Microbiology Flashcards
H. pylori Virulence Factors
- slender, curved gram - rods
- motile with polar flagella, microaerophilic
- VacA - vaculoating cytotoxin
- PAI encoding Type III secretion system
- Cag - rearranges cytoskeleton
- Urease
Diagnosis of H. pylori
endoscopy with biopsy & culture
- urea breath test
- serology useful to monitor recovery
Treatment of H. pylori
-omeprazole, metronidazole, clarithromycin
Campylobacter jejuni
-most common GI infection in developed nations
-only few hundred cells needed for infection
Reservoirs: sheep, cattle, chickens, wild birds, dogs
Source: undercooked poultry, unpasteurized milk, contaminated water
Micro: campylobacter jejuni
-thin, spiral shaped gram - rod
“gull-winged appearance”
microaerophilic
-1 week incubation
Symptoms of campylobacter jejuni
fever, appendicitis-like lower abdominal pain
- watery diarrhea that progresses to dysentery with blood and pus
- antecedent to Guillain-Barre
- self-limited: 3-7 days
Diagnosis of campylobacter jejuni
-culturing on media containing abx to prevent growth of resident bowel flora
Treatment of campylobacter jejuni
Erythromycin treatment
- fluoroquinolones (resistance is common)
- resistant to beta-lactams
Vibrio Micro
- curved, gram - rods
- motile, polar flagellum, oxidase +
- found in saltwater, disease in warm months
- sig: v. cholerae, v. papahaemolyticus, v. vulnificus
Cholera
5-10 million cases per year
- endemic in Asia, Africa, S. America, India subcont
- poor sanitation
- seven pandemics since 1817 (increased word travel)
- 1992 O139 outbreak is 8th
- spread by contaminated water and food
- human carriers and environmental reservoirs
Cholera Subtypes
> 200 based on O-antigen
O1 and O139 are responsible for epidemic/pandemic
-O1 serogroup subdivided into El Tor, & Classical
Cholera Pathogenesis
incubation 2-3 days
high infectious dose >10^8 CFU
-abrupt onset of vomiting & high volume watery diarrhea (20L/day), due to cholera toxin production, death by dehydration
-Rice-water stools: speckled with mucus, loaded with buds (10^9 cfu/mL)
Cholera Virulence Factors
- PAI-encoded pilus (TCP) attach to intestinal cells
- Phage-encoded toxin: AB toxin comprises 5B and 1A subunit, ADP-ribosylation of GTP-binding protein, activation of adenyl cyclase
Cholera Dx & Treatment
- stool culture on TCBS (thiosulfate or Citrate Bile salts Sucrose) or MacConkey agars
- treat with oral hydration therapy (+ doxycycline or erythromycin)
V. parahaemolyticus
- free-living sea water
- seafood-associated food poisoning (most common foodborne illness in Japan)
- Gulf/Pacific Coasts of US, warm months
- Watery diarrhea often with abdominal cramps, nausea, vomiting, low-grade fever, 24 hrs after exposure
- self-limiting, rare treatment needed
V. vulnificus
- free-living in sea water
- consumption of raw oysters or wound infection (cellulitis)
- vomiting, diarrhea, abdominal cramps
- immunocompromised or chronic liver pts (septicemia, bullae)
- rare, but 20% fatality
- doxycycline
Bacteroides fragilis
-gram - coccobacillus
-antiphagocytic capsule
-major in human GI tract
-opportunistic pathogen: intraabdominal infections, abscesses, PID, pulmonary infections
Treat: erythromycin, clindamycin, metronidazole, cephalosporins (3rd)
NOT: penicillin, aminoglycosides
Prevotella Melaninogenica
- gram - coccobacillus
- antiphagocytic capsule
- GI tract, nasopharyngeal & vaginal flora
- opportunistic pathogen, abscesses: pulmonary periodontal
Clostridium micro
- gram + spore-forming rods
- only anaerobic endospore-forming bacteria (resistant to heat/harsh environment)
- exotoxin & secreted hydrolytic enzymes responsible for pathogenesis
- colon and soil (spores)
C. perfrigens
-large “boxcar” gram + rods
-soil, human/animal intestine
-from spores in soil or food
-gas gangrene & cellulitis
-food poisoning
Treat: surgical debridement, large amounts of penicillin & protein-inhibiting antibiotic, hyperbaric oxygen chamber
C. perfrigens food poisoning
3ed most common in US
enterotoxin-producing strains
-rich meat dishes at low temperatures allow spores to germinate
8-24hrs post consumption: nausea, pain, diarrhea, no fever, vomiting rare
-full recovery in 24 hrs
C. tetani
-spore contamination of wounds
-tetanospasmia (toxin) is AB neurotoxin
-enters at neuromuscular junction and is transported by motor neurons to ganglia (incubation time depends on distance of wound from CNS)
-Cuts a V-snare (vesicle with neurotransmitter cannot fuse with neuron membrane)
prevents release of inhibitory neurotransmitters (glycine and GABA), blocking postsynaptic inhibition of spinal motor reflexes)
Tetanus
- trismus (lock jaw)
- risus sardonicus
- generalized intermittent spasms
- patient is aware and sensitive to stimuli
- death occur from exhaustino and respiratory failure
- Treat with HTIG to soak up excess toxin
C. botulinum
-contaminated food baby(from spores in carpet)
-infection of wounds with spres
-AB toxins: seven (A-G) antigenic types
may be most toxic bacterial exotoxin, 1g could kill 1 million people, cleave V- and/or T-snares, prevent release of ACh