Blood and Tissue protozoa, Biology tutorial


Blood protozoa of major biological/medical importance comprise members of genera

i) Trypanosoma (T. brucei and T. cruzi)

ii) Leishmania (L. donovani, L. tropica and L. braziliensis)

iii) Plasmodium (P. falciparum, P. ovale, P. malariae and P. vivax)

iv) Toxoplasma gondii; and

v) Babesia (B. microti).

1) Trypanosome:

The haemoflagellates all belong to family Trypanosomatidae, and comprise trypanosomes and leishmanias.


 Trypanosomes have leaf-like or rounded body containing the vesicular nucleus, and varying number of subpellicular microtubules lying under outer membrane. There is single flagellum arising from the kinetosome or basal granule. The undulating membrane is present in some genera and flagellum lies on its outer border. Posterior to kinetosome is the rod shaped or spherical kinetoplast having DNA.  Members of the genus Trypanosoma are heteroxenous and pass by amastigote, promastigote, epimastigote and tryptomastigote stages in life cycle. In some species only tryptomastigote forms are found in verteorate host; in others, apparently more primitive species, both amastigote and tryptomastigote forms are there.


Trypanosoma brucei gambiense is major in western and central regions of Africa, while Trypanosoma brucei rhodesiense is limited to eastern third of continent. 6,000 to 10,000 human cases are documented annually. 35 million people and 25 million cattle are at risk. Regional epidemics of disease are cause of main health and economic disasters.

Life cycle:

Infective, metacyclic form of trypanosome is injected in primary host during the bite by vector, tsetse fly. Organism transforms in dividing trypanosomal (trypomastigote) blood form as it enters draining lymphatic and blood stream. Trypanosomal form enters vector during blood meal and travels throughout alimentary canal to salivary gland where it proliferates as crithidial form (epimastigote) and matures to infectious metacyclic forms.

Trypanosomiasis is a disease caused by trypanosomes.

African trypanosomiasis (Sleeping sickness)

Etiology: There are two clinical forms of African trypanosomiasis:

1) A slowly developing disease caused by Trypanosoma brucei gambiense and

2) A rapidly progressing disease caused by T. brucei rhodesiense.

Symptoms: Clinical features of Gambian and Rhodesian disease are same; though they differ in severity and duration. Rhodesian disease progresses more quickly and symptoms are frequently more pronounced. Classically, progression of African trypanosomiasis can be divided in three stages: bite reaction (chancre), parasitemia (blood and lymphoid tissues), and central nervous system (CNS) stage.

Pathology and Immunology: The exact pathogenesis of sleeping sickness is not known, though immune complexes and inflammation have been supposed to be mechanism of damage to tissues. Immune response against organism does help to eradicate parasite but it is not protective, as parasite has unique skill of altering its antigens.

Diagnosis: Recognition of parasite in bloodstream, lymph secretions and enlarged lymph node aspirate gives definitive diagnosis in early (acute) stages. Parasite in blood can be concentrated by centrifugation or by use of anionic support media. Cerebrospinal fluid should always be observed for organisms.

Treatment and control: Blood stage of African trypanosomiasis can be treated with practical success with Pentamidine isethionate or Suramin. These drugs have been reported also to be efficient in prophylaxis though they may mask early infection and therefore increase risk of CNS disease. Most effective means of prevention is to evade contact with tsetse flies.

2) Leishmania:

Leishmania are ovoid organisms inside macrophage and have rod-shaped kinetoplast related with a rudimentary flagellum that, though, doesn't extend beyond cell margin. Parasites are found in amastigote stage in cells of vertebrate host and in promastigote stage in intestine of sandfly. In vertebrate host Leishmania is found in macrophages and other cells of reticuloendothelium system in bone marrow, skin, liver, spleen, lymph nodes and mucosa. It may also be found in leucocytes in blood.

This leishmanial, or amastigote form, after ingestion by the sandfly, transforms in promastigote form in insect gut in which kinetoplast is located at posterior end of body. Leishmania occur mainly in mammals, though ten species have been explained in Old World lizards. They cause disease in man, dogs and a variety of rodents. Leishmania have heteroxenous life cycle, are transsmitted by sandflies of genus Phlebotomus in Old World and Lutzomyia in New World.

Epidemiology: Leishmaniasis is common worldwide: ranging from south East Asia, Mediterranean, Indo-Pakistan, north and central Africa, and south and central America.

Morphology: In man, parasites takes place in amastigote form only, but in insect vector promastigote form is assumed. Amastigote forms are small, ovoid or round bodies (frequently called Leishman-Donovan bodies) approx 2-5μm in diameter by 1 - 3 μm while leptomonad estimates 14 - 20 microns by 1.5 - 4 microns, a similar size to trypanosomes.

Life cycle: Organism is transmitted by bite of numerous species of blood-feeding sandflies (Phlebotomus) that carry promastigote in anterior gut and pharynx. Parasites gain access to mononuclear phagocytes where they transform in amastigotes and separate until infected cell ruptures. Sandfly obtains organisms during blood meal; amastigotes transform in flagellate promastigotes and multiply in gut until anterior gut and pharynx are packed.

Leishmaniasis: It is a disease caused by Leishmania

Etiology: Many species of Leishmania are pathogenic for man: L. tropica (L. t. major, L. t. minor and L. ethiopica) cause cutaneous leishmaniasis (oriental sore, Delhi ulcer, Aleppo, Delhi or Baghdad boil) and L. donovani causes visceral leishmaniasis (Kalaazar, black disease, dumdum fever).

Symptoms: Visceral leishmaniasis (kala-azar, dumdum fever):L. donovani organisms in visceral leishmaniasis are quickly eradicated from site of infection therefore there is hardly ever local lesion. 1 to 4 months after infection, there is occurrence of fever, with daily rise to 102-104 degrees F, accompanied by chills and sweating. Spleen and liver increasingly become inflated. With evolution of diseases, skin develops hyperpigmented granulomatous areas (kala-azar means black disease).

Pathology: Pathogenesis of leishmaniasis is because of the immune reaction to organism, mainly cell mediated immunity. Laboratory examination reveals a marked leukopenia with relative monocytosis and lymphocytosis, anemia and thrombocytopenia.

Diagnosis: Diagnosis is based on the history of exposure to sandflies, symptoms and isolation of organisms from lesion aspirate or biopsy, by direct test or culture. Skin test (delayed hypersensitivity: Montenegro test) and detection of anti-leishmanial antibodies by immuno-fluorescence are indicative of exposure.

Treatment and Control: Sodium stibogluconate (Pentostam) is drug of choice. Pentamidine isethionate is utilized as the alternative. Control measures involve vector control and avoidance. Immunization hasn't been effectual.

3) Plasmodium:

Parasites of genus Plasmodium are accountable for disease malaria in both animals and man. Species also take place in other mammals like squirrels and bats and in amphibians and reptiles, but these haven't been much studied. Though it has been known for several years that some species of monkey malaria (like P. cynomolgi) are transmissible to man, it has been found that human malaria can be transmitted to numerous species of monkeys. Genus Plasmodium has true malarial parasites (in contrast to the haemoproteids).

Epidemiology: There are an expected 200 million global cases of malaria leading the mortality of more than one million people per year. P. falciparum (malignant tertian malaria) and P. malariae (quartan malaria) are the most widespread species of malarial parasite and are found in Asia and Africa. P. vivax (benign tertian malaria) predominates in Latin America, India and Pakistan, while, P. ovale (ovale tertian malaria) is about exclusively found in Africa.

Morphology: Malarial parasite trophozoites are usually ring shaped, 1-2 microns in size, though other forms (ameboid and band) may also exist. Sexual forms of parasite (gametocytes) are much larger and 7-14 microns in size.

Life cycle: Malarial parasites are transmitted by infected female anopheline mosquito that injects sporozoites present in saliva of insect. Sporozoites infect liver parenchymal cells where they may remain dormant (hypnozoites) or endure stages of schizogony to create schizonts and merogony to make merozoites (meronts). When parenchymal cells rupture, thousands of meronts are released in blood and infect red cells. Some merozoites transform in male and female gametocytes whereas others enter red cells to continue erythrocytic cycle. Gametocytes are ingested by female mosquito, the female gametocyte transforms in ookinete, is fertilized, and forms the oocyst in gut. The oocyte produces sporozoites (sporogony) which migrate to the salivary gland and are ready to infect another host.

Malaria is a disease caused by Plasmodim parasite.

Human malaria: It is not always realized that malaria is one of the world's supreme killers. It stays endemic in some 102 countries with more than half the world's population at risk. There are possibly more than 100 million cases of disease throughout world, of which maybe a million are fatal. Problem has grown worse in some rural areas that have undergone intensive economic development, particularly parts of Asia and in Amazon region of Latin America. It must also be emphasized that non-endemic countries are not immune to infection as cases of imported malaria were being reported.

Etiology: Four Plasmodium species are to blame for human malaria. These are P. falciparum, P. vivax, P. ovale and P. malariae.

Human malaria can develop in certain monkey species. Pattern of life cycles of these species follow general life cycle but there are significant physiological differences that are frequently reflected in nature of diseases produced.

Symptoms: Symptomatology of malaria depends on parasitemia, occurrence of organism in different organs and parasite burden. Incubation period differs normally between 10-30 days. As parasite load becomes important, patient develops lethargy headache, vague pains in bones and joints, chilly sensations and fever. As disease progresses, chills and fever become more prominent. Chill and fever follow the cyclic pattern (paroxysm) with symptomatic period lasting 8- 12 hours. Classical tertian paroxysm is rarely seen in P. falciparum and persistent spiking or a daily paroxysm is more usual.

Pathology and immunology: Symptoms of malaria are because of release of massive number of merozoites in circulation. Infection results in production of antibodies that are effective in containing parasite load. These antibodies are against merozoites and schizonts. Infection also results in activation of reticuloendothelial system (phagocytes). Cell mediated immunity also may develop and help in removal of infected erythrocytes. Malarial infection is related with immunosuppression.

Diagnosis: Diagnosis is on the basis of symptoms and detection of parasite in Giemsa stained blood smears. There are also antibody tests.

Treatment and Control: Treatment is helpful with different quinine derivatives (quinine sulphate, chloroquine, meflaquine and primaquine, etc.). Control measures are eradication of infected anopheline mosquitos.

4) Babesia:

Morphology: Trophozoite is very similar to ring form of Plasmodium species.

Life cycle: Organism (sporozoite) is transmitted by the tick and enters red cell where it goes through mitosis and organisms (merozoite) are released to infect other red cells. Ticks obtain organism during feeding on the infected individual. In tick, organism splits sexually in gut and migrates in salivary gland.

Babesiosis: It is a disease caused by Babesia parasite.

Etiology: Babesia microti is only member of the genus which infects man.

Symptoms: Babesiosis is related with hemolytic anemia, jaundice, fever and hepatomegaly, generally 1-2 weeks after infection.

Diagnosis: Diagnosis is on the basis of symptoms, patient history and detection of intraerythrocytic parasite in patient or transfer of blood in normal hamsters that can be heavily parasitized.

Treatment and control: Drugs of choice are clindamycin shared with quinine. Patient may recover impulsively. One must evade tick exposure and, if bitten, take away tick from skin instantly.

5) Toxoplasma:

This extraordinary species was known as the potential parasite of man for several years but its true nature as the coccidian was found not too long ago. It was known to happen in all warm-blooded animals - mammals and birds. The two stages known were trophozoite and cyst, also called as pseudocyst. Trophozoites were intracellular parasites that could invade almost any nucleated cell within the host.

Cysts had well-formed walls and contained organisms that multiplied inside cysts, as many as 1000-3000 organisms being found inside a single cyst. Trophozoite and cystic form appeared to be approximately identical in morphology, but they shown striking physiological difference in that trophozoites were quickly killed in acid pepsin while cystic forms could survive 1 h of acid pepsin digestion.

Epidemiology: Toxoplasma has global distribution and 20%-75% of population is seropositive devoid of any symptomatic episode. Though, infection poses the serious threat in immunosuppressed individuals and pregnant females.

Morphology: Intracellular parasites (tachyzoite) are 3x6 microns, pear-shaped organisms which are enclosed in the parasite membrane to create the cyst measuring 10-100 microns in size. Cysts in cat feces (oocysts) are 10-13 microns in diameter.

Life cycle: Natural life cycle of T. gondii takes place in cats and small rodents, though parasite can grow in organs (brain, eye, skeletal muscle, etc.) of any mammal or birds. Cats get infected by ingestion of cysts in flesh. Decystation takes place in small intestine, and organisms penetrate submucosal epithelial cells where they suffer many generations of mitosis, at last resulting in growth of micro- (male) and macro- (female) gametocytes. Infected cells eventually burst and release tachyzoites to enter other cells, comprising muscle and nerve cells, where they are protected from host immune system and multiply slowly (bradyzoites).

Toxoplasmosis is the disease caused by Toxoplasma parasite.

Etiology: Toxoplasma gondii is the organism responsible for toxoplasmosis

Symptoms: Though Toxoplasma infection is common, it hardly ever produces symptoms in normal individuals. Its serious results are restricted to pregnant women and immunodeficient hosts. Congenital infections happen in approx 1-5 per 1000 pregnancies of which 5-10% result in miscarriage and 8-10% result in serious brain and eye damage to fetus. 10-13% of babies will have visual handicaps. Though 58-70% of infected women will give birth to the normal offspring, small proportion of babies will develop active retino-chorditis or mental retardation in childhood or young adulthood. In immunocompetent adults, toxoplasmosis, may create flu-like symptoms, at times related with lymphadenopathy.

Immunology: Both humoral and cell mediated immune responses are stimulated in normal individuals. Cell-mediated immunity is protective and humoral response is of diagnostic value.

Diagnosis: Suspected toxoplasmosis can be confirmed by isolation of organism from tonsil or lymph gland biopsy.

Treatment: Acute infections advantage from pyrimethamine or sulphadiazine. Spiramycin is a successful alternative. Pregnant women are advice to avoid cat litter and to handle uncooked and undercooked meat cautiously.

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