Negative impact of prior influenza vaccination on current influenza vaccination among people infected and not infected in prior season: A test-negative case-control study in Japan.

BACKGROUND: Accumulating evidences indicate that repeated influenza vaccination has negative impact on the vaccine effectiveness (VE). However no published studies considered past influenza infection when assessing the VE of repeated vaccination. METHODS: Prospective surveillance was conducted from 2009 to 2012 at a community hospital on a small island in Japan. The study included all outpatients with an influenza-like illness (ILI) who attended the hospital, and a rapid diagnostic test (RDT) was used to diagnose influenza A/B infection. The VE of trivalent inactivated influenza vaccine (TIV) against medically attended influenza A (MA-fluA) was estimated using a test-negative case-control study design. The influence of TIV in the prior season on VE in the current season was investigated in the context of MA-fluA during the prior season. RESULTS: During the three influenza seasons, 5838 ILI episodes (4127 subjects) were analysed. Subjects who had an episode of MA-fluA in the prior season were at a significantly lower risk of MA-fluA in the current season (adjusted odds ratio: 0.38, 95% CI: 0.30-0.50). The overall adjusted VE was 28% (95% CI, 14-40). VE was substantially lower in subjects vaccinated in the prior season compared to those who had not been vaccinated in prior season (19%; 95% CI: 0-35 vs 46%; 95% CI: 26-60, test for interaction, P value <0.05). In subjects who did not have MA-fluA in the prior season showed the attenuation of VE due to repeated vaccination (13%; 95% CI: -7 to 30 vs 44%; 95% CI: 24-59, test for interaction, P<0.05). However this effect was not detected in subjects who had contracted MA-fluA in the prior season. CONCLUSIONS: Negative effects of repeated vaccination were significant among those without history of MA-fluA in the prior season.

[A case of rhabdomyolysis associated with Kaposi's varicelliform eruption].

Kaposi's varicelliform eruption is a common disease for dermatologists. In general, it is caused by Herpes simplex virus-1 (HSV-1) infection to skin which is affected by atopic dermatitis. There are some case reports which document a relationship between rhabdomyolysis and virus infection, in those cases, the major pathogenic virus of rhabdomyolysis is a influenza virus. It is exceedingly rare that rhabdomyolysis is caused by Herpes simplex virus. We introduce a case of rhabdomyolysis associated with Kaposi's varicelliform eruption induced by HSV-1. It was localized in the iliopsoas muscles. Since severe rhabdomyolysis may induce fatal acute renal failure, it is important to recognize that rhabdomyolysis can complicate Herpes simplex virus infection.

Essential contribution of monocyte chemoattractant protein-1/C-C chemokine ligand-2 to resolution and repair processes in acute bacterial pneumonia.

Neutrophil infiltration is the first step in eradication of bacterial infection, but neutrophils rapidly die after killing bacteria. Subsequent accumulation of macrophage lineage cells, such as alveolar macrophages (AMs), is essential to remove dying neutrophils, which are a source of injurious substances. Macrophage lineage cells can promote tissue repair, by producing potential growth factors including hepatocyte growth factor (HGF). However, it remains elusive which factor activates macrophage in these processes. Intratracheal instillation of Pseudomonas aeruginosa caused neutrophil infiltration in the airspace; subsequently, the numbers of total AMs and neutrophil ingested AMs were increased. Bronchoalveolar lavage (BAL) fluid levels of monocyte chemoattractant protein (MCP)-1/CC chemokine ligand-2 (CCL2), a potent macrophage-activating factor, were increased before the increases in the number of AM ingesting neutrophils and HGF levels in BAL fluid. Immunoreactive MCP-1 proteins were detected in alveolar type II epithelial cells and AMs only after P. aeruginosa infection. The administration of anti-MCP-1/CCL2 Abs reduced the increases in the number of AM-ingesting neutrophils and HGF levels in BAL fluid, and eventually aggravated lung tissue injury. In contrast, the administration of MCP-1/CCL2 enhanced the increases in the number of AM ingesting neutrophils and HGF levels in BAL fluid, and eventually attenuated lung tissue injury. Furthermore, MCP-1/CCL2 enhanced the ingestion of apoptotic neutrophils and HGF production by a mouse macrophage cell line, RAW 267.4, in a dose-dependent manner. Collectively, MCP-1/CCL2 has a crucial role in the resolution and repair processes of acute bacterial pneumonia by enhancing the removal of dying neutrophils and HGF production by AMs.