High-fat diet (HFD) induced obesity is associated not only with metabolic dysregulation, e.g., impaired glucose homeostasis and insulin sensitivity, but also with neurological dysfunction manifested with aberrant behavior and/or neurotransmitter imbalance. Most studies have examined HFD's effects predominantly in male subjects, either in the periphery or on the brain, in isolation and after a finite feeding period. In this study, we evaluated the time-course of selected metabolic, behavioral, and neurochemical effects of HFD intake in parallel and at multiple time points in female (C57BL/6) mice. Peripheral effects were evaluated at three feeding intervals (short: 5–6 weeks, long: 20–22 weeks, and prolonged: 33–36 weeks). Central effects were evaluated only after long and prolonged feeding durations; we have previously reported those effects after the short (5–6 weeks) feeding duration) [1]. Ongoing HFD feeding resulted in an obese phenotype characterized by increased visceral adiposity and, after prolonged HFD intake, an increase in liver and kidney weights. Peripherally, 5 weeks of HFD intake was sufficient to impair glucose tolerance significantly, with the deleterious effects of HFD being greater with prolonged intake. Similarly, 5 weeks of HFD consumption was sufficient to impair insulin sensitivity. However, sensitivity to insulin after prolonged HFD intake was not different between control, low-fat diet (LFD) and HFD-fed mice, most likely due to age-dependent decrease in insulin sensitivity in the LFD-fed mice. HFD intake also induced bi-phasic hepatic inflammation and it increased gut permeability. Behaviorally, prolonged intake of HFD caused mice to be hypoactive and bury fewer marbles in a marble burying task; the latter was associated with significantly impaired hippocampal serotonin homeostasis. Cognitive (short-term recognition memory) function of mice was unaffected by chronic HFD feeding. Considering our prior findings of short-term (5–6 weeks) HFD-induced central (hyperactivity/anxiety and altered ventral hippocampal neurochemistry) effects and our current results, it seems that in female mice some metabolic/inflammatory dysregulations caused by HFD, such as gut permeability, appear early and persist, whereas others, such as glucose intolerance, are exaggerated with continuous HFD feeding; behaviorally, prolonged HFD consumption mainly affects locomotor activity and anxiety-like responses, likely due to the advanced obesity phenotype; neurochemically, the serotonergic system appears to be most sensitive to continued HFD feeding.

A 15-month-old male neutered Wirehaired Pointer mixed-breed dog presented with fever and cervical pain. Cerebrospinal fluid (CSF) analysis showed neutrophilic pleocytosis with intracellular bacteria, and culture of CSF grew Bordetella bronchiseptica. The patient became non-ambulatory 3 days after CSF collection. He was treated with low-dose prednisone for 3.5 months and doxycycline for 1 year. Recheck CSF analysis 1 month after diagnosis showed reduction of inflammation and 3 months after diagnosis revealed only increased protein. The patient improved neurologically over several months and was weakly ambulatory 5 months and fully ambulatory 7 months after diagnosis. Whole genome sequencing of the bacterial isolate and a live modified intranasal vaccine similar to the one the dog had been vaccinated with 7 weeks before diagnosis was similar but not an exact match. Bacterial meningitis should be considered, and culture of CSF is recommended, in cases of neutrophilic pleocytosis of CSF.

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Case summaryA 3-year-old spayed female domestic shorthair cat developed a fever 1 week after starting the anticonvulsant phenobarbital. A diagnostic work-up for seizures and subsequent onset of fever of unknown origin, consisting of MRI of the brain, cerebrospinal fluid analysis and infectious disease testing, was unremarkable. The cat was switched from phenobarbital onto pregabalin with complete resolution of the fever within 24 h, consistent with a drug-induced fever following phenobarbital administration.Relevance and novel informationWhile anticonvulsant hypersensitivities have been reported and studied in veterinary medicine, phenobarbital-induced fever outside of the context of systemic clinical signs has not been documented in the veterinary scientific literature. Drug-induced fever secondary to anticonvulsants should be considered in patients that develop a fever after starting anticonvulsant therapy with an unrewarding diagnostic work-up for fever of unknown origin.

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