Parasitic Helminths - Hunter Flashcards

1
Q

What type of parasitic nematode causes Enterobiasis?

A

Enterobius vermicularis.

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2
Q

Describe the epidemiology of Enterobiasis.

A
  1. greater than 500 million human cases world wide.

2. most common helminth in the US.

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3
Q

What is the geographic distribution of Enterobiasis?

A

Worldwide - most common nematode infection in temperate zone.

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4
Q

Describe the pathology of Enterobiasis.

A
  1. presence alone of adult pinworm in colon causes no symptoms.
  2. heavy infections cause pruritus ani - scratching can lead to cellulitis.
  3. occasional aberrant infection of vagina - probability of reinfection is extremely high
  4. autoinfection - can result form egg hatching and larval migration back into colon.
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5
Q

What type of immunity is associated with Enterobiasis?

A
  1. IgE

2. mast cells involved in worm expulsion

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6
Q

How is Enterobiasis diagnosed?

A
  1. collect worm from perianal region - adhesive tape works

2. identification of characteristic pinworm eggs or adults.

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7
Q

How is Enterobiasis treated and prevented?

A
  1. Pyrantel pamoate - retreat after two weeks to kill new worms
  2. prevention - drug treatment, difficult to eliminate through hygiene alone
  3. no vaccine
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8
Q

Describe the life cycle of Enterobius vermicularis.

A
  1. humans ingest embryonated eggs that hatch in the small intestine.
  2. larvae migrate to colon and mature into adults - male and female
  3. after copulation, male worms die and female worms migrate to perianal region where they lay up to 10,000 fertilized eggs.
  4. after laying eggs the female dies.
  5. eggs embryonate on perianum and are spread or can hatch and auto-infect.
  6. eggs very resistant to desiccation.
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9
Q

What is the infective form of Enterobius vermicularis?

A

embryonated eggs

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10
Q

What is another name for Enterobius vermicualris?

A

Pinworm disease.

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11
Q

What nematode parasite causes Trichuriasis?

A

Trichuris trichiura.

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12
Q

Describe the epidemiology of Trichuriasis.

A

Greater than one billion cases world wide.

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13
Q

What is the distribution of Trichuriasis?

A

Worldwide.

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14
Q

Describe the pathology of Trichuriasis.

A
  1. light infections - asymptomatic
  2. heavy infections - usually in children, may present as acute dysentery of chronic colitis that resembles inflammatory bowel disease or Crohn’s disease.
  3. children can develop chronic malnutrition and anemia - causing short stature.
  4. In some cases, extensive swelling of rectal mucosa causes tenesmus, protracted tenesmus can cause rectal prolapse.
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15
Q

What type of immunity is associated with Trichuriasis?

A
  1. IgA

2. mast cells and IgE

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16
Q

How is Trichuriasis diagnosed?

A
  1. identification of characteristic bipolar eggs in stool sample
  2. eosinophilia - all roundworm diseases present with this
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17
Q

How is Trichuriasis treated and prevented?

A
  1. Mebendazole or Albendazole
  2. surgical intervention in cases of rectal prolapse
  3. prevention - sanitary disposal of feces
  4. no vaccine
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18
Q

Describe the life cycle of Trichuris trichuria.

A
  1. humans ingest embryonated eggs that hatch in small intestine
  2. larvae migrate to colon and form adult female and male worms.
  3. worms copulate in colon
  4. adults embed in columnar epithelium where females lay about 3-5,000 eggs per day.
  5. unembryonated eggs pass in feces.
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19
Q

What is the infective form of Trichuris trichuria?

A

embryonated eggs

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20
Q

What is another name for Trichuriasis?

A

Whipworm disease.

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21
Q

What nematode parasite causes Ascariasis?

A

Ascaris lumbricoides.

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22
Q

Describe the epidemiology of Ascariasis.

A

Greater than one billion cases worldwide.

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23
Q

What is the distribution of Ascariasis?

A

World wide.

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24
Q

What type of immunity is associated with Ascariasis?

A
  1. allergic responses are common

2. humoral immunity may play a role

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25
Q

Describe the disease and pathology of Ascariasis.

A
  1. larval migration phase may cause intense pneumonitis, hepatomegaly and generalized toxicity
  2. intestinal phase often asymptomatic, large numbers of long worms may cause obstruction, children may develop malabsorption.
  3. Hepatobiliary and pancreatic ascariasis result from migration of adult worms into common bile or pancreatic ducts, adult worms can be found in vomitus and stool.
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26
Q

How is Ascariasis diagnosed?

A
  1. identification of characteristic egg in stool sample
  2. radiography for extraintestinal infection
  3. lab results - eosinophilia and hyperimmunoglobulinemia G
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27
Q

How is Ascariasis treated and prevented?

A
  1. Albendazole
  2. surgery
  3. prevention - sanitary disposal of feces
  4. no vaccine
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28
Q

Describe the life cycle of Ascaris lumbricoides.

A
  1. human ingests embryonated egg
  2. egg travels to and hatches in small intestine
  3. 2nd stage larvae penetrate mucosa and migrate to liver
  4. larvae migrate to lungs and molt twice then 4th stage larvae break out into alveoalr spaces.
  5. larvae migrate up bronchial tree to trachea and are swallowed
  6. larvae return to small intestine, become adults and mate.
  7. females lay eggs and greater than 200,000 unembryonated eggs are passed in feces - approx. 25,000 tons of ascaris eggs are passed each year
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29
Q

What is the infective form of Ascaris lumbricoides?

A

embryonated eggs

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30
Q

Name some aberrant infections caused by dog and cat ascarids.

A

Visceral larva migrans -(worm dies in skin because human not natural host but sometimes can get to eye) caused by Toxocara canis and T. felis. There are greater than 10,000 cases per year with 40% prevalence in regions of Southern US.

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31
Q

What parasites cause Hook worm disease?

A
  1. Ancylostoma duodenale

2. Necator americanus

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32
Q

Which of the 2 parasites that causes Hookworm disease is more virulent?

A

Ancylostoma duodenale is more virulent because it is a better blood sucker.

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33
Q

Describe the epidemiology of Hookworm disease.

A

Greater than one billion human cases worldwide.

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34
Q

Describe the distribution of Hookworm disease.

A
  1. A. duodenale is found in Mediterranean region, N. Asia and parts of S. America
  2. N. americanus is found in Western hemisphere, Africa, S. Asia and the Pacific region
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35
Q

What disease and pathology is caused by Hookworm disease?

A
  1. skin penetration by filariform larvae may cause pruritic, papular, vesicular dermatitis.
  2. lung migration of larvae can cause pneumonitis.
  3. intestinal phase often asymptomatic
  4. heavy infections can cause epigastric pain, nausea, vomiting
  5. adult worms attach to mucosa of small intestine and cause severe mucosal damage with significant blood loss - about 7 million liters of blood lost per day.
  6. causes eosinophilia and anemia
  7. causes iron deficiency anemia - leading to congestive heart failure and death
  8. can cause edema and ascites via protein malnutrition - common in childen
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36
Q

How is Hookworm disease diagnosed?

A
  1. eggs in stool, must find adults or larvae to speciate hookworms
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37
Q

How is Hookworm disease treated and prevented?

A
  1. Albendazole
  2. oral iron sulfate supplementation for anemia
  3. prevention - sanitary disposal of human feces
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38
Q

Describe the life cycle of Hookworm disease parasites.

A
  1. humans are infected by stage 3 filariform larvae that penetrate skin
  2. larvae migrate to lung, enter trachea and are swallowed
  3. larvae mature into adults and copulate in the small intestine and unembryonated eggs (A. duodenal produces many more eggs than N. americanus) are passed in the feces
  4. in the soil, Rhabditiform larvae become infectious filariform larvae
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39
Q

What is he infective form of A. duodenale and N. americanus?

A

3rd stage filariform larvae.

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40
Q

What is cutaneous larva migrans?

A

Aberrant infection caused by dog hookworm - Ancylostoma caninum and others.

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41
Q

What nematode parasite causes Strongyloidiasis?

A

Strongyloides stercoralis.

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42
Q

Describe the epidemiology of Strongyloidiasis.

A

Greater than 200 million human cases worldwide.

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43
Q

Describe the distribution of Strongyloidiasis.

A
  1. tropical, subtropical
  2. temperate - S.Eastern US
  3. prevalent in Australia
  4. many animal reservoirs
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44
Q

What is the lifecycle of Strongyloides stercoralis?

A
  1. Stage 3 filariform larvae penetrate human skin, enter blood stream and migrate to lungs.
  2. larvae enter alveolar space, migrate up respiratory tree and are swallowed
  3. larvae mature in small intestine to egg-laying adult parthenogenetic females that reside in columnar epithelium.
  4. eggs hatch in small intestine, molt twice and 2nd stage Rhabditiform larvae are passed in feces and mature in soil to stage 3 filariform larvae.
  5. can have a free living cycle
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45
Q

What is the infective form of Strongyloides stercoralis?

A

3rd stage filariform larvae

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46
Q

What is the disease and pathology of Strongyloidiasis?

A
  1. larval migration may cause serpiginous, creeping urticarial eruptions in skin
  2. larval migration through lungs may cause pnemonitis
  3. intestinal disease characterized by water, mucous laden diarrhea
  4. autoinfection or hyperinfection - infective filariform larvae develop in colon, often seen in immuocompromised and can lead to disseminatd disease such as secondary bacterial infection and death
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47
Q

What type of immunity is associated with Strongyloidiasis?

A

T cell function critical but exact mechanism unknown.

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48
Q

How is Strongyloidiasis diagnosed?

A
  1. stool examination for 2nd stage rhabditiform larvae

2. eosinophilia

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49
Q

How is Strongyloidiasis treated and prevented?

A
  1. Ivermectin or Albendozole
  2. especially important to treat immunocompromised pt’s
  3. prevention - sanitary disposal of human/animal feces
  4. no vaccine
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50
Q

What nematode parasite causes Trichinellosis?

A

Trichinella spiralis.

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51
Q

Describe the epidemiology of Trichinellosis.

A

1.5 million harbor parasite in US.

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52
Q

What is the distribution of Trichinellosis?

A

Worldwide - infects any mammal.

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53
Q

What is the lifecycle of Trichinella spirals?

A
  1. human consumes poorly cooked meat bearing encysted larvae
  2. the larvae are liberated by digestive enzymes and then penetrate columnar epithelieal cells
  3. They molt four times and become adults within columnar epithelium of small intestine
  4. after copulation, the females deposit living larvae that spread via blood or lymph and must penetrate striated muscle to survive.
  5. infected muscle cells become ‘nurse cells’
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54
Q

What is the disease and pathology of Trichinellosis?

A
  1. humans acquire by eating improperly cooked pork - humans are dead end host since nurse cells calcify.
  2. intestinal stages - severe gastroenteritis with vomiting, diarrhea and abdominal pain
  3. larvae penetrate andkill many cell types before dying and may cause myocarditis and encephalitis.
  4. larvae in striated muscle cells survive but cause myositis with fever, myalgia and periborbital edema
  5. in extremely heavy infection muscles can become dysfunctional leading to paralysis - if of the diaphragm then can be fatal
  6. lab findings include - eosinophilia, and elevated muscle enzymes - CPK, LDH
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55
Q

What type of immunity is associated with Trichinellosis?

A

ADCC against free larvae, mast cell mediated expulsion of adult worms.

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56
Q

How is Trichinellosis diagnosed?

A
  1. enzyme immunoassay to determine anti-Trichinella antibodies
  2. definitive diagnosis via muscle biopsy and histopath
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57
Q

How is Trichinellosis treated and prevented?

A
  1. Prednisone for muscle inflammation
  2. Abendazole to kill adult worms
  3. prevention - cook or freeze pork, prevent pigs from eating meat scraps
  4. no vaccine
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58
Q

What is the infective form of Trichinella spirals?

A

Encysted larvae.

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59
Q

What nematode parasites cause Filariasis?

A

Wuchereria bancrofti

Brugia malayi

60
Q

Describe the epidemiology of Filariasis.

A

Greater than 120 million cases worldwide.

61
Q

Describe the distribution of Filariasis.

A

Tropics and Subtropics and Pacific islands.

62
Q

What is the life cycle of W. bancrofti and B. malayi?

A
  1. mosquito vector deposits stage 3 filariform larvae on skin when biting
  2. larvae enter bite wound and go to lymphatics
  3. long, slender adult worms mature and copulate in lymphatic vessels
  4. females produce microfilariae that circulate in blood stream.
  5. female mosquitoes acquire microfiliariae with blood meal
  6. microfilariae penetrate mosquito gut, migrate to flight muscles and molt twice.
  7. they then migrate to the probiscus.
63
Q

What is the infective form of W. bancrofti and B. malayi?

A

Stage 3 filariform larvae.

64
Q

What is the disease and pathology caused by Filariasis?

A
  1. many hosts are asymptomatic
  2. microfilaremia may cause ‘filarial’ fever - lymphangitis, lymphadenitis, cellulite, dermatitis with inguinal lymph nodes and testes often affected.
  3. chronic disease may result from lymphatic blockage by adult worms leading to lymphedema and elephantiasis.
65
Q

How is Filariasis diagnosed?

A
  1. find microfilaria on Giemsa stained blood film

2. blood concentration techniques available.

66
Q

How is filariasis treated and prevented?

A
  1. Diethylcarbamazine to kill microfilariae
  2. no affective therapy for adult worms
  3. surgery to relieve lymphedema
  4. prevention - mosquito control, mass chemotherapy for microfilaria
  5. no vaccine
67
Q

Name some other less important filaria species.

A
  1. Loa loa

2. Mansonella perstans

68
Q

What is a unique thing about microfilaria some strains?

A
  1. exhibit diurnal periodicity - only found in blood during the day
  2. other strains may exhibit nocturnal periodicity
  3. since vector is mosquito then biting habits must coincide with microfilarial periodicity.
69
Q

What nematode parasite causes Onchocerciasis?

A

Onchocerca volvulus.

70
Q

Describe the epidemiology of Onchocerciasis.

A
  1. 120 million at risk
  2. greater than 20 million human cases
  3. 270,000 blind
71
Q

What is another name for Onchocerciasis?

A

River blindness.

72
Q

What is the distribution of Onchocerciasis?

A
  1. Subsaharan Africa

2. Latin America

73
Q

Describe the life cycle of Onchocerca volvulus.

A
  1. blackfly deposits 3rd stage filariform larvae on skink while biting
  2. larvae enter bite wound and develop to adults in subQ tissue.
  3. long, slender adult worms copulate and females produce microfilaria that enter blood stream and eye
  4. microlilaria are acquired by the next blackly that bites infected host
    5 larvae penetrate gut of blackfly and migrate to flight muscles where they molt twice before migrating to proboscis.
74
Q

What is the disease and pathology caused by onchocercaisis?

A
  1. living microfilaria cause little pathology, dead cause intense host imflammatory response
  2. adult worms in subQ tissue nodules can causee lymphatic obstruction and edema
  3. dead microfilaria in eye often cause inflammation, sclerosing keratitis, blindness - 5th leading causee of blindness worldwide.
75
Q

What type of immunity is associated with River blindness?

A
  1. immunopathologic response to dead microfilaria

2. little response to adult worms

76
Q

What is the infective form of Onchocerca vulvulus?

A

3rd stage filariform larvae

77
Q

What is the vector for Onchocerca vulvulus?f

A

The blackly, Similium spp.

78
Q

How is onchocerciasis diagnosed?

A
  1. find microfilaria on Giemsa stained blood film

2. identification of adults or microfilaria from skin

79
Q

How is onchocerciasis treatead and prevented?

A
  1. Ivermectin
  2. nodulectomy
  3. prevention - blackfly control, mass chemotherapy
  4. no vaccine
80
Q

What nematode parasite causes Dracunculiasis?

A

Dracunculus medinensis.

81
Q

Describe the epidemiology of Dracunculiasis?

A

Nearly eradicated.

82
Q

What is the distribution of Dracinculiasis?

A
  1. Central Africa
  2. Yemen
  3. Pakistan
83
Q

Describe the life cycle of Dracunculus medinensis.

A
  1. human swallows copepod with 3rd stage infective larvae
  2. the larvae are freed from copepod in small intestine
  3. larvae penetrate mucosa and migrate within connective tissue for up to one year
  4. mature adults copulate then long, thin female migrates to skin of lower extremities where she induces a vesicle in skin overlying her vulvar region
  5. vesicle ruptures on contact with water and uterine prolapse releases living larvae
84
Q

What is the infective form of Dracunculus medinensis?

A

3rd stage larvae in copepod

85
Q

What is critical to the lifecycle of Dracunculus medinensis?

A

Water

86
Q

Describe the disease and pathology caused by dracunculiasis.

A
  1. no host response to initial migration of larval worms
  2. female worms secrete toxin that induces vesicle formation, local inflammation and ulceration.
  3. secondary bacterial infections and allergic reactions with urticaria and pruritus to worm products are common
87
Q

How is Dracunculiasis diagnosed?

A
  1. identify head of female worm in skin lesion

2. identify larvae

88
Q

How is Dracunculiasis treated and prevented?

A
  1. slow winding of adult worm on a thin stick to remove
  2. surgury
  3. Mebendazole with corticosteroids to reduce inflammation
  4. prevention - boil or filter drinking water, eliminate copepods
  5. no vaccine
89
Q

What is another name for Drucunculiasis?

A

Guinea worm disease.

90
Q

What trematode parasites cause Schistosomiasis?

A
  1. Schistosoma mansoni
  2. Schistosoma hematobium
  3. Schistosoma japonicum
91
Q

Describe the epidemiology of Schistosomiasis or Blood fluke.

A
  1. one sixth of world population at risk

2. greater than 200 million human cases

92
Q

What is the distribution of Schistosomiasis?

A

Tropics and Subtropics.

93
Q

Describe the lifecycle of the Blood fluke parasites.

A
  1. Cercariae penetrate skin and become schistosomules that migrate first to lungs then to portal veins near the liver
  2. adults migrate to mesenteric vessels (S. mansoni and S. japonicum) or to the venous plexus of the urinary bladder (S. haematobium)
  3. after copulation, female produces eggs that pass through blood vessel walls and gains access to colon or bladder and are passed in feces or urine
  4. eggs hatch on contact with water and release motile miracidia that penetrate foot process of intermediate host - the snail
  5. asexual reproduction in the snail yields fork-tailed cercariae that exit snail and fund human host
94
Q

What is the infective form of the Blood fluke parasites?

A

The fork-tailed cercaria.

95
Q

What is the intermediate host of the Blood fluke parasites?

A

A snail.

96
Q

Describe the disease and pathology caused by the Schistosoma parasites.

A
  1. cercarial penetration of skin can cause dermatitis - usually transient
  2. migration of schistosomules through the lungs can cause pneumonitis
  3. adult worms in blood vessels can cause no clinical symptoms
  4. onset of egg production causes Katayama fever
  5. intestinal or urinary bladder symptoms due to eggs passing through tissue to lumen
  6. eggs swept up portal circulation to liver cause granulomas, blockage of sinusoids, pipestem fibrosis and portal hypertension
  7. some eggs can reach lungs and cause granulomas
  8. clinical lab findings - hepatosplenomegaly, eosinophilia, hyperimmunoglobulinemia
  9. bird schistosomes can cause ‘swimmer’s itch’
97
Q

What type of immunity is associated with Schistosomiasis?

A
  1. T cell mediated delayed type hypersensitivity to eggs

2. antibody (IgE and mast cells) dependent cell-mediated cytotoxicity against schistosomules

98
Q

How is Schistosomiasis treated?

A

Praziquantel

99
Q

How can Schistosomiasis be prevented?

A
  1. sanitary disposal of feces and urine
  2. snail control
  3. no vaccine
100
Q

Name some other food and water borne trematodes.

A
  1. Clonorchis sinensis
  2. Paragonimus westermanni
  3. Opisthorchis spp.
  4. Fasciola hepatica
  5. Fasciolopsis buski
  6. Heterphyes heterophyes
  7. Metagonimus yokogawi
  8. Echinostoma spp.
101
Q

How is Schistosomiasis diagnosed?

A
  1. identification of characteristic eggs in feces or urine

2. eggs have spines - if see a lateral spine then this is diagnostic for S. mansoni

102
Q

What cestode parasites cause Taeniasis?

A
  1. Taenia saginata - in cows

2. Taenia solium - in swine

103
Q

The cestode Taenia parasites are also called what?

A

Cattle and Pork tapeworms.

104
Q

Describe the epidemiology of Taeniasis.

A

Prevalence is unknown but tens of millions of humans are at risk.

105
Q

What is the distribution of Taeniasis?

A

Tropics and subtropics - particularly in areas with cattle and swine.

106
Q

Describe the lifecycle of the Taenia parasites.

A
  1. human host ingests uncooked beef or pork with cysticercus larva
  2. larvae matures to adult tapeworm in small intestine
  3. tapeworm attaches to mucosal lining via its scolex with suckers an d hooks and produces eggs that pass in feces
  4. eggs embryonate in soil and are consumed by intermediate host - cow or pig
  5. eggs hatch and release onchospheres in animal small intestine that penetrate intestinal lining to blood stream where are carried to various organs and to muscle
  6. Cysticercus larvae develop in muscle tissue
107
Q

What is the infective form of the Taenia parasites?

A

Cysticercus larvae.

108
Q

What are the intermediate hosts of the Taenia parasites?

A

Cattle and Pigs.

109
Q

Describe the disease and pathology caused by Taenia parasites.

A
  1. adult tapeworm infection s are usually asymptomatic but can cause discomfort and mild diarrhea
  2. worms can reach up to 40 feet long
110
Q

What type of immunity is associated with Taeniasis?

A
  1. usually no response

2. can engage IgE and mast cell response to worm products

111
Q

How is Taeniasis diagnosed?

A
  1. identification or eggs or proglottids in fecal sample
112
Q

How is Taeniasis treated and prevented?

A
  1. Praziquantel - kills worm
  2. prevention - proper cooking of beef or pork
  3. freezing kills cysticerceri
  4. no vaccine
113
Q

Name some other related tapeworm species.

A
  1. Diphyllobothrium datum- broad fish tapworm up to 60 ft long
  2. Hymenolepsis nana - dwarf tapeworm
  3. Hymenolepsis diminuta - rat tapeworm
  4. Dipylidium caninum -dog tapeworm
114
Q

What cestode parasite causes Cysticercosis?

A

Taenia solium larvae.

115
Q

Describe the epidemiology of Cysticercosis.

A
  1. prevalence unknown

2. common problem where Taeniasis is found

116
Q

What is the distribution of Cysticercosis?

A

Worldwide - especially prevalent in Central and South America.

117
Q

Describe the life cycle of Taenia solium larvae.

A
  1. humans consume embryonated eggs that hatch in small intestine and release oncospheres
  2. oncosphere penetrates intestine and migrates to blood where it then travels to any organ or tissue where it grows in to a cysticercus enclosed in a cyst produced by the host
118
Q

What is the infective form of T. solium larvae?

A

Embryonated eggs.

119
Q

Describe the pathology and disease caused by Cysticercosis.

A
  1. a few cysticerci in muscle usually asymptomatic, pt may notice painless subQ nodules, larvae eventually die and calcify
  2. constellation of symptoms depending on location and number of cysts.
  3. neurocysticercosis - cysts in brain , prevalent in Central America - may present as brain tumor or epilepsy
  4. Cysticerci in eye can cause retinitis or uveitis.
120
Q

What type of immunity is associated with Cysticercosis?

A

Inflammation and fibrosis.

121
Q

How is Cysticercosis diagnosed?

A
  1. radiography
  2. MRI, CT scan
  3. serology
  4. eosinophila
122
Q

How is Cystiicercosis treated and prevented?

A
  1. Albendazole with corticosteroids for inflammation
  2. surgical removal
  3. prevention - sanitary disposal of human feces
  4. no vaccine
123
Q

What type of cestode parasite causes Echinococcosis?

A
  1. Echinococcus granulosus

2. Echinococcus multiocularis

124
Q

Describe the epidemiolgy of Echinococcosis.

A
  1. prevalence unknown

2. tens of millions of humans at risk

125
Q

What is the distribution of Echinococcosis?

A

Widespread in regions of the world with sheep raising.

126
Q

Describe the life cycle of Echinococcus parasites.

A
  1. human or animal such as sheep consumes embryonated eggs that hatch in small intestine and release oncospheres
  2. oncospheres penetrae mucosa and migrate through blood stream to liver, lungs and other organs
  3. oncoshperes develop into hydatid cyst in tissue
  4. canine carnivore consumes sheep parts containing hydatid cyst
  5. cyst ruptures in small intestine releasing tapeworm heads - called scolices
  6. Scolices attach to mucosal epithelium and small adult tapeworms develop in canine and eggs are produce that pass in the feces
  7. humans ingest these eggs passed from dog
127
Q

What is the infective form of the Echinococcus parasite?

A

embryonated eggs.

128
Q

What are dead end hosts in the life cycle of Echinococcus parasites?

A

Humans, the life cycle is naturally sheep to dog to sheep cycle.

129
Q

What is another name for Echinococcosis?

A

Hydatid disease.

130
Q

Describe the disease and pathology of Echinococcosis.

A
  1. E. granulosus is the most common in sheep to dog to sheep cycle, E. multilocularis most commonly seen in wild animals - in both cases humans interrupt the zoonotic cycle and serve as dead end hosts.
  2. humans do not harbor adult tapeworm - disease is due to larval tapeworms
  3. clinical manifestations depend on where the hydatid cyst is growing - most commonly liver cysts cause serious liver destruction
  4. hydatid cysts in other organs cause organ destruction and symptomology
  5. rupture of hydatid cyst can lead to anaphylactic shock and death
  6. E. multilocualris infections cause multilocular or alveolar cysts and cause more severe tissue distraction
131
Q

What type of immunity is associated with Echinococcosis?

A
  1. non-productive antibody response

2. host attempts to wall off hydatid cyst

132
Q

How is Echinococcosis diagnosed?

A
  1. serology

2. radiography

133
Q

How is Echinococcosis treated and prevented?

A
  1. Albendazole is marginally effective
  2. surgical removal if indicated
  3. prevention - avoid contact with dogs, prevent dogs from consuming offal
  4. no vaccine
134
Q

What are the parasitic arthropods?

A
  1. lice
  2. flies
  3. bedbugs
  4. fleas
  5. mites
  6. ticks
135
Q

Describe who head and body lice cause pathology.

A
  1. head and body lice afflict more than 12 million people a year - mostly school aged children
  2. infestation is associated with poor hygiene
  3. cause pediculosis - dermatitis, itching caused by hypersensitivity response to louse saliva
  4. diagnosed by clinical inspection - can see adult lice, nymphs and eggs or nits
  5. treat with Permethrin cream or ointment
136
Q

What are the 2 species of lice that cause human disease?

A
  1. Pediculus humanus capitis - on head

2. Pediculus humanus corporis - on body

137
Q

What bacterial disease can lice transmit?

A

Epidemic typhus.

138
Q

Describe infection by pubic lice.

A
  1. more than 3 million annual cases
  2. causes Phthiriasis - itching of area covered by pubic hair but may affect other areas of body as well
  3. itching may start soon after getting infected with lice or may not start for 2-4 weeks
  4. causes skin to turn bluish-gray in color and causes sores in genital area due to bites and scratching
  5. transmitted primarily by sexual contact
  6. diagnose - small gray-white oval eggs or nits attached to hair shaft, adult lice present too
  7. treat with 1% Permethrin cream
139
Q

What is the parasite that causes pubic lice?

A

Phthirus pubis.

140
Q

What is Myiasis?

A

Myasis is an ectoparasitic infestation of viable or necrotic tissues by the dipterous larvae of higher flies.

141
Q

Describe the pathology of Myiasis.

A
  1. rare in US but common in developing countries
  2. can cause furuncular myiasis - burrowing larvae cause pustular lesions that resemble boils or furuncles
  3. diagnosis - clinical in spection often with microscopy
  4. treatment - coaxing larvae from furuncles by smothering their respiratory spiracles with vaseline and give tetanus prophylaxis
  5. wound should be cleansed, debrided
  6. secondary bacterial infections common and can be treated by antibiotics
142
Q

What organism causes Myiasis?

A

Dermatobia hominis or Botfly

143
Q

Describe a case of bed bug infection.

A
  1. caused by Cimex lectularis in US
  2. this bed bug is oval, small and has a brownish body
  3. they reside in mattresses and crevices of wooden beds
  4. at night they come out and take a blood meal from humans
  5. main symptom is pruritic wheal caused by a hypersensitivity reaction to proteins in bug saliva
  6. can be asymptomatic
  7. treatment - Calamine lotion for itching, Malathion or Lindane used to treat mattresses and beds
144
Q

Describe Scabies.

A
  1. infestation by itch or scabies mite - Sarcoptes scabiei
  2. 300 million cases worldwide, associated with poor hygiene
  3. human scabies mite is an obligate parasite and completes entire life cycle on human host
  4. females burrow intradermally to lay eggs and larvae emerge and mature to re-infest same or new host
  5. diagnosis - examination with microscopy of a skin scraping with female mite
  6. may also detect scabies antibodies or DNA
  7. treatment - 5% Permethrin, Triamicinolone, and hydroxyzine - must treat entire family and house must be decontaminated
145
Q

What is Tick paralysis?

A
  1. a worldwide disease caused by more than 60 species of tick
  2. paralysis is due to a response to a neurotoxin secreted by salivary glands of tick
  3. this toxin inhibits presynaptic acetylcholine release at the neuromuscular junction
  4. pt develops ascending symmetrical flaccid paralysis and weakness in lower extremities
  5. death may follow paralysis of respiratory muscles
  6. treatment - removal of tick