Mycobacterium avium infection associated with sterile polyarthritis in a dog.

A 1-year-old male neutered Portuguese Podengo dog was presented for lameness, inappetence, pyrexia, diarrhoea and abdominal moderate to severe lymphadenomegaly. Cytology of synovial fluid revealed neutrophilic inflammation in multiple joints suggestive of immune-mediated polyarthritis. Cytology of fine-needle-aspiration material obtained from lymph nodes revealed macrophages with intracytoplasmic, rod-like Ziehl-Neelsen positive staining structures, indicative of mycobacteria. Four-month treatment with enrofloxacin, rifampicin and clarithromycin resulted in clinical improvement and resolution of polyarthritis as evidenced on repeat synoviocentesis, but diarrhoea recurred, Ziehl-Neelsen positive organisms were again found on lymph node cytology and analysis of the 16S rRNA-gene using the Basic Local Alignment Search Tool facility resulted in a match to Mycobacterium avium with 100% sequence identity. Treatment was adjusted to include pradofloxacin, doxycycline, rifampicin and ethambutol and 3 months later the dog is clinically normal. Based on the literature search, this is the first time canine Mycobacterium avium infection associated with immune-mediated polyarthritis is reported. Based on scoping searches, this is the first report of canine Mycobacterium avium infection associated with immune-mediated polyarthritis.

A gender-related defect in lipid metabolism and glucose homeostasis in peroxisome proliferator- activated receptor alpha- deficient mice.

The peroxisome proliferator-activated receptor alpha (PPARalpha) is a nuclear receptor implicated in the control of cellular lipid utilization. To test the hypothesis that PPARalpha is activated as a component of the cellular lipid homeostatic response, the expression of PPARalpha target genes was characterized in response to a perturbation in cellular lipid oxidative flux caused by pharmacologic inhibition of mitochondrial fatty acid import. Inhibition of fatty acid oxidative flux caused a feedback induction of PPARalpha target genes encoding fatty acid oxidation enzymes in liver and heart. In mice lacking PPARalpha (PPARalpha-/-), inhibition of cellular fatty acid flux caused massive hepatic and cardiac lipid accumulation, hypoglycemia, and death in 100% of male, but only 25% of female PPARalpha-/- mice. The metabolic phenotype of male PPARalpha-/- mice was rescued by a 2-wk pretreatment with beta-estradiol. These results demonstrate a pivotal role for PPARalpha in lipid and glucose homeostasis in vivo and implicate estrogen signaling pathways in the regulation of cardiac and hepatic lipid metabolism.