A type III protein secretion system encoded by Salmonella pathogenicity island 2 (SPI2) has been found to be required for virulence and survival within macrophages. Here, SPI2 was shown to allow Salmonella typhimurium to avoid NADPH oxidase-dependent killing by macrophages. The ability of SPI2-mutant bacteria to survive in macrophages and to cause lethal infection in mice was restored by abrogation of the NADPH oxidase-dependent respiratory burst. Ultrastructural and immunofluorescence microscopy demonstrated efficient localization of the NADPH oxidase in the proximity of vacuoles containing SPI2-mutant but not wild-type bacteria, suggesting that SPI2 interferes with trafficking of oxidase-containing vesicles to the phagosome.

Salmonella Pathogenicity Island 2—Dependent Evasion of the

Lower and upper respiratory infections are the fourth highest cause of global mortality (Lozano et al., 2012). Epidemic and pandemic outbreaks of respiratory infection are a major medical concern, often causing considerable disease and a high death toll, typically over a relatively short period of time. Influenza is a major cause of epidemic and pandemic infection. Bacterial co/secondary infection further increases morbidity and mortality of influenza infection, with Streptococcus pneumoniae, Haemophilus influenzae and Staphylococcus aureus reported as the most common causes. With increased antibiotic resistance and vaccine evasion it is important to monitor the epidemiology of pathogens in circulation to inform clinical treatment and development, particularly in the setting of an influenza epidemic/pandemic.

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Secondary Bacterial Infections Associated with Influenza Pandemics.

Q fever, a zoonotic disease caused by the bacterium Coxiella burnetii, can cause acute or chronic illness in humans. Transmission occurs primarily through inhalation of aerosols from contaminated soil or animal waste. No licensed vaccine is available in the United States. Because many human infections result in nonspecific or benign constitutional symptoms, establishing a diagnosis of Q fever often is challenging for clinicians. This report provides the first national recommendations issued by CDC for Q fever recognition, clinical and laboratory diagnosis, treatment, management, and reporting for health-care personnel and public health professionals. The guidelines address treatment of acute and chronic phases of Q fever illness in children, adults, and pregnant women, as well as management of occupational exposures. These recommendations will be reviewed approximately every 5 years and updated to include new published evidence.

Diagnosis and management of Q fever--United States, 2013: recommendations from CDC and the Q Fever Working Group

Sex steroid hormones play important physiological roles in reproductive and nonreproductive tissues, including immune cells. These hormones exert their functions by binding to either specific intracellular receptors that act as ligand-dependent transcription factors or membrane receptors that stimulate several signal transduction pathways. The elevated susceptibility of males to bacterial infections can be related to the usually lower immune responses presented in males as compared to females. This dimorphic sex difference is mainly due to the differential modulation of the immune system by sex steroid hormones through the control of proinflammatory and anti-inflammatory cytokines expression, as well as Toll-like receptors (TLRs) expression and antibody production. Besides, sex hormones can also affect the metabolism, growth, or virulence of pathogenic bacteria. In turn, pathogenic, microbiota, and environmental bacteria are able to metabolize and degrade steroid hormones and their related compounds. All these data suggest that sex steroid hormones play a key role in the modulation of bacterial-host interactions.

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Role of Sex Steroid Hormones in Bacterial-Host Interactions

The Summary of Notifiable Infectious Diseases and Conditions - United States, 2015 (hereafter referred to as the summary) contains the official statistics, in tabular and graphical form, for the reported occurrence of nationally notifiable infectious diseases and conditions in the United States for 2015. Unless otherwise noted, data are final totals for 2015 reported as of June 30, 2016. These statistics are collected and compiled from reports sent by U.S. state and territories, New York City, and District of Columbia health departments to the National Notifiable Diseases Surveillance System (NNDSS), which is operated by CDC in collaboration with the Council of State and Territorial Epidemiologists (CSTE). This summary is available at https://www.cdc.gov/MMWR/MMWR_nd/index.html. This site also includes summary publications from previous years.

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Summary of Notifiable Infectious Diseases and Conditions - United States, 2015.

Coxiella burnetii is the agent of Q fever, or ``query fever,'' a zoonosis first described in Australia in 1937. Since this first description, knowledge about this pathogen and its associated infections has increased dramatically. We review here all the progress made over the last 20 years on this topic. C. burnetii is classically a strict intracellular, Gram-negative bacterium. However, a major step in the characterization of this pathogen was achieved by the establishment of its axenic culture. C. burnetii infects a wide range of animals, from arthropods to humans. The genetic determinants of virulence are now better known, thanks to the achievement of determining the genome sequences of several strains of this species and comparative genomic analyses. Q fever can be found worldwide, but the epidemiological features of this disease vary according to the geographic area considered, including situations where it is endemic or hyperendemic, and the occurrence of large epidemic outbreaks. In recent years, a major breakthrough in the understanding of the natural history of human infection with C. burnetii was the breaking of the old dichotomy between ``acute'' and ``chronic'' Q fever. The clinical presentation of C. burnetii infection depends on both the virulence of the infecting C. burnetii strain and specific risks factors in the infected patient. Moreover, no persistent infection can exist without a focus of infection. This paradigm change should allow better diagnosis and management of primary infection and long-term complications in patients with C. burnetii infection.

https://hal.archives-ouvertes.fr/hal-01496178/document

From Q Fever to Coxiella burnetii Infection: a Paradigm Change.

Brill-Zinsser disease, the relapsing form of epidemic typhus, typically occurs in a susceptible host years or decades after the primary infection; however, the mechanisms of reactivation and the cellular reservoir during latency are poorly understood. Herein we describe a murine model for Brill-Zinsser disease, and use PCR and cell culture to show transient rickettsemia in mice treated with dexamethasone >3 months after clinical recovery from the primary infection. Treatment of similarly infected mice with cyclosporine failed to produce recrudescent bacteremia. Therapy with doxycycline for the primary infection prevented recrudescent bacteremia in most of these mice following treatment with dexamethasone. Rickettsia prowazekii (the etiologic agent of epidemic typhus) was detected by PCR, cell culture, and immunostaining methods in murine adipose tissue, but not in liver, spleen, lung, or central nervous system tissues of mice 4 months after recovery from the primary infection. The lungs of dexamethasone-treated mice showed impaired expression of β-defensin transcripts that may be involved in the pathogenesis of pulmonary lesions. In vitro, R. prowazekii rickettsiae infected and replicated in the murine adipocyte cell line 3T3-L1. Collectively these data suggest a role for adipose tissue as a potential reservoir for dormant infections with R. prowazekii.

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Adipose Tissue Serves as a Reservoir for Recrudescent Rickettsia prowazekii Infection in a Mouse Model

Epidemiological and experimental data suggest the association of gender and sex with susceptibility and severity of infectious diseases (Moss, 2005). Gender and sex likely affect viral and parasitic infectious diseases (Morales-Montor et al., 2004; Fish, 2008; Snider et al., 2009). Here we will review the effect of gender and sex on bacterial infectious diseases (sepsis, mycobacterial diseases and Q fever). We will differentiate gender and sex by considering that gender refers to differences determined by cultural and societal factors and sex refers to the biological differences between males and females (Fish, 2008). Indeed, variables such as poverty, occupational status and marital status affect differently men and women in different countries (Theobald et al., 2006), leading to different risks of exposition to infectious pathogens and accesses to efficient treatment. This is illustrated by the decreased prevalence of tuberculosis in industrialized countries associated with socioeconomic changes including reduced malnutrition and overcrowding, improved sanitary conditions in the workplaces before the use of chemotherapy (Davies et al., 1999). Sex-based differences in the susceptibility to pathogens include what is due to chromosome effect and sex hormones. Thus, it is critical to delineate the respective roles of gender and sex on bacterial infections. The present review focuses on four features of the association between sex and bacterial infections with a special attention for bacterial sepsis, mycobacterial infections and Coxiella burnetii infection.

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Sex Hormones and Bacterial Infections

Cytomegalovirus reactivation enhances the virulence of Staphylococcus aureus pneumonia in a mouse model

Macrophages are tissue immune cells involved in homeostasis and are considered as the first line of defense during bacterial infections. They are resident cells but may be recruited during inflammation and/or infection. Hence, their study is necessary not only to decipher innate immune mechanisms involved in bacterial infections but also to follow infected patients. Among the numerous functions of macrophages, their polarization into microbicidal or permissive cells has been an interesting concept to describe their responses to bacterial aggression. Numerous in vitro studies, including ours, have shown the ability of bacteria to induce different patterns of macrophage polarization. However, the studies of patients during infections have produced less convincing results. We propose in this review to take stock of the tools for studying the polarization of macrophages and to show their limits. We make recommendations for using macrophage polarization as a biomarker for measuring severity and response to treatment in bacterial infectious diseases.

/pdf/new-tools-for-studying-macrophage-polarization-application-s9gaxm4pw3.pdf

Jean-Louis Mege

Papers

From Q Fever to Coxiella burnetii Infection: a Paradigm Change.

Adipose Tissue Serves as a Reservoir for Recrudescent Rickettsia prowazekii Infection in a Mouse Model

Sex Hormones and Bacterial Infections

Cytomegalovirus reactivation enhances the virulence of Staphylococcus aureus pneumonia in a mouse model

New Tools for Studying Macrophage Polarization: Application to Bacterial Infections