GIT Infections – Flashcards

• Gram -, Vibrio shaped, rod
• motile
• acid tolerant
• microaerophilic
• non-invasive

• Ability to produce Cytoxin A (VacA) required for ulcer formation
• pathogenicity island produces CagA - induces IL-8->cancer
• LPS cross-reacts w/ host Ag -> Ab-> cancer
• Acid tolerent due to production of copious amts. of usease

• 1 of the most prevalent bacterial infections
• Humans = reservoir
• Transmission-> fecal-oral; gastric-oral; oral-oral
• Age+Gender-> carriage increases w/ age; NO gender differences
• Responsible for ALL type B gastric + duodenal ulcers (class I carcinogen, cancer can occur w/o ulcer)

• Abdominal pain
• Hematologic changes (idiopathic thrombocytopenic purpura, iron def., anemia

• Invasive(GOLD STANDARD) -> Endoscopy or esphagogastroduodenscopy
• Non-invasive: Breath test (¹³C) Urea; ELISA or LA; Stool Ag test detected by monoclonal Ab

• Combo, sequential, or both
• Bismuth salts
• Metronidazole or Tinidazole
• Tetracycline or amoxicillin
• Anti-secretory therapy may enhance healing
• protonix, clarithromycin, amoxicillin

TREAT ALL PERSONS INFECTED!!

• Vibrio cholerae
• Enterotoxigenic E. Coli
• Aeromonas Sp.

• Gram -, vibrio shaped, rod
• halophile
• falcultative anaerobe
• non-invasive

• O-Antigens
• Type O-1 - classical
• Type O139 - new

• Heat labile, ENTEROtoxin ->
• Stimulates activty of adenylatre cylase (which converts ATP to cyclic AMP -> Diarrhea)

• Humans + zooplankton = Resevoir
• Vehicle is FOOD + WATER
• Seasonality -> warmer months
• travelers to endemic or epidemic area are @ high risk!

• Incubation = 1-5d
• HIGH dose MO
• Diseae of small intestine - grows in lumen of small intestine + elaborates ENTEROtoxins -> fluid + electrolyte loss in feces (1L/h)
• hypovolemic shock
• metabolic acidosis
• hemoconcentration

• Abrupt onset
• effortless vomiting
• profuse water diarrhea assuming rice water appearance w/ flecks of floating mucus + possess a sweet fishy odor
• little if any fever
• Fluid loss in feces maybe 1L/h (hypovolemic shock, hemoconc., + metabolic acidosis)

• micorscopic exam of stool for presence fo commma-shaped MO + absence of fecal leukocytes
• culture
• serological confirmation

• Supportive -> rehydration
• Tetracycline is used to shorten the duration + carrier state

• Plasmid encoded ENTEROtoxins
• LT toxin
• heat labile, antigenically/strucaturally similar to + same moa as cholera enterotoxin
• ST toxin
• NON-antigenic -> stimulates guanylate cyclase -cGMP system

• WW incidence
• Cause of traveler's + weanling's disease
• Vehicle - FOOD + WATER
• Transmission -> Fecal-oral

• HIGH dose MO
• Incubation period -> 1-2d
• similar mechanism as V. cholerae

• Spectrum of clincal mani. is like cholera -NOT as severe
• aburpt onset of diarrhea which last 1-3d

• Prevention: pepto-bismol OR Rifaximin
• Treatment: TMZ + Rifaximin

• Staphlococcus aureus
• Bacillus cereus
• Clostridium perfringens, type A

• Characteristics: Coagulase +, Gram + cocci in clusters
• ENTEROtoxin: water-soluble, heat stable, colorless, odorless, + tasteless

• Humans = Reservoir + Source
• Mode of intoxication:
• toxin is produced by S. aureus growing in improperly prepared food
• Persons ingests the pre-formed toxin in: custard filled baked goods, potato salad, canned foods, processed meats, meat pies

• Incubation period = 1-6h post-ingestion
• Enterotoxin is absorbed in gut
• disseminates to the CNS
• acts on vomiting center

• symptoms last <12h
• nausea, acute salivation, pronounced vomiting, less pronounced diarrhea may occur, abdominal cramps, illness is SELF-LIMITING -> recovery 1-4d

• Short incubation period- NO neurological signs, NO fever
• Epidemiological investigations
• Test entertoxin
• Phage typing of MO

• Gram +, spore forming rod
• produces 2 ENTEROtoxins

• WW distribution, in soil
• spors are found on
• grains - rice
• potatoes
• vegis

• Emetic form: food poisining caused by heat-stable ENTEROtoxin produced in food
• Diarrheal form:food poisining caused by heat-labile ENTEROtoxin -> production of adenylate cyclase in small intestine
• symptoms 10-12h post ingestion + last <24h
• SELF- LIMITING
• profuse watery diarrhea, abdominal cramps, pain, less pronounced N/V may occur

• Suspect B. cereus food poisoning whenever upper GI illness develops 1-5 hours after eating, or lower-intestinal-tract illness develops 6-24h after eating
• Diagnosis is confirmed by detecting, quatitating, and identifying large #s of this aerobe in the incriminated food + pt's feces

• Gram +, spore forming rod
• anarobic
• produces ENTEROtoxin
• heat labile, acid labile, protein
• toxin produced in gut
• toxin inhibit glucose + Cl^- absorption

• WW - common in: soil + the gut of humans + other animals
• Food-borne disease is associated w/ ingestion of: meat, poultry, meat or poultry gravy

• Heat labile ENTEROtoxin produced in gut agter ingestion of food containing large # of MO

• Lower GI symptoms appear 10-12h after ingestion of contaminated food
• SELF-LIMITING
• symptoms last ;24h
• Symptoms -; profuse water diarrhea, abdominal cramps/pain, less pronounced N/V may occur

• confirmed by detecting, quantitating, and identifying larger #s in the incriminated food + pt's feces

• Giardia lamblia
• Cryptosporidium parvum
• Cyclospora spp. Isospora
• Microsporidia

• Trophozoites adhere to mucose of upper small intestine but do NOT invade - they interfere w/ absorption of fat + protein

• Asympotomatic cyst passers
• Acute infection-> 3-4d w/ little or no fever, watery, greasy, foul smelling stools, nausea, abdominal distension, flatulence
• Chronic infection-> ≤2yrs ->abdominal pain + distension, greasy foul-smelling stools (malabsorption), wt. loss

• Fecal-Oral route via FOOD or WATER

• Giardia lamblia + Cryptosporidium -> DIRECT contact OR sexually (oral-anal sex)

• Acid-fast
• broad host range
• Obligate intracellular parasite
• undergo sexual reproduction-> producing oocysts

• immunocompetent hosts
• explosive, profuse watery diarrhea w/ vomiting + flatulence + self-limiting
• duration ~2wks
• immunocompromised hosts
• prolonged, severe, watery diarrhea w/ wt. loss >2mo w/ dissemination to all of GI tract, liver, pancreas
• symptomatic resp. infections can occur

(LIKE crytosproidium)

• Mildly acid-fast
• have intracellular as well as extracellular existance 

• Highest incidence in natives + travelers to Asia + S. America 

• Microscopic examinations (LARGE oocytes)
• U.V floresence
•  Acid Fast +

Microsprodidians - Enterocytozoan bieneusi, Encephalitzoon spp. are causes of chronic diarrhea in the immnocompromised

They ARE the MOST COMMON cause of chronic diarrhea in HIV/AIDS pts.

• STEC - Shinga-producing E. Coli
• EHEC 0157:H7 - Enterohemorrhagic E. coli 

• Zoonosis
• Food-borne outbreaks + sporadic cases occur
• Childern + eldery more commonly affected
• peaks in warmer months
• RISK FACTORS: undercooked beef, raw milk, _ unpasteurized A.J., + poor personal hygiene 

• Afebrile bloody diarrhea
• Become bloody after 1-3d
• may have cramps, N/V, w/ fever in 1/2 pts.
• 1/3 of pts HAVE fecal leukocytes 

• HUS
• Microangiopathis hemolytic anemia
• thrombocytopenia
• acute renal failure
• CNS involvement
• Mortatlity is HIGH
• Toxemia
• Toxinn is potentiated by TMX-SMX in vitro + in vivo!!!

• invasive
• anarobic
• eucaryotic protzoan
• FORMS CYSTS;-- infectious form - LOW dose MO
• consumes human RBC
• Virulence Factors-> produce soluble cytotoxins -lyse PMNs

• Humans are the difinitve host and ONLY reservior
• LOW dose MO
• Transmitted -> fecal/oral(food/water), direct contact, sexually (oral/anal sex)
• RISK GROUPS: travelers to endemic coutnries SE Asia, persons who practice oral/anal sex 

• Acte amebic colitis (varies): bloody,loose watery diarrhea, abdominal pain, urgency to defecate, fever + constituational symptoms seen in many
• Extrainsetinal amoebiasis: Mostly necrotic amebic liver abscess (symptoms: upper right quadrent pain, fever, pleuritic pain, liver involvement-liver faulure s/s of hepatitis) 
• NOT self-limiting

Detection of trophozoites in diarrhea or cysts in formed stools

Few fecal RBC + WBC

• Gram + box car shaped rod
• spore former
• aerobic
• encapsulated
• facultative intracellular pathogen
• produced exotoxins 

TRUE

Enzootic disease:

• Sheep
• Goats
• Cattle
• Horses 

• Bacillus anthracis is excreted from infected animals in: feces, urine, + saliva
• Spores can surive for YEARS in the soil
• Disease requires DIRECT contact w/            -> contaminated soil, infected animals, or animal products bearing spores 

• fever
• N/V
• diarrhea
• GI pain
• bleeding 

Gram +, anaerobic, spore forming rod

Most produce cytotoxin (toxin A or Toxin B or BOTH)

person-to-person

Via fomites

• hospitalization (malnutrition, debilitation, bedridden)
•  Antibiotic therapy for ID
• antacids, PPI
• Elderly + females disproportionately affeted (more)

• short-term colonization
• acute diarrhea
• fulminant diarrhea
• recurrent C. difficle infection

Diarrhea

• Sometimes accompanied by lower abdominal cramping w/ NO systemic signs!

• Profuse, debilitating diarrhea (foul-smelling, greenish colored) w/ abdominal pain + cramping
• Systemic signs (fever, anorexia, malaise, dehydration)
• NO pseudomembrane 

• symptoms of AAC - MORE severe
• presence of classical pseudomemraneous colitis -> elevated yellowish plaques scattered over the inflamed areas of the muscose when viewed in sigmoid or coloic endoscopic exam 

• CDI should be suspected in any person w/ diarrhea who has recieved antibiotics <2mo +/or whom diarrhea began >72h after hosp.
• gram stain stool
• EIA + latex aggulation
• Cytotoxin assay - most specific
• stool culture - most sensitive
• endoscopy
• differential 

Supportive!

• STOP antibiotic treatment is possible
• vanco, metronidazole, or tinidaxole can be used
• probiotics 

• Barrier precautions
• isolation of pt
• careful cleaning - sporicidal agents (bleach)
• Hand hygiene (sanitizers do NOT eradicate Clostridium difficle) 

• Rotovirus -> winter
• Norwalk -> summer
• Norovirus -> summer (but ALL year round)

• fecal/oral route
• food + water can be vehicles 

• diarrhea
• acute vomiting
• fever
• abdominal pain
• Durations:
• Rotovirus 5-7d
• Norwalk 1-2d
• Norovirus 1-2d

Supportive!

** NOTE ** child can NOT digest disaccharides --            NO MILK!! 

• Surface 0 antigens (allows MO to INVADE)
• shiga toxins (irreversable inactivation of EF-1 + Y-interferon

• Gram -, NON-lactose fementing, non-motile, enteric bacilli
• facutlative intracellular pathogen
• 4 species based on serology
• S. dysenteriae, group a
• S. flexneri, group b **
• s. boydii, group c
• s. sonnei, group d **

**more common in US