Cerebral toxoplasmosis in HIV-infected patients over 2015-2018 (a case study of Russia)

Abstract

Cerebral toxoplasmosis is a leading cause of the central nervous system disorders in acquired immune deficiency syndrome. This study aimed to investigate the clinical course of cerebral toxoplasmosis in human immunodeficiency virus (HIV)-infected individuals. The study included 90 HIV-infected patients with cerebral toxoplasmosis, who underwent inpatient treatment. In case of positive enzyme immunoassay, HIV infection was confirmed with the immunoblot test. The HIV-1 ribonucleic acid level was determined using the polymerase chain reaction method. The flow cytometry was used for counting CD4 (cluster of differentiation 4 cells). Pathomorphological examination included the autopsy, gross and microscopic examination of internal organs, histological and other methods. The incidence of cerebral toxoplasmosis significantly increases at the CD4 count below 100 cells/μl, P < 0.001, and at the HIV viral load above 50 copies/ml, P < 0.05. The clinical picture of cerebral toxoplasmosis included focal symptoms, cognitive impairment, toxic syndrome, mild cerebral symptoms and a meningeal symptom. Given the absence of a specific clinical picture and the absence of abnormal laboratory and instrumental findings, the cerebral toxoplasmosis needs to be diagnosed with a number diagnostic methods combined: clinical examination, laboratory testing, immunological examination, molecular genetic testing and neuroradiological imaging.

Keywords: Cerebral toxoplasmosis; HIV infection; clinical picture; medical imaging; pathoanatomy.

Fig. 1.

Frequency of cerebral toxoplasmosis in terms of CD4 lymphocyte count, n = 90.

Fig. 2.

Frequency of cerebral toxoplasmosis in terms of viremia level, n = 90.

Fig. 3.

Cerebral toxoplasmosis. A – T2-VI; B – Т2 FLAIR; C, D – T1-VI. Multifocal brain damage (white arrows), with perifocal oedema (black arrows), and a ring accumulation pattern of the contrast agent (arrowheads).

Fig. 4.

Cerebral toxoplasmosis. A – T1-VI; B – Т2 FLAIR; C, D – T1-VI. Multifocal brain damage (white arrows), with perifocal oedema (black arrows), ring and nodular accumulation patterns of the contrast agent (arrowheads).

Fig. 5.

Cerebral toxoplasmosis. A – Т2 FLAIR; B – SWI; C – T1-VI. Multifocal brain damage with perifocal oedema (white arrows) and haemoglobin breakdown products (black arrows).

Fig. 6.

Cerebral toxoplasmosis. A – T2-VI; B – Т2 FLAIR; C – DWI; D – DCI; E – T1-VI; F – SWI. Multifocal brain damage with perifocal oedema (white arrows), with the absence of reduced diffusion in the central part (black arrows), and with the haemoglobin breakdown products (arrowheads).

Fig. 7.

Cerebral toxoplasmosis, haematoxylin-eosin stained. Spherical cyst (arrows) with multiple Toxoplasma.