Paper II
2023 July (Supplementary) (2019 Scheme) · 100 marks · 180 min

Question

Describe the pathogenesis, clinical features and laboratory diagnosis of Toxoplasmosis.

Q58 marksShort Essays

Answer

Toxoplasmosis

Pathogenesis: caused by the protozoan parasite Toxoplasma gondii. Humans are typically infected by ingesting oocysts (from food/water contaminated with cat faeces) or tissue cysts (in undercooked meat containing bradyzoites); after ingestion, the organism converts to rapidly dividing tachyzoites, which disseminate via the bloodstream/lymphatics to various tissues (particularly brain, eye, and muscle), where, under pressure from the developing host immune response, they convert to slowly dividing bradyzoites within tissue cysts, establishing a chronic, generally asymptomatic latent infection in the immunocompetent host. Reactivation of latent bradyzoites (with conversion back to tachyzoites) occurs particularly in immunocompromised individuals (e.g., AIDS with low CD4 count), causing active disease, most notably toxoplasmic encephalitis.

Clinical features:

  • In immunocompetent hosts: usually asymptomatic, or a mild, self-limiting mononucleosis-like illness with lymphadenopathy.
  • In immunocompromised hosts (e.g., AIDS): Toxoplasmic encephalitis — the most common cause of a focal brain mass lesion in AIDS patients, presenting with headache, fever, focal neurological deficits, and seizures.
  • Congenital toxoplasmosis: acquired transplacentally following primary maternal infection during pregnancy, causing the classical triad of chorioretinitis, hydrocephalus, and intracranial calcifications, along with other features (microcephaly, seizures).
  • Ocular toxoplasmosis: chorioretinitis, potentially causing visual impairment.

Laboratory diagnosis:

  • Serology — the mainstay for immunocompetent patients: IgM antibody indicates recent/acute infection, IgG antibody indicates past infection/immunity (and a rising IgG titre or IgG avidity testing helps date the infection, particularly important in pregnancy).
  • Molecular methods (PCR) — detection of T. gondii DNA in blood, CSF, or amniotic fluid (for suspected congenital infection); particularly valuable in immunocompromised patients, who may not mount a reliable antibody response.
  • Neuroimaging (CT/MRI) — in suspected cerebral toxoplasmosis, showing characteristic multiple ring-enhancing lesions, typically supported by clinical response to empirical anti-toxoplasma therapy.
  • Histopathology/tissue biopsy — demonstration of tachyzoites/tissue cysts, though rarely required given the reliability of serology/molecular methods.

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