Critical Care Medicine-Infections and Immunologic Disease>>>>>Infections in the Immunocompromised Host
Question 1#

A 38-year-old female with no significant past medical history was brought to the emergency department with confusion and lethargy. Her family noted that the patient had been complaining of worsening headaches for the last several days. On admission, she was afebrile and hemodynamically stable. Initial laboratory workup showed leukopenia (white blood cell [WBC] count of 3 000 cells/mL) with absolute lymphopenia. Human immunodeficiency virus (HIV) testing was positive with a ribonucleic acid (RNA) viral load of 68 000 copies/mL and CD4 count of 25 cells/µL. Magnetic resonance imaging (MRI) of the brain revealed multiple ring-enhancing lesions of different sizes with surrounding edema and mass effect.

What is the NEXT BEST step to diagnose her disease process?

A. India ink staining
B. Toxoplasma gondii IgG antibody
C. Stereotactic brain biopsy
D. Cytomegalovirus CSF polymerase chain reaction (PCR)
E. Quantiferon tuberculosis testing

Correct Answer is B


Correct Answer: B

This patient with newly diagnosed HIV/AIDS, and a CD4 count <100 cells/µL has central nervous system manifestation of toxoplasmosis. Clues to the diagnosis are compatible clinical features and multiple ringenhancing lesions with mass effect on MRI.

Toxoplasmosis, caused by the protozoan parasite Toxoplasma gondii, is the most common CNS opportunistic infection associated with HIV and is an AIDS-defining illness per the Centers for Disease Control and Prevention (CDC). Incidence of toxoplasmosis varies from 24% to 47% in T. gondii seropositive patients with a CD4 count <100 cells/µL. In immunosuppressed patients, disease is caused by the reactivation of latent infection and the CNS is the most common site of reactivation.

Toxoplasma encephalitis presents with fever, headache, mental status changes, focal neurologic deficits, or seizures. Mental status changes can result from global encephalitis and/or increased intracranial pressure.

In the appropriate clinical setting, a presumptive diagnosis can be made if the patient has a positive serology consistent with prior infection—a positive T. gondii immunoglobulin G (IgG)—and brain imaging (MRI) with multiple ring-enhancing lesions, often with surrounding edema. A presumptive diagnosis is sufficient to start anti-toxoplasma treatment. Identification of the organism on a tissue biopsy sample can confirm a suspected diagnosis but is not required especially given the morbidity and mortality associated with an invasive brain biopsy. Sulfadiazinepyrimethamine is the drug of choice. Clinical improvement is expected within 10 to 14 days of treatment initiation; if no improvement is observed by this time period, alternative diagnoses should be considered. 

The differential diagnosis for ring-enhancing lesions in the brain in a patient with known HIV includes primary CNS lymphoma, mycobacterial infections, cryptococcosis, and bacterial or fungal abscesses.

References :

  1. Renold C, Sugar A, Chave JP, et al. Toxoplasma encephalitis in patients with the acquired immunodeficiency syndrome. Medicine (Baltimore). 1992;71(4):224-239.
  2. Luft BJ, Remington JS. Toxoplasmic encephalitis in AIDS. Clin Infect Dis. 1992;15(2):211-222.
  3. Grant IH, Gold JW, Rosenblum M, Niedzwiecki D, Armstrong D. Toxoplasma gondii serology in HIV-infected patients: the development of central nervous system toxoplasmosis in AIDS. AIDS. 1990;4(6):519- 521.
  4. Zangerle R, Allerberger F, Pohl P, Fritsch P, Dierich MP. High risk of developing toxoplasmic encephalitis in AIDS patients seropositive to Toxoplasma gondii. Med Microbiol Immunol (Berl). 1991;180(2):59-66.