In many Leishmania-endemic regions of the world, infected dogs serve as a significant under local anesthesia using a current field radio-frequency generator. Canine leishmaniasis (CanL) is a parasitic disease caused by the can be diagnosed in approximately 50% of dogs with leishmaniasis using. Current treatment of canine Leishmaniasis leads to a notable and fast clinical Access to it as well as possible use of it will be the sole responsibility of the user.
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Spraying campaigns are inappropriate because of environmental considerations. Individual protection of dogs is advised. Dogs are to be kept indoors in the evening. Putting deltamethrin impregnated collars on all dogs has been demonstrated to reduce the prevalence of the infection. This could be a promising solution in the future. Whilst anti-leishmanial treatments of dogs are considered to achieve clinical cure unfortunately they do not result in the complete elimination of the parasite.
Pentavalent antimoniate Glucantime and Pentostam are widely used. They may inhibit leishmanial glycolytic enzymes. The most common protocol for Glucantime therapy is: After several injections, the therapy can be painful. It is expensive in the long term for large dogs. It may induce drug resistance. Allopurinol is an analogue of hypoxanthine. The product is incorporated into leishmanial RNA and alters protein synthesis.
The most common protocol for allopurinol is: The product is easy to administer orally. The treatment is usually appreciated by owners for its low cost and relative non toxicity. It can be administered for long periods of time.
It is nowadays widely used as monotherapy or in combination with pentavalent antimonials. Allopurinol is the therapy to be recommended.
The injections are painful. Amphotericine B is primarily an antifungal drug. It alters leishmanial cell membrane permeability. The conventional product has a toxic effect on canine kidneys.
The liposomal presentation AmBisome has reduced side effects. The treatment is expensive. Paromomycin Aminosidine inhibits ribosomal function. The product can be nephro- or oto-toxic.
Miltefosine is effective as anti-leishmanial therapy in mice and humans. A liposomal presentation is currently under evaluation in dogs. How to treat in practice: Before starting treatment, a complete blood count, a biochemical profile to assess renal function, and a protein electrophoresis are necessary.
For treatment, allopurinol is the author's personal recommendation. As relapses are common, periodic every six months monitoring of the patient has to be performed. Recent advances in techniques of diagnosis, control measures and therapy have changed the approach to CanL.
Improvement of the treatment is still needed to be able to eliminate the parasite from the canine host. The disease remains too often a frustrating problem for the practitioner and a danger to public health. E canis, E chaffeensis, A phagocytophila. PCR for Babesia canis. Cat Spermatozoa in the Female. Fixation of the Knee Joint. Protruding Third Eyelid Gland.
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Symptomatology The clinical signs of CanL are very variable. Diagnosis Diagnosis is based on non specific tools clinical signs and clinical laboratory findings and specific tools parasitology, serology and more recent molecular techniques. A parasitological cure is rarely achieved and clinical recurrences in CanL are frequent. Vaccination associated with the use of topical insecticides is undoubtedly the most effective form of prevention and control of the disease.
In order to integrate the most important scientific knowledge of the literature in one objective publication, this review proposes a short overview of the main points of CanL. Leishmaniasis is a group of diseases produced by the invasion of protozoan parasites of the genus Leishmania into the mononuclear phagocyte system of mammalian hosts. They are transmitted primarily by the hematophagous activities of female phlebotomine sand flies belonging to the genera Lutzomyia New World and Phlebotomus Old World.
These neglected diseases are prevalent in at least 98 countries and 3 territories on 5 continents, of which the majority are underdeveloped countries [ 1 , 2 ]. Approximately 12 million people are infected with a species of Leishmania at any given time [ 2 ]. About 70 species of mammals, including humans, are considered vertebrate hosts of different species of Leishmania around the world, and some of them are reservoirs of the parasite in nature [ 1 ].
Although the natural infection in rodents [ 3 , 4 ] and canids [ 5 — 10 ] is more common, the parasite is able to infect xenarthrans [ 11 , 12 ], hyraxes [ 13 ], marsupials [ 14 ], chiropterans [ 15 — 17 ], lagomorphs [ 18 — 21 ], procyonids [ 11 , 22 ], felids [ 23 — 26 ], Perissodactyla [ 27 , 28 ], and primates [ 11 , 29 ]. Determining the precise role played by each host in the transmission cycle remains a challenge.
These protozoans cause a wide variety of clinical forms ranging in severity from self-healing cutaneous leishmaniasis CL to fatal disseminated visceral leishmaniasis VL [ 30 ]. Among the recognized clinical forms of the disease, kala-azar, or VL, is the most severe and progressive form, as it is almost always fatal if untreated. In the rest of the world, particularly in the highlands of China, Central Asia, the Middle East, Transcaucasia, the Mediterranean, and Central and South America, VL is a zoonosis; that is, it is transmitted between animals and is secondarily transmitted to people [ 31 ].
Since the discovery of CanL in Tunisia, by Nicolle and Comte [ 33 ], the dog has been implicated as a major reservoir of the etiological agent of VL, playing a key role in its transmission [ 34 ].
Other infected mammals, such as the crab-eating fox Cerdocyon thous and opossums Didelphis spp. Maned wolves Chrysocyon brachyurus and bush dogs Speothos venaticus can be infectious to sand fly vectors even in the absence of clinical signs, but the epidemiological relevance of these findings has not yet been established [ 29 , 37 , 38 ].
The susceptibility of domestic cats Felis catus to infection by L. It seems that the immune response in cats is effective enough to control the infection and confer a certain degree of resistance, if there are not immunosuppressive events such as retroviruses [Feline Immunodeficiency Virus FIV and Feline Leukemia Virus FeLV ] [ 40 ], cancer, autoimmune disease, and others. Though infected domestic cats could be infectious to competent vectors of L.
Among the over phlebotomine sand fly species estimated to exist, about 98 species are currently proven or suspected vectors of leishmaniasis [ 41 ]. Like many other vector-borne diseases, transmission originates during blood meals that females require to develop a batch of eggs. The parasite has a digenetic life cycle, alternating between a mammalian host and insect vectors. In short and according to the literature, when a sand fly bites an infected host, it also ingests macrophages infected by rounded and nonmotile amastigote forms.
Then, the parasites transform from the amastigote to the flagellate promastigote stage, multiply by binary fission in the midgut, and migrate to the foregut and in mouth parts pharynx, cibarium, and proboscis of the infected sand fly vector. Subsequently, it can be transmitted to other new hosts, where these flies feed on blood meals, and the invertebrate cycle is concluded. They then evolve into the amastigote form, where reproducing asexually and continuously in macrophages until rupture occurs.
The parasites spread by invading mononuclear phagocytes in many organs, mostly spleen, liver, bone marrow, lymph node, and other tissues [ 7 , 42 — 47 ]. Intriguingly, the occurrence of autochthonous cases of VL in places where the presence of phlebotomine has not been proven suggests other routes of transmission. Although non-sand fly transmission is reputed to be low, several studies have clearly shown the potential impact of nontraditional transmission routes in CanL, particularly sexual venereal and transplacental vertical transmission, which may have epidemiological significance in the dissemination and maintenance of disease, especially in the absence of the biological insect vector [ 48 ].
Sexual and transplacental transmission of Leishmania has already been reported in mice [ 49 ], humans [ 50 — 54 ], and dogs [ 55 — 59 ]. Genital lesions associated with VL have been well documented in dogs [ 60 — 62 ] and it seems that sexual transmission in dogs tends to be more efficient from the infected male to a susceptible female [ 63 ].
Together these studies strongly support the notion that CanL is vertically transmitted. Other forms of transmission, such as infection during blood transfusion [ 70 ] or derivatives from infected donors [ 71 , 72 ], organ transplantation [ 73 , 74 ], and sharing of contaminated needles [ 75 ], should be carefully considered mostly in dog and human hosts.
Additionally, a suspected mode of transmission is the direct dog-to-dog transmission of the parasite by wounds or dog bites [ 76 , 77 ]. Other blood-feeding arthropods, such as ticks or fleas, have sometimes been suspected of transmitting Leishmania based on the association of CanL with the presence of these alternative vectors [ 78 , 79 ]. Despite there being no definitive conclusion about the role of these ectoparasites in the transmission cycle of the disease [ 79 , 80 ], it is nonetheless advisable to prevent and treat dogs against fleas, ticks, and mosquitoes [ 81 ].
The number and intensity of clinical signs are determined by a set of factors involving parasite strain, genetics, and the host immune status. In this way, some dogs are able to control the infection for many years, without the appearance of clinical signs, and sometimes may even evolve spontaneous cure. On the other hand, some infected dogs may display an acute evolution and severe disease, or progressive course that leads inexorably to death, if proper management and therapy are not adopted.
Moreover, when dogs are ill, they manifest a variable and nonspecific clinical spectrum [ 34 ], because CanL is a chronic and multisystemic disease that may potentially involve any organ [ 91 ].
Clinical manifestations of dogs naturally infected with L. Clinical signs may be present from three months to several years after dogs become infected [ 93 ]. In the classic cutaneovisceral form, one of the earliest and most common clinical signs of the disease is lymphadenopathy, mainly affecting the popliteal Figure 1 c , prescapular, and submaxillary lymph nodes [ 94 ].
Dermatological abnormalities occur later and are frequent and variable in their characterization and extension [ 95 ]. The classic dermatological patterns include nonpruritic exfoliative dermatitis with or without alopecia, which can be localized or disseminated Figures 1 b , 1 d ; erosive-ulcerative dermatitis Figure 1 e ; nodular, papular, or pustular dermatitis; nasal hyperkeratosis Figure 1 d ; nasal depigmentation and onychogryphosis Figure 1 f [ 93 , 97 , 98 ].
Other signs involve anorexia, chronic enteritis and weight loss, splenomegaly and hepatomegaly, ophthalmopathy, and hypotrophy muscle [ 91 , 93 , 97 , 99 ], as well as unusual or atypical signs like arthritis and neurological manifestations [ , ]. Renal disease may be the sole clinical manifestation of CanL and it can progress from mild proteinuria to nephrotic syndrome or to an end stage renal disease [ 91 ].
Chronic renal failure is a severe result of disease progression and is the most common cause of death [ 91 , 97 ]. There are two known clinical staging systems for CanL, with a good level of agreement between them [ ], which contribute to the establishment of a more accurate diagnosis, prognosis, and treatment [ ] by grouping the affected dogs according to the severity of their clinical presentation.
There remains no consensus on the exact relevance of each clinical form in the transmission cycle of the parasite. Some evidence suggests that the majority of transmission events to vectors result from a small proportion of infectious dogs with very high skin parasite loads, which would be correlated to severe disease [ , ].
On the other hand, asymptomatic dogs could be also highly infectious, indicating their role in maintaining and spreading the parasite in endemic areas [ ]. Despite these contradictory results and until specific and sensitive markers of infectiousness, whether direct or indirect, are available, it is prudent to consider that both symptomatic and asymptomatic dogs could be infectious to sand fly vectors and that they should therefore be considered equally when proposing control measures.
The immune mechanisms responsible for resistance or susceptibility to infection are not yet well known. The effectiveness of the immune response is a fundamental aspect in the pathogenesis of the disease and its progression [ ], playing a crucial role in clinical manifestations of CanL.
Conversely, the Ibizan Hound has been reported to be more resistant to Leishmania infection due to it displaying a predominantly cellular immune response [ , ]. The greater rate of infection in working dog breeds is possibly due to more contact time with the insect vector in outside environments. Although controversial, the length of the coat can probably influence the risk of infection, since it is a characteristic that varies greatly among canine breeds. In short, it seems that the chances of acquiring Leishmania infection are lower in mixed-breed female dogs, with long hair, maintained in domestic-restricted or restrained dogs raised indoors without the presence of green surroundings close to home [ ].
The laboratory analysis of parameters related to hematopoiesis, renal function, and serum electrophoretic profile must be used in the clinical routine as a complementary tool in diagnosis. The marked polyclonal humoral response that occurs after infection gives rise to visible changes in the electrophoretic plasma profile and contributes to the occurrence of organs damage, such as kidneys, eyes, and skin.
In addition, high parasite loads in the components of the mononuclear phagocyte system MPS , for example, in bone marrow and liver, triggering the occurrence of clinical pathology related to hepatic and hematopoietic functions [ 34 ].
Anemia is one of the main laboratory findings on the hemogram. It is likely that more than one factor is involved in the etiology of anemia, such as hemorrhage, hemolysis, chronic renal failure, bone marrow hypoplasia, or aplasia, and decreased lipid fluidity of the erythrocyte membrane [ 34 , , ]. Apparently, there is a relationship between anemia and clinical forms of the disease [ 34 , , ].
Bone marrow dysfunction does not usually involve precursor cells of leukocytes [ 34 , ], although dermatological lesions accompanied by secondary bacterial infections, or other comorbidities, can do so. Dysproteinemia is considered one of the most important changes in the disease [ 34 ]. The reduction of albumin levels is partly a result of renal excretion due to glomerular damage produced during the course of the disease and the low production by the liver in cases of liver failure.
Renal disease in CanL may manifest as mild proteinuria to nephrotic syndrome or chronic renal failure, in which there is glomerulonephritis usually associated with the deposition of immune complexes in the kidneys.
BioMed Research International
Vaccination associated with the use of topical insecticides is . The Canine Leishmaniasis Working Group (CLWG) System classifies dogs into. A vaccine used to prevent dogs from contracting the deadly, parasitic disease canine leishmaniasis also can be used to treat currently infected. The prevalence of canine leishmaniosis in the Autonomous Community of . using skin and spleen from dogs with natural Leishmania infantum infection. Vet.