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Scientific

parvum, and between C parvum isolates of human and animal origin. FEMSMicrobiol Lett 1997;150:209-217.17. Spano F, Putignani L, Crisanti A et al. A multilocus genotypic analysis ofCryptosporidium parvum from different hosts and geographical origin. J ClinMicrobiol 1988. In press.18. Vasquez JR, Gooze L, Kim K et al. Potential antifolate resistance determi-nants and genotypic variation in the bifunctional reductase-thymidylatesynthase gene from human and bovine isolates of Cryptosporidium parvum.Mol Biochem Parasitol 1996;79:153-165.19. Morgan UM, Sargent KD, Deplazes P et al. Sequence and PCR-RFLP anal-ysis of the internal transcribed spacers of the rDNA repeat unit in isolates ofCryptosporidium from different hosts. Parasitol 1998. In Press.20. Higgins DG, Bleasby AJ, Fuchs R. CLUSTAL V: improved software formultiple sequence alignment. Comput Appl Biosci 1991;8:189-191.21. Felsenstein J. PHYLIP. Phylogeny interface package (version 3.2).Cladistics 1989;5:164-166.22. Meloni BP, Thompson RCA. Simplified methods for obtaining purifiedoocysts from mice and for growing Cryptosporidium parvum in vitro. J Parasitol1996;82:757-762.23. Periera MC, Atwill ER, Crawford MR et al. DNA sequence similarity betweenCalifornia isolates of Cryptosporidium parvum. Appl Environ Microbiol1998;64:1584-1586.24. Atwill ER, Sweitzer RA, Periera MC et al. Prevalence and associated risk

factors for shedding Cryptosporidium parvum oocysts and Giardia cysts withinferal pig populations in California. Appl Environ Microbiol 1997;63:3946-3949.

(Accepted for publication 25 September 1998)

8. Olsen ME, Thorlakson CL, Deselliers L et al. Giardia and Cryptosporidium inCanadian farm animals. Vet Parasitol 1997;68:375-381.9. Awad-El-Kariem FM, Robinson HA, Dyson DA et al. Differentiation betweenhuman and animal strains of Cryptosporidium parvum using isoenzyme typing.Parasitol 1995;110:129-132.10. Carraway M, Tzipori S, Widmer G. New RFLP marker in Cryptosporidiumparvum identifies mixed parasite populations and genotypic instability inresponse to host change. Infect Immun 1997;65:3958-3960.11. Morgan UM, Constantine CC, O’Donoghue P et al. Molecular characterisa-tion of Cryptosporidium isolates from humans and other animals using RAPD(Random Amplified Polymorphic DNA) analysis. Am J Trop Med Hyg1995;52:559-564.12. Morgan UM, Constantine CC, Forbes DA et al. Differentiation betweenhuman and animal isolates of Cryptosporidium parvum using rDNA sequencingand direct PCR analysis. J Parasitol 1997;83:825-830.13. Morgan UM, Sargent KD, Deplazes P et al. Molecular characterisation ofCryptosporidium from various hosts. Parasitol 1998;117:31-37.14. Morgan UM, Pallant L, Dwyer B et al. Comparison of PCR and microscopyfor the detection of Cryptosporidium parvum in human fecal specimens -Clinical trial. J Clin Microbiol 1998;36:995-998.15. Peng MM, Xiao L, Freeman AR et al. Genetic polymorphism amongCryptosporidium parvum isolates: evidence of two distinct human transmissioncycles. Emerg Infect Dis 1997;3:567-573.16. Spano F, Putignani L, McLauchlin J et al. PCR-RFLP analysis of theCryptosporidium oocyst wall protein gene discriminates between C wrairi and C

Development of a lupinosis vaccine

Lupins have revolutionised dryland farming in Australia. They provide a cash seed crop, raise soil fertility,provide a disease break for cereal crops, and the stubble is a valuable summer feed. However, the bene-

fits of lupin grazing are greatly reduced by the occurrence of lupinosis or where management practices haveto be modified because of a high risk of disease in grazing stock.

After its first appearance in Western Australia in 1948 lupinosis soon developed into one of the majordiseases of sheep. This occurred at a time when the area sown to lupins was rapidly expanding throughoutAustralia. The disease, manifested principally as a hepatopathy, has a long history in Europe. It was welldescribed in the veterinary literature of last century and the probability of it being caused by a fungal toxinwas advocated by German investigators. This was not confirmed until the responsible fungus, Diaporthetoxica (formerly Phomopsis leptostromiformis), was isolated at about the same time in Western Australia andSouth Africa in the 1970s. In 1972 the CSIRO Division of Animal Health started to investigat the fungal toxin,isolated and named ‘phomopsin’ and its chemical structure was resolved. The development of an ELISA asan improved assay procedure for phomopsin in foodstuffs indicated that antibodies against the toxin couldbe produced in sheep and suggested that a protective vaccine might therefore be practicable. A recent pressrelease by CSIRO Animal Health reports that such a vaccine has been developed to the stage of beingtested. Results from these trials should be known by next June.

This research has its potential value in protecting against the losses caused by lupinosis. It is also ofconsiderable importance as the first demonstration of protection by vaccination against what is, immunologi-cally, a small chemical molecule. In the course of this work a new vaccine adjuvant was identified that isconsiderably more effective than Freund’s in inducing antibody responses. This type of vaccine might havefuture application in the protection of animals against other toxic chemicals.

Protection from lupinosis by vaccination could allow safe grazing on lupins stubble during February toApril when other feeds are in low supply and at a time when the risk of toxic fungal infection of the stubble isgreatest. Risks associated with the feeding of affected lupin seed or lupin hay could also be eliminated.

Carl Peterson