer's. Some viruses, known as oncoviruses, contribute to certain forms of cancer. The best studied example is the association between Human papillomavirus and cervical cancer: it is now acknowledged that almost all cases of cervical cancer are caused by certain strains of this sexually transmitted virus. Another example is infection with hepatitis B and hepatitis C viruses, which are associated with liver cancer. Some subviral particles also cause disease: the transmissible spongiform encephalopathies, which include Kuru, Creutzfeldt-Jakob disease and bovine spongiform encephalopathy ("mad cow disease"), are caused by prions, and hepatitis D is due to a satellite virus. The study of the manner in which viruses cause disease is viral pathogenesis. The degree to which a virus causes disease is its virulence. When the immune system of a vertebrate encounters a virus, it produces specific antibodies which bind to the virus and mark it for destruction. The presence of these antibodies is often used to determine whether a person has been exposed to a given virus in the past, with tests such as ELISA. Vaccinations protect against viral diseases, in part, by eliciting the production of antibodies. Specifically constructed monoclonal antibodies can also be used to detect the presence of viruses, with a technique called fluorescence microscopy. A second defense of vertebrates against viruses, cell-mediated immunity, involves immune cells known as T cells: the body's cells constantly display short fragments of their proteins on the cell's surface, and if a T cell recognizes a suspicious viral fragment there, the host cell is destroyed and the virus-specific T-cells proliferate. This mechanism is jump-started by certain vaccinations. RNA interference, an important cellular mechanism found in plants, animals and many other eukaryotes, most likely evolved as a defense against viruses. An elaborate machinery of interacting enzymes detects double-stranded RNA molecules (which occur as part of the life cycle of many viruses) and then proceeds to destroy all single-stranded versions of those detected RNA molecules. Every lethal viral disease presents a paradox: While it has been possible to prevent (certain) viral diseases by vaccination for a long time, the development of antiviral drugs to treat viral diseases is a comparatively recent development.

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21) Immunity Natural Resistance and Acquired Immunity Immunity is a biological term that describes a state of having sufficient biological defenses to avoid infection, disease, or other unwanted biological invasion. Immunity involves both specific and non-specific components. The non-specific components act either as barriers or as eliminators of wide range of pathogens irrespective of antigenic specificity. Other components of the immune system adapt themselves to each new disease encountered and are able to generate pathogen-specific immunity. Innate immunity, or nonspecific, immunity is the natural resistance with which a person is born. It provides resistance through several physical, chemical, and cellular approaches. Microbes first encounter the epithelial layers, physical barriers that line our skin and mucous membranes. Subsequent general defenses include secreted chemical signals (cytokines), antimicrobial substances, fever, and phagocytic activity associated with the inflammatory response. Adaptive immunity is often sub-divided into two major types depending on how the immunity was introduced. Naturally acquired immunity occurs through contact with a disease causing agent, when the contact was not deliberate, whereas artificially acquired immunity develops only through deliberate actions such as vaccination. Both naturally and artificially acquired immunity can be further subdivided depending on whether immunity is induced in the host or passively transferred from a immune host. Passive immunity is acquired through transfer of antibodies or activated T-cells from an immune host, and is short lived -- usually lasting only a few months -Passive immunity Passive immunity is the transfer of active immunity, in the form of readymade antibodies, from one individual to another. Passive immunity can occur naturally, when maternal antibodies are transferred to the fetus through the placenta, and can also be induced artificially, when high levels of human (or horse) antibodies specific for a pathogen or toxin are transferred to non-immune individuals. Passive immunization is used when there is a high risk of infection and insufficient time for the body to develop its own immune response, or to reduce the symptoms of ongoing or immunosuppressive diseases. Naturally acquired passive immunity Maternal passive immunity is a type of naturally acquired passive immunity, and refers to antibodymediated immunity conveyed to a fetus by its mother during pregnancy. Maternal antibodies (MatAb) are passed through the placenta to the fetus by an FcRn receptor on placental cells. This occurs around the third month of gestation. IgG is the only antibody isotype that can pass through the placenta. Passive immunity is also provided through the transfer of IgA antibodies found in Artificially acquired passive immunity Artificially acquired passive immunity is a short-term immunization induced by the transfer of antibodies, which can be administered in several forms; as human or animal blood plasma, as pooled human immunoglobulin for intravenous (IVIG) or intramuscular (IG) use, and in the form of monoclonal antibodies (MAb). Passive transfer is used prophylactically in the case of immunodeficiency diseases, Active immunity When B cells and T cells are activated by a pathogen, memory B-cells and T- cells develop. Throughout the lifetime of an animal these memory cells will gremember h each specific pathogen encountered, and are able to mount a strong response if the pathogen is detected again. This type of immunity is both active and adaptive because the body's immune system

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prepares itself for future challenges. Active immunity often involves both the cell-mediated and humoral aspects of immunity as well as input from the innate immune system. The human flora is the assemblage of microorganisms that reside on the surface and in deep layers of skin, in the saliva and oral mucosa, in the conjunctiva, and in the gastrointestinal tracts. 22- Immunity Natural Resistance and Acquired Immunity. Active and Passive Immunity. Inflammation is one of the first responses of the immune system to infection. The symptoms of inflammation are redness and swelling, which are caused by increased blood flow into a tissue. Inflammation is produced by eicosanoids and cytokines, which are released by injured or infected cells. Eicosanoids include prostaglandins that produce fever and the dilation of blood vessels associated with inflammation, and leukotrienes that attract certain white blood cells (leukocytes). Common cytokines include interleukins that are responsible for communication between white blood cells; chemokines that promote chemotaxis; and interferons that have anti-viral effects, such as shutting down protein synthesis in the host cell. Growth factors and cytotoxic factors may also be released. These cytokines and other chemicals recruit immune cells to the site of infection and promote healing of any damaged tissue following the removal of pathogens. The complement system is a biochemical cascade that attacks the surfaces of foreign cells. It contains over 20 different proteins and is named for its ability to gcomplement h the killing of pathogens by antibodies. Complement is the major humoral component of the innate immune response. Many species have complement systems, including non-mammals like plants, fish, and some invertebrates.In humans, this response is activated by complement binding to antibodies that have attached to these microbes or the binding of complement proteins to carbohydrates on the surfaces of microbes. This recognition signal triggers a rapid killing response. The speed of the response is a result of signal amplification that occurs following sequential proteolytic activation of complement molecules, which are also proteases. After complement proteins initially bind to the microbe, they activate their protease activity, which in turn activates other complement proteases, and so on. Leukocytes (white blood cells) act like independent, single-celled organisms and are the second arm of the innate immune system. The innate leukocytes include the phagocytes (macrophages, neutrophils, and dendritic cells), mast cells, eosinophils, basophils, and natural killer cells. These cells identify and eliminate pathogens, either by attacking larger pathogens through contact or by engulfing and then killing microorganisms. Innate cells are also important mediators in the activation of the adaptive immune system.Phagocytosis is an important feature of cellular innate immunity performed by cells called 'phagocytes' that engulf, or eat, pathogens or particles. Phagocytes generally patrol the body searching for pathogens, but can be called to specific locations by cytokines. Once a pathogen has been engulfed by a phagocyte, it becomes trapped in an intracellular vesicle called a phagosome, which subsequently fuses with another vesicle called a lysosome to form a phagolysosome. The pathogen is killed by the activity of digestive enzymes or following a respiratory burst that releases free radicals into the phagolysosome.Neutrophils and macrophages are phagocytes that travel throughout the body in pursuit of invading pathogens. Neutrophils are normally found in the bloodstream and are the most abundant type of phagocyte, normally representing 50% to 60% of the total circulating leukocytes. Dendritic cells (DC) are phagocytes in tissues that are in contact with the external environment; therefore, they are located mainly in the skin, nose, lungs, stomach, and intestines.[45] They are named for their resemblance to neuronal dendrites, as both have many spine-like projections, but dendritic cells are in no way connected to the nervous system. Dendritic cells serve as a link between the bodily tissues and the innate and adaptive immune

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systems, as they present antigen to T cells, one of the key cell types of the adaptive immune system. Mast cells reside in connective tissues and mucous membranes, and regulate the inflammatory response. They are most often associated with allergy and anaphylaxis. Basophils and eosinophils are related to neutrophils. They secrete chemical mediators that are involved in defending against parasites and play a role in allergic reactions, such as asthma. Natural killer (NK cells) cellsare leukocytes that attack and destroy tumor cells, or cells that have been infected by viruses. 23) Phagocytosis Phagocytosis in three steps: 1. Unbound phagocyte surface receptors do not trigger phagocytosis. 2. Binding of receptors causes them to cluster. 3. Phagocytosis is triggered and the particle is taken up by the phagocyte. . Phagocytosis is a specific form of endocytosis involving the vesicular internalization of solid particles,such as bacteria, and is, therefore, distinct from other forms of endocytosis such as the vesicular internalization of various liquids. Phagocytosis is involved in the acquisition of nutrients for some cells, and, in the immune system, it is a major mechanism used to remove pathogens and cell debris. Bacteria, dead tissue cells, and small mineral particles are all examples of objects that may be phagocytosed. Phagocytosis in mammalian immune cells is activated by attachment to Pathogen-associated molecular patterns (PAMPS), which leads to NF-B activation. Opsonins such as C3b and antibodies can act as attachment sites and aid phagocytosis of pathogens. It is possible for cells other than dedicated phagocytes (such as dendritic cells) to engage in phagocytosis. The inflammatory response is a series of local cellular and vascular responses which are triggered when the body is injured, or invaded by antigen. For instance, when you nick your skin, get a foreign object in your eye, or are stung by a bee, reactions occur in order to protect you. One such reaction is pain, which results from swollen tissue putting pressure on nerve endings, and which serves to alert you to the injury. Other functions of the inflammatory response are to prevent the spread of microorganisms or antigen to other areas, to dispose of any cellular debris, and to begin the healing process. Fever (also known as pyrexia or controlled hyperthermia) is a common medical sign characterized by an elevation of temperature above the normal range of 36.5 - 37.5 C (98.100 F) due to an increase in the body temperature regulatory set-point.[2] This increase in set-point triggers increased muscle tone and shivering. As a person's temperature increases, there is, in general, a feeling of cold despite an increasing body temperature. Once the new temperature is reached, there is a feeling of warmth. A fever is one of the body's immune responses that attempts to neutralize a bacterial or viral infection. A fever can be caused by many different conditions ranging from benign to potentially serious. Fever differs from uncontrolled hyperthermia, in that hyperthermia is an increase in body temperature over the body's thermoregulatory set-point, due to excessive heat production and/or insufficient thermoregulation. Hyperpyrexia a serious underlying condition or lead to significant side effects. The most common cause is an intracranial hemorrhage. Other possible causes include sepsis, Kawasaki syndrome,

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[14] neuroleptic malignant syndrome, drug effects, serotonin syndrome, and thyroid storm. [13] Infections are the most common cause of fevers, however as the temperature rises other causes become more common. Infections commonly associated with hyperpyrexia include: roseola, rubeola and enteroviral infections. [15] Immediate aggressive cooling to less than 38.9 C (102.0 F) has been found to improve survival. [16] Hyperpyrexia differs from hyperthermia in that in hyperpyrexia the body's temperature 24) The organs of the immune system either make the cells that participate in the immune response or act as sites for immune function. These organs include the lymphatic vessels, lymph nodes, tonsils, thymus, Peyer's patch, and spleen. The lymph nodes are small aggregations of tissues interspersed throughout the lymphatic system. White blood cells (lymphocytes) that function in the immune response are concentrated in the lymph nodes. Lymphatic fluid circulates through the lymph nodes via the lymphatic vessels. As the lymph filters through the lymph nodes, foreign cells of microorganisms are detected and overpowered. The tonsils contain large numbers of lymphocytes. Located at the back of the throat and under the tongue, the tonsils filter out potentially harmful bacteria that may enter the body via the nose and mouth. Peyer's patches are lymphatic tissues which perform this same function in the digestive system. Peyer's patches are scattered throughout the small intestine and the appendix. They are also filled with lymphocytes that are activated when they encounter disease-causing microorganisms. The thymus gland is another site of lymphocyte production. Located within the upper chest region, the thymus gland is most active during childhood when it makes large numbers of lymphocytes. The lymphocytes made here do not stay in the thymus, however; they migrate to other parts of the body and concentrate in the lymph nodes. The thymus gland continues to grow until puberty; during adulthood, however, the thymus shrinks in size until it is sometimes impossible to detect in x-rays. Bone marrow, found within the bones, also produces lymphocytes. These lymphocytes migrate out of the bone marrow to other sites in the body. Because bone marrow is an integral part of the immune system, certain bone cancer treatments that require the destruction of Colored scanning electron micrograph of a white blood cell (pink and white) attacking a Staphylococcus aureus bacterium (yellow). Photograph by Juergen Berger. Max-Planck Institute/Science Photo Library/Photo Researchers, Inc. Reproduced by permission. bone marrow are extremely risky, because without bone marrow, a person cannot make lymphocytes. People undergoing bone marrow replacement must be kept in strict isolation to prevent exposure to viruses or bacteria. The spleen acts as a reservoir for blood and any rupture to the spleen can cause dangerous internal bleeding, a potentially fatal condition. The spleen also destroys worn-out red blood cells. Moreover, the spleen is also a site for immune function, since it contains lymphatic tissue and produces lymphocytes. Immune response The immune response is how your body recognizes and defends itself against bacteria, viruses, and substances that appear foreign and harmful. Information The immune system protects the body from potentially harmful substances by recognizing

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and responding to antigens. Antigens are molecules (usually proteins) on the surface of cells, viruses, fungi, or bacteria. Nonliving substances such as toxins, chemicals, drugs, and foreign particles (such as a splinter) can also be antigens. The immune system recognizes and destroys substances that contain these antigens. 25) Antigens. Antibodies : Antigen is a substance/molecule that when introduced into the body triggers the production of an antibody by the immune system which will then kill or neutralize the antigen that is recognized as a foreign and potentially harmful invader. These invaders can be molecules such as pollen or cells such as bacteria. The term originally came from antibody generator[1][2] and was a molecule that binds specifically to an antibody, but the term now also refers to any molecule or molecular fragment that can be bound by a major histocompatibility complex (MHC) and presented to a T-cell receptor[3]. "Self" antigens are usually tolerated by the immune system; whereas "Non-self" antigens are identified as intruders and attacked by the immune system. Autoimmune disorders arise from the immune system reacting to its own antigens. Similarly, an immunogen is a specific type of antigen. An immunogen is defined as a substance that is able to provoke an adaptive immune response if injected on its own[4]. Said another way, an immunogen is able to induce an immune response, while an antigen is able to combine with the products of an immune response once they are made. The overlapping concepts of immunogenicity and antigenicity are thereby subtly different. According to a current text book: Antigenicity is the ability to combine specifically with the final products of the [immune response] (i.e. secreted antibodies and/or surface receptors on T-cells). Although all molecules that have the property of immunogenicity also have the property of antigenicity, the reverse is not true."[5] Antibodies (also known as immunoglobulins,[1] abbreviated Ig) are gamma globulin proteins that are found in blood or other bodily fluids of vertebrates, and are used by the immune system to identify and neutralize foreign objects, such as bacteria and viruses. They are typically made of basic structural units.each with two large heavy chains and two small light chains.to form, for example, monomers with one unit, dimers with two units or pentamers with five units. Antibodies are produced by a kind of white blood cell called a plasma cell. There are several different types of antibody heavy chains, and several different kinds of antibodies, which are grouped into different isotypes based on which heavy chain they possess. Five different antibody isotypes are known in mammals, which perform different roles, and help direct the appropriate immune response for each different type of foreign object they encounter.[2] Though the general structure of all antibodies is very similar, a small region at the tip of the protein is extremely variable, allowing millions of antibodies with slightly different tip structures, or antigen binding sites, to exist. This region is known as the hypervariable region. Each of these variants can bind to a different target, known as an antigen.[3] This huge diversity of antibodies allows the immune system to recognize an equally wide variety of antigens. The unique part of the antigen recognized by an antibody is called the epitope. These epitopes bind with their antibody in a highly specific interaction, called induced fit, that allows antibodies to identify and bind only their unique antigen in the midst of the millions of different molecules that make up an organism. Recognition of an antigen by an antibody tags it for attack by other parts of the immune system. Antibodies can also neutralize targets directly by, for example, binding to a part of a pathogen that it needs to cause an infection.[4 Monoclonal antibodies (mAb or moAb) are monospecific antibodies that are the same because they are made by identical immune cells that are all clones of a unique parent cell. Given almost any substance, it is possible to create monoclonal antibodies that specifically

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bind to that substance; they can then serve to detect or purify that substance. This has become an important tool in biochemistry, molecular biology and medicine. When used as medications, the non-proprietary drug name ends in -mab 26) Immune response: Cell mediated immunity (CMI). Cell-mediated immunity is an immune response that does not involve antibodies or complement but rather involves the activation of macrophages, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Historically, the immune system was separated into two branches: humoral immunity, for which the protective function of immunization could be found in the humor (cellfree bodily fluid or serum) and cellular immunity, for which the protective function of immunization was associated with cells. CD4 cells or helper T cells provide protection against different pathogens. Cellular immunity protects the body by: 1. activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in body cells displaying epitopes of foreign antigen on their surface, such as virusinfected cells, cells with intracellular bacteria, and cancer cells displaying tumor antigens; 2. activating macrophages and natural killer cells, enabling them to destroy intracellular pathogens; and 3. stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses. The term "cytokine" has been used to refer to the immunomodulating agents, such as interleukins and interferons. Biochemists disagree as to which molecules should be termed cytokines and which hormones. As we learn more about each, anatomic and structural distinctions between the two are fading. Classic protein hormones circulate in nanomolar (109) concentrations that usually vary by less than one order of magnitude. In contrast, some cytokines (such as IL-6) circulate in picomolar (10-12) concentrations that can increase up to 1,000-fold during trauma or infection. The effect of a particular cytokine on a given cell depends on the cytokine, its extracellular abundance, the presence and abundance of the complementary receptor on the cell surface, and downstream signals activated by receptor binding; these last two factors can vary by cell type. Cytokines are characterized by considerable "redundancy", in that many cytokines appear to share similar functions. [edit] Nomenclature Cytokines have been classed as lymphokines, interleukins, and chemokines, based on their presumed function, cell of secretion, or target of action. Because cytokines are characterised by considerable redundancy and pleiotropism, such distinctions, allowing for exceptions, are obsolete. [edit] Classification Several inflammatory cytokines are induced by oxidant stress.[7][8] The fact that cytokines themselves trigger the release of other cytokines[9][10] and also lead to increased oxidant stress makes them important in chronic inflammation. [edit] Cytokine receptors In recent years, the cytokine receptors have come to demand the attention of more investigators than cytokines themselves, partly because of their remarkable characteristics, and partly because a deficiency of cytokine receptors has now been directly linked to certain debilitating immunodeficiency states. In this regard, and also because the redundancy and pleiomorphism of cytokines are, in fact, a consequence of their homologous receptors,

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27) Hypersensitive response The hypersensitive response (HR) is a mechanism, used by plants, to prevent the spread of infection by microbial pathogens. The HR is characterized by the rapid death of cells in the local region surrounding an infection. The HR serves to restrict the growth and spread of pathogens to other parts of the plant. The HR is analogous to the innate immune system found in animals, and commonly precedes a slower systemic (whole plant) response, which ultimately leads to systemic acquired resistance (SAR).[1] Mechanism The HR is triggered by the plant when it recognizes a pathogen. The identification of a pathogen typically occurs when avirulence geneproducts, secreted by a pathogen, bind to, or indirectly interact with the product of a plant resistance (R) gene (gene for gene model). R genes are highly polymorphic, and many plants produce several different types of R gene products, enabling them to recognize virulence products produced by many different pathogens. In phase one of the HR, the activation of R genes triggers an ion flux, involving an efflux of hydroxide and potassium outside the cells, and an influx of calcium and hydrogen ions into the cell. In phase two, the cells involved in the HR generate an oxidative burst by producing reactive oxygen species (ROS), superoxide anions, hydrogen peroxide, hydroxyl radicals and nitrous oxide. These compounds affect cellular membrane function, in part by inducing lipid peroxidation and by causing lipid damage. The alteration of ion components in the cell, and the breakdown of cellular components in the presence of ROS, results in the death of affected cells and the formation of local lesions. Reactive oxygen species also trigger the deposition of lignin and callose, as well as the cross-linking of preformed hydroxyproline-rich glycoproteins such as P33 to the wall matrix via the tyrosine in the PPPPY motif. These compounds serve to reinforce the walls of cells surrounding the infection, creating a barrier and inhibiting the spread of the infection.[4] Allergy is a hypersensitivity disorder of the immune system.[1] Allergic reactions occur to normally harmless environmental substances known as allergens; these reactions are acquired, predictable, and rapid. Strictly, allergy is one of four forms of hypersensitivity and is called type I (or immediate) hypersensitivity. It is characterized by excessive activation of certain white blood cells called mast cells and basophils by a type of antibody known as IgE, resulting in an extreme inflammatory response. Common allergic reactions include eczema, hives, hay fever, asthma attacks, food allergies, and reactions to the venom of stinging insects such as wasps and bees Autoimmunity is the failure of an organism to recognize its own constituent parts as self, which allows an immune response against its own cells and tissues. Any disease that results from such an aberrant immune response is termed an autoimmune disease. Autoimmunity is often caused by a lack of germ development of a target body and as

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such the immune response acts against its own cells and tissues (Flowers 2009). Prominent examples include Coeliac disease, diabetes mellitus type 1 (IDDM), systemic lupus erythematosus (SLE), Sjogren's syndrome, Churg-Strauss Syndrome, Hashimoto's thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura, and rheumatoid arthritis (RA). See List of autoimmune diseases. Immunodeficiency (or immune deficiency) is a state in which the immune system's ability to fight infectious disease is compromised or entirely absent. Most cases of immunodeficiency are acquired ("secondary") but some people are born with defects in the immune system, or primary immunodeficiency. Transplant patients take medications to suppress their immune system as an antirejection measure, as do some patients suffering from an over-active immune system. A person who has an immunodeficiency of any kind is said to be immunocompromised. An immunocompromised 28) Immuno prophylaxis: Immunoprophylaxis against viral illnesses includes the use of vaccines or antibodycontaining preparations to provide immune protection against a specific disease. Active Prophylaxis (Vaccines): Active immunization involves administering a virus preparation that stimulates the body's immune system to produce its own specific immunity. Viral vaccines now available for use include the following types: (1) attenuated live viruses; (2) killed viruses; (3) recombinant produced antigens. A vaccinee is a person who has been vaccinated. Immune Response to Vaccines: Vaccination evokes an antibody response and stimulates T lymphocytes. Vaccine effectiveness is assessed in terms of percentage of recipients protected and the duration and degree of protection. Most effective viral vaccines protect more than 90 percent of recipients and produce fairly durable immunity. Hyperimmune sera and antivenoms . Anti-Bothropic . Anti-Crotalic . Anti-Bothropic-Crotalic . Anti-Elapidic . Anti-Bothropic-Lachetic . A stable, highly concentrated intravenously tolerable immunoglobulin preparation is described having an immunoglobulin content from 13.5 to 17.5% (w/v), an osmolarity from 250 to 600 mOs/l and a viscosity of no more than 9 cP. The immunoglobulin preparation possesses an exceptional imperishability and also is used as a highly concentrated preparation without problems due to its low viscosity.

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30) Staphylococcus The Staphylococcus genus includes at least forty species. Of these, nine have two subspecies and one has three subspecies.[2] Most are harmless and reside normally on the skin and mucous membranes of humans and other organisms. Found worldwide, they are a small component of soil microbial flora.[3] Biochemical identification Assignment of a strain to the genus Staphylococcus requires that it is a Grampositive coccus that forms clusters, produces catalase, has an appropriate cell wall structure ( One of the most important phenotypical features used in the classification of staphylococci is their ability to produce coagulase, an enzyme that causes blood clot formation. Coagulase-positive A seventh species has also been described - Staphylococcus leei - from patients with gastritis. . S. aureus (formerly also called Staphylococcus pyogenes) is coagulasepositive, meaning that it produces coagulase. However, while the majority of S. aureus are coagulase-positive, some may be atypical in that they do not produce coagulase. S aureus is also catalase-positive (meaning that it can produce the enzyme catalase) and able to convert hydrogen peroxide (H2O2) to water and oxygen, which makes the catalase test useful to distinguish Staphylococci from Enterococci and Streptococci. . S. pseudintermedius inhabits and sometimes infects the skin of domestic dogs and cats. This organism, too, can carry the genetic material that imparts multiple bacterial resistance. It is rarely implicated in infections in humans, as a zoonosis. Coagulase-negative . S. epidermidis, a coagulase-negative staphylococcus species, is a commensal of the skin, but can cause severe infections in immune-suppressed patients and those with central venous catheters. . S. saprophyticus, another coagulase-negative species that is part of the normal vaginal flora, is predominantly implicated in genitourinary tract infections in sexually-active young women. . In recent years, several other Staphylococcus species have been implicated in human infections, notably S. lugdunensis, S. schleiferi, and S. caprae. Common abbreviations for coagulase-negative staphylococcus species are CoNS and CNS.

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32.Streptococcus-Viridans streptococci,Streptococcus pneumoniae, Enterococcus The viridans streptococci include S mitis, S mutans, S salivarius, S sanguis, and others. Typically they are hemolytic, but they may be nonhemolytic. Their growth is not inhibited by Optochin, and colonies are not soluble in bile (deoxycholate). The viridans streptococci are the most prevalent members of the normal flora of the upper respiratory tract and are important for the healthy state of the mucous membranes there. They may reach the bloodstream as a result of trauma and are a principal cause of endocarditis on abnormal heart valves. Some viridans streptococci (eg, S mutans) synthesize large polysaccharides such as dextrans or levans from sucrose and contribute importantly to the genesis of dental caries. In the course of bacteremia, viridans streptococci, pneumococci, or enterococci may settle on normal or previously deformed heart valves, producing acute endocarditis. Rapid destruction of the valves frequently leads to fatal cardiac failure in days or weeks unless a prosthesis can be inserted during antimicrobial therapy. Subacute endocarditis often involves abnormal valves (congenital deformities and rheumatic or atherosclerotic lesions). Although any organism reaching the bloodstream may establish itself on thrombotic lesions that develop on endothelium injured as a result of circulatory stresses, subacute endocarditis is most frequently due to members of the normal flora of the respiratory or intestinal tract that have accidentally reached the blood. Hemolytic streptococci and enterococci vary in their susceptibility to antimicrobial agents. Particularly in bacterial endocarditis, antibiotic susceptibility tests are useful to determine which drugs may be used for optimal therapy. Aminoglycosides often enhance the rate of bactericidal action of penicillin on streptococci, particularly enterococci. Streptococcus pneumoniae The pneumococci (S pneumoniae) are gram-positive diplococci, often lancet-shaped or arranged in chains, possessing a capsule of polysaccharide that permits typing with specific antisera. Pneumococci are readily lysed by surface-active agents, which probably remove or inactivate the inhibitors of cell wall autolysins. Pneumococci are normal inhabitants of the upper respiratory tract of 540% of humans and can cause pneumonia, sinusitis, otitis, bronchitis, bacteremia, meningitis, and other infectious processes. The typical gram-positive, lancet-shaped diplococci are often seen in specimens of young cultures. In sputum or pus, single cocci or chains are also seen. Identifying points include almost uniform virulence for mice when injected intraperitoneally and the "capsule swelling test," or quellung reaction. Pneumococci form small round colonies, at first dome-shaped and later developing a central plateau with an elevated rim. Pneumococci are hemolytic on blood agar. Growth is enhanced by 510% CO2. Growth Characteristics :Most energy is obtained from fermentation of glucose; this is accompanied by the rapid production of lactic acid, which limits growth. Neutralization of broth cultures with alkali at intervals results in massive growth. The pneumococcal cell wall has peptidoglycan and teichoic acid, like other streptococci. The capsular polysaccharide is covalently bound to the peptidoglycan and to the cell wall polysaccharide. The capsular polysaccharide is immunologically distinct for each of the more than 90 types. When pneumococci of a certain type are mixed with specific antipolysaccharide serum of the same typeor with polyvalent antiserumon a microscope slide, the capsule swells

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markedly, and the organisms agglutinate by cross-linking of the antibodies. This reaction is useful for rapid identification and for typing of the organisms, either in sputum or in cultures. The polyvalent antiserum, which contains antibody to all of the types ("omniserum"), is a good reagent for rapid microscopic determination of whether or not pneumococci are present in fresh sputum. Pathogenesis Types of Pneumococci In adults, types 18 are responsible for about 75% of cases of pneumococcal pneumonia and for more than half of all fatalities in pneumococcal bacteremia; in children, types 6, 14, 19, and 23 are frequent causes. Pneumococci produce disease through their ability to multiply in the tissues. They produce no toxins of significance. The virulence of the organism is a function of its capsule, which prevents or delays ingestion by phagocytes. A serum that contains antibodies against the typespecific polysaccharide protects against infection. If such a serum is absorbed with the typespecific polysaccharide, it loses its protective power. Animals or humans immunized with a given type of pneumococcal polysaccharide are subsequently immune to that type of pneumococcus and possess precipitating and opsonizing antibodies for that type of polysaccharide. Loss of Natural Resistance Since 4070% of humans are at some time carriers of virulent pneumococci, the normal respiratory mucosa must possess great natural resistance to the pneumococcus. Among the factors that probably lower this resistance and thus predispose to pneumococcal infection are the following: (1) Viral and other respiratory tract infections that damage surface cells; abnormal accumulations of mucus (eg, allergy), which protect pneumococci from phagocytosis; bronchial obstruction (eg, atelectasis); and respiratory tract injury due to irritants disturbing its mucociliary function. (2) Alcohol or drug intoxication, which depresses phagocytic activity, depresses the cough reflex, and facilitates aspiration of foreign material. (3) Abnormal circulatory dynamics (eg, pulmonary congestion, heart failure). (4) Other mechanisms, eg, malnutrition, general debility, sickle cell anemia, hyposplenism, nephrosis, or complement deficiency. Pathology Pneumococcal infection causes an outpouring of fibrinous edema fluid into the alveoli, followed by red cells and leukocytes, which results in consolidation of portions of the lung. Many pneumococci are found throughout this exudate, and they may reach the bloodstream via the lymphatic drainage of the lungs. The alveolar walls remain normally intact during the infection. Later, mononuclear cells actively phagocytose the debris, and this liquid phase is gradually reabsorbed. The pneumococci are taken up by phagocytes and digested intracellularly. Treatment Since pneumococci are sensitive to many antimicrobial drugs, early treatment usually results in rapid recovery, and antibody response seems to play a much diminished role. Penicillin G is the drug of choice, but in the United States 510% of pneumococci are penicillin-resistant (MIC 2 g/mL) and about 20% are moderately resistant (MIC 0.11 g/mL). High-dose penicillin G with MICs of 0.12 g/mL appears to be effective in treating pneumonia caused by pneumococci but would not be effective in treatment of meningitis due to the same strains.

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Some penicillin-resistant strains are resistant to cefotaxime. Resistance to tetracycline and erythromycin occurs also. Pneumococci remain susceptible to vancomycin. Enterococci There are at least 12 species of enterococci. Enterococcus faecalis is the most common and causes 8590% of enterococcal infections, while Enterococcus faecium causes 510%. The enterococci are among the most frequent causes of nosocomial infections, particularly in intensive care units, and are selected by therapy with cephalosporins and other antibiotics to which they are resistant. Enterococci are transmitted from one patient to another primarily on the hands of hospital personnel, some of whom may carry the enterococci in their gastrointestinal tracts. Enterococci occasionally are transmitted on medical devices. In patients, the most common sites of infection are the urinary tract, wounds, biliary tract, and blood. Enterococci may cause meningitis and bacteremia in neonates. In adults, enterococci can cause endocarditis. However, in intra-abdominal, wound, urine, and other infections, enterococci usually are cultured along with other species of bacteria, and it is difficult to define the pathogenic role of the enterococci. A major problem with the enterococci is that they can be very resistant to antibiotics. E faecium is usually much more antibiotic-resistant than E faecalis. Intrinsic Resistance Enterococci are intrinsically resistant to cephalosporins, penicillinase-resistant penicillins, and monobactams. They have intrinsic low-level resistance to many aminoglycosides, are of intermediate susceptibility or resistant to fluoroquinolones, and are less susceptible than streptococci (10- to 1000-fold) to penicillin and ampicillin. Enterococci are inhibited by lactams (eg, ampicillin) but generally are not killed by them. Resistance to Aminoglycosides Therapy with combinations of a cell wall-active antibiotic (a penicillin or vancomycin) plus an aminoglycoside (streptomycin or gentamicin) is essential for severe enterococcal infections, such as endocarditis. Although enterococci have intrinsic low-level resistance to aminoglycosides (MICs of < 500 g/mL), they have synergistic susceptibility when treated with a cell wall-active antibiotic plus an aminoglycoside. However, some enterococci have high-level resistance to aminoglycosides (MICs > 500 g/mL) and are not susceptible to the synergism. This high-level aminoglycoside resistance is due to enterococcal aminoglycosidemodifying enzymes. The genes that code for most of these enzymes are usually on conjugative plasmids or transposons. The result is that only streptomycin or gentamicin (or both or neither) is likely to show synergistic activity with a cell wall-active antibiotic against enterococci. Enterococci from severe infections should have susceptibility tests for high-level resistance (MICs > 500 g/mL) to gentamicin and streptomycin to predict therapeutic efficacy. There are multiple vancomycin resistance phenotypes. The VanA phenotype is manifested by inducible high-level resistance to vancomycin and teicoplanin. VanB phenotypes are inducibly resistant to vancomycin but susceptible to teicoplanin. VanC strains have intermediate to moderate resistance to vancomycin. VanC is constitutive in the less commonly isolated species, Enterococcus gallinarum (VanC-1) and Enterococcus casseliflavus/Enterococcus flavescens (CanC-2/VanC-3). The VanD phenotype is manifested by moderate resistance to vancomycin and low-level resistance or susceptibility to teicoplanin. The VanE phenotype is moderately resistant to vancomycin and susceptible to teicoplanin.

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33-)genus staphylococus; The Staphylococcus genus includes at least forty species. Of these nine have two subspecies and one has three subspecies] Most are harmless and reside normally on the skin and mucous membranes of humans and other organisms. Found worldwide, they are a small component of soil microbial flora.[requires that it is a Gram-positive coccus that forms clusters, produces catalase, has an appropriate cell wall structure (including peptidoglycan type and teichoic acid presence) and G + C content of DNA in a range of 30-40 mol%. Staphylococcus species can be differentiated from other aerobic and facultative anaerobic gram positive cocci by several simple tests. Staphylococcus spp. are facultative anaerobes (capable of growth both aerobically and anaerobically). All species grow in the presence of bile salts and all are catalase positive . B) s aureus; S. aureus can cause a range of illnesses from minor skin infections, such as pimples, impetigo, boils (furuncles), cellulitis folliculitis, carbuncles, scalded skin syndrome, and abscesses, to life-threatening diseases such as pneumonia, meningitis, osteomyelitis, endocarditis, toxic shock syndrome (TSS), chest pain, bacteremia, and sepsis. Its incidence is from skin, soft tissue, respiratory, bone, joint, endovascular to wound infections. It is still one of the five most common causes of nosocomial infections, often causing postsurgical wound infections. Abbreviated to S. aureus or Staph aureus in medical literature, S. aureus should not be confused with the similarly named and similarly dangerous (and also medically relevant) species of the genus Streptococcus. 34-) streptococcus; is a genus of spherical Gram-positive bacteria belonging to the phylum Firmicutes[2] and the lactic acid bacteria group. Cellular division occurs along a single axis in these bacteria, and thus they grow in chains or pairs, hence the name from Greek streptos, meaning easily bent or twisted, like a chain (twisted chain). Contrast this with staphylococci, which divide along multiple axes and generate grapelike clusters of cells. Streptococci are oxidase- and catalase-negative, and many are B)S.Pyogenes; is a spherical grampositive bacterium that grows in long chains and is the cause of Group A streptococcal infections.[1] S. pyogenes displays streptococcal group A antigen on its cell wall. S. pyogenes typically produces large zones of betahemolysis (the complete disruption of erythrocytes and the release of hemoglobin) when cultured on blood agar plates and are therefore also called Group A (beta-hemolytic) 35) s.pneumonaiae; is gram-positive, alpha-hemolytic, bile-soluble aerotolerant anaerobe and a member of the genus Streptococcus.[1] A significant human pathogenic bacterium, S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century and is the subject of many humoral immunity studies. Despite the name, the organism causes many types of pneumococcal infection other than pneumonia, including acute sinusitis, otitis media,

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meningitis, bacteremia, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess. S. pneumoniae is the most common cause of bacterial meningitis in adults, children, and dogs, and is one of the top-two isolates found in ear infection, otitis media.[2] Pneumococcal pneumonia is more common in the very young and the very old. enterococus; is a genus of lactic acid bacteria of the phylum Firmicutes. Enterococci are Gram-positive cocci that often occur in pairs (diplococci) oEnterococci are facultative anaerobic organisms, i.e., they are capable of cellular respiration in both oxygen-rich and oxygen-poor environments.[2] Though they are not capable of forming spores, enterococci are tolerant of a wide range of environmental conditions: extreme temperature (1045C), pH (4.5-10.0) and high sodium chloride concentrations.[3] Enterococci typically exhibit gamma-hemolysis on sheep's blood agar.[4] r short chains and are difficult to distinguish from Streptococci on physical characteristics alone 38)neisseria gonorrhoae; is a species of Gram-negative coffee beanshaped diplococci bacteria responsible for the sexually transmitted infection gonorrhea.[1] Neisseria is usually isolated on Thayer-Martin agar an agar plate containing antibiotics (Vancomycin, Colistin, Nystatin, and SXT) and nutrients that facilitate the growth of Neisseria species while inhibiting the growth of contaminating bacteria and fungi. Further testing to differentiate the species includes testing for oxidase (all clinically relevant Neisseria show a positive reaction) and the carbohydrates maltose, sucrose, and glucose test in which N. gonorrhoeae will only oxidize (that is, utilize) the glucose. . gonorrhoeae can also cause conjunctivitis, pharyngitis, proctitis or urethritis, prostatitis and orchitis 6)neiiseria meningitidis; is a heterotrophic gram-negative diplococcal bacterium best known for its role in meningitis[1]and other forms of meningococcal disease such as meningococcemia. N. meningitidis is a major cause of morbidity and mortality during childhood in industrialized countries and is responsible for epidemics in Africa and in Asia.] N. meningitidis which acts as an endotoxin which is responsible for fever, septic shock, hemorrhage due to the destructions of red blood cells.[10] Other virulence factors include a polysaccharide capsule which prevents host phagocytosis and aids in evasion of the host immune response; and fimbriae which mediate attachment of the bacterium to the epithelial cells of the nasopharynx 40-family enterobacteriaceae; are a large family of bacteria, including many of the more familiar pathogens, such as Salmonella and Escherichia coli. Genetic studies place them among the Proteobacteria, and they are given their own order (EntMembers of the Enterobacteriaceae are rodshaped, and are typically 1-5 m in length. Like other Proteobacteria they have Gram30

negative stains,[1] and they are facultative anaerobes, fermenting sugars to produce lactic acid and various other end products. Most also reduce nitrate to nitrite, although exceptions exist (e.g. Photorhabdus). Unlike most similar bacteria, Enterobacteriaceae generally lack cytochrome C oxidase, although there are exceptions (e.g. Plesiomonas shigelloides). Most have many flagella used to move about, but a few genera are nonmotile. They are non-spore forming. Catalase reactions vary among Enterobacteriaceae b)escherchia coli; is a Gram negative rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but some, such as serotype O157:H7, can cause serious food poisoning in humans, and are occasionally responsible for product recalls.[1][2] The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2, and by preventing the establishment of pathogenic bacteria within the intestine. E. coli are not always confined to the intestine, and their ability to survive for brief periods outside the body makes them an ideal indicator organism to test environmental samples for fecal contamination.[6][7] The bacteria can also be grown easily and its genetics are comparatively simple and easily manipulated or duplicated through a process of metagenics, making it one of the best-studied prokaryotic model organisms, and an important species in biotechnology and microbiology. klebsiella; is a genus of non-motile, Gram-negative, oxidase-negative, rod shaped bacteria with a prominent polysaccharide-based capsule. Frequent human pathogens, Klebsiella organisms can lead to a wide range of disease states, notably pneumonia, urinary tract infections, septicemia, ankylosing spondylitis, and soft tissue infections b)SERRATA; is a genus of Gram-negative, facultatively anaerobic, rodshaped bacteria of the Enterobacteriaceae family. The most common species in the genus, S. marcescens, is normally the only pathogen and usually causes nosocomial infections. However, rare strains of S. plymuthica, S. liquefaciens, S. rubidaea, and S. odoriferae have caused diseases through infection.[1] Members of this genus produce characteristic red pigment, prodigiosin, and can be distinguished from other members of the family Enterobacteriaceae by its unique production of three enzymes: DNase, lipase, and gelatinase.[2] In the hospital, Serratia species tend to colonize the respiratory and urinary tracts, rather than the gastrointestinal tract, in adults. 42)shigella; is a genus of Gram-negative, non-spore forming rod-shaped bacteria closely related to Escherichia coli and Salmonella. The causative agent of human shigellosis, Shigella causes disease in primates, but not in other mammals.[1] It is only naturally found in humans and apes.[2] During infection, it typically causes dysentery.[ Shigella species are classified by four serogroups:

Serogroup A: S. dysenteriae (12 serotypes) 31

Serogroup B: S. flexneri (6 serotypes) Serogroup C: S. boydii (23 serotypes) Serogroup D: S. sonnei (1 serotype

41-)salmonella; is a genus of Gram-negative, facultatively anaerobic, rod-shaped bacteria of the Enterobacteriaceae family. The most common species in the genus, S. marcescens, is normally the only pathogen and usually causes nosocomial infections. However, rare strains of S. plymuthica, S. liquefaciens, S. rubidaea, and S. odoriferae have caused diseases through infection.[1] Members of this genus produce characteristic red pigment, prodigiosin, and can be distinguished from other members of the family Enterobacteriaceae by its unique production of three enzymes: DNase, lipase, and gelatinase.[2] Salmonella infections are zoonotic and can be transferred between humans and nonhuman animals. Many infections are due to ingestion of contaminated food[edit] Sources of infection

Unclean food, particularly in institutional kitchens and restaurants, Excretions from either sick or infected but apparently clinically healthy people and animals (especially endangered are caregivers and animals), Polluted surface water and standing water (such as in shower hoses or unused water dispensers), Unhygienically thawed fowl (the meltwater contains many bacteria), An association with reptiles (pet tortoises and snakes)(primarily aquatic turtles) is well described.

Salmonella bacteria can survive several weeks in a dry environment and several months in water; thus, they are frequently found in polluted water, contamination from the excrement of carrier animals being particularly important. Aquatic vertebrates, notably birds and reptiles, are important vectors of salmonella. Poultry, cattle, and sheep frequently being agents of contamination, salmonella can be found in food, particularly meats and eggs. 35) Neisseria gonorrhoeae as gonococci (plural), or gonococcus (singular), is a species of Gram-negative coffee bean-shaped diplococci bacteria responsible for the sexually transmitted infection gonorrhea.[1] Microbiology Neisseria are fastidious Gram-negative cocci that require nutrient supplementation to grow in laboratory cultures. Specifically, they grow on chocolate agar with carbon dioxide. These cocci are facultatively intracellular and typically appear in pairs (diplococci), in the shape of coffee beans. Of the eleven species of Neisseria that colonize humans, only two are pathogens. N. gonorrhoeae is the causative agent of gonorrhoea and is transmitted via sexual contact.[2] Neisseria is usually isolated on Thayer-Martin agar.an agar plate containing antibiotics (Vancomycin, Colistin, Nystatin, and SXT) and nutrients that facilitate the growth of Neisseria species while inhibiting the growth of contaminating bacteria and fungi. Further testing to differentiate the species includes testing for oxidase (all clinically relevant Neisseria show a positive reaction) and the carbohydrates maltose, sucrose, and glucose test in which N. gonorrhoeae will only oxidize (that is, utilize) the glucose. 32

N. gonorrhoeae are motile (twitching motility) and possess type IV pili to adhere to surfaces. The type IV pili operate mechanistically similar to a grappling hook. Pili extend and attach to a substrate which signals the pilus to retract, dragging the cell forward. N. gonorrhoeae are able to pull 100,000 times their own weight and it has been claimed that the pili used to do so are the strongest biological motor known to date, exerting one nanonewton.[3] "N. gonorrhoeae" is naturally competent for DNS transformation as well as being capable of conjugation. Both of these concepts allow for the DNA of N. gonorrhoeae the ability to undergo conformational changes. Especially dangerous to the health industry is the ability to conjugate since this can lead to antibiotic resistance. 34) Listeria, Gardnerella Listeria is a bacterial genus containing six species[1]. Named after the English pioneer of sterile surgery, Joseph Lister, the genus was given its current name in 1940. Listeria species are Grampositive bacilli and are typified by L. monocytogenes, the causative agent of listeriosis. Listeria ivanovii is a pathogen of ruminants, and can infect mice in the laboratory, although it is only rarely the cause of human disease.Listeria monocytogenes Listeria monocytogenes is a bacterium commonly found in soil, stream water, sewage, plants, and food.[2] Each bacterium is Gram-positive and rod-shaped. Listeria are known to be the bacteria responsible for listeriosis, a rare but potentially lethal food-borne infection: the case fatality rate for those with a severe form of infection may approach Listeria monocytogenes is a Gram-positive, rod-shaped bacterium. It is the agent of listeriosis, a serious infection caused by eating food contaminated with the bacteria. The disease affects primarily pregnant women, newborns, and adults with weakened immune systems. Listeriosis is a serious disease for humans; the overt form of the disease has a mortality greater than 25 percent. The two main clinical manifestations are sepsis and meningitis. Meningitis is often complicated by encephalitis, a pathology that is unusual for bacterial infections. Mechanism of infection The majority of Listeria bacteria are targeted by the immune system before they are able to cause infection. Those that escape the immune system's initial response, however, spread though intracellular mechanisms and are therefore guarded against circulating immune factors (AMI).[3] To invade, Listeria induces macrophage phagocytic uptake by displaying D-galactose in their teichoic acids that are then bound by the macrophage's polysaccharide receptors . Other important adhesins are the internalins.[4] Once phagocytosed, the bacterium is encapsulated by the host cell's acidic phagolysosome organelle.[2] Listeria, however, escapes the phagolysosome by lysing the vacuole's entire membrane with secreted hemolysin,[6] now characterized as the exotoxin listeriolysin O.[2] The bacteria then replicate inside the host cell's cytoplasm.[3] Gardnerella is a genus of gram-variable staining facultative anaerobic bacteria of which G. vaginalis is the only species. Once classified as Haemophilus vaginalis and afterwards as Corynebacterium vaginalis, Gardnerella vaginalis grows as small, circular, convex, gray colonies on chocolate agar; it also grows on HBT agar. A selective medium for G. vaginalis is colistin-oxolinic acid blood agar. Clinical significance Gardnerella vaginalis is a facultatively anaerobic gram-variable rod which can cause bacterial

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vaginosis in some women as a result of a disruption in the normal vaginal microflora. The resident anaerobic lactobacillus population in the vagina are responsible for the acidic environment. Once the anaerobes have supplanted the normal vaginal bacteria, prescription antibiotics with anaerobic coverage may have to be given to eliminate the G. vaginalis and allow the balance to be restored. While typically isolated in genital cultures, it may also be detected in other samples from blood, urine and pharynx. G. vaginalis is not sexually transmitted. Although a chief cause of bacterial vaginosis, it can also be isolated from women without any signs or symptoms of infection. It has a gram-positive cell wall[2], but because the cell wall is so thin it can appear either gram-positive or gram-negative under the microscope. It is associated microscopically with clue cells, which are epithelial cells covered in bacteria. G. vaginalis produces a pore-forming toxin, vaginolysin, which affects only human cells. Proteolysis acco

38)Salmonella is a genus of rod-shaped, Gram-negative, non-spore forming, predominantly motile enterobacteria with diameters around 0.7 to 1.5 m, lengths from 2 to 5 m, and flagella which project in all directions (i.e. peritrichous). They are chemoorganotrophs, obtaining their energy from oxidation and reduction reactions using organic sources, and are facultative anaerobes. Most species produce hydrogen sulfide,[1] which can readily be detected by growing them on media containing ferrous sulfate, such as TSI. Most isolates exist in two phases: a motile phase I and a nonmotile phase II. Cultures that are nonmotile upon primary culture may be switched to the motile phase using a Cragie tube.[citation needed] Salmonella is closely related to the Escherichia genus and are found worldwide in cold- and warm-blooded animals (including humans), and in the environment. They cause illnesses like typhoid fever, paratyphoid fever, and the foodborne illness.[2] Salmonella is typically pronounced /.salm..n.l./ voicing the initial letter "L," since it is named for pathologist Daniel Elmer Salmon. Salmonella as disease-causing agents Salmonella infections are zoonotic and can be transferred between humans and nonhuman animals. Many infections are due to ingestion of contaminated food. A distinction is made between enteritis Salmonella and typhoid/paratyphoid Salmonella, where the latter . because of a special virulence factor and a capsule protein (virulence antigen) . can cause serious illness, such as Salmonella enterica subsp. enterica serovar Typhi. Salmonella typhi. is adapted to humans and does not occur in animals. 37) Enterobacteriaceae E.coli and other opportunistic Enterobacteriaceae (Klebsiella,
Enterobacter, Serratia group KES; Proteus, Morganella, Citrobacter

Enterobacteriaceae are a large family of bacteria, including many of the more familiar pathogens, such as Salmonella and Escherichia coli. Genetic studies place them among the

34

Proteobacteria, and they are given their own order (Enterobacteriales), though this is sometimes taken to include some related environmental samples. Members of the Enterobacteriaceae are rod-shaped, and are typically 1-5 m in length. Like other Proteobacteria they have Gram-negative stains,[1] and they are facultative anaerobes, fermenting sugars to produce lactic acid and various other end products. Most also reduce nitrate to nitrite, although exceptions exist (e.g. Photorhabdus). Unlike most similar bacteria, Enterobacteriaceae generally lack cytochrome C oxidase, although there are exceptions (e.g. Plesiomonas shigelloides). Most have many flagella used to move about, but a few genera are non-motile. They are non-spore forming. Catalase reactions vary among Enterobacteriaceae. Many members of this family are a normal part of the gut flora found in the intestines of humans and other animals, while others are found in water or soil, or are parasites on a variety of different animals and plants. Escherichia coli (E. coli) is one of the most important model organisms, and its genetics and biochemistry have been closely studied. Most members of Enterobacteriaceae have peritrichous Type I fimbriae involved in the adhesion of the bacterial cells to their hosts. Escherichia coli (commonly abbreviated E. coli; pronounced /.....r.ki. .ko.la./, named after Theodor Escherich) is a Gram negative rodshaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but some, such as serotype O157:H7, can cause serious food poisoning in humans, and are occasionally responsible for product recalls.[1][2] The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2,[3] and by preventing the establishment of pathogenic bacteria within the intestine.[4][5] E. coli are not always confined to the intestine, and their ability to survive for brief periods outside the body makes them an ideal indicator organism to test environmental samples for fecal contamination.[6][7] The bacteria can also be grown easily and its genetics are comparatively simple and easily manipulated or duplicated through a process of metagenics, making it one of the best-studied prokaryotic model organisms, and an important species in biotechnology and microbiology. 36)Neisseria meningitidis Neisseria meningitidis is a heterotrophic gram-negative diplococcal bacterium best known for its role in meningitis[1] and other forms of meningococcal disease such as meningococcemia. N. meningitidis is a major cause of morbidity and mortality during childhood in industrialized countries and is responsible for epidemics in Africa and in Asia. [2] Meningococci only infect humans and have never been isolated from animals because the bacterium cannot get iron other than from human sources (transferrin and lactoferrin).[5] Meningococcus is spread through the exchange of saliva and other respiratory secretions during activities like coughing, kissing, and chewing on toys. Though it initially produces general symptoms like fatigue, it can rapidly progress from fever, headache and neck stiffness to coma and death. The symptoms are easily confused with those of meningitis due to other organisms such as Hemophilus influenzae and Streptococcus pneumoniae.[3] Death occurs in approximately 10% of cases.[7] Those with impaired immunity may be at particular risk of meningococcus (e.g. those with nephrotic syndrome or splenectomy; vaccines are given in cases of removed or non-functioning spleens). Septicaemia caused by Neisseria meningitidis has received much less public attention than meningococcal meningitis even though septicaemia has been linked to infant deaths. [9] Meningococcal septicaemia typically causes a purpuric rash that does not lose its color when

35

pressed with a glass ("non-blanching") and does not cause the classical symptoms of meningitis. This means the condition may be ignored by those not aware of the significance of the rash. Septicaemia carries an approximate 50% mortality rate over a few hours from initial onset. Many health organizations advise anyone with a non-blanching rash to go to a hospital emergency room as soon as possible.[citation needed] Note that not all cases of a purpura-like rash are due to meningococcal septicaemia; however, other possible causes need prompt investigation as well (e.g. ITP a platelet disorder or Henoch-Schonlein purpura). 40) Enterobacteriaceae Yersinia Yersinia is a genus of bacteria in the family Enterobacteriaceae. Yersinia are Gramnegative rod shaped bacteria, a few micrometers long and fractions of a micrometer in diameter, and are facultative anaerobes.[1] Some members of Yersinia are pathogenic in humans; in particular, Y. pestis is the causative agent of the plague. Rodents are the natural reservoirs of Yersinia; less frequently other mammals serve as the host. Infection may occur either through blood (in the case of Y. pestis) or in an alimentary fashion, occasionally via consumption of food products (especially vegetables, milk-derived products and meat) contaminated with infected urine or feces. Speculations exist as to whether or not certain Yersinia can also be spread via protozoonotic mechanisms, since Yersinia are known to be facultative intracellular parasites; studies and discussions of the possibility of amoeba-vectored (through the cyst form of the protozoan) Yersinia propagation and proliferation are now in progress.[2] Microbial physiology An interesting feature peculiar to some of the Yersinia bacteria is the ability to not only survive but actively proliferate at temperatures as low as 1-4 degrees Celsius (e.g., on cut salads and other food products in a refrigerator). Yersinia bacteria are relatively quickly inactivated by oxidizing agents such as hydrogen peroxide and potassium permanganate solutions. Pathogenesis Y. pestis is the causative agent of plague. The disease caused by Y. enterocolitica is called Yersiniosis. Y. pseudotuberculosis sometimes but rarely causes disease.[citation needed] Yersinia may be associated with Crohn's disease, an inflammatory autoimmune condition of the gut. Iranian sufferers of Crohn's disease were more likely to have had earlier exposure to refrigerators at home,[3] consistent with Yersinia's unusual ability to thrive at low temperatures. Yersinia is implicated as one of the causes of reactive arthritis worldwide. 39) Shigella is a genus of Gram-negative, non-spore forming rod-shaped bacteria closely related to Escherichia coli and Salmonella. The causative agent of human shigellosis, Shigella causes disease in primates, but not in other mammals.[1] It is only naturally found in humans and apes.[2] During infection, it typically causes dysentery.[3] The genus is named after Kiyoshi Shiga, who first discovered it in 1898. Shigella species are classified by four serogroups: . Serogroup A: S. dysenteriae (12 serotypes) . Serogroup B: S. flexneri (6 serotypes) . Serogroup C: S. boydii (23 serotypes) . Serogroup D: S. sonnei (1 serotype) Group A.C are physiologically similar; S. sonnei (group D) can be differentiated on the basis of biochemical metabolism assays.[4] Three Shigella groups are the major disease-causing species: S. flexneri is the most frequently isolated species worldwide and accounts for 60%

36

of cases in the developing world; S. sonnei causes 77% of cases in the developed world, compared to only 15% of cases in the developing world; and S. dysenteriae is usually the cause of epidemics of dysentery, particularly in confined populations such as refugee camps.[5] Shigella infection is typically via ingestion (fecal.oral contamination); depending on age and condition of the host as few as 100 bacterial cells can be enough to cause an infection.[6] Shigella causes dysentery that results in the destruction of the epithelial cells of the intestinal mucosa in the cecum and rectum. Some strains produce enterotoxin and Shiga toxin, similar to the verotoxin of E. coli O157:H7.[7] Both Shiga toxin and verotoxin are associated with causing hemolytic uremic syndrome. 43)Pseudomonas Pseudomonas is a genus of gamma proteobacteria, belonging to the larger family of pseudomonads. Because of their widespread occurrence in water and in plant seeds such as dicots, the pseudomonads were observed early in the history of microbiology. The generic name Pseudomonas created for these organisms was defined in rather vague terms in 1894 as a genus of Gram-negative, rod-shaped and polar-flagella bacteria. Soon afterwards, pseudomonads were isolated from many natural niches, and a large number of species names was originally assigned to the genus. New methodology and the inclusion of approaches based on the studies of conservative macromolecules have reclassified many strains.[3] Pseudomonas aeruginosa is increasingly recognized as an emerging opportunistic pathogen of clinical relevance. Several different epidemiological studies indicate antibiotic resistance is increasing in Characteristics Members of the genus display the following defining characteristics:[7] . Rod shaped . Gram-negative . One or more polar flagella, providing motility . Aerobic . Non.spore forming . positive catalase test Other characteristics which tend to be associated with Pseudomonas species (with some exceptions) include secretion of pyoverdine, a fluorescent yellow-green siderophore[8] under iron-limiting conditions. Certain Pseudomonas species may also produce additional types of siderophore, such as pyocyanin by Pseudomonas aeruginosa[9] and thioquinolobactin by Pseudomonas fluorescens,[10]. Pseudomonas species also typically give a positive result to the oxidase test, the absence of gas formation from glucose, glucose is oxidised in oxidation/fermentation test using Hugh and Leifson O/F test, beta hemolytic (on blood agar), indole negative, methyl red negative, Voges.Proskauer test negative, and citrate positive. Biofilm formation All species and strains of Pseudomonas are Gram-negative rods, and have historically been classified as strict aerobes. Exceptions to this classification have recently been discovered in Pseudomonas biofilms[12]. Pseudomonas have the ability to metabolise a variety of diverse nutrients. Combined with the ability to form biofilms, they are thus able to survive in a variety of unexpected places. For example, they have been found in areas where pharmaceuticals are prepared. A simple carbon source, such as soap residue or cap liner-adhesives is a suitable place for them to thrive. Other unlikely places where they have been found include antiseptics, such as quaternary ammonium compounds, and bottled mineral water. Antibiotic resistance Being Gram-negative bacteria, most Pseudomonas spp. are naturally resistant to penicillin and the

37

majority of related beta-lactam antibiotics, but a number are sensitive to piperacillin, imipenem, ticarcillin, tobramycin, or ciprofloxacin.[13] This ability to thrive in harsh conditions is a result of their hardy cell wall that contains porins. Their resistance to most antibiotics is attributed to efflux pumps, which pump out some antibiotics before the antibiotics are able to act. 42) Campylobacter Campylobacter (meaning 'twisted bacteria') is a genus of bacteria that are Gram-negative, spiral, and microaerophilic. Motile, with either uni- or bi-polar flagella, the organisms have a characteristic spiral/corkscrew appearance (see photo) and are oxidase-positive.[1] Campylobacter jejuni is now recognized as one of the main causes of bacterial foodborne disease in many developed countries.[2] At least a dozen species of Campylobacter have been implicated in human disease, with C. jejuni and C. coli the most common.[1] C. fetus is a cause of spontaneous abortions in cattle and sheep, as well as an opportunistic pathogen in humans.[3] Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence.[6] Nonmotile mutants do not colonize. Pathogenesis Campylobacteriosis is an infection by campylobacter.[7] The common routes of transmission are fecal-oral, ingestion of contaminated food or water, and the eating of raw meat. It produces an inflammatory, sometimes bloody, diarrhea, periodontitis[8] or dysentery syndrome, mostly including cramps, fever and pain. The infection is usually self-limiting and in most cases, symptomatic treatment by reposition of liquid and electrolyte replacement is enough in human infections. The use of antibiotics, on the other hand, is controversial. Helicobacter is a genus of Gram-negative bacteria possessing a characteristic helix shape. They were initially considered to be members of the Campylobacter Some species have been found living in the lining of the upper gastrointestinal tract, as well as the liver of mammals and some birds.[4] The most widely known species of the genus is H. pylori which infects up to 50% of the human population.[3] Some strains of this bacterium are pathogenic to humans as it is strongly associated with peptic ulcers, chronic gastritis, duodenitis, and stomach cancer. It also serves as the type species of the genus. Helicobacter spp. are able to thrive in the very acidic mammalian stomach by producing large quantities of the enzyme urease, which locally raises the pH from ~2 to a more biocompatible range of 6 to 7.[5] Bacteria belonging to this genus are usually susceptible to antibiotics 41) Vibrionaceae The Vibrionaceae are a family of Proteobacteria, given their own order. Inhabitants of fresh or salt water, several species are pathogenic, including the type species Vibrio cholerae, which is the agent responsible for cholera. Most bioluminescent bacteria belong to this family, and are typically found as symbiotes of deep-sea animals.[1] Vibrionaceae are Gram-negative organisms and facultative anaerobes, capable of fermentation. They contain oxidase and have one or more flagella, which are generally polar. Originally these characteristics defined the family, which was divided into four genera. Two of these, Vibrio and Photobacterium, correspond to the modern group, although several new genera have been defined. Genetic studies have shown the other two original members. Aeromonas and Plesiomonas.belong to separate families. The family Vibrionaceae currently comprises eight validly published genera: Aliivibrio[2], Catenococcus, Enterovibrio, Grimontia, Listonella, Photobacterium, Salinivibrio, and Vibrio; although the status of Listonella has been questioned.

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Pathology:A characteristic of the family is the broad host range susceptible to infection by vibrios. Pathogens of man, other than V. cholerae, include V. parahaemolyticus, a cause of gastroenteritis and V. vulnificus that can lead to acute and fatal septicaemia. Other species of Vibrionaceae are associated with disease in a wide variety of finfish, one of the most notable and commonly occurring pathogens being Vibrio anguillarum, the cause of septicaemia in farmed salmonids such as Atlantic salmon and rainbow trout.[5] Species such as V. tubiashii cause disease in larval stages of Pacific oyster (Crassostrea gigas) while V. harveyi causes luminous vibriosis in penaeid shrimps (prawns). The extent of the host range is seen with species such as V. mediterranei and V. coralliilyticus which can infect zooxanthellae, the plant symbiont of coral. These species of vibrio are thought to be a cause of coral bleaching [6][7] Vibrio cholerae (also Kommabacillus) is a gram negative comma-shaped bacterium with a polar flagellum that causes cholera in humans.[1][2] V. cholerae and other species of the genus Vibrio belong to the gamma subdivision of the Proteobacteria. There are two major biotypes of V. cholerae identified by hemaggluttination testing, classical and El Tor, and numerous serogroups. The classical biotype is found only in Bangladesh, whereas the El Tor is found throughout the world. Genomics and evolution The 4.0 Mbp genome of N16961, an O1 serogroup, (in America) El Tor biotype, 7th pandemic strain of V. cholerae, is composed of two circular chromosomes of unequal size that are predicted to encode a total of 3,885 genes[5]. The cholera toxin which causes the symptoms of cholera is encoded on the genome of a temperate bacteriophage, CTX-. The genomic sequence of this representative strain has furthered the understanding of the genetic and phenotypic diversity found within the species V. cholerae

44-)Bordetella :is a genus of small (0.2 - 0.7 m), Gram-negative coccobacilli of the
phylumproteobacteria. Bordetella species, with the exception of B. petrii, are obligate aerobes as well as highly fastidious, or difficult to culture. Three species are human pathogens (B. pertussis, B. parapertussis, B. bronchiseptica); one of these (B. bronchiseptica) is also motile.[1] B. pertussis and occasionally B. parapertussis cause pertussis or whooping cough in humans, and some B. parapertussis strains can colonise sheep. B. bronchiseptica rarely infects healthy humans though disease in immunocompromised patients has been reported.[2] B. bronchiseptica causes several diseases in other mammals, including kennel cough andatrophic rhinitis in dogs and pigs, respectively. Other members of the genus cause similar diseases in other mammals, and in birds (B. hinzii, B. avium).

Areas of infection - Mouth - Nose - Throat - Risk groups - - Unvaccinated children (especially infants) - Adolescents whose immunity has waned - Adults whose immunity has waned - Transmission - Direct contact with droplets from coughing or sneezing by an infected person - Can continue to transmit the bacteria three weeks after coughing spells have stopped - Can be carried by individuals who are immune and transmitted to those

39

who are not - Usual epidemic cycles in most countries is every two to five years Symptoms Incubation period is five to ten days - Infected person usually first shows cold symptoms (i.e. runny nose, sneezing, fever, and mild cough) - The cough worsens and comes in bursts - At the end of the cough, the infected person takes in air with a highpitched "whoop" from which the infection gets its name Complications Can cause death in infants - Convulsions - Dehydration - Inflammation of the middle ear - Lost of appetite - Seizures Treatment Antibiotic treatment, usually erythromycin - Increased fluids - Increased rest Prevention Immunization with pertussis vaccine

45) Francisella is a genus of pathogenic, Gram-negative bacteria. They are small coccobacillary or rod-shaped, non-motile organisms, which are also facultative intracellular parasites of macrophages.[1] Strict aerobes, Francisella colonies bear a morphological resemblance to those of the genus Brucella.[2] Pathogenesis The type species, F. tularensis, causes the disease tularemia or rabbit fever.[4] F. novicida and F. philomiragia (previously Yersinia philomiragia) are associated with septicemia and invasive systemic infections. The taxonomy of the genus is somewhat uncertain, especially in the case of F. novicida (may be a subspecies of F. tularensis). In general, identification of species is accomplished by biochemical profiling or 16S rRNA sequencing. 46) Brucella Electron micrograph of B. abortus located inside cisternae of Vero cell. Within the perinuclear envelope, the cisternae containing B. abortus are discontinuously lined by ribosomes (arrows). From Detilleux et al. Classification Higher order taxa: Bacteria; Proteobacteria; Alphaproteobacteria; Rhizobiales; Brucellaceae Species: Brucella abortus, Brucella canis, Brucella cetaceae, Brucella maris , Brucella melitensis, Brucella pinnipediae, Brucella sp. NCBI: Taxonomy Genomes Description and Significance 40

Brucella sp. causes brucellosis, a "zoonotic disease endemic in many areas of the world, characterized by chronic infections in animals leading to abortion and infertility, and a systemic, febrile illness in humans" (Paulsen et al. 2002). Brucella suis was the first pathogenic organism used by the U.S. military as a weapon backing in the 1950s. Although treatment is available for brucellosis, it is prolonged antibiotic therapy. In addition, early diagnosis is problematic and no acceptable vaccines have been made (Paulsen et al. 2002). Genome Structure Cell Structure and Metabolism Brucella is a Gram-negative pathogen that is distinguished from most other pathogens because it does not have "obvious virulence factors" like "capsules, fimbriae, flagella, exotoxins, exproteases, or other exoenzymes, cytolysins, resistance forms, antigenic variation, plamids, or lysogenic phages" (Moreno and Moriyon 2002). In addition to this, analyses of three Brucella species have shown that their genomes lack the functional sequences of so-called classical virulence factors, pathogenic islands, and a complete set of genes to mount, types I, II, and II secretion systems. It was found, however, that the bacterium recruits actin and activates small GTP-ases when in internalizes into cells (Moreno and

44)Bordetella Bordetella is a genus of small (0.2 - 0.7 m), Gram-negative coccobacilli of the phylum proteobacteria. Bordetella species, with the exception of B. petrii, are obligate aerobes as well as highly fastidious, or difficult to culture. Three species are human pathogens (B. pertussis, B. parapertussis, B. bronchiseptica); one of these (B. bronchiseptica) is also motile.[1] B. pertussis and occasionally B. parapertussis cause pertussis or whooping cough in humans, and some B. parapertussis strains can colonise sheep. B. bronchiseptica rarely infects healthy humans though disease in immunocompromised patients has been reported.[2] B. bronchiseptica causes several diseases in other mammals, including kennel cough and atrophic rhinitis in dogs and pigs, respectively. Other members of the genus cause similar diseases in other mammals, and in birds (B. hinzii, B. avium). The Bordetella genus is named after Jules Bordet. [edit] Pathogenesis The most often thoroughly studied of the Bordetella species are B. bronchiseptica, B. pertussis and B. parapertussis and the pathogenesis of respiratory disease caused by these bacteria has been reviewed.[3][4][5] Transmission occurs by direct contact, or via respiratory aerosol droplets, or fomites. Bacteria initially adhere to ciliated epithelial cells in the nasopharynx and this interaction with epithelial cells is mediated by a series of protein adhesins. These include filamentous haemaglutinin, pertactin, fimbriae, and pertussis toxin (though expression of pertussis toxin is unique to B. pertussis). As well as assisting in adherence to epithelial cells, some of these are also involved in attachment to immune effector cells. The initial catarrhal phase of infection produces symptoms similar to those of the common

41

cold and during this period, large numbers of bacteria can be recovered from the pharynx. Thereafter the bacteria proliferate and spread further into the respiratory tract, where the secretion of toxins causes ciliostasis and facilitates the entry of bacteria to tracheal/bronchial ciliated cells. One of the first toxins to be expressed is tracheal cytotoxin which is a disaccharide-tetrapeptide derived from peptidoglycan. Unlike most other Bordetella toxins, tracheal cytotoxin is expressed constitutively, being a normal product of the breakdown of the bacterial cell wall. Other bacteria recycle this molecule back into the cytoplasm, but in Bordetella and Neisseria gonorrhoeae it is released into the environment. Tracheal cytotoxin itself is able to reproduce paralysis of the ciliary escalator, inhibition of DNA synthesis in epithelial cells and ultimately killing of the same. One of the most important of the regulated toxins is adenylate cyclase toxin, 47-) Haemophilus : is a genus of Gram-negative, pleomorphic, coccobacilli bacteria belonging to the Pasteurellaceae family.[1][2] While Haemophilus bacteria are typically small coccobacilli, they are categorized as pleomorphic bacteria because of the wide range of shapes they occasionally assume. The genus includes commensal organisms along with some significant pathogenic species such as H. influenzae.a cause of sepsis and bacterial meningitis in young children.and H. ducreyi, the causative agent of chancroid. All members are either aerobic or facultatively anaerobic. Metabolism Members of the Haemophilus genus are typically cultured on blood agar plates as all species require at least one of the following blood factors for growth: hemin (factor X) and/or nicotinamide adenine dinucleotide (factor V). Chocolate agar is an excellent Haemophilus growth medium as it allows for increased accessibility to these factors.[3] Alternatively, Haemophilus is sometimes cultured using the "Staph streak" technique: both Staphylococcus and Haemophilus organisms are cultured together on a single blood agar plate. In this case, Haemophilus colonies will frequently grow in small "satellite" colonies around the larger Staphylococcus colonies because the metabolism of Staphylococcus produces the necessary blood factor by-products required for Haemophilus growth. 48-)Miscellaneous Gram-Negative Bacteria (Legionella, Bartonella, Streptobacillus and Spirillium) Legionella is a pathogenic Gram negative bacterium, including species that cause legionellosis or Legionnaires' disease, most notably L. pneumophila.[1][2] It may be readily visualized with a silver stain. Legionella is common in many environments, with at least 50 species and 70 serogroups identified. The side-chains of the cell wall carry the bases responsible for the somatic antigen specificity of these organisms. The chemical composition of these side chains both with respect to components as well as arrangement of the different sugars determines the nature of the somatic or O antigen determinants, which are essential means of serologically classifying many Gram-negative bacteria. Bartonella (formerly known as Rochalimaea) is a genus of Gram-negative bacteria. Facultative intracellular parasites, Bartonella species can infect healthy people but are considered especially important as opportunistic pathogens.[1] Bartonella are transmitted by insect vectors such as fleas, sand flies and mosquitoes. At least eight Bartonella species or subspecies are known to infect humans.[2] In June 2007, a new species under the genus, called Bartonella melophagi, was discovered.[3] This is the sixth species known to infect humans, and the ninth species and subspecies, overall, known to infect humans.

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Bartonella species have been infecting humans for thousands of years, as demonstrated by Bartonella quintana DNA in a 4000 year old tooth.[4] The genus is named after Alberto Leonardo Barton Thompson, a Peruvian scientist born in Argentina. Infection cycle The currently accepted model explaining the infection cycle holds that the transmitting vectors are blood-sucking arthropods and the reservoir hosts are mammals. Immediately after infection, the bacteria colonize a primary niche, the endothelial cells. Every five days, a part of the Bartonella in the endothelial cells are released in the blood stream where they infect erythrocytes. The bacteria then invade and replicate within a phagosomal membrane inside the erythrocytes. Inside the erythrocytes, bacteria multiply until they reach a critical population density. At this point, the Bartonella has simply to wait until it is taken with the erythrocytes by a blood-sucking arthropod. Although Bartonella DNA has been reported in ticks, there is no evidence that it can be transmitted by tick bites.[5] Streptobacillus is a genus of aerobic, gram-negative facultative anaerobe bacteria, which grow in culture as rods in chains. Spirillum in microbiology refers to a bacterium with a cell body that twists like a spiral.[1] It is the third distinct bacterial cell shape type besides coccus and bacillus cells. Spirillum is a genus of gram-negative bacteria. Spirillum minus is associated with rat-bite fever. Appearance It is a genus comprising elongated forms having tufts of flagellae at both poles and usually living in stagnant water rich in organic matter. They are twisted, and aerobic, certain species are pathogenic for humans.

49-)Anaerobic Gram-Positive Cocci and Nonspore-Forming Bacteria

Gram-positive anaerobic cocci (GPAC) are a heterogeneous group of organisms defined by their morphological appearance and their inability to grow in the presence of oxygen; most clinical isolates are identified to species in the genus Peptostreptococcus. GPAC are part of the normal flora of all mucocutaneous surfaces and are often isolated from infections such as deep organ abscesses, obstetric and gynecological sepsis, and intraoral infections. They have been little studied for several reasons, which include an inadequate classification, difficulties with laboratory identification, and the mixed nature of the infections from which they are usually isolated. Nucleic acid studies indicate that the classification is in need of radical revision at the genus level. Several species of Peptostreptococcus have recently been described, but others still await formal recognition. Identification has been based on carbohydrate fermentation tests, but most GPAC are asaccharolytic and use the products of protein degradation for their metabolism; the introduction of commercially available preformed enzyme kits affords a physiologically more appropriate method of identification, which is simple and relatively rapid and can be used in routine diagnostic laboratories. Recent reports have documented the isolation in pure culture of several species, notably Peptostreptococcus magnus, from serious infections. Studies of P. magnus have elucidated several virulence factors which correlate with the site of infection, and reveal some similarities to Staphylococcus aureus. P. micros is a strongly proteolytic species; it is increasingly recognized as an important pathogen in intraoral infections, particularly periodontitis, and mixed anaerobic deep-organ abscesses. Comparison of antibiotic susceptibility patterns reveals major differences between species. Penicillins are the antibiotics of choice, although some strains of P. anaerobius show broad-spectrum -lactam resistance.

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Non-Spore-Forming Bacteria Most of the non-spore-forming species of bacteria isolated from insects are in the families Enterobacteriaceae or Pseudomonidaceae. Non-spore-forming bacteria generally have low pathogenicity when they occur in the digestive tract of an insect, but may be very pathogenic if they are able to enter the insect's hemocoel. Thus, diseases caused by non-spore-forming bacteria generally rely on a conditional factor to gain entrance into the hemocoel. The general term "stress" encompasses many of these conditions. Stress results from unusually high temperatures, poor food quality, crowding, mechanical injury, or other factors. Nonspore- forming bacteria that are not active invaders may enter the hemocoel when the insect has been stressed and/or injured. Once in the hemocoel, many non-spore-forming bacteria multiply rapidly and may cause death of the insect from bacterial septicemia within one or two days. The digestive tracts of most insects contain non-spore-forming bacteria capable of producing bacterial septicemia if they are able to get into the hemocoel. These are known collectively as facultative pathogens.

50-)Anaerobic Spore-Forming Bacteria Clostridium Clostridium Pathology Clostridium consists of around 100 species[3] that include common free-living bacteria as well as important pathogens.[4] There are four main species responsible for disease in humans: . C. botulinum, an organism that produces botulinum toxin in food/wound and can cause botulism.[5] Honey sometimes contains spores of Clostridium botulinum, which may cause infant botulism in humans one year old and younger. The toxin eventually paralyzes the infant's breathing muscles.[6] Adults and older children can eat honey safely, because Clostridia do not compete well with the other rapidly growing bacteria present in the GI (Gastrointestinal) tract. This same toxin is known as "Botox" and is used cosmetically to paralyze facial muscles to reduce the signs of aging; it also has numerous therapeutic uses. . C. difficile, which can flourish when other bacteria in the gut are killed during antibiotic therapy, leading to pseudomembranous colitis (also known as antibiotic-associated diarrhea).[7] . C. perfringens, formerly called C. welchii, causes a wide range of symptoms, from food poisoning to gas gangrene. Also responsible for enterotoxemia (also known as "overeating disease" or "pulpy kidney disease") in sheep and goats.[8] C. perfringens also takes the place of yeast in the making of salt rising bread. The name perfringens means "breaking through, breaking in pieces". . C. tetani, the causative organism of tetanus.[9]. The name derives from "of a tension", referring to the tension (caused by tetanus) in the muscles.[citation needed] . C. sordellii has been linked to the deaths of more than a dozen women after

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Childbirth. 51-) Aerobic Spore-Forming Bacteria Bacillus Bacillus is a genus of Gram-positive rod-shaped bacteria and a member of the division Firmicutes. Bacillus species can be obligate aerobes or facultative anaerobes, and test positive for the enzyme catalase. [1] Ubiquitous in nature, Bacillus includes both free-living and pathogenic species. Under stressful environmental conditions, the cells produce oval endospores that can stay dormant for extended periods. These characteristics originally defined the genus, but not all such species are closely related, and many have been moved to other genera. [2] Industrial significance Many Bacillus species are able to secrete large quantities of enzymes. Bacillus amyloliquefaciens is a species of Bacillus that is the source of a natural antibiotic protein barnase (a ribonuclease), alpha amylase used in starch hydrolysis, the protease subtilisin used with detergents, and the BamH1 restriction enzyme used in DNA research. A portion of the Bacillus thuringiensis genome was incorporated into corn (and cotton) crops. The resulting GMOs are therefore resistant to some insect pests. Use as model organism Bacillus subtilis is one of the best understood prokaryotes, in terms of molecular biology and cell biology. Its superb genetic amenability and relatively large size have provided the powerful tools required to investigate a bacterium from all possible aspects. Recent improvements in fluorescence microscopy techniques have provided novel and amazing insight into the dynamic structure of a single cell organism. Research on Bacillus subtilis has been at the forefront of bacterial molecular biology and cytology. 52-) Anaerobic Gram-Negative Nonspore-Forming Bacteria and Cocci (Bacteroides,
Porphyromonas, Prevotella, Veilonella)

Bacteroides is a genus of Gram-negative, bacillus bacteria. Bacteroides species are non-endospore-forming, anaerobes, and may be either motile or non-motile, depending on the species.[1] The DNA base composition is 40-48% GC. Unusual in bacterial organisms, Bacteroides membranes contain sphingolipids. They also contain meso-diaminopimelic acid in their peptidoglycan layer. Bacteroides are normally mutualistic, making up the most substantial portion of the mammalian gastrointestinal flora,[2] where they play a fundamental role in processing of complex molecules to simpler ones in the host intestine.[3][4][5] As many as 1010-1011 cells per gram of human feces have been reported.[6] They can use simple sugars when available, but the main source of energy is polysaccharides from plant sources. Pathogenesis Bacteroides species also benefit their host by excluding potential pathogens from colonizing the gut. Some species (B. fragilis, for example) are opportunistic human pathogens, causing infections of the peritoneal cavity, gastrointestinal surgery, and appendicitis via abscess formation, inhibiting phagocytosis, and inactivating beta-lactam antibiotics.[8] Although Bacteroides species are anaerobic, they are aerotolerant and thus can survive in the abdominal cavity. Description and Significance Porphyromonas, which are commonly found in the human body and especially in the oral cavity, were originally classified in the Bacteroides genus. Porphyromonas gingivalis are an oral anaerobe associated with periodontal lesions, infections, and adult periodontal disease.

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Approximately 70-90% of people pubescent and older have gingivitis, an oral inflammatory process and a possible precursor to adult periodontal disease, which is associated with Porphyromonas gingivalis. Gingivitis allows Porphyromonas gingivalis to further infect the areas near the root of the teeth causing tooth decay and infection. 53) Mycobacterium is a genus of Actinobacteria, [Mycobacteria are aerobic and nonmotile bacteria (except for the species Mycobacterium marinum, which has been shown to be motile within macrophages) that are characteristically acid-alcohol fast.[1] Mycobacteria do not contain endospores or capsules and are usually considered Gram-positive. A recent paper in PNAS showed sporulation in Mycobacterium marinum and perhaps in M. bovis [2]. However, this has been strongly argued by other scientists [3]. While mycobacteria do not seem to fit the Gram-positive category from an empirical standpoint (i.e. they generally do not retain the crystal violet stain well), they are classified as an acidfast Gram-positive bacterium due to their lack of an outer cell membrane. All Mycobacterium species share a characteristic cell wall, thicker than in many other bacteria, which is hydrophobic, waxy, and rich in mycolic acids/mycolates. The cell wall consists of the hydrophobic mycolate layer and a peptidoglycan layer held together by a polysaccharide, arabinogalactan. The cell wall makes a substantial contribution to the hardiness of this genus. The biosynthetic pathways of cell wall components are potential targets for new drugs for tuberculosis.[4] Some species can be very difficult to culture (i.e. they are fastidious), sometimes taking over two years to develop in culture.[citation needed] Further, some species also have extremely long reproductive cycles . M. leprae, may take more than 20 days to proceed through one division cycle (for comparison, some E. coli strains take only 20 minutes), making laboratory culture a slow process.In addition, the availability of genetic manipulation techniques still lags far behind that of other bacterial species.[5] A natural division occurs between slowly. and rapidly.growing species. Mycobacteria that form colonies clearly visible to the naked eye within seven days on subculture are termed rapid growers, while those requiring longer periods are termed slow growers. Mycobacteria cells are straight or slightly curved rods between 0.2-0.6 m wide by 1.0-10 m long. [edit] Pigmentation Some mycobacteria produce carotenoid pigments without light. Others require photoactivation for pigment production. Photochromogens (Group I) Scotochromogens (Group II) Non-chromogens (Groups III & IV) [edit] Staining characteristics Mycobacteria are classical acid-fast organisms.[6] Stains used in evaluation of tissue specimens or microbiological specimens include Fite's stain, Ziehl-Neelsen stain, and Kinyoun stain. Mycobacteria appear phenotypically most closely related to members of Nocardia, Rhodococcus and Corynebacterium. Ecological characteristics Mycobacteria are widespread organisms, typically living in water (including tap water treated with chlorine) and food sources. Some, however, including the tuberculosis and the leprosy organisms, appear to be obligate parasites and are not found as free-living members of the genus. Pathogenicity Mycobacteria can colonize their hosts without the hosts showing any adverse signs. For example, billions of people around the world have asymptomatic infections of M. tuberculosis.

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. 54) Spirochaetes Treponema Genus: Treponema . Species: pallidum, pertenue, carateum GENERAL CONCEPTS: . Three "treponematoses" are discussed: syphilis, yaws and pinta. . Each of these diseases is characterized by distinct clinical stages. These stages are known as primary, secondary and tertiary. o The primary stage involves multiplication of the bacteria at the site of entry to produce a localized infection. o The secondary stage occurs following an asymptomatic period and involves dissemination of the bacteria to other tissues. o The tertiary stage may occur after 20-30 years. . The Treponema are highly invasive organisms; T. pallidum is the most invasive of the species, T. carateum the least invasive. DISTINCTIVE PROPERTIES: . The Treponema are motile, helically coiled organisms having a corkscrew-like shape. They stain very poorly because their thickness approaches the resolution of the light microscope. . Treponema are delicate organisms requiring pH in the range 7.2 to 7.4, temperatures in the range 30 C to 37 C and a microaerophilic environment. . The structure of these organisms is somewhat different: the cells have a coating of glycosamino-glycans, which may be host-derived, and the outer membrane covers the three flagella that provide motility. . In addition, the cells have a high lipid content (cardiolipin, cholesterol), which is unusual for most bacteria. Cardiolipin elicits "Wassermann" antibodies that are diagnostic for syphilis. . Treponema possess a complex antigenic makeup that is difficult to determine because the organisms cannot be grown in vitro. PATHOGENESIS: . Treponema pallidum is capable of infecting all body tissues. . The disease caused by T. pallidum is syphilis. This is a relatively painless, slowly evolving disease. The host-parasite relationship leads to short symptomatic periods when the organism multiplies, followed by prolonged asymptomatic periods when host responses produce healing. . Syphilis is strictly a person-person disease. 55-) Spirochaetes Borrelia Borrelia is a genus of bacteria of the spirochete phylum. It causes borreliosis, a zoonotic, vector-borne disease transmitted primarily by ticks and some by lice, depending on the species.[1] There are Lyme disease Main article: Lyme disease microbiology Of the 36 known species of Borrelia, 12 of these species are known to cause Lyme disease or borreliosis and are transmitted by ticks. The major Borrelia species causing Lyme disease are Borrelia burgdorferi, Borrelia afzelii, Borrelia garinii and Borrelia valaisiana. Relapsing fever Relapsing fever borreliosis often occurs with severe bacteremia.[2] Borrelia recurrentis is transmitted by the human body louse and no other animal reservoir of B. recurrentis is known. Lice that feed on infected humans acquire the Borrelia organisms that then multiply in

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the gut of the louse. When an infected louse feeds on an uninfected human, the organism gains access when the victim crushes the louse or scratches the area where the louse is feeding. B. recurrentis infects the person via mucous membranes and then invades the bloodstream. Other tick-borne relapsing infections are acquired from other species, such as Borrelia hermsii or Borrelia Parkeri, which can be spread from rodents, and serve as a reservoir for the infection, via a tick vector. Borrelia hermsii and Borrelia recurrentis cause very similar diseases although the disease associated with Borrelia hermsii has more relapses and is responsible for more fatalities, while the disease caused by B. recurrentis has longer febrile and afebrile intervals and a longer incubation period

56) Spirochaetes Leptospira Leptospira (Greek leptos, "fine, thin" and Latin spira, "coil")[1] is a genus of spirochaete bacteria, including a small number of pathogenic and saprophytic species.[2] Leptospira was first observed in 1907 in kidney tissue slices of a leptospirosis victim who was described as having died of "yellow fever."[3] Taxonomy Leptospira, together with the genera Leptonema and Turneria, is a member of the family Leptospiraceae. The genus Leptospira is divided into 20 species based on DNA hybridization studies.[4][5] Evolutionary relationships of the 20 recognized species of Leptospira The evolutionary history was inferred using the Minimum Evolution method [10]. The bootstrap consensus tree inferred from 1000 replicates is taken to represent the evolutionary history of the taxa analyzed [11]. Branches corresponding to partitions reproduced in less than 50% bootstrap replicates are collapsed. The percentage of replicate trees in which the associated taxa clustered together in the bootstrap test (1000 replicates) are shown next to the branches. The tree is drawn to scale, with branch lengths in the same units as those of the evolutionary distances used to infer the phylogenetic tree. The evolutionary distances were computed using the [edit] Morphology Although over 200 serotypes of Leptospira have been described, all members of the genus have similar morphology. Leptospira are spiral-shaped bacteria that are 6-20 m long and 0.1 m in diameter with a wavelength of about 0.5 m.[16] One or both ends of the spirochete are usually hooked. Because they are so thin, live Leptospira are best observed by darkfield

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microscopy. The bacteria have a number of degrees of freedom; when ready to proliferate via binary fission, the bacterium noticeably bends in the place of the future split. 57)- Mycoplasma and Ureaplasma Mycoplasma is a genus of bacteria that lack a cell wall.[1] Without a cell wall, they are unaffected by many common antibiotics such as penicillin or other beta-lactam antibiotics that target cell wall synthesis. They can be parasitic or saprotrophic. Several species are pathogenic in humans, including M. pneumoniae, which is an important cause of atypical pneumonia and other respiratory disorders, and M. genitalium, which is believed to be involved in pelvic inflammatory diseases. Origin of the name The name Mycoplasma, from the Greek mykes (fungus) and plasma (formed), was first used by A. B. Frank in 1889. He thought it was a fungus, due to fungus-like characteristics .[2] An older name for Mycoplasma was Pleuropneumonia-Like Organisms (PPLO), referring to organisms similar to the causative agent of contagious bovine pleuropneumonia (CBPP).[3] It was later found that the fungus-like growth pattern of M. mycoides is unique to that species. Characteristics There are over 100 recognized species of the genus Mycoplasma, one of several genera within the bacterial class Mollicutes. Mollicutes are parasites or commensals of humans, other animals (including insects), and plants; the genus Mycoplasma is by definition restricted to vertebrate hosts. Cholesterol is required for the growth of species of the genus Mycoplasma as well as certain other genera of mollicutes. Their optimum growth temperature is often the temperature of their host if warmbodied (e. g. 37 C in humans) or ambient temperature if the host is unable to regulate its own internal temperature. Analysis of 16S ribosomal RNA sequences as well as gene content strongly suggest that the mollicutes, including the mycoplasmas, are closely related to either the Lactobacillus or the Clostridium branch of the phylogenetic tree (Firmicutes sensu stricto). Cell morphology The bacteria of the genus Mycoplasma (trivial name: mycoplasmas) and their close relatives are characterized by lack of a cell wall. Despite this, the cells often present a certain shape, with a characteristic small size, with typically about 10% of the volume of an Escherichia coli cell. These cell shapes presumably contribute to the ability of mycoplasmas to thrive in their respective environments. Most are pseudococcoidal, but there are notable exceptions. Species of the M. fastidiosum cluster are rod-shaped. Species of the M. pneumoniae cluster, including M. pneumoniae, possess a polar extension protruding from the pseudococcoidal cell body. This tip structure, designated an attachment organelle or terminal organelle, is essential for adherence to host cells and for movement along solid surfaces (gliding motility), and is implicated in normal cell division. M. pneumoniae cells are pleomorphic, with an attachment organelle of regular dimensions at one pole and a trailing filament of variable length and uncertain function at the other end, whereas other species in the cluster typically lack the trailing filament. Other species like M. mobile and M. pulmonis have similar structures with similar functions. Clinical significance U. urealyticum is part of the normal genital flora of both men and women. It is found in about 70% of sexually active humans. 58-) Rickettsia, Coxiella and Ehrlichia Rickettsia is a genus of non-motile, Gram-negative, non-sporeforming, highly

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pleomorphic bacteria that can present as cocci (0.1 m in diameter), rods (1.4 m long) or thread-like (10 m long). Obligate intracellular parasites, the Rickettsia survival depends on entry, growth, and replication within the cytoplasm of eukaryotic host cells (typically endothelial cells).[1] Because of this, Rickettsia cannot live in artificial nutrient environments and are grown either in tissue or embryo cultures (typically, chicken embryos are used). In the past they were positioned somewhere between viruses and true bacteria. The majority of Rickettsia bacteria are susceptible to antibiotics of the tetracycline group. Rickettsia species are carried by many ticks, fleas, and lice, and cause diseases in humans such as typhus, rickettsialpox, Boutonneuse fever, African tick bite fever, Rocky Mountain spotted fever, Australian Tick Typhus, Flinders Island Spotted Fever and Queensland tick typhus.[2] They have also been associated with a range of plant diseases. Like viruses, they only grow inside living cells. The name rickettsia is often used for any member of the Rickettsiales. They are thought to be the closest living relatives to bacteria that were the origin of the mitochondria organelle that exists inside most eukaryotic cells. The method of growing Rickettsia in chicken embryos was invented by Ernest William Goodpasture and his colleagues at Vanderbilt University in the early 1930s. Coxiella burnetii is a species of intracellular, pathogenic bacteria, and is the causative agent of Q fever. The genus Coxiella is morphologically similar to Rickettsia, but with a variety of genetic and physiological differences. C. burnetii are small Gram negative bacteria with two growth phases, as well as a spore form which lies idle in soil.[1] It can survive standard disinfectants, and is resistant to many other environmental changes like those presented in the phagolysosome.[2] Ehrlichiosis is a tickborne[1] bacterial infection, caused by bacteria of the family Anaplasmataceae, genera Ehrlichia and Anaplasma. These obligate intracellular bacteria infect and kill white blood cells. The average reported annual incidence is 0.7 cases per million population.[2] Five species have been shown to cause human infection:[3] . Anaplasma phagocytophilum (which causes human granulocytic anaplasmosis, formerly known as human granulocytic ehrlichiosis). A. phagocytophilium is endemic to New England and the north central and Pacific regions of the United States. . Ehrlichia ewingii (which causes human ewingii ehrlichiosis). E. ewingii primarily infects deer and dogs (see Ehrlichiosis (canine)).[2] E. ewingii is most common in the south central and southeastern states. . Ehrlichia chaffeensis (which causes human monocytic ehrlichiosis). E. chaffeensis is most common in the south central and southeastern states. . Ehrlichia canis . Neorickettsia sennetsu 59) Chlamydia Chlamydia is a genus of bacteria that are obligate intracellular parasites. Chlamydia infections are the most common bacterial sexually transmitted infections in humans and are the leading cause of infectious blindness worldwide.[1] The three Chlamydia species include Chlamydia trachomatis (a human pathogen), Chlamydia suis (affects only swine), and Chlamydia muridarum (affects only mice and hamsters).[2] Prior to 1999, the Chlamydia genus also included the species that are presently in the genus Chlamydophila: Two clinically relevant species, Chlamydophila pneumoniae and Chlamydophila psittaci were moved to the Chlamydophila genus. Classification Because of Chlamydia's unique developmental cycle, it was taxonomically classified in a separate order.[3] Chlamydia is part of the Chlamydiales order, Chlamydiaceae family, along

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with Chlamydophila genus. As of March 2008, a new chlamydial agent has been proposed to be introduced into the Chlamidiaceae family, namely 'Candidatus Clavochlamydia salmonicola'.[4 60) Microbial Flora (Natural flora) in Health and Disease Normal Bacterial Flora of Humans (page 1) The Normal Flora In a healthy animal, the internal tissues, e.g. blood, brain, muscle, etc., are normally free of microorganisms. However, the surface tissues, i.e., skin and mucous membranes, are constantly in contact with environmental organisms and become readily colonized by various microbial species. The mixture of organisms regularly found at any anatomical site is referred to as the normal flora, except by researchers in the field who prefer the term "indigenous microbiota". The normal flora of humans consists of a few eucaryotic fungi and protists, but bacteria are the most numerous and obvious microbial components of the normal flora S. epidermidis. Scanning EM. CDC. (2) Many of the normal flora are either pathogens or opportunistic pathogens, The asterisks indicate members of the normal flora a that may be considered major pathogens of humans. S. aureus. Gram stain. 3) Streptococcus mutans is the primary bacterium involved in plaque formation and initiation of dental caries. Viewed as an opportunistic infection, dental disease is one of the most prevalent and costly infectious diseases in the United States. Streptococcus mutans. Gram stain. CDC 4) Enterococcus faecalis was formerly classified as Streptococcus faecalis. The bacterium is such a regular a component of the intestinal flora, that many European countries use it as the standard indicator of fecal pollution, in the same way we use E. coli in the U.S. In recent years, Enterococcus faecalis has emerged as a significant, antibiotic-resistant, nosocomial pathogen. Vancomycin Resistant Enterococcus faecalis. Scanning E.M. CDC (5) Streptococcus pneumoniae is present in the upper respiratory tract of about half the population. If it invades the lower respiratory tract it can cause pneumonia. Streptococcus pneumoniae causes 95 percent of all bacterial pneumonia. Streptococcus pneumoniae. Direct fluorescent antibody stain. CDC. (6) Streptococcus pyogenes refers to the Group A, Beta-hemolytic streptococci. Streptococci cause tonsillitis (strep throat), pneumonia, endocarditis. Some streptococcal diseases can lead to rheumatic fever or nephritis which can damage the heart and kidney. Streptococcus pyogenes. Gram stain. (7) Neisseria and other Gram-negative cocci are frequent inhabitants of the upper respiratory tract, mainly the pharynx. Neisseria meningitidis, an important cause of bacterial meningitis, can colonize as well, until the host can develop active immunity against the pathogen. (8) While E. coli is a consistent resident of the small intestine, many other enteric bacteria may reside here as well, including Klebsiella, Enterobacter and Citrobacter. Some strains of E. coli are pathogens that cause intestinal infections, urinary tract infections and neonatal meningitis. (9) Pseudomonas aeruginosa is the quintessential opportunistic pathogen of humans that can invade virtually any tissue. It is a leading cause of hospital-acquired (nosocomial) Gramnegative infections, but its source is often exogenous (from outside the host). Colonies of Pseudomonas aeruginosa growing on an agar plate. The most virulent

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Pseudomonas species produce mucoid colonies and green pigments such as this isolate 61) Laboratory Diagnosis of Viral Diseases 1. Organism present only in diseased individuals 2. Organism cultivated in pure culture from diseased individual 3. Organism causes disease when injected into healthy individuals 4. Organism re-isolated from infected individual from point 3. Isolate virus from diseased hosts. Cultivation of virus in host cells. Proof of filterability. Production of a comparable disease when the cultivated virus is used to infect experimental animals. Reisolation of the same virus from the infected experimental animal. Detection of a specific immune response to the virus. Cultivation of Viruses in the Laboratory . Viruses need a ghost h system. . Viruses can be grown in: o Animals o Embryonated eggs Cytopathic Effects . Visible results of viral infection . Cell death by . Multiplying viruses . Inhibition of DNA, RNA or protein synthesis . Effects on permeability of membrane Hemadsorption Test . Some viruses agglutinate RBCs o Mumps, measles, influenza o Hemagglutination . Clumps RBCs Viral Diagnostics in the Clinical Laboratory . Over 60% of all infectious disease cases seen by a physician are due to viral infections. Viral Serology . Enzyme-Linked Immunosorbent Assays (ELISAs) o Enzyme reacts with substrate to produce colored product o Very sensitive . HIV test . If positive twice, Western Blotting is performed next 62) Picornavirus A picornavirus is a virus belonging to the family Picornaviridae. Picornaviruses are nonenveloped, positive-stranded RNA viruses with an icosahedral capsid. The genome RNA is unusual because it has a protein on the 5' end that is used as a primer for transcription by RNA polymerase. The name is derived from pico, meaning small, and RNA, referring to the ribonucleic acid genome, so "picornavirus" literally means small RNA virus. Picornaviruses are separated into 12 distinct genera and include many important pathogens of humans and animals.[1] The diseases they cause are varied, ranging from acute "commoncold"like illnesses, to poliomyelitis, to chronic infections in livestock.

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] Classification Picornaviruses are classed under Baltimore's viral classification system as group IV viruses as they contain a single stranded, positive sense RNA genome of between 7.2 and 9.0 kb (kilobases) in length. Like most positive sense RNA genomes, the genetic material alone is infectious; although substantially less virulent than if contained within the viral particle, the RNA can have increased infectivity when transfected into cells. The genome itself is the same sense as mammalian mRNA, being read 5' to 3'. Unlike mammalian mRNA picornaviruses do not have a 5' cap but a virally encoded protein known as VPg. However, like mammalian mRNA, the genome does have a poly(A) tail at the 3' end. There is an untranslated region (UTR) at both ends of the picornavirus genome. The 5' UTR is longer, being around 600-1200 nucleotides (nt) in length, compared to that of the 3' UTR, which is around 50-100 nt. It is thought that the 5' UTR is important in translation and the 3' in negative strand synthesis; however the 5' end may also have a role to play in virulence of the virus. The rest of the genome encodes structural proteins at the 5' end and non-structural proteins at the 3' end in a single polyprotein. Experimental data from single step growthcurvelike experiments have allowed scientists to look at the replication of the picornaviruses in great detail. The whole of replication occurs within the host cell cytoplasm and infection can even happen in cells that do not contain a nucleus (known as enucleated cells) and those treated with actinomycin D (this antibiotic would inhibit viral replication if this occurred in the nucleus.)

63) Paramyxoviruses (from Greek para-, beyond, -myxo-, mucus or slime, plus virus, from Latin poison, slime) are viruses of the Paramyxoviridae family of the Mononegavirales order; they are negative-sense single-stranded RNA viruses responsible for a number of human and animal diseases. Physical structure Virions are enveloped and can be spherical, filamentous or pleomorphic. Fusion proteins and attachment proteins appear as spikes on the virion surface. Matrix proteins inside the envelope stabilise virus structure. The nucleocapsid core is composed of the genomic RNA, nucleocapsid proteins, phosphoproteins and polymerase proteins. Genome structure The genome consists of a single NOT segment negative-sense RNA, 15-19 kilobases in length and containing 6-10 genes. Extracistronic (non-coding) regions include: . A 3 f leader sequence, 50 nucleotides in length which acts as a transcriptional promoter. . A 5 f trailer sequence, 50-161 nucleotides long . Intergenomic regions between each gene which are three nucleotides long for morbillivirus, respirovirus and henipavirus, variable length (1-56 nucleotides) for rubulavirus and pneumovirinae. Each gene contains transcription start/stop signals at the beginning and end which are transcribed as part of the gene. Gene sequence within the genome is conserved across the family due to a phenomenon known as transcriptional polarity (see Mononegavirales) in which genes closest to the 3 f end of the genome are transcribed in greater abundance than those towards the 5 f end. This

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mechanism acts as a form of transcriptional regulation. The gene sequence is: . Nucleocapsid . Phosphoprotein . Matrix . Fusion . Attachment . Large (polymerase) 64) Orthomyoviruses Morphology: Influenza virus particles are highly pleiomorphic (variable), mostly spherical/ovoid, 80120nm diameter, but many forms occur, including long filamentous particles (up to 2000nm long x 80-120nm diameter). Different strains of virus vary in their tendency to form filaments - this property maps to the matrix protein. Host Range: . Influenza A viruses infect a wide variety of mammals, including man, horses, pigs, ferrets and birds. The main human pathogen, associated with epidemics and pandemics. There are 15 known haemagglutinin (H) serotypes and 9 known neuraminidase (N) serotypes. Pigs and birds are believed to be particularly important reservoirs, generating pools of genetically/antigenically diverse viruses which get transferred back to the human population via close contact between humans and animals. . Influenza B viruses infect mammals only and cause disease, but generally not as severe as A types. Unlike influenza A viruses, influenza B viruses do not have distinguishable serotypes. . Influenza C viruses also infect mammals only, but rarely cause disease. They are genetically and morphologically distinct from A and B types. Species barrier: The species which different types of influenza viruses are able to infect are determined by different forms of sialic acid present on the virus glycoproteins. In particular, this property depends predominately (but not exclusively) on the amino acid at position 226 of the haemagglutinin protein: This provides a considerable species barrier between birds and humans which is not easily overcome. However, pigs provide a "mixing pot" - able to be infected by both types of virus & thus allowing the passage of avian viruses to humans. 65-)Corornaviruses, Calicivirus Coronaviruses are species in the genera of animal virus belonging to the subfamily Coronavirinae in the family Coronaviridae.[1] Coronaviruses are enveloped viruses with a positive-sense single-stranded RNA genome and a helical symmetry. The genomic size of coronaviruses ranges from approximately 16 to 31 kilobases, extraordinarily large for an RNA virus. The name "coronavirus" is derived from the Greek meaning crown, as the virus envelope appears under electron microscopy (E.M.) to be crowned by a characteristic ring of small bulbous structures. This morphology is actually formed by the viral spike (S) peplomers, which are proteins that populate the surface of the virus and determine host tropism. Coronaviruses are grouped in the order Nidovirales, named for the Latin nidus, meaning nest, as all viruses in this order produce a 3' co-terminal nested set of subgenomic mRNA's during infection. Coronaviruses primarily infect the upper respiratory and gastrointestinal tract of mammals and birds. Four to five different currently known strains of coronaviruses infect humans. The most publicized human coronavirus, SARS-CoV which causes SARS, has a unique pathogenesis because it causes both upper and lower respiratory tract infections and can also cause gastroenteritis. Coronaviruses are believed to cause a significant percentage of

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all common colds in human adults. Coronaviruses cause colds in humans primarily in the winter and early spring seasons. The significance and economic impact of coronaviruses as causative agents of the common cold are hard to assess because, unlike rhinoviruses (another common cold virus), human coronaviruses are difficult to grow in the laboratory. Coronaviruses also cause a range of diseases in farm animals and domesticated pets, some of which can be serious and are a threat to the farming industry. Economically significant coronaviruses of farm animals include porcine coronavirus (transmissible gastroenteritis coronavirus, TGE) and bovine coronavirus, which both result in diarrhea in young animals. Feline Coronavirus: 2 forms, Feline enteric coronavirus is a pathogen of minor clinical significance, but spontaneous mutation of this virus can result in feline infectious peritonitis (FIP), a disease associated with high mortality. There are two types of canine coronavirus (CCoV), one that causes mild gastrointestinal disease and one that has been found to cause respiratory disease. Mouse hepatitis virus (MHV) is a coronavirus that causes an epidemic murine illness with high mortality, especially among colonies of laboratory mice. Feline calicivirus (FCV) is a virus of the family Caliciviridae that causes disease in cats. It is one of the two important viral causes of respiratory infection in cats, the other being feline herpesvirus. FCV can be isolated from about 50 percent of cats with upper respiratory infection.[1] Cheetahs are the other species of the family Felidae known to become infected naturally.[1] Viral structure and pathogenesis There are different strains of FCV that vary in virulence. Being an RNA virus, FCV has a high elasticity of its genome which makes it more adaptable to environmental pressures. This not only makes the development of vaccines more difficult, but allows for the development of more virulent strains.[2] In persistently infected cats, it has 66-) Reoviruses Reoviridae is a family of viruses that can affect the gastrointestinal system (such as Rotavirus) and respiratory tract. Viruses in the family Reoviridae have genomes consisting of segmented, double-stranded RNA (dsRNA).[1] The name "Reoviridae" is derived from respiratory enteric orphan viruses.[2] The term "orphan virus" means that a virus that is not associated with any known disease. Even though viruses in the Reoviridae family have more recently been identified with various diseases, the original name is still used. Reovirus infection occurs often in humans, but most cases are mild or subclinical. The virus can be readily detected in feces, and may also be recovered from pharyngeal or nasal secretions, urine, cerebrospinal fluid, and blood. Despite the ease of finding Reovirus in clinical specimens, their role in human disease or treatment is still uncertain. Some viruses of this family infect plants. For example, Phytoreovirus and Oryzavirus 67) Togaviruses, Flaviviruses The Togaviridae are a family of viruses, including the following genera: The Togaviridae family belong to group IV of the Baltimore classification of viruses. The genome is linear, single-stranded, positive sense RNA that is 10,000-12,000 nucleotides long. The 5'-terminus carries a methylated nucleotide cap and the 3'-terminus has a polyadenylated tail, therefore resembling cellular mRNA. The virus is enveloped and forms spherical particles (65-70 nm diameter), the capsid within is icosahedral, constructed of 240 monomers, having a triangulation number of 4. The receptors for binding are unknown, however the tropism is varied and it is known that the glycoprotein spikes act as attachment proteins. After virus attachment and entry into the cell, gene expression and replication takes place within the cytoplasm.

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Flavivirus is a genus of the family Flaviviridae. This genus includes the West Nile virus, dengue virus, Tick-borne Encephalitis Virus, Yellow Fever Virus, and several other viruses which may cause encephalitis. Flaviviruses are named from the yellow fever virus, a type virus for the Flaviviridae family; flavus means yellow in Latin. Yellow fever in turn was named because of its propensity to cause yellow jaundice in victims.[2] Flaviviruses share a common size (40-65 nm), symmetry (enveloped, icosahedral nucleocapsid), nucleic acid (positive-sense, single stranded RNA approximately 10,000. 11,000 bases), and appearance in the electron microscope. These viruses are transmitted by the bite from an infected arthropod (mosquito or tick). Human infections with these viruses are typically incidental, as humans are unable to replicate the virus to high enough titres to reinfect arthropods and thus continue the virus life cycle. The exceptions to this are yellow fever and dengue viruses, which still require mosquito vectors, but are well-enough adapted to humans as to not necessarily depend upon animal hosts (although both continue have important animal transmission routes as well).

68-) Bunyaviridae Buniavirus, Nairovirus Bunyaviridae is a family of negative-stranded RNA viruses. Though generally found in arthropods or rodents, certain viruses in this family occasionally infect humans. Some of them also infect plants. Bunyaviridae are vector-borne viruses. With the exception of Hantaviruses, transmission occurs via an arthropod vector (mosquitos, tick, or sandfly). Hantaviruses are transmitted through contact with deer mice feces. Incidence of infection is closely linked to vector activity,for example, mosquito-borne viruses are more common in the summer. Human infections with certain Bunyaviridae, such as Crimean-Congo hemorrhagic fever virus, are associated with high levels of morbidity and mortality, consequently handling of these viruses must occur with a Biosafety level 4 laboratory. Hanta virus or Hantavirus Hemorrhagic fever, common in Korea, Scandinavia, Russia, and the American southwest, is associated with high fever, lung edema and pulmonary failure. Mortality is around 55%. Virology Classification The family Bunyaviridae contains the genera: . Genus Hantavirus; type species: Hantaan virus . Genus Nairovirus; type species: Dugbe virus . Genus Orthobunyavirus; type species: Bunyamwera virus . Genus Phlebovirus; type species: Rift Valley fever virus . Genus Tospovirus; type species: Tomato spotted wilt virus Structure Bunyavirus morphology is somewhat similar to that of the Paramyxoviridae family; Bunyaviridae form enveloped, spherical virions with diameters of 90-100 nm. These viruses contain no matrix proteins.

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69) Rhabdoviruses Rhabdoviruses are viruses belonging to the family Rhabdoviridae, which is in the order Mononegavirales. The name is derived from the Greek rhabdos meaning rod referring to the shape of the viral particles. Rhabdoviruses infect a broad range of hosts throughout the animal and plant kingdoms. Animal rhabdoviruses infect insects, fish, and mammals, including humans. Virology Classification:Rhabdoviruses carry their genetic material in the form of negativesense single-stranded RNA. They typically carry genes for five proteins: large protein (L), glycoprotein (G), nucleoprotein (N), phosphoprotein (P), and matrix protein (M). Rhabdoviruses that infect vertebrates are bullet-shaped. . Genus Cytorhabdovirus; type species: Lettuce necrotic yellows virus . Genus Dichorhabdovirus; type species: Orchid fleck virus . Genus Ephemerovirus; type species: Bovine ephemeral fever virus . Genus Lyssavirus; type species: Rabies virus . Genus Novirhabdovirus; type species: Infectious hematopoietic necrosis virus . Genus Nucleorhabdovirus; type species: Potato yellow dwarf virus . Genus Vesiculovirus; type species: Vesicular stomatitis Indiana virus Replication:Replication of many rhabdoviruses occurs in the cytoplasm, although several of the plantinfecting viruses replicate in the nucleus. In order for replication, both the L and P protein must be expressed to regulate transcription. Transcription results in five monocistronic mRNAs being produced because the intergenic sequences act as both termination and promoter sequences for adjacent genes. During their synthesis the mRNAs are processed to introduce a 5' cap and a 3 f polyadenylated tail to each of the molecules. This structure is homologous to cellular mRNAs and can thus be translated by cellular ribosomes to produce both structural and non-structural proteins. 70) Poxviruses Poxviruses (members of the family Poxviridae) are viruses that can, as a family, infect both vertebrate and invertebrate animals. Four genera of poxviruses may infect humans: orthopox, parapox, yatapox, molluscipox. Orthopox: variola virus, vaccinia virus, cowpox virus, monkeypox virus, smallpox (eradicated); Parapox: orf virus, pseudocowpox, bovine papular stomatitis virus; Yatapox: tanapox virus, yaba monkey tumor virus; Molluscipox: molluscum contagiosum virus (MCV).[1] The most common are vaccinia (seen on Indian subcontinent) and molluscum contagiousum, but monkeypox infections are rising (seen in west and central African rainforest countries). Structure Poxviridae viral particles (virions) are generally enveloped (external enveloped virion- EEV), though the intracellular mature virion (IMV) form of the virus, which contains different envelope and is also infectious. They vary in their shape depending upon the species but are generally shaped like a brick or as an oval form similar to a rounded brick. The virion is exceptionally large, its size is around 200 nm in diameter and 300 nm in length and carries its genome in a single, linear, double-stranded segment of DNA.[2] By comparison, Rhinovirus is 1/10th as large as a typical Poxviridae virion.[3] Replication Replication of the poxvirus involves several stages. The first thing the virus does is to bind to a receptor on the host cell surface; the receptors for the poxvirus are thought to be Glycosaminoglycans (GAGs). After binding to the receptor, the virus enters the cell where it uncoats. Uncoating of the virus is a two step process. Firstly the outer membrane is removed as the particle enters the cell; secondly the virus particle (without the outer membrane) is uncoated further to release the core into the cytoplasm. The pox viral genes are expressed in

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two phases. The early genes are expressed first. These genes encode the non-structural protein, including proteins necessary for replication of the viral genome, and are expressed before the genome is replicated. The late genes are expressed after the genome has been replicated and encode the structural proteins to make the virus particle. The assembly of the virus particle occurs in the cytoskeleton of the cell and is a complex process that is poorly understood but is currently being researched. The replication of poxvirus is unusual for a virus with double-stranded DNA genome (dsDNA) because it occurs in the cytoplasm[4] Poxvirus encodes its own machinery for genome transcription, a DNA dependent RNA polymerase,[5] which makes replication in the cytoplasm possible. Taxonomy The name of the family, Poxviridae, is a legacy of the original grouping of viruses associated with diseases that produced poxes in the skin. Modern viral classification is based on phenotypic characteristics; morphology, nucleic acid type, mode of replication, host organisms, and the type of disease they cause. The smallpox virus remains as the most notable member of the family.

71) Human Herpesviruses Human Herpesvirus Six (HHV-6) is one of the eight known viruses that are members of the human herpesvirus family. It causes the disease exanthem subitum (Roseola), a nearuniversal childhood disease. After primary infection, latency is established in myeloid and bone marrow progenitors and exists for the life time of the host. The virus periodically re-activates from this latent state, with HHV-6 DNA being detectable in 20-25% of healthy adults in the United States. In the immunocompetent setting, these re-activations are often asymptomatic, but in immunosuppressed individuals there can be serious complications. HHV-6 re-activation causes severe disease in transplant recipients and can lead to graft rejection, often in consort with other betaherpesviridae. Likewise in HIV/AIDS, HHV-6 reactivations cause disseminated infections leading to end organ disease and death. Although up to 100% of the population are exposed (seropositive) to HHV-6, most by 3 years of age, there are rare cases of primary infections in adults. In the United States, these have been linked more with HHV-6A, which is thought to be more pathogenic and more neurotropic and has been linked to several central nervous system-related disorders. 72) Adenoviruses Adenoviruses are medium-sized (90.100 nm), nonenveloped (naked) icosahedral viruses composed of a nucleocapsid and a double-stranded linear DNA genome. There are 55 described serotypes in humans, which are responsible for 5.10% of upper respiratory infections in children, and many infections in adults as well. Viruses of the family Adenoviridae infect various species of vertebrates, including humans.

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Adenoviruses were first isolated in human adenoids, from which the name is derived, and are C Virology Classification This family contains the following genera: . Genus Atadenovirus; type species: Ovine adenovirus D . Genus Aviadenovirus; type species: Fowl adenovirus A . Genus Ichtadenovirus; type species: Sturgeon adenovirus A . Genus Mastadenovirus; type species: Human adenovirus C; others include AD-36 . Genus Siadenovirus; type species: Frog adenovirus Structure: yap Adenoviruses represent the largest nonenveloped viruses. Because of their large size, they are able to be transported through the endosome (i.e. envelope fusion is not necessary). The virion also has a unique "spike" or fiber associated with each penton base of the capsid (see picture below) that aids in attachment to the host cell via the coxsackie-adenovirus receptor on the surface of the host cell. In 2010 scientists announced that they had solved the structure of the human adenovirus at the atomic level, making the largest high resolution model ever. The virus is composed of around 1 million amino acid residues and weighs around 150 MDa.[2][3] Schematic diagram of the linear adenovirus genome, showing Early genes (E) and Late genes (L). The adenovirus genome is linear, non-segmented double stranded (ds) DNA which is between 26 and 45 Kbp. This allows the virus to theoretically carry 22 to 40 genes. Although this is significantly larger than other viruses in its Baltimore group it is still a very simple virus and is heavily reliant on the host cell for survival and replication. An interesting feature of this viral genome is that it has a terminal 55 kDa protein associated with each of the 5' ends of the linear dsDNA, these are used as primers in viral replication and ensure that the ends of the virus' linear genome are adequately replicated.

73-) Retroviruses The genome of retroviruses consists of RNA not DNA. HIV-1 and HIV-2, the agents that cause AIDS, are retroviruses.
In February 1997 it was reported that pig cells contain a retrovirus capable of infecting human cells (at least, in vitro). This is troublesome because of the efforts that are being made to transplant pig tissue into humans (e.g., fetal pig cells into the brains of patients with Parkinson's disease). Transplant recipients must have their immune systems suppressed if the transplant is to avoid rejection. Could immunosuppressed patients be at risk from the retroviruses present in the transplanted cells? The probability that the original hosts for HIV-1 and HIV-2 were some other primate suggests that retroviruses can move from one species to another. A typical, "minimal" retrovirus consists of:

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an outer envelope which was derived from the plasma membrane of its host many copies of an envelope protein embedded in the lipid bilayer of its envelope a capsid; a protein shell containing two molecules of RNA and molecules of the enzyme reverse transcriptase

Reverse transcriptase is a DNA polymerase that uses RNA as its template. Thus it is able to make genetic information flow in the reverse (RNA ->DNA) of its normal direction (DNA -> RNA). Infection of a host cell requires that the cell have a surface protein that can serve as a receptor for the envelope protein of the retrovirus. The envelope protein of HIV-1 binds to

CD4 molecules. It is this property that enables the virus to invade CD4+ T cells (and certain other cells that express CD4). CCR5 (CC chemokine Receptor 5) found on Th1 cells and macrophages.

All the proteins in the virus particle are encoded by its own genes. When a retrovirus infects a cell

its molecules of reverse transcriptase are carried into the cell attached to the viral RNA molecules. The reverse transcriptase synthesizes DNA copies of the RNA. These enter the nucleus and are inserted into the DNA of the host. These inserts are transcribed by the host's enzymes into fresh RNA molecules which re-enter the cytosol where o some are translated by host ribosomes the gag gene is translated into molecules of the capsid protein
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the pol gene is transcribed into molecules of reverse transcriptase the env gene is translated into molecules of the envelope protein other RNA molecules become incorporated into fresh virus particles

74-) Adenovirus What is adenovirus infection? Adenoviruses are a family of viruses. Infections from these viruses can cause illness in people and animals What are the signs and symptoms of adenovirus infection? Adenovirus often infects the airways this can appear as a cold (e.g., sore throat, sneezing, runny nose, cough, headache, chills), croup, or bronchitis. Illness usually lasts three to five days, but serious infections can last weeks. Complications can include middle ear infections, pneumonia, or meningitis. Some types of adenovirus cause other illnesses, such as skin rash, conjunctivitis (pink-eye,) bladder infections, or bowel infections (e.g., diarrhea). Who can get infected with adenovirus? Anyone can be infected by adenovirus. Most infections are mild. Serious illness can occur in young children, the elderly, or those with weak immune systems. Outbreaks can occur where people are in close quarters. How soon after exposure do symptoms appear? For airway infections, symptoms may develop 2 to 14 days after exposure to the virus. For intestinal tract infections, symptoms may develop 3 to 10 days after exposure to the virus. How is adenovirus spread? Adenovirus spreads very easily and can survive for a long time on objects. The virus may be spread through contact with droplets from the nose and throat of an infected person (e.g., during coughing or sneezing). Infection can occur while eating or touching the eyes, nose, or mouth if hands are contaminated with virus and not washed well. Infected persons may spread the virus if they do not wash their hands well and then they handle food that other people eat. Drinking from contaminated water sources (e.g., poorly maintained swimming pools) may also lead to infection. About Adenovirus Infections
Adenoviruses a group of viruses that infect the membranes (tissue linings) of the respiratory tract, the eyes, the intestines, and the urinary tract account for about 10% of acute respiratory infections in kids and are a frequent cause of diarrhea.

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Adenoviral infections affect infants and young children much more frequently than adults. Childcare centers and schools sometimes experience multiple cases of respiratory infections and diarrhea that are caused by adenovirus. Although these infections can occur at any time of the year, respiratory tract disease caused by adenovirus is more common in late winter, spring, and early summer. However, conjunctivitis and pharyngoconjunctival fever caused by adenovirus tend to affect older kids mostly in the summer. The majority of the population will have experienced at least one adenoviral infection by age 10. Although adenoviral infection in kids can occur at any age, most take place in the first years of life. Since there are many different types of adenovirus, repeated adenoviral infections can occur.

75) Hepatitis Viruses A retrovirus is an RNA virus that is replicated in a host cell via the enzyme reverse transcriptase to produce DNA from its RNA genome. The DNA is then incorporated into the host's genome by an integrase enzyme. The virus thereafter replicates as part of the host cell's DNA. Retroviruses are enveloped viruses that belong to the viral family Retroviridae. A special variant of retroviri are endogenous retroviri which are integrated into the genome of the host and inherited across generations. The virus itself stores its nucleic acid in the form of a +mRNA (including the 5'cap and 3'PolyA inside the virion) genome and serves as a means of delivery of that genome into cells it targets as an obligate parasite, and constitutes the infection. Once in the host's cell, the RNA strands undergo reverse transcription in the cytoplasm and are integrated into the host's genome, at which point the retroviral DNA is referred to as a provirus. It is difficult to detect the virus until it has infected the host. Simply, DNA is usually transcribed into RNA, and RNA is translated into protein. However, retroviruses function differently - their RNA is reverse-transcribed into DNA, which is integrated into the host cell's genome (when it becomes a provirus), and then undergoes the usual transcription and translational processes to express the genes carried by the virus. Therefore, the order of steps from a retroviral Structure Virions of retroviruses consist of enveloped particles about 100 nm in diameter. The virions also contain two identical single-stranded RNA molecules 7-10 kilobases (kb) in length. Although virions of different retroviruses do not have the same morphology or biology, all the 62

virion components are very similar.[1] The main virion components are: . Envelope: composed of a protein capsid, which is obtained from the host plasma membrane during budding process. . RNA: consists of a dimer RNA. It has a cap at 5' end and polyadenyle at 3' end. The RNA genome also has terminal noncoding regions, which are important in replication, and internal regions that encode virion proteins for gene expression. The 5' end includes four regions, which are R, U5, PBS, and L. R region is a short repeated sequence at each end of the genome during the reverse transcription in order to ensure correct end-to-end transfer in growing chain. U5, on the other hand, is a short unique sequence between R and PBS. PBS (primer binding site) consists of 18 bases complementary to 3' end of tRNA primer. L region is an untranslated leader region that gives signal for packaging of genome RNA. The 3' end includes 3 regions, which are PPT (polypurine tract), U3, and R. PPT is primer for plus-strand DNA synthesis during reverse transcription. U3 is a sequence between PPT and R, which has signal that provirus can use in transcription. R is the terminal repeated sequence at 3' end. . Proteins: consisted of gag proteins, protease (PR), pol proteins and env proteins. Gag proteins are major components of the viral capsid, which are about 2000-4000 copies per virion. Protease is expressed differently in different viruses. It functions in proteolytic cleavages during virion maturation to make mature gag and pol proteins. Pol proteins are responsible for synthesis of viral DNA and integration into host DNA

76) Laboratory Diagnosis of Fungal Diseases Several diseases of the liver, collectively known as hepatitis, are caused by viruses. The viruses involved, five of which have been reasonably well characterized, come from a wide range of virus families. Hepatitis A virus is a picornavirus, a small single strand RNA virus; hepatitis B virus belongs to the hepadnavirus family of double stranded DNA viruses; hepatitis C virus is a flavivirus, a single stand RNA virus; hepatitis E, also an RNA virus, is similar to a calicivirus. Hepatitis D which is also known as Delta agent is a circular RNA that is more similar to a plant a viroid than a complete virus. For a summary of the hepatitis viruses, see Table1. HEPATITIS A VIRUS This picornavirus (figure 1) is the causative agent of infectious hepatitis. Picornaviruses have a single strand, 3 f-polyadenylated, positive sense RNA genome surrounded by a naked (unenveloped) icosahedral capsid that is around 28 nm in diameter (figure 2). At the 5 f end of the RNA strand is a viral protein called VPg. There is only one serotype of HAV. Replication The virus binds to a receptor that is found on the surface of hepatocytes and a few other cells. HAV cellular receptor 1 (havcr-1) has an ectodomain that contains an N-terminal cysteine-rich immunoglobulin-like region, followed by a mucin-like region that extends the immunoglobulinlike

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region well above the cell surface. The immunoglobulin-like region is required for binding of HAV. The virus spends its entire life in the cytoplasm where it replicates using a virus-encoded RNA-dependent RNA polymerase. For further information on picornavirus replication see 78) Fungi, Etiological Agents of Opportunistic Mycoses Candida, Aspergillus, Zygomicetes
(Rhizopus, Absidia), Pneumocistis carinii

. Mycosis (pl., mycoses) - an infection caused by a fungus . Two broad categories of mycoses . Nosocomial (hospital acquired) . Community acquired . Nosocomial infections are considered opportunistic in origin . Community-acquired infections can be opportunistic, but also include endemic mycoses . Over the past 20 years, both nosocomial and community-acquired mycoses have increased dramatically . Excluding HIV/AIDS patients, mycoses are the 7th most common cause of infectious disease . Contributing factors to increased mycoses: . Growing population of immune compromised individuals . Mobile population/immigration . More older adults with chronic medical conditions . Aggressive medical therapies . Surgery . Antibiotics . Chemotherapies/Organ transplants .. Fungemia patients were more likely to die than those bloodstream infections by other types of microbes . Independent risk factors for fungemia (i.e., those determined to enhance infection alone) . Number and duration of antimicrobial agents . Chemotherapy . Previous colonization . Indwelling catheter . Neutropenia . Hemodialysis . Organ transplant patients experience the highest risk of fungal infection . Rates of fungal infection by type of transplant . Renal, <5% . Bone marrow, 2-30% . Heart, 10-35% . Liver, 28-42% . If different, probably reflect different sources or modes of infection . If same, infection is assumed to be cross-contamination from one patient to another, or from a common source . Typing methods can also help distinguish between a relapse of infection or the acquisition of an new one . Epidemiology data can also be used to help develop strategies of prevention and control which must consider if the origin of infection is

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. Endogenous - mainly yeast infections, particular Candida and Candida-like species . Exogenous - mainly mold species, but also yeasts from contaminated sources . Etiological agents of community-acquired fungal infections include . Endemic dimorphic fungi . Blastomyces dermatitidis . Coccidioides immitis and C. posadasii . Histoplasma capsulatum var. capsulatum and H. capsulatum var. dubosii . Paracoccidioides brasiliensis . Penicillium marneffei . Opportunistic pathogens 77) Fungi, Etiological Agents of Systemic Mycoses Criptococcus neoformans, Histoplasma
capsulatum, Blastomyces dermatitidis

Cryptococcus neoformans is composed of two varieties (v.): C. neoformans v. neoformans and v. grubii. A third variety, C. neoformans v. gattii, is now considered a distinct species, Cryptococcus gattii. C. neoformans v. grubii and v. neoformans have a worldwide distribution and are often found in soil which has been contaminated by bird excrement. The genome sequence of C. neoformans v. neoformans was published in 2005.[1] Recent studies suggest that colonies of Cryptococcus neoformans and related fungi growing on the ruins of the melted down reactor of the Chernobyl Nuclear Power Plant may be able to utilize the energy of radiation (primary beta radiation) for "radiotrophic" growth.[2] Characteristics Cryptococcus neoformans grows as a yeast (unicellular) and replicates by budding. C. neoformans does not exist in a hypae or pseudohyphae form. The only notable morphological change occurs as it develops a capsule at 37 C.[3] When grown as a yeast, C. neoformans has a prominent capsule composed mostly of polysaccharides. Microscopically, the India ink stain is used for easy visualization of the capsule. The particles of ink pigment do not enter the capsule that surrounds the spherical yeast cell, resulting in a zone of clearance or "halo" around the cells. This allows for quick and easy identification of C. neoformans. Cryptococcus neoformans seen in the lung of a patient with AIDS. The inner capsule of the organism stains red in this photomicrograph Pathology Infection with C. neoformans is termed cryptococcosis. Most infections with C. neoformans consist of a lung infection.[citation needed] However, fungal meningitis, especially as a secondary infection for AIDS patients, is often caused by C. neoformans making it a particularly dangerous fungus. Infections with this fungus are rare in those with fully functioning immune systems.[citation needed] For this reason, C. neoformans is sometimes referred to as an opportunistic fungus. Histoplasma is a genus of dimorphic fungi commonly found in bird and bat fecal material.[1] Histoplasma contains a few species, including.H. capsulatum.the causative agent of histoplasmosis;[2] and Histoplasma capsulatum var. farciminosum (old term, Histoplasma farciminosum), causing epizootic lymphangitis in horses.[3] Histoplasma capsulatum is most prevalent in the Ohio and Mississippi river valleys. It was discovered by Samuel Taylor Darling in 1906. Blastomyces is a fungal genus responsible for the medical condition blastomycosis. The most well known species of the genus is Blastomyces dermatitidis. B. dermatitidis is a dimorphic fungal pathogen, found primarily in the Mid-West and Northern United States and

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Canada. It exists in the soil in a filamentous form that produces spores directly upon the wall of the hyphae, lacking any kind of fruiting body to aid in aerosolization/dissemination of the spores. The natural reservoir of this organism in the environment is not clearly defined, but it seems to be associated with rivers and lakes. Blastomyces is endemic to the Mississippi and Ohio river valleys and the vicinity of the Great Lakes. Outbreaks of blastomycosis are often associated with disruptions of the soil that might lead to the artificial elevation of spore and/or hyphal fragments in the air. These agents infect human and animal hosts when they are inhaled. At the elevated temperature of 37 C in a host, the fungus undergoes a phase transition to the pathogenic yeast form. Yeast form cells multiply in the lung and may cause 78-)Fungi, Etiological Agents of Opportunistic Mycoses Candida, Aspergillus, Zygomicetes
(Rhizopus, Absidia), Pneumocistis carinii

Candida is a genus of yeasts. Many species of this genus are endosymbionts of animal hosts including humans. While usually living as commensals, some Candida species have the potential to cause disease. Clinically, the most significant member of the genus is Candida albicans, which can cause infections (called candidiasis or thrush) in humans and other animals, especially in immunocompromised patients. Many Candida species are members of gut flora in animals, including C. albicans in mammalian hosts, whereas others live as endosymbionts in insect hosts. The last decade has seen the sustained medical importance of opportunistic infections due to the worldwide increase in the number of immunocompromised patients, who are highly susceptible to opportunistic infections.Meanwhile, the genome sequences of several Candida species have been completed, enabling the detailed investigation of some aspects of their biology with the aid of post-genomic approaches. The basic knowledge gained from these investigations of pathogenic Candida, and related yeasts, can translate into innovations in the development of novel antifungal therapies, original approaches for targeted immuno-interventions, or highly sensitive diagnosis of fungal infections. The rise of yeast infections also parallels the rise in the use of antibiotics. Antibiotics are known to promote GI candida overgrowth, and even penetration of the GI mucosa. Some practitioners of alternative medicine have claimed that Candida overgrowth can cause various health problems, from fatigue to weight gain, but this is rejected by many doctors and there is little evidence to support the hypothesis. Candida antarctica is a source of industrially important lipases. Aspergillus (IPA: .asp..d..l.s) is a genus consisting of several hundred mold species found in various climates worldwide. Aspergillus was first catalogued in 1729 by the Italian priest and biologist Pier Antonio Micheli. Viewing the fungi under a microscope, Micheli was reminded of the shape of an aspergillum (holy water sprinkler), from Latin spargere (to sprinkle), and named the genus accordingly.Today "aspergillum" is also the name of an asexual spore-forming structure common to all Aspergilli; around one-third of species are also known to have a sexual stage. Zygomycota, or zygote fungi, is a phylum of fungi. The name comes from zygosporangia, where resistant spherical spores are formed during sexual reproduction. Approximately 1060 species are known. They are mostly terrestrial in habitat, living in soil or on decaying plant or animal material. Some are parasites of plants, insects, and small animals, while others form symbiotic relationships with plants. Zygomycete hyphae may be coenocytic, forming septa only where gametes are formed or to wall off dead hyphae
79-)Microbiological aspects of Skin, Wound, Joint and Bone Infections
Chapter 100Bone, Joint, and Necrotizing Soft Tissue Infections

Necrotizing Soft Tissue Infections 66

Etiology Anaerobic microorganisms such as Bacteroides species, Peptostreptococcus species, and Clostridiumspecies are largely responsible for these infections. Mixed infections by aerobic and facultative anaerobic organisms are common. Pathogenesis Susceptible persons have experienced trauma or surgery and frequently have diabetes and/or vascular insufficiency. Organisms gain entry via direct inoculation. Local hypoxia and decreased oxygen-reduction potentials favor anaerobic growth. Clinical Manifestations This signs of disease include production of tissue gas, a putrid discharge, tissue necrosis, fever, (occasionally) systemic toxicity, and absence of classic signs of inflammation. Microbiologic Diagnosis These infections are usually diagnosed by clinical presentation. Aerobic and anaerobic wound cultures help identify the major pathogens. Prevention and Treatment Immediate surgical debridement of all necrotic tissue is vital. High-dose parenteral antibiotic therapy should be started immediately. Hyperbaric oxygen therapy may be indicated. Joint Infections Etiology Neisseria gonorrhoeae and S taphylococcus aureus are responsible for most cases of bacterial arthritis. Pathogenesis Joint infections are usually a result of hematogenous spread, but may also arise from traumatic inoculation or by extension from an adjacent focus of infection. Proteolytic enzymes of polymorphonuclear leukocytes, bacterial toxins, and pressure from joint swelling all contribute to the damage of articular surfaces. Clinical Manifestations Joint swelling. pain, warmth (inflammation), decreased range of motion, and fever are the classic symptoms. Disseminated gonococcal infections may also cause migratory polyarthritis, dermatitis, and tenosynovitis. Microbiologic Diagnosis Aspiration and culture of synovial fluid usually provides the definite diagnosis. Prevention and Treatment Gonococcal arthritis may be prevented by techniques used to decrease the risk for sexually transmitted disease. The treatment for all septic arthritides is administration of parenteral antibiotics. Some cases may require aspiration and/or surgical debridement. Bone Infections Etiology Staphylococcus aureus is the most commonly isolated pathogen. Polymicrobic infections are frequent in contiguous-focus osteomyelitis. Pathogenesis Organisms may reach the bones by hematogenous spread, by direct extension from a contiguous focus of infection, or as a result of trauma. A cycle of increased pressure from infection, inflammation, local ischemia, and bone necrosis may establish itself and lead to a chronic infection. Clinical Manifestations Hematogenous osteomyelitis classically presents with high fever and pain around the involved bone. Sinus tracts with purulent drainage are evidence of chronic osteomyelitis. Microbiologic Diagnosis

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Bone biopsy and/or debridement cultures are mandatory with rare exceptions. Sinus tract cultures are unreliable. Prevention and Treatment Treatment consists of surgical debridement and long-term, culture-directed antimicrobial therapy. Hematogenous osteomyelitis in children may be treated with antibiotics alone

80-)Microbiological aspects of the Urinary Tract Infections


Current microbiological and clinical aspects of urinary tract infections

Abstract
OBJECTIVES: To evaluate some risk factors which could affect the isolation rates of various uropathogens and their in vitro susceptibility to antibiotics in ambulatory and hospitalized patients. PATIENTS AND METHODS: A prospective study was conducted in a microbiological laboratory at Pisa Hospital. Nine-hundred and seventy-two consecutive patients with documented urinary tract infection were enrolled from April 1996 to October 1999. Data on age, sex, current or previous bladder catheterization, some underlying diseases as diabetes mellitus, and previous antibiotic therapy were recorded. The distribution of bacteria isolates and their in vitro susceptibility to antibiotics was evaluated. RESULTS: Escherichia coli was responsible for 54.7% of urinary tract infections. Isolation of E. coli is decreasing in comparison to previous observations, especially in males and in patients with indwelling bladder catheters who instead show higher Pseudomonas spp. and Enterococcus spp. isolation rates than females and non-catheterized patients. Diabetes mellitus does not affect the isolation rate of uropathogens and their patterns of susceptibility. Multivariate analysis of multiresistant uropathogens showed a positive significant correlation with indewelling bladder catheter and age. An upward trend in the resistance of E. coli to cotrimoxazole, ampicillin and fluoroquinolones was observed from 1996 to 1999; more than 50% of Pseudomonas spp. strains were resistant to fluoroquinolones and gentamicin.

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CONCLUSIONS: The empirical antibiotic therapy of patients with urinary tract infection should be guided by an accurate anamnesis evaluating not only age and sex but also the presence of a bladder catheter at the moment of urine collection or a history of recent bladder catheterization and previous courses of antimicrobial drugs.

81) Microbiological aspects of Skin, Wound, Joint and Bone Infections The skin is the largest organ in the human body. It is the front line of defense against many types of pathogens, and remains disease-free over most of its area most of the time. However, breaks in the skin are particularly prone to invasion by microorganisms, and skin infections are a relatively common complaint. Skin infections may be bacterial, viral or fungal in nature. Among the more common bacterial skin infections is impetigo, a usually mild condition caused by staphylococcal or streptococcal bacteria. It causes small skin lesions and typically spreads among schoolchildren. Folliculitis results in pustules at the base of hairs or, in more serious cases, in painful boils. Often it is caused by Staphylococcus species. Among the more serious bacterial infections of the skin is cellulitis, a deep infection involving subcutaneous areas and the lymphatic circulation in the region as well as the skin itself. The affected area is painful, red, and warm to the touch, and the patient may be feverish. Viral skin infections typically show up as warts caused by the Human Papillomavirus (HPV). Common warts usually appear on the extremities, especially in children and adolescents. Plantar warts often grow on the heel or sole of the foot, surrounded by overgrown, calloused skin. When they develop on weight-bearing surfaces such as the heel, plantar warts may become painful. HPV also causes genital warts, or condylomata, which may increase the risk for cervical or penile cancer. Skin infections caused by fungi, including yeast, are called dermatomycoses. A common subcategory consists of the dermatophytoses, caused by Trichophyton species. These infections include tinea capitis ("cradle cap"), tinea corporis ("ringworm"), tinea cruris ("jock itch"), and tinea pedis ("athlete's foot"). Candida, which often affects the mucous membranes, may also be responsible for skin infections. Obese patients are prone to fungal infections in skin folds, as are uncircumcised men. Candida is also involved in some cases of diaper rash. Fungal infections are typically treated wit Causes The bacteria or other microorganisms that cause osteomyelitis can enter the bone through an injury, or can be carried through the bloodstream to the bones from another infection in the body. Although bones are usually well-protected against infection, they can become infected in several ways. Bacteria can enter the bone through an open fracture, penetration by a sharp, contaminated object (such as a nail that pierces through a shoe), orthopedic surgery, or a human bite. Wound infection due to disturbed coagulopathy. This patient has a pacemaker (visible below right clavicular space) and had previous cardiac surgery (median sternotomy wound visible) for a rheumatic mitral valve disorder, Pathophysiology Wound healing is a continuum of complex interrelated biological processes at the molecular level. Healing is divided into the following phases for descriptive purposes: inflammatory phase, proliferative phase, and maturation phase. Causes

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All surgical wounds are contaminated by microbes, but in most cases, infection does not develop because innate host defenses are quite efficient in the elimination of contaminants. A complex interplay between host, microbial, and surgical factors ultimately determines the prevention or 82) Microbiological aspects of the Urinary Tract Infections Urinary tract infection part of the urinary tract. Symptoms include frequent feeling and/or need to urinate, pain during urination, and cloudy urine.[1] The main causal agent is Escherichia coli. Although urine contains a variety of fluids, salts, and waste products, it does not usually have bacteria in it. When bacteria get into the bladder or kidney and multiply in the urine, they may cause a UTI. The most common type of UTI is acute cystitis often referred to as a bladder infection. An infection of the upper urinary tract or kidney is known as pyelonephritis, and is potentially more serious. Although they cause discomfort, urinary tract infections can usually be easily treated with a short course of antibiotics with all no significant difference between the classes of antibiotics commonly used. Signs and symptoms : Belirti ve semptomlar The most common symptoms of a bladder infection are burning with urination (dysuria), frequency of urination, an urge to urinate, no vaginal discharge, and no significant pain.[4] An upper urinary tract infection or pyelonephritis may also present with flank pain and a fever. Healthy women have an average of 5 days of symptoms.[4] The symptoms of urinary tract infections may vary with age and the part of the urinary system that was affected. In young children, urinary tract infection symptoms may include diarrhea, loss of appetite, nausea and vomiting, fever, and excessive crying that cannot be resolved by typical measures.[5] Older children on the other hand may experience abdominal pain, or incontinence. Lower urinary tract infections in adults may manifest with symptoms including hematuria ( Depending on the site of infection, urinary tract infections may cause different symptoms. Urethritis, meaning only the urethra has been affected, does not usually cause any other symptoms besides dysuria. Whereas in newborns the condition may cause jaundice and hypothermia, in the elderly, symptoms of urinary tract infections may include lethargy and a change in the mental status, signs that are otherwise nonspecific. Risk factors In young sexually active women, sex is the cause of 75.90% of bladder infections, with the risk of infection related to the frequency of sex.[4] Women are more prone to UTIs than men because, in females, the urethra is much closer to the anus than in males, and women lack the bacteriostatic properties of prostatic secretions. UTIs also more commonly progress to bladder infections in females due to the much shorter length of the female urethra.[8] Pathogenesis The bladder wall is coated with various mannosylated proteins, such as Tamm-Horsfall proteins (THP), which interfere with the binding of bacteria to the uroepithelium. As binding is an important factor in establishing pathogenicity for these organisms, its disruption results in reduced capacity for invasion of the tissues.[clarification needed] 83) Microbiological aspects of the Respiratory Tract Infections Upper respiratory tract infection

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Upper respiratory tract infections (URI or URTI) are the illnesses caused by an acute infection which involves the upper respiratory tract: nose, sinuses, pharynx or larynx. This commonly includes: tonsillitis, pharyngitis, laryngitis, sinusitis, otitis media, and the common cold. Definitions: Tanmlar Common URI terms are defined as follows: . Rhinitis - Inflammation of the nasal mucosa . Rhinosinusitis or sinusitis - Inflammation of the nares and paranasal sinuses, including frontal, ethmoid, maxillary, and sphenoid . Nasopharyngitis (rhinopharyngitis or the common cold) - Inflammation of the nares, pharynx,hypopharynx, uvula, and tonsils . Pharyngitis - Inflammation of the pharynx, hypopharynx, uvula, and tonsils . Epiglottitis (supraglottitis) - Inflammation of the superior portion of the larynx and supraglottic area . Laryngitis - Inflammation of the larynx . Laryngotracheitis - Inflammation of the larynx, trachea, and subglottic area . Tracheitis - Inflammation of the trachea and subglottic area Signs and symptoms : Belirti ve semptomlar Acute upper respiratory tract infections include rhinitis, pharyngitis/tonsillitis and laryngitis often referred to as a common cold, and their complications: sinusitis, ear infection and sometimes bronchitis (though bronchi are generally classified as part of the lower respiratory tract.) Symptoms of URI's commonly include cough, sore throat, runny nose, nasal congestion, headache, low grade fever, facial pressure and sneezing. Onset of the symptoms usually begins 1.3 days after the exposure to a microbial pathogen. The illness usually lasts 7.10 days. Group A beta hemolytic streptococcal pharyngitis/tonsillitis(strep throat) typically presents with a sudden onset of sore throat, pain with swallowing and fever. Strep throat does not usually cause runny nose, voice changes or cough. Pain and pressure of the ear caused by a middle ear infection (Otitis media) and the reddening of the eye caused by viral Conjunctivitis are often associated with upper respiratory infections. Lower respiratory tract is the part of the respiratory tract below the vocal cords. While often used as a synonym for pneumonia, the rubric of lower respiratory tract infection can also be applied to other types of infection including lung abscess and acute bronchitis. Symptoms include shortness of breath, weakness, high fever, coughing and fatigue. Lower respiratory tract infections place a considerable strain on the health budget and are generally more serious than upper respiratory infections. Since 1993 there has been a slight reduction in the total number of deaths from lower respiratory tract infection. However in 2002 they were still the leading cause of deaths among all infectious diseases, and they accounted for 3.9 million deaths worldwide and 6.9% of all deaths that year. declining. It has also become apparent the importance of atypical pathogens such as C. pneumoniae, M. pneumoniae and L. pneumophila, in CAP. 84) Infections of the Central Nervous System Headache Headache is the most common complaint of patients in a general neurology practice. The large majority of headaches are not life-threatening, and are due to migraine, tension, or chronic daily headaches. A small number have serious underlying causes: space-occupying intracranial lesions such as neoplasm or abscess, subarachnoid hemorrhage, hydrocephalus, meningitis, or encephalitis.

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Headache symptoms Migraine headache is the most common type of headache for which patients seek medical treatment.Diagnosis is purely clinical--there is no laboratory test. Migraine headache is more common in women than in men, and there is often a family history of migraine. The essential symptoms of migraine headache are severe, throbbing headache with nausea. Other common symptoms include unilateral headache, photophobia, and phonophobia. The patient usually wants to lie down in a dark room, and if she can go to sleep, feels better on awakening. In migraine with aura the headache is preceded by visual symptoms. This may be as nondescript as vague black spots, or as dramatic as "scintillating scotoma" or "fortification spectra"--brightly colored images with jagged lines. When clearly present, visual symptoms are invaluable for diagnosing migraine. Cluster headache is less common. The pain is nonthrobbing, unilateral, and retroorbital. An individual headache is brief, but recurs frequently, and the pain is said to be the most intense of all headache pain. Tension headache is very common, but not usually a cause for visits to the doctor's office. The pain is moderate, usually non-throbbing, and tends to be localized to the neck, occiput, and temples. Impaired consciousness Sudden onset of impaired or loss of consciousness has two main causes: syncope and seizure. Syncope due to fall in blood pressure is most common. It may be preceded by a feeling of lightheadedness, as in orthostatic hypotension, vasovagal syncope, or vasodepressor syncope, or there may be no warning at all, as in sudden ventricular fibrillation. Seizure is also common. A generalized tonic-clonic convulsion is usually easy to diagnose from the history. A complex partial seizure is more difficult to diagnose. There often is a sudden alteration of consciousness, unresponsiveness, often with purposeless repetitive behaviors, followed by postictal confusion. 1. Bulging fontanelle (infants) 2. Large head (infants) 3. Nausea Edema of the optic nerve head in papilledema is caused by disruption of fast axoplasmic transport. Axonal material "piles up" at the optic nerve head. It is thought that papilledema can become apparent within about six hours of an acute increase in ICP. Even when its appearance is dramatic, papilledema does not produce (initially) diminished vision. If increased ICP does cause diminished vision, the increase must have been severe and chronic, and a more likely ophthalmoscopic finding is optic atrophy due to degeneration of the nerve. In cases in which the optic nerve head is clearly swollen, and vision on the affected side is clearly diminished, a more likely condition is papillitis. This may be seen in acute optic neuritis, or in anterior ischemic optic neuropathy. In these conditions the papillitis is usually unilateral. B. Acute bacterial (septic) meningitis Signs and symptoms . Headache . Fever . Meningismus . Obtundation Early in the course of the illness, the patient with a purely meningeal infection will be awake, and painfully aware of his symptoms, so you may simply ask him about them. Later in the illness, if untreated, the meningeal inflammation will have led to diffuse brain dysfunction, ischemia or infarction, and the patient will be stuporous.

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Meningeal signs The stiff neck that occurs in meningitis is often striking--it is really stiff, almost boardlike, but not so painful as it is stiff. The stiffness is caused by reflex spasm of the neck muscles due to traction on inflamed cervical nerve roots. It is greatest with flexion, less with extension or rotation. Of course, a lot of older people have necks that are quite stiff due to osteoarthritis, and if they have a fever, this may occasionally lead to diagnostic concern for meningitis. Diagnosis 1. Suspicious clinical symptoms and signs. 2. CT of head to rule out abscess or other space-occupying lesion, if it can be done quickly. 3. Lumbar puncture (see below). 4. Blood cultures. Causes and therapy . S. pneumoniae . H. influenzae . L. monocytogenes . Group B streptococcus . N. meningitidis Streptococcus pneumoniae This organism is now the most common cause of bacterial meningitis in all age groups except newborns. It is a Gram-positive coccus that occurs in pairs (Click for micrograph [83k]). It has an external polysaccharide capsule that determines its serotype. Serotype is important for vaccine creation and epidemiology, but is not routinely performed on clinical isolates, and does not guide antibiotic therapy. For many years, S. pneumoniae was reliably sensitive to penicillin. Meningitis caused by these strains responds to meningitis doses of penicillin, ampicillin, cefotaxime, or ceftriaxone. Hemophilus influenzae H. influenzae is a small (1-2 micrometer diameter) Gram-negative coccobacillus (Click for micrograph [89k]). Strains causing meningitis in children almost all have an outer capsule, but non-meningitiscausing strains do not. The organism colonizes the upper respiratory tract of humans, who are its only natural host. Spread occurs through respiratory droplets or by direct contact with respiratory secretions. Treatment and prevention H. influenzae meningitis can be prevented by vaccination. Listeria monocytogenes Listeria monocytogenes is a facultatively anaerobic Gram-positive rod (Click for micrograph [137k]). The organism can be found in human feces, unpasteurized milk, cheeses, and other foods. Most cases are sporadic, and contaminated food is the source of infection. Treatment and prevention Listeria monocytogenes remains sensitive to penicillins, and ampicillin is the antibiotic of choice, but treatment must be prolonged--3 or 4 weeks. Trimethoprim-sulfamethoxasole is an alternative for the penicillin-allergic patient. Listeriosis results from food-borne transmission, so proper food handling measures markedly reduces infection risk. Neisseria meningitidis Neisseria meningitidis is an encapsulated Gram-negative organism that appears in pairs on Gram stain (Click for micrograph [80k]). It commonly colonizes the nasopharynx, and can

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spread rapidly from person to person through respiratory droplets. N. meningitidis often occurs in epidemics among persons living in close quarters like dormitories or barracks. The course of the illness is usually rapid and dramatic. A petechial rash on the trunk and lower body may coalesce into purpura, which is a sign of disseminated meningococcemia and disseminated intravascular coagulation. Distal extremity necrosis may also occur. C. Viral meningitis Signs and symptoms . Headache . Fever . Viral syndrome . Meningismus . This is the most common kind of meningitis, and the most benign. A systemic viral syndrome may be present, but fever and headache may suggest meningitis. Nuchal rigidity is usually present. It is highly unusual for focal neurologic signs to occur. Diagnosis Cerebrospinal fluid usually shows an "aseptic" picture--a lymphocytic pleocytosis with dozens to hundreds of WBCs, and normal glucose, protein and pressure. Viral culture may grow enterovirus, but is usually negative. D. Chronic meningitis Signs and symptoms . Headache . Fever . Meningismus . Confusion . Hydrocephalus. Causes There are a number of causes--bacterial, fungal, parasitic, and non-infectious. This is not a complete list, but includes organisms I have at least a little personal experience with: Mycobacterium tuberculosis M. tuberculosis is an acid-fast bacillus. It is passed between persons through respiratory droplets. Mycobacteria multiply in alveolar spaces or macrophages, and within 2 to 4 weeks hematogenous spread to extrapulmonary sites occurs. From there, tubercles develop, and if brain tubercles rupture into subarachnoid space, meningitis develops. Deeper tubercles become tuberculomas. Cerebrospinal fluid The CSF in tuberculous meningitis shows a lymphocytic pleocytosis with elevated protein and reduced glucose. Staining for mycobacteria is positive in 5 to 25%, and culture is positive in approximately 60% E. Encephalitis Symptoms and signs . Confusion . Personality change . Altered mental status . Fever . Seizures Brain Abscess Symptoms and signs 1. Headache 2. Focal neurologic deficits

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3. Fever, chills and other signs of infection usually do not occur 4. Papilledema (with increased ICP) 5. Nausea, vomiting (with increased ICP) 83) Microbiological aspects of the Intravascular infections, Bacteremia (Sepsis) and
Endotoxemia

of bacteria in the blood. The blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly with blood cultures) is always abnormal. Bacteria can enter the bloodstream as a severe complication of infections (like pneumonia or meningitis), during surgery (especially when involving mucous membranes such as the gastrointestinal tract), or due to catheters and other foreign bodies entering the arteries or veins (including intravenous drug abuse). Bacteremia can have several consequences. The immune response to the bacteria can cause sepsis and septic shock, which has a relatively high mortality rate. Bacteria can also use the blood to spread to other parts of the body (which is called hematogenous spread), causing infections away from the original site of infection. Examples include endocarditis or osteomyelitis. Treatment is with antibiotics,and prevention with antibiotic prophylaxis can be given in situations where problems are to be expected. Bacteremia is the presence of viable bacteria in the blood stream. Bacteremia is different from sepsis (so-called blood poisoning or toxemia), which is a condition where bacteremia is associated with an inflamma tory response from the body (causing systemic inflammatory response syndrome,characterised by rapid breathing, low blood pressure, fever, etc.). Common dental procedures, such as brushing teeth, are the most common cause of bacteremia, introducing a detectable amount of bacteria into the bloodstream, even if these rarely cause any clinical condition. Some patients with prosthetic heart valves however need antibiotic prophylaxis for dental surgery because bacteremia might lead to endocarditis (infection of the interior lining of the heart). Salmonella - which is assumed to only cause gastroenteritis in much of the middle-class or developed world - can cause a specific and virulent form of bacteremia in the developing world, especially in Africa. This form of bacteremia is particularly deadly to infants and people whose immune systems have been damaged by HIV, according to studies done by the Universities of Malawi and Liverpool at the Wellcome Trust Clinical Research Programme in Blantyre. Researchers announced in March 2008 in the Journal of Clinical Investigation that a study of 352 Malawian children had revealed antibodies against salmonella when the bacteria leaves the safety of the cells and moves into the bloodstream, and these antibodies may form the basis of an eventual vaccine. Causes : Nedenleri In the hospital, indwelling catheters are a frequent cause of bacteremia and subsequent nosocomial infections, because they provide a means by which bacteria normally found on the skin can enter the bloodstream. Other causes of bacteremia include dental procedures (occasionally including simple tooth brushing), herpes (including herpetic whitlow), urinary tract infections, peritonitis, Clostridium difficile colitis, intravenous drug use, and colorectal cancer. Bacteremia may also be seen in Endotoxins (not to be confused with enterotoxin) are toxins[1] associated with certain Gram-negative bacteria. An "endotoxin" is a toxin that is a structural molecule of the bacteria that is recognized by the immune system. The prototypical examples of endotoxin are lipopolysaccharide (LPS) or lipooligosaccharide (LOS), found in the outer membrane of various Gram-negative bacteria and are an important component of their ability to cause disease.[2] The term LPS is often used interchangeably with endotoxin, owing to its historical discovery. In the 1800s it became understood that bacteria could secrete toxins into their environment, which became broadly

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known as "exotoxin". The term "endotoxin" came from the discovery that portions of Gramnegative bacteria themselves can cause toxicity, hence the name endotoxin. Studies of endotoxin over the next 50 years revealed that the effects of "endotoxin" were, in fact, due to lipopolysaccharide. LPS consists of a polysaccharide (sugar) chain and a lipid moiety, known as lipid A, which is responsible for the toxic effects. The polysaccharide chain is highly variable amongst different bact Mechanism In humans, LPS binds to the lipid binding protein (LBP) in the serum which transfers it to CD14 on the cell membrane, which in turn transfers it to another non-anchored protein, MD2, which associates with Toll-like receptor-4 (TLR4). CD14 and TLR4 are present in several immune system cells (including macrophages and dendritic cells), triggering the signaling cascade for macrophage/endothelial cells to secrete pro-inflammatory cytokines and Nitric oxide that lead to "endotoxic shock".

86) Microbiological aspects of the Sexually Transmited Infections Sexually transmitted diseases Chlamydia Chlamydia is the most common and fastest-spreading sexually transmitted disease in the UK. It's caused by a bacterium, Chlamydia trachomatis. Unfortunately, many people (particularly females) have no symptoms at all. Where symptoms do occur, they may include pain in passing urine and a discharge. They usually appear approximately 7 to 21 days after infection. Chlamydia can also cause a form of conjunctivitis in adults. Also, this eye infection may occur in the newborn babies of mothers who have chlamydia. Gonorrhoea is caused by Neisseria gonorrhoeae, a bacterium that grows and multiplies quickly in moist, warm areas of the body . such as the cervix, urethra, mouth, or rectum. The cervix is the most common site of infection in women. However, the disease can also spread to the Fallopian tubes and other internal genital organs, causing such conditions as salpingitis and pelvic inflammatory disease. These may lead to to infertility. Gonorrhoea is most commonly spread during genital contact, but it can also be passed from the genitals of one partner to the throat of the other during oral sex. Gonorrhoea of the rectum can occur in people who practice anal sex. In pregnant women, gonorrhoea can be passed from an infected woman to her newborn infant during delivery. Genital herpes In 2009, over 30,000 new cases of gential herpes were seen at GUM clinics in Britain. In addition, it is

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believed that some thousands of other people developed herpes but were not seen at a clinic. Genital herpes is a highly contagious viral condition caused by the herpes simplex virus (HSV).It infects the skin and mucous membranes of the genitals or rectum, but it can also appear in areas such as the mouth, particularly the lips. Its chief symptom is an outbreak of small blisters, and these can be very HIV and AIDS HIV invades and destroys the immune system, which protects the body from infection. This means that a person who carries the HIV virus is prone to many different illnesses and may die from diseases that are harmless to healthy people. In some countries, particularly those located in Sub-Saharan Africa, the HIV rates are very high. For instance, in the Republic of South Africa it's estimated that about 11 per cent of the population is HIVpositive. Genital warts At the present time, British GUM clinics see about 91,000 new cases of genital warts a year. Many other people develop warts, but they are not seen at clinics. Many months can pass from the time of infection to the actual development of warts, so it may be very difficult to determine who you got them from. Trichomonas Trichomonas vaginalis (often known as 'TV') is a protozoan 'bug' that affects the vagina. Bacterial vaginosis BV is a common cause of vaginal discharge. The discharge is usually whitish or greyish or sometimes yellowish, and tends to have an off-putting efishy f odour. Unlike the discharges caused by thrush or trichomonas, it fs not usually associated with soreness, discomfort or itching.It's uncertain if BV is transmitted sexually, especially as there's no equivalent condition in males. Vaginal thrush (female

85) Microbiological aspects of Gastrointestinal Tract Infections The gastrointestinal tract contains a large number of bacteria of a wide variety. These range from organisms in the oral cavity to the organisms that form the bulk of faeces. The numbers and variety of bacteria in the mouth vary with food intake. Food provides an excellent substrate for bacterial growth. The bacterial flora of the mouth are notable for their role in the production of dental caries, resulting from the formation of acid as a byproduct of carbohydrate fermentation. Acid produced in this manner dissolves tooth enamel. There are a large number of bacteria in the oesophagus, but the stomach is relatively free of bacteria, because of the acidity of the gastric secretions. Organisms from the upper respiratory tract and mouth and those entrapped in food may survive if they are acid tolerant, and these constitute the stomach's transient flora. The anterior portion of the small intestine has very few bacteria associated with it, but numbers increase along its length and the distal portion has a rich microflora. Within the large bowel the numbers of bacteria reach 1013/g faeces, with a 10:1 to 100:1 predominance of anaerobes to aerobes. The main symptoms of gastrointestinal disease are vomiting and diarrhoea. These symptoms are non-specific and may have a cause unrelated to microorganisms. It is important, however, to exclude infection or intoxication before investigating diarrhoea further.

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