Filarial Worms PDF

FILARIAL WORMS The filarial worms have complex life cycles involving a developmental stage in an insect vector. They require an arthropod vector for their transmission. The worms inhabit either the lymphatic system or the subcutaneous tissues of man. The female worm gives rise to...

FILARIAL WORMS The filarial worms have complex life cycles involving a developmental stage in an insect vector. They require an arthropod vector for their transmission. The worms inhabit either the lymphatic system or the subcutaneous tissues of man. The female worm gives rise to a young worm called microfilaria. The microfilariae, when taken by the arthropod intermediate host during biting, develop into filariform larvae, which are the infective stages. Humans get infected when bitten by the infected arthropod intermediate host. Wuchereria bancrofti- ‫داء الفيل‬ Is a filarial nematode that causes Wuchereriasis or filariasis (commonly called elephantiasis) in human beings. The name of this worm is given Wuchereria bancrofti in honor of the two scientists Wucherer and Bancroft who made a considerable contribution in studying the disease caused by these worms. This is a parasite of lymph nodes and lymphatic vessels- causing lymphatic filariasis. This filarial worm is transmitted by the bite of various species of mosquitoes. It is believed that over 100 million people are infected. The microfilariae are nocturnal – seen in greatest numbers in peripheral blood in the night between 10 PM -2 AM. The physiological basis of this nocturnal periodicity is not understood. Morphology: These are long, hair-like, transparent, translucent, thread-like worms with smooth cuticle and tapering ends. These are filiform and cylindrical in shape with both ends tapering. Sexes are separate with distinct sexual dimorphism. The female is larger (70–100 × 0.25 mm) than the male (25–40 × 0.1 mm). The posterior end of the female worm is narrow and pointed that bears an anus, while that of the male is curved vertically and contains numbers of genital papillae two copulatory spicules of unequal length. Males and females remain coiled together usually in the abdominal and inguinal lymphatics and in the testicular tissues. The head end is slightly enlarged.  Mouth aperture is simple, without lips. The pharynx is divisible into an anterior muscular portion and a posterior glandular portion. An oesophageal bulb is lacking. The intestine is simple. The vulva of the female is located ventrally in the pharyngeal region and provided with a pyriform ejector mechanism. The female worm is viviparous and directly liberates sheathed microfilariae into the lymph. The adult worms live for many years, probably 10–15 years or more. Mode of transmission and pathogenesis The filariform larvae are introduced through the skin by the bite of the arthropod intermediate host. The larvae invade the lymphatics, usually the lower limb, where they develop into adult worms. The microfilariae are librated into the blood stream. They remain in the pulmonary circulation during day, emerging into the peripheral circulation only during night, to coincide with the biting habit of the vector. Presence of the adult worms causes lymphatic blockage and gross lymphedema, which sometimes lead to elephantiasis. The adult worm obstructs the flow of lymph in the lymph nodes and the lymphatic vessels draining the lower limbs and the external genitalia. The lower limbs and external genitalia become swollen. The skin becomes thick and fissured. The disease is called bancroftian elephantiasis. The major symptoms and findings include: lymphangitis, lymphedema, fever, headache, myalgia, hydrocele and chyluria. Epidemiology: W. bancrofti infection occurs in sub-Saharan Africa, Southeast Asia, the Indian subcontinent, many of the Pacific islands, and focal areas of Latin America and the Caribbean (including Haiti). B. malayi occurs mainly in China, India, Malaysia, the Philippines, Indonesia, and various Pacific islands. B. timori occurs on the Timor Island of Indonesia Pathogenecity and clinical features: Microfilaria The first stage larva is called microfilaria. They are colorless, transparent bodies with blunt anterior ends and pointed tails. They are very active and can move forward and backward within the sheath which is much longer than the embryo. They are microscopic and measure about250–300 μm in length and 6–10 μm in thickness. Its body is covered with a hyaline sheath followed by a cuticula being lined by flattened subcuticular cells or epidermis and an inner column of cytoplasm containing nuclei. Its cuticle has well-marked striations. Somatic cella or Nuclei appear as granules in the central axis of the body extended from head to tail except for the 5% terminal end of the tip. Their head-end has clear space devoid of granules known as cephalic space. Important structures from the anterior end downwards are future mouth or oral stylet, nerve ring: oblique area devoid of granules, nephridiopore, renette cell, dark-colored inner mass, and 4 cells of the future anus. They do not undergo further development in the human body unless they are taken up by their suitable host (mosquitoes). Their life span in the human body is probably 70 days. Third stage of the larva (infective form) The third stage larva is the infective form of the parasite is found only in mosquitoes. They are elongated, filariform, measures1.5mm in length, and 18-23 µm in diameter Life cycle of Wuchereria bancrofti: Wuchereria bancrofti is digenetic i.e. its life history is completed in two hosts Definitive host: Man. No animal host or reservoir is known for W. bancrofti Intermediate host: Female mosquitoes, belonging to genus Culex, Aedes, and Anopheles. Infective form: Actively motile third-stage filariform larva is infective to man.  Life cycle of W. bancrofti Diagnosis ♦ Blood film examination after staining by Giemsa or Leishman stain to detect microfilaria. The film should be taken by night. Treatment - Diethyl carbamazine (DEC): 2 mg/kg 3x daily for 2 weeks. Endemic non-filarial elephantiasis (Podoconiosis) Non-filarial elephantiasis of the lower limbs is common in Ethiopia. Silicon, aluminium and iron particles in the red clay soil are absorbed through skin abrasions in bare footed persons. The mineral particles cause obstruction of the lymphatics.  Microfilaria of W. bancrofti in blood smear Onchocerca volvulus: African River blindness Infection by this filarial worm is common in Africa. It causes onchocerciasis, and is the second-leading cause of blindness due to infection worldwide after trachoma Morphology: Male: Similar to that of Wuchereria bancrofti, measure 15-45 mm in length Female: The female measures 30-50 cm in length. It is present inside of a fibrous nodule (onchocercomata or onchocerca tumor) in subcutaneous tissue. Adult males of Onchocerca volvulus ; females are 30-50 cm. Intermediate Host and vector: Female Simulium, (Simulium damnosum) complex black flies, found around plantations following rivers or river basins. Backflies breed along fast-flowing rivers and streams, close to remote villages located near fertile land where people rely on agriculture. Microfilaria: Measures 300 microns in length. It is non-sheathed microfilaria. It is present in the subcutaneous tissue fluids and not in blood.  Life cycle of O. volvulus Life cycle: Onchocerca volvulus breed exclusively in the Simulium yahense black fly, found only in certain endemic areas near fast-flowing rivers and streams. The life cycle starts by a black fly biting an infected human host and ingesting microfilariae from the skin or blood. These microfilariae migrate from the gut to the thoracic flight muscles of the fly, where they develop from the initial larval phase into the infective microfilariae after one week (Stages J1 --> J2). They then migrate to the salivary glands of the fly and are ready to be transmitted again (Stage J3s). The third stage larvae are then introduced into the skin of the new human host via a fly bite, where over the next 6-12 months, they develop into mature adult parasites. The larger female nematode migrates to the subcutaneous or deeper fascial tissues and becomes encapsulated by a fibrous shell. The males migrate into these capsules in order to fertilize the females. It is these capsules that are the characteristic subcutaneous nodules of onchocerciasis. Fertilized adult females in these nodules produce millions of microfilariae, which are responsible for the systemic and ocular findings of onchocerciasis. While the most common mode of transmission is direct via insect bites, the disease can also be spread transplacentally from an infected mother to her fetus Pathogenicity and clinical manifestations: The disease, onchocerciasis or river blindness includes: Skin fibrous nodules (onchocercomata) enclosing female worms. The nodules are common in neck, iliac crest and the coccyx. Skin hypo- or hyper- pigmentation. Dermatitis is present. In advanced cases, the skin becomes thickened and wrinkled, showing lizard or leopard skin appearance. Diagnosis: Superficial biopsy (skin snip) is taken from the skin using sharp razor blade. The specimen is allowed to stand for 30 minutes in saline before it is examined microscopically for microfilariae. Microfilaria of O. volvulus Treatment Ivermectin: 50 mg/kg bodyweight, given every 6 or 12 months. Because it kills microfilariae but not adult worms, retreatment is necessary over a period of years. Prevention Vector control Mass treatment Establishment of villages away from Simulium breeding places. Use of repellents Protective clothing Loa loa: Loiasis, African eye worm The insect vectors include mango or mangrove flies of Chrysops - Chrysops silacea, Chrysops dimidiata. It spreads to people through the repeated bites of deerflies that breed in rain forests in West and Central Africa. Loiasis is endemic in Central and West Equatorial Africa. The abundant rubber plantations provide a favorable environment for the vector to transmit the disease. Morphology Adults of Loa loa are often isolated from the subconjunctiva. Adult females are 40-70 mm in length and 0.45-0.60 mm wide; males are smaller at 30- 34 mm long and 0.35-0.40 mm wide. The exterior of the cuticle lacks ridging seen in many Dirofilaria but contains irregularly- spaced elevations called “bosses Pathogenesis The microfilaria have a sheath. Their diurnal periodicity corresponds to the feeding pattern of the insect vector, which bites humans from 10:00 AM to 4:00 PM. The adult worms live in subcutaneous tissue and wander round the body, provoking localized reactions known as Calabar swellings and sometimes migrating across the front of the eye. The sheathed microfilariae of Loa loa exhibit diurnal periodicity, so that, unlike those of Wucheraria Microflora: Microfilariae of Loa loa are sheathed and measure 230-250 µm long in stained blood smears and 270-300 µm in 2% formalin. The tail is tapered and nuclei extend to the tip of the tail. Microfilariae circulate in the blood. Life Cycle: Clinical Features Incubation period is about one year. It causes calabar swelling beneath the skin due to parasites. There is fever, pain, pruritus, urticaria, allergic reactions, retinopathy, glomerulonephritis, meningo-encephalitis etc. Laboratory diagnosis: Detection of microfilaria in peripheral blood, urine, sputum, CSF - stained with Giemsa or unstained Eosinophilia Treatment: Diethylcarbamazine(DEC), 6 to 10 mg per kilogram per day for 2 to 3 weeks: but has side effects - allergic reactions. DRACUNCULUS MEDINENSIS (Guinea worm or Medina worm) - ‫تنينة مدينية‬ Dracunculus medinensis causes dracunculiasis. The infection is endemic to Asia and Africa: India, Nile Valley, central, western and equatorial Africa, lowlands of Ethiopia and Eritrea. Morphology This worm is the largest of the tissue parasite affecting humans. Gravid female worms measure 70-120 cm in length. Mature female worms can measure up to 1 meter in length and are 1 to 2 mm wide. Male worms measure 15 to 40mm in length and are 0.4 mm wide Their body cavity is almost fully occupied by a uterus greatly distended with rhabditiform larvae (250-750 μm in length). A digestive tube and cuticular annulations distinguish the larvae from microfilariae. The adult female, which carries about 3 million embryos, can measure 600 to 800 mm in length and 2 mm in diameter. When a person drinks contaminated water from ponds or shallow open wells, the small crustacean copepods (cyclops ) which contain the larvae of D. medinensis which is dissolved by the gastric acid of the stomach and the larvae are released and migrate through the intestinal wall. infected larvae released in the stomach penetrate the mucosa of the stomach and intestinal wall and migrate into the connective tissue. The larvae then mature into adult worms. After 100 days, the male and female meet and mate. The male becomes encapsulated and dies in the tissues while the female moves down the muscle planes. After about one year of the infection, the female worm emerges, usually from the feet, releasing thousands of larvae and thus repeating the life cycle. An alternative life cycle was proposed recently involving dogs and fish. After eating raw fish containing guinea worm larvae, dogs can get infected. By eating raw fish, humans can get infected; this reported alternative cycle had made the eradication of the disease more challenging, especially in Chad. Larvae of D. medinensis Pathogenicity and life cycle Infection is acquired by drinking unfiltered or not boiled water that contains Cyclops species. The larvae are released in the stomach, penetrate the intestinal wall and find their way to the subcutaneous tissue. Mating takes place in the axillary or inguinal regions 3 months after infection. The male worms then die in the tissue and the female worms move down to the limbs within 10 months. In about 1 year, female worms in the subcutaneous tissue provoke the formation of a burning blister in the skin of the legs. When in water, the blister bursts, and about 5 cm of the worm is extruded from the resulting ulcer - thus releasing many thousands of first stage larvae. The larvae swim in water and are ingested by the intermediate host - Cyclops species- within about 4 days. Inside the Cyclops, the larvae molt twice and become infective in 2 weeks Life cycle of Drancunculus medinesis Clinical feature: The female parasites in the subcutaneous tissue release toxic byproducts of histamine-like nature, which cause systemic allergic reactions, like erythema, urticaria, pruritus, fainting, asthma, dyspnea, etc. This is followed by the appearance of a blister on the legs, which ruptures on contact with water releasing larvae into the water by the female worm. The wound may ulcerate. The worms migrate into other tissues and may cause arthritis, pericarditis, abscesses etc. It occasionally penetrates the eyeball and causes loss of the eye. Diagnosis 1. Clinical: Observation of blister, worm or larvae 2. Histologic features of subcutaneous sinus tract 3. Eosinophilia and radiographic evidence Treatment Surgical excision when the worm is in the leg Niridazole (Ambilhar) or DEC Prevention Health education on: ♦ Boiling or filtering of drinking water ♦ Treating of patients and educating them not to enter water bodies ♦ Using insect larvicides to kill Cyclops in water. TRICHINOSIS ‫داء الشعرينات‬ Etiologic agent - Trichinella spiralis This is the only important species in this group. It causes trichinosis – a cosmopolitan infection. More than 100 different animal species can be infected with Trichinella species, but the major reservoir host for human infections is swine. These roundworm parasites (trichinella) use a host body to live and reproduce. These parasites infect animals such as bears, cougars, walruses, foxes, wild boars and domestic pigs. Human get the infection by eating the immature form of the roundworm (larvae) in raw or undercooked meat. When humans eat raw or undercooked meat containing trichinella larvae, the larvae grow into adult worms in the small intestine. This takes several weeks. The adult worms produce larvae that travel through the bloodstream to different parts of the body. They then bury themselves in muscle tissue. Morphology Adult female worm measures 3-4 mm in length and the adult male worm measures 1.4-2.6 mm in length. The encysted larvae measure 800-1300 μm in length. Pathogenicity and life cycle After ingesting infected meat, the capsule of the encysted larvae is digested by gastric juice, and the larvae are released in the duodenum or jejunum where they molt four times to become adult worm. After mating, the male worm dies and the female worm begins to deliver the embryos 4-7 days after the infection. The larvae penetrate the intestinal wall and migrate through the lymphatic vessels to the blood stream, which carries them to various organs. Skeletal muscles and diaphragm are most frequently parasitized. Others include the tongue, masseter and ocular muscles.  Life cycle of Trichinella spiralis Clinical features There are two clinical phases. 1. The intestinal phase: lasting 1-7 days - asymptomatic; sometimes cause nausea, vomiting, diarrhea, constipation, pain, etc, 2. The muscle phase: which causes myalgia, palpabral edema, eosinophilia, fever, myocarditis, meningitis, bronchopneumonia etc. Diagnosis: ♦ Muscle Biopsy ♦ Detection of larvae in blood or CSF ♦ Detection of larvae and adult worms in stool (rare). ♦ ELISA Treatment - Thiabendazol Prevention ♦ Cooking of all meat before consumption ♦ Inspection of pigs ♦ Pork must be stored at -150 C for 20 days.