Disseminated toxoplasmosis in a patient with advanced acquired immunodeficiency syndrome

Abstract

Extracerebral toxoplasmosis, with pulmonary involvement and shock, is a rare form of toxoplasmosis in patients with advanced AIDS. It can mimic pneumocystosis, histoplasmosis, and disseminated tuberculosis, and should be considered in the differential diagnosis of causes of respiratory failure and fulminant disease in this group of individuals, especially in areas where the Toxoplasma gondii infection is highly prevalent and in those without proper use of antimicrobial prophylaxis. We report the case of a 46-year-old male patient who presented to the emergency department with uremia, requiring urgent dialysis. During the laboratorial investigation, the patient had confirmed HIV infection, with a low CD4+ peripheral T-cell count (74 cells/µL). During hospitalization, the patient presented drug-induced hepatitis due to trimethoprim/sulfamethoxazole in a prophylactic dose, requiring interruption of this medication. On the 55th day of hospitalization, the patient developed refractory shock and died. At the autopsy, disseminated toxoplasmosis with encephalitis and severe necrotizing pneumonia were diagnosed, with numerous tachyzoites in the areas of pulmonary necrosis.

Keywords: AIDS; Autopsy; Toxoplasma gondii.

Figure 1. Radiological findings of pulmonary toxoplasmosis: A – supine chest x-ray showing diffuse bilateral pulmonary opacities and obliteration of left inferior hemithorax. Also note the tracheal tube and venous catheters; B – Axial computed tomography (lung window) showing bilateral centrilobular ground-glass opacities, consolidation of posterior portions of the lungs, and small bilateral pleural effusions.

Figure 2. Micrograph of pulmonary toxoplasmosis. A – Septal congestion, alveolar edema, foci of necrosis scattered in the lung parenchyma (arrows). Anthracosis is observed (H&E, 10X); B – Interstitial pneumonia and areas of intra alveolar exudate and lytic necrosis, T. gondii forms, not seeing at this magnification (H&E, 70X).

Figure 3. Micrograph of pulmonary toxoplasmosis. A – Areas of exudative pneumonia with free T. gondii tachyzoites (arrows) in the alveolar space. The inflammatory tissue reaction is weak, with few alveolar macrophages, lymphocytes, and neutrophils (H&E 630X); B – Rupture of a T. gondii cyst in a lung parenchymal cell (H&E 630X).

Figure 4. Micrograph of pulmonary toxoplasmosis. The immunohistochemistry revealed numerous intracellular and extracellular forms of T. gondii (Peroxidase, Rabbit Polyclonal Antibody, Cell Marque™ 400X).

Figure 5. Micrograph showing some histopathological aspects of AIDS-associated nephropathy. A – Collapse of glomerular capillaries, dilatation of the Bowman capsule, podocytes hypertrophy, tubular cystic dilatation, and interstitial chronic nephritis with interstitial fibrosis (H&E, 200X); B – The Masson’s Trichrome stain shows collagen deposition in the glomeruli, some with thick Bowman capsule (arrows) and others with glomerular sclerosis (arrowheads). On the bottom, interstitial fibrosis is evident (Masson’s trichrome, 90X).

Figure 6. Micrograph of diffuse T. gondii encephalitis. A – Glial nodule in the hippocampus associated with neuropil edema (H&E 100X); B – Glial nodule in the subcortical white matter. T. gondii forms were not seeing in the inflammatory reaction composed of histiocytes and lymphocytes (H&E 300X); C – Perivascular inflammatory infiltrate with discrete hemorrhage and edema (H&E 200X); D – The T. gondii antigen was detected by IHC in the cytoplasm of rare inflammatory cells (Peroxidase, Rabbit Polyclonal Antibody, Cell Marque™ 200X).