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Pre-Midterm Micro > Pre-midterm GI > Flashcards

Pre-midterm GI Flashcards

1
Q

What 2 parasites are coccidian protozoan, where are they seen?

A

Cyclospora cayetanensis- tropics and subtropics

Cryptoisospora belli- S. America, Africa, SEA

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2
Q

Infective and diagnostic forms of Cyclospora cayetanensis

A

Infective: Mature oocysts
Diagnostic: Unmature oocysts

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3
Q

Infective and diagnostic forms of Cryptoisospora belli

A

Infective: mature oocysts
Diagnostic: unmature oocyst

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4
Q

Entamoeba histolytica

A

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

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5
Q

Pathogenesis of Entamoeba histolytica

A

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)

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6
Q

3 outcomes of E. histolytica infection

A

1- asx
2- Intestinal Entamoebiasis (amoebic diarrhea and dysentry)
3- Extraintestinal amoebiasis (liver abscesses)

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7
Q

Giardia intestinalis

A

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

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8
Q

Pathogenesis of G. Intestinalis

A

Ingestion of cysts– 1-2wk incubation,
reaches the SI– forms trophozoites, multiply by binary fission.
Attach, but do NOT invade epithelium– causes watery diarrhea.

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9
Q

Dx of G. Intestinalis

A

Routine O&P- see bi-nucleat, pear-shaped flagellated trophozoites and cysts

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10
Q

Balantidium coli

A

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

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11
Q

Pathogenesis of B. coli

A

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.

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12
Q

Dx. of B. coli

A

Endoscopy- will see necrosis and ulceration– can get trophozoites from a scrapping.
Rare to get cysts on O&P

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13
Q

GI parasites associated with invasion

A

Entamoeba histolytica

Balantidium coli

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14
Q

S. Aureus

A 
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.
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15
Q

S. aureus food poisoning

A

<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

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16
Q

Bacillus cereus

A

G+
Aerobic
Spore former
Produces ST neurotoxin/emetic toxin- food poisoning
and LT enterotoxin- non-inflammatory diarrhea

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17
Q

B. cereus food poisoning

A

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.

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18
Q

Ciguatera poisoning

A

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

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19
Q

Scombroid poisoning

A

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.

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20
Q

Neurologic shellfish poisoning

A

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

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21
Q

Paralytic shellfish poisoning

A

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.

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22
Q

E. coli

A

G- rods
facultative anaerobes
Sorbitol fermentation (except STEC)
Normal GIT commensal

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23
Q

ETEC

A 
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
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24
Q

ETEC pathogenesis

A

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

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25
Q

Dx of ETEC

A

To distinguish from other E. coli- inoculate mouse adrenal cells and the LT/ST will stimulate adenylate cyclase

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26
Q

EPEC

A

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

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27
Q

Vibrio cholerae (and dx/identificaiton)

A 
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)

28
Q

Pathogenesis of V. cholerae (Presentation and Complications)

A

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

29
Q

How to differentiate V. cholerae from other vibrios

A

V. cholerae is the only Sucrose +, so grow on TCBS agar

30
Q

Clostridium perfringens

A

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)

31
Q

Pathogenesis of C. perfringens

A

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

32
Q

Bacillus cereus

A

G+ rods
Facultative aerobe
Spore forming
ST Emetic neurotoxin and LT enterotoxin

Foods assoc: Rice, and pastas. Also: meat, veggies, and dairy

33
Q

Pathogenesis of B. cereus LT

A

SI colonization, production of LT enterotoxin, activates AC and increases cAMP–> watery diarrhea.

34
Q

Rotavirus

A

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

35
Q

Pathogenesis of Rotavirus

A

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.

36
Q

Norovirus

A

Caliciviridae family
non-enveloped +ssRNA
Winter seasonality. Typically in older children and adults.
Associated with cruise ships and raw shellfish/mollusks

37
Q

Pathogenesis of Norovirus

A

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

38
Q

Adenovirus in non-inflame diarrhea

A

non-enveloped, dsDNA
group F serotypes assoc with disease
Replicates in SI and is present in the stool
Watery diarrhea with/without vomiting

39
Q

Astrovirus

A

non-enveloped +ssRNA
Peak is in winter
Watery diarrhea

40
Q

Cryptosporidium spp.

A

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

41
Q

Cryptosporidium pathogenesis

A

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

42
Q

Non-invasive pathogens that cause inflammatory diarrhea

A

EAEC

STEC

43
Q

Virulence factors of Shigella spp.

A

Endotoxin/ O-Ag
Exotoxin- acts as neurotoxin: coma meningismus, ulceration
NAD glycohydrolase: destroys NAD causes cell death.
Actin filaments- for cell-cell transfer

44
Q

Pathogenesis of shigella spp.

A

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

45
Q

S. dysenteriae

A

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

46
Q

Shigellosis

A

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

47
Q

Shigella spp.

A

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

48
Q

EIEC

A

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.

49
Q

Salmonella spp.

A 
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

50
Q

Salmonella enterocolitis

A

Spp: S. typhimurium, S. enteritis, S. newport
Sxs: N/V/watery D
- stool cultures, + blood cultures

51
Q

Typhoid fever

A

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

52
Q

Pathogenesis of Salmonella spp.

A

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

53
Q

Campylobacter spp.

A

curved G- Motile(single polar flagella) rods.
Non-spore forming
Microaerophilic
Catalase +
Oxidase +
Zoonotic: poultry, cows, sheep, pigs, cats and dogs

54
Q

Pathogenesis of Campylobacter

A

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

55
Q

Complications of C. jejuni

A

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

56
Q

Yersinia enterocolytica

A

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

57
Q

Complications of yersinia infection

A

Post-Infective reactive arthritis (AI arthritis)

Invasion binds B1-integrins on T lymphocytes.

58
Q

V. parahaemolyticus

A

Invasive. Halophilic
From raw seafood
Sxs: acute abdominal pain, vomiting, and watery diarrhea
Dx: Oxidase +, Sucrose - on TCBS agar

59
Q

V. vulificus

A

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

60
Q

EAEC

A

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

61
Q

Life-threatening conditions of STEC

A

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.

62
Q

STEC

A

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.

63
Q

Amoebic liver abscesses

A

Caused by entamoeba histolytica
Mostly in R lobe,
Mostly in males
v. rare in travelers

64
Q

Toxins that activate adenylate cyclase

A

LT of ETEC
Cholera toxin (V. Cholerae)
CPE (C. perfringens)
LT of Bacillus cereus

65
Q

Toxins that activate guanylate cyclase

A 
ST of ETEC
Yersinia toxin (ST of Y. enterocolytica)
66
Q

Toxins that inactivate the 28S RNA of 60S ribosomal subunit

A 
Shiga toxin (S. dysenteriae)
Cholera toxin (V. cholerae)

Pre-Midterm Micro (8 decks)

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