pathology of infectious diseases IV - lecture notes - julia Flashcards

(26 cards)

1
Q

what is entamoeba histolytica?

A
  • parasitic ameoba that can infect GI tract
  • creates ulcers - characteristic lesion due to necrosis
  • protozoan
  • has both infectous form (stable cyst that contaminates food and water) and invasive trophozoite form in GI tract
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2
Q

what allows entamoeba histoytica to adhere?

A

has a surface lectin that allows adherance to colonic epithelium, invasion, and confers complement resistance

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3
Q

how does entamoeba histolytica cause disease?

A
  • kills PMNs
  • liquefies tissues
  • causes “sterile abscesses” - ameobas are in there so not really sterile, but no bacteria
  • causes collitis with “flask-shaped ulcers”, liver abscess with liquefied necrotic material
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4
Q

what would an ulcer due to entameoba histolytica look like?

A

flask-like

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5
Q

what are pseudopods?

A
  • pathogenic amebi that move in one direction put out separate area that engulfs cells that they come up against
  • bottom right darker area in picture
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6
Q

what is the pathologic consequence of acute amebic colitis?

A
  • ruptured bowel
  • organisms can get into lymph and blood stream and get to other organs
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7
Q

where in an amebic liver abscess would you find the amebi?

A
  • around the edge, where they’re eating the still living tissue
  • if you put a needle into the center of the abscess, won’t get any bacteria or ameba
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8
Q

what is clostridium difficile?

A
  • toxin-producing, gram positive, spore-forming anaerobic bacillus
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9
Q

how does clostridium difficile spread?

A
  • normal component of bowel flora
  • when give antibiotics, can overgrow
  • also widespread in nature
  • spores stable in environment
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10
Q

how does clostridium difficile cause disease?

A
  • releases cytotoxins A and B
  • these kill cells
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11
Q

what is the pathologic effect of clostridium difficile?

A
  • fever
  • gi pain
  • diarrhea
  • pseudomembrane formation
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12
Q

how is C. dif diagnosed?

A
  • look for toxin itself or the genetic material responsible for the toxin - most strains produce both kinds of toxins
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13
Q

what does a pseudomembrane formation consist of?

A
  • fibrin
  • inflammatory cells
  • bacteria
  • dead cells
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14
Q

what does a pseudomembrane look like histologically?

A

pile of cellular debris that contains bacteria, dead cells, fibrin - not a true cellular membrane

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15
Q

what causes cryptococcal meingitis?

A

cryptococcus neoformans = encapsulated yeast

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16
Q

where is cryptococcus neoformans found? how is it spread?

A
  • found worldwide in high nitrogen soils
  • aerosol spread
17
Q

what does cryptococcus neoformans cause?

A
  • common respiratory infection (primary infection always always respiratory)
  • immunosuppresed tend to disseminate to meninges, bone, skin
  • can cause chronic meningitis, hydorcephalus
18
Q

how does cryptococcus neoformans cause disease?

A
  • has polysaccharide capsule
  • no toxin
  • little acute inflammatory diagnosis
  • but eventually causes loose granulomas
19
Q

how is cryptococcal meningitis diagnosed?

A
  • polysaccharide capsule used for diagnosis - gets broken down in body and gets into CSF with meningitis or can be in serum of patients
  • stain for mellanin cause it uses tryptophan to make a mellanin-like pigment
  • silver impregnation technique
20
Q

how is malaria transmitted?

A
  • mosquito
  • species feed with body at 45 degree angle to surface
21
Q

what causes malaria?

A

various species of plasmodium

22
Q

how does malaria infect the body?

A
  • infecious forms (sporozites) are in mosquito
  • bite injects form that infects hepatocytes
  • parasite forms that infects erythrocytes matures in the liver
  • break out
  • infects RBCs
23
Q

how does malaria cause disease?

A
  • infected RBCs lyse => acute anemia and toxicity due to hemoglobin that’s been released
  • release infectous merozoites
  • these attach to and invade new RBCs
  • => periodic fevers correlated to RBC infection and lysis cycle
  • a few gametocytes, infectious for mosquitoes, are eventually formed
  • binding of infected RBC to endothelium via integrin and thrombospondin receptors - parasite changes membrane of RBCs so it doesn’t stay in circulation
  • => clogging of tiny capillaries and huge cytokine response
24
Q

what are the clinical features of malaria?

A
  • fever (can be periodic - more likely to be periodic in patients living in endemic areas)
  • high parasitemia
  • severe anemia
  • cerebral dysfunction
  • renal failure due to toxicity of Hb and sludging in capillaries
  • => pulmonary edema and death
  • cerebral malaria can evolve very rapidly and be fatal
25
what are the patterns of morphologic change caused by malaria? (what would you expect to see in the spleen, liver, brain)
* enlargement of spleen and liver because they pick up remnants of RBCs so in chronic malaria will have enlargement * cerebral malaria will have small vessels clogged with parasitized RBCs, can have hemorrhage around these vessels * little inflammatory infilatrate * brain can swell = cerebral edema picture = spleen on left, liver on right
26
how is malaria diagnosed?
* examination of blood films - look at the RBCs