bioRxiv ScienceSearch

Biology subjects

Johnson, A. F.

Publications and source records attributed to Johnson, A. F..

2 recordsLinked to original sources

Factors contributing to the disease ecology of brown crab (Cancer pagurus) in a temperate marine protected area.

Marine ecosystems are affected by multiple, well-known stressors like fishing and climate change, but a less documented concern is disease. Marine reserves have been successful in replenishing stocks and aiding recruitment but studies have shown that high population abundances in marine reserves may lead to unwanted secondary effects such as increase in predators and competition, altering trophic webs, and disease. Here, we investigate factors contributing to disease prevalence in a brown crab (Cancer pagurus) population around Lundy Island (the UKs first MPA) after 7 years of no-take protection. Population parameters (size, sex, and abundance), disease (shell disease, Hematodinium spp. infection) and injury presence (a known precursor to some disease conditions) were assessed over two years in both fished and unfished areas of the MPA. We found no significant difference in prevalence between the disease prevalence in fished and unfished areas, however overall, the number of injured crabs increased significantly over the two years (12%), as did the prevalence of shell disease (15%). The probability of crabs having shell disease increased significantly in male crabs, and in those missing limbs. The probability of crabs being injured increased significantly in crabs below the minimum landing size. In terms of population parameters, crabs were more prevalent in the fished area compared to the unfished area, thought to be a result of an increase in the predatory European lobster. The findings of the present study highlight potential secondary community changes as a result of MPA implementation. Therefore, surveillance for such changes, as part of MPA management, would provide useful information on the health and overall function of the protected ecosystem.

ecology

Group A Streptococcus Infection of the Nasopharynx Requires Proinflammatory Signaling Through the Interleukin-1 Receptor

Group A Streptococcus (GAS) is the etiologic agent of numerous high morbidity and high mortality diseases which commonly have a highly proinflammatory pathology. One factor contributing to this inflammation is the GAS protease SpeB, which directly activates the proinflammatory cytokine interleukin-1{beta} (IL-1{beta}), independent of the canonical inflammasome pathway. IL-1{beta} drives neutrophil activation and recruitment that limits bacterial growth and invasion during invasive skin and soft tissue infections like necrotizing fasciitis. GAS also causes pharyngitis (strep throat), and the upper respiratory tract is its primary nidus for growth and transmission. Since the fitness selection for the species is likely primarily for this site, we examined the process of IL-1{beta} activation in the murine nasopharynx. SpeB still activated IL-1{beta}, which was required for neutrophil migration, but this inflammation instead increased GAS replication. Inhibiting IL-1{beta} or depleting neutrophils, which both promote invasive infection, prevented GAS infection of the nasopharynx. Prior antibiotic exposure increased GAS growth in the murine nasopharynx, and antibiotics were sufficient to reverse the attenuation previously observed when IL-1{beta}, neutrophils, or SpeB were not present to drive inflammation. Therefore, the same fundamental mechanism has opposing effects on virulence at different body sites. Invasive disease may be limited in part due to specific adaptations for inducing host inflammation that are beneficial for pharyngitis. IMPORTANCEOur previous reports showed that Group A Streptococcus (GAS) protease SpeB directly activates the host proinflammatory cytokine IL-1{beta} and this restricts invasive skin infection. The upper respiratory tract is the primary site of GAS colonization and infection, but the host-pathogen interactions at this site are still largely unknown. We provide the first evidence that IL-1{beta}-mediated inflammation promotes upper respiratory tract infection. This provides experimental evidence that the notable inflammation of strep throat, which presents with significant swelling, pain, and neutrophil influx, is not an ineffectual immune response, but rather is a GAS-directed remodeling of this niche for its pathogenic benefit.

microbiology