Background: Prior reports suggest that osteoarticular infections may be increasing over time. Questions/Purposes: We sought to determine if incidence rates, median in-hospital costs, and length of stay (LOS) of osteomyelitis, septic arthritis (SA), and combined infections have changed over time for pediatric patients, and how they compare to previously reported rates. Methods: The Kids' Inpatient Database (KID), a US national sample of pediatric hospital discharge records from 1997, 2000, 2003, 2006, 2009, and 2012, was used to determine yearly estimated counts of infections in children 20 years of age or younger. US census data was used to calculate yearly incidence rates. Trend tests using linear contrast analysis were used to compare estimated median LOS and inflation-adjusted median costs over time for each type of infection. Results: From 1997 through 2012, the incidence rate of osteomyelitis increased from 7.9 to 10.5 per 100,000, SA was unchanged from 5.3 to 5.2 per 100, and combined infections increased from 0.8 to 1.3 per 100,000. Median LOS from 1997 to 2012 showed no significant change for osteomyelitis (5.0 to 4.9 days), SA (4.4 to 4.1 days), or combined infections (6.

To investigate the independent and interactive effects of opiate addiction and HIV on neuroinflammation, we measured microglial/macrophage activation and astrogliosis in multiple regions of human brain. Samples of thalamus, frontal gray matter, and frontal white matter were obtained from 46 individuals categorized as: HIV negatives, HIV-negative opiate addicts, HIV positives, HIV-positive opiate addicts, HIV encephalitis (HIVE), and HIVE opiate addicts. Activated brain microglia/macrophages and astrocytosis were quantified by morphometric analysis of immunohistochemical stains for CD68, HLA-D, CD163, and GFAP. The effects of HIV grouping, opiate addiction, and their interaction on expression of the markers were examined in a series of two-way ANOVAs. In opiate addicts, there was generally higher baseline expression of CD68 and HLA-D in HIV negatives, and lower expression in HIV and HIVE, compared to individuals without opiate abuse. Thus, for these markers, and for GFAP in frontal gray, opiates were associated with attenuated HIV effect. In contrast, for CD163, opiates did not significantly alter responses to HIV, and HIV effects were variably absent in individuals without opiate abuse. The divergent impact that opiate addiction displays on these markers may suggest a generally immunosuppressive role in the CNS, with decreased HIV-associated activation of markers CD68 and HLA-D that potentially reflect neurotoxic pathways, and preservation of CD163, thought to be an indicator of neuroprotective scavenger systems. These results suggest a complex impact of opiates on neuroinflammation in baseline and virally stimulated states.

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