Pre-midterm GI Flashcards
What 2 parasites are coccidian protozoan, where are they seen?
Cyclospora cayetanensis- tropics and subtropics
Cryptoisospora belli- S. America, Africa, SEA
Infective and diagnostic forms of Cyclospora cayetanensis
Infective: Mature oocysts
Diagnostic: Unmature oocysts
Infective and diagnostic forms of Cryptoisospora belli
Infective: mature oocysts
Diagnostic: unmature oocyst
Entamoeba histolytica
Pseudopod forming protozoa
In temperate climates: C and S American, Africa and India
Diagnostic: O&P- mature cysts, PCR, Ag-testing (IHA/EIA)
Infective: Mature cysts with 4 nuclei
Pathogenesis of Entamoeba histolytica
Ingestion of mature cysts w 4 nuclei
Excitation into flask-shaped trophozoites (motile w pseudopods)
Multiply in LI and attach to colonic mucosa via Lectin
Encystation and released into stool
OR
Released into portal v. system– infect liver and create abscesses. Can also go to lungs or CNS (meningitis)
3 outcomes of E. histolytica infection
1- asx
2- Intestinal Entamoebiasis (amoebic diarrhea and dysentry)
3- Extraintestinal amoebiasis (liver abscesses)
Giardia intestinalis
Main cause of parasitic diarrhea. Seen in US in travelers from endemic countries– Caribbean and tropics.
H2O and food-borne. Associated with recreational water.
Sxs: flattulance, foul-smelling steattorrhea, watery diarrhea
Pathogenesis of G. Intestinalis
Ingestion of cysts– 1-2wk incubation,
reaches the SI– forms trophozoites, multiply by binary fission.
Attach, but do NOT invade epithelium– causes watery diarrhea.
Dx of G. Intestinalis
Routine O&P- see bi-nucleat, pear-shaped flagellated trophozoites and cysts
Balantidium coli
Ciliated Protozoan
SEA, Pap NG, Lat. America, some of Mid. E.
Reservoir: PIGS– fecal contaminated drinking water
Sxs: intermittent diarrhea, abd. pain and weight loss
Complication: fulminant colitis– rare
Pathogenesis of B. coli
Ingestion of cysts
excystation in the SI
trophozoites colonize the LI, replicate and some INVADE the colon.
Some trophozoites then encyst, and both ciliated trophozoites and cysts are then released into the stool.
Dx. of B. coli
Endoscopy- will see necrosis and ulceration– can get trophozoites from a scrapping.
Rare to get cysts on O&P
GI parasites associated with invasion
Entamoeba histolytica
Balantidium coli
S. Aureus
G+ Aerobic/Facultative Coagulase + Catalase + B-hemolytic Produces ST enterotoxin- produces watery diarrhea, and acts as a neurotoxin- stimulates Vagu and SNS nn. induces vomiting.
S. aureus food poisoning
<6hr incubation–> emesis
Other sxs: abd. cramps, HA/N/Watery D
Foods assoc: cooked meats, cream desserts, dairy, produce
Occurs from poor food handling
Dx: Mannitol salts agar– turns it yellow
Bacillus cereus
G+
Aerobic
Spore former
Produces ST neurotoxin/emetic toxin- food poisoning
and LT enterotoxin- non-inflammatory diarrhea
B. cereus food poisoning
Associated with rice and pastas
Found in soil- spread via cross-contamination
2-3 hr incubation, 6-24hr duration.
Often mistaken for S. aureus
Dx: dry, wrinkly colonies, flat to agar surface on blood agar. Will also find large amounts of bacteria in the implicated food.
Ciguatera poisoning
Caribbean and tropical pacific
ST Ciguatoxin produced in grouper, barracuda and amberjacks
Sxs:
GI- 3-6hrs after ingestion watery diarrhea, abdominal pain and nausea.
Neuro- circumoral and extremity paresthesia, severe pruritus and temperature reversal
Scombroid poisoning
aka non-allergic histamine
Bacteria convert histamine into histamine and create ST Scombrotoxin neurotoxin in fish: tuna, mahi and marlin
1st sx: normally burning sensation in mouth and metallic taste
GI sxs: mins- 3hrs after get watery diarrhea, Nausea lasts 3-6 hrs
Other sxs: dizzy, urticaria, facial flushing, pruritus, and paresthesias.
Neurologic shellfish poisoning
Common in SE and FL
Brevetoxin in mollusks responsible
Short incubation
Sxs: paresthesias, mouth numbness, mouth and extremity tingling, and upset GI
More common to see GI sxs than with saxitoxin
Paralytic shellfish poisoning
Common on W coast
Saxitoxin in mollusks responsible
Short incubation
Same sxs as brevetoxin, but have more sever neuro sxs (ataxia) and less common GI
Complications: muscular and respiratory paralysis.
E. coli
G- rods
facultative anaerobes
Sorbitol fermentation (except STEC)
Normal GIT commensal
ETEC
Enterotoxigenic E. coli Main cause of traveler's diarrhea Has CFA pili for attachment, LT and ST toxins Large dose required Rapid onset of profuse watery diarrhea Resolution in 24-72 hours
ETEC pathogenesis
Ingestion of contaminated food–> colonization of SI by CFA pili __> produces LT and ST toxins
LT- similar to cholera, activates adenylate cyclase and increases cAMP.
ST- heat stabile, activates guanylate cyclase and increases cGMP.
Both are 1A5B toxins- B binds GM1R on brush border and allows A access.
Hyper secretion occurs–> watery diarrhea
Dx of ETEC
To distinguish from other E. coli- inoculate mouse adrenal cells and the LT/ST will stimulate adenylate cyclase
EPEC
Enteropathogenic E. coli
Cause of “infantile Diarrhea” high mortality <5
Pathogenesis: Colonization of SI by EAF plasmid, and then effacement of microvilli by BFP. Causes osmotic imbalance and watery diarrhea.
Tx: may use antibiotics bc of high mortality rate
Vibrio cholerae (and dx/identificaiton)
G- motile rods Non-spore forming "S-shapes" Oxidase + Ferment: Sucrose and Mannose Acid sensitive, but Halotolerant
Dx: grown on TCBS agar (thiosulfate-citrate-bile salts-sucrose agar)
Pathogenesis of V. cholerae (Presentation and Complications)
Colonization of SI
Produce bacteriophage encoded AB cholera toxin–> binds GM1R: adenylate cyclase activated, and cAMP increased
Presents with: profuse watery diarrhea with mucus flecks, severe dehydration, hypokalemia, metabolic acidosis, mm. cramps.
Complications: death by uremia (from ATN), hypovolemic shock
How to differentiate V. cholerae from other vibrios
V. cholerae is the only Sucrose +, so grow on TCBS agar
Clostridium perfringens
G+
Spore forming
Strain type C- Necrotic enterocolitis (in Papau NG from uncooked pork)
Strain type A- Type A food borne infection (seen in US, assoc w meat and meat assoc dishes- gravy)
Pathogenesis of C. perfringens
Colonization of SI
Sporulation of C. perfringens–> release of CPE (LT C. perfringens enterotoxin)–> pore formation in membrane–> watery diarrhea
Will see a large number of spores in the feces.
Sxs: watery diarrhea and severe abdominal pain
Bacillus cereus
G+ rods
Facultative aerobe
Spore forming
ST Emetic neurotoxin and LT enterotoxin
Foods assoc: Rice, and pastas. Also: meat, veggies, and dairy
Pathogenesis of B. cereus LT
SI colonization, production of LT enterotoxin, activates AC and increases cAMP–> watery diarrhea.
Rotavirus
Reoviridae family
segmented, enveloped, dsRNA
Common in <5yrs. Main cause of diarrheal hospitalizations worldwide.
Risks: unsafe water/inadequate sanitation, day care, children <5.
Seasonality: Winter in temperate climates.
Summer in tropical
Pathogenesis of Rotavirus
Fecal-oral transmission primary route
Replicates in SI epithelial cells–> causes shortening and blunting of the microvilli (similar to EPEC)
Decreases absorptive area causes watery diarrhea.
Sxs: sudden, watery diarrhea, with or without vomiting.
Norovirus
Caliciviridae family
non-enveloped +ssRNA
Winter seasonality. Typically in older children and adults.
Associated with cruise ships and raw shellfish/mollusks
Pathogenesis of Norovirus
Fecal oral, food and water transmission
Multiplies in SI, causes transient lesions in intestinal mucose, but does NOT reach the LI, so will have NO fecal leukocytes in the stool.
Presents: abd. cramps, watery diarrhea, myalgia, malaise, HA, nausea, low-grade fever, vomiting
Adenovirus in non-inflame diarrhea
non-enveloped, dsDNA
group F serotypes assoc with disease
Replicates in SI and is present in the stool
Watery diarrhea with/without vomiting
Astrovirus
non-enveloped +ssRNA
Peak is in winter
Watery diarrhea
Cryptosporidium spp.
Coccidian protozoa
C. parvum and hominis cause disease in humans
Risk: children in tropics, IMCP’d, vets
Source: contaminated drinking and recreational water, and animals
Dx: Modified Ziehl-Neelsen stain
Cryptosporidium pathogenesis
oocyte ingestion
Sporozoite release in SI–> attach and invade epithelia
Develop into trophozoites:
Asex cycle: Type I meront–>reattaches and infects SI
Sexual cycle: Type II meront–>micro/macrogamonts–> fertilization==> zygotes–> produce 2 oocysts:
1- thin-walled, auto-infect
2- Thick-walled, excreted in stool and used for diagnosis
Non-invasive pathogens that cause inflammatory diarrhea
EAEC
STEC
Virulence factors of Shigella spp.
Endotoxin/ O-Ag
Exotoxin- acts as neurotoxin: coma meningismus, ulceration
NAD glycohydrolase: destroys NAD causes cell death.
Actin filaments- for cell-cell transfer
Pathogenesis of shigella spp.
vv. small infective dose (as few as 10)
colonizes LI
invades M cells via plasmid-induced endocytosis–> lysis of phagosome–> moves back to LI with help of actin filaments–> Releases Il-1–> apoptosis
S. dysenteriae
Type 1 shigella- group A O-Ag
Produces bacillary dysentry
Shiga toxin (cytotoxin/neurotoxin)- inactivates 28s RNA in 60 ribosomal subunit– haunts protein synthesis– cell death.
Enterotoxin leads to a watery diarrhea by inhibits sugar and AA absorption in the SI and
Blood, WBCs, and mucus in stool
Shigellosis
Caused by:
S. sonnei- least sever, seen in children <5
S. fleneri- most like S. dysenteriae, fairly severe, seen in homosexual men
S. boydii- rare
Transmission by 4 Fs
Shigella spp.
G- non-motile rods
No H2S production (exception: flexneri)
Grown on S-S agar- differentiates from Salmonella
No lactose fermentation
Pale colonies on MacConkey- differentiates from E.coli
No gas produced from glucose
No citric acid use
EIEC
Enteroinvasive E. coli
SEA and S. America
Similar to shigella, but less severe
Starts as watery diarrhea, then becomes bloody
Pathogenesis: LI invasion–> lyses phagosome, replicates in the cytoplasm, spreads through the cells and destroys colonic cells.
Salmonella spp.
Motile, G- rods
no lactose fermentation
Pale on macconkies
Produces H2S
Differentiates from shigella on S-S agar
Produces gas from glucose
Dx: isolate from stools, water or food. travel hx, + tidal reaction
Salmonella enterocolitis
Spp: S. typhimurium, S. enteritis, S. newport
Sxs: N/V/watery D
- stool cultures, + blood cultures
Typhoid fever
Enteric fever: S. typhi, and S. paratyphi A, B (tartrate -) or C
7-20d incubation, duration is weeks
Sxs: early constipation, bloody diarrhea, gradual fever w high plateau.
Blood cultures + 1st-2nd week, stool + from 2nd week on
May have maculopaplar rash on trunk, anemia, leukopenia, absence of eosinophils in stools.
May also have reptile assoc salmonellosis
Pathogenesis of Salmonella spp.
Colonize SI and sometimes LI– invade via M cells–> multiply in vacuole and then release into the blood/lymph
end of first stage
S. typhi then in the blood stream is engulfed by macros and taken to the liver, spleen and bone marrow (can cause organomegaly)–> colonizes the gallbladder and replicates in the bile –> secreted and re-enters the intestines.
Asx carriers shed for life– cholecystectomy is only way to prevent further infection.
** Travel hx is key for typhoid fever
Campylobacter spp.
curved G- Motile(single polar flagella) rods.
Non-spore forming
Microaerophilic
Catalase +
Oxidase +
Zoonotic: poultry, cows, sheep, pigs, cats and dogs
Pathogenesis of Campylobacter
Invades both LI and SI–> mucosal damage–> toxin production
Enterotoxin- watery diarrhea
Verotoxin (cytotoxin) - similar to Shiga, bloody diarrhea
Sxs: profuse bloody and watery diarrhea and vomiting, severe abd. pain and pyrexia
Complications of C. jejuni
Reactive arthritis
GBS (acute inflammatory demyelinating polyneuropathy): anti-LPS Abs are formed to campylobacter, but cross-react with GM1-gangliosides in the myelin sheath–> n. damage–> loss of conduction and paralysis
Yersinia enterocolytica
Causes gastritis in cold climates (psychrotroph)
Mimics appendicitis
Seen in refrigerated foods: carrots and lettuce
Invades SI and causes inflammatory rxn from GALT. Also affects adjacent tissues and mesenteric lymph nodes.
ST enterotoxin activates GC and increases cGMP–> watery diarrhea.
V. severe abdominal pain
Dx: specialized yersinia MacConkey agar- pinpoint colonies >48hrs. Paired Ab titers
Complications of yersinia infection
Post-Infective reactive arthritis (AI arthritis)
Invasion binds B1-integrins on T lymphocytes.
V. parahaemolyticus
Invasive. Halophilic
From raw seafood
Sxs: acute abdominal pain, vomiting, and watery diarrhea
Dx: Oxidase +, Sucrose - on TCBS agar
V. vulificus
Virulent strain. Halophilic
Diarrhea and infected cuts
From contaminated seafood, or contact with seawater in an open wound.
Sxs: intense skin lesions, gastroenteritis, and severe cases bacteremia
Risks: Liver diseases!! (also DM)
Dx: oxidase+, sucrose - on TCBS agar
EAEC
Enteroaggregative E. coli
Non-invasive, so no leukocytes in the stool.
Possesses AAF (aggregative adherence factor)
3 Stages:
1- Adherence to intestinal mucosa
2- enhanced mucus production/ biofilm formation
3- cytotoxin prdn- damages intestinal cells.?? maybe
Sxs: watery or bloody diarrhea, but don’t know what causes bloody– is NOT INVASIVE
Life-threatening conditions of STEC
1- Hemorrhagic colitis: in adults/elderly. Starts as watery diarrhea, goes to bloody. Abd pain
2- Hemolyticuremic syndrome: seen in children. microangiopathic hemolytic anemia, thrombocytopenia and ARF. See blood in urine
3- Thrombotic thrombocytopenia purpura: Elderly. HUS + fever + neurologic sxs.
STEC
Shiga-toxin producing E. coli. NON INVASIVE
Attaches to epithelial cells of LI (similar to EPEC), Releases verotoxin (cytotoxin)–> B subunit binds to surface and allows entry of A subunit–> inactivates 28S RNA of 60S ribosomal subunit–stops protein synthesis –> hemorrhagic colitis
Toxin then enters circulation and binds endothelial glomerular cells –> endothelium swells–> fibrin is deposited –> hemolytic anemia and renal damage –> ARF.
NEVER give antibiotics–will kill cells and release more toxins, making the sxs worse.
Amoebic liver abscesses
Caused by entamoeba histolytica
Mostly in R lobe,
Mostly in males
v. rare in travelers
Toxins that activate adenylate cyclase
LT of ETEC
Cholera toxin (V. Cholerae)
CPE (C. perfringens)
LT of Bacillus cereus
Toxins that activate guanylate cyclase
ST of ETEC Yersinia toxin (ST of Y. enterocolytica)
Toxins that inactivate the 28S RNA of 60S ribosomal subunit
Shiga toxin (S. dysenteriae) Cholera toxin (V. cholerae)
