Micro Intestinal Flora2

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Gastroenteritis

Back 1

Syndrome characterized by nausea, vomiting, diarrhea, and abdominal discomfort

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Diarrhea

Back 2

i. Abnormal fecal discharge characterized by frequent and/or fluid stool
ii. From disease of the small intestine
iii. Increased fluid and electrolyte loss
iv. Acute, brief (1-3 days)
v. Often due to enterotoxin-secreting bacterium

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Dystentry

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i. Inflammatory disorder of the GI tract associated with blood and pus in the feces
ii. Frequent evacuations but stools smaller than with diarrhea
iii. Accompanied by pain, fever, and abdominal cramps
iv. From disease of the large intestine
v. Minimal fluid loss
vi. Usually lasts 2-7 days

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Enterocolitis

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i. Inflammatory disorder affecting the mucosa of both the small and large intestine

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Endemic infections

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i. Sporadic during usual living circumstances
ii. Some worldwide, some geographically limited
iii. Maybe seasonal variations
iv. More common in infants and children

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Epidemic infections

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i. Spread beyond the family unit
ii. Related to failure of public health sanitary measures (typhoid fever, cholera, shigellosis)
iii. Spread through the water supply (salmonellosis , cholera, giardiaosis, crytptosporidosis)
iv. Outbreaks due to meats, fruit juices, and fresh veggies (EHEC)

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Traveler’s diarrhea

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i. 20-50% who travel to less developed countries will develop a diarrheal illness in the 1st week of travel
ii. 50% of cases = ETEC
iii. 10-20% of cases = Shigella spp.
iv. Uncooked or undercooked foods, water

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Enteric fever

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i. Systemic infection with origin and focus in GI tract
ii. Fever and abdominal pain
iii. Develops gradually over days
iv. Due to penetration of microbe into cells of small intestine with spread outside the bowel
v. Bacteremia common
vi. Example = typhoid fever by S. typhi

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Escherichia coli
i. Bacteriology

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1. Facultative, Gram-negative, motile bacillus
2. Classified based on O (LPS), H (flagella), and K (capsule) antigens
3. Pathogenesis

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Enteropathogenic E. coli (EPEC)

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a. Produce bundle-forming pili, intimin, Tir (translocated intimin receptor)
b. Attach to epithelium of small intestine
c. Disrupt microvillus
d. Attaching-effacing mechanism

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Enterotoxigenic E. coli (ETEC)

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a. Produce plasmid-associated enterotoxins
b. LT = heat-labile enterotoxin
c. Similar in structure and action to cholera toxin
d. ST = heat-stable enterotoxin
e. Activates guanylate cyclase activity
f. Increases cyclic GMP and fluid secretion

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Enterohemorrhagic E. coli (EHEC)

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a. Verotoxin = similar to Shiga toxin
b. After attach to large intestine epithelium (attaching-effacing) toxin is produced and acts on epithelium
c. Causes hemmorhagic colitis and hemolytic-uremic syndrome
d. Most common form is O157:H7

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Enteroinvasive E. coli (EIEC)

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a. Invade cells by endocytosis
b. Lyse endocytic vacuole, multiply and spread to adjacent cells
c. Causes tissue destruction, inflammation, necrosis, and ulceration

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Enteroaggregative E. coli (EAEC)

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a. “stacked brick” formation
b. Act in small intestine aggregative adherence due to plasmid-associated fimbriae

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Salmonella sp.
i. Bacteriology

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1. Facultative, Gram-negative, motile bacillus
2. Large number of O and K antigens
3. H antigens undergo phase variation
4. Multiple pili

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Salmonella--Manifestations

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Salmonella enterica serovar typhimurium
Salmonella enterica serovar typhi =

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Salmonella enterica serovar typhi =

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typhoid fever
a. Incubation 1-4 weeks
b. Bacteria multiply in liver and spleen
c. Large number of bacteria in bloodstream
d. Lasts 2-3 weeks
e. High fever, anorexia
f. Bacteria move to gall bladder and are shed in bile and then into intestines
g. Asymptomatic carriers
h. Human-specific pathogen
i. Vi antigen = capsular polysaccharide of N-acetylglucosamine uronic acid

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Salmonella enterica serovar typhimurium

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= gastroenteritis
a. Transmitted via contaminated food, esp. chicken and eggs
b. Incubation period = 6-24h
c. Nausea and vomiting initially followed by abdominal pain and diarrhea
d. Ingested bacteria enter via M cells in Peyer’s patches
e. Bacteria grow in macrophages
f. cAMP levels raise = leads to diarrhea

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Campylobacter jejuni
i. Bacteriology

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1. Curved or S-shaped, motile, Gram-negative rod
2. Polar flagella
3. Microaerophilic and thermophilic (42°C)
4. Low infecting dose

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Campylobacter jejuni--Epidemiology

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1. Primary reservoir = animals
2. Common source = undercooked poultry
3. Also caused by contaminated water supplies
and unpasteurized milk
4. Association with Guillain-Barre syndrome

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Campylobacter jejuni--Manifestations

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1. Disease starts 1-7 days after ingestion with fever and lower abdominal pain
2. Dysenteric stools with blood and pus
3. Self-limiting after 3-5 days
4. Ulceration and inflamed bleeding mucosal surfaces of jejunum, ileum, and colon
5. Only severe cases require antibiotic treatment

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Shigella sp.
i. Bacteriology

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1. Gram-negative bacillus
2. Symptoms range from mild to severe depending on species
a. S. sonnei = mild
b. S. flexneri and S. boydii = more severe
c. S. dysenteriae = most severe

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Shigella--Epidemiology

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1. Spread person-to-person by fecal-oral route and contaminated food or water
2. Require small infectious dose (10-100 organisms)
3. Spread easily where sanitation and personal hygiene are poor
4. Primarily pediatric disease

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Shigella--Manifestations

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1. Bacillary dysentry
a. Diarrhea is watery at first then contains mucus and blood
2. Can lead to hemolytic-uremic syndrome

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Shigella--Pathogenesis

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1. Bacteria attach to and invade mucosal epithelium of distal ileum and colon causing inflammation and ulceration

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Vibrio cholera
i. Bacteriology

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1. Curved, highly motile, Gram-negative bacillus
2. Oxidase positive
3. Aerobic or anaerobic
4. Free-living inhabitant of fresh water
5. Over 150 O antigen serotypes, but only 2 cause cholera

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Vibrio cholera--Pathogenesis

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1. Long, filamentous pili that form bundles on
bacterial surface
2. Colonizing factor = toxin-coregulated pilus (TCP)
3. Cholera toxin = ADP-ribosylating toxin
4. ZOT = toxin that loosens tight junctions
5. ACE toxin
6. Capsule present in O139 strain
7. Siderophores
8. Hemolysin

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Vibrio parahaemolyticus
i. Bacteriology

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1. Curved, Gram-negative rod
2. Highly motile via single polar flagellum
3. Facultative anaerobe
4. Highly salt tolerant – found in coastal seawater

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Vibrio parahaemolyticus--epidemio

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1. From ingesting contaminated, raw seafood
2. Outbreaks on cruise ships
3. Common in Japan

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Vibrio parahaemolyticus--manifestations

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1. Produces bowel inflammation
2. Watery diarrhea, occasionally dysentery

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Vibrio parahaemolyticus--path

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Production of heat‐stable, hemolytic cytotoxin

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Yersinia enterocolitica
i. Bacteriology

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1. Coccobacillus with bipolar end staining
2. Multiple O and H antigens
3. Prefers to grow at 22-25°C

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Yersinia enterocolitica--epidemio/manifestations

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ii. Epidemiology
1. Found in rodents, rabbits, pigs, sheep, cattle, horses, and domestic pets
2. Food-associated infections in children and colder climates
iii. Manifestations
1. Causes superficial necrosis of the small intestine mucosa and ulceration

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c.perfrigens

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add or check image

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Clostridium difficile
i. Bacteriology

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1. Gram-positive, sporeforming bacillus
2. Obligate anaerobe
3. Present in stool of 2-5% of population

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Clostridium difficile--manifestations

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Antibiotic-associated diarrhea
1. Usually 5-10 days after start of antibiotic but can range from first day to weeks after cessation of the med
2. Hospital outbreaks possible
3. Ranges from a few days of intestinal fluid to pseudomembranous colitis
a. Intense inflammation and formation of pseudomembranes composed of inflammatory debris on the mucosal surface

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Clostridium difficile--Path

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1. 2 large polypeptide toxins, A and B
a. Released in late growth phases
b. A toxin = causes cell rounding and disruption of intercellular tight junctions followed by altered membrane permeability and fluid secretion
c. B toxin = cytotoxic potency 10X that of A
d. Toxins act synergistically

Front 38

bacillus cerceus

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check image

Front 39

Staphylococcus aureus

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Food poisoning
1. 8 enterotoxins
2. Heat stable toxins
3. Resistant to destruction by enzymes in stomach and small intestine
4. Generally behave as superantigens
5. Cause severe vomiting within 3-6h
6. Recovery is usually within 24h
7. Enterotoxin A = most commonly associated with food poisoning
8. Entertoxin B = staphylococcal enterocolitis (rare)
9. Entertoxins C-E = associated with contaminated milk products
10. Entertoxin D = second most common; alone or in combination with A
ii. Up to 50% of S. aureus strains produce enterotoxin
iii. Food contaminated by human carriers
iv. Bacteria grow at room temp and release toxin
v. Toxin is detected by latex agglutination test

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Clostridium botulinum

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i. Caused by exotoxin of Clostridium botulinum
ii. Seven serologically distinct toxins
1. A, B, E, and F associated with human disease
2. Toxins blocks neurotransmission

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Food-borne botulism

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a. Toxin elaborated by organisms in food
b. Toxins ingested in food, usually canned or reheated
c. Organisms may produce toxin in gut after ingestion
d. Absorbed from the gut into the bloodstream and on to the peripheral nerve synapses

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Infant botulism

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a. Organism is ingested and toxin elaborated in vivo
b. Associated with feeding babies honey contaminated with spores
c. Most common form of botulism

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Wound botulism

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a. Organism implanted in wounds and toxin elaborated in vivo
4. Flaccid paralysis leading to progressive muscle weakness and respiratory arrest
5. Life-threatening

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Laboratory diagnosis--botulin

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1. Demonstration of presence of toxin by injecting feces or food into mice that have been give antitoxin and others not given antitoxin
2. Culture of feces, food, or wound may be done

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Antitoxin--botulism

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1. Toxins inactivated and used to produce antitoxin in animals
2. Given as soon as botulism is suspected
3. Supportive care also necessary

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Listeria monocytogenes--i. Bacteriology

Back 46

Food-associated infections
1. Gram-positive coccobacillus
2. β-hemolytic colonies on blood agar
3. Catalase positive
4. Tumbling motility below 30°C
5. 11 serotypes based on flagellar and surface antigens
6. Widespread in animals and the environment
7. Can grow slowly at refrigeration temperatures

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Listeria monocytogenes--Pathogenesis

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1. Internalin – attaches to host receptor (E-cadherin) and internalizes into endocytic vacuole
2. Listerolysin O (LLO) – pore-forming cytotoxin that allows for escape from phagosome into the cytosol
3. Propels through cytosol via actin polymerization
4. Survival within macrophages

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Listeria monocytogenes--manifestations

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1. Associated with uncooked foods like pate, contaminated milk, soft cheeses, coleslaw
2. Usually presents as meningitis
3. Populations at risk
a. Pregnant women
b. Immunocompromised individuals
c. Elderly individuals