1

1. Important features Characteristic Cells Approximate diameter ( m)1 Nucleic Acid Type of nucleus Ribosomes Mitochondria Nature of outer surface Motility Method of replication Viruses No 0.02- 0.2 Either DNA or RNA None Absent Absent Protein capsid and lipoprotein envelope None Not binary fission

BASIC BACTERIOLOGY
A. Bacteria compared with other microorganisms

Bacteria Yes 1-5 Both DNA and RNA Prokaryotic 70S Absent Rigid wall containing peptidoglycan

Fungi Yes 3-10 (yeast)

Protozoa and Helminths Yes 15-25 (trophozoites)

Both DNA Both DNA and RNA and RNA Eukaryotic Eukaryotic 80S Present Rigid wall containing chitin 80S Present Flexible membrane Most Mitosis

Some None Binary fission Budding or mitosis

Eukaryotes and Prokaryotes Eukaryoticfungi and protozoa Prokaryoticbacteria Characteristics DNA within a nuclear membrane DNA associated with histones Mitotic division Chromosome number Membrane-bound organelles, such as mitochondria and lysozomes Size of ribosome Cell wall containing peptidoglycan Presence of sterols in cell membrane Prokaryotic bacterial cells No No No One No Eukaryotic Human cells Yes Yes Yes More than one Yes

70S Yes No

80S No Yes

Motility- most protozoa and some bacteria are motile, whereas fungi and viruses are non-motile.
-

the protozoa are heterogenous group that possess three different organs of locomotion: flagella, cilia, and pseudopods. The motile bacteria move only by means of flagella

STRUCTURE OF BACTERIAL CELLS

Classification: According to shape: Bacteria are classified by shape into 3 basic groups: cocci, bacilli and spirochetes 1. Cocci- round 2. Bacilli- rod-shaped 3. Spirochetes- spiral-shaped According to arrangement: 1. Cocci> pairsdiplococci Chainsstreptococci Grape-like clustersstaphylococci

Comparison of cell walls of gram (+) and gram (-) bacteria: COMPONENT GRAM (+) CELLS Thicker; multi layer Yes No GRAM (-) CELLS Thinner; single layer No Yes

Peptidoglycan Teichoic acid Lipopolysaccharide

Structure
Essential components Cell wall Peptidoglycan

Chemical composition
Sugar backbone with peptide side chains that are crosslinked Teichoic acid Lipid A Polysaccharide

Function
Gives rigid support, protects against osmotic pressure; is the site of action of penicillins and cephalosphorins and is degraded by lysozyme Major surface antigen but rarely used in laboratory diagnosis Toxic component of endotoxin Major surface antigen used frequently in laboratory diagnosis Site of oxidative and transport enzymes. Protein synthesis; site of action of aminoglycosides, erythromycin, tetracyclines and chloramphenicol Genetic material Participates in cell division and secretion Contains many hydrolytic enzymes, including lactamases Protects against phagocytosis Two types: (1) mediates attachment to cell surfaces (2) sex pilus mediates attachment of two bacteria during conjugation Motility Provides resistance to dehydration, heat, and chemicals Contains a variety of genes for antibiotic resistance and toxins Site of nutrients in cytoplasm Mediates adherence to surfaces

Surface fibers of gram(+) bacteria Outer membrane of gram(-) bacteria Cytoplasmic membrane Ribosome

Lipoprotein bilayer without sterols RNA and protein in 50S and 30S subunits DNA Invagination of plasma membrane Space between plasma membrane and outer membrane Polysaccharide Glycoprotein

Nucleoid Mesosome Periplasm Non-essential components Capsule Pilus or fimbriae

Flagellum Spore Plasmid Granule Glycocalyx

protein Keratin-like coat, dipicolinic acid DNA Glycogen, lipids, polphosphates Polysaccharide

3
GROWTH CYCLE

BACTERIAL GROWTH

Bacteria reproduce by binary fission, a process by which one parent cell divides to form two progeny cells. Bacteria are said to undergo exponential growth. No. of cells 1 2 4 8 16 32 64 128

Exponential 20 21 22 23 24 25 26 27 The doubling time or the generation time of bacteria ranges from as little as 20 minutes to more than 24 hrs. The short doubling time and the exponential growth of some organisms results in rapid production of very large number of bacteria. The doubling time varies not only with the species but also with the amount of nutrients, temperature, the pH and other environmental factors. THE GROWTH CURVE The growth cycle of bacteria has 4 phases. A curve could be plotted if a bacterial population has been determined and plotted. There are 4 phases of the cycle: 1. LAG PHASE - vigorous metabolic activity - period of cell adaptation and adjustment after metabolites are depleted. - cells do not divide - this can last for a few minutes up to many hours 2. LOG PHASE or Exponential Phase - rapid cell division occurs in this stage - cells are in a steady state - new cell materials are being synthesized - cell mass increases in number

- Beta-lactam drugs such as penicillin act during this phase because the drugs are effective when cells are making peptidoglycan ie. When they are dividing. 3. STATIONARY PHASE - slowing of growth - living cells equals dead cells - production of spores (sporulation) which are resistant to radiation because of the cystine-rich keratin-like spore coat. They resist also desiccation because of very low water content. Dipicolinic acid helps stabilize the nucleic acids. 4. DEATH PHASE OR PHASE OF DECLINE - final phase or phase of decline - marked by a decline of the number of viable bacteria - dead bacteria more than viable bacteria

AEROBIC AND ANAEROBIC GROWTH For most organisms, an adequate supply of oxygen enhances metabolism and growth. The oxygen acts as the hydrogen acceptor in the final steps of energy production catalyzed by the flavoproteins and cytochromes. Oxygen generates 2 toxic molecules, hydrogen peroxide (H2O2) and the free radical superoxide (O 2), bacteria requires 2 enzymes to utilize oxygen. Superoxide dismutase, which catalyzes the reaction: 2 O 2 + 2H+ H2O2 + O2 Catalase, which catalyzes: 2H2O2 2H2O + O2 One important criterion in classifying bacteria is its response to oxygen

- Obligate anaerobes > organism that cannot grow in the presence of oxygen > lacks either superoxide dismutase or catase or both. - Obligate aerobes > require the presence of oxygen for growth > the ATP generating system of these bacteria is dependent on oxygen as the hydrogen acceptor. - Facultative > can grow either in the presence or absence of oxygen. > they utilize oxygen to generate energy by respiration if it is present, but they can use the fermentation pathway to synthesize ATP in the absence of sufficient oxygen.

NORMAL FLORA

NORMAL OR INDIGENOUS FLORA - microorganisms that are frequently found in particular sites of the body in normal healthy individual. Types of organisms that interact with a host: 1. Parasite- lives at the expense of the host 2. Symbiont- benefits the host 3. Commensal- with neutral relationship to the host. a. Resident flora- consist of relatively fixed types of microorganisms regularly found in a given area at a given age. b. Transient flora- consist of non-pathogenic or potentially pathogenic microorganisms that inhabit the skin mucous membrane for hours, days or weeks. - establishes itself briefly for colonization or infection without disease but tend to be excluded by competition from residents or by hosts innate or immune defense mechanism. - derived from the environment. Origin of Normal Flora: 1. healthy fetus- sterile until birth membrane ruptures 2. during and after birth a. flora of the mothers genital tract b. skin and respiratory tract of those handling it c. environment NORMALLY STERILE IN HEALTH: - blood- occasionally, there is transient low level bacteremia due to physiologic trauma (e.g. streptococci) - body fluids- CSF etc. - tissues: urinary bladder, uterus, fallopian tubes, middle ear, paranasal sinuses

NORMAL FLORA OF THE DIFFERENT SITES: 1. Skin - flora are most abundant in moist areas a. Aerobic and anaerobic diphtheroid - Corynebacterium, Propionibacterium b. Nonhemolytic aerobic and anaerobic staphylococci - Staphylococcus epidermidis, Peptococcus c. Alpha- hemolytic streptococci - Streptococcus viridans, Streptococcus fecalis d. Gram (-) coliform bacilli and Acinetobacter e. Fungi and Yeast - Pityrosporum ovale, Pityrosporum orbiculare, Torulopsis glabrata Candida albicans f. Non-pathogenic mycobacteria Factors that eliminate non-resident microorganisms from the skin 1. Fatty acids in sebaceous secretions 2. Presence of lysozyme 2. THE MOUTH AND THE RESPIRATORY TRACT A. Mouth - tongue and buccal mucosa- Viridans streptococci - gingival crevices and tonsillar cryptsanaerobic flora Bacteroides melaninogenicus, Treponemas, Fusobacteria, Clostridia, Actinomyces, Peptostreptococcus B. Nasopharynx- oral organisms - there is also transient carriage of: S.pneumoniae, Hemophillus species, N.meningitidis 3. THE CONJUNCTIVAL SAC- very scanty - held in check by the flow of tears which contain lysozyme = Corynebacterium xerosis = Moraxella species = Staphylococci
9

= Non-hemolytic streptococci 4. THE DIGESTIVE TRACT A. Esophagus- transient mouth flora B. Stomach- rapidly becomes sterile after meals C. Small intestines- scanty resident flora except in the lower ileum (streptococci, Lactobacilli, Yeast) D. Colon- anaerobes-96 to 99%; Bacteroides, anaerobic (lactobacilli, Clostridium, anaerobic streptococci); Facultative- 1 to 4% (E.coli, Proteus and other Enterobacteriaceae, Enterococci, Pseudomonas, Lactobacilli, Candida in breastfed babies: 99% anaerobic (Bifidobacterium) in bottle-fed babies: lactobacillus acidophilus predominates 5. GENITO-URINARY TRACT urinary tract- sterile above the distal 1 cm of the urethra vagina- a. Before puberty and post-menopausal stage - derived from the flora of the skin and colon b. Childbearing age - Lactobacilli: aciduric streptococci and yeast BENEFICIAL EFFECTS OF NORMAL FLORA 1. Intestinal flora are involved in the synthesis of Vit.K and other vitamins like: Niacin, Thiamine, Riboflavin, Pyridoxine, Folic Acid, Panthotenic acid, Biotin 2. Defense against microbial pathogens

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a. Bifidobacteria and breastfeeding- inhibit colonization by enteric pathogens (breastmilk has a maternal IgA; Bifidobacteria lower the pH to 5) b. Vaginal flora, particularly Lactobacillus provides protection against gonococcal vulvovaginitis c. Prolonged oral antibiotic use alter rhe flora of the GIT; antibiotic resistant organisms will have an opportunity to increase in number and produce disease: Candida- causes diarrhea, superficial infection; Staphylococcus aureus- causes necrotizing enterocolitis; Clostridium deficilepseudomembranous colitis 3. Priming of the Immune system- it is shown that animals placed in sterile environment soon after birth have very little immunity and easily succumb when transferred to non-sterile environment. ROLE OF THE NORMAL FLORA IN DISEASE: - cause opportunistic infection if they reach protected areas of the body in sufficient numbers and if local or generalized host defense mechanisms are compromised. Summary of the members of normal flora and their anantomic locations Members of the normal flora Bacteroides species Candida albicans Corynebacterium sp. (diphtheroids) Clostridium species E.coli and other coliforms Gardnerella vaginalis Hemophilus sp. Lactobacillus sp. Neisseria sp. Propionibacterium acnes Pseudomonas aeruginosa Staphylococcus aureus Staphylococcus epidermidis Enterococcus faecalis Anatomic location Colon, throat, vagina Mouth, colon, vagina Nasopharynx, skin, vagina Colon Colon, vagina, outer urethra Vagina Nasopharynx, conjunctiva Mouth, colon, vagina Mouth, nasopharynx Skin Colon, skin Nose, skin Skin,nose,mouth,vagina,urethra Colon

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Viridans streptococci

Mouth, nasopharynx

PATHOGENESIS

KOCHS POSTULATES 1. The same organism must be found in all cases of a given disease. 2. The organism must be isolated and grown in pure culture from the infected person. 3. the organisms from the pure culture must reproduce the disease when inoculated into a susceptible animal. 4. The organism then must be isolated in pure culture from the experimentally infected animal. DISEASE - undesirable host-parasite relationship resulting in interruption in the normal functioning of a body structure. INFECTION - invasion of the body by pathogenic microorganisms. COMMENSALS are organisms that routinely colonize body surfaces without doing harm. PATHOGENS organisms that damage human host either by direct invasion and injury or by the production of harmful toxic products. PATHOGENICITY ability to produce disease VIRULENCE degree of pathogenicity

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BACTERIA CAUSE DISEASE BY 2 BASIC MECHANISM: 1. Invasion of tissues or surfaces a. Colonization of epithelial surfaces (V.cholera, B.pertussis, C.diptheriae b. Penetration of epithelial cells (Shigelle dysenteriae) c. Penetration of deeper tissues (Salmonella typhi) Invasiveness may be attributed to: 1. Surface molecules- which act either by: a. promoting adherence to susceptible cells by means of the common pili or fimbriae and b. promoting resistance to phagocytosis through its capsule or slime layer. 2. Extracellular enzymes a. Collagenases- breakdown of the collagen framework of the muscles (C.perfringens) b. Other enzymes- Streptokinase and Staphylokinase- catalyze the lysis of fibrin. c. Coagulase- cause plasma to clot d. Leukocidins- destroy WBC e. Protease- hydrolyze immunoglobulins 2. Toxin production- falls into two general categories: a. Exotoxins- are polypeptides released by the cell b. Endotoxins- are lipopolysaccharides which form an integral part of the cell wall. A. TYPES OF BACTERIAL INFECTIONS 1. Epidemic- if it occurs much more frequently than usual. 2. Pandemic- if it has a worldwide distribution 3. Endemic- if it is constantly present at a low level in a specific population B. STAGES OF BACTERIAL PATHOGENESIS

13

1. Transmission from an external source into the portal of entry 2. Evasion of primary host defenses such as skin or stomach acid 3. Adherence to mucous membranes usually by bacterial pili 4. Colonization by growth of the bacteria at the site of adherence 5. Disease symptoms caused by toxin production or invasion accompanied by inflammation 6. Host responses, both non-specific and specific (immunity) during steps 3, 4, 5 7. Progression or resolution of the disease.

C. DETERMINANTS OF BACTERIAL PATHOGENESIS 1. Transmission The mode of transmission of many infectious diseases is human to human, but infectious diseases are also transmitted from nonhuman sources such as soil, water, and animals. Pathogens exit the infected patient most frequently from the respiratory and gastrointestinal tracts, hence, transmission to the new host usually occurs via airborne respiratory droplets or fecal contamination of food and water. Organisms can also be transmitted by sexual contact, urine, skin contact, blood transfusions, contaminated needles, or biting insects. There are four important portals of entry: Repiratory, GI, Genital tract and Skin. Animals can also be an important source of organisms that infect humans. They can either be the source (reservoir) or the mode (vector) of transmission of certain organisms. Disease for which animals are the reservoir are called zoonoses.

14

Important modes of transmission

Mode of transmission

Clinical example

Comment

15

B. I. Human to Human A. Direct contact

Gonorrhea

Intimate contact: eg. Sexual or passage through birth canal Fecal-oral: eg. Excreted in feces then ingested in food or water. Spores in soil enter wound in skin. Bacteria in water aerosol are inhaled into lungs Bacteria enter the cat scratch Bacteria enter in tick bite

Dysentery B. No direct contact II. Non human to human A. Soil source B. Water source C. Animal source 1. Directly 2. Via insect vector

Tetanus Legionnaires disease

Cat-scratch fever Lyme disease

Portals of entry of some common pathogens

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Portal of entry Respiratory tract

Pathogen

Streptococcus pneumonia Neisseria meningitides Haemophilus influenzae M. tuberculosis Influenza virus Rhinovirus Epstein-Barr virus Coccidioides immitis Histoplasma capsulatum Gastrointestinal Shigella dysenteriae Tract Salmonella typhi Vibrio cholera Hepatitis A virus Poliovirus Trichinella spiralis Skin Clostridium tetani Rickettsia rickettsii Rabies virus Trichophyton rubrum Plasmodium vivax Genital tract Neisseria gonorrhea Treponema pallidum Chlamydia trachomatis Human papilloma virus Candida albicans

Type of organis m B B B B V V V F F

Disease Pneumonia Meningitis Meningitis PTB Influenza Common cold Infectious mononucleosis Coccidioidomycosis Histoplasmosis

B B B V V P B B V F P B B B V F

Dysentery Typhoid fever Cholera Infectious hepatitis Poliomyelitis Trichinosis Tetanus Rocky Mountain S.F. Rabies Tinea pedis(athletes foot) Malaria Gonorrhea Syphilis Urethritis Genital warts Vaginitis

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Bacterial diseases transmitted by food Bacterium I. Diarrheal disease Gram (+) cocci Staphylococcus aureus Gram (+) rods Bacillus cereus Clostridium perfringens Gram (-) rods E.coli Salmonella enteritidis Shigella sp. Vibrio cholera Vibrio parahaemolyticus Campylobacter jejuni Yersinia Enterocolitica Various foods and water Seafoods and water Seafood Various foods Various foods Reheated rice Cooked meat, stew and gravy Various foods and water Poultry, meat and eggs Soil Soil, animals or humans Humans Domestic animals esp. poultry Humans Humans Warm salt water Domestic animals Domestic animals Diarrhea Diarrhea Typical food Main Reservoir Disease

Custard-filled pastries, potato, egg, or tuna fish salad

Humans

Food poisoning esp. vomiting

Diarrhea Diarrhea Diarrhea (dysentery) Diarrhea Diarrhea Diarrhea Diarrhea

II. Non-diarrheal Disease Gram (+) rods Clostridium botulinum Improperly canned vegetables, smoked fish Soil Botulism

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Listeria monocytogenes Gram (-) rods Brucella sp.

Cows Unpasteurized milk products

Sepsis in neonates or mothers

Meat

Francisella Meat Tularensis Mycobacteria Mycobacterium bovis Milk

Domestic animals Rabbits

Brucellosis Tularemia

cows

Intestinal tuberculosis

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Bacterium Gram (+) rods

Bacillus anthracis Listeria monocytogenes

Main reservoir Domestic animals Domestic animals Domestic animals

Mode of transmission Direct contact Ingestion of unpasteurized milk products Ingestion of unpasteurized milk products; contact with animal tissue Ingestion of contaminated meat Fecal-oral

Disease Anthrax Sepsis in neonates or mother Brucellosis

Gram (-) rods

Brucella sp.

Campylobacter jejuni E.coli 0157:H7 Francisella tularensis Pasteurella multocida Salmonella enteritidis Yersinia enterocolitica Yersinia pestis

Diarrhea Domestic animals Cattle Rabbits Cats Poultry, eggs and cattle Domestic animals Rodents esp. rats and prairie dogs Hemorrhagic colitis Tularemia Tick bite, direct contact Cellulitis Cat bite Diarrhea Fecal-oral Diarrhea Fecal-oral Sepsis Rat flee bite

Mycobacteriu m
Mycobacterium bovis

Cows

Ingestion of unpasteurized milk products

Intestinal tuberculosis

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Spirochetes
Borrelia borgdorferi Leptospira interrogans

Mice Rats and dogs

Tick bite Urine

Lyme disease Leptospirosis

Chlamydiae
Chlamydia psittaci

Birds

Inhalation of aerosols

Psittacosis

Rickettsiae
Rickettsia rickettsii Coxiella Burnetti

Rats and dogs Sheep

Tick bite Inhalation of aerosols of amniotic fluid

Rocky mountain spotted fever Q-fever

Zoonotic disease caused by bacteria

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2. ADHERENCE TO CELL SURFACES

- certain bacteria have specialized structures or produce certain substances that allow them to adhere to the surface of human cells thereby enhancing them their ability to cause disease. - These adherance mechanisms are essential for microorganisms that attach to mucous membranes. 3. INVASION, INFLAMMATION, AND INTRACELLULAR SURVIVAL - One of the two mechanisms by which bacteria cause disease is invasion of tissue followed by inflammation. - Several enzymes secreted by invasive bacteria play a role in pathogenesis: 1. Collagenase and Hyaluronidase- degrades collagen and hyaluronidase respectively thereby allowing the bacteria to spread through subcutaneous tissue. - important in cellulitis caused by Streptococcus pyogenes. 2. Coagulase- produced by Staph aureus - accelerates the formation of fibrin clot from its precursor, fibrinogen. 3. Immunoglobulin A (IgA) protease- degrades IgA, allowing the organism to adhere to mucous membranes and is produced chiefly by N.gonorrheae, H.influenza, and S.pneumoniae. 4. Leukocidins- can destroy both neutrophilic leukocytes and macrophages VIRULENCE FACTOR; a. Capsule- prevents the phagocyte from adhering to the bacteria
22

- anticapsular antibodies allow more effective phagocytosis to occur ( a process called opsonization) b. M protein- antiphagocytic - found in Group A streptococci (S.pyogenes) protein A- binds to IgG and prevents the activation of complement. TYPES OF INFLAMMATION: 1. Pyogenic- pus producing - neutrophils are the predominant cells - produced by Gram (+) and Gram (-) cocci 2. Granulomatous- macrophage and T-cells predominate - no bacterial enzymes or toxins that induce granuloma have been identified. - bacterial antigens stimulate the cell mediated immune system resulting in sensitized T-lymphocytes and macrophage activity. - Phagocytosis by macrophages kills most of the bacteria but some survive and grow within the macrophages in the granuloma.

INTRACELLULAR SURVIVAL- an important attribute of certain bacteria that enhances their ability to cause disease - intracellular pathogens - commonly cause granulomatous lesion - Best known bacteria: Mycobacterium, Legionella Brucella and Listeria - Best known fungi: Histoplasma
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4. TOXIN PRODUCTION - the second major mechanism by which bacteria cause disease is the production of toxins. Comparison of Properties Exotoxin Endotoxin Certain species of Cell wall of most gram (-) some gram (+) and bacteria gram (-) bacteria Yes No Polypeptide Plasmid or bacteriophage High (fatal dose on the order of 1 ug) Various effects Various modes Lipopolysaccharide Bacterial chromosome Low (fatal dose on the order of hundreds of micrograms) Fever, shock Includes TNF and interleukin-1 Poorly antigenic No toxoids formed and no vaccine available Stable at 100C for 1 hour

Property
Source

Secreted from cell Chemistry Location of genes Toxicity Clinical effects Mode of action Antigenicity

Induces high titer antibodies called antitoxin Vaccines Toxoids used as vaccines Heat stability Destroyed rapidly at 60C (except staphylococcal enterotoxin) Typical diseases Tetanus, botulism, diphtheria

Meningococcemia, sepsis by gram (-) rods

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Important bacterial exotoxins Bacterium Gram (+)

Corynebacterium diphtheriae Clostridium tetani Inactivates EF-2 by ADP ribosylation Tetanus Blocks release of the inhibitory neurotransmitter glycine Clostridium Botulism Blocks release of botulinum acetylcholine Clostridium difficile Pseudomembranous Exotoxin B is cytotoxic to colitis enterocytes. Clostridium Gas gangrene Alpha toxin is lecithinase. perfringens Enterotoxin is a super antigen Bacillus anthracis Anthrax One of the toxins is an adenylate cyclase Staph.aureus Toxic shock Is a superantigen; binds to class II MHC protein and T cell receptor ; induces IL-1 and IL-2 Strep.pyogenes Scarlet fever Is a superantigen; action similar to toxic shock syndrome toxin of S.aureus Diphtheria Yes Yes Yes No No No No

Disease

Mode of action

Toxoid vaccine

No

Gram (-)
Escherichia coli 1. watery diarrhea - labile toxin stimulates adenylate cyclase by ADP ribosylation; stable toxin stimulates guanylate cyclase. -Verotoxin is cytotoxic to enterocytes Stimulates adenylate cyclase by ADP-ribosylation Stimulates adenylate cyclase by ADP-ribosylation; inhibits chemokine receptor No

2. bloody diarrhea Vibrio cholera Bordetella pertussis Cholera Whooping cough

No No Yes

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D. TYPICAL STAGES OF AN INFECTIOUS DISEASE

1. Incubation Period- time between the acquisition of the organism and

the beginning of symptoms. 2. Prodromal period- non-specific symptoms such as fever, malaise and loss of appetite occur. 3. Specific-illness period- the overt characteristic signs and symptoms of the disease occur. 4. Recovery period- during which the illness abates and the patient returns to the healthy state.

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6
INNATE (NON-SPECIFIC) IMMUNITY 1. Skin and Mucuos membranes

HOST DEFENSES

- intact skin is the first line of defense against many organisms. - Fatty acids secreted by the sebaceous glands in the skin have antibacterial and antifungal activity. - Resp.tract > cilia, mucus, alveolar macrophages, lysozyme in tears and mucus, hairs in the nose, and cough reflex. - GIT > hydrolytic enzymes in saliva, acid in the stomach, various degradative enzymes and macrophages in the small intestine Vagina > low pH generated by lactobacilli

2. Inflammatory response and Phagocytosis - characterized by the clinical findings of redness, swelling, warmth and pain.at the site of infection. - these signs are due to: a. increase blood flow b. increase capillary permeability- due to histamine, prostaglandins, and leukotrienes. - Bradykinin is an important mediator of pain c. escape of fluid and cells into tissue space
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- Neutrophils predominate in acute pyogenic infection - Macrophage are more prevalent in chronic or granulomatous infections.

- Phagocytosis > involves 3 steps: 1. Migration 2. Ingestion 3. Killing

Bacteria enter skin

Activation of complement pathway

Phagocytosis by

C5a attracts neutrophils

C3b opsonizes bacteria, which enhances phagocytosis by neutrophils

C5, 6, 7, 8, 9 form membrane attack complex that lyses bacteria

Neutrophils

Macrophages

Cytokine production

Present epitopes and stimulate

Tumor necrosis factor induces inflammation

IL-1 induces fever

IL-6 induces acute phase proteins

Chemokines(eg.IL8, MIP) attract neutrophils and macrophages Antibody mediated immunity Cell 28 mediated immunity