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Letter
HIV and Lacaziosis, Brazil
Marilia B. Xavier,* Marcia M.R. Ferreira,* Juarez A.S. Quaresma,*
and Arival C. de Brito*
*Federal do Para University, Belem, Para, Brazil
Suggested
citation for this article
To the Editor: Jorge Lobo disease (lacaziosis) is a chronic deep
mycosis for which prognosis is good in terms of survival but unclear in
terms of regression of the lesions (1). No involvement
of internal organs or mucous membranes is observed. The causative agent
is Lacazia loboi (2), a fungus of uncertain
phylogeny, which causes an inflammatory infiltrate accompanied by the
formation of a granuloma in which giant cells phagocytose a larger number
of fungi (3,4). Pecher and Funchs suggested that
patients with lacaziosis have a cellular immunodeficiency (5).
The disease is more frequent in men and persons 21–40 years of age. It
is found exclusively in Latin America; only 1 case has been diagnosed
in Europe, and that was due to accidental contamination with material
from a dolphin (4).
Trauma and injuries or sites of insect bites facilitate penetration of
the fungus. Lesion progression is slow, with new lesions arising by contiguity
with other lesions or through the lymphatic route (6,7).
Clinically, lacaziosis manifests as keloidal lesions of solid consistency
and variable size that contain small scales and crusts (6).
The lesions are most frequently located in the auricle and on the upper
and lower limbs. Cutaneous dissemination of the disease is observed in
a relatively small number of cases. We describe a patient with Jorge Lobo
disease.
The patient was a 59-year-old man, a storeroom employee, who was seen
at the Tropical Medical Center in Belem, Brazil, in April 2004. A papula
had developed near his right knee in 1992 after a wood splinter had penetrated
the skin. The lesion increased in size, and a histopathologic diagnosis
of Jorge Lobo disease was made. The lesion was then surgically removed.
Approximately 2 years later, the lesion recurred. The patient then went
to a dermatology service and was treated with clofazimine, after which
the lesion disappeared. However, the lesion reappeared 1 year later.
HIV serologic analysis was performed in 2002, and the results were positive.
The patient then began treatment for HIV infection. He is currently being
monitored at the specialized referral unit in Belem. He does not have
any opportunistic infections and is not taking any antiretroviral drugs.
The patient came to the dermatology service of the Tropical Medical Center,
where dermatologic and histopathologic examinations were conducted and
CD cell counts and HIV viral load were measured. Dermatologic aspects
of the lesion included an erythematous-infiltrated, hypertrophic plaque
with a verrucous surface ≈4 cm long in the distal third of the medical
aspect of the right thigh (Figure). A punch biopsy
specimen of brown smooth skin 0.35 cm in diameter in an epidermal disk
was fixed in formalin. Microscopy of skin sections containing epidermis
showed compact keratinization, parakeratotic foci, and irregular hyperplasia
with a pseudoepitheliomatous area. A highly dense, nodular, diffuse inflammatory
infiltrate was observed at all levels of the dermis. It consisted of macrophages
and numerous multinucleated cells, most of them of the foreign body type.
Fibroplasia was also noted. Abundant, round parasitic elements surrounded
by a double membrane and containing a basophilic nucleus were found in
tissues, as well as other anucleated, intracellular, and free parasites
that formed chains of >2 cells (Appendix
Figure). Jorge Lobo disease was diagnosed. Laboratory results showed
146 CD4 cells/μL, 251 CD8 cells/μL, a CD4:CD8 ratio of 0.42, and
60,000 copies of HIV viral RNA/mL.
Since a cytotoxic response is observed in Jorge Lobo disease (7),
HIV infection may increase the susceptibility to infection with L.
loboi. Patients with AIDS show a predisposition to diverse fungal
infections that classically affect different organs and systems. An association
between Jorge Lobo disease and AIDS has not been reported. However, since
Jorge Lobo disease is restricted to specific areas of the world and the
number of AIDS cases is increasing, especially in Latin America, a possible
correlation between HIV infection and Jorge Lobo disease should be considered
because of the associated cellular immunodeficiency.
The patient showed no signs of other opportunistic infections classically
associated with AIDS, and he was not taking any antiretroviral drugs.
His initial infection manifested as cutaneous lesions that occur in Jorge
Lobo disease. Despite the cellular immunodeficiency, we did not observe
atypical dissemination of the lesions. Further studies should be conducted
to evaluate the relationship between the cellular immunosuppression of
AIDS and secondary infection with L. loboi. In addition, epidemiologic
studies are needed to determine the association of AIDS with Jorge Lobo
disease.
References
- Restrepo A. Treatment
of tropical mycosis. J Am Acad Dermatol. 1994;31:S91–102.
- Taborda PR, Tabora VA, McGinnis MR. Lacazia
loboi gen. nov., comb. nov., the etiologic agent of lobomycosis.
J Clin Microbiol. 1999;37:2031–3.
- Kwon-Chung C. Phylogenetics
of fungi that are pathogenic to humans. Clin Infect Dis. 1994;19:S1–7.
- Haubold EM, Aronson JF, Cowwan DF. Isolation
of fungal rDNA from bottlenose dolphin skin infected with Loboa loboi.
Med Mycol. 1998;36:263–7.
- Funchs J, Milbradt R, Pecher SA. Lobomycosis
(keloidal blastomycosis): case reports and overview. Cutis. 1990;46:227–34.
- Elsayed S, Kuhn SM, Barber D, Church DL, Adams S, Kasper R. Human
case of lobomycosis. Emerg Infect Dis. 2004;10:715–18.
- Pecher SA, Funchs J. Cellular
immunity in lobomycosis (keliodal blastomycosis). Allergol Immunopathol
(Madr). 1988;16:413–5.
Suggested citation
for this article:
Xavier MB, Ferreira
MMR, Quaresma JAS, de Brito AC. HIV and lacaziosis, Brazil [letter]. Emerg
Infect Dis [serial on the Internet]. 2006 Mar [date cited]. Available
from http://www.cdc.gov/ncidod/EID/vol12no03/05-1426.htm
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