Biological Sciences
Leishmaniasis
Leishmaniasis is a parasitic disease caused by the Leishmania parasite, transmitted through the bites of infected sandflies. It can manifest in different forms, including cutaneous, mucocutaneous, and visceral leishmaniasis, with symptoms ranging from skin ulcers to organ damage. The disease is prevalent in tropical and subtropical regions, posing a significant public health concern.
Written by Perlego with AI-assistance
Related key terms
1 of 5
10 Key excerpts on "Leishmaniasis"
- Dongyou Liu(Author)
- 2012(Publication Date)
- CRC Press(Publisher)
91 8 8.1 INTRODUCTION Leishmaniasis. is. a. group. of. infectious. diseases. caused. by. protozoan. parasites. of. the. genus. Leishmania ,. of. which. there.are.more.than.20.species.that.affect.humans . .Several. clinical.syndromes.are.subsumed.under.the.term.leishmani-asis—visceral,. cutaneous,. and. mucocutaneous. leishmani-asis—which.result.from.the.replication.of.the.parasite.within. macrophages.in.the.mononuclear.phagocyte.system,.dermis,. and. nasopharyngeal. tissue,. respectively . . These. parasitoses. are.widely.distributed.in.all.continents.except.in.Antarctica,. representing. a. grave. problem. for. world. health,. as. mobility. and.mortality.are.rising.[1] . Knowledge. of. these. New. World. diseases. dates. to. pre-Columbian. times,. as. shown. in. the. sculpture. of. the. Mochica. (330. BC–500. AD). and. Chimú. (1000–1400. AD). cultures. . The. first. clinical. descriptions. of. the. diseases. appeared. during. the. Spanish. colonization. in. texts. of. the. period.(Fernando.de.Oviedo,.1535,.Pedro.Pizarro,.1571,.and. Fernando.de.Santillán,.1572),.which.mentioned.the.risk.suf-fered. by. farmers. who. returned. from. the. Andes. with. skin. ulcers,.known.as.the.valley.sickness.or.Andean.disease . .In. the. eighteenth. century,. Cosme. Bueno. and. Hipólito. Ruiz. described.for.the.first.time.the.role.of.the.insects.in.transmit-ting.the.disease . .These.authors.mentioned.a.corrosive.blister. that.was.difficult.to.cure,.called.“uta,”.which.appeared.on.the. face.[2] . .Alexander.Russel.(1756).masterfully.described.the. clinical.form.of.cutaneous.Leishmaniasis.of.the.striking.scars. of.a.Turkish.patient,.calling.it.the.“Aleppo.boil .” .Throughout. history,.Leishmaniasis.has.received.different.names:.Jericho. button,.Delhi.boil,.salek,.and.uta.[3] . In.1901,.the.disease.began.to.be.known.as.Leishmaniasis. when. William. Boog. Leishman. identified. ovoid. organisms. extracted. from. the. spleen. of. an. Irish. soldier.
eBook - ePub- Felipe Kierzenbaum(Author)
- 2013(Publication Date)
- Academic Press(Publisher)
In this chapter, we follow the course of Leishmaniasis in mammalian hosts from the point of entry of the parasite to the point of eradication of host or pathogen. In the course of this odyssey, it is frequently difficult to determine which side, the parasite or the host, causes a particular event to occur. Our perspective, however, is that the prolonged host–parasite interaction in Leishmaniasis is a battle, with each contender a versatile and clever proponent of its own survival: A situation beneficial to the parasite is a consequence of an effective parasite action; one detrimental to the parasite is a consequence of an effective host reaction.II Parasites and the Diseases They Cause
A Parasites
Leishmania are members of the protozoan family Trypanosomatidae in the order Kinetoplastida. They are ovoid unicellular eukaryotic cells, with a defined nucleus and prominent rod-shaped organelle called a kinetoplast, which is an extranuclear package of DNA. As a group, they cause a spectrum of diseases in humans and other mammals that ranges from simple, self-curing cutaneous lesions to visceral infections associated with parasitism of the reticuloendothelial system. Unlike other spectral diseases (i.e., leprosy), different clinical forms of Leishmaniasis are usually associated with distinctly different species of the parasite (Table I ). Despite overt differences in geographic distribution and disease manifestations, the many different species of Leishmania lead remarkably similar lives. Members of the genus exhibit a heteroxenous life cycle consisting of an extracellular, flagellated stage (promastigote) that replicates within the gut of an invertebrate vector and a sessile, intracellular stage (amastigote) that replicates within monocytes and macrophages of the vertebrate host. A generalized life cycle can be applied to virtually all species of Leishmania (Fig. 2
eBook - PDF- Mark F Wiser(Author)
- 2010(Publication Date)
- Garland Science(Publisher)
Several species of Leishmania are capable of infecting humans and cause a myriad of disease manifestations ranging from self-limiting cutaneous lesions to more serious disseminated diffuse and mucocutaneous disease as well as visceral disease. This wide range of disease manifestations depends somewhat on the specific parasite species. However, host responses and poorly understood host–parasite–vector interactions also contribute to the disease. In addition, transmission of the various species, and thus the vari-ous clinical outcomes, are also dependent on the geographic area and eco-logical setting. For example, many of the species are also capable of infecting other mammals and in many situations Leishmaniasis is a zoonotic disease, whereas anthroponotic transmission predominates in other areas. Leishmaniasis is endemic in tropical and subtropical areas through-out the world. Transmission occurs in settings ranging from rain forests to deserts and can be found in rural or peri-urban areas. Leishmaniasis is a focal disease in both space and time. Distinct species of parasites, vectors, and reservoir hosts maintain the transmission cycle in any given area. The number of reported cases and geographical range of endemic leishmania-sis is increasing, and thus Leishmaniasis can be considered as an emerging disease. Life Cycle Leishmania are transmitted by a small biting fly known as a sand fly (Figure 10.1). Two different genera of phlebotomine sand flies transmit Leishmania : Phlebotomus in the eastern hemisphere (i.e., Old World including Africa, Asia, and Europe) and Lutzomyia in the western hemisphere (i.e., New World including South and Central America). Only the females take blood meals and thus the males play no direct role in transmission.
eBook - PDF- David Mabey, Geoffrey Gill, Eldryd Parry, Martin W. Weber, Christopher J. M. Whitty(Authors)
- 2013(Publication Date)
- Cambridge University Press(Publisher)
Section 7 Chapter 42 Protozoal infections Leishmaniasis Ed E. Zijlstra and Ahmed M. Musa The leishmaniases are a group of diseases that are caused by the protozoan parasite Leishmania which belongs to the order of Kinetoplastidae. Infection affects the skin, mucosal surfaces, causes disseminated disease or a combination. The clinical manifestations and prevalence in each geographical area are determined by the strain of Leishmania, the susceptibility of the population, the pres- ence of the reservoir and the sand fly vector; socioeconomic factors, changes in the ecology and population movements all play a role. World-wide, 88 countries are affected with a global annual inci- dence 1.5–2 10 6 cases of which 1–1.5 10 6 cases of cutaneous Leishmaniasis and 500 000 cases of visceral Leishmaniasis and 70 000 deaths (WHO, 2010). The problem in Africa There are five major clinical syndromes of Leishmaniasis, all of which may be found in Africa (Table 42.1); of these, VL and CL are by far the most common. Although scattered cases of VL and CL have been reported from all parts of Africa, the endemic areas are mainly in the Table 42.1. Frequency, principal endemic areas, morbidity, mortality and type of Leishmanial parasite involved in various types of Leishmaniases found in Africa VL PKDL CL ML DCL LR Frequency Common Common Common Rare Rare Rare Endemic area Sudan Sudan Sudan Sudan Ethiopia Kenya Kenya Kenya Kenya Kenya Ethiopia Ethiopia Morocco Morocco Algeria Algeria Tunisia Tunisia Libya Libya Somalia Mauritania Senegal Mali Burkina Faso Niger Nigeria Morbidity High Variable Mild High Moderate Moderate Mortality High Absent Absent Low Low Absent Parasite L. donovani L. donovani L. major L. major L. aethiopica L. tropica L. infantum L. infantum L. tropica* L. donovani L.
eBook - PDF- Garg, Sudhi Ranjan(Authors)
- 2021(Publication Date)
- Daya Publishing House(Publisher)
8 Leishmaniases M.B. Chhabra 1 and L.D. Singla 2 1 Department of Veterinary Parasitology, College of Veterinary Sciences, Hisar – 125 004 2 Department of Veterinary Parasitology, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana – 141 004 Leishmaniases are vector-transmitted parasitic zoonoses caused by over 25 obligatory intracellular protozoa Leishmania spp. They represent a spectrum of diseases with clinical and epidemiological diversity. Leishmaniases are anthropozoonotic metazoonoses caused by kinetoplastid flagellates of the genus Leishmania , within protozoa. Geographical Distribution Leishmaniases are endemic in 88 countries spread over five continents. Of these, 72 are developing countries, in the tropics and subtropics. According to estimates, 12 million people are affected worldwide and an estimated 1.5-2 million new cases occur annually (Bhunia et al . 2011). Of these, the estimated yearly incidence of cutaneous leishmaniases (CL) is 1-1.5 million cases and the visceral form of the disease accounts for 5,00,000 new cases annually (Desjeux 2001). An overwhelming majority (>90 per cent) of visceral leishmaniases (VL) occur in only six countries, namely, Bangladesh, India, Nepal, Sudan, Ethiopia and Brazil. The disease complex This ebook is exclusively for this university only. Cannot be resold/distributed. causes over 75,000 deaths per year worldwide (Morgan 2000). Etiologic Agents and Vectors The genus Leishmania belongs to a group of blood and tissue flagellates. The genus was created by Ross in 1903 to include the causal parasite of Indian kala-azar, Leishmania donovani . Blood sucking phlebotomine sandflies are the obligatory vectors. Host Range The primary hosts of Leishmania are sylvatic mammals of several orders (Rodentia, Marsupalia, Carnivora etc.) but under peri-domestic and domestic transmission foci, synanthropic and domestic animals can act as source of infection for phlebotomine sandfly vectors.
- Julius Kreir(Author)
- 2012(Publication Date)
- Academic Press(Publisher)
Since technical failure, such as loss of virulence of the vaccinating strain in the interim between the two trials, cannot be ruled out, this promising lead will doubtless be further explored in the future. VII. Epidemiology Much of the epidemiology of the leishmanias infecting man has in-evitably been considered in dealing with the separate parasites in Section III on taxonomy. Here we shall discuss the broader aspects, with particu-lar reference to medical and economic importance. A. Zoonoses It will have been seen from the foregoing pages that most of the leish-manias are parasites of wild animals, among which they are transmitted by phlebotomine sandflies (Diptera: Phlebotominae). When man in- 3. Leishmania 113 trudes into their natural habitat he may become an accidental host of some of these organisms. In such cases the disease is referred to as a zoonosis and is rarely, if ever, transmitted directly from man to man. Good examples of this are rural oriental sore, due to L. major, with its reservoir in the burrowing rodents of the Middle East, southern Russian, and African desert regions; L. mexicana mexicana in the wild rodents of the tropical rain forest in northern Central America; L. braziliensis braziliensis, L. b. guyanensis, and L. mexicana amazonensis in South American forests; L. b. panamensis in sylvatic animals of Panama; and L. infantum and L. chagasi in dogs and foxes of the Eastern Hemisphere and Western Hemisphere, respectively. The infection rates of these parasites in man clearly depend on a com-plex of epidemiological factors. Thus, in Belize, the log cutters and collectors of chewing-gum latex (chicleros) live in the forest for nearly 6 months of the year. This period coincides with the rainy season, maxi-mum sandfly activity, and therefore a high rate of transmission of L. m. mexicana. Few of the forest workers escape infection. In Brazil, on the other hand, the closely related parasite L.
eBook - PDFCanine Medicine
Recent Topics and Advanced Research
- Hussein Abdelhay Elsayed Kaoud(Author)
- 2016(Publication Date)
- IntechOpen(Publisher)
2. Epidemiology Visceral Leishmaniasis (VL), also known as kala-azar, is a disease caused by an obligate intracellular protozoon belonging to the family Trypanosomatidae, genus Leishmania . It is transmitted through the bite of infected female sand flies and is widely distributed throughout the world ( Figure 2 ). Currently, the World Health Organization considers VL as a neglected disease. An estimated 500,000 new cases of human VL occur per year [2]. Its epidemiology is extremely complex and depends on social and environmental variables, the species of Leishmania and the vector involved, and the behavior of reservoirs and hosts ( Table 1 ). Canine Medicine - Recent Topics and Advanced Research 20 Figure 2. World distribution of human visceral Leishmaniasis, 2013 [3]. Species Region Vector Host/reservoir Leishmania (L.) infantum Old World: Europe Asia Africa Phlebotomus perniciosus P. ariasi Humans Dogs Wild canids Leishmania (L.) donovani Old World: Asia Africa P. argentipes P. orientalis Humans Leishmania (L.) infantum (syn. of L. chagasi ) New World: South, Central, and North America Lutzomyia longipalpis Lu. cruzi Lu. forattinii Lu. evansi Humans Dogs Wild canids Felines Marsupials Adapted with permission from Refs. [4–6]. Table 1. Visceral Leishmaniasis: species, region of occurrence, vectors, reservoirs, and mammal hosts. 2.1. Biological cycle The life cycle of L. infantum is heteroxenic, that is, the parasite develops in two types of hosts: in the intermediate host, or the vector, the promastigote form develops in the insect gut; once in the definitive host, the amastigote develops as an obligate intracellular parasite in macro-phages. During blood meals, vectors ingest macrophages containing Leishmania amastigotes, Canine Visceral Leishmaniasis in Brazil http://dx.doi.org/10.5772/65956 21 which will then multiply by binary division and differentiate into promastigotes.
- Michael J. Day(Author)
- 2016(Publication Date)
- CRC Press(Publisher)
The mech-anisms underlying this polarization remain unclear. However, there is a clear genetic influence on the disease Fig. 9.2 The life cycle of Leishmania infantum in the sand fly vector and its mammalian hosts (canines and man). (1) During a blood meal taken by the female sand fly, promastigotes are injected with saliva into the skin of the vertebrate host. (2, 3) Promastigotes are phagocytosed by macrophages in the skin and multiply by binary fission to amastigotes. (4) The macrophage ruptures and free amastigotes penetrate adjacent host cells and disseminate to the visceral organs. (5) Cells containing amastigotes are taken up by the sand fly during a blood meal. (6) Amastigotes are released from host cells, transform to promastigotes and multiply. (7) Promastigotes attach to the gut wall of the sand fly where they continue to multiply and eventually reach the proboscis before infecting a naïve host. 1 2 3 4 5 6 7 Fig. 9.3 Transmission electron micrograph of a mac-rophage showing amastigote forms of Leishmania within a cytoplasmic compartment. Chapter 9 128 investigations of cutaneous lesions have shown reduced expression of MHC class II by epidermal Langerhans cells and keratinocytes and fewer infiltrating T lym-phocytes within severe generalized nodular lesions, compared with milder alopecic dermatitis. The little information on the immunological response to Leishmania infection in the cat is mainly related to humoral response. One cat with cutaneous leishmaniosis in southern Texas failed to respond to intradermal leish-manin injection, although other parameters of immune competence were reported as normal. Studies of cellular immunity in cats with leishmaniosis are lacking. This immunological background helps explain the clinicopathological features of overt leishmaniosis as it presents in the dog. In animals that develop dissemi-nated infection, lesions and clinical signs develop over a period of 3 months to several years after infection.
eBook - PDFLeishmaniasis
Trends in Epidemiology, Diagnosis and Treatment
- David M. Claborn(Author)
- 2014(Publication Date)
- IntechOpen(Publisher)
Introduction Tissue parasites such as Leishmania are transmitted from host to host through a vector species, and transmission can be from human to vector to animal or vice versa (zoonotic transmission), which occurs in rural and periurban environments or from human to vector to human (anthroponotic transmission), which occurs in urban environments. Lutzomyia and Phleboto‐ mus species have long been known as the primary transmitters of Leishmaniasis. However, in recent decades, evidence has been building for the existence of alternative transmission pathways. These pathways involve direct contact with infected tissues, such as may be encountered during surgical/therapeutic procedures, biological/reproductive activities, certain work-related practices and by unsafe drug use, all of which are reviewed below. 2. Transmission forms 2.1. The life cycle of Leishmania spp.: the vector transmission Leishmania spp. is a parasite with a dimorphic life cycle that is controlled by the passage from vector to host [1]. As such, the parasite has developed novel adaptations to survive within the vector [2]. The vector phase of the life cycle begins when the vector ingests blood containing the parasites. Following ingestion, the parasites eventually reach the midgut, where they are held for approximately 4 hours in the peritrophic matrix. There, the amastigote cells differen‐ tiate into small, motile cells with short flagella, a form known as the procyclic promastigote. Next, Leishmania initiates the first stage of the vector life cycle, which occurs over the following 24-48 hours. The body of the parasite elongates in the next 72 hours to form the nectomonad © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- David Claborn(Author)
- 2017(Publication Date)
- IntechOpen(Publisher)
Each of the New World species of Leishmania has unique ecological and geographical distributions [17]. From an epidemiological point of view and disease‐control stand‐point, to know whether an organism, causing the Eco-Epidemiological and Immunological Features of Localized Cutaneous... http://dx.doi.org/10.5772/66130 141 disease in a given area, is of the same species as that found in suspected mammalian reservoirs and insect vectors, is very important [18]. Based on both the clinical and epidemiological features of the disease, as well as on the biological characteristics of the parasite in laboratory animals [19–21], L. (L.) mexicana Biagi, 1953 emend. Garnham, 1962, was considered the main agent of LCL in the Yucatan Peninsula. Nevertheless, its characterization at the genus and sub-genus level was not done in those studies. Therefore, from January 1990 to July 1992, 153 patients with LCL determined by both clinical diagnosis and parasite visualization (smear, biopsy and/or isolation-culture) were studied. All of them were infected in the state of Campeche. Parasite isolation by needle aspirates taken from the edge of the lesions was positive in 49%. Isolates were characterized by isoenzyme markers (glucose phosphate isomerase, mannose phospate isomerase, nucleoside hydrolase, phosphoglucomutase, 6-phosphogluconate dehydrogenase and glucose-6-phosphate dehy-drogenase). Seventy (93.3%) were identified as L. (L.) mexicana Biagi, 1953 emend. Garham, 1962 and 5 (6.7%) as Leishmania (Viannia) braziliensis Viannia 1911 emend. Matta, 1916 [22]. Later on, a study to identify Leishmania parasites isolated from humans and wild rodents from the state of Campeche, using IFA with Mabs was carried out. The main purpose was to determine if the parasites of both types of hosts were of the same biotype. All the isolates obtained from wild rodents reacted with monoclonal antibodies M7 and M8 and were thus identified as L.
Index pages curate the most relevant extracts from our library of academic textbooks. They’ve been created using an in-house natural language model (NLM), each adding context and meaning to key research topics.
