Serum albumin concentration was low in all 10 blood samples collected during the chronic phase of the outbreak. This probably resulted from severely impaired liver function, although the possibility of dietary protein deficiency or binding of amino acids by gossypol or other components of CSM products cannot be disregarded. Hypoalbuminaemia has also been observed in lactating cows fed CSM (Lindsey et a1 1980).

Other laboratory investigations were of little value. Vitamin A concentrations were marginally depressed and vitamin A injections had no effect on the condition of the treated calves. Deficiency of vitamin A in animals being fed CSM has been suggested by some authors as a cause of so-called ‘CSM injury’ (Reed et a1 1928; Blood et a1 1983), but our findings do not support this hypothesis.

Haemoglobinuria has been reported in young calves fed CSM (Rogers et a1 1975) and in adult cows (Lindsey e t a1 1980), but in our cases no haemoglobinuria was observed.

Calves being fed a concentrate diet should be regarded as func- tionally similar to monogastric animals, as long fibre is required for rumen development. Calves are susceptible to gossypol poisoning as demonstrated in this outbreak, with 2 animals dying after being fed grain concentrate containing 33% CSM for 8 days at the rate of 2 kg/day, with a lower intake before weaning. Individual variation in susceptibility is high, some animals surviving 8 weeks on the diet. Withdrawal of CSM from the diet did not alleviate the problem of gossypol poisoning. We recommend that CSM should not be used as a protein supplement for preruminant calves because concentra- tions as low as 100 mg free gossypol per kg of feed may be toxic.

We thank Mrs D Russek for allowing us to make observations on her property and for her valuable suggestions. We also thank Mr S Lambert and Cargll Processing Ltd, Narrabri, and SGS Quan- tum, Brisbane, for testing feed samples for gossypol content and the staff of the Regional Veterinary Laboratory, Glenfield, for process- ing the tissue samples.

References Abou-DoniaMB (1976) Residue Rev 61: 125 Adams R, Geissman TA and Edwards JD (1960) Chem Rev 60: 555 Blood DC, Radostits OM, Henderson JA, Arundel JH and Gay CC (1983)

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Morgan SE (1989) Vet Clin North Am Food Anim Pract5:251 Orgad-Klopfer U and Adler H (1986) Isr J Vet U e d 42: 16 Reed OE, Huffman CF and Addington LH (1928) J Dairy Sci 11: 488 Reiser R and Fu HC (1 962) J Nutr 7 6 21 5 Rogers PAM, Henaghan TP and Wheeler B (1975) Irish Vet 57: 9 Sharma MP, Smith FH and Clawson AJ (1966) J Nutr 88: 434 Smith HA (1957) Am J Pathol 33: 353 Tanksley TD and Knabe DA (1981) Feedstufls 21: 24 West JL (1940) J Am Vet Med Assoc 9 6 74

Vet Res 4 9 493

(Accepted for publicarion 13 December 1994)

CORRESPONDENCE

I11 literacy

Animal and Veterinary Science

University of Idaho, 1020 E Homedale Road, Caldwell ID 83605-8098, USA

BRUCE C ANDERSON Department,

I continue to be distressed by the equating of lesion withpathology. Myriad examples of this grating misuse exist, as exemplified in your journal, volume 72(4) April 1995, page 121. There, Tisdall et a1 mention the Maltese dogs having “hepatic pathology”.

If the dogs had worms, would you state they had parasitology? If you were dealing with immune deficits, would you uncover lots

Please. Pathology is not lesion. Through the practice of pathology,

of immwology?

lesions are discovered and characterised.

(Mea, in magnum partum, culpa - Ed)

Salmonella Enteritidis:

Denmans Lane, Fontwell, Arundel, West Sussex BN18 OSU, UK

the egg and I

OLAF SWARBRICK

There are three further points that should be made about the epidemiology of S Enteritidis (Cox JM 1995 Aust Vet J 72:108), particularly in the UK. First, the incidence of S Enteritidis PT4 in the UK started to rise in humans in 1983/84 some two years before the increased incidence in poultry became apparent in 1985 (Chief Veterinary Officer, MAW, Report 1987). Before 1985 there were up to 5 or 10 recoveries of S Enteritidis annually from UK poultry; the records do not show whether these were from clinical incidents, from carcases or from environmental samples. After 1985 the number of reported incidents rose sharply into the hundreds (with human incidents in the low thousands, although I am aware this is not a fair comparison). This appears to indicate that it was the humans that infected the poultry, and not the other way round. The medical authorities were clearly using a different type of epidemiology to the veterinarians!

This leads to the next point. The medical authorities allow human sewage containing S Enteritidis to be disseminated throughout the rivers, estuaries and foreshores of the UK. Doctors are then surprised that salmonellae are present in farm livestock and criticise veterinary efforts for control as inadequate. There are several examples of human sewage causing salmonella infections in farm livestock, let alone in other humans. I am always surprised that doctors believe that zoonoses pass solely from animals to humans, and never the other way.

The third is that no one section of the professions involved in public health can on their own deal with the complex problem of salmonellosis. Every profession must help the others in a situation and spirit of total cooperation. Local inter-professional criticism is not acceptable. The public expect the professions to deal with sal-

398 Australian Veterinary Journal Vol. 72, No. 10, October 1995