Coccidians Flashcards
Class Sporozoea
Coccidia
Infect the intestinal tracts of animals.
Coccidian parasites
obligate, intracellular parasites, which means that they must live and reproduce within an animal cell.
Coccidian
with no definite organ of locomotion.
Coccidia
It may have body flexion, gliding or undulating of longitudinal ridges.
Coccidia
Characterized by thick-walled oocysts excreted in feces.
Coccidians
[5] Coccidian in Humans
- Cryptosporidium
- Isospora
- Cyclospora
- Toxoplasma
- Sarcocystis
[3] Only a single direct cycle of transmission occurs, both the asexual and sexual stages of multiplication occurs in a single host and that is to man.
Cryptosporidium
Isospora
Cyclospora
[2] The sexual stages are usually in the intestinal mucosa of a carnivorous host (the predator). The result in an oocyst or sporocyst that passes out in the feces to infect an intermediate host (the prey) in which asexual multiplication of the parasite occur.
Toxoplasma
Sarcocystis
[3] Life cycle of Coccidians
- Merogony
- Gametogony
- Sporogony
schizogony
[life cycle of coccidians]
Merogony
produce merozoites.
[life cycle of coccidians]
Merogony
gamogony or gametocytogenesis.
[life cycle of coccidians]
Gametogony
produce micro- and macrogametes.
[life cycle of coccidians]
Gametogony
produce sporozoites.
[life cycle of coccidians]
Sporogony
completed on host cell.
[life cycle of coccidians]
Sporogony
thin (autoinfection) or thick walled oocysts.
[life cycle of coccidians]
Sporogony
cosmopolitan distribution.
Toxoplasma Gondii
seropositive prevalence rates vary — generally 20-75%
Toxoplasma Gondii
Generally causes very benign disease in immunocompetent adults.
Toxoplasma Gondii
tissue cyst forming coccidia.
Toxoplasma Gondii
It has been coined for the first, actively multiplying merozoites that develop within the intermediate host, irrespective of whether infection is from oocysts or tissue cysts.
Tachyzoites
non-infectious
[metrocytes, bradyzoites]
Metrocytes
infectious
[metrocytes, bradyzoites]
Bradyzoites
These [2] are merozoites that develop within tissue cysts.
Metrocytes and Bradyzoites
Ingestion of sporulated oocysts (cat feces + incubation)
Human transmission — Toxoplasma Gondii
Ingestion of zoites (tachyzoite & bradyzoites (undercooked meat)
Human transmission — Toxoplasma Gondii
Congenital infection (only during acute stage)
Human transmission — Toxoplasma Gondii
Blood transfusions (only during acute stage) .
Human transmission — Toxoplasma Gondii
The organisms can grow in any organs or tissues, developing in the brain, eyes and skeletal muscles.
Pathogenesis — Toxoplasma Gondii
There is localized proliferation of the organisms and immunologic hypersensitivity reaction.
Pathogenesis — Toxoplasma Gondii
Multiplication of the organisms within the infected cell leads to death and rupture of the cell.
Pathogenesis — Toxoplasma Gondii
A clinical manifestations of Toxoplasma Gondii that is often severe and even fatal.
Congenital toxoplasmosis
Sabin syndrome (tetrad of signs)
Clinical Manifestations — Toxoplasma Gondii
[3] Other forms of Toxoplasmasis
- Typhus-like exanthematous form
- Cerebrospinal form
- Non-congenital retinochoroiditis infection
May produce myocarditis, meningoencephalitis and atypical pneumonia.
[other forms of toxoplasmasis]
Typhus-like exanthematous form
There is involvement of the CNS and the CSF is xanthochromic.
[other forms of toxoplasmasis]
Cerebrospinal form
The ocular lesion originates in the retina and spread to the choroids.
[other forms of toxoplasmasis]
Non-congenital retinochroiditis infection
likely due to both active parasite proliferation and immune hypersensitivity.
[ocular toxoplasmasis]
Retinochroiditis
generally a recrudescence-rarely from primary infection.
Ocular toxoplasmasis
most lesions are focal and self-limiting.
Ocular toxoplasmasis
rapidly destructive in AIDS patients.
Ocular toxoplasmasis
Inoculation into mice or cell culture (only acute stage).
Diagnosis — Ocular Toxoplasmasis
Very sensitive and specific but requires maintenance of live organism.
Sabin-Feldman methylene blue dye test
Serological test: to detect antibodies
Diagnosis Diagnosis — Ocular Toxoplasmasis
[3] Treatments for Ocular Toxoplasmasis
- Pyrimethamine and Sulfadiazine
- Corticosteroids
- Trimethroprim-sulfamethoxazole
controls Toxoplasma but do not kill it.
[treatments for ocular toxoplasmasis]
Pyrimethamine and Sulfadiazine
prevent occurrence of hypersensitivity.
[treatments for ocular toxoplasmasis]
Corticosteroids
prophylaxis for immunocompromised.
[treatments for ocular toxoplasmasis]
Treimethoprim-sulfamethaxazole
pyrimethamine can cause lower blood counts.
Leucovorin
Causes allergic reaction but can be substituted by clindamycin.
Sulfadiazine
