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.

The erm gene product confers clindamycin resistance on Staphylococcus aureus. We report a clindamycin clinical failure where resistance developed on therapy in a D-test-positive strain. D tests of 91 clindamycinsusceptible, erythromycin-resistant S. aureus isolates showed that 68% of methicillin-susceptible and 12.3% of methicillin-resistant S. aureus strains were D-test positive.Clindamycin-susceptible, erythromycin-resistant Staphylococcus aureus (clindamycin-erythromycin discordant) may develop clindamycin resistance (7,8). The erm gene product is a ribosome methylase whose expression is normally minimal. Erythromycin induces the production of this methylase, which is why these strains are erythromycin resistant, but mutations in the promoter region of erm allow production of methylase without an inducer (18,19). These mutants are stably erythromycin and clindamycin resistant. Since erythromycin resistance can occur with other mechanisms (e.g., efflux pumps and enzymatic modification) (15), the D-test identifies inducible resistance that might presage mutational clindamycin constitutive resistance. The D-test is performed by placing clindamycin and erythromycin disks at an edge-to-edge distance of 15 to 20 mm and looking for flattening of the clindamycin zone nearest the erythromycin disk (2). A positive D-test suggests the presence of an erm gene that could result in constitutive clindamycin resistance and clinical failure.There are few published clinical failures of clindamycin with emergence of resistance (1,3,9,12,16). However, there are also reports of successful use of clindamycin in treating patients with D-test-positive isolates (3, 9). We report a clinical failure with documented emergence of resistance. In order to avoid poor clinical outcomes but retain the usefulness of clindamycin, it would be helpful to know the prevalence of inducible resistance in clindamycin-erythromycin discordant bacteria. This prevalence varies by geographic location, patient age, bacterial species, and bacterial susceptibility profile (4,5,10,11,13,14,16). For example, a pediatric population in Houston, Tex., with methicillin-resistant S. aureus (MRSA) had a D-test positivity rate of 2.2% (9) compared to a similar population of children with MRSA in Chicago, Ill., whose D-test positivity rate was 94% (3). We determined the prevalence of D-test positivity in clindamycin-erythromycin discordant S. aureus isolates in our institution in early 2004. We tested isolates from infected body sites where clindamycin might be considered for therapy.The patient was a 44-year-old man with fever, chills, and increased low back pain 10 days after a lumbar discectomy. At admission he had a temperature of 102.4°F and complained of 3 days of erythema, bloody drainage, and pain along his incision. He had a wound exploration, and the tissue Gram stain showed white blood cells and gram-positive cocci. Fluid and blood cultures grew clindamycin-erythromycin discordant methicillin-susceptible S. aureus (MSSA), which was treated with 2 weeks of ox...

Gram-negative sepsis and subsequent endotoxic shock remain major health problems in the United States. The present study examined the role of morphine in inducing sepsis. Mice administered morphine by the subcutaneous implantation of a slow-release pellet developed colonization of the liver, spleen, and peritoneal cavity with gram-negative and other enteric bacteria. In addition, the mice became hypersusceptible to sublethal endotoxin challenge. The effects were blocked by the simultaneous implantation of a pellet containing the opioid antagonist naltrexone. These findings show that morphine pellet implantation in mice results in the escape of gram-negative organisms from the gastrointestinal tract, leading to the hypothesis that morphine used postoperatively or chronically for analgesia may serve as a cofactor in the precipitation of sepsis and shock. In addition, morphine-induced sepsis may provide a physiologically relevant model of gram-negative sepsis and endotoxic shock.

Cerebral phaeohyphomycosis caused by Cladophialophora bantiana is a rare disease. We describe a heart and bilateral lung transplant recipient who was unsuccessfully treated for a C. bantiana brain abscess. This report compares the present case to those of other solid-organ transplant recipients with the same infection and to those of patients who did not receive transplants

Background Previous studies have found fewer clinical infections in wounds closed with monofilament suture compared with braided suture. Recently, barbed monofilament sutures have shown improved strength and increased timesavings over interrupted braided sutures. However, the adherence of bacteria to barbed monofilament sutures and other commonly used suture materials is unclear.

Understanding the consequences of drug withdrawal on immune function and host defense to infection is important. We, and others, previously demonstrated that morphine withdrawal results in immunosuppression and sensitizes to lipopolysaccharide-induced septic shock. In the present study, the effect of morphine withdrawal on spontaneous sepsis and on oral infection with Salmonella enterica serovar Typhimurium was examined. Mice were chronically exposed to morphine for 96 h by implantation of a slow-release morphine pellet. Abrupt withdrawal was induced by removal of the pellet. In the sepsis model, bacterial colonization was examined and bacterial species were identified by necropsy of various tissues. It was found that at 48 h postwithdrawal, morphine-treated mice had enteric bacteria that were detected in the Peyer's patches (4/5), mesenteric lymph nodes (4/5), spleens (4/10), livers (6/10), and peritoneal cavities (8/10). In placebo pelletwithdrawn mice, only 2/40 cultures were positive. The most frequently detected organisms in tissues of morphine-withdrawn mice were Enterococcus faecium followed by Klebsiella pneumoniae. Both organisms are part of the normal gastrointestinal flora. In the infection model, mice were orally inoculated with S. enterica 24 h post-initiation of abrupt withdrawal from morphine. Withdrawal significantly decreased the mean survival time and significantly increased the Salmonella burden in various tissues of infected mice compared to placebo-withdrawn animals. Elevated levels of the proinflammatory cytokines were observed in spleens of morphine-withdrawn mice, compared to placebo-withdrawn mice. These findings demonstrate that morphine withdrawal sensitizes to oral infection with a bacterial pathogen and predisposes mice to bacterial sepsis.

Biofilms were present on tracheostomy tubes in greater than 90% of tracheostomy tubes collected as early as 7 days after insertion in both the inpatients and outpatients. Although a variety of bacteria were identified in the biofilm, they often appeared as discrete microcolonies that appeared to be monospecies biofilm on confocal microscopy. There was a statistically significant inverse correlation between the number of colony forming units found and frequency of inner cannula change.

No abstract