Nematodes

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INTESTINAL HELMINTHS

Intestinal nematodes of importance to man are Ascaris lumbricoides (roundworm), Trichinella spiralis (trichinosis), Trichuris trichiura (whipworm), Enterobius vermicularis (pinworm), Strongyloides stercoralis (Cochin-china diarrhea), Ancylostoma duodenale and Necator americanes (hookworms) and Dracunculus medinensis (fiery serpents of the Israelites). E. vermicularis and T. trichiura are exclusively intestinal parasites. Other helminths listed above have both intestinal and tissue phases.

Ascaris lumbricoides (Large intestinal roundworm)

Epidemiology

The annual global morbidity due to ascaris infections is estimated at 1 billion with a mortality of 20,000. Ascariasis can occur at all ages, but it is more prevalent in the 5 to 9 years age group. The incidence is higher in poor rural populations.

Morphology

The average female worm measures 30 cm x 5 mm. The male is smaller.

Life cycle

The infection occurs by ingestionof food contaminated with infective eggs which hatch in the upper small intestine. The larvae (250 x 15 micrometers) penetrate the intestinal wall and enter the venules or lymphatics. The larvae pass through the liver, heart and lung to reach alveoli in 1 to 7 days during which period they grow to 1.5 cm. They migrate up the bronchi, ascend the trachea to the glottis, and pass down the esophagus to the small intestine where they mature in 2 to 3 months. A female may live in the intestine for 12 to 18 months and has a capacity of producing 25 million eggs at an average daily output of 200,000. The eggs are excreted in feces, and under suitable conditions (21 to 30 degrees C, moist, aerated environment) infective larvae are formed within the egg. The eggs are resistant to chemical disinfectant and survive for months in sewage, but are killed by heat (40 degrees C for 15 hours). The infection is man to man. Auto infection can occur.

Symptoms
Symptoms are related to the worm burden. Ten to twenty worms may go unnoticed except in a routine stool examination. The commonest complaint is vague abdominal pain. In more severe cases, the patient may experience listlessness, weight loss, anorexia, distended abdomen, intermittent loose stool and occasional vomiting. During the pulmonary stage, there may be a brief period of cough, wheezing, dyspnea and sub-sternal discomfort. Most symptoms are due to the physical presence of the worm.

Diagnosis
Diagnosis is based on identification of eggs (40 to 70 micrometers by 35 to 50 micrometers - figure 2) in the stool.

Treatment and Prevention
Mebendazole, 200 mg, for adults and 100 mg for children, for 3 days is effective. Good hygiene is the best preventive measure.

Trichinella spiralis (Trichinosis)
Epidemiology
Trichinosis is related to the quality of pork and consumption of poorly cooked meat. Autopsy surveys indicate about 2 percent of the population is infected. The mortality rate is low.

Morphology
The adult female measures 3.5 mm x 60 micrometers. The larvae in the tissue (100 micrometers x 5 micrometers) are coiled in a lemon-shaped capsule.

Life cycle

Infection occurs by ingestion of larvae, in poorly cooked meat, which immediately invade intestinal mucosa and sexually differentiate within 18 to 24 hours. The female, after fertilization, burrows deeply in the small intestinal mucosa, whereas the male is dislodged (intestinal stage). On about the 5th day eggs begin to hatch in the female worm and young larvae are deposited in the mucosa from where they reach the lymphatics, lymph nodes and the blood stream (larval migration). Larval dispersion occurs 4 to 16 weeks after infection. The larvae are deposited in muscle fiber and, in striated muscle, they form a capsule which calcifies to form a cyst. In non-striated tissue, such as heart and brain, the larvae do not calcify; they die and disintegrate. The cyst may persist for several years. One female worm produces approximately 1500 larvae. Man is the terminal host. The reservoir includes most carnivorous and omnivorous animals.

Symptoms

Trichinosis symptoms depend on the severity of infection: mild infections may be asymptomatic. A larger bolus of infection produces symptoms according to the severity and stage of infection and organs involved.

Pathology and Immunology

Trichinella pathogenesis is due the presence of large numbers of larvae in vital muscles and host reaction to larval metabolites. The muscle fibers become enlarged edematous and deformed. The paralyzed muscles are infiltrated with neutrophil, eosinophils and lymphocytes. Splenomegaly is dependent on the degree of infection. The worm induces a strong IgE response which, in association with eosinophils, contributes to parasite death.

Diagnosis

Diagnosis is based on symptoms, recent history of eating raw or undercooked meat and laboratory findings (eosinophilia, increased serum creatine phosphokinase and lactate dehydrogenase and antibodies to T. spiralis).

Treatment and Control

Steroids are use for treatment of inflammatory symptoms and Mebendazole is used to eliminate worms. Elimination of parasite infection in hogs and adequate cooking of meat are the best ways of avoiding infection.

Trichuris trichiura (whipworm)

Epidemiology

Trichuriasis is a tropical disease of children (5 to 15 yrs) in rural Asia (65% of the 500-700 million cases). It is, however, seen in the two Americas, mostly in the South and is concentrated in families and groups with poorer sanitary habits.

Morphology

The female organism is 50 mm long with a slender anterior (100 micrometer dia,eter) and a thicker (500 micrometers diameter) posterior end. The male is smaller and has a coiled posterior end. The Trichuris eggs are lemon or football shaped and have terminal plugs at both ends.

Life cycle

Infection occurs by ingestion of embryonated eggs in soil. The larva escapes the shell in the upper small intestine and penetrates the villus where it remains for 3 to 10 days. Upon reaching adolescence, the larvae pass to the cecum and embed in the mucosa. They reach the ovipositing age in 30 to 90 days from infection, produce 3000 to 10,000 eggs per day and may live as long as 5 to 6 years. Eggs passed in feces embryonate in moist soil within 2 to 3 weeks. The eggs are less resistant to desiccation, heat and cold than ascaris eggs. The embryo is killed under desiccation at 37 degrees C within 15 minutes. Temperatures of 52 degrees C and -9 degrees C are lethal.

Symptoms

Symptoms are determined largely by the worm burden: less than 10 worms are asymptomatic. Heavier infections (e.g., massive infantile trichuriasis) are characterized by chronic profuse mucus and bloody diarrhea with abdominal pains and edematous prolapsed rectum. The infection may result in malnutrition, weight loss and anemia and sometimes death.

Diagnosis

Diagnosis is based on symptoms and the presence of eggs in feces (50 to 55 x 20 to 25 micrometers).

Treatment and Control

Mebendazole, 200 mg, for adults and 100 mg for children, for 3 days is effective. Accompanying infections must be treated accordingly. Improved hygiene and sanitary eating habits are most effective in control.

Enterobius vermicularis (pinworm)

Epidemiology

Enterobiasis is by far the commonest helminthic infection in the US (18 million cases at any given time). The worldwide infection is about 210 million. It is an urban disease of children in crowded environment (schools, day care centers, etc.). Adults may get it from their children. The incidence in whites is much higher than in blacks.

Morphology

The female worm measures 8 mm x 0.5mm; the male is smaller. Eggs (60 micrometers x 27 micrometers) are ovoid but asymmetrically flat on one side.

Life cycle

Infection occurs when embryonated eggs are ingested from the environment, with food or by hand to mouth contact. The embryonic larvae hatch in the duodenum and reach adolescence in jejunum and upper ilium. Adult worms descend into lower ilium, cecum and colon and live there for 7 to 8 weeks. The gravid females, containing more than 10,000 eggs migrate, at night, to the perianal region and deposit their eggs there. Eggs mature in an oxygenated, moist environment and are infectious 3 to 4 hours later. Man-to-man and auto infection are common. Man is the only host.

Symptoms

Enterobiasis is relatively innocuous and rarely produces serious lesions. The most common symptom is perianal, perineal and vaginal irritation caused by the female migration. The itching results in insomnia and restlessness. In some cases gastrointestinal symptoms (pain, nausea, vomiting, etc.) may develop. The conscientious housewife's mental distress, guilt complex, and desire to conceal the infection from her friends and mother-in-law is perhaps the most important trauma of this persistent, pruritic parasite.

Diagnosis

Diagnosis is made by finding the adult worm or eggs in the perianal area, particularly at night. Scotch tape or a pinworm paddle is used to obtain eggs.

Treatment and Control

Two doses (10 mg/kg; maximum of 1g each) of Pyrental Pamoate two weeks apart gives a very high cure rate. Mebendazole is an alternative. The whole family should be treated, to avoid reinfection. Bedding and underclothing must be sanitized between the two treatment doses. Personal cleanliness provides the most effective in prevention.

Strongyloides stercoralis (Threadworm)

Epidemiology

Threadworm infection, also known as Cochin-China diarrhea, estimated at 50 to 100 million cases worldwide, is an infection of the tropical and subtropical areas with poor sanitation. In the United States, it is prevalent in the South and among Puerto Ricans.

Morphology

The size and shape of threadworm varies depending on whether it is parasitic or free-living. The parasitic female is larger (2.2 mm x 45 micrometers) than the free-living worm (1 mm x 60 micrometers). The eggs, when laid are 55 micrometers by 30 micrometers.

Life cycle

The infective larvae of S. stercoralis penetrate the skin of man, enter the venous circulation and pass through the right heart to lungs, where they penetrate into the alveoli. From there, the adolescent parasites ascend to the glottis, are swallowed, and reach the upper part of the small intestine, where they develop into adults. Ovipositing females develop in 28 days from infection. The eggs in the intestinal mucosa, hatch and develop into rhabditiform larvae in man. These larvae can penetrate through the mucosa and cycle back into the blood circulation, lung, glottis and duodenum and jejunum; thus they continue the auto infection cycle. Alternatively, they are passed in the feces, develop into infective filariform larvae and enter another host to complete the direct cycle. If no suitable host is found, the larvae mature into free-living worm and lay eggs in the soil. The eggs hatch in the soil and produce rhabditiform larvae which develope into infective filariform larvae and enter a new host (indirect cycle), or mature into adult worms to repeat the free-living cycle.

Symptoms

Light infections are asymptomatic. Skin penetration causes itching and red blotches. During migration, the organisms cause bronchial verminous pneumonia and, in the duodenum, they cause a burning mid-epigastric pain and tenderness accompanied by nausea and vomiting. Diarrhea and constipation may alternate. Heavy, chronic infections result in anemia, weight loss and chronic bloody dysentery. Secondary bacterial infection of damaged mucosa may produce serious complications.

Diagnosis

The presence of free rhabditiform larvae in the feces is diagnostic. Culture of stool for 24 hours will produce filariform larvae.

Treatment and control

Ivermectin or thiabendozole can be used effectively. Direct and indirect infections are controlled by improved hygiene and auto-infection is controlled by chemotherapy.

Necator americanes and Ancylostoma duodenale (Hookworms)

Epidemiology

Hookworms parasitize more than 900 million people worldwide and cause daily blood loss of 7 million liters. Ancylostomiasis is the most prevalent hookworm infection and is second only to ascariasis in infections by parasitic worms. N. americanes (new world hookworm) is most common in the Americas, central and southern Africa, southern Asia, Indonesia, Australia and Pacific Islands. A. duodenale (old world hookworm) is the dominant species in the Mediterranean region and northern Asia.

Morphology

Adult female hookworms are about 11 mm x 50 micrometers. Males are smaller. The anterior end of N. americanes is armed with a pair of curved cutting plates whereas A. duodenale is equipped with one or more pairs of teeth. Hookworm eggs are 60 micrometers x 35 micrometers.

Life cycle

The life cycle of hookworms is identical to that of threadworms, except that hookworms are not capable of a free-living or auto-infectious cycle. Furthermore, A. duodenale can infect also by oral route.

Symptoms

Symptoms of hookworm infection depend on the site at which the worm is present and the burden of worms. Light infection may not be noticed.

Diagnosis

Diagnosis is made by identification of hookworm eggs in fresh or preserved feces. Species of hookworms cannot be distinguished by egg morphology.

Treatment and control

Mebendazole, 200 mg, for adults and 100 mg for children, for 3 days is effective. Sanitation is the chief method of control: sanitary disposal of fecal material and avoidance of contact with infected fecal material.

Dracunculus medinensis (Guinea worm; fiery serpent of the Israelites)

Drancunculis Guinea Worm

Epidemiology

Guinea worm is estimated to infect about 50 million people in North, West and Central Africa, southwestern Asia, the West Indies and northeastern South America.

Morphology

The adult female worm measures 50-120 cm by 1 mm and the male is half that size.

Life cycle

The infection is caused by ingestion of water contaminated with water fleas (Cyclops) infected with larvae. The rhabtidiform larvae penetrate the human digestive tract wall, lodge in the loose connective tissues and mature into the adult form in 10 to 12 weeks. In about a year, the gravid female migrates to the subcutaneous tissue of organs that normally come in contact with water and discharges its larvae into the water. The larvae are picked up by Cyclops, in which they develop into infective form in 2 to 3 weeks.

Symptoms

If the worm does not reach the skin, it dies and causes little reaction. In superficial tissue, it liberates a toxic substance that produces a local inflammatory reaction in the form of a sterile blister with serous exudation. The worm lies in a subcutaneous tunnel with its posterior end beneath the blister, which contains clear yellow fluid. The course of the tunnel is marked with induration and edema. Contamination of the blister produces abscesses, cellulitis, extensive ulceration and necrosis.

Diagnosis

Diagnosis is made from the local blister, worm or larvae. The outline of the worm under the skin may be revealed by reflected light.

Treatment

Treatment includes the extraction of the adult guinea worm by rolling it a few centimeters per day or preferably by multiple surgical incisions under local anaesthesia. Metronidazole is effective in killing the worm. Protection of drinking water from being contaminated with Cyclops and larvae are effective preventive measures.

Toxocara canis and T. catti (visceral larva migrans)

These are roundworms of dogs and cats but they can infect humans and cause damage of the visceral organs. Eggs from feces of infected animals are swallowed by man and hatch in the intestine. The larvae penetrate the mucosa, enter the circulation and are carried to liver, lungs, eyes and other organs where they cause inflammatory necrosis. Symptoms are due to the inflammatory reaction at the site of infection. The most serious consequence of infection may be loss of sight if the worm localizes in the eye. Treatment includes Mebendazole to eliminate the worm and prednisone for inflammatory symptoms. Avoidance of infected dogs and cats is the best prevention

Ancylostoma braziliensis (cutaneous larva migrans, creeping eruption)

Creeping eruption is prevalent in many tropical and subtropical countries and in the US especially along the Gulf and southern Atlantic states. The organism is primarily a hookworm of dogs and cats but the filariform larvae in animal feces can infect man and cause skin eruptions. Since the larvae have a tendency to move around, the eruption migrates in the skin around the site of infection. The symptoms last the duration of larval persistence which ranges from 2 to 10 weeks. Light infection can be treated by freezing the involved area. Heavier infections are treated with Mebendazole. Infection can be avoided by keeping away from water and soil contaminated with infected feces

BLOOD AND TISSUE HELMINTHS

The major blood and tissue parasites of man are microfilaria. These include Wuchereria bancrofti and W. (Brugia) Malayi, Onchocerca volvulus, and Loa loa (eye worm).

Wuchereria bancrofti and W. (Brugia) malayi (elephantiasis)

Epidemiology

W. bancrofti is strictly a human pathogen and is distributed in tropical areas worldwide, whereas B. malayi infects a number of wild and domestic animals and is restricted to South-East Asia. Mosquitoes are vectors for both parasites.

Morphology

These two organisms are very similar in morphology and in the diseases they cause. Adult female W. bancrofti found in lymph nodes and lymphatic channels are 10 cm x 250 micrometers whereas males are only half that size. Microfilaria found in blood are only 260 micrometers x 10 micrometers. Adult B. malayi are only half the size of W. bancrofti but their microfilaria are only slightly smaller than W. bancrofti.

Life cycle

Filariform larvae enter the human body during a mosquito bite and migrate to various tissues. There, they may take up to a year to mature and produce microfilaria which migrate to lymphatics and, at night, enter the blood circulation. Mosquitos are infected during a blood meal. The microfilaria grow 4 to 5 fold in the mosquito in 10 to 14 days and become infective for man.

Symptoms

Symptoms include lymphadenitis and recurrent high fever every 8 to 10 weeks, which lasts 3 to 7 days. There is progressive lymphadenitis due to an inflammatory response to the parasite lodged in the lymphatic channels and tissues. As the worm dies, the reaction continues and produces a fibro-proliferative granuloma which obstructs lymph channels and causes lymphedema and elephantiasis. The stretched skin is susceptible to traumatic injury and infections. Microfilaria cause eosinophilia and some splenomegaly. Not all infections lead to elephantiasis. Prognosis, in the absence of elephantiasis, is good.

Diagnosis

Diagnosis is based on history of mosquito bites in endemic areas, clinical findings and presence of microfilaria in blood samples collected at night.

Treatment and control

Diethylcarbamazine quickly kills the adults worms or sterilizes the female. It is given 2 mg/kg orally for 14 days. Steroids help alleviate inflammatory symptoms. Cooler climate reduces the inflammatory reaction.

Onchocerca volvulus (Blinding filariasis; river blindness)

Epidemiology

Onchocerciasis is prevalent throughout eastern, central and western Africa, where it is the major cause of blindness. In the Americas, it is found in Guatemala, Mexico, Colombia and Venezuela. The disease is confined to neighborhoods of low elevation with rapidly flowing small streams where black flies breed. Man is the only host.

Morphology

Adult female onchocerca measure 50 cm by 300 micrometers, male worms are much smaller. Infective larvae of O. volvulus are 500 micrometers by 25 micrometers.

Life cycle

Infective larvae are injected into human skin by the female black fly (Simulium damnosum) where they develop into adult worms in 8 to 10 months. The adults usually occur as group of tightly coiled worms (2 to 3 females and 1 to 2 males). The gravid female releases microfilarial larvae, which are usually distributed in the skin. They are picked up by the black fly during a blood meal. The larvae migrate from the gut of the black fly to the thoracic muscle where they develop into infective larvae in 6 to 8 days. These larvae migrate to the head of the fly and then are transmitted to a second host.

Symptoms

Onchocerciasis results in nodular and erythematous lesions in the skin and subcutaneous tissue due to a chronic inflammatory response to persistent worm infection. During the incubation period of 10 to 12 months, there is eosinophilia and urticaria. Ocular involvement consists of trapping of microfilaria in the cornea, choroid, iris and anterior chambers, leading to photophobia, lacrimation and blindness.

Diagnosis

Diagnosis is based on symptoms, history of exposure to black flies and presence of microfilaria in nodules.

Treatment and control

Diethylcarbamazine is effective in killing the worm. Destruction of microfilaria produces extreme allergic reaction which can be controlled with corticosteroids. Prevention measures include vector control, treatment of infected individuals and avoidance of black fly.

Loa loa (eye worm)

Loasis is limited to the areas of African equatorial rain forest. The incidence in endemic areas varies greatly (8 to 75 percent). The larger, female organisms are 60 mm by 500 micrometers; males are 35mm by 300 micrometers in size. The circulating microfilaria are 300 micrometers by 7 micrometers; the infective larvae in the fly are 200 micrometers by 30 micrometers. The life cycle of Loa loa is identical to that of onchocerca except that the vector for this worm is the deer fly. The infection results in subcutaneous (Calabar) swelling, measuring 5 to 10 cm in diameter, marked by erythema and angioedema, usually in the extremities. The organism migrates under the skin at a rate of up to an inch every two minutes. Consequently, the swelling appears spontaneously, persists for 4 to 7 days and disappears, and is known as fugitive or Calabar swelling. The worm usually causes no serious problems, except when passing through the orbital conjunctiva or the nose bridge. The diagnosis is based on symptoms, history of deer fly bite and presence of eosinophilia. Recovery of worms from the conjunctiva is confirmatory. Treatment and control are the same as those for onchocerciasis.