64, 2^ Correspondence^ 171

REFERENCES1. BECK, J. S., ABBOT, N. C., SAMSON, P. D., BUTLIN,

C. R., GRANGE, J. M., CREE, 1. A., FORSTER, A. andKHAN, F. Impairment of vasomotor reflexes in thefingertips of leprosy patients. J. Neurol. Neurosurg.Psych. 54 (1991) 965-971.

2. BELL-KROTOSKI, J. A. "Pocket" filaments andspecifications for the Semmes-Weinstein monofi-laments. J. Hand Ther. 3 (1990) 26-31.

3. BRANDSMA, W. Basic nerve function assessment inleprosy patients. Lepr. Rev. 52 (1981) 161-170.

4. BURTE, N. P., CHANDORKAR, A. G., MULEY, M. P.,BAL-SARA, J. J. and BULAKH, 1'. M. Effect of oneyear treatment on autonomic functions in lepro-matous leprosy with lepra (ENL) reaction. Lepr.India 55 (1983) 278-285.

5. KARANTH, S. S., SPRINGALL, D. R., LUCAS, S., LEVY,D., ASHBY, P., LEVENE, M. M. and POLAK, J. M.

Changes in nerves and neuropeptides in skin from100 leprosy patients investigated by immunocyto-chemistry. J. Pathol. 157 (1989) 15.26.

6. Low, P. A. Autonomic nervous system function.J. Clin. Neurophysiol. 10 (1993) 14-27.

7. Low, P. A., NEUMANN, C., DYCK, P. J. and FEALEY,R. D. Evaluation of skin vasomotor reflexes byusing laser doppler velocimetry. Mayo Clin. Proc.58(1983) 583-592.

8. MEYERS, W. M. and MARTY, A. M. Current con-cepts in the pathogenesis of Leprosy. Drugs 41 (1991)832-856.

9. SOLIVEN, B. C., MASELLI, R. A., JASPAN, J. B., GREEN,A. J., GRAZIANO, H., PETERSEN, NI. and SPIRE, J. P.Sympathetic skin response in diabetic neuropathy.Muscle Nerve 10 (1987) 711-716.

Leprosy and AIDS in the Amazon Basin

To THE EDITOR:The state of Amazonas in Brazil is a hy-

perendemic area of leprosy. Although therehas been a control program in action forabout the last 20 years, the prevalence rateand the detection rate were 39.4 per 10,000and 67 per 100,000 inhabitants in 1994,respectively. The first case of AIDS in thestate was diagnosed in 1986. Although thereis a low incidence rate of AIDS in the stateof Amazonas (9.5/100,000), 63% of the caseswere diagnosed within the last 3 years (Min-isterio da Saude do Brasil. Boletim Epide-miologico D.S.T./AIDS, Brasilia, 1995. AnoVII). This shows an increased trend of Al DSin the region. Despite an existing possibilityof an interaction between Mycobacteriumleprac and the HIV infection(' -3 ' 6 ' 7 ), fewclinical reports have been written and theeffects of this co-infection have not yet beendefined( 4 . 5 ).

In this letter, the clinical aspects and pro-gression of four patients who were identifiedas having leprosy and HIV infection [HIV1-HIV 2 antibodies by enzyme immuno-assay (Genelavia-Sanofi, France, and im-munolluorescence)], one of them with AIDSwhich was identified by the presence of Ka-posi's sarcoma, are described.

Case 1. JCLN, a 25-year-old marriedmale, presented with a hypochromic lesionon the left arm, was skin-smear negative,intradermal reaction was Mitsuda positiveand a histopathological examination of thelesion showed tuberculoid infiltrate. This ledto the diagnosis of the tuberculoid form ofleprosy in October of 1992. A drug com-bination treatment, including ofloxacin, wasgiven to the patient who had agreed to takepart in a double-blind trial for a period of6 months. The patient took the treatmentregularly and had no side effects or leprosyreactions. A routine serologic exam showeda positive result for HIV on 27 October1993. Only after that did the patient say thathe had known he was infected with HIVsince 1991 but that he had ignored the factand had not taken any preventative mea-sures. The leprosy lesion has disappeared,and a general clinical exam and laboratoryexams have not shown any abnormalities.

Case 2. VNA, a 27-year-old, male ho-mosexual hairdresser. A diagnosis of bor-derline lepromatous leprosy was made on15 September 1994. The patient presentedwith skin infiltration and disseminatedplaques. The first skin-smear exam showeda bacterial index (B1) of 3.2 with 1% of intact

172^ International Journal of Leprosy^ 1996

bacilli. Multidrug therapy (MDT-WHO) wasstarted, and a month later the patient pre-sented with a type 1 reaction which re-sponded well to prednisone. In February1995, a nodule-like lesion, reddish-purpleand shiny in appearance, developed on thesole of the patient's right foot. Histopatho-logical examination of the lesion was com-patible with Kaposi's sarcoma. A serologicexam showed a positive result for HIV inMarch 1995. At present, the leprosy lesionsare decreasing in size and number, and thepatient is still taking MDT-WHO and AZT.

Case 3. RLS, a 27-year-old, married malewas diagnosed as having lepromatous lep-rosy on 3 October 1978, having presentedwith anesthesia in the lower limbs, ulnarclawing in the left hand, and ulnar and com-mon peroneal nerve enlargement. He had apositive skin smear, and histopathologicalexamination showed histocytes with vacu-olated cytoplasm with acid-fast bacilli.Treatment with sulfone was introduced butchanged to MDT-WHO in June of 1986.After 2 years, the patient was released fromtreatment. Because his wife was detected ashaving HIV, he was advised to have the testwhich proved scropositive in March of 1995.At present, he has lost weight and has anulcer on the sole of his foot.

Case 4. RM, a 30-year-old, male ho-mosexual had anesthetic tuberculoid plaqueson the thoracic region and the neck and leftarm, a negative skin smear, a positive Mit-suda reaction, and histopathology of the le-sion showed tuberculoid infiltrate. The pa-tient was diagnosed as having tuberculoidleprosy, and MDT-WHO was started. HIVwas detected in a routine serologic exam.At the moment, the patient has only resid-ual patches and his general clinical and lab-oratory examinations are normal.

The high prevalence of leprosy and theincreased trend of HIV infection in the Am-azon region suggest that the co-existence ofthese two infections is not a rare event.However, there is a lack of epidemiologicalstudies evaluating the prevalence of HIV inleprosy patients in the region. The clinicalevolution or the response to treatment ofthe leprosy patients described above havenot changed from those without HIV infec-tion. However, two of them have not yetcompleted treatment. Only one patient had

type 1 reaction and he responded satisfac-torily to prednisone. Epidemiological stud-ies are necessary to better understand theprevalence of the co-infection (leprosy andAIDS), and the progression of existing andnew cases will need to be closely monitored.A probable hypothesis is that in the Ama-zon region these two infections are occur-ring in different social classes, which wouldexplain the low incidence of sufferers of co-existing leprosy and HIV.

Antonio Pedro M. Schettini, M.D.

Institute of Tropical Dermatologyand renereology Alfredo da Alatta

.11anaus, Amazonas, Brazil

Jonas Ribas, M.D.

Institute of Tropical Dermatologyand Venereology Alfredo da Matta

Manaus, Amazonas, Brazil, andAmazonas University School of MedicineAlanaus, Amazonas, Brazil

Paula F. Bessa Rebello, M.D.Carla Barros da Rocha Ribas, M.D.

Maria da Conceicao A. Schettini, M.D.

Institute of Tropical Dermatologyand Venereology Alfredo da Matta

Manaus, Amazonas, Brazil

Reprint requests to Antonio Schettini,M.D., Caixa Postal 1505, Manaus, Ama-zonas, Brazil.

REFERENCES1. BASKIN, G. B., GORMUS, B. J., MARTIN, L. N.,

MURPHEY-CORB, M., WALSH, G. P. and MEYERS,W. M. Pathology of dual Mycobacterium lepraeand simian immunodeficiency virus infection inrhesus monkeys. Int. J. Lepr. 58 (1990) 3358-3364.

2. BORGDORFF, M. W., VAN DEN BROEK, J., CHUM, H.J., KLOKKE, A. N., GRAF, P., BARONGO, L. R. andNEWELL, J. N. HIV-1 infection as a risk factor forleprosy; a case-control study in Tanzania. Int. J.Lepr. 61 (1993) 556-562.

3. KAWUMA, S.J.H., BWIRE, R. and ADATU-ENGWAU,F. Leprosy and infection with the human immu-nodeficiency virus in Uganda; a case-control study.Int. J. Lepr. 62 (1994) 521-526.

4. LUCAS, S. Human immunodeficiency virus andleprosy. (Editorial) Lepr. Rev. 64 (1993) 97-103.

5. MILLER, R. A. Leprosy and AIDS: a review of theliterature and speculations on impact of CD4 + lym-

64,2^ Correspondence^ 173

phocyte depletion on immunity to Mycobacteriumleprae. Int. J. Lepr. 59 (1991) 639-644.

6. PONNIGHAUS, J. M., MWANJASI, L. J., FINE, P. E.M., SHAW, M.-A., TURNER, A. C., OXBORROW, S.M., LUCAS, S. B., JENKINS, P. A., STERNE, J. A. C.

and Buss, L. Is HIV infection a risk factor forleprosy? Int. J. Lepr. 59 (1991) 221-228.

7. TURK, J. L. and REES, R. J. W. AIDS and leprosy.Lepr. Rev. 59 (1988) 193-194.

TT Leprosy: Does It Indicate Percutaneous Infection?

To THE EDITOR:

The subepidermal zone (SEZ) is a narrowstrip of dermis which lies just below thebasal layer of the epidermis. Histologicalchanges in the SEZ find mention even in theearly literature, and the SEZ is regarded asa differentiating point between tuberculoidand lepromatous leprosy. A free SEZ is alsoknow as the band of Unna, who first statedthat this zone is free of bacilli when com-pared to the lepromatous granuloma ( 12 ).Complete obliteration of the SEZ by epi-thelioid cell granuloma is exclusively a fea-ture of tuberculoid (TT) leprosy as per theRidley-Jopling classification ( 7 ). Hence, thispiece of histologic change isolates TT fromalmost all other types of leprosy. While wehave some convincing explanation about thefree grenz zone of lepromatous leprosy (4 ),the significance of its obliteration in TT lep-rosy is not adequately explained. Evolutionof a granuloma in the most superficial partof the dermis makes more sense as a startingpoint of the granuloma and, more impor-tantly, might indicate the cutaneous routeof infection.

Although inhalation of bacilli-rich drop-lets is at present regarded as the most com-mon mode of entry by leprosy bacilli ( 3 ),infection through the skin, as advocated inearlier studies ( 1, 2 ' ), has not been discard-ed. Can the evolution of TT leprosy be at-tributed to the percutaneous entry of thebacilli? Will the route by which the antigengains access to the biological system decidethe nature of the immune response? An im-portant study by Ridley ( 5 ) states that gran-uloma in the SEZ and the epidermis is foundin cases with high resistance which detectsand mounts an immune attack at the site ofentry of Mycobacterium leprae. Now thereare pieces of evidence which attribute an

antigen-processing function to the epider-mal Langerhans' cells in many delayed-typehypersensitivity (DTH)-mediated diseases,including leprosy (to's.) These mononuclearphagocytes are known to process and trans-port M. leprae antigens through the sub-epidermal lymphatics to regional lymphnodes and lymphocytes on the route for aneffective immune response ( 8 . 9 ).

On the basis of these observations, one istempted to interpret the pathogenesis of TTand other types of leprosy mainly aroundthe route of infection. If the organism isdetected by the antigen-processing cells,there is an effective immune response, re-sulting in a localized TT leprosy. If this checksystem is bypassed due to entry throughroutes other than the skin, an entirely dif-ferent course of the disease may ensue. Anepithelioid cell granuloma, including that ofTT, is a manifestation of DTH. We cannotthink of its evolution without a phase ofacute inflammation. Type 1 reaction in-volving the SEZ and the epidermis appearsto represent this acute state. In other words,TT cases with involvement of both the SEZand the epidermis may have started out witha type 1 reaction although they arc now im-munologically stable, i.e., TT patients mayhave started out as borderline. This alsomay explain the occurrence of type 1 reac-tion, which is a strong borderline feature,in some TT cases which as a whole arc con-sidered immunologically stable. The appar-ent low lymphocyte density and the lack offocalization (Fig. 1) were due to massiveinflammatory edema. These reacting gran-ulomas probably indicate a recent sensiti-zation and a persisting antigenic stimula-tion. As the acute phase subsides, the gran-uloma attains the compact histology usuallydescribed for TT leprosy. It is logical to sup-pose that in TT leprosy DTH follows an

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