Intestinal Parasite Infections From Roundworms -- Description, Diagnosis, Treatm

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Intestinal Parasite Infections From Roundworms -- Description,

Diagnosis, Treatment

 

With over 500,000 species, nematodes constitute the second largest

class in the animal kingdom. Nematodes are elongated, cylindrical,

non-segmented worms with rounded anterior and pointed posterior ends.

The species commonly infecting humans include the Ancylostoma

duodenale and Necator americanus (hookworms), Ascaris lumbricoides,

Anisakis marina, Capillaria philippinensis, Enterobius vermicularis

(pinworm), Strongyloides stercoralis, and Trichuris trichiura (whip worm).

HOOKWORMS

 

A. duodenale (Old World hookworm) and N. americanus (New World

hookworm) affect approximately one quarter of the world's population.

Both species have a worldwide distribution. A. duodenale is most

common in areas bordering the Mediterranean Sea, southeast Asia,

India, Australia, and Oceania. N. americanus is most common in the

southern United States, Central and South America, Africa, southeast

Asia, and the South Pacific.

 

Hookworm larvae inhabit moist, shady soil. Infection generally occurs

in areas where human feces are used as fertilizer. Barefoot children

and agricultural workers are at highest risk of hookworm infection.

Although N. americanus is acquired exclusively by skin penetration, A.

duodenale may be acquired percutaneously, orally, and in a

transmammary fashion.

 

Life cycle. The life cycles of both worms are identical. Humans are

infected when filariform larvae inhabiting contaminated soil penetrate

the skin and pass through the venous system to the lungs. Larvae

migrate from the lungs up through the trachea and into the esophagus

where they are swallowed and enter the stomach and small intestine. In

the upper small intestine, particularly the jejunum, the young worms

attach to the intestinal wall and mature, copulate, and produce eggs.

The female worm produces 10,000 to 20,000 eggs per day. The eggs are

passed in the feces to warm, moist soil where they rapidly develop and

hatch in 1 to 2 days. The newly hatched rhabditiform larvae feed on

bacteria in the soil and become infectious filariform larvae in 7 to

10 days.

 

Clinical manifestations. The clinical manifestations of hookworm

infection are related to the life cycle of the worm. Initial skin

penetration causes a localized pruritic rash accompanied by

papulovesicular eruptions. This symptom complex is called " ground

itch " and is more common in N. americanus infection. As larvae pass

through the lungs, bronchitis or pneumonitis may occur.

 

Abdominal pain, nausea, vomiting, pica, and anorexia can occur when

worms enter the intestinal tract. Diarrhea with mucus and blood may

occur, while some patients may complain of constipation. The hallmark

of hookworm infection is iron deficiency anemia. This occurs as worms

attach to the intestinal mucosa and engorge with blood, as well as

through continued seepage of blood from previous attachment sites.

Daily blood loss secondary to N. americanus is estimated to be 0.03

mL/d per worm, and that of A. duodenale is estimated to be 0.15 mL/d

per worm. Chronic fatigue, weakness, lassitude, and depression often

develop as a consequence of anemia. More severe complications of the

anemia include cardiomyopathy, tachycardia, and failure to thrive. The

anemia of hookworm infection is distinctly uncommon in the United

States, but is common in third world countries. A protein-losing

enteropathy leading to hypoalbuminemia and facial and pedal edema

occurs although the pathogenesis remains controversial.

 

Diagnosis, treatment, and prevention. The diagnosis of hookworm

infection is based on the identification of eggs in the stool.

Hookworm eggs are ovoid with bluntly rounded ends and possess a

colorless, thin hyaline shell. It is difficult and impractical to

attempt to differentiate the eggs of the two hookworm species

microscopically, as they appear identical, and treatment for both

species is the same.

 

The drug of choice for hookworm infection is mebendazole, 100 mg BID

for 3 days. The adult and pediatric doses of mebendazole are the same.

Pyrantel pamoate at a dosage of 11 mg/kg (maximum 1 g) for 3 days or a

single 400-mg dose of albendazole is also effective.

 

Oral iron therapy should be given to all patients with iron deficiency

anemia, and a diet rich in protein and iron should be recommended to

all patients. Pregnant women with hookworm infection and iron

deficiency anemia should be initially treated with iron replacement,

and anthelminthic therapy should be reserved for after delivery.

 

Prevention of hookworm infection can be achieved through improvement

in methods of rural sanitation and personal hygiene. Educating the

public to the importance of using latrines and wearing proper footwear

is vital to the control of this parasite.

A. MARINA

 

Anisakiasis, or herringworm disease, was first identified in 1966.

Although the majority of cases have been reported in Japan, Holland,

and the Pacific coast of South America, anisakiasis has a worldwide

distribution. Infection with this nematode must be considered wherever

raw fish is consumed. The popularity of sushi restaurants in the

United States and Japan, herring in Holland, and ceviche in South

America has increased public awareness of this condition.

 

Life cycle. The life cycle of A. marina is not completely known. The

adult worm inhabits the intestinal tracts of marine mammals and birds.

Eggs are passed in the host feces and the larvae hatch in the sea. The

larvae are taken up by various crustaceans and develop into an

infective stage. The crustaceans enter the food chain and are eaten by

fish. When an infected fish is eaten by a human, larvae burrow inside

the human stomach or intestine.

 

Clinical manifestations. Anisakiasis may cause colicky abdominal pain,

nausea, vomiting, and fever. Occasionally, pain may be so severe as to

mimic peritonitis or appendicitis and lead to surgical intervention.

A. marina is an invasive organism and may cause ulceration, abscess,

eosinophilic granuloma, or intestinal perforation. These symptoms may

be mistaken for Crohn's disease.

 

Diagnosis, treatment, and prevention. The diagnosis of anisakiasis is

difficult to make and should be considered whenever abdominal symptoms

follow ingestion of raw saltwater fish. The diagnosis is usually made

at the time of laparoscopy or endoscopy. Occasionally, the patient

will present vomiting worms.

 

There is no proven therapy for anisakiasis. If the diagnosis is made

prior to surgical intervention, treatment with thiabendazole can be

tried. Anisakiasis can be prevented with proper handling of saltwater

fish. Fish should be cooked for at least 10 minutes at 60°C or frozen

to –20°C for 60 hours.

C. PHILIPPINENSIS

 

Intestinal capillariasis caused by C. philippinensis, a nematode

related to T. trichiura, was first described in the northern

Philippines in the 1960s. Since this initial report, more than 1000

cases occurring in the Philippines, Thailand, Japan, Korea, Indonesia,

Taiwan, Iran, Egypt, Spain, and Colombia have been reported.

 

Life cycle. The life cycle of C. philippinensis includes fish as

intermediate hosts and fish-eating birds as probable hosts.

Fish-eating birds ingest fish infected with larvae, and the larvae

become adults in the bird's GI tract. Eggs pass from the bird's feces

into freshwater, where they embryonate. Embryonated eggs are ingested

by freshwater fish and develop into larvae in the fish intestine.

Humans acquire the infection by eating raw, small, freshwater fish,

crustaceans, or snails. Adult worms inhabit the small intestine,

predominantly the jejunum.

 

Clinical manifestations. The most common presenting symptoms are

anorexia, nausea, vomiting, diarrhea, borborygmus, and abdominal pain.

Chronic infection can lead to severe malabsorption with an

accompanying protein-losing enteropathy, electrolyte abnormalities,

steatorrhea, and edema. Untreated infection has a mortality rate of

about 10%.

 

Diagnosis, treatment, and prevention. Diagnosis is based on the

identification of eggs in the feces of a symptomatic patient.

Asymptomatic infection and autoinfection can occur. The treatment of

choice in the American literature is 200 mg of mebendazole BID for 20

days. The pediatric dose is the same. The treatment of choice in the

Philippines, where the disease is endemic, is 200 mg of albendazole

BID for 10 days. Thiabendazole, 25 mg/kg per day given in two dosages

for 30 days, is a less effective alternative. In addition to

anthelminthic therapy, electrolyte replacement and an antidiarrheal

agent should be given. C. philippinensis can be prevented by avoiding

the ingestion of raw or partially cooked freshwater fish, snails, and

crustaceans.

E. VERMICULARIS

 

E. vermicularis has a worldwide distribution and is the most common

intestinal nematode seen in North America. This parasite most

commonly affects children 5 to 14 years of age and is more common in

temperate and cold climates, secondary to less frequent bathing and

changing of undergarments. Transmission within families is common, and

high rates have been reported in homosexual men. Despite its high

prevalence, pinworm rarely causes severe disease.

 

Life cycle. The life cycle takes place entirely within the lumen of

the GI tract. Transmission of pinworm occurs via direct infection from

the anal canal to the mouth by finger contamination, via airborne eggs

that dislodge from bed linens and clothes, and via contaminated dust

containing embryonated eggs (fomites). After ingestion, eggs hatch in

the stomach and small intestine and migrate to the ileum, cecum,

appendix, and ascending colon where they attach to the mucosa. The

worms mate in these areas and the gravid female becomes engorged with

eggs. During the night, the gravid females migrate out of the anus and

deposit mature eggs in the perianal and perineal regions by a process

known as oviposition.

 

Clinical manifestations. The most common symptom of pinworm infection

is pruritus ani; however, most pinworm infections are asymptomatic.

Other symptoms that have been described include abdominal pain,

irritability, restlessness, insomnia, and fatigue. Some children

develop feelings of shame and guilt that may manifest as anorexia,

depression, enuresis, or emotional instability. Pinworm infection has

been linked to appendicular pain and chronic inflammation; however,

there appears to be no relationship with acute appendicitis.

Ulcerations of colonic mucosa have been described in areas of pinworm

infestation.

 

Complications of pinworm infection include secondary bacterial

dermatitis and folliculitis. Vulvovaginitis may occur with worm

migration to the vagina.

 

Diagnosis, treatment, and prevention. Pinworm infection is diagnosed

by identifying the adult worm or eggs from the perineum. This is

usually done at night as the female passes through the anal canal to

deposit her eggs. Alternatively, a strip of adhesive tape can be

applied sticky side down to the uncleaned perianal area in the morning

prior to defecation or bathing in order to capture characteristic

eggs. The adhesive side of the tape is then placed onto a glass slide,

and the slide is examined for eggs.

 

E. vermicularis is quite responsive to drug therapy, although the

relapse rate is high. In addition to drug therapy, proper personal

hygiene, sterilization of bed linens, and dust removal must be

performed. The treatment of choice for pinworm is a single dose of

pyrantel pamoate, 11 mg/kg (maximum 1 g), with another dosage given in

2 weeks. A single dose of either 100 mg of mebendazole or 400 mg of

albendazole, with a repeat dosage given in 2 weeks, is adequate

alternative therapy. The entire family should be treated simultaneously.

 

Prevention of pinworm infection depends on maintaining adequate

personal hygiene and clean living quarters. Hand washing and

fingernail cleaning should be done as much as possible. Frequent

washing of the toilet seat should be performed. Linens or clothing

should not be shaken prior to washing. Thumb sucking, fingernail

biting, and anal scratching should be discouraged.

S. STERCORALIS

 

S. stercoralis is a soil-dwelling nematode with a worldwide

distribution that is commonly found in the tropics and subtropics. In

temperate climates, S. stercoralis is commonly found in the setting of

group homes, mental hospitals, prisons, and settlements of refugees

from endemic areas. As a result of autoinfection, strongyloidiasis may

be found years later in veterans from the wars in Vietnam, Korea, and

World War II.

 

Possible risk factors for the development of S. stercoralis infection

include corticosteroid use, leukemia, lymphoma, prior gastric surgery,

protein-calorie malnutrition, chronic alcoholism, and immunosuppression.

 

Life cycle. The life cycle of S. stercoralis is more complicated than

that of other nematodes as it has the unique ability to perpetuate

itself in both the human host and soil. Under appropriate soil

conditions, free living worms produce rhabditiform larvae that become

infective filariform larvae after several months. The filariform

larvae penetrate the skin and enter the lymphatic and venous systems

where they are carried through the heart into the lungs. In the lungs,

the larvae penetrate the alveolar spaces and migrate up the trachea

and into the esophagus where they are swallowed and migrate to the

duodenum and upper jejunum. The larvae mature into adult worms in the

small intestine and lay eggs, which are either expelled in feces or

take up residence in the colon. The rhabditiform larvae in the colon

transform into filariform larvae, penetrate the bowel wall, and

complete the life cycle. Other rhabditiform larvae may transform into

filariform larvae in fecal matter that adheres to the skin, penetrate

the skin in that area, and complete the life cycle.

 

Clinical manifestations. The majority of acute S. stercoralis

infections are asymptomatic. Pulmonary symptoms such as cough,

wheezing, or the development of Löffler's syndrome may occur as larvae

invade the lungs. Acute GI symptoms include epigastric pain and

diarrhea. Pseudo-obstruction, bleeding gastric ulcer, colonic

ulceration, and concomitant enteric bacterial infections may occur

with S. stercoralis infection.

 

Chronic strongyloidiasis may be asymptomatic, although patients can

present with lower abdominal cramping, biliary colic, intermittent or

persistent diarrhea, pruritus ani, or malabsorption.

 

Hyperinfection or overwhelming strongyloidiasis may develop in

patients with impaired host-defense systems due to corticosteroid

therapy.

 

Diagnosis, treatment, and prevention. The diagnosis of

strongyloidiasis is made by identifying rhabditiform larvae in the

stool. The peripheral eosinophil count is markedly elevated in acute

disease (up to 85% of the white blood cell count), moderately elevated

in chronic disease, and absent in overwhelming infection.

 

The treatment of choice for strongyloidiasis is 25 mg/kg per day of

thiabendazole BID (maximum 3 g/d) for 2 days. Ivermectin, 200 mg/kg

per day given for 2 days, has also been shown to be effective.

Preventive measures include the sanitary disposal of human feces and

the wearing of appropriate footwear.

T. TRICHIURA

 

T. trichiura, or whipworm, is found in areas of poor sanitation and

overcrowding, primarily in the tropics and subtropics. In the United

States, whipworm is seen mostly in immigrants from tropical regions

and in rural areas of the southeast.

 

Life cycle. T. trichiura is transmitted by ingestion of embryonated

eggs from feces-contaminated soil. Eggs hatch and produce larvae that

attach to the mucosa of the small intestine and mature. After a period

of maturation of up to 3 months, the worms migrate to the colon and

attach to the colonic mucosa, predominantly in the cecum. The worms

produce eggs that are excreted in the feces.

 

Clinical manifestations. Symptoms of whipworm infection are dependent

upon worm load. Light infections (fewer than 100 worms) are the most

common and are usually asymptomatic. Lower abdominal pain, nausea,

flatulence, weight loss, and diarrhea may occur with light infection.

Infections with increased worm load (hundreds of worms) may cause

periumbilical pain, vomiting, anorexia, pica, and dysentery. Rectal

prolapse, although uncommon in the United States, is occasionally seen

in third world nations. Whipworm has been reported to simulate rectal

Crohn's disease. Iron deficiency anemia, growth retardation, and

clubbing have all been noted in T. trichiura infection. Severe

trichuriasis is frequently associated with a secondary intestinal

infection such as shigellosis, amebiasis, ascariasis, or

strongyloidiasis.

 

Diagnosis, treatment, and prevention. The diagnosis of T. trichiura is

made by identifying eggs in the stool, which are bile-stained and have

a characteristic mucus plug on each end. Worms can occasionally be

seen on proctosigmoidoscopy or embedded in prolapsed rectal mucosa.

Eosinophilia is uncommon in T. trichiura infection and when present

may indicate massive or concomitant infection.

 

The treatment of choice for T. trichiura infection is 100 mg of

mebendazole BID for 3 days. The dose is the same in adults and

children. Albendazole, given at a single dosage of 400 mg daily is an

alternative therapy. Prevention of T. trichiura infection requires

proper personal hygiene and adequate facilities for feces disposal.

A. LUMBRICOIDES

 

A. lumbricoides is the most common helminthic infection in humans and

is found on all continents, with the exception of Australia and

Antarctica. It is most common in Asia as a source of disease. The

organism is found in areas of poor hygiene and especially in places

where human feces are utilized as fertilizer. A. lumbricoides may

affect all age groups, but is most common in children. Contamination

of soil in playgrounds and utilization of garbage as toys contribute

to the increased incidence in this patient population.

 

Life cycle. An adult A. lumbricoides is a creamy white worm measuring

15 to 35 cm in length that typically inhabits the jejunum and middle

ileum. The female lays approximately 200,000 eggs per day that are

passed in host feces. The ova require 2 weeks of incubation in soil

for maturation before becoming infective. Infective eggs must be

ingested for human infection to occur. This may occur from the

ingestion of contaminated soil, vegetables, or water. After ingestion,

the ova hatch in the duodenum. The resulting larvae then enter the

portal circulation and pass to the lungs, where they migrate across

pulmonary and capillary beds, up the respiratory tree, and are

swallowed as mature worms. These worms live intraluminally but may

migrate into the ampulla of Vater, entering the common bile duct

and/or pancreatic duct.

 

Clinical manifestations. The clinical manifestations of A.

lumbricoides infection can be divided into two clinical stages: larval

migration and adult worm infection.

 

As larvae migrate through the venules, they may produce hepatitis,

although it is rare. Larvae migrating through the lungs may cause

cough, hemoptysis, dyspnea, pulmonary edema, or Löffler's syndrome.

 

Symptoms of adult worm infection of the GI tract are dependent upon

worm load. Light infections tend to be asymptomatic although patients

may complain of vague abdominal pain, anorexia, or malaise. Infections

with multiple worms may lead to more serious complications, such as

intestinal obstruction or perforation.

 

Intestinal obstruction typically presents with nausea, vomiting, and

colicky abdominal pain. A palpable abdominal mass that changes in size

and location on serial examinations is typical of ascariasis.

Obstruction is most common at the ileocecal valve. Untreated

intestinal obstruction can lead to volvulus, perforation, and

peritonitis. The incidence of intestinal obstruction is approximately

2 in 1000 cases in children.

 

A. lumbricoides may migrate up the common bile duct or pancreatic duct

and cause cholangitis or pancreatitis; in addition, it may migrate

into the appendix, leading to appendicitis. Tapeworms also cause

intussusception of the small intestine.

 

Diagnosis, treatment, and prevention. The diagnosis of ascariasis is

based on observation of an adult worm passed in the stool. The

identification of ova in the host stool or the vomiting of worms is

also diagnostic of A. lumbricoides infection. Eosinophilia is common.

 

The treatment of choice for A. lumbricoides is 100 mg of mebendazole

BID for 3 days. Albendazole, 400 mg given once a day for 2 days, or a

single 11-mg/kg dose of pyrantel pamoate (maximum 1 g) are alternative

therapies.

 

Intestinal obstruction can generally be treated conservatively with IV

fluids and nasogastric suction, followed by the administration of

anthelminthic therapy via a nasogastric tube. Obstruction associated

with fever or a distended abdomen usually requires surgical

intervention.

 

The prevention of A. lumbricoides infection is dependent upon

improving sanitary conditions and personal hygiene in areas of high

prevalence.

 

Source: Dr. David Bernstein, M.D.