Lecture 4 Nematodes

8/12/2019 Lecture 4 Nematodes

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INTESTINAL NEMATODES

I. Ascaris lumbricoides

A. Epidemiology: Worldwide. 1 billion people infected. U.S. incidence is

highest in the southeast (warm, moist climate).

B. Mode of transmission:

Ingestion of food/water contaminated with embryonated oocysts (eggs

mature in the soil). Thousands of eggs can be laid by the worms daily; these

are passed in the feces of infected hosts.

C. Clinical manifestations: Ascariasis

1. Mostly asymptomatic. Heavy adult worm burden in the intestines may

cause malnutrition. These are the largest of the Nematodes, growing upto 25 cm or more; however, intestinal obstruction is rare.

2. Migration of larvae causes the most morbidity. Lung is the major

destination for migrating larvae. Ascaris pneumonia with fever, cough

and eosinophilia may occur with heavy larval burden.

D. Pathology:

1. Ingested eggs release larvae; larvae leave the small intestine by

penetrating the wall and escaping into the circulatory system. Larvae

travel to the lung, cross the alveoli and are coughed up and swallowed.

2. Once back in the small intestine, larvae mature into adult worms that live

in the lumen and derive nutrients from hosts digestive process. No

attachment of penetration of the adult worms occurs.


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E. Laboratory diagnosis: Microscopic examination stool sample for eggs

having the characteristic irregular surface.

F. Treatment: Mebendazole and pyrantel pamoate.

II. Trichuris trichuria: Causes whipworm infection. Humans are the definitive

hosts.

A. Epidemiology: Occurs worldwide, mainly in the tropics and subtropics.

B. Mode of transmission: Same as for Ascaris: ingestion of fecally-

contaminated soil, food, etc.

C. Clinical manifestations: Mostly asymptomatic. Rarely (with heavy

infections) whipworm may produce mild anemia, abdominal pain, diarrhea

and rectal prolapse

D. Pathology: Eggs develop into immature forms in the small intestine and

migrate to the cecum and ascending colon. Here they mature, and produce

thousands of eggs which are passed in the feces. Adult worms bury their

hairlike anterior ends into the intestinal mucosa, which may cause localized

inflammation.

E. Laboratory diagnosis: Microscopic examination of stool sample for the

presence of barrel-shaped eggs, each polar plugs.

F. Treatment: Mebendazole.

III. Enterobius vermicularis also known as pinworm


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A. Epidemiology: Worldwide distribution, especially in the temperate zones.

350 million infected worldwide. Particularly common among children and

institutionalized individuals. Can spread among family members.

B. Mode of transmission: Ingestion of eggs from fingers contaminated by

scratching, or through contact with contaminated linens or clothing.

C. Clinical manifestations: Perianal and perineal pruritis (itching) is the

most common complaint. Many cases are asymptomatic.

D. Pathology: Eggs mature in hours and remain viable for months in the

environment of infected individuals. Adult worms live in the cecum and thefemale migrates at night to the perianal area to lay eggs. This is the cause of

the major symptom, the pruritis.

E. Laboratory diagnosis: Eggs are not found in the stools, but are recovered

using the Sellotape slide or Scotch tape method from the perianal region

just after rising in the morning. A single exam is about 50% reliable.

F. Treatment: Thiabendazole. Eggs are not killed, so retreatment after 2weeks is advisable. Family members should be treated concomitantly.

Reinfection is common.

IV. Strongyloides stercoralis

A. Epidemiology: Worldwide in the tropics and subtropics; southeastern U.S.

Patients exposed to Strongyloidesin endemic regions may be affected by

severe disease produced even after many years if the patient is

immunosuppressed.

B. Mode of transmission: Direct skin contact with free-living soil larvae

(e.g. walking barefoot). Larvae penetrate the skin and migrate to the lungs.


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C. Clinical manifestations: Many cases are asymptomatic. With heavy

worm burden, symptoms include abdominal pain, diarrhea, and

malabsorption. Massive infection can occur in the immunosuppressed.

D. Pathology:

1. Larvae are passed in the feces and undergo a free-living phase. Infective

(filarial) larvae migrate to the lungs, pass through the alveoli and up the

trachea, where they are swallowed. Larvae mature into adults in the

small intestine, enter the mucosa and begin producing eggs.

2. Eggs hatch into rhabditiform larvae in the intestines and are passed in thefeces. Autoinfection is caused by rhabditiform larvae that mature

without leaving the host and penetrate the intestinal wall to migrate to

the lungs. Infection can persist for decades by autoinfection without

producing symptoms. Hyperinfection results from an autoinfection cycle

in a person whose immunity is compromised by AIDS, T-cell deficiency,

or malnutrition.

3. Direct infection cycles can be set up in which individuals in close

contact become infected with the rhabditiform larvae from the primary

host without the parasites free-living phase occurring.

E. Laboratory diagnosis: Examination of stool samples for the characteristic

rhabditiform larvae. Eosinophilia can be measured by CBC.

F. Treatment: Thiabendazole.

V. ecator americanus&Ancylostoma duodenale: Hookworms

A. Epidemiology: Worldwide in the tropics and subtropics; southeastern U.S.

. americanus(New World hookworm) andA. duodenale(Old World

hookworm)


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B. Mode of transmission: Direct skin contact with free-living soil larvae

(e.g. walking barefoot). Larvae penetrate the skin and migrate to the lungs.

C. Clinical manifestations: Many cases are asymptomatic. "Ground itch"

may occur at the site of larval penetration. Pneumonitis and intestinal

malabsorption may occur. Iron deficiency anemia may result from bleeding

from the intestinal mucosa.

D. Pathology:

1. Similar to Strongyloides, except that eggs are passed by the infected host

and the rhabditiform larvae develop into the filariform larvae as the free-living phase. Infective filarial larvae migrate to the lungs, pass through

the alveoli and up the trachea, where they are swallowed.

2. Larvae develop into adults in the small intestine, attaching to the

intestinal wall with either cutting plates (ecator) or teeth (Ancylostoma).

Adults feed on blood from the capillaries of the small intestine.

Mechanical injury to the mucosa causes additional blood loss.

E. Laboratory diagnosis: Examination of stool samples for the characteristic

thin-shelled eggs. Eosinophilia can be measured by CBC. Anemia is also

an indicator.

F. Treatment: Mebendazole.

DISEASES CAUSED BY NEMATODE LARVAE (Also Called Phasmid

Nematodes)

I. Toxocara sp.: Visceral larva migrans


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A. Epidemiology: Worldwide. Eggs from definitive hosts are found in the

soil. Children who play in dirt contaminated with animal feces are most at

risk.

B. Mode of transmission: Ingestion of eggs from contaminated soil.

C. Clinical manifestations: Mostly asymptomatic. Symptomatic infections

are associated with fever, cough, wheezing (lung symptoms), hepatomegaly,

leukocytosis and eosinophilia.

D. Pathology:

1. The definitive host for these parasites is usually a dog or cat. The adult

worm lives in the intestine of this host and eggs are passed in the feces,

similar to the human cycle with parasites like Trichuris.

2. In humans, ingested eggs release larvae which migrate through tissues

causing a host inflammatoryresponse. Granulomatousnodules are

typical when the larvae settle in the liver, small intestine, brain and retina.

Visceral larva migrans.

E. Laboratory diagnosis: Serologic testing is common. Definitive diagnosis

depends upon visualizing the larvae in tissue. Hypergammaglobulinemia and

eosinophilia.

F. Treatment: Diethylcarbamazine.

II. Ancylostoma braziliense: Cutaneous larva migrans

A. Epidemiology: Worldwide, tropical and subtropical zones. Dog and cat

hookworms. Children who play in dirt contaminated with animal feces are

most at risk.

B. Mode of transmission: Exposure of bare skin to contaminated soil.


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C. Clinical manifestations: Serpiginous, pruritic lesions of the skin on parts

of the body which have contacted the soil.

D. Pathology:

1. The definitive host for these parasites is usually a dog or cat. The adult

worm lives in the intestine of this host and eggs are passed in the feces,

similar to the human cycle with parasites likeecator americanus.

2. Infective filariform larvae penetrate the skin and migrate through tissues

causing an intense host inflammatoryresponse. Itching, redness and

swelling associated with the characteristic lesions are the hallmarks ofcutaneous larva migrans.

E. Laboratory diagnosis: Diagnosis is made on clinical observation alone.

Lesions are very characteristic and the larvae migrate so persistently (0.5 to 1

inch per day) that accurate diagnosis is certain.

F. Treatment: Thiabendazole. Deworming pet dogs and cats and avoiding

barefoot travel in infested areas are both good preventative measures.

DISEASES CAUSED BY TISSUE NEMATODES

I. Trichinella spiralis: Trichinosis

A. Epidemiology: Worldwide in many carnivores. Among domestic

animals, pigs are the most commonly infected, acquiring the infection byfeeding on rats or uncooked meat containing cysts. Infection of swine

has dropped in the U.S. due to the industrialization of pig farming (i.e.,

pigs are not feed uncooked garbage).

B. Mode of transmission: Ingestion of undercooked meat, usually

pork, containing encysted larvae.

C. Clinical manifestations: Mostly asymptomatic. About 1-2 million peoplein the U.S. are infected, but there are only about 100 symptomatic cases


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reported to the CDC per year. With heavy infection, symptoms include

fever, muscle pain, weakness, eosinophilia and periorbital edema.

Cardiac or CNS invasion may result in cardiac arrest or respiratory

paralysis.

D. Pathology: Larvae are released and mature into adult worms in the

small intestine. Eggs hatch within adult females and are released.

Larvae are distributed via the bloodstream to various organs, but encyst

only within striated muscle. Cysts remain viable for many years, but

eventually calcify. Symptomatology usually due to host inflammatory

response.

E. Laboratory diagnosis: Muscle biopsy shows larvae within striated

muscle. Serologic testing (flocculation) positive 3 weeks postinfection.

F. Treatment: Steroids plus mebendazole for extreme cases may be

therapeutic. Generally, no effective therapy. Disease can be prevented

by adequately cooking meats.

II. Anisakis species

A. Epidemiology: Worldwide; definitive host is saltwater fish. . The recent

increase in popularity of sushi (sashimi) has resulted in increased incidence of

this disease in the U.S.

B. Mode of transmission: Ingestion of inadequately cooked saltwater fish

C. Clinical manifestations: Nausea and vomiting, usually within 24 hours

after eating the contaminated fish. Gastroenteritis with blood in the stool may

be present. Severe cases may resemble appendicitis or GI cancer (chronic

form).

D. Pathology: Humans are incidental hosts. Saltwater fish and shellfish are

intermediate hosts; larvae mature into adults in the definitive hosts (marine

carnivores). Larvae penetrate the submucosa of the stomach or intestine.


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E. Laboratory diagnosis: No serology or treatment available. Surgical

removal may be necessary.

DISEASES CAUSED BY BLOOD NEMATODES

I. Wuchereria bancroftiandBrugia malayi: Filariasis

A. Epidemiology: Found in all tropical regions, (Brugia only in certain areas

of Asia). Mosquito vector varies. Over 250 million people infected

worldwide. Humans are the definitive hosts.

B. Mode of transmission: Female mosquito (esp.Anophelesand Culexsp.)

deposits infective larvae on the skin while taking a blood meal. Since the

adult worms do not multiply in humans and larvae do not multiply in

mosquitoes, disease severity depends on the number larvae-transmitting bites

an individual receives.

C. Clinical manifestations: Early infections are asymptomatic. Later, fever,

lymphangitis and cellulitis develop. Nocturnal periodicity of microfilariae

present in the blood dictates when blood samples are drawn.

D. Pathology: Larvae penetrate the skin and migrate to the lymph nodes.

When mature, adults produce microfilariae which circulate in the blood and

are ingested by mosquitoes to complete the cycle. Edema in the legs and

genitalia results from obstruction. Elephantiasis occurs in patients who have

been repeatedly infected over long periods of time.

E. Laboratory diagnosis: Thick blood smears (samples drawn at night)

reveal microfilariae. Serologic tests are not useful.

F. Treatment and Prevention: Diethylcarbamazine is only effective against

microfilariae (Ivermectin used also). No therapy for adult worms. Prevention

involves mosquito control (insecticides, repellents, netting and protective

clothing). Disfiguration caused by the edema cannot be reversed.

II. Onchocerca volvulus


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A. Epidemiology: Africa, Central, and South America. Over 40 million

people infected.

B. Mode of transmission: The bite of the blackfly transmits infective larvae

that migrate into the subcutaneous tissue. Onchocerciasis is also called river

blindness because the backflies that transmit the disease develop in rivers and

most infected individuals live near these waterways.

C. Clinical manifestations: Pruritic nodules and papules form due to the

host inflammatory response to adult worm proteins. Dermatitis, inflammatory

lesions such as keratitis, iritis and chorioretinitis and eosinophilia result.

D. Pathology: Female adult worms produce microfilariae that migrate through

the subcutaneous tissue. Fibrous nodules develop around the adult worms,

especially over the iliac crests. Microfilariae concentrate in the eyes, causing

lesions that can lead to blindness. Some lymphatic obstruction has been

documented, esp. in Africa. Elephantiasis results.

E. Laboratory diagnosis: No serology or blood smears done, since filariae

are never blood-borne. Biopsy of affected skin reveals microfilariae.

F. Treatment and Prevention: Ivermectin is effective against microfilariae.

No therapy for adult worms. Prevention involves vector control (insecticides,

repellents, netting and protective clothing). Ivermectin is preventative as well.

III. Loa loa

A. Epidemiology: West and Central Africa; Congo and Niger river basins.

B. Mode of transmission: The bite of the deerfly or mangofly (Chrysopssp.)

transmits infective larvae that migrate into the subcutaneous tissue.


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C. Clinical manifestations: There is no host inflammatory response to the

microfilariae or adults. Transient localized, nonerythematous, nodules

(Calabar swellings) form due to host hypersensitivity reaction. Adult worms

observed migrating across the conjunctiva is the most dramatic finding.

D. Pathology: Female adult worms migrate through the subcutaneous tissue

producing microfilariae. Calabar swellings develop around the adult worms.

Microfilariae do not appear in the blood until years after the adult worms

appear in some cases. (Maturation time~1 year; lifespan 1-15 years).

E. Laboratory diagnosis: Blood smears from samples collected during the

day demonstrate microfilariae. Occasionally biopsy of swellings can recover

adults.

F. Treatment and Prevention: Ethylcarbamazine eliminates microfilariae and

may kill adults. Ivermectin is effective against microfilariae. Prevention

involves vector control (insecticides, repellents, netting and protective

clothing).

IV. Dracunculus medinensis

A. Epidemiology: Tropical regions, especially Africa, the Middle East and

India. Most problematic in regions where the same source of water is used for

bathing and drinking. Tens of millions people are infected.

B. Mode of transmission: Ingestion of contaminated drinking water.

Crustaceans (copepods) containing infective larvae are swallowed. Humansare the definitive hosts.

C. Clinical manifestations: Causes Guinea Worm Disease.

D. Pathology: Larvae contained within swallowed crustaceans are released,

penetrating stomach and small intestine and migrate into the body, where they

develop into adults. After maturation and copulation, males die and females

migrate to the subcutaneous regions. Females up to a meter long cause theskin to ulcerate due to host inflammatory response. Adult worms produce a


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substance that causes blistering and ulceration of the skin, usually of the lower

extremities. Motile larvae are released into fresh water when infected hosts

bathe or seek the comfort of soaking in water. Infectios larval forms develop

in the crustacean host to complete the cycle.

E. Laboratory diagnosis: Characteristic presentation of the ulcerated papule.

The head of the worm can sometimes be found within the skin ulcer.

F. Treatment and Prevention: Metronidazole or niridazole aids in making the

worm easier to extract, but does not eradicate the worms. Adult worms can be

physically removed by winding onto a stick. Disease can be prevented by

boiling or filtering drinking water.

Lecture 4 Nematodes

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