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Block 6 Week 5 > Parasitic Helminths (Nematodes i.e roundworms) > Flashcards

Parasitic Helminths (Nematodes i.e roundworms) Flashcards

1
Q

What is the common name for Enterobiasis?

A

Pinworm disease

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2
Q

What is the prevalence of enterobiasis?

A

greater than 500 million cases worldwide

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3
Q

What is the most common helminth in the U.S.

A

Enterobiasis (pinworm disease)

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4
Q

What is the geographic distribution of enterobiasis (pinworm disease)?

A

world-wide

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5
Q

What is the most common nematode infection in temperate zone?

A

enterobiasis (pinworm disease)

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6
Q

What is the life cycle of enterobiasis (pinworm disease)?

A
  • humans ingest embryonated eggs that hatch in small intestine.
  • Larvae migrate to colon, mature to adult male and female worms
  • After copulation females migrate to perianal region and lay 10,000 fertilized eggs and then die.
  • eggs embryonate on perianum
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7
Q

Are enterobiasis suceptible to drying out?

A

no they are very resistant to dessication

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8
Q

If you have enterobiasis in the colon what are the symptoms?

A

no symptoms

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9
Q

What will a heavy enterobiasis infection cause?

A

pruritis ani. scratching may lead to cellulitis; occasional aberrant infection of vagina; probability of reinfection is extremely high

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10
Q

(blank) can result from egg hatching and larval migration back into the colon in enterobiasis

A

autoinfection

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11
Q

How does your immune system respond to enterobiasis?

A

IgE and mast cells involved in worm expulsion

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12
Q

What is the treatment fr enterobiasis?

A

pyrantel pamoate (retreat after 2 weeks to kill new worms)

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13
Q

How do you prevent and control enterobiasis?

A

drug treatment; difficult to eliminate through hygiene; NO Vaccine

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14
Q

WHat is the common name for trichuriasis?

A

whipworm disease

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15
Q

What is the prevalence of trichuriasis?

A

greater than one billion human cases worldwide

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16
Q

What is the parasite that causes trichuriasis?

A

trichuris trichuria

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17
Q

What is the geographic distribution of trichuriasis?

A

worldwide

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18
Q

WHat is the life cycle of trichuriasis?

A

humans ingest embryonated eggs that hatch in small intestine
larvae migrate to colon where adult female and male worms mature and copulate. Adults embedded in columnar epithelium wher they lay fertilized eggs (3-5,000 eggs/day) that pass (unembryonates) in feces.

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19
Q

What do light trichuriasis infections look like?

A

asymptomatic

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20
Q

What do heavy trichuriasis infections look like?

A

may present as acute dysentery or a chronic colitis that resembles inflammatory bowel disease (e.g chrons disease); children develop chronic malnutrition, anemia, short stature
can cause tenesums which causes rectal prolapse

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21
Q

How does your immune system handle trichuriasis (whipworm disease)?

A

IgA, mast cells and IgE

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22
Q

How do you diagnose trichuriasis?

A

identification of characteristic bipolar eggs in stool sample; eosinophilia

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23
Q

How do you treat trichuriasis?

A

mebendazole or albendazole; surgical intervention for rectal prolapse

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24
Q

How do you prevent trichuriasis?

A

sanitary disposal of feces; NO vaccine

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25
Q

What is this:
Aberrant infections caused by the dog and cat ascarids Toxocara canis, T. felis and others (>10,000 cases/year in the U.S.; 40% prevalence in regions of Southern U.S.)

A

Visceral Larva Migrana

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26
Q

if a worm picture has teeth what is it?

A

ancylostoma duodenale

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27
Q

If a worm picture has a big toothless mouth?

A

necator americanus

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28
Q

What is the prevlance of hookworm disease?

A

greater than one billion human cases worldwie

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29
Q

What parasites cause hookworm disease?

A 
ancylostoma dodenal (most virulent)
necator americanus (less virulent)
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30
Q

What is the geographic distribution of hookworm disease?

A

A. duodenale is found in the mediterranean region, N. asia and part of s. America.
N. americanus previals in the W. hempsiphere but is also found in Africa, S. America and the pacific region

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31
Q

What is the life cycle of hookworm disease?

A
  • Humans are infected by 3rd stage filariform larvae that penetrate skin
  • Larvae migrate to lung, enter alveoli, then migrate up to trachea and are swallowed
  • Adult male and female copulate in small intestine and unembryonated eggs are passed in feces (egg production: A. duodenal»N. americanus)
  • Rhabditiform larvae in soil become infectious filiariform larvae.
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32
Q

What type of hookworm parasite produces more eggs, A. duodenal or N. americanus?

A

A duodenale

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33
Q

What is the clinical manifestation of hookworm disease?

A

pneumonitis
pruitic, papular, vesicular dermatitis
IN intestins-> severe infections cause blood loss, epigastric pain and nausea

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34
Q

What is the est. its of blood lost per day from humans infected with severe case of hookworm?

A

7 million liters

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35
Q

How does your immune system respond to hookworm disease?

A

IgA, mast cells, IgE

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36
Q

How do you diagnose hookworm disease?

A

eggs in stool; must find adults or larvae to sepciate hookworms

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37
Q

How do you treat hookworm disease?

A

albendazole; oral iron sulfate supplementation for anemia

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38
Q

What are the lab and clinical findings in hookworm disease?

A
  • eosinophilia
  • anemia
  • iron deficiency anemia (CHF and death)
  • edema and ascites (caused by protein malnutrition; common in children)
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39
Q

How do you prevent and control hookworm disease?

A

sanitary disposal of human feces?

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40
Q

What is this:

Aberant infections caused by the dog hookworm Ancylostoma caninum and others

A

cutaneous larva migrans

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41
Q

What is the prevalence of strongyloidiasis?

A

greater than 200 milion human cases worldwide

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42
Q

What is the parasite that causes strongyloidiasis?

A

strongyloides stercoralis

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43
Q

What is the geographic distribution of stronyloidiasis?

A

tropical, subtropical and temperate (southeastern U.S); animal reservoirs

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44
Q

What is the life cycle/biology of strongyloidiasis?

A

both parasitic and free-living phase

  • 3rd stage filariform larvae go to human skin->blood-> lungs.
  • get swallowed and go to small intestine
  • adult parthenogentic lay eggs
  • larvae molt twice
  • 2nd stage rhabditiform larvae pass in feces
  • S. stercoralis can have free-living cycle
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45
Q

What are the clinical manifestations of strongyloidiasis?

A

skin- seroiginous, creepingm urticarial eruptions
lungs- pneumonitis
GI- water, mucous-laden diarrhea
Autoinfection or hyperinfection in colon can lead to disseminated disease and death

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46
Q

How does your immune system respond to strogyloidiasis?

A

T cell function critical, but exact mechanism is unknown

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47
Q

How do you diagnose strongyloidiasis?

A

stool examination for 2nd stage rhabditifom larvae; eosinophilia

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48
Q

How do you treat strongyloidiasis?

A

ivermectin or albendazole

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49
Q

How do you prevent or control strongyoidiasis?

A

sanitary disposal of human/animal feces; no vaccine

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50
Q

What is the prevalence of trichinellosis?

A

1.5 million harbor parasites in US

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51
Q

What is the parasite that causes trichenellosis?

A

trichinella spiralis

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52
Q

What is the geographic distribution of trichinellosis?

A

worldwide (infects any mammal)

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53
Q

What is the life cycle/biology of trichinellosis?

A
  • Humans acquire T spiralis by consuming poorly cooked meat bearing encysted larvae.
  • -the larvae are liberated by digestive enzymes, penetrate columnar epithelial cells, molt four times, become female and male within columnar epithelium of s. intestine
  • After cpulation, females deposite living larvae that spread via blood or lymph an must penetrate striated muscle cells to survive.
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54
Q

What do you call muscle cells that are infected with trichinellosis?

A

nurse cells

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55
Q

Humans often acquire trichinellosis by consuming improperly cooked (blank); humans are usually (blank) hosts (nurse cells calcify)

A

pork

dead end

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56
Q

What is the clinical manifestations of trichenellosis?

A
  • severe gastroenteritis (diarrhea, vomiting, abdominal pain)
  • larvae penetrate and kill cell types before death (myocarditis and encephalitis)
  • larvae in striated muscle cells survive but cause a myositis (fever, myagia, periorbital edema)
  • in extremly heavy infections-> muscles may become dysfunction (paralysis of diaphragm can be fatal)
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57
Q

What will the lab findings be like in trichinellosis?

A

eosinophils

elevated muscle enzymes (CPK, LDH)

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58
Q

How does your immune system respond to trichinellosis?

A

ADCC against free larvae; mast cell-mediated expulsion of adult worms)

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59
Q

How do you diagnose trichinellosis?

A

enzyme immunoassay to detect anti-Trichinella antibodies; definitive by muscle biopsy, squash prep and histopathology

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60
Q

How do you treat trichinellosis?

A

Prednisone for muscle inflammation; albendazoe to kill adults

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61
Q

How do you prevent and control trichinellosis?

A

cook or freeze pork; prevent pigs from eating meat scraps; no vaccine

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62
Q

What is this:

  • female mosquito vector deposits 3rd stage filariform larvae on skin while biting
  • larvae enter bite wound and go to lymphatics
  • long, slender adult female and male worms mature and couplate in lymphatic vessels, then females produce microfiaria that circulate in bloodstream.
  • Female mosquitos acquires microfilaria with blood meal. -Microfilariae penetrat gut, migrate to flight muscles then molt twice, migrate to probiscus.
A

Filariasis

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63
Q

What are the parasites that cause filariasis?

A

Wuchereria bancrofti and Brugia malavi

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64
Q

What is the geographic distributon of filariasis?

A

tropics and subtropics (pacific islands)

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65
Q

What is the prevalence of filariasis?

A

greater than 120 million human cases worldwide

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66
Q

In some strains of filariasis, microfilaria are found in the blood only during the (bank), while other strains only exhibit (blank)

A

day (diurnal periodicity)

nocturnal peridicity

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67
Q

What are the vector mosquitos of filariasis?

A

Aedes, Culex, Anopheles

68
Q

For filariasis, biting habits must coincide with (blank)

A

microfilarial periodicity

69
Q

What is the clinical manifestations of filriasis (not chronic)?

A
  • filarial fever
  • lymphangitis
  • lymphadenitis
  • cellulitis
  • dermatitis (inguinal lymph nodes and tested often affected).
70
Q

What are the clinical manifestations of chronic filariasis?

A

lymphatic blockage by adult worms leads to lymphedema; elephantiasis (most profound late stage sequella)

71
Q

What wil filariasis laboratory findings show?

A

elevated IgE; eosinophilia

72
Q

How do you diagnose Filariasis?

A

microfilaria on Giemsa-stained blood film (consider periodicity);
blood concentration techniques

73
Q

How do you treat Filiariasis?

A

diethylcarbamzine to kill microfilariae; no effective therapy for adult worms; surgery to relieve lymphedema

74
Q

How do you prevent and control filariasis?

A

mosquito contro; mass chemotherapy for microfilaria; NO VACCINE

75
Q

What are some other filarids of minor medical importance?

A

Loa loa; Mnsonela perstans

76
Q

What is this:

  • blackfly vector deposits 3rd stage filariform larvae on skin while biting
  • larvae enter bite wound and develop to adults in subcutaneous tissues
  • Long slender worms copulate
  • produce microfilaria that enter bloodstream and tissue (eye)
  • backfly acquires microfilaria with bloodmeal, larvae penetrat gut and migrate to flight muscles where they molt twice before migrating to probosciscerciasis?
A

Onchocerciasis (river blindness)

77
Q

What is the parasite that caues onchocerciasis?

A

Onchocerca volvulus

78
Q

What is the geographic distribution of onchocerciasis?

A

subsaharan africa and latin america

79
Q

What is the vector for onchocerciasis?

A

black fly vector

80
Q

What are the clinical manifestations of Onchocerciasis (river blindness)?

A

Living microfillaria-no problem
Dead microfillaria- intest host inflammatory response
-lympatic obstruction and edema

81
Q

What is the prevalence of ochocerciasis (river blindness)?

A

120 million at risk, greater than 20 million human cases, 270,000 blind

82
Q

How does your immune response react to onchocerciasis?

A

immunopathologic response to microfilariae, little response to adult worms

83
Q

How do you diagnose Onchocerciasis?

A

find microfilaria on Giemsa-stained blood film; identification of adults or microfilaria from skin snip near nodules

84
Q

How do you treat onchocerciasis?

A

ivermectin, nodulectomy

85
Q

How do you prevent Onchocerciasis?

A

blackfly control, mass chemotherapy NO VACCINE

86
Q

What is this:
human swallows copepod with infective 3rd stage larvae. Larvae are freed from copepod in small intestine. Penetrate mucosa and migrate w/in CT for up to 1 year. Worms copulated and migrate to skin of lower extremities where they make a vesicle in skin. Vesicle ruptures on contact with water and uterine prolapse releases living larvae.

A

Dracunculiasis (guinea worm disease)

87
Q

If you see a string coming out of a foot, what is it?

A

dracunculiasis

88
Q

What is the parasite that causes dracunculiasis?

A

dracunculus medinensis

89
Q

Where do you find dracunuculiasis?

A

central africa, yemen, pakistan

90
Q

What does the worm of dracunculiasis look like?

A

very long an thin (100 cm X 1.5 mm)

91
Q

What is the clinical manifestations of Dracunculiasis disease?

A

worm secretes toxin that induces vesicle local inflammation and ulceration; secondary bacterial infections; allergic reactions (urticaria and pruritus) to worm products

92
Q

What does your immune system do in response to Dracunculiaiss?

A

has no acquired immunity

inflammatory response to adult worms

93
Q

How do you diagnose dracunculiasis?

A

identify head of female worm in skin lesion, identify larvae

94
Q

How do you treat dracunculiasis?

A

slow winding of adult worm on a thin stick; surgery, mebendazole with corticosteroids to reduce inflammation

95
Q

How do you prevent and control dracunculiasis?

A

boil or filter drinking water, eliminate copepods; NO VACCINE

96
Q

What is this:
Cercariae penetrate skin and become schistosomules that migrate to lungs-> portal veins near liver.
Adults travel to mesenteric vessels (mansni and japonicum) or to the venous plexus of urinary bladder (haernatobium). After copulation, produces eggs that pass through blood vessel walls and gain access to colon or bladder and are passed in feces or urine. Eggs hatch on contact w/ water and release motile miracidia that penetrate food process of intermediate host snail. Asexual reproduction in snail yields fork-tailed cercariae that exit snail and find human definitive host.

A

Schistosomiasis (Blood fluke)

97
Q

What are the parasites that cause Schistosomiasis?

A

Schistosoma mansoni; S. japonicum. S, haernatobium

98
Q

What is the geographic distribution of schistosomiasis (blood fluke)?

A

tropics and subtropics

99
Q

What are the clinical manifestations of schistosomiasis?

A 
transient dermatitis
pneumonitis
cercarial dermatitis
Katayama fever
Liver granulomas
portal hypertension
pipestern fibrosis
100
Q

What are the cinica and lab findings of schistosomiasis (blood fluke)?

A

hepatosplenomegaly, eosinophilia, hyperimmunoglobulenimia

101
Q

How does the immune system respond to schistosomiasis?

A

T-cell mediated delayed hypersensitivity reaction to eggs; antibody-dependent cell mediated cytotoxicity against schistosomules (IgE and eosinophils)

102
Q

How do you diagnose Schistosomiasis?

A

identification of chracterstic eggs in feces or urine

103
Q

How do you treat schistosomiasis?

A

praziquantel

104
Q

How do you prevent/control shicstosomiasis?

A

sanitary disposal of feces/urine; snail control NO VACINe

105
Q

What are these:
Clonorchis sinensis;
Paragonimus westermanni; Opisthorchis spp.;
Fasciola hepatica;
Fasciolopsis buski;
Heterophyes heterophyes; Metagonimus yokogawi;
Echinostoma spp.

A

Related Food and Water-borne Trematode Species:

106
Q

This parasite is caused by eating undercooked beef or pork product with cysticercus larva that matures to adult tapeworm in small intestine. Tapeworm attached to mucosal lining via its scolex (suckers and hooks) and produces eggs taht pass in feces. Eggs embryonate on soil and are consumed by intermediate host cow or pig. Eggs hatch and releases onchospheres in small intestine that penetrate intestinal lining to blood stream and are carried to various organs (muscle) Cystericercus larvea develop in muscle

A

Taeniasis (cattle and pork tapeworms)

107
Q

What are the parasites taht cause Taeniasis?

A 
Taenia saginata (cows)
T soilum (swine)
108
Q

Where do you find taeniasis?

A

tropics and subtropics

109
Q

What is teh clinical disease and pathology of taeniasis?

A

adult tapeworm infections (up to 40 ft long) usually asymptomatic; abdominal discomfort and mild diarrhea

110
Q

How does your body respond to taeniasis?

A

worm produced may engage IgE and mast cells

111
Q

How do you diagnose Taeniasis?

A

identification of eggs or proglottids in fecal sample

112
Q

How do you treat Taeniasis?

A

Praziquantel, psychological support

113
Q

HOw do you prevent/ control taeniasis?

A

proper cooking of beef and pork; freezing kills cystericercerci; NO VACCINE

114
Q

What are some related tapeworm species to Taeniasis?

A

Diphyllobothrium latum (broad fish tapeworm…60 ft. long!);
Hymenolepis nana
(dwarf tapeworm); Hymenolepis diminuta (rat tapeworm);
Dipylidium caninum (dog tapeworm)

115
Q

What is this:
humans consume embryonated eggs that hatch in s. intestine to release oncospheres. Oncosphere penertates intestines and migrates via blood to any organ or tissue where it grows into a cystericerus (bladder worm) enclosed in a produced by the host.

A

Cystericercosis

116
Q

If you see a worm in the eye what is it?

A

cysticercosis (taenia solium larvae)

117
Q

What is the parasite that cauess cysticercosis?

A

T. solium larvae

118
Q

Where do you find cystericerosis?

A

Worldwide (especiallly prevalent in central and south america)

119
Q

What are the clinical manifestations of cystericerosis?

A

-painless subcutaneous nodules
-larvea die and calcify
-neurocysticercosis (central america)
-retinitis or uveitis
(may present as a brain tumor or epilepsy)

120
Q

What is the immune response to cysticercosis?

A

inflammation and fibrosis

121
Q

How do you diagnose cysticercosis?

A

radiography
MRI and CT
serology
eosinophilia

122
Q

How do you treat cysticercosis?

A

albendazole, add corticosteroids; surgical removal in certain cases; no vaccine

123
Q

how do yo prevent cysticercosis?

A

sanitary disposal of human feces

124
Q

If you see a CT with hole in it what is it?

A

cysticercus

125
Q

What is this:
can have human or animal host that consumes embryonated eggs that hatch is s. intestine to release oncospheres.
Oncospheres penetrate intestine and migrate through blood stream to liver, lungs, and other organs.
Oncospheres develop into hydatid cyst. Canine carnivore consumes sheep (rarely human) host bearing hydatid cysts that rupture in small intestine releasing tapeworm heads (scolices) that attach to mucosal epithelium. Small adult tapeworms develop in canine, eggs are produced that pass in feces.

A

Echinococcosis (hydatid disease)

126
Q

What does echinococcosis look like

A

fish eggs

127
Q

Where do you find echinococcosis (hydatid disease)?

A

widespread in regions of world with sheep raising

128
Q

What parasite causes echinococcosis?

A

Echinococcus granulosus. E multilocularis

129
Q

What host do you most commonly see echinococcosis granulosus in?

A

domestic sheep> dog > sheep cycles

130
Q

Where do you most commonly see e. multilocularis?

A

in wild animals (sylvatic cycles);

in both cases, human interrupt these zoonotic cycles and serve as “dead end” hosts

131
Q

In echinococcosis, do humans harbor adult tapeworms?

What is disease due to then?

A

no

presents of larval tapeworms

132
Q

What do the clinical manifestations of echinococcosis depend upon?

A

where the unilocular hydatid cyst is growing, most commonly, liver cysts cause serious liver destruction; hydatid cysts in other organs can cause organ destruction and symptomology.

133
Q

What can rupture of a hydatid cysts (caused by Echnococosis) cause?

A

anaphylactic shock and death

134
Q

E. multicularis infections cause (blank) or (blank) cysts; moer severe tissue destruction seen in these destructions

A

multilocular or alveolar cysts

135
Q

How does your immune system respond to echinococcosis?

A

non-protective immune response, host attempts to wall of hydatid cyst

136
Q

How do you diagnose echinococcosis?

A

serologic tests are available, radiography

137
Q

How do you treat echinococcosis?

A

alendazole is marginally effecive; surgical removal is indicated

138
Q

How do you prevent and control echinococcosis?

A

avoid contact with dogs; prevent dogs from consuming offal; no vaccine

139
Q

(blank) is a parasite, such as a flea, that lives on the outside of its host.

A

ectoparasite

140
Q

What kind of parasites are ectoparasites?

A

arthropods

141
Q

Name 4 insects that are ectoparasites?

A

lice
flies (myiasis)
bedbugs
fleas

142
Q

Name 2 arachnids that are ectoparasites

A

mites

ticks

143
Q

What is the fancy name for lice and tell me the common features?

A
  1. pediculus humanus (head or body lice)- pruritis of scalp or trunk; nits seen on hair shaft
  2. phthirus pubis (pubic louse)-pruiritis in pubic area; nits seen on hair shaft
144
Q

What is the fancy name for flies and what are the common features of disease?

A

Dermatobia hominis (botfly)-> pruitic, painful, and erythematous nodule; larva may be seen emerging from nodule

145
Q

What is the fancy name for bedbugs and what are the common features of disease?

A

cimex letularius-> pruritic, erythematous wheal

146
Q

What is the fancy name for fleas and what is the common feature of the disease?

A

Ctenocephalides felis (cat flea)-> pruritic; erythematous wheal

147
Q

What is the fancy name for mites and what are the common features of disease?

A

sarcoptes scabiei (itch mite)-> pruiritic, erythematous papules, and linear tracks

148
Q

What is the fancy name for ticks and what are the common features of disease?

A

dermacentor species-> ascending paralysis

149
Q

How do you treat lice?

A

permethrin

150
Q

How does pubic lice (crabs) spread?

A

sexual intercourse

151
Q

What is this:

reaction causes skin to turn bluish-gray in color, sores in the genital area

A

crabs!

152
Q

How do you treat crabs?

A

permethrin cream

153
Q

(blank) is an ectoparasitic infestation of viable or necrotic tissues by the dipterous larvae of higher flies

A

Myiasis

154
Q

In (blank) myiasis burrowing larvae cause pustular lesions that resemble boils or furuncles

A

furuncular

155
Q

Furuncular myiasis may be treated conservatively by coaxing embedded larvae from furuncles by smothering their respiratory spiracles with occlusive coatings of (blank)

A

petrolatum (Vaseline)

156
Q

Myiasis wounds should be cleansed and débrided, (blank) should be administered, and bacterial secondary infections treated with antibiotics

A

tetanus prophylaxis

157
Q

What is the most common bedbug found in the US?

A

cimex lectularius

158
Q

What bug has an oval, brownish body?

A

bedbugs

159
Q

The main symptom of a bedbug bite is a (blank) caused by a hypersensitivity reaction to proteins in the bug saliva

A

pruritic wheal

160
Q

How do you treat a bed bug?

A

calamine lotion for itching

malation or lindane for mattresses and beds

161
Q

Scabies is an infestation by the itch or scabies mite called (blank)

A

Sarcoptes scabiei

162
Q

The human scabies mite is an (blank) parasite and completes its entire life cycle on its human hosts as females burrow intradermally to lay eggs and larvae emerge and mature to reinfest the same or new hosts

A

obligate

163
Q

TIck (blank) is a worlwide disease that is caused by ticks, but only a handful of species can cause this. It is caused by a neurotoxin secreted by the salivary glans of the arachnid/

A

paralysis

164
Q

In tick paralysis what happens?

A

The patient develops ascending symmetrical flaccid paralysis and weakness in the lower extremities.
(death may follow if you get paralysis of respiratory muscles)

165
Q

How do you treat tick paralysis?

A

removal of tick

Block 6 Week 5 (10 decks)

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