Skip to main content

Concurrent pulmonary tuberculosis and lepromatous leprosy in a newly diagnosed HIV positive patient: a case report

Abstract

Background

The leprosy-tuberculosis (TB) co-infection is rarely reported in recent times. However, this dual comorbidity is associated with high mortality and major morbidity. Unrecognised leprosy-TB co-infection may predispose affected patients to rifampicin monotherapy and subsequent drug resistance.

Case presentation

A 35 year old migrant, human immunodeficiency virus (HIV) positive male worker presented with 6 month history of symmetric infiltrative nodular plaques of the face and distal, upper extremities. A few days after initial dermatology presentation, a sputum positive pulmonary tuberculosis diagnosis was made at his base hospital. Subsequent dermatology investigations revealed histology confirmed lepromatous leprosy and a weakly reactive rapid plasma reagin test. The presenting clinical features and laboratory results were suggestive of lepromatous leprosy coexisting with pulmonary tuberculosis in an HIV positive patient.

Conclusions

This case illustrates the occurrence of leprosy with pulmonary tuberculosis in an HIV infected patient and the difficulties in interpreting non-treponemal syphilis tests in these patients. This case also highlights the need for a high index of suspicion for co-infection and the need to exclude PTB prior to initiation of rifampicin containing multi-drug therapy (MDT). Interdisciplinary management and social support are crucial in these patients.

Peer Review reports

Background

Tuberculosis (TB) and leprosy are chronic granulomatous infectious diseases resultant from aerosol spread of the intracellular gram positive, aerobic bacilli - Mycobacterium tuberculosis and Mycobacterium leprae respectively. Both diseases are of public health importance as they cause significant morbidity and mortality. In addition, there are concerns of drug resistance especially for M. tuberculosis [1]. These infections share similar transmission dynamics and are more prevalent in low socio-economic settings characterized by overcrowding, poor sanitation and malnutrition [2,3,4]. A significant proportion of the population in Asia and Africa are latently infected by M. tuberculosis and/or M. leprae, however only around 5 % of these infected individuals develop overt clinical TB or leprosy [4]. Both diseases show polarity ranging from pauci-bacillary to multi-bacillary disease depending on the host’s cell mediated immune response [5]. Unlike TB, the level of host systemic immunosuppression due to HIV infection does not appear to significantly modify the natural course and/or the clinical presentation of leprosy [6,7,8]. However, the immune reconstitution inflammatory syndrome (IRIS) can complicate the management of both infections in patients on antiretroviral treatment [6, 7].

HIV has rarely been reported in a patient co-infected with pulmonary tuberculosis (PTB) and nodular leprosy [9]. Infrequently, nodular syphilitic plaques have been misdiagnosed as lepromatous, tuberculoid or borderline leprosy in HIV positive [10,11,12] as well as immunocompetent patients [13, 14]. On the other hand patients with leprosy may present with biologically false positive (BFP) results; conversely 16 % of leprosy patients with BFP results have treponemal disease suggestive of present or past syphilis infection [15]. In this case report, we describe a newly HIV diagnosed patient co-infected with nodular appearing, histologically confirmed lepromatous leprosy, pulmonary TB (PTB) and suspected secondary syphilis. This case highlights the diagnostic challenges during patient work-up and the therapeutic challenges encountered in the patient’s PTB treatment given the previously undiagnosed leprosy.

Case presentation

A 35 year old Malawian single, self-employed immigrant presented as a referral to the Edendale hospital dermatology clinic for non-pruritic rash on his face, forearms and hands. He had also been referred to our hospital’s ophthalmology clinic for a corneal opacification in his left eye. The rash had been present for the past 6 months. On his index dermatology consultation, it was noted that he had been recently diagnosed and initiated on highly active antiretroviral therapy (HAART) - a week prior to the visit. The initial CD4 count and viral load were not available from his base hospital. History revealed that at the time of HIV diagnosis, he had presented to his base hospital with a generalized illness associated with malaise, night sweats and fever without an associated cough. Unbeknown to our dermatology team, in the week after the initial dermatology consult, he was subsequently started on a 6 month course of anti-tubercular medications for GeneXpert MTB/Rif Ultra® sputum positive PTB sensitive to rifampicin at his base hospital. The rest of his past medical and surgical history was unremarkable. He reported that he occasionally traveled to visit his family in Malawi and that his last visit was 3 years previously.

On examination, the patient had symmetric infiltrated skin coloured plaques and nodules on the nasal bridge, the forehead, the forearms and the dorsum of both hands as shown in Fig. 1. The palms of both hands displayed a keratoderma characterized by brownish plaques and there was a healed burn scar on the dorso-lateral surface of the right hand. An appreciable flexion deformity of the right little finger was also observed. A left eye corneal opacification accompanied by bilateral episcleritic red eyes was also evident. Apart from the keratoderma, no other stigmata of secondary syphilis were observed. The patient had a normal gait and the rest of the examination was unremarkable. A 5 mm punch biopsy of his forehead lesions along with blood tests were performed as indicated in Additional file 1: Table 1. Our initial differential diagnosis of the infiltrative nodulo-papular plaques included amongst others sarcoidosis, leprosy, syphilis, deep fungal infections and scleromyxoedema [16]. His serum angiotensin converting enzyme (SACE) result was 91U/L (range 20.0–70.0U/L) and whilst awaiting histology results our primary diagnosis was sarcoidosis. We started the patient on topical dovate ointment, chloroquine 200 mg/day. On his next review, a weakly reactive RPR result with a titre of 1:2 dilutions was noted. As the World Health Organisation (WHO) recommended benzathine penicillin was not available, the patient was initiated on ceftriaxone 1 gram intramuscularly stat and doxycycline 100 mg bd per oral daily for 1 month.

On his third review, 2 months after initial presentation, we noted that the forearm lesions had disappeared while the facial plaques were significantly regressing. The patient’s RPR was no longer reactive and his biopsy results revealed a histopathological diagnosis of lepromatous leprosy as shown in Fig. 2. This prompted a re-examination of his neurological system which revealed glove and stocking loss of sensation in both hands and feet respectively. The posterior tibial and radial nerves were also noted to be palpable in the upper and lower limbs respectively. Our patient was started on the WHO recommended MDT for leprosy. A month later, he experienced worsening of his facial lesions which led us to believe that the combination of ceftriaxone and doxycycline had been more efficacious than the current therapy. A paradoxical, leprosy associated IRIS reaction and a type I reversal leprosy reaction were considered in the differential diagnosis of the worsening facial plaques. Both present similarly making a diagnosis difficult [7], however, in our patient, the type I reversal reaction was favoured over a leprosy-associated IRIS reaction in the current case report as the later did not meet the specified definition for the condition [7]. Unfortunately, the patient was not re-biopsied and no specific treponemal test such as TPHA was done.

Fig. 1
figure 1

Clinical images of the facial (a, b) and hand lesions (c, d) on initial presentation

Fig. 2
figure 2

Histopathology images of the facial lesions: hematoxylin and eosin stain showing the granulomatous inflammation in the dermis (a) and fite stain demonstrating mycobacterium leprae bacilli (b, c)

Discussion and conclusions

We have presented a case of concurrent lepromatous leprosy and PTB in an HIV positive patient with suspected secondary syphilis. HIV, PTB and leprosy coinfection has not been reported in the literature [17]. However, a case of reactivated cutaneous TB and leprosy in an HIV patient has been reported [9]. Similarly, a few cases of leprosy coinfection with syphilis in an HIV positive patient have previously been reported [18,19,20]. Meanwhile, M. tuberculosis and M. leprae coinfection has rarely been reported in the same patient even in countries where both diseases are endemic, but it has increased mortality and morbidity [4, 5, 21,22,23]. The reported leprosy-TB coinfected cases presented with pulmonary and/or extra-pulmonary TB—cutaneous, lymph nodal, perianal and peritoneal lesions [4, 21, 23,24,25,26,27]. Speculative hypotheses have indicated that leprosy, especially the anergic/pauci-bacillary form predisposes to TB whereas others have postulated an antagonistic relationship between the two mycobacterial infections [5]. Leprosy-TB coinfection is rare possibly due to the different mycobacterial reproduction rates and the possible cross-immunity between the two organisms [24, 28]. In the last 15 years, the leprosy-TB coinfection case reports have been described in the setting of systemic corticosteroids for a lepromatous type I reversal reaction in a patient initially diagnosed as either borderline or lepromatous leprosy [21]. In most leprosy-TB coinfections, TB follows leprosy infection [23, 29]. An undiagnosed leprosy-TB coinfected patient runs the risk of receiving rifampicin monotherapy and the subsequent development of rifampicin-resistant TB during leprosy therapy [21, 23]. Sputum and a chest radiograph to exclude PTB are required in the initial work-up of a patient with leprosy [21]. Furthermore, the substitution of minocycline for rifampicin whilst awaiting the TB screening results, directly observed therapy and intensive medical monitoring may be necessary to prevent poor treatment outcomes [21, 23].

Both leprosy and syphilis were considered in the clinical differential diagnosis of our patient’s infiltrative plaques. However, leprosy and syphilis may present a challenging differential diagnosis [19]. Both diseases have polymorphous presentations and occasionally present unclear laboratory tests which hinder definitive clinical diagnosis of the presenting lesions [14, 19]. Syphilis,” the great imitator” [30], normally presents as a papulo-squamous rash, but in HIV positive patients it may present atypically as annular, nodular or granulomatous plaques [10, 14]. In fact, nodular and granulomatous syphilis has occasionally been clinically and/or histopathologically misdiagnosed as indeterminate [31] or tuberculoid [10] or borderline [11, 12, 14] lepromatous [32] leprosy especially in HIV infected patients [10]. Given the aforementioned confusion in earlier cases even on histology, the weakly reactive RPR result and the initial improvement on ceftriaxone and doxycycline, syphilitic palmar keratoderma and ocular lesions [33] remained a possible diagnosis in our patient. The initial improvement following the institution of ceftriaxone and doxycycline for the suspected syphilis was probably just due to rifampicin monotherapy for leprosy whilst the patient was receiving PTB treatment from his base hospital. Whilst this regimen is effective for early syphilis [34], it is not effective for leprosy. Of the tetracyclines, only minocycline is effective for leprosy [35].

Even though our patient was HIV positive, his HIV status neither increased his risk for leprosy nor for lepromatous leprosy as previously feared [7]. In fact, HIV does not alter the clinical, immunological nor histopathological spectrum of leprosy features even in patients with advanced immunodeficiency [8, 19, 20]. In fact, upgrading reactions characterized by organized granulomas and a competent cellular immune response involving activated macrophages, CD4+ and CD8+ cells have been described in leprosy-HIV coinfected patients [36]. Borderline and tuberculoid leprosy presentations may actually be more common in HIV infected compared to HIV uninfected patients [7, 36, 37]. However, leprosy may aggravate HIV infection though data is limited in this regard [5, 7]. These observations suggest that cell-mediated immune responses are preserved at the site of M. leprae infection whereas they are abrogated systemically in contrast to TB [8]. Leprosy co-infection with either HBV, HCV, HTLV-1 is associated with increased risk for inflammatory and nerve damage complications as well as leprosy relapse [38]. Furthermore, immune dysregulation with exacerbation of either disease may result in the HIV-leprosy patient coinfected with a third infectious pathology such as syphilis [20]. Moreover, HIV positive patients have an increased risk for leprosy type I reversal reactions and paradoxical leprosy-IRIS especially when they are on HAART [5, 7, 8]. Thus, stricter monitoring is needed in HIV-leprosy coinfected patients compared to those without HIV. On the other hand, HIV and syphilis coinfection occurs more frequently as both infections affect a similar patient profile [20]. In addition, syphilis increases the chances of HIV transmission and/or infection [39]. In HIV positive patients, syphilis often presents atypically, with shortened time between primary and disproportionately aggressive secondary syphilis [20, 39]. Thus, it is always prudent to include syphilis in the differential diagnosis of any rash and especially papulo-nodular rashes in an HIV positive patient [16].

However, several case reports have indicated that treponemal specific tests may have high false negative results whereas non-treponemal tests may can have high rates of false positive, non-falling results or falsely non-reactive [33]. Similarly, the weakly reactive RPR not only suggested syphilis, it could simply have been a biologically false positive (BFP) result due to leprosy, TB and/or HIV infection [30, 39]. Lepromatous and borderline leprosy are highly associated with BFP results [40]. There is a distinct possibility that the initial partial leprosy treatment with rifampicin reduced the chance of an RPR BFP result on retest in our patient. Studies have demonstrated that leprosy patients may have an inordinately higher frequency of concurrent syphilis, though the results supporting this notion still require more analysis for verification [41,42,43]. BFP results have also been noted to be significantly higher in HIV infected individuals compared to non-HIV infected individuals [44]. However, HAART appears to decrease the odds of biologically false positive RPR results in HIV infected individuals [41, 45]. Confusingly, false-negative syphilis results have also been noted in primary and secondary syphilis [39]. Moreover, our patient’s raised SACE levels could also be explained by leprosy, sarcoidosis, TB as well as HIV infection amongst a host of other diseases [46].

In conclusion, clinicians ought to be aware that leprosy and PTB may occur concurrently and they may need to rule out one if the other is present [21]. A thorough history and examination coupled with good clinico-pathological correlation is necessary in diagnosing atypical or unusual dermatoses [12]. Undiagnosed leprosy-TB coinfection runs the risk of rifampicin monotherapy which subsequently increases the chances of developing resistant mycobacterial strains [21, 47]. In this and other HIV positive patients, it is important to screen and start treatment for PTB before the institution of HAART in accordance with the guidelines to prevent PTB IRIS reactions [48, 49]. In addition, all pts with HIV should be screened for syphilis and vice versa [39]. Furthermore, a treponemal antibody test is required in a patient with leprosy to disprove a reactive non-treponemal test such as an RPR [41, 43]. Leprosy patients with both reactive treponemal and non-treponemal syphilis tests should be treated for syphilis [41]. Though not significantly relevant in the presented case, in migrant populations, it is prudent to review RPR results in light of the endemic treponemal diseases in their home country so as not to miss other treponemal diseases such as yaws and pinta. Finally, there is need for better communication on patient management between primary and referral hospitals to optimize therapeutic outcomes and prevent mismanagement. Both infections should be notified.

Availability of the data and material

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Abbreviations

CD:

Cluster of Differentiation

CRP:

C Reactive Protein

ESR:

Erythrocyte Sedimentation Rate

HAART:

Highly Active Anti-retroviral Therapy

HIV:

Human Immunodeficiency Virus

IRIS:

Immune Reconstitution Inflammatory Syndrome

MDT:

Multi-drug Therapy

RPR:

Rapid Plasma Reagin

PTB:

Pulmonary Tuberculosis

VDRL:

Venereal Diseases Research Laboratory

WHO:

World Health Organisation

References

  1. 1.

    Kurz SG, Furin JJ, Bark CM. Drug-resistant tuberculosis: challenges and progress. Infect Dis Clin N Am. 2016;30(2):509–22.

    PubMed  PubMed Central  Article  Google Scholar 

  2. 2.

    Narasimhan P, Wood J, Macintyre CR, Mathai D. Risk factors for tuberculosis. Pulm Med. 2013;2013:828939. https://doi.org/10.1155/2013/828939.

  3. 3.

    Pescarini JM, Strina A, Nery JS, Skalinski LM, Andrade KVF, Penna MLF, Brickley EB, Rodrigues LC, Barreto ML, Penna GO. Socioeconomic risk markers of leprosy in high-burden countries: A systematic review and meta-analysis. PLoS Negl Trop Dis. 2018 Jul 9;12(7):e0006622. https://doi.org/10.1371/journal.pntd.0006622.

  4. 4.

    Parise-Fortes MR, Lastória JC, Marques SA, et al. Lepromatous leprosy and perianal tuberculosis: a case report and literature review. J Venom Anim Toxins Incl Trop Dis. 2014;20:38. https://doi.org/10.1186/1678-9199-20-38.

  5. 5.

    Trindadae M, Miyamoto D, Benard G, Sakai- valente N, Vasconcelos D, Naafs B. Case report: Leprosy and tuberculosis co-infection: clinical and immunological report of two cases and review of the literature. Am J Trop Med Hyg. 2013;88(2):236–40.

    Article  Google Scholar 

  6. 6.

    Massone C, Talhari C, Ribeiro-Rodrigues R, Sindeaux R, Mira M, Talhari s BN. Leprosy and HIV coinfection: a critical approach. Expert Rev Anti Infect Ther. 2011;9(6):701–10.

    PubMed  Article  Google Scholar 

  7. 7.

    Lockwood D, Lambert S. Leprosy and HIV, where are we at? Lepr Rev. 2010;81(3):169–75.

    PubMed  Article  Google Scholar 

  8. 8.

    Ustianowski A, Lawn S. D L: Interactions between HIV infection and leprosy: a paradox. Lancet. 2006;6(6):350–60.

    Article  Google Scholar 

  9. 9.

    Arora V, Johri A. Reactivation of tuberculosis and leprosy in an HIV-positive case. Tuber Lung Dis. 1994;75(3):237–8.

    CAS  PubMed  Article  Google Scholar 

  10. 10.

    Fernandez-Nieto D, Ortega-Quijano D, Jimenez-Cauhe J, Fernandez-Gonzalez P, Moreno-Moreno E, Bea-Ardebol S. Secondary syphilis mimicking tuberculoid leprosy in an HIV-positive individual: a case report. Int J STD AIDS. 2019;30(12):1235–38. https://doi.org/10.1177/0956462419869136.

  11. 11.

    Fonseca E, et al. Syphylis in an HIV infected patient misdiagnosed as leprosy. J Cut Pathol. 1999;26(1):51–4.

    CAS  Article  Google Scholar 

  12. 12.

    Mani M, Kanish B, Kwatra K, Chaudhary P, Bhatia A. A case of secondary syphilis with HIV, resembling borderline lepromatous leprosy. Indian J Sex Transm Dis AIDS. 2015;36(2):182–4.

    PubMed  PubMed Central  Article  Google Scholar 

  13. 13.

    Son J, Park S, Chung B, Kim H, Cho H, Park C. Nodular secondary syphilis in an immunocompetent woman: case report and literature review. Dermatologica Sinica. 2018;36(1):36–41.

    Article  Google Scholar 

  14. 14.

    Dupnik, Martins M, Souza A, Jerenimo S, Nobre M. Nodular secondary syphilis simulating lepromatous leprosy. Lepr Rev. 2012;83:389–93.

    PubMed  Article  Google Scholar 

  15. 15.

    Scotti AT, Mackey DM, Trautman JR. Syphilis and biologic false positive reactors among leprosy patients. Arch Dermatol. 1970;101(3):328–30.

    CAS  PubMed  Article  Google Scholar 

  16. 16.

    Lee G, Gru A, Wong H, Nagarajan P. Granulomatous syphilis: a pattern to remember. Case report and systematic review of the literature. Clin Microbial. 2015;4:184.

    Google Scholar 

  17. 17.

    Al-Mendawi M. Muliti-drug resistant tuberculosis and leprosy: an unsolved mystery. Lung India. 2017;34:579–80.

    Article  Google Scholar 

  18. 18.

    Graf von Ballestrem W, Alvarenga A, et al. Leprosy in HIV-positive and syphilitic young Paraguayan man. Acta Leprol. 1992;8:103–4.

    Google Scholar 

  19. 19.

    Souza C, Bornhausen-Demarch E, Prata A, de Andrade A, Fernandez M, Lopes M, Nery J. Syphilis, leprosy and human immunodeficiency virus coinfection: a challenging diagnosis. Cutis. 2013;92(2):71–6.

    PubMed  Google Scholar 

  20. 20.

    Pires C, Soares J, dos Santos M, Cordeiro H, Lodi V, Rocha R, Chichester A, Carneiro F. Leprosy in a patient coinfected with HIV and syphyillis. Am J Infect Dis. 2019;15(2):72–7.

    Article  Google Scholar 

  21. 21.

    Mangum L, Kilpatrick D, Stryjewska B, Sampath R. Tuberculosis and Leprosy Coinfection: A Perspective on Diagnosis and Treatment. Open Forum Infect Dis. 2018;5(7):ofy133. https://doi.org/10.1093/ofid/ofy133.

  22. 22.

    Choubey S, Sharma M, Agrawal B. Pulmonary tuberculosis and lepromatous leprosy co-infection in a single individual: a case report. J Assoc Chest Phys. 2014;2(1):40–2.

    Article  Google Scholar 

  23. 23.

    Rajagopala S, Devaraj U, D’Souza G, Aithal V. Co-infection with M. tuberculosis and M. leprae: case report and systematic review. J Mycobact Dis. 2012;2:118.

    Google Scholar 

  24. 24.

    Verma A, Singh A, Prakask V, Bhatia A, Kant S. Coexistence of leprosy and pulmonary tuberculosis: an uncommon entity. Med J DY Patil Univ. 2015;8(5):675.

    Article  Google Scholar 

  25. 25.

    Dey B, Gochhait D, Prabhakaran N, Chandrashekar L, Behera B. A rare case of coexistence of borderline lepromatous leprosy with tuberculosis verrucosa cutis. Case Rep Infect Dis. 2016;2016:1–4.

    Article  Google Scholar 

  26. 26.

    Kodali S, Kodali M. Coexistence of lepromatous leprosy, cutaneous tuberculosis and pulmonary tuberculosis: a rare occurrence. J NTR Univ Health Sci. 2019;8(1):55–8.

    Google Scholar 

  27. 27.

    Sherpa P, Amatya a, Kakshapati T. Borderline tuberculod leprosy, lupus vulgaris and pulmonary tuberculosis: a rare assiciation. J Pathol Nepal. 2019;9:1505–7.

    Article  Google Scholar 

  28. 28.

    Geluk A, van Meijgaarden K, Franken K, Wieles B, Arend S, Faber W, Naafs B, Ottenhoff T. Immunological crossreactivity of the mycobacterium leprae CFP-10 with its homologue in Mycobacterium tuberculosis. Scand J Immunol. 2004;59(1):66–70.

    CAS  PubMed  Article  Google Scholar 

  29. 29.

    Sendrasoa F, Ranaivo I, Raharolahy O, Andrianarison M, Ramarozatovo L, Rabenja F. Pulmonary tuberculosis and lepromatous leprosy coinfection. Case Rep Dermatol Med. 2015;2015:1–4.

    Article  Google Scholar 

  30. 30.

    Birnbaum N, Goldschmidt R, Buffet W. Resolving the common clinical dilemmas of syphilis. Am Fam Phys. 1999;59(8):2233–40.

    CAS  PubMed  Google Scholar 

  31. 31.

    Job C, Anandhan G, Jayakumar J, et al. A case of secondary syphilis with a remarkable resemblance in histopathologic appearence to inderterminate leprosy. Int J lepr Other Mycobact Dis. 1994;62:433–5.

    CAS  PubMed  Google Scholar 

  32. 32.

    Pandhi D, Reddy B, Khurana N, Agarwal S. Nodular syphilis mimicking histiod leprosy. J Eur Acad Dermatol Venereol. 2005;19:256–7.

    CAS  PubMed  Article  Google Scholar 

  33. 33.

    Kirby J, Goreshi R, Mahoney N. Syphilitic palmoplantar keratoderma and ocular disease: a rare combination in an HIV-positive patient. Cutis. 2009;84:305–10.

    PubMed  Google Scholar 

  34. 34.

    Psomas K, Moing V. Efficacy of ceftriaxone and doxycycline in the treatment of early syphilis. Medicine et Maladies Infectieuses. 2012;42(1):15–9.

    CAS  Article  Google Scholar 

  35. 35.

    Prasad P, Kaviarasan PK. Leprosy therapy, past and present: can we hope to eliminate it? Indian J Dermatol 2010;55(4):316–24.

  36. 36.

    Deps P, Lucas S, Porro A, Maeda S, Tomimori J, Guidella C, Reuter T, Oliveira N, Madureira B, Souza V, et al. Clinical and histological features of leprosy and human immunodeficiency virus co-infection in Brazil. Clin Exp Dermatol. 2013;38(5):470–7.

    CAS  PubMed  Article  Google Scholar 

  37. 37.

    Lockwood D, Lambert S. Human immunodeficiency virus and leprosy: an update. Dermatol Clin. 2011;29(1):125–8.

    CAS  PubMed  Article  Google Scholar 

  38. 38.

    Machado P, Machado L, Shibuya M, Rego J, Johnson W, Glesby M. Viral co-infection and leprosy outcomes: a cohort study. PLoS Negl Trop Dis. 2015;9(8):e0003865.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  39. 39.

    Lynn W, Lightman S. Syphilis and HIV: a dangerous combination. Lancet. 2004;4(7):456–66.

    CAS  Article  Google Scholar 

  40. 40.

    Bolognia J, Jorizzo J, Schaffer J, et al. Dermatology. 3rd ed. New York: Elsevier Saunders; 2012.

    Google Scholar 

  41. 41.

    Murray K. Syphilis in patients with Hansen’s disease. Int J Lep Other Mycobact Dis. 1982;50(2):152–8.

    CAS  Google Scholar 

  42. 42.

    Felman Y. Syphilis and leprosy: reply. JAMA. 1982;247(15):2097.

    Article  Google Scholar 

  43. 43.

    Murray K. Syphils and leprosy. JAMA. 1982;247(15):2097.

    CAS  PubMed  Article  Google Scholar 

  44. 44.

    Joyanes P, Borobio MV, Arquez JM, Perea EJ. The association of false-positive rapid plasma reagin results and HIV infection. Sex Transm Dis. 1998;25(10):569-71. https://doi.org/10.1097/00007435-199811000-00013.

  45. 45.

    Oboho IK, Gebo KA, Moore RD, Ghanem KG. The impact of combined antiretroviral therapy on biologic false-positive rapid plasma reagin serologies in a longitudinal cohort of HIV-infected persons. Clin Infect Dis. 2013;57(8):1197–1202. https://doi.org/10.1093/cid/cit445

  46. 46.

    Muller B. Analysis of serum angiotensin-converting enzyme. Ann Clin Biochem. 2002;39:426–43.

    Article  Google Scholar 

  47. 47.

    Lipsitch M, Levin B. Population dynamics of tuberculosis treatment: mathematical models of non-compliance and bacterial heterogeneity in the evolution of drug resistence. Int J Tuberc Lung Dis. 1998;2(3):187–99.

    CAS  PubMed  Google Scholar 

  48. 48.

    Lanzafame M, Vento S. Tuberculosis: immune reconstitution inflammatory syndrome. J Clin Tuberc Other Mycobact Dis. 2016;3:6–9.

    PubMed  PubMed Central  Article  Google Scholar 

  49. 49.

    Chelkeba L, Fekadu G, Tesfaye G, Belayneh F, Melaku T, Mekonnen Z. Effects of time of initiation of antiretroviral therapy in the treatment of patients with HIV/TB co-infection: a systemic review and meta-analysis. Ann Med Surg (Lond). 2020;55:148–58.

    Article  Google Scholar 

Download references

Acknowledgements

The authors are grateful for the assistance provided by Sr. Z. Ndlovu, Sr. P. Muzila and Sr. L. Ndaba and other staff at Edendale Hospital in preparing this manuscript.

Funding

No external sources of funding were used for this study.

Author information

Affiliations

Authors

Contributions

JM and ZM collected the clinical information around the presented case report. JM drafted the manuscript with input/modifications from AM, SP and ZM. ZM and AM supervised the report. All the authors reviewed the manuscript and approved the final version.

Corresponding author

Correspondence to Josiah T. Masuka.

Ethics declarations

Ethics approval and consent to participate

This case report was approved by the Edendale Hospital Ethics Committee. All patient data was de-identified.

Consent for publication

Written informed consent for publication of the patients’ clinical details and/or clinical images was obtained from the patients/guardians/ relative of the patients. Copies of the consent forms are available for review by the Editor of this journal.

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

This article belongs to the Topical Collection: Infectious, Rare and Idiopathic Pulmonary Diseases.

Supplementary Information

Additional file 1

. Table 1: Tabulated laboratory results.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Masuka, J.T., Mkhize, Z., Pillay, S. et al. Concurrent pulmonary tuberculosis and lepromatous leprosy in a newly diagnosed HIV positive patient: a case report. BMC Pulm Med 21, 207 (2021). https://doi.org/10.1186/s12890-021-01572-w

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12890-021-01572-w

Keywords

  • Leprosy
  • Pulmonary tuberculosis
  • Syphilis
  • HIV
  • Coinfection