Lobomycosis 

  • Author: Kyle L Horner; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jan 26, 2012
 

Background

Lobomycosis (lacaziosis) is a self-limited, chronic fungal infection of the skin endemic in rural regions in South America and Central America. Natives of the Brazilian rain forest call this disease miraip or piraip, meaning "that which burns."

Jorge Lobo first described this infection in the medical literature[1] as keloidal blastomycosis in a patient from the Amazon Valley of Brazil. Since the original report, lobomycosis has been reported in many South American countries, in North American travelers to endemic regions, in 2 species of Atlantic dolphins, and in 1 marine park dolphin trainer.

The condition was called Lobo disease in 1938, in 1958 the name lobomycosis was applied, and in 2005 the name lacaziosis was suggested.[2, 3, 4]

Three species names have been recommended: Loboa loboi[5] ; Paracoccidioides loboi[6] because of its antigenic relationship to Paracoccidioides brasiliensis; and Lacazia loboi[7] in deference to Lacaz, who contributed much to the knowledge of the disease. Other names that have been used are Glenosporella loboi and Blastomyces loboi. Based on recent molecular studies, the name Lacazia loboi is the current recommended name.[4] As is common in medical mycology, the name of the disease is taken from the genus of the etiologic agent, and therefore, lacaziosis has been proposed for the disease name rather than lobomycosis.[4]

Phylogenetic and genomic analyses indicate that it is a sister taxon of the human dimorphic fungal pathogen P brasiliensis and that both species belong to the order Onygenales.[4, 8, 9, 10]

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Pathophysiology

The organism responsible for lobomycosis has yet to be cultured in vitro. The infection has been transmitted to an armadillo,[11] to the footpads and cheek pouches of golden hamsters,[12, 13] and to tortoises.[14] Live organisms have been maintained for 18 months in the footpads of BALB/c mice.[15, 16, 17] However, most of our knowledge of the etiologic agent of lobomycosis is derived from histopathologic, electron microscopic, and molecular studies.[4]

The fungus is abundant in lobomycotic skin lesions. It is a spherical intracellular yeast 6-12 μm diameter.[18] The fungus is remarkably homogeneous, with an average diameter of 9 μm. Although debate exists as to whether nuclei and organelles of fungal origin have been definitively identified,[18, 19, 20] 2 lines of evidence support the fungal nature of the etiologic agent of lobomycosis. First, immunologic studies show cross-reactivity of the antiserum obtained from patients affected by lobomycosis with several antigens prepared from cultures of P brasiliensis[21, 22] Second, sequence analysis of ribosomal RNA (rRNA) obtained from skin lesions in dolphins are highly homologous to rRNA sequences from the genus Cladosporium[23] and from P brasiliensis.[8]

L loboi is predominantly an intracellular pathogen. Organisms, singly or in chains, reside predominantly in macrophage vacuoles. They probably reproduce by budding; linear or radiating chains of as many as 20 organisms linked by tubules have been observed.[18] The melanin-containing birefringent 1-μm-thick cell wall[24] resists digestion by macrophages and may be central in contributing to the chronicity of the infection.[18]

The cytokines secreted in vitro by mononuclear cells of patients with lobomycosis showed increased interleukin-4 and interleukin-6 and decreased interleukin-2 production compared with mononuclear cells from normal patients. Mononuclear cells from patients with generalized disease produce higher levels of interferon-gamma than those from patients with localized disease. Taken together, these results suggest that mononuclear cells from patients with lacaziosis are predominantly of the Th2 profile. Further studies are needed to assess the significance of these observations.[25] When compared to healthy control subjects of the same ethnic group no human leukocyte antigen (HLA) susceptibility or resistance could be demonstrated in 21 patients with lobomycosis.[26] However, HLA-DR7 was found to be potentially protective.

The natural reservoir of L loboi is unknown. Its likely habitat is somewhere in the rural environment because of the observed distribution of the disease. Soil and vegetation seem to be likely sources of infection.

L loboi has also been recovered from lobomycotic lesions of the Guiana dolphin Sotalia guianensis from the Surinam River estuary[27, 28] and Tursiops truncatus dolphins in Florida, Hawaii, North Carolina, and the Bay of Biscay in Europe[29, 30, 31, 32, 28, 33] ; these findings imply that some aquatic reservoir also exists. Recently, 2 west coast Florida bottlenose dolphin (Tursiops truncatus) populations had a prevalence of lacaziosis of 2-3%.[34]

Lobomycosis is similarly manifested in humans and in dolphins; the skin lesions and morphologic features of the organism are nearly identical, and at least one case of dolphin-to-human transmission has been documented.[30] However, the organism in dolphins is somewhat smaller than that seen in humans, and it may not prove to be identical.[35]

Lobomycosis often develops at sites of minor trauma, but sometimes, no history of trauma can be recalled.[30] The disease has been associated with ear lesions in persons who carry natural materials on their shoulder, with snake and insect bites,[36] and in one case, with trauma associated with exposure to high-pressure falling water.[24] Human-to-human transmission has not been documented, though the inoculation of a tissue homogenate reproduced the disease,[37] and 1 case in Europe may have been caused by occupational exposure to an infected dolphin[30] . Murine-to-human transmission has been postulated but not proven.[38]

Although L loboi is generally considered a deep-seated mycosis, it has shown the potential for transepidermal elimination of infectious organisms.[39] Dissemination within an individual may occur by means of lymphatic spread[40] or autoreinfection.[12]

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Epidemiology

Frequency

United States

Only 1 case of lobomycosis has been reported in the United States. The patient was exposed to a waterfall in Venezuela years before presentation.[24]

International

Approximately 64% of all known cases have occurred in Brazil[25, 41] and though lobomycosis is uncommon, it occurs in as many as 8.5% of the members of some tribes indigenous to South America, for example, the Amoruas tribe of the Casanare state in Colombia and the Caiabi Indians of Brazil.[42, 43] The first report[44] of imported human lobomycosis in Canada was published in 2004 and in South Africa in 2008.[45]

Mortality/Morbidity

No deaths from lobomycosis have been reported. One patient in whom squamous cell carcinoma developed in a lobomycotic nodule later died from lung metastases.[46]

Race

Other than a few tribes in South America (eg, the Amoruas, the Caiabi), no racial prevalence is known. One case has been reported in the United States, but the patient was exposed to a waterfall in Venezuela years before his or her presentation.[24] The case in Europe was reported in a handler of an affected dolphin.[30]

  • The disease has been reported in many areas: Costa Rica,[36] Panama,[47] Venezuela,[6] Colombia,[43] Guyana,[48] Surinam,[12] French Guyana,[49] Ecuador,[6] Peru,[50] Bolivia,[6] Honduras,[6] Mexico,[51] Holland,[30] the United States,[24] and Canada.[44]
  • The disease is usually found in areas higher than 200 m with tropical, humid, or subtropical forests; an average temperature of 24°C; and more than 2000 mm of annual rainfall.[40]

Sex

  • Lobomycosis is more common in men (68-92% of cases) than in women.[52]
  • The disease is most common in farmers, rubber workers, hunters, and prospectors.[53]
  • The high prevalence among women of some tribes is attributed to their active participation in farming activities.

Age

The age of onset is 1-70 years, with an average patient age of 38 years.[12]

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Contributor Information and Disclosures
Author

Kyle L Horner  MD, MS, Staff Physician, Silver Falls Dermatology, Corvallis, OR

Kyle L Horner is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, and American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Gregory J Raugi, MD, PhD  Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

David P Fivenson, MD  Associate Director, St Joseph Mercy Hospital Dermatology Program, Ann Arbor, Michigan

David P Fivenson, MD is a member of the following medical societies: American Academy of Dermatology, Medical Dermatology Society, Michigan Dermatological Society, Michigan State Medical Society, Photomedicine Society, Society for Investigative Dermatology, and Wound Healing Society

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD  Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Celgene Honoraria Safety Monitoring Committee

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Dr. Kord Honda, MD, to the development and writing of this article.

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Keloidal nodule on the leg. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.
Lobomycosis in this patient appears as a flat plaque lesion. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.
Separate keloidal lesions in a localized area. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.
Characteristic histologic appearance of the organism. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.
 
 
 
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