Find more content written by:  Anil H. Patki
  • Volume 59 , Number 2
  • Page: 331–2

Some possible interactions of M. leprae and HIV in the peripheral nerves

Anil H. Patki

To the Editor:

Infection with the human immunodeficiency virus (HIV) has affected millions of people in the African continent (5) where leprosy is also endemic. The association of the acquired immunodeficiency syndrome (AIDS) with leprosy has seldom been reported (3), probably because of the prolonged incubation period of leprosy. A patient with AIDS who gets infected with Mycobacterium leprae succumbs to other (opportunistic or nonopportunistic) infections before he develops clinical leprosy. The possible interactions between the two infections have also been discussed (6). The possible results of the defective cell-mediated immunity due to HIV infection include conversion of subclinical leprosy cases into tuberculoid cases, downgrading of pauci-bacillary cases to multibacillary cases, and an increased incidence of type 2 lepra reactions (6).

However, interactions of two infectious agents at the level of peripheral nerves is a distinct possibility with which those involved in the care of leprosy patients must be prepared to deal. This is so because the HIV is not only lymphotrophic but also neurotrophic (2). In addition to the subacute encephalitis, peripheral neuropathy has also been recognized as a neurologic manifestation of HIV infection. The peripheral nerve syndromes found in patients with HIV infection include chronic inflammatory polyneuropathy and distal symmetric sensorimotor neuropathy (4). The etiologic role of the HIV in these nerve affections has been demonstrated by culture of the virus from the sural nerve of a patient with peripheral neuropathy (2) and, more recently, by the demonstration of HIV replication in infiltrating mononuclear cells in the peripheral nerves by in situ hybridization (1). Nerve biopsies in these patients revealed vasculitis and inflammatory infiltrates in the epineu-rium and endoneurium. What is more interesting is that this neurologic involvement could occur before or in the absence of immunodeficiency (2).

The implications of these findings are grave for patients with leprosy who may get infected with HIV. In addition to the immunodeficiency, they could suffer from additional nerve damage as a result of either a downgrading reaction or necrotizing vasculitis of the nerves due to the HIV infection. The deterioration of nerve function may occur while the patient is on antilep-rosy treatment, and it will have to be differentiated from a type 1 reaction. The management of peripheral neuropathy caused by HIV infection is far from clear. The HIV infection can also lead to Bell's palsy (4) which will have to be differentiated from leprous facial palsy. The investigations suggested for the evaluation of a patient with HIV-induced peripheral neuropathy include the examination of the cerebrospinal fluid, electromyography, nerve conduction velocity, and nerve biopsy (4). None of these may be available in the field and, when available, may not differentiate the nerve dysfunction due to a lepra reaction from that caused by the HIV in a patient infected with both M. leprae and HIV. The only direct confirmation of the fact that the HIV is responsible for the neuropathy will be by the demonstration or culture of the virus.

Another problem in these patients will be the treatment of lepra reactions. Systemic corticosteroids which are often needed for the control of reactions may have an adverse effect on the course of HIV infection by causing immunodeficiency.

The possible interaction of M. leprae and HIV in the peripheral nerves is a distinct possibility which will require careful study and follow up of the patients who may get infected with both of these agents.


- Anil H. Patki. M.D., D.N.B.

Indira Medico Clinic
Banali Apartments
8/4 Karve Road
Pune 411004, India



1. Gherardi, R., Lebargy, F., Gaulard, P., Mhiri, C., Uernaudin, J. F. and Gray, F. Necrotizing vasculitis and HIV replication in peripheral nerves. (Letter) N. Engl. J. Med. 321(1989)685-686.

2. Ho, D. D., Rota, T. R„ Schooley, R. T., Kaplan, J. C, Allan, J. D., Groopman, J. E., Resnick, L., Felsenstein, D., Andrews, C. A. and Hirsch, M. S. Isolation of HTLV-HI from cerebrospinal fluid and neural tissues of patients with neurologic syndromes related to the acquired immunodeficiency syndrome. N. Engl. J. Med. 313(1985)1493-1497.

3. Lamfers, E. J. P., Bastiaans, A. H., Mravunac, M. and Rampen, F. H. J. Leprosy in the acquired immunodeficiency syndrome. Ann. Intern. Med. 107(1987)111-112.

4. Levy, R. M., Bredesen, D. E. and Rosenblum, M. L. Neurological manifestations of the acquired immunodeficiency syndrome (AIDS): experience at UCSF and review of literature. J. Neurosurg. 62(1985)475-495 (159 rcf).

5. Quinn, T. C, Mann, J. M., Curran, J. W. and Piot, P. AIDS in Africa: an epidemiologic paradigm. Science 234(1986)955-963.

6. Turk, J. L. and Rees, R. J. W. AIDS and leprosy. Lepr. Rev. 59(1988)193-194.

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