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Human Parasitology > Foodborne Trematode Infections > Flashcards

Foodborne Trematode Infections Flashcards

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?

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?

A

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

23
Q

What are parasite secretions?

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?

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
Q

What is the common name of fasciola hepatica?

A

sheep liver fluke

26
Q

What occurs during fasciola hepatica’s life cycle?

A

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
Q

What structures make up the digestive tract of fasciola hepatica?

A
  1. oral sucker 2. gastrodermis
28
Q

What is the function of an oral sucker?

A

suction to break capillaries and allow blood to flow into worm

29
Q

What is the gastrodermis?

A

single layer of epithelia cells that lines worm digestive tract w/ surface lamellae (projections)

30
Q

What 2 phases do cells go through during cyclical transformation in the digestive tract of fasciola hepatica?

A
  1. absorptive phase 2. secretory phase
31
Q

What occurs during the absorptive phase?

A

surface lamellae are long & numerous. increased SA for absorption of blood. few secretory bodies

32
Q

What occurs during the secretory phase?

A

surface lamellae are shorter & less numerous. many secretory bodies. enzymes -> digest blood

33
Q

What pathology can fasciola hepatica juveniles induce?

A

ulcers in ectopic sites (eye, skin, brain, lungs). acute fasioliasis = liver necrosis, hepatomegaly, ~8 weeks

34
Q

What is chronic fasioliasis?

A

> 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
Q

What is cirrhosis?

A

replacement of normal liver tissue w/ fibrous tissue

36
Q

What is jaundice?

A

yellowish pigmentation of skin. increased bilirubin in blood. normally excreted in bile & urine

37
Q

What is fascioliasis?

A

emerging parasite disease due to environmental change -> human made modifications

38
Q

What is the common name of paragonimus westernani?

A

oriental lung fluke

39
Q

Describe the life cycle of paragonimus westernani?

A

1st IH = snail 2nd IH = crabs & crayfish (metacercaria) DH = humans (reservoir hosts)

40
Q

What occurs inside the DH of paragonimus westernani? (humans)

A
  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
Q

What 2 pathologies can rise from paragonimus westernani?

A
  1. lung tissue necrosis - cough, chest pain, blood in sputum 2. ectopic sites - migrating juveniles (ex: abdominal wall, heart, brain)
42
Q

How can you diagnosis the pathologies relating to paragonimus westernani?

A
  1. egg in sputum & feces 2. x-ray
43
Q

How can trematodes be treated? What is the exception to this?

A

PZQ (except fasciola hepatica)

44
Q

What happens upon exposure to PZQ?

A
  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
Q

Why is PZQ not effective in treating fasciola hepatica?

A

thick tegument

46
Q

What does triclabendazole treat (TCBZ)?

A

fasciola hepatica = 1980s very effective against juveniles

47
Q

What are some of the effects of TCBZ?

A
  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
Q

How can we control infection?

A
  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
Q

How can we control molluscicides?

A

cooper sulfate & sodium pentachloraphenate

50
Q

How can we control fasciola hepatica?

A

don’t use watercress in salads

51
Q

How can we control C. sineusis & O. viverrini?

A

proper preparation of fish - cooking, salting, picking, smoking, drying -> metacercaria survives. no night soil in fish ponds

52
Q

How can we control P. Westernani?

A

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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