Mid Infectious Diarrhea

Front 1

What is the attack rate of diarrhea in children?

Back 1

-10-18 illnesses per child per year in the developed world
-1-3 illnesses per child per year in the developed world

Front 2

What causes most cases of acute infectious diarrhea?

Back 2

Viruses

Front 3

What are the most commonly isolated bacterial pathogens in diarrhea? Which are spread person to person?

Back 3

-Campylobacter (42%)
-Salmonella (32%)
-Shigella (19%)
-E. coli O157:H7 (7%)
-Vibrio (1%)

Person to Person:
-Shigella
-Salmonella typhi

Front 4

Describe Vibrio

Back 4

-Gram negative bacilli
Grow in esturarine and marine environments
-Survive in contaminated waters with increased salinity and temperature
-Subclassed based on O antigens
-Can cause cholerae (V. cholerae O1 and O139)
-Cholera is spread by contaminated food or water

Front 5

What are the clinical manifestions of cholera? What is treatment?

Back 5

-Variable
-75% asymptomatic
-20% abrupt watery diarrhea
-5% Severe watery diarrhea, vomiting, and dehydration
-No tenesmus, strain, abdominal pain, or fever
-Severe dehydration, metabolic acidosis (bicarbonate loss), hypokalemia (low potassium) an hypovolumic shock
-Occurs 2-3 days after ingestion of bacilli
-Duration: 1-3 days
-Mortality: 60% treated, >1% untreated
-Treatment: Rehydration: IV followed by oral rehydration solution (glucose and electrolytes) and doxycycline

Front 6

Describe shigella. What are the species of shigella?

Back 6

Small gram negative bacilli/rods
S. sonnei (developed countries)
S. flexneri (developing countries)
S. dysenteriae (most severe)
S. boydii

Front 7

What is the reservoir for Shigella?

Back 7

Humans

Front 8

Describe the pathogenesis of Shigella

Back 8

-Transmitted fecal-pral
-Low innoculum (<200 organisms)
-Invasion of intestinal mucosa, moving from small to large intestines, with multiplication in the cells lining the mucosa and mucosal destruction
-Cytotoxin elaboation
-Penetration beyond the mucosa is rare

Front 9

What are the clinical manifestions of Shigella?

Back 9

-12 hours after ingestion, bacterial multiplication begins in small intestines resulting in abdominal pain, cramping, watery diarrhea and fever
-Resolution of fever in a few days
-Onset of severe lower abdominal pain, accompanied by urgency, tenesmus, and blood mucoid stools
-Illness lasts on average 7 days
-Colonic shedding 1-4 weeks
-S. dysenteriae results in more serious diarrhea with risk of Hemolytic Uremic Syndrome (HUS)

Front 10

What enterotoxin does S. dysenteriae produce?

Back 10

Shiga Toxin, which disrupts protein synthesis and produces endothelial damage

Front 11

Describe EIEC

Back 11

Causes bloody diarrhea by causing destruction of the epithelial cells in the large intestines

Front 12

Describe the clinical presentation of EHEC

Back 12

-Mild, uncomplicated diarrhea to hemorrhagic colitis with severe abdominal pain
-Bloody diarrhea
-Little or no fever
-Associated with Hemolytic Uremic Syndrome (acute renal failure, thrombocytopenia, microangiopathic hemolytic anemia) (Stx-2, 10% of children under 10, Mortality: 3-5% of children with HUS)
-Severe neurological and renal sequelae can occur in as many as 30% of patients

Front 13

Describe campylobacter?

Back 13

-Small, comma-shaped gram negative bacilli
-Microaerophilic

Front 14

What are the most common causes of campylobacter gastroenteritis? Where do the bacteria come from?

Back 14

C. jejuni
C. coli
C. upsaliensis

C. jejuni and C. coli infections occur through consumption of contaminated poultry, milk, and other foods

Front 15

What is the pathogenesis of C. jejuni?

Back 15

-Produces histologic damage throihg invasion into intestinal cells
-Exact role of the adhesions, cytotoxins, and nterotoxins are not well defines
-Rarely associated with Guillaine-Barre syndrome
-Pathogenesis believed to be related to antigenic cross-reactivity between the oligosaccharides of Campylobacter and glycosphiniolipids present on neural tissues

Front 16

Describe salmonella

Back 16

-Gram negative bacilli
More than 2400 unique serogroups
-Typhoid species: S. typhi and S. paratyphi
-Nontyphoidal species: S. enteritidis and S. typhimurium

Front 17

Explain the pathogenesis of S. typhi

Back 17

-Only reservoir is human
-Causes typhoid fever
-Produces a febrile illness
-Passes through the intestinal lining
-S. typhi is engulfed by macrophages, where it replicates and is sent to the liver, spleen, and marrow
-5-21 days later patients experience fever, headache, malaise, myalgias, and a salmon pink rash on the abdomen

Front 18

Explain the pathogenesis of S. enteritidis

Back 18

-Colonized the GI tract of virtually all animals
-Large inoculum required for development of symptomatic disease
-Infections occur in people when contaminated foods are improperly stored
-However in high risk populations (elderly, immunocompromised)
-Characterized by fever, nausea, vomiting, bloody or non-bloody diarrhea, abdominal cramps

Front 19

Describe E.coli

Back 19

-Gram negative bacillus
-Facultative anaerobe
-6 groups
-Enterotoxigenic (ETEC)
-Enteropathogenic (EPEC)
-Enteroinvasive (EIEC)
-Enterohemorrhagic
-Shiga-like toxin producing E. coli (STEC)
-Enteroaggregative (EAEC)
-Diffusely adherent E. coli (DAEC)

Front 20

Describe ETEC

Back 20

-Traveler's diarrhea
-Produces heat-labile, heat-stable enterotoxins which affect the small intestine sand cause a secretory diarrhea
-Seen mostly in infants in developing countries

Front 21

Describe EHEC

Back 21

-Inoculum <1000 organisms
-Hemorrhagic colitis, associated with HUS in children
-Produces cytotoxic Shiga Toxins (Stx-1 and 2) that destroy intestinal villi and cause dysentery
-Serotype O157:H7 is responsible for most of the E. coli gastroenteritis in the US
-More common in warm months from meats, water, milk or fruit juice

Front 22

Describe EPEC

Back 22

-Children's diarrhea
-Causes diarrhea by destroying microvilli in the small intestine
-Seen mostly in infants in developing countries

Front 23

Describe EIEC

Back 23

Causes bloody diarrhea by causing destruction of the epithelial cells in the large intestines

Front 24

Describe the clinical presentation of EHEC

Back 24

-Mild, uncomplicated diarrhea to hemorrhagic colitis with severe abdominal pain
-Bloody diarrhea
-Little or no fever
-Associated with Hemolytic Uremic Syndrome (acute renal failure, thrombocytopenia, microangiopathic hemolytic anemia) (Stx-2, 10% of children under 10, Mortality: 3-5% of children with HUS)
-Severe neurological and renal sequelae can occur in as many as 30% of patients

Front 25

Describe the Cholera Toxin

Back 25

-Enterotoxin
-A subunit: enzymatic activity
-B subunit: binds to enterocyte surface receptor, the ganglioside Gm1
-After binding to enterocyte, A subunit translocates across cell membrane, catakyzed ADP ribosylation of a GTP-binding protein resulting in persistent activation of adenylate cyclase
-Inhibits Na reabsorption and new flux of fluid from the gut
-Doesnt affect sodium glucose transport

Front 26

Describe Shiga toxin

Back 26

-Produced by S. dysenteriae
-B subinit binds to host cell glycolipid (Gb3) and facilitates transfer of A subunit
-A subunit disrupts protein sunthesis by preventing binding of aminoacyl-transfer RNA to the 60S ribosomal subunit
-Results in destruction of intestinal cells and villi, decreasing intestinal absorption

Front 27

Describe S. aureus enterotoxin

Back 27

-Neurotoxin
-Heat-stable
-Increases peristalsis by autonomic activation, results in intense vomiting

Front 28

Describe Bacillus Cereus enterotoxic

Back 28

-Two enterotoxins
-Emetic: incubation period of 1-6 hours
-Diarrheal: Incubation period of 10-12 hours

Front 29

Describe ETEC toxin

Back 29

-LT-1
-Similar to cholera toxin
-1 A subinit
-5 B subunites

Front 30

Describe EHEC Shiga toxin

Back 30

-Stx-1 identical to Shigella Shiga toxin
-Stx-2 has 60% homology, A internalized and binds to 28S ribonucleic acid, disrupting protein synthesis

Front 31

Which bacteria can invade tissues? What is the mechanism?

Back 31

-E. coli, Shigella, and Salmonella all share a common effector system
-Type III secretion system
-Salmonella has two: SPI-1 and 2
-After binding M cells, SPI-1 secretion system introduces salmonella-secreted invasion proteins (Sips and Ssps) into M cells
-Results in rearrangement of host cell actin and subsequent membrane ruffling
-Ruffled membrane engulfs Salmonella
-Salmonella replicates in host cel and spreads to adjacenet cells
-Shigella system has 4 proteins (IpaA-D)
-Shigella lyses phagocytic vacuole and replicates in host cell cytoplasm

Front 32

Contrast watery diarrhea, Dysentery and enteric fever

Back 32

-Watery diarrhea is usually localized to the small intestines and is enterotoxin-mediated
-Dysentery is localized to large intestine and is caused by secreted cytotoxins or bacterial invasion
-Enteric fever is from bacterial invasion and systemic dissemination

Front 33

What causes watery diarrhea?

Back 33

-V. cholerae
-ETEC
-Bacillus cereus
-C. perfringens

Front 34

What causes dysentery?

Back 34

-Shigella
-EHEC
-C. jejuni
-C. difficile
-E. histolytica

Front 35

What causes enteric fever?

Back 35

-Salmonella
-Yersinia

Front 36

What bacteria is in beef/gravy? Shellsfish? Sushi?

Back 36

Beef gravy: Salmonella, Campylobacter, EHEC

Sushi: Campylobacter

Shellfish: Vibrio species

Fried rice: B. cereus

Front 37

What bacteria is in water? milk? Eggs? Undercooked chicken?

Back 37

Water: Giardia, Norwalk virus, Campulobacter

Milk: Salmonella, Campylobacter, Yersinia

Eggs: Salmonella

Chicken: Salmonella, Campylobacter

Front 38

For which cases are antibiotics recommended? What is used?

Back 38

-Traveler's diarrhea (ETEC)
-Fluoroquinolones

-Empiric therapy for those with moderate to severe disease in the absence of C. difficile and EHEC
-3-7 day course of fluoroquinolone