10 - Bacterial Infections of the GI Tract Flashcards
Which gut bacteria cause systemic disease and penetration through an intact mucosa?
Listeria and Salmonella typhi
Which pathogens invade cells/cause inflammatory or cytotoxic destruction of the ilial or colonic mucosa?
Shigella, enterohemorrhagic E. coli, nontyphoidal Salmonella serotypes, and campylobacter/helicobacter
Which bacteria causes a shift in bidirectional water and electrolyte fluxes in the upper small bowel by intraluminal toxins or minimally invasive organisms?
Vibrio cholerae.
What is the ultrastructure of the small intestine? What type of cells are present?
Villi are sites of terminal digestion and absorption.
Mucus produced by goblet cells for protection and lubrication.
Vili and crypts lined by single layer of columnar epithelial cells.
Describe the ultrastructure of the large intestine? What type of cells are present.
Absorbs most water from chyme and compacts material into feces.
Vili are absent, but the colonic mucosa is fill of crypts of lieberkhun that are make of columnar epithelial cells.
How much fluid enters the GI tract each day? What is the avg fecal excretion each day? Where does 90% of net absorption occur?
8.5 L of fluid enters the GI tract each day.
Avg daily fecal excretion is about 150 mL (requires absorption of 8L)
90% absorption occurs in small bowel (lg intestine can’t absorb more than 2-3 L a day)
What are the six barriers to invading pathogens?
- Epithelial barriers and intestinal motility: rapid epithelial turn over
- Structural barrier: adherins and tight junctions
- Chemical barrier: gastric acidity
- Paneth cells (in crypts): secrete AMPs like lysozyme and a-defensins.
- Adaptive immunity: MALT makes IgA
- Microbial recognition: PRRs recognize bacterial PAMPs.
What is the role of normal commensals? When do we get them?
- Colonize neonates following delivery; drives maturation of mucosal immune system
- Monopolizes physical and nutritional niches at mucosal surface
- Contributes to nutrient acquisition by fermenting non-digestable dietary components; synthesis of VitK and B
- Provides host defense to limit ability to pathogens to take-up residence and invade the human body
What are the characteristics of listeria monocytogenes? What is the organism associated with this? In what conditions does it grow?
Aerobic, non-spore forming gram + rod.
Motile at room temp; tumble in solns.
1-45 C and high salt concentrations.
In what populations is listeriosis found in humans? How does it cause disease?
- Neonates
- Elderly
- Pregnant women
- People with defects in cellular immunity
Penetration through intact mucosa to the reticuloendothelial system.
What is the pathogenesis of listeria? How does it replicate?
- Can survive stomach acid and bile salts.
- Adherence to host cells via InIA, internalin.
- Enters enterocytes in peyers patches
- pH drop in phagosome activates listeriolysin O and PLC
- Bacteria replicate in cytoplasm; ActA located on one pole of bacterium and polymerizes host actin for movement to get to new uninfected cell to repeat process.
- Systemic effects occur with entry into macrophages and spreading through reticuloendothelial system (sleen, liver).
What is the epidemiology of listeria? How is it spread?
Sporadic and associated with undercooked means, unpasteurized milk, and contaminated cheese, and unwashed raw vegetables.
Can grow in wide range of temps, even during prolonged refridge.
Human to human transmission occurs from mother to child.
What is the clinical appearance of listeria in neonates?
Early onset in utero: abortion, stillbirth, premature birth.
Granulomas may form in organs
Late onset: 2-3 wks after birth, characterized by meningitis or meningoencephalitis with septicemia.
What is the clinical appearance in pregnant women? What about in healthy and immunocompromised adults?
Pregnent: usually during 3rd trimester when cellular immunity most impaired; influenza like symptoms with fever
Adults: Healthy-mild flu-like illness, self-limited gastroenteritis. Immunocompromised-meningitis, high mortality and neurological disease.
How would you diagnose listeria in the lab?
Gram stain CSH for meningitis pts - 10^4/ml to detect
Culture 1-2 days, cold enrichment in fridge
Biochem or serological tests for 13 serotypes.
Pulse-field gel electrophoresis.
What is the treatment and prevention for listeria?
Control difficult because it’s in environment. No vaccine.
High risk individuals should avoid: raw or partially cooked food from animals, soft cheese, unwashed raw vegetables.
Treatment: gentamicin w/ penicillin or ampicillin (naturally cephalosporin resistant).
What is the prevalance of salmonellosis in the US?
1 million cases/year
19,000 hospitalizations and 380 deaths
What are the characteristics of salmonella? What does it do in the body?
Gram - rod found in soil, water, and intestinal flora.
H antigen: for flagellar proteins
K and Vi capsular antigens: for E. coli and S. typhi respectively
O antigen for LOS.
Penetration through intact mucosa and inflamm or cytotoxic destruction or colonic mucosa.
Does not ferment lactose
What is the host range of salmonella? What is it resistant to?
Broad range: birds, mammals, reptiles, rodents EXCEPT typhi and paratyphi which are highly adapted to humans
Can resist stomach acid and can invade M cells and enterocytes in peyers patches.
What is the pathogenesis of salmonella?
Once it invades the mucosa, it replicates within the endocytic vacuoles, which are modified and stabilized by the injection of bacterial proteins through type III secretion systems (spacious vacuole).
Pathogenicity island 1 genes: invasion (SPI-1)
Pathogeniticy island 2 genes: evasion of immune response
What is the clinical appearance of gastroenteritis due to salmonella caused by serotypes other than typhi and paratyphi?
6-48 post eating contam food.
Nausea, emesis, non-bloody diarrhea. Fever, abdominal cramps, headache.
Symptoms can persist 7-10 days, spontaneous resolution.
What is the epidemiology of the gastroenteritis caused by salmonella? Who is most likely to get it? (this is only for serotypes other than typhi and paratyphi).
From contaminated food such as poultry, eggs, dairy products, and ground beef. (or pet turtles!)
Incidence greatest in children under five and adults older than 60.
Freq during summer months.
High infectious dose.
What is the pathogenesis or enteric or typhoid fever?
Invade cells and replicated as in gastroenteritis.
Typhi also replicates in macrophages and spreads through the reticuloendothelial system to liver, spleen, blood, and BM.
Bacteremia causes fever and may lead to localized infections (osteomyelitis, endocarditis, arthritis) or rarely in bowel perf.
For typhoid/enteric fever, what is the inoculum? How is it transmitted? Where is it endemic?
Inoculum for Typhi is low (this differs from the non-infectious salmonella).
Transmission is person to person and fecal.
Endemic in India, south/central America, Africa. Travelers should be vaccinated.
What are the three clinical diseases associated with salmonella?
Salmonella gastroenteritis
Salmonella septicemia
Enteric fever
What are the symptoms of salmonella gastroenteritis?
Symptoms for 6-48 hrs after food consumption.
Fever, cramps, myalgias, headaches, nausea, emesis, and non-bloody diarrhea.
Symptoms for 2-7 days but self limiting.
What species are associated with salmonella septicemia? Who is at risk?
ALL SALMONELLA SPECIES CAN CAUSE A BACTEREMIA.
But, they generally don’t unless you have a compromising condition like HIV or age extremes.
What are symptoms of enteric fever caused by salmonella typhi?
10-14 days after ingestion, gradual fever, headache, myalgias, malaise, anorexia, rose spots (bacteremic phase).
After bacteremic phase GI symptoms occur (GI phase)
Colonization of gall bladder and reinfection of the intestines.
How do you diagnose salmonella in the lab? What are some properties of it?
Stool culture using selective medium.
Lactose -, motile, makes H2S (makes dark black colonies)
Also can use pulse electrophoresis.
What is the treatment for salmonella?
Symptom relief, no Abx for gastroenteritis.
Ampicillin, trimethoprim-sulfamethoxazole or ciprofloxacin for systemic infections.
