Yersiniosis then and now

Download Yersiniosis then and now

Post on 22-Jul-2016




0 download

Embed Size (px)


  • ScientificScientificScientificScientific









    The Australian Veterinary Journal welcomesoriginal contributions on all aspects ofveterinary science.

    Submission of a manuscript for publicationwill be held to imply that it is a record ofunpublished original work of the author(s)and, if accepted will not be published else-where in whole or part without permission.The Journal reserves the right to reject anymanuscript.

    Send contributions to the Scientific Sectionof the AVJ to: Editor,AVA House, 272 Brunswick Road,Brunswick, Victoria 3056.

    Telephone: (03) 9387 2982International +61 3 9387 8808Telefax: (03) 9388 0112International +61 3 9388 0112Email:

    Instructions for authors and Statisticalguidelines for authors were published in the January,February 2004 issue. Both are available on

    Authors, please note that from July 1st the manuscript handling feewill be $55, including GST.

    Contact the Scientific editor(, 03 9387 2982) in advance if you wish to submit an obituary.

    S C I E N T I F I C S E C T I O N



    556 Australian Veterinary Journal Volume 83, No 9, September 2005

    Yersiniosis then and now

    CR WILKSSchool of Veterinary Science, The University of Melbourne, Victoria 3010

    Yersiniosis, due to infection with either Yersinia enterocolitica or Y pseudotuberculosis,is well recognized as a cause of enteritis and pseudotubercular granulomas in live-stock and several other species of domesticated and wild animals, including birds.These yersiniae are associated also with important zoonoses; disease in humans includesmesenteric lymphadenitis, terminal ileitis, food poisoning and, rarely, septicaemia.Although not as well known as Y pestis, the bacterial cause of bubonic plague, there aremany studies on the other species of Yersinia that have been published over the yearsincluding recent studies on the interaction of Y pseudotuberculosis and phagocytic cells,which have improved our understanding of pathogenesis. However, when exploring theearly literature one needs to be aware of several changes in nomenclature of these speciesduring the past 70 years. Reports from the early part of the 20th century of diseaseoutbreaks in sheep and goats, apparently caused by infection of Y pseudotuberculosis, recog-nized the important association with other stressors, particularly exposure to cold wetweather. It is now known that, at low temperature, these yersiniae grow well, and haveenhanced production of enterotoxin.

    Two papers in this issue of the journal (pages 563 to 571) add to our knowledge of theepidemiology of yersinia infections in goats under farmed conditions. Yersiniosis hasemerged as an important health concern in both goats and deer as these animals have beenmore intensively managed in geographical areas where at least part of the year is both coldand wet.

    A scientific report contained in the minutes of the 56th regular meeting of the VeterinaryAssociation of Victoria, 30 October 1931, provides an insight into the understanding ofyersiniosis at that time. It also provides an historical perspective to the current papers. Thereport was presented by Mr EM Pullar of the Veterinary Research Institute in the form ofan illustrated lecture outlining the recent advances in the study of Pyaemic Hepatitis ofSheep.

    A severe epidemic of this rare disease occurred in the late winter of this year (1931) in twoisolated districts, one in the Mallee, the other in the Western District. The condition has beenobserved twice before. First by Gilruth at Werribee in 1909 and some two years ago byHindmarsh at Albury and Cootamundra.

    The disease is characterized by the presence of tubercles in the liver and spleen and occasionallythe associated lymphatic glands. These tubercles vary in size from a pins head to that of a splitpea and contain a small quantity of caseous pus.

    The causal organism is a small round ended gram negative bacillus that grows in long chains influid cultures and is very closely related, if not identical with Pseudotuberculosis rodentium.Owing to the fact that in primary culture the organism shows bipolar staining both of theearlier workers described it as a Pasteurella.

    The clinical signs of the disease are vague. As a rule the affected sheep lags behind the rest of theflock and shows a disinclination to move rapidly, and after walking a short distance will standquite still in a characteristic attitude with the head and neck elevated, and the back arched.Diarrhoea and excessive thirst and shedding of wool are quite common symptoms. The animalfinally becomes comatose and dies without struggling. As a rule the sheep is found lying on itsventral surface with the head and neck extended straight in front. Early in the outbreak thetime from the appearance of clinical symptoms, to death was as a rule only a few hours; but laterinfected sheep would linger for several days or even a week. Long standing cases generally showedsigns of jaundice.


    AvjSept05.qxd 17/08/2005 9:44 AM Page 556

  • ScientificScientificScientificScientific

    557Australian Veterinary Journal Volume 83, No 9, September 2005

    The mortality in the affected flocks ran as high as 10% and thesusceptibility varied considerably. About 90% of the fatal casesoccurred amongst 6-tooth sheep, particularly big framed good condi-tioned animals. Both sexes suffered equally. The only sheep on theinfected farms were merinos.

    The mode of natural infection was at first surmised to be by ingestionas the situation of the lesions indicates a portal infection but experi-ments have since shown that the liver and spleen are the predilectionsites for the organism, as these organs are the site of the chief lesionsfollowing subcutaneous, intramuscular and intraperitoneal inocula-tions. It is possible that the organism is picked up by cells of thereticulo-endothelial system although bone marrow cultures frominfected guinea pigs have frequently been negative.

    Intestinal lesions were observed in only two out of ten natural cases,although guinea pigs develop typical bowel lesions following oral inoc-ulation. Injury to the alimentary mucosa by parasites does not appearto play an important part as the natural cases were almost free ofintestinal helminths.

    It would appear that the sheep is not the natural subject for thisdisease, as only three epidemics have been recorded and these confinedto Australia. In addition there is no record of the lesions ever havingbeen seen at the post mortems during other investigations or at abat-toirs. The natural host of this organism is possibly a rodent or somenative game. Magpies were found to be dying in greater numbers inthe affected district, and on examination twenty six out of twentynine birds showed lesions of pyaemic hepatitis from which the causalorganism was recovered. This, however, is not conclusive evidence thatthe magpie is the natural host as they could easily have becomeinfected through eating carrion.

    Experimental vaccination of some of the sheep in the district wasperformed, but the results are useless as the epidemic ceased entirelyabout a week after the second dose had been administered.

    A vote of thanks to Mr Pullar was moved and carried with acclama-tion.

    The meeting terminated at 10.15 p.m. and adjourned to supper.

    Equine Nutrition and Feeding. 3rd edition. Frape D, editor, Blackwell Publishing Asia, 2004, 650 pages. Price A$116.00. ISBN 1 4051 0598 4.

    In the 3rd edition of Equine Nutrition & Feeding, David Frape has again demonstrated his mastery and depth of understanding of his subject. In addition to clear,concise descriptions of the anatomy and physiology of the digestive system, Frape reframes existing knowledge and recent research findings in the context ofevolutionary development and clinical diseases. This is a valuable expansion of the previous editions with an extra 100 pages of information.The first paragraph introduces the special anatomical features of the order Perissodactyla, which includes horses, asses, zebras, rhinoceroses andtapirs. This is a valuable addition to previous editions as it encourages the reader to view the information in the subsequent chapters against a back-ground of evolution. Given that from 20 million years until 6000 years ago, fossil records provide no evidence of navicular disease, sesamoiditis, splints(except for one sample from Bolivia), spavin, chronic laminitis, arthrosis or osteochondrosis in any site, it is timely that current feeding strategies areexamined in the context of what is natural for the horse and how current practices contribute to the occurrence of clinical conditions.In Chapter 1 includes concise and clear descriptions of the physiology and function of each segment of the gut, making this a useful text for all students.As he does throughout the text, Frape relates the results of recent gastro-intestinal research to the predisposing modern feeding practices. Chapters 1and 2 follow the metabolic pathways of the products of protein and energy digestion, interlinking with recent research on carbohydrate digestion, theeffect of grain processing on caecal microbiology and fibre degradability, Cushings syndrome, insulin resistance, blood glucose and laminitis.Chapter 3 provides useful and important details of revised mineral and trace element requirements. Up-to-date information on zinc, chloride, iodine andthe risks of seaweed