pathology of infectious diseases IV - lecture notes - julia Flashcards

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
Q

what are the patterns of morphologic change caused by malaria? (what would you expect to see in the spleen, liver, brain)

A
  • 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
Q

how is malaria diagnosed?

A
  • examination of blood films
    • look at the RBCs