Paper II
2024 March (Supplementary) (2019 Scheme) · 100 marks · 180 min

Question

Pathogenesis, clinical manifestations and laboratory diagnosis of Toxoplasmosis (PTO)

Q78 marksShort Essays

Answer

Toxoplasmosis

Pathogenesis: caused by the protozoan parasite Toxoplasma gondii. Humans are infected by ingesting oocysts (food/water contaminated with cat faeces, the definitive host) or tissue cysts (undercooked meat containing bradyzoites). After ingestion, the organism converts to rapidly dividing tachyzoites, disseminating via the bloodstream/lymphatics to various tissues (brain, eye, muscle); under host immune pressure, tachyzoites convert to slowly dividing bradyzoites within tissue cysts, establishing chronic, generally asymptomatic latent infection. Reactivation (bradyzoites converting back to tachyzoites) occurs particularly in immunocompromised individuals (e.g., AIDS with low CD4 count).

Clinical manifestations:

  • Immunocompetent hosts: usually asymptomatic, or a mild, self-limiting mononucleosis-like illness with lymphadenopathy.
  • Immunocompromised hosts (AIDS): Toxoplasmic encephalitis — the most common cause of a focal brain mass lesion in AIDS, 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 microcephaly and 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; IgG avidity testing helps date 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 multiple ring-enhancing lesions, typically supported by clinical response to empirical anti-toxoplasma therapy.
  • Histopathology/tissue biopsy — demonstration of tachyzoites/tissue cysts, rarely required given the reliability of serology/molecular methods.

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