INTRODUCTION

During HIV (human immunodeficiency virus) infection, the occurrence of opportunistic infections (viral, parasitic, etc.) is closely linked to CD4 T-cell counts [1,2]. Among viral opportunistic diseases, herpes zoster (reactivation of the varicella-zoster virus) is the most common. It is considered an indicator of decreased immunity. Clinically, in immunocompromised individuals, it manifests as extensive, disseminated, and chronic lesions [3–5]. In the group of parasitic opportunistic diseases, cutaneous leishmaniasis, caused by a protozoan of the Leishmania group (an intracellular parasite), is frequently reported in tropical and subtropical regions [6]. Clinically, cutaneous leishmaniasis in immunocompetent individuals presents as a single, painless papulonodular lesion on sun-exposed areas. After a several weeks, it evolves into an ulcerocrustous lesion with raised edges; spontaneous healing is often obtained after a few months of evolution [8]. However, in an immunocompromised field due to HIV, the skin lesions are multiple, polymorphic, atypical [10,1], sometimes disseminated [12,13].

While the occurrence of shingles or cutaneous leishmaniasis in an immunocompromised individual due to HIV is frequently described in the literature [1,4,10,11], their association is rarely reported. Herein, we report a case observed at the Dermatology Department of the National Hospital of Niamey of an HIV-immunocompromised patient presenting with thoracic shingles and cutaneous leishmaniasis with nasal involvement.

CASE REPORT

Mrs. K.S., a 55-year-old widow residing in a rural area of Dosso (140 km from Niamey), was diagnosed as HIV-1 positive and had been receiving antiretroviral therapy (ART) according to the Tenofovir-Lamivudine-Dolutegravir (TDF-3TC-DTG) protocol for eight months. She presented with a budding lesion on her nose that had been developing for 6 months (2 months after initiating ART). The initial asymptomatic papulonodular lesion, located on the left side of her nose, had progressed to a budding, crusted plaque. This plaque, obstructing her nasal passages, had spread onto her upper lip without epistaxis or rhinorrhea. She also presented with a painful, unilateral band-like lesion on her trunk that began to develop three months after the onset of the nasal budding lesion. She also reported a history of chickenpox during childhood, complicated by a presternal keloid treated with corticosteroids (intralesine infiltration) more than ten years ago. On admission, the patient was afebrile. The conjunctival mucosal color was normal. Her vital signs were as follows: BP = 133/85 mmHg, HR = 73 bpm, RR = 16 breaths/min. Her weight was 52 kg, her height was 168 cm, and her BMI was 18.42 kg/m².

Dermatological examination revealed a raised, budding tumor on the face with a verrucous and hyperkeratotic surface, dotted with crusts in places (yellowish, thick, and adherent crusts). This tumor was bordered superiorly on both sides by a lichenoid inflammatory halo extending to the malar regions. It, thus, occupied the mid-facial region, extending from the root of the nose and covering the entire upper lip (Fig. 1a). As a sequela of the shingles, a band-like ulcerated and crusted plaque was found; this plaque extended from the sternum, covering the upper half of the left breast and ending on the anterior aspect of the left shoulder (Fig. 1b). The hair, nails, and skin were unremarkable. An otolaryngological examination revealed an infiltrated, dry nasal mucosa with yellowish crusts obstructing the nasal passages, which bled at the slightest touch. The examination of the cervicofacial lymph node areas was normal. The rest of the physical examination was unremarkable. Paraclinical tests for leishmaniasis on a skin smear were positive (without specifying the type of leishmaniasis); the erythrocyte sedimentation rate (ESR) was 122 mm in the first hour. The tuberculin skin test (TST) was negative. HIV serology was positive for HIV type 1, and the CD4 count was 158 cells/mm³.

Figure 1: (a) Close-up view of the nasolabial involvement before treatment. (b) Day 0 before treatment.

The complete blood count was generally normal: WBC = 5.0 x 10⁹/L (neutrophils: 2870/mm³, lymphocytes: 1050/mm³, monocytes: 790, eosinophils: 280, basophils: 20, RBC = 4.51 x 10¹², MCV = 88.1 fL, MCHC = 27.6 pg; platelets = 208,000/mm³), Hb = 12.4 g/dL. Liver serology was negative. TPHA/VDRL tests were negative. Blood glucose was 5.24 mmol/L. CRP was 24 mg/L. Creatinine was 59 μmol/L. Liver transaminases were normal (AST = 25 IU/L and ALT = 36 IU/L). Alpha amylase was 87 IU/L, and the blood ionogram was normal. The chest X-ray was normal (no parenchymal or pleural abnormalities). The abdominal and pelvic ultrasound was normal (no deep lymphadenopathy, and the kidneys, liver, and spleen were unremarkable). The diagnosis of co-infection with nasal cutaneous leishmaniasis, left thoracic herpes zoster, and HIV infection was made based on clinical and paraclinical findings. Treatment was both local and systemic. Topical trolamine was applied twice daily to the herpes zoster and leishmaniasis lesions. Systemic treatment included metronidazole 1 g/24 h for eight weeks, azithromycin 1500 mg for one week, and paracetamol 3 g/24 h until pain resolved. No treatment-related side effects were noted.

After four weeks of treatment, pigmented, adherent keratotic lesions persisted on the nasolabial folds and the tip of the nose. For the herpes zoster lesions, healing was complete, leaving a unilateral, band-like hypertrophic scar associated with signs of early keloid lesions (Fig. 2). Complete healing of both the herpes zoster and leishmaniasis lesions was achieved after eight weeks of treatment, leaving an unsightly post-scarring hyperpigmentation on the nose; the patient’s general condition was also good (Fig. 3), while antiretroviral therapy continued.

	Figure 2: 28 days during treatment.
	Figure 3: Eight weeks at the end of treatment.

DISCUSSION

This case illustrates the possibility of coinfection involving opportunistic viral (such as shingles) and parasitic (such as leishmaniasis) diseases in HIV-infected patients, which, to our knowledge, is the first such case. The occurrence of opportunistic diseases in HIV-infected individuals is closely linked to the CD4 T lymphocyte count (the main cells of the cellular immune response) [2,4,10,12]. The common feature of this association in the context of HIV is the collapse of the cell-mediated immune system (the selective destruction of CD4+ T lymphocytes), leading to an inability of the body to activate either effector cells (macrophages) against intracellular pathogens (leishmania) or an inability to maintain varicella-zoster virus latency through the activation of cytotoxic cells (CD8) [12–14]. Indeed, without antiretroviral treatment, varicella-zoster virus reactivation occurs due to a decrease in the number of CD4+ (helper) T lymphocytes, which work with CD8+ (cytotoxic) T lymphocytes to ensure the inactivity of the varicella-zoster virus. This destruction leads to a breakdown in immune surveillance, hence the reactivation of the virus [4,5]. In cutaneous leishmaniasis, the atypical, polymorphic, and sometimes highly extensive or tumoral clinical presentations in immunocompromised individuals, such as our patient, also result from a decrease in the CD4+ cell count [14,15].

The collapse of the immune system in our patient (CD4 count of 158 cells/mm³), likely linked to the slow action of antiretroviral therapy (ART), testifies to the severity of this leishmaniasis and the delayed healing of the herpes zoster lesions. Had it not been for the reactivation of the immune system and the good response to metronidazole treatment [8,9], this nasal form would have been life-threatening due to mucocutaneous involvement, as reported in Latin America [16]. The diagnostic challenge in this case is to avoid confusing cutaneous leishmaniasis in its pseudotumoral and verrucous form with verrucous cutaneous tuberculosis of the nose [17], rhinophyma [18,19], nasal Kaposi’s sarcoma [20,21], or squamous cell carcinoma [22]. Successful treatment in such a case depends on well-managed and closely monitored antiretroviral therapy. The therapeutic challenge is to be able to use effective molecules with fewer side effects, given the antiretroviral treatment [23].

After two months, the shingles had reached the healing stage, justifying the use of paracetamol alone for managing postherpetic neuralgia. Metronidazole has been one of the most widely used molecules in the management of leishmaniasis in Niger for several years [8,9]. Unlike meglumine antimoniate [24], metronidazole may be used without the risk of renal toxicity [8,9,24]. Good adherence to antiretroviral therapy is essential to ensure immune reconstitution and treatment efficacy [1]. Having been on antiretroviral therapy for eight months, taking metronidazole for eight weeks resulted in complete healing of the leishmaniasis lesions in our patient. The application of trolamine topically also led to complete healing of the shingles lesions.

CONCLUSION

The coinfection of cutaneous leishmaniasis and herpes zoster in an immunocompromised individual with HIV reflects profound immunosuppression. To our knowledge, this type of coinfection has not been reported in the literature. The cornerstone of treatment is well-managed antiretroviral therapy, which is essential for restoring immunity and enabling a cure for both leishmaniasis and herpes zoster.

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