Tissue nematodes ppt for Medical undergraduates

Tissue nematodes lecture for MBBS.

1. Tissue Nematodes

2. Introduction to Helminths Elongated flat or round worm like parasites measuring few milimeters to meters

3. Classification of helminths based on habitat

4. (Somatic Nematodes) Somatic nematodes inhabit in the extra intestinal sites They can be grouped into filarial and non-filarial nematodes

5. WUCHERERIA BANCROFTI: LYMPHATIC FILARIAL NEMATODES Lymphatic filariasis is caused by Wuchereria bancrofti , Brugia malayi and B. timori Microfilariae are the diagnostic forms, found in the blood vessels The nuclei are present throughout the body except near the head and the tail end W hen stained with Giemsa or other Romanowsky stains they look pink with a column of violet nuclei

6. Epidemiology Filarial W. bancrofti , is the most widely distributed parasite of humans It is found throughout the tropics and subtropics with highest prevalence in Asia (India-5 %, China) and Sub-saharan Africa (8%) Highly endemic states are Uttar Pradesh, Bihar , Jharkhand, Odisha, Andhra Pradesh, Tamil Nadu, Kerala and Gujarat Host: 1 . Definitive host: Man 2. Intermediate host: Mosquito named Culex quinquefasciatus is the principle vector worldwide Infective form: Third stage filariform larvae found in the proboscis of the mosquito. Mode of transmission: L3 filariform larvae get deposited in skin by the insect bite

7. Life cycle

8. Clinical Features Incubation period is about 8–16 months Clinical manifestations can be categorized into: 1. Lymphatic filariasis 2. Tropical pulmonary eosinophilia (TPE ) / ( Occult filariasis ) 3. Immune complexes mediated manifestations

9. Lymphatic Filariasis These are the normal people residing in endemic area This might be due to: Insufficient exposure Immunological resistance Prepatent period at the time of study

10. Asymptomatic microfilaraemia In endemic area, many infected individuals don’t exhibit any symptoms of filarial infection . Microfilaremia demonstrated in their peripheral blood Microscopic hematuria and/or proteinuria Dilated and tortuous lymphatics ( visualized by imaging) Filarial dance sign (ultrasound showing motile adult worm in scrotal lymphatics )

11. Acute filariasis (acute adenolymphangitis ) It is characterized by recurrent episodes of: Filarial fever (high-grade fever) Lymphatic inflammation ( lymphangitis and lymphadenitis) Transient local edema: Early pitting edema; reversible on limb elevation Dermatolymphangitis : Plaque like lesion is formed over the affected skin with fever, chill and lymphatic inflammation

12. Chronic filariasis It develops 10–15 years after infection Chronic host immune response against the dead worm leads to enhanced granuloma, thrombi formation and fibrosis of the lymph vessels leading to severe lymphatic obstruction and pedal edema

13. Occult Filariasis or Tropical pulmonary Eosinophilia ( TpE ) Also called as Weingarten’s syndrome: in infected individuals of endemic places R eported from India , Pakistan, Sri Lanka, Brazil, Guyana, and Southeast Asia Nocturnal paroxysmal cough and wheezing (due to nocturnal periodicity of microfilariae), weight loss , low-grade fever Laboratory Diagnosis Blood eosinophilia (absolute eosinophil count more than 3000/ μ L) Chest X-ray: Shows diffuse infiltration Elevated serum IgE levels Pulmonary function test shows obstructive changes in lungs. Treatment It responds well to Diethylcarbamazine (DEC ), 4–6 mg/kg for 14 days. Relapse may occur in 12–25% of cases.

14. Laboratory Diagnosis Microscopy (To detect Microfi lariae ) Sample: Microfilariae can be found in blood , and occasionally in hydrocele fluid, urine or other body fluids Direct wet mount: Demonstrates serpent tine movement of microfi lariae Thick smear stained with Leishman’s , Giemsa or hematoxylin and eosin stain can be performed to observe the sheath and nuclei of microfilaria

15. Collection time: It is critical and should be based on the periodicity of the microfilariae . For nocturnal periodicity, blood should be collected between 9 pm and 2 am. DEC provocation test: day time Patient takes a tablet of DEC orally (2mg/kg ) so that the nocturnal microfilariae are stimulated and come to peripheral blood within 30 minutes QBC (Quantitative buffy coat examination ): It involves centrifugation of blood, staining with acridine orange stain and examined under fluorescent microscope. This technique is more sensitive than smear microscopy Antigen detection: by using monoclonal antibodies against Og4C3 and AD12 antigens Laboratory Diagnosis Microscopy (To detect Microfilariae )

16. Management Various formats are used like indirect hemagglutination (IHA), indirect fluorescent antibody test (IFA) and ELISA Imaging Methods Ultrasound: Filarial dance sign; Serpentine movement of adult worms within the lymphatic vessels of scrotum—positive in 80% of cases Treatment: Diethylcarbamazine ( DEC) It is the drug of choice for the treatment of Filariasis It is given 6 mg/kg daily for 12 days

17. Filariasis control programme Elimination of lymphatic filariasis by 2015: Launched in India in 2002, by National Health Policy Strategies employed are — ( 1) Annual mass administration of DEC or DEC + Albendazole (2 ) Home based management for lymphedema cases and up scaling of hydrocele operations

18. Brugia Malayi In India, the major states involved are Kerala , Odisha, Assam and West Bengal . Vector: Mansonia ( M. annulifera and M. uniformis ) is the main vector for the nocturnal strains, Anopheles and Aedes also can transmit the infection Reservoir: Humans

19. OTHER FILARIAL NEMATODES: Loa loa Loa loa (also called as African eye worm ) was first reported in West Indies in 1770 Epidemiology Loa loa is restricted to the rain forests of West and Central Africa . Life cycle is similar to that of W. bancrofti except the vector is female Chrysops species(deerflies , mango flies , red flies or tabanid flies)

20. Pathogenesis and Clinical Feature C alabar Swellings This is the most common form of loiasis , also called as fugitive swelling It is a subcutaneous swelling developing on the extremities (knee or wrist) and less frequently at other sites It occurs due to host inflammatory response to the migrating adult worm (at a speed of 1cm/min) or its metabolic products Microfilariae are not pathogenic

21. Management Ocular Manifestations It includes conjunctival granuloma, edema of eye lid leading to proptosis (bulging ) Microscopy Definite diagnosis of loiasis requires: Detection of microfi lariae in the peripheral blood Diethylcarbamazine (DEC) is the drug of choice Dose: DEC is given in a dose of 8–10 mg/ kg per day for 21 days It is effective against both the adult and the microfilarial forms of L. loa

22. ONCOCERCA VOLVULUS Onchocerca volvulus is the causative agent of “river blindness” in man . Sub Saharan Africa, particularly West Africa The infection is also found in Yemen and in part of central and South America Microfilaria They are usually found in skin dermis (90 %) or rarely in the subcutaneous nodules, blood, sputum or urine Life Cycle Life cycle is similar to that of W. bancrofti except the vector Simulium (black flies )

23. Clinical Features I n heavy infections the major manifestations include skin (dermatitis ), subcutaneous fibrous nodule ( onchocercoma ), lymphadenitis and ocular changes. Skin (dermatitis ) Onchocercoma (Subcutaneous Nodules ) Conjunctivitis with photophobia Lymphadenopathy

24. Lab diagnosis Detection of microfi lariae —skin snip technique Skin snips technique; Most common sites: Both iliac crests or sometimes from calves and the shoulders Procedure : Skin is lifted by a needle and a small piece (1 to 3 mm) is excised with a sterile scalpel blade Detection of adult worm—biopsy of subcutaneous nodule

25. Serology—IgG-4 specifi c dip stick assay Molecular method—PCR Mazzoti skin test (DEC patch test) Eosinophelia and elevated serum IgE Ivermectin is the drug of choice for onchocerciasis Given orally in a single dose of 150 μg /kg , either yearly or semiannually Lab diagnosis

26. Dracunculus medinensis Dracunculus medinensis causes Guinea worm disease or dracunculiasis Reported from Sub-Saharan Africa such as Sudan (the highest burden), Ghana, Mali, and Niger It is eliminated from India (and also from Pakistan )

27. Epidemiology Host: There are two types of hosts: 1 . Definitive host: Man 2. Intermediate host: Copepods ( Cyclops ) Infective form: Third stage filariform larvae Mode of transmission: Man gets infection by drinking fresh water from stagnant pools containing minute fresh water crustaceans ( Cyclops ) infected with L3 larvae

28. Clinical features The initial presentation is a painful papule that enlarges over hours to days to form a blister from which the worm emerges The most common site—lower leg, ankle and foot The manifestations are seasonal (June to September)

29. Lab diagnosis Detection of adultworm (from blister) Detection of L1 larvae Antibody detection—ELISA Peripheral blood Eosinophilia There are no anti-helminthic drugs known to be effective against D. medinensis Symptomatic t/t: application of wet compresses, administration of analgesics, prevention of secondary bacterial infection by the use of topical antibiotics

30. TRICHINELLA SPIRALIS Trichinella spiralis causes trichinellosis ( or trichinosis ) which is a zoonotic infection acquired from domestic pigs or other carnivores T. spiralis was first detected by James Paget and Richard Owen (1835) from a cadaver muscle In India Few cases of animal trichinellosis has been reported The first case was reported from the Punjab In 2010, an outbreak of human trichinellosis had occurred in Uttarakhand It is one of the smallest intestinal nematode

31. Life cycle Pig is the optimum host and is the principal reservoir of infection Animals like rats horses or other carnivores can also serve as the host Transmission usually occurs in nature from one flesh eating animal to other Common cycles are pig to pig, rat to rat, pig to rat Man is an accidental host and acts as dead end Infective form: First stage (L1) larvae Mode of transmission: By ingestion of raw or uncooked pork or other animal meat containing L1 larvae

32. Clinical features Clinical symptoms of trichinellosis depend on the phase of parasitic invasion — Enteric invasion , larval migration, and muscle encystment Most of the light infections are asymptomatic Symptoms appear in the second week after infection Periorbital and facial edema is common Hemorrhages are seen in the sub-conjunctiva, retina and nail beds (“splinter” hemorrhages) Maculopapular rash

33. Stage of Muscle Encystment Occurs 2–3 weeks after infection Common symptoms are myositis with myalgia , muscle edema, and weakness Most commonly involved muscles: extraocular muscles followed by biceps; and muscles of the jaw, neck, lower back, and diaphragm

34. Lab diagnosis Demonstration of larvae in muscle biopsies—By direct slide technique and H and E stain Serology (antibody detection)—ELISA, CIEP Bachman intradermal test: Intradermal injection of Bachman antigen (prepared from Trichinella larva obtained from rabbit muscle) causes an immediate small induration surrounded by erythema of 5 cm diameter in 15–20 minutes Animal inoculation in rats Other method—blood eosinophilia, elevated WBC count, elevated muscle enzyme, etc

35. Treatment Moderate infection: Mebendazole and albendazole are active against enteric stages of the parasite Severe infection: Glucocorticoid is added which is beneficial for severe myositis and myocarditis

36. Thank you