| An obligate coccidian parasite that is asymptomatic in humans but causes disease in congenitally infected infants and immunodeficient and occasionally in immune competent individual? | TOXOPLASMA GONDII |
| TOXOPLASMA GONDII life cycle in non feline phase | 1) Oocyst she in cat feces sporulate in 1-5 days
2) intermediate host ingest Oocyst contaminated food, water
3)Oocyst transform into TACHYZOITES. In nueral and muscle tissue, they develop into tissue Cyst.
4) cats become reinfected
5) human become infected. |
| humans get infected by TOXOPLASMA GONDII by | 1) ingestion of raw/ undercooked meat containing cyst
2) ingestion of Oocysts in contaminated water or food
3) blood transfusion or organ transplant (less common)
4) from mother to fetous
5)accidental sticks with contaminated needles or exposure of lesions/ mucosal surface to parasite |
| trophozoite infect all cells in host except? | RBCs |
| pheline phase os life cycle of TOXOPLASMA GONDII | 1) sex gametes mate to form Oocyts
2) Oocyst pass in cat feces
3) after 2-3 days Oocyst become sporozoites ingested by feline to continue life cycle |
| human infection of TOXOPLASMA GONDII from cats occurs | sporozoites infect humans when cleaing cat litter |
| in transplantation transmission of TOXOPLASMA GONDII ,low risk transmission to fetus if mother is infected? | more than 6 months before conception |
| high risk transmission if mother is infected | lee than 6 months before conception |
| infection of TOXOPLASMA GONDII in first trimester is at ? | 15% |
| infection of TOXOPLASMA GONDII in 3rd trimester | 65% |
| infected infants with TOXOPLASMA GONDII are usually asymptomatic. infant can later suffer from? | chronic leaning difficulty and neurological sequelae |
| most infected women are asymptomiatic so screening should occur? | in women who intend to become pregnant |
| TOXOPLASMA GONDII bradyzoites and Oocyst are found in ? | Bradyzoites are found in tissue, Oocyst are found in cat feces |
| host response include | Secretory IgA, cell death, necrosis and inflammatory response. |
| host response in immunocompromised individuals where Tarchyzoites persist? | necrotisisnf encephalitis, pneumonia, myocarditis |
| pathology of tachyzoites and bradyzoites | tachyzoites: cell death, necrosis, mononuclear inflammatory response.
bradyzoites: yield only inflammatory response. cyst eventually rupture. |
| infected organs in TOXOPLASMA GONDII include | lymph nodes, eyes, brain. lungs, heart and GIT |
| clinical features and pathology of TOXOPLASMA GONDII | 1) in immunocompromised pts: toxoplasmic encephalitis most frequently seen in AIDS due to recrudescence. altered mantal status, seizures, fever and nerological findings. pneumonia, h. failure, liver failure and retinitis. |
| clinical pathology in immunocompetent patients | 80/90 % show no symptoms but lymphadenopathy, malaise, headahes, fever <40 degrees celcius. infectious mono syndrome.
vary rare : fever polymyositis, encephalitis, pnemonia and myocarditis |
| congenital toxoplasmosis include | hypoxia, hypoglycemia, hydrocephalus, visual impairment and death |
| occular infection of TOXOPLASMA GONDII due to congenital infection show symptoms such as? | blurred vision, scotoma, photophobia and glaucoma |
| lab diagnosis of TOXOPLASMA GONDII | culture, serology, PCR, ELISA, Immunoassays. amniotic fluid analysis for B1 gene, igg/igm titres |
| acute/Prior infection of TOXOPLASMA GONDII is associated wiht which form of the parasite? | TACHYZOITES: acute infection
BRADYZOITES: Prior infection |
| treatment of congenital TOXOPLASMA GONDII infection | PYRIMETHAMINE AND SULFADIAZINE FOR I YR |
| TRETEMENT OF TOXOPLASMOSIS IN IMMUNOCOMPETENT INDIVIDUAl | PYRIMETHAMINE AND SULFADIAZINE OR CLINDOMYCIN insever presentations. |
| toxoplasmosis in immunocompromised individual | primary prophylaxis (before infection): compromoxazole and pyrimethamine- sulfadiazine or depsone pyrimethamine or atovaqone. |
