You are on page 1of 6

Eur Arch Otorhinolaryngol

DOI 10.1007/s00405-007-0533-4

LARYNGOLOGY

Infectious granulomatous laryngitis: a retrospective


study of 24 cases
Leonardo Silva · Edward Damrose · Fernanda Bairão ·
Mayra L. Della Nina · James C. Junior ·
Henrique Olival Costa

Received: 20 June 2007 / Accepted: 29 October 2007


© Springer-Verlag 2007

Abstract The diagnostic and treatment of verrucous prognosis aspects. Twenty-four patients were identiWed.
lesions of the larynx involves a high level of suspicion by Mycobacterium tuberculosis and Paracoccidiodis brasili-
the physician attending the patient. The causes may go ensis accounted for ten cases each, and Leishmania brazili-
from unspeciWc laryngitis to neoplasia and granulomatous ensis the remaining four. Hoarseness was the most common
diseases. This kind of lesion is uncommon and the presen- symptom of infection. Up to one-third of patients with
tation aspects may vary broadly. The lesions in larynx are laryngeal involvement lacked laryngeal symptoms. The
signiWcant source of morbidity. The onset of symptoms is average delay from onset of symptoms to diagnosis was
insidious and the diagnosis is usually delayed. Symptoms 7 months. All patients underwent direct laryngoscopy and
include dysphonia, dyspnea, dysphagia and odynophagia. biopsies. Caseating granulomas was the key histopatho-
Proper treatment depends upon tissue biopsy, identiWcation logic Wnding. IdentiWcation of the causative organism was
of the causative organism, and the appropriate pharmaco- uncommon. No evidence of concomitant malignancy was
therapy. As there are few papers presenting the clinical fea- seen on biopsy. Despite treatment, almost 40% of patients
tures of infectious granulomatous laryngitis (IGL) as had permanent sequelae of infection, including hoarseness,
leishmaniasis, tuberculosis and paracoccidiodomycosis dyspnea, and dysphagia. Mycobacterium tuberculosis, P.
aVecting the larynx, we considered important to show the brasiliensis, and L. braziliensis accounted for all cases of
experience of a big Brazilian Laryngology Service in deal- IGL. Patients may have laryngeal infection but lack laryn-
ing with this potential worldwide problem. We present a geal symptoms. Prompt diagnosis relies upon a high index
retrospective chart review showing our institution’s experi- of suspicion, especially when evaluating patients from
ence with IGL focusing in the diagnostic, treatment and endemic areas. Given the degree of tissue destruction,
which accompanies infection, timely intervention may be
important in the prevention of late sequelae. Despite appro-
priate therapy, a signiWcant number of patients may have
L. Silva (&) · H. O. Costa permanent sequelae of infection.
Department of Otolaryngology,
Santa Casa Medical School, Rua Martiniano de Carvalho,
864, suite 1001, Bela Vista, São Paulo, SP 01321 000, Brazil
Keywords Granulomatous · Laryngitis · Clinical aspects
e-mail: leosilva@uol.com.br

E. Damrose Introduction
Stanford Voice Center, Stanford, CA, USA

F. Bairão · M. L. D. Nina Infectious granulomatous laryngitis (IGL) is an uncommon


Otolaryngology Resident, yet important cause of chronic laryngitis. Because of its rar-
Santa Casa Medical School, São Paulo, SP, USA ity, it may be overlooked in the diVerential diagnosis of
J. C. Junior
voice disorders [1–4]. Its spectrum of presentation may
Otolaryngology Resident Stanford Voice Center, vary, from hoarseness, to dysphagia and odynophagia [5–
Stanford, CA, USA 7]. In Brazil, Mycobacterium tuberculosis, Paracoccidiodis

123
Eur Arch Otorhinolaryngol

brasiliensis, and Leishmania braziliensis are the most com- Treatment


mon causative agents of ILG. A delay in the diagnosis of
IGL may lead to inadequate or incorrect treatment, and Patients found to have M. tuberculosis subsequently under-
worsened prognosis [7, 8]. When the causative agent is, for went combined therapy with rifampin (10 mg/kg/day), hid-
example, tuberculosis, delaying the diagnosis could lead to razide (10 mg/kg/day), and pyrazinamide (35 mg/kg/day)
serious consequences regarding transmission of the disease for 2 months, followed by 4 months of rifampin (10 mg/kg/
to other individuals [4]. day) and hidrazide (10 mg/kg/day).
As the global community is becoming increasingly more In patients diagnosed with paracoccidioidomycosis,
connected, the regional infectious diseases are being shared treatment was accomplished with sulfamethoxazole
through the entire world, leading to a public health concern (800 mg bid) for a minimum of 3 months. Treatment was
[9–11]. continued until complete resolution of laryngeal and chest
While the organism responsible for the infection may not lesions. Patients not responding to sulfamethoxazole some-
necessarily be seen microscopically, the hallmark histologi- times require treatment with amphotericin B. All patients in
cal Wnding in ILG is that of the caseating granuloma [12, this series responded to treatment with sulfamethoxazole.
13]. This particular type of inXammatory reaction is only Patients diagnosed with leishmaniasis were treated with
encountered in a select number of diseases. Thus, the iden- methyl glucamine antimoniate 20 mg/kg/day given intra-
tiWcation of the classic chronic granulomatous inWltrate by muscularly as 20–30 day cycles. Patients typically undergo
tissue biopsy is an important part of the ILG work out. three to four cycles until a complete clinical response is
Physical Wndings of laryngeal involvement by ILG are observed. Patients were considered cured when all systemic
variable, and there is no single speciWc feature that could symptoms have resolved and there was no evidence of
call for the diagnostic of the infection. Every compartment residual lesions.
of the larynx can be aVected, along with adjacent sites in
the head and neck such as the nasal and oral cavities.
Therefore, a high index of clinical suspicion is necessary Results
for the proper and timely diagnosis of the disease [5].
As the recognition of the disease depends upon the pre- Twenty-four patients with ILG were identiWed between
vious clinical experience of the physician, and being the 1997 and 2006, divided as follows: 10 patients with tuber-
ILG an uncommon medical situation, the aim of this study culosis, 10 with leishmaniasis, and 4 with paracoccidioido-
was to share the experience gathered by our institution, pre- mycosis. There were 17 males and 7 females. The average
senting a retrospectively review of the clinical aspects and age at diagnosis was 37.8 years for tuberculosis (range 7–
outcome of 24 patients diagnosed with ILG. 58 years), 47.9 years for leishmaniasis (range 23–65 years)
and 44 years for paracoccidioidomycosis (range 39–
48 years). Etiology, symptoms and initial site of presenta-
Materials and methods tion are summarized in Table 1.
All patients were found to have laryngeal involvement,
Permission to conduct this study was given by the Institu- although not all patients presented with laryngeal symp-
tional Clinical Research Committee of the Central Hospi- toms as the initial complaint. The average time to diagnosis
tal of Santa Casa Medical School of São Paulo, in Brazil. from the initial onset of symptoms was 7 months (range
A retrospective chart review was performed from 1997 to 1 month to 2 years) although the time varied according to
2006 for patients diagnosed with ILG. The charts were the organism (tuberculosis, 1–20 months; paracoccidiod-
reviewed for the following information: gender, age, pre- omycosis, 8–24 months; leishmaniasis, 4–9 months).
senting complaints and symptoms, laryngeal Wndings on All patients underwent direct laryngoscopy with biop-
laryngoscopy, and the period of time between the onset of sies. Histopathology in 20 patients (83.3%) revealed non-
symptoms and diagnosis. Charts were also reviewed for caseating granulomas with chronic inXammation, but no
the response to therapy and persistent sequelae or symp- organisms. In the remaining four patients (16.7%) the caus-
toms. ative organism could be seen, and in all of these cases it
Patients underwent a complete head and neck examina- was paracoccidiodomycosis.
tion including Xexible laryngoscopy. Chest radiography Dysphonia was the most frequent post-treatment symp-
was performed to evaluate the pulmonary involvement. All tom (Table 2). Nine of 24 patients (37.8%) had permanent
patients subsequently underwent direct laryngoscopy to sequelae of infection despite therapy (Table 3). One patient
evaluate carefully the extent of laryngeal involvement, to required a tracheostomy for subglottic stenosis, Wve
obtain a tissue specimen for pathological analysis, and to patients had permanent dysphonia secondary to vocal fold
exclude the possibility of malignancy. scarring, one patient acquired a vocal fold paresis, and two

123
Eur Arch Otorhinolaryngol

Table 1 Distribution of organ-


Organism Number of Symptom Presenting site Laryngeal
isms, symptoms and presenting
patients (%) (N, %) of involvement lesion
site of head and neck involve-
(N, %)a
ment
Mycobacterium tuberculosis 10 (41.7) Dysphonia Nose Supraglottis
Dyphasia Mouth Glottis
Odynophagia Larynx Subglottis
Dyspnea Pharyx
Leishmania braziliensis 10 (41.7) Dysphonia Nose Supraglottis
a
All patients had laryngeal Dyphasia Mouth Glottis
involvement, but not all patients Odynophagia Larynx Subglottis
presented with laryngitis as the Dyspnea Pharyx
initial complaint Paracoccidiodes brasiliensis 4 (16.7) Dysphonia Nose Supraglottis
Nose 5 20.8%; Mouth 2 8.4%; Dyphasia Mouth Glottis
Larynx 16 66.6%; Neck 1 4.2%; Odynophagia Larynx Subglottis
Silva 3 Dyspnea Pharyx

Table 2 Distribution of post-


Organism Dyspnea Dysphonia Dysphagia Odynophagia
treatment symptoms
Mycobacterium tuberculosis 1(10%) 5(50%) 1(10%) 0
Leishmania braziliensis 1(25%) 1(25%) 1(25%) 0
Paracoccidiodes brasiliensis 0 1(10%) 0 0

Table 3 Complications of
Patient Organism Percent Outcome
infection
(%)a

1 Leishmania braziliensis Subglottic stenosis, tracheostomy dependence


2 Leishmania braziliensis Bilateral vocal fold scarring, permanent dysphonia
3 Leishmania braziliensis 30 Chronic dysphagia
4 Mycobacterium tuberculosis Bilateral vocal fold scarring, permanent dysphonia
5 Mycobacterium tuberculosis Bilateral vocal fold scarring, permanent dysphonia
6 Mycobacterium tuberculosis Bilateral vocal fold scarring, permanent dysphonia
7 Mycobacterium tuberculosis Bilateral vocal fold scarring, permanent dysphonia
a 8 Mycobacterium tuberculosis 50 Chronic odynophagia
Percent of total patients infect-
ed by a given organism 9 Paracoccidiodes brasiliensis 25 Bilateral vocal fold scarring, permanent dysphonia

patients had persistent dysphagia or odynophagia. The maximum of 2 years. In the majority of cases a diagnosis
remaining 15 patients developed complete resolution of was established within 8 months of the onset of symptoms.
their laryngeal disease, with no further evidence of laryn- Poor access to medical care, the ineYciency of the
geal abnormality found on repeat endoscopy. health care system, and the insidious nature of early disease
all may contribute to a delay in diagnosis and treatment.
In the diagnosis of granulomatous laryngitis, the diVer-
Discussion ential diagnosis includes other infectious entities such as
blastomycosis, hanseniasis, syphilis, coccidioidomycosis,
In this series, M. tuberculosis, P. brasiliensis, and L. brazi- actinomycosis, and histoplasmosis; non-infectious disor-
lienses accounted for all cases of IGL. When dealing with ders such as sarcoidosis, lupus erythematosus and
infectious diseases with signiWcant transmission rates, Wegener’s granulomatosis; and neoplasias [7, 14–21]. Tis-
prompt diagnosis and treatment is essential to prevent the sue biopsy is key in the establishment of the diagnosis, and
spread of infection to others. also in ruling out associated neoplasia [16, 20].
The delay between the onset of the symptoms and the The causative organism may be seen in the tissue speci-
diagnosis reXects the access to health care services and the men [8, 21, 22]. All patients in this series underwent tissue
timeliness of the diagnosis. In our study, the minimum biopsy. In all patients, histology revealed caseating granu-
period of time to reach a diagnosis was 1 month with a lomas and chronic inXammation, but only in the four

123
Eur Arch Otorhinolaryngol

patients diagnosed with paracoccidioidomycosis was the


organism seen. Several biopsies demonstrated epithelial
hyperplasia with atypia, but no patient was found to have a
concomitant malignancy, as has been reported in other
series [21, 22].
Histologically, all tissue samples should reveal caseating
granulomas (Fig. 1a). Ziehl Neelsen stain may be used to
identify M. tuberculosis (Fig. 1b). Paracoccidiodis brasili-
ensis can be seen as a spherical element on routine hema-
toxylin/eosin staining (Fig. 2a) but the Wnding of the marine
pilot’s wheel with Grogott’s stain is pathognomonic for P.
brasiliensis (Fig. 2b). A robust inXammatory reaction and
neovascularization can be seen with L. brazieliensis infec-
tion (Fig. 3a), and Giemsa staining can reveal the organism
(Fig. 3b).
In general, laryngeal tuberculosis and paracoccidioido-
mycosis develop secondarily from primary pulmonary
infection. Laryngeal infection occurs through direct inocu-
lation of the larynx by aerosolized droplets containing the
organism. In leishmaniasis, laryngeal infection is secondary

Fig. 2 a Spherical fungal elements of paracoccidioidomicosis (ar-


rows) interspersed among granulomas and chronic inXammatory cells
(400£). b Grogott (silver) staining revealing the marine pilot’s wheel
appearance of paracoccidioidomicosis (1,000£)

to contamination from the nasal and oropharyngeal mucous


membranes. Thus, laryngeal involvement by tuberculosis
and paracoccidioidomycosis is said to be an ascendant pro-
cess, while that by leishmaniasis is thought to be a descen-
dant process [24–26]. Therefore, the site of initial infection
is helpful in determining the diagnosis, with nasal involve-
ment seen initially with leishmaniasis, and pulmonary
involvement seen initially with M. tuberculosis and P.
brazieliensis.
Laryngeal tuberculosis shows a predilection for adult
males, and rarely occurs in children [27, 28]. Although
tuberculosis is highly contagious, its incidence of laryngeal
infection in this series was equal to that of paracoccidioido-
mycosis. Some authors consider a chest X-ray and laryn-
geal biopsy to be the most valuable diagnostic tests for
laryngeal tuberculosis, with a diagnostic accuracy that
Fig. 1 a The caseating granuloma with epithelioid and giant cells as approaches 100% [29]. A milliary inWltrate and cavitary
seen in M. tuberculosis infection (100£). b Ziehl Neelsen staining lesions in the apices of the lungs can be seen in patients
demonstrating numerous M. tuberculosis bacilli (arrows) (1,000£) with acute tuberculosis. Although laryngeal tuberculosis in

123
Eur Arch Otorhinolaryngol

vitro inhibiting action of 17- estradiol on the transforma-


tion of the yeast mycelium and the existence of a receptor
for 17- estradiol in the yeast’s cytoplasm [31].
Most patients with laryngeal paracoccidioidomycosis
have concomitant active lung infection, although isolated
laryngeal infection can also occur. Laryngeal involvement
may be diVuse or localized, and when localized may resem-
ble a carcinoma. Dissemination from the lungs occurs
through the bloodstream or directly by infection from pul-
monary secretions [23]. The disease can show long latent
periods, with some patients having developed active dis-
ease as long as 30 years after leaving endemic areas [32].
The clinical presentations of tuberculosis and paracoccidi-
oidomycosis are similar and may be diYcult to diVerentiate
from each other. Fever, cough, and weight loss are common
in both disease states, and both diseases aVect men in of
lower socio economic standing. Both diseases behave path-
ologically similar, with primary lung infection ascending to
involve the larynx secondarily. Laryngeal symptoms are
identical and include dysphonia, odynophagia and dyspnea
[33]. Cavitary lesions and interstitial inWltrates can be seen
on chest X-ray, and usually involve the central and basal
portions of the lungs. Unlike tuberculosis, the apices are
usually spared.
Leishmaniasis is the second most common parasitary
condition in the world, with 600,000 new cases per year
[34]. In the western hemisphere the highest prevalence is in
Brazil, with 65,000 new cases diagnosed annually [34–36].
In the last few years, the epidemiology of the disease has
Fig. 3 a InXamatory reaction with intensive neovascular formation changed, with a shift in the patient population from those
and abundant plasmacitic cells as seen in leishmaniasis (400£). b Gi-
emsa staining demonstrating the organism L. braziliensis (arrows)
that live in areas undergoing active deforestation, to those
(1,000£) residing in the outskirts of large urban centers and rural
areas that have already been deforested. Leishmaniasis
involves the mucous membranes of the nasal and oral cavi-
general is associated with signiWcant lung disease, the chest ties Wrst, before descending to involve the larynx. Because
X-ray can be normal when destruction of pulmonary tissue pulmonary involvement is not seen in the disease, the chest
has not had an opportunity to progress signiWcantly, as can X-ray is normal. The Wndings of nasal lesions and a normal
be seen in children [28]. chest X-ray are therefore extremely helpful in distinguish-
In the setting of advanced pulmonary disease, cytology ing leishmaniasis from tuberculosis and paracoccidioido-
can reveal the organism in sputum or gastric Xuid cytology. mycosis.
The most common deep infectious mycosis in Latin While all patients responded to therapy and were cured
America, paracoccidioidomycosis causes an acute intersti- of their disease, almost 40% of our patients experienced
tial pneumonitis after inhalation of the fungus. A chronic permanent sequelae as a result of IGL. Hoarseness was usu-
form can surface many years after initial infection. The dis- ally secondary to atrophy of the vocal folds and loss of the
ease is endemic to many regions of the United States, mucosal wave. Two patients experienced dysphagia follow-
Europe and Asia [16, 24, 30]. The disease most commonly ing apparent clinical resolution of active disease, but the
aVects adults between the ages of 29 and 49, and children etiology as to the exact nature of the dysphagia has
only rarely. remained uncertain.
Males are 14 times more likely to be aVected than Subglottic stenosis was seen in one patient, which
females. Apparently, this diVerence is due to a greater required placement of a tracheostomy. While most patients
exposure to the agent, mainly among the male rural worker who present with IGL will be eVectively treated with no
population, and possibly due to a protective action of estro- long term laryngeal sequelae, it is important to recognize
gen [24]. Some experimental studies have shown the in this clinical entity and institute prompt treatment in order to

123
Eur Arch Otorhinolaryngol

minimize injury to the laryngeal tissues as well as to mini- 15. Thaller SR, Gross JR, Pilch BZ (1987) Laryngeal tuberculosis as
mize the opportunity for spread of the disease to other indi- manifested in the decades 1963–83. Laryngoscope 97(7 Pt1):848–
850
viduals [37]. 16. Swallow CE, McAdams HP, Colon E (1984) Tuberculosis mani-
fested by a laryngeal mass on CT scans. AJR (1994) 163:179–180.
Laryngoscope 94:608–611
Conclusions 17. Cantarella G, Pagani D, Fasano V, Scaramellini G (2007) Glottic
tuberculosis masquerading as early multifocal carcinoma. Tumori
93(3):302–304
Mycobacterium tuberculosis, P. brasiliensis, and L. brazili- 18. Sant’Anna GD, Mauri M, Arrarte JL, Camargo H Jr. (1999) Laryn-
ensis accounted for all cases of IGL. Patients may have geal manifestations of paracoccidioidomycosis (South American
laryngeal infection but lack laryngeal symptoms. Prompt blastomycosis). Arch Otolaryngol Head Neck Surg 125(12):1375–
1378
diagnosis relies upon a high index of suspicion, especially 19. Tristano AG, Díaz L (2007) A case of laryngeal paracoccidioido-
when evaluating patients from endemic areas. Given the mycosis masquerading as chronic obstructive lung disease. South
degree of tissue destruction which accompanies infection, Med J 100(7):709–711
timely intervention may be important in the prevention of 20. Payne J, Koopmann CF (1984) Laryngeal carcinoma or is it laryn-
geal blastomycosis? Laryngoscope 94(5 Pt1):608–611
late sequelae. Despite appropriate therapy, a signiWcant num- 21. Bailey CM, Windle-Taylor PC (1981) Tuberculous laryngitis: a
ber of patients may have permanent sequelae of infection. series of 37 patients. Laryngoscope 91:93–100
22. Ibarra A, Arellano L (1983) Tuberculosis laringea: experiencia en
16 casos. Rev Med Chil 111:39–42
23. Maymo Arganaraz M, Luque AG, Tosello ME et al (2003) Para-
References coccidioidomycosis and larynx carcinoma. Mycoses 46:229–232
24. Londero AT (1982) Paracoccidioidomicose. In: Del Negro G,
1. Wang CC, Lin CC, Wang CP, Liu SA, Jiang RS (2007) Laryngeal Lacaz CS, Fiorillo AM (eds) São Paulo, Sarvier, pp 85–90
tuberculosis: a review of 26 cases. Otolaryngol Head Neck Surg 25. Reder PA, Neel HB 3rd (1993) Blastomycosis in otolaryngology:
137(4):582–588 review of a large series. Laryngoscope 103(1 Pt 1):53–58
2. Prasad KC, Sreedharan S, Chakravarthy Y, Prasad SC (2007) 26. Ebeo CT, Olive K, Byrd RP Jr, Mirle G, Roy TM, Mehta JB (2002)
Tuberculosis in the head and neck: experience in India. J Laryngol Blastomycosis of the vocal folds with life-threatening upper air-
Otol 121(10):979–985 way obstruction: a case report. Ear Nose Throat J 81(12):852–855
3. Rizzo PB, Da Mosto MC, Clari M, Scotton PG, Vaglia A, Marchi- 27. Ulloa R, Avila ML, Soto M et al (1998) Laryngeal tuberculosis.
ori C (2003) Laryngeal tuberculosis: an often forgotten diagnosis. Pediatr Infect Dis J 17:758–760
Int J Infect Dis 7(2):129–131 28. Ramadan HH, Wax MK (1995) Laryngeal tuberculosis. A cause of
4. Thompson St. C (1924) Tuberculosis of larynx: its signiWcance to stridor in children. Arch Otolaryngol Head Neck Surg 121: 109–
physician. Lancet 2:948–949 112
5. Silva L, Klautau GB, Costa HOO (2002) Laringites EspecíWcas. 29. Castro CC, Benard G, Ygaki Y et al (1999) MRI of head and neck
In: Otacílio & Campos Tratado de Otorrinolaringologia, vol 4 paracoccidioidomycosis. Br J Radiol 72: 717–722
(ed1), São Paulo, Roca, pp 393–415 30. Sarazin F, Sainte-Marie D, Demar M, Aznar C, Sarrouy J, Pradin-
6. Lim JY, Kim KM, Choi EC, Kim YH, Kim HS, Choi HS (2006) aud R, Carme B, Couppié P (2005) Cutaneous-mucosal paracoc-
Current clinical propensity of laryngeal tuberculosis: review of 60 cidio-domycosis: the Wrst case diagnosed in French Guiana. Ann
cases. Eur Arch Otorhinolaryngol 263(9):838–842 Dermatol Venereol 132(2):136–139
7. Manns BJ, Baylis BW, Urbansky SJ et al (1996) Paracoccidioido- 31. Negroni R (1993) Paracoccidioidomycosis. Int J Dermatol
mycosis: case report and review. Clin Infect Dis 23:1026–1032 32:847–859
8. Marques AS (1998) Paracoccidioidomicose. An Bras Dermatol 32. Franco MF, Mendes RP, Moscardi-Bacchi TV et al (1989) Para-
73(2):455–469 coccidioidomycosis. Clin Trop Med Commun Dis 4:185–220
9. Morales Puebla JM, Padilla Parrado M, Díaz Sastre MA, Chacón 33. Mendes RP (1994) The gamut of clinical manifestations. In: Gran-
Martinez J, Galán Morales JT, Lasso Luis MO, Jiménez Antolin co M, Lacaz CS, Restrepo-Moreno A, Del Negro G (eds) Paracoc-
JA, Menéndez Loras LM (2006) Laryngeal tuberculosis. Incidence cidioidomycosis. CRC, Boca Raton, pp 233–258
between 1994 and 2004. An Otorrinolaringol Ibero Am 34. Grimaldi G, Tesh RB, McMahon-Pratt D (1989) A review of the
33(6):591–598 geographic distribution and epidemiology of leishmaniasis in the
10. Menon K, Bem C, Gouldesbrough D, Strachan DR (2007) A clin- new world. Am J Trop Med Hyg 41:687–725
ical review of 128 cases of head and neck tuberculosis presenting 35. Martins R, Marques SA, Alves M, Fecchio D et al. (1997) Sero-
over a 10-year period in Bradford, UK. J Laryngol Otol logical follow-up of patients with paracoccidioidomycosis treated
121(4):362–368 with itraconazole using dot-blot and Western-blot. Rev Inst Med
11. Krecicki T, Zalesska-Krecicka M, Zatonski T, Jankowska R, Trop São Paulo 39:261–269
Skrzydlewska-Kaczmarek B (2004) Laryngeal tuberculosis. Lan- 36. Passos VMA, Falcao AL, Marzochi MCA (1993) Epidemiological
cet Infect Dis 4(1):57 aspects of American cutaneous leishmaniasis in a periurban area of
12. Motta AC, Lopes MA, Ito FA, Carlos-Bregni R, de Almeida OP, the metropolitan region of Belo Horizonte, Minas Gerais, Brazil.
Roselino AM (2007) Oral leishmaniasis: a clinicopathological Mem Inst Oswaldo Cruz 88:103–110
study of 11 cases. Oral Dis 13(3):335–340 37. Díaz Sastre MA, Padilla Parrado M, Morales Puebla JM, Jiménez
13. Couldery AD (1990) Tuberculosis of the upper respiratory tract Antolín JA, Caro García MA, Chacón Martínez J, Menéndez Lo-
misdiagnosed as Wegener’s granulomatosis––an important dis- ras LM, Orradre Romeo JL (2007) Laryngeal leishmaniasis. An
tinction. J Laryngol Otol 104:255–258 Otorrinolaringol Ibero Am 34(1):17–25
14. Flanagan PM, McIlwain JC (1993) Tuberculosis of the larynx in a
lepromatous patient. J Laryngol Otol 107:845–847

123

You might also like