bacterial causes of gastroenteritis Flashcards

Escherichia coli
Terms Definitions
what things are often found in a pts food consumption hx if subject to a foodborne illness?
raw/poorly cooked food, unpasteurized milk/juices, or home-canned food
what clinical factors are important to examine in a pt with a hx/symptoms of foodborne illnesses?
incubation period, duration of illness, predominant symptoms (vomiting/diarrhea/fever?), and pt populations
what social factors are important to examine in a pt with a hx/symptoms of foodborne illnesses?
pets/visits to a petting farm, daycare, travel, consumption of untreated water, and group picnics
what should vomiting as a primary symptom in gastroenteritis lead a dr to consider?
enteric viral infection (in a day or so) or food poisoning due to preformed toxins (in a few hrs or so: *staph aureus enterotoxin or *bacillus cereus heat-stable enterotoxin)
what should watery, noninflammatory diarrhea point a physician to in terms of a dx?
enteric viruses, ETEC (enterotoxigenic E coli), vibrio cholerae, and parasites (except entamoeba histolytica)
what should persistent diarrhea point a physician to in terms of a dx?
parasitic infection
what should inflammatory diarrhea point a physician to in terms of a dx?
shigella, campylobacter, salmonella, STEC (EHEC); EIEC, clostridium difficle, yersinia entercolitica, vibrio parahaemolyticus, and entamoeba histolytica (parasite)
what are the most common bacterial causes of gastroenteritis in the US?
salmonella, campylobacter, and shigella (in order)
what are the most common overall causes of gastroenteritis in the US (in order)?
calivirus (norovirus), salmonella, STEC, campylobacter, clostridium perfringens (preformed toxin), staph enterotoxin, shigella, and vibrio parahaemolyticus
what characterizes diarrhea due to staph aureus food poisoning?
food is usually contaminated by a human carrier by *preformed toxin - doesn't taste contaminated, incubation period is 4 hrs, diarrhea is watery (not bloody), pts present with severe vomiting/abdominal pain/nausea/no fever for
what is the MOA of the staph aureus enterotoxin?
the staph aureus enterotoxin is a superantigen which *activates T cells, stimulating cytokine release, and *acts on neuronal receptors in the upper GI, stimulating the vomiting center in the brain. the staph aureus enterotoxin is *heat stabile (unlike the organism), and the organism need not be present to cause the disease.
what is bacillus cerus?
a spore-forming gram positive bacillus (all spore-forming bacteria are gram positive, but the reverse is not always true)
what are the 2 toxins produced by bacillus cereus?
a heat-stable and a heat-labile toxin
what is the MOA of the *heat-stable enterotoxin produced by bacillus cereus?
what is the MOA of the *heat-labile enterotoxin produced by bacillus cereus?
it resembles the heat-labile toxin of E. coli & vibrio cholerae and stimulates cAMP, resulting in *hypersecretion of water and electrolytes
what characterizes the *heat-stable enterotoxin produced by bacillus cereus?
implicated food: rice. incubation hrs: ~2. symptoms: n/v, cramps. duration hrs: 8-10.
what characterizes the *heat-labile enterotoxin produced by bacillus cereus?
implicated food: meat/veggies. incubation hrs: ~9. symptoms: diarrhea, nausea, cramps. duration hrs: 20-36.
what characterizes the clostridium spp?
clostridium spp are an *anerobic, spore-forming bacillus and associated with many clinical diseases.
what GI diseases are associated with clostridium spp?
antibx-associated diarrhea (C. difficile), food poisoning (C. perfringens)
what characterizes food poisoning due to C. perfringes?
outbreaks usually involve *meat, *spores are heat resistant* (withstand initial cooking and revert to vegetative form if food is not refrigerated/rewarmed), and enterotoxin is *heat-labile (released after ingestion of organism/pre-formed in left-overs)
what is the MOA for food poisoning due to C. perfringes? what part of the GI is most affected.
the enterotoxin alters membrane permeability, resulting in fluid secretion. the ileum is most severely involved.
what characterizes food poisoning due to C. perfringens?
incubation in 8-24 hrs (longer than staph aureus toxin), nausea, abdominal pain, diarrhea (similar to bacillus cereus heat-labile toxin), no fever/rare vomiting, resolution in
what characterizes vibrio spp?
gram negative (along w/campylobacter, does not belong to enterobacteriaceae), highly motile curved rods
what do vibrio cholera subgroups O1 and O139 produce?
cholera toxin, which causes more severe gastroenteritis, however this is uncommon in the US
what are the more common forms of vibrio seen in the US? where are they seen geographically?
V. parahaemolyticus, V. vulnificus (does not cause gastroenteritis) and nontoxigenic V. cholera. vibrio likes saltwater and therefore is seen mostly in the gulf of mexico and can contaminate shellfish/seafood
is noncholera vibrio illness a notifiable disease?
no, only cholera
what is gastroenteritis due to vibrio usually due to?
sewage contaminated water near costal waters - often associated with consumption of raw oysters/other shellfish
how can vibrio parahaemolyticus outbreaks still occur in monitored coastal areas?
the organism multiplies rapidly and low levels can reach infectious levels if not handled properly.
what characterizes gastroenteritis due specifically to vibrio parahaemolyticus?
gastroenteritis due specifically to vibrio parahaemolyticus is transmitted by eating undercooked seafood, has a 5-72 hr incubation period and produces watery diarrhea for 1-3 days (less severe than cholera, though bloody in severe cases). pts co-present with nausea, vomiting, low-grade fever, and headache.
does V. parahaemolyticus produce enterotoxins?
this is unclear
can V. parahaemolyticus infect wounds?
occasionally, though V. vulnificus (which does not cause GI disease) is usually more responsible for this kind of infection, and lead to systemic/life-threatening disease.
what characterizes gastroenteritis due to nontoxigenic V. cholerae?
diarrhea due to nontoxigenic V. cholerae ranges from mild to severe watery and does not cause epidemics like V. cholera O1 or O139. nontoxigenic V. cholerae has also not been associated with wound infections.
what is the MOA of the enterotoxin produced by V. cholera O1 or O139?
it is a typical exotoxin w/A (active) and B (binding) subunits. the toxin binds GM1 cells receptors, the A subunit gets into the cell and *activates adenylyl cylase to generate a lot of cAMP. the *cAMP then activates ion pumps, causing secretion of Na, Cl, K, and carbonate.(same as the heat-labile enterotoxin produced by bacillus cereus as well as the labile E. coli toxin)
what characterizes the enterobacteriaceae family?
enterobacteriaceae are a ubiquitous *gram negative bacilli which *ferment glucose and are oxidase negative. they are found as normal intestinal flora in humans/animals and can cause the following clinical diseases: sepsis, UTIs, and GI/pulmonary infections as either primary or opportunistic pathogens
which members of the enterobacteriaceae family are associated with gastroenteritis?
escherichia, shigella, salmonella, and yersinia
what is the serological classification of the enterobacteriaceae (and other gram negagive bacteria) based on?
O, H, or K antigens. O antigens are found on the end of LPS (lipopolysaccharide) endotoxins. H antigens have to do with flagella (implies motility). K antigenicity has to do with the capsule.
what characterizes Escherichia coli?
nonpathogenic E. coli are normal flora of the GI tract and both pathogenic/nonpathogenic forms are lactose fermenters. specific O (somatic) and H (flagellar) antigens are associated with pathogenic E. coli. (O157:H7 is associated with E.coli causing hemolyticuremic syndrome (HUS))
what are the virulence factors associated with E. coli?
*adhesins which allow organisms to attach to certain cells where they can do damage, examples are fimbriae, colonization factor antigens, intimin, and bundle forming pili. *enterotoxins including heat-labile toxin (LT), heat-stabile toxin (ST), and the shiga toxin (STEC).
what pathogen is the leading cause of traveler's diarrhea?
enterotoxigenic E. coli
what is the leading mode of transmission of enterotoxigenic E. coli?
contaminated drinking water, food washed w/contaminated water
what types of enterotoxins are produced by enterotoxigenic E. coli?
heat-stable (STa & STb) and heat-labile (LT-I & LT-II)
what is the MOA for enterotoxigenic E. coli enterotoxin LT-I?
ADP-ribosylates adenylate cyclase regulatory protein, increases cAMP, which alters electrolyte channels (same as cholera toxin, causes watery diarrhea)
what is the MOA for enterotoxigenic E. coli enterotoxin STa?
same as cholera toxin/LT-I - but activates cGMP rather than cAMP. (leads to watery diarrhea)
what is the MOA for enterotoxigenic E. coli enterotoxin STb?
STb increases intracellular Ca++, increases HCO3- secretion, and induces villous atrophy. (leads to watery diarrhea)
what is the clinical disease associated w/enterotoxigenic E. coli?
non-inflammatory diarrhea, (watery - no blood/mucus), low-grade fever/nausea/abdominal cramping all of mild to moderate severity for 2-5 days
what is the older name for shiga toxin-producing E. coli (STEC)?
enterohemorrhagic E. coli (EHEC)
what is the most common subtype of shiga toxin-producing E. coli (STEC) in the US?
O157:H7 (though some non-O157 subtypes can express the shiga toxin)
what is shiga toxin-producing E. coli (STEC) a common pathogen of?
livestock - often STEC infections will result from beef contaminated during slaughter or direct contact with animals
what is the primary route of transmission for shiga toxin-producing E. coli (STEC)?
ground beef, unpasteurized milk/juice, and spinach/lettuce (prob due to contaminated irrigation water)
what forms of the shiga toxin are produced by shiga toxin-producing E. coli (STEC)?
Stx-1 and Stx-2 (one or both may be produced)
what is the effect of intimin production by shiga toxin-producing E. coli (STEC)?
intimin is responsible for attachment/effacement lesions and destruction of microvilli (more invasive)
what is the MOA for the shiga toxin as produced by STEC?
the A subunit enters the cell and A1 cleaves the 28s rRNA in the 60S ribosomal subunit, preventing binding of tRNA to the ribosome - *disrupting protein synthesis. the B subunit binds globotriasosylceramide receptors on intestinal/renal epithelium (*potential hemolytic uremic syndrome*). (1 A and 5 B subunits total).
what characterizes the clinical disease associated with shiga toxin-producing E. coli (STEC)?
after a 3-4 day incubation period, watery diarrhea starts, initially mimicking ETEC infection. however, w/in 2 days the diarrhea becomes bloody (though not many WBCs unlike shigella) and is accompanied by severe abdominal pain/sometimes vomiting. severity of disease ranges from mild to hemorrhagic colitis and is usually self-limiting between 4-10 days.
what is hemolytic uremic syndrome (HUS)?
HUS can be caused by STEC, more commonly in younger children and characterized by renal failure/thrombocytopenia/hemolytic anemia and has a mortality rate of 3-5% and a sequelae (renal impairment/HTN) rate of 30%. HUS occurs when STEC toxin enters the bloodstream, attaches to glomerular endothelium (blood vessel cell lining of kidney), causing damage to blood vessels (not just in the kidneys but in all tissues of the body), and initiates a non-inflammatory reaction leading to acute renal failure (ARF) and platelet activation that causes thrombocytopenia (low platelet count).
what is often the mechanism for STEC/HUS outbreaks in petting zoos & raw milk?
fecal isolates of STEC match those found on animals in zoos and in raw mild, implying inadequate washing
what characterizes enteroinvasive E. coli?
enteroinvasive E. coli is more invasive, causing inflammatory diarrhea. it is transmitted via contaminated food/water and is less common in the US. enteroinvasive E. coli resembles Shigella in that it is non-motile, ferments lactose slowly (shigella does not ferment lactose), and can cross react with shigella antiserum.
what characterizes clinical disease due to enteroinvasive E. coli?
enteroinvasive E. coli invades cells and spreads, leading to cell death/sloughing/inflammatory response. it starts as watery diarrhea and becomes dysenteric (mucus in stool/lots of fecal WBCs) and is associated with fever/cramping
what characterizes enteropathogenic E. coli?
enteropathogenic E. coli often causes infant diarrhea in developing countries which is non-inflammatory, watery, and associated with possible vomiting.
what is the pathogenesis of enteropathogenic E. coli?
like w/STEC, enteropathogenic E. coli cause attachment/effacement lesions by initially attaching via bundle forming pili and more securely via intimin receptors. enteropathogenic E. coli modify the cytoskeleton to form pedestals and disrupt the microvilli (leading to impaired absorption, though no invasion)
what characterizes enteroaggregative E.coli?
enteroaggregative E.coli can cause protracted diarrhea in children/infants for >14 days in developing countries. enteroaggregative E.coli attaches via fimbria (no A/E lesions), stimulates mucin production, forms a biofilm, and causes watery to mucoid diarrhea. vomiting is rare.
what characterizes the shigella spp?
shigella spp are non-motile, non-lactose fermenting bacteria which can either cause dysentery or watery diarrhea. S. sonnei is the most common in the US and causes watery diarrhea (as does S. boydii), while S. dysenteria/S. flexerni cause dysentery, but are not generally found in the US
what is the most common mode of transmission for shigella spp in the US?
*person-person, as it only requires a low infectious dose and can be spread via contaminated food/water and has no animal reservoir
what is the pathogenesis of gastroenteritis due to shigella?
shigella spp invade the *intestinal mucosa (M cells) and the bacteria express proteins that then enable *spread to enterocytes via induction of phagocytosis, phagolysosome escape, and mediation of cellular actin rearrangement (formation of actin tails propel bacteria into adjacent cells).
what about shigella spp contributes the most to the severity of the disease they cause?
the shiga toxin, of which S. dysenteria type I is the most potent producer. the shiga toxin is capable of causing HUS (same as STEC).
can shigella produce enterotoxin along with shiga toxin?
yes, shigella spp can produce enterotoxins which cause watery diarrhea.
why do shigella spp infection sometimes result in abscesses, ulcer, and inflammatory reactions?
b/c shigella spp invade enterocytes
how is dysentery typically spread? who does it typically affect?
dysentery typically spreads person-person via the fecal/oral route, and is less commonly spread via contaminated food. usually children
after an incubation period of 1-3 days, how does dysentery present initially?
usually initially as watery diarrhea (prob due to enterotoxin production)
what is the definition of dysentery? how does it present?
dysentery = inflammatory colitis and bloody diarrhea involving of small stools with mucus and tenesmus (painful straining to pass stools). cramping, fever, and pain in the lower abdomen are common co-presentations and there may be pseudomembrane formation (sloughed off epithelial cells, bacterial, fibrin, and inflammatory cells)
how does the incidence of shigella-induced gastroenteritis compare to that of salmonella or campylobacter?
shigella-induced gastroenteritis is common, but less so than campylobacter and salmonella
after norovirus, what is the next most common cause of gastroenteritis?
what is the single spp of salmonella called? what is the classification w/in this spp?
salmonella enterica which is then broken down into serotypes, such as typhimurium and enteritidis, which are the most commonly seen in the US. (for ex. these serotypes are written as S. typhimurium - not in italics)
what is salmonella arizonae?
a serotype of salmonella associated with reptiles
what are the 2 most common serotypes of enteritis (diarrhea) producing salmonella in the US?
S. enteritidis and S. typhimurium
what serotypes of salmonella can produce enteric (typhoid) fever, a systemic disease?
S. typhi and S. paratyphi
what is the most common route of salmonella transmission?
exposure to undercooked chicken or eggs, as seen in food prepared in advance and poorly refrigerated. exposure to turtle/rodents also possible routes of transmission.
why has it been illegal to sell small turtles as pets since 1975?
this was done in an attempt to cut down on rate of salmonella transmission via turtle contact, however attempts to treat turtles, their eggs, and breeding grounds w/antibx to eliminate salmonella have not been successful and have resulted in a high prevalence of antibx resistance
what was learned about salmonella in the 2009 outbreak?
salmonella can persist in high-fat and low water food and withstand temperatures as high as 194 F (90 C) for 50 min – can be very difficult to inactivate
what is significant about the alfalfa salmonella outbreak?
all alfalfa sprouts infected were traced back to a single seed grower
what is the pathogenesis of salmonella-induced gastroenteritis?
the enterotoxin activates cAMP, leading to watery diarrhea (like cholera), and its adhesin also disrupts the membrane, "ruffling" it, triggering its own phagocytosis. once salmonella is intracellular, it can travel from cell to cell (apical -> basolateral surface) and cause an inflammatory response, it may even invade the bloodstream and produce a systemic response (enteric/typhoid fever - not all salmonella can do this)
how does gastroenteritis due to salmonella typically present?
after a 24-48 hr incubation period, n/v, abdominal cramps, and diarrhea (predominant symptom - starts watery, can become hemorrhagic/dysenteric). self-resolution occurs w/in a week.
what characterizes enteric/typhoid fever as caused by salmonella? where are endemic areas for salmonella capable of causing enteric fever?
the reservoirs are gall bladders of chronic carriers, and from there, salmonella can be transmitted in a water supply contaminated with sewage. endemic areas include latin america, asia, and india.
what characterizes the yersinia spp?
yersinia are bipolar staining coccobacilli which are animal pathogens presumably transmitted to humans via consumption of contaminated food or water. Y. pestis is the best known as it causes plague, but the enteric spp are *Y. enterocoltica and Y. pseudotuberculosis*
what is the pathogenesis of gastroenteritis due to yersinia spp?
yersina invade the M cells of peyer's patch and can also replicate within the RES. virulence factors trigger *cytotoxic events and *impair PMN & macrophage activity (damages peyer's patches and mesenteric lymph nodes).
what does gastroenteritis due to yersinia spp mimic? beyond that, what are other presentations of pts w/enteric yersina spp infections?
yersinia spp infections can mimic appendicitis (fever, abdominal pain, mesenteric lymphadenitis). gastroenteritis due to yersinia also may include diarrhea, and enteric fever - polyarthritic syndrome. the infection is eventually self-limiting.
what is the major cause of inflammatory diarrhea in the US?
campylobacter spp
how do campylobacter spp appear morphologically?
curved, gram negative rods (though not a part of enterobacteriaceae) that resemble vibrio
what is the most common campylobacter spp?
C. jejuni
where are campylobacter spp found? what is the route of transmission?
campylobacter is normal flora of the GI & GU tracts in animals and is transmitted via contaminated food/water. undercooked chicken is the most common source - also unpasteurized milk.
what characterizes clinical disease due to campylobacter spp?
dysenteric stools are common (invasive, triggers inflammatory response), fever, lower abdominal pain, all lasting for ~1 week.
what syndrome is campylobacter jejuni infection associated with?
guillain-barre syndrome, which is an autoimmune acute demyelinating syndrome often preceded by an infection due to the antibody induced by ganglioside-like structures in the campylobacter LPS core
what kind of disease is gastroenteritis due to clostridium difficile?
gastroenteritis due to clostridium difficile is antibx-associated, as it can be normal intestinal flora/nosocomia - but when pts are on antibx, C. diff can take over the intestine completely.
what characterizes the gastroenteritis due to clostridium difficile?
gastroenteritis due to C. diff can either be simply self-limited diarrhea or can progress to pseudomembranous colitis (fibrin, mucus, inflammatory cells) in more serious cases.
what are virulence factors for C. diff?
toxin A - enterotoxin and toxin B - cytotoxin
what characterizes helicobacter spp as a cause of gastroenteritis in humans?
helicobacter pylori is the human pathogen, and resembles campylobacter (gram negative, curved rods)
what virulence factors does helicobacter possess?
*urease (allows persistence at low pH, useful in dx of H. pylori), *vacuolating cytotoxin (VacA) which induces apoptosis, and the *Cag protein which reorganizes actin (activates multiple celluar proteins)
what is the presumed route of transmission for H. pylori?
person-person, fecal-oral
what is the most common bacterial cause of gastritis, gastric ulcers, and duodenal ulcers?
H. pylori
how does H. pylori colonization change as pts age?
colonization increases with age and can persist for years, possibly for life
what other diseases are H. pylori linked to?
gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphomas
how does H. pylori utilize its virulence factors?
low pH avoidance in the stomach is accomplished via: good motility allowing the organism to get below the mucus layer and urease activity which produces ammonia (*neutralizes microenvironment). surface proteins also mediate adherence to epithelial cells and NAP (neutrophil activating protein), urease, VacA, and Cag protein all have toxic activity.
what characterizes gastritis due to H. pylori?
the infection is limited to stomach mucosa, an inflammatory response is induced (abcesses & ulcers), and the pt may be asymptomatic for decades. clinically, pts will present with pain in the upper abdoment, n/v.
what are complications associated w/H. pylori mediated gastritis?
perforation of ulcers - leading to internal bleeding and peritonitis
how are H. pylori infections diagnosed?
endoscopic examinations can yield a bx/cx of gastric mucosa, upon which urease tests are performed. the urea breath test can also performed, where pts ingest 13C or 14C-urea, and if urease-equipped H. pylori are in the stomach, that labeled CO2 will be exhaled
what is the fecal leukocyte test?
this is done to test for WBCs to determine if the diarrhea is inflammatory. it consists of a *methylene blue stain and requires a fresh stool sample for wet mount
what is the lactoferrin stool sample test?
more sensitive than a fecal leukocyte test, this tests for the iron-binding glycoproteins (lactoferrin) present in PMNs to determine whether the diarrhea is inflammatory. it is available commercially as a latex agglutination test for convenience.
what test is appropriate for diagnosing pts with persistent diarrhea?
ova & parasite (O&P) test - needs to be performed ~3x consecutively
what bacteria are tested for in a routine stool cx?
C. jejuni, salmonella spp, shigella spp, and perhaps vibrio (along coastal areas) are tested for in routine stool cxs. vibrio cholera and STEC (culture and/or toxin) tests can be requested.
if a pt has been on antibx, what is an important bacteria to look for in their stool?
C. diff and/or its toxin
what can the macconkey agar be used to differentiate?
between lactose fermenters and non-lactose fermenters. E. coli is a lactose fermenter, but many other GI pathogens are not.
what is an important application of the sorbitol macconkey agar test?
screening for E. coli O157, an enterohemorrhagic non sorbitol fermenter, which will appear clear while other fermenters will appear pink.
what is hekton enteric agar (HE agar) selective for?
shigella or salmonella
what is the cefoperazone-vancomycin-amphotericin B agar (campy CBA) agar selective for?
what is the thiosulfate-citrate-bile salts-sucrose (TBCS) agar selective for?
vibrio - likes bile salts
if a sorbitol macconkey test is positive (indicating presence of E. coli 0157), what should also then be tested for?
the shiga toxin, either stx1 or stx2 via EIA or PCR
what are the CDC recommendations for identifying STEC?
include STEC O157 in routine enteric bacterial panels, screen stool samples for Stx (via EIA or PCR), cx simultaneously or cx Stx-positive samples, if Stx-positive broth is negative for STEC 0157 - send to public health lab for identification of non-O157 STEC
what route of transmission is rotavirus more associated with?
what route of transmission is norovirus more associated with?
food contamination
what route of transmission is ETEC more associated with?
what route of transmission is vibrio more associated with?
coastal areas, shellfish
what route of transmission is C. jejuni more associated with?
contaminated poultry/water/milke - big in the US
what route of transmission is STEC more associated with?
undercooked meat, spinach/lettuce
what route of transmission is C. diff more associated with?
immunocomprimised/heavy antibx load
what route of transmission is salmonella more associated with?
what route of transmission is shigella more associated with?
contaminated food, water, daycare/travel
what route of transmission is yersinia more associated with?
contaminated pork/tofu/raw milk
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