Hd Test 3 - Enteric Pathogens

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Inflammatory diarrhea

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low-volume w/ blood/pus/WBC in stool.

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causes of inflammatory diarrhea

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organisms that invade cells of intestinal epithelium, and non-invasive organisms that colonize lower bowel and produce cytotoxins

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Secretory Diarrhea

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high volume, water, no blood/pus

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causes of secretory diarrhea

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organisms that bind mucosal epithelium and disrupt host cell processes or secrete endotoxins.

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Food poisoning

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from consumption of preformed microbial toxin

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types of toxins

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enterotoxin - targets enteric cells (shiga, cholera toxin); exotoxin - any secreted toxin (TSS, botulinum); endotoxin - LPS (part of gram neg OM)

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enteroinvasive pathogens

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facultative intracellular pathogens. Invasion of host cells key to causing disease. Shigella, salmonella enterica, yersinia, campylobacteria, listeria, enteroinvasive e. coli

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enterotoxic pathogens

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bacteria that make enterotoxin. invasion not a factor. C difficile, vibrio cholera

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enteropathogenic pathogens

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bacteria that destroy epithelium. invasion not a factor. H pylori, EPEC, EHEC

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enteroinvasive - virulence and sx

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based on ability to invade/replicate

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mechanisms of invasion

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trigger and zipper

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trigger

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attach to host, inject effector protein into host that induces cytoskeletal rearrangement >> membrane ruffling and uptake of bacteria. Ex: T3SS

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zipper

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attach to host and engage specific receptor >> receptor-mediated endocytosis.

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where replication occurs

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in vacuole or in cytoplasm

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Salmonellae

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gram negative rod w/ flagella; facultative anaerobe; lactose negative

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where salmonellae lives

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Gi tract of many animals

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Typhoid fever

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systemic infection w/ Salmonella enterica serovar Typhi that begins as GI infection from contaminated food.

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typhoid fever sx

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gastroenteritis, slowly-progressing fever, profuse sweating

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typhoid fever transmission

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person-person; human reservoir. carrier state exists. highly virulent

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salmonella enteric serovar typhi pathogenesis

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high acid tolerance >> survives stomach; invades intestinal epithelial and M cells via T3SS. Prevents vacuole/lysosome fusion. highly resistant to macrophages. capsule helps elude immune system.

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dissemination

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spreads via Reticulo-endothelial system to liver/spleen. May colonize biliary dict and lead to chronic carrier state.

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typhoid fever treatment

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long-term AB.

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non-typhoid salmonella

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spread from livestock, reptiles, birds, via contaminated food. Larger ID. V/D, cramps, but septicemia is rare.

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differences w/ non-typhoid salmonella

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similar entry mechanism, but no capsule. Bacteria do not disseminate. AB not recommended to treat.

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Shigella

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gram-negative bacilli; lactose neg

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reservoir

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mainly human; also infects primates

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Shigellosis

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low ID, person-person spread; syx range from mind diarrhea to dysentery. treat w/ rehydration

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shigella pathogenesis

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invades M cells and can move w/in and btw cells using actin-based mobility.

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shiga toxin

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made by shigella dysenteriae and EHEC. enterotoxic, blocks abs of glucose, electrolytes, AA. Cytotoxic to some cells.

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campylobact jejuni

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gram negative curved rod (corkscrew); motile, microaerophilic; selective for charcoal medium **most common bacterial cause of diarrheal disease in US

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host ranges

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normal flora in human, birds, cattle, pets

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sx and treatment

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inflammatory diarrhea; rehydration and AB

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campylocat jejuni virulence

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flagellar motility, invasion, cytolethal distending toxin damages host cell DNA and causes death

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Listeria monocytogenes

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gram pos bacilli; actin-based motility, can grow at 4 degrees celcius

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where is listeria often found

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contaminated dairy, processed meat.

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listeria sx

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fever, muscle ache, N/V

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special population concerns

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pregnant women, fetuses, neonates

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concerns re: pregnancy

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mild flulike symptoms but can spread across the placenta and cause miscarriage or preterm birth OR spread at delivery and cause meningitis

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early neonates

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resembles group B strep >> can cause meningitis

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vibrio cholera

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gram neg, comma-shaped rods; "darting motility"

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where cholera is found

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aquatic environments; only infects humans

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cholera disease

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abrupt onset of watery diarrhea, loss of fluid/electrolytes; dehydration and shock lead to death. No systemic disease. Sensitive to stomach acid, so buffering acid lowers ID.

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cholera treatment

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oral rehydration and antibiotics

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cholera toxin

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enterotoxin (causes net fluid secretion in gut) 5 B subunits that bind; A subunit enters cell and stimulates adenylate cyclase, increases cAMP, increases ion transport into lumen

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H pylori

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gram negative rod, spiral, flagellated found in stomach of 50% of population.

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H pylori pathogenesis

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produces urease that converts urea to ammonia and CO2, increasing pH. mucinases damage epithelium and cause inflammation

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H pylori treatment

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antibiotics, proton pump inhibitor, bismuth subsalicylate

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E coli

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facultative gram negative rod; lactose fermenter

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enterotoxigenic E coli

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choleralike disease but no darting motility. treat like cholera

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enteroinvasive EC

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bacteria invade, escape phagosome; similar to shigella; invades/multiplies in epithelium, causes inflammatory diarrhea. No toxin. person-person spread

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EPEC and EHEC

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enteropathogenic, cause diarrhea. attach and form lesion, cause inflammation