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my with dog on Leishmaniasis Using



  • my with dog on Leishmaniasis Using
  • BioMed Research International
  • chapter and author info
  • 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.

    my with dog on Leishmaniasis Using

    It currently occurs from southern Canada [ 45 ] and the United States [ 46 , 47 ] to northern Argentina [ 48 , 49 ]. In North America, it was first reported on hunting kennels of Foxhound dogs in New York, in [ 46 ]. Since then, CVL has been spreading and has so far been diagnosed in 18 North American and two Canadian states, totaling 58 kennels with positive Foxhounds, but with no reports of human cases.

    Isozyme characterization showed that the isolated agents from 46 Foxhounds are Leishmania infantum MON1 [ 45 ]. High mortality and transmissibility rates associate with these foci in North America. It is believed that the disease was imported from Southern Europe due to dog travel history between these regions [ 50 ].

    Direct transmission forms are associated with these outbreaks: Among Brazilian cities and states, variation in prevalence of CVL is huge, ranging from 0. CVL urbanization correlates with increasing global mobility [ 54 ] associated with demographic and ecological factors. Louis, Sobral, Teresina, and Salvador. They then proceed to live in suburban areas with unsanitary conditions and malnutrition. Migrants often bring along their dogs and raise chicken and pigs around their homes, all ultimately serving as a feed source for the vector.

    According to Moreno et al. In the same year, Lutzomyia longipalpis was found in urban areas of San Borja, a species not previously reported in the Southern region [ 58 ].

    Since then, new cases were reported: Of these 34 reports, 20 were autochthonous, showing that it is an emerging zoonosis in the state [ 59 ]. Prevalence of CVL in the world varies widely, and such variation also applies to different locations within the same city, suggesting that different ecosystems favor maintenance of vectors in different manners [ 60 ].

    As noted by Azevedo et al. Migration of humans and their pets, disorderly occupation, poor living conditions, deforestation, and climate change associated with vector-adaptive capacity are some of the causes of the global urbanization of leishmaniasis [ 54 ]. The best example of the phenomenon of urbanization of zoonotic visceral leishmaniasis is happening in Brazil [ 54 , 63 ]. VL has invaded urban centers and large capitals with no previous record of autochthonous cases [ 12 ].

    The prevalence of human VL caused by L. There is no consensus on the risk factors associated with CVL, as results differ between the studied Brazilian regions and between countries. In Portugal, risk factors are outdoor rearing, age over two years , short fur, pure breeds, and location dogs in the hinterlands are more likely to be affected [ 29 ]. In Brazil, Belo et al.

    Another study in Brazil defined risk factors as outdoor rearing, contact with poultry, dogs living in rural areas, the presence of organic matter, the absence of environmental management, and proximity to forests [ 65 ]. As for dogs in the countryside, in an endemic area of Northeastern Brazil, the only identified risk factor found was sex, as male dogs were twice as likely to develop the disease [ 66 ].

    The components of the immune system act in a complex and coordinated manner to prevent entry and survival of foreign agents in the body. The first line of defense is the innate immunity, which responds immediately and unspecifically to a range of pathogens, and further presents them to the constituents of adaptive immunity when needed.

    Adaptive immunity will then generate a specific response and develop memory cells against such antigen. Performance of these defense mechanisms can control infection and ensure the least possible damage to host tissues.

    In visceral leishmaniasis, the result of the relationship between parasite and host is determined by complex factors involving saliva components of the vector insect, agent-secreted surface proteins, and different responses produced by the host [ 67 ]. It ultimately promotes inhibition of immune response by either stimulating the development of regulatory T cells [ 69 ] or exerting some degree of control over the complement system, exploring its opsonic properties to facilitate adherence with phagocytic cells and preventing their lytic effects through the action of gp63 glycoprotein expressed on the parasite surface [ 70 ].

    It has been documented that resistance to infection by L. Progression of the infection, however, relates to exaggerated humoral response and cellular immune depression, consequently bringing up an onset of clinical signs [ 71 — 74 ].

    Asymptomatic animals also exhibit lower parasitism, whereas the symptomatic generally carry high parasite load in different tissues such as the skin, bone marrow, spleen, liver, and lymph node [ 73 — 76 ].

    Through antigen presentation, the cells of innate immunity stimulate the acquired response. Antigen-presenting cells have receptors that recognize pathogen-associated molecular patterns PAMPs expressed by the parasite. Among these, the Toll-like receptor TLR is one of the most studied. Stimulation of these receptors culminates with the activation of signaling pathways in infected cells, which results in induction of antimicrobial genes and inflammatory cytokines IL, TNF while increasing the ability of cells to present antigen.

    Thus, pathogen recognition by TLR receptors helps conducting adaptive immune response against the presented antigen [ 77 ]. Expression of TLR genes in dogs infected with L. In spleen samples, decreased transcription for TLR4 and IL has been observed when infected groups were compared with controls. Decrease in transcription of TLRs, Th17, and FoxP3 cytokines is suggestive of silent establishment of infection [ 78 ].

    In peripheral blood samples from infected dogs, the highest expression of TLR2 and its receptor CD11b CR3 by monocytes correlates with reduced parasitic load and higher resistance to leishmaniasis [ 79 ].

    Studies have shown that both inlet and survival of Leishmania spp. The agent reaches the interior of macrophages when they phagocyte apoptotic bodies of previously infected neutrophils, where it can survive and multiply. The main effector mechanism involved in protective immune response against Leishmania spp.

    Antigen-presenting cells submit Leishmania spp. It is reported, however, that control of infection depends on Th1 cells that activate macrophages, promoting elimination of intracellular parasites [ 86 ], whereas Th2 cells direct the immune system toward humoral response and negatively regulate cellular immunity, promoting Th1 cell anergy [ 87 ].

    They play an important role in resistance to infection. The findings suggest that Treg cells are a major source of IL in the spleen and participate in the modulation of immune response, while a small percentage of these cells in infected dogs may be related to persistent immune activation [ 90 ].

    The role of B cells in CVL is unclear. Although the relationship between a pattern of anti- Leishmania humoral response and resistance or susceptibility to LV is not well defined [ 92 ], immunoglobulin profile may appear as a biomarker for monitoring clinical prognosis and tissue parasitic density, as it is associated with the progression of clinical signs and increase of parasites in lymphoid organs [ 73 ]. Cytokine patterns for CVL have not been well established.

    Studies are inconclusive, so the pattern of immune response associated with resistance or susceptibility in infected animals is yet to be established. One of the first studies on cytokine profiling in CVL was performed by Pinelli et al. Since then, much research has been done in order to elucidate the cytokine profiles found in various tissue compartments of infected dogs.

    They revealed contrasting cytokine profiles among different tissues, indicating that the immune response in LVC occurs in an organ-specific manner [ 71 ]. Profile of cytokines in peripheral blood mononuclear cells PBMC culture from asymptomatic dogs experimentally infected with L. After evaluating expression of cytokines in spleen cells from dogs naturally infected with L. Do Nascimento et al. Increased expression of IL-5 and IL in the skin of healthy dogs and negative correlation of the latter with clinical disease progression were also observed.

    Regarding cytokine profile in the bone marrow, Quinnell et al. However, some infected dogs had detectable expression of mRNA for IL-4 significantly correlated with more severe clinical signs.

    Moreover, expression of mRNA for IL was not detected either in control or in infected dogs, and unlike in human infection, immunosuppressive activity of IL was not observed in CVL [ 94 ].

    Dogs infected with L. Deficiency in IL mRNA expression was evident in the symptomatic dogs compared to the asymptomatic. Reduction in cytokine expression results in decreased iNOS expression and therefore higher parasite load. The increase in IL expression in the liver of asymptomatic dogs and its correlation with elevated expression of iNOS indicates a protective role of that cytokine in canine infection by L.

    However, Michelin et al. Another subject lacking clarification is the participation of chemokines and their receptors in resistance or susceptibility to LVC. Knowledge surrounding the role of these modulators in response to L. On the other hand, CCL24 expression negatively correlated with parasitism [ ]. After connecting clinical findings in naturally infected dogs with liver and spleen parasitism and expression levels for cytokines, chemokines, and their receptors, Albuquerque [ 67 ] showed that symptomatic dogs exhibit low expression of these modulators, alongside lower inflammatory response, and higher parasite load—primarily in the liver—than asymptomatic animals.

    CXCL10 was the only chemokine found at a much higher concentration in both the liver and the spleen of symptomatic animals. It also positively correlated with clinical score. The author indicates that expression profiles of hepatic and splenic chemokines and their receptors are essential for induction of correct cell inflammatory profile, as it has potential to contain the infection and the disease. Impaired cell migration facilitates replication of the parasite and development of CVL symptoms [ 67 ].

    Understanding of the immune response in canine visceral leishmaniasis may reveal the factors involved with the onset and severity of clinical signs and the damage to host tissues. Additionally, it takes place as an indispensable tool for development of an effective vaccine.

    Classical symptomatic case with emaciation, thickened skin, cutaneous lesions, exfoliative dermatitis, fur loss, and cutaneous ulcers. At first, kala-azar signals can be rather discrete and easily confused with other diseases. Clinical leishmaniasis may appear quickly after infection or within two years. Partial paralysis of hindquarters is often seen in the final stage of the disease.

    The most common skin lesions in dogs with kala-azar are exfoliative dermatitis generalized, regional, or localized ; ulcerative dermatitis, onychogryphosis, and papular dermatitis.

    Focal or multifocal nodular forms have a high amastigote load and may indicate either inefficient or strong cellular immunity by the host [ , — ]. Ocular disease occurs in CVL, with anterior uveitis being the most common ocular manifestation, characterized by conjunctivitis, blepharitis, periocular alopecia, exophthalmia, keratitis, keratoconjunctivitis sicca, anterior uveitis, glaucoma, and retinal detachment [ ]. The nosebleeding epistaxis occurs due to thrombocytopenia and is often confused with ehrlichiosis, a bacterial disease transmitted by ticks, which in many cases might associate with leishmaniasis.

    In endemic areas, it is advisable that any diagnosis of ehrlichia or anaplasma in dogs must be accompanied by differential diagnosis of kala-azar. In general, dogs in endemic areas are poly-infected and malnourished, particularly stray dogs or those who frequently wander on the streets, leading to a plurality of overlapping clinical pictures. Among other conditions, furfuraceous flaking due to scabies, weight loss as consequence of other infections or lymphomas, and autoimmune diseases, such as systemic lupus erythematosus, often confuse diagnosis since clinical signs are usually not pathognomonic.

    Therefore, differential diagnosis must be a concern for the small animal clinician [ , ]. Treating seropositive dogs for canine visceral leishmaniasis CVL is a controversial practice in Brazil and, above all, not recommended by the World Health Organization, mainly because it does not lessen the importance of the dog as a reservoir, and utilizes drugs used in human treatment of visceral leishmaniasis VL [ ].

    Nevertheless, European countries legally established treatment since the twentieth century [ ]. Frequent usage of these drugs in veterinary clinics may select resistant parasites due to variation in sensitivity of leishmania species, in addition to providing low parasiticide effect, thus interfering negatively in human treatment [ ].

    The lack of success for parasitological cure occurs mainly because it is an intracellular parasite and is located in less vascularized tissues where it can be difficult to obtain therapeutic doses, such as the vitreous body [ ]. Many studies have been conducted in order to find an effective treatment for CVL, but drugs currently available are still inefficient, only allowing temporary remission of clinical signs.

    Besides, some have a high cost and produce toxic effects. A variety of drugs, such as amphotericin B, pentamidine isethionate, ketoconazole, fluconazole, miconazole, itraconazole, has been used either isolated or in combination and produced different results [ ].

    Due to the possibility of parasitic resistance to first-choice drugs, chemotherapeutic treatment options are limited. In addition, due to the high cost and long-term use, chemotherapy becomes an undesirable option for owners.

    In veterinary medicine, the first choice as chemotherapy for treatment of CVL is allopurinol, a leishmaniostatic drug that acts by inhibiting leishmania growth through DNA modification. It has low cost, but parasite resistance to it remains unknown. Allopurinol is however the only drug recommended by the World Health Organization, especially since it is little used for treatment of human leishmaniasis [ ].

    Antimonials are leishmanicidal drugs that hinder promastigote metabolism by inhibiting glycolytic activity. These are drugs of choice for human treatment of VL but are chemically similar to those that have been used in therapeutic protocols in dogs. Their toxicity and efficacy are related to the antimony content [ ]. When assessing the therapeutic efficacy of Glucantime alone or associated with an antigenic extract of L.

    Yet, upon using meglumine antimoniate and allopurinol—alone and in combination—in dogs naturally infected by L. Despite clinical improvement of treated animals, however, the combination was not able to eliminate the parasite in all dogs. Thus, this protocol is not recommended, since treated dogs would go on as a source of infection for humans and other dogs, similar to results obtained using antimoniate, which promoted hematologic normalization and bone marrow recovery, but not parasitological cure, and to findings from another study wherein dogs showed increased parasitic load in lymph nodes [ — ].

    In accordance with Ikeda-Garcia et al. Therapy resulted in clinical improvement accompanied by reduction in parasite burden, but even after a long period of treatment with allopurinol alone, parasites remained in tissues [ , ]. Miltefosine is another drug used in human treatment that has been evaluated for canine treatment in recent years.

    It is a phospholipid antibiotic of broad spectrum with leishmanicide effect that improves the activation of both macrophages and T cells [ ]. After evaluating efficacy of three treatment protocols for dogs naturally infected with L. Hence, miltefosine alone is not recommended for treatment. There was a decrease of IL-4, indicating possible resolution of the infection and efficacy of the treatment, since this cytokine is a good marker for the occurrence of active disease [ , ]. Some studies seek to associate chemotherapeutic treatment to immunomodulatory drugs, which plays a role in therapeutic protocols by controlling clinical signs and in prevention protocols by enhancing the immune cell-mediated response through activation of macrophages via helper T cells, in order to destroy phagocytized microorganisms.

    Domperidone is a receptor antagonist of dopamine D2 that has been used as well. When orally given to naturally infected dogs, results showed a reduction of clinical signs and titers of anti-leishmania antibodies [ ].

    Nevertheless, further clinical trials are needed to determine the optimal dose, as well as posttreatment investigations to check for parasitological cure, since the drug is a good choice for infected animals with kidney failure due to its route of administration, and it is a low-cost option [ ]. Amphotericin B is a broad-spectrum macrolide antibiotic produced by actinomycete Streptomyces nodosus [ ], available for usage in VL treatment.

    According to Solano-Gallego et al. Additionally, it is frequently used in the treatment of both human and canine VL for being inexpensive. They observed reduction in clinical signs and parasite density, in antibody titers through indirect immunofluorescence, and in prevalence of positive dogs using PCR 3 months after the end of the experiment. These findings can be explained by direct action of the drug as well as activation of cellular immunity. However, more studies are required to prove its therapeutic efficacy for CVL, especially considering its affordable price to owners and market availability [ ].

    Despite the research on efficacy of different classes of medications for CVL treatment, no great progress has been done regarding toxicity or parasitological cure, highlighting the necessity for evaluation of new formulations and medicaments to be used exclusively for treatment of CVL.

    Immunotherapy can be an effective addition to chemotherapy, as it induces effector immune response faster than the isolated use of chemotherapeutic drugs [ ]. This combination enables reduction of chemotherapy doses, consequently lowering the risks of toxicity and death. However, the use of multiple recombinant antigens could provide better results [ ]. In animals treated with vaccine associated to SSG, there was a They concluded that immunochemotherapy protocols may be effective, but further studies are needed in different animal models in order to better understand the immune response [ ].

    Immunotherapy is often considered for CVL prevention and control as a preferable alternative to euthanasia, due to the absence of a low-toxicity chemotherapy treatment and increasing resistance. 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. The activity of hepatic enzymes is generally within the reference values for the canine species, although biochemical findings in infected dogs can include alterations in aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase [ , ]. To improve the prognosis and to avoid both human and dog transmission from false negative cases and unnecessary euthanasia from false-positive cases , diagnosis should be established as soon as possible, even on the basis of only a few or even a single clinical sign [ 42 ].

    The diagnosis is made considering the epidemiological origin and the set of clinical signs presented by the dog [ 91 ]. Due to the large number of asymptomatic dogs and the absence of pathognomonic clinical signs, the diagnosis depends on laboratory support. All the parasitological, immunological, and molecular techniques available for diagnosis are important and need to be interpreted according to their benefits and limitations.

    Parasitological diagnosis is the unique definitive method, which is often based on observations of amastigotes, preferentially in lymphoid organs such as bone marrow, lymph nodes, and spleen, as well as the liver and skin.

    According to the literature, splenic aspirates are considered as the method of choice for parasitological diagnosis in CanL [ ]. Molecular techniques have high sensitivity and specificity, and PCR and qPCR are currently part of the veterinary diagnostic routine, which are especially useful for follow-up and may be performed on various biological samples, such as peripheral blood, bone marrow aspirate or lymph nodes, skin fragment, and others [ 91 , , ].

    CanL is frequently diagnosed through the detection of specific antibodies against Leishmania sp. However, serological tests present important limitations, such as cross-reactions with Trypanosoma parasites, cutaneous leishmaniasis species, and other hemoparasites [ , ], as well as false negative results in anergy cases or low titers dubious reactions [ ].

    Recently, immunochromatographic assays have been employed as routine laboratory tests in veterinary clinics for the detection of dozens of diseases including CanL. These tests are quick and easy about 15 minutes to perform, require no trained personnel or specialized laboratory training to interpret the results, and present reliable indexes of sensitivity and specificity.

    For CanL, usually recombinant proteins of the parasite, like rK39, are impregnated onto nitrocellulose membranes, and serum samples are applied in the rapid test platform. From the point of view of public health, positive results in serological tests are used as a criterion for indication of euthanasia in suspected dogs based on the elimination program for control of VL adopted in Brazil. Even though parasitological cures are rarely achieved, and clinical recurrences in CanL often occur after therapy, it is necessary to consider that the available protocols can promote clinical cure, increase the life expectancy, and improve the quality of life, in addition to reducing the parasite load and infectiousness to sand fly vectors.

    Thus, the decision to treat a diseased dog is the result of a discussion between the dog owner and the veterinarian. According to the literature, the clinical response to treatment can vary from poor to good depending on their overall initial clinicopathological status and their specific response to therapy.

    For instance, dogs with renal insufficiency are expected to have a lower recovery rate in comparison to those without compromised kidneys or only mild proteinuria [ 91 ]. Current treatment protocols are summarized in Table 1. In addition to the drugs mentioned, there are other products that are proposed to modulate the immune response, immunostimulating the animal organism, such as domperidone, cytokines, and vaccines immunotherapy.

    However, in veterinary medicine, allopurinol a purine analog is considered the major first line drug for long-term treatment of CanL, often in combination with pentavalent antimonials or miltefosine for the first month and then continued alone [ 91 , ].

    While it is rarely used for the treatment of human leishmaniasis, as allopurinol is the only drug recommended by the WHO for the treatment of CanL, recently the first report of resistance to allopurinol was published in L. However, after a six-year follow-up, clinical and laboratory findings indicated that meglumine antimoniate plus allopurinol had better clinical efficacy than miltefosine plus allopurinol in CanL [ ].

    The duration of the treatment depends on the severity of the disease, individual tolerance of drugs, and clinical response to treatment. There are also several side effects, such as xanthinuria, renal mineralisation, and urolithiasis in the case of long-term treatment with allopurinol, and meglumine antimoniate can be potentially nephrotoxic and miltefosine can produce gastrointestinal upset [ 91 , , ].

    Some immunomodulator-based treatments, like domperidone, can enhance innate defense mechanisms, activating phagocytic cells and potentiating the intracellular killing of the parasites, which can help to prevent CanL and reduce the risk of developing the clinical disease [ ].

    Recently, a study unprecedentedly registered the parasitological cure of dogs with VL treated with an innovative combined therapy with liposome-encapsulated meglumine antimoniate and allopurinol [ ]. Knowledge about host—parasite relationships in dogs is increasing and signals the existence of factors inherent to the host, such as immunological differences in response to infection, which would influence the efficacy of the treatment.

    With this in mind, research groups seek the cure of dogs through new formulations of existing drugs or by associating them with immunostimulants and immunotherapeutics.

    The observed results indicate improved treatment in the future. Considering that the sand fly bite is the most important route of transmission of CanL, the infection control measures should be primarily focused on preventing contact with the insect vector, either through physical barriers fine mesh nets in windows and kennels , chemical barriers repellents , or handling avoiding exposure to twilight, eliminating organic peridomiciliary material.

    Predicting a large possibility of failure of these measures, the dog still needs to be able to respond to the infection challenge caused by the bites of infected sand flies, preferentially by an adaptive immune response previously developed through vaccination, or as a last alternative, by chemotherapeutics, which can boost the immune system to help fight infection. Current prophylactic measures used for the prevention and control of CanL are summarized in Table 1. Repellent products available for preventing CanL contain synthetic pyrethroids deltamethrin, permethrin, or flumethrin alone or in combination with other insecticides, which displays a synergistic effect on insects.

    There is no scientific evidence that seropositive dog culling could reduce the incidence of VL [ , ], and wherever this has been applied e. Therefore, vaccination against Leishmania associated with topical insecticides is undoubtedly the most effective form of prevention and control of CanL. CanL is a zoonotic chronic disease transmitted mostly by infected sand flies and can be potentially fatal to humans and dogs.

    Their epidemiological, clinical, and laboratory aspects are very variable, which makes it difficult for veterinary practitioners to complete a diagnosis and then treat and control the disease, especially due to the lack of more effective drugs and vaccines. However, considerable efforts are being made by professionals from multidisciplinary areas in order to improve the knowledge about this parasitic disease, so that prevention, treatment and control may be improved in the future.

    The authors declare that there are no conflicts of interest regarding the publication of this article. Indexed in Science Citation Index Expanded.

    Subscribe to Table of Contents Alerts. Table of Contents Alerts. Abstract Canine leishmaniasis CanL is a vector-borne disease caused by Leishmania infantum and is transmitted by female phlebotomine sand flies primarily between animals and secondarily to humans.

    Introduction 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. Transmission and Life Cycle 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 ].

    Immunology and Clinical Signs The number and intensity of clinical signs are determined by a set of factors involving parasite strain, genetics, and the host immune status. Clinical manifestations of dogs naturally infected with Leishmania Leishmania infantum: Current treatment protocols and prophylactic measures used for the prevention and control of canine leishmaniasis. View at Google Scholar J. De Almeida Curi, I. Parasites and Wildlife , vol. Trypanosoma cruzi , T.

    View at Google Scholar R. View at Google Scholar V.

    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.

    chapter and author info


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