Objectives Leishmaniosis is a vector-borne disease and in European countries is caused by Leishmania infantum. Cats are considered secondary reservoirs of the infection in endemic areas. The objective of this retrospective study is to describe the clinical findings, diagnosis, treatment and outcome of feline leishmaniosis (FeL) in 16 cats in Spain. Methods Medical records of cats diagnosed with leishmaniosis were retrospectively reviewed for cases that met the following inclusion criteria: identification of Leishmania organisms and/or DNA on cytological and/or histological specimens and/or a high anti- Leishmania antibody titre, compatible clinical findings and pathological abnormalities. Results Sixteen cats met the inclusion criteria, all of which were living in areas endemic for canine leishmaniosis. Systemic signs were present in 11 cases (68.8%). The most common clinical signs on presentation included cutaneous lesions in 12 cats (75%), ocular disease in six cats (37.5%) and anorexia in six cats (37.5%). A polyclonal gammopathy was noted in 12 cats (85.7%). Non-regenerative anaemia and renal abnormalities were present in six (37.5%) and five patients (31.3%), respectively. In nine cats (56.3%), immunosuppressive conditions/comorbidities were identified. The diagnosis was made in eight of the cats (50%) by cytology, but a combination of diagnostic tests was needed for definitive diagnosis in the remaining patients. Twelve cats (75%) were treated specifically for leishmaniosis. Five of the 12 cats (41.7%) did not improve with treatment. The median survival time in the group of patients treated specifically for leishmaniosis was 17 months. Median survival of patients treated with concomitant diseases was 13 months vs 41 months in those without, although this was not statistically significant ( P = 0.557). Conclusions and relevance Presentation of FeL appears to be similar to canine leishmaniosis but with some specific features: ulcerative and nodular skin lesions are the predominant cutaneous signs; cats with immunosuppressive conditions or co-existing diseases were more commonly present than typically seen in dogs (mainly feline immunodeficiency virus). A combination of diagnostic tests may be needed for definitive diagnosis.
Using a real-time PCR technique, Demodex mites, albeit in very low numbers, were found to be normal inhabitants of haired areas of the skin of healthy dogs.
Demodex injai mites were detected on trichoscopic examinations and/or deep skin scrapings in eight wirehaired fox terrier dogs with dorsal greasy skin and hair. Histological examination performed in five dogs revealed marked sebaceous gland hyperplasia with lympho-plasmacytic periadnexal dermatitis in all of them. One mite section was observed in one patient. Seven dogs were parasitologically cured after 2 to 7 months of oral ivermectin treatment. Greasy skin and hair resolved in four dogs, was partially reduced in two dogs and persisted in the remaining dog. Skin biopsies were repeated after parasitological cure in two dogs and revealed the persistence of sebaceous gland hyperplasia with mild lympho-plasmacytic periadnexal dermatitis and no parasites. Based on the findings in this case series, the terrier dog breed might be at increased risk for the development of D. injai mite infestation associated with dorsal greasy skin and hair, and microscopically with sebaceous gland hyperplasia. Persistence of sebaceous gland hyperplasia after parasitological cure in some patients suggested that this histological finding may not always be resulting from Demodex infestation. Moreover, low numbers of adult mites and variable clinical responses to acaricidal therapy suggested a contributory rather than a major role of D. injai in this skin condition. Dermatopathological diagnosis of sebaceous gland hyperplasia, particularly in case of dorsal trunk specimens from terrier dog breeds, warrants the search for D. injai mites on trichoscopic examinations and/or deep skin scrapings.
Demodex canis and D. injai are two different species, with a genetic distance of 23.3%. It would seem that the short-bodied Demodex mite D. cornei is a morphological variant of D. canis.
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