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Age- and sex-specific mortality patterns in an emerging wildlife epidemic: the phocine distemper in European harbour seals.

Artikel i vetenskaplig tidskrift
Författare Tero Harkonen
Karin C. Harding
Thomas Dau Rasmussen
Jonas Teilmann
Rune Dietz
Publicerad i PLoS ONE
Volym 2
Nummer/häfte 9
Sidor e887
ISSN 1932-6203
Publiceringsår 2007
Publicerad vid Institutionen för marin ekologi
Sidor e887
Språk en
Länkar dx.doi.org/10.1371/journal.pone.000...
Ämneskategorier Biologiska vetenskaper

Sammanfattning

Analyses of the dynamics of diseases in wild populations typically assume all individuals to be identical. However, profound effects on the long-term impact on the host population can be expected if the disease has age and sex dependent dynamics. The Phocine Distemper Virus (PDV) caused two mass mortalities in European harbour seals in 1988 and in 2002. We show the mortality patterns were highly age specific on both occasions, where young of the year and adult (>4 yrs) animals suffered extremely high mortality, and sub-adult seals (1-3 yrs) of both sexes experienced low mortality. Consequently, genetic differences cannot have played a main role explaining why some seals survived and some did not in the study region, since parents had higher mortality levels than their progeny. Furthermore, there was a conspicuous absence of animals older than 14 years among the victims in 2002, which strongly indicates that the survivors from the previous disease outbreak in 1988 had acquired and maintained immunity to PDV. These specific mortality patterns imply that contact rates and susceptibility to the disease are strongly age and sex dependent variables, underlining the need for structured epidemic models for wildlife diseases. Detailed data can thus provide crucial information about a number of vital parameters such as functional herd immunity. One of many future challenges in understanding the epidemiology of the PDV and other wildlife diseases is to reveal how immune system responses differ among animals in different stages during their life cycle. The influence of such underlying mechanisms may also explain the limited evidence for abrupt disease thresholds in wild populations.

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