A model of spatially evolving herpesvirus epidemics causing mass mortality in Australian pilchard Sardinops sagax

Abstract

In 1995 mass mortality of pilchards Sardinops sagax occurred along > 5000 km of Australian coast; similar events occurred in 1998/99. This mortality was closely associated with a herpesvirus. The pilchard is an important food source for larger animals and supports commercial fisheries. Both epidemics originated in South Australian waters and spread as waves with velocities of 10 to 40 km d -1. Velocity was constant for a single wave, but varied between the epidemics and between the east-and west-bound waves in each epidemic. The pattern of mortality evolved from recurrent episodes to a single peak with distance from the origin. A 1-dimensional model of these epidemics has been developed. The host population is divided into susceptible, infected and latent, infected and infectious, and removed (recovered and dead) phases; the latent and infectious periods are of fixed duration. This model produces the mortality patterns observed locally and during the spread and evolution of the epidemic. It is consistent with evidence from pathology. The wave velocity is sensitive to diffusion coefficients, viral transmission rates and latent period. These parameters are constrained using the local and large-scale patterns of epidemic spread. The relative roles of these parameters in explaining differences between epidemics and between east-and west-bound waves within epidemics are discussed. The model predicts very high levels of infection, indicating that many surviving pilchards recovered following infection. Control appears impracticable once epidemics are initiated, but impact can be minimised by protecting juvenile stocks. KEY WORDS: Epidemic · Model · Herpesvirus · Mass mortality · Pilchard · Australia Resale or republication not permitted without written consent of the publisherDis Aquat Org 54: [1][2][3][4][5][6][7][8][9][10][11][12][13][14] 2003 this species. The mortality occurred as a locally shortlived outbreak, forming waves that travelled at very high and near-constant velocities. Mortality also occurred from June in New Zealand (Smith 1995). The outbreak was unprecedented in scale for an observed epidemic (Gaut 2001), although Californian sedimentary records imply collapses have occurred over the centuries (Baumgartner et al. 1992). The scale of mortality provided a generally clear picture of the spread of the epidemic.In November 1998 a second occurrence of such mass mortality events began (Gaughan et al. 2000). Mortality spread over the same area, again starting in South Australia, but at about half the velocity of 1995. Hence this epidemic lasted for over 6 mo, although again the duration at most localities was brief. On this occasion New Zealand was not affected. Mortality, however, was probably even greater than during the 1995 epidemic.No features of the physical environment (Griffin et al. 1997) or unusual or toxic algae were associated with the 1995 mass mortality events. There is also no evidence of any environmental linkage in 1998/99. The only common feature of the mortality events was he...

Herpesviruses of Fish, Amphibians and Invertebrates

“…In several months it spread thousands of kilometres bidirectionally along the Australian coastline, and then to New Zealand . A similar event occurred a few years later in 1998/1999 (Murray et al, 2003). Affected pilchards showed progressive gill inflammation followed by epithelial hypertrophy and hyperplasia .…”

Comparison of three molecular methods for the detection of Pilchard herpesvirus in archived paraffin-embedded tissue and frozen tissue

“…Pilchards surviving the epizootic had lesions consistent with infection by PHV. This suggested that they had survived, rather than avoided, infection (Murray et al 2003). These survivors showed few signs of disease 8 d after the front had passed .…”

“…Models have been proposed to explain how the virus spread so quickly. The most recent research proposed that the schooling patterns of pilchards, involving contact within and also between schools, allowed the rapid spread of the disease from a point source (Murray et al 2003). During the disease outbreak, affected pilchards were observed to exhibit signs of stress only a few minutes before dying , allowing infected and uninfected fish to school together (Murray et al 2003).…”

“…These survivors showed few signs of disease 8 d after the front had passed . Modeling by Murray et al (2003) suggested the incubation period of infection to be 4 to 12 d, depending on the epidemic-wave speed.…”

Risk of introducing viral hemorrhagic septicemia virus (VHSV) to the Chilean South Pacific via sardine imports from Europe

“…Concentrations of the virus in sardine from these fisheries may be low, especially in healthy, wild-caught fish (Arkush et al 2006). Despite these large volumes of imported and likely VHSVinfected bait, there has been no indication of the spread of the virus among wild fish, salmonids or other pen-raised fish populations in Australia, although mass mortalities by herpesvirus of Australian pilchard Sardinops sagax have been reported (Murray et al 2003). However, a key difference between the Chilean and Australian marine environments is water temperature: southern Chile is much cooler and thus potentially more conducive to VHSV infection compared to South Australia.…”