Feline Leishmaniosis

Edited June, 2018

The Leishmaniosis in cats guidelines were first published in the J Feline Med Surg 2013, 15: 638-642 by Maria Grazia Pennisi et al. The present guidelines were updated by Maria Grazia Pennisi.





Leishmania infection is less known in cats than in dogs and humans; felids were traditionally considered as resistant, and canids as the main reservoir. Only sporadic feline disease cases have been reported worldwide, mainly caused by L. infantum. Epidemiological investigations have confirmed, however, that feline infections are not rare and that disease occurrence might be underestimated in endemic areas.


Cats are infected by the same Leishmania species that infect dogs and humans in tropical and subtropical areas worldwide. Sand fly vectors take blood meals from cats and are competent vectors for L. infantum, as shown experimentally.


Skin lesions (ulcerative, crusty, nodular or scaly dermatitis) are the most frequent clinical manifestation and sometimes the only findings at physical examination. Lymph node enlargement, weight loss, ocular involvement (nodular blepharitis, uveitis, panophthalmitis), decreased appetite, chronic gingivo-stomatitis and lethargy are the most frequent non-cutaneous findings, alone or in combination.


Direct confirmation of Leishmania infections can be obtained by cytology, histology, isolation or by PCR, performed on samples taken from the skin, lymph nodes, blood or any affected tissues. Serology using validated immunofluorescence tests, ELISA, direct agglutination or Western blot have been used to assess infection frequencies or to support the diagnosis in affected cats.


The information available for treatment is based only on case reports. Despite clinical improvements following long term oral administration of allopurinol (10-20 mg/kg q12h or q24h), the infection is not cleared, and recurrence of clinical signs may occur after cessation of therapy, similar to dogs (EBM grade IV). Meglumine antimoniate (50 mg/kg SID SC and as well in association with allopurinol) is less frequently used and led to good clinical responses, but long term follow-up is lacking (EBM grade IV).


Preventative tools (ectoparasiticides effective against sand flies and vaccines) are licensed for dogs only, however flumethrin collars, which are available for cats, were effective in reducing the incidence of feline Leishmania infection in an endemic area.





After malaria and lymphatic filariasis, leishmaniosis is the third most important vector-borne disease in people; it is caused by several Leishmania species, most of zoonotic concern (Solano-Gallego et al., 2009). In veterinary medicine, canine leishmaniosis caused by L. infantum is of primary interest, because dogs are the main reservoir of the parasite for humans, and management of the canine disease may be challenging (Baneth et al., 2008).


Cats are naturally infected by the same Leishmania species that affect dogs and humans in tropical and subtropical areas worldwide: L. infantum in the Mediterranean basin, Iran and Brazil; L. tropica and L. major in Turkey, L. mexicana in Texas (USA) and Venezuela; L. braziliensis in Brazil and French Guiana; L. amazonensis in Brazil; L. venezuelensis in Venezuela (Attipa et al., 2017; Bonfante-Garrido et al., 2001; Can et al., 2016; Schubach et al., 2004; de Souza et al., 2005; Hatam et al., 2009; Paşa et al., 2015; Rivas et al., 2018; Trainor et al., 2010; Vides et al., 2011; Rougeron et al., 2011; Pennisi et al., 2015a).


The susceptibility of cats has been confirmed by experimental studies (Kirkpatrick et al., 1984; Simoes-Mattos et al., 2005).

Fig. 1. Life cycle of Leishmania donovani. Wikipedia, public domain.

Fig. 1. Life cycle of Leishmania infantum. Wikipedia, public domain.


Life cycle and transmission


Leishmania spp. are protozoan parasites, the natural history of which involves two hosts: the phlebotomine sand fly and a vertebrate (Fig. 1). The vector harbours flagellated extracellular promastigote forms and transmits them to a vertebrate host; there, the parasite changes into the amastigote form that is able to survive and replicate in intracellular vacuoles within macrophages. Haematophagous female sand flies transmit the promastigotes or may take up amastigotes from an infected vertebrate host.


There is no evidence that ticks and fleas are involved in natural Leishmania transmission (Baneth et al., 2008; Solano-Gallego et al., 2009). The risk for transmission in the absence of sand flies is negligible, but transplacental infection occurs as a rare event in both dogs and humans (Baneth et al., 2008; Solano-Gallego et al., 2009). Venereal transmission is a potential way of infection (da Silva et al., 2009). Other types of direct transmission have been suggested to explain the spread of the infection among kennel dogs in the USA, in the absence of sand fly vectors (Baneth et al., 2008; Solano-Gallego et al., 2009). The risk of transmission by blood transfusion is important for humans and dogs in endemic areas (Baneth et al., 2008; Solano-Gallego et al., 2009; Kaplan et al., 2009) and it may occur also in cats, as healthy cats can be found positive, when testing EDTA-blood  samples with PCR or even with cytological evaluation of blood smears (Persichetti et al., 2016; Attipa et al., 2017; Brianti et al., 2017; Diakou et al., 2017; Metzdorf et al., 2017; Otranto et al., 2017).


Many studies have demonstrated that sand flies take blood meals from cats and they  have been found infected by L. infantum  after feeding on naturally infected cats (Maroli et al., 2006; da Silva et al., 2010).





Leishmaniosis, caused by L. infantum, is a globally  emerging disease (Baneth et al., 2008; Solano-Gallego et al., 2009). Using molecular diagnostic techniques on dogs in endemic areas, it was shown that the prevalence of the infection is much higher than that of the disease manifestation (Lombardo et al., 2012). The same is true for people: in some endemic areas, latent infections approach 30% of the population, based on a positive Leishmanin Skin Test, LST (Kaplan et al., 2009). Feline leishmaniosis is sporadically reported worldwide, usually from the same areas where the disease occurs in dogs or humans (Pennisi et al., 2015a). In the Old World, feline L. infantum infection has been detected in Mediterranean countries (Italy, Spain, Portugal, France, Greece, Turkey, Cyprus) and Iran and characterized feline isolates are similar to those obtained from dogs or humans (Pennisi and Persichetti, 2018). Cases have been seen in Switzerland, in cats imported from Spain; increased pet movement throughout Europe will likely lead to more disease also in non-endemic areas (Rüfenacht et al., 2005; Richter et al., 2014).


Epidemiological studies have been performed during the last 20 years in endemic areas using serological (immunofluorescence, ELISA, Western blot, direct agglutination) and/or parasitological methods (cytology, immunohistochemistry, PCR); the rates of infection vary widely, which may be due to the methodology used, the geographic area, and population under study. Positive blood PCR rates range between 0.43 and 61% of the cat population tested, and antibody prevalence between 3 and 59% (Pennisi et al., 2015a) but feline positivity is usually lower compared to dogs (Pennisi et al., 2015a; Otranto et al., 2017).





Disease development is primarily influenced by immunological factors, which are linked to the complex genetic background of the hosts, as demonstrated by studies in laboratory animals, dogs and humans (Baneth et al., 2008). In people, L. infantum can induce various clinical manifestations, ranging from a local skin lesion to severe visceral disease. The latter form is the typical presentation in immunocompromised patients (Kaplan et al., 2009). In dogs, leishmaniosis is a multisystemic disease with a wide spectrum of severity that reflects the balance between the protective cell-mediated, and the non-protective humoral, immune response. In humans and dogs a dynamic range of disease severities can be observed, varying from subclinical infection to self-limiting mild and non-self-limiting severe disease (Baneth et al., 2008; Solano-Gallego et al., 2009).


In all host species, macrophages play a central role in the control of the infection. Cytokines such as IFN-γ, IL-2 and TNF-α, secreted by activated T cells, stimulate macrophages to kill intracellular Leishmania amastigotes. The presence of Leishmania-infected macrophages is usually associated with a granulomatous inflammatory reaction (Baneth et al., 2008). Lymphoid hyperplasia is also common. A massive antibody response is associated with severe disease and responsible for immune complex deposition in the kidney, with glomerulonephritis and subsequent renal failure (Baneth et al., 2008; Solano-Gallego et al., 2009).


Histopathology of feline skin lesions mainly shows a diffuse granulomatous dermatitis with macrophages containing many Leishmania parasites, or a granulomatous perifolliculitis and lichenoid tissue reaction/interface dermatitis, with a lower parasite load (Navarro et al., 2010; Puleio et al., 2011). Granulomatous inflammation has also been seen in the liver and in the kidneys (Puleio et al., 2011).


Leishmania infection of cats is more common than the associated disease and cats may remain PCR and antibody positive for a long time without  manifestation of clinical disease (Pennisi et al., 2015a). This means that cats may be more resistant than dogs to developing disease but also that they could be reservoirs for L. infantum.



Clinical signs


Canine leishmaniosis is usually chronic and progressive, with an incubation period lasting for months or even years. Any tissue or organ may be involved, but skin lesions are most suggestive, and renal disease is most important prognostically (Solano-Gallego et al., 2009).


Fig. 2. Leishmania infantum associated ulcerative dermatitis in a cat (courtesy Maria Grazia Pennisi)

Fig. 2. Leishmania infantum associated ulcerative dermatitis in a cat (courtesy Maria Grazia Pennisi)


Feline leishmaniosis caused by L. infantum has been documented mainly in the last twenty years in Europe or Brazil (Pennisi et al., 2015a). Cases have been reported in adult or old cats, almost all domestic shorthair, with no gender predilection, but quite often FIV or dual FIV and FeLV infections are also detected. Some cats have concurrent diseases such as squamous cell carcinoma, or have been treated with immunosuppressive drugs before developing clinical manifestations of L. infantum infection.

Skin lesions are the most frequent clinical manifestation, and they are sometimes the only findings at physical examination. Ulcerative, crusty, nodular or scaly dermatitis are seen mainly on the head and on the neck (Fig. 2, 3) or symmetrically on distal limbs, less often on the trunk. Pruritus is usually absent; however, alopecia or a poor coat condition are reported. Conversely some cats do not show any skin lesions and lymph node enlargement, ocular involvement (nodular blepharitis, uveitis, panophthalmitis), chronic gingivo-stomatitis, decreased appetite, weight loss and lethargy are the most frequent non-cutaneous findings. Dehydration, pale mucous membranes, vomiting, hepatomegaly, fever, jaundice, polyuria/polydipsia, spleen enlargement, nasal discharge, recurrent abortion, dyspnoea are also reported, though less commonly.


Fig. 3. Leishmania infantum associated hemorrhagic nodule in a cat (courtesy Maria Grazia Pennisi)

Fig. 3. Leishmania infantum associated haemorrhagic nodule in a cat (courtesy Maria Grazia Pennisi)


Information on clinico-pathological abnormalities in feline leishmaniosis is scarce, however non-regenerative anaemia, hyperglobulinaemia and proteinuria are most frequently reported. In a few cases followed up until death or euthanasia, chronic kidney disease developed and it was the cause of death (Pennisi et al., 2004).


Clinical and clinico-pathological abnormalities can obviously be influenced also by concurrent diseases as well as retroviral infection.





Leishmania immunity is complex. In the dog, a susceptible species, protective immunity against L. infantum is CD4 T cell-mediated, and the release of IFN-γ, IL-2 and TNF-α is associated with anti-Leishmania activation of macrophages. A combination of high antibody levels and a reduced cell-mediated response are found in dogs developing the disease (Baneth et al., 2008; Solano-Gallego et al., 2009).


Cats with L. infantum associated clinical disease have high blood parasitaemia, low to very high antibody levels and hyperglobulinaemia, but the relationship between specific IFN-γ production and the severity of disease was not investigated in cats.  However, it was recently evidenced that, as in other hosts, humoral and cell-mediated adaptive immune responses are elicited by L. infantum in exposed cats from endemic areas. Interferon-γ was in fact detected in 21% of these cats and they all were negative at Leishmania PCR  performed on DNA extracted from whole EDTA-blood and negative or border-line antibody positive (Priolo et al., 2017).  

As reported for dogs, Leishmania PCR-positive healthy cats may be seronegative for anti-Leishmania antibodies (Pennisi et al., 2012, 2015a).


Infection experiments with L. braziliensis have shown that the development of skin lesions usually precedes antibody appearance, and seroconversion occurs when the lesions are healing (Simoes-Mattos et al., 2005).


An association between FIV and L. infantum infections has been found in endemic areas. Most cats developing clinical signs are suspected to have an impaired immune system because of concurrent FIV infection, dual FIV and FeLV infection, neoplasia (e.g. squamous cell carcinoma), diabetes mellitus, autoimmune disease (e.g. pemphigus foliaceus) or treatment with immunosuppressive drugs such as corticosteroids (Pennisi et al., 2000, 2012; Sobrinho et al., 2012).


Fig. 4. Lymph node smear from a cat: Leishmania amastigotes in a macrophage (MG-G stain; x64 objective). Photomicrograph courtesy Maria Grazia Pennisi)

Fig. 4. Lymph node smear from a cat: Leishmania amastigotes in a macrophage (MG-G stain; x64 objective; Photomicrograph courtesy Maria Grazia Pennisi)




A diagnosis can be confirmed by parasitological (cytology, histology, PCR or culture) and serological methods (immunofluorescence antibody test [IFAT], ELISA, direct agglutination or Western blot [WB]). In most feline cases where cytology, culture and PCR were performed, a diagnosis was confirmed using lymph node, skin, bone marrow or blood samples (Fig. 4). Ocular disease caused by L. infantum was diagnosed by histology after enucleation of the affected eye. Upon post mortem examination, parasitological evidence of infection was obtained also from samples of the spleen, liver, kidney, pancreas, and gastro-intestinal tract (Pennisi et al., 2015a).


Immunohistochemistry has been used on skin biopsies (Navarro et al., 2010; Puleio et al., 2011). Serological tests for leishmaniosis are not commercially available but IFAT has been validated for usage on feline samples and cut off was set at 1:80 dilution (Pennisi et al., 2012; Persichetti et al., 2017). Recently, diagnostic performance of IFAT, ELISA and WB was examined and all three techniques were reliable, with WB being the most accurate (Persichetti et al., 2017).





The available information is mostly based on single case reports or case series of feline leishmaniosis caused by L. infantum, not always with an appropriate follow-up (EBM grade IV) (Pennisi et al., 2015a). Treatment of cats with clinical leishmaniosis is still empirically based and off label by using the most common drugs administered to dogs. Therefore, cats under therapy should be carefully monitored for adverse effects. Long-term administration of allopurinol (10-20 mg/kg SID or BID) is usually clinically effective, even in FIV infected cats; however, the L. infantum infection is not cleared and clinical signs may recur after stopping therapy, as is the case in dogs (Pocholle et al., 2012; Pennisi et al., 2015a; Pennisi et al., 2016; Attipa et al., 2017). In a few cases allopurinol was given as maintenance therapy after a course of meglumine antimoniate (usually 50 mg/kg SID SC), domperidone or miltefosine, all resulting in a good clinical responses (Pennisi et al., 2015a; Maia et al., 2015; Bardagi et al., 2016; Basso et al., 2016). It should however be considered that propylene glycol is among the excipients of the miltefosine oral formulation licensed for the treatment of dogs with leishmaniosis and that it can theorethically cause Heinz body formation and decreased life span in feline red blood cells. Surgical excision of nodules was performed in two cats but this was followed by recurrence (Costa Durao et al., 1994; Rüfenacht et al., 2005).

The life expectancy for cats with leishmaniosis after diagnosis is usually good, unless concurrent conditions or complications as chronic kidney disease or neoplasia occur. Based on a retrospective evaluation of 14 cases, prognosis was not significantly influenced by therapy or FIV co-infection (Pennisi et al., 2016).





In dogs, prevention of leishmaniosis is based on prevention of the bite of sand flies obtained with topical pyrethroids.   Since recent years, vaccination is also available and it is an optional measure aiming to prevent the development of clinical disease (Miró et al., 2017). Almost all pyrethroids are toxic to cats, but flumethrin is licenced for cats as a collar and it was able to reduce the incidence of L. infantum infection in cats as it was seen in dogs (Brianti et al., 2014, 2017). According to current knowledge, testing of blood donors by antibody detection and Leishmania PCR performed on DNA extracted from whole EDTA-blood is the only reasonable measure for preventing non-vectorial transmission to cats (Pennisi et al., 2015b).



Zoonotic risk


Leishmania species reported in cats are of zoonotic concern but no information is available on the risk associated for owners of infected cats. Vectorial transmission is considered the main way of transmission for L. infantum and dogs are considered the main peridomestic reservoir. In any case, only one study performed in Iran found that owners of infected dogs have a higher risk for leishmaniosis caused by L. infantum (Gavgani et al., 2002).




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