The medical records of 158 dogs with visceral leishmaniasis confirmed cytologically and/or serologically were reviewed. Ages of affected dogs varied from nine months to 15 years, with a male-to-female ratio of 1.3. The most common clinical manifestations of the disease were variable cutaneous lesions such as exfoliative dermatitis and skin ulcerations, chronic renal failure, peripheral lymphadenopathy or lymph node hypoplasia, masticatory muscle atrophy (i.e., chronic myositis), ocular lesions (i.e., conjunctivitis, keratoconjunctivitis sicca, blepharitis, and uveitis), and poor body condition. Ascites, nephrotic syndrome, epistaxis, polyarthritis, and ulcerative stomatitis were seen only in a small number of cases. Clinical splenomegaly was not a common finding. The clinicopathological abnormalities were nonregenerative anemia, hyperproteinemia, glomerular proteinuria, and symptomatic or asymptomatic azotemia. In this study, an indirect immunofluorescence assay's diagnostic sensitivity was found to be higher than that of lymph node aspiration cytology.
The CADESI-4 is simpler to use and quicker to administer than its previous version. The ICADA recommends the CADESI-4 instead of the CADESI-3 to score skin lesions of AD in dogs enrolled in clinical trials.
Canine leishmaniosis caused by Leishmania infantum (Syn. L. chagasi) is an important zoonosis with a complex pathogenesis. Parasite transmission occurs via female sandflies that inject promastigotes into the skin of the host. The interaction between the parasite and skin immune system is influenced by the repeated infectious bites and the simultaneous intradermal injection of sandfly saliva. Amastigotes are transported via infected macrophages to the regional lymph nodes and finally dissemination may occur. The outcome of the infection depends on host factors (genetic background, cell-mediated and humoral immune response, cytokine milieu, concurrent diseases) and parasite virulence. Resistance may be breed-associated; it is characterized by low to undetectable antibody production and effective cell-mediated immunity, and is orchestrated by cytokines such as interleukin-2, interferon-gamma and tumour necrosis factor-alpha. Susceptibility may be genetically determined or acquired (advanced age, concurrent diseases); in these dogs, parasite multiplication goes unrestricted and overproduction of specific and nonspecific antibodies occurs, leading to multiple organ pathology. Resistance or susceptibility is not an all-or-nothing phenomenon and many intermediate phenotypes may be found. From a diagnostic point of view, although clinical cases are readily identified using microscopy and serology, investigation should not stop at this point and an extensive search for underlying diseases is advised, especially in aged dogs. Conversely, microscopy and conventional serology are frequently negative in asymptomatic infected dogs; to identify such dogs, polymerase chain reaction, evaluation of cutaneous delayed-type hypersensitivity, in vitro lymphocyte proliferation test to Leishmania antigen, and Western blotting may be employed.
The objective of this retrospective study was to investigate in 100 dogs with otitis externa (OE) the possible associations between signalment, history, clinical and laboratory findings and the various primary, secondary and perpetuating causative factors of ear canal inflammation. The age of the dogs ranged from 3 months to 14 years (median: 4.75 years) and they included 45 males and 55 females. Cocker spaniels, Jura des Alpes and Brittany spaniels were significantly overrepresented among dogs with OE when compared to the hospital canine population. In the majority of the cases, OE was chronic-recurrent (63%) or bilateral (93%). Allergic dermatitis (43/100 dogs), grass awns (12/100) and otoacariasis (7/100) were the most common primary causative factors; no primary factor could be incriminated in 32 cases and more than one was found in three dogs. Malassezia spp. (66/100 dogs), cocci (38/100) and rods (22/100) were the secondary causative factors, while ear canal stenosis (38/100) and tympanic membrane perforation-otitis media (25/100) were the most important perpetuating factors. Atopic dermatitis and adverse food reactions-associated OE was more common in females and dogs with a history of pruritic skin disease, while grass awn-induced OE occurred in cocker spaniels and acute cases. Tympanic membrane perforation was less frequent in atopic dermatitis and adverse food reactions-associated OE, but more common when otoscopic and ear canal cytological examination revealed the presence of grass awns and rods, respectively. Finally, cocci overgrowth was positively associated with ear canal stenosis.
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