Normal Intestinal Flora

• Escherichia coli
• Proteus species
• Providencia species
• Klebsiella species
• Enterobacter species
• Citrobacter species

1. Gram negative bacilli
2. Facultatively ananerobic
3. Non-spore-forming
4. Most are coliforms
5. Many of them are motile
6. They differ by their biochemical properties and their specific antigenic components

• Fall into two broad categories
  • Those infections caused by ingestion of viable bacteria
    • Usually in contaminated food or water
    • These bacteria reproduce and increase in number
    • Result is gastroenteritis
    • Examples: typhoid fever, salmonellosis, shigellosis, cholera
  • Those intoxications caused by ingestion of preformed toxins
    • Produced by bacteria growing in contaminated food or water
    • Called an intoxication
    • These toxins are exotoxins,
    • Examples: botulism (neurotoxin), staphylococcal food poisoning (enterotoxin), clostridial food poisoning (enterotoxin)

• Cause one of two disease states
  1. Bacteria multiply in intestinal mucosa and submucosa
  2. Bacteria multiply AND produce harmful toxins
• Basic clinical syndrome is abdominal distress, diarrhea, nausea, vomiting
• There is an incubation period
• Mild fever, chills, headache are usually present

• Salmonellosis (p.240)
• Shigellosis (p. 242)
• Campylobacter jejuni
• Helicobacter pylori
• Yersinia entercolitica (p. 255)

• Gram negative, facultatively anaerobic rod
• Acquired by:
  • Ingesting food or water that is fecally contaminated
  • OR by the placement of the organism in the mouth by soiled hands
  • OR Eggs, shellfish, turtles may serve as a source of infection
• Incubation: 12-36 hours
• To diagnose: isolate pathogen from stool or food
• ID50 is small, about 1000 bacteria
• Symptoms include fever, nausea, abdominal pain, diarrhea
• One serotype, S. typhi, is extremely virulent
  • Multiplies in phagocytic cells, rather than intestinal cells
  • Called typhoid fever, and it is a systemic illness
  • Transmission is human to human

• AKA as bacillary dysentery
• Liquid stools often contain blood and mucus
• Most Shigella species inflict damage by microbial multiplication in intestinal mucosa
  • HOWEVER, one species, S. dysenteriae, also secretes a toxin called Shiga toxin
  • S. dysenteriae may go systemic, invading bloodstream
• Reservoir: human intestinal tract (infected feces are always the source)
• Transmission: fecal-oral route; indirectly through contaminated objects; use standard precautions, unless patient is incontinent (then, use contact also)
• ID50 is very small; not affected by stomach acidity
• Incubation: 1-4 days

• Probably the most common bacterial agent of diarrhea in children
• Incubation: 2-4 days
• Reservoir: zoonotic (commensals in GI tract of cattle, sheep, poultry)
  • Humans get this by eating contaminated food/water
  • Outbreaks traced to unpasteurized milk, undercooked poultry, and direct transmission between cats (or dogs) and humans

• Microaerophilic, Gram negative, curved rod
• Major cause of gastritis and peptic and duodenal ulcer disease
• When not properly diagnosed and treated, develops into chronic gastritis that places patient at risk for stomach cancer
• To diagnose:
  1. Biopsy tissue, treated with silver stain
  2. Breath test (drink C isotope-labeled urea; look for C-labeled carbon dioxide)
  3. Indirect enzyme immunoassays

• Gram negative bacillus
• Psychrotroph (4^o C.) that rarely may contaminate blood supply
• Reservoir is animals; also isolated from water, fruits, vegetables
• Does not normally survive pasteurization (large numbers may, however)
• Causes diarrhea, abdominal pain, fever
• Transmission: fecal-oral

1. Cholera Vibrio cholera)
2. Vibrio parahaemolyticus
3. Clostridum perfringens
4. Bacillus cereus
5. Clostridium difficile
6. Escherichia coli

• Gram negative, comma-shaped rod
• Colonizes the small intestine
  1. Secretes enterotoxin
  2. It binds to intestinal epithelial cells
  3. It activates an enzyme in mucosal cells
  4. This increases cAMP production
  5. Increased cAMP alters the permeability of the mucosa
  6. Result is an outpouring of fluid and salts--profuse diarrhea with classic "rice water" stools (1L/hour)
• Collapse, shock, and death may follow
• Source is contaminated water supplies; shellfish are a reservior
• Immunity: active, either from disease or vaccine
• Standard precautions; use contact precautions if diapered/incontenent

• Halophile; Gram negative
• Source is raw oysters and crustaceans (especially sushi)
• Present in coastal waters of continental US and Hawaii
• Symptoms include abdominal pain, vomiting, watery stools that arise after colonization by the bacteria and subsequent enterotoxin production

• Gram positive, anaerobic endospore-forming bacillus that is also responsible for gas gangrene
  • Anaerobic infection that arises in necrotizing tissue
• Source is meat, poultry, or gravy that is contaminated with C. perfringens
  • Produces heat-resistant endospores that survive cooking temperatures
  • If food stands at room temperature, spores germinate and bacilli grow rapidly
• Once ingested, bacilli form endospores in intestinal tract and produce enterotoxin
• Symptoms appear 8-24 hours after food ingestion
• Disease is mild and brief

• Aerobic, Gram positive, endospore-forming bacillus
• Source is grain and vegetable dishes
• After cooking, room temperature storage allows endospores to germinate
• Incubation period is about 10 hours and illness is brief
• Causes nausea, abdominal pain, profuse watery diarrhea with rectal spasm (tenesmus)
• ID50 is very high, but once organisms are colonized, two enterotoxins are produced

• Gram positive, endospore-forming, anaerobic rod
• Administration of any antimicrobial agent may result in mild to severe diarrhea with or without intestinal pathologic changes
  • Growth of normal intestinal flora is suppressed, allowing an overgrowth of C. difficile (is more resistant to antimicrobials), which produces two toxins (Toxin A: enterotoxin; Toxin B: cytotoxin)
  • It is also thought that normal intestinal flora prevent the production of, or inactivate, C. difficile toxins
• In mild cases, diarrhea, fever, and abdominal pain result
• In severe cases, pseudomembranous colitis results
  • To treat, stop antimicrobial therapy; in severe cases, vancomycin/metronidazole
• Use contact precautions as C. difficile endospores contaminating environment easily spread to susceptible patients

• E. coli is normal flora within intestinal tract
• HOWEVER, there are different strains of E. coli that are known to produce at least five types of diarrheal disease
  1. Enterotoxigenic E. coli (ETEC)
  2. Enteroinvasive E. coli (EIEC)
  3. Enteropathogenic E. coli (EPEC)
  4. Enterohemorrhagic E. coli (EHEC)
  5. Enteroaggregative E. coli (EAggEC)
• These strains are different from the E. coli that infect the urinary tract and wounds
• These bacteria harbor plasmids (extrachromosomal DNA fragments) that contain the genetic instructions for microbial attachment to intestinal epithelial cells and subsequent invasion and/or elaboration of toxins

• Largely responsible for "traveler’s diarrhea" (turista)
  • Develops in persons visiting underdeveloped countries and who do not take proper precautions with food and drink
  • Onset is within 1-2 weeks after arrival
  • Abdominal pain, malaise, loss of appetite, watery diarrhea, low grade fever lasting 3-5 days
• Enterotoxin resembles the cholera toxin in that it causes a watery diarrhea
• To prevent: travelers should eat well-cooked food and water treated by chemicals/boiling (bottled water may not be safe to drink)
• Immunity: people living in endemic areas develop immunity to these strains

• These actually invade the intestinal tissue, producing a marked inflammatory response
• Symptoms include severe abdominal cramps, malaise, fever, bloody stools
• Bloody diarrhea in the absence of other enteric pathogens is a clue
• Toxin is similar to Shigella dysenteriae toxin

• Cause of epidemic infant diarrhea in hospital nurseries and communities, mostly in developing countries
• Bacteria attach to intestinal epithelia cells, causing a severe, water diarrhea with dehydration and shock
• Infants acquire this from contaminated formula (mixed with water containing organisms) or by transmission on hands of hospital personnel

• Serotype O157:H7 is main serovar (O is an outer membrane antigen; H is a flagellar antigen detectable by serologic methods)
• Symptoms include abdominal cramps, watery diarrhea, followed by a bloody intestinal discharge
  • Diarrheal fluid does not contain white blood cells
  • Patients do not have fever
• In some patients, especially children, diarrhea is followed by a syndrome called "hemolytic uremic syndrome" (HUS)
  • HUS results in acute renal failure, decreased platelets, and a hemolytic anemia
• Toxins are called Shiga-like toxin 1 and 2 (AKA verotoxins 1 and 2)
• This particular strain does not ferment sorbitol
• Use immunologic assays to detect toxins or serological tests to detect 0157 and H7 antigens
• Reservoir: cattle
• Transmission: poorly cooked beef, raw milk, unpasteurized apple juice; also direct contact; ID50 IS LESS THAN 10 BACTERIA

• AKA as enteroadherent E. coli
• Another cause of traveler’s diarrhea in developing countries
• Symptoms include water diarrhea, vomiting, dehydray, fever; sometimes bloody stools
• Risk factors for acquiring this infection are unknown, although probably similar to other causes of traveler’s diarrhea

1. Staphylococcal enterotoxin poisoning
2. Botulism

• Intoxication induced by consuming preformed toxin produced by Staphylococcus aureus multiplying actively in food before it is consumed
• Symptoms appear 1-6 hours after ingestion
• Onset is abrupt and often violent
  • Nausea, vomiting, cramps, diarrhea
• Diagnosis depends upon isolation of S. aureus from food (if bacteria are still alive)
  • Cooking kills the organisms, but toxin is heat stable
• Source: usually a person with an infected lesion; also healthy carriers
• Staphylococci require a few hours to grow and make the toxin
• Treatment: toxin is preformed, so antibiotics don’t help

• Clostridium botulinum is a Gram positive anaerobic, endospore-forming rod found in soil and freshwater sediments
• In anaerobic environments (e.g., sealed cans), microbe produces an exotoxin that is a neurotoxin
  • Toxin is specific for synaptic end of the nerve
  • It blocks the release of acetylcholine (which is necessary for transmission of nerve impulses across synapses)
  • Victims develop a progressive flaccid paralysis
  • Toxin is destroyed by boiling
• Ingestion of endospore does not lead to botulism in adults
• C. botulinum does not colonize successfully with normal intestinal microbiota
  • In infants, however, intestinal microbiota is not well-established, and they are at risk for infant botulism
• Treatment: toxin is preformed, so antibiotics don’t help; supportive care and antitoxin

1. Mumps: pp. 388-389
2. CMV: pp. 418-419
3. Hepatitis: pp. 405-411
4. Viral Gastroenteritis: pp. 412-413
   • Rotavirus: p. 412
   • Norwalk agent: p. 413

• Vaccine-preventable disease
• Infects the parotid glands, one of three pairs of salivary glands of the digestive system
• Transmission: droplets
• Portal of entry: respiratory tract
• Symptoms include inflammation and swelling of parotid glands, fever, pain during swallowing
• Orchitis can occur in males past puberty

• Fecal-oral transmission
• Source: contaminated food, shell fish
• 2-6 weeks incubation
• Vaccine available
• To diagnose: look for IgM

• AKA serum hepatitis
• Transmission: body fluids, especially sexual (STD)
• 4-26 weeks incubation
• Vaccine available
• Anti-HBs found in vaccinated people
• 10% become chronic carriers
  • These people at high risk for liver cancer

• Transmission similar to hepatitis B, although not sexual transmission is not as efficient
• 90% become chronic carriers
  • Number one reason for liver transplant
  • These people at high risk for liver cancer