VI- GI Bacterial Flashcards
1-8 hour bacterias
- Staph aureus
- Bacillus cereus (emetic)
- Clostridium botulinum
aka have preformed toxins
8-16 hour bacterias
- bacillus cereus (diarrheal)
- clostridium perfringens
- clostridium botulinum
toxins are produced in vivo
16+ hour bacterias
- shigella spp
- salmonella spp
- listeria monocytogenes
- E. Coli
- campylobacter spp
- vibrio
attachment, growth, and virulence factors produced
general presentation of food poisoning
- diarrhea
- vomitting
- NO FEVER
bacterias that give food poisoning
- Staph. aureus
- Clostridium botulinum
- clostridium perfringens
- Bacillus cereus
Staph. Aureus presentation
- severe vomiting, diarrhea, abdom pain within 1-8 hours
- resolves in 24 hours
Staph. Aureus toxins
ingestion of preformed enterotoxins (A most common) that are all heat stable aka will survive cooking
foodborne botulism presentation
- non specific signs less than 8 hours after toxin or 16 hours of spore ingestion
- 1-3 days later affect cranial nerves so bilateral ptosis, ophthalmoplegia, blurred vision, dilateral descending weaking > flaccid paralysis
Clostridium botulinum toxin
botulism toxin
-ingestion of either preformed toxin or spores that germinate in intestine
-directly causes flaccid paralysis by binding motor end plates of muscle fibers
foodborne botulism treatment
IV anti-toxin ASAP to stop progression of paralysis + ventilation for respiratory dysfunctions + supportive therapy
infant botulism presentation
ingestion of spores from honey or contaminated formula between birth - 6 mo
constipation, weak cry, failure to thrive, flaccid paralysis so floppy baby
C. perfringens presentation
- diarrhea and abdom cramps 8-16 hours after ingestion
- last for 24 hours
from enterotoxin
emetic Bacillus cereus features
- from reheated rice
- ingest preformed heat stable toxin
- onset 15 min - 8 hrs
- vomiting, nausea, abdom cramps, NO DIARRHEA
diarrheal Bacillus cereus features
- meat, veggies
- spores germinate in intestine, heat liable toxin
- onset 8-16 hours
- diarrhea, nausea, abdom cramps, NO VOMIT
H. pylori characteristics
- gram neg flagellated curved rod
- microaerophilic, like 5% oxy
- exclusive to humans
H. pylori presentations
- gastritis
- ulcers
- stomach cancer
gastritis prez
feeling fullness, upset stomach, nausea, vomiting
ulcers prez
dull stomach pain, heart burn, nausea, vomit, stomach bleeding
BLACK OR TARRY STOOLS
H. pylori pathogenesis
- flagella based motility penetrates gastric mucosa and adhere to epithelium
- powerful urease enzyme to convert urea to ammonia = inc toxic levels
- VacA for accumulation of vacuoles
- CagA oncogenic protein by T4SS
H. pylori diagnosis
- urea breath test - detect CO2 via gas chromatography if urease present
- biopsy
H. pylori treatment
- antibiotics
- proton pump inhibitor or antacid to control acid and prevent further mucosal damage
non inflammatory bacterias
- EPEC
- ETEC
- vibrio cholerae
inflammatory ish bacterias
- listeria monocytogenes
inflammatory bacterias
- EHEC
- salmonella spp
- campylobacter
- shigella spp
- C. difficile
- vibrio parahaemolyticus
- yersinia enterocolitica
MacConkey positive
red colonies
-lactose fermentation
-E. Coli
MacConkey agar negative
white or translucent colonies
-salmonella, shigella
indole positive
red color change - indole production
-E. Coli, Vibrio spp
indole negative
no color change
-salmonella
hydrogen sulfate production black colonies
Salmonella (typhi and NT) bc H2S producer
-shigella is not black bc not produce H2S
use Hektoen agar or SS agar
intestinal pathogenic E. Coli’s
- ETEC - enterotoxigenic
- EHEC - enteropathogenic
- STEC - shiga toxin producing
ETEC features
- LT and ST toxins cause electrolyte loss
- @ small intestine
- travelers, infants
- watery diarrhea
EPEC features
- A/E lesions, loss of microvilli, NO TOXINS
- small intestine
- infants and peds
- watery diarrhea
EHEC features
- A/E lesions, Stx production (shig toxin)
- @ large intestine
- bloody diarrhea, HUS sequelae (kidney)
EPEC adhesions
- BfpA - bundle forming pilus
- intimin on bacterial surface
- T3SS injects Tir into host so can bind intimin to adhere
ETEC toxins
- LT = heat liable toxin, inc cAMP, AB toxin
- ST = heat stable toxin, inc cGMP, non AB so does not enter cell
adherence via pili
vibrio cholerae diseases
gastroenteritis
vibrio parahaemolyticus diseases
- gastroenteritis
- bacteremia
- wound infection
vibrio cholerae presentation
- asymptomatic to severe watery diarrhea RICE WATER STOOL
- 2-3 day incubation, 7 day duration
can kill within hours from dehydration
vibrio cholerae epidemiology
- spread easily thru contaminated water
- long term immunity from O antigen
- associated with natural disasters, pop displacement, poor sanitary conditions
vibrio cholerae toxin
- Tcp for adherence to enterocytes
- cholera toxin = massive fluid efflux, AB toxin that inc cAMP, encoded on prophage
vibrio cholerae treatment
rehydration therapy IV and oral, no antibiotics
-prevent transmission with clean water and proper sanitation
-oral vaccines but not great
listeria monocytogenes survival traits
- intracellular pathogen
- wide growth range
- resistant to high salt concentrations
- wide pH range
listeria monocytogenes presentation
- healthy - asymp or non specific
- immunocomp - bacteremia, meningitis, encephalitis (stiff neck, persistent headache
- pregnant women - non specific but risk of transmission to neonate
fetal listeriosis
- early onset - premature babies with flu like illness before delivery mother, in utero infection, onset 0-7 days after birth, blood infection + pneumonia + meningitis
- late onset - full term, mo no sign of illness, unclear infection, 5-30 days onset, blood infection + meningitis
listeria pathogenesis
- internalin A protein to mediate adherence and induce uptake
- listeriolysin O LLO disrupts vacuole membrane so can escape to cytosol for rep
- ActA allows intracellular motility to disseminate liver/spleen/CNS, jet packs
listeria diagnosis
culture from normally sterile sites (blood, CSF)
1. cold enrichment selectin
2. weak beta hemolysis blood agar
3. pos motility test
listeria treatment
- antibiotics
- properly cook animal products, ready to eat meats, wash raw veggies
EHEC found in
- hamburgers, ground beef
- raw veggies or fruit
EHEC presentation
- hemorrhagic colitis aka bloody diarrhea
- little to no fever
- marked abdom tender
- HUS sequelae (hemolytic uremic syndrome) so anemia and kidney failure
EHEC toxin
shiga toxin (AB toxin) that inhibits protein syn > cell death = bloody diarrhea
EHEC diagnosis
does not ferment sorbitol so will be colorless on MacConkey’s culture
EHEC treatment
supportive therapy only NOT antibiotics bc may be harmfuul by inc toxin production
Salmonella Typhi characteristics
- gram neg facultative anaerobe
- motile flagellated rods with H antigen
- intracellular pathogen
- highly adapted to humans, humans only reservoir
S. Typhi presentation
- fever with headache, rises over 3 days
- fever persists for 4 weeks
- infection of gall bladder > reinfection of intestine so diarrhea
rise in rever coincides with rise of pos blood cultures
S. Typhi pathogenesis
adheres to M cells and enterocytes
-causes apical membrane of M cell to ruffle indicating endocytic uptake
-M cells @ ileum for immune presentation
S. Typhi pathogenesis
- T3SS mediates uptake into M cells + injects Ssps salmonella invasion proteins
- Vi antigen polysac capsule promotes extended intracell rep
- LPS endotoxin induces fever from septicemia
S. Typhi diagnoses
culture stool and blood
-white on MacConkeys (non lactose fermenting)
-black on SS or Hektoen agar (prod H2S)
S. Typhi treatment
- antibiotic therapy
- avoid sources of infection (drink bottled water in endemic areas, no ice, fully cook veggies, avoid raw fruits/veggies)
- vaccination for travelers
nontyphoidal salmonella presentation
- nausea + vomit + abdom cramps
- diarrhea - can be loose or severe dysentery with blood/pus for 3-4 days
- maybe fever (50%)
NT salmonella pathogenesis
- like S. typhi with T3SS into M cells then ruffles
- enter macrophage and kill rapidly by massive inflammatory resp
- can disseminate and show focal infections like arthritis, endocarditis
NT Salmonella diagnosis
- white on MacConkeys bc not ferment lactose
- black precipitate on hektoen agar bc produces H2S
NT Salmonella treatment
- supportive
- NO antibiotics bc can induce carrier state unless severe case
Camp. jejuni features
- sea gull shaped curved rods
- motile with flagella
- microaerophilic
- grow at 42 celcius
Camp. jejuni presentation
- low abdom pain
- fever
- diarrhea (watery or pus/blood)
- complicate to guillain barre syndrome
Camp. jejuni pathogenesis
- flagella mediated adherence to intestinal epithelium
- produce toxins
- cause acute inflamm, crypt abscess, entry into bloodstream from intestine
vibrio parahaemolyticus presentation
SHELL FISH
1. common- watery diarrhea, nausea, vomit, abdom cramps, some fever/chills
2. dysentery- severe cramps, nausea, vomit, bloody stools
Vibrio. para pathogenesis
two major hemolysin toxins
-thermostable direct hemolysin
yersinia enterocolitica features
- bi polar safety pin staining on giemsa
- gram neg coccobacilli
yersinia entero presentation
- weeks of abdom pain and cramps
- diarrhea - water to bloody
- acute mesenteric lymphadenitis - can be confused with acute appendicitis
pork
yersinia entero diagnosis
- NAAT
- culture
C. diff features
spores!
gram pos anaerobe
CDAD
c. diff associated diarrhea
- watery diarrhea with leukocytes and occult blood
- nausea, anorexia, fever, dehydration, leukocytosis left shift
- abdom distension, tenderness
- diffuse or patchy nonspecific colitis
pseudo membrane colitis
- profuse watery diarrhea with leukocytes and occult blood
- same CDAD symps but more severe
- marked abdom distension, tenderness
- adherent yellow plaques
fulminant colitis
C-Diff
- severe OR diminished diarrhea, needs surgery
- lethargy, fever, tachycardia, dilated colon
- acute abdom sudden/severe/pain
- no sigmoidoscopic exam
C.diff pathogenesis
- antibiotics alter/destroy normal intestinal microbiota
- c.diff survive then germinate in open niches
- toxin A and B produced
- mucosal cell injury and inflamm
C.diff tests
- EIA test for toxin A, B or both in stool
- glutamate dehydrogenase detection
- NAAT/PCR for toxin B
c.diff treatment
- initial infection/1st recurrence use antibiotics
- 2nd recurrence or if antibiotic resistance then different antibiotic or fecal microbiota transplant
in isolation NO hand santizer bc not work
shigella epidemiology
- extremely low infectious dose
- incidence directly related to hygiene so poor sanitary, crowded healthcare system, day cares
shigella presentation
- majority will be fever + malaise+ watery diarrhea from S. sonnei
- can be dysentery with freq feeling need to defecate (tenesmus) from S. flexerni or S. dysenteriae
shigella pathogenesis
- T3SS uptake into M cells
- phagocytosed by macrophages
- rapid escape from phagosome and induce macrophage apoptosis
- spread to neighboring cells from actin
- ulcers in infected areas
shiga toxin!!
shigella treatment
- rehydration
- antibiotics okay to shorten duration of illness
enteroinvasive E. Coli all about
- gram neg facultative anaerobe
- milder form of dysentery shigellosis
- same patho as shigella but no toxin
not very common
