Brugia malayi Malayan filariasis Morphology Microfilaria Presence of

Brugia malayi Malayan filariasis

Morphology Microfilaria: Presence of two distinct nuclei at tail end is characteristic feature.

Life cycle is essentially same as W bancrofti. Nocturnal periodic B malayi transmitted by Anopheles and Mansonia, while sub periodic strains are transmitted by Coquilletcidia and Mansonia. Not transmitted by Culex. Man is definitive host and main reservoir of infection. Leaf monkeys are definitive hosts and reservoirs for sub-periodic B malayi

Clinical manifestations Acute stage: Characterised by recurrent attacks of lymphadenitis associated with fever chills and rigors. Attacks are usually precipitated after hard physical work Inguinal lymph nodes are commonly involved Often the infected lymph nodes suppurate to form abscesses Chronic stage: Elephantiasis commonly seen below knee only.

Epidemiology Restricted distribution. Nocturnal periodic strains common seen in rice growing areas of coastal regions. In India; Kerala, Orissa, Assam, West Bengal, and Madhya Pradesh.

Laboratory diagnosis Capillary blood is taken from patient during • 10 pm and 4 am: Nocturnal periodic strains, • 8 -10 pm in night for sub periodic strains

Onchocerca volvulus (Blinding filaria – 2 nd most common cause of infectious blindness) • Definitive host: Man • Intermediate host: Black flies (simulium) • Infective form: L 3 Larva • Mode of transmission: Inoculation • Site of localization: Subcutaneous tissue, dermis & eye

Geographic Distribution Onchocerca volvulus, occurs mainly in Africa, with additional foci in Latin America and the Middle East.

Life Cycle

Microfilaria invade the midgut of the fly, advance to the thoracic muscles where they undergo differentiation into L 1 larva within 28 hours after the blood meal. They moult twice producing L 2 and L 3 larva (infective larva). Infective L 3 larva migrates to the proboscis for future deposition into human skin during the next blood meal. When the Fly bites another person, Infective L 3 larvae are injected into subcutaneous tissue.

The larvae move under the skin and form nodules where they develop into adult worms in 12 to 18 months. Adult worms pair and mate in the human host. Female Onchocerca gives birth daily to thousands of microscopic larvae (microfilaria) Microfilaria released from the nodules traverse the skin and connective tissue easily. The most common migration sites are subepidermal lymphatics and the anterior chamber of the eye.

Onchocerciasis also known as river blindness and Robles' disease, Skin involvement typically consists of intense itching, swelling, and inflammation Skin atrophy - loss of elasticity, the skin resembles tissue paper, 'lizard skin' appearance, and depigmentation. May involve any part of the eye from conjunctiva and cornea to uvea and posterior segment, including the retina and optic nerve

Clinical features Incubation period - 10 to 12 months Eosinophilia and urticaria. Nodular and erythematous lesions (Onchocercomata) in the skin and subcutaneous tissue Photophobia, lacrimation, keratitis and blindness – due to trapping of microfilaria in the cornea, choroid, iris and anterior chambers.

27/04/08 Dr Ekta, Microbiology

Diagnosis The best method for diagnosis is identification of microfilariae in bloodless skin snips. Buttocks and legs are often most heavily infected and are most likely to yield microfilariae. A small piece of skin is raise with a needle and clipped with a razor or scissors.

27/04/08 Dr Ekta, Microbiology

Diagnosis & Treatment Nodular biopsy – adult worm Skin snip – unsheathed microfilaria with no nuclei Treatment – Ivermectin, surgical removal, DEC in non ocular onchocercosis

Diagnosis In heavily infected individuals, microfilariae can even be found in the blood, sputum and urine. Living microfilariae of Onchocerca volvulus on urine sample Living microfilariae of Onchocerca volvulus in blood sample

Loa the filarial nematode that causes Loa loa filariasis. It is commonly known as the “African eye worm". Its geographic distribution includes Africa and India

Loa loa (African eye worm) • Definitive host: Man • Intermediate host: Chrysops (deer fly, Mango fly) • Infective form: L 3 Larva • Mode of transmission: Inoculation • Site of localization: Subcutaneous & deep connective tissue

Life cycle Three species involved in the life cycle include the parasite Loa loa, the fly vector, and the human host. A vector fly bites an infected human host and ingests microfilariae. Microfilariae move to the fat body of the insect host. Microfilariae develop into first stage larvae, second stage, then third stage larvae. Third stage larvae (infective) travel to the proboscis of fly.

Life cycle An infected vector fly bites an uninfected human host and the third stage larvae penetrates the skin and enters human subcutaneous tissue. Larvae mature into adults, who produce microfilariae that have been found in spinal fluid, urine, peripheral blood, and lungs Maturing larvae and adults occupy the subcutaneous layer of the skin

Clinical features Subcutaneous swelling – Calabar or fugitive swelling, measuring 5 to 10 cm, marked by erythema and angioedema, usually in the extremities Migrating worm in sub- conjunctival tissue

Diagnosis Examination of blood samples will allow identification of microfilariae of Loa loa. It is important to time the blood collection with the known periodicity of the microfilariae. The blood sample can be a thick smear, stained with Giemsa or haematoxylin and eosin

Diagnosis & Treatment • Peripheral blood smear - Sheathed microfilaria with nuclei upto rounded tail tip • Isolation of worms from the conjunctiva or subcutaneous biopsy • Treatment - Ivermectin, surgical removal, DEC (effective against adult & microfilaria)

DRACUNCULUS MEDINENSIS FIERY SERPENT/ MEDINA WORM/ THREAD WORM

Introduction Known as guinea worm disease. Also called serpent/medina/Thread worm. Vector borne parasitic disease. Involves subcutaneous tissues(leg and foot). Caused by nematode parasite, Dracunculus medinensis. Its not lethal but disable its victim temporarily.

Transmitted exclusively when people drink stagnant water contaminated with parasite infected water cyclops. It affects people in rural, deprived and isolated communities who depend mainly on open surface water sources such as ponds and wells. In India, the last case was reported in July 1996. On completion of three years of zero incidence, India was declared free of guineaworm disdease.

Dracunculus medinensis (Guinea Worm) Adult worms: Male 2 to 4 cm, Female 70 – 120 cms, viviparous Definitive host: Human: Intermediate host: Cyclops Infective form: Larva inside Cyclops Mode of transmission: Ingestion of water contaminated with cyclops Site of localization: Subcutaneous tissue

Cyclops

Epidemiology AGENT: Dracunculus medinensis Adult parasite inhabits subcutaneous tissue mainly of legs but other parts are also included. Female worm is 55 to 120 cm long as compare to male 2 to 3 cm long. HOST: Man is the definitive host. Multiple and repeated infections may occur in the same individual. Habit of washing and bathing in surface water and using step-well makes them prone to infection.

27/04/08 Dr Ekta, Microbiology

LIFE CYCLE Adult females are found in the sub-cutaneous tissues of man, especially in the regions around the ankle, back and intermuscular connective tissues of the lower extremities of the body like arms and legs. The male and female attain their sexual maturity in the retroperiotoneal connective tissues and undergoes the process of copulation. The male die after fertilising the female and gets calcified to remain there for about six months before getting disappeared.

A fertilized female migrates to reach the selected parts of the host’s body which are liable to come in contact with water like arms, legs, knee, ankle joint and back (in case of water carriers). The adult female acquires its place in subcutaneous tissues of these parts. On reaching the skin surface, female secretes a toxin which produces a blister of about 5 to 7 cm in diameter on the skin surface. The blister eventually breaks and an ulcer is formed. At the base of the ulcer appears a minute pore.

Contact with water stimulates the worm to protrude its head and causes a reflex discharge of milky fluid, containing large number of embryos. The female bear a large uterus in which several embryos remain lodged in coiled form. When the worm comes in contact with water, these embryos are liberated into outside water from the prolapse uterus. D. medinensis are viviparous because instead of producing eggs they discharge embryos. Further development of embryo occurs only when it reaches into the body of intermediate host.

After being liberated from the mother’s body the embryo wait for few days for its intermediate host. Cyclops belonging to class crustacea act as intermediate host for D. medinensis. The embryos are ingested by cyclops, 15 to 20 embryos can be ingested and accommodated in the stomach of a single cyclop without causing much inconvenience. The normal life span of cyclop is about 3 to 4 months, but the infected cyclop die in about 42 days in ordinary infection and in about 15 days in case of heavy infection.

Fresh water crustacean called cyclops take these larvae. Larvae require 15 days for their development in these cyclops. Cyclops act as INTERMEDIATE HOST. Man acquires infection by drinking water containing infected cyclops.

In human body digested by gastric juice, parasites are released. These parasites can penetrate the duodenal wall. Migrate through the viscera to the subcutaneous tissues of various parts of the body. Grow into adult worms in 10 -14 months.

Gravid female goes down infected persons lower limb near skin surface. Worm penetrates into the dermis and induces an inflammatory reaction and blister formation. Upon contact with water the worm bursts releases up to 1 million microscopic, free swimming larva in water. Larvae remain active in water for 3 -6 days.

Clinical Features Disease – Dracunculosis Intense burning pain localized to path of travel of worm(the fiery serpent). Fever, Nausea, Vomiting Allergic reaction Arthritis and paralysis (due to death of adult worm in joint).

Clinical Features Clinical features develop an year after infection following the migration of worm to the subcutaneous tissue of the leg Blister formation – rupture of blister when in contact with water - ulceration – release of larvae by adult female worm Secondary bacterial infection of ulcer

Diagnosis Detection of adult worm – when it appears at the surface of skin Detection of larva – in milky fluid released by worm on exposure to water Radiology – calcified worm in deeper tissues

Treatment • Thiabendazole/ Metronodazole – symptomatic relief, easy removal of worm • Gradual extraction of worm by winding of a few cms on a matchstick per day, over 3 to 4 weeks Worms are removed by sequentially rolling them out over a small stick. ‘ROD OF ASCLEPIUS” • • Surgical excision

Prevention Provision of safe water supply Education to discourage people from entering water source Filtering water through a double folded cloth Boiling water before drinking Discouraging the use of step wells