Leishmania infantum AS A CAUSATIVE AGENT OF CUTANEOUS LEISHMANIASIS IN THE STATE OF MATO GROSSO DO SUL, BRAZIL

Cutaneous leishmaniasis is caused by different species of theLeishmania genus. Leishmania(Leishmania) infantum, causing cutaneous leishmaniasis, has been described in patients living in areas where visceral leishmaniasis is endemic. In this study, it was possible to characterize this species in seven slides from cutaneous tissue imprints from patients with cutaneous leishmaniasis in the State of Mato Grosso do Sul, Brazil.

Attempts using cryotherapy to achieve more rapid healing in patients with cutaneous leishmaniasis due to L. braziliensis braziliensis

The use of cryotherapy as an adjunct to systemic antimonial therapy (Clucantime) was studied in 17 patients with a total of23 skin lesions of leishmaniasis in an area where L. braziliensis braziliensis is the species in circulation. Cryotherapy did not speed healing and has been discarded as an auxiliary therapeutic measure in our practice. However this technique may be suitable for species o/Leishmania causing more limited superficial lesions in man without the danger of metastasis.

Human mucocutaneous leishmaniasis in Três Braços, Bahia - Brazil: an area of Leishmania braziliensis braziliensis transmission. II. Cutaneous disease. Presentation and evolution

The clinical records of 182 patients with cutaneous leishmaniasis probably due to Leishmania braziliensis braziliensis are analysed. 68% had a single lesion which was usually an ulceron the lower anterior tibial third. Many had short histories of one to two months and all age groups were represented 13% had closed lesions of a verrucose or plaque like nature. Evolution of these skin lesions after treatment was related to the regularity of antimony therapy. Although healing usually occurred in three months, the time to scarring after commencing treatment was variable and related to the size ofthe lesion (p < 0.01). Usually if sufficient antimony treatment was given the lesion closed. Seven of the ten patients with initially negative leishmanin skin tests converted to positive after treatment. A significant decline of indirect fluorescent antibody titres occurred in patients followed, during and after therapy.

The use of different concentrations of leishmanial antigen in skin testing to evaluate delayed hypersensitivity in american cutaneous leishmaniasis

Three concentrations of Leishmania mexicana amazonensis sonicated whole promastigote antigen (30, 9.6 and 3 ug N in 0.1 ml) wereprepared and 0.1 ml of each inoculated intradermally intopatients who live in one endemic leishmaniasis region in Brazil. Patients were divided into groups with active cutaneous leishmaniasis (ACL), healed cutaneous leishmaniasis (HCL), mucosal leishmaniasis (ML), and Controls (C). Skin reactions were recorded by measuring induration 48 hours after inoculation. Skin tests using 9.6 ugN/0.1 mlyielded the best diagnostic resultssince 97% of 30 patients with active lesions (cutaneous or mucosal) and 83% with HCL showed reactions of 5 mm orgreater as compared with 4% Controls. Tests using 30ug N/O. 1 ml causedan unacceptable levei of skin reactions with necrosis (10% of ACL patients tested and 17% of HCL, respectively). Tests using 3 ug N/O. 1 ml were less sensitive since only 87% of patients with active lesions and 68% with HCL had reactions of 5mm orgreater. The 3 ug N/O. 1 ml dose was utilized to ask the questions whether skin delayed hypersensitivity decreased with time after the initial lesion and whether mucosal involvement is associated with enhaced hypersensitivity to leishmanial antigen. Decreased delayed hypersensitivity was noted only in those patients who had an initial lesion more than 30 years ago. The mean induration of the reaction in 10 patients with ML was 11.3 mm ± 7.15, in 41 patients with HCL, 9.27 mm ± 6.78 and in 20patients with ACL 10. 7 mm ± 6.10 mm. The percent of patients with 5 mm orgreater induration was ML 80%, HCL 71%, ACL 90%. Thus, we could not confirm an association between enhanced delayed hypersensitivity and mucosal involvement in leishmaniasis.

Leishmania mexicana in Proechimys iheringi denigratus Moojen (Rodentia, Echimyidae) in a region endemic for American cutaneous leishmaniasis

Three isolates of Leishmania were recovered from five of 27 specimens of the rodent Proechimys iheringi denigratus Moojen captured near Três Braços in the Atlantic Forest region of Bahia, Brazil. Two of these isolates were recovered from hamsters inoculated with a pooled triturate of liver, spleen and skin tissue from apparently healthy P. i. denigratus. The third isolate was recovered from a triturate of only skin tissue from another. Metastasis was observed in the inoculated hamsters, the parasites grew abundantly in artificial media and a typical suprapylarial pattern of infection in Lutzomyia longipalpis was produced indicating that the parasites belong to the Leishmania mexicana complex. All isolates reacted with Leishmania mexicana mexicana and Leishmania mexicana amazonensis monoclonal antibodies. The isoenzyme analysis differentiated these isolates from standard isolates of L. m. mexicana, L. m. amazonensis, L. m. aristedesi, L. m. pifanoi, L. m. garnhami and L. m. ssp.(Goiás-W. Barbosa). These isolates seem to be a subspecies of L. mexicana very closely related to L. m. amazonensis from which they differ by decreased electrophoretic mobility of GPI, PEP and ALAT. This is the first record of the isolation of a parasite of thegenus Leishmania in a rodent captured in the State of Bahia.

American cutaneous leishmaniasis: presentation and problems of patient management

We report our experience with the diagnosis and treatment of 60 patients with American cutaneous leishmaniasis. They were infected in Panama (55), Brazil (4) or Colombia (I). Among 35 patients with a 3 week exposure in Panama, the mean maximum incubation period was 33 days (range 4-81 days). Diagnosis was delayed an average of 93 days after onset of skin lesions, due to the patient's delay in seeking medical attention (31 days), medical personnel's delay in considering the diagnosis (45 days), and the laboratory's delay in confirming the diagnosis (17 days). Forty-four patients (73%) developed ulcers typical of cutaneous leishmaniasis. Sixteen additional patients (27%) had atypical macular, papular, squamous, verrucous or acneiform skin lesions that were diagnosed only because leishmanial cultures were obtained. Of the 59 patients treated with pentavalent antimonial drugs, only 34 (58%) were cured after the first course of treatment. Lesions which were at least 2 cm in diameter, ulcerated, or caused by Leishmania braziliensis were less likely to be cured after a single course of treatment than were lesions smaller than 2 cm, nonulcerated or caused by Leishmania mexicana or Leishmania donovani.

Spontaneous regional heading of extensive skin lesions in diffuse cutaneous leishmaniasis (DCL)

The authors report a case of diffuse cutaneous leishmaniasis, with longstanding evolution and presenting with diffuse infiltrated lesions rich in amastigotes in the absence of mucosal involvement. In situ characterization with monoclonal antibodies revealed Leishmania amazonensis. Large regional lesions have presented spontaneous healing without specific therapy. Considering that DCL presents with a defect in the cellular immune response, thisfact demonstrate that this patient may develop a regional cellular immune response enough to destroy the parasites and to produce clearing of some lesions.

Evaluation of a direct immunofluorescent antibody (difma) test using Leishmania genus - specific monoclonal antibody in the routine diagnosis of cutaneous leishmaniasis

A direct immunofluorescent antibody (DIFMA) test using a Leishmania genus- specific monoclonal antibody was evaluated in the routine diagnosis of cutaneous leishmaniasis (CL) in Ecuador. This test was compared with the standard diagnostic techniques of scrapings, culture and histology. Diagnostic samples were taken from a total of 90 active dermal ulcers from patients from areas of Ecuador known to be endemic for cutaneous leishmaniasis. DIFMA was positive in all lesions. It was shown to be significantly superior to standard diagnostic methods either alone or in combination. The sensitivity of DIFMA did not diminish with chronicity of lesions. This test proved to be extremely useful in the routine diagnosis of CL because it is highly sensitive, is easy to use and produces rapid results.

Diabetes melutus associated with pentamidine isethionate in diffuse cutaneous leishmaniasis

The authors report a case of a male patient from Bacabal, MA with diffuse cutaneous leishmaniasis (DCL), for at least nine years, with 168 lesions on his body. These were tumour-like nodules with some ulceratmi. He usedpentavalent antimonial (glucantime®) and an association of gamma interferon plus glucantime with improvement of the lesions but relapsed later. Recently, pentamidine isethionate (pentacarinat®) was given a dosage of 4mg/kg/weight/day on alternate days for 20 applications. After 3 months a similar course of 10 application was given 2 times. Later he developed diabetic signs with weight loss of 10kg, polydypsia, polyuria and xerostomia. The lower limbs lesions showed signs of activity. Blood glucose levels normalised and remain like this at moment. Attention is drawn to the fact that pentamidine isethionate should be used as a therapy option with care, obeyng rigorous laboratory controls including a glucose tolerance test.

Histopathology of human American cutaneous leishmaniasis before and after treatment

Chemical therapy for the treatment of leishmaniasis is still inadequate, and a number of drugs and therapeutic programs are being tested. Besides treatment, the ultimate goal is an effective cure, and histopathological analyses of the lesion cicatrices constitute an important measure of treatment success, or otherwise, in this respect. In this paper, we describe histopathological patterns in cases of American cutaneous leishmaniasis in 32 patients from the municipality of Caratinga, Minas Gerais, Brazil, before and after treatment with the following therapeutic methodos: l) leishvacin + glucantime; 2) leishvacin + BCG associated with glucantime; 3) glucantime; 4) leishvacin + BCG. Lesion fragments were collected from all patients by biopsy prior to, and approximately 30 days after, each treatment which resulted in a clinical diagnosis of cure. Following the analysis of slides, the preparations were described from a histopathological point of view and grouped taking into account the prevalence or significance of the characteristic elements. This process resulted in the following classification: 1. exsudative reaction (ER); 2. exsudative giant cell reaction (EGCR); 3. exsudative productive reaction (EPR); 4. exsudative productive giant cell reaction (EPGCR); 5. exsudative productive necrotic reaction (EPNR); 6. necrotic exsudative reaction (NER); 7. productive exsudative reaction (PER), 8. productive giant cell reaction (PGCR); 9. productive exsudative giant cell reaction (PEGCR); 10. productive exsudative giant cell granulomatous reaction (PEGCGR); 11. productive reaction (PR) and 12. productive cicatricial (cure) reaction (PCR). After this analysis, it was noted that clinical cure did not always coincide with histopathological cure.

Mefloquine in the treatment of cutaneous leishmaniasis

Three cases of cutaneous leishmaniasis were treated orally with a mefloquine dose of 4.2mg/kg/day for six days in the Teaching Hospital of the Faculdade de Medicina do Triângulo Mineiro, Uberaba, MG, Brazil. Three weeks later a new series was repeated. No patient was cured.

Evaluation of IFN-gamma and TNF-alpha as immunological markers of clinical outcome in cutaneous leishmaniasis

To evaluate if IFN-gamma and TNF-alpha levels could be used as markers of therapeutic response in cutaneous leishmaniasis, 54 patients with history of one ulcerated cutaneous lesion, with up to 30 days onset, were enrolled in the study. IFN-gammaand TNF-alpha were measured by ELISA in lymphocyte cultures supernatant before and 60 days after initiating therapy. Cure was considered to be a complete healing of lesion 60 days after treatment. IFN-gamma and TNF-alpha levels were similar in both groups of patients before therapy. There was a tendency to increase IFN-gamma levels in patients that were cured in 60 days, however the values did not reach statistical significance. In both groups of patients, TNF-alpha levels were similar before therapy and fell significantly after treatment, irrespective of cure or maintenance of active lesion.