|Year : 2014 | Volume
| Issue : 2 | Page : 124-126
Leprosy-HIV co-infection in a Nigerian male
Tahir Chubado1, Terna-Yawe H Edith1, Nggada A Haruna2, Galadima G Bala3, Mohammed Yahaya3, Kefas M Mbaya1
1 Department of Surgery, Division of Plastic Surgery, University of Maiduguri Teaching Hospital (UMTH), Maiduguri, Borno, Nigeria
2 Department of Human Pathology, University of Maiduguri Teaching Hospital (UMTH), Maiduguri, Borno, Nigeria
3 Department of Medical Microbiology and Parasitology, University of Maiduguri Teaching Hospital (UMTH), Maiduguri, Borno, Nigeria
|Date of Web Publication||16-Oct-2014|
Department of Medical Microbiology, University of Maiduguri Teaching Hospital, PMB 1414, Maiduguri, Borno
Source of Support: None, Conflict of Interest: None
There is paucity of data regarding studies on leprosy and HIV/AIDS co-infection. We present a case of lepromatous leprosy in a known HIV/AIDS patient that presented with chronic leg ulcers. This case report is presented because of its rarity and the fact that physicians managing HIV/AIDS patients are likely to miss leprosy in such patients due to the decreasing prevalence of leprosy worldwide. Informed written consent was obtained from the patient for the purpose of this study.
Keywords: HIV/AIDS, leg ulcers, leprosy
|How to cite this article:|
Chubado T, Edith TYH, Haruna NA, Bala GG, Yahaya M, Mbaya KM. Leprosy-HIV co-infection in a Nigerian male
. Arch Int Surg 2014;4:124-6
| Introduction|| |
Leprosy otherwise known as "Hansen's Disease" is a chronic mildly but debilitating infectious disease caused by Mycobacterium leprae, an acid-fast bacillus that mainly affects the skin, peripheral nerves, mucosa of the upper respiratory tract, and the eyes, apart from other structures.  Acquired immunodeficiency syndrome (AIDS), first described in 1981, is caused by the Human immunodeficiency virus (HIV), which belongs to the lentivirus subfamily of the retroviridae.  There is profound immunosuppression seen in AIDS due to the depletion of T4 helper lymphocytes, and eventually, the immune system succumbs. AIDS develops when killed CD4 cells can no longer be replaced and consequently, opportunistic infections may occur. Many diseases are known to be either related or associated with HIV.  Patients with HIV are more susceptible to infection with Mycobacteriae such as Mycobacterium tuberculosis. However, the same is not true with M. leprae. 
| Case Report|| |
A 41-year-old male farmer presented to the plastic surgery clinic of the university of Maiduguri teaching hospital with a 3-year history of bilateral chronic leg ulcers. These started as nodular lesions, which gradually increased in size, ruptured spontaneously discharging serous fluid, and associated with severe pain. The resulting ulcers gradually increased in size. The patient is married to three wives and has eighteen children, all alive. He denied any history of risky sexual behavior. He does not smoke cigarettes or consume alcohol.
Physical examination revealed multiple ulcers on the lower limb, the smallest measuring 4 cm × 4 cm and the largest 10 cm × 6 cm, irregular with punched out edges, dirty floor, indurated base, and hyperpigmented surrounding skin. The peripheral pulses (dorsalis pedis and posterior tibial arteries) were palpable. There was no peripheral lymphadenopathy.
Biopsy specimens were taken for culture and histopathology. The results were in keeping with chronic non-specific ulcer. Other investigations including chest X-ray, fasting blood sugar, and Mantoux test were all unremarkable. However, the patient tested positive for HIV-1 and HIV-2 antibodies and was commenced on highly active antiretroviral therapy (HAART). The leg ulcers slowly but gradually improved on daily wound dressing with honey.
However, four weeks on admission, patient developed multiple hypo-and hyperpigmented patches and nodules of various sizes distributed on the face, upper limbs, and trunk. Leprosy was suspected. The medical microbiology team was invited to review patient because of these findings.
On examination, papules and nodules of varying sizes 0.5-2 cm were present, as well as hypo- and hyperpigmented patches, distributed asymmetrically over the face, upper limbs, and trunk. Nasal septum had collapsed and there was bilateral loss of eye lashes with a typical leonine facie [Figure 1]. There was neither oral candidiasis nor generalized lymphadenopathy. The vital signs were normal. Patient had loss of sensation on the upper back, ventral aspect of the forearm with thickened ulnar nerve bilaterally.
|Figure 1: Leonine facie with hypo/hyperpigmented patches seen four weeks into admission|
Click here to view
Hematological parameters showed hematocrit of 30%, white blood cells count 6.4 × 10 6 /L, differential of neutrophils 64%, lymphocytes 35%, and monocytes 1%. There was hypochromasia and macrocytosis with thrombocytosis. Erythrocytes sedimentation rate was 131 mm/hour using the Westergreen method. The venereal disease research laboratory (VDRL) test was negative.
Fine needle aspirates from ear lobes, nodules, and nasal smear using modified Ziehl neelsen technique  yielded numerous globi of acid-fast bacilli [Figure 2] with a bacteriologic index of 4+. Histopathology of skin biopsy showed ill-defined dermal granuloma with occasional multinucleated giant cells of langhan's type. Fite fraco stain revealed numerous globi of M. leprae. These features are consistent with lepromatous leprosy. Hence, a diagnosis of lepromatous leprosy in HIV/AIDS patient was made.
|Figure 2: Numerous globi seen following modified Ziehl neelsen-stained nasal smear (×1000)|
Click here to view
Based on the WHO-MDT program recommendations, patient was classified into multi-bacillary category and hence placed on Rifampicin 600 mg monthly with Clofazimine 300 mg monthly (all supervised) and Dapsone 100 mg daily with Clofazimine 50 mg daily (self-administered) in addition to the highly active antiretroviral therapy he was administered.
| Discussion|| |
The resolution to "eliminate leprosy as a public health problem" by the year 2000 was passed at the 44 th World Health Assembly in 1991. The elimination was defined as reducing the leprosy prevalence to less than one case per 10,000 populations.  Nigeria achieved national elimination target by end of 1998.  Leprosy is no longer a public health challenge in Nigeria and consequently, there is generally a low index of suspicion amongst clinicians for its diagnosis. Our index case would have been missed if he had not presented to a tertiary health centre where a definitive diagnosis of leprosy could be done with microscopic examination of aspirates and skin specimens - a procedure that is not readily available in most facilities in Nigeria. In addition, very few clinicians may differentiate other opportunistic infections that characterized HIV/AIDS from leprosy.
A study by Moses and colleagues reported that among different classes of leprosy patients co-infected with HIV in Maiduguri, there is a slight preponderance of paucibacillary than multibacillary leprosy and that HIV-infected leprosy patients are more likely to manifest advance stages of the disease than HIV seronegative patients.  Although our index patient presented with multibacillary type of leprosy. However, a Tanzanian study by Burgdorff et al.  concluded that HIV-1 infection is significantly associated with multibacillary type of leprosy.
Mantoux test was negative in our index patient implying that he was negative to M. tuberculosis bacilli based on preliminary screening. The VDRL test was also negative, meaning that the patient does not have syphilis, which could be a differential diagnosis of the ulcers he presented. There was no alteration in the histopathological appearances of the leprosy lesion from our patient as compared to other seronegative patients. This is consistent with a study by Chandra Gupta et al.  in Andhra Pradesh and Bhargava et al.  in Jaipur, both in India, which showed that there was no alteration in the histopathology of leprosy in HIV. A study by Jacob et al.  reported that HIV does not influence the course of M. leprae infection. However, there are documented reports of leprosy after HAART initiation from countries where leprosy is not endemic as part of an immune reconstitution inflammatory syndrome (IRIS).  Several studies have shown that lower CD4 + T-cell counts at the time of HAART initiation increase the risk of developing IRIS.  However, there appears to be so few cases of leprosy presenting as IRIS in contrast to tuberculosis where there are substantial numbers of cases being reported.  IRIS could not be accessed in our index case because the CD4 + T-cell count at the time of initiation of HAART was not done due logistic reasons.
Physicians might likely miss diagnosing patients presenting with leprosy-HIV co-infection and such patients might die of HIV/AIDS complications, even before leprosy has manifested. Therefore, a routine history and examination to rule out leprosy in all HIV-positive patients is suggested.
| Conclusion|| |
In any patient presenting with chronic ulcers and background HIV/AIDS, a detailed history, clinical examination, and relevant diagnostic test should be done to rule out the possibility of leprosy.
| References|| |
Brooks GF, Carroll KC, Butel JS, Morse SA, Mietzner TA, editors. Mycobacteria. Jawetz, Melnick & Adelbergs medical microbiology. 25 th
ed. New York; 2010. p. 328-9.
Mandell, Douglas, and Bennett's principles and practice of infectious diseases. In: Mandell GL, Bennett JE, Dolin R, editors. 7 th
ed., Elsevier Inc. 2009. pp. 2323-4.
Bhargava RK, Agrawal US, Kanodia R. HIV and leprosy - A case report. Indian J Sex Transm Dis 2005;26:89-90.
The International Federation of Anti-Leprosy Associations (ILEP). WHO/CDS/CPE/CEE/2000; Learning Guide 3.14 First Edition. Geneva; 2000.
World Health Assembly. Elimination of leprosy; resolution of the 44 th
World Health Assembly, World Health Organisation, Geneva, 1991 (resolution No WHA 44.9).
Federal Ministry of Health Abuja, Department of Public Health. National TB & Leprosy Control programm, Annual report; 2008.
Moses AE, Adelowo KA, Nwankwo EA. Effect of HIV infection on the clinical spectrum of leprosy in Maiduguri.
Niger Postgrad Med J 2001;8:74-7.
Borgdorff MW, van den Broek J, Chum HJ, Klokke AH, Graf P, Barongo LR, et al
. HIV-1 infection as a risk factor for leprosy; a case-control study in Tanzania. Int J Lepr Other Mycobact Dis 1993;61:556-62.
Chandra Gupta TS, Sinha PK, Murthy VS, Swarna Kumari G. Leprosy in an HIV-infected person. Indian J Sex Transm Dis 2007;28:100-2.
Jacob M, George S, Pulimood S, Nathan N. Short-term follow up of patients with multibacillary leprosy and HIV infection. Int J Lepr Other Mycobact Dis 1996;64:392-5.
Martiniuk F, Rao SD, Rea TH, Glickman MS, Giovinazzo J, Rom WN, et al
. Leprosy as immune reconstitution inflammatory syndrome in HIV-positive persons. Emerg Infect Dis 2007;13:1438-40.
Deps P, Lockwood DN. Leprosy presenting as immune reconstitution inflammatory syndrome: Proposed definitions and classification. Lepr Rev 2010;81:59-68.
[Figure 1], [Figure 2]