Bug Parade – Flashcards
Unlock all answers in this set
Unlock answersquestion
| Vibrio cholerae biology |
answer
| comma-shaped, G- rod, 2 chromosomes, oxidase+, single polar flagellum, akali tolerant, O1 and O139 strains cause disease |
question
| Vibrio cholerae virulence factors |
answer
| mucinase, flagellum, pili (adherence and prevent elimination) cholera toxin and regulation by ToxR |
question
| Vibrio cholerae pathogenesis |
answer
| entry: fecal-oral, large inoculum attach: epithelial of small intestine, no invastion incubate: 2-3 days Symp: abrupt onset, non-inflammatory diarrhea and vomit, "rice water" stool, rapid fluid loss, dehydration Resolve: self-limiting if dehydration controlled, 60% mortality w/o tx |
question
| Vibrio cholerae epidemiology |
answer
| underdeveloped countries due to poor sanitation U.S.: contaminated seafood, travel to endemic areas |
question
| Vibrio cholerae diagnosis |
answer
| culture stool: grows on alkaline pH clinical: exposure, diet, diarrhea volume and description, outbreak detection |
question
| Vibrio cholerae treatment |
answer
| fluid and electrolyte replacement antibiotics: erythromycin, (tetracylcine) |
question
| Vibrio cholerae prevention |
answer
| no vaccine available sanitary water sources don't eat poop |
question
| Vibrio parahaemolyticus biology |
answer
| curved, G- rod, halophilic, motile |
question
| Vibrio parahaemolyticus virulence factors |
answer
| cytotoxins with enterotoxic activity |
question
| Vibrio parahaemolyticus pathogenesis |
answer
| self-limiting gastroenteritis incubate: 5-72 hours, abrupt onset watery diarrhea and vomiting |
question
| Vibrio parahaemolyticus epidemiology |
answer
| seafood-associated diarrhea (summer) case clusters (common source) |
question
| Vibrio parahaemolyticus therapy |
answer
| supportive only antibiotics - only if severe, doxycycline, criprofloxacin |
question
| Vibrio vulnificus biology |
answer
| curved, G- rod, halophilic, motile |
question
| Vibrio vulnificus virulence factors |
answer
| acidic polysaccharide capsule (antiphagocytic, resist C') pore-forming cytotoxin, proteases |
question
| Vibrio vulnificus pathogenesis |
answer
| primary sepsis: contaminated seafood causes invasive gastroenteritis, invades gut wall to blood stream, mortality >40% w/ tx rapid progress cellulitis: contaminated wound, inflammation of skin and subcutaneous tissue, rapid spread causes blisters and bullae (flaccid), bloodstream access, sepsis |
question
| Vibrio vulnificus epidemiology |
answer
| U.S.: costal waters, contaminated seafood or water Increased risk: liver disease, alcoholism, hermochromatosis, hematopoietic disease, or other chronic diseases |
question
| Vibrio vulnificus treatment |
answer
| antibiotics: doxycyline, cirprofloxacin support for sepsis |
question
| Vibrio vulnificus prevention |
answer
| avoid undercooked seafood proper wound care |
question
| Helicobacter pylori biology |
answer
| spiral/S-shaped G-, motile, microaerophile, oxidase+, catalase+ |
question
| Helicobacter pylori virulence factors |
answer
| flagella (polar tuft) mucinase, adhesions (non-pilus) hemagglutinin, sialic acid-binding protein, Lewis blood group adhesion, cytotoxins, urease (breaks urea to CO2 and NH4) |
question
| Helicobacter pylori pathogenesis |
answer
| entry: fecal-oral target: stomach disease: chronic gastritis 90% of duodenal ulcers, 50-80% of gastric ulcers predisposes to gastric carcinoma and gut-associated lymphoma |
question
| Helicobacter pylori epidemiology |
answer
| 50% of U.S. population has |
question
| Helicobacter pylori diagnosis |
answer
| non-invasive: urea breath test, serology, stool Ag test invasive: biopsy for histology and rapid urease test |
question
| Helicobacter pylori treatment |
answer
| cocktail antibiotics (metronidazole + tetracyline or macrolide), acid-inhibitor, anti-inflammatory med |
question
| Campylobacter jejuni biology |
answer
| curved, G- rod, motile, microaerophilic, oxidase+, catalase+, grows at 42* but not at 25*C |
question
| Campylobacter jejuni virulence factors |
answer
| toxins, adhesins LPS O-Ag sialic acid mimices ganglioside on neural tissue (Abs to will cause autoimmunity) |
question
| Campylobacter jejuni pathogenesis |
answer
| entry: oral disease: invasive, inflammatory gastroenteritis incubate: 1-7 dyas symps: fever, chills, myalygia, headache, then acute onset of watery diarrhea (+/- blood), cramps mild to severe sequelae: Guillan-Barre syndrome (nerve autoimmune disease) |
question
| Campylobacter jejuni epidemiology |
answer
| leading cause of bacterial-food poisoning undercooked/raw poultry and unpasteurized milk |
question
| Campylobacter jejuni diagnosis |
answer
| stool culture, selective media: grows at 42* but not 25*C gram-stain (G- rod) |
question
| Campylobacter jejuni treatment |
answer
| supportive severe, antibiotics: tetracycline, macrolides, quinolones |
question
| Campylobacter fetus biology |
answer
| curved, G- rod, motile, microaerophilic, oxidase+, catalase+, grows at 25* but not 42*C |
question
| Campylobacter fetus virulence factors |
answer
| protein capsule (S-layer) |
question
| Campylobacter fetus pathogenesis |
answer
| entry: oral route disease: systemic infections (sepsis) that follow gastroenteritis episodes |
question
| Campylobacter fetus epidemiology |
answer
| rare in U.S., usually only immunocompromised contaminated food (undercooked) or water |
question
| Campylobacter fetus diagnosis |
answer
| stool culture, selective media: grows at 25* but not 42*C gram-stain (G- rod) |
question
| Campylobacter fetus treatment |
answer
| antibiotics: tetracyclines, macrolides, quinolones support for sepsis |
question
| Clostridium perfringens biology |
answer
| large, G+ bacilli, spore forming, anaerobes, hisototoxic, non-motile, aerotolerant, 5 types (A-E) based on toxins, Type A is most human infections |
question
| Clostridium perfringens virulence factors |
answer
| major toxins: alpha, beta, epsilon, iota enterotoxin is superantigen for T cells |
question
| Clostridium perfringens pathogenesis |
answer
| Gastroenteritis: oral entry, large inoculum, target small intestine, heat-labile enterotoxin from spores, adominal cramps, watery diarrhea Cellulitis: subcutanenous tissue infection, multiply and release toxins, discoloration, gas formation, bullae, edema, non-pain, no necrosis Supprative myositis: faciitis, wound contam with spores, toxin release, accumulation of pus, no necrosis or systemic involvement Clostridial myonecoris: gas gangrene, wound with spores, toxin release, acute onset, severe pain, extensive muscle necrosis, skin discoloration, tachycardia, fever, intravascular hemolysis, shock, organ failure, 40-100% mortality Necrotizing Enteritis: caused by Type C, necosis in jejunum, Beta-toxin, acute abdominal pain, vomiting, bloody diarrhea, perforation -> peritonitis and shock |
question
| Clostridium perfringens epidemiology |
answer
| soft tissue: wound, trauma, surgery, vascular insufficiency increases risk gastro: comtaminated meats, cook then cooling period (spores germinate and multiply) |
question
| Clostridium perfringens diagnosis |
answer
| soft tissue: large G+ rods, lack of WBC invasion, gas in tissues (Xray or palp) gastro: recovery from food or feces |
question
| Clostridium perfringens treatment |
answer
| soft tissue: penicillin gas gangrene: surgical debridement, amputation, penicillin, clindamycin, metronidazole gastro: supportive, no antibiotics |
question
| Clostridium perfringens preventation |
answer
| proper wound care judicious prophalaxis refrigerate food quickly, heat leftovers thoroughly |
question
| Clostridium difficile biology |
answer
| large, G+ bacilli, spore forming, strict anaerobes, hisotoxic, oxidase+, catalase+, motile |
question
| Clostridium difficile virulence factors |
answer
| adhesins for colonic epithelial toxin A: damage tight junctions, increase permeability of gut, chemoattract for PMNs toxin B: cytotoxin, destroys cytoskeleton, kills enterocytes spores: longer survival in hospital setting |
question
| Clostridium difficile pathogenesis |
answer
| disease: antibiotic associated colitis endogenous or exogenous infectio bns entry: oral-fecal (spores or germination) bacteria adhesins and toxins cause local damage with inflammation, self-limiting Pseudomembranous colitis: fever, abdominal pain, bloating, cramping, fulminant watery diarrhea with WBC, inflammatory plaques can progress to Toxin Megacolon |
question
| Clostridium difficile epidemiology |
answer
| high association with antibiotic use (5-10 d after start or 2-10weeks after finish) hospitalized and elderly |
question
| Clostridium difficile diagnosis |
answer
| detect toxin A or B in stool (immunoassay) |
question
| Clostridium difficile treatment |
answer
| discontinue causitive antibiotic tx antibiotic: metronidazole or ORAL vancomycin |
question
| Clostridium difficile prevention |
answer
| rapid diagnosis contact precautions rigorous hospital room cleaning |
question
| Clostridium botulinum biology |
answer
| large, G+ bacilli, spore forming, strict anaerobes, neurotoxic, motile, 7 serotypes (A-G) Group I: A, B or F Group II: B, E or F produce botulinum toxin |
question
| Clostridium botulinum virulence factors |
answer
| spore formation botulinum toxin: flaccid paralysis, heat-labile, AB toxin B toxin - protects from degradation in gut A - Zn-dependent endopeptidase; targets NMJ, no ACh release, flaccid |
question
| Clostridium botulinum pathogenesis |
answer
| Food-borne: intoxication; ingestion of toxin, enters blood stream, goes to peripheral nerves; incubate 12-71 hrs; dry mouth, diplopia, ptosis, pupil dilation, dyphagia, nausea, vomit; progresses to bilateral, descending wekanes; death from resp. failure; toxin binds irreversible, long reovery Infant: infection; ingest spores, infects gut (poor NF); initially: constipation, weak cry, lethargy, poor feed/drink; progress: flaccid paralysis, floppy baby, respiratory distress; 1-2% die, in SIDS Wound: infection; spores contaminate wound, produce toxin; incubate 4-14 days; similar to food-borne plus fever, leukocytosis, and co-infections |
question
| Clostridium botulinum epidemiology |
answer
| Food-borne: canned food, preserved fish Infant: honey, dust Wound: IV drug users |
question
| Clostridium botulinum diagnosis |
answer
| Food-borne: bioassay for toxin activity (serum, feces, gastric fluid, and implicated food) Infant: culture from feces |
question
| Clostridium botulinum treatment |
answer
| respiratory support antitoxin (equine >1y/o, human <1y> wound only: penicillin metronidazole to follow antitoxin |
question
| Clostridium botulinum prevention |
answer
| heat food >60* avoid honey for infants, breast feeding can be protective proper wound care |
question
| Clostridium tentani biology |
answer
| large, G+ bacilli, spore forming, strict anaerobes, neurotoxin, motile, round terminal spores (tennis racket) |
question
| Clostridium tentani virulence factors |
answer
| spore formation tetanolysin (oxygen-labile hemolysin) tetanospasmin - heat-labile, AB toxin, B binds motor neurons, A is Zn-dependent endopeptidase |
question
| Clostridium tentani pathogeneis |
answer
| Tetanus: spastic paralysis; infection of spores in wound; incubate 1-21days, usually <8days; anaerobic causes germination, vegatative bacteria produce tetanospasmin, travels to blood, binds motor nerve endings, travels to CNS, blocks release of GABA, unregualted spastic activity; binds irreversibly, long recovery Generalized: most common, trismus, risus sardinocus, body-wide spasms, opisthotonos, can progress to autonomic nerves Localized: spasms at 1* infection site, indicates partial immunity or is the prodrome of generalized Cephalic: head is 1* infection site Neonatal: 1* infection at umbilical cord, becomes generalized, >90% mortality from apnea or sepsis |
question
| Clostridium tentani epidemiology |
answer
| rare in U.S., developing countries more prevalent 30-50% mortality |
question
| Clostridium tentani diagnosis |
answer
| clinical presentation, history of wound or prior vaccination |
question
| Clostridium tentani treatment |
answer
| debride 1* wound passive immunization (TIG) metronidazole vaccinate with tetanus toxoid supportive therapy until recovery |
question
| Clostridium tentani prevention |
answer
| vaccine: DTAP, 5 childhood, booster/10yr prophilaxis: depends on vaccine hisotry educate: about hygiene for cutting and cleaning umbilical cord |
question
| Corynebacterium diphtheriae biology |
answer
| G+ rod, nonmotile, aerobic, normal flora on skin, irregular club-shapted, "chinese leters", short chain myocolic acids in wall |
question
| Corynebacterium diphtheriae virulence factors |
answer
| diphtheria toxin - AB toxin, encoded on phage (lysogenic conversion), produced at site, travels in blood, targets heart and nerve cells A - ADP-ribosylation enzyme, shuts down protein synthesis, host cell death |
question
| Corynebacterium diphtheriae pathogenesis |
answer
| Respiratory: 2-4 day incubate; sudden onset of malaise, low fever, sore throat, exudative pharyngitis (thick pseudomembrane that is adherent); systemic complications include myocarditis (1-2weeks) or neurophathy (10-30days) at oculomotor and ciliary nerves Cutaneous: asymptomatic on carrier, trans by direct contact; papule --> pustule --> nonhealing ulcer that may have grayish membrane; co-infection with G+ cocci usually |
question
| Corynebacterium diphtheriae epidemiology |
answer
| Respiratory: poor urban areas around world, seen in elderly Cutaneous: homeless, alcoholics, poor areas, reservations |
question
| Corynebacterium diphtheriae diagnosis |
answer
| clincal findings: start intial treatment Grow on tellurite medium -> black colonies toxin production (immunoassay, PCR tox gene) takes a long time for confirmation |
question
| Corynebacterium diphtheriae treatment |
answer
| Respiratory: keep airway open, antitoxin from CDC Cutaneous and resp: penicillin, macrolide, tetracycline after recover, immunize with toxoid |
question
| Corynebacterium diphtheriae prevention |
answer
| DTaP vaccine prophylaxis of close contacts isolate respiratory pts contact precautions with cutaneous pts |
question
| Bordetella pertussis biology |
answer
| G- coccobacillus, strict anaerobe, very small, nonmotile |
question
| Bordetella pertussis virulence factors |
answer
| tracheal cytotoxin (TCT) - disacch tetrapeptide like PG, binds and kills epithelial cells, induces IL-1 and fever pertussis toxin (PT) - AB5 toxin, ribosylates G-protein, cAMP increase, increase mucus secretion hemolysin - increases cAMP directly, inhibits chemotaxis and phagocytosis by PMNs adhesins (ciliated brochial epithelial), filamentous hemagglutinin, pertactin, fibriae Type III secretion (proctects against host) |
question
| Bordetella pertussis pathogenesis |
answer
| disease: Whooping cough entry: respiratory incubate: 7-10days Catarrhal stage - 1-2weeks, resembles common cold, most contagious, highest load Paroxysmal: 1-6 weeks, ciliated cells dying, mucus clearance impaired, deep violent coughing followed by inspiratory whoop and possible vomiting Convalescent: paroxysms diminish in # and severity, secondary complications still possible (pneumonia) |
question
| Bordetella pertussis epidemiology |
answer
| endemic worldwide pretty common, rising incidence in U.S. due to incomplete vaccine regemine |
question
| Bordetella pertussis diagnosis |
answer
| PCR (culture) |
question
| Bordetella pertussis treatment |
answer
| supportive b/c recognized after peak load macrolides if severe |
question
| Bordetella pertussis prevention |
answer
| DTaP vaccine prophylaxis to close contacts to reduce carriage |
question
| Bacillus antracis biology |
answer
| G+ bacillus, pairs or long chains, large, spore-forming, aerobic, nonmotile, nonhemolytic, grow rapidly in culture |
question
| Bacillus antracis virulence factors |
answer
| Capsule - poly-D-glutamic acid, invasive Toxins (EF/PA or LF/PA) Edema factor - adenylate cyclase, increases [cAMP], hypersecretion, edema in tissues Lethal factor - Zn-dependent endopeptidase, induces apoptosis, necrosis of cells, tissue damage Protective antigen - binding component, combines with and delivers EF or LF |
question
| Bacillus antracis pathogenesis |
answer
| Inhalation: spores in, move to LRT, multiply in lymph nodes; incubate 1-7days; initally flu-like, later worse pulm (necrosis, hemorrhage, effusion), elargemetn of lymph nodes, meningitis (50%), high fever, shock; die in 3 days w/o tx Cutaneous: spores in cut, painless pustule surrounded by vesicles, regional lymphadenopathy, black/painless eschar with massive edema; 20% die w/o tx, rare with tx GI: enter oral route; incubate 2-5days; abdominal pain, messenteric lymphadenopathy, nausea, vomit, diarrhea, GI necrosis, ulcer of mouth/throat, progresses to sepsis and shock; mortality 100% w/in few days |
question
| Bacillus antracis epidemiology |
answer
| Inhalation: rare in U.S., bio-terrorism organism, wool-sorters Cutaneous: 95% of natural cases of this microbe GI: very rare, herbivores |
question
| Bacillus antracis diagnosis |
answer
| microscopy/culture: grows fast to high numbers, motile, hemolytic PCR - new, faster |
question
| Bacillus antracis treatment |
answer
| 1st line: penicillin, doxycyline, ciprofloxacin combo with other antibiotics |
question
| Bacillus antracis prevention |
answer
| Vaccine: for animals, humans in military and handling imported animal products prophylaxis for 60days if exposed |
question
| Bacillus cereus biology |
answer
| G+ bacillus, large, spore-forming, aerobic, hemolytic, transient colonize skin |
question
| Bacillus cereus virulence factors |
answer
| heat-stable and heat-labile toxins |
question
| Bacillus cereus pathogenesis |
answer
| Emetic food: ingest contaminated rice; spores survive cook, germinate during cooling, produce toxins; incubate 30min-6hrs, heat-stable enterotoxin inudces nauesea, vomiting, abdominal cramps; duration 8-12 hours Diarrheal Food: ingest contaminated meat, vegetables, sauces; spores survive cooking, germinate in gut; incubation 9-18hrs; heat-labile toxin acts like cholera toxin, induces [cAMP] causing water diarrhea, duration 20-36 hrs |
question
| Bacillus cereus treatment |
answer
| supportive no antibiotics severe: vancomycin or clindamycin |
question
| Bacillus cereus prevention |
answer
| proper food handling and storage |
question
| Pseudomonas aeruginosa biology |
answer
| G- rod, aerobic, non-fermentative, oxidase+, fluorescein pigments: pyocyanin and pyoverdin, sweet culture odor; forms clear colony on MacConkey |
question
| Pseudomonas aeruginosa virulence factors |
answer
| multi-drug resistant, simple growth requirements, versatile pilus, flagella ETA - inhibits protein synthesis S and T exoenzymes - cytotoxic, manipulate actin rearrangment, secreted by T3SS elastase, protease, hemolysins, pyocyanin, pyoverdin, quorum sensing, capsule, biofilm |
question
| Pseudomonas aeruginosa pathogenesis |
answer
| Normal hosts: foliculitis, otitis externa, eye infections, endocarditis (IV drug users), pneumonia (ventilator, high mortality), UTIs, IV-line sepsis Abnormal hosts: Chronic colonization: pulmonary infection; increased mucus secretion from CF pts, long-term infection; loses pili, flagella and O antigesn, upregulates biofilm w/ quorom sensing; loss of lung function from inflammatory destruction Invasive mode: malignant otitis externa (diabetics) Systemic infection: ecthyma gangrenosum, hemorrhagic lesions on skin due to elastase production |
question
| Pseudomonas aeruginosa epidemiology |
answer
| Oppportunistic: antibiotic treatment, foreign body, VAP, IMC, burn pts, CF pts Chronic - cystic fibrosis Invasive - diabetes mellitus Systemic - neutropenic, burn pts, pneumonia, and CF pts |
question
| Pseudomonas aeruginosa diagnosis |
answer
| green pigmentation of culture fruit odor oxidase+ clear growth on MacConkey |
question
| Pseudomonas aeruginosa treatment |
answer
| aminoglycoside + anti-pseudomonas B-lactam |
question
| Pseudomonas aeruginosa prevention |
answer
| avoid broad spectrum antibiotics in general prevent contamination of sterile objects |
question
| Escherichia coli biology |
answer
| G- rod, oxidase- |
question
| Escherichia coli virulence factors |
answer
| O antigen, H antigen, K/Vi antigen, endotoxin, capsule, antigenic phase variation, T3SS, antibiotic resistance plasmids |
question
| Escherichia coli pathogenesis |
answer
| UTI: normal flora of GI travel up to kidney, uropathogenic E coli more virulent (P pili and HlyA) Neonatal: 2nd most common cause of meningitis, K-1 capsular antigen strain, not normal flora but found in pregger GI, high mortality Bacteremia and sepsis |
question
| Escherichia coli epidemiology |
answer
| UTI - women, newly married, elderly, urinary catheters |
question
| Escherichia coli diagnosis |
answer
| UTI - gram stain, oxidase test (-) Neonatal - ultrasound, showing brain abnormality |
question
| Escherichia coli treatment |
answer
| UTI - trimethoprim |
question
| Escherichia coli prevention |
answer
| UTI - cleaning urethral meatus, cranberries, blueberries |
question
| Enteropathogenic E. coli (EPEC) virulence factors |
answer
| T3SS, intimin, Tir, pili |
question
| Enteropathogenic E. coli (EPEC) pathogenesis |
answer
| loose attachment by pili, pestal formation induced by T3SS: injects Tir which is expressed by host then and is receptor for intimin adhesin on bacterium attaches to epithelial cells of small intestine, destroys microvilli, cause watery diarrhea, incubates 2-6days, acute onset, lasts 1-3 weeks |
question
| Enteropathogenic E. coli (EPEC) epidemiology |
answer
| developing countries, esp. infant diarrhea |
question
| Enteropathogenic E. coli (EPEC) diagnosis |
answer
| lactose fermentation, green sheen on EMB agar, culture, serotype, probe for exotocins |
question
| Enteropathogenic E. coli (EPEC) treatment |
answer
| treat symptoms disseminated: fluoroquinolone and susceptibility testing |
question
| Enterotoxigenic E. coli (ETEC) virulence factors |
answer
| high ID(50); heat-labile (LT-I and LT-II) - like cholera, increases cAMP -> increase solute secretion heat-stable (STa and STb) - cGMP mediated fluid secretion |
question
| Enterotoxigenic E. coli (ETEC) pathogenesis |
answer
| 1-2 day incubation diarrhea for 3-4 days |
question
| Enterotoxigenic E. coli (ETEC) epidemiology |
answer
| developing coutries, traveler's diarrhea, feces-contaminated food or water |
question
| Enterotoxigenic E. coli (ETEC) diagnosis |
answer
| lactose fermenation, green sheen on EMB agar, culture, serotype, probe for exotoxins |
question
| Enterotoxigenic E. coli (ETEC) treatment |
answer
| treat symptoms disseminated: fluoroquinolones and susceptibility testing |
question
| Enterohermorrhagic E. coli (EHEC, STEC, VTEC) virulence factors |
answer
| low ID(50), shiga-like verotoxin Stx1 - binds to 28S rRNA, destroys intestinal villi, Stx2 - targets and destroys endothelial cells |
question
| Enterohermorrhagic E. coli (EHEC, STEC, VTEC) pathogenesis |
answer
| Hermorrhagic colitis: incubate: 3-4 days; watery diarrhea with abdominal pain, vomit (50%), after 2 days, bloody diarrhea, intense ab pain, no fever; requires hospitaliztion, resolves ~1wk HUS: shiga-toxin enters systemic circulation; acute renal failure, hemolytic anemia, thrmobocytopenia; 5-10 days after dairrhea onset |
question
| Enterohermorrhagic E. coli (EHEC, STEC, VTEC) epidemiology |
answer
| developed countires "hamburger disease", unpasteurized milk, fruit juice, uncooked vegetables, fruits |
question
| Enterohermorrhagic E. coli (EHEC, STEC, VTEC) diagnosis |
answer
| MacConkey agar with sorbitol, serology O157 antigen, stool containing Shiga-like toxin |
question
| Enterohermorrhagic E. coli (EHEC, STEC, VTEC) treatment |
answer
| supportive, monitor for HUS no antibiotics b/c would increase toxin release |
question
| Enteroinvasive E. coli (EIEC) virulence factors |
answer
| pInv genes - for invasion of colonic epithelium |
question
| Enteroinvasive E. coli (EIEC) pathogenesis |
answer
| 2-3day incubation, water diarrhea to dysentery-like syndrome (mucoid, bloody diarrhea, cramps, fever), lasts 1-2wks |
question
| Enteroinvasive E. coli (EIEC) epidemiology |
answer
| rare in US, uncommon in developing countries |
question
| Enteroinvasive E. coli (EIEC) diagnosis |
answer
| lactose fermentation, green sheen on EMB agar, culture, serotype, probe for exotoxins |
question
| Enteroinvasive E. coli (EIEC) treatment |
answer
| treat symptoms disseminated: fluoroquinolone and susceptibility testing |
question
| Enteroaggregative E. coli (EAEC) virulence factors |
answer
| bundle-forming fimbriae causes autoagglutination |
question
| Enteroaggregative E. coli (EAEC) pathogenesis |
answer
| persistent watery diarrhea causes dehydration and growth retardation in children |
question
| Enteroaggregative E. coli (EAEC) epidemiology |
answer
| developing countries |
question
| Enteroaggregative E. coli (EAEC) diagnosis |
answer
| lactose fermentation, green sheen on EMB agar, culture, serotype, probe for exotoxins |
question
| Enteroaggregative E. coli (EAEC) treatment |
answer
| treat symptoms disseminated: fluoroquinolones and susceptibility testing |
question
| Shigella dysenteriae biology |
answer
| G- rod, oxdiase-, faculative anaerobe, non-lactose fermentor, nonmotile, low ID(50) |
question
| Shigella dysenteriae virulence factors |
answer
| invasion plasmid IpaD - recognizes receptors on enterocytes IpaA and IpaB - promotes invasion T3SS - injects IpaA and IpaB IL-1b - secreted by infected cells, attracts PMNs and leukocytes Shiga toxin - inhibits protein synthesis by cleaving 28S rRNA |
question
| Shigella dysenteriae pathogenesis |
answer
| Trans: fecal-oral (contaminated salads, like potato, shrimp, chicken, tuna), raw veggies, dairy products, meat, water, food handlers incubate: 1-7dyas small volume diarrhea, mild abdominal discomfort to full-blown dysentery (cramps, fever, diarrhea, vomit, blood, pus or mucous in stools), mucosal ulceration, rectal bleeding dehydration |
question
| Shigella dysenteriae epidemiology |
answer
| daycare outbreaks, children |
question
| Shigella dysenteriae diagnosis |
answer
| fecal leukocytes, culture stool |
question
| Shigella dysenteriae treatment |
answer
| FQ and guided susceptibility |
question
| Salmonella enteritidis biology |
answer
| G- rod, oxidase-, motile, non-lactose fermentors, high ID(50) |
question
| Salmonella enteritidis virulence factors |
answer
| T3SS - SPI-1 and SPI-2, resistance to acid (ATR gene) |
question
| Salmonella enteritidis pathogenesis |
answer
| Trans: contaminated poultry, eggs, water or contact with contaminated pet; target: infection limited to lumen of intestine incubate: 18-36hrs symps: abdominal pain, diarrhea, fever, headache, chil, self-limiting in few days |
question
| Salmonella enteritidis epidemiology |
answer
| major cause of gastroenteritis 3rd most common food-poisoning agent in elderly and infants, can be life-threatening |
question
| Salmonella enteritidis treatment |
answer
| no antibiotics, might prolong disease |
question
| Salmonella typhi biology |
answer
| G- rod, oxidase-, motile, non-lactose fermentors |
question
| Salmonella typhi virulence factor |
answer
| TS3 - SPI-1 and SPI-2, resistant to acid (ATR gene), low ID(50), replication/spread in macrophages, persistent in gallbladder |
question
| Salmonella typhi pathogenesis |
answer
| trans: fecal-oral, contaminated food or water, person-to-person Typhoid fever: severe systemic, sustained fever and abdominal symptoms 1st week - rising, stepwise fever, bacteremia 2nd week - abdomen pain and rose spot rash on abdomen and trunk 3rd week - hepatomegaly, splenomegaly, intestinal bleeding |
question
| Salmonella typhi epidemiology |
answer
| developing countries |
question
| Salmonella typhi diagnosis |
answer
| culture from blood or marrow |
question
| Salmonella typhi treatment |
answer
| FQ or chloramphenicol |
question
| Salmonella typhi prevention |
answer
| vaccines: capsule or live |
question
| Klebsiella pneumoniiae biology |
answer
| G- rod, oxidase negative, nonmotile, ferments lactose, normal flora in GI and URT 5% |
question
| Klebsiella pneumoniiae virulence factors |
answer
| prominent capsule with mucoid appearance |
question
| Klebsiella pneumoniiae pathogenesis |
answer
| common cuase of community acquired primary lobar pneumonia thick bloody sputum with currant-jelly appearance |
question
| Klebsiella pneumoniiae epidemiology |
answer
| alcoholics with compromised pulmonary function |
question
| Klebsiella pneumoniiae treatment |
answer
| cephalosporins |
question
| Enterobacter biology |
answer
| G- rod, oxidase negative |
question
| Enterobacter virulence factor |
answer
| ESBL - expended spectrum beta-lactamases effective against 3rd generation beta-lactams |
question
| Enterobacter pathogenesis |
answer
| UTI in patients with urinary catheters Bacteremia in ICU |
question
| Enterobacter epidemiology |
answer
| urinary catheters and ICU |
question
| Serratia biology |
answer
| G- rod, oxidase- |
question
| Serratia pathogenesis |
answer
| nosocomial pneumonia |
question
| Proteus biology |
answer
| G- rod, oxiase- |
question
| Proteus pathogenesis |
answer
| nosocomial and community-acquired pylonephritis and cytitis kideny stones |
question
| Proteus diagnosis |
answer
| swarming motility powerful urease activity |
question
| Yersinia enterocolitica biology |
answer
| G- rod, faculatative anaerobic, siderophilic |
question
| Yersinia enterocolitica virulence factors |
answer
| grows at 4* C Yop proteins - encoded on plasmids, injected via T3SS, prevent phagocytosis, induces apoptosis of macrophages, suppresses cytokine production |
question
| Yersinia enterocolitica pathogenesis |
answer
| Gastroenteritis with contaminated foods Blood-transfusion related bateremia |
question
| Yersinia pestis biology |
answer
| G- rods, facultative anaerobes, siderophilic, zoonotic |
question
| Yersinia pestis virulence factors |
answer
| Yop proteins - encoded on plasmids, injected via T3SS, prevent phagocytosis, induces apoptosis of macrophages, suppresses cytokine production Capsule, plasminogen activating protease (rapid spread), serum resistant factor |
question
| Yersinia pestis pathogenesis |
answer
| Urban plague, Black Death, Sylvatic plague Trans: aerosol, fleas are host, rodents are reservoir Bubonic plague: incubate 7 days; sudden onset of fever, chills, weakness, headache, painful bulbo in groin/axilla, bacteremia, subepidrual hemorrhages, necrosis of extremities; 75% fatality Pneumonic plague: 2* from bubonic or 1* from inhalation; rapid progressive necrotic pneumonia, highly infectious, 90% fatality |
question
| Yersinia pestis epidemiology |
answer
| Category A bioterrorism agent |
question
| Yersinia pestis diagnosis |
answer
| Suspicion when: fever and painful lymphadenopathy, traveled to endemic area, contact with vector Culture and bipolar staining RPT: F1 antigen detection, high specificity and sensitivity |
question
| Yersinia pestis treatment |
answer
| streptomycin or tetracyline respiratory isolation (until pneumonia is ruled out, 48 hrs of therapy, and sputum culture is negative) |
question
| Bacteroides fragilis biology |
answer
| G- rod, strict anaerobic, endogenous (normal flora) |
question
| Bacteroides fragilis virulence factors |
answer
| capsule B. fragilis toxin extracellular enzymes |
question
| Bacteroides fragilis pathogenesis |
answer
| Abdominal abscesses and bacteremia Wound exudates have strong, foul-smelling discharge due to organic acid production |
question
| Bacteroides fragilis diagnosis |
answer
| growth in 20% bile collect and transport in oxygen-free environment |
question
| Bacteroides fragilis treatment |
answer
| Metronidazole + surgery + antibiotics for G- aerobic infection if mixed resistant to kanamycin, vancomycin and colistin |
question
| Peptostreptococcus biology |
answer
| G+ cocci, strict anaerobe, endogenous to mouth, GI tract and genital tract |
question
| Peptostreptococcus pathogenesis |
answer
| wound infections, aspiration pneumonia, lung abscesses, brain abscesses, chronic otitis media, OBGYN infections |
question
| Actinomyces israellii biology |
answer
| G+ rod, strict anaerobe, filamentous, not acid fast |
question
| Actinomyces israellii pathogenesis |
answer
| colonize URT and GI tracts Chonic granulmatous lesions: become supprative and form abscesses connected by sinus tract Cervicofacial abscesses: patients with poor oral hygine or recent invasive dental procedure |
question
| Actinomyces israellii diagnosis |
answer
| sulfur granules: macroscopic colonies like grains of sand |
question
| Actinomyces israellii treatment |
answer
| penicillin + surgical intervention |
