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Human Parasitology > Foodborne Trematode Infections > Flashcards

Foodborne Trematode Infections Flashcards

(52 cards)

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1
Q

What causes food-borne diseases?

A
  1. enteric pathogens 2. chemical contaminants 3. biotoxins 4. parasites
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2
Q

What are foodborne trematode infections?

A

food contaminated w/ larval stages of parasite. all are zoonotic infections

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3
Q

What is a zoonotic infection?

A

primarily affect domestic or wild animals. when human enters life cycle -> replaces natural DH

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4
Q

What are the main genera that cause pathology in humans?

A

clonorchis, opisthorchis, faciola, paragonimus

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5
Q

What is the distribution of foodborne trematode infections?

A

east & southeast asia, central and south america

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6
Q

What is the prevalence of foodborne trematode infections?

A

~40 million people infected ~665,000 DALYs per year

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7
Q

What is the common name of clonorchis sinesis?

A

oriental liver fluke

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8
Q

Describe the life cycle of clonorchis sinesis.

A

1st IH = snail 2nd IH = fish DH = fish eating mammals

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9
Q

What happens during the transmission stage of clonorchis sinesis?

A
  1. metacercaria 2. reservoir hosts are non-human DH & source of infection 3. excysts in duodenum 4. migrates to bile duct (not liver)
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10
Q

What is the pathology of clonorchis sinesis?

A
  1. adult worms live in bile duct = damage to lining 2. degree of damage depends on # of worms 3. cholangitis
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11
Q

What occurs when <100 worms are present?

A

asymptomatic

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12
Q

What occurs when 100 - 1,000 worms are present?

A

nausea, diarrhea, pain

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13
Q

What occurs when >1,000 worms are present?

A

fever, pain, jaundice, thickening and blockage of bile duct, hepatomegaly, cholangitis

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14
Q

What is cholangitis?

A

bacterial infection of bile duct

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15
Q

How can clonorchis sinesis be diagnosed?

A

detection of eggs in feces (abopercular knob) or ultrasound

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16
Q

What is the common name of opisthorchis viverrini?

A

cat liver fluke

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17
Q

How can you differentiate clonorchis sinesis vs. opisthorchis viverrini?

A

clonorchis sinesis has branched testes vs. opisthorchis viverrini has lobed testes

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18
Q

What is true about the life cycle of and diagnosis of opisthorchis viverrini?

A

very similar to clonorchis sinesis

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19
Q

What is the pathology assoicated with opisthorchis viverrini?

A

liver fluke induced malignancies and infections: source of preventable malignancies

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20
Q

What malignancies are associated with opisthorchis viverrini?

A
  1. CCA 2. mechanical injury 3. ulcers 4. parasite secretions 5. immunopathology
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21
Q

What mechanical injury can result from opisthorchis viverrini?

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A

fluke in bile duct -> feeding & movement -> oral & ventral suckers attach to epithelium lining of bile duct

22
Q

How do ulcer from parasites form?

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A

egg of parasite gets trapped in tissue results in granulomatous response by host -> inflammation

23
Q

What are parasite secretions?

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A

metabolic products that are toxic to host. mitogenic - stimulates host cell proliferation and results in transcriptional changes in host cell

24
Q

What is the immunopathology associated with opisthorchis viverrini?

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A

damage in bile duct & liver results in host’s immune response. inflammation (response to antigens). NO released by certain immune cell -> excess of NO is cytotoxic & mutagenic (inhibits DNA repair)

25
What is the common name of fasciola hepatica?
sheep liver fluke
26
What occurs during fasciola hepatica's life cycle?
inside host: 1. excysts in small intestine (juvenile penetrates through intestinal) 2. migrates through abdominal cavity 3. penetrates Glisson's capsule (that surrounds the liver) 4. juveniles in liver: move, feed, grow -> liver rot 5. to bile duct = adult worms
27
What structures make up the digestive tract of fasciola hepatica?
1. oral sucker 2. gastrodermis
28
What is the function of an oral sucker?
suction to break capillaries and allow blood to flow into worm
29
What is the gastrodermis?
single layer of epithelia cells that lines worm digestive tract w/ surface lamellae (projections)
30
What 2 phases do cells go through during cyclical transformation in the digestive tract of fasciola hepatica?
1. absorptive phase 2. secretory phase
31
What occurs during the absorptive phase?
surface lamellae are long & numerous. increased SA for absorption of blood. few secretory bodies
32
What occurs during the secretory phase?
surface lamellae are shorter & less numerous. many secretory bodies. enzymes -> digest blood
33
What pathology can fasciola hepatica juveniles induce?
ulcers in ectopic sites (eye, skin, brain, lungs). acute fasioliasis = liver necrosis, hepatomegaly, ~8 weeks
34
What is chronic fasioliasis?
>12 adult worms in bile duct. secrete proline that stimulates host to produce & deposit collagen & fibrous tissue so duct can handle less bile. results in back pressure: cirrhosis & jaundice
35
What is cirrhosis?
replacement of normal liver tissue w/ fibrous tissue
36
What is jaundice?
yellowish pigmentation of skin. increased bilirubin in blood. normally excreted in bile & urine
37
What is fascioliasis?
emerging parasite disease due to environmental change -> human made modifications
38
What is the common name of paragonimus westernani?
oriental lung fluke
39
Describe the life cycle of paragonimus westernani?
1st IH = snail 2nd IH = crabs & crayfish (metacercaria) DH = humans (reservoir hosts)
40
What occurs inside the DH of paragonimus westernani? (humans)
1. excyst in small intestine & penetrate through intestinal wall 2. embed in abdominal wall for ~1 week 3. migrate in abdominal cavity 4. penetrates diaphragm 5. enters lungs: adult worms, secrete enzymes that digest host antibodies
41
What 2 pathologies can rise from paragonimus westernani?
1. lung tissue necrosis - cough, chest pain, blood in sputum 2. ectopic sites - migrating juveniles (ex: abdominal wall, heart, brain)
42
How can you diagnosis the pathologies relating to paragonimus westernani?
1. egg in sputum & feces 2. x-ray
43
How can trematodes be treated? What is the exception to this?
PZQ (except fasciola hepatica)
44
What happens upon exposure to PZQ?
1. rapid, sustained muscular contractions = paralysis, flushed out of intestine 2. tegumental disruption = exposure to parasite antigens on surface 3. disruption of voltage-gated Ca2+ channels in tegument -> rapid influx of Ca2+
45
Why is PZQ not effective in treating fasciola hepatica?
thick tegument
46
What does triclabendazole treat (TCBZ)?
fasciola hepatica = 1980s very effective against juveniles
47
What are some of the effects of TCBZ?
1. swelling of tegument (damage to ion pumps) 2. swelling of mitochondria 3. microtubule inhibitor = disrupts formation of cytoskeleton -> disrupts movement of vesicles into distal cytoplasm 4. bithionol - mode of action unclear
48
How can we control infection?
1. drug treatment 2. don't use night soil (human feces as fertilizers -> need proper sanitation) 3. snail control (physical removal) 4. control of reservoir hosts
49
How can we control molluscicides?
cooper sulfate & sodium pentachloraphenate
50
How can we control fasciola hepatica?
don't use watercress in salads
51
How can we control C. sineusis & O. viverrini?
proper preparation of fish - cooking, salting, picking, smoking, drying -> metacercaria survives. no night soil in fish ponds
52
How can we control P. Westernani?
properly cook crack/crayfish. don't make "drunken crab" - rice wine for 12 & crab juices for medicinal purposes

Human Parasitology (22 decks)

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