CASE NOTES


Yersiniosis or more?

David Thomson - District Veterinarian, Grafton

Posted Flock & Herd October 2011

Introduction

Sudden and acute deaths appear to be comparatively common and significant amongst beef and dairy cattle in the Grafton area, including within herds under relatively regular, experienced producer observation. Anecdotally, losses occur more commonly during the period July to October each year coinciding with the worst period for season pastures (cattle in lower body condition; more feed supplementation via winter fodder crops such as rye grass, conserved silages, hay and concentrates; calving). Losses involve both sporadic individual deaths and multiple-death outbreaks. Losses are also sometimes associated with at least some evidence of diarrhoea within affected mobs. The following report details two acute, multiple-death outbreaks affecting beef herds during August 2011 where yersiniosis (Y. pseudotuberculosis) was diagnosed in one of the mortalities from each herd event.

HISTORY

Farm 1

This farm is located on a flood plain. The mob is reportedly under a minimum of once daily owner observation. Mob reportedly vaccinated against clostridial diseases once at weaning (3-4 months previously) using 5-in-1 vaccine. Affected group of weaners-yearlings were in condition score 2-3, initially grazing on somewhat flood-affected sown rye grass with access to a damp paddock with very short, flood-affected kikuyu and paspalum pasture. Initial deaths (No's 1 and 2) occurred in animals approximately 8 months of age after a short illness (2-3 days). Prior to death, the affected animals separated themselves from others, stood under trees for shelter (1-2 days), went down and then died soon after. The mob was subsequently moved to a new dry paddock with relatively bulky, hayed-off, frost-affected kikuyu/clover/paspalum (fresh growth coming underneath) and supplemented with some corn silage and mineral/salt lick blocks. Death No. 3, occurred suddenly without any premonitory signs in an animal approximately 12 months of age, 14 days after deaths No's. 1 and 2 and 10 days after relocating to the dry paddock. Death No. 4 occurred 5 days after death No. 3 in an animal in the same paddock and mob approximately 8 months of age. This animal was initially depressed for approximately 3 days with some mild scours, progressing rapidly over further 2 days to severe watery brownish-green scours before going down (immediately after gentle yarding) and dying.

Farm 2

Located on low forest ridges falling to low swamp and lagoon traversed by deep drains. Affected group mixed ages, condition score 2 under twice daily owner observation associated with supplementary feeding. Pastures on ridges and low-lying ground very short with no body - obviously flood-affected, paspalum dominant on low-lying areas, but with some fresh growth evident. The mob was relocated from floodplains approximately 2-3 months previously. History of a multi-death outbreak of clostridial septicaemia in the herd (diagnosed clinically by LHPA veterinarian) before that move and all stock had received two vaccinations with 7-in-1 clostridial/leptospirosis vaccine. The mob was supplemented with cereal straw hay, some cottonseed meal and mineral/urea/salt lick blocks. Individual animals in the affected and a nearby mob were observed wading in drains and lagoons eating water plants. Death No. 1 apparently a sudden death of a late pregnant first calf heifer approximately 10 days prior to visit. The animal was found dead in the water in a drain. Death No. 2 apparently a sudden death of a 15 month unjoined heifer 7 days prior to visit with reported evidence of mild scours on the rear of the carcass. Death No. 3 apparently a sudden death of an aged (9yrs), late pregnant cow with some evidence of scours on the rear of the carcass. Two other young stock in the mob (1-2yrs) were observed with watery greenish scours at the time of the visit. They were subsequently treated with oxytetracycline injections (X 2 each at three days interval) and have since reportedly recovered uneventfully.

Physical Examination

Farm 1

After deaths No's 1 and 2, the cohorts appeared bright, alert and physically healthy with minimal evidence of scours or other ailments. Carcass of death No. 1 was in lateral recumbency, more than 1 day old and had evidence of scavenger feeding about the head. There was no obvious evidence of scours affecting the hind end of the carcass prior to death. An autopsy was not performed on this carcass. Carcass of death No. 2 was in lateral recumbency, there was no evidence of terminal struggling and it had been dead less than 12 hours. Externally there was minimal evidence of loose faeces on caps of the hocks and in brush of the tail. Eyes were, however, somewhat sunken and mucus membranes relatively pale (inconclusive after death). Carcass of Death No. 3 was in lateral recumbency with no evidence of terminal struggling and had been dead less than 4 hours (based on owner reports). There was no evidence of ante mortem scouring, but eyes were somewhat sunken. Death No. 4 was examined immediately before death and specimens of blood and faeces collected at that time. It was in lateral recumbency, with obviously sunken eyes, leathery skin tone, mild fever (40C after yarding) and obvious evidence of watery scours on the perineum, hocks and tail brush.

Farm 2

All deaths occurred in low swampy areas of pasture and cattle were obviously pressuring these areas for the fresh new pick. Carcasses of deaths No's. One and two were more than 7 days old and decomposing (on a woodpile waiting to be burned). Carcass of death No. 1 had been found in water in a large, deep drain. It was a springing first calf heifer, but there had not been overt evidence of dystocia (owner report). Death No. 2 had been found in lateral recumbency at the side of a drain with no evidence of terminal struggling, but some suggestion of green scours on its perineum (owner report). The carcass of death No. 3 (aged cow) had been found in lateral recumbency with no evidence of terminal struggling (owner report) and had been dead approximately 8-12 hours. Eyes were sunken, skin felt dry, there was a small rectal prolapse with very inflamed mucosal surfaces (indicative of acute enteritis and straining ante-mortem) and there was dried evidence of watery clearish scours on caps of the hocks and brush of the tail. This cow was also springing, but there was no evidence of dystocia.

Necropsy Findings

Farm 1

Death No. 2 - mild pleural and pericardial effusion, moderate ascites suggestive of hypoproteinaemia. A modest burden of Haemonchus placei attached to the mucosal lining of the abomasum. Some modest congestion of the GIT from jejunum to colon. Otherwise grossly unremarkable considering apparent time since death. Death No. 3 - mild pleural effusion and mild ascites. Liver slightly enlarged. Lining of the rumen and abomasum stripped very readily, but contents primarily pasture (no evidence of corn silage engorgement). Mesenteric lymph nodes grossly swollen and oedematous. GIT, particularly ileum and upper colon, congested and hyperaemic with suggestion of fine sub-mucosal haemorrhages. Haemorrhages evident in the thymus. Otherwise grossly unremarkable. Death No. 4. - faeces watery brownish-green. PCV of blood (when spun down) apparently normal despite clinical dehydration. Generally dehydrated carcass, but modest ascites. Liver slightly enlarged. Mesenteric lymph nodes enlarged and oedematous. Obvious, severe, acute enteritis and GIT congested and hyperaemic from mid jejunum through colon - most severe in ileum and upper colon. Otherwise grossly unremarkable.

Farm 2

Death No. 3 only - mild ascites and pleural effusion suggestive of hypoproteinaemia. Heart relatively normally sized, but somewhat flabby to handle. Liver somewhat shrunken (but not grossly cirrhotic) due apparently to chronic toxic insult. Late third trimester of pregnancy - cotyledons somewhat autolysed in appearance, but membranes clear. GIT from mid jejunum to rectum grossly congested and hyperaemic. Visible 'freckling' of the ileum suggestive of sub-serosal/sub-mucosal haemorrhages. Inner mucosal surfaces very inflamed with patches of apparent villous necrosis fibrin-like casts adherent to the mucosa and free-floating within the contents. Contents from ileum to rectum very watery and clear yellowish with many fibrinous casts. Otherwise unremarkable.

LABORATORY RESULTS

Farm 1

Death No. 2 - Low FEC (60/gm), negative BVDV, conclusion of 'unconfirmed enteric signs'. Death No. 3 - mild lymphoid and neutrophil infiltrates of the heart, lung (bronchioles) - suggestive of a viral illness -, autolytic changes of the GIT and related lymph nodes (possibly incomplete fixation) and patchy congestion and some haemorrhages of the mucosal and sub-mucosal surfaces of the ileum and colon with moderate numbers of bacilli present; Salmonella negative. Death No. 4 - Yersinia +++ in rectal contents; AST, CK, Urea, Creatinine, Ure/Crea and Alb/Glob ratios all high (suggestive of renal shut-down/shock due to dehydration); protein, albumin, globulin and Ca all low (suggestive of hypoproteinaemia due, at least in part to enteritis losses and low calcium possibly partly due to inanition); PCV, RBC and WBC all high; protein-RTS low. Conclusion was protein losing enteropathy and prolonged recumbency (but the latter had not been the case as animal had only just gone down under gentle handling immediately before specimen collection).

Farm 2

Death No. 3 - Yersinia +++ in ileum and colon contents.

DISCUSSION

Although a relatively definitive diagnosis of yersiniosis was concluded in one case from each of the two farm outbreaks studied, the occurrence of multiple sudden deaths in mobs that appeared to be under regular observation by experienced beef cattle producers, both of whom are familiar with 'mud scours' as a disease entity, is not necessarily consistent with that diagnosis. The probability of a multi-factorial disease complex manifesting in part as clinical yersiniosis warrants consideration and possibly, further investigation, particularly as some of the cases at Farm 2 appeared to depart somewhat from the classical picture of a 'young cattle' disease. Necropsy findings in deaths No's 2 and 3 at Farm 1 were not consistent with clinical yersiniosis, although in both cases, 'enteric' syndromes were somewhat evident at necropsy and in death No. 2, those non-specific suspicions were supported by the laboratory conclusion. Laboratory findings for Death No. 3 at Farm 1 were, however, more indicative of other disease processes and may have been confused in part by sub-optimal fixation of tissue specimens with autolysis when specimens were, in fact, collected relatively soon after death. In this case, the findings of mucosal and sub-mucosal haemorrhages in the ileum and colon could be quite significant.

At farm 2, the occurrence of apparently acute deaths in two nutritionally challenged cases during the latter third trimester of pregnancy may be significant in that it would be reasonable to expect both cases to have somewhat compromised immune systems. Whilst speculative without further evidence, the occurrence of sudden deaths associated with an enteric syndrome involving haemorrhages and bacilliary infiltration of the mid and lower intestines and/or acute enteritis may be more consistent with Clostridium perfringens Type C infection than classical yersiniosis due to Yersinia pseudotuberculosis, but the former disease is not generally considered to be prevalent in Australian cattle. Unfortunately, in these cases more targeted investigations of this possibility were neither requested by myself nor pursued by the laboratory. Cattle in affected mobs at both farms had been vaccinated with classical 5-in-1 clostridial vaccine, but this does not include Cl. perfringens Type C immunogen. Type C has only recently become available in the form of "Tasvax 7" (NB. potentially confusing with classical "7-in-1" from other vaccine manufacturers that contains 2 serotypes of leptospirosis combined with classical 5-in-1 clostridial vaccine) and "Tasvax 8" vaccines. Protein and mineral deficiencies and imbalances in clinical and sub-clinical forms, including their indirect impact on blood, biochemical the immunological competence, are also well-recognized throughout the region and likely to be at their most obvious during the period from July to October when pasture feed is generally at its worst. The possibility of a regionally significant disease complex involving mineral deficiency/imbalance, immunological compromise, acute clostridial disease and sub-acute yersiniosis complications may warrant further consideration and investigation.

 


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