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x. ID > 4/10 Parasitology and Travel Med I > Flashcards

4/10 Parasitology and Travel Med I Flashcards

1
Q

2 kinds of worms

A
  • Roundworms (intestinal and tissue)
  • Flatworms (tapeworms, flukes)
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2
Q

indication of worm infection?

A

eosinophilia

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3
Q

T/F worms multiply in hosts

A

mostly false. most do not multiply in hosts

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4
Q

in worm infections, what is disease state determined by?

A

disease is determined by infecting numbers

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5
Q

general life-cycle of roundworm

A
  • All produce and release eggs; some eggs mature and are released as larvae
  • Do not multiply in host (must ingest more eggs in order to get more worms)
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6
Q

standard trmt of roundworms?

A

Bendazole – inhibits microtubule function, immobilizes and kills worms

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7
Q

What is this?

A

Pinworm

Enterobius vermicularis

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8
Q

What is this?

A

Pinworm

Enterobius vermicularis

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9
Q

What is the life cycle of the pinworm?

A
  • EGG ingestion –> intestines where larvae mature in into adults. Female pinworms migrate to anal verge to expel eggs via feces
  • Eggs remain infectious in the environment for 2wks – requires repeated treatments
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10
Q

Where do pinworms occur?

A

Worldwide (
children (30%), adults (15%))

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11
Q

How are Enterobius vermicularis diagnosed?

A

EGG, clear scotch tape prep from perianal area

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12
Q

Enterobius vermicularis treatment?

A

Bendazole - treat entire family for 2 weeks due to high recurrence of infection

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13
Q

Strongyloides stercoralis general life cycle?

A
  • LARVAE penetrates skin -> transported to the lungs where it penetrate alveolar spaces -> swallowed -> small intestines
  • Adult F deposit their eggs into the intestinal mucosa, from which larvae hatch and migrate to the lumen (no eggs in stool!!)
  • Larvae produced in small bowel can either be
    • passed into stool as the non-infectious form
    • become infectious and penetrate the intestinal mucosa, taking gram (-) bacteria with them, into the blood stream, resulting in a hyperinfection (+bacterial sepsis) where it goes on to reinfect the lungs, starting the cycle again
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14
Q

How long can Strongyloides stercoralis last in the body?

When is it usually reactivated?

A

Latent period (up to 30 years); can be reactivated by steroids -> hyperinfection

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15
Q

What is hyperfinection? What is it caused by?

A

Strongyloides stercoralis - occurs when it penetrates the intestinal mucosa, taking gram (-) bacteria with them, into the blood stream, resulting in a hyperinfection (+bacterial sepsis) where it goes on to reinfect the lungs, starting the cycle again

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16
Q

Where is Strongyloides stercoralis found?

A

Worldwide - warm, moist climates

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17
Q

symptoms of Strongyloides stercoralis?

A
  • Asxs
  • GI symptoms - nausea, diarrhea, cutaneous/pulmonary sx
  • Hyperinfection – fever, pulm, sepsis
  • Symptoms related to invasion (itchy rash)
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18
Q

what bug is this?

A

Strongyloides stercoralis

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19
Q

How is Strongyloides stercoralis diagnosed?

A
  • LARVA (non-infectious; feces), serology
  • Hyperinfection
    • blood culture - gram (-) rods
    • sputum exam with microscopic ring worm larvae
20
Q

How is Strongyloides stercoralis treated?

A
  • Bendazole (or Ivermectin)
  • Wear shoes!
21
Q

What worm is this?

A

Ascaris lumbricoides

22
Q

Life-cycle of this bug?

A
  • EGG ingestion > develops into larvae that penetrates the bowel wall > migrates to the lungs and break into alveoli space > coughed up and swallowed
  • Mating occur in the small bowel g produces egg that are shed in feces (can contaminate agriculture)
23
Q

Where does ascaris usually affect?

A
  • SE USA
  • Northeast pigs
  • Tropics (haiti)
24
Q

What are the symptoms of Ascaris?

A
  • Light infection = Asxs; excreted into stool (usually freaks people out)
  • Heavy infection > gut/bile obstruction, malabsorption
  • Hemorrhagic pneumonitis (eosinophilic pneumonia) in lung
25
Q

What is this? How is it diagnosed

A

ascaris lumbricoides

EGG (feces) – see lumpy bumpy coat

26
Q

How do you treat Ascaris lumbricoides?

A

Piperazine – paralyzes the worm

27
Q

What are the two types of Larva Migrans?

what is it also known as?

A
  • Visceral Larva Migrans
  • Ocular Larva Migrans
  • aka Dog/cat Ascarid “Toxocariasis”
28
Q

Life cycle of Visceral Larva migrans?

A
  • EGG ingested from dog/cat feces in soil
  • Eggs hatch > larvae penetrates the intestinal wall, travel with the blood stream to various organs ((liver, heart, lungs, brain, muscle, eyes) and cause local reactions
29
Q

What are the dead end hosts for visceral larva? Why?

A

humans are dead-end, accidental hosts (it can infect but not mature/complete its life cycle in humans; ie no eggs in stool; usually completes its life cycle in dogs)

30
Q

Who does visceral larva migrans affect?

A

Mostly kids

31
Q

Clinical presentation of visceral larva migrans?

A
  • Asxs that progresses to fever, hepatomegaly
  • Retinoblastoma-like in eye (blood work shows eosinophilia compared to Rb)
32
Q

How do you diagnose visceral larva migrans?

A
  • Serology
  • Tissue Bx - eosinophilic granuloma
33
Q

What is this?

A

Visceral Larva Migrans

34
Q

Treatment for Visceral Larva Migrans?

A
  • Bendazole
  • Diethylcarbamazine
35
Q

two types of flatworms?

A
  • Flukes – reproduce sexually in humans, asexually in snails
  • Tapeworms – scolex/head, mucosal attachment by sucker/hooklets, proglttids produce eggs, distal most mature, absorb nutrients in intestine through entire length of body
36
Q

What is this?

A

Schistosomiasis (Flukes)

S. mansoni (lateral spike)

37
Q

What is this?

A

Schistosomiasis (Flukes)

S. hematobium (apical)

38
Q

What is this?

A

Schistosomiasis (Flukes)

S. japonicum (smallest)

Jen remembers this one because it looks like the Japanese flag.

39
Q

What is the general life cycle of Schistosomiasis (Flukes)?

A
  • CERCARIA (released from snails) penetrates unbroken skin and enters circulatory system to reach the portal vein, where it mature into adults.
  • Paired adult worms migrate to mesenteric/bladder veins and mature to adult form -> produce EGGS that
    • burrow through the intestinal wall and shed in stool/urine, back to water to snails
    • cause disease by circulating back to the liver
40
Q

Why is it that there is no host immune reaction against Schistosomiasis (Flukes)?

A

Adults adopt host antigens, rapidly turnover their surface coat = NO host immune reaction!

41
Q

Where does schistosomes usually occur?

A

Freshwater

Tropics

Egypt

42
Q

symptoms of schistosomiasis??

A
  • Early Sx: fever, eosinophilia
    Liver – “pipestem fibrosis” = cirrhosis, portal HTN, ascites and esophageal varices
    • biosynthetic function is maintained eg. clotting factors and albumin levels are not markedly changed
  • Egg granulomas in lung, brain, spinal cord
  • Bladder: hematuria or SCC (due to chronic inflammation)
  • Swimmer’s Itch – cercariae in skin
43
Q

What worm causes Pipestem fibrosis?

What is the immune response like?

A

Schistosomiasis (Flukes) - acute TH1 response with IFNG and TNF, but as chronic disease supervenes, shift toward TH2 with eosinophilia, fibrosis

44
Q

How do you diagnose Schistosomiasis (Flukes)?

A
  1. EGG (O&P of stool, biopsy)
  2. Rectal Biopsy – detect old infections
45
Q

How is Schistosomiasis (Flukes) treated?

A

Praziquantel (does not work as prophylaxis)

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