Esthesioneuroblastoma with bilateral metastases to the parotid glands.

BACKGROUND: Esthesioneuroblastoma (ENB) is a rare, poorly characterized, intranasal cancer arising from olfactory neuroepithelium. METHODS: This case report reviews the underlying pathophysiology, clinical presentation, and diagnosis of primary ENB and parotid metastases. RESULTS: We present the case of a 43-year-old man who was referred to our practice with radiographically and biopsy confirmed ENB. After neoadjuvant chemotherapy, radiation, and open surgical resection, he returned to the clinic 30 months postoperatively with a right parotid mass, which was found to be a recurrence of his primary cancer. A parotidectomy was performed; however, he returned 10 months later with a new left parotid mass. Subsequent imaging and biopsy confirmed recurrence of ENB and a second parotidectomy was performed. CONCLUSION: This case illustrates that delayed metastases in the setting of ENB are not limited to the cervical lymph nodes and, in rare instances, may involve the parotid glands. Surveillance should include the parotid lymph node basin with a high clinical index of suspicion in the setting of parotid lymphadenopathy after primary surgical therapy. © 2016 Wiley Periodicals, Inc. Head Neck 38: E2457-E2460, 2016.

Isolation and characterization of "Pseudomonas andersonii" from four cases of pulmonary granulomas and emended species description.

"Pseudomonas andersonii" is a Gram-negative bacillus initially isolated from a granulomatous lung lesion. Novel species status has not been validated for this single strain. We report four additional cases of pulmonary granuloma involving P. andersonii and further characterize the organism. These patients had pulmonary nodules that were surgically resected and which grew P. andersonii on routine culture. Mycobacterium avium complex was concomitantly isolated in two cases, and fungal structures were identified histopathologically in two other cases. The five P. andersonii strains described to date were similar in growth characteristics, biochemical reactions, matrix-assisted laser desorption ionization-time of flight mass spectrometry protein profiles, and susceptibility to antimicrobial agents. Their 16S rRNA genes were 99.9 to 100% identical but less than 95.0% similar to those of all other known bacteria. The gyrA genes of these strains were 99.5 to 100% identical. These shared features illustrate P. andersonii as a unique and distinct bacterium and support the novel species status of the organism.

Enhancement of cellular and humoral immune responses to human immunodeficiency virus type 1 Gag and Pol by a G/P-92 fusion protein expressing highly immunogenic Gag p17/p24 and Pol p51 antigens.

OBJECTIVES: Immunity to the human immunodeficiency virus type-1 (HIV-1) G/P-92 fusion protein consisting of highly immunogenic regions of Gag (p17 and p24) and Pol (p51) expressed in recombinant vaccinia virus (vG/P-92) was compared with responses to the entire viral Gag-Pol precursor protein (vVK1). STUDY DESIGN/METHODS: We analyzed the level of Gag and Pol protein expression in vG/P-92-infected cells as well as the ability of the G/P-92 fusion protein to form virus-like particles (VLP) in infected cultures. The efficacy of vG/P-92 and vVK1 vaccines was evaluated in a murine model by measuring T helper (Th), cytotoxic T lymphocyte (CTL), and antibody responses to Gag and Pol antigens. RESULTS: The deletion of a frameshift site resulted in an increased level of Pol in cells expressing the G/P-92 fusion protein. Particles budding from the plasma membrane were detected in both vG/P-92- and vVK1-infected cells, but the release of VLP was less efficient from cells expressing the G/P-92 fusion protein than the entire gag-pol gene product. Immunization with vG/P-92 vector elicited a higher level of cellular and humoral responses to both Gag and Pol antigens than the vVK1 vaccine. CONCLUSIONS: The enhanced immunogenicity of the G/P-92 fusion protein compared with the entire viral gag-pol gene product might be related to a higher intracellular level of Pol and Gag expression due to the deletion of a frameshift site and less efficient transport of VLP from vG/P-92-infected cells, respectively.