eMedicine Specialties > Dermatology > Fungal Infections

Lobomycosis

Author: Kyle L Horner, MD, MS, Staff Physician, Department of Dermatology, Penn State Milton S Hershey Medical Center
Coauthor(s): Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle
Contributor Information and Disclosures

Updated: Oct 6, 2009

Introduction

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 literature1 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 loboi5 ; Paracoccidioides loboi6 because of its antigenic relationship to Paracoccidioides brasiliensis; and Lacazia loboi7 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

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 brasiliensis21,22 Second, sequence analysis of ribosomal RNA (rRNA) obtained from skin lesions in dolphins are highly homologous to rRNA sequences from the genus Cladosporium23 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 wall24 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 estuary27,28 and Tursiops truncatus dolphins in Florida, Hawaii, North Carolina, and the Bay of Biscay in Europe29,30,31,32,28,33 ; these findings imply that some aquatic reservoir also exists. 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.34

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,35 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,36 and 1 case in Europe may have been caused by occupational exposure to an infected dolphin30 . Murine-to-human transmission has been postulated but not proven.37

Although L loboi is generally considered a deep-seated mycosis, it has shown the potential for transepidermal elimination of infectious organisms.38 Dissemination within an individual may occur by means of lymphatic spread39 or autoreinfection.12

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 Brazil25 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.40,41 The first report42 of imported human lobomycosis in Canada was published in 2004 and in South Africa in 2008.43

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.44

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,35 Panama,45 Venezuela,6 Colombia,41 Guyana,46 Surinam,12 French Guyana,47 Ecuador,6 Peru,48 Bolivia,6 Honduras,6 Mexico,49 Holland,30 the United States,24 and Canada.42
  • 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.39

Sex

  • Lobomycosis is more common in men (68-92% of cases) than in women.50
  • The disease is most common in farmers, rubber workers, hunters, and prospectors.51
  • 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

Clinical

History

Skin lesions develop slowly. For example, the incubation time in the patient who acquired the disease from an affected dolphin was 3 months,30 and the incubation period in the American who had traveled to Venezuela was 2.5 years.24

When a volunteer was inoculated with the etiologic agent, the lesion was 1 X 2 mm in the first month, and then it waxed and waned. At 5 months, the lesion was a 2- to 3-mm, red papule. At 15 months, it measured 1 cm, with a small telangiectasis. At 25 months, the lesion was 15 X 10 mm, and at 4 years, it measured 33 mm in diameter, and a 4-mm satellite lesion developed.36

  • Because of this slow growth, patients do not present for many years, or they may present only after the lesions become large.
  • The lesions often begin as small papules or pustules, and they may occur at sites of minor trauma.36
  • The lesions may be mildly pruritic, or they may burn.50
  • Single lesions occasionally regress and form scars. However, the disease never disappears, and organisms are identifiable in the scar tissue.52
  • Aside from occasional lymphadenopathy, patients lack other systemic symptoms.51

Physical

  • The disease predominately affects exposed areas and extremities. Examples include the ears, buttocks, lumbosacral area, scapular area, elbows, and lower limbs.53 The scalp and mucosae are spared.
  • Lesions, papules, or plaques are most often described as keloidal, but the adjectives gummatous, verrucous, or ulcerative have also been applied.12
  • Lesions have well-defined lobulated margins and are not attached to deeper structures.54
  • The epidermis may be shiny, atrophic, and discolored.12
  • The disease may spread proximally from the extremities and fungal cells have been found in the lymph nodes, indicating lymphatic spread.41,55
  • Lymph nodes that drain the affected regions may be enlarged and infected with the organism in 0-25% of patients.12
Keloidal nodule on the leg. Courtesy of Dr Robert...

Keloidal nodule on the leg. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.

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Keloidal nodule on the leg. Courtesy of Dr Robert...

Keloidal nodule on the leg. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.


Lobomycosis in this patient appears as a flat pla...

Lobomycosis in this patient appears as a flat plaque lesion. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.

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Lobomycosis in this patient appears as a flat pla...

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. Co...

Separate keloidal lesions in a localized area. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.

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Separate keloidal lesions in a localized area. Co...

Separate keloidal lesions in a localized area. Courtesy of Dr Roberto Baruzzi, Sao Paulo, Brazil.


Causes

Other than geography and possible implantation of organisms through skin trauma,56 no predisposing factors have been identified.

  • Important data regarding the interplay among genetic, cultural, and geographic factors have been derived from studies of the Caiabi Indians of Brazil.
    • After they relocated to a geographic area similar to their former one, no new cases have been reported.
    • Furthermore, their original neighbors did not have similar prevalence rates.57
  • Immunodeficiencies appear to occur in patients with lobomycosis.
    • These immunodeficiencies include a delayed skin allograft rejection, a failure to sensitize to dinitrochlorobenzene, and an anergy to Candida species.58
    • Whether the immunodeficiencies are primary and predispose patients to infection or secondary and the result of infection is not known.
    • Based on the large number of fungal cells in the infected tissue and the disorganized cell arrangement in the granuloma, it has been hypothesized that patients with lobomycosis have immunoregulatory disturbances, which are likely to be specific and perhaps responsible for the lack of containment of the pathogen.59
    • One patient infected with the HIV has been reported to have lobomycosis.60

More on Lobomycosis

Overview: Lobomycosis
Differential Diagnoses & Workup: Lobomycosis
Treatment & Medication: Lobomycosis
Follow-up: Lobomycosis
Multimedia: Lobomycosis
References
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Further Reading

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Keywords

lacaziosis, keloidal blastomycosis, Amazonian blastomycosis, blastomycoid granuloma, Lobo's disease, Lobo disease, fungal infection of the skin, miraip, piraip, Loboa loboi, Paracoccidioides loboi, Paracoccidioides brasiliensis, Lacazia loboi, Glenosporella loboi, Blastomyces loboi

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Contributor Information and Disclosures

Author

Kyle L Horner, MD, MS, Staff Physician, Department of Dermatology, Penn State Milton S Hershey Medical Center
Kyle L Horner, MD, MS is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Pennsylvania Academy of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle; 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.

Medical Editor

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.

Pharmacy Editor

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.

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, 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; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting; Medicis Honoraria Consulting; Celgene Honoraria Consulting

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine 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, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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