|
   |
|
CASE REPORT |
|
|
|
| Year : 2020 | Volume
: 41
| Issue : 1 | Page : 108-110 |
| |
Human immunodeficiency virus encephalitis
Nitin Sinha, Sahil Sareen, Ashwini Kumar Malhotra, Sanchit Singh
Department of Medicine, Post Graduate Institute of Medical Education and Research, Dr. Ram Manohar Lohia Hospital, New Delhi, India
| Date of Submission | 28-Dec-2016 |
| Date of Acceptance | 05-Dec-2019 |
| Date of Web Publication | 18-Jun-2020 |
Correspondence Address:
Dr. Nitin Sinha
10-B, Himalaya Legend, Nyay Khand-1, Indirapuram, Ghaziabad, Uttar Pradesh - 201 014
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijstd.IJSTD_112_16
 Abstract | | |
Here, we present a case of pyrexia with altered sensorium in a young healthy male individual. On evaluation, he was detected to have human immunodeficiency virus infection with low CD4. He had no opportunistic infection or any other acquired immunodeficiency syndrome-defining illnesses although his magnetic resonance imaging brain showed features of encephalitis. He recovered tremendously within 3 months of antiretroviral therapy.
Keywords: Human immunodeficiency virus, human immunodeficiency virus encephalitis, low CD4, and encephalitis
How to cite this article:
Sinha N, Sareen S, Malhotra AK, Singh S. Human immunodeficiency virus encephalitis. Indian J Sex Transm Dis 2020;41:108-10 |
| Introduction | |  |
Human immunodeficiency virus (HIV) has been shown to have primary neurotropic properties.[1] Neurological lesions with HIV can occur in patients with acquired immunodeficiency syndrome (AIDS) or in asymptomatic individuals.[1]
The widespread use of efficacious antiretroviral therapy has tremendously influenced the natural history of the HIV infection. The frequency of the central nervous system (CNS) opportunistic infections, which were accompanied with high mortality, has decreased dramatically in countries where antiretroviral agents are available.[2] Two clinical neuropsychiatric disorders remain prevalent following the introduction of antiretrovirals, the first is a major depressive disorder,[3] and the second is HIV-associated neurocognitive disorder (HAND).[4] Bell et al. noted that HIV encephalitis (HIVE) occurred independently of opportunistic infections and lymphomas and showed different associations with risk groups, immunosuppression, and antiviral treatment.[5] Compared to the pretreatment era, in the post highly active antiretroviral therapy (HAART) era, there has been shift in the HIVE from a subacute to a chronic protracted form probably due to the increased longevity of HIV-infected patients and more exposure to HIV proteins and emergence of resistant HIV strains.[6]
| Case Report | | |
Our patient, a 35-year-old right-handed male, a soldier by occupation and a resident of Greater Noida, Uttar Pradesh, India, presented with the complaints of fever for the past 2 weeks and altered sensorium for the past 4 days following an episode of generalized tonic–clonic seizure. There was no associated upper or lower respiratory tract symptoms, no burning micturation, ear discharge, rashes, or other skin lesions or head trauma. His investigations showed that he was HIV-1 reactive. He had a history of prolonged fever for 1 month a year back and had been diagnosed with tubercular lymphadenitis by the fine-needle aspiration study. He was prescribed rifampicin, isoniazid, pyrazinamide, and ethambutol for the same, and he was continuing to take all of them till date. There was no history of addictions. He was married for 7 years and had two children. Examination revealed normal vitals in a conscious but disoriented patient with a staring look and a Glasgow Coma Scale score of 11/15. General examination revealed pallor and oral thrush. Neurological examination revealed a Folstein's Mini-Mental State Examination (MMSE) score of 12/30 with no signs of meningismus. Due to the condition of the patient, whatever restricted examination of motor system, sensory system, and cranial nerves was possible was normal. Examination of cardiovascular, respiratory, abdominal, and musculoskeletal system was within normal limits.
Investigations revealed an erythrocyte sedimentation rate of 33 mm (1st h) and a mild normocytic normochromic anemia (hemoglobin – 10.4 g%). Other biochemical parameters (liver function, kidney function, and blood sugar) were normal. Urine examination was also normal. A repeat testing of HIV by the ELISA confirmed the presence of antibodies against HIV-1. The CD4 count was 156/mm3, with a CD4 percentage of 14%. The differential diagnosis includes HIV with the likelihood of CNS opportunistic infections or HIV encephalopathy. Cerebrospinal fluid (CSF) examination reveals 10 cells, all mononuclear, with a sugar of 56 mg%, and a protein of 46 mg%. The adenosine deaminase levels were found to be 10 IU/L (within normal limits), and the CSF did not show any organism on Gram stain or Ziehl–Neelsen stain. The India ink staining for Cryptococcus was also negative. The polymerase chain reaction (PCR) in CSF was negative for Mycobacterium tuberculosis, human herpesvirus-6/herpes simpex virus, Toxoplasma gondii, and Cytomegalovirus. The PCR for JC virus could not be carried out due to financial constraints. Serum Widal, venereal disease research laboratory, hepatitis B surface antigen, Hepatitis C RNA, and IgG antibodies against toxoplasma were all negative.
Imaging of the brain revealed bilaterally symmetrical, T2/FLAIR hyperintensities noted in the white matter, involving the bilateral centrum semiovale, periventricular, posterior limb of the internal capsule, and midbrain (cerebral peduncle) suggestive of encephalitis on magnetic resonance imaging [Figure 1]. | Figure 1: T2-weighted image of magnetic resonance imaging brain showing encephalitis
Click here to view |
The patient's attendant did not give consent for a brain biopsy. The final diagnosis was made to be HIVE in a treatment-naïve patients with a CD4 count of 156/mm3 with oral candidiasis.
He was started on antiretroviral therapy with triple-drug regimens of tenofovir, lamivudine, and efavirenz along with antieplieptics and fluconazole. After 3 months of follow-up, he was seizure free, and his MMSE revealed marked improvement (from 12/30 to 20/30). The CD4 count also showed improvement from 156/cumm to 325/cumm.
| Discussion | | |
Infection of the CNS by HIV is associated with neurologic conditions, from HIV-associated dementia (HAD) to milder HANDs.[7] HAART helps to prolong the life of infected patients, reducing the incidence of HAD.[2] Although cases with severe HIV-related cognitive impairment have decreased, the frequency of HIVE, characterized by the presence of infected macrophages in the CNS, microgliosis, astrogliosis, and myelin loss, has remained the same or slightly increased.[5]
Brain, in particular, represents a sanctuary for HIV-1 latency, where the provirus can persist due to the variable and poor penetration of antiretroviral drugs.[7]
Neuroinflammatory responses play an important role in neurodegeneration in HIV1 latent and HIVE groups.[8],[9],[10]
There is no single test that can confirm the diagnosis of HIVE. Diagnosis is made largely by exclusion, ruling out other possible causes for the impairment such as herpes simplex virus encephalitis, toxoplasmosis, progressive multifocal leukoencephalopathy, Cytomegalovirus encephalitis, and CNS lymphoma.
Although the exclusion of other possibilities in our case (by imaging and serology testing) coupled with characteristic imaging properties of HIVE makes the diagnosis of the same almost certain.
The aim of presenting this case was to highlight a rare presentation of HIV infection with only acute impaired mentation without evidence of any severe AIDS-defining illness or opportunistic infection and to demonstrate the tremendous response to the ART.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Ho DD, Rota TR, Schooley RT, Kaplan JC, Allan JD, Groopman JE, et al. Isolation of HTLV-III from cerebrospinal fluid and neural tissues of patients with neurologic syndromes related to the acquired immunodeficiency syndrome. N Engl J Med 1985;313:1493-7.  |
| 2. | Price RW, Spudich S. Antiretroviral therapy and central nervous system HIV type 1 infection. J Infect Dis 2008;197 Suppl 3:S294-306. |
| 3. | Bing EG, Burnam MA, Longshore D, Fleishman JA, Sherbourne CD, London AS, et al. Psychiatric disorders and drug use among human immunodeficiency virus-infected adults in the United States. Arch Gen Psychiatry 2001;58:721-8. |
| 4. | Grant I. Neurocognitive disturbances in HIV. Int Rev Psychiatry 2008;20:33-47. |
| 5. | Bell JE, Donaldson YK, Lowrie S, McKenzie CA, Elton RA, Chiswick A, et al. Influence of risk group and zidovudine therapy on the development of HIV encephalitis and cognitive impairment in AIDS patients. AIDS 1996;10:493-9. |
| 6. | Langford TD, Letendre SL, Larrea GJ, Masliah E. Changing patterns in the neuropathogenesis of HIV during the HAART era. Brain Pathol 2003;13:195-210. |
| 7. | Alexaki A, Liu Y, Wigdahl B. Cellular reservoirs of HIV-1 and their role in viral persistence. Curr HIV Res 2008;6:388-400. |
| 8. | Irish BP, Khan ZK, Jain P, Nonnemacher MR, Pirrone V, Rahman S, et al. Molecular mechanisms of neurodegenerative diseases induced by human retroviruses: A review. Am J Infect Dis 2009;5:231-58. |
| 9. | Roulston A, Lin R, Beauparlant P, Wainberg MA, Hiscott J. Regulation of human immunodeficiency virus type 1 and cytokine gene expression in myeloid cells by NF-kappa B/Rel transcription factors. Microbiol Rev 1995;59:481-505. |
| 10. | Yang B, Akhter S, Chaudhuri A, Kanmogne GD. HIV-1 gp120 induces cytokine expression, leukocyte adhesion, and transmigration across the blood-brain barrier: Modulatory effects of STAT1 signaling. Microvasc Res 2009;77:212-9. |
[Figure 1]
|
