Despite being common causes of febrile illness in northern Tanzania, Q fever and SFGR are not diagnosed or managed with targeted antimicrobials. C. burnetii does not appear to be an HIV-associated co-infection.

Coxiella burnetii is an obligate intracellular bacterium that causes the zoonotic disease Q fever. Because C. burnetii is highly infectious, can survive under a variety of environmental conditions, and has been weaponized in the past, it is classified as a select agent and is considered a potential bioweapon. The agent is known to be present in domestic livestock and in wild animal populations, but the background levels of C. burnetii in the environment have not been reported. To better understand the amount of C. burnetii present in the environment of the United States, more than 1,600 environmental samples were collected from six geographically diverse parts of the United States in the years 2006 to 2008. DNA was purified from these samples, and the presence of C. burnetii DNA was evaluated by quantitative PCR of the IS1111 repetitive element. Overall, 23.8% of the samples were positive for C. burnetii DNA. The prevalence in the different states ranged from 6 to 44%. C. burnetii DNA was detected in locations with livestock and also in locations with primarily human activity (post offices, stores, schools, etc.). This study demonstrates that C. burnetii is fairly common in the environment in the United States, and any analysis of C. burnetii after a suspected intentional release should be interpreted in light of these background levels. It also suggests that human exposure to C. burnetii may be more common than what is suggested by the number of reported cases of Q fever.

This study provides Class I evidence that for patients with FTD, intranasal oxytocin is not significantly associated with adverse events or significant changes in the overall neuropsychiatric inventory.

No abstract

Coxiella burnetii is a gram-negative bacterium that causes the zoonotic disease Q fever. Traditionally considered an obligate intracellular agent, the requirement to be grown in tissue culture cells, embryonated eggs, or animal hosts has made it difficult to isolate strains and perform genetic studies on C. burnetii. However, it was recently demonstrated that the attenuated Nine Mile Phase 2 (NM2) C. burnetii strain will grow axenically in acidified citrate cysteine medium (ACCM) in a 2.5% oxygen environment. The current study was undertaken to determine whether more virulent C. burnetii strains could be grown in ACCM, and whether virulence would be maintained after passage. The ACCM medium supported an ?1000-fold expansion of Nine Mile Phase 1 (NM1), NM2, M44, and Henzerling strains of C. burnetii, whereas the Priscilla (Q177) strain expanded only 100-fold, and the K strain (Q154) grew poorly in ACCM. To determine if passage in ACCM would maintain the virulence of C. burnetii, the NM1 strain was grown for up to 26 weekly passages in ACCM. C. burnetii maintained in ACCM for 5 or 8 passages maintained full virulence in a mouse model, but NM1 passaged for 23 or 26 times was somewhat attenuated. These data demonstrate that virulent strains of C. burnetii can be successfully passaged in ACCM; however, some strains can lose virulence after extended passage, and other strains grow poorly in this medium. The loss of virulence in axenic culture was associated with some truncation of lipopolysaccharide chains, suggesting a possible mechanism for attenuation.

IMPORTANCE Schizophrenia spectrum disorders (SSDs) and autism spectrum disorder (ASD) both feature social cognitive deficits; however, these disorders historically have been examined separately using a range of tests and subdomain focus and at different time points in the life span. Moving beyond diagnostic categories and characterizing social cognitive deficits can enhance understanding of shared pathways across these disorders.OBJECTIVE To investigate how deficits in social cognitive domains diverge or overlap between SSDs and ASD based on the extant literature.

In this paper, quantitative methods were used to evaluate the weight of evidence regarding a causative relationship between cobalt-chromium (CoCr)-containing hip implants and increased cancer risk. We reviewed approximately 80 published papers and identified no-observed-adverse-effect level (NOAEL) and/or lowest-observed-adverse-effect level (LOAEL) values for specific endpoints of interest: genotoxic effects from in vitro studies with human cell lines as well as genotoxicity and tumor formation in animal bioassays. Test articles included Co particles and ions, Cr particles and ions, and CoCr alloy particles as well as CoCr alloy implants. The NOAEL/LOAEL values were compared with body burdens of Co/Cr particles and ions we calculated to exist in systemic tissues of hip implant patients under normal and excessive wear conditions. We found that approximately 40 tumor bioassays have been conducted with CoCr alloy implants or Co/Cr particles and ions at levels hundreds to thousands of times higher than those present in hip implant patients, and none reported a statistically significant increased incidence of systemic tumors. Results from in vitro and in vivo genotoxicity assays, which are relatively less informative owing to false positives and other factors, also indicated that DNA effects would be highly unlikely to occur as a result of wear debris from a CoCr implant. Hence, the toxicological weight of evidence suggests that CoCr-containing hip implants are unlikely to be associated with an increased risk of systemic cancers, which is consistent with published and ongoing cancer epidemiology studies involving patients with CoCr hip implants.

These results uniquely indicate that distinct lower- and higher-level aspects of social cognition exist across SSDs and healthy controls. Further, mentalizing may be particularly linked to negative symptoms and functional outcome. This informs future studies of the neural circuitry underlying social cognition and the development of targeted treatment options for improving functional outcome.