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ID Week 5 > ICL 3.3: Nematodes > Flashcards

ICL 3.3: Nematodes Flashcards

1
Q

what’s the common name for nematodes?

A

roundworms

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2
Q

what are the two groups of nematodes?

A
  1. intestinal nematodes

2. tissue nematodes

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3
Q

what are intestinal nematodes?

A

adults live in GI tract, maturing usually in small intestine or colon

some species get to intestine after larval migration via internal organs (e.g. lung)

usually direct infection by eggs or larvae

almost all have direct life cycle needing humans

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4
Q

what are tissue nematodes?

A

adults live in lymphatics or in subcutaneous tissues – release larvae

arthropod vectors needed for transmission of infection (i.e. indirect life cycle with human as definitive host)

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5
Q

which nematodes are transmitted by ingestion and cause intestinal infection?

A
  1. A. lumbriocoides
  2. E. vermicularis
  3. T. trichiura
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6
Q

which nematodes are transmitted by ingestion and cause tissue infection?

A
  1. T. spiralis

2. D. medinensis

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7
Q

which nematodes are transmitted by contact and cause intestinal infection?

A
  1. S. stercoralis
  2. A. duodenale
  3. N. americanus
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8
Q

which nematodes are transmitted by bite and cause tissue infection?

A
  1. O. volvulus

2. W. bancrofti

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9
Q

which nematodes are transmitted by ingestion and cause tissue infection in the wrong host?

A
  1. toxocara cani
  2. toxocara cati
  3. anisakis simplex
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10
Q

which nematodes are transmitted by contact and cause tissue infection in the wrong host?

A
  1. A. caninum

2. A. braziliensis

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11
Q

what’s the common name for enterobius vermicularis?

A

pinworm

transmitted by ingestion –? intestinal infection

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12
Q

what is the life cycle of enterobius vermicularis?

A
  • direct life cycle
    1. eggs on perianal folds; larvae inside the eggs mature within 4-6 hours
    2. embryonated eggs are ingested by humans
    3. larvae hatch in small intestine
    4. adults in lumen of colon
    5. gravid female migrates to perianal region at night to lay eggs
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13
Q

what age group is often infected with enterobius vermicularis?

A

children

it’s found

infections more frequent in school- or preschool-children and in crowded conditions

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14
Q

where in the world are enterobius vermicularis infections more common?

A

worldwide

enterobiasis appears to be more common in temperate than tropical countries

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15
Q

what is the most common helminthic infection in the united states?

A

enterobius vermicularis

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16
Q

what are the symptoms of enterobius vermicularis infection?

A

enterobiasis is frequently asymptomatic

perianal pruritus (itch), especially at night

this may lead to excoriations and bacterial superinfection

includes anorexia, irritability, and abdominal pain

occasionally, there’s invasion of the female genital tract with vulvovaginitis

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17
Q

how do diagnose enterobius vermicularis infection?

A

eggs on anal skin

you can detect them using clear sticky tape = scotch tape test

sometimes the worms are also seen in feces –> look like a grain of rice with a clear outer membrane and then speckled inside

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18
Q

how do you treat enterobius vermicularis infection?

A

pyrantel pamoate

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19
Q

what’s the common name for trichuris trichiura?

A

whipworm

they literally look like a whip

transmitted by ingestion –> intestinal infection

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20
Q

where are trichuris trichiura found in the body?

A

they live in the cecum and ascending colon

the adult worms are FIXED in that location

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21
Q

how long does it take for trichuris trichiura to become infectious?

A

eggs take ~3-4 weeks to become infectious (embryonate)

best in warm conditions and sandy soils

females survive 1-2 years

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22
Q

how do you get a trichuris trichiura infection?

A

by ingesting embryonated eggs

it takes eggs 3-4 weeks to become infectious/embryonate

you also often be co-infected with hookworm and Ascaris

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23
Q

what’s the life cycle of trichuris trichiura?

A
  1. unembryonated eggs passed in feces
  2. 2-cell stage
  3. advanced cleavage
  4. embryonated eggs are ingested by humans
  5. larvae hatch in small intestine
  6. adults in cecum
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24
Q

where in the world are trichuris trichiura found?

A

worldwide

infections more frequent in areas with tropical weather and poor sanitation practices, and among children

trichuriasis occurs in the southern United States.

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25
Q

what are the symptoms of trichuris trichiura infection?

A

usually asymptomatic

heavy infections like in children often cause GI problems like abdominal pain, diarrhea, or rectal prolapse and possible growth retardation

you may also see anemia, bloody diarrhea, with profuse mucus, stunting of growth, or abdominal pain with tenesmus

rectal prolapse = part of the rectum protrudes from the anus (so gross, looks like a cupcake on someones anus)

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26
Q

how do you diagnose trichuris trichiura infection?

A

microscopic identification of whipworm eggs in feces is evidence of infection

footbal-shaped eggs that have a pair of polar “plugs” at each end

kinda looks like a double sided nipple

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27
Q

how do you treat trichuris trichiura infection?

A

mebendazole

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28
Q

what is the largest nematode parasitizing the human intestine?

A

ascaris lumbricoides

transmitted by ingestion –> intestinal infection

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29
Q

what type of life cycle does ascaris lumbricoides have?

A

direct life cycle

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30
Q

how long does it take ascaris lumbricoids to become infectious?

A

eggs released in feces require 2-4 week incubation in soil to become infective (embryonated eggs)

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31
Q

what is the pathogenesis of ascaris lumbricoides?

A

eggs released in feces require 2-4 week incubation in soil to become infective (embryonated eggs)

larvae hatch in small intestine (pH bile) and enter lamina propria and mesenteric capillaries

they then migrate via liver, heart to lung

in the lungs they enter alveoli, molt and then migrate up bronchioles, bronchi and trachea to epiglottis and then swallowed

after entry to small intestine, larvae mature into adults; mating occurs with 6 weeks

adults feed on digested food in intestine

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32
Q

what’s the life cycle of ascaris lumbricoides?

A
  1. adults mate in the small intestines and release eggs in feces
  2. eggs released in feces require 2-4 week incubation in soil to become infective (embryonated eggs)

unfertilized eggs will not undergo biological development

  1. embryonated egg is consumed by human
  2. larvae hatch in small intestine
  3. larvae enter lamina propria and mesenteric capillaries

they then migrate via liver, heart to lung

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33
Q

what happens when the ascaris lumbricoides larvae reach the lungs?

A

larval migration and molt in lung induces Ig (IgE and IgG) antibody and eosinophilia

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34
Q

where is ascaris lumbricoides found in the world?

A

worldwide

highest prevalence in tropical and subtropical regions, and areas with inadequate sanitation

occurs in rural areas of the southeastern United States

it’s the most common human helminthic infection

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35
Q

what are the symptoms of ascaris lumbricoides infection?

A
  1. large number of larval migration can cause pneumonitis & liver enlargement
  2. adult worms are rarely problem but if there’s alot of them they can cause intestinal blockage
  3. eosinophilia

aberrant migration can also occur to the bile duct, liver or penetrate the intestinal wall and cause peritonitis

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36
Q

how do you diagnose ascaris lumbricoides?

A

eggs are characteristic

they’re rounded and have a thick shell with an external mammillated layer

looks like an avocado with a giant pit = unfertilized

fertilized still looks like an avocado but the pit looks like an 8

occasionally the whole worm is expelled…

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37
Q

how do you treat ascaris lumbricoides?

A

there’s no effective drug to treat larval migration

but for the adults you can use mebendazole or albendazole

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38
Q

how is trichinella spiralis transmitted and what kind of infection does it cause?

A

transmitted by ingestion and causes tissue infection

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39
Q

how do you get a trichinella spiralis infection?

A

infection after ingestion of larvae in meat

in most environments it’s kept in circulation by rodents being eaten by carnivores

otherwise, adults are small and have a short life (7 days)

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40
Q

what are the definitive hosts of trichinella spiralis?

A
  1. pigs
  2. rodents
  3. humans
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41
Q

what is the life cycle of trichinella spiralis?

A
  1. encysted larva in striated muscle is ingested by animals or humans
  2. larva are released in small intestine
  3. adults mate in small intestine
  4. larva are deposited in mucasa
  5. larva enter circulation and encysted larva enter striated muscle
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42
Q

where in the world do you find trichinella spiralis?

A

most common in parts of Europe and the United States

now incidence is rare since original main source (pork) subject to many regulations and main source now is wild animals

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43
Q

what are the symptoms of a trichinella spiralis infection/

A

1st week = intestinal symptoms like NVD

2nd week = extraintestinal like:

  1. muscle invasion = myalgia, weakness, malaise
  2. petechiae from invasion of other organs
  3. myocarditis; uncommon but potentially fatal
  4. CNS invasion = fits, paralysis, coma, etc.

3rd week = larvae begin to encyst

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44
Q

when do you see eosinophilia during a trichinella spiralis infection?

A

starts during 2nd week

peaks during 3rd week

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45
Q

how do you diagnose a trichinella spiralis infection?

A
  1. specific diagnostic tests = EIA
  2. muscle biopsy, microscopy
  3. based on clinical symptoms like myositis and eosinophilia

myositis = inflammation of the muscles that you use to move your body

diet should also raise suspicion = wild boar, polar bear, walrus, cougar, fox, non-commercial home raised pork

46
Q

how do you treat trichinella spiralis infection?

A

Treatment should begin ASAP with steroids which are used for infections with severe symptoms, plus mebendazole and albendazole

the decision to treat is based on symptoms, exposure to raw or undercooked meat, lab test results

47
Q

how do you prevent trichinella spiralis infection?

A

proper cooking of meat

deep freezing meat

48
Q

what’s the common name for dracunculus medinensis?

A

guinea worm

transmitted by ingestion and causes tissue infection

it’s a deep tissue nematode

49
Q

which groups are at risk for dracunculus medinensis?

A

Anyone who drinks standing pond water contaminated by persons with Dracunculiasis is at risk for infection

people who live in villages where the infection is common are at greatest risk

50
Q

what’s the life cycle of dracunculiasis medinensis?

A
  1. humans drink unfiltered water containing copepods with L3 larvae (definitive host)
  2. larvae are released when copepods die – larvae penetrate the host’s stomach and intestinal wall; they mature and reproduce
  3. fertilized female worm migrates to surface of skin, causes a blister and discharges larvae
  4. female worm begins to emerge from skin one year after infection; L1 larvae released into water from the emerging female worm
  5. L1 larvae consumed by a copepod
  6. larvae undergoes two molts in the copepod and becomes an L3 larvae
51
Q

what is the geographic distribution of drunculiasis medinensis?

A

an ongoing eradication campaign has dramatically reduced the incidence of dracunculiasis, which is now restricted to rural, isolated areas in a narrow belt of African countries

that’s what those fancy straws are for!

52
Q

how do you diagnose drunculiasis medinensis?

A

1st you’ll see a painful blister

2nd you’ll see a worm emerging from the blister as a white filament 1-3 weeks later

the clinical manifestations are localized but incapacitating.

53
Q

how do you treat drunculiasis medinensis?

A
  1. local cleansing of the lesion and local application of antibiotics, if indicated because of bacterial superinfection
  2. mechanical, progressive extraction of the worm over a period of several days

no curative antihelminthic treatment is available

54
Q

which helminth species are hookworms?

A
  1. ancylostoma duodenale
  2. necator americanus

transmitted by contact and cause intestinal infection

55
Q

which helminth species are threadworms?

A

Strongiloides stercoralis

transmitted by contact and cause intestinal infection

56
Q

what is the pathology of hookworms?

A

dggs hatch within 2 days on warm sandy soil

filariform larvae climb on vegetation (grass, etc)

on contact with bare skin, filariform larvae PENETRATE skin, usually entering via hair follicle -> enter capillaries

they then migrate via lung, bronchi and trachea to epiglottis and are swallowed (~ to Ascaris)

adults (~1 cm) in small intestine live 4-5 years

57
Q

what is the life cycle of an intestinal hookworm?

A
  1. eggs in feces
  2. rhabditiform larva hatches
  3. filariform larva
  4. filariform larva penetrates skin –> blood vessels to the heart and then to the lungs where they ascend the bronchial tree to the pharynx and are swallowed
  5. adults in small intestine
58
Q

where are hookworms found in the world?

A

worldwide

mostly in areas with moist, warm climate

necator americanus predominates in the Americas and Australia, while only Ancylostoma duodenale is found in the Middle East, Africa

59
Q

what are the phases of a hookworm infection?

A
  1. cutaneous phase
  2. pumonary phase
  3. intestinal phase
60
Q

what is the cutaneous phase of a hookworm infection?

A

aka invasive phase

hookworm penetrates the skine = irritation and itching

“ground itch”

61
Q

what is the pulmonary phase of a hookworm infection?

A

during the period when the larvae are bursting out of capillaries in the lungs into alveolar spaces

there’s local hemorrhage but it’s rarely symptomatic except if heavy infection which could then cause pneumonitis and eosinophilia, cardiac complication, GI and neutrional/metabolic symptoms

62
Q

what is the intestinal phase of a hookworm infection?

A

adult worms usually restricted to the anterior third of the small intestine, but where infections are very heavy they can occupy the whole length of the small intestine

63
Q

what’s the most common symptom of a hookworm infection?

A

iron deficiency anemia

it’s caused by blood loss at the site of intestinal attachment of the adult worms

this can be accompanied by eosinophilia and low ferritin as well as elevated serum transferrin

64
Q

how do you diagnose a hookworm infection?

A

Microscopic identification of eggs in the stool is the most common method for diagnosing hookworm infection

egg looks like a blunty (segmented) ovoid egg with transparent shell

it’s RARE to see larvae

in the migratory phase you’ll see eosinophilia

65
Q

how do you prevent hookworm infection?

A
  1. good sanitation; avoid feces on soil

2. wear shoes

66
Q

how do you treat hookworm infections?

A

if it’s a light infection or in an endemic area it’s often ot treated

in the US use albendazole

67
Q

what’s the common name for strongiloides stercoralis?

A

threadworm

68
Q

what are the reservoires for strongiloides stercoralis?

A

humans, monkey s, dogs

69
Q

how are threadworms different from hookworms?

A

threadworms:

  1. have non-human reservoir hosts (monkey, dogs)
  2. eggs hatch in the intestine and before they are passed into the feces
  3. larvae can mature into filariforms in the intestine and cause autoinfection
  4. a free-living, non-parasitic cycle outside the host can exist
  5. rhabditiform larvae in feces (diagnostic)
70
Q

how are threadworms transmitted?

A

contact

filariform larvae penetrate the human host skin to initiate the parasitic cycle (~ to hookworm).

71
Q

what’s the life cycle of strongiloides stercoralis?

A

direct life cycle

  1. rhabditiform larvae in the intestine are excreted in stool
  2. development into free living adult worms
  3. eggs are produced by fertilized female worms
  4. rhabditiform larvae hatch from embryonated eggs
  5. the rhabditiform larvae develop into infective filariform
  6. infective filariform larvae penetrate the intact skin initiated the infection
  7. the filariform larvae enter the circulatory system, are transported to the lungs and penetrate the alveolar spces. they are carried to the trachea and pharynx, swallowed and reach the small intestine where they become adults
  8. adult female worm in the intestine
  9. eggs deposited in intestinal mucosa, hatch and migrate to lumen
  10. autoinfection: rhabditiform larvae in large intestine, become filariform larvae, penetrate intestinal mucosa or perianal skin and follow the normal infective cycle
72
Q

where in the world is strongiloides stercoralis?

A

Tropical and subtropical areas, but cases also occur in temperate areas (including the South of the United States)

more frequently found in rural areas, institutional settings, and lower socioeconomic groups

73
Q

what are the symptoms of strongiloides stercoralis infection?

A

frequently asymptomatic

  1. GI symptoms = abdominal pain and diarrhea
  2. pulmonary symptoms = pulmonary eosinophilia during pulmonary migration of the filariform larvae
  3. dermatologic manifestations: urticarial rashes on buttocks and waist areas.
  4. disseminated strongyloidiasis occurs in immunosuppressed patients = abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia -> potentially fatal
74
Q

how do you diagnose strongiloides stercoralis infection?

A
  1. microscopic identification of larvae: Rhabditiform larvae in feces / duodenal fluid. (relatively insensitive)
  2. hyperinfection: sputum smears are recommended in disseminated autoinfection
  3. antibody test = ELISA, IFA

consider possibility if no other explanation for long-term eosinophilia exists.

75
Q

how do you treat strongiloides stercoralis infection?

A

ivermectin

patients at risk for disseminated strongyloidiasis should be treated

76
Q

which nematodes cause filariasis?

A
  1. wuchereria bancrofti
  2. onchocerca volvulus

both transmitted by bite and cause tissue infection

77
Q

what disease does wuchereria bancrofti cause?

A

lymphatic filariasis/elephantiasis

78
Q

which disease does onchocerca volvulus cause?

A

river blindness

79
Q

what is the vector for lymphatic filariasis/elephantiasis?

A

caused by wuchereria bancrofti

vector = intermediate host = mosquito

adults grow to large size within humans and release microscopic larvae that are transmitted by arthropod vectors

80
Q

what is the vector for river blindness?

A

caused by onchocerca volvulus

vector = intermediate host = black fly

adults grow to large size within humans and release microscopic larvae that are transmitted by arthropod vectors

81
Q

which is the vector for loiasis?

A

aka african eye worm caused by filariasis

vector = intermediate host = tabanid fly

adults grow to large size within humans and release microscopic larvae that are transmitted by arthropod vectors

82
Q

what’s the impact of lymphatic filariasis?

A

25,000,000 men have genital elephantitis disease

15,000,000 people have lymphoedema = elephantiasis of the leg/limb

treatment can slow or stop disease progression but lymphatics may have permanent damage

major employment discrimination

83
Q

what’s the life cycle of wuchereria bancrofti?

A
  1. moquito m takes blood meal –> L3 larvae enter skin of human (definitive host)
  2. adults in lymphatics
  3. adults produce sheathed microfilariae that migrate into lymph and blood channels
  4. mosquito takes a blood meal and ingest microfilariae
  5. microfilariae shed sheaths, penetrate mosquito’s midgut, and migrate to throracic muscles
  6. L1 larvae
  7. L3 larvae
  8. migrate to head and mosquito’s proboscis
84
Q

what is the pathology of wuchereria bancrofti?

A

there’s a long time where it’s just asymptomatic

but there are recurring attacks of lymphangitis and “filarial fever” over a period of years

this leads to lymphatic blockage and lymphedema

= super swollen arms, legs, testicles, etc.

85
Q

where is wuchereria bancrofti found?

A

Among the agents of lymphatic filariasis, Wuchereria bancrofti is encountered in tropical areas worldwide

lymphatic filariasis is found throughout the tropics and subtropics

86
Q

what are the symptoms of wuchereria bancrofti?

A
  1. acute manifestions of lymphatic filariasis = adenolymphagitis and episodic attacks of fever, inflammation inguinal lymph nodes, testis, spermatic cord, lymphedema.
  2. Hydrocele (scrotum swelling): most common manifestation in males in endemic areas. Individuals who are chronically infected -> Chyluria (“milky” urine due to lymphatic fluid)
  3. repeated episodes of inflammation and lymphedema lead to lymphatic damage, chronic swelling, and elephantiasis of the legs, arms, scrotum, vulva, and breasts
  4. tropical pulmonary eosinophilia (TPE) = scattered wheezes and crackles are heard
  5. lymphadenopathy and hepatomegaly may be present
87
Q

how do you diagnose wuchereria bancrofti?

A

1.demonstrate microfilariae in the peripheral blood –> but they appear periodically (timing of sample collection is critical)

microfilariae may be absent in adenolymphangitis or in late chronic lymphatic disease

  1. detection of filarial antigen in blood; with or without microfilariae is still considered diagnostic
  2. urine examination and microscopy: should be examined macroscopically for chyluria, then concentrated (microfilariae)
  3. CBC count: eosinophilia is marked
  4. serum immunoglobulin concentrations: elevated serum immunoglobulin E and immunoglobulin G4 may be observed with active filarial disease
  5. recently, PCR testing has been described
88
Q

what’s the easiest method for wuchereria bancrofti diagnosis?

A

blood smear or most easy method now for detecting Wuchereria is via antigen in blood

can be done at any time of day/night

89
Q

how do you treat wuchereria bancrofti?

A

asymptomatic microfilaremia -> oral Ivermectin and also Diethylcarbamazine (DEC) therapy

inpatient care for adenolymphangitis (ADL) and chronic filariasis -> Antihistamines, corticosteroids (reduce swelling), pain relief, and intravenous antibiotics for secondary infections

bed rest, limb elevation, and compression bandages (chronic lymphedema)

for large hydroceles and scrotal elephantiasis do surgical excision

however, correction of gross limb elephantiasis is less successful and may require multiple procedures and skin grafting

90
Q

which parasite causes river blindness?

A

onchocerca volvulus

transmitted by bite and causes tissue infection

onchocerciasis is the second-leading infectious cause of blindness in the world

it affects subcutaneous nodules -> intensely pruritic

91
Q

how is onchocerca volvulus transmitted?

A

larvae transmitted by bites from Simulium blackflies that live on rocks with fast moving water

92
Q

where in the world is onchocerca volvulus found?

A

Occurs mainly in Africa, in Central and South America and the Middle East

93
Q

what’s the life cycle of onchocerca volvulus?

A
  1. blackfly takes blood meal and L3 larvae enter bite wound in human (definitive host)
  2. subcutaneous tissues
  3. adults in subcutaneous nodule
  4. adults produce unsheathed microfilariae that typically are foundin skin and in lymphatics of connective tissues, but also occasionally in peripheral blood, urine and sputum
  5. blackfly takes a blood meal and ingests microfilariae from human
  6. microfilariae penetrate blackfly’s midgut to throacic muscles
  7. L1 larvae
  8. L3 larvae
  9. migrate to head and blackfly’s proboscis
94
Q

what are the symptoms of onchocerca volvulus infection?

A

microfilariae live 1-2 years -> die in skin or eyes = inflammation

adult O. volvulus live 10-15 years in nodules

aymptoms appear between 9 months and 2 years

once developed, adult worms cluster in subcutaneous nodules = onchocercomata

generalized pruritus may occur early in the infection and may be severe

onchodermatitis may be present

itchy eyes, redness, or photophobia may be early symptoms of ocular onchocerciasis –> over the years, scarring progresses and you’ll have visual loss and eventually blindless

skin examination -> subcutaneous nodules, diffuse onchodermatitis, lymphedema, leopard skin of the shins (white patches)

skin atrophy may cause drooping of the inguinal skin, termed hanging groin

in the eye, the inflammatory response to dying microfilariae -> punctuate keratitis = red pupils (snowflake opacities)

95
Q

how do you diagnose onchocerca volvulus infection?

A
  1. pathological diagnosis = microfilariae in a skin-snip biopsy sample and direct examination of excized nodules
  2. immunodiagnosis = antibody detection, antigen detection
  3. PCR = uncommon
  4. DEC patch test
96
Q

what is the DEC patch test?

A

Diethylcarbamazine (DEC) patch test

topical application of DEC (DEC patch) elicits localized cutaneous reactions (pruritus, maculopapular eruptions, dermal edema) in response to dying microfilaria.

based on the principle of Mazzotti reaction

used to diagnose onchocerca volvulus

97
Q

how do you treat onchocerca volvulus?

A
  1. Ivermectin (rIVERmectin) -> long treatment

dying microfilaria-> pruritus and adenopathy (Mazzotti reaction), ocular inflammation -> angioedema = corticoides + ivermectin

ivermectin -> little effect on adult worms-> reduces burden of microfilaria and risk of complications (does not cure)

  1. targeting endosymbiotic bacteria Wolbachia = new approach in the control of onchocerciasis-> Doxycycline
  2. nodulectomy can result in cure only if excision eliminates all adult worms (not practical in patients with multiple nodules or in patients in whom nodules are not clinically evident).
98
Q

what is the common name for anisakiasis?

A

larvae wander

transmitted by ingestion and infects tissue in the wrong host!!

99
Q

how do you get anisakiasis?

A

consumption of infected raw or undercooked fish with larvae

100
Q

how does anisakiasis infect a human?

A

consumption of infected raw or undercooked fish with larvae

larvae penetrate the gastric and intestinal mucosa

within hours violent abdominal pain, nausea, and vomiting may occur

if the larvae pass into the bowel severe eosinophilic granulomatous response may also occur 1-2 weeks following infection -> symptoms mimicking Crohn’s disease

101
Q

how do you diagnose anisakiasis?

A

gastroscopic examination and biopsy

102
Q

how do you treat anisakiasis?

A

surgical or endoscopic removal

103
Q

what are the two parasites that cause toxocariasis?

A
  1. toxocara cani
  2. toxocara cati

transmitted by ingestion and cause tissue infection in the wrong host!

104
Q

what is the life cycle of the parasites that cause toxocariasis?

A
  1. eggs passed in feces of dog/cat
  2. eggs become embryonated egg with larva
  3. dog ingests embryonated egg
  4. adults in lumen of intestine
  5. transplacental or transmammary to baby puppy

the other option is the embryonated egg with larva is ingested by a buny = intermediate host

then the dog eats the bunny

or the human can accidentally ingest the eggs or the intermediate host (bunny)

then the eggs will hatch and larvae penetrate the gut wall and migrate into various tissues where they encyst

105
Q

what are the symptoms of toxocariasis?

A

asymptomatic (only eosinophilia and positive serology)

the main clinical presentations = visceral larva migrans (VLM)

these cause episodes of fever, coughing and wheezing, anemia, eosinophilia, hepatomegaly, and positive toxocara titers; symptoms depend of tissue affected

ocular larva migrans is uncommon

106
Q

how do you diagnose toxocariasis?

A

serology or finding the larvae in biopsy specimens

107
Q

how do you treat toxocariasis?

A

VLM = albendazole + antiinflammatory medications

108
Q

which parasites cause cutaneous larva migrans?

A
    • Ancylostoma caninum (Dog hookworm)
    • Ancylostoma braziliense (Dog+Cat hookworm)

they’re both transmitted by contact and cause tissue infection in the wrong host!

109
Q

what’s the life cycle of A. braziliense and A. caninum?

A

incomplete cycle

  1. eggs in feces of dog/cat
  2. rhabditiform larva hatches
  3. rhabditiform larva develops into filariform larva in the environment
  4. cat/dog ingest rhabditiform larvae
  5. adults in small intestines

OR

rhabditiform larvae can penetrate the skin of humans accidentally and migrate aimlessly

the most common manifestation of this is cutaneous larva migrans = ground itch

110
Q

how do you treat A.braziliense / A. caninum

infections?

A

usually self limiting

if severe infection-> albendazole, ivermectin and surgical removal of the parasite.

111
Q

is A.braziliense / A. caninum

infection of humans a complete or incomplete cycle?

A

incomplete

no adults are formed once inside humans!!

112
Q

what reaction do humans have to A.braziliense / A. caninum

infection?

A

larvae wander in tissues

absence of sensing correct signals for migration-> Intense inflammation and irritation-> death

intensely pruritic serpiginous track in upper dermis

ID Week 5 (13 decks)

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