1. HELMINTHIC INFECTION
Objectives:Upon completion this lecture ,the student will be able to :
Classify worms that cause human infection
Determine types of round worms
Identify mode of transmission of round worms
Recognize the clinical feature of each worm
Management of each worm

2. INFECTIONS CAUSED BY HELMINTHS
worm large multicellular organisms with complex tissues and organs.
Helminths (from the Greek Helmins, meaning worm) include three groups:
Nematodes(round worms)
Trematodes(flukes)
Cestodes(tape worms)

3. NEMATODES
The nematodes, or roundworms, that are of medical significance can be classified as either tissue or intestinal parasites.

4. HELMINTHIC INFECTIONS
Intestinal human nematodes: Ancylostoma duodenale, Necator americanus, Strongyloides stercoralis, Ascaris lumbricoides, Enterobius vermicularis, Trichuris trichiura
Tissue-dwelling human nematodes: Wuchereria bancrofti, Brugia malayi, Loa loa, Onchocerca volvulus, Dracunculus medinensis, Mansonella perstans, Dirofilaria immitis
Zoonotic nematodes: Trichinella spiralis

5. TRICHINELLOSIS Etiology: T
TRICHINELLOSIS Etiology: T. spiralis and six other Trichinella species cause human infection

6. Life Cycle and Epidemiology: Infection results when humans ingest meat (usually pork) that contains cysts with Trichinella larvae. During the first week of infection, the larvae invade the small-bowel mucosa; during the second and third weeks, they mature into adult worms, which release new larvae that migrate to striated muscle via the circulation and encyst.

8. Clinical Features:
Light infections (<10 larvae per gram of muscle) are asymptomatic. A burden of >50 larvae per gram can cause fatal disease. • Week 1: diarrhea, abdominal pain, constipation, nausea, and/or vomiting.

9. • Week 2: hypersensitivity reactions with fever and hypereosinophilia; periorbital and facial edema; hemorrhages in conjunctivae, retina, and nail beds; maculopapular rash; headache; cough; dyspnea; dysphagia. Deaths are usually due to myocarditis with arrhythmias or CHF and are less often caused by pneumonitis or encephalitis.

10. Weeks 2–3: myositis, myalgias, muscle edema, weakness (especially in extraocular muscles, biceps, neck, lower back, and diaphragm). Symptoms peak at 3 weeks; convalescence is prolonged.

11. Diagnosis: • Eosinophilia in >90% of pts, peaking at a level of >50% at 2–4 weeks. • Elevated IgE and muscle enzyme levels; increase in specific antibody titers by week 3. • A definitive diagnosis is made by the detection of larvae on biopsy of at least 1 g of muscle tissue. Yields are highest near tendon insertions.

12. TREATMENT: Drugs are ineffective against muscle larvae, but mebendazole and albendazole may be active against enteric-stage parasites. Glucocorticoids (1 mg/kg daily for 5 days) may reduce severe myositis and myocarditis.

13. Prevention: Cooking pork until it is no longer pink or freezing it at _15◦C for 3 weeks kills larvae and prevents infection.

14. VISCERAL AND OCULAR LARVA MIGRANS Etiology: Most cases of larva migrans are caused by Toxocara canis.

15. Life Cycle and Epidemiology: Infection results when humans—most often preschool children—ingest soil contaminated by puppy feces that contain infective T. canis eggs. Larvae penetrate the intestinal mucosa and disseminate hematogenously to a wide variety of organs (e.g., liver, lungs, CNS), provoking intense eosinophilic granulomatous responses.

16. Clinical Features: Heavy infections may cause fever, malaise, anorexia, weight loss, cough, wheezing, rashes, and hepatosplenomegaly. Ocular disease usually develops in older children or young adults and may cause an eosinophilic mass that mimics retinoblastoma, endophthalmitis, uveitis, or chorioretinitis.

17. Diagnosis: • No eggs are found in the stool because larvae do not develop into adult worms. • Blood eosinophilia up to 90%, leukocytosis, and hypergammaglobulinemia may be evident. • Toxocaral antibodies detected by ELISA can confirm the diagnosis.

18. TREATMENT: Glucocorticoids can reduce inflammatory complications
TREATMENT: Glucocorticoids can reduce inflammatory complications. Only ocular infections require treatment: albendazole (800 mg bid for adults and 400 mg bid for children) for 5–20 days in conjunction with glucocorticoids.

19. CUTANEOUS LARVA MIGRANS This disease is caused by larvae of animal hookworms, usually the dog and cat hookworm Ancylostoma braziliense. Larvae in contaminated soil penetrate human skin; erythematous lesions form along the tracks of their migration and advance several centimeters each day. Pruritus is intense. Vesicles or bullae may form. Ivermectin (a single dose of 200 g/kg) or albendazole (200 mg bid for 3 days) can relieve the symptoms of this self-limited infestation.

20. Intestinal Nematode Infections Intestinal nematodes infect >1 billion persons worldwide in regions with poor sanitation, particularly in developing countries in the tropics or subtropics. These parasites contribute to malnutrition and diminished work capacity.

21. ASCARIASIS Etiology: Ascariasis is caused by Ascaris lumbricoides, the largest intestinal nematode, which reaches lengths up to 40 cm. The parasite is transmitted via fecally contaminated soil.

22. Life Cycle: Swallowed eggs hatch in the intestine, larvae invade the mucosa, migrate to the lungs, break into the alveoli, ascend the bronchial tree, are swallowed, reach the small intestine, mature, and produce up to 240,000 eggs per day that pass in the feces.

23. Clinical Features: Most infections have a low worm burden and are asymptomatic. During lung migration of the parasite, patients may develop a cough and substernal discomfort, occasionally with dyspnea or blood-tinged sputum, fever, and eosinophilia. Eosinophilic pneumonitis (Lo¨ffler’s syndrome) may be evident. Heavy infections occasionally cause pain, small-bowel obstruction, perforation, volvulus, biliary obstruction and colic, or pancreatitis

24. Laboratory Findings: Ascaris eggs (65 by 45 µm) can be found in fecal samples. Adult worms can pass in the stool or through the mouth or nose. During the transpulmonary migratory phase, larvae can be found in sputum or gastric aspirates.

25. TREATMENT: A single dose of albendazole (400 mg) or mebendazole (500 mg) is effective. Pyrantel pamoate (a single dose of11 mg/kg, up to 1 g) is safe in pregnancy.

26. HOOKWORM Etiology: One-fourth of the world’s population is infected with one of two hookworm species: Ancylostoma duodenale or Necator americanus.

27. Life Cycle: Infectious larvae penetrate the skin, reach the lungs via the bloodstream, invade the alveoli, ascend the airways, are swallowed, reach the small intestine, mature into adult worms, attach to the mucosa, and suck blood and interstitial fluid.

28. Clinical Features: Most infections are asymptomatic
Clinical Features: Most infections are asymptomatic. Chronic infection causes iron deficiency and—in marginally nourished persons—progressive anemia and hypoproteinemia, weakness, shortness of breath, and skin depigmentation.

29. Laboratory Findings: Hookworm eggs (40 by 60 µm) can be found in the feces. Stool concentration may be needed for the diagnosis of light infections.

30. TREATMENT: Albendazole (400 mg once), mebendazole (500 mg once), or pyrantel pamoate (11 mg/kg daily for 3 days) is effective. Nutritional support and iron replacement are undertaken as needed.

31. STRONGYLOIDIASIS Etiology and Epidemiology: Unlike other helminthes, Strongyloides stercoralis can replicate in the human host, permitting ongoing cycles of autoinfection from endogenously produced larvae. Autoinfection is most common among immunocompromised hosts, including those receiving glucocorticoids. Hyperinfection and widespread larval dissemination can occur in these patients. However, severe disease due to Strongyloides is unusual in HIV-infected patients.

32. Life Cycle: Infection results when filariform larvae in fecally contaminated soil penetrate the skin or mucous membranes. Larvae travel through the bloodstream to the lungs, break through alveolar spaces, ascend the bronchial tree, are swallowed, reach the small intestine, mature into adult worms, and penetrate the mucosa of the proximal small bowel; eggs hatch in intestinal mucosa.

33. Rhabditiform larvae can pass with the feces into the soil or can develop into filariform larvae that penetrate the colonic wall or perianal skin and enter the circulation to establish ongoing autoinfection.

35. Clinical Features: Uncomplicated disease is associated with mild cutaneous and/or abdominal manifestations such as urticaria, larva currens (a pathognomonic, pruritic, erythematous eruption along the course of larval migration that may advance up to 10 cm/h), abdominal pain, nausea, diarrhea, bleeding, and weight loss. Colitis, enteritis, or malabsorption can develop.

36. Diagnosis: Eosinophilia is common, with levels that fluctuate over time. Eggs are rarely found in feces because they hatch in the colon. A single stool examination detects rhabditiform larvae (200–250 µm long) in about one-third ofuncomplicated infections. If stool examinations are negative, duodenojejunal contents can be sampled. Antibodies can be detected by ELISA. In disseminated infection, filariform larvae (550 µm long) can be found in stool or at sites of larval migration.

37. TREATMENT: Ivermectin (200 µg/kg daily for 1 or 2 days) is more effective than albendazole (400 mg daily for 3 days, repeated at 2 weeks) and is better tolerated than thiabendazole (25 mg/kg bid for 2 days). Disseminated disease should be treated for 5–7 days.

38. ENTEROBIASIS Etiology: Enterobiasis (pinworm) is caused by Enterobius vermicularis.

39. Life Cycle: Adult worms dwell in the bowel lumen and migrate nocturnally out into the perianal region, releasing immature eggs that become infective within hours. Autoinfection results from perianal scratching and transport of infective eggs to the mouth. Person-to-person spread occurs. Pinworm is common among schoolchildren and their household contacts and among institutionalized populations.

40. Clinical Features: Perianal pruritus is the cardinal symptom and is often worst at night. Diagnosis: Eggs in the perianal region are detected by application of cellulose acetate tape in the morning. Eggs measure 55 by 25 µm and are flattened on one side.

41. TREATMENT: One dose of mebendazole (100 mg), albendazole (400 mg), or pyrantel pamoate(11 mg/kg; maximum, 1 g) is given, with the same treatment repeated after 10–14 days. Household members should also be treated.

42. Filarial and Related Infections Filarial worms are nematodes that dwell in the SC tissue and lymphatics. More than 170 million people are infected worldwide. Infection is established only with repeated and prolonged exposures to infective larvae. Disease tends to be more intense and acute in newly exposed individuals than in natives of endemic areas.

43. Elephantiasis of the lower extremity associated with Wuchereria bancrofti infection.

44. Life Cycle: Insects transmit infective larvae to humans
Life Cycle: Insects transmit infective larvae to humans. Adult worms reside in lymphatics or SC tissues; their offspring are microfilariae (200–250 µm long, 5–7 µm wide) that either circulate in the blood or migrate through the skin. Subperiodic forms are those that are present in peripheral blood at all times and peak in the afternoon.

45. Nocturnally periodic forms are scarce in peripheral blood by day and increase by night. Adult worms live for years; microfilariae live for 3–36 months.

46. LYMPHATIC FILARIASIS Etiology: Wuchereria bancrofti, Brugia malayi, or B. timori can reside in lymphatic channels or lymph nodes. W. bancrofti is most common and usually is nocturnally periodic.

47. Pathology: Adult worms cause inflammatory damage to the lymphatics.

48. Clinical Features: Asymptomatic microfilaremia, hydrocele, acute adenolymphangitis (ADL), and chronic lymphatic disease are the main clinical presentations. ADL is associated with high fever, lymphatic inflammation, and transient local edema. W. bancrofti particularly affects genital lymphatics. ADL may progress to lymphatic obstruction and elephantiasis with brawny edema, thickening of the SC tissues, and hyperkeratosis. Superinfection is a problem.

49. Diagnosis: Detection of the parasite is difficult, but microfilariae can be found in peripheral blood, hydrocele fluid, and occasionally other body fluids. Timing of blood collection is critical. Two assays are available to detect W. bancrofti circulating antigens, and a PCR has been developed to detect DNA of both W. bancrofti and B. malayi in the blood.

50. High-frequency ultrasound of the scrotum or the female breast can identify motile adult worms. Patients have eosinophilia and elevated IgE levels. The presence of antifilarial antibody supports the diagnosis, but cross-reactivity with other helminthic infections makes interpretation difficult.

51. TREATMENT: Diethylcarbamazine (DEC) given at 6 mg/kg daily for 12 days is the standard regimen, but one dose may be equally efficacious. An alternative is albendazole (400 mg bid for 21 days).

52. Prevention: • Mosquito control or personal protective equipment can minimize bites. • Mass annual distribution of albendazole with DEC or ivermectin for community- based control reduces microfilaremia and interrupts transmission.