• View in gallery

    The granular erythematous appearance of patient’s gingival. This figure appears in color at www.ajtmh.org.

  • View in gallery

    Diffuse nodular appearance of the patient’s palate with multiple superficial fissuring and intact mucosa. This figure appears in color at www.ajtmh.org.

  • View in gallery

    The mucosal enlargement involving hard palate, the soft palate, and the uvula. This figure appears in color at www.ajtmh.org.

  • View in gallery

    kDNA/PCR amplification of the isolated parasite. Lane 1, molecular weight control; Lane 2, isolate from the patient; Lane 3, L. major positive control; Lane 4, L. donovani positive control.

  • View in gallery

    Four weeks after treatment with liposomal amphotericin B (L-AMB), the upper lip was back to normal and the gums were back to their pinkish normal color and texture. This figure appears in color at www.ajtmh.org.

  • 1

    Kharfi M, Fazaa B, Chaker E, Kamoun MR, 2003. [Mucosal localization of leishmaniasis in Tunisia: 5 cases]. Ann Dermatol Venereol 130 :27–30.

    • Search Google Scholar
    • Export Citation
  • 2

    Motta AC, Lopes MA, Ito FA, Carlos-Bregni R, de Almeida OP, Roselino AM, 2007. Oral leishmaniasis: a clinicopathological study of 11 cases. Oral Dis 13 :335–340.

    • Search Google Scholar
    • Export Citation
  • 3

    el-Hassan AM, Meredith SE, Yagi HI, Khalil EA, Ghalib HW, Abbas K, Zijlstra EE, Kroon CC, Schoone GJ, Ismail A, 1995. Sudanese mucosal leishmaniasis: epidemiology, clinical features, diagnosis, immune responses and treatment. Trans R Soc Trop Med Hyg 89 :647–652.

    • Search Google Scholar
    • Export Citation
  • 4

    Abbas K, el Toum IA, el Hassan AM, 1992. Oral leishmaniasis associated with kala-azar. A case report. Oral Surg Oral Med Oral Pathol 73 :583–584.

    • Search Google Scholar
    • Export Citation
  • 5

    Dupond JL, Chobaut JC, Barale T, Billerey C, Mallet H, Pretot L, Leconte des Floris R, 1984. [Laryngeal leishmaniasis in a patient from the Jura. Unusual cause of epitheloid and giant cell granulomatosis]. Presse Med 13 :149–151.

    • Search Google Scholar
    • Export Citation
  • 6

    Ferlito A, Pesavento G, Visona A, Recher G, Meli S, Bevilacqua P, 1986. Leishmaniasis donovani presenting as an isolated lesion in the larynx. ORL J Otorhinolaryngol Relat Spec 48 :243–248.

    • Search Google Scholar
    • Export Citation
  • 7

    Tomson N, Symonds RP, Moir AA, Kendall CH, Wiselka MJ, 2002. New World leishmaniasis from Spain. Postgrad Med J 78 :757–758.

  • 8

    Barnetson RS, Ridley RS, Wheate HW, 1978. A form of mucocutaneous leishmaniasis in the Old World. Trans R Soc Trop Med Hyg 72 :516–518.

  • 9

    Ibrahim M, Suliman A, Hashim FA, el Khalil TA, Evans DA, Kharazmi A, el Hassan AM, 1997. Oronasal leishmaniasis caused by a parasite with an unusual isoenzyme profile. Am J Trop Med Hyg 56 :96–98.

    • Search Google Scholar
    • Export Citation
  • 10

    Mahdi M, Elamin EM, Melville SE, Musa AM, Blackwell JM, Mukhtar MM, Elhassan AM, Ibrahim ME, 2005. Sudanese mucosal leishmaniasis: isolation of a parasite within the Leishmania donovani complex that differs genotypically from L. donovani causing classical visceral leishmaniasis. Infect Genet Evol 5 :29–33.

    • Search Google Scholar
    • Export Citation
  • 11

    Habibzadeh F, Sajedianfard J, Yadollahie M, 2005. Isolated lingual leishmaniasis. J Postgrad Med 51 :218–219.

  • 12

    el Harith A, Slappendel RJ, Reiter I, van Knapen F, de Korte P, Huigen E, Kolk AH, 1989. Application of a direct agglutination test for detection of specific anti-Leishmania antibodies in the canine reservoir. J Clin Microbiol 27 :2252–2257.

    • Search Google Scholar
    • Export Citation
  • 13

    Smith DF, Searle S, Ready PD, Gramiccia M, Ben-Ismail R, 1989. A kinetoplast DNA probe diagnostic for Leishmania major: sequence homologies between regions of Leishmania minicircles. Mol Biochem Parasitol 37 :213–223.

    • Search Google Scholar
    • Export Citation
  • 14

    el-Hassan AM, Zijlstra EE, 2001. Leishmaniasis in Sudan. Mucosal leishmaniasis. Trans R Soc Trop Med Hyg 95 (Suppl 1):S19–S26.

  • 15

    Camuset G, Remy V, Hansmann Y, Christmann D, Gomes de Albuquerque C, Sena Casseb GA, 2007. [Mucocutaneous leishmaniasis in Brazilian Amazonia.]. Med Mal Infect 37 :343–346.

    • Search Google Scholar
    • Export Citation
  • 16

    Ghalib HW, Eltoum EA, Kroon CC, el Hassan AM, 1992. Identification of Leishmania from mucosal leishmaniasis by recombinant DNA probes. Trans R Soc Trop Med Hyg 86 :158–160.

    • Search Google Scholar
    • Export Citation
  • 17

    Wysluch A, Sommerer F, Ramadan H, Loeffelbein D, Wolff KD, Holzle F, 2007. [The leishmaniasis—a parasite infection as differential diagnosis of malignant tumours of oral mucosa. A case report and review of literature.] Mund Kiefer Gesichtschir 11 :167–173.

    • Search Google Scholar
    • Export Citation
  • 18

    Evans TG, 1993. Leishmaniasis. Infect Dis Clin North Am 7 :527–546.

  • 19

    Chaudhry Z, Barrett AW, Corbett E, French PD, Zakrzewska JM, 1999. Oral mucosal leishmaniasis as a presenting feature of HIV infection and its management. J Oral Pathol Med 28 :43–46.

    • Search Google Scholar
    • Export Citation
  • 20

    Milian MA, Bagan JV, Jimenez Y, Perez A, Scully C, 2002. Oral leishmaniasis in a HIV-positive patient. Report of a case involving the palate. Oral Dis 8 :59–61.

    • Search Google Scholar
    • Export Citation
  • 21

    Mota Sasaki M, Matsumo Carvalho M, Schmitz Ferreira ML, Machado MP, 1997. Cutaneous leishmaniasis coinfection in AIDS patients: case report and literature review. Braz J Infect Dis 1 :142–144.

    • Search Google Scholar
    • Export Citation
 
 
 

 

 

 

 

 

 

Mucosal Leishmaniasis in a Sudanese Patient

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  • 1 Department of Oral and Maxillofacial Surgery, Department of Orthodontics, Genetics Section, University of Khartoum, Faculty of Dentistry, Khartoum, Sudan; Department of Medicine, University of Khartoum, Khartoum, Sudan; Institute of Endemic Diseases, University of Khartoum, Faculty of Medicine, Khartoum, Sudan; University of Alnellen, Khartoum, Sudan; Institute of Endemic Diseases, Faculty of Medicine, University of Khartoum, Khartoum, Sudan

Mucosal leishmaniasis (ML) is an oral disease caused by the parasite Leishmania donovani. The disease has been proven to be pandemic in many areas of the world. It affects young men living in leishmaniasis-endemic areas. ML might be accompanied or proceeded by visceral leishmaniasis (VL), although in most of the cases seen in Sudan, ML occurs as a primary lesion. ML can mimic oral cancer or fungal infections, with ulceration as the most common finding in ML lesions. In this report, the patient came from an area known to be endemic for VL. Although the lesions were not ulcerative, the patient history was indicative for ML. Early detection and proper diagnosis were of great help in the cure and prognosis of the disease.

INTRODUCTION

Leishmaniasis is a group of diseases caused by the protozoan parasites of the Genus Leishmania. Leishmania prevails in four continents and is endemic in 88 countries. The clinical presentation ranges from simple cutaneous ulcer, mucocutaneous lesions, to the severe fatal visceral form. The disease is transmitted by the bite of a female sand fly infected with Leishmania parasites.1 Mucosal leishmaniasis (ML) is a chronic infection that affects the upper respiratory tract and/or oral mucosa. The oral lesions classically appear as mucosal ulcerations, mainly in the hard or soft palate. 2,3

In many areas endemic for leishmaniasis, ML is usually accompanied by a cutaneus or a visceral form of the disease.4 Although ML is frequent in the New World, few cases are reported in the Old World. 1,58 In Sudan, ML occurs as a primary mucosal disease that is not preceded or accompanied by a cutaneous lesion.9 This may indicate that the parasite that invades the oral mucosa is divergent from other parasites causing visceral leishmaniasis (VL). 10 The disease is caused by Leishmania donovani and prevails in areas of the country endemic for VL, where health services are usually very scare and primitive.3 Oral ML can lead to loss of teeth4 or respiratory obstruction that might be fatal. ML can be confused with fungal infections or oral cancer and might be an early or only sign of HIV infection. When detected early, ML can be easily treated before inflecting irretrievable damage to the oral and nasal tissues. Proper identification of the mucosal lesion in its early course may help in the early diagnosis of the disease and proper treatment. 11

CASE REPORT

A 49-year-old male patient was referred by The ENT Unit at Khartoum General Hospital to the Dental Hospital for evaluation and treatment of an intraoral mucosal lesion. The patient’s complaint started 7 months before with nasal congestion accompanied by non-specific vague pain localized mainly to the soft palate. The pain sometimes radiated to the tongue and the larynx. Three months later, the patient noticed a diffuse growth of his gingival and palatal mucosa. The condition had progressively increased in size over that period, causing difficulty in eating and swallowing. In addition, the patient reported obstruction of his left nostril, but there was no bleeding or nasal discharge. The patient’s medical history showed nothing significant apart from having VL 5 years ago, which was treated with Pentostam (GlaxoSmithKline UK, Stockley Park West, Uxbridge, Middlesex) at a dose of 20 mg/kg for 28 days.

The patient was married with four children and lived in an area known to be endemic for Kala-Azar (VL). He denied any use of tobacco or alcohol. The only notable feature in his family history was that three of his sons had VL during the past 10 years with no history of any mucosal involvement. On extraoral examination, the 49-year-old man looked pale and lethargic, with sunken eyes. There was a diffuse swelling on his left cheeks. His left nostril was red, edematous, and blocked with crusted material. A mild generalized swelling was also noticed on the patient’s upper lip. Neck examination showed bilaterally enlarged, non-tender submandibular and submental lymph nodes.

Intraorally, there was generalized gingival enlargement, involving both the maxillary and the mandibular gingiva. The labial gingiva appeared red in color, smooth, and shiny, with an irregular granular surface (Figure 1). Visible plaque accumulation along the cervical margins of the upper and lower teeth was also seen. The patient had marked nodular infiltration and granular appearance on the upper labial gingiva, particularly the left quadrant. A small single ulcer of ~1–2 mm in diameter was detected adjacent to the left maxillary canine and first premolar. The ulcer had a yellowish floor and was surrounded by raised granular margins.

The patient had a substantial swelling of his palatal mucosa with marked erythema and shiny appearance. The mucosal enlargement was diffuse and spread to involve the hard palate, the gingiva, the soft palate, and the uvula. The mucosa had a firm consistency with extensive granular changes, raised nodular surface, and multiple superficial fissuring. The palatal gingiva was extensively swollen, covering almost the entire palatal surface of the maxillary teeth (Figure 2). A pedunculated growth arising form the soft palate was also noticed, and the patient had a reduced palatal mobility (Figure 3). No areas of ulceration or necrosis were seen on the palatal mucosa. Examination of the patient’s buccal mucosa and tongue did not show any similar specific changes to those seen on the gingiva and palatal mucosa apart of migratory glossitis.

The patient was fully dentate with poor oral hygiene and visible deposition of materia alba around the cervical margins of almost all his teeth. Inspection of the teeth showed no mobility, no sulcular exudates, and no tenderness to percussion. False pockets measuring 4.0–6.0 mm were detected. Intraoral radiographs showed interproximal bone loss in the posterior maxillary teeth. The bone loss was horizontal and limited to few teeth.

Three milliliters of venous blood was collected in plain blood collection tubes for laboratory investigation. These included the detection of anti-leishmania antibodies in the serum using the direct agglutination test (DAT) as described earlier, 12 as well as HIV testing. A biopsy was taken from the mucosal lesion for parasite culture and histopathology examination. The cultured parasite was characterized based on the results of the polymerase chain reaction (PCR) amplification of parasite kDNA.13

Significant anti-leishmania antibodies were detected in the patient serum (titer of 104,800), indicating Leishmania infection. The patient was HIV negative. The diagnosis was confirmed by histologically detecting amastigotes in phagocytic cells from the biopsy taken from the mucosal lesion. kDNA/PCR amplification of the parasite DNA amplified an 800-bp DNA fragment identical to the L. donovani reference strain (Figure 4).

Under strict oral hygiene instructions, chlorhexidine gluconate mouthwash, and brushing, the patient was referred for medical opinion and care. He was started on liposomal amphotericin B (L-AMB) 3 mg/kg body weight every other day for a total of 7 doses.

Four weeks later, the patient was examined for his orofacial lesions. The facial swelling had notably subsided, and the upper lip was back to normal. His gums had a pinkish normal color. The gum swelling disappeared (Figure 5). The hard palate was slightly swollen, but the irregular fungating appearance had disappeared. The uvula was back to normal. The patient was followed up monthly for the first 3 months and then bimonthly for 1 year. The patient’s medical report indicated that he was generally well with normal vital signs and had no lymphadenopathy or skin lesions. He had hepatosplenomegaly that was related to his previous history of VL.

DISCUSSION

In our case report, the patient is a 49-year-old man with a typical presentation of ML in Sudan. 14,15 The patient had a history of VL that was completely treated 10 years before. ML can be a primary disease or could follow an episode of VL as seen in our case. The majority of cases presented in Sudan are the isolated mucosal form that is not accompanied by the visceral form. Many have speculated that the visceral and mucosal forms are connected because they are caused by the same parasite. 9,16 Recently, it has been found that ML in Sudan is caused by a different subspecies of the L. donovani complex than the one causing VL. 10

The mucosal lesions classically appear as an ulcerations, mainly in the hard or soft palate.2 In our report, the patient had no ulcerations, but there was a diffuse mucosal enlargement spreading to the gingiva, hard palate, soft palate, and uvula. The soft palate and the uvular pedunculated growth made eating very difficult, which affected the patient’s nutritional uptake. In many cases and because of lack or delay of medical care, such enlargements can be fatal through airway obstruction. The mucosal changes can be easily mistaken with an oronasal malignancy. In areas endemic for leishmaniasis, ML should be considered early in the differential diagnosis when considering gingival ulcerations or hypertrophy. 17 Gingival hypertrophy and the false deep pockets will definitely lead to periodontitis and loss of teeth.4

Our patient is from eastern Sudan, which is a well-known endemic area for VL and is endemic for HIV infection. The HIV/AIDS prevalence rate among the general population in the Sudan is on the increase. It has reached 2.6% among the adult population, which makes the country fall under a generalized epidemic according to the WHO classification. An association between ML and HIV has recently been described. 18 ML can be the only sign of an HIV infection, which is something to be considered closely by dental practitioners because they might be the only ones to discover new HIV cases in the population. 1921 Leishmaniasis can develop in any stage of HIV infection, although the clinical manifestations—and hence the diagnosis—tend to coincide with periods of maximum immune depression. The patient was tested for HIV seroreactivity, and he had no anti-HIV antibodies. He did not have any form of an immunocompromised state as shown by his medical history and examination.

The patient responded to AmBisome treatment, indicating the efficacy of liposomal amphotericin B in the treatment of Sudanese ML. A remarkable improvement in oral lesions and the hepatomegaly regressed to the costal margin.

ML is becoming a pandemic. In Sudan, ML occurs as a primary lesion that is not accompanied or preceded by VL.

Appropriate laboratory tests and histopathologic examination should be used to rule out other diseases that can clinically mimic ML, including tumors of the oronasal cavity, primary paranasal aspergillus granulomatosis, leprosy, histoplasmosis, and rhinoscleroma. If detected early, the disease is easily curable without causing severe damage to the oral and nasal mucosal tissues.

Figure 1.
Figure 1.

The granular erythematous appearance of patient’s gingival. This figure appears in color at www.ajtmh.org.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 80, 6; 10.4269/ajtmh.2009.80.935

Figure 2.
Figure 2.

Diffuse nodular appearance of the patient’s palate with multiple superficial fissuring and intact mucosa. This figure appears in color at www.ajtmh.org.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 80, 6; 10.4269/ajtmh.2009.80.935

Figure 3.
Figure 3.

The mucosal enlargement involving hard palate, the soft palate, and the uvula. This figure appears in color at www.ajtmh.org.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 80, 6; 10.4269/ajtmh.2009.80.935

Figure 4.
Figure 4.

kDNA/PCR amplification of the isolated parasite. Lane 1, molecular weight control; Lane 2, isolate from the patient; Lane 3, L. major positive control; Lane 4, L. donovani positive control.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 80, 6; 10.4269/ajtmh.2009.80.935

Figure 5.
Figure 5.

Four weeks after treatment with liposomal amphotericin B (L-AMB), the upper lip was back to normal and the gums were back to their pinkish normal color and texture. This figure appears in color at www.ajtmh.org.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 80, 6; 10.4269/ajtmh.2009.80.935

*

Address correspondence to Kamal Abbas, Department of Oral and Maxillofacial Surgery, University of Khartoum, Faculty of Dentistry, PO Box 102, Khartoum, Sudan 11111. E-mail: kamalabbas@hotmail.com

Authors’ addresses: Kamal Abbas, Department of Oral and Maxillofacial Surgery, University of Khartoum, Faculty of Dentistry, PO Box 102, Khartoum, Sudan. Mayson A. Musatafa, Department of Oral and Maxillofacial Surgery, University of Khartoum, Faculty of Dentistry, PO Box 102, Khartoum, Sudan. Shaza Abass, Department of Orthodontics, University of Khartoum, Faculty of Dentistry, PO Box 102, Khartoum, Sudan. Musa M. Kheir, Department of Medicine, University of Khartoum, PO Box 102, Khartoum, Sudan. Maowia M. Mukhtar, Institute of Endemic Diseases, University of Khartoum, Faculty of Medicine, PO Box 102, Khartoum, Sudan. Elwaleed M. Elamin, University of Alnellen, Khartoum, Sudan. Ahmed M. Elhassan, Institute of Endemic Diseases, Faculty of Medicine, University of Khartoum, PO Box 102, Khartoum, Sudan.

Acknowledgments: The American Committee on Clinical Tropical Medicine and Travellers’ Health (ACCTMTH) assisted with publication costs.

REFERENCES

  • 1

    Kharfi M, Fazaa B, Chaker E, Kamoun MR, 2003. [Mucosal localization of leishmaniasis in Tunisia: 5 cases]. Ann Dermatol Venereol 130 :27–30.

    • Search Google Scholar
    • Export Citation
  • 2

    Motta AC, Lopes MA, Ito FA, Carlos-Bregni R, de Almeida OP, Roselino AM, 2007. Oral leishmaniasis: a clinicopathological study of 11 cases. Oral Dis 13 :335–340.

    • Search Google Scholar
    • Export Citation
  • 3

    el-Hassan AM, Meredith SE, Yagi HI, Khalil EA, Ghalib HW, Abbas K, Zijlstra EE, Kroon CC, Schoone GJ, Ismail A, 1995. Sudanese mucosal leishmaniasis: epidemiology, clinical features, diagnosis, immune responses and treatment. Trans R Soc Trop Med Hyg 89 :647–652.

    • Search Google Scholar
    • Export Citation
  • 4

    Abbas K, el Toum IA, el Hassan AM, 1992. Oral leishmaniasis associated with kala-azar. A case report. Oral Surg Oral Med Oral Pathol 73 :583–584.

    • Search Google Scholar
    • Export Citation
  • 5

    Dupond JL, Chobaut JC, Barale T, Billerey C, Mallet H, Pretot L, Leconte des Floris R, 1984. [Laryngeal leishmaniasis in a patient from the Jura. Unusual cause of epitheloid and giant cell granulomatosis]. Presse Med 13 :149–151.

    • Search Google Scholar
    • Export Citation
  • 6

    Ferlito A, Pesavento G, Visona A, Recher G, Meli S, Bevilacqua P, 1986. Leishmaniasis donovani presenting as an isolated lesion in the larynx. ORL J Otorhinolaryngol Relat Spec 48 :243–248.

    • Search Google Scholar
    • Export Citation
  • 7

    Tomson N, Symonds RP, Moir AA, Kendall CH, Wiselka MJ, 2002. New World leishmaniasis from Spain. Postgrad Med J 78 :757–758.

  • 8

    Barnetson RS, Ridley RS, Wheate HW, 1978. A form of mucocutaneous leishmaniasis in the Old World. Trans R Soc Trop Med Hyg 72 :516–518.

  • 9

    Ibrahim M, Suliman A, Hashim FA, el Khalil TA, Evans DA, Kharazmi A, el Hassan AM, 1997. Oronasal leishmaniasis caused by a parasite with an unusual isoenzyme profile. Am J Trop Med Hyg 56 :96–98.

    • Search Google Scholar
    • Export Citation
  • 10

    Mahdi M, Elamin EM, Melville SE, Musa AM, Blackwell JM, Mukhtar MM, Elhassan AM, Ibrahim ME, 2005. Sudanese mucosal leishmaniasis: isolation of a parasite within the Leishmania donovani complex that differs genotypically from L. donovani causing classical visceral leishmaniasis. Infect Genet Evol 5 :29–33.

    • Search Google Scholar
    • Export Citation
  • 11

    Habibzadeh F, Sajedianfard J, Yadollahie M, 2005. Isolated lingual leishmaniasis. J Postgrad Med 51 :218–219.

  • 12

    el Harith A, Slappendel RJ, Reiter I, van Knapen F, de Korte P, Huigen E, Kolk AH, 1989. Application of a direct agglutination test for detection of specific anti-Leishmania antibodies in the canine reservoir. J Clin Microbiol 27 :2252–2257.

    • Search Google Scholar
    • Export Citation
  • 13

    Smith DF, Searle S, Ready PD, Gramiccia M, Ben-Ismail R, 1989. A kinetoplast DNA probe diagnostic for Leishmania major: sequence homologies between regions of Leishmania minicircles. Mol Biochem Parasitol 37 :213–223.

    • Search Google Scholar
    • Export Citation
  • 14

    el-Hassan AM, Zijlstra EE, 2001. Leishmaniasis in Sudan. Mucosal leishmaniasis. Trans R Soc Trop Med Hyg 95 (Suppl 1):S19–S26.

  • 15

    Camuset G, Remy V, Hansmann Y, Christmann D, Gomes de Albuquerque C, Sena Casseb GA, 2007. [Mucocutaneous leishmaniasis in Brazilian Amazonia.]. Med Mal Infect 37 :343–346.

    • Search Google Scholar
    • Export Citation
  • 16

    Ghalib HW, Eltoum EA, Kroon CC, el Hassan AM, 1992. Identification of Leishmania from mucosal leishmaniasis by recombinant DNA probes. Trans R Soc Trop Med Hyg 86 :158–160.

    • Search Google Scholar
    • Export Citation
  • 17

    Wysluch A, Sommerer F, Ramadan H, Loeffelbein D, Wolff KD, Holzle F, 2007. [The leishmaniasis—a parasite infection as differential diagnosis of malignant tumours of oral mucosa. A case report and review of literature.] Mund Kiefer Gesichtschir 11 :167–173.

    • Search Google Scholar
    • Export Citation
  • 18

    Evans TG, 1993. Leishmaniasis. Infect Dis Clin North Am 7 :527–546.

  • 19

    Chaudhry Z, Barrett AW, Corbett E, French PD, Zakrzewska JM, 1999. Oral mucosal leishmaniasis as a presenting feature of HIV infection and its management. J Oral Pathol Med 28 :43–46.

    • Search Google Scholar
    • Export Citation
  • 20

    Milian MA, Bagan JV, Jimenez Y, Perez A, Scully C, 2002. Oral leishmaniasis in a HIV-positive patient. Report of a case involving the palate. Oral Dis 8 :59–61.

    • Search Google Scholar
    • Export Citation
  • 21

    Mota Sasaki M, Matsumo Carvalho M, Schmitz Ferreira ML, Machado MP, 1997. Cutaneous leishmaniasis coinfection in AIDS patients: case report and literature review. Braz J Infect Dis 1 :142–144.

    • Search Google Scholar
    • Export Citation
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