Parasitology BZO6T14

Syllabus topics (RTMNU)

• Basic Concepts of Parasitology and Host–Parasite Relationships: Definition and scope of parasitology
• types of parasites based on habitat, host dependence, degree of pathogenicity, and host specificity
• Types of hosts (Stages of Parasite’s Development, Conditions for Parasite’s Development, Transmission Agents of Parasites)
• Evolution of host–parasite relationships, parasite life cycle patterns, and mechanisms of pathogenesis
• Distribution, Transmission, and Zoonotic Diseases: Sources of parasitic infection including soil, water, food, and animals (zoonoses)
• Modes of transmission—direct and indirect transmission
• Course of infection: incubation period, prodromal period, illness period, decline period, and convalescence period
• Clinical manifestations including morphological, behavioral, and physiological symptoms
• Diagnosis, Prevention, and Control of Parasitic Diseases: Methods of diagnosis including faecal examination (ova and parasite detection), blood tests, imaging techniques, immunodiagnostic tests, and laboratory culture methods
• Principles of prevention and control of parasitic infections in humans and animals
• Host Immunity and Parasite Adaptations: General immune responses against parasites—humoral immunity and cell-mediated immunity
• Hypersensitivity reactions and regulation of immune responses
• Self-defense mechanisms of the host
• Adaptations in parasites including immunological, morphological, nutritional, biochemical, and life cycle adaptations that facilitate survival within the host

Basic Concepts of Parasitology

Parasitology is the branch of biology that studies parasites, their hosts and the relationship between them. Parasitism is a close association in which one organism (the parasite) lives on or in another (the host), gets food and shelter from it and usually harms it.

Scope: medicine (malaria, filariasis, amoebiasis), veterinary science (livestock parasites), agriculture (plant nematodes), public health, immunology, drug and vaccine development, evolution and ecology.

Types of parasites:

• By habitat: ectoparasites live on the body surface (lice, ticks); endoparasites live inside (tapeworm, Plasmodium).
• By host dependence: obligate – cannot live without a host (Taenia); facultative – can live free or as parasite (Naegleria); temporary/intermittent – visits host only for food (mosquito, bedbug); permanent – whole life in host; accidental – enters an unusual host; aberrant/wandering – reaches an unusual site.
• By pathogenicity: pathogenic – cause disease (E. histolytica); non-pathogenic/commensal – little or no harm (Entamoeba coli); opportunistic – cause disease when immunity is low (Toxoplasma, Cryptosporidium in AIDS).
• By host specificity: monoxenous (one host, e.g., Ascaris, Entamoeba), heteroxenous (two or more hosts, e.g., Plasmodium, Taenia); stenoxenous (narrow host range) and euryxenous (wide host range).

Types of Hosts

• Definitive (final) host: where the adult or sexual stage lives (mosquito for Plasmodium; man for Taenia solium).
• Intermediate host: where larval or asexual stages develop (man for Plasmodium; pig for T. solium; snail for flukes).
• Reservoir host: an animal that keeps the parasite in nature and is a source of human infection (dogs for Leishmania).
• Paratenic (transport) host: parasite survives but does not develop.
• Vector: a living transmission agent, usually an arthropod – biological vector (parasite develops inside, e.g., Anopheles) or mechanical vector (just carries, e.g., housefly).

Conditions for parasite development: suitable host and site, right temperature and moisture outside (for eggs/larvae), presence of the correct intermediate host or vector, and a host whose immunity allows survival.

Evolution of Host–Parasite Relationships, Life Cycle Patterns and Pathogenesis

Parasitism probably evolved from free-living ancestors through commensalism. Over long co-evolution, a well-adapted parasite tends to cause less harm because killing the host also kills the parasite; new or unusual hosts often suffer more.

Life cycle patterns: direct (simple) – one host, infective stage passes from host to host (Ascaris, Giardia); indirect (complex) – one or more intermediate hosts or vectors (Fasciola, Plasmodium, Wuchereria).

Mechanisms of pathogenesis: mechanical damage (blocking ducts or intestine – Ascaris; lymph blockage – filaria), tissue destruction (amoebic ulcers), robbing nutrients (vitamin B₁₂ loss), toxic and allergic products, inflammation and immune damage, and opening the way for secondary bacterial infections.

Distribution, Transmission and Zoonotic Diseases

Sources of infection: soil (hookworm, Ascaris eggs), water (Giardia cysts, schistosome cercariae), food (undercooked pork – Taenia; raw vegetables), animals and insects.

Zoonoses are diseases naturally transmitted between vertebrate animals and man, e.g., toxoplasmosis (cats), taeniasis (pigs, cattle), leishmaniasis (dogs), hydatid disease (dogs).

Modes of transmission: direct – contact, sexual (Trichomonas), congenital/transplacental (Toxoplasma), faeco-oral by hands; indirect – through contaminated food/water, vectors (mosquito, sandfly), skin penetration (hookworm, cercariae), blood transfusion.

Course of infection: (1) incubation period – from entry to first symptoms; (2) prodromal period – mild, general symptoms; (3) illness period – full symptoms; (4) decline period – symptoms reduce; (5) convalescence – recovery.

Clinical manifestations: morphological (swelling, elephantiasis, anaemia, cysts), behavioural (weakness, itching, sleepiness in trypanosomiasis), physiological (fever, diarrhoea, malabsorption).

Diagnosis, Prevention and Control

• Faecal (stool) examination: saline and iodine mounts for ova, cysts and trophozoites; concentration methods.
• Blood tests: thick and thin smears (malaria, filaria – night blood); eosinophil count.
• Imaging: X-ray, ultrasound, CT/MRI (cysticercosis, hydatid cyst, liver abscess).
• Immunodiagnosis: ELISA, rapid diagnostic tests (malaria antigen), antibody detection; PCR for parasite DNA.
• Culture: NNN medium for Leishmania; culture of Trichomonas.

Principles of prevention and control: break the life cycle at its weakest point – treat infected persons (reduce source), sanitation and safe water, proper cooking of meat, vector control, health education, deworming of animals, meat inspection.

Host Immunity and Parasite Adaptations

Host immune responses: innate defences (skin, stomach acid, phagocytes, complement); humoral immunity – B cells make antibodies (IgG, IgM; IgE against helminths with eosinophils and mast cells); cell-mediated immunity – T-helper and cytotoxic T cells, macrophage activation (important against intracellular parasites like Leishmania, Toxoplasma). Hypersensitivity – overreaction causing damage (e.g., allergic reactions to worms, granulomas around schistosome eggs). Regulatory T cells control the response.

Parasite adaptations:

1. Immunological: antigenic variation (trypanosomes change surface coat; Plasmodium), hiding inside cells, coating with host molecules (schistosomes), suppressing host immunity.
2. Morphological: loss of sense organs and locomotion; hooks, suckers (tapeworm scolex); thick cuticle or tegument resisting digestion.
3. Nutritional: absorb digested food through body surface (tapeworm has no gut).
4. Biochemical: anaerobic respiration; anti-enzymes against host digestive enzymes.
5. Life cycle: huge egg output, hermaphroditism, asexual multiplication in larval stages, resistant cysts, use of intermediate hosts.

Likely exam questions

1. (Long, 8 marks) Define parasitism. Classify parasites and hosts with suitable examples.
2. (Long, 8 marks) Describe host immune responses against parasites and the adaptations of parasites for survival in the host.
3. (Short, 4 marks) What are zoonotic diseases? Give examples.
4. (Short, 4 marks) Describe the course of a parasitic infection.
5. (Short, 4 marks) Write a note on laboratory diagnosis of parasitic diseases.

Syllabus topics (RTMNU)

• Intestinal Protozoan Parasites: Study of Giardia lamblia and Entamoeba histolytica with reference to their morphology, life cycle, mode of transmission, pathogenesis, clinical manifestations, diagnosis, and treatment
• Urogenital and Tissue Protozoan Parasites: Study of Trichomonas vaginalis and Toxoplasma gondii including morphology, life cycle, transmission, pathogenesis, clinical manifestations, diagnosis, and preventive measures
• Blood and Tissue Flagellates: Study of Trypanosoma spp. (African and American trypanosomiasis) and Leishmania spp. (leishmaniasis), including life cycle, mode of transmission through vectors, pathogenesis, prevention, and treatment
• Sporozoan Parasites and Coccidia: Study of Plasmodium spp. (malaria parasite) and Cryptosporidium spp., focusing on life cycle, transmission, pathogenicity, clinical manifestations, diagnosis, prevention, and treatment

Giardia lamblia

Morphology: Trophozoite – pear-shaped, bilaterally symmetrical, 10–20 µm, with two nuclei, a ventral sucking disc, four pairs of flagella, two median bodies (looks like a "face"). Cyst – oval, four nuclei, thick wall; infective stage.

Life cycle (one host – man): cysts swallowed in contaminated water/food → excystation in duodenum → trophozoites attach to intestinal wall with sucking disc and multiply by binary fission → encystation in colon → cysts passed in stool.

Transmission: faeco-oral route, contaminated water. Pathogenesis and symptoms (giardiasis): trophozoites cover the mucosa and damage villi → malabsorption of fat → foul-smelling, greasy diarrhoea (steatorrhoea), bloating, weight loss, especially in children. Diagnosis: cysts/trophozoites in stool, stool antigen test. Treatment: metronidazole, tinidazole.

Entamoeba histolytica

Morphology: Trophozoite (15–40 µm) – one nucleus with central karyosome, finger-like pseudopodia, ingested RBCs (key sign of invasive form). Cyst – round, up to four nuclei, chromatoid bars; mature four-nucleate cyst is infective.

Life cycle: mature cysts swallowed → excystation in lower ileum → one cyst gives eight small amoebae → trophozoites live in colon and multiply by binary fission → some invade the mucosa → others encyst and pass out in stool.

Pathogenesis (amoebiasis): trophozoites secrete enzymes and destroy tissue → flask-shaped ulcers in colon → amoebic dysentery (stool with blood and mucus, abdominal pain). They may reach the liver through the portal vein → amoebic liver abscess (fever, pain in right upper abdomen). Many carriers are symptom-free and spread cysts.

Diagnosis: stool microscopy, antigen ELISA, ultrasound for liver abscess. Treatment: metronidazole followed by a luminal drug (diloxanide furoate). Prevention: safe water, hand washing, sanitation.

Trichomonas vaginalis

Morphology: only trophozoite stage (no cyst); pear-shaped, 10–25 µm, four anterior flagella, an undulating membrane with a fifth flagellum, axostyle.

Life cycle and transmission: single host (man); lives in vagina (women) and urethra/prostate (men); multiplies by binary fission; transmitted mainly by sexual contact – a sexually transmitted infection.

Pathogenesis and symptoms: vaginitis with frothy yellow-green discharge, itching, burning urination; men are often symptom-free carriers (urethritis). Diagnosis: wet mount showing jerky moving trophozoites, culture, rapid antigen/PCR tests. Prevention: treating both partners (metronidazole), safe sex, condoms.

Toxoplasma gondii

Morphology: three forms – tachyzoite (crescent-shaped, rapidly multiplying), bradyzoite in tissue cysts (slow, in brain and muscle), oocyst (in cat faeces).

Life cycle: definitive host – cat (sexual cycle in intestine, oocysts passed); intermediate hosts – man and other mammals and birds (asexual cycle).

Transmission: eating oocysts from cat faeces (soil, vegetables), undercooked meat containing tissue cysts, transplacental (mother to foetus), transplant/transfusion.

Pathogenesis: usually mild or silent in healthy people; dangerous in pregnancy (congenital toxoplasmosis: abortion, hydrocephalus, eye damage) and in AIDS patients (brain infection). Diagnosis: IgG/IgM antibody tests, PCR. Prevention: cook meat well, wash vegetables, pregnant women should avoid cleaning cat litter.

Trypanosoma and Leishmania (Blood and Tissue Flagellates)

Life cycle (Leishmania): sandfly bites → promastigotes enter skin → engulfed by macrophages → change to amastigotes and multiply → sandfly sucks infected macrophages → promastigotes in fly gut. Kala-azar is found in Bihar, Jharkhand, West Bengal. Prevention: vector control (insecticide spraying, bed nets), early treatment.

Plasmodium and Cryptosporidium

Plasmodium (malaria parasite): species – P. vivax, P. falciparum (most dangerous), P. malariae, P. ovale, P. knowlesi. Definitive host: female Anopheles mosquito; intermediate host: man.

1. In man (asexual – schizogony): sporozoites injected by bite → liver cells (exo-erythrocytic schizogony) → merozoites → enter RBCs → ring stage → trophozoite → schizont → RBC bursts releasing merozoites and toxins (haemozoin) → fever with chills; repeats every 48 h (vivax, falciparum – tertian) or 72 h (malariae – quartan). Some merozoites form gametocytes. P. vivax and P. ovale form dormant hypnozoites in liver (relapse).
2. In mosquito (sexual – gametogony and sporogony): gametocytes taken with blood → gametes → zygote → ookinete → oocyst on stomach wall → sporozoites → salivary glands.

Clinical features: cold stage, hot stage, sweating stage; anaemia, enlarged spleen; falciparum can cause cerebral malaria. Diagnosis: peripheral blood smear, rapid diagnostic test. Treatment: chloroquine + primaquine (vivax), artemisinin-based combination therapy (falciparum). Prevention: bed nets, repellents, removing stagnant water, larvivorous fish.

Cryptosporidium spp.: tiny coccidian parasite of intestinal cells; transmitted by oocysts in contaminated water (resistant to chlorine), food, contact with animals. Life cycle completes in one host. Causes watery diarrhoea; severe and long-lasting in AIDS patients and malnourished children. Diagnosis by modified acid-fast stain of stool, antigen tests; treatment – rehydration, nitazoxanide; prevention by safe drinking water.

Likely exam questions

1. (Long, 8 marks) Describe the life cycle of Plasmodium vivax in man and mosquito. Add a note on its pathogenicity.
2. (Long, 8 marks) Describe the morphology, life cycle and pathogenesis of Entamoeba histolytica.
3. (Short, 4 marks) Write a note on Giardia lamblia.
4. (Short, 4 marks) Describe the life cycle of Leishmania donovani.
5. (Short, 4 marks) Write a note on toxoplasmosis.

Syllabus topics (RTMNU)

• Introduction to Helminths: General morphology, structure organization and classification of parasitic helminths with special reference to the phylum Platyhelminthes
• Overview of adaptations for parasitic mode of life
• Trematodes (Flukes) – I: Study of blood flukes (Schistosoma spp.) with reference to morphology, life cycle, mode of transmission, pathogenesis, clinical manifestations, and control of schistosomiasis
• Trematodes (Flukes) – II: Study of Fasciola hepatica (liver fluke) including life cycle, transmission, pathogenesis, diagnosis, prevention, and treatment
• Cestodes (Tapeworms): Study of Taenia species with emphasis on morphology, life cycle, transmission, pathogenicity, preventive measures, and treatment

Introduction to Helminths and Phylum Platyhelminthes

Helminths are parasitic worms – multicellular, bilaterally symmetrical, often large enough to be seen with naked eye. Main groups: Platyhelminthes (flatworms: flukes and tapeworms) and Nematoda (roundworms).

General features of Platyhelminthes:

1. Dorso-ventrally flattened, bilaterally symmetrical, triploblastic, acoelomate (space filled with parenchyma).
2. Body covered by a living syncytial tegument (absorbs food, resists host enzymes).
3. Digestive system incomplete (flukes) or absent (tapeworms).
4. Excretion by flame cells (protonephridia).
5. Mostly hermaphrodite (except schistosomes); complex reproductive organs; huge egg output.
6. No respiratory or circulatory system; mostly anaerobic respiration.

Classification of parasitic flatworms:

• Class Trematoda (flukes): leaf-like, unsegmented, with oral and ventral suckers; complex life cycle with snail as first intermediate host. Examples: Fasciola hepatica, Schistosoma, Clonorchis.
• Class Cestoda (tapeworms): long, ribbon-like, segmented (proglottids), scolex with suckers/hooks, no gut. Examples: Taenia solium, T. saginata, Echinococcus granulosus.
• (Class Monogenea – mostly ectoparasites of fish gills, single host.)

Adaptations for parasitic life: hooks and suckers for attachment; thick tegument and anti-enzymes; loss of locomotory and sense organs; absorption of food through body surface; anaerobic metabolism; hermaphroditism and self-fertilisation; enormous fertility; larval multiplication (polyembryony in flukes); resistant egg shells; use of intermediate hosts to reach new hosts.

Blood Flukes – Schistosoma spp.

Species: S. haematobium (urinary bladder veins; urinary schistosomiasis), S. mansoni and S. japonicum (mesenteric veins; intestinal/hepatic schistosomiasis).

Morphology: unlike other flukes, sexes are separate. Male is short and stout (about 1–1.5 cm) with a ventral groove, the gynaecophoric canal, in which the long, slender female lies. Both have oral and ventral suckers. Eggs have a spine (terminal in S. haematobium, lateral in S. mansoni).

Life cycle: adults live in veins → eggs pass through bladder or gut wall into urine/stool → in fresh water, eggs hatch into miracidia → enter snail (intermediate host, e.g., Bulinus, Biomphalaria) → sporocysts → cercariae with forked tails → leave snail → penetrate human skin while bathing or working in water → become schistosomula → travel in blood through lungs and liver → mature in veins.

Pathogenesis and clinical features: "swimmer's itch" (cercarial dermatitis) at entry; fever, cough (Katayama fever); main damage from eggs trapped in tissues causing granulomas and fibrosis – blood in urine (haematuria), bladder damage (and higher risk of bladder cancer) in S. haematobium; bloody diarrhoea, enlarged liver and spleen, portal hypertension in S. mansoni/S. japonicum.

Control: praziquantel treatment (mass drug administration), snail control (molluscicides), safe water supply, sanitation (no urination/defecation in water), avoiding contact with infested water, health education.

Liver Fluke – Fasciola hepatica

Morphology: leaf-shaped, about 2–3 cm × 1 cm, with an anterior cephalic cone, oral and ventral suckers, spiny tegument, branched intestine, branched testes and ovary; hermaphrodite. Lives in bile ducts of sheep and cattle (definitive hosts); man is an occasional host.

Life cycle (two hosts): eggs in bile → passed in faeces → in water, miracidium hatches → enters snail (Lymnaea) → sporocyst → redia (two generations) → cercaria → leaves snail → encysts on water plants as metacercaria (infective stage) → eaten by sheep/man with grass or watercress → excysts in duodenum → penetrates gut wall → enters liver through capsule → wanders in liver tissue → settles in bile ducts and matures (about 3–4 months).

Pathogenesis (fascioliasis / "liver rot"): migrating young flukes destroy liver tissue (fever, pain, enlarged liver); adults cause bile duct inflammation, thickening and blockage, jaundice, anaemia; heavy losses of meat, wool and milk in sheep and cattle.

Diagnosis: eggs in stool or bile, ELISA, ultrasound/CT. Treatment: triclabendazole. Prevention: avoid eating raw water plants, snail control, draining wet pastures, deworming livestock.

Tapeworms – Taenia spp.

Species: Taenia solium (pork tapeworm) and T. saginata (beef tapeworm). Man is the definitive host.

Morphology (T. solium): long (2–3 m), ribbon-like; body divided into scolex (head with four suckers and a rostellum bearing two rows of hooks – armed), short neck (growth zone), and strobila of about 800–1000 proglottids – immature, mature (with male and female organs) and gravid (uterus full of eggs, with 7–13 lateral branches). T. saginata is longer, scolex without hooks (unarmed), gravid uterus with 15–30 branches.

Life cycle (T. solium): gravid proglottids/eggs pass in human stool → eaten by pig (intermediate host) → onchosphere (hexacanth embryo) hatches → enters blood → settles in muscles → cysticercus (bladder worm) → man eats undercooked "measly" pork → scolex evaginates and attaches to intestine → adult in 2–3 months.

Pathogenicity: Taeniasis (adult in gut) – mild abdominal discomfort, indigestion, weight loss. Cysticercosis – if man swallows T. solium eggs (contaminated food, hands, autoinfection), cysticerci form in muscles, eyes and brain; neurocysticercosis is a common cause of epilepsy (seizures) in India.

Diagnosis: proglottids or eggs in stool; CT/MRI and serology for cysticercosis. Treatment: praziquantel or niclosamide for adult worm; albendazole (with steroids) for neurocysticercosis. Prevention: cook pork and beef well, meat inspection, sanitary latrines, hand hygiene, keep pigs away from human faeces.

Likely exam questions

1. (Long, 8 marks) Describe the life cycle of Fasciola hepatica with its larval stages.
2. (Long, 8 marks) Describe the morphology and life cycle of Taenia solium. Add a note on cysticercosis.
3. (Short, 4 marks) Write the general features of Platyhelminthes.
4. (Short, 4 marks) Write a note on parasitic adaptations of helminths.
5. (Short, 4 marks) Describe the pathogenesis of schistosomiasis.

Syllabus topics (RTMNU)

• Intestinal Nematodes: Study of Ascaris lumbricoides with reference to morphology, life cycle, mode of transmission, pathogenic effects, clinical manifestations, diagnosis, prevention, and treatment
• Tissue Nematodes: Study of Wuchereria bancrofti including life cycle, transmission through mosquito vectors, pathogenesis, clinical features of filariasis, preventive measures, and treatment
• Ectoparasites of Medical and Veterinary Importance: Study of important ectoparasites including flies (bot flies, black flies, sand flies), mosquitoes (vectors of Japanese encephalitis, and dog heartworm), ticks, mites, lice, and fleas
• Emphasis on pathogenicity, symptoms, diagnostic approaches, and public health significance
• Treatment and Control of Parasitic Diseases: Principles of parasite treatment and control with emphasis on understanding parasite life cycles for effective management
• Overview of antiparasitic drugs and characteristics of an ideal antiparasitic agent
• Basic concepts of vaccines against parasitic diseases (attenuated, killed, recombinant, toxoid, and DNA vaccines)
• Strategies for prevention and control including environmental modification, vector control, eradication and elimination programs, public health measures, legislation, and the role of organizations and modern tools such as GIS in disease surveillance

Ascaris lumbricoides (Intestinal Nematode)

General features of nematodes: unsegmented, cylindrical, tapering at both ends, covered by tough cuticle, pseudocoelom, complete gut, separate sexes.

Morphology: largest intestinal roundworm of man. Female 20–35 cm, straight tail; male 15–30 cm, curved tail with two copulatory spicules. Mouth with three lips. Eggs – fertilised eggs are oval with thick mamillated (bumpy) coat, bile-stained brown.

Life cycle (one host, direct): adults in small intestine → female lays about 2 lakh eggs per day → eggs pass in stool → embryonate in moist soil in 2–3 weeks (infective egg with second-stage larva) → swallowed with contaminated food, water or hands → larvae hatch in intestine → penetrate gut wall → liver → heart → lungs (moult, grow) → move up trachea → swallowed → mature in intestine (about 2–3 months).

Pathogenic effects and clinical features (ascariasis): larval stage – lung inflammation, cough, fever, eosinophilia (Loeffler's syndrome); adult stage – abdominal pain, nausea, malnutrition and stunted growth in children; heavy worm load may cause intestinal obstruction; wandering worms may block bile duct or appendix.

Diagnosis: eggs in stool; adult worm passed; X-ray/ultrasound. Treatment: albendazole, mebendazole, pyrantel pamoate. Prevention: latrine use, hand washing, washing vegetables, periodic deworming of school children (India's National Deworming Day).

Wuchereria bancrofti (Tissue Nematode) and Filariasis

Morphology: thread-like white adults living in lymphatic vessels and lymph nodes; female (about 8–10 cm) longer than male (about 4 cm). Female gives birth to sheathed larvae called microfilariae.

Life cycle (two hosts): man – definitive host; female Culex quinquefasciatus mosquito (in India) – intermediate host/vector. Microfilariae circulate in peripheral blood mainly at night (nocturnal periodicity, about 10 pm–2 am) → mosquito sucks blood → in mosquito they develop in thoracic muscles (L1 → L2 → L3 infective larvae in 10–14 days) → move to proboscis → enter man's skin during bite → reach lymphatics → adults in about a year.

Pathogenesis and clinical features (lymphatic filariasis): adult worms and inflammation block lymph vessels → fever, lymphangitis, lymphadenitis → lymphoedema → elephantiasis of legs, scrotum (hydrocele), breasts; chyluria; tropical pulmonary eosinophilia. Many infected people show no symptoms but carry microfilariae.

Diagnosis: night blood smear for microfilariae; rapid antigen test; ultrasound ("filarial dance sign").

Prevention and treatment: mass drug administration (diethylcarbamazine (DEC) + albendazole, with ivermectin in some areas), mosquito control (removing stagnant drains, larvicides, bed nets), care of affected limbs (washing, hygiene). India runs a programme to eliminate lymphatic filariasis.

Ectoparasites of Medical and Veterinary Importance

• Bot flies: larvae develop inside animal tissues – myiasis (e.g., Dermatobia in man, Oestrus ovis in sheep nasal cavity, Hypoderma warble fly in cattle; damages hides).
• Black flies (Simulium): painful bites; vector of Onchocerca volvulus – river blindness.
• Sand flies (Phlebotomus): vector of kala-azar (leishmaniasis), sandfly fever.
• Mosquitoes: Culex (especially C. tritaeniorhynchus) transmits Japanese encephalitis virus (pigs and wading birds act as amplifying/reservoir hosts) – brain inflammation in children; mosquitoes (Aedes, Culex, Anopheles) transmit dog heartworm (Dirofilaria immitis), which lives in the dog's heart and pulmonary arteries.
• Ticks: blood-sucking arachnids; transmit Kyasanur Forest Disease (Karnataka), babesiosis and theileriosis in cattle, tick paralysis; cause anaemia and hide damage.
• Mites: Sarcoptes scabiei – scabies (intense itching, burrows); chigger mites – scrub typhus; mange in animals.
• Lice: head louse, body louse (Pediculus humanus) – pediculosis, itching; body louse transmits epidemic typhus and relapsing fever.
• Fleas: rat flea Xenopsylla cheopis transmits plague (Yersinia pestis) and murine typhus; dog flea carries dog tapeworm.

Diagnosis: visual inspection, skin scraping (mites), lice/nits in hair, larvae in wounds. Public health significance: vectors of many serious diseases; economic losses in livestock.

Treatment and Control of Parasitic Diseases

Principle: knowing the life cycle shows the weak link – the stage outside the host, the vector, or the intermediate host – where the cycle can be broken.

Antiparasitic drugs (overview): antiprotozoal – metronidazole, chloroquine, artemisinin, miltefosine; anthelmintics – albendazole, mebendazole, praziquantel, ivermectin, DEC; ectoparasiticides – permethrin.

Characteristics of an ideal antiparasitic drug: kills all stages of the parasite; safe with few side effects; effective in a single or short dose; cheap and easily available; oral; stable in storage; no resistance develops; safe for children and pregnant women.

Vaccines against parasites (basic concepts):

• Attenuated (live, weakened): e.g., irradiated sporozoite malaria vaccines (experimental); live vaccines for cattle theileriosis.
• Killed (inactivated): whole dead organisms.
• Recombinant (subunit): one parasite protein made by genetic engineering – the malaria vaccines RTS,S/AS01 and R21/Matrix-M (WHO-recommended for children in endemic areas).
• Toxoid: inactivated toxin used to raise antibodies (mainly used for bacterial diseases; concept applied to parasite toxins).
• DNA vaccines: a gene coding for a parasite antigen is injected; host cells make the antigen (under research).

Parasite vaccines are difficult because parasites have complex life cycles and change their antigens.

Strategies for prevention and control: environmental modification (drainage, filling breeding sites, sanitation); vector control (insecticide spraying, larvicides, larvivorous fish Gambusia, bed nets); eradication (complete global removal) and elimination (removal from a region) programmes – e.g., India's National Vector Borne Disease Control Programme for malaria, filaria and kala-azar; mass drug administration; public health measures (safe water, health education, meat inspection); legislation (food safety, quarantine); organisations – WHO, ICMR, NCDC; modern tools – GIS (Geographic Information System) and remote sensing to map cases and breeding sites and plan control.

Likely exam questions

1. (Long, 8 marks) Describe the life cycle of Wuchereria bancrofti and the clinical features of filariasis.
2. (Long, 8 marks) Describe the strategies for prevention and control of parasitic diseases.
3. (Short, 4 marks) Describe the life cycle of Ascaris lumbricoides.
4. (Short, 4 marks) Write a note on ticks and mites as ectoparasites.
5. (Short, 4 marks) Give the characteristics of an ideal antiparasitic drug.