How Staphylococcus aureus Adapts to Its Host

Columbia University College of Physicians and Surgeons, New York, USA.
New England Journal of Medicine (Impact Factor: 55.87). 05/2011; 364(21):1987-90. DOI: 10.1056/NEJMp1100251
Source: PubMed
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    • "Interestingly, anemia was also more common in the group of women with mastitis, since women suffering from anemia might be more vulnerable to infections. In addition, iron supplements enhance growth and virulence of Staphylococcus aureus and other mastitis-associated species [34]; as a consequence, women receiving them may also be more prone to mastitis. No clinical trials have evaluated the impact of iron supplementation on mastitis but the study of iron acquisition pathways seems to be a good target to define the underlying mechanisms of mastitis severity [35]. "
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    ABSTRACT: Background The purpose of this study was to identify potential predisposing factors associated with human infectious mastitis. Methods We conducted a case–control study among breastfeeding women, with 368 cases (women with mastitis) and 148 controls. Data were collected by a questionnaire designed to obtain retrospective information about several factors related to medical history of mother and infant, different aspects of pregnancy, delivery and postpartum, and breastfeeding practices that could be involved in mastitis. Bivariate analyses and multivariate logistic regression model were used to examine the relationship between mastitis and these factors. Results The variables significantly- and independently-associated with mastitis were cracked nipples (P < 0.0001), oral antibiotics during breastfeeding (P < 0.0001), breast pumps (P < 0.0001), topical antifungal medication during breastfeeding (P = 0.0009), mastitis in previous lactations (P = 0.0014), breast milk coming in later than 24 h postpartum (P = 0.0016), history of mastitis in the family (P = 0.0028), mother-infant separation longer than 24 h (P = 0.0027), cream on nipples (P = 0.0228) and throat infection (P = 0.0224). Conclusions Valuable factors related to an increased risk of infectious mastitis have been identified. This knowledge will allow practitioners to provide appropriate management advice about modifiable risk factors, such as the use of pumps or inappropriate medication. They also could identify before delivery those women at an increased risk of developing mastitis, such as those having a familial history of mastitis, and thus develop strategies to prevent this condition.
    BMC Pregnancy and Childbirth 06/2014; 14(1):195. DOI:10.1186/1471-2393-14-195 · 2.19 Impact Factor
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    • "Although these studies have provided important information regarding immune responses and pathogen virulence, they are highly limited for the investigation of pathogenic mechanisms at the cellular level. Additionally, murine models do not necessarily reflect the situation in humans because the action of PVL is species specific and restricted to human neutrophils [9, 24]. To overcome these limitations, we developed an experimental model system that provides relevant advantages: it is based on cells of human origin, and it includes well-defined cell types, such as neutrophils and epithelial cells, which are both essentially involved in the pathogenesis of pneumonia, thus enabling us to study separately the effect of the pathogens on the different cell types. "
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    ABSTRACT: Staphylococcus aureus necrotizing pneumonia is a life-threatening disease that is frequently preceded by influenza infection. The S. aureus toxin Panton-Valentine leukocidin (PVL) is most likely causative for necrotizing diseases, but the precise pathogenic mechanisms of PVL and a possible contribution of influenza virus remain to be elucidated. In this study, we present a model that explains how influenza virus and PVL act together to cause necrotizing pneumonia: an influenza infection activates the lung epithelium to produce chemoattractants for neutrophils. Upon superinfection with PVL-expressing S. aureus, the recruited neutrophils are rapidly killed by PVL, resulting in uncontrolled release of neutrophil proteases that damage the airway epithelium. The host counteracts this pathogen strategy by generating PVL-neutralizing antibodies and by neutralizing the released proteases via protease inhibitors present in the serum. These findings explain why necrotizing infections mainly develop in serum-free spaces (eg, pulmonary alveoli) and open options for new therapeutic approaches.
    The Journal of Infectious Diseases 07/2012; 206(7):1138-48. DOI:10.1093/infdis/jis468 · 6.00 Impact Factor

  • The Journal of Bone and Joint Surgery 09/2011; 93(18):e109. DOI:10.2106/JBJS.K.00785 · 5.28 Impact Factor
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