The causes of LUTD found in cats in this study are similar to those that have been previously documented, and idiopathic LUTD is the most frequent diagnosis. However, the rate of urethral obstruction, particularly in cats with idiopathic LUTD, was higher than in other reports. The cause of this difference is unknown.
Aelurostrongylus abstrusus parasitizes the respiratory tract and can heavily affect the breathing and general condition of cats. Experimental infections of six cats were initiated by intragastric administration with 100 or 800 third-stage larvae (L3) obtained from the terrestrial snail Helix aspersa. First-stage larvae were isolated from faecal samples after 35-41 days post infection (dpi) in five animals and until end of study (84 dpi) in two cats. Cough and respiratory sounds were observed starting from 28 to 41 dpi and dyspnoea and panting starting from 52 dpi. All cats had enlarged lymph nodes and, starting from 56 dpi, reduced body weight, and four cats showed intermittent reduced general condition with apathia and anorexia. Eosinophilia and leucocytosis partially with massive lymphocytosis, and occasional basophilia and monocytosis were observed. Mild anaemia was present in five cats, while alterations in coagulation parameters suggested stimulation of the coagulation cascade with increased consumption of coagulation factors (delayed PT, hypofibrinogenemia). Adult A. abstrusus specimens were isolated from the five patent cats at necropsy and all six cats showed pathological changes in the lungs, including disseminated inflammatory cell infiltrates, often associated with incorporated larvae and eggs. There was some degree of overlap between the severity and the inoculation doses. Infections starting from 100 L3 of A. abstrusus had an impact on the lung tissues and on the health of the cats, despite the presence of only mild haematological abnormalities. Due to the worldwide occurrence of feline lung worms, parasitic infections should be considered in the differential diagnosis of lung diseases regardless of the presence of clinical signs and larval excretion.
The prevalence of infection with Bartonella henselae was investigated in cats from different areas of Switzerland. Serum samples of 728 cats were examined for antibodies to B. henselae by immunofluorescent antibody testing, and the results were analyzed with a view to a possible correlation between a positive titer and signalment, clinical signs, infection with feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), feline coronavirus (FCoV), or feline spumavirus (FeSFV), and the living environments of the cats. The seroprevalence in all cats was 8.3%. No significantly different prevalence was found in sick versus healthy cats (9.2 versus 7.2%); however, in sick cats seropositive for B. henselae, there was an increased frequency of stomatitis and a variety of diseases of the kidneys and the urinary tract. There was an increased prevalence of B. henselae in cats positive for FCoV (P ؍ 0.0185) or FeSFV (P ؍ 0.0235) and no statistically significant increased prevalence in cats infected with FeLV or FIV. There was no correlation between a positive titer and sex or breed. The same prevalence of B. henselae antibodies was found in cats with and without access to the outdoors and in cats from single-and multicat households. The seroprevalence was increased in cats living south of the Alps (12.1%); however, this difference was not significant (P ؍ 0.0616).
Ninety-seven pure-bred Akitas were examined clinically and histologically for sebaceous adenitis. The diagnosis was established histologically in 23 Akitas by demonstrating an inflammatory reaction targeted against the sebaceous glands or a reduction in the number of glands. The clinical course of sebaceous adenitis in the Akita was similar to that seen in other breeds. The first skin lesions occurred mainly on the dorsal midline and ears. Compared with the Poodle, the age at first onset of the disease was more variable and the hair loss affected mainly the undercoat. The progression of sebaceous gland destruction varied between dogs and was not seen in all cases. Because bud-like sebaceous gland proliferation could be identified, it seems that regeneration of the sebaceous glands may occur. An autosomal recessive inheritance appears to be possible. Apart from a genetic background, immune-mediated factors possibly influence the onset and course of sebaceous adenitis.
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