export_gi bacteria i Flashcards
Diagnosis of diarrhea
Passage of 3 or more loose or liquid stools per day
Diarrhea is the leading cause of ___ in children under 5
Malnutrition
What is the most likely mode of transmission of GI infections?
Fecal-oral route
Which GI host defenses can actually trigger bacterial virulence
Mucus
Bile
Benefits of GI microbiota
Competitive exclusion
Digest indigestible materials
Negatives of GI microbiota
Effects on immunity
Can digest food into carcinogens
Gastritis
Inflammation of the stomach
Gastroenteritis
Inflammation of the stomach and intestines
Diarrhea
Frequent loose and fluid-filled stools
Dysentery
Inflammatory disorder of the GI tract
Blood/pus in feces, pain, fever, abdominal cramps
Enteritis
Inflammation of the intestines, especially the small intestine
Enterocolitis
Inflammation of the mucosa of the small and large intestine
Colitis
Inflammation of the large intestine
Symptoms of patient with inflammatory GI bacteria
More likely to see occult or visible blood
More likely to see fecal leukocytes
Non-inflammatory GI bacteria
Some do not produce known toxins and just bind to epithelial cells
OR
Some secrete non-cytotoxic toxins
Both result in increased electrolyte and water efflux
1-8 hours after ingestion of GI bacterial-infected food
Preformed toxin
S. aureus, Bacillus cereus, Clostridium botulinum
8-16 hours after ingestion of GI bacterial-infected food
Production of toxin after ingestion
Bacillus cereus, Clostridium perfringens, Clostridium botulinum
16+ hours after ingestion of GI bacterial-infected food
Adherence, growth, and virulence factor production
Shigella, Salmonella, Listeria monocytogenes, EHEC, EPEC, ETEC, EIEC, Campylobacter, Vibrio
Two types of food poisoning
Preformed toxins
Spore ingestion/germination
Symptoms of food poisoning
Diarrhea, vomiting, or both
NO FEVER
Four causes of food poisoning
S. aureus (not spore forming) Clostridium botulinum (spore forming)
Clostridium perfringens (spore forming)
Bacillus cereus (spore forming)
All are Gram+
S. aureus features and disease causative agent
Gram-positive cocci, non-spore forming
Ingestion of a preformed toxin
S. aureus pathogenesis and treatment for food poisoning
Vomiting, diarrhea, and abdominal pain 1-8 hours after consumption
Heat-stable toxin
Supportive therapy
Clostridium botulinum features and disease causative agents
Gram-positive rod, spore forming
Botulism toxin
Clostridium botulinum pathogenesis for food poisoning
Vomiting, diarrhea, abdominal pain 1-8 hours (preformed toxin) or 8-16 hours (spores)
Progresses to flaccid paralysis, muscle weakness, respiratory arrest
Clostridium botulinum complications and treatment for food poisoning
Lingering weakness and dyspnea up to 1 year after primary disease
Supportive therapy and IV anti-toxin administration
Clostridium perfringens features and disease causative agents for food poisoning
Gram-positive rod, spore forming
C. perfringens enterotoxin
Clostridium perfringens pathogenesis and treatment for food poisoning
Enterotoxin associated with meat held at below recommended temperatures
8-16 hours, diarrhea and abdominal cramps lasting for about 24 hours
Supportive therapy
Bacillus cereus features and causative agent for food poisoning
Gram-positive, spore forming Preformed toxin (emetic form)
Production of toxins (diarrheal form)
Bacillus cereus emetic food poisoning pathogenesis
Vomiting, nausea, abdominal cramps 1-8 hours after ingestion
Heat-stable enterotoxin associated with rice
Bacillus cereus diarrheal food poisoning pathogenesis
Diarrhea, nausea, and abdominal cramps 8-16 hours after ingestion
Heat-liable enterotoxin is produced in the intestine, associated with meat and vegetables
Bacillus cereus food poisoning treatment
Supportive therapy
H. pylori features and disease
Gram-negative, curved rod, microaerophilic
Ulcers and chronic gastritis
H. pylori pathogenesis
Flagella
Urease
Cytotoxin - VacA
Adhesins
Diagnosis and treatment of H. pylori
Urea breath test, biopsy
Combo of antibiotics and proton pump inhibitors
Listeria monocytogenes features and resistances
Gram positive rods, facultative anaerobes
Intracellular pathogen
Wide temperature growth range, resistance to high salt concentration, and wide pH range
Clinical manifestations of Listeria monocytogenes in healthy adults
Usually asymptomatic
May have fever, nausea, and/or diarrhea
Clinical manifestations of Listeria monocytogenes in immunocompromised adults
Bacteremia
Meningitis and encephalitis
Clinical manifestations of Listeria monocytogenes in pregnancy
There is a risk of transmission to neonate
Granulomatosis infantiseptica
Pyogenic granulomas distributed over the whole body
In utero transmission can result in premature birth or abortion, or have a later onset (2-3 weeks after birth)
Listeria monocytogenes pathogenesis
Adhesion and uptake
Internalized into endocytic vacuole
Acidification and escape
Replication in cytosol
Spread to other cells
Disseminated infection
Internalin-A
Adherence and induced uptake for Listeria monocytogenes
LLO
Disrupt vacuole membrane to allow for escape into cytosol for Listeria monocytogenes
ActA
Mediates actin polymerization, which allows bacteria to spread to neighboring cells and blood stream
Listeria monocytogenes diagnosis
Microscopy is INSENSITIVE
Cold enrichment selection of CSF culture, weak beta-hemolysis on blood agar
Listeria monocytogenes treatment and prevention
Beta-lactam or trimethoprim-sulfamethoxazole
No vaccine
Non-inflammatory GI Bacteria Spp.
EPEC, ETEC, listeria monocytogenes, vibrio cholera
Inflammatory GI Bacteria Spp.
samonella spp., campylobacter jejuni, C. difficile (severe cases), EHEC, EIEC, Shigella spp., vibrio parahaemolyticus, yersinia enterocolitica
watery, sometimes bloody or often bloody diarrhea
EHEC, campylobacter jejuni, shigella spp., yersinia enterocoliticia, EIEC, clostridium difficile, vibrio parahaemolyticus
Watery, rarely bloody diarrhea
EPEC, ETEC, food-poisoning, Clostridium perfringens, bacillus cereus, vibrio cholerae, samonella spp., listeria monocytogenes
