Different clinical presentation of community-onset bacteremia among human immunodeficiency virus-infected and human immunodeficiency virus-uninfected adults in the ED

Lee, Ching Chi; Chu, Feng Yuan; Ko, Wen Chien; Hsien, Chih

doi:10.1016/j.ajem.2014.07.028

Cited by 3 publications

(3 citation statements)

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“…In fact, male gender is considered as one of the four risk factors associated with the development of sepsis in general surgical and post-traumatic patients, with a hospital mortality rate of 70% in male and 26% in female patients [ 18 , 165 , 166 ]. Moreover, it has been reported that male gender along with HIV infection is a risk factor for bacteremia, suggesting an important role of immune suppression [ 167 ]. The pathological response to trauma-hemorrhage in rodent males, ovariectomized females, and testosterone-treated females is characterized by a severe suppression of the immune response and multiple organ dysfunctions, leading to a high incidence of sepsis [ 168 – 170 ].…”

Section: Sexual Dimorphism and Bacterial Sepsismentioning

confidence: 99%

“… Gastroenteritis and wound infections [ 57 , 200 , 245 , 246 ] Women Enterohemorrhagic Escherichia coli Hemolytic–uremic syndrome and irritable bowel syndrome [ 59 , 60 ] Respiratory tract infections Men Streptococcus pneumoniae Community-acquired pneumonia [ 79 ] Mycobacterium tuberculosis Tuberculosis [ 93 – 100 ] Legionella spp. Legionnaires’ disease [ 131 , 132 , 141 , 133 – 140 ] Bloodstream infections Men Many bacterial species Septic shock, organ dysfunction, severe sepsis [ 18 , 162 , 177 , 163 , 165 – 167 , 173 – 176 ] Urinary tract infections Women Escherichia coli Acute cystitis, inflammation, and sepsis [ 229 , 231 ] Lyme borreliosis Women Borrelia burgdorferi Erythema migrans and facial nerve palsy [ 232 , 233 ] Sexually transmitted infections Women Chlamydia trachomatis Infertility, ectopic pregnancy, and pelvic inflammatory disease [ 235 , 237 ] Neisseria gonorrhea …”

Section: Introductionmentioning

confidence: 99%

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Sexual dimorphism in bacterial infections

et al. 2018

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BackgroundSex differences are important epidemiological factors that impact in the frequency and severity of infectious diseases. A clear sexual dimorphism in bacterial infections has been reported in both humans and animal models. Nevertheless, the molecular mechanisms involved in this gender bias are just starting to be elucidated. In the present article, we aim to review the available data in the literature that report bacterial infections presenting a clear sexual dimorphism, without considering behavioral and social factors.Main bodyThe sexual dimorphism in bacterial infections has been mainly attributed to the differential levels of sex hormones between males and females, as well as to genetic factors. In general, males are more susceptible to gastrointestinal and respiratory bacterial diseases and sepsis, while females are more susceptible to genitourinary tract bacterial infections. However, these incidences depend on the population evaluated, animal model and the bacterial species. Female protection against bacterial infections and the associated complications is assumed to be due to the pro-inflammatory effect of estradiol, while male susceptibility to those infections is associated with the testosterone-mediated immune suppression, probably via their specific receptors. Recent studies indicate that the protective effect of estradiol depends on the estrogen receptor subtype and the specific tissue compartment involved in the bacterial insult, suggesting that tissue-specific expression of particular sex steroid receptors contributes to the susceptibility to bacterial infections. Furthermore, this gender bias also depends on the effects of sex hormones on specific bacterial species. Finally, since a large number of genes related to immune functions are located on the X chromosome, X-linked mosaicism confers a highly polymorphic gene expression program that allows women to respond with a more expanded immune repertoire as compared with men.ConclusionNotwithstanding there is increasing evidence that confirms the sexual dimorphism in certain bacterial infections and the molecular mechanisms associated, further studies are required to clarify conflicting data and to determine the role of specific hormone receptors involved in the gender bias of bacterial infections, as well as their potential as therapeutic targets.

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Section: Sexual Dimorphism and Bacterial Sepsismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sexual dimorphism in bacterial infections

et al. 2018

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“…Empirical administration of appropriate antimicrobials to septic or infective individuals has remained challenging because of the increased antibiotic resistance in both hospitals and communities [1] as well as atypical presentations in the specific population, such as the elderly [2] and human immunodeficiency virus-infected adults [3]. Particularly in septic patients presenting with a critical illness, inappropriate empirical therapy is associated with increased mortality [4, 5].…”

Section: Introductionmentioning

confidence: 99%

Beneficial effects of early empirical administration of appropriate antimicrobials on survival and defervescence in adults with community-onset bacteremia

et al. 2019

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BackgroundBloodstream infections are associated with high morbidity and mortality, both of which contribute substantially to healthcare costs. The effects of early administration of appropriate antimicrobials on the prognosis and timing of defervescence of bacteremic patients remain under debate.MethodsIn a 6-year retrospective, multicenter cohort, adults with community-onset bacteremia at the emergency departments (EDs) were analyzed. The period from ED arrival to appropriate antimicrobial administration and that from appropriate antimicrobial administration to defervescence was regarded as the time-to-appropriate antibiotic (TtAa) and time-to-defervescence (TtD), respectively. The primary study outcome was 30-day mortality after ED arrival. The effects of TtAa on 30-day mortality and delayed defervescence were examined after adjustment for independent predictors of mortality, which were recognized by a multivariate regression analysis.ResultsOf the total 3194 patients, a TtAa-related trend in the 30-day crude (γ = 0.919, P = 0.01) and sepsis-related (γ = 0.909, P = 0.01) mortality rate was evidenced. Each hour of TtAa delay was associated with an average increase in the 30-day crude mortality rate of 0.3% (adjusted odds ratio [AOR], 1.003; P < 0.001) in the entire cohort and 0.4% (AOR, 1.004; P < 0.001) in critically ill patients, respectively, after adjustment of independent predictors of 30-day crude mortality. Of 2469 febrile patients, a TtAa-related trend in the TtD (γ = 0.965, P = 0.002) was exhibited. Each hour of TtAa delay was associated with an average 0.7% increase (AOR, 1.007; P < 0.001) in delayed defervescence (TtD of ≥ 7 days) after adjustment of independent determinants of delayed defervescence. Notably, the adverse impact of the inappropriateness of empirical antimicrobial therapy (TtAa > 24 h) on the TtD was noted, regardless of bacteremia severity, bacteremia sources, or causative microorganisms.ConclusionsThe delay in the TtAa was associated with an increasing risk of delayed defervescence and 30-day mortality for adults with community-onset bacteremia, especially for critically ill patients. Thus, for severe bacteremia episodes, early administration of appropriate empirical antimicrobials should be recommended.

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