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 ::  Abstract
 ::  Epidemiology
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Year : 2003  |  Volume : 49  |  Issue : 1  |  Page : 50-4

Cutaneous leishmaniasis: an overview.

Consultant Dermatologist, Lincoln County Hospital Lincoln LN2 5QY United Kingdom.

Correspondence Address:
N C Hepburn
Consultant Dermatologist, Lincoln County Hospital Lincoln LN2 5QY United Kingdom.

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0022-3859.928

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 :: Abstract 

Leishmaniasis is a major world health problem, which is increasing in incidence. In Northern Europe it is seen in travellers returning from endemic areas. The protozoa is transmitted by sandflies and may produce a variety of clinical syndromes varying from a simple ulcer to fatal systemic disease. This review considers the management of simple cutaneous leishmaniasis. Patients usually have a single ulcer that may heal spontaneously, requiring only topical, or no treatment at all. Lesions caused by Leishmania braziliensis may evolve into the mucocutaneous form, 'espundia', and should be treated with systemic antimony. Sodium stibogluconate 20mg/kg/day i.v. for 20 days is the appropriate first line treatment in these cases. Although it may cause transient bone marrow suppression, liver damage, a chemical pancreatitis, and disturbances in the electrocardiogram, it appears safe. The success of treatment should be assessed 6 weeks after it has been completed and patients should be followed up for 6 months.

Keywords: Animal, Antimony Sodium Gluconate, therapeutic use,Antiprotozoal Agents, therapeutic use,Cryotherapy, Human, Leishmania, classification,Leishmaniasis, Cutaneous, diagnosis,epidemiology,pathology,therapy,Meglumine, therapeutic use,Organometallic Compounds, therapeutic use,

How to cite this article:
Hepburn N C. Cutaneous leishmaniasis: an overview. J Postgrad Med 2003;49:50

How to cite this URL:
Hepburn N C. Cutaneous leishmaniasis: an overview. J Postgrad Med [serial online] 2003 [cited 2023 May 28];49:50. Available from:

Cutaneous Leishamaniasis, first descriptions of which can be traced back to the 9th century (Balkh sore), remains a major world health problem in the 21st century. The Leishmaniases are caused by the protozoa leishmania, which is transmitted by the bite of an infected female sandfly. The result of infection can vary from a chronic skin ulcer, to erosive mucosal disease with progressive destruction of the nasopharynx and severe facial disfigurement, to a life threatening systemic infection with hepato-splenomegly. The resulting syndrome depends upon a complex interaction between a specific species of leishmania and the genetic and immunological status of the host [Figure - 1].

  ::   Epidemiology Top

There are about 1.5 million new cases of cutaneous leishmaniasis (CL) each year of which over 90% occur in Afghanistan, Algeria, Iran, Iraq, Saudi Arabia, Syria, Brazil and Peru.[1] However, CL often occurs in specific pockets – not only of place but also in time – for example Delhi boil affected 40,000 people in the early 1940s but is rarely seen in Delhi today.

The geographical distribution of CL is mainly determined by the sandfly vectors (Phlebotomus sp and Lutzomyia sp). They live in dark, damp places, and are relatively weak flyers, with a range of only 50 metres from their breeding site. Unlike mosquitos, they fly silently and their small size (2-3mm long) allows them to penetrate mosquito nets. They are most active in the evening and at night. Sandfly numbers are related to natural factors such as rainfall,[1],[2] and may increase with global warming. Decreased insecticide spraying for malaria, poor waste disposal and heaps of construction waste encourage breeding has led to an increase in the prevalence of peri-domestic cases.[3],[4]

Most infections exist as zoonoses amongst wild animals, such as rodents and dogs, and are most prevalent in rural or forest areas. Whilst man is usually an incidental host, such infections are by no means uncommon – in endemic areas up to 9% of the healthy population may have positive leishmanin skin test - indicative of an earlier, often asymptomatic, infection.[5] In India simple CL is usually due to L. tropica and man is the most common reservoir.

In India Post Kala Azar Dermal Leishmaniasis (PKDL) is the most common cutaneous manifestation of leishmaniasis. Although not a strictly a form of CL it is important particularly in North Eastern India (particularly in Bihar State) where Visceral Leishmaniasis is epidemic.[6] This type occurs in patients who were treated for visceral leishmaniasis, caused by L. donovani, some months or years earlier. The aetiology is unknown but possibilities include inadequate treatment or re-infection of patients previously cured of visceral leishmaniasis. Lesions are variable but often consist of hypo-pigmented macules, papules or nodules; they do not ulcerate, and may persist for months or years. These patients may play an important role as reservoirs of infection.[7]

In Southern Europe, where leishmaniasis is endemic, the incidence of visceral disease is increasing, often in association with HIV-1 infection. Many such patients develop unusual cutaneous manifestations.[8],[9]

In North America and Northern Europe CL is a disease seen in returning travellers, such as those conducting rural field studies, tourists and the military. Unfortunately many of those infected are ignorant of the risks, take no personal protective measures and experience delays in diagnosis followed by inappropriate treatment upon their return.[10]

  ::   Pathology Top

The life-cycle consists starts with inoculated promastigotes which are phagocytosed by macrophages, once inside they loose their flagella and become amastigotes which multiply by binary fission. Infected macrophages then burst, releasing their amastigotes to infect other macrophages. The subsequent fate of the amastigotes depends upon parasite and host factors, which are poorly understood. Viscerotrophic species, such as L. donovani, migrate throughout the reticulo-endothelial system, giving rise to visceral leishmaniasis; whereas dermotrophic species, such as L. major, usually remain close to the inoculation site, causing cutaneous disease. Any spread of dermotrophic species tends to be late, and only to adjacent skin (producing satellite lesions), or to lymphatics and regional lymph nodes. These phenotypic distinctions are not absolute. L. braziliensis is able to migrate to the oropharyngeal mucosa where it may remain dormant for many years before reactivating to cause the destructive mucocutaneous form ‘espundia’. There are reports of L. tropica causing visceral disease.[11] In post-kala-azar dermal leishmaniasis the viscerotrophic parasite becomes dermotrophic as a consequence of treatment,[12] as it may in those with HIV infection.[9]

In all forms of leishmaniasis the presence of amastigotes within the cells of the mononuclear phagocytic system remains the hall mark of the disease, although at times they may be difficult to detect. Infected macrophages measure 20-30 ?m across whereas amastigotes (known as Leishman-Donovan bodies) are round to oval structures measuring only 2-5 ?m. They are surrounded by a plasma membrane and contain both a relatively large, deeply basophilic, nucleus and a smaller, deeply staining, rod-shaped kinetoplast of extra-nuclear DNA (from the base of the flagellum which is lost in the conversion from promastigote to amastigote). Although H & E will demonstrate amastigotes, a Giemsa stain is preferred by many - as it stains the flagellum bright red.[13],[14]

In early cutaneous lesions, the dermal infiltrate is mainly made up of macrophages filled with amastigotes. There are relatively few lymphocytes and plasma cells. As the lesion develops more lymphocytes and plasma cells appear and the superficial dermis becomes oedematous. The overlying epidermis becomes hyperkeratotic and subsequently breaks down to form an ulcer covered with a coagulum of hyperkeratotic debris, dried exudate, dead cells and a mixture of live and dead organisms. Over the following months, there is a gradual decrease in the number of amastigotes and macrophages, leaving a granulomatous infiltrate consisting of lymphocytes, epithelioid cells and multinucleate giant cells. At this stage it may be difficult or impossible to detect organisms in H&E, or Giemsa, stained sections. Ultimately, either the patient’s immune response is able to eliminate the infection and effect a spontaneous cure, or it fails and a chronic form of leishmaniasis develops.

  ::   Clinical features Top

Infection, following a bite from an infected sandfly, may remain sub-clinical or develop, after an incubation period of 1 to 12 weeks, into a papule that enlarges and then ulcerates. A typical lesion is a painless ulcer with a raised, indurated, margin and a necrotic base that is often covered with an adherent crust of dried exudate. Most patients have 1 or 2 lesions, usually on exposed sites, varying in size from 0.5 to 3 cm in diameter.[15] There is, however, considerable variation: some lesions do not ulcerate, others develop sporotrichoid nodular lymphangitis. Secondary bacterial infection is common which can lead to pain. Most lesions heal over months or years, leaving an atrophic scar. In general half those lesions caused by L. major or L. mexicana will have healed in 3 months, those caused by L. tropica take longer – about 10 months - and those due to L.brazilinesis persist much longer.[16],[17] Natural resolution leads to partial resistance to re-infection.[18]

  ::   Diagnosis Top

The diagnosis is often made on the basis of a clinically typical lesion in conjunction with an appropriate history of exposure. However, there are a number of mimics [Table - 1], and the treatment may be toxic, so pathological confirmation should be sought - preferably by demonstrating the organism in tissue and /or culture. Unfortunately this is not always possible in practice. In a study of 475 cases due to L. major in Saudi Arabia the parasite was demonstrated by smear in 50-80% (depending on the investigator and the technique used), by skin biopsy in 70% and by culture in only 50%. When all 3 methods were combined the parasite was still not detected in 10-20% of cases.[19] The problem is often greater in New World disease, particularly in lesions over 6 months old.[20],[21] The best approach is to use several methods.

Take a full thickness biopsy from the infiltrated margin of the lesion and divide it into 3 parts: to prepare an impression smear, for histological examination and for culture. Try to select a lesion, which is not secondarily infected, clean it thoroughly with 0.9% saline, or 70% alcohol, to remove the crust and any pus. If infection is present, a second clean with 6% hydrogen peroxide is helpful prior to injecting 2% lignocaine with adrenaline. Although a punch may be used, I prefer an elliptical biopsy taken with a scalpel. Haemostasis is achieved by pressure as sutures generally pull through.

Impression smears are made by gently pressing the skin biopsy against a glass microscope slide 4-5 times after which the slide is dried in air then fixed in 95% ethanol for 3 minutes. They can then be stained with Giemsa or H & E and examined for the presence of amastigotes.

Specimens for culture should be transported in ‘sloppy Evans’ media and subsequently cultured on Evans Modified Tobies media or NNN media.[22] Cultured organisms may be typed by isoenzyme analysis.[22]

Alternative methods of obtaining tissue for diagnosis include needle aspirates and slit skin smears. A needle aspirate is obtained by using a 2ml leur lock syringe with a 20 gauge needle, containing 0.3ml 0.9% saline. The needle is inserted through intact skin and 0.1 ml is injected into the edge of the lesion. The needle is then moved back and forth rotating it and applying suction at the same time to cut small pieces of tissue from the edge of the needle track, which are then aspirated. The aspirate can be used to inoculate cultures and prepare smears. Slit-skin smears are made by squeezing the edge of the lesion between thumb and forefinger, making a shallow slit 1mm deep in the pinched skin with a scalpel and then scrapping the cut edge.[22]

Attempts have been made to utilise molecular technology to improve diagnostic speed, convenience and specificity -but they remain research tools. Monoclonal antibodies can demonstrate parasites in paraffin sections but are often species specific.[23] PCR methods are useful for confirming the diagnosis and offer improved sensitivity over microscopy and culture,[24] however, problems exist with the identification of individual species, particularly causing American CL.

Serology is unhelpful for cutaneous disease because antibodies tend to be undetectable or present in low titre.[6] The Leishmanin skin test, which is analogous to the tuberculin test, detects cell-mediated immunity; becomes positive once the lesions begin to crust and remains so indefinitely. It cannot distinguish between past and present infection.[5]

  ::   Treatment Top

There is no single optimal treatment for all forms of CL. Indeed, the natural diversity of the parasites, together with the wide spectrum of clinical disease that they produce, means one is unlikely to evolve in the foreseeable future. In an ideal world each endemic area would establish its own optimum treatment regimen based on efficacy and toxicity, without neglecting the practical difficulties of administration and cost. In reality data tends to be extrapolated from one situation to another with variable results.

The situation is complicated by the self-healing nature of CL. Adequately controlled therapeutic trials are therefore essential to assess the efficacy of any new treatment. Unfortunately, the literature abounds with reports of ‘effective’ treatments, based on case reports and uncontrolled, small, series making it difficult to assess their efficacy.

Fortunately, there are some guiding principles. Lesions due to different species vary in both their severity and response to treatment – American CL tends to be more severe and longer lasting than Old World CL. As most Old World lesions heal rapidly without treatment an expectant approach may be appropriate – particularly for those patients living in endemic areas because spontaneous healing is associated with the development of protective immunity. Lesions on cosmetically or functionally important sites, such as the face or hands, those with associated lymphangitis and those with multiple or persistent lesions are best given active treatment. Local treatment is appropriate for those with early non-inflamed lesions and systemic therapy for those with multiple or more complicated lesions.

In American CL the crucial first step is to decide whether or not L.braziliensis could be the infecting organism because, until further information is available, all such cases must be considered capable of progressing to mucocutaneous disease and therefore require adequate systemic therapy. Hence, if the patient contracted CL in any area in which L.braziliensis occurs (i.e. Belize, Colombia, Costa Rica, Guiana, Honduras, Surinam, Panama, Venezuela, the western slopes of the Andes and the Argentinean highlands),[25] the parasite must be identified before alternatives to optimal systemic therapy can be considered.

The pentavalent antimony derivatives sodium stibogluconate (Pentostam,Glaxo Wellcome, UK) and meglumine antimoniate (Glucantime, Rhone-Poulenc Rorer, France), developed in the 1940s, remain the mainstay of systemic treatment. They are similar in both efficacy and toxicity – any reported differences can be explained by their differing antimony concentrations (Pentostam 100mg/ml; Glucantime 85mg/ml). Their mode of action is not known, although they inhibit glycolysis and fatty acid oxidation in leishmania.[7] Their efficacy is well established - provided they are given in adequate doses and for an adequate length of time.[16],[26]

In American CL sodium stibogluconate, 20mg/kg/day for 20 days is an appropriate course curing over 90% of cases in a single course.[6],[15],[27],[28] Shorter courses may be adequate for Old World disease. It is best given once daily by slow i.v.(or i.m.) injection. Toxicity is common, and appears dose related, most patients develop malaise, anorexia, myalgia and arthralgia after 14 days treatment. This is associated with elevations in serum aminotransferases, a chemical pancreatitis, a mild leucopenia, thrombocytopenia, and flattening of the T-waves on the ECG. Treatment should be monitored but in most cases these abnormalities settle rapidly once treatment is stopped.[16],[27] Lesions become less indurated, flatten, then re-epithelialise as they respond to treatment. However, healing continues after treatment has stopped so the need for additional treatment should delayed for 4-6 weeks. This also allows patients to recover from the toxicity.[28],[29] A protocol is suggested in [Figure - 2].

Rifampicin has been reported to be efficacious but there are no good controlled trials to support its use and furthermore its use in areas where tuberculosis and leprosy are endemic should be avoided.[17] Alternative systemic agents include aminosidine (paromomycin), pentamidine and ketoconazole, but they have yet to find a place in routine clinical practice.[7] The most promising oral drug today is miltefosine. In an open label study in Colombia, four weeks treatment with 133 and 150mg of miltefosine daily cured 100% and 89% respectively.[29]

Local and topical therapy is an important option for those patient not at risk of mucocutanous disease. Local injection of sodium stibogluconate, or meglumine antimoniate, is useful for early, non-inflamed lesions. Technique is important – infiltrate 1-3ml around the lesion to produce complete blanching at the base. It may be repeated on alternate days or given weekly until they heal.[16],[30],[31] Aminosidine (paromomycin) ointment (15% paromomycin, 12% methyl benzethonium chloride in white soft paraffin) applied twice daily for 10 days is effective for L.major.[31] and may also be useful for L.mexicana.[7] It causes considerable local irritation, but less irritant derivatives have been less effective. Cryotherapy is also useful for small lesions (<1cm diameter). Apply two 20s freeze-thaw cycles to the whole lesion, assess response at intervals of 3 weeks and repeat once or twice if necessary.[31] Lesions can also be treated by local excision, curettage or by electrodessication but are probably associated with a higher risk of relapse.[7] The most recent topical agent to be investigated is the topical immunomodulator, Imiquimod, which was developed to treat genital warts. It produced a 90% cure rate in patients who had failed to respond to antimonials alone when it was used in conjunction with antimonials in Peru.[32] A treatment protocol is suggested in [Figure - 2].

  ::   Follow-up Top

Patients should be monitored until the lesions have fully healed and the infiltration has resolved. Most relapses occur within 3-6 months after successful treatment,[15],[31] so follow up at 6 months is appropriate. Thereafter patient should be warned that relapse is possible and observe their scar for thickening, crusting or ulceration. Those who relapse should be given a full course of systemic antimony in the first instance.

 :: References Top

1.Ashford RW, Desjeux P, de Raadt P. Estimation of population at risk of infection and number of cases of leishmaniasis. Parasitol Today 1992;8:104-5.  Back to cited text no. 1    
2.Gonzalez R, De Sousa L, Devera R JA, Ledezema E. Seasonal and nocturnal domiciliary human landing/biting behaviour of Lutzomyia (lutzomyia) evansi and Lutzomyia (Psychodopygus) panamensis (diptera; Psychodidae) in a periurban area of a city on the Caribbean coast of eastern Venezuela (Barcelona; Anzoategui State). Trans R Soc Trop Med Hyg 1999;93:361-4.  Back to cited text no. 2    
3.Tayeh A, Jalouk L, Cairncross S. Twenty years of cutaneous leishmaniasis in Aleppo, Syria. Trans R Soc Trop Med Hyg 1997;91:657-9.  Back to cited text no. 3    
4.Brandao-Filho SP, Campbell-Lendrum D, Brito ME, Shaw JJ, Davies CR. Epidemiological surveys confirm an increasing burden of cutaneous leishmaniasis in north-eastern Brazil. Trans R Soc Trop Med Hyg 1999;93:488-94.  Back to cited text no. 4    
5.Weigle KA, Valderrama L, Arias AL, Santrica C, Saravia NG. Leishmanin standardization and evaluation of safety, dose, storage, longevity of reaction and sensitization. Am J Trop Med Hyg 1991;44: 260-71.  Back to cited text no. 5    
6.Herwaldt BL. Leishmaniasis. Lancet 1999;354:1191-9.  Back to cited text no. 6    
7.Gilles HM (Ed). Protozoal Diseases. Arnold, London: 1999.  Back to cited text no. 7    
8.Rosenthal E, Marty P, Poizot-Martin I, Reynes J, Pratlong F, Lafeuillade A, et al. Visceral leishmaniasis and HIV-1 co-infection in southern France. Trans R Soc Trop Med Hyg 1995;89:159-62.  Back to cited text no. 8    
9.Ara M, Maillo C, Peon G, Clavel A, Cuesta J, Grasa MP, et al. Visceral leishmaniasis with cutaneous lesions in a patient infected with human immunodeficiency virus. Br J Dermatol 1998;139:114-7.  Back to cited text no. 9    
10.Herwaldt BL, Stokes SL, Juranek DD. American cutaneous leishmaniasis in U.S. travellers. Ann Intern Med 1993;118:779-84.  Back to cited text no. 10    
11.Magill AJ, Grogl M, Gasser RA, Sun W, Oster CN. Visceral infection caused by Leishmania tropica in veterans of Operation Dessert Storm. N Engl J Med 1993;328:1383-7.  Back to cited text no. 11    
12.Kubba R, Al-Gindan Y. Leishmaniasis. Dermatol Clinics 1989;7:331-51.  Back to cited text no. 12    
13.Kalter DC. Cutaneous and mucocutaneous leishmaniasis. Progr Derm 1989;23:1-11.  Back to cited text no. 13    
14.Lever WF, Schamberg-Lever G. Histopathology of the skin. 7th edn. Philadelphia: Lippincott; 1990.  Back to cited text no. 14    
15.Hepburn NC, Tidman MJ, Hunter JAA. Cutaneous leishmaniasis in British troops from Belize. Br J Dermatol 1993;128:63-8.  Back to cited text no. 15    
16.Bryceson A. Therapy in Man In: Peters W, Killick-Kendrick R edrs. The leishmaniases in biology and medicine. London: Academic Press; 1987. pp. 847-907.  Back to cited text no. 16    
17.Herwaldt BL, Arana BA, Navin TR. The natural history of cutaneous leishmaniasis in Guatemala. J Infect Dis 1992;165:518-27.  Back to cited text no. 17    
18.Locksley RM, Louis JA. Immunology of leishmaniasis. Curr Opin Immunol 1992;4:413-8.  Back to cited text no. 18    
19.Kubba R, Al-Gindan Y, El-Hassan AM, Omer AHS. Clinical diagnosis of cutaneous leishmaniasis (oriental sore). J Am Acad Derm 1987;16:1183-9.  Back to cited text no. 19    
20.Navin TR, Arana FE, de Merida M, Avana BA, Castillo AL, Silvers DN. Cutaneous leishmaniasis in Guatemala: comparison of diagnostic methods. Am J Trop Med Hyg 1990;42:36-42.  Back to cited text no. 20    
21.Herwaldt BL, Arana FE, Navin TR. The natural history of cutaneous leishmaniasis in Guatemala. J Infect Dis 1992;165;518-27.  Back to cited text no. 21    
22.Evans D. Handbook on Isolation, characterisation and cryopreservation of Leishmania. Geneva: UNDP/World Bank/WHO(TDR); 1989.  Back to cited text no. 22    
23.Biddlestone LR, Hepburn NC, McLaren KM. A clinico-pathological study of cutaneous leishmaniasis in British troops from Belize. Trans R Soc Trop Med Hyg 1994;88:672-6.  Back to cited text no. 23    
24.Andresen K, Gaafar A, El-Hassan, AM Ismail A, Dafalla M, Theander TG, et al. Evaluation of the polymerase chain reaction in the diagnosis of cutaneous leishmaniasis due to Leishmania major: a comparison with direct microscopy of smears and sections from lesions. Trans R Soc Trop Med Hyg 1996;90:133-5.  Back to cited text no. 24    
25.Lainson R, Shaw JJ. Evolution, classification and geographical distribution. In: Peters W, Killick-Kendrick R (eds). The leishmaniases in biology and medicine, vol 1. London: Academic Press; 1987.   Back to cited text no. 25    
26.Berman JD. Chemotherapy for leishmaniasis: Biochemical mechanisms, clinical efficacy and future strategies. Rev Infect Dis 1988;10:560-86.  Back to cited text no. 26    
27.Hepburn NC, Tidman MJ, Hunter JAA. Aminosidine versus sodium stibogluconate for the treatment of American cutaneous leishmaniasis. Trans R Soc Trop Med 1994;88:700-3.  Back to cited text no. 27    
28.Herwaldt BL, Berman JD. Recommendations for treating leishmaniasis with sodium stibogluconate (Pentostam) and review of pertinent clinical studies. Am J Trop Med Hyg 1992;46:296-306.   Back to cited text no. 28    
29.Soto J, Toledo J, Gutierrez P, Nicholls RS, Paddilla J, Engel J, et al. Treatment of American cutaneous leishmaniasis with miltefosine, an oral agent. Clin Infect Dis 2001;33:e57-61.  Back to cited text no. 29    
30.WHO. Control of the leishmaniases. Technical report series 793. Geneva: WHO; 1990.  Back to cited text no. 30    
31.Uzun S, Uslular C, Yucel A, Acar MA, Ozpoyraz M, Memisoglu HR. Cutaneous leishmaniasis: evaluation of 3074 cases in the Cukurova region of Turkey. Br J Derm 1999;140:347-50.  Back to cited text no. 31    
32.Arevalo I, Ward B, Miller R, Meng TC, Najar E, Alvarez E, et al. Successful treatment of drug resistant cutaneous leishmaniasis in humans by use of Imiquimod, an immunomodulator. Clin Infect Dis 2001;33:1847-51.  Back to cited text no. 32    


[Figure - 1], [Figure - 2]


[Table - 1]

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18 Mucocutaneous leishmaniasis in an 11-year-old girl with ataxia telangectasia – case report
Safa S. Elfaituri,Idris Matoug,Hanan Elsalheen,Yousif Belrasali,Fatma Emaetig
Libyan Journal of Medicine. 2015; 10(0)
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19 Contact dermatitis-like cutaneous leishmaniasis in a Libyan HIV patient
Hamida Al-Dwibe,Aisha Gashout,Abdu-Maged Morogum,Said El-Zubi,Ahmad Amro
Parasites & Vectors. 2014; 7(1): 401
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20 Mucocutaneous leishmaniasis must be included in the differential diagnosis of midline destructive disease: Two case reports
R. Crovetto-Martínez,J.M. Aguirre-Urizar,C. Orte-Aldea,I. Araluce-Iturbe,J. Whyte-Orozco,J. Crovetto-De la Torre
Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology. 2014;
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21 Patología dermatológica importada
Roser Savall Lòpez-Reynals
FMC - Formación Médica Continuada en Atención Primaria. 2013; 20(1): 4
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22 Molluscicidal and Leishmanicidal Activity of the Leaf Essential Oil ofSyzygium cumini(L.)Skeelsfrom Brazil
Clarice N. Dias,Klinger A. F. Rodrigues,Fernando A. A. Carvalho,Sabrina M. P. Carneiro,Jose G. S. Maia,Eloisa H. A. Andrade,Denise F. C. Moraes
Chemistry & Biodiversity. 2013; 10(6): 1133
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23 Cheminformatic models based on machine learning for pyruvate kinase inhibitors of Leishmania mexicana
Salma Jamal,Vinod Scaria
BMC Bioinformatics. 2013; 14(1): 329
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24 Lack of association between Gly82Ser, 1704G/T and 2184A/G of RAGE gene polymorphisms and retinopathy susceptibility in Malaysian diabetic patients
Z.X. Ng,U.R. Kuppusamy,R. Poh,I. Tajunisah,A.C.A. Koay,K.C.S. Fong,K.H. Chua
Genetics and Molecular Research. 2012; 11(1): 455
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25 Acute New World cutaneous leishmaniasis presenting as tuberculoid granulomatous dermatitis
Daniel D. Miller, Barbara A. Gilchrest, Amit Garg, Lynne J. Goldberg, Jag Bhawan
Journal of Cutaneous Pathology. 2012; : no
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26 Efficacy of CO2 laser for treatment of anthroponotic cutaneous leishmaniasis, compared with combination of cryotherapy and intralesional meglumine antimoniate : Efficacy of CO2 laser for treatment of anthroponotic cutaneous leishmaniasis
S Shamsi Meymandi, S Zandi, H Aghaie, A Heshmatkhah
Journal of the European Academy of Dermatology and Venereology. 2011; 25(5): 587
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27 Clinical pleiomorphism in human leishmaniases, with special mention of asymptomatic infection : Leishmaniases and clinical pleiomorphism
A. L. Bañuls, P. Bastien, C. Pomares, J. Arevalo, R. Fisa, M. Hide
Clinical Microbiology and Infection. 2011; 17(10): 1451
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28 An experimental approach to studying the effectiveness and safety of meglumine antimoniate formulations
G. Delgado, Y. Sánchez, D. Plaza, A. Mariño, D. Granados
Biomedicine & Pharmacotherapy. 2011;
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29 The influence of natural rubber/Au nanoparticle membranes on the physiology of Leishmania brasiliensis
Carlos G. Barboza-Filho, Flávio C. Cabrera, Renivaldo J. Dos Santos, Jose Antonio De Saja Saez, Aldo E. Job
Experimental Parasitology. 2011;
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30 The influence of natural rubber/Au nanoparticle membranes on the physiology of Leishmania braziliensis
Carlos G. Barboza-Filho, Flávio C. Cabrera, Renivaldo J. Dos Santos, Jose Antonio De Saja Saez, Aldo E. Job
Experimental Parasitology. 2011;
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31 Cutaneous sporotrichoid leishmaniasis resistant to pentavalent antimonial therapy: complete resolution with itraconazole : Cutaneous sporotrichoid leishmaniasis: complete resolution with itraconazole
E. Cozzani, R. Satta, V. Fausti, F. Cottoni, A. Parodi
Clinical and Experimental Dermatology. 2011; 36(1): 49
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32 Photodynamic Therapy: Current Evidence and Applications in Dermatology
Yoojin Lee, Elma D. Baron
Seminars in Cutaneous Medicine and Surgery. 2011; 30(4): 199
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33 New World cutaneous leishmaniasis: Updated review of current and future diagnosis and treatment
Panagiotis Mitropoulos,Pete Konidas,Mindy Durkin-Konidas
Journal of the American Academy of Dermatology. 2010; 63(2): 309
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34 Leishmaniasis in the knee area
Bava Amadeo Javier,Rossi Maria Laura,Seley Celeste,Troncoso Alcides
Asian Pacific Journal of Tropical Medicine. 2010; 3(4): 330
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35 A family with skin lesions
Ozaras, R., Polat, E., Aygun, G., Yemisen, M., Mete, B., Goksugur, N., Tabak, F.
Netherlands Journal of Medicine. 2010; 68(1): 41+-44
36 Leishmaniasis in the knee area
Javier, B.A., Laura, R.M., Celeste, S., Alcides, T.
Asian Pacific Journal of Tropical Medicine. 2010; 3(4): 330-331
37 A chronic mutilating rhinopathy with a delayed diagnosis of mucocutaneous leishmaniasis
Sujith Kumar Karimbil, Sobhana Kumari, Machiyanickel Isac Celine, Augustine Joy
International Journal of Dermatology. 2010; 49(4): 426
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38 Management of Old World Cutaneous Leishmaniasis in Refugee Children :
Joanne Crogan, Hasantha Gunasekera, Nicholas Wood, Mohamud Sheikh, David Isaacs
The Pediatric Infectious Disease Journal. 2010; 29(4): 357-359
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39 Trends in the epidemiology of cutaneous leishmaniasis in a young adult population in Israel: a long-term survey
Daniel Mimouni,Ran D. Balicer,Hagai Levine,Eyal Klement,Yael Bar-Zeev,Nadav Davidovitch,Salman Zarka
International Journal of Dermatology. 2009; 48(6): 611
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40 Immunohistochemistry and polymerase chain reaction on paraffin-embedded material improve the diagnosis of cutaneous leishmaniasis in the Amazon region
Valdir Sabbaga Amato, Felipe Francisco Tuon, Heitor Franco de Andrade, Helio Bacha, Carla Pagliari, Elaine Raniero Fernandes, Maria Irma Seixas Duarte, Vicente Amato Neto, Ricardo Andrade Zampieri, Lucile Maria Floeter-Winter
International Journal of Dermatology. 2009; 48(10): 1091-1095
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41 Correlation of parasitic load with interleukin-4 response in patients with cutaneous leishmaniasis due toLeishmania tropica
Rajesh Kumar,Ram Awatar Bumb,Poonam Salotra
FEMS Immunology & Medical Microbiology. 2009; 57(3): 239
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42 Delay in diagnosis: trauma- and coinfection-related cutaneous leishmaniasis because of Leishmania guyanensis infection
Patrick Mulvaney, Gazelle Aram, Peter R. Maggiore, Heinz Kutzner, John Andrew Carlson
Journal of Cutaneous Pathology. 2009; 36(1): 53-60
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43 Leishmania OligoC-TesT as a Simple, Rapid, and Standardized Tool for Molecular Diagnosis of Cutaneous Leishmaniasis in Peru
Diego Espinosa, Andrea K. Boggild, Stijn Deborggraeve, Thierry Laurent, Cristian Valencia, Rosa Pacheco, Ce´sar Miranda-Vera´stegui, Alejandro Llanos-Cuentas, Thierry Leclipteux, Jean-Claude Dujardin, Philippe Bu¨scher, Jorge Are´valo
Journal of Clinical Microbiology. 2009; 47(8): 2560
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44 Whatman paper (FTA cards) for storing and transferring Leishmania DNA for PCR examination
Fata, A., Khamesipour, A., Mohajery, M., Hosseininejad, Z., Afzalaghaei, M., Berenji, F., Ganjbakhsh, M., Amin-Mohammadi, A.
Iranian Journal of Parasitology. 2009; 4(4): 37-42
45 Correlation of parasitic load with interleukin-4 response in patients with cutaneous leishmaniasis due to Leishmania tropica
Kumar, R., Bumb, R.A., Salotra, P.
FEMS Immunology and Medical Microbiology. 2009; 57(3): 239-246
46 Antiparasitic drugs. Review of the useful drugs in the treatment of classic and emergent parasitic diseases | [Antiparasitarios. Revisión de los fármacos útiles en el tratamiento de parasitosis clásicas y emergentes]
Pérez Arellano, J.L., Carranza, C., Mateos, F.
Revista Espanola de Quimioterapia. 2009; 22(2): 93-105
47 Fissure leishmaniasis: A new variant of cutaneous leishmaniasis
U Bari, A., Ul Bari, A., Ejaz, A.
Dermatology Online Journal. 2009; 15(10): art no 13
48 Tropical dermatology: Tropical diseases caused by protozoa
Lupi, O., Bartlett, B.L., Haugen, R.N., Dy, L.C., Sethi, A., Klaus, S.N., Machado Pinto, J.,Tyring, S.K.
Journal of the American Academy of Dermatology. 2009; 60(6): 897-925
49 Clinical spectrum of nasal leishmaniasis in Muzaffarabad
Journal of the College of Physicians and Surgeons Pakistan. 2009; 19(3): 146-149
50 Leishmania OligoC-TesT as a simple, rapid, and standardized tool for molecular diagnosis of cutaneous leishmaniasis in Peru
Espinosa, D., Boggild, A.K., Deborggraeve, S., Laurent, T., Valencia, C., Pacheco, R., Miranda-Verástegui, C.,Arévalo, J.
Journal of Clinical Microbiology. 2009; 47(8): 2560-2563
51 Cutaneous leishmaniasis with unusual presentation
Yaghoobi, R., Maraghi, S., Bagherani, N.
Iranian Journal of Parasitology. 2009; 4(2): 67-69
52 Trends in the epidemiology of cutaneous leishmaniasis in a young adult population in Israel: A long-term survey
Mimouni, D., Balicer, R.D., Levine, H., Klement, E., Bar-Zeev, Y., Davidovitch, N., Zarka, S.
International Journal of Dermatology. 2009; 48(6): 611-613
53 Cutaneous leishmaniasis in Iraq
AlSamarai, A.M., AlObaidi, H.S.
Journal of Infection in Developing Countries. 2009; 3(2): 123-129
54 Tropical dermatology: Tropical diseases caused by protozoa
Omar Lupi,Brenda L. Bartlett,Reshma Nair Haugen,Lady C. Dy,Aisha Sethi,Sidney N. Klaus,Jackson Machado Pinto,Francisco Bravo,Stephen K. Tyring
Journal of the American Academy of Dermatology. 2009; 60(6): 897
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55 Malaria and leishmaniasis: Current status of chemotherapy, new leads and targets for drug discovery
Pathak, R., Batra, S.
Anti-Infective Agents in Medicinal Chemistry. 2009; 8(3): 226-267
56 Cutaneous leishmaniasis in Damascus
Daæaboul, M.W.T.
Eastern Mediterranean Health Journal. 2009; 15(5): 1084-1097
57 Evaluation of permethrin treated clothing for personal protection against Phlebotomus papatasi (Diptera: Psaychodidae)
Khoobdel, M.
Journal of Entomology. 2008; 5(1): 51-55
58 Efficacy of a weekly cryotherapy regimen to treat Leishmania major cutaneous leishmaniasis
Ibrahim M. Mosleh,Eid Geith,Lina Natsheh,Gabrielle Schönian,Nabil Abotteen,Saæad Kharabsheh
Journal of the American Academy of Dermatology. 2008; 58(4): 617
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59 Is the amastigote form of Leishmania the only form found in humans infected with cutaneous Leishmaniasis?
Daboul, M.W.
Laboratory Medicine. 2008; 39(1): 38-41
60 Leishmaniasis: Drug resistance and natural products (review)
Polonio, T., Efferth, T.
International Journal of Molecular Medicine. 2008; 22(3): 277-286
61 The relationship between leishmaniasis and AIDS: The second 10 years
Alvar, J., Aparicio, P., Aseffa, A., Den Boer, M., Cañavate, C., Dedet, J.-P., Gradoni, L.,Moreno, J.
Clinical Microbiology Reviews. 2008; 21(2): 334-359
62 Efficacy of a weekly cryotherapy regimen to treat Leishmania major cutaneous leishmaniasis
Mosleh IM, Geith E, Natsheh L, et al.
63 The Relationship between Leishmaniasis and AIDS: the Second 10 Years
Jorge Alvar, Pilar Aparicio, Abraham Aseffa, Margriet Den Boer, Carmen Can~avate, Jean-Pierre Dedet, Luigi Gradoni, Rachel Ter Horst, Rogelio Lo´pez-Ve´lez, Javier Moreno
Clinical Microbiology Reviews. 2008; 21(2): 334
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64 Evaluation of Permethrin Treated Clothing for Personal Protection Against Phlebotomus papatasi (Diptera: Psaychodidae)
Mehdi Khoobdel .
Journal of Entomology. 2008; 5(1): 51
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65 Special Infectious Disease Risks of Expatriates and Long-Term Travelers in Tropical Countries. Part II: Infections Other Than Malaria
Stephen Toovey,Filip Moerman,Alfons van Gompel
Journal of Travel Medicine. 2007; 14(1)
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66 Monocyte cytokine and costimulatory molecule expression in patients infected with Leishmania mexicana
Parasite Immunology. 2007; 29(3): 117
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67 Liver transplant recipient with concomitant cutaneous and visceral leishmaniasis
Deren Özcan, Deniz Seçkin, Adil M. Allahverdiyev, Peter J. Weina, Hakan Aydin, Figen Özçay, Mehmet Haberal
Pediatric Transplantation. 2007; 11(2): 228
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68 Monocyte cytokine and costimulatory molecule expression in patients infected with Leishmania mexicana
Carrada, G., Cañeda, C., Salaiza, N., Delgado, J., Ruiz, A., Sanchez, B., Gutiérrez-Kobeh, L., (...), Becker, I.
Parasite Immunology. 2007; 29(3): 117-126
69 Evaluation of meglumine antimoniate effects on liver, kidney and pancreas function tests in patients with cutaneous leishmaniasis
Kashani MN, Firooz A, Eskandari SE, et al.
70 Special infectious disease risks of expatriates and long-term travelers in tropical countries. part II: Infections other than malaria
Toovey S, Moerman F, van Gompel A
JOURNAL OF TRAVEL MEDICINE. 2007; 14 (1): 50-60
71 Butterfly rash due to cutaneous leishmaniasis
Qureshi, F.A., Suliman, M.I., Sarwar, J.
Journal of the College of Physicians and Surgeons Pakistan. 2007; 17(10): 624-625
72 Therapeutic options for cutaneous leishmaniasis
Mahajan, V.K., Sharma, N.L.
Journal of Dermatological Treatment. 2007; 18(2): 97-104
73 Atypical disseminated cutaneous leishmaniasis in a patient with HIV infection
Khan, I., Mohsin, K., Ahmed, S.A.
Journal of Pakistan Association of Dermatologists. 2007; 17(4): 263-267
74 Can you identify this condition?
Nguyen, C.
Canadian Family Physician. 2007; 53(8): 1307+-1317
75 Identification of serine proteases from Leishmania braziliensis
Guedes HLM, Neto JM, Fonseca MA, et al.
V Rastogi, PS Nirwan
Indian Journal of Medical Microbiology. 2007; 25(3): 272
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77 Therapeutic options for cutaneous leishmaniasis
Vikram K. Mahajan,Nand Lal Sharma
Journal of Dermatological Treatment. 2007; 18(2): 97
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78 Clinical diagnosis of cutaneous leishmaniasis: A comparison study between standardized graded direct microscopy and ITS1-PCR of Giemsa-stained smears
A. Al-Jawabreh,G. Schoenian,O. Hamarsheh,W. Presber
Acta Tropica. 2006; 99(1): 55
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79 Improving the safety of intravenous admixtures: Lessons learned from a Pentostam® overdose
Just, S., Schepers, G., Piotrowski, M.M., Saint, S., Kauffman, C.A.
Joint Commission Journal on Quality and Patient Safety. 2006; 32(7): 366-372
80 Clinical diagnosis of cutaneous leishmaniasis: A comparison study between standardized graded direct microscopy and ITS1-PCR of Giemsa-stained smears
Al-Jawabreh A, Schoenian G, Hamarsheh O, et al.
ACTA TROPICA. 2006; 99 (1): 55-61
81 New formulations and derivatives of amphotericin B for treatment of leishmaniasis
Golenser J, Domb A
82 Cutaneous leishmaniasis: A case confirmed by both histopathologic examination and polymerase chain reaction
Yeh, M.-H., Ho, M.-C., Wu, Y.-H., Hu, S.-L.
Dermatologica Sinica. 2006; 24(1): 58-62
83 Polymerase chain reaction with lesion scrapping for the diagnosis of human American tegumentary leishmaniasis
Venazzi EAS, Roberto ACBS, Barbosa-Tessmann IP, et al.
84 Double blind, randomized controlled trial, to evaluate the effectiveness of a controlled nitric oxide releasing patch versus meglumine antimoniate in the treatment of cutaneous leishmaniasis [NCT00317629]
Silva SY, Rueda LC, Lopez M, et al.
TRIALS. 2006; 7: Art. 14
85 PCR in the investigation of canine American tegumentary leishmaniasis in northwestern Paraná State, Brazil
Velasquez, L.G., Membrive, N., Membrive, U., Rodrigues, G., Reis, N., Campana Lonardoni, M.V., Teodoro, U., (...), Silveira, T.G.V.
Cadernos de Saude Publica. 2006; 22(3): 571-578
86 Imiquimod
Jobanputra, K.S., Rajpal, A.V., Nagpur, N.G.
Indian Journal of Dermatology, Venereology and Leprology. 2006; 72(6): 466-469
87 Old World cutaneous leishmaniasis in American soldiers deployed to Iraq highlights diagnostic and therapeutic options
Walsh, D.S.
Giornale Italiano di Dermatologia e Venereologia. 2006; 141(4): 393-399
88 Double blind, randomized controlled trial, to evaluate the effectiveness of a controlled nitric oxide releasing patch versus meglumine antimoniate in the treatment of cutaneous leishmaniasis [NCT00317629]
Sandra Y Silva, Ligia C Rueda, Marcos López, Iván D Vélez, Christian F Rueda-Clausen, Daniel J Smith, Gerardo Muñoz, Hernando Mosquera, Federico A Silva, Adriana Buitrago, Holger Díaz, Patricio López-Jaramillo
Trials. 2006; 7(1)
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89 Old World cutaneous leishmaniasis in American soldiers underscores diagnostic and therapeutic options
Douglas S Walsh
Expert Review of Dermatology. 2006; 1(3): 355
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90 Papular dermatitis due to Leishmania spp. infection in dogs with parasite-specific cellular immune responses
Veterinary Dermatology. 2005; 16(3): 187
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91 Isolated Lingual Leishmaniasis
Habibzadeh F, Sajedianfard J, Yadollahie M
J Postgrad Med. 2005; 51(3): 218-219
92 Cutaneous leishmaniasis
Manzur, A.
Journal of Pakistan Association of Dermatologists. 2005; 15(2): 161-171
93 Old World eyelid cutaneous leishmaniasis: A case report
Mencía-Gutiérrez, E., Gutiérrez-Díaz, E., Rodríguez-Peralto, J.L., Monsalve-Córdova, J.
Dermatology Online Journal. 2005; 11(3): art no 29
94 Host humoral immune response to Leishmania lipid-binding protein
Maache M, Azzouz S, De La Guardia RD, Alvarez P, Gil R, De Pablos LM, Osuna A
PARASITE IMMUNOLOGY. 2005; 27 (6): 227-234
95 Cutaneous leishmaniasis in soldiers from Fort Campbell, Kentucky returning from Operation Iraqi Freedom highlights diagnostic and therapeutic options
Willard RJ, Jeffcoat AM, Benson PM, Walsh DS
96 Papular dermatitis due to Leishmania spp. infection in dogs with parasite-specific cellular immune responses
Ordeix L, Solano-Gallego LS, Fondevila D, Ferrer L, Fondati A
VETERINARY DERMATOLOGY. 2005; 16 (3): 187-191
97 Cutaneous leishmaniasis in soldiers from Fort Campbell, Kentucky returning from Operation Iraqi Freedom highlights diagnostic and therapeutic options
Robert J. Willard,Anelia M. Jeffcoat,Paul M. Benson,Douglas S. Walsh
Journal of the American Academy of Dermatology. 2005; 52(6): 977
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98 Host humoral immune response to Leishmania lipid-binding protein
Parasite Immunology. 2005; 27(6): 227
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99 Another Hazard of War: Infectious Diseases : Leishmaniasis, malaria threaten troops, millions worldwide.
Barbara A. Goldrick
AJN American Journal of Nursing. 2004; 104(12): 64
[VIEW] | [DOI]
100 Treatment of protozoan infections
Sra, K.K., Sracic, J., Tyring, S.K.
Dermatologic Therapy. 2004; 17(6): 513-516
101 Skin ulceration in a returning traveler
Coutinho, B., Kolb, N.R., Markle, W., Berkenblit, G.V.
Advanced Studies in Medicine. 2004; 4(10): 560-561
102 Another hazard of war: Infectious diseases
Goldrick BA
AMERICAN JOURNAL OF NURSING. 2004; 104 (12): 64-66
103 Treatment of protozoan infections
Karan K. Sra,Julie Sracic,Stephen K. Tyring
Dermatologic Therapy. 2004; 17(6): 513
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Online since 12th February '04
© 2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
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