GI Flashcards
Common Infectious Causes of Esophagitis
Candida albicans (most common), CMV, HSV
Candida albicans (esophagitis)
Risk: immunocompromised
Diagnosis: endoscopy (whitish plaques), double contrast esophogram (discrete linear plaque-like lesions)
HSV-1 (Esophogitis)
Diagnosis: endoscopy/double contrast esophogram (multiple superficial flat ulcers w/ raised edges that look “volcano-like”)
Cytopathic effects: syncitia (multinucleated giant cells)
CMV (Esophagitis)
Risk: solid organ transplant pt’s
Diagnosis: endoscopy/double contrast esophogram showing giant/flat ulcers in upper/mid esophagus
Cytopathic effect: “owl’s eye” inclusion bodies
Gastritis
Course: acute or chronic
Causes: NSAIDs, ETOH, tobacco, B12 deficiency
Infectious causes: H. pylori, CMV, Candida, Histoplasma
(No erosion w/ H. pylori
Peptic Ulcer Dz (PUD)
Causes: H. pylori (or NDSAIDs)
Gastric ulcers: pain briefly after eating
Duodenal ulcers: pain a few hours after eating
Diagnosis: endoscopy required to differentiate btwn duodenal and gastric
Helicobacter pylori
G-ve, non spore forming
Motile: 5-6 polar flagella (assist in invasion of mucosa)
Catalase +ve
Urease +ve
H. pylori Pathogenesis
Flagella: (5-6) mobility and chemotaxis to colonize under mucosa
Urease: neutralize gastric acid and gastric mucosal injury caused by the ammonia
LPS: adhere to host cells; inflammation
Vacuolating toxin (vacA): gastric mucosal injury
Type IV secretion system: pili-like structure that injects effectors
H. pylori Diagnosis
Serology: non-invasive, most sensitive, checks for IgG Abs
Fecal ag: non-invasive, determines current infection, used to check response/efficacy of tx
Gastric biopsy: invasive, most specific
Carbon Urea breath test: expensive, based on urease activity, pt will exhale labeled CO2 if urease is active in stomach
Most common cause of food born illness?
Norovirus (Norwalk - caliciviridae family)
Acute Non-inflammatory Diarrhea
Duration: < 2wks Type: watery, not bloody Mechanism: mucosal hypersecretion or decreased absorption w/o mucosal destruction Location: generally SI Onset: abrupt Cause: viral or non-invasive bacteria
Acute Inflammatory Diarrhea
Duration: < 2wks
Type: contains blood and/or pus
Mechanism: mucosal invasion resulting in inflammation
Location: usually colon
Cause: invasive bacteria, toxin-producing bacteria
Persistent Diarrhea
Duration: 2-4 weeks
Chronic Diarhea
Duration: > 4wks
Type: secretory, osmotic, steatorrheal, inflammatory, dysmotile factitial, iatrogenic
Cause: medication, non-infectious, parasites
Stool lactoferrin WBCs
Indicates inflammatory diarrhea
Stool Osmolar Gap
Indicates lactose intolerance/laxative use
Routine organisms to look for
- Campylobacter sp.
- E. coli
- Shigella
- Salmonella
Toxemia (Food Poisoning)
Consumption of food containing toxins
*shorter incubation than food-born
Food-born Infection
Consumption of food containing organism
Organisms requiring low infective dose?
Shigella - shiga toxin, invades Peyer’s Patches
EIEC - no toxin
*only about 10 organisms
Organisms associated with poultry exposure
Campylobacter - microaerophilic, curved organism, oxidase +ve, cytotoxin (shiga like), catalase +ve
Salmonella - motile, produce H2S, invades Peyer’s patches, N/V/D @ onset
Organisms associated with travel to Asia?
Salmonella - poultry, motile, H2S production, invasive (Peyer’s patches)
EIEC - low infectious dose, no toxin, invasive
Vibrio cholera - cholera toxin, “rice water” stool, oxidase +ve, S-shape colonies, non-invasive
Organisms invading Peyer’s Patches?
Shigella - shiga toxin, low infective dose
Salmonella - motile, produce H2S gas
Organisms producing LT enterotoxin (acting on adenylate cyclase)
ETEC - travel hx
Bacillus cereus - G+ve, spore forming
Vibrio cholera - halotolerant, “rice water” stool, TCBS agar
Organisms that produce ST enterotoxin (activating guanylate cyclase)
ETEC - travel hx, no fever
Yersinia - refrigerated food, cold countries, mild fever
Ciguatera toxin
Food: predatory reef fish
ROS: acute GI sx’s 3-6h after ingestion + parasthesias, puritis & hot/cold temp reversal
Scrombroid toxin
Food: tuna, mahi-mahi, marlin
ROS: burning in mouth w/ metallic taste, acute GI sx’s <1h after ingestion (+ sx’s like dizziness, paresthesias, rash)
Brevetoxin
Food: shellfish
Condition: Neurologic Shellfish Poisoning
Incubation: <1-3h
ROS: paresthesia, mouth numbness, tingling of mouth/extremities, + GI sx’s
Saxitoxin
Food: shellfish
Condition: Paralytic Shellfish Poisoning
Incubation: <2h
ROS: tingling and numbness of mouth spreading to extremities, ataxia (GI sx’s less common), muscular or respiratory paralysis possible in rare situations
Aflatoxin
Food: nuts & seeds
ROS: necrosis, cirrhosis, HCC (liver stuff)
Non-invasive inflammatory diarrheal diseases?
EAEC - include production of copious amounts of mucous
STEC - non-sorbitol fermenting, shiga toxin
Fecal fat
Malabsorption caused by chronic diarrhea (or Giardiasis bc it colonizes the upper SI and blocks small bile ducts)
ETEC
“Traveler’s Diarrhea”
Pathogenesis: LT (👆🏽cAMP), ST (👆🏽cGMP)
ROS: acute onset profuse watery diarrhea, NO fever, can have N/V and malaise
Recovery: <72h (self-limiting)
EPEC
“Infantile Diarrhea” (children <5yo)
Pathogenesis: efface surface of microvilli causing impaired absorptive properties which allows efflux of H2O/electrolytes
ROS: watery diarrhea
Vibrio cholera
Halotolerant, acid sensitive, motile, S-shaped colonies
Risk: travel to developing countries (Africa, Haiti, India)
Pathogenesis: cholera toxin binds to GM1 receptor activating adenylate cyclase (👆🏽intracellular [cAMP])
ROS: abrupt onset of profuse watery diarrhea WITH vomiting, “rice water” stool (aka flecks of mucous)
Diagnosis: TCBS agar (sucrose is differentiating from other vibrios bc cholera is sucrose +ve)
*rotavirus is the only other diarrheal illness that leads to the same amt of fluid loss
Clostridium perfringens
G+ve, spore forming
Acquired: meat & meat dishes (gravy)
Pathogenesis: colonization of SI w/ release of clostridium perfringens enterotoxin (CPE) which has cytotoxic activity causing pore formation in membranes
ROS: watery diarrhea + SEVERE abd pn (NO N/V)
Diagnosis: stool sample w/ CPE
Bacillus cereus (diarrheal)
G+ve, spore forming
Acquired: rice
Pathogenesis: LT enterotoxin activating adenylate cyclase (👆🏽cellular [cAMP])
ROS: watery diarrhea w/ abd pn
Rotavirus
Acquired: fecal-oral (poor hygiene)
Prevalence: children <5yo
Pathogenesis: shortening/blunting of microvilli decreasing surface area so they lose absorptive qualities
ROS: sudden onset watery diarrhea w/ or w/o vomiting lasting up to 6 days, excessive fluid loss like cholera
Diagnosis: latex agglutination, EIA
Norovirus
Acquired: fecal-oral, food-borne (raw shellfish)
Prevalence: older children & adults
Seasonality: winter months
Pathogenesis: multiplies in SI and causes transient lesions in mucosa
ROS: 1-2d diarrhea/vomiting, abd cramps, myalgia, malaise, HA, low fever
Diagnosis: RT-PCR
Adenovirus
Pathogenesis: URT is main target
ROS: watery diarrhea, + or - vomiting, URI, and conjunctivitis
Cryptosporidium parvum/hominis
Acquired: recreational waters
Infectious and diagnostic stage: thick walled oocyst
ROS (healthy): watery diarrhea, N/V, abd cramps, resolves w/in 10 days
ROS (immunocompromised): severe sx’s, chronic diarrhea, up to 50 BMs/day, wt loss
Diagnosis: modified Ziel-Neelson stain
Shigella sonnie
Non-motile, no lactose fermentation, low infective dose
Prevalence: <5yo (day care)
Pathogenesis: colonize LI then attach to M cells and plasmid encoded protein triggers cell to endocytose the organism, eventually induces cell apoptosis which leads to ulcers
ROS: watery diarrhea @ onset then becomes bloody, can have N/V later on
Shigella dysenteriae
non-motile, no lactose fermentation
Pathogenesis: produces shiga toxin that binds to 28S subunit of 60S ribosome inhibiting protein synthesis leading to cell death, this causes blood mucous and WBCs in stool due to capillary thrombosis
ROS: bloody diarrhea with mucous, abd pn, fever
EIEC
Low infectious dose
Prevalence: SE Asia and South America
Pathogenesis: invasion of LI then attachment/endocytosis in M cell by plasmid encoded protein, eventually induces cell apoptosis (NO toxins produced)
ROS: watery diarrhea progressing to bloody type (less severe than Shigellosis)
Enterocolitis (S. typhirium)
Acquired: poultry (eggs, chicken)
ROS: watery diarrhea @ onset + N/V, low to mild fever
Duration: 2-5d
Diagnosis: colorless colonies on MacConkey’s bc no lactose fermentation
Stool culture: +ve soon after sx’s start
Enteric Fever (S. typhi)
Incubation: 7-20d (insidious onset)
Fever: gradual w/ HIGH plateau
ROS: early constipation followed by bloody diarrhea eventually
Pathogenesis: disseminates into blood where it’s engulfed by macrophages –> transported to RES organs (liver) it colonizes the bladder and replicates and eventually reenters the SI via bile
Stool culture: +ve after 2nd wk
*vaccine: oral live attenuated and capsular polysaccharide IM
Campylobacter jejuni
G-ve curved rod, microaerophilic, catalase +ve
Acquired: poultry, eggs, zoonotic
Prevalence: children <5yo
Pathogenesis: colonizes/invades LI and SI, enterotoxin (watery diarrhea) and cytotoxin (similar to shiga toxin, causes bloody diarrhea)
ROS: onset 3-5d after ingestion, profuse watery diarrhea at onset then bloody + severe abd pn
Diagnosis: colonies appear mucous and gray
Complications: GBS or reactive arthritis
Yersinia enterolitica
Acquired: refrigerated foods
Prevalence: cold countries (children <7yo)
Pathogenesis: invasive, induces inflammatory response that mimics appy (messenteric adenitis) produces chromosomally encoded enterotoxin (ST) that 👆🏽[cGMP]
ROS: severe abd pn, watery diarrhea, mild fever
Complication: post-infective arthritis
Diagnosis: pinpoint colonies on MacConkey’s
Post-infective Guillan-Barre Syndrome
Causative agent: campylobacter
Pathogenesis: Ab’s against the O ag in the bacterium cross-react w/ the GM1 ganglioside in the myelin sheath of peripheral nerves
ROS: demyelination causing ascending paralysis
Vibrio parahemolyticus
Acquired: poorly cooked or raw seafood
Prevalence: Japan
Pathogenesis: invade epithelial cells and reaches lamina propria but doesnt go further
ROS: acute abd pn, watery diarrhea (sometimes bloody), N/V
Diagnosis: sucrose -ve
Vibrio vulnificius
Acquired: saltwater abrasions Prevalence: coastal US Pathogenesis: highly invasive ROS (immunocompetent): gastroenteritis ROS (liver dz'd pt): can be complicated, causes fluid filled blisters
EAEC
NON-INVASIVE
Pathogenesis: aggregation adherence factor (AAF) are fimbriae that allow adherence to cells of LI, once bound they induce production of copious amounts of mucous which forms a biofilm
ROS: can be watery or bloody diarrhea
STEC
NON-INVASIVE, no sorbitol fermentation
Prevalence: northern US
Pathogenesis: attachment in LI, produces verotoxin a cytotoxin similar to shiga toxin so it inactivates the 28S of the 60S ribosome subunit
Tx: NEVER ABX (killing the organism will just release more toxin)
Hemorrhagic Colitis (STEC)
Prevalence: adults/elderly
ROS: watery diarrhea at onset w/ abd pn then becomes bloody
Hemolytic Uremic Syndrome (STEC)
Prevalence: children
ROS: microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure
Thrombotic Thrombocytopenia Purpura (STEC)
Prevalence: elderly
ROS: anemia, acute renal failure (HUS) + fever + neuro involvement
Salmonella serotypes
Motile, produce H2S gas
Pathogenesis: colonize SI and LI, invade epithelial cells then replicate in M cells of Peyer’s patches in terminal SI –> after replication they travel through cell to BM and enter lamina propria, it can then enter lymph and then disseminates into blood via capillaries
Staphylococcus aureus (GIT)
Coagulase +ve, catalase +ve
Acquired: foods requiring excessive handling
Prevalence: summer/holidays
Toxin: ST enterotoxin acts neurologically (emesis), and enteritic (diarrhea)
ROS: emesis w/in 6h of ingestion
Diagnosis: beta-hemolytic, mannitol salts, confirm w/ coagulase
Bacillus cereus (food Intoxication)
Spore forming Acquired: contaminated rice Pathogenesis: emetic (neurotoxin) is ST causing vomiting, shorter incubation than S. aureus ROS: predominantly vomiting w/in 4h Diagnosis: flat colonies on blood agar
Giardia labmia
Binucleate, pear-shaped, flagellated trophozoite and cyst
Acquired: water from hiking/camping
Pathogenesis: attach to epithelial cells in SI (non-invasive)
Infective: cyst
Diagnostic: cyst/trophozoite
ROS: 3-4 wks of diarrhea
Diagnosis: 3 stools over several days
Cystiosospora belli
ROS: watery diarrhea, persistent if untreated
Diagnosis: autofluorescent, multiple samples
Entamoeba histolytica
Acquired: travel back from developing endemic countries
Infectious: mature cysts
Diagnostic: mature cysts/cysts and trophozoites in stool
Intestinal sx’s: watery diarrhea and bloody
Extraintestinal sx’s: liver abscess (of right lobe 1-3 mo after onset)
Balantidium coli
Acquired: pig reservoir
Prevalence: developing countries
Infectious/diagnostic: cyst
ROS: intermittent diarrhea/abd pn/wt loss
Complication: Fulminant Colitis (rare) = bloody diarrhea w/ mucus
Trichuris trichuria (whipworm)
Pathogenesis: ingestion of barrel shaped egg
ROS: abd pn, diarrhea, iron deficiency, finger clubbing, rectal prolapse (“coconut cake prolapse”)
Diagnosis: eggs in feces
Enterobius vermicularis (pinworm)
Epidemiology: most common worm infection in US
Pathogenesis: ingest oval shaped eggs, worm matures, female worm goes to perinatal area @ night to deposit eggs then dies (causing itching)
ROS: anal itching
Dx: cellotape for eggs
Diphyllobothrium latum
Fish tapeworm
ROS: diarrhea, B12 deficiency (megaloblastic anemia)
Ascaris lumbricoides
*round worm
Transmission: fecal-oral
Pathogenesis: nodular eggs hatch inSI then larvae go to lungs, swallowed and back to SI
ROS: dry cough, CP, fever = Loffler Syndrome
Complication: bowel obstruction
Dx: fertilized egg in stool
Hymenolepsis nana
Transmission: person-to-person
Epidemiology: most common tape worm (in US seen in institutionalized, immunocompromised, malnourished)
Dx: eggs in feces
Necatur americanus and Ancylostoma duodenal (American dude)
*hook worm
Transmission: skin penetration (feet) by filariform larvae
Pathogenesis: filariform larvae to SI then lungs, swallowed and back to SI
ROS: iron deficiency anemia, abd pn (problematic in pregnant women)
Dx: eggs in feces (oval, clear-shelled), eosinophilia
Strongyloides stercoralis (Strong guy)
*thread worm
Transmission: skin penetration (feet) by filariform larvae
Pathogenesis: filariform larvae to SI then lungs, swallowed and back to SI
ROS: urticaria and rashes a few days s/p skin penetration, pulmonary sx’s, diarrhea/abd pn weeks later
Dx: rhabditiform larvae in stool
Clostridium difficile
G+ve bacilli
Pathogenesis: Toxin A (enterotoxin = watery diarrhea d/t fluid accumulation), Toxin B (similar to diphtheria toxin so causes decrease of protein synthesis and cell death = bloody diarrhea)
ROS: pseudomembranous colitis
Dx: toxin in stool
Whipple’s Dz
Etiology: Tropheryma whipplei Transmission: soil/sewage Prevalence: farm/sewage workers ROS: wt loss and arthralgia, then diarrhea, steatorrhea, fever, malabsorption, CNS and CVS sx's (culture -ve endocarditis) Dx: biopsy w/ PAS+ macrophages, PCR
HAV
Most common cause of acute hepatitis
Epidemiology: developing world
Transmission: undercooked shellfish (imported strawberries, green onions)
ROS: aversion to cigarette smoke
Prevention: vaccine (and virus is inactivated by bleach and UV radiation)
HBV
Genome: partially circular dsDNA (Dane particle)
Transmission: blood-borne
Pathogenesis: produces decoys (HBsAg), causes CD8+ T-cells to induce apoptosis of infected cells
ROS: acute or chronic hepatitis, aversion to cigarette smoke
Prevention: vaccine (virus inactivated by 10% bleach)
HCV
Transmission: blood-borne
Pathogenesis: error prone RNA-dependent RNA pol, inhibits apoptosis in the infected cell = persistent infection, inhibits IFN-α = chronic infection
ROS: chronic carrier status is common
Prevention: donor screening (since 1981 in US), no vaccine bc of ag variation
Co-infection w/ HBV + HDV
Mechanism: HBV + delta ag present acutely
Better prognosis
Fasciola hepatica/gigantica
Aka Sheep Liver Fluke leaf-shaped
Transmission: ingestion of infected plants (like fuggin watercress)
Pathogenesis: metacercariae ingested, larvae migrate (2-4mo), parasite matures (wks to yrs during latent)
ROS: liver sx’s, malabsorption bc no bile, etc.
Dx: eggs in feces
Clonorchis sinensis
Aka Chinese Liver Fluke
Transmission: ingestion of undercooked/pickled freshwater fish containing cysts
Pathogenesis: metacercariae ingested resides in biliary tree
ROS: choly probs (fever, jaundice, diarrhea, pain, hepatomegaly); chronically can lead to adenocarcinoma of bile duct
Dx: operculated eggs in feces
Anti-HBc IgM
“Window period” (no HBsAg or Anti-HBs would be present yet), could have some Anti-HBe Ig present
*about 5mo s/p initial infection
Anti-HBc IgG
Chronic infection
*OR seen in full recovery (if no HBsAg present but Anti-HBs is present)
HBeAg
Marks active replication so measures transmissibility/infectivity, seen in acute or chronic infection
Anti-HAV IgG
Immune d/t vaccine or previous recovery from prior HAV infection
Anti-HCV Ig
Tells you there was exposure to HCV whether the pt recovered or still has virus you’d have to do PCR for # of viral particles present
Superinfection w/ HBV + HDV
Mechanism: chronic HBV infection then superimposed HDV infection = rapid dz progression, eventual hepatic encephalopathy
POOR prognosis
