World Journal of AIDS, 2011, 1, 28-30
doi:10.4236/wja.2011.12005 Published Online June 2011 (
Copyright © 2011 SciRes. WJA
Perforation of the Nasal Septum and Nasal Ulcers
Maria Pilar Martín-Fortea1, Isabel Sanjoaquín-Conde2, Santiago Letona-Carbajo2,
Maria José Crusells-Canales2, Julián Cuesta-Muñoz2, Juan Antonio Amiguet-García2
1Department of Internal Medicine, Hospital Clínico Universitario “Lozano Blesa”, Zaragoza, Spain; 2Department of Infectious Dis-
eases, Hospital Clínico Universitario “Lozano Blesa”, Zaragoza, Spain.
Received April 27th, 2011; Revised May 14th, 2011; Accepted May 21st, 2011.
A case about a HIV woman with nasal ulcers is described in this paper. In every inmunodepressed patient who has mu-
cosal or cutaneous ulcers, infection by leishmanial parasites need s to be ruled out, especially when ulcers have not re-
gression with usual treatments. The Leishmanial nasal disease usually shows swelling and mucosal ulcers, that may
progress to necrosis. Delaying in appropriate therapy might cause irreversible damage.
Keywords: Mucocutaneous Leishmaniasis, Leishmania/HIV Co-Infection, Nasal Ulcer
1. Introduction
This is a case about a 36-years-old Paraguayan woman,
resident in Spain from 2004. She occasionally consumed
cocaine during 2007. In 2008 she was diagnosed as HIV
A2 infection (225 CD4/mm3 [18%], Viral Load: 8.82 ×
105 copies/mm3). She was treated with Nevirapine and
Emtricitabine/Tenofovir and presented a good response
to treatment. Six months later, she reported rhinorrhea
and nasal congestion and she was treated with Levoflox-
acin (500 mg/day) and Ibuprofen 600 mg/8 h empirically.
After 2 weeks nasal septum perforation was proven. Ini-
tially that perforation was related to the previous history
of cocaine addiction. The patient was treated with Cefu-
roxime 500 mg/12h and topical Mometasone every 12h.
However, the symptoms got worse, with vesicles, oe-
dema and redness of nasal skin. After the collection of
nasal samples for cultures (fungus, bacterium and myco-
bacterium) and investigation for Herpes for PCR, the
treatment was then changed to Famciclovir 250 mg/8h,
but vesicles and oedema showed progression with nose
and upper lip deformity, increase of nasal septum perfo-
ration and ulcerations of nasal mucosa (Figure 1). Cul-
tures of nasal samples and PCR for herpes were negative.
New samples were taken for cultures. Intravenous ther-
apy commenced with Acyclovir 500 mg/8h, Fluconazole
400 mg/day, Imipenem 1 gr/8h and Amikacin 1 g/day.
The autoimmunity study was negative. Facial CT ruled
out the existence of a tumour. A biopsy of nasal-lip skin
showed abundant granulomatosis, with epithelioid cells.
Serological tests to Trypanosoma cruzi and Herpes 1-2
were negative, but were positive to Leishmania by using
ELISA IgG 2 (positive over 1.1). Serological tests, his-
tology and skin lesion appearance, led to the considera-
tion of a diagnosis of Mucosal Leishmaniasis. New skin
samples were co lle cted in or der to be s ent to Ref erenc e
Figure 1. View of nasal septum perforation (a) and ulcera-
tions of nasal mucosa (b).
Perforation of the Nasal Septum and Nasal Ulcers29
Centre for PCR study and specific Leishmania culture.
Pending the outcome of specific cultures, empirical
therapy was replaced with liposomal amphotericin B 3
mg/kg/day (six weekly doses with a received dose of 900
mg). During the second week of treatment, the oedema
decreased and the ulcerations started to heal (Figure 2).
After treatment, the nose and upper lip skin healed, and
nasal mucosa was recovered but the nasal septum perfo-
ration remained. Secondary prophylaxis was not pro-
posed due to cellular immunity preservation. After an
excellent response to treatment, negative results of PCR
and specific culture were received, so that could not
identify the etiolog ical specie.
2. Discussion
Cutaneous-mucosal leishmaniasis is endemic in Latin
America, mainly in Brazil [1], and in most cases it is due
to L. braziliensis [2,3]. Around 5% - 7% of affected pa-
tients present mucosal leishmaniasis [4]. Both clinical
presentations may be simultaneous, but the mucosal
presentation may appear months or years after healing of
the cutaneous presentation [1,4]. Cases of mucosal leish-
maniasis have been reported in the Mediterranean basin,
but this is uncommon [5,6]. This disease will be found
most frequentl y i n t he HIV immigrati on po pul at i on [7] .
The clinical diagnosis of mucosal leishmaniasis was
based on lesion appearance and epidemiological analysis
[8]. Differential diagnosis arises with other infectious
diseases (mycobacterium, paracoccidioidomycosis, his-
toplasmosis, blastomycosis, Klebsiella rhinoescleroma-
tis), tumours (lymphomas, carcinoma, midline granu-
loma), relapsing polichondritis, sarcoidosis and Wegener
disease [2,4]. If middle line necrosis is observed, cocaine
Figure 2. Aspect of the nose and nasal mucosa after two
weeks of treatment.
addiction must be suspected [9]. However, in a necrosis
caused by cocaine use there is not granulomas neither
inflammation [10].
Identification of the parasites in tissue biopsy materials
obtained from skin or mucosal ulcers is the best method
of diagnosis confirmation, but local parasitism must be
abundant, and this is not usual in the mucosal presenta-
tion [2,3,8]. A diagnostic choice is parasite DNA detec-
tion by using PCR. Its sensitivity reaches around 89% -
100%, but it is only available in specialized laboratories
[3,8]. Mucocutaneous leishmaniasis does usually not
develop a significant antibody response [11], conse-
quently serological response in HIV patients offers less
diagnostic value, because up to 40% of co-infected HIV/
Leishmania patients may present negative values in ac-
cordance with their immunological status [12]. An ex-
cellent response after treatment supports the diagnosis
[13]. There are no specific treatment guidelines in mu-
cosal leishmaniasis [2], but currently availab le therapy is
based on pentavalent antimony and amphotericin B.
In the case of an immunodepressed patient who pre-
sents torpid evolution of mucocutaneous ulcers, it is nec-
essary to rule out infection by Leishmania parasites. It
may occur, as in our patient, that PCR and specific cul-
tures turn out negative. A low level of parasites and the
previous active therapy against the protozoa (such as
Fluconazole) may lead to this. In our patient, after ruling
out a cross-reaction with T. cruzi, increased value was
given to Leishmania positive serology, observing that
mucocutaneous forms and co-infected HIV patients usu-
ally present negative values.
[1] M. M. Lessa, H. A. Lessa, T. W. Castro, A. Oliveira, A.
Scherifer, et al., “Mucosal Leishmaniasis: Epidemo-
logical and Clinical Aspects,” Revista Brasileira de Otor-
rinolaringologia, Vol. 73, No. 6, 2007, pp. 843-847.
[2] E. Shwart, C. Hatz and J. Blum, “New World Cutaneous
Leishmaniasis in Travellers,” Lancet Infectious Diseases,
Vol. 6, No. 6, 2006, pp. 342-349.
[3] M. Mateo, I. Cruz, M. D. Flores and R. López-Vélez,
“Slowly Progressing Skin Ulcers Following a Stay in
Costa Rica,” Enfermedades Infecciosas y Microbiología
Clínica, Vol. 23, No. 4, 2005, pp. 243-244.
[4] B. Herwaldt, “Leishmaniasis,” Lancet, Vol. 354, 1999, pp.
1191-1199. doi:10.1016/S0140-6736(98)10178-2
[5] J. Alvar, J. A. Ballesteros, R. Soler, A. Beniro, G. J. van
Eys, et al., “Mucocutaneous Leishmaniasis due to
Leishmania (Leishmania) Infantum: Biochemical Char-
acterization,” The American Journal of Tropical Medicine
and Hygiene, Vol. 43, No. 6, 1990, pp. 614-618.
Copyright © 2011 SciRes. WJA
Perforation of the Nasal Septum and Nasal Ulcers
Copyright © 2011 SciRes. WJA
[6] P. A. van Damme, M. Keuter, S. Van Assen, P. M.
De-Wilde and P. J. A. Beckers, “A Rare Case of Oral
Leishmaniasis,” Lancet Infectious Diseases, Vol. 4, No. 1,
2004, p. 53. doi:10.1016/S1473-3099(03)00861-2
[7] J. M. Ramos, Z. Zube ro and J. Ena, “Inmigración y VIH.
Aproximación a las Enfermedades Parasitarias y Vira-
les,”Enfermedades Infecciosas y Microbiología Clínica,
Vol. 26, No. 3, 2008, pp. 42-53.
[8] M. Gallego and C. Riera, “Las Leishmaniasis Humanas.
Control de Calidad de la Sociedad Española de Enfer-
medades Infecciosas y Microbiología Clínica.”
Consulted in June 6th, 2010.
[9] M. Trimarchi, G. Gregorini, F. Facchetti, M. L. Morassi,
C. Manfredini, R. Maroldi, et al., “Cocaine-Induced Mid-
line Destructive Lesions: Clinical, Radiographic, Histo-
pathologic, and Serologic Features and Their Differentia-
tion from Wegener Granulomatosis,” Medi ci ne, Vol. 80,
No. 6, 2001, pp. 391-404.
[10] C. B. Bonner and I. Y. Castillo, “Lesión Destructiva de la
Línea Media Inducida por Cocaína: Comunicación de un
Caso,” Anales de Otorrinolaringología Mexicana, Vol.
54, No. 1, 2009, pp. 32-35.
[11] Centers for Disease Control & Prevention, “National
Center for Infectious Diseases, Division of Parasitic Dis-
eases,” Consulted in 19 September 2010.
[12] J. Alvar, C. Cañavete, B. Gutiérrez-Solar, M. Jiménez, F.
Laguna, et al., “Leishmania and Human Immunodefi-
ciency Vírus Coinfection: The Firts 10 Years,” Clinical
Microbiology Reviews, Vol. 10, No. 2, 1997, pp. 298-319.
[13] M. Ara, C. Mailo, G. Peon, A. Clavel, J. Cuesta, et al.,
“Visceral Leishmaniasis with Cutaneous Lesions in a Pa-
tient Infected with Human Immunodeficiency Virus,” The
British Journal of Dermatology, Vol. 139, No. 1, 1998,
pp. 114-117. doi:10.1046/j.1365-2133.1998.02326.x