In a murine model of acute fatal pneumonia, we previously showed that nasal immunization with a live-attenuated aroA deletant of Pseudomonas aeruginosa strain PAO1 elicited LPS serogroup-specific protection, indicating that opsonic Ab to the LPS O Ag was the most important immune effector. Because P. aeruginosa strain PA14 possesses additional virulence factors, we hypothesized that a live-attenuated vaccine based on PA14 might elicit a broader array of immune effectors. Thus, an aroA deletant of PA14, denoted PA14ΔaroA, was constructed. PA14ΔaroA-immunized mice were protected against lethal pneumonia caused not only by the parental strain but also by cytotoxic variants of the O Ag-heterologous P. aeruginosa strains PAO1 and PAO6a,d. Remarkably, serum from PA14ΔaroA-immunized mice had very low levels of opsonic activity against strain PAO1 and could not passively transfer protection, suggesting that an antibody-independent mechanism was needed for the observed cross-serogroup protection. Compared with control mice, PA14ΔaroA-immunized mice had more rapid recruitment of neutrophils to the airways early after challenge. T cells isolated from P. aeruginosa ΔaroA-immunized mice proliferated and produced IL-17 in high quantities after coculture with gentamicin-killed P. aeruginosa. Six hours following challenge, PA14ΔaroA-immunized mice had significantly higher levels of IL-17 in bronchoalveolar lavage fluid compared with unimmunized, Escherichia coli-immunized, or PAO1ΔaroA-immunized mice. Antibody-mediated depletion of IL-17 before challenge or absence of the IL-17 receptor abrogated the PA14ΔaroA vaccine’s protection against lethal pneumonia. These data show that IL-17 plays a critical role in antibody-independent vaccine-induced protection against LPS-heterologous strains of P. aeruginosa in the lung.

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pathology departments at hospitals across Boston, Massachusetts received numerous amputated limbs, as well as other surgical specimens from trauma surgeries. In the absence of clear guidelines, each department faced uncertainties in performing gross examination of these specimens.Objective.-To develop a protocol for processing surgical specimens with forensic evidence.Design.-We collaborated with representatives who knew the practices at 3 major Boston hospitals, the Office of the Chief Medical Examiner of Massachusetts, and a senior team leader for the evidence response team for the Boston, Massachusetts division of the US Federal Bureau of Investigation to construct a protocol for processing specimens with forensic evidence.Results.-A simple and robust protocol approved by experts in forensic evidence collection was developed. Important points in this protocol include (1) assigning the task of processing the specimens to one individual or one team of individuals, (2) photographing all specimens before and after washing, (3) obtaining a radiograph of each specimen, and (4) identifying a secure area to store forensic evidence.Conclusions.-When acts of terror occur, protocols provide order and clarification to the processing of surgical specimens. We propose a protocol that provides guidance for pathology departments across the country to handle trauma-related surgical specimens with forensic evidence in an efficient manner to allow optimal patient care and a secure way of gathering forensic evidence.

A 40-year-old man with no significant past medical history developed fever, dry cough, night sweats, chills, and malaise 1 week after hiking in the mountains in Michigan. He visited his primary care physician (PCP) and was treated with oral azithromycin for 5 days with no improvement. The patient then traveled to Europe for 2 weeks. During this trip, he had daily fevers, chills, cough, and sweats. After returning to Massachusetts, he went to the emergency department, where a chest X-ray examination showed diffuse bilateral airspace consolidation. He was admitted to our hospital and initially treated with levofloxacin, vancomycin, and cefepime for presumptive community-acquired pneumonia. His white blood cell count was 20.8 ϫ 10 3 cells/mm 3 (normal range, 4 ϫ 10 3 to 11 ϫ 10 3 cells/mm 3 ), with 86.6% neutrophils (normal range, 50 to 70% neutrophils), 7.4% lymphocytes (normal range, 18 to 42% lymphocytes), 5.2% monocytes, 0.3% eosinophils, and 0.5% basophils. Organisms of 8 to 10 m in diameter were seen on Gram (Fig. 1A) and KOH-calcofluor white (Fig. 1B) stain preparations of bronchoalveolar lavage and sputum samples. The patient was subsequently treated with antimicrobial agents appropriate for these findings. Despite intensive medical therapy, the patient developed acute respiratory distress syndrome (ARDS) and expired. Histological preparations of autopsy lung tissue samples stained with hematoxylin and eosin (H&E) (Fig. 1C) or Gomori methenamine silver (GMS) (Fig. 1D) showed the same organism morphology. What is your diagnosis?