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E. Kalavsky – One of the best experts on this subject based on the ideXlab platform.
Multidrug-resistant Acinetobacter baumannii.Emerging infectious diseases, 2007Co-Authors: Vladimir Krcmery, E. KalavskyAbstract:
To the Editor: In the January 2007 issue of Emerging Infectious Diseases, Sunenshine et al. (1) described their finding of an independent association between patients with multidrug-resistant (MDR) Acinetobacter Infection and increased hospital and intensive care unit (ICU) length of stay compared with that for patients with antimicrobial drug–susceptible Acinetobacter Infection. The authors did not, however, find a statistically significant difference in mortality rates between the 2 groups of patients.
Toby K. Eisenstein – One of the best experts on this subject based on the ideXlab platform.
Morphine, but not trauma, sensitizes to systemic Acinetobacter baumannii Infection.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2011Co-Authors: Jessica M. Breslow, M. Alexandra Monroy, John M. Daly, Joseph J. Meissler, John P. Gaughan, Martin W. Adler, Toby K. EisensteinAbstract:
Acinetobacter baumannii is an important nosocomial pathogen in civilian intensive care units. Recently the incidence has increased in wounded military personnel. Morphine is documented in numerous animal studies to be immunosuppressive and to sensitize to Infection. The hypotheses were tested that morphine, administered for analgesia in the battlefield, predisposes to Acinetobacter Infection, and that the opioid may have an additive or synergistic effect with trauma. To test these hypotheses, an intraperitoneal Infection model was established in mice using several Acinetobacter strains. Morphine administered for 48 h by implantation of a slow-release morphine pellet increased mortality compared to animals receiving a placebo pellet, an effect that was blocked by the mu-opioid receptor antagonist, naltrexone. Acinetobacter burdens in the blood, spleens, livers, and lungs of morphine-treated mice, were significantly higher than those in placebo-treated animals, confirming that mortality was due to potentiated growth of the bacteria. There were also elevated levels of pro-inflammatory cytokines in morphine-treated versus placebo-treated mice. Morphine caused a reduction in the total number of cells in the peritoneal cavity, a decrease in the percentage and total numbers of neutrophils, and a decrease in the total number of macrophages. Morphine treatment also suppressed levels of the neutrophil-inducing molecules, IL-17A and KC/CXCL1. However, IL-17A−/− mice given morphine were not sensitized to Acintobacter Infection to a greater degree than similarly treated wild-type mice. Trauma alone did not sensitize to Acinetobacter Infection, and there was no additive effect between morphine and trauma. These results support the hypothesis that morphine potentiates Acinetobacter Infection.
Innate Immune Responses to Systemic Acinetobacter baumannii Infection in Mice: Neutrophils, but Not Interleukin-17, Mediate Host ResistanceInfection and immunity, 2011Co-Authors: Jessica M. Breslow, Joseph J. Meissler, John P. Gaughan, Rebecca R. Hartzell, Phillip B. Spence, Allan L. Truant, Toby K. EisensteinAbstract:
Acinetobacter baumannii is a nosocomial pathogen with a high prevalence of multiple-drug-resistant strains, causing pneumonia and sepsis. The current studies further develop a systemic mouse model of this Infection and characterize selected innate immune responses to the organism. Five clinical isolates, with various degrees of antibiotic resistance, were assessed for virulence in two mouse strains, and between male and female mice, using intraperitoneal Infection. A nearly 1,000-fold difference in virulence was found between bacterial strains, but no significant differences between sexes or mouse strains were observed. It was found that microbes disseminated rapidly from the peritoneal cavity to the lung and spleen, where they replicated. A persistent septic state was observed. The Infection progressed rapidly, with mortality between 36 and 48 h. Depletion of neutrophils with antibody to Ly-6G decreased mean time to death and increased mortality. Interleukin-17 (IL-17) promotes the response of neutrophils by inducing production of the chemokine keratinocyte-derived chemoattractant (KC/CXCL1), the mouse homolog of human IL-8. Acinetobacter Infection resulted in biphasic increases in both IL-17 and KC/CXCL1. Depletion of neither IL-17 nor KC/CXCL1, using specific antibodies, resulted in a difference in bacterial burdens in organs of infected mice at 10 h postInfection. Comparison of bacterial burdens between IL-17a(-/-) and wild-type mice confirmed that the absence of this cytokine did not sensitize mice to Acinetobacter Infection. These studies definitely demonstrate the importance of neutrophils in resistance to systemic Acinetobacter Infection. However, neither IL-17 nor KC/CXCL1 alone is required for effective host defense to systemic Infection with this organism.
Keith S Kaye – One of the best experts on this subject based on the ideXlab platform.
multidrug resistant Acinetobacter baumannii an emerging pathogen among older adults in community hospitals and nursing homesClinical Infectious Diseases, 2010Co-Authors: D M Sengstock, R Thyagarajan, J Apalara, A Mira, Teena Chopra, Keith S KayeAbstract:
Background. Drug-resistant Acinetobacter species are problematic in tertiary-care hospitals. We describe the epidemiology, resistance patterns, and outcomes of older adults with Acinetobacter Infection in community hospitals.Methods. We queried the microbiology databases of the Oakwood Healthcare System (4 hospitals with 632, 259, 199, and 168 beds) for clinical Acinetobacter cultures obtained in 2003-2008. Patients aged ⩾60 years who were admitted from home or nursing homes were included. We recorded the initial Acinetobacter isolate and susceptibility to 8 antibiotics. Cultures obtained 48 h after hospitalization were categorized as “nosocomial.” Administrative databases provided patients’ origins (home or nursing home) and discharge destinations (home, nursing home, long-term acute-care facility, another hospital, or hospice care or death).Results. During the 6-year period, 560 community-dwelling (mean age ± standard deviation, 74±8.6 years) and 280 nursing home-dwelling (78 ± 9.1 years) patients had Acinetobacter isolated. During this period, Acinetobacter prevalence increased 25% (P < .001, by trend test). In comparison of 2003 with 2008, Acinetobacter resistance to imipenem and ampicillin/sulbactam increased (from 1.8% to 33.1%; P < .001), as did “panresistance” (ie, resistance to all 8 antibiotics; increase from 0.0% to 13.6%; P < .001). Although resistance was stable in community-acquired isolates (resistance to ∼4.2 antibiotics), resistance increased among nursing home-acquired and nosocomial-acquired isolates (from 4.5 to 5.7 and from 5.0 to 6.0 antibiotics, respectively;P < .01). At discharge, only 25% of community-dwelling and 50% of nursing home-dwelling patients returned to their place of origin; the remainder required higher levels of care or died. After adjustment for age, length of stay, and origin, resistance to each additional antibiotic predicted a 120% increased risk for discharge to higher levels of care or death (odds ratio, 1.23; 95% confidence interval, 1.11-1.36).Conclusions. The prevalence and resistance of Acinetobacter species are increasing in the community. Patients with resistant isolates are selectively discharged to nursing homes and long-term acute-care facilities, introducing resistance to new facilities.