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Perforation of the Hard Palate

Educational Objective
Based on this clinical scenario and the accompanying image, understand how to arrive at a correct diagnosis.
1 Credit CME

A 45-year-old man was admitted to the hospital following 3 weeks of dysphagia; 1 week of nasal regurgitation, nonproductive cough, and breathy voice; and a 25-pound weight loss over the preceding 2 months. He had been diagnosed a year earlier with HIV infection and hepatic tuberculosis. Baseline CD4 count was 7 cells/μL, and following treatment with HAART (highly active antiretroviral therapy) consisting of dolutegravir, emtricitabine, and tenofovir-disoproxil-fumarate, he achieved full virological suppression; however, CD4 counts remained low at 31 cells/μL. He had completed 12 months of directly observed therapy with ethambutol, moxifloxacin, and rifabutin—a liver-sparing regimen—owing to toxic effects from the first-line regimen 1 month prior to admission. Physical examination revealed evidence of perforation of the hard palate (Figure, A). A computed tomographic scan of the chest revealed necrotic lymph nodes, and a palatine biopsy was performed (Figure, B and C).

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C. Histoplasmosis

Histoplasmosis, caused by a soil-based fungus,1 is the most common endemic mycosis in the United States, with a reported in-hospital crude mortality rate of 5% for children and 8% for adults.2 Clinical manifestations of histoplasmosis range from asymptomatic infection to rapidly progressive fatal illness.3 Oral histoplasmosis is an important entity to recognize because it is often a manifestation of disseminated disease.4 Moreover, the appearance may mimic other local or systemically manifested oral disease resulting in misdiagnosis.5

Disruption of soil by activities such as spelunking, excavation, outdoor construction, and remodeling of old buildings inhabited by birds or bats1 results in aerosolization of Histoplasma spores, which are then inhaled by human hosts causing infection. The vast majority of these primary infections are either asymptomatic or result in self-limited influenzalike illness, depending on the intensity of exposure.6 Cellular immunity develops approximately 2 weeks after infection in immunocompetent hosts, producing granulomas3 that either resolve spontaneously or persist as calcifications most commonly seen in mediastinal lymph nodes, liver, and spleen.4 In approximately 8% cases of histoplasmosis, the fungus disseminates.1 Risk of dissemination is greatest in individuals with a compromised immune system, especially those with AIDS and hematological malignant conditions, and in individuals using immunosuppressive medications.7 Dissemination can cause an acute, rapidly fatal sepsis syndrome with low blood pressure and multiorgan failure7 or a more subacute to chronically progressive disease with presence of focal lesions in various organs including the oropharynx.1

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Article Information

Corresponding Author: Udip Dahal, MD, Division of Allergy, Immunology and Infectious Diseases, Rutgers Robert Wood Johnson Medical School, 125 Paterson St, New Brunswick, NJ 08901 (drudip@gmail.com).

Published Online: May 30, 2019. doi:10.1001/jamaoto.2019.0926

Conflict of Interest Disclosures: None reported.

Additional Contributions: We thank the patient’s next of kin for granting permission to publish this information.

References
1.
Deepe  GS  Jr. Histoplasma capsulatum (histoplasmosis). In: Bennett  JE, Dolin  R, Blaser  MJ, eds.  Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Disease. 8th ed. Philadelphia, PA: Elsevier; 2015:2949-2962.
2.
Chu  JH, Feudtner  C, Heydon  K, Walsh  TJ, Zaoutis  TE.  Hospitalizations for endemic mycoses: a population-based national study.  Clin Infect Dis. 2006;42(6):822-825. doi:10.1086/500405PubMedGoogle ScholarCrossref
3.
Hage  CA, Wheat  LJ. Histoplasmosis. In: Kasper  DL, Fauci  AS, eds.  Harrison’s Infectious Diseases. 3rd ed. New York, NY: McGraw-Hill; 2017:996-999.
4.
Young  LL, Dolan  CT, Sheridan  PJ, Reeve  CM.  Oral manifestations of histoplasmosis.  Oral Surg Oral Med Oral Pathol. 1972;33(2):191-204. doi:10.1016/0030-4220(72)90389-1PubMedGoogle ScholarCrossref
5.
Toth  BB, Frame  RR.  Oral histoplasmosis: diagnostic complication and treatment.  Oral Surg Oral Med Oral Pathol. 1983;55(6):597-600. doi:10.1016/0030-4220(83)90376-6PubMedGoogle ScholarCrossref
6.
Rubin  H, Furcolow  ML, Yates  JL, Brasher  CA.  The course and prognosis of histoplasmosis.  Am J Med. 1959;27(2):278-288. doi:10.1016/0002-9343(59)90347-XPubMedGoogle ScholarCrossref
7.
Kauffman  CA.  Histoplasmosis: a clinical and laboratory update.  Clin Microbiol Rev. 2007;20(1):115-132. doi:10.1128/CMR.00027-06PubMedGoogle ScholarCrossref
8.
Fowler  CB, Nelson  JF, Henley  DW, Smith  BR.  Acquired immune deficiency syndrome presenting as a palatal perforation.  Oral Surg Oral Med Oral Pathol. 1989;67(3):313-318. doi:10.1016/0030-4220(89)90362-9PubMedGoogle ScholarCrossref
9.
Miller  RL, Gould  AR, Skolnick  JL, Epstein  WM.  Localized oral histoplasmosis: a regional manifestation of mild chronic disseminated histoplasmosis.  Oral Surg Oral Med Oral Pathol. 1982;53(4):367-374. doi:10.1016/0030-4220(82)90437-6PubMedGoogle ScholarCrossref
10.
MacFarlane  TW, Samaranayake  LP. Systemic infections. In: Jones  JH, Mason  DK, eds.  Oral Manifestations of Systemic Diseases. 2nd ed. London, England: Balliere Tindall; 1990:339-386.
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