Protozoal Infections Morphology Disease Pathogenesis Clinical Manifestation Microscopic Macroscopic Cerebral Toxoplasmosis Toxoplasma Abscess formation During an acute infection, patients can be either usually appear assymptomatic pseudocyst Often present with Acquired Toxoplasmosis But when the cysts forms in the CNS, with multiple foci of patients will develop Congenital bradyzoites calcification Fever Toxoplasmosis With/out Ingestion of the cysts will Headache granuloma lead to infection Lethargy Toxoplasmic The initial infection takes Altered mental status place at the intestion and Encephalitis neurological deficits regional lymph nodes Convulsions The formation occurs at May end with fatality the Single or multiple lesions can be seen CNS at the Eyes Basal Ganglia Cardiac muscle Junction between the white and Skeletal muscle gray matter Prions Diseases Morphology Disease Pathogenesis Clinical Manifestation Microscopic Macroscopic Prions Diseases Groups of diseases with abnormal form Spongiform atrophy Most patients of a specific protein, Prion Protein (PrP) The progression of develop Dementia cerebral cortex It is itself transmissable particles Small disease can be either Disease Can be directly inoculated Very slow vacoules in (CJD) PrP undergoes conformational change dendritic Rapid from cytoplasm Normal isoform (PrPc) α-helix-containing Syndrome Abnormal sheet isoform β-helix-pleated cluster (GSS) (PrPsc) Astrocytocis PrPsc is located at the Chromosome 20 Fatal familial Neuronal loss Accumulation of PrPsc in the neurons insomnia appear to be the cause of pathology Kuru Largely how does this happens, remains unknown
Protozoal Infections Disease Pathogenesis Morphology Clinical Manifestation Microscopic Macroscopic Toxoplasmic Encephalitis Cerebral Toxoplasmosis can be either Acquired Toxoplasmosis Congenital Toxoplasmosis Ingestion of the cysts will lead to infection The initial infection takes place at the intestion and regional lymph nodes The formation occurs at the CNS Eyes Cardiac muscle Skeletal muscle Toxoplasma pseudocyst with bradyzoites With/out granuloma Abscess formation Often present with multiple foci of calcification During an acute infection, patients usually appear assymptomatic But when the cysts forms in the CNS, patients will develop Fever Headache Lethargy Altered mental status neurological deficits Convulsions May end with fatality Single or multiple lesions can be seen at the Basal Ganglia Junction between the white and gray matter Prions Diseases Disease Pathogenesis Morphology Clinical Manifestation Microscopic Macroscopic Prions Diseases Disease (CJD) Syndrome (GSS) Fatal familial insomnia Kuru Groups of diseases with abnormal form of a specific protein, Prion Protein (PrP) It is itself transmissable particles Can be directly inoculated PrP undergoes conformational change from Normal α-helix-containing isoform (PrPc) Abnormal β-helix-pleated sheet isoform (PrPsc) PrPsc is located at the Chromosome 20 Accumulation of PrPsc in the neurons appear to be the cause of pathology Largely how does this happens, remains unknown Spongiform cerebral cortex Small vacoules in dendritic cytoplasm cluster Astrocytocis Neuronal loss atrophy The progression of disease can be either Very slow Rapid Most patients develop Dementia
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