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Principles and practice of Clinical parasitology - Gillespie S.

Gillespie S. Principles and practice of Clinical parasitology - Wiley publishing , 2001. - 675 p.
ISBN 0-471-97729-2
Download (direct link): principlesandpracticeofclin2001.pdf
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Large numbers of cases of visceral leishmaniasis due to L. (L.) donovani occur in India, particularly in the states of Assam and Bihar, and in Bangladesh (Addy and Nandy,
1992). Humans are the only reservoir there; anthropophilic P. argentipes is the major vector. Historically, children and young adults were the most frequently affected, but the mean age has risen to 20 years, possibly due to a fall in herd immunity (Basu and Mallik, 1995). Endemic foci of L. (L.) donovani are found in Kenya. Infection has been associated with termite hills, which serve as breeding sites for P. martini and other Phlebotomus species. The reservoir is uncertain. A major epidemic of visceral leishmaniasis has been reported among refugees in the Sudan (Zijlstra et al., 1994). Phlebotomus orientalis is a vector. The reservoirs include rats, gerbils, small carnivores and possibly humans. Visceral leishmaniasis is also endemic in southern China, but the number of cases is now small (Guan, 1991). L. (L.) donovani or L. (L.) infantum are occasionally isolated from persons with simple cutaneous leishmaniasis (Mebrahtu et al., 1993; Jimenez et al., 1995).
Leishmaniasis is a spectral disease (Pearson and Sousa, 1996). The clinical manifestations depend on complex interactions between the virulence characteristics of the infecting Leishmania spp. and the genetically determined cell-mediated immune responses of its human host. There are three major clinical syndromes: cutaneous, mucosal or visceral leishmaniasis. Variations occur in each of these, and many Leishmania spp. can cause more than one syndrome.
Cutaneous Leishmaniasis Simple Cutaneous Leishmaniasis
In simple cutaneous leishmaniasis, lesions develop where promastigotes are inoculated by sand flies feeding on exposed areas of skin. They may be single or multiple. The incubation period varies from 2 weeks to several months. In rare cases it has been as long as 3 years. The morphology of the lesions varies, even among persons infected with the same Leishmania sp. They typically begin as papules that progressively enlarge and, in the majority of cases, ulcerate. In
Fig. 13-5 Cutaneous leishmaniasis due to L. (V.) braziliensis in north-eastern Brazil. The lesion has a ‘pizza-like’ morphology: it is round with a raised border, red granulating base and overlying yellowish exudate
some cases lesions are papular, acneiform or nodular, with minimal or no ulceration.
Many lesions develop a ‘pizza-like’ appearance (Figure 13.5), with a circular, raised outer border, beefy, red, granulating base and overlaying yellow exudate. These are sometimes referred to as ‘wet’ lesions. ‘Dry’ lesions tend to be smaller, with less pronounced ulceration and an overlying crust. In a few cases a hard excrescence forms at the center of the lesion, which may take the form of a cutaneous horn. Satellite lesions may be seen, and secondary staphylococcal or streptococcal cellulitis of adjacent skin can develop. Regional lymph-adenopathy may accompany skin lesions, particularly in persons infected with L. (V.)
guyanensis. In some persons with L. (V.)
braziliensis, regional lymphadenopathy, fever and constitutional symptoms precede the development of skin lesions and resolve as the lesion develops.
After a variable period of time, cutaneous lesions heal, leaving flat, atrophic, burn-like scars as evidence of disease. In general, lesions of L.
(L.) mexicana and L. (L.) major tend to heal
within several months, while those of L. (V.) braziliensis and L. (L.) tropica persist longer. After lesions resolve, persons are usually immune to the infecting Leishmania spp.
On rare occasions, persons infected with L. (V.) braziliensis develop a large number of skin lesions, suggesting hematogenous dissemination. Disseminated cutaneous disease has also been
reported in persons with concurrent HIV infection, but the number is small in comparison to HIV-associated visceral leishmaniasis.
Diffuse Cutaneous Leishmaniasis
In diffuse cutaneous leishmaniasis, plaque-like or nodular lesions develop on the face or other exposed areas and slowly spread. They do not ulcerate. Large numbers of amastigote-filled macrophages are found at biopsy, the leishmanin skin test is negative, and peripheral blood mononuclear cells neither proliferate nor produce IFNy or IL-2 in response to leishmanial antigens. The disease persists over a period of many years and responds poorly to chemotherapy. Diffuse cutaneous leishmaniasis is most frequently associated with L. (L.) aethiopica in Africa and L. (L.) amazonensis in Latin America.
Leishmaniasis recidiva
Leishmaniasis recidiva is a chronic, localized process associated with L. (L.) tropica in the Middle East. Lesions expand slowly and frequently persist for years, healing at the center as the margins expand. They are typically found on the face or other exposed areas. Biopsies reveal a chronic granulomatous response with few parasites.
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