Introduction Lucilia cuprina (Wiedemann) was first recorded in Australia at Albany between 1864 and 1867, and the fly was probably not introduced to the eastern Australian states until the 1880s or 1890s (Norris 1990). Adaptation of the fly to parasitism of woolled sheep and the introduction of the highly susceptible Vermont Merino genotypes are considered to have preceded the emergence of widespread cutaneous myiasis in sheep (fly strike) in the early 1900s (Norris 1990). It was soon realised that conformation of the withers and breech, wool characteristics and susceptibility to bacterial dermatitis (fleece rot) were predisposing factors for susceptibility of sheep to fly strike and that these traits were heritable (Gilruth et al. 1933). Moderate heritability of resistance to fleece rot was confirmed by Hayman (1953) and this observation led to several decades of work on genetics of resistance to fleece rot and fly strike. Divergent selection of sheep on an index of natural fleece rot and fly strike, and fleece rot and fly strike induced by simulated rainfall, was used to establish two lines of sheep that diverged at an annual rate of 2.8% for natural fleece rot and 0.4% for natural fly strike over 17 years of selection (Mortimer et al. 1998). The effects of this selection program on fleece traits and host defence mechanisms have been the subject of intensive investigation (reviewed by Colditz et al. 2001; James 2006). The fleeces of resistant animals contained less moisture after artificial wetting and dry more quickly than fleeces of susceptible animals (Raadsma 1989). In addition, wool colour, variability of fibre diameter, staple thickness, crimp frequency, mean fibre diameter and birth coat were associated with resistance (Raadsma 1993). Numerous components of the immune system differ between the selection lines. Importantly, resistant animals had higher antibody titres to Pseudomonas aeruginosa (Gogolewski et al. 1996); however, following experimental infection, larvae of L. cuprina exhibited comparable survival and growth on sheep from both lines (Colditz et al. 1996). Recently, substantial differences between the lines in bacterial flora on skin were found both before and after simulated rainfall (Dixon and Norris 2007). Results from the selection lines support earlier conclusions that dermatitis and fly strike usually occur as a disease complex. The predominant impact of selection using an index of fleece rot 0816-1089/08/091210 10.1071/EA07301 © CSIRO 2008 J. L. Smith A,B , I. G. Colditz A,B,C , L. R. Piper A,B , R. M. Sandeman A,C and S. Dominik A,B A Australian Sheep Industry CRC. B CSIRO Livestock Industries, F.D. McMaster Laboratory, Locked Bag 1, Post Office, Armidale, NSW 2350, Australia. C LaTrobe University, Bundoora, Vic. 3086, Australia. D Corresponding author. Email: ian.colditz@csiro.au Abstract. Cutaneous myiasis (fly strike), caused by Lucilia cuprina, is a major ectoparasitic infection of sheep. Previous research has identified contributions of body conformation, wool characteristics and resistance to bacterial dermatoses to resistance to fly strike. This paper investigates whether genetic variation occurs amongst sheep in growth of larvae on skin. Mixed sex Merino sheep in 27 half-sibling groups were challenged with freshly hatched Lucilia cuprina larvae, and survival and growth of larvae were measured after 50 h. Growth but not survival of larvae had moderate heritability (0.29 ± 0.22), comparable to that seen for resistance to nematode parasites in sheep. Phenotypic correlations between resistance to larval growth and wool traits, skin wheal response to intradermal injection of larval excretory secretory products and resistance to internal parasites were negligible; however, there was a significant negative phenotypic correlation with fleece rot score after exposure of sheep to simulated rain at a time independent to that of measurement of larval growth. Larval growth was negatively correlated with peripheral blood eosinophil numbers measured either before or after larval challenge. In addition, larval growth in vitro on serum collected from challenged sheep was moderately associated with larval growth in vivo. A search for quantitative trait loci (QTL) for larval survival and growth was conducted in data from 94 half-sibling progeny of a Merino × Romney sire backcrossed to Merino ewes. Potential QTL for larval growth were identified on chromosome 11 and for larval survival on chromosome 18, although phenotyping greater numbers of sheep and a higher marker density on these chromosomes is necessary to confirm the result. We conclude that this study has identified a novel level of resistance of Merino sheep to growth of L. cuprina larvae that may be mediated in part through actions of anti-larval factors in serum and eosinophils. Further studies are required to establish the impact of growth retardation on the severity of systemic responses of sheep to fly strike and on the biology of adult flies. Genetic resistance to growth of Lucilia cuprina larvae in Merino sheep Australian Journal of Experimental Agriculture, 2008, 48, 1210–1216 www.publish.csiro.au/journals/ajea CSIRO PUBLISHING