Combined HIV-CMV encephalitis presenting with brainstem signs

Acta Neuropathologica, 1990

A 25-year-old homosexual male with AIDS presented with a cauda equina syndrome clinically suggestive of cytomegalovirus (CMV) myeloradiculitis. He was treated with ganciclovir with transient improvement of neurological signs and died 4 months after onset of neurological signs. Neuropathological examination revealed human immunodeficiency virus (HIV) encephalitis, CMV subependymal encephalitis and CMV myeloradiculitis. The latter was characterised by myelin loss, Schwann cell proliferation and presence of CMV early antigens in the nuclei of S-] 00 protein-positive cells in the spinal roots. In the subependymal regions, morphologically characteristic multinucleated giant cells, positive for CD68, contained early CMV antigens (El3) in their nuclei and HIV antigens (gp41 and p24) in their cytoplasm. The observation that HIV and CMV can co-infect the same cell in vivo raises the possibility of a direct synergistic interaction of both viruses at cell level. This suggests that CMV may play a role as a co-factor in the pathogenesis of HIV encephalopathy.

Revista do Instituto de Medicina Tropical de São Paulo

Neurological disorders caused by Cytomegalovirus (CMV) in patients with Acquired Immunodeficiency Syndrome (AIDS) are rarely reported in the Highly Active Antiretroviral Therapy (HAART) period. The objective of this study was to describe the main clinical and laboratory features of patients with CMV-related neurological complications in HIV-infected patients admitted to a referral center in São Paulo, Brazil. CMV disease requires the identification of the virus in the cerebrospinal fluid (CSF) using Polymerase Chain Reaction (PCR). Thirteen cases were identified between January, 2004 and December, 2008. The median age of patients was 38 years and nine (69%) were men. At admission all patients were aware of their HIV status and only four (31%) patients were on HAART. Patients who were not on antiretroviral therapy before admission received HAART while inpatients. CMV disease was the first AIDS-defining illness in eight (62%) patients. The neurologic syndromes identified were diffuse ...

Journal of Neurology, 1996

Pediatric Neurology, 1999

The present report concerns a vertically human immunodeficiency virus type 1 (HIV-1)-infected 7-year-old child, in whom a neurodegenerative disease occurred after an acute neurologic disorder that was in all likelihood symptomatic of HIV-1 encephalitis. At the steady state the neurologic disease fulfilled the accepted criteria of HIV-related progressive encephalopathy of childhood and was characterized by involvement of multiple neural systems and subcortical dementia. The neurologic disease displayed, however, atypical presentation and course, and its acute focal onset led the authors to postulate an acute and direct involvement of the brain in HIV-1 infection. The correlation between the cliniconeuroradiologic data and levels of HIV-RNA in the cerebrospinal fluid and the response to different antiretroviral treatments are also discussed.

Annals of the New York Academy of Sciences, 1994

Virus-associated diseases of the central nervous system (CNS) commonly occur in patients with human immunodeficiency virus (HIV) infection. These include CMV infection (reported in up to 30% of cases), progressive multifocal leukoencephalopathy (PML, 2-7%), herpes simplex virus (HSV, 0-2%) and varicellazoster virus (VZV, 0-2%) infections. Primary CNS lymphoma (4-lo%), furthermore, has been shown to be associated with Epstein-Barr virus (EBV) in 100% of cases. The current diagnostic procedures for these diseases include virus isolation (possible for CMV, HSV, and VZV), and examination of cerebrospinal fluid (CSF) " Address correspondence to Paola Cinque, M.D., Centro Ricerca e Cura patologie HIVcorrelate,

International Journal of Infectious Diseases, 2007

Antiviral Therapy, 2014

Cytomegalovirus (CMV) central nervous system involvement is uncommon and hardly diagnosed because it can mimic many different conditions. We here present a case of an HIV-positive patient with neurological signs and symptoms (headache, asthenia, confusion, hallucinations, ataxia) with concurrent opportunistic diseases (neurotoxoplasmosis, disseminated Kaposi's sarcoma, disseminated CMV infection). CMV CNS involvement was not initially considered given the observed multiple comorbidities: antiviral treatment duration was probably not adequate given the end-organ disease. Concomitantly, plasma CMV DNA was undetectable while cerebrospinal fluid viral load was 31,340 copies/ml. Ganciclovir treatment followed by oral valganciclovir maintenance was associated with the slow disappearance of symptoms, the improvement of MRI images and the persistent undetectability of CMV DNA. The case here reported highlights the challenges of diagnosing CMV encephalitis in HIV-positive patients (with several cerebral comorbidities), the incomplete knowledge of the appropriate treatment for such a disease and the possibility of CMV replication in the cerebrospinal fluid despite undetectable plasma CMV DNA.

Acta Neuropathologica, 1995

Unlike cytomegalovirus (CMV) ventriculoencephalitis, herpes simplex virus type 1 necrotizing encephalitis has only rarely been observed in AIDS patients. A 40-year-old bisexual man was followed for an HIV1 infection from 1987 onwards. In June 1993 he was referred for sudden confusion, left hemiparesia and fever. The blood contained less than 10 CD4 lymphocytes/mm 3. The patient remained comatose and febrile, and died 4 weeks later. In coronal sections of the brain there was necrosis of the internal parts of the left temporal lobe, necrosis of certain areas of the ventricular walls and a small tumor at the top of the right frontal lobe, which proved to be a polymorphic high-grade lymphoma. CMV ventriculoencephalitis lesions were prominent in the ventricular walls of the occipital lobes and there was a strong nuclear signal for CMV using in situ hybridization. Herpes simplex virus type 1 was shown in the nuclei and cytoplasm of certain neurons and astrocytes in the borders of the necrotized temporal lobe areas by immunohistochemistry, in situ hybridization and electron microscopy, whereas in situ hybridization and immunohistochemistry for CMV were negative in such areas. Necrotizing type 1 encephalitis must not be overlooked in immunodeficient patients.

Curēus, 2024

We present a case of cytomegalovirus (CMV) polyradiculopathy which occurred concomitantly with CMV encephalitis and CMV retinitis in a patient with HIV/AIDS. Our patient is a 43-year-old male who was admitted with progressive changes in mentation. Cerebrospinal fluid (CSF) analysis showed elevated white blood cell (WBC), low glucose, and elevated protein. The polymerase chain reaction (PCR) panel of CSF was positive for CMV, and other microbiology results were negative. Extensive bilateral CMV retinitis was also noted. The patient was started on ganciclovir and foscarnet, and two weeks after, highly active antiretroviral therapy (HAART) was initiated using Truvada and dolutegravir. The hospital course was complicated by urinary retention and bilateral lower extremity weakness with hypotonia, severe hyperalgesia, and allodynia. An electromyography (EMG) study demonstrated bilateral lumbosacral root dysfunction at L2-S1 with active neurologic changes indicating significant axon loss. Neurology was consulted, and the patient was diagnosed with CMV-induced polyradiculopathy. After three months of treatment, no improvement was noted on lower limbs as he continued with intravenous (IV) ganciclovir. The therapeutic response to induction therapy was discordant as improvement of encephalitis was noted, but not on polyradiculopathy after 180 days of treatment. This highlights the lack of data and treatment guidelines for established CMV polyradiculopathy and not only the necessity for prolonged treatment of CMV polyradiculopathy but also the difficulty in recovery of function once it has developed.

Acta Neurologica Scandinavica, 1988