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47 Cards in this Set
- Front
- Back
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clinical manifestations of diarrhea
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Systemic – malaise, myalgias, fever
Upper GI – nausea, vomiting Lower GI – cramping, diarrhea, tenesmus |
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non-specific barriers in the GI tract
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Mucins – gel formation, physical barrier, molecular sieve, reduces shear stress, blocks chemical insults, binding site for normal flora
Gastric acid – antimicrobial Tight junctions – prevent penetration between cells and bacterial products Defensins, lysozymes, phospholipases, DNAases, trypsin from Paneth cells Found in small bowel villi Resident Flora Direct competition TLR conditioning of normal immune system by normal flora Keep immune system healthy Normal flora constitutively signal TLR |
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systemic immunity triggered in the gut
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M cell
Sample environment Specialized epithelial cells Concentrated over peyer’s patches Gut Dendritic cells Fed antigens from M cells When from M cell, can make T cells tolerant to antigen (there is not co-stimulation of dendritic cell to activate If not from M cell, T cell knows it is malignant (get from break in tight junctions)… get costimulation and activation of dendritic cells Feed to immature T cells B cell – produce antibodies Class switching requires T cells IgA is the most common isolated deficiency because it is the last one to switch Protective affects Mostly benign See it in chronic parasitic infection – have trouble clearing pathogens |
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M cell in gut
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Sample environment
Specialized epithelial cells Concentrated over peyer’s patches |
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Gut dendritic cells
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Fed antigens from M cells
When from M cell, can make T cells tolerant to antigen (there is not co-stimulation of dendritic cell to activate If not from M cell, T cell knows it is malignant (get from break in tight junctions)… get costimulation and activation of dendritic cells Feed to immature T cells |
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b cells in gut
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Class switching requires T cells
IgA is the most common isolated deficiency because it is the last one to switch Protective affects Mostly benign See it in chronic parasitic infection – have trouble clearing pathogens |
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abnormal immune activation in gut
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Abnormal immune activation:
Leaky tight junctions, get T cells that are activated against normal flora Balance of T cells: Different T cell responses Pro-inflammatory and anti-inflammatory responses |
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extra intestinal manifestations of gut infection
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Extra-intestinal manifestations –
T cell migration – can migrate to skin or joints Causing systemic illnesses |
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common G - rods
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Salmonella
Shigella E coli Campylobacter Yersinia |
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IgA deficiency predisposes to what infections
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IgA deficiency
Giardia Cryptosporidiosis |
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risk factors for c. difficile colitis
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C. difficile colitis
Major risk factor is loss of normal flora Antibiotic treatment |
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enterotoxigenic bacteroides fragilis
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Minor strain of normal flora B. fragilis
Causes inflammatory diarrhea w/out much fever/systemic symptoms Very toxic to colonic epithelium and disrupts tight junctions Causes chronic inflammation |
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intestinal protozoa
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entamoeba histolytica
giardia lamblia cryptosporidium |
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entamoeba histolytica life cycle
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Life cycle – ingest cyst, stomach acid releases protozoa, travels to large bowel
Causes diarrhea with dysentery (bloody stool) Fever and abdominal tenderness |
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entamoeba histolytica distribution and infection
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Worldwide distribution
Developed world – institutionalized adults, recent immigrants, gay males Fecal oral contamination Many types, but need special stains to determine type |
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complications of entamoeba histolytica infection
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Complications – constrictions, perforations
Can escape through portal system to liver and form abscess |
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dx of entamoeba histolytica
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dx.
3 stool exams for cysts or trophozoites Stool antigen detection – ELISA Test Most have positive serum serologies Clinical picture + serologies Aspiration of cyst |
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tx of entamoeba histolytica
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Tx.
Metronidazole affects only trophozoites not cysts Paromomycin, iodoquinol – for cysts |
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giardia lamblia distribution
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Worldwide distribution in surface water
Mammals are reservoir Also common in daycare outbreaks Swimming pools and wading pools common |
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giardia lamblia type of infection
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Causes malabsorptive diarrhea in small intestine
No mucus No blood No fever Incubation 7-14 days Infection vary widely from asymptomativ to chronic Symptomatic more common in children Non-inflammatory |
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dx of giardia lamblia
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dx.
ELISA test for antigen Microscopic exam for stool cysts/trophozoites |
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tx of giardia lamblia
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Tx
Metronidazole Prevent with hygiene and sanitation |
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cryptosporidium distribution
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Coccidian parasite
Worldwide distribution fecal-oral Disease in immunocompetent – self limiting Immunocompromised – much more difficult Outbreaks in daycare and water, food borne possible Reservoir – cattle Chlorine does not kill, so can get large outbreaks in tapwater |
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cryptosporidium type of infection
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Intracellular pathogen affecting microvilli of small intestine
Atrophy Clinical presentation: 7-10 incubation Watery Diarrhea, crampy, abdominal pain Self limited in immunocompetent |
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dx of cryptosporidium
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Dx.
Microscopic – acid fast ELISA stool antigen detection |
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tx of cryptosporidium
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Tx
Symptomatic support |
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ascaris distribution
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More common in tropical regions
Children Fecal oral transmission |
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ascaris life cycle
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Eat egg, hatches, travels to lung then to airway, swallowed, and back down to intestine
Can cause disease in lung or in small intestine |
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ascaris pathogenesis
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Asymptomatic
Hypersentivity pneumonitis Adult worms – vague crampy abdominal pain most common problem can cause obstruction |
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ascaris dx
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Ova parasite stool examination
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ascaris tx
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Tx
Mebendazole Albendazole Prevention – improved sanitation |
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enterobius vermicularis (pinworm) distribution
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Most widely prevalent nematode of man
Temperate more likely than tropical Children – daycare, school |
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enterobius vermicularis (pinworm) life cycle
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Egg hatches, and worm hangs around anus
Itchy anus at night |
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dx of enterobius vermicularis (pinworm)
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Dx. Scotch tape test
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tx of enterobius vermicularis (pinworm)
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Tx
Mebendazole |
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hookworms distribution
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Vary geographically
Ancylostoma duodenale – Mediterranean countries Necator americanus – north and south America Common in tropics, subtropics, southeast US Risk – skin exposure to focally contaminated soil Transmission is not fecal oral |
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hookworm life cycle
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Life cycle – larva in soil
Contact with skin, penetrates to venous to lungs, then trachea, swallow, transforms in small intestine Get small amount of blood loss With heavy infestation, get ulcer and anemia from blood loss |
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hookworm clinical manifestation
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Clinical – initial intestinal infection with abdominal pain and eosinophilia
Eosinohilia with migration of worms |
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dx of hookworm infection
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Dx look for eggs in stool
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tx for hookworm infection
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Tx
Mebendazole Prevention – don’t expose skin |
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strongyloides stercoralis distribution
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Tropic and subtropic distribution
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strongyloides stercoralis life cycle
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Life cycle – skin to lung to intestine
Can get into skin around anus, travel to lung, then back to intestine |
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strongyloides stercoralis pathogenesis
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Pathogenesis
Adult worms embedded in small intestinal mucosa lead to local inflammation Chronic infections long lasting (can autoinfect) |
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strongyloides stercoralis clinical
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Clinical
Diarrhea Hyperinfection syndrome – carrying bacteria to blood |
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strongyloides stercoralis dx and tx
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Dx look for eggs in stool
Tx ivermectin |
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cestodes - tapeworms
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Taeniasis –
t. saginata - beef t. solium - pork diphyllobothriasis – fish tapeworm |
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clinical manifestation of tapeworm infections
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adult tapeworms – minimal symptomatic
larva – cause serious disease when humans are intermediate host with T. solium muscle and brain damage cause seizure – common in new immigrants diphyllobothriasis – fish tapeworm causes vitb12 deficiency |
