Parasitology for competitive examinations

virusDr. Sabitha Vijayan BHMS, MD

Parasites are organisms that infect other living beings. Medical parasitology deals with the parasites which infect man and diseases they produce.
Human parasites may be either unicellular microbes – the protozoa or larger organisms – the metazoan.
Parasites may be either ecto or endo parasites.
Ectoparasites inhabits body surfaces only without penetrating into tissues   Eg. Lice, tick, mites

They are important as vectors Transmitting pathogenic microbes.

The term infestation is employed for parasitation with ectoparasites while infection for endoparasites.

The host in which the adult stage lives or sexual mode of reproduction take place is called definitive host. The species in which larval stage of parasites live or asexual reproduction takes place is called intermediate host.

Paratenic host– a vertebrate host in which a parasite remains viable without development or multiplication is called paratenic host. Such a host may serve to pass on the infection to another is called a transport host.

Anthroponosis : Infection with a parasitic species that are maintained in man alone.Eg. Malaria, filaria

Premunition –  once a parasitic infection is completely eliminated, host become again susceptible to re infection, this type of immunity to re infection depends on the continued presence of residual parasites . this is called premunition.

The PROTOZOA are classified into 4 groups

  • Amoeba –  can assume any shape and crawl by means of pseudopodia
  • Flagellates – possess whip like appendages called flagella for locomotion
  • Sporozoa – production of spore like oocysts
  •  Ciliates – motile by means of cilia which covers entire body surface.


Entamoeba histolytica :- found in human colon. Infection is acquired though contaminated food and water containing mature cyst. Entire life cycle is completed in one host. Lumen dwelling amoeba when invade intestinal tissue cause disease.

Amoebic penetration of colon causes necrosis and abscesses. The abscesses breaks down into form an ulcer numerous in caecum. Superficial ulcers heal without scarring and deep ulcers form scars leading to strictures. Chronic ulcer leads to granuloma mistaken for malignant tumour

Parasite invade portal vein leading to multifocal hepatic invasion with liver enlargement. This is the stage of amoebic hepatitis. Peripheral extension leads to amoebic abscess. The centre of abscess contain thick chocolate brown pus  ‘ the anchovy sauce pus’ with liquefied necrotic tissues.

Amoebiasis of lung usually occurs in right lung. A hepatobronchial fistula develops with chocolate brown sputum.

Cutaneous amoebiasis occurs by direct spread from rectum ,perianally and colostomy openings and sinuses draining liver abscesses. Trophozoets can be demonstrated in leisions. Also occurs as a venereal infection of penis following anal intercourse.

The typical presentation of intestinal amoebiasis is amoebic dysentery, similar to bacillary dusentery.

Charcot-Leyden crystals are demonstrable in stool.

If diarrhea does not occur there may be vague abdominal symptoms called uncomfortable belly’ or growling abdomen’


1. Charcot-leyden crystals are found in microscopic faecal examination. ( also occur in malignancy  and ulcerative colitis)

2. In extraintestinal amoebiasis, LATEX agglutination and ELISA

Entamoeba gigivalis

Is a commensal in unhygienic mouths. Not reported to cause any disease.

Two pathogenic free living amoeba are 1. Naegleria and 2. acanthamoeba.

Species Naegleria fowleri causes acute purulent meningitis acquired by swimming in contaminated ponds.

Acanthamoeba causes acute meningoencephalitis and granulomatous leisions in skin, lungs, eyes or gastric mucosa; transmitted through inhalation, ingestion, or traumatized skin.

Both Naegleria and Acanthamoeba cause allergic pneumonitis acquired from amoeba growing in humidifiers of air conditioning plants.


 Intestinal flagellates

  • Giardia lamblia
  • Trichomonas vaginalis
  • Giardia lamblia was first observed by Leuwenhook in his own stool. It is the only protozoan parasite in the lumen of human small intestine.
  • Infection acquired by ingestion of cyst in the contaminated food and water.
  • Giardia L do not invade tissues but remain tightly attached by means of sucking disc.usually no clinical illness result but mucous diarrnoea, dull epigastric pain and flatulence.
  • But children may develop spruce like symptoms with chronic diarrhea.
  • Enhanced susceptibility to giardia associated with blood group A, achlorhydria, use of cannabis, chronic pacreatitis and AIDS.

Trichomonas vaginalis

Occurs in vagina and cervix and Bartholin’s gland, urethra and bladder in female and in anterior urethra, prostate and preputial sac in male.

Usually asymptomatic but may cause pruritic vaginitis in female and urethritis in male.

Haemoflagellates :  Lives in blood and tissues of man and  vertebrae and gut of insect vectors.

Haemoflagellates infecting man belong to 2 genera – Trypanosoma,  Leishmania

Haemoflagellates have two or more morphological stages such as amastigote, promastigote, epimastigote and trypomastigote

Trypomastigote stage lacking in leishmania

The important trypanosomes are the following

            1.T. brucci Gambians

            2. T. brucci rhodensis

            3. T. cruzi

  • T.brucei causes Nagana in cattle
  • T. gambiens –  west African sleeping sickness
  • T. rhodensis –  East African sleeping sickness
  • The human infection acquired by metacyclic trypomastigote form.
  • West African sleeping sickness(Gambian)
  • Vectors are glossina palpate and g. tachinoides
  • Incubation period – 1-2 weeks

Illness is chronic

Initial parasitemia following which they are predominantly located in lymph nodes.

Intermittent fever, chills, headache mark the stage.  There is hepatosplenomegaly with lymphadenopathy particularly in the post cervical region. With the invasion of CNS which occur after several months a sleeping sickness stage starts. Patient falls into coma and death.

East African (Rhodesian ) sleeping sickness

It is more acute form and may end fatally with in one year before involvement of CNS. Fever, weakness, rapid loss of weight and myocarditis.

Typical sleeping sickness not seen.

South American Trypansomiasis (Chaga’s disease) 

T.cruzi  Vector –  reduviid bug

These are night biting bug which defaecate while feeding. The faeces of infected bugs contain mitocyclic trypomastigote which are infective forms. Trypomastigote induce local inflammatory reaction called chogomas. When they enter through conjunctiva, unilateral oedematous swelling of eyelids results. This is Romana’s sign.

This disease ends fatally with myocarditis or meningoencephalitis.


Named after Sir. William leishman. Leishmania produce 2 broad type of clinical diseases. – Visceral and Cutaneous.

Mainly 4 type are parasitic to man

L. donovani- kala azar/ visceral leishmaniasis/ dumdum fever/ tropical splenomegaly.

L. tropica –  oriental sore/ old world cutaneous leishmaniasis.

L. braziliensis  or L. mexicana – new world cutaneous leishmaniasis or epsundia

Amastigote form of Leishmania donovani are seen smears of patients called L.D bodies, in giemsa or wright stain. Habitat is reticuloendothelial system.

Kala azar

Visceral leishmaniasis –  first characterized in India.

Vector- sand fly (phlebotomus argentipes)

PKDL – post kala azar dermal leishmaniasis –  is characterized by depigmented macules and erythematous patches on face- butterfly patches. Cut surface of liver shows nutmeg appearance. Leucopaenia , anaemia, neutropenia and thrombocytopaenia are common.

Diagnostic test for kala azar

  • Napier’s aldehyde test
  • Chopra’s antimony tes
  • Montenegro skin test(leishmanian skin test) this is negative in kala azar positive in dermal leishmaniasis and in persons who have recovered from kala azar. But not in active cases( the first two diagnostic tests are based on the increased globulin content of serum in the disease)

The antigen used in the serological test for non-leishmanial antigen is WKK antigen.

Three distinct patterns of old world cutaneous leishmaniasis are

1. Zoonotic rural type causing moist ulcers which are inflamed and often multiple- L. tropica major

2. Anthroponotic urban type causing painless dry ulcerating lesions often single leading to desquamating scars –  L. tropica minor

3. Non ulcerative  often diffuse lesions caused by L. aethiopica.

Leishmaniasis recidivans :- is a type of leisions seen in persons with a high degree of cell mediated immunity to the parasite . it resemble lupus or tuberculoid leprosy. Parasites are very scanty in the leisions, leishmanian test is strongly positive.

Mucocutaneous leishmaniasis or Epsundia is a late consequence of the cutaneous leishmaniasis due to L. brazieliensis. 


Syn; paludism in latin ; palus = marsh

Causative agent discovered in 1880 by Laveran , French army surgeon.

In 1886 Golgi described asexual development in the RBC – Golgi cycle

Romanowsky in Russia developed method of staining malarial parasite in blood films. Human malaria transmitted by female Anopheles mosquito. Chimpanzees act as reservoir hosts .

Mainly 4 species

  1. Plasmodium vivax
  2. Plasmodium malaria
  3. Plasmodium falciparum
  4. Plasmodium ovale
  • In life cycle of malaria parasite, asexual phase occurs in man and sexual phase occurs in mosquito. (the sexual phase takes place in female anopheles mosquito, even though sexual forms of the parasite origin in human RBC
  • In falciparum malaria ecrudescences are seen for one or two years;while in P.malariae infections they may last for even 50 years.
  • The periodicity of malarial fever depends on the erythrocytic schizogenic cycles to become synchronized so that all the mature shizonts in the body burst at the same time releasing merozoites and other pyrogens into the circulation causing febrile paroxysms.
  • P. vivax- benign tertian or BT malaria.fever recur after 48 hours
  • P. falciparum –  malignant tertian or MT malaria (also called subtertian. Fever paroxysm recur at less than the expected 48 hours. It is called pernicious malaria because of its lethal nature and active autumnal referring to its seasonal prevalence)
  • p.malariae –  Quartan malaria – 72 hours periodicity
  • P.ovale –  ovale tertian – 48 hours periodicity

Note:- sometimes in early P.vivax infection, there may be two independent broods of parasites with overlapping cycles so that there may be daily paroxysms. This is called quotidian periodicity

  • The infected erythrocytes show Schoffner’s dots on the surface in p.vivax infections.
  • Shortest incubation period is in P.falciparum infections
  • Longest incubation period is seen in p. malariae infections.
  • The minimum level of parasitaemia for their microscopic detection, is called microscopic threshold
  • The typical picture of malaria consist of periodic bouts of fever with rigor, followed by anaemia and splenomegaly.
  • All clinical manifestations  in malaria are due to the products of erythrocytic shizogony and host’s reactions to them.
  • The new malarial attack that appear after a period of latency, usually within eight weeks after the culmination of primary attack and resulting from persistence of erythrocytic cycle of parasite is called ecrudescence.
  • The most serious and fatal type of malaria MT malaria caused by P. falciparum . they may present in various forms, the most important of which are cerebral, algid, and septicaemic varieties.
  • Cerebral malaria is characterized by hyperpyrexia, coma, and paralysis.
  • Algid malaria resembles surgical shock.
  • In septicaemic malaria, characterized by high degree of prostration, high fever with involvement of various organs.
  • A syndrome called Black water fever is seen in falciparum malaria particularly in patients who have experienced repeated infections and inadequate treatment with quinine. It is malarial haemoglobunuria, seen in P.falciparum infections. It is due to massive intravascular haemolysis.
  • TSS- tropical splenomegaly syndrome- is a chronic benign condition seen in endemic areas. It is an abnormal immunological response to malaria characterized by splenomegaly, high titres of circulatory antimalarial antibody and absence of malarial parasite in peripheral blood smear.
  • National Malaria Eradication Programme – 1958
  • The immune depression caused by endemic malaria is responsible for the Buckett’s  lymphoma seen in African children.
  • Diagnosis :    ISB stain, Field’s stain
  • Several serological tests include immunofluorescence test, indirect haemagglutination, ELISA.


  •  Toxoplasma gondi
  • Cat is the definitive host
  • Congenital toxoplasmosis results when infection is transmitted trasplacentally from mother to foetus. Clinical manifestation may be developed after months or years, such as chorioretinitis, strabismus, blindness, deafness, epilepsy or mental retardation.
  • Sometimes acute disease manifestation occur such as fever, jaundice, hydrocephalus, pneumonitis or myocarditis.
  • Post nasal infection is usually asymptomatic. Commonest manifestation of acquired toxoplasmosis is lymphadenopathy particularly in post cervical lymph nodes
  • May become fatal in immunodeficiency diseases.
  • Diagnostic test is Sabin –Fieldman dye test.
  • Cryptosporidium causes intractable diarrhea in AIDS patients.
  • Pneumocystis carini causes pneumonia which become fatal in immuno compromised patients.
  • The only ciliate protozoan parasite of man is Balantidium coli. – largest protozoan parasite in man. It lives in large intestine. Infection acquired from pigs. Clinically resembles amoebiasis.
  • Helminthes are metazoan parasite with an outer covering
  • Trimatodus (flukes) are unsegmented helmiths which are flat and broad.
  • Flukes are hermaphrodites except schistostomes.

Clinically important trematodes infecting man are

1.     Schistosomes (which live inside veins)
a.     s. haematobium – in vesical or pelvic venous plexus
b.     s. mansoni – in inferior mescenteric vein
c.     s. japonicum –  in superior mescenteric vein

B. In various locations

            a. Biliary tract –    clonorchis sinensis

            b. fasciola hepatica

s. haematobium

            Formerly known as Bilharzia haematobium.

Endemic in Egypt. Adult worm lives in vesical and pelvic plexus of vein. Eggs passed to lumen of urinary bladder and discharged in urine particularly at the end of urination.

  • Intermediate host is snail
  • Man is the definitive host
  • Clinical illness result by skin penetration, egg deposition, tissue proliferation.
  • Clinical picture include local ——-carial dermatitis or general anaphylactic or toxic symptoms with fever, head ache, malaise, and urticaria. This is called katayama fever.
  • Typical manifestation is endemic haematuria or painless terminal haematuria.
  • In chronic cases, there is hyperplasia and fibrosis of vesical mucosa with granular appearance – sandy patch.
  • Schistosomiasis favours urinary carriage of typhoid bacilli
  • Diagnosis is by intradermal allergic test called fairley’s test.
  • S. mansoni causes intestinal Bilharziasis or Schistosomal dysentery.
  • S. japonicum- seenin superior mesenteric vein and intrahepatic portal vein.
  • Disease is otherwise called oriental schistosomiasis or katayama disease.
  • Acute illness include fever, abdominal pain, diarrhea, allergic manifestation called Katayama fever.
  • In chronic illness liver is maximally infected with hepatomegaly and fibrosis. There occurs periportal cirrhosis called Simmer’s pipestem fibrosis with portal hypertension and splenomegaly.

Liver fluke

Clonorchis sinensis – Chinese liver fluke . dogs and fish eating canines acts as reservoir host.

Migration of larva to bile duct causes hyperplasia and adenomatous change leading to cholangitis. Chronic infection leads to calculus formation, primary biliary cirrhosis and portal hypertension.

Fasciola hepatica

Sheep liver fluke –  first trematode to have been discovered and it is the largest and commonest liver fluke.

Intermediate host is snail of genera Lymnae. Present with fever, oesinophils, tender hepatomegaly.  cholelithiasis is a late complication.

Halzoun- ingestion of raw liver of infected sheep results insuffocation.

Lung fluke:-  Paragonimus westermani

Chronic disease resembles tuberculosis


  1. Fish tapeworm – diphyllobothrium latum
  2. Taenia saginata –  beef tape worm
  3.  Taenia solium – pork tape worm
  4. Echinococcus granulosus –  dog tape worm. Larval form causes hydatid disease in man
  5. Hymenolepis nana –  dwarf tape worm
  6. Hymenolepis diminuta  –  rat tape worm

Fish tape worm infection usually asymptomatic but sometimes causes mechanical obstruction. It causes a kind of pernicious anaemia called Bothrioceps anaemia.

Sparganosis – Ectopic infection by Sparganum (plerocercoid) larvae of tapeworm in abnormal host.

Taenia Saginata –  Beef tapeworm

            Mainly in small intestine

Larvae – bladder worm or cysticercus bovis

Human infection follows consumption of raw or undercooked beef

Taenia solium : When eggs are ingested by man or pig larval stage develops in muscles called cysticercus cellulosae. Pig flesh containing larvae is called measly pork.

Cysticercosis of brain cause epileptic manifestations

Ocular cysticercosis causes blurring of vision, uveitis, iritis and blindness ultimately.

Echinococcus granulosus :   Dog tapeworm or hydatid worm causes hydatid cyst.

Diagnostic test is Casoni’s intradermal test

When hydatid cyst forms inside bones, erode bony tissue and form osseous hydatid. Primary site is liver.

Trichinella spiralis :   Trichinia worm –  trichinosis

Infection acquired through consumption of inadequately cooked pork.

Trichuris trichuria :  Whipworm – infective larvae is rhabdiform larvae. Mechanical effect due to heavy infection is appendix causes appendicitis and in children cause rectal prolapse.

Strongyloides stercoralis : Causes strongyloidasis – usually benign but severe form is seen in immunocompromised persons called hyper infection.

Cutaneous form –  dermatitis, erythrema and itching 

Hook worms

  • Ancylostoma duodenale and necator americanus
  • Ancylostoma duodenale – infection is acquired when walking barefooted on soil containing filariform larvae
  • No multiplication in host
  • Necator americanus – is smaller than Ancylostoma duodenale.
  • When filariform larva enter the skin, they give rise to severe itching  at the site; scratch causes bacterial infection and forms the ground itch
  • Larva sometimes causes creeping eruption called cutaneous larva migricans.
  • When larva break out in pulmonary capillaries and enter alveoli causing minute local haemorrhages. Pulmonary lesion is called loeffler’s syndrome.(more common in ascariasis)
  • Adult worm in intestine sucks the blood and cause ulceration , second degree anaemia, hypoproteinaemia, odema and effusion
  • Single ancylostoma sucks 0.2 ml blood a day and necator 0.03 ml/day 

Enterobius vermicularis

  • Pinworm, thread worm or seatworm
  • Formerly called oxyuris vermicularis
  • Enterobiasis is usually a group  infection.
  • Diagnosis :- NIH swab

 Round worms

  • Ascaris lumbricoides- largest nematode parasite in human intestine
  • Larval migration causes allergic reaction. Migrating larvae in lungs cause ascaris pneumonia with fever, cough and wheezing.  Sputum contains charcto-leyden crystals. Larva may occur in sputum but more in gastric  washings. This is called loeffler’s syndrome
  • Ascaris contribute to PEM, Vit. A deficiency.



Mainly classified into

1.     Lymphatic filariae           site of adult       site of microfilaria          vector

Wuchereria bancrofti   lymph nodes           blood                          culex mosquito

Brugiya malay               lymph nodes      blood                mansoni

Brugiya timori                lymph node       blood

2.     Subcutaneous filarial

Loa loa                          connective tissue            blood                chrysops

Onchocercha volvularis   subcutaneous     skind and          similium

                                                nodule               eyes

3.     Serous cavity

Mansonilla ozadis

Mansonilla pestani

Occult filariasis
In some persons immune process to filarial antigens may produce clinical conditions unrelated to lymphatic lesions. Microfilaria not demonstrable in blood

Clinical features
Worms inside lymphnode and vessel causes granuloma formation with subsequent scarring and even calcification, increased permeability of vessel wall causes leakage of protein rich lymph into tissue causing typical hard pitting or brawny oedema.

Clinical features include lymphadenitis, lymphangitis, filarial fever, lymphorrhagia, hydrocele, lymphoedema, elephantiasis

Diagnostic kit : DEC provocation test

Small quantity of diethyl carbazine induce microfilaria to appear in peripheral blood even during day time. (microfilaria usually have a nocturnal periodicity in peripheral circulation being seen only at night, between 10 pm and 4 am)

Onchocerca volvulus :  Convoluted filaria

Or blinding filaria- causes blindness

Here subcutaneous nodule called onchocercoma occurs due to fibroblastic reaction around worms.


  • Fiery serpent
  • Incubation period – 1 year
  • No illness until gravid female worm comes to lie under skin ready to discharge embryos.
  • A few hours before blister formation there is constitutional symptoms of nausea, vomiting, intensive pruritus and urticarial rash.
  • The term Larva currens (racing larva) has been applied to rapidly progressing linear urticarial track caused by migrating larvae
  • Larvae migrans – sometimes nematode larvae appear to lose their way and wander aimlessly. Infections are abortive.
  • Cutaneous larva migrans are mainly due to Ancylostoma braziliensis and A. caninum.

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