Modelling the spread of infectious salmon anaemia among salmon farms based on seaway distances between farms and genetic relationships between infectious salmon anaemia virus isolates.

Infectious salmon anaemia (ISA) is an important infectious disease in Atlantic salmon farming causing recurrent epidemic outbreaks worldwide. The focus of this paper is on tracing the spread of ISA among Norwegian salmon farms. To trace transmission pathways for the ISA virus (ISAV), we use phylogenetic relationships between virus isolates in combination with space-time data on disease occurrences. The rate of ISA infection of salmon farms is modelled stochastically, where seaway distances between farms and genetic distances between ISAV isolates from infected farms play prominent roles. The model was fitted to data covering all cohorts of farmed salmon and the history of all farms with ISA between 2003 and summer 2009. Both seaway and genetic distances were significantly associated with the rate of ISA infection. The fitted model predicts that the risk of infection from a neighbourhood infectious farm decreases with increasing seaway distance between the two farms. Furthermore, for a given infected farm with a given ISAV genotype, the source of infection is significantly more likely to be ISAV of a small genetic distance than of moderate or large genetic distances. Nearly half of the farms with ISA in the investigated period are predicted to have been infected by an infectious farm in their neighbourhood, whereas the remaining half of the infected farms had unknown sources. For many of the neighbourhood infected farms, it was possible to point out one or a few infectious farms as the most probable sources of infection. This makes it possible to map probable infection pathways.

Intrauterine growth pattern by the tendency to repeat small-for-gestational-age births in successive pregnancies.

BACKGROUND: Fetuses of women who repeat small-for-gestational-age births in successive pregnancies may have a different intrauterine growth pattern than SGA birth of non-repeater mothers. Also repeated SGA births may grow differently depending on whether the tendency to repeat is due to some external factors such as cigarette smoking ("false repeaters") or due to genetic or intrinsic factors ("true repeaters"). MATERIAL AND METHODS: Fetal growth were compared in a "nested case-control" study within a longitudinal (cohort) study, comparing three types of SGA births, 23 of "true repeater" mothers, 46 of "false repeater" mothers and 65 of non-repeater mothers, and these were compared with 1017 non-SGA births. Fetal growth was compared using a regression analysis based on repeated measurements (four for each woman). RESULTS: For mean abdominal diameter the "true repeater" SGA births grew more slowly towards the end of pregnancy. However, the growth curves show only minor differences between the three types of SGA births, but the patterns are grossly different from the growth of non-SGA births (controls). CONCLUSION: The intrauterine growth retardation starts early in pregnancy, and is not strikingly different between births of repeater and non-repeater mothers.