- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
International Common Names
- English: cutaneous leishmaniasis; cutaneous leishmaniasis in horses and sheep; cutaneous leishmaniasis, leishmaniosis, in horses and sheep; leishmaniasis; visceral leishmaniasis
OverviewTop of page
The leishmaniases are a group of infectious diseases that affect humans, domestic and wild animals and are caused by members of the genus Leishmania. Visceral leishmaniosis caused by Leishmania infantum, the most severe disease form, is a frequent cause of chronic and potentially fatal clinical illness in dogs and humans in some regions, and it is less common in cats and rare in horses (Baneth et al., 2008; Solano-Gallego et al., 2009; Ready, 2014). Dogs are considered the major reservoir for human L. infantum infection, in an area that stretches from Portugal to China and across South America. Canine leishmaniosis (CanL) is also important in non-endemic countries due to importation of dogs from endemic areas and dog travel with owners to countries where its vectors are not present (Baneth et al., 2008).
Visceral leishmaniosis is a major zoonosis in the Mediterranean basin, Middle East and South America. A World Health Organization (WHO) report from 2014 indicates that there are approximately 200,000-400,000 new human cases of visceral leishmaniosis annually with 20,00 to 30,000 deaths annually and the population at risk globally is about 200 million people (http://www.who.int/mediacentre/factsheets/fs375/en/). Anthroponotic visceral leishmaniosis caused by Leishmania donovani mainly in India and East Africa is responsible for a large part of the fatalities in people. However, visceral leishmaniosis with the dog as a major reservoir for the parasite is the main form of the disease in other parts of the world including Brazil, China and the Mediterranean region (Ready, 2014). Visceral leishmaniosis caused by L. infantum in the Mediterranean basin was traditionally predominantly a disease of young children and the name of the causative agent of this disease reflects the predilection to infants. Malnutrition has been recognized as a risk factor for infantile leishmaniosis, and may explain why this disease is more prevalent among children in poor countries as compared with affluent ones despite high prevalence rates in the dog populations. AIDS patients are currently an important risk group for human visceral leishmaniosis in Southern Europe (van Griensven et al., 2014).
Other species of Leishmania infect canines and additional mammal hosts, including Leishmania braziliensis in South America and Leishmania tropica, in the Old World, however, these are not the focus of this datasheet, as these infections are less frequent and paramount to human health and welfare (Baneth et al., 2008; Solano-Gallego et al., 2009).
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Canis aureus||Wild host|
|Canis familiaris (dogs)||Domesticated host|
|Canis lupus (wolf)||Wild host|
|Carollia perspicillata||Wild host|
|Cerdocyon thous||Wild host|
|Didelphis albiventris||Wild host|
|Didelphis marsupialis (common opossum)||Wild host|
|Equus caballus (horses)||Domesticated host|
|Felis catus (cat)||Domesticated host|
|Genetta genetta||Wild host|
|Herpestes ichneumon||Wild host|
|Lepus granatensis||Wild host|
|Lepus yarkandensis||Wild host|
|Lynx pardinus||Wild host|
|Martes martes||Wild host|
|Meles meles||Wild host|
|Monachus monachus||Wild host|
|Mustela nivalis||Wild host|
|Ovis aries (sheep)|
|Rattus norvegicus (brown rat)||Wild host|
|Rattus rattus (black rat)||Wild host|
|Sus scrofa (pigs)||Domesticated host|
|Vulpes vulpes (red fox)||Wild host|
Hosts/Species AffectedTop of page
Visceral leishmaniosis caused by L. infatum or its synonym in Latin America, Leishmania chagasi is a disease that involves mainly humans and dogs. Dogs are considered the main peridomestic reservoir host for human infection, and also suffer from severe clinical disease. In addition, natural L. infantum infection has been recorded in cats, horses, pigs and in a variety of wild mammal and marsupial species including: golden jackals (Canis aureus), red foxes (Vulpes vulpes), gray wolves (Canis lupus), crab-eating foxes (Cerdocyon thous), opossums (Didelphis albiventris and D. marsupialis), lynx (Lynx pardinus), hares (Lepus granatensis and L. yarkandensis), badgers (Meles meles), mongooses (Herpestes ichneumon), pine martens (Martes martes), genets (Genetta genetta),weasels (Mustela nivalis), a seal (Monachus monachus), bats (Carollia perspicillata), rats (Rattus rattus and R. norvegicus) and other rodent species (reviewed in Quinnell and Courtenay, 2009). Not every infected animal species may serve as a reservoir host, e.g. be responsible for parasite transmission to humans or animals. Reservoir hosts for Leishmania should have several characteristics in order to serve as efficient sources of blood meals with parasites for sandfly vectors: they should be abundant, infected at a high rate, attractive and infectious to sandflies, and able to maintain infection year round. The identification of blood meal belonging to a certain animal host in a considerable number of naturally-infected sandflies in a survey of an endemic region may provide evidence for the potential of this host to serve as reservoir. Apart from dogs and humans, only a small number of animal host species have been studied for their capacity to infect sandflies with L. infantum by xenodiagnoses (feeding sandflies on an infected host). Studies have shown that domestic cats, hares, black rats, opossums and crab-eating foxes can infect sandflies under experimental conditions (Quinnell and Courtenay, 2009; Molina et al., 2012). However, the mere ability to infect sandflies does not imply that the host is an epidemiologically-important reservoir which plays a role in sylvatic or domestic transmission at the population level. The transmission of L. infatnum from domestic dogs undoubtedly constitutes the main route for human infection in most endemic areas globally. In these areas people share the same habitat with dogs infected for long durations. Although sub-clinically infected dogs are infectious to sandflies, dogs with clinical signs of disease have been shown to have high parasite loads and be more infectious (Michalsky et al., 2007).
In dogs, susceptibility or resistance to clinical disease is influenced by genetics. The presence of overt CanL among Ibizian hounds in the Balearic islands is rare and significantly lower than among other breeds and it has been shown that this breed mounts a predominantly cellular immune response against L. infatnum (Solano-Gallego et al., 2000). Other breeds that originate from regions that are not enzootic for leishmaniosis such as the Boxer, Rottweiler and German Shepherd are overrepresented in CanL surveys. A study on the polymorphism of the canine Slc11a1 (NRAMP1) gene, which encodes an iron transporter protein involved in the control of intraphagosomal replication of parasites and macrophage activation, has implied that susceptible dogs have mutations in this gene (Sanchez-Robert et al., 2008). A DLA class II DLA-DRB1 genotype, which is a dog major histocompatibility complex (MHC) class II allele, has been linked to the risk of being infected in an endemic area in Brazil (Quinell et al., 2003).
In the USA, CanL has mainly been described in foxhounds, and it has been shown that transplacental transmission of this infection is responsible for some of the disease which occurs in dogs from this breed, in an environment that apparently lacks clear transmission of infection by sandfly vectors (Boggiatto et al., 2011).
Systems AffectedTop of page skin and ocular diseases of small ruminants
DistributionTop of page
CanL is a major zoonotic disease endemic in more than 70 countries in the world. It is enzootic in regions of southern Europe, Africa, Asia, South and Central America and is sporadic in the USA. CanL is also an important concern in non-endemic countries where imported disease constitutes a veterinary and public health problem. Dogs are the primary animal reservoir for human visceral leishmaniosis and the disease is usually fatal if not treated in people (Baneth et al., 2008; Solano-Gallego et al., 2009). Phlebotomine sandflies are the vectors of Leishmania infantum, the causative agent of CanL in the Old World and for its New World synonym L. chagasi. Seroprevalence rates for CanL found in studies carried out in the Mediterranean basin range between 10 and 37% of the dogs in disease foci. Surveys using the polymerase chain reaction (PCR) for the detection of leishmanial DNA in canine tissues, or combining serology and PCR, have revealed higher infection rates approaching 70% in some foci (Baneth et al., 2008; Solano-Gallego et al., 2009). It has been estimated based on seroprevalence studies from Italy, Spain, France and Portugal that 2.5 million dogs in these countries are infected (Moreno and Alvar, 2002). The number of infected dogs in South America is also estimated in millions with high infection rates in some areas of Brazil and Venezuela.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease not reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||Present||OIE, 2009; Alam et al., 2013|
|Bhutan||No information available||OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||Localised||OIE, 2009; Alam et al., 2014|
|-Gansu||Localised||Zhang et al., 2013; Alam et al., 2014|
|-Hebei||Localised||Alam et al., 2014|
|-Henan||Localised||Alam et al., 2014|
|-Hong Kong||No information available||OIE, 2009|
|-Shandong||Localised||Alam et al., 2014|
|-Sichuan||Localised||Zhang et al., 2013; Alam et al., 2014|
|-Xinjiang||Localised||Alam et al., 2014|
|Georgia (Republic of)||Widespread||OIE Handistatus, 2005; Babuadze et al., 2014|
|India||Restricted distribution||OIE, 2009|
|Indonesia||Disease not reported||OIE, 2009|
|Iran||Widespread||OIE, 2009; Mohebali, 2013|
|Iraq||Widespread||Sukkar et al., 1981; OIE, 2009|
|Israel||Localised||Baneth et al., 1998; OIE, 2009|
|Japan||No information available||OIE, 2009|
|Jordan||No information available||OIE, 2009|
|Kazakhstan||Disease not reported||OIE, 2009|
|Korea, DPR||Disease not reported||OIE Handistatus, 2005|
|Korea, Republic of||No information available||OIE, 2009|
|Kuwait||Disease not reported||OIE, 2009|
|Kyrgyzstan||Disease never reported||OIE, 2009|
|Laos||Disease never reported||OIE, 2009|
|Lebanon||Localised||Nuwayri-Salti et al., 1997|
|Malaysia||Disease never reported||OIE, 2009|
|-Peninsular Malaysia||No information available||OIE Handistatus, 2005|
|-Sabah||Disease never reported||OIE Handistatus, 2005|
|-Sarawak||No information available||OIE Handistatus, 2005|
|Maldives||Disease never reported||OIE, 2012|
|Mongolia||Disease never reported||OIE, 2009|
|Myanmar||No information available||OIE, 2009|
|Nepal||No information available||OIE, 2009|
|Oman||Localised||Elnour et al., 2001|
|Pakistan||Present||Rab et al., 1995|
|Philippines||No information available||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||Localised||Al-Zahrani et al., 1988|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease not reported||OIE, 2009|
|Syria||Widespread||Dereure et al., 1991|
|Taiwan||Disease never reported||OIE Handistatus, 2005|
|Tajikistan||Widespread||Alam et al., 2009|
|Thailand||Disease never reported||OIE, 2009|
|Turkey||Widespread||OIE, 2009; Toz et al., 2013|
|Turkmenistan||Present||Lesnikova et al., 1990|
|United Arab Emirates||Disease not reported||OIE, 2009|
|Uzbekistan||Widespread||Kovalenko et al., 2011|
|Vietnam||No information available||OIE, 2009|
|Yemen||Present||Rioux et al., 1989|
|Algeria||Widespread||Aït-Oudhia et al., 2011; OIE, 2012|
|Angola||Present||OIE, 2012; Vilhena et al., 2014|
|Benin||Disease never reported||OIE, 2012|
|Botswana||Disease never reported||OIE, 2012|
|Burkina Faso||No information available||OIE, 2009|
|Burundi||Disease never reported||OIE Handistatus, 2005|
|Cameroon||No information available||OIE Handistatus, 2005|
|Cape Verde||Disease not reported||OIE, 2012|
|Central African Republic||Disease not reported||OIE, 2012|
|Chad||No information available||OIE, 2009|
|Congo||No information available||OIE, 2009|
|Congo Democratic Republic||Disease not reported||OIE Handistatus, 2005|
|Côte d'Ivoire||No information available||OIE Handistatus, 2005|
|Djibouti||Disease not reported||OIE, 2012|
|Egypt||Present||OIE, 2009; Rosypal et al., 2013|
|Eritrea||No information available||OIE, 2009|
|Ethiopia||Present||Bashaye et al., 2009|
|Gabon||Disease not reported||OIE, 2012|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||Disease never reported||OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||Present||S. Muriuki, Africa, personal communication, 2012|
|Lesotho||Disease never reported||OIE, 2012|
|Libya||Present||Postigo, 2010; OIE, 2012|
|Madagascar||Disease never reported||OIE, 2009|
|Malawi||No information available||OIE, 2009|
|Mali||Disease not reported||OIE, 2012|
|Mauritius||Disease never reported||OIE, 2012|
|Morocco||Widespread||Natami et al., 2000|
|Mozambique||Disease not reported||OIE, 2009|
|Nigeria||No information available||OIE, 2009|
|Réunion||No information available||OIE Handistatus, 2005|
|Rwanda||No information available||OIE, 2009|
|Sao Tome and Principe||No information available||OIE Handistatus, 2005|
|Senegal||Localised||OIE, 2009; Faye et al., 2010|
|Seychelles||Disease never reported||OIE, 2012|
|Sierra Leone||Disease not reported||OIE, 2012|
|Somalia||No information available||OIE Handistatus, 2005|
|South Africa||No information available||OIE, 2009|
|Sudan||Widespread||Dereure et al., 2000|
|Swaziland||Disease never reported||OIE, 2012|
|Tanzania||No information available||OIE, 2009|
|Togo||Disease not reported||OIE, 2012|
|Tunisia||Widespread||OIE, 2012; Zoghlami et al., 2014|
|Uganda||No information available||OIE, 2009|
|Zambia||Disease not reported||OIE, 2012|
|Zimbabwe||Disease never reported||OIE, 2012|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Disease not reported||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease never reported||OIE, 2009|
Central America and Caribbean
|Barbados||Disease never reported||OIE Handistatus, 2005|
|Belize||Disease not reported||OIE, 2009|
|British Virgin Islands||Disease not reported||OIE Handistatus, 2005|
|Cayman Islands||Disease never reported||OIE Handistatus, 2005|
|Costa Rica||Localised||Mendoza et al., 1983|
|Cuba||Disease never reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||No information available||OIE Handistatus, 2005|
|Dominican Republic||No information available||OIE, 2009|
|El Salvador||Absent, reported but not confirmed||OIE, 2009|
|Guadeloupe||No information available||OIE, 2009|
|Guatemala||No information available||OIE, 2009|
|Haiti||Disease never reported||OIE, 2009|
|Honduras||No information available||OIE, 2009|
|Jamaica||No information available||OIE, 2009|
|Martinique||Disease never reported||OIE, 2009|
|Nicaragua||No information available||OIE, 2009|
|Panama||No information available||OIE, 2009|
|Saint Kitts and Nevis||Disease never reported||OIE Handistatus, 2005|
|Saint Vincent and the Grenadines||Disease never reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Disease never reported||OIE Handistatus, 2005|
|Argentina||Localised||OIE, 2009; Cruz et al., 2010|
|Bolivia||No information available||OIE, 2009|
|-Bahia||Widespread||Almeida et al., 2005|
|-Ceara||Widespread||Schubach et al., 2014|
|-Espirito Santo||Present||Tonini et al., 2012|
|-Goias||Present||Azevedo et al., 2008|
|-Maranhao||Widespread||Ponte et al., 2011|
|-Mato Grosso do Sul||Widespread||Sousa et al., 2013|
|-Minas Gerais||Widespread||Coura-Vital et al., 2013|
|-Para||Present||Lima et al., 2010|
|-Parana||Localised||Thomaz-Soccol et al., 2009|
|-Pernambuco||Widespread||Almeida et al., 2005|
|-Piaui||Present||Silva et al., 2012|
|-Rio de Janeiro||Widespread||Honse et al., 2013|
|-Rio Grande do Norte||Widespread||Lima et al., 2012|
|-Rio Grande do Sul||Widespread||Almeida et al., 2005|
|-Rondonia||Localised||Santos et al., 2014|
|-Santa Catarina||Present||Maziero et al., 2014|
|-Sao Paulo||Widespread||Motoie et al., 2013|
|Chile||Disease never reported||OIE, 2009|
|Colombia||Present||Travi et al., 2001|
|Ecuador||Disease never reported||OIE, 2009|
|Falkland Islands||Disease never reported||OIE Handistatus, 2005|
|French Guiana||Absent, reported but not confirmed||OIE, 2009|
|Guyana||Disease never reported||OIE Handistatus, 2005|
|Paraguay||Localised||OIE Handistatus, 2005; Pangrazio et al., 2009|
|Peru||Disease never reported||OIE, 2009|
|Uruguay||Disease never reported||OIE, 2009|
|Venezuela||Widespread||Zerpa et al., 2000|
|Albania||Widespread||Lazri et al., 2008|
|Andorra||Reported present or known to be present||OIE Handistatus, 2005|
|Austria||No information available||OIE, 2009|
|Belarus||Disease never reported||OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Bosnia-Hercegovina||Present||OIE Handistatus, 2005; Alvar et al., 2012|
|Bulgaria||Present||OIE, 2009; Harizanov et al., 2013|
|Croatia||Widespread||Zivicnjak et al., 2005; OIE, 2009|
|Cyprus||Widespread||Deplazes et al., 1998; OIE, 2009|
|Czech Republic||Disease not reported||OIE, 2009|
|Denmark||No information available||OIE, 2009|
|Estonia||Disease never reported||OIE, 2009|
|Finland||Disease not reported||OIE, 2009|
|France||Present||OIE, 2009; Bourdeau et al., 2014|
|-Corsica||Widespread||Neogy et al., 1992|
|Germany||Disease not reported||OIE, 2009|
|Greece||Widespread||OIE, 2009; Bourdeau et al., 2014|
|Hungary||Localised||OIE, 2009; Tánczos et al., 2012|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease not reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||Widespread||OIE, 2009; Bourdeau et al., 2014|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Disease never reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease never reported||OIE, 2009|
|Luxembourg||Disease not reported||OIE, 2009|
|Macedonia||Widespread||OIE, 2009; Alvar et al., 2012|
|Malta||Widespread||Headington et al., 2002; OIE, 2009|
|Moldova||Disease not reported||OIE Handistatus, 2005|
|Netherlands||Disease not reported||OIE, 2009|
|Norway||Disease not reported||OIE, 2009|
|Poland||Disease never reported||OIE, 2009|
|Portugal||Widespread||OIE, 2009; Bourdeau et al., 2014|
|Romania||Present||OIE, 2009; Mircean et al., 2014|
|Russian Federation||Present||OIE, 2009|
|San Marino||Present||Salvatore et al., 2013|
|Serbia||Present||Dakic et al., 2009; OIE, 2009|
|Slovakia||Disease not reported||OIE, 2009|
|Slovenia||Disease not reported||OIE, 2009|
|Spain||Widespread||OIE, 2009; Bourdeau et al., 2014|
|-Balearic Islands||Widespread||Solano-Gallego et al., 2001|
|Switzerland||Disease not reported||OIE, 2009|
|-Northern Ireland||Disease never reported||OIE Handistatus, 2005|
|Ukraine||Disease not reported||OIE, 2009|
|Yugoslavia (former)||No information available||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||No information available||OIE Handistatus, 2005|
|French Polynesia||Disease never reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease never reported||OIE, 2009|
|Samoa||Disease never reported||OIE Handistatus, 2005|
|Vanuatu||Disease never reported||OIE Handistatus, 2005|
|Wallis and Futuna Islands||No information available||OIE Handistatus, 2005|
PathologyTop of page
CanL is the result of a chronic infection which may potentially involve any organ. Clinical manifestation of disease may develop three months to seven years after infection. As with other chronic persistent intracellular infections, the immunoglobulin response to infection is usually excessive but not protective, and can eventually be detrimental. T-lymphocyte regions in the lymphoid organs become depleted, and antibody-producing B-cell regions proliferate. The proliferation of B lymphocytes, plasma cells, histiocytes, and macrophages results in generalized lymphadenomegaly, splenomegaly, and consistent hyperglobulinemia. Increased B-cell activity results is the generation of large amounts of specific and non-specific antibodies and circulating immune complexes. Immune complex deposition may cause vasculitis, polyarthritis, uveitis, and glomerulonephritis (Baneth et al., 2008; Solano-Gallego et al., 2009).
The type of inflammatory infiltrate found in tissue cytology or histopathology specimen of organs such as skin, liver, intestine, eye, spleen, lymph nodes, striated muscles, synovium,and nasal mucosa, is commonly either pyogranulomatous to granulomatous or lymphoplasmacytic. Typically, there is lymphoid reactive hyperplasia in lymphoid organs such as lymph nodes and spleen along with histiocytic hyperplasia in the bone marrow and spleen associated with variable numbers of Leishmania amastigotes (Baneth et al., 2008; Miro et al., 2008; Solano-Gallego et al., 2009).
Immune complex glomerulonephritis results in renal failure, which is the main cause of death in dogs with leishmaniosis. Glomerulonephritis is mainly membranoproliferative or mesangioproliferative. Other histological types of glomerular disease including membranous, focal segmental, chronic, and minimal change glomerulonephritis, have also been described in CanL. Membranoproliferative glomerulonephritis is more frequently associated with clinically-manifested kidney disease, whereas in dogs without clinicopathological evidence of renal disease, histopathological evaluation usually reveals mesangioproliferative lesions and minimal change glomerulonephritis (Baneth et al., 2008; Solano-Gallego et al., 2009).
Skin lesions are one of the main clinical manifestations of CanL. A variety of skin lesions have been reported in CanL and they are frequently generalized rather than local because L. infantum disseminates all over the body. In addition, microscopical lesions and presence of parasite may also be detected in healthy-looking normal-appearing skin from sick dogs and not only necessarily in dermal lesions. Dermal manifestation of CanL include exfoliative dermatitis with alopecia which can be generalized or localized over the face, ears and limbs (See pictures: Dermal manifestations of canine leishmaniosis; Exfoliative dermatitis and pinneal ulceration); ulcerative dermatitis over bony prominences, and in mucocutaneous junctions, paws, and the ear pinnae; focal or multifocal nodular dermatitis; mucocutaneous proliferative dermatitis; and papular dermatitis (Solano-Gallego et al., 2009).
Ocular lesions in CanL consist of anterior uveitis, conjunctivitis, keratoconjunctivitis sicca, blepharitis or a combination of these. In keratoconjunctivitis sicca, inflammatory infiltrates located around the lacrimal ducts cause secretory retention and a decrease in tear production. Muscle pathology is attributed to immune mediated mechanisms and inflammatory responses associated with CanL. Muscle weakness is observed in CanL and is associated with mononuclear myositis, neutrophilic vasculitis and IgG immune complexes in muscle tissues in conjunction with serum anti-myofiber antibodies. This includes masseter muscle atrophic myositis, polymyositis, myocarditis and pericarditis (Baneth et al., 2008; Miro et al., 2008; Solano-Gallego et al., 2009; Noli and Saridomichelakis, 2014).
Dogs with leishmanioasis may show signs of hemorrhagic diathesis manifested primarily as epistaxis, and less commonly as hematuria and hemorrhagic diarrhoea. Hemorrhagic diathesis is associated with tissue ulceration and alterations in primary and secondary hemostasis. Epistaxis appears to be the result of thrombocytopathy, hyperglobulinemia-induced serum hyperviscosity, and lymphoplasmacytic or granulomatous rhinitis with or without nasal mucosa ulceration. Anemia usually develops as a sequel to the decreased erythropoiesis of chronic disease or to chronic kidney disease but may be aggravated by blood loss.
More rare pathologic findings in CanL include mucosal lesions of the oral cavity, tongue and genital organs; joint swelling with erosive or non-erosive polyarthritis; osteolytic and osteoproliferative bone lesions; chronic hepatitis; chronic relapsing colitis, neurological disease due to meningitis, and systemic vasculitis with thromboembolism or serum hyperviscosity syndrome (Baneth et al., 2008; Miro et al., 2008; Solano-Gallego et al., 2009).
DiagnosisTop of page
The clinical manifestations of CanL vary as a consequence of the numerous pathogenic mechanisms of the disease process, the different organs affected, and the diversity of immune responses mounted by individual dogs. Pertinent clinical history, a thorough physical examination and several routine diagnostic tests such as complete blood count, biochemical profile, urinalysis and serum electrophoresis can help to raise the suspicion index for this disease and determine its severity. Accurate diagnosis of CanL often requires an integrated approach consisting of clinicopathological diagnosis and specific laboratory tests (Solano-Gallego et al., 2011).
The main clinical findings found on physical examination in typical CanL include skin lesions, generalized lymphadenomegaly, progressive weight loss, muscular atrophy, exercise intolerance, decreased appetite, lethargy, splenomegaly, polyuria and polydypsia, ocular lesions, epistaxis, abnormal nail growth (onychogryposis), lameness, and less frequently vomiting and diarrhoea. Additional variable clinical signs make the list of differential diagnosis to CanL extensive (Solano-Gallego et al., 2009; Solano-Gallego et al., 2011; Noli and Saridomichelakis, 2014).
About 60-80% of the dogs with clinical CanL admitted to veterinary care have dermal manifestations of the disease. Dermal involvement in CanL caused by L. infantum is associated with a visceral infection, and dissemination of the parasite to internal organs, in addition to its presence in the skin. Skin patterns of lesions include: non-pruritic exfoliative dermatitis, ulcerative dermatitis, focal or multifocal nodular dermatitis, mucocutaneous proliferative dermatitis and papular dermatitis. Atypical cutaneous manifestations such as depigmentation, panniculitis, digital and nasal hyperkeratosis, pustular eruption, and erythema multiforme are relatively uncommon.
Up to 80% of the dogs diagnosed with CanL have ocular lesions, including conjunctivitis, blepharitis, keratoconjunctivitis and uveitis. In some cases, ocular abnormalities are the only clinical signs.
Most dogs with clinical CanL will have mild to moderate non-regenerative anemia and less commonly thrombocytopenia. The most consistent serum biochemistry findings in dogs with clinical CanL are serum hyperproteinemia with hyperglobulinemia and hypoalbuminemia resulting in a decreased albumin/globulin ratio. Marked hyperglobulinemia with no apparent cause in dogs from Leishmania-endemic regions should also be investigated for CanL. Grossly elevated activities of liver enzymes or azotemia are found in only a minority of dogs with CanL. However, some degree of renal pathology is present in most dogs with clinical CanL. Azotemia with increased serum creatinine and urea levels usually develops with increased progression toward severe kidney disease. However, proteinuria and an abnormal urine protein/creatinine ratio may be present prior to the development of azotemia (Baneth et al., 2008; Miro et al., 2008; Solano-Gallego et al., 2009; Solano-Gallego et al., 2011; Noli and Saridomichelakis, 2014).
Diagnosis of CanL infection is usually performed for two main reasons: (1) to confirm ’disease‘, e.g. to find out if a dog with clinical signs and/or clinicopathological abnormalities compatible with CanL has the disease; and (2) to investigate the presence of ’infection‘ for epidemiological studies, for screening clinically healthy dogs living in endemic regions usually requested by the owners, to prevent transmission of infection from subclinical carriers by blood transfusion, to avoid importation of infected dogs to non-endemic countries, and to monitor response to treatment. Therefore, it is important to separate subclinical Leishmania infection from disease and to apply different diagnostic techniques accordingly (Solano-Gallego et al., 2011).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly||Diagnosis|
|Digestive Signs / Melena or occult blood in faeces, stools||Sign|
|Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears||Diagnosis|
|Digestive Signs / Polyphagia, excessive appetite||Sign|
|Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears||Sign|
|Digestive Signs / Vomiting or regurgitation, emesis||Sign|
|General Signs / Exercise intolerance, tires easily||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Diagnosis|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Diagnosis|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Diagnosis|
|General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass||Sign|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Sign|
|General Signs / Polydipsia, excessive fluid consumption, excessive thirst||Sign|
|General Signs / Swelling skin or subcutaneous, mass, lump, nodule||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weight loss||Sign|
|Ophthalmology Signs / Abnormal corneal pigmentation||Sign|
|Ophthalmology Signs / Abnormal pigmentation, colour, iris||Sign|
|Ophthalmology Signs / Blepharospasm||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, laceration, cut, tear, injury||Sign|
|Ophthalmology Signs / Conjunctival, scleral, papules||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Ophthalmology Signs / Corneal edema, opacity||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Ophthalmology Signs / Obstruction of nasolacrimal duct||Sign|
|Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding||Diagnosis|
|Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules||Diagnosis|
|Respiratory Signs / Sneezing, sneeze||Sign|
|Skin / Integumentary Signs / Absence of skin||Diagnosis|
|Skin / Integumentary Signs / Alopecia, thinning, shedding, easily epilated, loss of, hair||Sign|
|Skin / Integumentary Signs / Cracked skin, fissure||Sign|
|Skin / Integumentary Signs / Defective growth of nail, claw, hoof||Diagnosis|
|Skin / Integumentary Signs / Dryness of skin or hair||Diagnosis|
|Skin / Integumentary Signs / Foul odor skin, smell||Sign|
|Skin / Integumentary Signs / Hyperkeratosis, thick skin||Diagnosis|
|Skin / Integumentary Signs / Overgrown nail, claw, hoof||Diagnosis|
|Skin / Integumentary Signs / Pruritus, itching skin||Sign|
|Skin / Integumentary Signs / Purulent discharge skin||Diagnosis|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Diagnosis|
|Skin / Integumentary Signs / Scarred skin||Sign|
|Skin / Integumentary Signs / Skin crusts, scabs||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Diagnosis|
|Skin / Integumentary Signs / Skin hyperpigmentation, excess pigment||Sign|
|Skin / Integumentary Signs / Skin hypopigmentation, decreased pigment, vitiligo||Sign|
|Skin / Integumentary Signs / Skin laceration, cut, tear, bite||Sign|
|Skin / Integumentary Signs / Skin papules||Sign|
|Skin / Integumentary Signs / Skin plaque||Sign|
|Skin / Integumentary Signs / Skin pustules||Sign|
|Skin / Integumentary Signs / Skin scales, flakes, peeling||Diagnosis|
|Skin / Integumentary Signs / Skin ulcer, erosion, excoriation||Sign|
|Skin / Integumentary Signs / Splitting nail, claw, hoof, breaking, brittle, cracked||Diagnosis|
|Urinary Signs / Increased frequency of urination, pollakiuria||Sign|
|Urinary Signs / Oliguria or anuria, retention of urine||Sign|
|Urinary Signs / Polyuria, increased urine output||Sign|
|Urinary Signs / Proteinuria, protein in urine||Diagnosis|
Disease CourseTop of page
Canine leishmaniosis is primarily a chronic disease that develops months to years after the initial infection with L. infantum. Infected dogs experience a long sub-clinical infection before the appearance of clinical disease. And, only a small part of the dogs that become persistently infected develop overt clinical manifestations of disease, while the majority of infected dogs appear to remain sub-clinically infected for long period, often for their life time (Baneth et al., 2008; Solano-Gallego et al., 2009).
Population studies in Leishmania-endemic areas have shown that a proportion of the canine population develops a clinical disease, another fraction has persistent subclinical infection, while yet another fraction is resistant to the infection or intermittently resolves it without developing clinical signs. The immune responses mounted by dogs during infection is an important factor in determining if they will develop a lasting infection and whether and when it will progress from a subclinical state into clinical disease. Dogs that are able to resist infection and either resolve it and eliminate the parasite, or restrict the infection and remain constantly asymptomatic, have been termed "clinically resistant". Animals that are predisposed and will develop symptomatic disease are considered "susceptible" (Baneth et al., 2008).
A broad range of immune responses, pathologic and clinical manifestations have been described in CanL. Leishmania infection in dogs may be a subclinical infection, or manifested as a self-limiting disease, or a non-self-limiting disease associated with severe illness. In dogs, the two opposite extremes of this clinical spectrum are characterized by: (1) protective immunity that is CD4 T cell mediated by the release of IFN-gamma, IL-2 and TNF alpha that induce macrophage anti-Leishmania activity, or, (2) disease susceptibility that is associated with the production of a marked humoral non-protective immune response and a reduced or depressed cell mediated immunity with a mixed Th1 and Th2 cytokine production. Within this spectrum, clinical disease can range from a mild papular dermatitis associated with specific cellular immunity and low degree humoral responses to a severe disease associated with a massive humoral response and high parasite loads frequently associated with glomerulonephritis (Baneth et al., 2008; Solano-Gallego et al., 2009).
Specific immune responses play a major role in susceptibility to infection. During infection, dogs become increasingly immunosuppressed and may develop decreased CD4+ lymphocyte counts and a decrease in the CD4+/CD8+ ratio. Moreover, it has been demonstrated that the infectiousness of dogs with leishmaniosis to sandflies increases with the decrease in CD4+ counts (Guarga et al., 2000). Immune-mediated mechanisms are responsible for much of the pathological findings in CanL. Circulating immune complexes and antinuclear antibodies have been detected in animals with CanL. Glomerulonephritis associated with the deposition of immune complexes in the kidneys is a hallmark of the disease. Renal pathology is present, even if not manifested clinically, in the majority of infected seropositive dogs (Baneth et al., 2008).
EpidemiologyTop of page
The natural life cycle of Leishmania infection involves a sandfly vector and a vertebrate host. Phlebotomine sandflies of the genus Phlebotomus in the Old World and Lutzomyia in the New World are the natural vectors of leishmaniosis. In the Mediterranean region and Asia, sandflies are primarily active from spring to late autumn, while in Latin America, some sandfly species are active throughout the year. Sandflies in general do not move long distances, and studies have shown that they are seldom dispersed more than 2 km away from their initial location of previous detection (Maroli et al., 2010). Many species of sandfly exist, but only some of them are competent vectors of Leishmania able to transmit infection. Different vector species may be found in distinct geographic regions and ecologic niches. Some sandfly species exclusively transmit only one Leishmania species, whereas others are permissive vectors able to transmit several species. The capacity of different sandfly species to act as vectors appears to be related to the ability of Leishmania parasites to specifically bind to ligands in the sandfly digestive system. When they do not bind to the sandfly gut, the parasites that initially replicated in the gut lumen are excreted with the digested blood and do not transmit during a second blood meal (Dostálová and Volf, 2012).
The Leishmania life cycle includes two life forms: the promastigote, which is a flagellated free form that develops in the sandfly, and the amastigote, which is the parasite’s intracellular form found in the cytoplasm of host macrophages (Solano-Gallego et al., 2009). During the sandfly’s bite, blood from the vertebrate host with intracellular amastigotes is taken up by the sandfly. The vertebrate host’s infected macrophages rupture in the sandfly’s gut and release amastigotes which transform under the change in temperature and pH into promastigotes. Promastigotes bind to the sandfly gut, replicate in large numbers, and migrate toward the anterior gut close to the valve that separates the gut from the pharynx. They evolve into metacyclic promastigotes and are injected to the skin of the vertebrate host with saliva during the infected sandfly’s subsequent blood meal (Dostálová and Volf, 2012). In the skin, promastigotes invade macrophages and transform in to the amastigote intracellular form. Invasion of the macrophage is mediated via binding to a membrane receptor, phagocytosis into a phagosome, and continued survival in cytoplasmic vesicles, inhibiting destruction of the parasite by the lysosome enzymes and oxidative burst. The promastigotes are rapidly transformed into amastigotes in the macrophage cytoplasms. Amastigotes replicate by binary fission and fill the macrophage with more parasites until it ruptures, and then amastigotes invade additional macrophages and disseminate. Dissemination and parasite replication initially takes place in the skin, and then infected macrophages reach the local draining lymph nodes and in the case of visceralzing Leishmania species, such as L. infantum, they disseminate further via the blood and lymph to internal organs including the spleen, liver and to the bone marrow. Cells with amastigotes can also be found widespread in the host’s skin distantly from the original infectious bite site, due to parasite migration and dissemination from other infected organs. Further transmission of the parasite takes place when additional sandfly females feed on the infected hosts’ skin and uptake infected cells in their blood meal (Solano-Gallego et al., 2009).
Impact: EconomicTop of page
No formal figures are published for the economic loss due to CanL. Losses would include expenses for prevention of the disease via vaccination and use of insecticides; expenses for the diagnosis of infection and for its treatment.
Zoonoses and Food SafetyTop of page
Visceral leishmaniois is a severe human disease that may be fatal if untreated. It primarily affected young children and infants in the past, but now it is also often a complication in adults infected with human immunodeficiency virus (HIV) or those receiving immunosuppressive therapy. Transmission of L. infantum from dogs to humans via sandflies is considered to be the main route of this zoonotic infection. Several studies have investigated the association between canine and human leishmaniosis in the same region and examined to what degree infection in dogs poses a risk for human disease. An increased prevalence of infection in the canine population is associated with increased incidence of human leishmaniosis, poor socioeconomic conditions are risk factors for the association between canine and human infections, and dog density and infected dog ownership are risk factors for infantile human leishmaniosis. The link between dog and human infections probably differs from one region and life style to another and could depend on factors such as human nutrition, time spent outdoors, the density of dogs, and the behaviour of local sandfly vectors (Baneth et al., 2008; Miro et al., 2008).
In southern Europe, where human disease is often sporadic and the ratio between clinically affected humans and infected dogs is low, the ownership of dogs is usually not observed as being associated with an increased risk to humans. Despite this, effective control of canine leishmaniosis could lead to a decrease in human leishmaniosis in endemic regions.
Infected pets may remain disease carriers despite treatment. In areas where sandfly vectors are found, this poses a problem to owners, veterinarians, and local public health and environmental agencies who are concerned with the risk to humans and animals. Before deciding on the fate of an infected pet, owners should be consulted and educated about the disease, its zoonotic nature, the prognosis for their dog, what should be expected from therapy, and safety precautions that should be taken (Miro et al., 2008; Solano-Gallego et al., 2011).
Disease TreatmentTop of page
The main drugs used for treatment of CanL include: (1) the pentavalent antimony meglumine antimoniate (Glucantime®) which selectively inhibits leishmanial glycolysis and fatty acid oxidation; (2) allopurinol which acts by inhibiting protein translation through interfering with RNA synthesis; (3) Miltefosine (Milteforan®) which is an alkylphospholipid with a direct toxic effect on Leishmania parasites impairing signalling pathways and cell membrane synthesis. Treatment with these drugs is frequently combined, with allopurinol administered together with meglumine antimoniate or with miltefosine for 4 weeks initially and then allopurinol continued alone for long term therapy of at least 6 months and often a year or longer (Solano-Gallego et al., 2011; Noli and Saridomichelakis, 2014).
Amphothericin B which acts by binding to ergosterol in the parasite's cell membrane and altering its permeability is also effective but it is highly nephrotoxic and therefore not recommended.
The WHO recommends that drugs used against leishmaniosis in people should not be used in animals due to the possibility of provoking resistance and development of drug-resistant strains (http://whqlibdoc.who.int/trs/WHO_TRS_949_eng.pdf). Allopurinol is not used again leishmaniosis in humans and therefore it is good choice for the fulfillment of the WHO requirements.
Anti-leishmanial treatment often achieves only temporary clinical improvement in dogs with leishmaniosis and it is frequently not associated with the complete elimination of the parasite. Treated dogs often remain carriers of the disease, may be infectious to sandflies and may experience clinical relapses. Owners must receive a thorough and realistic explanation about the disease, its zoonotic potential, the prognosis for their dog, and what should be expected from treatment.
The indications for stopping treatment are fulfillment of all the following terms: complete disappearance for the clinical signs of disease, normalization of the hematology and serum biochemisty paramaters, and a negative serological titer by a quantitative antibody test, such as the IFAT or ELISA (Solano-Gallego et al., 2011).
Prevention and ControlTop of page
Decrease of sandfly bites and subsequent infection can be achieved by keeping dogs indoors during the sandfly season from dusk to dawn, reducing the microhabitats favourable to sandflies in the vicinity of the house or in locations where the dog spends time, and use of insecticides. The use of topical insecticides against CanL in collars or spot-on formulation containing pyrethroids has been shown to be effective in reducing disease transmission. Deltamethrin-impregnated collars and permethrin with imidacloprid spot on drops have been shown to significantly reduce the number of sandfly bites to dogs under experimental transmission and demonstrated decreased transmission of infection in field studies. It is also recommended that dogs travelling from a non-endemic region for CanL to an endemic region would wear collars against sandfly bites or be treated with some other topical insecticide with approved efficacy against sandfly bites (Miro et al., 2008; Solano-Gallego et al., 2009; Maroli et al., 2010).
Commercial vaccines against CanL have been approved in Brazil and Europe, however they do not completely prevent infection but rather decrease the occurrence of clinical disease. The only commercial vaccine currently available in Europe is CaniLeish® manufactured by Virbac, which consists of excreted-secreted products obtained by in vitro culture of L. infantum promastigotes with the QA-21 saponin adjuvant. The first immunization consists of 3 subcutaneous injections at 3-week intervals in dogs above 6 months of age seronegative to L. infantum based on a negative rapid serological test supplied by the vaccine manufacturer. Booster vaccination is recommended every year (Gradoni, 2015).
In Brazil, the Leishmune® vaccine manufactured by Zoetis is a fucose-mannose ligand (FML) extract from L. donovani with a saponon adjuvant. The LeishTec® is a second approved canine vaccine in Brazil produced by Hertape Calier and based on recombinant protein A2 and saponin (Gradoni, 2015).
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24/02/15 Original text by:
Gad Baneth, Professor of Veterinary Medicine, The Rybak-Pearson Chair in Veterinary Medicine, School of Veterinary Medicine, Hebrew University, P.O. Box 12, Rehovot 76100, Israel.
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