Cattle Practice 8.2

CATTLE PRACTICE State Veterinary Journal 20: 3-5. Nicholas R.A.J. and Baker S. (1998) Recovery of mycoplasmas from animals. In: Mycoplasma Protocols, Methods in Molecular Biology vol. 104, Miles R.J. and Nicholas R.A.J. Eds. Totowa, New Jersey; Humana Press. pp 37-44. Nicholas R A J., Ayling R.D and Miles R.J. (1999) Prevalence of mycoplasmas in respiratory disease in cattle in Britain. In COST 826 Agriculture and Biotechnology. Mycoplasmas of ruminants: pathogenicity, diagnostics, epidemiology and molecular genetics. Eds. L. Stipkovits, R. Rosengarten & J. Frey. EUR 18756 EN Luxembourg. pp 94-96. Pfutzner H.and Sachse K (1996) Mycoplasma bovis as an agent of mastitis, pneumonia, arthritis and genital disorders in cattle. Rev. sci. tech. Off. int. Epiz 15 1477-1494 Rebhun W.C., Guard C. and Richards C.M. (1995). Respiratory Diseases. In: Diseases of Dairy Cattle. Ed. W.C. Rebhun. Baltimore, Williams and Wilkins p.79. BCVA 2000 VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION The farm in west Cornwall carried 100 Holstein milking cows together with 150 dairy and beef followers. The herd was well managed and well fed. Some replacement heifers, cows and a bull had been bought in over the last two years. Cows and youngstock were fed on silage, straw and bought in concentrates alone. Calves were fed on hay, straw and bought in concentrates together with raw milk, in buckets, including mastitic milk withheld from the bulk tank. Between November 1998 and March 1999 eight young cows had aborted two to three months before full term. In June and July 1999 two calves had been born apparently blind and one of these was ataxic. The surrounding area had a history of TB in cattle and badgers but this farm had no experience of TB during the last 20 years. In July 1999, however, the eventual slaughter of an inconclusive reactor milking cow revealed tuberculous lesions in the retropharyngeal lymph nodes from which M. bovis was isolated. A herd TB test followed on the 24th of August 1999 and this identified 11 reactors, eight of which showed visible lesions of TB. Two of these were adults in which the lesions were confined to the lymphatic glands of the head and chest. The other six were calves, between six and two months of age, and in four of these the tuberculous lesions were again confined to the lymphatic glands of the head and chest. However, two also showed miliary caseous lesions in the apical lobes of the lungs. M. bovis was isolated from the tuberculous lesions of the two cows and five of the six calves. M. bovis was also isolated from the lungs of one which showed no visible lesions of TB but acute pneumonic changes were present. Three weeks after the herd TB test a three month old calf developed pneumonia and died three days later despite veterinary treatment. Unfortunately post mortem examination was not carried out and the carcase was removed to the local hunt kennels. The following week a three month old calf (No. 400) developed hypernoea, dyspnoea and a temperature of 103°F. It showed a mucopurulent nasal discharge, developed a cough and again, despite veterinary treatment, it died 24 hours later. The calf was submitted to VLA Truro for post mortem examination on the 21st of September and this revealed caseous foci in sub-mandibular, retropharyngeal, bronchial and mediastinal lymph nodes as well as extensive tuberculous pneumonia of the lungs. Acidfast bacilli were present in smears prepared from the lesions and M. bovis was subsequently isolated from these. Histological examination of the lungs showed a granulomatous and necrotising mycobacterial pneumonia and lymphadenitis. Because of the apparent rapid onset of disease, the age of the calves and the severity of the changes seen, a visit was made to examine the remainder of the calves on the farm. This was carried out on the 29th of September 1999. MATERIALS AND METHODS Clinical Examination of the In-Contact Calves Twenty two calves were present on the farm and these were kept in two houses both of which were open at one end to the cows covered yard and separated only by a gate. The calves, therefore, shared air space and had nose to nose contact with the cows. Fourteen 1-3 month old calves were kept in one house and eight 3-4 month old calves were in the other. There had been frequent movements of calves between the houses in both directions. A number of the calves showed respiratory signs including hypernoea, coughing and nasal discharge. In addition five calves showed either developmental abnormalities or central nervous signs which were suggestive of in-utero Bovine Viral Diarrhoea Virus infection (BVDV) and these signs are summarised :- Tuberculous Pneumonia and BVD in Housed Calves Monies R.J., Veterinary Investigation Officer, Veterinary Laboratories Agency, Truro, Polwhele, Truro, Cornwall, TR4 9AD. ABSTRACT A three-month-old calf showing signs of pneumonia died within 48 hours of the first clinical signs becoming apparent despite veterinary treatment. The calf was submitted to VLA Truro for post mortem examination which revealed extensive lesions of tuberculous pneumonia from which Mycobacterium bovis (M. bovis) was subsequently isolated. This case report describes the clinical, post mortem and laboratory findings in a group of 22 "in -contact" calves. KEYWORDS: Bovine Tuberculosis (TB), calves, Bovine Viral Diarrhoea Virus (BVDV), Immunosuppression.

CATTLE PRACTICE The Animal Health Office decided to slaughter all 22 calves as TB contacts. Heparin and plain blood samples were collected from all the calves prior to their slaughter on the 30th of September 1999. Post Mortem Examination Post mortem examinations of all 22 calves was carried out. The five calves showing central nervous signs and developmental abnormalities were taken to VLA Truro for more detailed post mortem examination, including removal of the brain, and these calves will be referred to as group A. Post mortem examination of the remaining 17 calves was carried out at the slaughter house, these calves will be referred to as group B. In this group the brains were not examined. Histology Tissue samples of lung lesions and brains from the five calves in group A were collected and fixed in formal saline for histopathological examination. Additional samples of lung lesions were collected from six of the calves in group B. Sections were stained with haematoxylin and eosin and in addition sections of lung tissues were stained by the ZiehlNeelsen method. Lung and brain sections were also examined by immune staining for pestivirus antigen. BCVA 2000 Bacteriology Samples of affected lungs from all calves showing lung lesions were taken aseptically and innoculated onto 5 per-cent sheep blood agar and MacConkey agar. In addition, the samples were innoculated onto modified Middlebrook 7H11 agar semi-solid slopes and any suspect colonies were innoculated onto specialised Lowenstein Jensen and Stonebrinks media at different temperatures (Gallagher and Horwill, 1977). Serology Serum samples were examined by the compliment fixation test for antibody to Haemophilus somnus and by the ELISA test for antibody to Mycoplasma bovis. Serum samples were screened by the ELISA tests for antibodies to Respiratory Syncitial Virus (RSV), Infectious Bovine Rhinotracheitis (IBR), Parainfluenza 3 (PI3) and Bovine Virus Diarrhoea (BVD). Virus Isolation Heparin blood samples were screened for BVD antigen and clots from all the blood samples were screened for BVD virus by virus isolation. Pooled samples of thymus and spleen tissue from the five calves in Group A were also screened for BVD virus by virus isolation. RESULTS Post Mortem Examination The significant post mortem changes seen in calves of Groups A are summarised below:- VOL 8 PART 2 Animal I/D Clinical signs Date of Birth 396 Drooping of ears, hypernoea. 18/6/99 397 Blind, circling, ataxia, short tail. 30/6/99 398 Blind, bilateral cataracts. 1/7/99 411 Hypernoea, cough, undersize, dejected. 18/8/99 420 Short tail. 5/9/99 Animal I/D Group A - PM Findings (slaughter date 30/9/99) Date of Birth 396 Miliary granulomatous nodules in apical lobes of lungs. 18/6/99 397 Short tail. Miliary granulomatous lesions in apical and cardiac lobes of lungs. Cerebellar hypoplasia. 30/6/99 398 Miliary granulomatous lesions in apical and cardiac lobes of lungs. Caseous pus in BM/LNs. Cerebellar aplasia. 1/7/99 411 Granulomatous foci in one consolidated apical lobe of lungs. Other apical lobe congested. 18/8/99 420 Short tail. One granulomatous focus in BM/LN and two small white foci in an apical lobe of lungs. 5/9/99 BM/LNs = Bronchial and Mediastinal lymph nodes.

CATTLE PRACTICE The significant post mortem changes seen in calves of group B are summarised below:- BCVA 2000 RP/LNs = Retropharyngeal lymph nodes. BM/LNs = Bronchial and Mediastinal lymph nodes. NSL = No specific lesions. VOL 8 PART 2 Animal I/D Group B - PM Findings (slaughter date 30/9/99) Date of Birth 385 Nodular granulomatous lesions throughout lungs. 27/5/99 386 Caseous abscess in BM/LNs. 28/5/99 388 NSL. 31/5/99 390 Nodular granulomatous lesions throughout lungs. 14/6/99 391 NSL 14/6/99 394 Caseous abscess in lungs and BM/LNs. 18/6/99 396 Miliary granulomatous nodules in apical lobes of lungs. 18/6/99 397 Short tail. Miliary granulomatous lesions in apical and cardiac lobes of lungs. Cerebellar hypoplasia. 30/6/99 398 Miliary granulomatous lesions in apical and cardiac lobes of lungs. Caseous pus in BM/LNs. Cerebellar aplasia. 1/7/99 402 Caseous nodules in RP/LNs. Caseous lung abscess. 5/7/99 404 Caseous abscess in lungs, caseous nodules in BM/LNs. 6/7/99 405 Caseous lung abscess (5 cm in diameter) Caseous nodules in BM + RP/LNs. 6/7/99 407 Congestion and consolidation of apical lobe of lungs. 30/7/99 408 NSL. 10/8/99 409 NSL. 8/8/99 410 NSL. 9/8/99 418 NSL. 19/8/99 419 NSL. 2/9/99 421 NSL. 6/9/99 422 Nodular granulomatous foci (1-2 mm in diameter) in apical lobes of lungs. 6/9/99 Bacteriology Pasteurella multocida was isolated from the lung lesions of one of the calves only - 398. Mycobacterium bovis was isolated from the lesions in nine of the calves - 386, 394, 396, 398, 402, 404, 405, 411, 422. Virology BVD antigen was detected in a heparin sample taken from one calf (385) and BVD virus (type I) was isolated from whole blood samples taken from two calves (385 and 411). In addition BVD virus (type I) was isolated from a pooled sample of thymus and spleen tissues from two calves (411 and 420). Serology Serum samples showed no evidence of antibody to either Haemophilus somnus or Mycoplasma bovis. ELISA examination for antibody to RSV, IBR and PI3 viruses showed titres to all three viruses and these are shown in the graphs below. ELISA examination for antibody to BVD virus showed that all except three had titres greater than 0.4 OD units. One (385) had no titre and calves 411 and 390 had titres between 0.2 and 0.3 OD units. The results are represented in the Tables 1, 2, 3 and 4.

CATTLE PRACTICE BCVA 2000 VOL 8 PART 2 P13 Antibody 0 0.2 0.4 0.6 0.8 422 421 420 419 418 411 410 409 408 407 405 404 402 398 397 396 394 391 390 388 386 385 IBR Antibody 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 422 421 420 419 418 411 410 409 408 407 405 404 402 398 397 396 394 391 390 388 386 385 RSV Antibody 0 0.5 1 1.5 422 421 420 419 418 411 410 409 408 407 405 404 402 398 397 396 394 391 390 388 386 385 BVD Antibody 0.2 0.4 0.6 0.8 1 1.2 Tables 1-4.

CATTLE PRACTICE BCVA 2000 Histology The results of histological examination of brain and lung tissues from five calves in Group A are summarised below:- VOL 8 PART 2 Group A Histology Immune Staining Animal I/D Lung Brain Lung Brain 396 Chronic bronchopneumonia with bronchiolitis obliterans. (No acid-fasts seen but M. bovis isolated) Localised granuloprival-type cerebellar dysgenesis consistent with mid-gestational BVDV infection. Negative Negative 397 Chronic bronchopneumonia with bronchiolitis obliterans and marked lymphoid cuffing (no acid-fasts seen) Severe granuloprival-type cerebellar dysgenesis consistent with mid-gestational BVDV infection. Negative Negative 398 Granulomatous and mycobacterial pneumonia (acid-fasts seen) Severe granuloprival-type cerebellar dysgenesis consistent with mid-gestational BVDV infection. Negative Negative 411 Chronic bronchopneumonia with bronchiectasis (no acidfasts seen but M. bovis isolated.) No specific lesions Positive Positive Pattern consistent with persistent pestivirus infection. 420 No specific lesions No specific lesions Positive Positive Pattern consistent with persistent pestivirus infection. Samples of lung lesions from six of the calves in Group B were examined and the findings are shown below:- Group B Lung Animal I/D Histology Immune staining 385 Chronic bronchopneumonia with bronchiolitis obliterans. No evidence of acid-fast bacilli. Positive (pattern suggestive of persistent pestivirus infection). 390 Chronic bronchopneumonia with bronchiolitis obliterans. No evidence of acid-fast bacilli. Positive (pattern suggestive of persistent pestivirus infection). 404 Focal granulomatous pneumonia (no acid-fasts seen but lesions small and typical of mycobacterial infection – M. bovis isolated). Negative 405 Granulomatous and necrotising mycobacterial pneumonia (acid-fast bacilli seen). Negative 407 Sub-acute exudative bronchopneumonia. Negative 422 Focal severe necrotising mycobacterial pneumonia (acid-fast seen). Negative FURTHER INVESTIGATIONS Whilst awaiting the 60 day tuberculin test the farmer culled a cow because of persistent mastitis. The cell count had risen from 500 (x 1,000/ml) to 2,558 (x 1,000/ml) over the previous four months. The affected quarter was swollen and firm and during several periods of antibiotic treatment the milk had been withheld from the bulk tank and fed to the calves. At post mortem several small caseous abscesses were present in the liver and a mesenteric lymph node, showing caseation and calcification, was enlarged to 5 cms in diameter. Multiple tuberculous miliary abscesses were present throughout one quarter of the udder. Examination of Ziehl-Neelsen stained smears from the udder lesions showed very large numbers of acidfast bacilli. Histological examination of mammary tissue showed sheets of epitheloid macrophages together with extensive areas of necrosis and central mineralisation. A Ziehl-Neelsen stained section showed numerous acidfast bacilli within the lesions and also within occasional ducts. M. bovis was subsequently isolated from the lesions. Examination of the udders of all the cows in the herd and scrutiny

CATTLE PRACTICE of their individual cell count records was then carried out. Milk samples were collected from any cows showing abnormal udders or persistently high cell counts. The samples were centrifuged and microscopic and cultural examinations of the sediments for acidfast bacilli were carried out. All of these proved negative. A further eight cows were culled before the next 60 day herd test and the carcases of these were examined. Two showed lesions of TB which were confined to the retropharyngeal lymph nodes and liver of one cow. Caseous abscesses were present in the lungs and liver of the other cow. The 60 day herd test identified a further five reactor cattle. Three of these were older cattle showing tuberculosis lesions in the lymphatic glands of the head or liver. Two, however, were calves aged four and six weeks old both of which showed extensive pulmonary tuberculosis. The two calves were part of a group of four which were the last animals to receive milk from the cow with tuberculous mastitis before it's eventual slaughter. The remaining two calves of the four were slaughtered but showed no lesions of TB. Blood samples were also collected from all the cattle on the farm at the same time as the TB herd test was carried out. Samples were screened for both BVD antigen and BVD antibody. Antigen was detected in only one animal - an 18 month old steer which was then removed from the herd. Surprisingly 15% of the herd had remained sero-negative to BVD virus. At the time of writing the herd is awaiting a further 60 day tuberculin test. DISCUSSION The significant feature of this case is the high morbidity and severity of the tuberculous disease in the calves. Advanced and disseminated lesions were found in calves which had passed the TB test less than one month previously. The youngest calf showing lung lesions from which M. bovis was isolated was only 25 days old. This would suggest that bovine TB is not always a slow and chronic disease, rapid progression resulting in clinical disease can occur, especially in calves. It is also of note that, despite good evidence that infection was introduced orally to one calf at least, none of the calves showed alimentary tract lesions. However, feeding milk in buckets to calves may well create aerosols resulting in respiratory infection. It cannot be assumed that all of the calves were infected from the milk. It is likely that airborne spread also occurred between the calves, the lung lesions in some of the calves would have been an abundant source of bacilli for respiratory infection of other contact calves. The position of the calf houses meant that the spread of infection from the calves back to the cows was also likely to result. BCVA 2000 Involvement of other pathogens in the respiratory syndrome of the calves has not been demonstrated. It is unfortunate that it was not possible to collect paired serum samples from the calves. The identification numbers are in chronological order, 385 being the oldest and 422 the youngest. A decline in antibody titres to RSV, PI3 and RSV viruses is seen with the increasing age of the calves. This would suggest that, with the exception of calf 388 - a four month old calf showing a high titre to RSV virus, they are most likely the result of maternally derived antibody. A combination of antigen detection and virus isolation techniques on blood samples together with virus isolation and immune staining procedures on tissue samples identified three calves which were persistently infected with BVD virus and one calf which may have been persistently infected. A further three calves showed post mortem changes resulting from in-utero BVD infection. The presence of an 18 month old viraemic animal suggests that BVD virus had been circulating in the herd for approximately two years at least. The titres to BVD virus seen in these group of calves relate well to the accepted understanding of BVD in cattle (Duffell and Harkness, 1985). Calves born with cerebellar anomalies would be expected to have antibody to BVD virus but not to be viraemic (396, 397 and 398). Calves infected at an earlier gestation age would be expected to be viraemic but to have no antibody to BVD virus (385). There are also those calves which fall in between the two groups. In this case these are represented by the two animals from which virus was recovered and the one calf in which virus was demonstrated by immune staining. These calves (411, 420 and 390) all showed varying levels of antibody to BVDV. The importance of BVD virus and its role in immunosuppression and intercurrent disease has been recognised for some time (Potgieter et al, 1984). It is known that acute BVD virus infection in calves can influence the onset of bovine respiratory tract disease. Could a calf which is either persistently or acutely infected with BVD virus quickly develop extensive tuberculous lesions when challenged with M. bovis? Also, would such a calf present a high level of challenge to in-contact calves which may themselves be transiently infected with BVD virus? Such calves may also, as a result of their suppressed immune response, produce a lowered response to the intradermal skin test for bovine tuberculosis. Calves 385, 390 and 420 were demonstrated to be persistently infected with BVD virus but cultural and histological examination failed to confirm the lung changes were caused by M. bovis. Calf 411 was also demonstrated to be persistently infected and in this instance M. bovis was isolated from the lung lesions. However, as one of the younger animals the opportunity of calf 411 to influence the older calves VOL 8 PART 2

CATTLE PRACTICE in the group would have been limited. Before the group of 22 calves were investigated in detail six calves with tuberculous lesions had been removed from the farm. A further two calves, one a confirmed case of tuberculous pneumonia, had died. Unfortunately, at that stage, the involvement of BVD virus had not been suspected and the BVD status of those calves remains unknown but it is likely to have been similar to the BVD status of the 22 calves described here. ACKNOWLEDGEMENTS The assistance of Roger Sainsbury, BVM&S MRCVS (Animal Health Office, MAFF), John Head, BVet Med MRCVS (Head and Head, Helston) and Stephen Trethewey BVet Med MRCVS (Head and Head, Helston) for bringing the case to my attention and assisting in examining and collecting blood samples from calves is gratefully acknowledged. I author would also like to thank Dr Sandra Scholes BCVA 2000 BVM&S, MRCPath, MRCVS, VLA Lasswade, for carrying out histological examinations of tissues, the Virology Department of VLA Weybridge for virological investigations, S. Waterhouse HWC(MLS),VLA Langford, for serological investigations and the laboratory staff at VLA Truro and Starcross for bacterological examinations. The author would also like to thank Lyn Penrose for typing the manuscript. REFERENCES Gallagher J., Horwell D.M. (1977) Journal of Hygiene (Cambridge) 79: 155 Duffell S.J., Harkness J.W. (1985) Bovine virus diarrhoea - mucosal disease infection in cattle. Veterinary Record, 117: 10. Potgieter L.N.D., Mccracken M.D., Hopkins M.F., Walker R.D., Guy J.S. (1984). Experimental production of bovine respiratory tract disease with Bovine Diarrhoea Virus. American Journal of Veterinary Research, 45: 1582-1585. VOL 8 PART 2

CATTLE PRACTICE BCVA 2000 VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION The way that we describe the prevalence or the cost of pneumonia in cattle is immaterial; the losses are substantial. Furthermore, the losses have been occurring annually in spite of the extensive resources which farmers, the veterinary profession and researchers have applied to tackle the problem. This short paper will present a summary of the losses, and then focus on the environmental component of the problem. Data will be presented which suggests that a large and significant proportion of our cattle buildings are either inappropriate for the current conditions, or managed in an inappropriate manner. The solution to our current building problems lies in understanding the basics of how buildings function and thereafter the application of good design. In terms of managing animal disease and supporting animal health, good design refers to the ability to meet the needs of the livestock - a dry, clean bed, protection from the elements, and a plentiful supply of clean air. We have the solutions; what we need is application. COSTS Calf pneumonia is the cause of the most significant economic losses in calves more than ten days old. A number of estimates have been carried out in this complex subject and values vary widely. AFRC estimated a potential annual benefit from applied research into calf pneumonia of £60m (AFRC 1989), whilst more targeted studies have put the cost at an average of £75 per calf with symptoms and £22 per calf within an exposed group (Gunn & Stott, 1996). These values are supported by the latest data from Andrews (2000) with losses from suckler herd case studies calculated at an average of £82.10 per ill calf. The same study calculated costs within the exposed groups as an average of £74.10 per animal, due to high morbidity. These estimated losses must be considered alongside the various reports of the widespread presence of the various pathogens and the number of clinical infections. A study by Peters (1986) reputed that almost 50% of calves suffered at least one period of clinical pneumonia. A two year epidemiological study of beef cattle in Scotland found that 93% (28/30) herds had rising antibody titres to at least one of the 6 monitored pneumonia pathogens (Robertson, 1994). However, this evidence of multiplication of the viruses was not always associated with outbreaks of respiratory disease. The latest data from Pfizer suggests that more than 63% of herds tested have elevated antibodies to PI3 and RSV in one or more animals (Pfizer, 1999). None of the estimates above include a value for the welfare costs endured by the infected calves, nor the emotional cost to the stockman and others within the industry. However, our understanding of the real costs have improved and we can now be more confident of the value that is attached to any activity which has a good probability of reducing the risk of clinical infections. Investment in serology and vaccination can be balanced against estimated losses. Investment in whole herd management and especially the housing environment can likewise be approached as a means to reducing costs on farms. CATTLE HOUSING The building is often cited as the "cause" of pneumonia problems and there is significant evidence that some aspect or aspects of the built environment contribute to the impact of the various pathogens. MacCormack, Clark and Knowles (1984) found that approximately 50% of naturally ventilated cattle buildings had insufficient ventilation openings for the number of cattle housed. In a more detailed study (Robertson, 1994) found that 33% of buildings were outwith their design limits for the number of Building Designs to Optimise Health Robertson J.F., Aberdeen University Centre for Organic Agriculture, MacRobert Building, Old Aberdeen, AB24 5UA. ABSTRACT Respiratory disease in cattle is widespread, and there is significant evidence that the majority of UK herds have seroconversion to one or more of the relevant pathogens. Previous work has also described that approximately 50% of naturally ventilated cattle buildings subjected to analysis of design parameters are inadequate for the weight and number of livestock housed. The reasons for failure are varied, but the evidence suggests that the basic principles of building function and especially ventilation are not clearly understood by the industry. Design solutions are available through computer models that consider animal heat production, building dimensions, and the location and dimensions of air inlets and exhausts. Design problems seen in practice are discussed. It is suggested that better information transfer of existing information to the industry can achieve a significant improvement in management of cattle pneumonias. KEYWORDS: Pneumonia, ventilation, design factors.

CATTLE PRACTICE cattle housed and a further 13% would be unable to provide an adequate ventilation pattern throughout the building. It is appropriate to go back to the basics to understand the reasons for part of the current building problem. The vast proportion of UK cattle buildings were built more than 40 years ago. Many were constructed appropriate to the needs and understanding of cattle production at that time. However, there have been three vital and significant changes relevant to the environment/disease interface over the past decades. First, the prevalence of the relevant viruses and bacteria has increased. It is probable that more animals are exposed to more pathogens than before. Second, stocking densities will have increased as herd sizes have increased. The increase may not always be at individual housing level, but any increase in numbers within a single farm unit must increase the potential for aerial transmission of disease at a local level. The third, and possible greatest change, has occurred with feeding and growth rates. Thirty or more years ago the genetics and feeding regimes of both dairy and beef cattle meant that the energy throughput of livestock was significantly less than in modern practice. Many housed cattle would have been fed a winter ration based on hay and straw, with many stock at or just above maintenance feed levels. Growing cattle had target growth rates of 2 - 3 lb. (0.91 - 1.36) kg per day, compared with modern targets of 2-3 kg per day. The classic studies of Blaxter and his colleagues demonstrated that, amongst other things, the heat output of ruminants as a proportion of metabolisable energy rises from 0.41 below maintenance to 0.75 above maintenance for certain roughages (from 0.26 to 0.45 for concentrates) (Table 1). Current systems of feeding mean that the heat output from growing cattle can be 2.5 times greater than typical systems of 40 years ago. There will also be a significant increase in the moisture output per animal in the modern situation, giving a potential increase in absolute humidity levels within a building. Thus the heat and moisture throughput of buildings has significantly increased, leading to the current situation where there is an imbalance between the designed capabilities of many buildings and the BCVA 2000 environmental requirements of the livestock. In addition, any accumulation of waste heat will raise air temperatures and, when linked to increased moisture concentrations will have the potential for increasing the survival rates of airborne microorganisms. DESIGN SOLUTIONS Buildings can be designed to provide an adequate, naturally ventilated environment for most livestock situations. The role of mechanical ventilation systems will be discussed only briefly in this paper. The industry can take design guidance from the British Standards BS5502; part 40 (1990), which covers all aspects of cattle building design in 14 pages. A bargain and very useful as guidance for quality assurance visits. The standards give direction on ventilation rates per kilogram liveweight for different weight ranges and are therefore most useful for situations where mechanical ventilation will be used. A major difficulty in practice is not the description of desired ventilation rates, but the design of apertures within a naturally ventilated building that will give the required ventilation rate. However, the information already exists to design natural ventilation systems based on the laws of physics, our knowledge of animal metabolism and a wide respect for the UK climate. THERMAL BUOYANCY Animal health requirements dictate that a minimum ventilation rate is required in naturally ventilated buildings that are independent of wind. Natural convection (or stack effect) can provide this minimum ventilation rate if the ventilation inlets and outlets are in the right place. In effect, the heat produced by the housed livestock can drive the ventilation system if the warmed air is allowed to rise and escape from the building, creating a negative pressure inside the building that draws in outside air without the assistance of external wind. Bruce (1978) presented a theory of natural convection and its application to cattle buildings which has never been substantially superseded, and which has been applied to a computer model. The model is able to define, for VOL 8 PART 2 Table 1. Heat increment of feeding associated with the ingestion of high and low quality feeds. Heat produced as a proportion (J/J) of Metabolizable energy Diet Type Metabolizable energy/ gross energy* Digested energy/ gross energy* Below maintenance Above maintenance Roughage 0.40 0.50 0.41 0.75 Concentrates 0.70 0.82 0.26 0.45 Ratio ME/DE = 0.8 for roughages 0.85 for concentrate From: Blaxter K 1980. Feeds as Sources of Energy for Ruminant Animals. The Massey-Ferguson Papers

CATTLE PRACTICE any stated number and liveweight of stock, the required apertures in the sidewalls, gables or roof structure to provide adequate minimum ventilation by thermal buoyancy. INLETS AND OUTLETS In practice the design and location of apertures may be restricted by an adjoining building or, in the case of existing buildings, a myriad of technical reasons. The value of a computer model is that the parameters of an existing building can be applied to the model and the effect of various design changes observed. Porous cladding of known airflow properties can be used to restrict large openings, with the designer balancing the available aperture with the known porosity of different materials to give a required inlet area. The influence of opening up a ridge in the roof can be estimated. Inlets are best provided around a building below eaves height and the programmes can be used to visualise the effect of removing layers of blocks from walls and inserting protected openings of known airflow properties. A balanced distribution of clean inlet air is a difficulty frequently seen in naturally ventilated buildings used as calf housing. The common problems are:- •no high level exhausts to assist the stack effect. •inadequate inlet areas. •inlet areas to shared air space used by older animals. •low heat production from low numbers of calves in large volume spaces. •high moisture levels from inadequate ventilation and/or hygiene practice. •poor location of mechanical ventilation equipment. The use of mechanical ventilation in 'problem' buildings is often used as a low cost solution. A fan of known capacity can be used with a plastic perforated duct to introduce clean air to a space, but the provision of outlets is too often forgotten. Exhaust air contains not only the products of animal metabolism but also any respiratory pathogens present. It is essential that the pathogens are not distributed around the breathing zone of vulnerable stock by positive pressure ventilation. DESIGN FAILURE A primary recommendation is to check whether buildings are constructed and managed according to any available design specification. Thereafter, any building without an exhaust in the roof will not function simply by stack effect and openings in the sidewalls of the building will be required to operate as both inlets and outlets. The active inlet area is therefore reduced in such a situation. The roof space will have the potential to accumulate heat and BCVA 2000 moisture, leading to condensation and a fine environment for promoting the potential survival of microorganisms. Many such buildings use door apertures for ventilation, which gives loss of control of internal air speeds when external wind speed increases. There is also the risk that a door is closed or partially closed during poor weather and is not opened immediately the weather improves, for example at night. Cattle are thereafter left in a building with inadequate ventilation and exposed to an inevitable increase in the concentration of airborne moisture and micro-organisms. DISCUSSION Original models of animal metabolism and output have been increasingly refined and heat production, latent and sensible heat outputs, moisture and gas production can all be determined with relative ease. It is therefore possible to refine the existing ventilation models to take dietary changes into account, for example. However, the major difficulty facing the industry is not one of refinement of existing processes, but a radical improvement in the understanding of basic principles. Important factors to recognise and understand include:- •diet and stocking density will influence energy outputs within buildings. •animal behaviour influences daily heat production (van Ouwerkerk and Pedersen, 1994). •thermal buoyancy, or stack effect, is the driving force of minimum ventilation rates. •minimum natural ventilation rates rely on negative pressure within buildings obstruction of air inlets will increase back pressure. •cold surfaces and dampness can absorb heat from air, reducing stack effect. •ambient temperature, humidity and air speed all influence heat loss mechanisms. None of these mechanisms are particularly difficult to describe. The question I wish to ask is, how can we present the information to the industry in such a way that they understand the principle factors? Should we apply resources to information transfer, and if so, what are the priorities? The improved understanding of the costs of chronic respiratory disease are part of the answer in that we can help to justify the investment required to improve buildings and management. Design principles can be applied to new and existing buildings for a cost of approximately £300 per building and changes to existing structures may cost from zero to some thousands of pounds. These costs can be balanced against estimated losses to help the decision process. We have most of the necessary information; we need to learn how to apply it more effectively. There is a VOL 8 PART 2

CATTLE PRACTICE need for farmers, veterinarians and the animal health industry to work together and to embrace the skills of epidemiologists and extension specialists. We have the skills and technology; we need the cohesion and resources to apply them effectively. REFERENCES AFRC (1989) Agricultural and Food Research Council Corporate Plan 1989-1994 Andrews T. (2000) How to cost out a pneumonia outbreak. Cattle Practice (In press) Bruce (1978) Natural convection through openings and its application to cattle building ventilation. Journal of Agricultural Engineering Research. 23: 151-167. BS 5502 part40. (1990). Code of practice for the design and construction of cattle buildings. BSI 2 Park Street, London W1A 2BS Gunn G. J., Stott A.W. (1996) Combining economic arguments BCVA 2000 and active surveillance to promote better management of endemic cattle disease. Society for Veterinary Epidemiology and Preventative Medicine, Meeting March 27-29. Proceedings, 1-7. MacCormack J.A.D., Clark J. J., Knowles L. C. (1984). Survey of naturally ventilated buildings for beef cattle. Farm Buildings Progress 78: 31-35 Ouwerkerk E. N. J. van and Pedersen S. (1994) Application of the carbon dioxide mass balance method to evaluate ventilation rates in livestock buildings. XII World Congress on Agricultural Engineering, Milano, August 29 - September 1, Proceedings, 516- 529 Peters A.R. (1986) Veterinary Record 119: 355 Pfizer (1999) Rispoval 1998-1999 Seasons. The Rispoval range. Protection from viral pneumonia. Robertson J. F, (1994) Ventilation capacity of naturally ventilated buildings and ventilation requirements of beef cattle: problems associated with calf pneumonia. Presented at 1994 International Winter meeting, Paper no. 944588, American Society of Agricultural Engineers, 2950 Niles Road, St. Joseph, MI USA. VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION Bovine respiratory disease, also known as cattle pneumonia or acute undifferentiated respiratory disease, is a multi-agent, multi-factorial condition. The very fact that no uniform terminology is accepted for the disease hints at the problem in identifying the precise agents involved. Since many clinical trials have shown that successful clinical management of acute outbreaks requires antibiotic treatment anyway, it is reasonable to question the need for an accurate diagnosis. However, treating an outbreak, irrespective of the degree of success is costly and prevention is desirable to: improve animal welfare, increase productivity and reduce treatment costs. The additional pressure to reduce antibiotic use in food producing animals must also be recognised. Specific surveys and surveillance data have demonstrated that bovine respiratory syncytial virus (BRSV), followed closely by parainfluenza 3 virus (Pi3) with bovine herpes virus 1 (BHV1) a distant third are the initiating agents in the majority of outbreaks (Stott and others, 1980, Verhoeff and van Nieuwstadt 1984, Caldow and others 1993). Effective vaccines exist for these agents and there are also control strategies to minimise exposure to the contributory immunosuppressive effects of acute bovine virus diarrhoea (BVD). Therefore control programmes can be implemented to manage the risks of bovine respiratory disease and so reduce clinical disease without having recourse to laboratory diagnosis on an individual farm. However, despite the logic of a standard approach to prevention, laboratory diagnosis still has the following important roles in the management of the disease:- • To convince the client (or the clinician) that viruses are involved in order to justify a vaccination programme. • To confirm a clinical diagnosis of infectious bovine rhinotracheitis (IBR) early in an outbreak. • To monitor antibiotic sensitivity during an outbreak. • Troubleshooting in the event of the failure of a control programme. To achieve these objectives there are a number of standard techniques at the clinician's disposal: virus antigen detection or isolation, bacteriology, serology and pathology. These can be costly and therefore the clinician must be aware of their limitations and the most appropriate sampling method. VIRUS DETECTION Virus detection systems have a relatively small window of opportunity. In BRSV infections virus is shed for 9 days beginning three days after exposure (Sharma and Woldehiwet 1991). While BRSV virus can be isolated from lung lavage fluids during that time it is far less frequently detected in nasal secretions (Kimman and others 1989). In contrast, BHV1 can be isolated with ease from nasal secretions for up to eleven days after exposure (Gibbs and Rweyemamu 1977). Virus antigen can also be detected by the fluorescent antibody test (FAT) performed on nasopharyngeal swabs. This offered promise as a rapid diagnostic technique, which could deliver results on the day of sample collection and was less demanding technically (Edwards and others 1988). However, the value of this technique for BRSV had been shown to be limited by non-specific fluorescence observed in nasopharyngeal samples, a problem not observed when material from the lower airways or lung tissue was used (Thomas and Stott 1981 and Kimman and others 1986). In practice nasopharyngeal swabs have proved to be of little value for the diagnosis of BRSV or Pi3 infections using either virus isolation techniques or fluorescent antibody tests, but extremely useful for the diagnosis of BHV1. An improvement in the success of BRSV and Pi3 detection can be made if broncho-alveolar lavage (BAL) is performed on acute cases (Kimman and others 1986). Various sampling techniques can be used which are simple and quick and cause little more discomfort to the calf than nasopharyngeal swabbing (Caldow 1997). The samples collected can be used for either FAT or virus isolation, but for the latter, best results are observed when cell cultures are inoculated within one to two hours of collection. When attempting to detect viruses it is important to Pneumonia: Identifying the Causal Agent Caldow G.L1., Nettleton P.F.2., 1SAC VSD, St Boswells, TD6 0EQ. 2Moredun Research Institute, Pentlands Science Park, Bush Loan, Edinburgh, EH26 0PZ. ABSTRACT The diagnostic tests available for determining the aetiological agents involved in outbreaks of calf pneumonia are discussed. Reasons for pursuing a diagnosis are explained and an investigation strategy is outlined. KEYWORDS. calf pneumonia, diagnostic tests.

CATTLE PRACTICE limit the sampling to acute cases, if the animal already has a purulent nasal exudate it should not be sampled. It is recommended that a minimum of four animals should be sampled. When using nasopharyngeal swabs examination should be limited to BHV1 and swabs should be placed in virus transport medium on collection. In the future other techniques for virus antigen detection on nasopharyngeal swabs and other clinical material may become available. Enzyme linked immunosorbant assay (ELISA) antigen capture systems for the detection of BRSV and Pi3 antigens are used in other European countries and also for human RSV diagnosis, but are not routinely available in veterinary laboratories in Britain. Such tests may provide a more sensitive antigen detection system than the FAT. Polymerase chain reaction (PCR), a technique used to amplify genetic material has been developed for the detection of a range of viruses including BRSV (Vilcek and others 1994) and could offer a highly sensitive and specific test on clinical samples such as nasopharyngeal swabs, although the cost of these tests may limit their use. An added advantage of PCR is that the amplified region of nucleic acid can be readily sequenced and compared to that of other virus isolates allowing detailed epidemiological studies (Elvander and others 1998) BACTERIOLOGY Bacteriological examination is straightforward when compared to virus detection systems. As the nasal passages, trachea and lower airways are continuous, bacterial pathogens isolated from the nasopharynx correlate well to those isolated from the lower airways (Allen and others 1991). Furthermore, the agents are robust and culture techniques sensitive. As all of the commonly involved bacterial agents are commensals and can be found in the nasal passages of healthy cattle the value of bacteriological examination does not rest on isolation and identification of a particular organism, but rather in the antimicrobial resistance pattern of the isolate. Resistance to antibiotics has been demonstrated in Pasteurellae isolates from cases of bovine respiratory disease in the UK (Allan and others 1985). And although the value of in vitro antibiotic sensitivity testing in relation to in vivo response is generally questioned (Clarke and others 1991) it may be necessary to exclude antibiotic resistance as a factor in treatment failure or relapse, particularly as the pathology of the condition is such that rapid cures cannot always be expected. Nasopharyngeal swabs collected prior to treatment usually allow successful isolations in over 50% of samples, but once treatment has been initiated the chances of isolating bacterial pathogens from nasal swabs falls significantly. Swabs should be placed in bacterial transport medium. Mycoplasma bovis can BCVA 2000 also be isolated with ease but for this an extra swab should be taken and placed in mycoplasma transport medium. SEROLOGY Serological tests offer the most straightforward method of determining whether or not an animal has been exposed to an organism. When seroconversion is demonstrated it further allows a fairly exact idea of when that exposure occurred. The major drawback with paired serology is the time lag between the acute episode and receiving results, a period of 3-4 weeks in most outbreaks. This need not be a limitation if the results can then be used to alter preventive medicine programmes for succeeding batches of animals. Justification for the use of a vaccine against any one virus is sometimes sought by investigating one disease outbreak on a particular unit and then assuming that in subsequent outbreaks the same agent or agents will be involved. Therefore any serological investigation carried out is usually targeted specifically at those viruses for which a commercial vaccine is available, BRSV, Pi3, BHV1 and BVD. Only when severe outbreaks occur in the face of a vaccination programme is examination widened to include agents such as Adenovirus, Haemophilus somnus or Mycoplasma bovis. Serology in Young Calves Adequate colostral antibody is essential for the health of young calves and many studies have shown an inverse relationship between serum IgG concentration in the neonate and the incidence of respiratory disease, ie passively acquired antibody has a protective effect against respiratory disease in young cattle. This protection is finite as the half-life of colostral antibody is around 14 to 21 days and has mostly disappeared by 3 to 4 months of age. The colostrum of course contains antibodies against the respiratory viruses and in one study where sera from 500 market purchased 10day old calves were examined 95% were found to be seropositive to BRSV, 91% to Pi3 and 51% to BHV1 (Caldow and others, 1993). The relevance of this is twofold: it underlines the high seroprevalence to these viruses that exists in the dairy herd in Britain and therefore that when dairy bred calves are assembled from several sources it is probable that one or more of these viruses will turn up with them. Also systemic antibody responses to BRSV infection in particular are suppressed in calves with passively acquired specific antibody despite the occurrence of clinical signs and virus shedding. Subsequent re-infection results in seroconversion without clinical disease (Kimman and others 1987). The same has been observed in field outbreaks of Pi3 (Caldow 1996). Therefore at least in the first 3 to 4 months of life VOL 8 PART 2

CATTLE PRACTICE seroconversions will underestimate the amount of active virus infection and serological investigation can give disappointing results. To overcome this limitation a large sample size is recommended (at least 10-12 calves) and the first samples must be collected only in the acute stages of disease. This allows assessment of the level of maternally derived antibody and to use that to interpret the subsequent lack of seroconversion or otherwise. The suggested diagnostic criteria are for 25% of calves to show seroconversion to any single agent plus some with static titres. Calves older than 4 months Bovine respiratory disease causes severe problems in older calves housed after their first grazing season and in Scotland respiratory disease outbreaks occur most frequently 2-6 weeks after housing with a second peak around late December. Animals may be assembled from different sources and therefore different viruses can be expected to be circulating in a mixed population of immune and naïve animals. The seroconversion rate in these animals can be high, but a large proportion of these seroconversions are not associated with disease (Caldow and others 1988). For this reason acute clinical cases only should be sampled. The recommended sample size is six and the diagnostic criterion is for at least 50% of the sample to show seroconversion to one virus. Serological investigation of outbreaks will lead to the point where it is possible to exclude infections, but in many investigations a decision on the relative importance of two or more viruses has to be made. Currently that is difficult and while most studies implicate BRSV as the more significant virus in the bovine respiratory disease complex, experience in Scotland shows that Pi3 can be the important virus in around a third of outbreaks. The antibody detection ELISAs used detect mostly immunoglobulin of the IgG subclass, but IgM production has been shown to be less suppressed by maternal antibody and therefore serological tests specific for IgM can be of value in younger calves (Westenbrink and Kimman 1987). As IgM is produced only for a short time after infection with the respiratory viruses and has a short half life, if blood samples are collected 10 days after infection it would appear to offer a single test for infection in both the young and older calves. However, the dynamics of this response are also a weakness for a diagnostic test as the antibody peak is only present for a short period of time and can easily be missed. It is also important to avoid false positive results due to the influence of IgM rheumatoid factor and false negative results due to lack of sensitivity. Pre-treatment of sera with protein-G agorose has been advocated to overcome this (Graham and others 1999). IgM specific assays BCVA 2000 are not routinely available in Britain, although they are used in some other European countries. PATHOLOGY Necropsy limited to a gross examination allows confirmation that the animal died from respiratory disease, but it is surprising how little such examinations can add to the investigation. Certainly the severe consolidation and interlobular emphysema of acute BRSV infection is distinctive enough to be considered diagnostic as is the marked tracheitis seen in IBR, but often all that is observed is severe anterior pneumonia with extensive consolidation. Nevertheless, necropsy of acute cases is worth doing and in such cases the best approach is to submit the entire pluck or carcase to a veterinary investigation laboratory. Where that is not possible samples should be taken from the advancing lesions at the junction between diseased and unaffected tissue. Slices 1cm thick should be presented, both fresh and fixed in 10% formal saline. The FAT for BRSV and Pi3 on impression smears made from these samples is quite often successful. Similarly, swabs from tracheal mucosa may be used to screen for BHV1 involvement. The value of bacteriology may be limited if the animal has received antibiotic treatment, but otherwise this may be useful. Histological examination, with the exception of tracheal mucosa for IBR, often yields non-specific findings of virus involvement with secondary bacterial disease and frequently any evidence of the viral pathology has been obliterated by the damage caused by the bacteria. Specific immunostaining of fixed tissues may allow identification of the agent involved, however it is not widely used in the UK. The examination of chronic cases in an outbreak is unhelpful and should be avoided unless you wish to screen for mucosal disease. OUTBREAK INVESTIGATION For best results investigations should be initiated early in an outbreak where herds are known to have a perennial problem, it can be of value to prime the client prior to the pneumonia risk period and encourage them to seek veterinary advice as soon as sick animals are observed. In this way acute sera can be collected and if more intensive examinations are required the best cases can be selected. CONCLUSION The diagnostic tests available are sufficient to identify the majority of the agents involved in cattle pneumonia if applied to acute cases. However, the information collected can be difficult to interpret and the clinician should be clear at the outset why the investigation is being undertaken, what results can be expected and how those results will be used. VOL 8 PART 2

CATTLE PRACTICE BCVA 2000 Graham D. A., Foster J.C., Mawhinney K.A., Elvander M., Adair B.M. and Merza M. 1999 Detection of IgM responses to bovine respiratory syncytial virus by indirect ELISA following experimental infection and re-infection of calves ; abolition of false positive and false negative results by pre-treatment of sera with protein-G agarose. Veterinary Immunology and Immunopathology 71: 41-51 Kimman T.G., Westenbrink F. & Straver P.J. 1989 Priming for Local and Systemic Antibody Memory Responses to Bovine Respiratory Syncytial Virus: Effect of Amount of Virus, Virus Replication, Route of Administration and maternal Antibodies. Veterinary Immunology and Immunopathology 22: 145-160 Kimman T.G., Westenbrink F., Schreuder B.E.C. & Straver P.J. 1987 Local and Systemic Antibody Response to Bovine Respiratory Syncytial Virus Infection and Reinfection in Calves with and without Maternal Antibodies. J. Clin. Microb. 25: 1097- 1106 Kimman T.G., Zimmer G.M., Straver P.J. & Leeuw P.W. 1986 Diagnosis of bovine respiratory syncytial virus infections improved by virus detection in lung lavage samples. Am. J. Vet. Res. 47:143-147 Sharma R. & Woldehiwet Z. 1991 Bovine Respiratory Syncytial Virus: A Review. Vet. Bulletin, 61: 1117-1131 Stott E.J., Thomas L.H., Collins A.P., Crouch S., Jebbett J., Smith G.S., Luther P.D. & Caswell R. 1980 A survey of virus infections of the respiratory tract of cattle and their association with disease. J. Hygiene, 85: 257-269 Thomas L.H. & Stott E.J. 1981 Diagnosis of respiratory syncytial virus infection in bovine respiratory tract by immunofluorescence. Vet. Rec. 108: 432-435 Verhoeff J. & van Nieuwstadt A.P.K.M.I. 1984 BRS virus, Pi3 virus and BHV1 infections of young stock on self-contained dairy farms: Epidemiological and clinical findings. Vet. Rec. 114: 288- 293 Vilcek S., Elvander M., Ballagiporday A., Belak S. 1994 Development of nested PCR assays for detection of bovine respiratory syncytial virus in clinical samples. J. Clin. Microb. 32: 2225 - 2231 Westenbrink F. & Kimman T.G. 1987 Immunoglobulin Mspecific enzyme-linked immunosorbent assay for serodiagnosis of bovine respiratory syncytial virus infection. Am. J. Res. 48: 1132- 1137 VOL 8 PART 2 Table 1. Laboratory Investigation Procedures. Investigation Test Sample Size Evidence of Virus Involvement Paired Serology <4 months: sample 12 >4 months: sample 6 To Confirm IBR FAT on nasopharyngeal swabs 4 acute cases To Monitor Antibiotic Sensitivity Bacteriology on nasopharyngeal swabs Minimum of 4 untreated cases Trouble shooting in event of Failure of Control Programme Paired Serology; FAT & bacteriology on BAL Minimum of 4 acute cases REFERENCES Allan E.M., Wiseman A., Gibbs H.A. and Selman I.E. 1985 Pasteurella species isolated from bovine respiratory tract and their antibicrobial sensitivity patterns. Vet. Rec. 117: 629-631 Allen J.W., Viel L., Bateman K.G. & Rosendal S. 1992 Changes in the Bacterial Flora of the Upper and Lower Respiratory Tracts and Bronchoalveolar Lavage Differential Cell Counts in Feedlot Calves Treated for Respiratory Diseases. Can. J. Vet. Res. 56: 177-183 Caldow G.L., Edwards S., Nixon P. & Peters A.R. 1988 Associations between viral infection and respiratory disease in young beef bulls. Vet. Rec. 122: 529-531 Caldow G.L., Edwards S., Peters A.R., Nixon P., Ibata G. & Sayers R. 1993 Associations between viral infections and respiratory disease in artificially reared calves. Vet. Rec. 133: 85-89 Caldow G.L. 1996 Diagnostic Field Results in Bovine Respiratory Disease in Scotland, XIX World Buiatrics Conference, Edinburgh 1996, 3: 48-49 Caldow G.L., 1997 Broncho Alveolar Lavage in the Investigation of Bovine Respiratory Disease. Cattle Practice 5: 39-40 Clarke C.R., Burrows G.E. & Ames T.R 1991 Therapy of Bovine Bacterial Pneumonia. Vet. Clin. N.Amer. Food An. Prac. 7: 669- 695 Edwards S., White H., Newman R.H. & Nixon P. 1988 State Vet. J. 42: 41-47 Elvander M., Vilcek S., Baule C., Uttenthal A., Ballagi-Pordany A. and Belak S. 1998 Genetic and antigenic analysis of the G attachment protein of bovine respiratory syncytial virus strains. J. Gen. Virol. 79: 2939-2946 Gibbs E.P.J. & Rweyemamu M.M. 1977 Bovine herpes viruse 1. Vet Bulletin, 47: 317-343

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 pasteurellosis associated with Mannheimia (Pasteurella) haemolytica A1 (Gibbs et al 1983) and increasingly, other serotypes such as A2 and A6 (Donachie 2000). However, the complex situation of mixed infections has led to the development of 'blanket' terms such as 'Enzootic Pneumonia' often being used without precise case definition. Respiratory disease is usually associated with the rearing of calves in a housed environment. However, pneumonic pasteurellosis has also been described in calves at pasture (Wiseman et al 1976), as has pleuritis and pneumonia caused by infection with Haemophilus somnus (Radostits et al 1999). Growing cattle at pasture may also seroconvert to viral respiratory pathogens (Barrett 1997), raising the possibility of complex mixed respiratory infections occurring in both housed and non-housed cattle under certain conditions. The lack of specificity of clinical signs related to individual pathogens, and the delay between clinical presentation and receiving the results of diagnostic tests, mean that the clinician must often instigate treatment before a definitive diagnosis is reached. In reality, many respiratory disease cases are treated without a definitive diagnosis ever being made. THE CHOICE OF AN ANTIMICROBIAL The selection of antimicrobials for the treatment of respiratory disease from a pharmacological standpoint has been extensively reviewed previously by Clarke and others (1991), Bateman (1993) and Apley (1997, 1999) and will not be discussed further here. The veterinary profession in the UK is fortunate to have a large selection of antimicrobial products at its disposal for the treatment and control of bovine The Calf Pneumonia Complex - Treatment Decisions Barrett D. C., Department of Veterinary Clinical Studies, University of Glasgow Veterinary School, Bearsden Road, Bearsden, Glasgow, G61 1QH. INTRODUCTION There is increasing concern about the use of antibiotics in food-producing animals and the contribution they might make to antibacterial resistance in human pathogens (Anon 1998). Furthermore, the current increasing importance and prevalence of quality assurance schemes, encompassing better animal health monitoring and promoting preventive medicine programmes, emphasises the need to develop and monitor alternative strategies of disease control. Bovine respiratory disease is costly to farmers, detrimental to animal welfare and is reported to result in the greatest use of antimicrobials in cattle husbandry (Bateman 1993). It is therefore timely to review the selection criteria used in choosing an antimicrobial for the treatment and control of respiratory disease. RESPIRATORY DISEASE IN CALVES AND GROWING CATTLE In the early 1990s it was estimated that infectious respiratory disease in calves cost the agricultural industry £50 million per annum in the UK and $750 million per annum in North America (Bryson 1991). More recent estimates include a cost to the US beef industry approaching $1 billion per annum (Griffin 1997) and £80 million per annum to the UK cattle industry (Barrett 1997). Respiratory disease thus represents a significant loss to the cattle industry world-wide. Respiratory disease in growing cattle is associated with one or more of a collection of viruses, bacteria, mycoplasma and/or parasites and can present as a number of specific clinical syndromes such as cuffing pneumonia associated with Mycoplasma dispar (Jarrett et al 1953) and pneumonic ABSTRACT With tight profit margins in the livestock industry there is a growing need to understand the financial costs of animal disease and the cost-benefit of interventions to treat or control disease. In addition, the use of antimicrobials in food-producing animals is under public scrutiny, due to concerns that their use may, in the long term, be detrimental to human health. It is therefore timely to look at and rationalise antimicrobial use within the herds under our care, and attempt to maximise the financial return to the farmer on investment in respiratory disease treatment and control. This paper outlines criteria for antimicrobial selection based on good clinical practice and sound economics. It also suggests that these principles be integrated into herd health plans. KEYWORDS: Respiratory Disease, pneumonia, treatment, cost-effective, animal health economics, prevention, vaccination, quality assurance

CATTLE PRACTICE respiratory disease. When a veterinary surgeon is choosing an antimicrobial therapy, he/she should firstly ask him/herself if antimicrobial treatment is justified on welfare and/or economic grounds. Having established that an antimicrobial treatment is justified the following further questions should be considered in order that a rational selection be made:- • Are the probable bacterial pathogens likely to be sensitive to the antimicrobial in vitro? • Can the product be expected to reach therapeutic concentrations in the infected tissues for a sufficient period of time? • Is the antimicrobial available in a preparation which is licensed for use in this specific class of animal? • Is the route of administration appropriate to the animal, and does the dosing interval suit the management situation? • What are the required minimum withdrawal periods, and are meat and/or milk residues likely to be a problem? • Are there any risks to human health in the use of this product? • Has he/she had previous success when using the product? • Where appropriate have animals on the same farm previously shown a good clinical response to treatment with the product? • What is the cost of the product? • What is the likely cost-benefit of using this product over another? In vitro sensitivity and resistance Current data on the antibiotic resistance patterns of a range of bovine respiratory pathogens isolated in the UK are largely unavailable. There are recent publications that consider the antibiotic susceptibility of Mycoplasma bovis isolates from the UK and Ireland (Ball et al 1995, Ayling and others 1998) but not for other common pathogens such as M. haemolytica, Pasteurella multocida, M. dispar, H. somnus, Arcanobacterium pyogenes and other secondary bacterial invaders. Product licenses and withdrawal periods Those products licensed specifically for bovine respiratory disease have appropriate pharmacokinetics and have shown good efficacy, at least at the time that the initial trial work was undertaken. However, reliable data on changing resistance patterns are unavailable, thus limiting the criteria that can be used in product selection. One of the criteria on which a product choice may be made is the withdrawal period. In the beef sector the meat withdrawal period is an important consideration as farmers wish to market animals at a time when financial returns can be optimised. Very short BCVA 2000 withdrawal periods such as those applicable to ceftiofur may therefore give financial advantages over products with much longer withdrawal periods in animals close to slaughter. Ease of administration and potential for tissue damage and pain The route and requisite frequency of administration of a product are important selection criteria. There are sound animal welfare and economic reasons to limit the use of intramuscular injections, especially in meat producing animals. The oral, intravenous and subcutaneous routes of administration should therefore be used when appropriate. Oral, in-feed administration is currently possible with oxytetracycline and may in the future be feasible with other products such as tilmicosin (Thomas et al 1996, Reeve-Johnson 1998). However, this may not be practical in a disease outbreak, either because cattle are anorexic, or because the delay between needing to initiate treatment and obtaining medicated feed is unacceptably long. Oral sulphadimethoxine/ baquiloprim boluses are available for growing cattle, with up to four days duration of action. Their use eliminates both the need to handle cattle daily and the risk of injection reactions. However, neither oral bolus administration nor intravenous injection are easy in large numbers of cattle and for this reason there is increased interest in the use of subcutaneous products. Currently tilmicosin, enrofloxacin and marbofloxacin are licensed for subcutaneous use in cattle, and florfenicol has been shown to be effective via the subcutaneous route (Varma et al 1998). It is desirable, in most instances, to limit the number of times an animal has to be restrained for treatment. The labour costs of administering repeat treatments are often overlooked when comparing the cost of various therapeutic regimens and may outweigh the price differential between different products. Monitoring clinical responses and pathogen specific sensitivity patterns Clinical resistance occurs when a decrease in efficacy against a pathogen or pathogens shows up as a decreased treatment response rate, increased case fatality rate, or increased re-treatment rate of animals previously considered to be cured (Apley 1997). Quantitative assessment of clinical response to respiratory disease therapy is not commonly undertaken. Most farm and veterinary practice records would be insufficient to allow the clinician to calculate accurately the above parameters and thus monitor changing response patterns, especially as definitive diagnosis is the exception rather than the rule. This is unfortunate because accurate clinical data at herd, veterinary practice, regional or national level would provide a means of monitoring changes VOL 8 PART 2

CATTLE PRACTICE in disease patterns and the development (if any) of antimicrobial resistance. In addition to monitoring clinical responses to treatment, if veterinary surgeons are to select from the available products in an informed way and limit the development of antimicrobial resistance in the future, there is a need for independently generated data on in vitro sensitivity in the public domain. These data should represent the antibiotic susceptibility of as many pathogen isolates as possible to a range of the commonly used antimicrobials. PRODUCTION LOSSES AND THE ECONOMICS OF TREATMENT The common practice of considering only the cost of a disease in terms of drugs, veterinary fees, labour, additional feed costs etc. is only the first step in the economic analysis of the problem and should be replaced with economically sound analyses which estimate the economic benefit of control measures (Morris 1997). The comparative economic benefit of different treatment/control measures should be considered as part of the veterinary herd health plan, before an outbreak of disease occurs on a farm. However, after the appearance of disease, economic judgements are still important in the selection of a treatment protocol and future control strategy. Having acknowledged that the financial benefits of disease prevention should be considered, it is important that the potential losses due to disease are first quantified. Respiratory disease costs can be broken down into the following sections:- • Prevention and treatment with drugs and vaccines. • Veterinary professional fees. • Farm labour, including opportunity costs. • Mortality, replacement costs and loss of genetic potential. • Loss of production from chronic cases and culls. • General production inefficiency, reduced live weight gains and poor food conversion rates, leading to an extended rearing period. • Reduced sale value of finished beef cattle, due to poor appearance at the time of sale and poorer grading of carcasses. • Delay in age of first service and calving in replacement heifers and subsequent depression of milk yield in dairy herd replacements. Ideally veterinary surgeons would be in a position to use sound animal health economic principles (Dijkhuizen et al 1995) in treatment selection for respiratory disease based on: accurate quantification of the financial effects of disease, optimal decision analysis at the individual and herd level and, accurate determination of the costs and benefits of various BCVA 2000 treatments. Unfortunately our level of knowledge at the present time does not allow this and a compromise has to be made using the information currently available. In the case of dairy calves, the cost of respiratory disease has been estimated at between £3824 and £4732 per one hundred calves at risk (Esslemont et al 1998). The treatment and veterinary costs are estimated to make up 24%-30% of the total cost. Of note is the fact that, under certain circumstances, farm labour expenses may exceed the total veterinary costs and that the main losses are consistently associated with reduced calf performance. The majority of estimates of the cost of respiratory disease are based on morbidity and mortality. Estimates of morbidity are usually based on the clinical appearance of the animals. The assumption is therefore made that animals which do not appear to be clinically ill are not affected by disease and will not contribute to the economic impact of the disease outbreak. However, it is recognised that many animals in a cohort infected with respiratory pathogens will seroconvert without showing overt clinical signs (Barrett 1997). If this infection and seroconversion is associated with sub-clinical disease and negative effects on performance, then the costs are likely to have been underestimated. This argument is supported by Griffin (1997) who reported that, in one study, 50% of cattle that had never been diagnosed as having BRD during life had gross lung lesions at slaughter. Griffin (1997) also reported a significant difference in average daily gain between those with and without lung lesions. It would appear that cattle with lung pathology significant enough to reduce performance may go undiagnosed and untreated. This underlines the economic and animal welfare importance of disease prevention. HERD HEALTH PLANS AND DISEASE PREVENTION Herd health plans within quality assurance schemes provide an incentive to revise and improve farm management practices and to minimise pathogen burdens and hence the risk of infection. Our first priority should be to maximise animal welfare and profitability by disease prevention. In a recent report from the SAC Veterinary Science Division the following pathogens were reported to have been diagnosed in calf pneumonia outbreaks in November 1999; M. haemolytica (19%), Respiratory Syncytial Virus (18%), Parainfluenza 3 Virus (15%), Bovine Herpes Virus-1 (15%), P. multocida (9%), H. somnus (1%) (Anon 2000). There were a further 23 per cent of cases where no diagnosis was made. There are now vaccines available in the UK against the majority of these pathogens, suggesting that we VOL 8 PART 2

CATTLE PRACTICE could do more to prevent respiratory disease on many farms. In so doing we may also reduce the use of antimicrobials in cattle rearing. CONCLUSION This paper has discussed antibiotic selection criteria and possible ways of reducing total antimicrobial usage such as better disease prevention and control. It has also highlighted the lack of hard evidence upon which to base some decisions when considering antibiotics in the treatment and control of respiratory disease. There is a similar lack of clinical and economic evidence upon which to base other decisions relating to respiratory disease prevention, treatment and control, for example the use and selection of non-steroidal anti-inflammatory preparations and the optimisation of vaccination strategies. Despite the lack of definitive evidence to support some decisions, the selection of antimicrobials for the treatment of respiratory disease in cattle should be made on as sound a scientific and economic basis as possible. There is no justification for selecting a product which is likely to result in a suboptimal clinical response, on the basis of economy. While we should strive to increase the level of knowledge upon which we base our decisions, at the present time one should probably select a licensed product which has proven efficacious on the farm in the past, has a convenient withdrawal period, has a suitable route and frequency of administration and which is unlikely to result in the further development of antimicrobial resistance in human pathogens. All those involved in prescribing for cattle with respiratory disease should be striving to improve the accuracy of their diagnoses, the efficacy of their treatment and the efficiency of disease control measures on farms. (This article summarises a more extensive paper recently published in the Veterinary Record (Barrett 2000)). ACKNOWLEDGEMENTS The author would like to thank Dr D. Mellor and Dr N. Jonsson for their helpful and constructive comments on this paper, Elanco Animal Health, Eli Lilly and Company Ltd for commissioning the original full length paper and the Veterinary Record for allowing this summary paper to be published in Cattle Practice. REFERENCES Anon (1998) A review of antimicrobial resistance in the food chain. A technical report for MAFF July 1998; MAFF PB3901 Anon (2000) SAC Veterinary Science Division report. Veterinary Record 146: 88-90 BCVA 2000 Apley M. (1997) Antimicrobial therapy of bovine respiratory disease. In The Veterinary Clinics of North America - Food Animal Practice 13: 549-574 Apley M. (1999) Respiratory disease therapeutics. In Current Veterinary Therapy 4 - Food Animal Practice. Philadelphia, W.B. Saunders Company Ltd. Ed: Howard J.L, & Smith R.A. pp 462- 471 Ayling R.D., Baker S.E., Nicholas R.A.J., Peek M.L. & Simon A.J. (1998) Comparison of the minimum inhibitory concentrations and mycoplasmacidal activities of danofloxacin, florfenicol, oxytetracycline, spectinomycin and tilmicosin against Mycoplasma bovis and M. mycoides subspecies mycoides small colony type. Proceedings XX World Buiatrics Congress, Sydney 2, 1136 Ball H.J., Reilly G.A.C. & Bryson D.G. (1995) Antibiotic susceptibility of Mycoplasma bovis strains isolated in Northern Ireland. Irish Veterinary Journal 48: 316-318 Barrett D.C. (1997) A serological survey of viral respiratory pathogens in growing calves on a multi-system cattle unit. Diploma in Cattle Health and Production thesis. RCVS Barrett D.C. (2000) Cost-effective antimicrobial drug selection for the management and control of respiratory disease in European cattle. Veterinary Record 146: (In Press) Bateman K.G. (1993) Antimicrobial drug use in cattle. In Antimicrobial Therapy in Veterinary Medicine. ed. J.F. Prescott & J.D. Baggot 2nd Edn. Iowa State University Press. pp 456-468 Bryson D.G. (1991) The inter-relationship between viral and bacterial pneumonias of calves. In Proceedings of the Royal Veterinary College / Pfizer Ltd Symposium on Respiratory Disease in Cattle and Pigs, RVC July 1991 Clarke C.R., Burrows G.E. & Ames, T.R. (1991) Therapy of bovine bacterial pneumonia. In The Veterinary Clinics of North America - Food Animal Practice 7: 669-694 Dijkhuizen A.A., Huirne R.B.M. & Jalvingh A.W. (1995) Economic analysis of animal diseases and their control. Preventive Veterinary Medicine 25: 135-149 Donachie W., (2000) Bacteriology of bovine respiratory disease. Cattle Practice 8: 5-7 Esslemont R.J., Kossaibati M.A. & Reeve-Johnson, L. (1998) The cost of respiratory diseases in dairy heifer calves. Proceedings XX World Buiatrics Congress, Sydney 2: 685-691 Gibbs H.A., Allen M.J., Wiseman A. & Selman I.E. (1983) Pneumonic pasteurellosis in housed, weaned, single suckled calves. Veterinary Record 112: 87 Griffin D. (1997) Economic impact associated with respiratory disease in beef cattle. In: The Veterinary Clinics of North America - Food Animal Practice 13: 367-377 Jarrett W.F.H., Mcintyre W.I.M. & Urquhart, G.M. (1953) Recent work on husk - A preliminary report on an atypical pneumonia. Veterinary Record 65: 153-156 Morris R.S. (1997) How economically important is animal disease and why ? In Animal Health Economics - Principles and Application. ed. A.A. Dijkhuizen & R.S. Morris. University of Sydney. pp 1-11 Radostits O.M., Gay C.C., Blood D.C. & Hinchcliff, K.W. (1999) In: Veterinary Medicine, 9th ed. London, W.B. Saunders Company Ltd. pp 421-477 Reeve-Johnson L. (1998) A field trial series investigating the efficacy of orally delivered tilmicosin in calves. Proceedings XX World Buiatrics Congress, Sydney 2: 1029-1030 Thomas,E., Aitken I.A. & Reeve-Johnson L.G. (1996) Efficacy of oral Tilmicosin for the control of pneumonic Pasteurellosis in young milk replacer fed calves. Proceedings XIX World Buiatrics Congress, Edinburgh Poster Presentations 43-44 Varma K.J., Lockwood P.W., Cosgrove S.B. & Rogers E.R. (1998) Pharmacology, safety, and clinical efficacy of Nuflor® (Florfenicol) following subcutaneous administration to cattle. Proceedings XX World Buiatrics Congress, Sydney 1: 511 Wiseman A., Selman I.E. Pirie H.M. & Harvey I.M. (1976) An outbreak of acute pneumonia in young, single-suckled calves. Veterinary Record 98: 192-195 VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION Growing cattle require adequate dietary mineral and vitamin intake to support the increasing body mass. Rapidly growing animals on high intensity diets are susceptible to disease associated with a dietary mineral or vitamin imbalance. Proprietary concentrate feeds are likely to have adequate mineral/vitamin inclusion, although errors in compounding may result in a deficient diet. Home mixed rations, however, based on straight feeds more commonly lead to mineral/vitamin deficiency related disorders. This may be due to omission, sub optimal inclusion or inadequate mixing of the supplement. Diseases in growing cattle commonly reported to VLA, Regional Laboratories include osteodystrophies associated with inappropriate dietary levels of calcium, phosphorus or Vitamin D. Deficiency of vitamin A and copper may also affect development of bone. However, clinical presentation of deficiency may be due to an effect on other tissues e.g. change in coat colour or scouring in copper deficiency or a secondary consequence of deficiency such as blindness in Vitamin A deficiency caused by bony compression of optic nerves. Other conditions regularly reported to VLA, Regional Laboratories include white muscle disease, urolithiasis, cobalt deficiency and hypomagnesaemia. This paper limits discussion to the osteodystrophies (including the effect of copper and Vitamin A deficiency), urolithiasis and white muscle disease. The number of diagnoses of white muscle disease, urolithiasis and Vitamin A deficiency for the years 1994 through to November 1999 were collected from VIDA for animals aged 0-12 and 13-24 months. Details of the number of cases of osteodystrophies such as rickets or osteoporosis are more difficult to obtain, as these are not individually recorded on VIDA. Information relating to these conditions was collected from VLA regional laboratory monthly reports for the years 1998 through to November 1999. OSTEODYSTROPHY Lameness and stiffness in growing cattle due to nutritional osteodystrophies are regularly reported to VLA, Regional Laboratories. Deficiency of specific mineral components in the diet may lead to recognised disease conditions, eg rickets (vitamin D or phosphorus deficiency) or osteoporosis (calcium, copper or phosphorus deficiency). Rickets is characterised by defective calcification of growing bone. Enlargement of the epiphyses and the costochondral junctions result from failure of calcification with persistence of hypertrophic cartilage. The poorly mineralised bones are susceptible to distortion and fractures (Radostits and others, 1994). Osteoporosis means a deficiency in the amount of bone tissue in the skeleton or part of the skeleton. Bone may be fragile and susceptible to fractures. The condition results from an imbalance between formation and resorption of bone in favour of resorption. Specific deficiencies of calcium, copper and phosphorus may induce osteoporosis (Palmer, 1993). Osteochondrosis may affect the growth cartilage of young rapidly growing cattle. The aetiology of this condition is poorly understood, although lack of dietary mineral and vitamin supplementation (Davies and Munro, 1999) and lack of calcium in relation to daily weight increase (Reiland et al, 1978) have been considered as predisposing factors. Rapid growth, high calorific diet, inheritance, gender and hard flooring have also been implicated as predisposing factors (Palmer, 1993). Lesions of osteochondrosis may be seen in cattle with no recognised clinical signs (Jensen et al 1981). However, clinical disease may be seen when secondary manifestations such as osteochondritis dissecans with flapping of joint cartilage or epiphysiolysis (separation of an epiphysis from the metaphysis) occur. Skeletal and Other Disorders Associated with Inadequate Dietary Mineral and Vitamin Supplemention in Growing Cattle Davies I.H., Veterinary Laboratories Agency, Kendal Rd, Harlescott, Shrewsbury, SY1 4HD. ABSTRACT Osteodystrophies due to inadequate inclusion of calcium, phosphorus or vitamin D in the diet are regularly reported to Veterinary Laboratories Agency (VLA), Regional Laboratories. Vitamin A and copper are also required for normal growth of bone, although clinical presentation of deficiency may be related to the secondary effect on another organ system, eg blindness with vitamin A deficiency or more significant effects on other organ systems in copper deficiency. Other conditions in growing cattle in which inadequate dietary mineral and vitamin intake is thought to have been a contributing factor include urolithiasis and white muscle disease. These conditions, with particular emphasis on skeletal disorders, are discussed with use of information collected from VLA, Regional Laboratory monthly reports and Veterinary Investigation Diagnosis Analysis (VIDA) database for England and Wales.

CATTLE PRACTICE Confirmation of rickets, osteoporosis or osteochondrosis usually requires histopathology of bone or joint. In practice the underlying pathology is not always sought when the clinical picture suggests the presence of an osteodystrophy and analysis of the diet suggests inadequate mineral and vitamin inclusion. Furthermore, in the field it is unlikely that clinical disease is associated with deficiency of a single component as there may be varying deficiency of calcium, phosphorus, vitamin D, vitamin A or copper, all of which may influence bone development. Deficiency of copper and Vitamin A are discussed separately. SUMMARY OF CASES REPORTED TO THE VLA The following is a summary of 12 outbreaks of osteodystrophy in cattle from January 1998 to November 1999 in which inadequate mineral/vitamin inclusion in the diet was considered to be the primary cause:- Clinical signs Clinical presentation in a group of animals can vary in severity with some animals apparently unaffected, others appearing stiff and the most severely affected recumbent. Typical presenting signs include:- • Recumbency/reluctance to rise. • Stiffness. • Long bone fractures. • Joint swelling (especially hocks). • Rupture of the gastrocnemius tendon. • Ill-thrift. • Swelling of the epiphyses. In this series the age of affected animals ranged from 4-12 months, although 5-7 month old cattle were most commonly affected. In nine of the outbreaks bull beef animals were affected, two involved Friesian Holstein heifers and one Friesian/Ayrshire heifers. In seven of the outbreaks there was no mineral inclusion in the diet and in the others mineral inclusion was thought to be inadequate. In each case the diet was home mixed with often barley, wheat or maize gluten forming the main components. Each of these feeds has an excess of phosphorus to calcium. Dietary analysis is, therefore, an important part of the investigation of these cases. Caldow et al, 1995 consider evaluation of the ration as the single most important element in confirming the diagnosis. The feeding of proprietary rations, however, does not exclude the possibility of a nutritional osteodystrophy as errors in compounding may occur. BCVA 2000 Laboratory Findings Post-mortem examination is useful to identify the underlying pathology. Histopathology can be used to further support the diagnosis. Ulceration and flapping of cartilage particularly in hock and stifle joints may be evident in cases of Osteochondritis dissecans. In classical rickets swollen joints, enlargement of the costochondral junctions and bending and softening of bones which easily fracture are typical features. Thin cortical bone and bone fractures may be seen with osteoporosis, a deficiency in the amount of bone tissue in the skeleton. In this series where post mortem examination was carried out, in five of the outbreaks bilateral fracture of the femur was identified. Joint cartilage lesions were identified in two outbreaks and rupture of the achilles tendon with pliable ribs in another case. Low blood calcium concentrations and elevated serum alkaline phosphatase (SAP) concentrations are potentially useful indicators of bone pathology due to dietary mineral imbalance. The results should be interpreted with some caution as SAP concentrations may be elevated due to normal bone growth. Low blood calcium concentrations were reported on two occasions and raised serum alkaline phosphatase in three outbreaks. Bone calcium, phosphorus and ash concentrations can also be helpful indicators of mineral deficiency, although in some outbreaks of mineral/vitamin responsive lameness concentrations are within the reference range. Low calcium concentrations in bone were identified in three cases and in another two incidents, calcium and phosphorus concentrations were within the reference range. Examination of joint fluid from animals with swollen joints is a useful tool in distinguishing degenerative joint conditions from those due to infection with, for example, Mycoplasma bovis. Infected joint fluid is likely to have an elevated cell count (>70,000 cells/ml) and appear turbid. Joint fluid in a degenerative joint condition such as osteochondrosis will have a low cell count, relatively clear appearance but may be amber or red in colour due to haemorrhage. Treatment Recumbent animals may have severe underlying pathology. The presence of long bone fractures or a ruptured tendon will require emergency slaughter. Cattle affected with severe osteochondritis dissecans with ulceration of joint cartilage and swollen joints have a poor prognosis and casualty slaughter may be required. Less severely affected animals are likely to respond well to the addition of a balanced mineral/vitamin supplement to the diet and should show significant improvement over a two to three week period. VOL 8 PART 2

CATTLE PRACTICE HYPOVITAMINOSIS A Vitamin A is required for the normal development of bone and deficiency leads to abnormalities of modelling of membranous bones. Irreversible blindness, a common manifestation of vitamin A deficiency is due to stenosis of the optic foraminae causing compression of the optic nerves. Other signs of deficiency in growing cattle include night blindness, oedema of the brisket and limbs and the neurologic effects of increased intra cranial pressure (Palmer, 1993). Night blindness, an inability to see in dim light conditions, occurs because Vitamin A is required for the regeneration of visual purple. In housed cattle in familiar surroundings this sign is unlikely to be recognised by the owners. An increase in cranial pressure occurs because the size of the cranial cavity is reduced as a consequence of abnormal bone remodelling and because of impaired absorption of CSF. Nervous signs include collapse and convulsions in calves, which are not usually blind (Radostits et al, 1994). Figure 1 shows incidents of vitamin A deficiency in cattle recorded on VIDA for the years 1994 - November 1999 (cattle aged 0-12 and 13-24 months). There is a higher incidence recorded in the younger age group, although five of six cases detailed in monthly reports involved beef bulls aged between 10 and 15 months and one involved an 18 month old Limousin heifer. BCVA 2000 Unsupplemented barley based diets were consistent features in these outbreaks. Green feeds are a good source of vitamin A, although vitamin A content in old hay or silage is likely to be poor. Laboratory Findings Serum or liver vitamin A concentrations are useful as confirmatory tests. However, as blindness is irreversible due to optic nerve damage, vitamin A concentrations may be normal in affected cattle which have recently had their diets supplemented. Gross pathology demonstrating stenosis of the optic foraminae and constriction of the optic nerves may also be of value. The pathognomonic microscopic lesion is squamous metaplasia of the parotid salivary duct but this lesion resolves within a few weeks following vitamin repletion (Palmer, 1993). Treatment Animals that are blind will not respond to Vitamin A supplementation, although any apparently unaffected animals in the group will require supplementation. Calves with clinical signs due to increased CSF pressure will usually return to normal in 48 hours following parenteral treatment (Radostits et al, 1994). COPPER DEFICIENCY Primary or secondary copper deficiency can induce abnormalities in the skeleton of growing calves. Osteoporosis and abnormalities of cartilage may result (Jubb et al). Clinical signs include stiffness of gait, lameness, and enlargement of the distal ends of metacarpus and metatarsus. Epiphyses may be painful on palpation. Other signs of copper deficiency such as ill thrift, changes in coat colour and diarrhoea may also be evident (Radostits et al, 1994). Copper deficiency is more likely to be seen in young cattle at grass, particularly on pastures containing copper antagonists such as molybdenum, sulphur and iron. However, copper deficiency may contribute to the clinical signs of osteodystrophy in housed cattle on un-supplemented rations. OTHER CONDITIONS White Muscle Disease White Muscle Disease is most commonly reported in the 0-12 month age group Figure 2. There is a peak of diagnoses in April and May Figure 3, which is likely to be associated with turn out. Figure 4 shows the percentage of serum samples, which were considered deficient in vitamin E (< 2.3 mmol/l), from cattle of all ages submitted to the Veterinary Investigation Centres for the years 1994 and 1995. Figure 5 shows the percentage of blood samples submitted from cattle of all ages in 1999, which were VOL 8 PART 2 Figure 1. Incidents of Vitamin A Deficiency in Cattle Recorded on VIDA for the years 1994-Nov 1999 (Ages 0-12 months, 13-24 months) 0 2 4 6 8 10 12 14 16 1994 1995 1996 1997 1998 1999 0-12m 13-24m Incidents The most common presenting sign in cases reported to the VLA is blindness with dilation of the pupils, which are unresponsive to light. A striking feature may be reflection of light from the tapetum, which can be observed from a distance. Papilloedema may be seen with an opthalmoscope. The owner often reports blindness as sudden in onset, but as animals accommodate to their surroundings any abnormality may not have been noticed. In one outbreak blindness was first recognised when one animal in a group was being loaded for slaughter. Subsequent examination of other animals in the group then revealed further affected cases.

CATTLE PRACTICE considered to have deficient GSHPx concentrations (<30 u/ml RBC @ 37°c). The percentage of samples with low vitamin E status peaks in April whereas the percentage of samples with low GSHPx concentrations rises slightly during the summer and autumn. Six cases detailed in monthly reports each reported low vitamin E status with four showing concurrent low GSHPx concentrations, two of which were considered marginal. BCVA 2000 Vitamin E and selenium are likely to have a cross protective effect although disease can be seen with deficiency of either selenium or vitamin E alone or a combination of both. There are usually pre-disposing factors such as excess dietary unsaturated fatty acids, unaccustomed exercise or rapid growth in young animals (Radostits et al, 1994). Clinical presentation in cases reported to VLA regional laboratories are typical and include muscle weakness/stiffness dyspnoea, recumbency, stilted gait some of which are associated with turnout. Serum CPK and AST concentrations are valuable in confirming the presence of a myopathy. CPK concentrations may be extremely high, and are often in the order of tens of thousands. Age range of reported cases is predominantly 0-12 months with cases reported as young as 4 weeks of age. One incident involved an 18 month old bull turned out to serve heifers. Selenium deficiency is likely to be seen in young calves fed on home grown rations in selenium deficient areas. Vitamin E concentrations are likely to be low in poor quality hay and straw and 'prop corn' treated barley. Parenteral treatment with vitamin E/selenium combinations is likely to be successful unless there is myocardial involvement (Radostits et al, 1994). VOL 8 PART 2 Figure 2. Incidents of White Muscle Disease in Cattle. Recorded on VIDA for the years 1994-Nov 1999 (0-12 months and 13-24 months of age) 0 5 10 15 20 25 30 35 1994 1995 1996 1997 1998 1999 0-12 M 13-24 M Incidents Figure 3. Incidents of White Muscle Disease in Cattle. (ages 0-12 months) Recorded on VIDA by month (Totals for 1994-Nov 1999) 0 5 10 15 20 25 30 35 Jan Feb Mar Apr May Jun July Aug Sept Oct Nov Dec Incidents Figure 4. Vitamin E Levels in Cattle -% Deficient 194 294 394 494 594 694 794 894 994 1094 1194 1294 195 295 395 495 595 695 795 895 995 10951195 1295 0 10 20 30 40 50 60 70 Month/Year % Figure 5. % of Blood Samples from Cattle (all ages). Submitted to VLA, RL’s with Low GSH-Px (1999) 0 5 10 15 20 25 Jan Feb Mar Apr May Jun Jul Aug Sept Oct Nov Dec Incidents

CATTLE PRACTICE Urolithiasis Incidents of urolithiasis are occasionally reported to VLA, Regional Laboratories (Fig.6). Cases of urolithiasis may not be reported due to the typical clinical appearance of affected animals, although uroliths may occasionally be submitted for chemical estimation. Struvite (Magnesium ammonium phosphate) is the most commonly identified crystal in uroliths from growing steers submitted to the VLA. Clinical signs in affected animals with obstruction relate to abdominal pain and include grinding of the teeth, grunting, straining, kicking at the abdomen, frequent attempts to urinate and possible dribbling of blood stained urine from the prepuce. Symptoms of pain will subside if the bladder ruptures, but uraemia will develop and death will occur within 2-3 days. Fine crystals are often present on the hairs of the prepuce of an affected BCVA 2000 animal and may be seen in many of the other apparently normal animals in the rest of the group. Rectal palpation may be required to identify a tense bladder. Predisposing factors include heavy concentrate feeding, with an excess of phosphate to calcium and high magnesium content, and low water intake in castrated male animals. Laboratory examination can be used to confirm the nature of the crystal and blood urea to assess uraemia. Treatment is surgical. Prevention involves ensuring adequate calcium to phosphorus ratio in the diet (at least 1.2:1) with up to 4% salt added, as well as free access to water. Ammonium chloride may be added to the ration to acidify the urine (Radostits et al, 1994). REFERENCES Caldow G., Wain B., Grant A. & Lewis M. (1995) Bovine osteodystrophies. Veterinary Record 136: 80 Davies I.H. & Munro R. (1999) Osteochondrosis in bull beef cattle following lack of dietary mineral and vitamin supplementation. Veterinary Record 145: 232-233 Jensen R., Park R. D., Lauerman L. H., Braddy P. M., Horton D. P., Flack D. E., Cox M. F., Einerston N., Miller G. K. & Rehfeld C. E. (1981) Osteochondrosis in Feedlot Cattle. Veterinary Pathology 18: 529-535 Palmer N. (1993) Diseases of bones. In Pathology of Domestic Animals. Eds K. V.F. Jubb P.C. Kennedy N. Palmer. 4th edn. Vol I, London, Academic Press. pp58-64, 87-88,118-125 Radostits O.M., Blood D.C., & Gay C.C. (1994) A textbook of the diseases of cattle, sheep, pigs, goats and horses. 8th edn. London, Baillere Tindall pp 453-454, 1386, 1408-1448 Reiland S., Stromberg B., Olsson S., Dreimanis I. & Olsonn I.G. (1978) Osteochondrosis in growing bulls. Acta Radiologica (Supplement) 358: 179-196 VOL 8 PART 2 Figure 6. Incidents of Urolithiasis in Cattle (0-24 months). Recorded on VIDA for the years 1994 - Nov 1999 0 1 2 3 4 5 6 1994 1995 1996 1997 1998 1999 Incidents

CATTLE PRACTICE BCVA 2000 VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION I suspect that the very mention of bovine lameness immediately brings to mind the dairy cow, and subsequently sole ulcers, white line disease and digital dermatitis. Kossaibati et al in a survey of 50 Daisy recorded herds (July 1995 to June 1996) lameness affected 26% of cows, but there was a tremendous variation between farms (3.8% to 68.8%). A large proportion of this paper is drawn from personal unpublished observations thus will not have references. Most of the conditions are not of national economic importance and have no great incidence with the possible exceptions of laminitis, oesteochondritis dessicans and oestedystrophies resulting from nutritionally induced hyperparathyroidism. However, for pedigree breeders selling replacement stock and stock bulls, there can be a tremendous financial impact on a particular enterprise. However, it is important to distinguish between the terms congenital and inherited, as there appears to be a tendency to use them synonymously. A congenital defect may well be inherited but alternatively may be due to toxin or viral insults during pregnancy. Breeders require an opinion as to whether the presenting condition is or could be inherited. If the answer is yes there are several sequelae. 1) If as a result of an AI bull it is reported to the AI company. BUT however, if there are numerous normal progeny of this bull within the herd there may be no reporting due to the probable adverse effects on the value of the herd and selling replacements. 2) If the sire and dam are homebred the affected calf may vanish without trace, and the clients discourage contact with the relevant breed society. The conditions will be listed from birth to the point of calving and not on their relative incidence or importance. Outbreaks of digital dermatitis and foul-in-the-foot are not restricted to older cattle and can occur in youngstock but will not be discussed. DIAGNOSIS AND PROGNOSIS At times this can be difficult and may require several examinations before a definitive diagnosis (if a diagnosis can be achieved) can be made let alone whether the condition is inherited. a) Is it lameness (i.e. manifestation of pain) and does if affect one or more limbs. b) Is it a conformation fault which alters gait. c) Is the locomotor disorder not the primary concern but part of generalised systemic problem. Many observations/examinations are best carried out:- a) At 5 metres rather than 5cms. b) On a non-bedded area. c) Non-slip smooth area. d) Of a non-agitated animal. e) Not led by an experienced stockman. Under these circumstances. (see Lameness in Cattle 1997) the conformation and posture can be assessed ("The dimensions and shape of an animal are referred to collectively as its CONFORMATION. POSTURE is the manner in which an animal stands as distinct from its shape"). Abnormal posture is acquired in an attempt to relieve pain or to adjust to a mechanical influence. The posture may become habitual after the cause is no longer present. Posture is important, first as an indication of the seat of pain, and second, because individuals who are evaluating body characteristics confuse abnormal posture with abnormal conformation. Figures 6-1 to 6-5, (Copyright W.B.Saunders) are included as a reference to conformation and posture. Miscellaneous "Locomotor" Disorders in Young Cattle Borsberry S., 608 Warwick Road, Solihull, West Midlands, B91 1AA. ABSTRACT Much emphasis is placed on lameness and its effect on milk production. This paper is a reminder that there is a plethora of conditions which affect young cattle. KEYWORDS: bovine, youngstock, congenital defects, inherited defects, conformation, posture.

CATTLE PRACTICE BCVA 2000 VOL 8 PART 2 Figure 6-1. Anatomical landmarks of the body. Tuber ischiadicum (2), trochanter major (3), tuber coxae (4) ligamentum patellae laterale (5), tuber calcanei (6) lateral tubercle of the proximal end of the metatarsus (7) and tuberculum majus (10). Figure 6-2. Common body measurements. Loin height (A), withers height (B) shoulder height (C) body length (D) and pelvic length and slope of rump (E). Figure 6-3. Common claw measurements. Claw length (A) claw height (B) heel height (C) claw diagonal (D) toe angle (E) claw width (F and G). F + G = digit width. Figure 6-4. Camping forward. The hind limb is advanced so that the tuber calcanei is located in a vertical plane anterior to the tuber ischiadicum. A similar imbalance of the forelimb is referred to as protraction of the limb. Figure 6-5. Camping back. The hind limb is retracted so that the tuber calcanei is located in a vertical plane posterior to the ischiadicum. A similar imblance of the forelimb is referred to as retraction of the limb. The purpose is to examine the animal in its natural state. From 5 metres in a non-agitated state, on a non-slip surface, the posture can be gauged. A non-bedded area allows the appreciation of the conformation below the fetlock. An experienced "show" herdsperson will subconsciously lead an animal in such a manner as to disguise posture and gait abnormalities. Observation on a soft surface e.g. grass compared to a hard surface may alleviate "hoof pain". Comparing posture and gait between the two surfaces may well aid diagnosis. Agitated animals may well "hide" postural gait abnormalities and early signs of disease such as spastic paresis. The clinician must also be aware that animals which are accustomed to grass and straw bedded yards may well be apprehensive when faced with a concrete surface thus, the initial gait and posture may well be dissimilar to that which is expressed when the animal has "gained its confidence on this type of surface". In my opinion, one of the major concerns is that large animal veterinary surgeons must enjoy "looking at" the species they deal with, appreciate the norm in order to recognise the abnormal.

CATTLE PRACTICE Arthrogryposis (0 days) Can be inherited as in the Charolais breed. Jackson (1978) states:- "The defect is recessive, showing incomplete penetrance. There is high probability that the pure Charolais sires may be able to survive in the homozygous recessive state without showing changes in the phenotype. Affected calves are more common in Charolais cross animals". Ingestion of toxins e.g. lupin and infection by akabane virus during pregnancy can result in congenital arthrogryposis. “Bucked knees” congenital flexure of the carpus (0 days) Most cases are mild, bilateral and tend to improve over a two week period. Many cases will not be brought to veterinary attention as many breeders believe that the lack of extension of the carpi is due to the calf "learning to walk". Contracted flexor tendons (0 days) Is the most common congenital abnormality in cattle, bilateral and severity can vary from being upright in the pastern to the anterior aspect of the fetlock touching the ground. Mild cases are self correcting whereas more severe cases may require manual extension of the fetlock. Where manual extension fails splinting is helpful (removal of the splint at least once daily for two hours is essential to prevent joint rubs). Andrews (2000) suggests the response to 3g of oxytetracycline intravenously is a good prognostic indicator. Femoral nerve paralysis (0 days) Can be unilateral or bilateral and in many cases occurs where dystocia has not been recorded although most texts refer to forced extraction during parturition as the probable cause. The femoral nerve supplies the extensor muscles of the stifle which are the major weight-bearing muscles of the pelvic limb (Fig 3). The calf is unable to bear weight on the affected limb and there is generally no swelling of the affected limb. "Outbreaks" of femoral nerve paralysis can occur in the absence of dystocia which has led some clinicians to believe that there may be an inherited component to this disorder. Fractured Femur (0 days) This can mistakenly be diagnosed as femoral nerve paralysis but, fracture and paralysis can occur together. Where the fracture involves the BCVA 2000 Fracture of metacarpus/metatarsus (0 days) Often due to excessive traction during parturition. Low hind pasterns (0 days) Calves can be born with excessive extension of the rear fetlock joints to the extent that the plantar aspect can rest on the floor. Over a period of 10 days they improve to a normal or near normal stance. Parallel hindleg deviation (Fig 8) (0 days) Tends to occur when the hind legs are relatively long. All cases I have seen have recovered over a period of 10 to 14 days. VOL 8 PART 2 Figure 3. Femoral Nerve Paralysis. Figure 8. Parallel Hindleg Deviations. Syndactyly (0 days) Can be differentiated from monodactyly by radiography (syndactyly is the fusion or nondivision of functional digits, appears to be inherited; monodactyly is an inherited agenesis of digital structure). (Some texts state that it is of unknown cause) Partial syndactyly may well not be noticed at birth except by the most observant stockpersons. There are rumours that there is currently an AI Holstein Bull which is producing mule foot (monodactyly). distal femur it may be difficult to detect crepitus and radiography may be required to confirm the diagnosis.

CATTLE PRACTICE Foot and Mouth (0 days onwards) This is not to be discussed in detail but a reminder that in most outbreaks lameness is the first reported sign. Strabismus (0 days onwards) Relatively rare and I have observed convergent strabismus in several Charolais cross calves. All have shown a high head carriage and hypermetria of the forelimbs. Recumbent Calf (0-3 days) Examination reveals no apparent physical or systemic cause, with sensation in the distal limbs being apparently normal, are generally beef calves with a relatively large birth weight and dystocia not necessarily being reported. There are no obvious signs of bruising and attempts to "stand" these animals may not aid diagnosis. Lifting manually with hands cupped under the ventral abdominal wall tends to result in a crescent shaped calf which once asked to stand makes no attempt and simply crumples to the ground. Prognosis is difficult as within 72 hours these animals may rise as though there had been nothing wrong with them. Joint-ill (3 days to 4 weeks) More commonly affects one joint but can affect two or more joints but is rarely bilaterally symmetrical. The most common joints affected are the carpus and tarsus. Cases which fail to respond to systemic antibiotics are candidates for joint flushing with Hartmann's solution as suggested by Jackson et al (1996). They reported that hock treatment had the best prognosis and the stifle had the poorest. Proximal Tibia (1 week to 4 weeks) This tends to occur in the larger beef breeds and there is sudden onset of acute lameness (up to 9/10ths). The calf stands with a partial-flexed abducted stifle with the hock adducted (Fig 5a). Palpation reveals pain on extension and rotation of the stifle, the joint capsule and patella are clinically normal. Manual compression of the proximal tibia localises the pain to that area. I suspect that violent movement or an abnormal external force causes a partial separation of the epiphysis. Fig 5b shows the three centres of ossification of the proximal tibia. Provided there is no further trauma, the leg gradually returns to normal over a period of 3 to 4 weeks. BCVA 2000 A Diaphysis of femur B Distal epiphysis of femur C Patella D Proximal epiphysis of tibia E Tibial tuberosity F Diaphysis of tibia VOL 8 PART 2 Figure 5a. Proximal Tibia Pain. Figure 5b. Stifle Joint (from Burt et al 1968). Collapsing Calf (2 weeks to 10 weeks) The reason for the inclusion in this paper is due to the reporting of the condition to the veterinary "The calf walks for a few strides and then its legs buckle as though there is intermittent paralysis". Calves with bloat tend to be reported as such but calves with mesenteric torsion do show these signs of collapse but once lying in the prone position show signs of abdominal discomfort (which include rolling and hind leg kicking). Tibial Nerve Paralysis (4 weeks to 8 weeks) The tibial nerve supplies the muscles that extend the hock and flex the digits. I have only encountered this on four occasions, all in tethered calves which have recovered over a period of two to eight weeks (Fig 4).

CATTLE PRACTICE Tetanus (2 months plus) Outbreaks can occur e.g. after batch surgical castration but the disease mainly affects an individual. Many publications cite "rocking horse" stance (Fig 1), ruminal tympany and prolapse of the third eyelid. However, where signs are slow to develop the major signs will be stiffness, reluctance to move and lock jaw. BCVA 2000 Fractured Femur (5 -12 months) Can be difficult to diagnose but on manipulation of the affected limb(s) crepitus can generally be detected. Outbreaks can occur due to imbalance of Ca:P which result in nutritionally induced parathyroidism (Borsberry 1994) Hind Limb Paralysis (5 - 12 months) Can occur with outbreaks of bilateral fractured femurs and is probably due to a compression on the spinal cord. Spastic Paresis (5 - 12 months) Characterised by hypertonia of the gastrocnemius muscle. The condition, which is probably inherited, can be bilateral but more commonly affects one limb. I have seen it in pedigree Holsteins, but mainly in pure bred Charolais, Parthenaise and cross bred Charolais (with Charolais as part of the pedigree of both sire and dam). Signs can develop as early as 2 months but only the most observant stockperson may notice the early stages. The calf will stand slightly straight-legged but with its heel very slightly raised. (This raised heel can be used to differentiate the condition from a conformation fault of some cattle where at rest there is reduced flexion of the stifle, and increased extension of the hock (Fig 7) but the heel is in contact with the floor). VOL 8 PART 2 Figure 4. Tibial nerve paralysis. Figure 1. “Rocking horse”. Laminitis (4 months plus) Acute and subcute laminitis tend to occur in young stock which have been over supplied with rapidly fermentable carbohydrate without an adequate supply of fibre. When all four limbs are affected the animal tries to reduce pressure on the toes and tends to bear weight on the heels (Fig 2). However, if only the fore limbs are affected, the stance can resemble that of the early signs of tetanus. One differentiating feature is that the carpi tend to be flexed similar to a cat walking on a "hot tin roof" which may be exacerbated when the animal is asked to move on a hard surface compared to a bedded area, whereas in tetanus the limbs appear stiff. Figure 2. Laminitis Posture. Figure 7. Straight Hind Leg. As the condition progresses the hock extends to an angle of approximately 180° due to the contraction of the gastrocnemius muscle. In the early stages the signs can appear intermittently, however, with moderate excitement, the affected limb(s) will become "fixed" and on forward progress, the weight will be borne by the toes with little flexion of the hock and stifle and the movement of the leg appears to be as rotation of the hip. Various treatments have been suggested:- 1) Complete tenotomy of the gastrocnemius tendon and partial tenotomy of the superficial flexor tendon.

CATTLE PRACTICE 2) Partial tenectomy of two insertions of the gastrocnemius muscle onto the calcaneus. 3) Complete tibial neurectomy. The author has only experience of the tendon surgery. The complete method resulted in dropped hock which is aesthetically unpleasant and could possibly have welfare implications. The partial tenectomy is better but gait does not return to normal. Ergotism (6 months onwards) The onset of clinical signs generally are hind leg lameness. There is swelling of the distal hind limbs, diagnosis on initial examination may not be conclusive. After 3 to 4 days the hooves separate and begin to slough (abortion in pregnant cattle is not the presenting sign and occurs two to three weeks after the initial signs of lameness). This condition needs to be distinguished from a unilateral swelling of a distal limb where a constricting foreign body e.g. wire wraps around the leg. Hind Limb Subluxation of the Pasterns (Clicky Pasterns) (6 months onwards) This occurs in the larger beef breeds where the individual's natural posture is camping forward and as the animal walks and bears weight on the hind limbs there is flexion of the pastern joint and there is an audible "clonk". Breeders believe this condition to be of little significance. Oeteochondrosis Dessicans (6 months to 12 months) See previous speaker. Davies et al (1996) reported several outbreaks. "The affected animals were reluctant to move and showed difficulty rising and appeared stiff when walking. Joint swelling due to increased synovial fluid was a variable feature. Carpal and tarsal joints were the most obviously affected although in some cases joint swelling was not detected. The owner reported that appetite was BCVA 2000 reduced and several calves showed considerable weight loss. No gross lesions were detected in the feet. Rectal temperature of the calves was normal and there was no evidence of ocular-nasal discharge or pneumonia". The condition needs to be distinguished from laminitis. Pedal Bone Fracture (15 months onwards) Tends to occur at pasture with the onset of acute foreleg lameness. Generally affects the medial clay with the animal exhibiting marked abduction of the shoulder leading many owners to believe that there is dislocation of the shoulder joint. Corkscrew Claw (18 months plus) Most texts report that the condition is not obvious until 3 to 4 years of age. However, it has been observed bilaterally on the foreleg medial claws of Simmentals. ACKNOWLEDGMENT Figures 6-1 to 6-5 are the copyright of W.B. Saunders (1997) From Lameness in Cattle 3rd Edition. I am most grateful for allowing their reproduction. REFERENCES Andrews A.H. (2000) Personal communication Borsberry S. (1994) Vet Rec 135: 607 Burt J.K., Myers V.S., Hillmann D.J. and Getty R. (1968) JAVMA 152: 168-174 Davies I.H., Bain M.S., Munro R. and Livesey C.T., (1996) Cattle Practice Vol 4 Part 3 243-245 Diseases of Dairy Cattle (1995) Pub. Williams and Wilkins Jackson A.E. (1978) Vet Rec 102: 149 -150 Jackson P.G.G., Strachan W.D., Tucker A.W., Martin-Smith N., Watts T.C., Knudsen S.B., and Jones P.M.D (1996) Proceedings X1X World Buiatrics Congress Vol 2 p 554-558 Kossaibati M.A., Esslemont R.J. and Watson C. (1998) Understanding and tackling lameness in dairy herds Pub. NMR Information Partnerships. p18. Lameness in cattle, 3rd Edition (1997) Pub W.B. Saunders Co. Veterinary Genetics (1987) Pub Clarendon Press VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION BSE and vCJD are new, acquired prion diseases or sub-acute, transmissible spongiform encephalopathies, first reported in Great Britain (GB) in 1986 and 1996 respectively. Both are progressive neurological and fatal diseases requiring post mortem examination of the brain to make a definitive diagnosis. No tests are available to detect infected individuals before clinical onset. GEOGRAPHICAL DISTRIBUTION Up until December 1999, countries with BSE in native-born cattle, mostly dairy cattle, are (cumulative numbers of confirmed cases): Belgium (10), France (78), Liechtenstein (2), Luxembourg (1), Netherlands (6), Northern Ireland (1,788), Portugal (353), Republic of Ireland (424), Switzerland (323), GB (176,069) and other British Isles (1,277). By contrast, up until December 1999, there is a total of 52 definite and probable cases of vCJD in the UK and one each in France and the Republic of Ireland. ORIGIN OF BSE BSE has originated from either sheep or cattle infected with a scrapie-like agent. The source of infection is feed and the vehicle is meat-and-bonemeal (MBM). Commercially and safety-stimulated changes in the processing of animal waste around 1980 in the UK apparently permitted an increase of infectivity to enter the MBM, sufficient to cause detectable disease by 1986, after the mean 60 month incubation period was complete. Recycling BSE infection from cattle via MBM exacerbated the epidemic. BSE ASSOCIATED, NATURALLY OCCURRING DISEASES IN OTHER SPECIES There is currently no evidence for the BSE agent causing scrapie in sheep or goats anywhere in the world. However, agents with the same biological strain type as the BSE agent have been incriminated in the occurrence of TSE in several captive, wild species of BOVIDAE and FELIDAE in the UK. A closely similar agent has also been isolated from domestic cats in the UK with feline spongiform encephalopathy (FSE). One case each of FSE has also occurred in Norway and Liechtenstein. The same biological strain type of agent as occurs in cattle with BSE has been isolated also from three human patients in the UK with vCJD but not from patients with other forms of CJD (Bruce et al 1997). ANIMAL HEALTH CONTROL MEASURES The main measures to protect ruminants from BSE are a ban on the inclusion of ruminant protein (subsequently mammalian MBM) in ruminant diets and the elimination of rendering processes that were ineffective in inactivating the BSE and scrapie agents. In the UK a ban on the use of certain specified bovine offals (SBO) thought most likely to contain BSE infectivity in cattle incubating BSE, originally introduced to protect public health in 1989, was extended in 1990 to protect all species of animal and bird. More recently, an extended ban to further protect public and animal health, the specified risk materials or SRM ban, (that includes some tissues from sheep and goats) has been introduced in the UK. A similar ban in regard to certain sheep and goat tissues is also in place in France. A Commission Decision (97/534/EC), that would establish an EUwide SRM ban, will become effective from 30 June 2000 unless it is postponed, as it has been in the past. Alternatively it may be substituted by a more rigorous ban. The feed ban has a sound scientific basis but was incompletely effective in reducing exposure from feed sources, such that some cases of BSE have occurred in animals born after the ban was introduced. In the UK new exposures from feed have now been prevented entirely by banning the use of mammalian MBM in the feed for any food animal species including horses and fish. The epidemic in the UK is now declining towards elimination as it is in Switzerland. The OIE has produced a Code to facilitate safe trading in cattle and cattle products. PUBLIC HEALTH CONTROL MEASURES In addition to the SBO ban mentioned above, all cattle suspected to have BSE are compulsorily slaughtered and totally destroyed so they can enter no food or feed chain. The WHO has provided recommendations on the global surveillance and diagnosis of all forms of CJD. Bovine Spongiform Encephalopathy (BSE) and Variant Creutzfeldt-Jakob Disease (vCJD) Bradley R., Veterinary Laboratories Agency (VLA), New Haw, Addlestone, KT15 3NB.

CATTLE PRACTICE ORIGIN OF vCJD AND RISK FACTORS A new form of CJD (vCJD) was observed during 1995 and early 1996. This was identified by an unusual and uniform presentation in young people. The clinical phase was long and there was consistent and pathognomonic neuropathology. Ten cases of this new variant form of CJD were announced on 20th March 1996. It was suggested that, in the absence of any other plausible explanation, the disease had resulted from exposure to the BSE agent prior to the SBO ban in 1989. Subsequently, it was shown by biological and molecular strain typing that the agents causing BSE and vCJD were indistinguishable and were distinct from strains of agent that caused scrapie and from strains causing other forms of CJD. However, analyses of data from vCJD cases to the end of 1998 reveal no increased risk of vCJD as a result of occupation, dietary factors or medical interventions. Uncertainties in key epidemiological parameters such as the extent of effective exposure, patient susceptibility and the length of the incubation period, make predictions of the size and duration of the vCJD epidemic difficult. THE UK BSE SITUATION CONTRASTED WITH THAT IN OTHER EUROPEAN COUNTRIES It is clear that the total number of cases of BSE and the incidence of BSE in the UK exceeds, by far, the number of cases and the incidence in other countries. Indeed more cases have been reported in 1999 in the UK (>2,000) than collectively in all other countries in a period of more than ten years. However, the annual number of suspect cases reported and confirmed in the UK has declined since 1992 and is still declining. Furthermore, the residual risk to humans and animals is probably lower in the UK than anywhere else. This is because of the extensive interlocking measures applied and enforced to protect animal and human health. A significant measure applied after March 1996 is the scheme that prohibits the consumption of products from all slaughtered cattle over thirty months (OTM) of age. This OTM scheme exists in no other country. Cattle from herds in the UK beef assurance scheme may be slaughtered for human consumption up to 40 months of age. Because cattle in these closed herds are mainly grass fed and have not received MBM in their diet, they present a low risk from BSE. Following the announcement of ten cases of vCJD in March 1996 several countries reported an increase in the number of BSE cases. For example, all three Benelux countries reported their first BSE cases in 1997. In France, Ireland and Portugal the number of confirmed cases increased and they continue to BCVA 2000 increase, though the numbers reported are much less than are currently reported in the UK. Some British and continental veterinarians have expressed concern that there could be more cases of BSE occurring outside the UK than were being officially reported. Indeed, Schreuder et al, (1997) investigated the expected incidence of BSE in cattle imported from the UK to other Member States. It was concluded that it was likely that BSE cases had occurred in cattle in Member States that had been imported cattle from the UK. The (average) number of potential cases in animals imported between 1985 and 1989 was estimated to be 1642, a much higher number than had been officially reported to the EC or OIE. BSE cases in imported cattle could also have been the source of secondary cases of BSE. Such cases could have resulted from the recycling of infected cattle tissues through the rendering system (depending on the efficacy of the processing in the country in question) and then back to cattle via contaminated feed. FEED BANS IN OTHER EUROPEAN COUNTRIES It is only since 1994 that a uniform MBM feed ban (for ruminants) and rendering control has been determined by EC legislation. Switzerland (who alone adopted an SBO ban like the UK), Denmark, France, Ireland, The Netherlands and some other countries imposed a national ruminant feed ban from 1990. In at least one country, the ban was applied to cattle feed only, and not to other ruminant feed thus potentially exposing sheep and other ruminants to infected MBM via feed until the law was changed some years later. Other than Belgium, all other Member States with BSE in native-born cattle have had, like the UK, cases in animals born after the respective dates of the feed ban in their own country. Most agree these probably result from crosscontamination of ruminant feed with infected MBM intended for monogastric species. Mammalian MBM, including ruminant MBM, is permitted for feeding to non-ruminant farm animals in all other Member States than the UK and Portugal. OFFALS BANS IN OTHER EUROPEAN COUNTRIES There still are, in 2000, no uniform SRM controls in the EU though all countries with BSE in native-born animals have some form of ban. Nowhere is the ban so extensive as in the UK. There is no clear indication that such bans, where they exist, are as rigorously enforced as they are now in the UK. Some Member States have no SRM ban at all. There could be an EU-wide SRM ban by 1 July 2000 (see above). VOL 8 PART 2

CATTLE PRACTICE PASSIVE SURVEILLANCE For the most part, the surveillance for BSE in all Member States is passive, relying on the clinical identification of suspect animals by farmers and veterinarians. Such surveillance relies for its success on the observer vigilance and awareness of the clinical signs of the illness. Such surveillance is likely to underestimate the real number of cases. ACTIVE SURVEILLANCE As a result of developing confirmatory tests for BSE by detecting prion protein (PrP) in the brain or spinal cord of BSE-affected cattle, a number of suitable tests have come forward. Using one of these tests, in January 1999, the Swiss State Veterinary Service initiated a targeted, active surveillance system for three categories of cattle (Doherr et al, 1999, Schaller et al, 1999). These are fallen stock, cattle slaughtered in emergency and a proportion of healthy cattle slaughtered for human consumption. Eighteen additional cases of BSE, that otherwise would not have been detected, had been identified by this method before the end of 1999 (Doherr et al, 1999). This was about the same number of cases detected by conventional passive surveillance in that period. The under-reporting of BSE in 1999 in Switzerland was thus estimated to be about 50%. Two out of 4,847 healthy slaughter animals were positive, probably because they were in the last few months of incubation. Twelve out of 4,868 tested fallen stock were positive and four out of 2,274 tested emergency slaughter animals were positive. FUTURE OUTLOOK A successful EC-funded comparative validation of four rapid tests for PrP using brain or spinal cord tissue for the post-mortem confirmation of BSE in clinically affected cattle has been reported (Moynagh and Schimmel, 1999). It is proposed to use the approved tests throughout the Union, initially probably on fallen stock and cattle sent for emergency slaughter and over a certain age. On the basis of the Swiss experience this should, if effectively carried out on a sufficiently large population, determine once and for all the occurrence of BSE in Member States. This form of testing might also perhaps, give an indication of the true incidence of the disease and the extent of any under-reporting. Though not currently validated for use in clinically healthy cattle, studies are in progress to determine how effective some of these tests are for detecting BCVA 2000 pre-clinical cases of BSE. This will be done by using CNS tissue derived from an experimental study of BSE pathogenesis in cattle. Contrary to the situation in scrapie-infected sheep, the distribution of BSE infectivity in cattle is restricted to inaccessible tissues even in the clinical phase of disease. Therefore, the prospect of a reliable and practical test being soon available to detect pre-clinical BSE in live cattle is remote. CONCLUSIONS The epidemic of BSE in the UK is clearly under control and heading for elimination as predicted. It is probably similarly heading for elimination in Switzerland. The situation in other countries is less certain but provided the lessons learned in the UK are adopted by all those countries at risk, the future prospects for the elimination of BSE are also good. The critical issue is to ensure that ruminant feed is not contaminated with infected MBM. This is a difficult task and interlocking and enforced measures are essential to success. In regard to vCJD, uncertainties in key epidemiological parameters make predictions of the size and duration of the vCJD epidemic difficult. New exposures from infected cattle tissues are now unlikely in the UK. The medical profession has the additional responsibility for ensuring that public health is fully protected from possible accidental, man to man transmissions. The potential risks from blood transfusions, for example, have been addressed and appropriate risk management procedures have been applied. REFERENCES Bruce M.E., Will R.G., Ironside J.W., McConnell I., Drummond D., Suttle A., McCardle L., Chree A., Hope J., Birkett C., Cousens S., Fraser H., Bostock C.J., (1997). Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature; 389: 498-501. Doherr M.G., Oesch B., Moser M., Vandevelde M., Heim D., 1999. Targeted surveillance for bovine spongiform encephalopathy. Veterinary Record, 145: 672. Moynagh J., Schimmel H., 1999. Tests for BSE evaluated. Nature, 400: 105. Schaller O., Fatzer R., Stack M., Clark J., Cooley W., Biffinger K., Egli S., Doherr M., Vandevelde M., Heim D., Oesch B., Moser M., (1999). Validation of a Western immunoblotting procedure for bovine PrPSc detection and its use as a rapid surveillance method for the diagnosis of bovine spongiform encephalopathy (BSE). Acta Neuropathology; 98: 437-443. Schreuder BEC, Wilesmith JW, Ryan JBM, Straub OC, 1997. Risk from BSE from the import of cattle from the United Kingdom into countries of the European Union. Veterinary Record, 141: 187- 190. VOL 8 PART 2

CATTLE PRACTICE BCVA 2000 VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 animals. Any substance or combination of substances which may be administered to animals with a view to making a medical diagnosis or to restoring, correcting or modifying physiological functions in animals is likewise considered a veterinary medicinal product." The Medicines (Restrictions on the Administration of Veterinary Medicinal Products) Regulations 1994 came into force on 31 December, 1994 and were amended in 1997. They implement some of the requirements of Articles 4.3 and 4.4 of Directive 81/851/EEC (as amended). In accordance with these Regulations certain records must be kept by Veterinary Surgeons when prescribing for food producing animals the off data-sheet use of a veterinary medicinal product authorised for a different species or condition to that being treated, a medicine licensed for use in humans or an extemporaneously prepared product in accordance with the "cascade". These records must be kept for a period of three years from the end of the calendar year to which the records relate and be made available to any statutory enforcement agency. Details of the records which must be kept are shown at Appendix 1. The Medicated Feedingstuffs Regulations 1998 implement Council Directive 90/167/EEC and control the manufacture and distribution of medicated feedingstuffs. Medicated feedingstuffs are those that contain veterinary medicinal products on the advice of a veterinary surgeon and with one exception, on a veterinary prescription. A medicated feeding stuffs prescription "MFS prescription" replaces the former "Veterinary Written Prescription" (VWD). Copies of MSF prescriptions are required to be kept for a period of 3 years beginning with the date specified in the prescription as the "to be used before" date. The Retailers Records for Veterinary Medicinal Products Regulations 2000 came into force on 1 February 2000. These implement Article 50b .2 and .3 of Directive 81/851 as amended and require the keeping of records of each incoming and outgoing transaction by anyone supplying by retail veterinary medicinal products intended for use in food producing animals other than those on the general sales list (GSL) or in respect of which a withdrawal The State Veterinary Service Inspection Kirk K., Veterinary Advisor, National Assembly for Wales, Cathays Park, Cardiff. CF10 3NQ. INTRODUCTION This paper describes what may be expected when a Veterinary Officer (VO) of the State Veterinary Service (SVS) carries out a practice inspection of the records requiremed to be kept with regard to veterinary medicines. The relevant domestic legislative requirements are listed. It must be emphasised that procedures described here for an inspection are those at the time of submission of this paper. To date inspections have been carried out on an informal and advisory basis. Discussion and consultation is currently underway for the further structuring and formalising of inspections. DESCRIPTION OF A VO INSPECTION OF THE DISPENSING RECORDS OF A VETERINARY PRACTICE The Legislation The Veterinary Medicines Directorate (VMD) enforce the following legislative requirements with regard to the dispensing, prescribing, administration and sale of veterinary medicinal products by veterinary practices:- a. The Medicines (Restriction on the Administration of Veterinary Medicinal Products) Regulations 1994 as amended. b. The Medicated Feedingstuffs Regulations 1998 c. The Retailers' Records for Veterinary Medicinal Products Regulations 2000 d. The Animals and Animal Products (Examination for Residues and Maximum Residue Limits) Regulations 1997 The SVS, on behalf of the VMD, carries out these inspections in order to assess compliance with this legislation. VO’s already visit Local Veterinary Inspector (LVI) practices to audit procedures related to their LVI responsibilities. Inspections of dispensing records are carried out at this time. The definition of a veterinary medicinal product used for the purpose of the above regulations is that of European Community law (as opposed to that of section 130 of the Medicines Act 1968) and is as follows:- "Any substance or combination of substances presented for treating or preventing disease in

CATTLE PRACTICE period (other than zero) must be observed. A further requirement of these Regulations is that at least annually a detailed audit is performed and incoming and outgoing veterinary medicines are reconciled with current stores and discrepancies recorded. The Animals and Animal Products (Examination for Residuess and Maximaum Residue Limits) Regulations 1997 implement Directive 96/22 and Directive 96/23. These concern the prohibition of use in food producing animals of certain substances which have an hormonal or thyrostatic action and beta agonists and the implementation of a surveillance scheme to monitor certain substances and their residues in animals and animal products intended for human consumption. Regualations 25 to 29 allow specific hormones and beta agonists to be used under specified conditions in food producing animals. These conditions and the records that must be kept are given in Appendix 2. Regualation 32(1) requires anyone who by way of business rears, produces or treats animals intended for human consumption or who has any commercial operation carried out with respect to animals intended for human consumption to keep a record relating to the administration of any veterinary medicinal product to such animals. The records required to be kept by this Regulation are given in Appendix 3. THE INSPECTION VO’s visit LVI practices (both large animal, equine, mixed and companion animal) to carry out an annual audit and to ensure that office procedures are maintained as required by the Conditions of Appointment of LVI’s. Inspections of dispensing records are usually carried out at these visits. In addition, visits are made to any non-LVI large animal, equine or mixed practices specifically in order to inspect dispensing records. Assuming that a practice has nominated a Veterinary Surgeon to be responsible for ensuring the observance of the BVA Code of Practice on Medicines and the RCVS Guide to Professional Conduct covering the prescribing of medicinal products by veterinary surgeons, an inspection is carried out by appointment in the presence of that nominee. It is expected that veterinary surgeons at a practice will have, at least, easy access to the BVA Code of Practice on Medicines, RCVS Guide to Professional Conduct 2000 and "AMELIA 8" (July 1998 revision) - VMD's guidance note on the Medicines (Restrictions on the Administration of Veterinary Medicinal Products) Regulations 1994 (as amended). The VO may well request sight of these. The VO will expect to be shown records that are kept following the use of drugs in food producing species BCVA 2000 used under the "cascade", copies of MFS prescriptions and details of the method employed by the practice to comply with the "Retailers Regulations". The VMD has advised that it expects practices to be making reasonable efforts to comply with the latter regulations. As an interim measure, it is prepared to accept the recording of batch numbers on a time basis and is prepared to accept an annual audit on the basis of inward transaction of veterinary medicines into a practice compared with those held in the practice pharmacy and those recorded out of the practice pharmacy. There should be an adequate paper trail in order that medicines which have left the practice pharmacy can be traced. All discrepancies must be noted. Whatever system of recording is used must allow the recall of drugs if necessary. Similarly, the VO will need to be demonstrated the way in which the practice complies with the record keeping requirements of the Animals and Animal Products (Examination for Residues and Maximum Residue Limits) Regulations 1997. The VO will complete an inspection report form which will be discussed during the inspection. A copy of this will be sent to the practice with a letter giving details of the findings of the inspection. Where minor non-compliances are found the VMD has indicated that a timescale may be agreed with the VO for these to be rectified. A re-inspection may follow at which progress will be assessed. Where major non-compliance is found the findings will be referred to the VMD who will consider enforcement action. APPENDIX 1 Records required to be kept under The Medicines (Restrictions on the Administration of Veterinary Medicinal Products) Regulations 1994 (as amended) when medicines are prescribed for food producing animals in accordance with the prescribing "cascade":- • date of examination. • owner's name and address. • number of animals treated. • diagnosis. • product prescribed. • dosage administered. • duration of treatment. • withdrawal period recommended. APPENDIX 2 The conditions under which certain hormonal substances and beta agonists may be used in food producing animals under The Animals and Animal Products (Examination for Residues and Maximum Residue Limits) Regulations 1997 are as follows:- VOL 8 PART 2

CATTLE PRACTICE • Such a product must have a marketing authorisation. • A beta agonist must have a withdrawal period of less than 28 days after the end of treatment. • A hormonal product must not act as a deposit or have a withdrawal period of more than 15 days and must not have been authorised before 1 January 1995. A veterinary medicinal product which meets the above requirements and which contains oestrodiol 17 beta, testosterone or progesterone or a derivative and readily yields the parent compound after absorption at the site of application may be administered for a therapeutic purpose to a clearly identifiable farm animal by a veterinary surgeon who makes an appropriate record of treatment, by injection for the treatment of ovarian dysfunction in the form of vaginal spirals. Administration may also be carried out for the synchronisation of oestrus or the preparation of donor or recipients for the implantation of embryos by, or under the direct responsibility of a veterinary surgeon, and in any other case by a veterinary surgeon. The records required to be kept are as follows:- • type of treatment • the product authorised or prescribed BCVA 2000 • date of treatment • identity of animals treated • any applicable withdrawal period APPENDIX 3 Records required to be kept under Regulation 32 (1) of the Animals and Animal Products (Examination for Residues and Maximum Residue Limits) Regulations 1997 are as follows:- • date of administration • identity and quantity of veterinary medicinal product • name and address of supplier of veterinary medicinal product • identification of the animal or batch of animals to which the veterinary medicinal product was administered. REFERENCES British Veterinary Association Code of Practice on Medicines Royal College of Veterinary Surgeons Guide to Professional Conduct "AMELIA 8" (July 1998 revision) VMD's Guidance Note to the Veterinary Profession on The Medicines (Restrictions on the Administration of Veterinary Medicinal Products) Regulations 1994 (as amended). VOL 8 PART 2

CATTLE PRACTICE BCVA 2000 VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 THE RETAILER'S RECORDS FOR VETERINARY MEDICINAL PRODUCTS REGULATIONS These regulations have been out for consultation to interested parties but essentially are an EEC Directive drafted in to UK law. Directive 81/851/EEC requires member states to take all appropriate measures to ensure that the retail supply of veterinary medicinal products is conducted only by the persons who are permitted to by the legislation of the member state concerned. The directive then details the records we need to keep as veterinary surgeons. Small animal transactions have been excluded from the batch recording requirements. GSL products are the only category not covered by the regulations, unless that GSL product is for food producing species and has a withhold period. RECORD KEEPING For each incoming and outgoing transaction a record shall be kept of:- 1) The date of transaction. 2) The identity of the product. 3) The manufacturer's batch number. 4) The quantity received or supplied. 5) The name and address of the supplier or recipient. 6) The name and address of the prescribing veterinarian and a copy of the prescription. At least once a year a detailed audit of all transactions shall be carried out and recorded, with incoming and outgoing products reconciled with those held in stock and any discrepancies recorded. Sounds easy you think? It is certaily not a stocktake! All records must be kept for three years. I would like to run through various aspects of the regulations and suggest how our practice can comply with them. The aim is to make practical suggestions and hope that discussion will follow. Each practice needs to carefully consider their own situation and decide how to practically and realistically comply with this required recording. Remember that although small animal transactions are excluded from these regulations, there is still a need to be able to "audit" these products. In order to perform a detailed medicines audit you will need to account for the items used on the small animal side of a mixed practice. RECORDING 1) Date: see wholesaler's invoice or clients invoice/delivery note. 2) Product I/D: see invoice or delivery note (as above). 3) Batch Number: a) Outgoing Stock Either by computer recording- see your software supplier for suggestions as of the easiest method. Bar-coding of medicines is a recent development which should prove very useful, or manual longhand system- write B.N. on delivery note or invoice. Someone must be prompted to record a batch number or else it probably will not happen. Accuracy of recording is vital- It is pointless and potentially dangerous to incorrectly record batch numbers. Any system that makes it easier to record batch numbers is worth considering e.g. Bar-code scanners. b) Incoming Stock Keep a copy of the wholesaler's invoice/delivery note and record on this the batch numbers of stock delivered. Keep these in a separate file. 4a) Quantity received: copy of wholesaler's invoice in separate file (see above). 4b) Quantity supplied: see practice delivery note/ invoice. 5) Name & address of supplier or recipient: see invoices & delivery notes and file in a logical manner e.g. Date order. 6) Name & address of prescribing veterinary surgeon and a copy of the prescription-refers to pharmacists. POTENTIAL PROBLEMS 1) Consumables e.g.. Pentobarbitone Injection? 2) Open bottles 3) Car boot stock/on farm recording. I would advise that you have a detailed inventory of your car boot stock that includes batch numbers and expiry dates. As a bottle is used from car stock, then it has a line struck through it and the replacement bottle goes on to the end of the sheet. The use of a clip board for the sheets allows batch numbers to be retrieved easily by recording into the car rather than out of the car. Batch Recording in Veterinary Practice Vernon R., Linden House Veterinary Centre, 22a Victoria Road, Diss, Norfolk, IP22 3HW.

CATTLE PRACTICE 4) Dispensing products that are remote from the computer. For example when products are dispensed before items are on the surgery premises. 5) Dispensing from bulk items. 6) Inaccurate transposing of information. 7) Software supply problems/information retrieval. DETAILED AUDIT This should be done at least annually. It should be easy to look at incoming and outgoing stock since you should already have that information from your accounts and with the help of your supplier. You also need to record:- 1) Breakages. 2) Out of date stock. Then note any discrepancies and be able to account for them. This will not be very easy for most Practices. I suggest you speak nicely to your wholesaler and your software supplier. Our practice has devised a report that will satisfy the detailed audit when a stocktake is done. It should be easy IF you have a stock control programme on your computer to reconcile all that is specified in the detailed audit. Our computer system traces each product in and out of the practice. Several "new clients" have been set up e.g. out of date stock, breakages, stock correction and operating room. All the above "new client" cards are set not to charge out items but do de-stock the BCVA 2000 system. This allows us to account for out of date stock & breakages. The op room card allows staff to order consumables as they are used. The stock correction card allows for the human error side e.g. if someone bills out the wrong item relative to the item dispensed, you can use this card to correct the stock levels and record these transactions. As an order arrives into the practice it is entered onto the computer, including the batch number & expiry date of each product. Then for each product, every time the item is ordered or dispensed it shows on that stock history card. Then at any time you can reconcile stock held with those sold and bought. But what if you are non-computerised? Then a detailed audit will be extremely onerous and potentially inaccurate. SUMMARY Each practice needs to devise S.O.P.s to cope with these new regulations and I have described our practice system. I do not suggest it is the best system, just that it will hopefully work for us. In some cases I would suggest that you should ensure that you can "Product Recall" and then be able to satisfy the idea behind the regulations. The recording of the dates of opening bottles on the side of the container would be essential as would the recording of the date a specific batch of the product arrived at the practice. Accurate recording of batch numbers of incoming items into the practice will allow you to trail a product through your practice without the need to record every batch number during large animal visits. Each practice will have to devise a different system and the system must be a realistic one in order that it will work! VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION The success rate after bovine caesarian is not something that we as a profession can be proud of. What is apparent is that good surgeons get away with not so good surgical procedures. We need to adopt a system of doing Caesars which minimises the likelihood of a bad outcome, and one which any veterinary surgeon can use. Having said this, there is plenty of scope for constructive debate between vets who have a good success rate. A number of variations in technique are only a matter of personal preference, and do not have a major effect on outcome. How do you make the decision that a caesarian is necessary? • Assessment of relative foetal-maternal proportions. Use complex formulae or gut-feeling and clinical acumen. • No progress being made. • Cannot do it any other way. • Previous farm history. • Note that making the decision to caesar early improves your success rate no end. Also, if the cow has been subjected to traction before the caesar is carried out she is much more likely to go down during it. Preparation of cow and surgeon. • Should the operation be carried out with the cow up or down? Most surgeons prefer the cow standing, the incision is further away from the floor, the uterus is easier to exteriorise, the calf is easier to remove, and your back won't be so sore the next day! • Should we use sedatives? Xylazine, ACP, other unlicensed products? Remember that the safety of the surgeon is important. • Should we give Clenbuterol? If so should we use an ecbolic to reverse? • Local anaesthetic patterns, preferences explored. • Should we give an epidural? • Do we need to give antibiotics? If so, What? When? And for how long? • Shaving, clipping etc. of op site. • Clothing for surgeon. Needs to be effectively sterile, not the gown you have worn earlier that day for a putrid cleansing or lame cow. • Scrub up routine. Remember not only does the side of the cow need to be sterile, so do the hands, arms, upper arms and chest of the surgeon. • Drapes. Few people use them routinely but they may save the cow's life. Incision to delivery • Where do you make the hole? We need to balance considerations of wound healing with ease of delivery of the calf. Also, we need to minimise abdominal contamination if the foetus is 'fizzy'. Beware of animals which have had a previous left flank laparotomy! • Exteriorise part of the uterus prior to incising it. Easy if there is a hind limb of the foetus just inside your abdominal incision. Much more difficult if the calf's backbone towards you. Made easier if Clenbuterol has been given. Beware of long fingernails! You only want to have to sew up one hole in the uterus. Make sure you incise along the line of muscle fibres, and keep the incision as far away from the cervix as possible. Make the hole big enough. A Kruuse knife is safer than a scalpel. • Remove the calf. Often easier said than done. We always carry a pair of sterile calving ropes in the caesar kit. It is much safer to put these on and hand them to the farmer to pull on than expect him to have your knowledge of surgical sterility when grabbing the calf's legs with his hands. • Decide whether the calf or the cow is your priority. • Exteriorise uterine incision for suturing. Delivery to last stitch. • How to hold the uterus for suturing. We use a Glock's clamp. • Patterns of uterine closure. NB. Much easier if you made the incision correctly in the first place. The Utrect method will be described. • Cleaning out of the abdomen is important. Remove major blood clots etc. If there has been contamination don't be afraid of copious quantities of water as a uterine lavage. Wipe uterine incision clean with sterile swabs. We carry an autoclaved hand towel in the caesar kit to help with this. • Close up the abdomen. Preferences of suture patterns will be discussed. How many layers? Continuous or interrupted for the skin sutures? How long to leave them in? Post operative considerations. • What antibiotic should we give and for how long? What about Dimetridazole into the abdomen? • What about some analgesia? • Whose responsibility is it to see that the calf gets colostrum? • Revisit? What criteria do we adopt to recognise that all is not as it should be? Are we prepared to open them up again? Caesarean Section in the Bovine Bee D., St Peters Veterinary Group, Petersfield, Hants.

CATTLE PRACTICE BCVA 2000 VOL 8 PART 2

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION These are my notes for guidance and discussion at the workshop session on Calving and Caesars. Section 1 • History of the clinical case. • Physical examination including internal. • Foeto-maternal disproportion. • Traction. Section 2 • Malpresentation. • Torsion. • Fizzy calves! • Embryotomy. • Therapeutics. SECTION 1 •The most important factor in assessing this is whether there is PROGRESSION in the calving process. • With reasonable traction (see later) there should be progression, if not DO SOMETHING ELSE which will probably mean caesarean section. Traction • A prerequisite to traction is correct position and thorough lubrication. • Correct position is very desirable but not always possible. It may only come straight after traction. But get it the best you can before. • Lubrication is THE MOST VALUABLE TOOL in bovine obstetrics. Bottles of liquid lubricant are good for the arms but just try and keep it in the cow! Some method must be used to get the lubricant to where it is needed which usually means cranial to where you've got the calf stuck! So unless it is a very fresh calving with plenty of fluids get some lubrication around the tight bits before traction. Different materials will be discussed. • Ropes or Chains? Both hurt like mad if you put them round your own wrists and pull! Ropes produce a tourniquet, slip easily but are softer. Chains are easier to clean and de-knot. There is obviously personal preference. • Always get a rope or chain around the head before you start traction. • The calving aid. The most important factor in their use is they are AN AID, NOT A WINCH! Most also do not pull in the correct direction. This will be discussed! • Other forms of traction still have their place. • Direction of pull. If you get stuck in a cave you don't just push, you wriggle so do the same to the calf. • The casting rope. This is often under used. Traction on a down cow is easier. • Remember that PROGRESSION must still occur. If not then do something else. SECTION 2 Malpresentation There can be no doubt that the monkeys among us are at an advantage here. The longer your arms the easier it will be. If you've got narrow shoulders so that you can get both arms in easily, then you're the best. And by the way some strength can also help! • Front feet back This is usually common sense. • Head back If you can't reach it don't be afraid to use hook or get your shoulder in as well. Calvings and Caesars Singleton G., Manor Farm House, Manor Road, Martock, Somerset. TA12 6JJ. History of the Clinical Case Parity Heifers need considerably more time than cows Condition score The fat animal makes an easy calving difficult Stage of lactation Premature, on time or overdue Duration How long has she been on, what has already happened? What is the sire Who is causing the trouble? Other dystocia Is there an ongoing problem with this animal or herd? Physical examination including internal Restraint Avoid a crush, she may go down. If using a chain around the neck then put some string in it Is the animal ill? She may be hypocalcaemic or exhausted Cleaning the perineum Dry-wiping or wet! State of the tract Vagina & cervix are definitely abnormal if they don’t feel normal! A torsion is easily missed Identification Hocks feel like elbows, take your time! How many calves Check all the bits belong to one calf Assessing the size Have you got foeto-maternal disproportion? All of these should be checked out before attempting delivery. Foeto-maternal disproportion • Very difficult to assess. • Extremes are fairly obvious but there is a grey area in the middle. As one gets more experienced this grey area narrows BUT IT IS STILL THERE!

CATTLE PRACTICE • The swan neck head back can be one of the most difficult calvings around. It is often quicker, easier and less traumatic to the cow to cut the calf's head off. If so then protect the cervical stump when delivering the rest of the calf. • Posterior presentation without a breech is not abnormal and on its own should not cause a problem. The direction of pull perhaps needs to be more towards the tail. • Breech Although I have never seen it written, my, and many of my colleagues, experience, is that tears in the uterus are common after correcting this condition. So great care must be take when manipulating a breech calf. It is taught that one must protect the uterus from a foot when bringing it straight. But the common tear I have found is in the dorsal uterine wall. Is retropulsion of the calf causing this or does the breech position cause a weakness in this area of uterus? • The full breech as opposed to the hock breech is obviously harder to correct. The use of rope and an epidural should be considered. Someone else's arm can also be useful. It can be easier to cut off the legs rather than correct their position. Remember to remove the legs BELOW the hock so that you can still pull securely from above it! • Back and side presentations If large and dried out these can be near to impossible and one may have to resort to caesarean. Casting and rolling can sometimes help, but be prepared for it to be made worse! Torsion • This with the breech often presents as the cow that was going to calve a few days ago, then stopped and now has a smelly discharge. • Once a torsion has been felt and recognised as such it is seldom forgotten. • A useful tip is to teach the farmer what it feels like and to call us so that traction is not applied before correction. • Unless you have the attributes of the "complete bovine obstetrician" and can swing them back, rolling is usually needed. • Remember you have to roll the cow in the same direction as the torsion. BCVA 2000 • Surfing the plank! The use of a wooden plank with someone stood on it pressed on the cow's abdomen helps correction whilst rolling. • Even after all this physical stuff still be prepared to do a caesarean as the cervix may still not want to dilate. Fizzy calves! This is a wonderful name for the emphysematous calf and an awful lot easier to spell and say. •The vets nightmare. This can really test your physical fitness. If its big and fizzy you've got a job on your hands. • Unless the calf is the small side of average, some cutting is likely to be involved. • If the cow is clinically well then caesarean is a option. If not then either slaughter or embryotomy will be necessary. • If there is to be a per-vaginal delivery then thorough lubrication is a must. Lubricating fluids need to be infused around the whole calf. Embryotomy All the various bits of the embryotomy kit together with every day alternatives will be demonstrated and discussed. • A full embryotomy of an over sized calf should not be contemplated by the light-hearted. It takes a long time and is exhausting! • Part embryotomies on the other hand are extremely useful and make a difficult calving much easier. i.e. • The removal of a swan necked head back. • Partial removal of hind legs with a breech • The splitting of the hips for a hip-locked calf. Therapeutics VOL 8 PART 2 Epidural What drugs, when, where and how much? Clenbuterol Indications. Does it need reversing? Oxytocin How much and how often? When contra-indicated Calcium Does it have a role in the non hypocalcaemic case? Glucose Or is the borogluconate the same? Antibiotics Treatment and prophylaxis Anti-inflammatories Steroid or NSAIDs

BCVA 2000 CATTLE PRACTICE VOL 8 PART 2 INTRODUCTION Lameness has assumed even more importance as reducing the incidence of this condition is now firmly embedded in the National Dairy Farm Assurance Scheme. In order to avoid lameness we must first understand it! Unfortunately, this knowledge is still far from complete and although we are considerably wiser than we were 10 years ago there are still substantial gaps in our understanding of the problem. Defining these various risk factors and deciding which has the greatest impact on dairy cow hoof health and lameness has been an integral part of our SAC research programme. This paper puts claw horn lameness in the context of lameness in general, relates it to "laminitis" and the functional anatomy of the claw, summarises some of our recent work and connects this to other studies in the field. In particular it refers to recent work reported in the attached Proceedings of the Scottish Lameness Group 1999 (see Appendix 1). These proceedings illustrate that there is an increasing amount of work on lameness being undertaken throughout the UK. Finally, using this information we make some suggestions as to how our present knowledge might be used to tackle claw horn lameness problems in the field. OVERALL LAMENESS ASSESSMENT Incidence and Prevalence of lameness Studies associated with earlier workshops have confirmed that the farmer or his herdsperson treats most lameness. Furthermore they have also given further confirmation that the real incidence of lameness in our dairy cattle in the UK is high, probably 50 cases per 100 cows per year, with over one quarter of the cows in the average herd being lame at least once in any year and that this may well be increasing (Bosberry et al 1999). There are a large number of individual conditions that cause lameness in the dairy cow but they can be simply categorised into four and ranked in order of frequency reported in the UK as:- 1. Claw lesions. 2. Digital and interdigital (skin) conditions. 3. "Non-foot" (upper limb, back etc.) conditions. 4. Lameness of unknown or uncertain origin. The digital/interdigital problems are dominated by foul in the foot and digital dermatitis. These vie with each other for importance, both causing roughly 9% of recorded lameness each. In the claw lesion section sole ulcer and problems of the white line are the major contributors. In the UK, these two categories account for over 50% of all lameness and are recorded at a ratio of roughly 2:1. While we will concentrate upon these claw horn lesions we remind the reader that it is often forgotten how frequently cows in the UK have fluid filled swellings or adventitious bursae over the hocks and knees. Similarly, the skin around and between the digits is particularly prone to damage by rough and uneven surfaces and when it is additionally subject to constant dirty and unhygienic surroundings, this area often proves unequal to the challenge and Foul in the Foot and Digital Dermatitis, are the result. For this reason it is essential that we should pay more attention to increasing the repair and cleanliness of the underfoot conditions in our cattle housing and walkways and use a footbath regularly. Recording lameness Research is indicating that for a good definition of just how the farm is affected by lameness we need the sort of information detailed in Table 1. If the farmer REALLY wants to tackle lameness then firstly the cause of each individual case of lameness must be accurately identified and recorded and subsequently a summary produced that defines the main lesions causing lameness. Such information will improve the quality of advice markedly. We appreciate that this level of recording looks horrendously complicated but in fact using "hoof maps" it is very easy. Quite a number of UK groups (and others) have now had plenty of experience of using and handling the results from these. Laminitis & Lameness: Putting Science into Practice! Logue D.N., Offer J.E., SAC Veterinary Science Division, Dairy Health Unit, SAC Auchincruive, KA6 5AE.

CATTLE PRACTICE CLAW HORN LAMENESS Functinal anatomy of the Foot In order to understand lameness involving the foot it is important to appreciate its functional anatomy. There are differences between the front and hind feet, the fore feet bear more weight when stationary, but the hinds supply more propulsive power. Furthermore, in the adult dairy cow the inner claw bears more stresses in the front foot while in the hind foot it is the outer that bears most of these burdens. Within the foot itself there is a complex arrangement of bone, ligaments, soft tissues and specialised epithelium, either skin (between and around the digits) or horn. The last bone of the digit is embedded within the horny hoof capsule and moreover is virtually suspended within it. In other words most of the forces that the cow generates when she walks are transferred to the ground initially by the heel and then by the wall. The sole is not primarily designed as a weight bearing area nor indeed is the interdigital area. Thus, where this support is reduced for whatever reason, unnatural pressures can occur which result in unusual forces being exerted on any or all of these areas but particularly on the sole and the white line (see Figure 1). BCVA 2000 It can be seen from this diagram that the laminae are a very specific region of the claw. It is increasingly thought that the use of the term "laminitis" in relation to claw horn disruption as shown in Figure 2 is incorrect (see Kempson & Mgasa and Mgasa & Kempson 1999 in Appendix 1) VOL 8 PART 2 Table 1: Information needed to understand lameness on the farm. Type of record How recorded Prevalence of lameness Quarterly Locomotion score Incident of lameness Record of cases seen Recording of lesions associated with lameness (In order of need) Main site information Extent Other important details further Overgrowth Infected/not Site - Claw-which? & where? - sole etc. Under-running Mild/severe Site - Claw-which? & where? - sole etc. Ulcer (corium exposed) Infected/not mild/severe Site - Claw-which? & where? - sole etc. Septic penetration Cause? Site - Claw-which? & where? - sole etc. Claw Heel erosion Mild/severe Site - Claw-which? “Skin” of foot Foul Mild/severe Site - Foot Interdigital dermatitis Mild/severe Site - Foot Digital dermatitis Mild/severe Site - Foot Limb/other Traumatic Uncertain origin Mild/severe Infected Site - Hock etc. “Uncertain” Site uncertain Mild/severe Action taken Block Bandage Other (full description) Figure 1: Simple diagram of the structure of the claw of the cow. White Line Laminar Corium Sole Corium (After Leach 1996)

CATTLE PRACTICE Claw horn lesions and “laminitis” Whatever the underlying cause of claw horn lesions (and there is still debate about this) there is little doubt that the presence of haemorrhages in the claw horn (especially sole and white line), are, in severe cases, the precursors to more severe lesions such as sole ulcers. These haemorrhages are most frequently seen in cattle some 3 months post-calving. This type of claw horn disruption coupled with the challenge from the environment determines the distribution of claw lesions and explains the 'typical lesions" such as sole ulcers and white line lesions. Risk factors for claw horn lesion Development of claw horn lesions (including haemorrhages) post calving Early researchers drew a strong similarity between some of the lesions affecting the claw of the cow (such as those in Figure 2) with those of laminitis in the horse. Since "grain overload" could cause laminitis in horses it was widely considered twenty years ago that nutrition was the major influence on claw horn lesion formation and lameness in the cow. However, more recent work has not really confirmed this. Over the past decade we have returned to basics and along with other groups, attempted to describe what occures on the feet of the “normal” cattle. We have concentrated on observing how lesions develop with time and the relationship of this development with various risk factors. This was undertaken initially in a cohort of just over 30 dairy cows at the SAC Crichton Royal Farm, Acrehead Unit between 1989 & 1995. Recently we have finalised the statistical modelling of the data related to claw horn lesion development (Figure 3). In summary, this showed that lesions in the first lactation animal were significantly less severe than in the more mature animal and that there was a difference in the development of sole and white line lesions with time. By lactation 4, sole lesions and lesions of the white line were more severe and occurring more widely BCVA 2000 throughout the lactation. More detailed analysis has also shown that those lesions that occur in the first lactation may reappear in subsequent lactations suggesting chronic damage to the underlying tissues of the cow's foot (Offer et al in press). These results agree very well with recent epidemiological modelling of lameness events from herds in the Liverpool study (Ward & French 1997). They showed that cows that were lame as first calving heifers were much more likely to be lame in the second lactation than those that did not exhibit lameness in the first. VOL 8 PART 2 Figure 2: Severe claw horn disruption or sole haemorrhages. Figure 3: White line (W.L.) and sole lesion (sole) formation in Holstein Friesian cattle for lactations 1 and 4 (lact 1 and lact 4). 20 25 30 35 40 sole lact4 W.L. lact4 Recently we have reported preliminary results from a similar set of observational studies that were carried out over the subsequent four years (1994-98). This study investigated the effect of two dairy cow management extremes in Scotland on lesion formation and lameness and their inter-relationship with behaviour and social interactions (Logue et al 1999, Offer et al 1999). The study was again conducted at SAC Acrehead Dumfries and was part of an extensive SERAD funded study on Metabolic Stress in the Dairy Cow (see Cattle Practice 1999 Vol 7 Part 1). In this study the performance of 2 herds under the same personnel and with a similar physical environment was compared. One herd was designated 'low input'(LI) herd (0.5t/cow/year concentrate, milked x2/day, yielding approximately 5500l/lactation), and the other was a 'high output'(HO) herd (2t/cow/year concentrate, milked x2/day in 1994-95 and milked x 3/day from 1995-98, and yielding some 8500l/lactation). Both herds had two calving seasons: autumn (AC) and spring (SC). This design allowed a 2x2 factorial design for herd and season of calving to be used. Lameness was assessed in all cows from both herds fortnightly by locomotion scoring and the examination of all four feet of any lame cow. All first calving heifers were routinely examined for hoof lesions from autumn 1994 until spring 1997 and additionally those animals surviving into later lactations were re-examined during this period.