Gram Positive Cocci

Treatment Staphylococcus aureus Characteristics Gram + cocci in clusters,immotile human skin and nares,body walls off infection w/a fibrinous barrier; S. aureus causes pus formation. Associated Disease(s) Invasive: suppurative skin infections: minor trauma pimples ,carbuncles, impetigo; major osteomyelitis, fasciitis, cellulitis. hematogenous inf., nosocomial infection. Toxinoses: Food Poisoning (enterotoxin), exfoliative skin disease (Ritters disease of newborns), TSS Pathogenesis Multifactorial; secrete 4 hemolysins that lyse cells; hemolysin lyses cell similar to pore form. by complement, also:coagulase +, exfoliatin. Protein A is a surface molecule that binds IgG to camouflage the bacterium. Also able to respond to env. w/signal molecule. Treatment penicillin vancomycin [erythromycin] (Many strains are multi-abx resistant. and make lactamase)

Staphylococcus epidermidis

Gram + cocci in clusters, human skin (always),

Staphylococcus saprophyticus Streptococcus pyogenes (Group A, -hemolytic)

Gram + cocci in clusters, skin/genitourinary tract Gram + cocci in chains, catalase neg., Group A causes most strep disease, asymptomatic carriers, causes suppurative infections.

Opportunistic infections, large number of nosocomial infections: bacteremia, endocarditis, endophthalmitis, osteomyelitis (following surgery), infections of indwelling foreign devices, neonatal necrotizing enterocoloitis. Infections outside of hospital, causes 20% of all urinary tract infections in young women. Suppurative: Pharyngitis, Scarlet Fever, erysipelas, streptococcal pyoderma (impetigo). Non-suppurative: Acute Rheumatic Fever, Acute Glomerulonephritis.

Coagulase negative

Coagulase negative Surface molecules confer adherence to tissues and resistance to phagocytosis. M-protein(prevents phag.), Protein F (adherencefibronectin), Fc receptor (like Prt.A), C5a peptidase, etc. Secreted exotoxins: erythrogenic toxin, Streptolysin S, Streptolysin O, Streptokinase, DNAse. Capsular polysaccharide (prevent phag.), Hemolysin (like streptolysin S), IgA receptor (camouflage), Fibronectin binding protein (adherence). Very sensitive to penicillin. If patient is allergic, give erythromycin.

Streptococcus agalactiae (Group B, -hemolytic) Viridans Streptococci (-hemolytic) Enterococcus faecalis (-hemolytic, non-hemolytic) Streptococcus pneumoniae (the pneumococcus)

Gram + cocci in chains, catalase neg., lower GI tract & female genital tract. Gram + cocci in chains, catalase neg., oral cavity (up to 60% of normal oral flora) Gram + cocci, low pathogenicity, normal flora of human gut, very hardy. Gram +, encapsulated, lancet shaped cocci in pairs, usually community acquired, sporadic. Transmitted by droplet nuclei or aspiration by carrier. Facultative anaerobes, -hemolytic.

Puerperal sepsis (after childbirth) , neonatal meningitis (early onset w/50% mortality or late onset w/20% fatality) dental caries, subacute bacterial endocarditis (on preexisting heart valve lesions),enter bloodstream via decayed teeth or following oral surgery. subacute bacterial endocarditis, female urinary tract infections, peritoneal abscess, bacteremia (from above foci). Pneumonia (Lobar and Bronchopneumonia, most common cause of meningitis in adults, most common cause of otitis media and sinusitis in children, can cause septicemia, esp. in the very old or very young. (Immunity to reinfection is type-specific against capsule.)

penicillin vancomycin chloramphenicol penicillin

Antibiotic resistance to every known antibiotic due to conjugal transfer of antibiotic resistance genes within and across species Capsule confers path: inhibits phagocytosis by inhibiting alt.pathway, must be present for virulence. Capsule also stimulates production of type-specific opsonic Ab that results in killing by PMNs. No toxins involved in path. 85 different serotypes.

???

penicillin amoxicillin cephalosporins vancomycin Vaccine for people at risk available.

Gram Positive Rods

Organism Listeria monocytogenes Characteristics Gram+, non-encapsulatedrod w/a characteristic tumbling motility, facultative intracellular parasite, grows under many conditions, found nearly everywhere, transmitted through improperly pasteurized milk/products, oral-fecal contamination of any source (ie- H20 contamination, vegetable fertilized w/manure, meat, etc). Disease(s) Listeriosis is disease. Rarely causes disease but when it does is severe esp to fetus, newborn, pregnant women and the immuno- compromised. 70-90% fatality if untreated, 30-50% fatality w/treatment depending on status of host and clinical signs. Can be carried in GI tract or female genital to lead to disease. Is able to enter a wide variety of cells where it can survive and multiply. Immunity to reinf w/ survivors. Septicemia, meningitis, abscesses, granulomas, lymphadenitis. Lead cause of meningitis in CA/renal tp patients Anthrax (cutaneous or inhalational).Mostly a disease of animals or people who work with animals.Cutaneous enters thru cut on skin, causes a malignant pustule that is a necrotic black lesion then rapidly disseminates and causes death very quickly. Inhalational is from organisms directly to lung that release exo-toxin and cause pulmonary necrosis, septicemia, meningitis and death w/in 24h. Self limiting type of food poisoning. Incubation period and clinical sx. resemble staph. food poisoning. Can also cause disseminated, usually fatal, disease in immuno compromised pts.(usually post-operatively). Diphtheria. Fever, chills, pharyngitis, cervical lymphadenitis, massive neck edema (severe cases) and a thick, closely adherent dirty gray pharyng., tonsillar or laryng. pseudomembrane Death due to resp. paralysis or myocarditis. Cutaneous diphtheria results in an ulcerative lesion w/a dirty gray pseudomembrane. W/both there can be toxemic degeneration and death. Can cause septicemia in rare instances in immunosuppressed individuals with a high fatality rate. Pathogenesis Extracellular product listeriolysin O is responsible for pathogenicity- a cytolysin that specifically dissolves the endosomal membrane so that it evades the major antibacterial activity of the cell, this way the org. can also get into cytoplasm. Cell surface virulence includes Internalin for attachment and invasion and Act A for directional actin polym. of host cells actin. Actin polym. allows bacteria to move in cytoplasm and is required for cell-cell spread, also makes it resistant to humoral immunity. Treatment Ampicillin, penicillin with an aminoglycoside, erythromycin. Use only pasteurized milk products b/c of this bacterium!!!

(see HO, lots of details for this one) Bacillus anthracis

Gram +, sporeforming, non motile rod with characteristic square cut ends (boxcar), encapsulated, spores can live in the soil for 30 years, found carried in GI tract of animals, transmitted by spores or respiratory droplets.

Exotoxin produces pathogenesis. Toxin is a heat labile protein composed of 3 components: protective antigen, lethal or toxic factor and edema factor. Polypeptide capsule made exclusively of D-glutamic acid gives anti-phagocytic activity but does not stimulate protective antibody

Vaccine (but is only 50% eff) Penicillin and tetracycline are effective only when given early

Bacillus cereus

Corynebacterium diphtheriae

Gram+, motile, non encapsulated, beta hemolytic, exists as a saprophyte in water and soil, trans. in contaminated rice or meat dishes Gram +, non sporeforming, non motile, vy. distinct (beaded, barred or clubbed), facultative anaerobes, obligate parasite of humans, carried in URT, transmitted by droplet nuclei or contaminated milk, people can be carriers.

Secretes enterotoxins

K antigen on surface is anti-phagocytic. Exotoxin is of 2 polypeptide fragments: B fragment is for transport into cell and A frag ment is toxin for ADP-ribosylation and inactivation of elongation factor EF-2 which inhibits protein synthesis. Lysogeny w/ a beta prophage carrying the tox gene is essential for toxigenicity.

Vaccination prevents disease Active disease: give anti-toxin immediately, penicillin or eryth romycin for killing bacteria.

Diphtheroids

Same habitat, may have same morphological and biochemical properties as C.diphtheriae but they do not produce exotoxin

Often have multiple antibiotic resistance, but do not produce exotoxin

Gram Positive, Anaerobic, Sporeforming Rods

Organism Clostridium botulinum Characteristics Gram+, anaerobic, spore form- ing, multiplies in uncooked meat, sausage, fish and badly canned items, dx. by animal injection, cultures show characteristic light bulb appearance. Spores do not produce toxin, only vegetative form does. Gram+, anaerobic, spore formi-ing, found all over the place, typical entry through wounds (puncture wound or laceration, but also burns, ulcers, cpd fx, operative wounds, injection sites of IVDAs, Dx. is clinical, appear on culture as gram+ rods w/spore formation at tip forming a drumstick Gram+, anaerobic, spore forming, occur normally in soil and sewage, normal in human GI, box shaped organisms with gram stain, positive blood cultures(for gas gangrene), found also in feces for other infections Disease(s) Botulism. Caused by intoxication w/bacteria. Clinical sx. 18-36h after ingestion, ptosis, mydriasis, blurred vision, dysphagia, dysphonia, urinary retention, muscle weakness (descending), respiratory paralysis. Death can occur w/in 18h. This results from Ach presynaptic blockade. Infant Botulism results in floppy infant, may be cause of SIDS in some cases. Tetanus. Caused by intoxication, may take several days to weeks for symptoms to occur. Onset of sx. may be muscular contractions in the vicinity of the wound followed by spastic contraction of the masseter muscle (trismus) resulting in locked jaw, generalized rigidity and severe spasms of the limbs and trunk. Later signs: risus sardonicus, spasmic contractions of back(opisthotonus) and of the resp.muscles which may lead to death. Gas gangrene. Destroys tissues esp. muscle,Infects poorly perfused, injured tissues, incubation 6-72h, severe edema, bronze discoloration, bullous lesions w/dark thin fluid, then H2 gas production leading to crepitations, ischemia, shock and death. Most common organism to cause gas gangrene. Also: Anaerobic cellulitis, uterine infection, necrotizing enteritis, food poisoning (self limiting diarrhea). Pathogenesis Botulinus toxin causes path. Released by lysis of bacterial cells in medium. Toxin has two subunits:H-chain causes receptor mediated endocytosis by host cell, once in cell the H and L-chain are separated and the L-chain moves by retrograde transport to the presynaptic terminal where it prevents fusion of the synaptic vesicles w/the presynaptic membrane. All toxins are destroyed by boiling at 100C for 10 minutes. Secretes tetanus toxin which is a dimer similar to botulinus toxin (H and L chain) L chain functions as a synaptobrevin on the surface of synaptic vesicles that inhibits their fusion with the presynaptic membrane. Tetanus toxin specifically blocks the inhibitory neurons of spinal motor neurons preventing release of GABA and glycine which results in uninhibited transmission of excitatory impulses and muscular spasms. Produces extotoxins. Most important toxin is -toxin which cleaves lecithin in host cell membranes and is lethal and necrotizing on injection. Perfringolysin O (similar to strep-tolysin O, pore complexes). The combined action of -toxin and streptolysin O may be the cause for the intravascular hemolysis associated w/ infections. b-toxin important in necrosis of necrotizing enteritis. Spores in food germinate & release toxin in food pois. Produces two heat labile toxins: A and B. The toxins are released by vegetative cells and together cause fluid loss, mucosal damage and necrosis of intestinal mucosa. Toxin can be id by ELISA. Free toxin can be inactivated with a specific antiserum. Give a polyvalent antitoxin. Do not give penicillin b/c it causes cell lysis and more toxin. Immunization @ 2,4,6 mos. and boosters every 5-10 y. Antitoxin + immune globu-lin given to wounded people w/o immun. immediately!

Clostridium tetani

Clostridium perfringens

surgical excision of inf. skin and muscle, limb amp utation, hyperbaric O2. Abx to well perfused tissues, no time to wait for cultures! Surg.for bowel in enteritis. Stop previous abx tx. Vancomycin or metronidazol to stop inf. Surg-ery for megacolon

Clostridium dificile

Gram+, anaerobic, spore forming, normal commensal of human gut, results from superinfection following antibiotic treatment

Pseudomembranous colitis. Diarrhea and toxic megacolon. Endoscopy shows multiple small pseudomembranous colon plaques. Milder form is antibiotic associated diarrhea w/ same clinical findings but less severe

Gram Negative Coccobacilli

Organism Bordetella pertussis Characteristics Gram neg, coccobacillus, non motile, non sporeforming, piliated, LPS, obligate aerobe, slow growing, hard to grow, human respiratory tract, no known animal or environment-al reservoir, transmitted by respiratory droplets, highly communicable, mostly children Gram neg, coccobacillus, non spore, non motile, encapsulated and nonencapsulated strains, fastidious, facultative anaerobe, requires hemin and NAD, found in human respiratory tract, transmitted by respiratory droplets. Disease(s) Pertussis (whooping cough). 4 phases: 1. incubation; 2. catarrhal (mild cold-like sx. , mild cough of severity,most infectious phase) 3. paroxysmal (severe, forceful, spasmodic coughing w/ whoop following and then vom-iting, complicated by otitis media, seizures, apnea, pneumonia); 4. convalescent (less fr. paroxysms, recovery). 1% death rate, mental retardation and paralysis can occur. Meningitis, epiglottitis (in kids), not seen often any more b/c of vaccine, 75% unencapsulated causes otitis media, sinusitis, bronchopneumonia, 5% encapsulated causes pneumonia, epiglottitis, bacteremia, meningitis Most common from 3mos to 4 yr after maternal abs have worn off and T cell response not active. Complications are severe. Pathogenesis Attaches (firmly) to ciliated resp.epithelial cells(using FHA,pili and peritactin), secretes toxins to inhibit phago.cells (adenylate cyclase toxin, pertussis toxin )& inhibit muco-ciliary defense(tracheal toxin), multiplies and causes local damage, systemic disease results (lymphocytosis, insulin, glycemia) See HO for details of toxins. Capsule is antiphagocytic major virulence factor (PRP polymer, most adults have anti- PRP Ab), pili may have a role in attachment, LPS, outer membrane proteins, IgA protease (specific role not yet established) Treatment Erythromycin for active disease. Vaccination to prevent disease. Vaccine can cause some ses but is safe and prevents epidemics. Vaccination For active disease give cephalospor-ins, ampicillin + chloramphenicol.

Haemophilus influenzae

Gram Negative Cocci

Name Neisseria meningitidis Characteristics gram-, diplococci, fastidious, habitat is human mucosal surfaces, poor environmental survival, symptomatic & asymp inf. Spread by respiratory droplets. Detect by gram st, serum Ag, culture, clinical dx. gram- diplococci, fastidious, human mucosa/poor environ. survival, sympt/asympt inf. Spread by sexual contact or perinatal inf. Gram st of exudate in males can dx. but for sure culture to confirm from any source. Disease(s) Meningococcal disease: meningitis and/or septicemia(fever,ha,chills, malaise, wkness, hemorrhagic skin lesions/petechiae/purpura, DIC, Thrombocytopenia, leukocytosis, hypotension, septic shock (LPS-A). Can be epidemic, bacteremia in susceptible people (asplenic pts, children), carrier state in others Gonorrhea: Urethritis (males), cervicitis (females), rectal inf, pharyngeal inf, ophthalmia neonatorum (mother to infant gonococcal conjunctivitis). Complications: PID, Disseminated gonococcal infection (DGI, only 0.5-3% of inf) leading to arthritis, dermatitis, tenosynovitis(Lovers heels), fever, often mild systemic toxicity. Pathogenesis Attaches to non-ciliated cells of the nasopharyngeal mucosa and undergo TRANSCYTOSIS to cross the basement membrane. Features: Pilus(attachment), IgA1 protease(cleaves IgA), antiphagocytic capsule, LipidA(septic shock). Attachment: by a pilus that shows Ag variation to effectively evade the immune system and by an opacity protein that also has Ag variation, Lipooligosaccharide(LOS) toxic also shows Ag variation, IgA1 protease to evade IgA on mucosal surfaces, P1 porin shows resistance. Inflammation is intense, dissemination can occur but not as prone as in N.meningitidis Treatment IV antibiotics, manage complications, prophylaxis during epidemics

Neisseria gonorrheae

Uncomplicated ceftriaxone + doxycycline. Many pcnase producing strains, tx for chlamydia too, tx for sexual partner, no vax, use a condom

Gram Negative Rods (Enteric)

Organism Vibrio cholerae Characteristics gram-,curved rod, single polar flagellum(motile), endemic, epidemic, pandemic, trans in contaminated food/H20 (fecal-oral trans),lives in brackish water/shellfish, human is transitory habitat. Halophilic (salt loving), marine habitat (coastal waters) Seawater gram-,curved,spiral or comma shaped rods, motile, micro-aerophilic, worldwide zoonosis in GI tract of dom. animals, trans by cont food/water, common, est 2Mcases/yr in US fairly rare gram-,spiral rods, motile, produce urease, habitate the gastric epithelium Gram- rods, motile, facultative intracellular, usually aquired by contaminated food or animals esp. poultry meat or eggs, infections are typically animal associated, fecal oral transmission as well. Associated Disease(s) Cholera: Inf. is asymptomatic to acute in nature, can be spread by asymp people, early signs: vomiting, cramps, then PROFUSE secretory diarrhea (rice water stools), massive fluid loss of 10L/day leads to dehydration, electrolyte deficiency and hypovolemic shock. W/o tx. 60% fat., w/tx. only 1% fat. Food poisoning: undercooked seafood, causes secretory diarrhea Septicemia in compromised host, cellulitis in healthy host Common cause of diarrhea. Acute enteritis: diarrhea, malaise, fever, abd. pain. Range of diarrhea from loose to watery to bloody. Ususally self limiting, bacteremia rare, dx. by stool culture. Pathogenesis Raising pH of stomach encourages infection. 1)colonization: ingestion, gastric acid barrier, attachment to sm.bowel (microvilli) 2) cholera toxin: ADP ribosylates G prt. to turn on adenylate cyclase, loss of salt and H20 by diffusion into lumen, loss of bicarb can lead to acidosis. Treatment Replace fluids & electrolytes po or iv, tetracycline duration, vaccine under dev. Tx. is very effective & easy to give.

Vibrio parahaemolyticus Vibrio vulnificus Campylobacter jejuni

Pathogenic mechanisms uncertain

Fluid and electro-lyte replacement, antibiotics may be indicated(bloody stool), usually no tx is necessary. triple tx: pepto, metronidazole, amoxicillin. Antibiotics not recommended for uncomplicated enterocolitis, ceftriaxone for sepsis. Prevent w/ public health measures (ie restaurant safety) no vaccine available Ceftriaxone (1st ), ampicillin or cotrimoxazole if not severe. Prevent by public health measures. Killed and live -attenuated vaccine available.

Campylobacter fetus Helicobacter pylori

Salmonella enterica (serotypes referred to as if they are species)

Salmonella typhi

Gram - rods, motile, facultative intracellular, infects only man, get from people who are chronic carriers and excreters (Typhoid Mary) a condition that occurs in 1-3% of untreated cases. Fecal oral transmission

Systemic disease in immunocompromised host Gastritis/ulcers: thought to be cause of much gastritis and predisp to stomach CA, abx. tx. against clears up ulcers and gastritis. Acute enterocolitis: Most common disease syndrome of salmonella, follows 6-8 hr incub-ation, most pts. have nausea, vomiting, diarrhea. Fever and abd cramping also common, inf involves small bowel and colon (different site from shigella), Fecal PMNs are present, dx. by stool culture for enteric pathogens, death is rare. Infections can spread beyond intestinal mucosa to produce bacter-emia and seed distant tissues that can result in later focal infections (osteomyelitis in sickle cell pts. occurs w/ increased frequency) Typhoid fever (enteric fever): Incubation 1-3 weeks, gradual onset of fever, abd pain and hepatosplenomegaly, duration usually 4 weeks w/o tx. Dx. by culture of blood, bone marrow and stool. bone marrow gives the highest yield of organisms b/c it is a systemic infection of mononuclear phagocytes. Death may occur despite use of antibiotics b/c of the fatal comp-lication of intestinal perforation and peritonitis Shigellosis: suspect in any diarrhea lasting > 48 hours. Abd cramps, may have fever. Stools have PMNs, blood, mucous. 1wk is avg. time. Dx. by stool culture, produce disease at very low inoculation.

Virulence: motility, urease, cytotoxin, exact cause of inflammation is unknown, infection remains for life if not treated. Invades epithelial cells by contact w/ micro-villi of host, then bact cell assembles invasomes (invasion organelles) which triggers host cell memb. ruffling, the bact then shed their invasomes followed by host cell uptake. Salmonella can turn on and off genes according to if they are in a host cell or not, PhoQ is a sensor molecule (ex: low pH inside a phagolysosome) that regulates genes for transcriptional regulation and turns off other genes. Pag C is essential for resistance to killing by macrophages. S. typhi first invades small bowel epithelial cells or M cells in Peyers patches trans-cytosis across epithelial cellsendocytosis by lamina propria M. Bact survive in spacious phagosomes and reach systemic circulation via thoracic duct reticuloendo-thelial system (phagocytes in liver, spleen and bone marrow). Gall bladder inf leads to the chronic carrier state. Inf dose is large. Intracellular, 1st invades M cells of gut lymphoid follicles, kill resident macrophages invade intestinal epith cells on basolateral surface, then spread cell-cell. Use host cells actin to rocket from cell-cell (like Listeria), express IcsA protein. Invasion plasmid is essential for pathogenicity. Secrete shiga toxin, causes endothelial damage. Expression of proteins is temp. controlled.

Shigella (dysenteriae, flexneri, boydii or sonnei)

Gram- rods, not normal flora, facultative intracellular,motile exclusive to primates, vy few needed to infect, evade host def like gastric acid, fecal-oral transmission: The Four Fs: food, fingers, feces, flies. Only person to person.

Gram Negative Rods (Nosocomial)

Name Escherichia coli (extraintestinal infections) Characteristics Gram - rods, facultative anaerobes, ferment lactose, found in human colon, vagina, urethra. Transmitted during birth in neonatal meningitis, travels from urethra in UTI and pyelonephritis. Disease(s) Meningitis of newborn Uropathogenic:UTI(cystitis or pyelonephritis) Untreated pyelonephritis is a chronic infection that can last for many months. (Different strains of E.coli have acquired traits that allow them to be infective to these regions) Pathogenesis Meningitis of newborn: Strains w/K1 polysaccharide,forms a capsule that is poorly immunogenic(like N.meningitidis).Mom w/ E.coli K1(carrier)confers risk to the newborn Cystitis:Have common pili that allow binding to Dmannose on bladder epithelial surfacesecrete hemolysin,a cytotoxic prt. that damages bladder & causes sx.of cystitis. Pyelonephritis:Bind to renal epithelium by a Pap pilus:binds to ,1-4 digalactoside (only on renal epith), has PapG adhesin only on tip, (very small), also secretes hemolysin. Attachment by EPEC: 3 stages; 1st nonintimate adherence to the epithelial cell surface by pili. 2nd is induction of microvilli effacement (flattening out). 3rd is intimate adherence and host cell cytoskeletal rearrangement by intimin, a bacterial adhesin encoded by the eaeA gene. E.coli O157:H7 is probably from acquisition of the Shiga toxin gene by EPEC (maybe via bacteriophage), transforming it into EHEC Treatment

Escherichia coli (enteric pathogens)

Gram - rods, facultative anaerobes, ferment lactose, enterotoxigenic E.coli are not usually part of the normal flora of the human gut. Enterotoxigenic strains are found in parts of the world w/ poor sanitation and can also be in food (fecal-oral).

Pseudomonas aeruginosa

gram- rod, obligate aerobe,ubiquitous in environment, not found in GI tract of healthy people, an opportunistic infection and a common nosocomial pathogen.

Legionella pneumophila

(See HO, lots of info for this one)

gram- aerobic, tough to stain, flagellated,intracellular path, catalase+, oxidase+, gelatinase+, -lactamase+, lots of branched chain fatty acids, transmitted by aerosolization of contaminated water, reservoir is aquatic unicellular organisms, humans are accid-ental hosts

Infant diarrhea: Enteropathogenic E.coli (EPEC). Chronic diarrhea of children, can cause dehydration and malnutrition. Non-inflammatory enteritis w/ watery diarrhea w/o fecal leukocytes. Travelers diarrhea (dehydrating diarrhea): Enterotoxigenic E.coli (ETEC). Non-inflammatory enteritis (as for infant diarrhea) Hemolytic Uremic Syndrome, blood and non bloody diarrhea: Enterohemorrhagic E.coli (EHEC). Diarrhea is dysenteric w/fecal leukocytes. HUS is hemolytic anemia, renal failure w/ uremia, thrombocytopenia and neurological sx. (E.coli 0157:H7) Dysentery:Enteroinvasive E.coli (EIEC), similar to shigellosis, fecal leukocytes present. Very rare in healthy people, causes life threat-ening and fatal infections in burn pts, Cystic fibrosis, and immunocompromised pts. Also a common cause of surgical wound infection. Causes rapid tissue destruction and/or sepsis, foci of infection on man made devices (indwelling catheters, prosthetic heart valves, prosthetic joints) is very difficult to cure. Legionnaires Disease: Pneumonia, often severe and fatal;Stage 1:mild illness (flu like), Stage 2:moderately serious pneumonia, non remitting fever, bradycardia, chest pain, hemoptysis, cxr:diffuse or lobar infiltrate, Stage 3:Severe multilobar pneumonia, resp failure, disorientation, liver abnormalities, hyponatremia and hypophosphatemia. Pontiac Fever: Febrile illness w/o pneumonia, mild and non-fatal

Rehydration is effective for travelers diarrhea, cotrimoxazole can shorten duration of sx. Only eat cooked food and boiled water in certain countries, prophy-lactic Pepto Bismol or doxycycline may be preventive.

Antibiotic resistance is very common and tends to develop during the course of therapy, so two antibiotics are always used. Multifactorial virulence: secretes a slime that inh. WBC activities, secretes hemolysins and proteolysins that damage cells and tissues, also secretes exotoxin A (m.a. is the same as diphtheria toxin w/inhibition of prt synthesis Lung: alveoli filled w/pmns, M, & fibrin, many intra and extra cellular bacteria in M (inside vacuoles) and pmns. Multiplies intra cellularly in alveolar M and monocytes until host cell destroyed, enters by coiling phagocytosis mediated by complement rec. on phagocyte and C3 component on bact called Major Outer Membrane Protein, inh fusion of phagosome w/host cell lysosomes, inhibits acidification of phagosome.needs Fe

Combination antibiotic chemotherapy

Erythromycin (or newer analogs), and rifampin, only bacteriostatic Host immune system must kill maybe by cytotoxic T cells?

Gram Negative Rods (Zoonotic)

Name Brucella melitensis (and suis and abortus) Characteristics gram- nonmotile coccobacilli, aerobic (may require CO2 for growth), all are pathogenic in their natural host, pasteuriz-ation kills, people in close contact w/animals are most likely to be infected Disease(s) Brucellosis: Undulating fevers (daily cycling), night sweats, malaise, chills, weakness, myalgia, HA. May have enlaged spleen and liver, vertebral spondylitis, bacteremia (20%) and epididymitis Neurological sx. may occur as may endocarditis. Causes chronic illness w/ an acute onset. Pathogenesis Enter through alimentary tract, conjunctivae, or skin and are engulfed by PMNs that carry bact to the lymphatics, there they enter mononuclear cells and multiply w/in by inh. of phagolysosomal fusion, cells die, bact are released into blood and go to reticuloendo-thelial system, cause granulomatous lesions Treatment Ususally combo tx w/tetracycline and streptomycin or rifampin; or cotrimoxazole, vacc for cattle but not people.

Francisella tularensis Pasteurella multocida Yersinia pestis

gram- bacillus, short non-motile, nonspore forming, tends to stain bipolar (safety pin), rats are the primary reservoir and trans. is by the bite of their fleas, bact multiply in flea gut and cause flea to regurgitate onto next animal, also can be spread by people via respiratory droplets.

Plague: Bubonic form is by bacteria spreading to regional lymph nodes causing a very painful swelling (bubo) high fever, malaise, then bacteria spread to liver, spleen and lungs. DIC can occur. Secondary pneumonia leads trans. by respiratory droplets.Pneumonic form from resp drops is very conta-gious and 100% fatal w/o tx. Septicemic plague is caused by bite but no bubo forms and pt presents w/fever and dies of bacteremia since hard to dx. all very fatal!

In flea gut at lower temps and low Ca the bact can multiply but does not secrete toxins. In host @ 37 and incr Ca, chaperone prts allow the translocation of YOPS (virulence factors) out of the cell. Two cytotoxins are also secreted into the host cell as well as YopM that binds to human a-thrombin and is thought to produce the hemorrhagic lesion Killing fleas w/insecticide and quarantining victims is effective for prevention

Yersinia pseudotuberculosis

Yersinia enterocolitica

Does not display bipolar staining, more motile at 22C but not at 37C, reservoir in wild and domesticated animals and fowl. Does not display bipolar staining, in contaminated food and water, mostly milk and meat

Mesenteric adenitis and pseudoappendicitis syndrome, usually a sporadic infection

On entry the bact bind to integrin receptors on the host cell with invasin proteins on their surface, this allows them to be phagocytosed. same as above

Diarrhea in children: acute self-limiting gastroenteritis, enterocolitis and lymphadenitis Adults, exudative pharyngitis, Reiter syndrome and erythema nodosum in pts. w/HLA B-27 marker

start asap, for pneumonic, give streptomycin, tetracycline(good prophylactic) or chloramphenicol for meningitis. Reduces mortality if started vy early, vaccine available. ampicillin, chloramphenicol, tetracycline, or aminoglycosides tetracycline, chloramphenicol, cotrimoxazole, and gentamicin

Obligate Intracellular Parasites

Name Chlamydia trachomatis Characteristics only grows in eukaryotic cells, developmental cycle with two growth forms, spread by sexual contact, peripartum or close personal contact only grows in eukaryotic cells, developmental cycle with two growth forms, aerosol spread, zoonosis (in certain birds) obligate intracellular of vascular endothelium, trans by tick bite, southeast and south central US Disease(s) Genitourinary tract infection:cervicitis, non gonococcal urethritis, PID, neonatal ophthalm-orrhea and pneumonia, lymphogranuloma venereum, Trachoma (ocular inf), chronic sequelae: tubal infertility, ectopic preg-nancy, blindness. Psittacosis: fever, respiratory symptoms, systemic infection Pathogenesis (Dx: serology, culture, PCR, direct hybridization, LCR w/ urine) Treatment Tetracycline or doxycycline, erythromycin, azithromycin, atypical pneum-onia d/dx Tetracycline

Chlamydidophila psittaci

Rickettsia rickettsii

Rickettsia prowazekii

Rickettsia typhi

Rickettsia tsutsugamushi

Coxiella burnetii

obligate intracellular of vascular endothelium, trans by human louse (close personal contact), unsanitary cond, military campaigns obligate intracellular of vascular endothelium, trans by the rat flea, in urban and suburban dep on rodent expos. obligate intracellular of vascular endothelium, trans by chiggers (larval mites), humans are accidental hosts (usually rodents) obligate intracellular pathogen, in urine,feces, milk and birth products of cattle, sheep and goats, trans by inhalation of contaminated aerosols

Rocky Mountain Spotted Fever: Affects vascular endothelium (vasculitis), multi-system presentation w/fever, myalgias, HA, rash on palms/soles 3-5 days post fever, serious compl: gangrene, renal failure, neurological involvement, DIC in very severe cases. Epidemic Typhus: vasculitis leading to intense HA, chills,fever, myalgia (w/o eshcar), rash begins in axillary folds and the upper trunk. Endemic Typhus: HA, myalgia and fever, a rash occurs in 60-80% of cases and is central in distribution

(Dx. by serology, isolation, direct immunofluorescence)

Chloramphenicol, tetracyline, rifampin, ciprofloxacin

(Dx. by serology, clinical hx)

Chloramphenicol & tetracycline. Control human body louse and sanitation same as other typhus

Scrub Typhus: Bite site ulcerates and forms a black crust called an eschar, regional lymphadenopathy next 4-5 days, fever, HA and myalgia, rash occurs on the trunk and spreads to extremities, may be CNS symptoms Q fever: Typically an acute self-limiting febrile illness:HA,fever,chills,fatigue,myalgia; rash almost never occurs, may cause atypical or rapidly progressive pneumonia. Chronic inf can result in endocarditis or hepatitis w/ a donut granuloma of a fibrin ring around a central lipid vacuole.

same as other typhus

Tetracycline Dx. by serology and history

Mycoplasma (Wall-less Cells)

Name Mycoplasma pneumoniae Characteristics no cell wall, require sterols for growth, many commensal mucosal species, 1020% of pneumonias, 50% of summer pneumonias, school children and young adults. no cell wall, require sterols for growth, able to metabolise urea (have urease), genital mycoplasm same as above, colonization rates 0-31% Disease(s) Atypical pneumonia: a prolonged flu or bronchitis, cxr shows lower lobe bronchial pneumonia, PMNs; malaise, cough may persist for 2-6 weeks, tracheobronchitis is most common complication. Nongonococcal urethritis: can progress to prostatitis/epididymitis, or postpartum fever/abortion/chorioamnionitis(?) Pyelonephritis, PID, salpingitis, postabortal/ postpartum fever, may contribute to nongonococcal urethritis Pathogenesis (Dx. by culture, serology with rising titers, complement fixation is the gold standard serology) Treatment Erythromycin or tetracycline resistant to penicillin b/c lacks cell wall Tetracycline (10% resist) or erythromycin Tetracycline

Ureaplasma urealyticum

Mycoplasma hominis

Spirochetes (Flexible, thin walled cells)

Name Borrelia burgdorferi Characteristics highly motile(by endo-flagella in periplasmic space), cork-screw shaped (spirochete), must use darkfield microscope, does not have LPS. Worldwide, spread by bite of Ixodes tick,it winters in the fur of deer and feeds on the white-footed mouse, inf in mouse skin is major reservoir of bact. Most common in mid west and northeast US. (as above for spirochetes), predominantly found the western US, most often at elevations above 5000 ft. (as above for spirochetes) rare in US, often in developing nations spirochete characteristics, stains well with Silver stain. obligate parasite of humans, does not appear in nature or in animals. Can be sexually trans-mitted or congenital, trans. is greatest during 1 or 2 stage, exogenous routes, endogenous activation of latent disease may also occur Disease(s) Lyme disease: Chronic infection, disseminates to many organs. Erythema migrans (EM) is most distinctive feature (60%). Early disease shows localized EM, disseminated lympho-cytoma (swelling ear or nipple), arthritis attacks, migratory musculoskeletal and joint pain, chronic meningitis, heart problems, severe malaise and fatigue. Chronic disease on skin shows ACA. Musculoskeletal recurrent oligoarthritis or chronic arthritis, chronic parenchymal brain inf. Chronicity defined by >1yr of joint infection. Assoc w/HLA-DR-4. Relapsing fever (alternating periods of fever and illness alternate with periods of wellness) an uncommon infection Acute febrile illness, sometimes fatal systemic illness marked by hepatic invovement in fatal cases. Syphilis: 1: appearance of painless, indurated, well circumscribed ulcer (chancre) and regional lymphadenopathy (disease is communicable at this stage), lesions heal. 2: bact in circulation (septicemia) go to lymph nodes and tissues:fever, HA, lymphaden-opathy, generalized rash (palms/soles), mucous patches in oral cavity, condylomata (commun-icable lesions), alopecia. Also hepatoslpenomegaly, nephritis, periostitis. Latency: 2 stage may occur again. AIDS pts have higher rate of recur, rapidly progr CNS involvement. 3 (or late stage): anywhere from months to >50 years. neurosyphilis from treponemes in CNS, CV (aneurysm, aortic endocarditis), benign gummas. Pathogenesis Hallmarks of Lyme disease are dissemin-ation and persistence of bacteria, dissem-ination is mediated by the spirochetes ability to invade endothelial intercellular junctions, relative low amounts of outer membrane spanning proteins is possibly a factor in ability of bacteria to cause chronic disease. Treatment Therapies are being developed

Borrelia hermsii

Leptospira interrogans Treponema pallidum (this one has a lot too)

Has the capacity to undergo antigenic variation of Variable Major Protein (VMP), periods of illness and wellness alternate as bact goes through antigenic repertoire Contains a lipopolysaccharide like material (LLS) in the outer membrane Enter through abraded skin or mucous membranes, attach by their tips to host cells and colonize, w/in hours organisms go to lymph nodes, then disseminate to liver, spleen & bone marrow via circulation, bact exit through tight junctions of endothelial cells sets up chronic inflammatory response. [Congenital syphilis: Thru placenta 18th week, damage depends on stage of disease in mom/# of treponemes. Ususally miscarriage or stillbirth. 1Sx. can present up to age 2. Mucous membrane lesions, osteochondritis, anemia, organomegaly, CNS disease. Late sx: keratitis, 8th nerve deaf., abn 2nd tooth dvlp (raspberry molars), abn long bones (sabre shins), perf nasal septum, gummas.]

Dx. by blood smear and serology

Dx: Hx. of pt, can mimic other diseases. Dark-field microscopy. VDRL or RPR serology tests, 30% may show false neg, false + w/autoimmune diseases (SLE). Tx: penicillin or doxycycline, tetracycline, erythromycin. Educate, cond-oms, screening.

Mycobacteria (Acid fast, aerobic rods, facultative intracellular)

Name Mycobacterium tuberculosis (see HO for sure, this one has a lot of detail!) Characteristics Facultative,intracellular, obligate aerobe, slightly bent rods, slow growing, four unique surface layers,trans. by respiratory droplets, acid-fast (red) bacilli, dry cauliflower like colonies Positive PPD: documents infection but not state of TB Negative TB: doesnt say much pt. may be anergic (AIDS), have to re-test if still suspected Disease(s) Tuberculosis: 1TB: exudative response, bacteria are phagocytized by PMNs but remain inside the cytoplasm, followed by form-ation of a productive lesion w/granuloma and tubercule resulting(caseous necrosis). Ghon complex is hilar lymph node granuloma, caseous lesions can heal w/fibrosis. Humoral immunity makes dormant but doesnt elim.bact Reactivation TB: from caseous lesion can be-come active, liquefaction, spread through lung, fever,cough, malaise, wt.loss, night sweats Miliary TB when bacteria disseminates (AIDS) Tuberculosis in cattle. In man enters through GI, infects lymph nodes (scrofula), can also infect vertebrae and joints, collapse of vertebrae (Potts disease) Tuberculoid leprosy: Annular lesions in extremities (cooler) w/ red, raised border. Red area has most bact. Lesioned areas have sensitivity. Destructive lesions.Damage to fingers can occur b/c of sensation. CMI is effective at stemming spread of bacteria. Lepromatous leprosy:More contagious. CMI lost or allowing spread of bacteria.Sx:diffuse thickening of skin: eyebrow alopecia, enlarged earlobes, broadening of nose, swelling of fingers, hypopigmentation. Reversal Reaction(lepromatoustuberculoid) Erythema Nodosum Leprosum (systemic) Lucios reaction(hemorrhagic infarcts) Pathogenesis Chronic asymptomatic infections: bact. enter and multiply inside macrophages and never escape. Unknown cues cause multiplication of bacteria and release from macrophages. Survival: resistance to oxidative killing, inhibition of phagosome-lysosome fusion, resistance to lysosomal enzymes. AIDS is a common cause of reactivation by mechanisms unknown. Also: stress, overcrowding, age, silicosis Best treatment is prevention. Exact pathogenesis unknown. Treatment 4 drug regimen: INH, rifampin, pyrazinamide, ethambutol (last 2 for only 1st 3 mo) give for 9mos, 12 mos in AIDS pts Combination tx. b/c of MDR. Check w/cxr and sputum culture.

Mycobacterium bovis

same characteristics as M.TB, caused by infected dairy products, eradicated by pasteurization Acid-fast rods, aerobic, facultative intracellular,cannot be cultured in vitro, very slow growing, optimal growth at less than body temperature, carried on armadillos (low body temp), also trans by nasopharyngeal secretions or contact of skin wounds w/bacilli in the soil. Very long incubation of 1-20 years, hard to contract. Must have prolonged contact. Found in human skin and nerves.

Disease is pretty much eradicated in the US due to pasteurization.

source of BCG vaccine, no longer used, only 70% effective

Mycobacterium leprae

M. leprae is an intracellular pathogen. The clinical sx. correlate with the immune response to the pathogen. Tuberculoid pts have good CMI, lepromatous pts have decr CMI and their disease is disseminated. CMI is assessed by skin testing: Fernandez rxn, Mitsuda rxn:characterized by presence of granulomas, org. lymphocytes and macro-phages (competent CMI), + in tuberculoid pts/neg. in lepromatous pts. In reversal rxn Mitsuda goes from neg to + (DTH). Pts w/ HLA-DR 2,3 tend to get tuberculoid form, HLA-DQ 1 assoc w/ lepromatous form.

Dapsone + rifampin for the tuberculoid form. Clofazimine is added for lepromatous form or if organism is resistant to dapsone. Tx. is for at least 2 yr. Give dapsone for close family contacts, vaccine being researched.