<p>CHAPTER 53 Intestinal Nematodes</p><p>Six intestinal nematodes commonly infect humans: Enterobius vermicularis (pinworm), Trichuris trichiura (whipworm), Ascaris lumbricoides (large roundworm), Necator americanus and Ancylostoma duodenale (hookworms), and Strongyloides stercoralis. Together they infect more than one fourth of the human race, producing embarrassment, discomfort, malnutrition, anemia, and occasionally death. General Features</p><p>1. The intestinal nematodes have cylindric, fusiform bodies covered with a tough, acellular cuticle 2. Tubular alimentary tract consists of a mouth, esophagus, midgut, and anus 3. Highly developed reproductive produce thousands of offspring in the form of eggs 4. Eggs incubate or embryonate outside of the human developing into an adolescent form known as a larva 5. In some species, the egg hatches outside of the host, releasing a larva capable of penetrating the skin 6. Adults can survive for months or years within the lumen of the gut 7. Disease severity is related to the number of adult worms harbored by the host 8. Nematodes do not multiply within the human so the frequency and intensity of reinfection determines the worm burden Enterobius vermicularis (PINWORM)</p><p>I. PARASITOLOGY</p><p>1. The adult female is cream-colored worm with a sharply pointed tail 2. Common name is pinworm 3. Clear, thin-shelled, ovoid eggs are flattened on one side </p><p>A. LIFE CYCLE</p><p>1. The adult female migrates down the colon, slips unobserved through the anal canal and deposits sticky eggs on the host's perianal skin 2. Scratching of the perianal area to relieve the associated itching results in adhesion of the eggs to the fingers 3. The eggs are near maturity so transfer to the oral cavity allows them to hatch in the upper intestine 4. Entire adult-to-adult cycle is completed in 2 weeks II. ENTEROBIASIS</p><p>A. EPIDEMIOLOGY</p><p>1. Single most common cause of human helminthiasis 2. The eggs are relatively resistant to desiccation and may remain viable in linens, bedclothes, or house dust for several days</p><p>B. PATHOGENESIS AND IMMUNITY</p><p>1. No significant intestinal pathology 2. Do not appear to induce protective immunity III. ENTEROBIASIS: CLINICAL ASPECTS</p><p>A. MANIFESTATIONS</p><p>1. Nocturnal anal itching 2. Occasional infection of female genitourinary tract</p><p>B. DIAGNOSIS</p><p>1. Diagnosis is suggested by the clinical manifestations and confirmed by the recovery of the characteristic eggs from the anal mucosa 2. Anal cellophane tape test detects ova when placed on a slide</p><p>C. TREATMENT AND PREVENTION</p><p>1. All family members may need treatment with pyrantel pamoate and mebendazole 2. Reinfection common Trichuris trichiura (WHIPWORM) I. PARASITOLOGY</p><p>1. The adult whipworm is thin and threadlike 2. The tail of the male is coiled; that of the female is straight 3. Eggs are of the same size as pinworm eggs but have a distinctive thick brown </p><p>A. LIFE CYCLE</p><p>1. Life cycle that differs from the pinworm only in its external phase 2. Adults inhabit cecum and release eggs to lumen 3. Eggs must mature in soil for 10 days II. TRICHURIASIS</p><p>A. EPIDEMIOLOGY</p><p>1. Associated with defecation on soil and warm, humid climate 2. Adult worms live for years</p><p>B. PATHOGENESIS AND IMMUNITY</p><p>1. Local colonic ulceration provides entry point to bloodstream for bacteria 2. An IgE-mediated immune mucosal response is demonstrable, but is insufficient to cause appreciable parasite expulsion. III. TRICHURIASIS: CLINICAL ASPECTS</p><p>A. MANIFESTATIONS</p><p>1. Colonic damage with abdominal pain and diarrhea 2. Colonic or rectal prolapse with heavy worm load</p><p>B. DIAGNOSIS</p><p>1. Stools examined for characteristic eggs 2. In light infections, stool concentration methods may be required</p><p>C. TREATMENT AND PREVENTION</p><p>1. Infections not treated unless symptomatic 2. Mebendazole is the drug of choiceAscaris Ascaris lumbricoides I. PARASITOLOGY</p><p>1. Earthworm-sized roundworm produces elliptical eggs 2. Eggs viable up to 6 years</p><p>A. LIFE CYCLE</p><p>1. Adults inhabit small intestine 2. Eggs must mature for 3 weeks in soil 3. Larvae from ingested eggs enter bloodstream and pass through alveoli and via respiratory tract and esophagus to intestines II. ASCARIASIS</p><p>A. EPIDEMIOLOGY</p><p>1. Epidemiology similar to that of Trichuris 2. Parasite may also be acquired through ingestion of egg-contaminated food by the host</p><p>B. PATHOGENESIS AND IMMUNITY</p><p>1. Hypersensitive pulmonary reactions to larval migration through the lung is an immediate hypersensitivity reaction 2. Ascariasis induces a protective immune response in the host III. ASCARIASIS: CLINICAL ASPECTS</p><p>A. MANIFESTATIONS</p><p>1. Clinical manifestations may result from either the migration of the larvae through the lung include fever, cough, wheezing, and shortness of breath 2. Intestinal infections asymptomatic with small worm loads 3. Malabsorption and occasional obstruction produced with heavy worm loads</p><p>B. DIAGNOSIS</p><p>1. Stool examination readily reveals characteristic eggs 2. Pulmonary phase of ascariasis is diagnosed by the finding of larvae and eosinophils in the sputum</p><p>C. TREATMENT AND PREVENTION</p><p>1. Albendazole, mebendazole and pyrantel pamoate are highly effective 2. Control requires adequate sanitation facilities. Hookworms: ANCYLOSTOMA AND NECATOR</p><p>I. PARASITOLOGY</p><p>A. LIFE CYCLE 1. In soil, eggs mature and release rhabditiform larvae that molt to produce infective filariform larvae 2. Filariform larvae penetrate skin and then follow same path as Ascaris larvae to gut B. HOOKWORM DISEASE</p><p>A. EPIDEMIOLOGY</p><p>1. Larvae require hot, moist conditions 2. Limited to tropical areas and southern United States</p><p>B. PATHOGENESIS AND IMMUNITY</p><p>1. Adult worms live in gut for years 2. Blood loss significant 3. Produce peripheral and gut eosinophilia III. HOOKWORM DISEASE: CLINICAL ASPECTS</p><p>A. MANIFESTATIONS</p><p>1. Most infections asymptomatic depending on worm load 2. Pruritus at site of skin penetration 3. Iron deficiency anemia caused by blood loss from intestinal worms</p><p>B. DIAGNOSIS</p><p>1. Diagnosis is made by examining direct or concentrated stool for the distinctive eggs 2. Eggs of both species look the same</p><p>C. TREATMENT AND PREVENTION</p><p>1. The anemia must be corrected 2. Pyrantel pamoate, mebendazole and albendazole, are all highly effective 3. Prevention requires improved sanitation Strongyloides stercoralis</p><p>I. PARASITOLOGY 1. S. stercoralis adults measure only 2 mm in length, making them the smallest of the intestinal nematodes 2. eggs hatch quickly, releasing rhabditiform larvae that reenter the bowel lumen and are subsequently passed into the stool 3. Larvae differ slightly from hookworm</p><p>A. LIFE CYCLE</p><p>1. Primary cycle resembles hookworm except rhabditiform larvae develop in gut 2. Development of filariform stage in gut produces autoinfection 3. Adults can develop in soil, producing sustained life cycle II. STRONGYLOIDIASIS</p><p>A. EPIDEMIOLOGY</p><p>1. Distribution similar to hookworm but less common 2. Infection by ingestion of filariform larvae also occurs</p><p>B. PATHOGENESIS AND IMMUNITY</p><p>1. Damage to intestinal mucosa may cause malabsorptive syndrome 2. Immunosuppression enhances risk of autoinfection by accelerating larval development III. STRONGYLOIDIASIS: CLINICAL ASPECTS</p><p>A. MANIFESTATIONS</p><p>1. Pulmonary and intestinal manifestations can be similar to hookworm, ascaris infections 2. External autoinfection causes lesions over buttocks and back 3. Massive hyperinfection occurs in immunosuppressed but uncommon in AIDS</p><p>B. DIAGNOSIS</p><p>1. Rhabditiform larvae detected in stool or duodenal aspirates 2. When absent from the stool, larvae may sometimes be found in duodenal aspirates or jejunal biopsy specimens</p><p>C. TREATMENT AND PREVENTION</p><p>1. Drugs of choice are ivermectin and thiabendazole 2. Treatment essential to prevent autoinfection cycle 3. Medical personnel can be infected with filariform larvae</p>