Enteropathic Bacteria/Clostridia Flashcards
Enteropathic Bacteria
E. Coli Cholera Shigella Salmonella Campylobacter Yersinia Toxins - Staph aureus, Botulism
Enteropathic viruses
Enteroviruses
Norwalk virus
Polio virus
Enteropathic parasites
Giardia
Amoebae
Ascaris
Cryptosporiosis
Which enterpathic bacteria causes disease by ingestion of enterotoxins
Staphylococcus aureus, Vibrio, Clostridium perfringens, Clostridium botulinum
Characteristics of disease by ingestion of enterotoxins
very short incubation times, self-limited explosive diarrhea (except botulism which is a neurotoxin)
Secretory enterotoxin causes
secretory diarrhea and dehydration
Cytotoxic enterotoxin causes
dysentery (bloody diarrhea)
Describe direct invasion of the gut wall by enteroinvasive organisms
organisms proliferate, invade and destroy mucosal cells
results in dysentery
incubation time extended days-weeks
Levels of tissue involvement that cause diarrhea
toxin only ( no bacteria)
Superficial colonization + toxin
Superficial colonization + inflammation
Levels of tissue involvement that cause dysentery
mucosal invasion
mucosal necrosis
submucosal invasion
systemic spread
Important virulence factors of enteropathic organisms
adherence to mucosal cells
production of enterotoxins
capacity to invade
Adherence to mucosal cells
pili, flagella
mediated by plasmid-encoded adhesins
prototype secretagogue toxin
Vibrio cholerae
Traveler’s diarrhea
E. coli
cytotoxins - results in epithelial cell necrosis
Shiga toxin - Shigella, E. coli O157H7
T cell superantigens
Staphylococcal enterotoxins
secretion of cytokines from activated T cells that cause intestinal motility and fluid secretion
capacity to invade
microbe-stimulated endocytosis
intracellular proliferation, cell lysis and cell-to cell spread
invasion and cytolysis result in bloody diarrhea or dysentery
Predisposing factors to enteropathogens
fecal contamination, age, other ivnasive disease, immunosuppression, antispasmodic drugs, antacids
Cholera causes
secretory diarrhea
Shigella causes
dysentery
Typhoid fever causes
systemic illness
Characteristics of E. coli
coliform - ferment lactose
non-spore forming facultative anaerobe
commensals vs. pathogens
characteristics of disease caused by E. coli
watery diarrhea, cramping pain, fever, malaise; invasive or cytolytic disease - dysentery; verotoxin - hemolytic uremic syndrome
ETEC
watery “traveler’s” diarrhea from consumption of food contaminated with enterotoxin-producing strain
EHEC
severe blood colitis from consumption of hamburger, dairy products, contaminated with invasive, shiga/vero-toxin-producing strain (mainly O157:H7)
EPEC/EIEC
enteropathogenic/enteroinvasive
Enteroaggregative (EAEC)
primarily pediatric diarrhea in impoverished nations
What differentiates EHEC from other E. coli
does not ferment sorbitol or grow at 45 C
source of EHEC O157:H7
cattle and beef products including hamburger and unpasteurized milk
other agricultural products contaminated by manure
outbreaks - hamburger, spinach, sprouts
O157H7 EHEC MOA
shiga-like toxin (verotoxin)
mucosal invasion
O157H7 EHEC disease presentation
dysentery
hemolytic uremic syndrome
hemolytic uremic syndrome
hemolysis and acute renal failure - obstruction of glomeruli by microthromi
Describe the salmonella organisms
flagellated, gram neg. non coliforms, H2S produciton
Name the salmonellas
S. typhi S. enteritidis S. typhimurium S. paratyphi S. cholerae-suis
Three characteristic forms of salmonella disease
- typhoid (typhoid mary)
- enteric fever
- salmonella food poisoning
only host of typhoid fever
humans
transmission of typhoid fever
fecal-oral transmission of infected water and food
disease of developing countries, poor sanitation, disasters
pathogenesis of typhoid fever relies on
invasion, bacteremia, and distant tissue colonization
Pathology of typhoid fever
rose spots hepatosplenomegaly invasive mucosal lesions oval plaques which later ulcerate typhoid nodules in liver
Symptoms of typhoid fever
fever, chills, bacteremia in the first week
widespread mononuclear phagocytic involvement with rash (second week)
neutrophenia in peripheral blood
typhoid fever and the gallbladder
gallbladder infection associated with carrier state
organism can survive bile salts which allows for colonization of the gallbladder with shedding of the bacteria in the feces
enteric fever
S. typhinurium, S. paratyphi, S. cholerae-suis
fever, bacteremia, local lesions
assocaited with sickle cell disease, schistosomiasis
Transmission of salmonella
shed in urine/feces, vomitus/oral secretions by infected humans, convalescents, chronic carriers
undercooked food
REPTILES
Pathologic mechanisms of salmonella
invasive disease - invade mucosal cells and cause mucosal ulceration
do not produce enterotoxins
multiply within neutrophils and macrophages
Shigella organism
gram neg, nonmotile, non coliform bacteria
pathogenesis of shigella
organism escapes phagolysosome and destroys the host cell
invasive lesions of colonic mucosa that spread to lymph nodes
exotoxin (shigatoxin) causes mucosal necrosis
Cholera organism
comma-shaped, gram neg.; alkali tolerant (salt water)
pathogenesis of Cholera
no invasive lesions, pathogenicity entirely due to enterotoxin; induces secretion of isotonic fluid
Cholera toxin
subunit A binds with ADP-ribosylation factors to activate GTP-activated adenylate cyclase resulting in cAMP formation; stimulates secretion of chloride and bicarbonate
Campylobacter organism
comma-shaped, gram neg.; flagellated
disease manifestations of campylobacter
most common cause of gastritis, diarrhea, and dysentery in US
Guillain Barre
transmission of campylobacter
ingestion of undercooked chicken or contaminated liquid of solid food, usually from animals
pathogenesis of campylobacter
foul-smelling stools with blood or exudate
enteric fever with toxin/invasive lesions
Yersinia Enteritis
mostly pediatric population upper/lower GI ulcerative intestinal lesions like typhoid fever microabscess and granuloma formation deeply invasive and may be lethal
Clostridia organism
gram-positive sporulating anaerobes; highly stable in environment, produce large amounts of fermentation products and degradative enzymes
method of transmission of clostridia
contamination of wounds by spores, particularly those with low oxygen tension such as necrotic tissues or puncture wounds
Tetanus
neurotoxin tetanospasmin
severe convulsive contractions
loss of sympathetic inhibition
Gangrene (C. perfringens)
extracellular necrotizing enzymes, myonecrosis
invasion of traumatic or surgical wounds
gas gangrene
C. perfringens enteritis
food poisoning - spores
abdominal cramps and watery diarrhea, incubation period 6-24 hours
Pseudomembranous colitis (C. diff)
severe colitis with pseudomembrane formation
enterotoxin (toxin A) and cytotoxin (toxin B)
Botulism
preformed neurotoxin - cleaves synaptobrevin
blocks release of acetylcholine, descending forms of paralysis
honey
Pathologic mechanisms of clostridia
- local proliferation of sporulating organisms with DISTANT DISSEMINATION OF TOXIN
- specific exotoxins cause specific disease w/o infection
- spores long0lasting/difficult to kill; growth favored in necrotic tissue, anaerobic, or no competing organisms
- growth accompanied by necrosis/damaging bacterial enzymes
