PARASITES OF MEDICAL IMPORTANCE 2008 By Dr Tony Oni Dept. of Medical Microbiology & Parasitology, College of Medicine, University of Ibadan/

Parasitic diseases – causative agents Protozoa. Helminths (worms). Arthropods (insects & arachnids).

Effects of parasite infection: Due to Parasites themselves. Consequences of host response to the invader.  

Nature and Extent of the pathological effects depend on: Site of infection. Mode of infection. Level of the parasite burden.

Pathogenic mechanisms: Mechanical tissue damage. Physical obstruction of anatomical sites leading to loss of function. E.g. Ascariasis, tapeworm – in intestine. & Filaria worm in the lymphatics.

Pathogenic mechanisms (contd): Physiological effects. Malabsorption especially of fat from intestine caused by Giardia spp. Competition by parasite for essential nutrients eg Diphyllobothrium latum for Vitamin B12 in intestine leading to pernicious anaemia. Hookworm sucking blood. Production of metabolites that have profound effects in the body e.g. Trypanosoma cruzi; Production of vasoconstrictor by malaria parasites.

Pathogenic mechanisms (contd): Tissue damage. Presence of parasite can release proteolytic enzymes that damage host tissues e.g. ulceration of intestine in amoebiasis. Host reaction to parasite can evoke immunological reactions.

HELMINTHS Responsible for a large burden of community health problems worldwide. Few are life-threatening. Most have no independent existence outside the host.

HELMINTHS :Classification:- Nematodes (Roundworms). Intestinal nematodes. Tissue nematodes. Platyhelminths (Flatworms). Trematodes (flukes). Cestodes (tapeworms)

Intestinal nematodes Predisposing factor to infection: poor hygiene. Common in the tropics and subtropics. Low worm burden are asymptomatic. Heavy infection problematic especially in children where they are associated with impaired development

Ascaris lumbricoides. Common roundworm Common in the tropics and subtropics. Low worm burden are asymptomatic. Heavy infection problematic especially in children where they are associated with impaired development Predisposing factor to infection: poor hygiene.

Ascaris lumbricoides. Infection : by the ingestion of the egg, which hatch in the duodenum. Larvae penetrate the gut mucosa to the bloodstream, getting to pulmonary circulation and the lung, where they undergo two moults. They migrate via the trachea to the intestinal tract. Maturity occur in the gut lumen and they live in there for several years.

Ascaris lumbricoides. Pathogenic effects Pneumonic symptoms due to migration in the lungs. Invasion of the biliary and pancreatic tracts by the adult worms. Intestinal obstruction by heavy infection.

Ascaris lumbricoides: ova

Ascaris lumbricoides: ova

Ascaris lumbricoides: adult

Toxocara canis Dog ascarid. Accidental infection in man. Egg hatch in the small intestine, penetrates the gut mucosa but can not complete the migratory phase. They find their way to remote parts of the body causing visceral larva migrans. It can cause serious retinal lesion if it reaches the eye. Visceral larvae migrans is associated with other roundworms like Angiostrongylus, Gnathostoma and Anisakis

Trichuris trichiura Whipworm. Often found together with ascaris. Adult : The head (whip) end embedded in colonic mucosa. Each female lay thousands of characteristic “tea-tray” eggs every day. These develop infective larvae in warm moist condition. After ingestion , ova hatch in the in intestine and mature in the large intestine. There is no migratory phase. Effect of infection: Trivial. Rectal prolapse in children with associate type of dysentery.

Trichuris trichiura: ova

Hookworm Ancylostoma duodenale Necator americana Widely distributed in tropics and subtropics. Eggs hatch in the soil into larvae which undergo several moults before the infective larvae are formed. Infection by penetration of unbroken skin, into the bloodstream and then migrate like ascaris. On reaching the small intestine they attach to the mucosa with the monthparts.

Hookworm Effect: Ingestion of blood causing Iron deficiency anaemia. Small bleeding mucosal ulcers as a result of movement of the worm from site to site in the small intestine.

Ancylostoma caninum Dog hookworm. Larvae may penetrate human skin, but do not migrate. They cause cutaneous larva migrans.

Hookworm: ova

Strongyloides stercoralis Related to hookworm but differ by having a distinct free-living phase in the life cycle, during when male and female reproduce. Human infection: penetration of the skin by the infective larvae of the female worm. Migratory phase involving the lungs follows and the worms attach to gut mucosa.

Strongyloides stercoralis Production of eggs containing fully developed larvae. Hatching within the intestinal lumen and the larvae (not eggs) are found in faecal samples. Some of these larvae develop into infective forms and penetrate the gut mucosa to start another cycle of infection (auto-infection) . Effect: Hyperinfection in debilitated individuals.

Strongyloides stercoralis

Enterobius vermicularis Threadworm Infect children worldwide. Has the simplest life-cycle of all the intestinal worms. Adults live in large intestine, may be found in the appendix. Mature gravid females crawl to the anus at night and lay egg in peri-anal area. Characteristically, the eggs are flatten on one side and usually contain fully developed larvae. Infection : by ingestion of the eggs.

Enterobius vermicularis Threadworm Effect: Pruritus ani due to deposition of eggs. Faecal samples examination not appropriate for diagnosis, but swabs from unwashed perianal area or sellotape impression for the characteristic eggs. In addition the adult threadworm can be found on the surface of well formed stool.

Enterobius vermicularis:ova

Treatment of intestinal nematodes. Determinants: Severity of symptoms Re-infection. Scarce medical resources.

Treatment of intestinal nematodes. Drugs: Effective against all Pyrante pamoate Albendazole Mebendazole Effective against all expect Trichuris trichiura Thiabendazole Levamisole - not good for Strogyloides stercoralis, Trichuris trichiura and Enterobius vermiculairs. Good against Ascaris lubricoides and Enterobius vermicularis Piperazine

TISSUE NEMATODES Filarial worms. Guinea worm (Dracunculus medinensis). Trichinella spiralis

Filarial worms Complex life cycle involving developmental stages in an insect vector. Varied pathological effects. Some have major impact on communities living in endemic areas.

Wuchereria bancrofti Transmission is by bite of various species of mosquito in the tropical belt of the world. Effect: invasion of larvae into the lymphatics, usually of the lower extremities. Adult worms cause lymphatic blockage and gross lymphoedema (elephantiasis, bancroftian filariasis).

Wuchereria bancrofti Microfilaria, the embryonic form, are liberated into the bloodstream, they remain the elastic egg membrane as a sheath Filarial worms covering the whole larva. They remain in the pulmonary circulation during the day, but get to the peripheral circulation at night during when biting by the vector occurs. Blood samples for microfilaira are better taken at night between 12 and 2 am because of this nocturnal periodicity

Wuchereria bancrofti:microfilaria

Elephantiasis

Loa loa Distribution: Central and Western tropical Africa, where the vector Chrysops species live. Adult live in subcutaneous tissue and wanders round the body provoking local reaction Calabar swellings. It sometimes migrate across the front of the eye. The sheathed microfilaria exhibits diurnal periodicity

Loa loa microfilaria crossing the conjunctiva

Brugia malayi Distribution: India, far east and south east Asia. Transmitted by mosquito. Causes elephantiasis. Exhibits nocturnal periodicity.

Onchocerca volvulus Distrubution : Tropical Africa and Central America. Vector: Simulium damnosum and related species of black-fly. Adult : live in the subcutaneous tissue, and may be encapsulated in bony parts of the body like the ankle, hip, elbow, shoulder. In central America, this occur in the head. The microfilaria are not in blood but in the subcutaneuos tissue. The eye may be invaded by microfilaria leading to corneal and retinal lesion, causing blindness (River blindness). Irritation of the skin result to hypopigmentation (leopard skin).

Onchocerca volvulus Diagnosis: excision and identification of worm in the nodule. Skin snip for microfilaria.

Onchocerca volvulus: Subcutaneus nodules

Onchocerca volvulus: River blindness

Mansonella species Mansonella species Distribution: Mansonella perstans –Tropical Africa and part of South America. Mansonella ozzardi –West Indies and part of South America. Transmission: by biting midges Culicoides species. The unsheathed microfilaria are in the bloodstream and has no periodicity.They are generally regarded as nonpathogenic. However Mansonella streptocerca causes skin lesions similar to Onchocerca volvulus, but with milder symptoms. Infection is West and Central Africa.

Treatment of filariasis Chemotherapy: Diethylcarbamazine (DEC) kills microfilaria but not effective against adult worms. It is non-toxic. Death of the microfilaria can evoke allergic reaction (Mazzotti reaction) especially in onchocarciasis. Suramin: -kills adult worms. Ivermectin.- especially for onchocercaiasis. Ivermectin and albendazole..

Dracunculus medinensis Guinea worm. Distribution: Poor hygienic environment, with lack of portable water. Vector : Cyclops (water flea). Infection : drinking water flea infected water.

Dracunculus medinensis Guinea worm. Effect: Larvae penetrate the gut mucosa and develop in the connective tissue, usually of the lower limb. The gravid female emerges from the skin in a blister in readiness to deliver. when the blister is immerged in water the worm bust to release about 1 million larvae which are ingested by the Cyclops to continue the life-cycle. The blister may be secondarily infected by gram positive cocci. Chemotherapy not helpful.

Dracunculus medinensis Vector : Cyclops (water flea).

Guinea worm: worm on matchstick

Trchinella spiralis Host : wide range Infection: by eating undercooked pork products. Infected larvae lie dormant in skeletal muscle, release at digestion. Male and female mature attached to mucosa of small intestine. The female is viviparous, producing numerous larvae during the short life period lasting weeks. The larvae penetrate the gut wall and migrate to the skeletal muscle, when they remain dormant.. Treatment : Mebendazole.

Trchinella spiralis in skeletal muscle

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