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Biology with Genetics > Parasites 2 > Flashcards

Parasites 2 Flashcards

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1
Q

Leishmania donovani - Geographic Distribution

A

China, India, Middle East, Africa, Latin America.

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2
Q

Leishmania donovani - Morphology

A

Amastigote: Small (round, ~1.5 µm), large nucleus, rod-shaped kinetoplast, short internal flagellum.
Promastigote: Elongated, large nucleus, anterior kinetoplast, long free flagellum.

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3
Q

Leishmania donovani - Life Cycle

A

Amastigotes multiply in the reticuloendothelial system (spleen, liver, bone marrow).
Sandfly ingests amastigotes, which transform into promastigotes in the sandfly’s gut. Promastigotes multiply and are injected into humans during feeding, transforming into amastigotes in macrophages.

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4
Q

Leishmania donovani - Diagnostics

A

Demonstration of Leishman-Donovan bodies in spleen, liver, bone marrow.
Giemsa stain of smears.
Culture in special media.
PCR and serological tests also used.

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5
Q

Leishmania donovani - Pathogenicity

A

Visceral leishmaniasis (kala-azar):
Affects spleen, liver, bone marrow. Leads to anemia, hepatosplenomegaly, bone marrow suppression, hyperglobulinemia, and wasting.

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6
Q

Leishmania braziliensis - Geographic Distribution

A

Central and South America (Brazil, Peru, etc.)

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7
Q

Leishmania braziliensis - Morphology

A

Amastigote: Small, ovoid, large nucleus, kinetoplast.
Promastigote: Elongated, large nucleus, anterior kinetoplast, long flagellum.

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8
Q

Leishmania braziliensis - Life Cycle

A

Amastigotes multiply in the mucosal tissues.
Promastigotes develop in sandflies and are transmitted during feeding.

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9
Q

Leishmania braziliensis - Diagnostics

A

Biopsy of mucosal tissue or skin.
PCR for species identification.
Serological tests may be used, but biopsy of mucosal lesions is definitive.

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10
Q

Leishmania braziliensis - Pathogenicity

A

Mucocutaneous leishmaniasis:
Destroys mucosal tissues (nose, mouth), leading to disfigurement and secondary infections.

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11
Q

Leishmania tropica - Geographic Distribution

A

Urban areas of Mediterranean, Soviet Union (Armenia, Azerbaijan, etc.), Afghanistan, India, Turkey.

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12
Q

Leishmania tropica - Morphology

A

Morphology is identical to L. donovani:
Amastigote: Small, ovoid, large nucleus, rod-shaped kinetoplast.
Promastigote: Elongated, large nucleus, anterior kinetoplast, long flagellum.

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13
Q

Leishmania tropica - Life Cycle

A

Amastigotes multiply in macrophages and live within tissues. Transmitted by sandflies. Amastigotes remain in infected tissues, causing cutaneous lesions, which may leave scars when healed.

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14
Q

Leishmania tropica - Diagnostics

A

Microscopic examination of material from the edge of ulcerated lesion may reveal parasites.
Culture of skin scrapings.
PCR may confirm species.

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15
Q

Leishmania tropica - Pathogenicity

A

Cutaneous leishmaniasis (Oriental sore, Aleppo button):
Characterized by skin ulcers, which may leave scars after healing. In some cases, ulcers may become secondarily infected.

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16
Q

Toxoplasma gondii - Geographic Distribution

A

Worldwide

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17
Q

Toxoplasma gondii - Morphology

A

Trophozoites: Crescent-shaped, 4–8 µm, single central nucleus.
Cysts: Form in brain and muscles, contain bradyzoites.
Oocysts: Passed in cat feces, infective.

18
Q

Toxoplasma gondii - Life Cycle

A

Definitive host: Cats. Humans are accidental hosts.
Oocysts shed in cat feces. Humans become infected by ingesting oocysts in undercooked meat. Tachyzoites disseminate through the bloodstream, invading cells and causing necrosis. Cysts form in organs like the brain and muscles, leading to chronic infection.

19
Q

Toxoplasma gondii - Diagnostics

A

Serological tests: Detect IgG/IgM antibodies.
Direct Toxoplasma DNA in body fluids by PCR.
Histology: Tachyzoites or cysts in tissue biopsies.
Tissue inoculation in animals (e.g., mice) to confirm infection.

20
Q

Toxoplasma gondii - Pathogenicity

A

Toxoplasmosis: Mostly asymptomatic but can cause disseminated disease in immunocompromised patients (AIDS, transplant recipients) or congenital toxoplasmosis. In severe cases, brain necrosis, encephalitis, and damage to the eye can occur.

21
Q

Trichinella spiralis - Geographic Distribution

A

Worldwide

22
Q

Trichinella spiralis - Morphology

A

Adult female: 3–4 mm long.
Adult male: 1.4–1.6 mm long.
Larvae: 0.8–1.0 mm long (in muscle tissue).

23
Q

Trichinella spiralis - Life Cycle

A

Infection acquired by ingesting undercooked meat (usually pork) containing encysted larvae. After ingestion, larvae are released into the intestines, penetrate intestinal wall, and migrate through the lymphatic vessels into the bloodstream. Larvae then migrate to striated muscles (e.g., diaphragm, tongue, limb muscles), where they become encapsulated and encysted.

24
Q

Trichinella spiralis - Diagnostics

A

Diagnosis is based on clinical symptoms and history of ingestion of poorly cooked meat (especially pork).
Serological tests and muscle biopsy can reveal infection.
Elevated serum muscle enzymes (creatine phosphokinase, aldolase) may indicate muscle damage.

25
Q

Trichinella spiralis - Pathogenicity

A

Trichinosis:
Caused by ingestion of larvae encysted in muscle tissue from undercooked meat (usually pork). Symptoms include fever, myalgia, palpebral edema, diarrhea, and eosinophilia. Severe infections can cause myocarditis, encephalitis, and neurological disturbances in severe cases, leading to death.

26
Q

Trichomonas vaginalis - Geographic Distribution

A

Worldwide

27
Q

Trichomonas vaginalis - Morphology

A

Trophozoites: Pear-shaped, 7–23 µm, 4 anterior flagella, 1 posterior flagellum along an undulating membrane. No cyst stage.

28
Q

Trichomonas vaginalis - Life Cycle

A

Trophozoite stage only (no cyst stage). Parasites live in the genital tracts of females and the prostate gland in males. Transmission occurs through sexual intercourse. Reproduces by longitudinal binary fission.

29
Q

Trichomonas vaginalis - Diagnostics

A

Diagnosed by microscopic examination of vaginal secretions, urethral discharges, or urine.
Culture and PCR can improve detection in cases of chronic infection.

30
Q

Trichomonas vaginalis - Pathogenicity

A

Causes vaginitis, characterized by foul-smelling discharge, itching, and burning in females. In males, it is associated with prostatitis, urethritis, and epididymitis.

31
Q

Trichomonas tenax - Geographic Distribution

A

Worldwide

32
Q

Trichomonas tenax - Morphology

A

Trophozoites: Small, flagellated protozoa, inhabiting the mouth. No cyst stage.

33
Q

Trichomonas tenax - Life Cycle

A

Trophozoites are found in tartar, in various oral cavities, and in gingival margins. Transmission occurs through direct contact, and occasionally it can be aspirated into the lungs.

34
Q

Trichomonas tenax - Diagnostics

A

Identified by microscopic examination of oral samples from tartar or gingival margins.

35
Q

Trichomonas tenax - Pathogenicity

A

Non-pathogenic commensal of the human mouth. Occasionally causes opportunistic infections when aspirated.

36
Q

Schistosoma haematobium - Geographic Distribution

A

Africa (sub-Saharan regions), Middle East.

37
Q

Schistosoma haematobium - Morphology

A

Adult fluke: 12–14 mm long with oral and ventral suckers.
Eggs: Characterized by a terminal spine.

38
Q

Schistosoma haematobium - Life Cycle

A

Waterborne transmission. Free-swimming cercariae infect humans through penetration of intact skin. The parasites enter the bloodstream and mature. Adult flukes settle in bladder blood vessels, where eggs are excreted in urine, leading to infection of freshwater snails, the intermediate host, where cercariae hatch into water.

39
Q

Schistosoma haematobium - Diagnostics

A

Detection of eggs with a terminal spine in urine samples.
Serology and PCR confirm diagnosis in early stages.

40
Q

Schistosoma haematobium - Pathogenicity

A

Urinary schistosomiasis:
Eggs cause inflammation and fibrosis in the bladder, leading to hematuria, bladder inflammation, and cancer in severe cases.

Biology with Genetics (4 decks)

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