Enteric Bacteria Flashcards
Shigella bacteriology
- gram stain and shape
- fermentation
- mobility
- respiration
- intra vs extracellular
gram (-) rods non-lactose fermenting and not H2S producing -non motile -facultative anaerobe -facultative intracellular
If you have a GI infection, what is going to be the general bacteriology (stain)? What is the exception? What is the general respiration?
Gram (-) bugs; Listeria is the exception; facultative anaerobic
On culture, how can you distinguish between shigella and e. coli?
E coli ferments lactose (bright pink on MacConkey), shigella does not
Shigella Pathogenicity
- disease names (3)
- infectious dose
- presentation
- mortality risk
- complication
shigella enterocolitis, bacillary dysentery, and shigellosis
- very low (~100 IUs)
- bloody diarrhea, local inflammation, ulceration
- worse with poor nutrition
- Reactive Arthritis (Reiter’s syndrome)
Reactive Arthritis
“Can’t see, can’t pee, can’t climb a tree.”
- associated w/ HLA-B27
- conjuctivitis, urethritis, and arthritis
- shigella and chlamydia
Shigella pathogenesis
- target
- cause of presentation
- immune evasion
- populations most at risk
- invade epithelium of distal ileum and colon and secrete exotoxins
- exotoxins kill adjacent cells
- necrosis, apoptosis, host immune response and hemorrhage lead to bloody diarrhea
- survive phagocytosis and cause macrophage apoptosis
- children under 5, HIV+, MSM
Main Shigella virulence factor
- seen in what other bacteria?
- secretion system
shiga toxin: protein-synthesis-inhibiting shiga toxin is plasmid-encoded
- can be picked up by E coli
- type 3
Hemolytic uremic syndrome
begins when shiga toxin escapes into bloodstream, causes hemolysis, renal failure, uremia, and DIC
Dx Shigella: Exam
Very young/very old: fever, dehydration, severe headache, lethargy, watery diarrhea w/ bloody mucous
Dx HUS: Exam
hemolysis, thrombocytopenia, uremia requiring dialysis
Dx Shigella: Lab
Strain via immunoassays (agglutination); methylene blue stain of fecal sample to determine if neutrophils are present (Shigella, salmonella, campylobacter)
Dx HUS: Lab
schistocytes, decreased platelets, increased PMNs, increased lactate dehydrogenase
Shigella treatment
fluids/elect replacements; ceftriazone, fluoroquinolone, azithromycin, cefixime; NO antidiarrheal meds
Shigella prevention
sewage disposal, water chlorination, handwashing
E. coli bacteriology
- stain and shape
- fermentation
- respiration
- mobility
- straight gram (-) rod
- lactose fermentor, H2S/urease negative
- facultative anaerobe
- may be mobile (flagella) or nonmobile
E. coli pathologies (6)
- enterotoxigenic diarrhea
- enterohemorrhagic diarrhea
- UTI
- meningitis
- pneumonia
- intra-abdominal escape after GI perforation
Enterotoxigenic E coli (ETEC)
Traveler’s diarrhea
Enteropathogenic E coli (EPEC)
childhood diarrhea
Enteroinvasive E coli (EIEC)
causes shigella-like dysentery
Enterohemorrhagic E coli (EHEC)
infected by phage STX, produces shiga toxin, causes hemorrhagic colitis or HUS
Enteroaggregative E coli (EAggEC)
primarily associated w/ persistent diarrhea in children in developing countries
Enteroadherent E coli (EACE)
cause of childhood diarrhea and traveler’s diarrhea in Mexico and N. Africa
Enterotoxigenic diarrhea pathogenesis
- pili attach to jejunum and ileum
- enterotoxins (exotoxin that acts on the GI tract)
- enterotoxin LT forces host ion channels to export, host loses fluid, potassium, and chloride
Enterohemorrhagic diarrhea pathogenesis
- attach to mucosal epithelial cells of the colon and may invade
- lysogenic phage STX encodes shiga toxin which becomes active inside gut cells, shuts down protein synthesis, destroys some
- inflammation, bloody diarrhea
- if toxin hits blood stream > HUS
When does HUS become a threat in EHEC
when antibiotics are used to treat bloody diarrhea
How does shiga toxin cause renal injury and anemia?
binds to Gb3 on RBCs and uses RBCs as transport to kidney, RBCs/toxin complex clog capillaries in the kidney via platelet-fibrin thrombi (shistocytes)
Dx E coli: exam
bloody or nonbloody diarrhea, dehydration, recent travel abroad
Dx E coli: lab
stool culture, EIA test colonies for shiga toxin
Enterotoxic diarrhea treatment
self limited, hydrate
Enterohemorrhagic diarrhea treatment
NO antidiarrhea or antibiotics! Just hydrate
Types of bacteria that can cause gastroenteritis with their toxins but not their virulence? How do you separate these from others clinically.
Staph aureus, bacillus cereus, and botulinum. Onset within hours
Salmonella bacteriology
- stain and shape
- fermentation
- oxidase, urease, H2S
- mobility
- gram (-) rods
- seldom lactose
- oxidase (-), urease (-), H2S (+)
- motile
Salmonella pathologic presentations (4)
enterocolitis, enteric fever (typhoid fever), septicemia (rare and in combo w/ sickle cell), and reactive arthritis
Salmonella Enterocolitis
- who and where
- presentation
- infectious dose
- children and nursing homes, ppl on antacids
- inflammation, diarrhea, N/V
- high (100K)
Salmonella enterocolitis pathogenesis
-salmonella selectively attach to M cells of Peyer patches, are internalized by receptor mediated endocytosis
salmonella virulence factors (5)
- Ipf operon (enhances adhesion to M cell)
- Type 3 secrection
- SipB (causes macrophage apoptosis)
- Spi2 (‘spy’- S. typhi uses this to turn macrophages into trojan horses for systemic spread)
- Vi antigen (S typhi capsule for immune evasion
Salmonella Enteric and Typhoid fevers
- onset
- progression
- presentation
human restricted fecal-oral infections with S typhi or paratyphi
- fever, pain, constipation
- 3-4wks: cough, stupor, delerium, GI hemorrhage, bowel perforation, myocarditis, death
- recent travel, hotel stay, high fever, headache, anorexia
treat salmonella enterocolitis
only for very young, very old, or HIV+ (Ab sensitivity before admin)
treat salmonella enteric fever or septicemia
ceftriaxone or ciprofloxacin; drain abscesses
Yersinia enterocolitica and pseudotuberculosis bacteriology
- stain and shape
- fermentation
- mobility
gram (-) oval rods
- non lactose, urease (+)
- motile at 25*C but not at body temp
Yersinia enterocolitica pathogenicity
- what does it cause
- infectious dose
- virulence factors
- enterocolitis by invading intestinal mucosa and destroying tissue through the Peyer patches
- very high (10^9)
- carried on plasmids and chromosomes
Yersinia enterocolitica virulence factors
- pili and Inv adhesin (binding to M cells)
- CNF (dermonecrotic toxin destroys tissues)
Yersinia enterocolitica presentation
- who? where?
- complication?
- most common in young children, risk increased with iron overload
- cooler climates without food processing
- reactive arthritis
Yersinia pseudoTB pathogenesis
- adult presentation
- child presentation
- similar, more rare, seen in Immunocomp or pre-existing liver disease
- Izumi fever: vasculitis w/ fever, rash, inflammation of oral cavity, erythema/edema of hands and feet
Dx yersinia: Exam
diarrhea, dehydration, “false appendicitis”, recent travel
Dx yersinia: labs
- culture from stool, blood, or CSF
- grow in cold-enrichment on CIN agar
How do you distinguish between Y. enterocolitica and pseudoTB
pseudoTB ferments sorbitol and has ornithine decarboxylase activity
Treat yersinia
- fluids
- if complications then trimethoprim, sulfamethoxazole, cipro
Using Hektoen Enteric Agar to differentiate
- no growth?
- Blue-green growth?
- orange growth?
- Black growth?
- listeria
- no lactose or H2S (Shigella)
- Lactose w/o H2S (E coli)
- H2S (Salmonella
Listeria bacteriology
- stain and shape
- respiration
- mobility
- colony on blood and nonblood agar
- gram (+) rod
- facultative anaerobic
- tumbling motility
- beta hemolytic, blue-green colonies
Listeria virulence (2) -immune evasion?
- listerolysin (exit macrophage lysosomes)
- ActA (rocket thing via actin)
- intracellular pathogen, cell to cell spread via ActA
Listeria presentation
- who?
immunosuppressed, pregnant
-eating environmentally contaminated food
Listeria outside of GI
meningitis, abscess, endocarditis, septic arthritis, osteomyelitis, pneumonia
Listeria in pregnancy
bacteria escape GI and begin to grow in the placenta, esp in the third trimester (CMI is lowest)
- cause preterm labor, abortion, still birth, intrauterine infection
Listeria in neonate
- transmission across placenta: early onset sepsis and premature birth w/ abscesses and/or granulomas in major organs
- transmission from vagina: late onset meningitis w/ sepsis
Dx listeria: exam
- pregnancy
- CNS
- fever, arthralgia, back pain, headache
- mental status change, seizure, cranial nerve deficits, strokelike hemiplegia, tremor, myoclonus, ataxia, brain abscess
Dx listeria: lab
blood culture, Wet mount of CSF
- gram stain
Treat listeria
Abs, IV if CNS or bacteremic
- amp and gentamicin
- reportable
V. cholerae bacteriology
- stain and shape
- respiration
- fermentation
- mobility
- reservoirs
- gram (-), curved comma-shape rod
- aerobic, facultatively anaerobic
- sucrose fermenting, slightly lactose, oxidase (+)
- mobile
- humans and plankton (indian ocean)
What marker indicated vimbrio pathogenecity
O cell wall antigen (O1 and O139)
V cholerae pathogenesis
- transmission
- infectious dose
- risk factors
- virulence factors (3)
- fecal-oral transmission
- high
- ppl on antacids, w/ gastrectomy, or with H pylori infection
- mucinase, toxin-coregulated pilus (TCP), cholera toxin
Cholera toxin
- receptor
- mechanism
A-B subunit enterotoxin
- GM1 on intestinal lining
- perisistant activation of adenylate cyclase > loss of H2O and ions
How does V. cholera encode the toxin
carried by lysogenic bacteriophage CXT
Electrolyte imbalance in cholera
acidosis and hypokalemia > cardiac and renal failure in hours
Dx Cholera: exam
-children
-drowsy, coma, fever, hypoglycemic convulsion
Treat cholera
IV lactated Ringer solution
Non-cholera vibrio infections (2)
- which is more common? presentation?
- which is more lethal? presentation
parahaemolyticus, vulnificus
- parahaemolyticus: gastroenteritis from undercooked shellfish
- vulnificus: cellulitis after seawater infected wound
campylobacter bacteriology
- stain and shape
- mobility
- oxidase, catalase
- respiration
- gram (-), comma or S-shaped rod
- motile (flagella)
- (+)
- microaerophilic
Campylobacter transmission
fecal-oral, raw milk, undercooked chicken, sexual contact, sick pets (puppies)
C. jejuni strongly predisposes pts to what?
Guillain-Barre syndrome, Reactive arthritis, HUS
Campylobacter presentation in children
presents w/ watery foul-smelling diarrhea > progressing to bloody stool w/ fever and abd pain
Dx Campylobacter: lab
- how can you tell it apart from salmonella, listeria, yersinia
- campylobacter cannot grow at low temp
- grows better under low oxygen atmosphere
Treat campylobacter
- simple gastroenteritis
- children, pregnancy
- adults w/ worsening symptoms
- meningitis
- rehydrate
- erythromycin
- azithromycin, tetracycline, clindamycin
- meropenem, ampicillin, chloramphenicol
H pylori bacteriology
-stain and shape
curved gram (-) rod
H pylori pathogenicity
peptic ulcer disease, MALT lymphoma, gastric lymphoma, adenocarcinoma of the stomach
H pylori virulence
- flagella as attachment
- urease (break down urea into ammonia > neutral pH)
- Vac-A (vacuolating cytotoxin)
- Cag-A (chemotaxis of neutrophils)
Dx H pylori: exam
urea breath test, biopsy, PCR for stool
Treat H pylori
reduce irritation with pepto, PPIs
-kill bacteria w/ triple therapies
(omeprazole+amoxicillin+clarithromycin)
(bismuth subsalicyclate+metronidazole+tetracycline)
(lansoprazole+amoxicillin+clarithromycin)
