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396 Cards in this Set
- Front
- Back
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morphology of genus Clostridium?
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anaerobic Gm(+) spore-forming rods
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where are clostridium found?
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soil and occassionally in the intestinal tract
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morphology and characteristics of C. perfringens?
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moderate anaerobes; large, nonmotile rod with 'boxcar' ends
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which toxin type is responsible for most human disease with c. perfringens?
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Type A or alpha toxin
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properties of alpha toxin of c. perfringens?
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phospholipase C, major lethal toxin
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transmission of c. perfringens?
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traumatic or nontraumatic, exogenous or endogenous
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characteristics of anaerobic cellulitis caused by c. perfringens?
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localized with no invasion to healthy muscle
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describe myonecrosis and its pathogenesis
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necrotizing invasion of healthy muscle due to major alpha toxin production
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treatment of c. perfringens infections?
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debridement of necrotic tissue, penicillin, with possible hyperbaric oxygen
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is there a vaccine for c. perfringens?
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no
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third most common cause of food poisoning?
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C. perfringens
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food poisoning from C. perfringens involving ingestion of?
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mixture of the organisms and the enterotoxins
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symptoms of C. perfringens food poisoning?
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diarrhea with rare vomiting and short duration fever
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mechanism of action of C. perfringens enterotoxin?
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stimulate fluid secretion in intestines
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which organism sporulates well in the intestines?
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C. dificile
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main virulence factors of c. dificile?
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exotoxins, specifically toxin A and B
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pathogenesis of toxins A and B of c. dificile?
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fluid accumulation, cell death, inflammation
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why are new NAP1 strains of c. dificile so severe?
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produce 20x more of both toxin A and B
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what toxin is highly associated with NAP1 strains of c. dificile causing more severe disease?
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binary toxin
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is c. dificile normal flora?
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in 70% of newborns but only 1-8% of health adults, increasing during hospitalization
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where is c. dificile commonly found?
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soil, water, intestines of animals
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what induces classic disease from c. dificile?
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antibiotic treatment
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which antibiotics are commonly associated with c. dificile overgrowth?
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clindamycin, amphicillin/amoxicillin
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which antibiotics are uncommonly related and often used as treatment for c. dificile overgrowth?
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vancomycin, metronidazole
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what is the classical disease caused by c. dificile?
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nosocomial diarrhea
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what populations are susceptible to c. dificile infection?
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recent antimicrobial use, length of stay in healthcare facility, >60 yo, underlying illness
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clinical manifestations of c. dificile infection?
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inflammatory diarrhea with formation of yellow pseudomembrane in colon, may lead to ulceration
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how is c. dificile infection diagnosed?
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A/B toxins in stool with antigen detection kit and yellow pseudomembrane on colonoscopy
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what are strategies to re-establish normal flora following c. dificile infection?
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probiotics or fecal transplantation
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prevention strategies for c. dificile infection?
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non-toxigenic c. dificile, soap and water handwashing
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what disease is seen with c. septicum?
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necrotizing disease of the colon
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what are symptoms of c. septicum infection?
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sudden onset of abdominal pain, fever, diarrhea
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what makes patients more susceptible to c. septicum infection?
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neutropenia and immunosuppression, NOT antibiotic induced
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are anaerobes commonly found as normal flora?
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yes
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what predisposes infection with anaerobes?
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reduction of tissue oxidation-reduction potential (loss of blood supply, growth of facultative anaerobes to use of oxygen)
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what is a key clinical clue to possible infections with anaerobes?
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foul-smelling lesion or discharge
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what is the most commonly isolated anaerobe?
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bacteriodes fragilis
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oxygen tolerance of bacteriodes fragilis?
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moderate anaerobe
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major virulence factor for bacteriodes fragilis?
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polysaccharide capsule
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which organism has LPS but shows no endotoxin activity (aka bacteremia without sepsis)?
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bacteroides fragilis
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what are common clinical manifestations of anaerobes?
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abscesses, peritonitis, wound infection, cervico-facial infections, necrotizing pneumonia, pelvic inflammatory disease, bite wounds
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which organism and toxin has potential to cause diarrhea in young children and is associated with inflammatory bowel disease?
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enterotoxin-producing b. fragilis (ETBF)
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which anaerobe has many antibiotic resistances, including penicillin, aminoglycosides, etc.?
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b. fragilis
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what is the most commonly recommended antibiotic for b. fragilis infection?
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metronidazole
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what is recommended treatment for abscesses?
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surgical drainage
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fusobacterium is normal flora of which locations?
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oral cavity and/or intestinal tract
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morphology of fusobacterium nucleatum?
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pleomorphic, Gm(-) long thin bacilli with pointed ends (fusiform)
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morphology of peptostreptococcus?
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Gm(+) cocci in chains
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peptostreptococcus is normal flora of which locations?
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skin, mouth, female genital tract, intestinal tract
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clinically is peptostreptococcus found in isolation?
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no, usually part of a mixed infection
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morphology of actinomyces?
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Gm(+) filamentous branching bacilli, not acid-fast
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what is characteristic of pus from an actinomyces infection?
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sulfur granules
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where is actinomyces normal flora?
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oral cavity, intestinal tract, vagina
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what are the most common clinical manifestations of actinomycosis?
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cervicofacial lesions, abdominal lesions, salpingitis
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where is eikenella corrodens normal flora?
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oral cavity, URT, other mucosal surfaces
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why is it often considered with anaerobes?
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often found in mixed infections with anaerobes
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morphology of eikenella corrodens?
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Gm(-) bacilli
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clinical manifestations of eikenella corrodens?
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human bite infections, bloodstream invasion with subacute endocarditis
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treatment for what infection must include aerobic and anaerobic coverage?
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human bite infections
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50% of clinically significant isolates?
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enterobacteriacae
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lactose fermentation distinguishes which population of enterobacteriaceae?
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escherichia, (coliforms)
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major virulence factor of e. coli?
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pili (fimbrae) used for adherence
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ETEC strains of e. coli produce which toxin and what does it cause?
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enterotoxins; watery diarrhea
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EHEC strains of e. coli produce which toxin and what does it cause?
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shiga-like toxin; enterohemorrhagic colitis
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where is e. coli normal flora?
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intestinal tract
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which diarrhea-causing e. coli are transmitted via animal-to-human (food supply)?
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EHEC
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clinical manifestations of EHEC?
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watery diarrhea with progression to copious blood diarrhea, possible development of HUS in children <5 yo
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pathogenesis of EHEC?
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local infection with systemic and local toxemia - destruction of renal endothelial and glomerular cells leads to development of HUS
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antibiotic therapy for EHEC?
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none, may enhance toxin release and make HUS worse
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prevention of EHEC infection?
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no vaccine, block transmission of animal feces into food/water
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what disease is associated with ETEC?
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Travelers diarrhea - watery diarrhea
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which population is susceptible to ETEC infection?
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infants and children of developing countries or tourists
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how is ETEC transmitted?
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person-to-person through contaminated food or water
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what are clinical features of ETEC?
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watery diarrhea, absent fever
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where do ingested ETEC adhere?
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small intestines
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where is shigella considered normal flora?
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never considered normal flora
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major virulence factor of shigella?
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shiga toxin
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what are the effects of shiga toxin?
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lethal toxin locally causing bloody diarrhea and systemically killing renal endothelial cells leading to kidney failure
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how does shigellosis differ from dysentery?
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much milder with less shiga toxin production, more common in the US
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how is shigella transmitted?
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fecal oral route
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what populations are more commonly infected with shigellosis?
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pediatric with spread in day-care centers and elementary schools
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what are the clinical characteristics of bacterial dysentery?
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frequent, small volume bloody, mucoid discharge with pus (leukocytes) and fever
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where does shigella reproduce?
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invasion and intracellular replication within colonic epithelial cells
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what are severe complications of bacterial dysentery?
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HUS and extensive ulceration
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antibiotic treatment for dysentery?
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none with HUS, makes it worse
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prevention for shigella infection?
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no vaccine, handwashing
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most serotypes of salmonella cause?
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gastroenteritis, exceptions are s. typhi, s. paratyphi, s. cholerasius
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major virulence factor for gastroenteritis serotypes of salmonella?
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adhesion and invasion antigens for intracellular growth
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the primary target cell of gastroenteritis serotypes of salmonella is?
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macrophage
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primary reservoir for gastroenteritis serotypes of salmonella?
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intestinal tract of animals
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clinical characteristics of salmonella gastroenteritis?
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abdominal pain and diarrhea, fever
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where is salmonella normal flora?
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not normal flora
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vaccine for salmonella?
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none
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salmonella typhi is considered what type of serotype?
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invasive
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major virulence factor of salmonella typhi and its function?
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vi capsular antigen which aids in bloodstream spread
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transmission of salmonella typhi and importance of carriers?
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person to person via fecal oral; carriers important - Typhoid Mary
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pathogenesis of salmonella typhi?
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multiplication intracellularly within macrophage with dissemination to liver, spleen, bone marrow
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where do carriers of salmonella typhi have bacteria?
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gall bladder
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secondary bacteremia with salmonella typhi clinical manifestations?
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sustained bacteremia with high fever, spread to kidney, gall bladder, peyer's patches, skin leading to diarrhea, inflammation, perforation, rose spots, and sepsis in severe cases
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what are the vaccine options for salmonella typhi and when recommended?
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-purified Vi capsular polysaccharide
-live attenuated s. typhi strain ty21a -recommended for travelers to developing countries |
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morphology of vibrio species?
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Gm(-) curved rods with single polar flagellum
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preferred pH for vibrio?
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prefer alkaline, killed at low pH
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where is vibrio found?
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surface waters worldwide
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major virulence factor of v. cholerae and what is its cause?
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cholera enterotoxin causing increase in cAMP stimulating fluid secretion in intestinal epithelial cells
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habitat for v. cholerae?
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environmental water, amplified by cholera diarrhea contamination
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transmission of v. cholerae?
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human to human via fecal-oral but can also survive and grow in environmental water; eating contaminated shellfish
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clinical manifestations of v. cholerae infection?
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massive diarrhea leading to dehydration and electrolyte imbalance (hypovolemic shock)
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where does v. cholerae colonize?
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small intestine with no invasion
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treatment for v. cholerae?
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fluid replacement
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vaccines for v. cholerae?
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-oral live, attenuated strain of v. cholerae
-killed cells + toxin B subunit |
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morphology of campylobacter jejuni?
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Gm(-) slender, spirally curved rods
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habitat of campylobacter jejuni?
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normal intestinal flora of many animals
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transmission of campylobacter jejuni?
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food-borne gastroenteritis from milk, water, food
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clinical symptoms of acute infection with campylobacteriosis?
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some invasion with diarrhea and high persistent fever
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sequelae of campylobacteriosis?
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-Guillain-Barre syndrome
-Reiter's syndrome |
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vaccine for campylobacter jejuni?
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none
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h. pylori morphology?
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Gm(-) spirally curved rods
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what conditions are commonly associated with h. pylori?
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chronic gastritis and peptic ulcers
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what virulence factor of h. pylori is important to penetrating the gastric mucosa?
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flagella
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what virulence factors of h. pylori is important to stimulating inflammation?
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CagA protein and VacA cytotoxin
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what is the mechanism of inflammation of CagA protein of h. pylori?
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injected into host cells and kills the cell
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what enzyme allows h. pylori to exist in the acidic stomach?
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urease
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what is the mechanism of the VacA cytotoxin of h. pylori?
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induces vacuolation and cell death stimulating neutrophil migration and overall inflammation
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where is h. pylori found as normal flora?
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human stomach mucosa
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how is h. pylori transmitted?
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person-to-person via fecal-oral
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what are chronic gastritis and ulcers strongly associated with?
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gastric cancer
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how is diagnosis of h. pylori confirmed?
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histological exam of gastric biopsies
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what is a rapid, less invasive test for h. pylori infection?
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breath test for conversion of labeled urea to CO2
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why is it important to confirm eradication of h. pylori?
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there is frequent antibiotic resistance and treatment failure
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vaccine for h. pylori?
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none
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which virulence factor of e. coli is important to ascent in urinary tract?
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pili (fimbrae) is used for adherence to mucosal surfaces
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Gal-Gal on P blood-group antigen make individuals susceptible to which strain of e. coli?
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those with P fimbriae
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major virulence factor of e. coli for invasion of the body?
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capsule
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what is the mechanism of hemolysin from e. coli?
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pore-forming kills phagocytic cells
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which organisms causes 80-90% of all UTIs?
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e. coli
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how does e. coli cause inflammation?
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invasion and replication in epithelial cells
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besides UTI, what other conditions can be caused by e. coli?
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neonatal meningitis and bacteremia/septic shock
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vaccine for e. coli?
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none
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major virulence factor of klebsiella pneumoniae?
|
large mucoid capsule
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what is characteristic of klebsiella pneumoniae pneumonia?
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'currant jelly' sputum
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what diseases are caused by klebsiella pneumoniae infection?
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UTI, pneumonia, bacteremia
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what diseases are caused by proteus infection?
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UTI, kidney stone formation, bacteremia
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what are morphology and characteristics of proteus?
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urease production and swarming motility on agar
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what rare subtype of enterobacter causes rare but occasional outbreaks of neonatal sepsis, meningitis, necrotizing enterocolitis associated with powdered infant formula?
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e. sakazakii
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what diseases are caused by enterobacter infection?
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UTI, bacteremia
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which organisms are opportunistic enterobacteriaceae?
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klebsiella pneumonia, proteus, enterobacter, providencia, serratia
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characteristics of chlamydia?
|
obligate intracellular parasites
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chlamydia has tropisms for which cells?
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columnar epithelial cells of genital tract, repiratory tract, conjunctiva
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transmission of chlamydia?
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human-to-human or bird-to-human, no arthropod vector
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cellular location of chlamydia?
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phagosome of host cell
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pathogenesis of chlamydia?
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persistent infection due to alternating life cycles of host cell destruction and chlamydial growth
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the infectious form of chlamydia?
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eb (elementary body)
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eb (elementary body) pathogenesis?
|
attachment and entry with rigid cell wall; infectious and able to survive environmental stress
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metabolically active form of chlamydia?
|
rb (reticulate body)
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characteristics of rb (reticulate body)?
|
divides by binary fision; Gm(-) outer membrane
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why is LPS valuable to diagnosis of chlamydia?
|
genus-specific - all chlamydia have same major LPS antigen
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phase 1 of chlamydia life cycle?
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eb attachment to host cell --> endocytosis
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phase 2 of chlamydia life cycle?
|
primary differentiation of ebs to rbs
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phase 3 of chlamydia life cycle?
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growth and binary fission of rbs
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phase 4 of chlamydia life cycle?
|
secondary differentiation of rbs to ebs
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phase 5 of chlamydia life cycle?
|
release of infectious ebs
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what is the benefit of PCR of cervical swab?
|
detect both chlamydia and n. gonorrhoeae
|
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c. trachomatis servars A-C cause which disease?
|
trachoma, leading cause of blindness
|
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what is disease progression of c. trachomatis servars A-C?
|
purulent conjunctivitis --> scarring and contraction --> turning in of eyelashes --> abrasion of cornea
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vaccine for c. trachomatis servars A-C?
|
none
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c. trachomatis servars D-K causes which disease?
|
genital tract infections
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c. trachomatis servars D-K cause what disease in men?
|
nongonococcal urethritis
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what disease does c. trachomatis servars D-K cause in females?
|
cervicitis
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what is the danger in asymptomatic infections of c. trachomatis servars D-K in males?
|
as many as 50% have no pain or noticeable discharge so unknowingly spread it to their sexual partners
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what is danger in asymptomatic infections of c. trachomatis servars D-K in females?
|
75% asymptomatic and can contribute to transmission but also to complications
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what is most common bacterium seen in Reiter's syndrome?
|
c. trachomatis servars D-K
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what diseases are seen with c. trachomatis serovars D-K in neonates?
|
inclusion conjunctivitis and pneumonia
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what are the clinical manifestations of c. trachomatis serovars L1-L3?
|
small painless ulcer at site of sexual contact followed by painful lymphadenopathy
|
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how is c. pneumoniae transmitted?
|
person-to-person via respiratory secretions
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what disease is seen with c. pneumoniae infection?
|
community-acquired pneumonia
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how is psittacosis transmitted?
|
inhalation from infected birds and their droppings
|
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what does c. psittaci infection cause?
|
psittacosis or atypical pneumonia
|
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morphology of genus neisseria?
|
Gm(-) diplococci
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neisseria natural habitat?
|
mucosal surfaces of the body, fragile and survive poorly outside the body
|
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what is the oxidase status of neisseria?
|
oxidase(+)
|
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growth media required for neisseria?
|
chocolate agar and increased CO2
|
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major virulence factor of n. gonorrhoae and its function?
|
pili (fimbriae): major adhesin
|
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why is n. gonorrhoae less invasive than n. meningitidis?
|
no capsule
|
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which organism causes painful urethritis in males?
|
n. gonorrhoae
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what is the uncomplicated infection of n. gonorrhoae in females?
|
often asymptomatic with infection of the endocervix, not painful
|
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what is a complication of n. gonorrhoae infection in females?
|
PID
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arthritis and/or tenosynovitis with dermatitis is diagnostic of what disseminated infection?
|
n. gonorrhoae
|
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how diagnose n. gonorrhoae infection in males?
|
Gm stain
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how is n. gonorrhoae detected in females?
|
DNA probe technology
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what is new treatment protocol for uncomplicated n. gonorrhoae infection in females?
|
two drug therapy due to multi-drug resistance and co-infections with chlamydia
|
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vaccine for n. gonorrhoae?
|
none
|
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most distinct property of spirochetes?
|
periplasmic flagella
|
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morphology of spirochetes?
|
helically coiled Gm(-) like organisms
|
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spirochetes include which genuses?
|
treponema, borrelia, leptospira
|
|
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what is used to visualize treponema and leptospira?
|
dark-field microscopy or silver impregnation
|
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are spirochetes intracellular or extracellular?
|
extracellular
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what disease is seen with treponema pallidum?
|
syphilis
|
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habitat of t. pallidum?
|
humans with disease
|
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transmission of t. pallidum?
|
person-to-person via sexual contacts
|
|
|
what characterizes primary syphilis?
|
a painless, hard chancre at site of sexual contact that is highly infectious
|
|
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what characterizes secondary syphilis?
|
dissemination with development of muco-cutaneous lesions including: rash on palms and soles, alopecia, genital papules, mouth and skin lesions; highly infectious
|
|
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when does primary syphilis occur and resolve?
|
development of chancre at 2-10 weeks and spontaneous healing within 3-6 weeks
|
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when does secondary syphilis occur and resolve?
|
within 1-3 months after primary chancre and lasting 2-6 weeks
|
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what characterizes the latency period of syphilis?
|
no clinical symptoms but positive serology
|
|
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what characterizes tertiary syphilis?
|
development of gummas in skin and bone, cns, cardiovascular system
|
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what are gummas?
|
granulomatous lesions
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when is there positive serology in the progression of syphilis?
|
all except late latency and tertiary
|
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when is the fetus infected with congenital syphilis?
|
after the 16th week of gestation
|
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what are early congenital symptoms of syphilis?
|
low birthwt, cutaneous lesions and mucoid patches on palms and soles, snuffles, hepatosplenomegaly, nephritis, long bone involvement, multiple organ failure, similar to secondary
|
|
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what are late congenital symptoms of syphilis?
|
stigmata: Hutchinson's teeth, saddle nose
|
|
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what is primary screening test for syphilis?
|
non-treponemal antigen tests with cardiolipin-lecithin-cholesterol suspension as antigen to detect nonspecific IgM and IgG antibodies called reagin
|
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what is the confirmatory test for syphilis?
|
treponemal antibody tests with fluorescent treponemal antibody absorbed with t. pallidum as antigen
|
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what is treatment for syphilis?
|
penicillin
|
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|
what is the Jarish-Herxheimer reaction and what disease is it seen in?
|
acute febrile reaction <24 hours after start of penicillin following treatment of syphilis
|
|
|
vaccine to syphilis?
|
none
|
|
|
what are the other treponemal diseases and how are they transmitted?
|
spread by non-venereal contact - Bejel, Pinta, Yaws
|
|
|
morphology of listeria?
|
Gm(+) coccobacilli
|
|
|
what is the usual transmission of l. monocytogenes?
|
contaminated commercially-prepared food
|
|
|
what characteristics make l. monocytogenes effective at growing in commercially prepared foods?
|
facultative anaerobes and psychrophilic (like colder temps)
|
|
|
what cell is l. monocytogenes found in and what does it utilize to move?
|
macrophage using ActA (actin polymerization)
|
|
|
what is the habitat of l. monocytogenes?
|
widespread in nature and from feces of domestic animals
|
|
|
what are modes of transmission of l. monocytogenes?
|
food-borne via contaminated food and transplacentally
|
|
|
what is progression of disease pathogenesis in l. monocytogenes?
|
ingestion --> replication in intestinal epithelial cells with submucosa invasion --> replication in macrophages --> asymptomatic or flu-like, nausea, vomiting --> bloodstream invasion with spread to meninges in immunocompromised
|
|
|
l. monocytogenes infection incubation and clinical manifestations in healthy adults?
|
incubation of 1-2 days following large dose with 'listeria gastroenteritis' (fever, headache, nausea, vomiting)
|
|
|
l. monocytogenes infection incubation and clinical manifestations in immunocompromised, elderly, neonates?
|
incubation of 2-3 weeks following small dose with bloodstream invasion, septicemia, meningitis
|
|
|
risk of l. monocytogenes infection in pregnant women and fetus and clinical manifestations?
|
20x higher risk of infection in pregnant women with bloodstream invasion (no systemic symptoms) with transplacental spread to fetus
|
|
|
which organisms can be spread transplacentally?
|
l. monocytogenes, t. pallidum, b. burgdorferi
|
|
|
what characterizes early onset listerosis in neonates?
|
acquired transplacentally with septicemia, pneumonia, meningitis <2 days postpartum; high mortality
|
|
|
what characterizes late onset listerosis in neonates?
|
acquired at or soon after birth with bloodstream invasion and meningitis 1-2 weeks postpartum most likely from hospital acquired infections
|
|
|
how is diagnosis of listerosis made?
|
monocytosis, CSF Gm, and recognized as part of food-borne outbreaks
|
|
|
prevention of listerosis?
|
no vaccine, limit types of foods given to immunocompromised or pregnant persons
|
|
|
what is a severe progression of c. trachomatis servars D-K in females?
|
acute PID
|
|
|
the rickettsial group are associated with which types of infections?
|
bloodstream infections (vector-borne and/or zoonotic infections)
|
|
|
what is the intracellular location of rickettsia?
|
cytoplasm
|
|
|
what is the host target cell of rickettsia?
|
vascular endothelium
|
|
|
what disease is associated with rickettsia rickettsii?
|
rocky mountain spotted fever
|
|
|
how is r. ricketsii transmitted?
|
from rodents and dogs by bite of dog tick
|
|
|
what age group is typically affected with rmsf?
|
children under the age of 15 years
|
|
|
which disease presents with severe frontal headache and centripetal petechial rash?
|
rmsf
|
|
|
what symptoms are typically seen with r. rickettsii infection?
|
fever, frontal headache, centripetal petechial rash commonly on palms and soles, vasculitis
|
|
|
how diagnose rmsf?
|
clinical presentation of rash with history of tick bite
|
|
|
what is important with treatment of r. rickettsii infection?
|
early treatment in order to get good response
|
|
|
vaccine and prevention for r. rickettsii?
|
none, tick protection
|
|
|
how is rickettsial pox transmitted?
|
from house mice by mite
|
|
|
where is the highest risk of rickettsial pox?
|
urban areas with mice infestations
|
|
|
what distinguishes other spotted fever groups from rmsf?
|
black, crusty scab at site of tick or mite bite and less severe than rmsf
|
|
|
what organism causes epidemic typhus?
|
r. prowazekii
|
|
|
how is epidemic typhus transmitted?
|
human to human from louse vector - louse feces rubbed into bite, superficial abrasion, or inhaled
|
|
|
what organism is implicated with sylvatic typhus?
|
r. prowazekii
|
|
|
what animal is associated with sylvatic typhus and how is it transmitted?
|
flying squirrels from louse or flea vector
|
|
|
r. prowazekii is associated with which two conditions and what is their difference?
|
epidemic typhus and sylvatic typhus; sylvatic is less severe and thought to be caused by less virulent form
|
|
|
what is brill-zinsser?
|
re-occurence of a mild disease months or years after primary epidemic typhus
|
|
|
what organisms cause endemic typhus?
|
r. typhi and r. felis
|
|
|
what is transmission of endemic typhus or murine typhus?
|
flea-borne from rodents
|
|
|
which disease presents with centrifugal macular, maculopapular rash and generalized headache?
|
typhus
|
|
|
what clinical symptoms will be seen with typhus?
|
centrifugal rash, generalized headache, vasculitis and systemic inflammation
|
|
|
orientia tsutsugamushi causes what disease?
|
scrub typhus
|
|
|
how is scrub typhus transmitted?
|
mite (chigger) vector from mice or other rodents
|
|
|
what are the clinical manifestations of orientia tsutsugamushi?
|
typhus-like disease with centrifugal rash, fever, localized escher
|
|
|
what disease does coxiella burnetii cause?
|
q fever
|
|
|
rickettsial disease rarely associated with an insect vector?
|
coxiella burnetii - q fever
|
|
|
how is coxiella burnetii transmitted?
|
inhalation of aerosols or contaminated dust from placental products or excreta of infected animals
|
|
|
which organism is one of the most infectious known bacteria and is a potential biological warfare agent?
|
coxiella burnetti
|
|
|
what is the typical presentation of q fever?
|
mild, atypical lobar or interstitial pneumonia with flu-like symptoms with systemic spread --> hepatomegaly, splenomegaly; no rash
|
|
|
which cell does coxiella burnetti replicate in and in which organs?
|
macrophages of lung, liver, spleen
|
|
|
what is important in history for diagnosis of q fever?
|
exposure to animals = farmers, woolsorters, tanners, veterinarians, meat handlers
|
|
|
what are the high risk groups for coxiella burnetti infection?
|
farmers, woolsorters, tanners, veterinarians, meat handlers; patients with prosthetic or damaged heart valves
|
|
|
vaccine for coxiella burnetti?
|
killed whole cell preparation available in Australia but not US
|
|
|
HME (human monocytic ehrlichiosis) is caused by what organism?
|
ehrlichia chaffeensis
|
|
|
how is HME transmitted?
|
from deer by lone star tick and dog ticks
|
|
|
what cell does ehrlichia chaffeensis replicate in?
|
bloodstream monocytes and tissue macrophages
|
|
|
HGA (human granulocytotropic anaplasmosis) is caused by which organism?
|
anaplasma phagocytophilum
|
|
|
how is HGA transmitted?
|
deer ticks
|
|
|
what cell type does anaplasma phagocytophilum replicate in?
|
circulating granulocytes
|
|
|
which system do HME and HGA effect and what are their general clinical manifestations?
|
hematopoietic system, presenting with leukopenia, thrombocytopenia, and systemic inflammation; HME has uncommon rash (<50%) and HGA has rare rash
|
|
|
what differentiates HME and HGA interms of symptomology?
|
HME is more like to have a rash but is less severe; HGA is less likely to have a rash but is more severe
|
|
|
vaccine for ehrlichiosis/anaplasmosis?
|
none
|
|
|
what organism causes cat scratch disease?
|
bartonella henselae
|
|
|
how is bartonella henselae transmitted?
|
saliva of cat from bite or scratch
|
|
|
where does bartonella henselae replicate?
|
primarily extracellular
|
|
|
how does cat scratch disease present in normal individuals?
|
primary skin papule or pustule at inoculation site; painful lymphadenopathy with fever
|
|
|
what are clinical conditions of cat scratch disease in immunocompromised?
|
bacillary angiomatosis, bacillary peliosis hepatitis (also spleen), bacteremia and sepsis, endocarditis
|
|
|
what is bacillary angiomatosis?
|
vascular proliferative disorder of skin and viscera; red, nodular lesions similar to Kaposi's sarcoma
|
|
|
what is bacillary peliosis hepatitis, which may also affect the spleen?
|
cystic, blood-filled spaces in the liver
|
|
|
what is the challenge of treating immunocompromised individuals with cat scratch disease?
|
treatment is slow and replases are common
|
|
|
what organism causes trench fever?
|
bartonella quintana
|
|
|
how is trench fever transmitted?
|
human to human via body lice
|
|
|
what symptoms are associated with trench fever?
|
bone pain, especially in shins; macular rash, headache, fever
|
|
|
which organism causes oroya fever?
|
bartonella bacilliformis
|
|
|
where is bartonella bacilliformis found in the body?
|
intracellular in rbcs
|
|
|
how is oroya fever transmitted?
|
human to human via sandfly, above certain altitudes in the Andes
|
|
|
what is clinical manifestation of oroya fever?
|
severe hemolytic anemia with high fatality
|
|
|
are spirochetes intracellular and intracellular?
|
extracellular
|
|
|
what is the primary tick-borne disease in the US?
|
lyme disease
|
|
|
what organism causes lyme disease?
|
borrelia burgdorferi
|
|
|
what are the reservoirs for borrelia burgdorferi?
|
white-footed mouse and white-tailed deer
|
|
|
which tick transmitts borrelia burgdorferi?
|
deer tick in northeast and upper midwest; western black-legged tick in california
|
|
|
which point of the tick life cycle causes the most cases?
|
nymphal tick (80%)
|
|
|
what characterizes primary stage of lyme disease?
|
erythema migrams with bulls-eye skin rash about 1 week following bite with proliferation of the bacteria in tissue at the site of bite and initial dissemination
|
|
|
what characterizes secondary stage of lyme disease?
|
neurologic and cardiac symptoms about 2 weeks to 3 months after initial bite as result of dissemination and replication with chronic fatigue
|
|
|
what neulogic symptoms are seen with secondary stage lyme disease?
|
facial nerve palsy, peripheral neuropathy, meningitis
|
|
|
what cardiac symptoms are seen with secondary stage lyme disease?
|
carditis, AV block
|
|
|
what characterizes tertiary stage of lyme disease?
|
arthritis
|
|
|
what is origin of arthritis seen with lyme disease?
|
immuno-pathological process
|
|
|
how can lyme disease be transmitted?
|
tick-borne or transplacental
|
|
|
when is treatment indicated for lyme disease?
|
empiric because very treatable in early stages but arthritis is not antibiotic treatable
|
|
|
how is lyme disease prevented?
|
tick exposure and control deer population
|
|
|
vaccine for borrelia borgedorfi?
|
LYMErix vaccine against outer surface protein was discontinued due to reported side effects (arthritis, myalgia)
|
|
|
what organisms cause relapsing fever?
|
borrelia (b. recurrentis, b. hermsii, b. parkeri)
|
|
|
how are b. recurrentis transmitted?
|
human to human by body lice
|
|
|
how are b. hermsii and b. parkeri transmitted?
|
soft ticks
|
|
|
what is the pathogenesis of the relapsing fevers?
|
antigenic variation
|
|
|
what are reservoirs for leptospira interrogans?
|
dogs are major source but other domestic animals (hogs, cattle)
|
|
|
how is leptospira interrogans transmitted?
|
direct contact with urine of infected animals or contaminated water
|
|
|
what lesion develops with leptospirosis?
|
none
|
|
|
which organism causes a biphasic disease?
|
leptospira interrogens
|
|
|
what is characteristic of primary disease in leptospirosis?
|
mild septicemia with flu-like symptoms
|
|
|
what is characteristic of secondary disease in leptospirosis?
|
return of symptoms with anicteric or icteic presentation
|
|
|
what is seen if anicteric in secondary disease of leptospirosis?
|
fever, mild meningitis, uveitis, other organ
|
|
|
what is seen if icteric in secondary disease of leptospirosis?
|
jaundice, hemorrhage, renal failure, death 5-40% of cases
|
|
|
morphology of genus bacillus?
|
aerobic large, Gm(+) rods producing endospores
|
|
|
where are bacillus distributed?
|
soil, water, and dust samples
|
|
|
what organisms cause anthrax?
|
bacillus anthracis
|
|
|
which organism has a capsule composed of polypeptide?
|
bacillus anthracis
|
|
|
what is exotoxin for bacillus anthracis?
|
edema factor, protective antigen, lethal factor
|
|
|
what is edema factor and which organism is it associated with?
|
exotoxin protein of bacillus anthracis that increased cAMP
|
|
|
what is protective antigen and which organism is it associated with?
|
exotoxin protein of bacillus anthracis that facilitates entry of EF and LF into cells
|
|
|
what is lethal factor and which organism is it associated with?
|
exotoxin protein of bacillus anthrasis that is a protease that cleaves MAPK disrupting signal transduction
|
|
|
how is b. anthracis transmitted?
|
direct contact with spores on animal products or sick animals; inhalation of dust containaing anthrax spores
|
|
|
what are three general diseases caused by b. anthracis?
|
cutaneous, pulmonary, intestinal
|
|
|
what are clinical features of cutaneous anthrax?
|
small painless papule develops into enlargin black eschar surrounded by vesiculation and edema; localized and low fatality
|
|
|
where on the body will you see cutaneous anthrax?
|
anywhere there is a cut or scrape coming in contact with spores; typically hands, forearms, men's faces
|
|
|
what is the most common form of anthrax?
|
cutaneous
|
|
|
what are clinical features of pulmonary anthrax?
|
initially non-specific, secondarily developing abruptly with fever, acute respiratory distress, pulmonary edema, pleural effusion followed by cyanosis, shock, coma, common meningitis; high mortality (90%)
|
|
|
what is pathogenesis of pulmonary anthrax?
|
phagocytosed by alveolar macrophages with germination --> migrate to draingin mediastinal lymph nodes --> intracellular replication --> lysed macrophage --> extracellular replication --> bloodstream spread --> massive local inflammation (mediastinitis) with massive edema, respiratory failure, septic shock, meningitis
|
|
|
treatment of b. anthrasis?
|
penicillin, etc; mAb against anthrax PA
|
|
|
vaccine of b. anthrasis and who uses it?
|
purified PA with primary use by military
|
|
|
what disease does bacillus cereus cause?
|
food poisoning
|
|
|
what does the heat-stable enterotoxin of bacillus cereus cause?
|
vomiting
|
|
|
what does heat-labile enterotoxin of bacillus cereus cause?
|
diarrhea
|
|
|
how is bacillus cereus transmitted?
|
food contamination, commonly fried rice
|
|
|
what are clinical manifestations of emetic form of bacillus cereus?
|
nausea and vomiting due to ingesting toxins [2-4 hours or shorter]
|
|
|
what are clinical manifestations of diarrheal form of bacillus cereus?
|
diarrhea and abdominal cramps with incubation of 10-18 hr due to bacterial growth and toxin production in intestines
|
|
|
what other infections besides food poisoning are caused by bacillus cereus?
|
eye trauma, iv catheters or CNS shunts infections, pneumonia and bacteremia (in welders who are exposed to large amounts of dust)
|
|
|
morphology of yersinia?
|
Gm(-) rods and coccobacilli that have bipolar staining
|
|
|
what disease does yersinia pestis cause?
|
bubonic and pneumonic plague
|
|
|
what disease does yersinia entercolitica cause?
|
acute entercolitis
|
|
|
where does yersinia pestis grow in the body?
|
intracellular growth in macrophages followed by extracellular growth
|
|
|
what are virulence factors of yersinia pestis?
|
endotoxin and capsule
|
|
|
what is the habitat of yersinia pestis?
|
zoonotic reservoir is wild rodents
|
|
|
how is yersinia pestis transmitted?
|
bites of rodent fleas, direct contact with dead or infected animals, aerosols from other humans with disease
|
|
|
what is typical of the bubonic phase of yersinia pestis?
|
2-6 days after bite; travels via lymphatics to lymph nodes where survives and grows in macrophages --> production of bubo --> eventual bloodstream spread extracellularly
|
|
|
what is typical of the septicemic phase of yersinia pestis?
|
extracellular causing DIC (black death) and septic shock
|
|
|
what is typical of the pneumonic phase of yersinia pestis?
|
extracellular systemic spread to lungs; pneumonia with organisms in alveolar spaces and sputum; can also be acquired by inhalation from bioterrorism or person to person
|
|
|
how is diagnosis made for yersinia pestis infection?
|
immunofluorescence using Fra1 antibody
|
|
|
old and new vaccine for yersinia pestis and when is it used?
|
old = killed, whole bacteria; new = recombinant Fra1 fragments; only used in high risk situations
|
|
|
how are y. enterocolitica and y. pseudotuberculosis different from y. pestis?
|
no capsule
|
|
|
habitat for y. enterocolitica and y. pseudotuberculosis?
|
aquatic and animal reservoirs (pigs, cattle, dogs)
|
|
|
how are y. enterocolitic and y. pseudotuberculosis transmitted?
|
fecal oral via ingestion of feces contaminated food/water
|
|
|
what are clinical manifestations of yersinia entercolitis?
|
watery diarrhea with fever ~salmonella or campylobacter; enter mesenteric lymph nodes to cause intense inflammation (pain resembling appendicitis)
|
|
|
what organism causes tularemia?
|
francisella tularensis
|
|
|
morphology of francisella tularensis?
|
small, Gm(-) coccobacillus with bipolar staining
|
|
|
where is francisella tularensis located in the body?
|
facultative intracellular parasite in macrophages
|
|
|
habitat of francisella tularensis?
|
animals, particularly rabbits
|
|
|
transmission of francisella tularensis?
|
handling of infected animals, tick bites from infected animals
|
|
|
who is at high risk of tularemia?
|
hunters (esp skinning rabbits) and job-related working outdoors
|
|
|
what is most common disease of tularemia and what are its manifestations?
|
ulceroglandular: focal ulcer at site of entry with regional lymphadenopathy (intracellular in macrophages)
|
|
|
what are possible clinical manifestations of tularemia?
|
ulceroglandular disease, typhoidal disease, oropharyngeal disease, oculorglandular disease with possible extracellular bloodstream infection
|
|
|
vaccine for tularemia and indication?
|
live, attenuated vaccine only for persons at high-risk of exposure
|
|
|
morphology of brucella?
|
small, weakly staining Gm(-) coccobacilli, NOT bipolar staining
|
|
|
growth of brucella is enhanced by what compound and why does this matter?
|
enhance by erythritol which is found in uterus and placenta leading to spontaneous abortion
|
|
|
where is brucella found in the body?
|
facultative intracellular parasite within macrophages
|
|
|
habitat of brucella?
|
wild and domestic animals
|
|
|
transmission of brucella?
|
direct contact with infected materials (urine, milk, vaginal secretions, placental tissue), ingestion of unpasteurized milk products, inhalation of contaminated dust
|
|
|
brucellosis is aka?
|
undulant fever, malta fever, bang's disease
|
|
|
clinical manifestations/target organs of brucellosis?
|
chronic, febrile illness with series of relapses; targets lungs (if inhaled), lymph nodes, spleen, liver, bone marrow
|
|
|
what is the hallmark lesion of brucellosis?
|
minute granulomas (similar to TB)
|
|
|
how is diagnosis of brucellosis established?
|
based on immunological reactions: serology, brucellergin DTH test
|
|
|
prevention of brucellosis?
|
live, attenuated vaccine for animal immunization; pasteurization; gloves and protective clothing
|
|
|
morphology of pasteurella?
|
small, Gm(-) coccobacilli or rods with bipolar staining
|
|
|
is pasteurella found intracellularly or extracellularly?
|
extracellularly with no intracellular phase
|
|
|
habitat for pasteurella?
|
normal flora in variety of animals
|
|
|
transmission of pasteurella?
|
animal bites (typically cats) or inhalation of infected animal materials (less common)
|
|
|
clinical presentation of pasteurellosis?
|
cellulitis with osteomyelitis as complication, respiratory tract infection, spread to bloodstream (only immunocompromised)
|
|
|
what are examples of structural mechanisms of bacteria contributing to pathogenesis?
|
LPS, pili, capsule, toxins, exoenzymes
|
|
|
what are examples of genetic mechanisms of bacteria contributing to pathogenesis?
|
lysogency and plasmids
|
|
|
what is lysogency?
|
temperate bacteriophage bring in toxins and modify innocuous bacteria to toxin producers
|
|
|
what different plasmids are there?
|
transfer, resistance, and pathogenic factors
|
|
|
what are examples of pathogenic factors?
|
those that carry toxin genes or encode pili
|
|
|
what are pathogenicity islands?
|
encode a variety of pathogenic factors that can make any innocuous bacterium a pathogen in one fell swoop
|
|
|
what defines a pathogenicity island?
|
encode several virulence genes, are present in pathogens but not in nonpathogens, are usually (75%) associated with tRNA genes on chromosome, often bounded by transposons or insertion sequences, differ in G+C content from rest of chromosome, often are unstable
|
|
|
what is the mechanism of the 2 component system?
|
signal changes the conformation of the sensor --> exposes for phosphorylation --> phosphorylated --> sensor changes conformation of responder --> responder active and often is positive transcription regulator
|
|
|
what can a bacteria respond to?
|
sugar and amino acid, temp and pH, population responses (sporulation, etc)
|
|
|
what does secretion capability give a bacteria?
|
better ability to transmit toxins and other molecules to eukaryotic cells
|
|
|
what is a type IV secretion?
|
protein machinery contacts mammalian cells and directly transmits toxins (similar to conjugation)
|
|
|
what is a type III secretion?
|
channel opener to eukaryotic cells
|
