The document discusses various parasites of medical importance, focusing on their classifications, pathogenic mechanisms, and effects on human health. It highlights the impact of helminths, especially in tropical regions, detailing specific worms like Ascaris lumbricoides, Trichuris trichiura, and different filarial species. Treatment options for intestinal nematodes and filariasis are also outlined, emphasizing effective medications and challenges in management.

1. PARASITES OF MEDICAL
IMPORTANCE

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

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

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

5. 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.

6. 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.

7. 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.

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

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

10. 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

11. 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.

12. 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.

13. 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.

14. Ascaris lumbricoides: ova

15. Ascaris lumbricoides: ova

16. Ascaris lumbricoides: adult

17. 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

18. 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.

19. Trichuris trichiura: ova

20. 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.

21. 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.

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

23. Hookworm: ova

24. 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.

25. 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.

26. Strongyloides stercoralis

27. 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.

28. 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.

29. Enterobius vermicularis:ova

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

31. 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

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

33. 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.

34. 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).

35. 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

36. Wuchereria bancrofti:microfilaria

37. Elephantiasis

38. 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

39. Loa loa
microfilaria crossing the conjunctiva

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

41. 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).

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

43. Onchocerca volvulus: Subcutaneus nodules

44. Onchocerca volvulus: River blindness

45. 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.

46. 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..

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

48. 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.

49. Dracunculus medinensis Vector :
Cyclops (water flea).

50. Guinea worm: worm on matchstick

51. 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.

52. Trchinella spiralis in skeletal muscle

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