Annals of Indian Academy of Neurology
: 2007  |  Volume : 10  |  Issue : 2  |  Page : 109--111

Multiple opportunistic infections in an unusual patient with human immunodeficiency virus infection

Ravindra Kumar Garg, Vimal Paliwal, Rohitash Sharma, Parthiv Desai, Alok Mohan Kar 
 Department of Neurology, King George Medical University, Lucknow, India

Correspondence Address:
Ravindra Kumar Garg
Department of Neurology, King George Medical University, Lucknow - 226003


A marked decrease in incidence has been observed for most central nervous system opportunistic infections after the use of highly active antiretroviral therapy. In developing countries, where highly active antiretroviral therapy is still unavailable, unusual patients are encountered. We are reporting an untreated patient who, in addition to progressive multifocal leukoencephalopathy, also had disseminated tuberculosis and oral candidiasis. Neuroimaging showed a very extensive white matter and gray matter involvement producing a picture of źDQ╗JC virus encephalitisźDQ╗.

How to cite this article:
Garg RK, Paliwal V, Sharma R, Desai P, Kar AM. Multiple opportunistic infections in an unusual patient with human immunodeficiency virus infection.Ann Indian Acad Neurol 2007;10:109-111

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Garg RK, Paliwal V, Sharma R, Desai P, Kar AM. Multiple opportunistic infections in an unusual patient with human immunodeficiency virus infection. Ann Indian Acad Neurol [serial online] 2007 [cited 2020 Oct 20 ];10:109-111
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Full Text


Progressive multifocal leukoencephalopathy (PML) is an important opportunistic infection in patients with human immunodeficiency virus (HIV) infection caused by the human polyomavirus JC. PML is a fatal demyelinating disease of the central nervous system (CNS). It is a late manifestation of HIV infection and is seen in approximately 4% of patients. Although PML and miliary tuberculosis are common in immunosuppressed patients; their concomitant occurrence in an untreated patient is rarely seen. Here, we describe an unusual co-occurrence of PML, miliary tuberculosis and other infective complications in a single patient.

 Case Report

A 33-year-old man presented with history of intermittent low-grade fever, cough, weight loss and recurrent oral ulceration for the past one year. Patient had progressive painless vision loss of one month duration. From the same duration he also had unsteadiness of gait and tendency to fall. He had sudden onset left hemiparesis 15 days back, marked vision loss and altered sensorium. Subsequently his sensorium further deteriorated.

On examination, he had pallor, clubbing and oral candidiasis. He was not responding to verbal commands but was responding to painful stimuli (Glasgow coma score E 2 M 3 V 4 ). He had no light perception in either eye with preserved pupillary reaction to light. Patient had left supranuclear facial palsy, left hemiparesis, bilateral extensor plantar and neck rigidity. Respiratory system examination revealed coarse crepitations and occasional ronchi diffusely in both the lungs. Other systemic examination was normal.

In laboratory evaluation haemogram serum electolytes, liver function tests and renal function tests were normal. Chest X-ray revealed miliary mottling scattered throughout both the lungs [Figure 1]. HIV ELISA was reactive from two different laboratories at two different occasions. CD4+ cell count was >200 cells/mm 3 . Lumbar puncture yielded clear CSF under normal pressure with 35 mg/dL glucose, 206 mg/dL proteins and 34 lymphocytes per mm 3 . Gram's, India ink and acid-fast bacillus staining in CSF sediments were negative. Computed tomographic scan showed asymmetrical hypodense lesions without any mass effect, predominantly involving cerebral white matter. There was no contrast enhancement. On magnetic resonance imaging (MRI), lesions were hypointense in T1-weighted images, hyperintense in T2-weighted and fluid attenuated inversion recovery (FLAIR) sequences. The lesions were located in the subcortical white matter, mostly in the parieto-occipital regions. Lesions were also seen extensively in brain stem, thalamus, basal ganglia and cerebellum. MR imaging did not show any mass effect or contrast enhancement [Figure 2]. Polymerase chain reaction (PCR) for JC virus DNA as well as PCR for Mycobacterium tuberculosis was positive in CSF. Antinuclear antibodies and VDRL testing were negative. patient was treated with antituberculous drugs and was being planned for antiretroviral treatment. His condition deteriorated and he expired after short hospital stay.


Our case is unusual because of two reasons. Firstly, patient exhibited multiple opportunistic infections in the course of disease (on different occasions). This patient, in addition to PML, had disseminated tuberculosis (miliary pulmonary tuberculosis and tuberculous meningitis) and oral candidiasis. Secondly, patient was having very extensive involvement of brain resembling a picture previously described as "JC virus encephalitis", because there was an involvement of gray matter and infratentorial structures along with extensive involvement of cortical and subcortical white matter. The parieto-occipital and frontal lobes are most commonly affected.

Primarily, PML is a demyelinating disease of the CNS caused by lytic infection of oligodendrocytes by JC polyomavirus. HIV infection accounts for 85% of all PML cases and 5% of patients with AIDS ultimately develop the disease.[1] PML is clinically characterized by progressive cognitive decline, hemiparesis, sensory loss, visual field defects, ataxia, aphasia and cranial nerve deficits. MRI findings in progressive multifocal leukoencephalopathy consists of altered signal in subcortical and deep white matter, most clearly evident on T2-weighted and FLAIR sequences. PML lesions may exhibit gadolinium enhancement in a minority of cases. Less commonly, there is cortical gray matter involvement. Gray matter involvement in PML has been reported in various studies, it is thought to be a secondary phenomenon related to white matter destruction. Basal ganglia involvement, when it occurs, is possibly due to the involvement of white matter tracts coursing through these structures.[2],[3],[4] Before highly active antiretroviral therapy, 5% of AIDS patients developed PML with CD4 counts usually below 100/mm 3 .[5] However, the exact effect of highly active anti-retroviral therapy on the incidence of PML is not known. Paradoxically, highly active antiretroviral therapy -induced immune reconstitution can lead to worsening of PML. There are several reports of PML developing shortly after the introduction of highly active anti-retroviral therapy even with improvement in the CD4 cell count and HIV viral load. This phenomenon is called immune reconstitution inflammatory syndrome.[6]

Tuberculosis is one of the most important infectious complications in HIV-infected individuals. In a series, HIV-infected group of patients with tuberculosis had a significantly higher proportion of miliary shadowing.[7] Tuberculosis can appear at any stage of HIV infection and its presentation varies with the stage. Miliary tuberculosis is a potentially lethal form of tuberculosis resulting from massive lymphohaematogeneous dissemination of Mycobacterium tuberculosis bacilli. Impaired cell-mediated immunity underlies the disease's development. Paradoxical clinical deterioration of miliary tuberculosis, characterized by pulmonary and abdominal manifestations, is reported in a patient with the acquired immunodeficiency syndrome, after initiation of treatment with highly active antiretroviral therapy.[8]

A marked decrease in incidence has been observed for most CNS opportunistic infections after the use of highly active antiretroviral therapy. The incidence rates of commonly encountered CNS opportunistic infections (cryptococcal meningitis, toxoplasmosis, progressive multifocal leukoencephalopathy) and primary CNS lymphoma have decreased since the introduction of highly active antiretroviral therapy.[9] A recent study assessed the incidence of CNS diseases in 9,803 patients across Europe in the period 1994 to 2002. In this study, 568 patients (5.8%) had a new CNS disease. Incidence decreased significantly from 5.9 per 100-person-year in 1994 to 0.5 in 2002.[10] Overall, the decrease was calculated as 40% per calendar year. Highly active antiretroviral therapy reduced the incidence of HIV-associated tuberculosis by more than 80% in an area endemic with tuberculosis and HIV-1.[11] The incidence of toxoplasmic encephalitis has also been reported to decline from 3.9 cases per 100 person-years in to 1.0 cases per 100 person-years in post highly active antiretroviral therapy era.[12] A 46% decrease in the incidence of cryptococcosis during the post- highly active antiretroviral therapy era (1997-2001, n = 292) compared to the prehighly active antiretroviral therapy era (1985-1996, n = 1352) has been noted.[13] So, in developing countries, where highly active anti-retroviral therapy is scantly available, several such unusual patients are likely to be encountered. There is a need to remain vigilant.


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