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CASE NOTES


Spinal abscess caused by Trueperella pyogenes in a bull

Sophia Johnson & Julianna Brailey, University Sydney Veterinary students, Dr Lyndell Stone, District Veterinarian, Hunter Local Land Services and Dr Mark Hazelton, Veterinary Pathologist, Elizabeth Macarthur Agricultural Institute

Posted Flock & Herd August 2021

INTRODUCTION

This case report describes a spinal abscess caused by Trueperella pyogenes in a two-year-old Limousin bull, which had been intended to be used as a sire in a beef cattle herd in the Mid North Coast of NSW. The owner suspected the bull was affected by Bovine Ephemeral Fever Virus (BEF), also known as 'three-day sickness'.

Due to the drought and several previous years of either limited or no known seasonal BEF transmission, this property, along with many others in the region, had several younger age cohorts of BEF naïve stock. Thus, BEF vaccination was performed for high-value animals including the bull in December 2019.

The BEF virus reached the region in late March/early April 2020. Young cattle displayed clinical signs consistent with BEF, in mid-April, when the bull began to also show clinical signs, so veterinary attention was not initially sought. At first, BEF was a reasonable differential diagnosis, however, as the case deteriorated over time, it was considered less likely. Initial clinical signs progressed to hind limb ataxia, which is consistent with a thoracolumbar spinal lesion. The cause of the clinical signs was confirmed to be a spinal abscess at post-mortem.

CASE REPORT

In early Autumn of 2020, a two-year-old Limousin bull was noted to be lame by the owner. The lameness continued for 11 days and the bull was observed to be intermittently recumbent and spending large amounts of time lying in the shade. This behaviour may have been indicative of pyrexia. A further 10 days later, the bull was described as 'miserable', having swollen joints, continuing to seek shade, and displaying hind-limb ataxia. The bull continued to eat, drink, urinate, and defecate normally at this time. A private veterinarian was contacted and based on a distance exam in the paddock, a provisional diagnosis of BEF was made.

Over the next 5 days the owner administered penicillin, anti-inflammatories, and VAM® and there appeared to be some improvement. However, after a further nine days the bull deteriorated and became recumbent more frequently or was observed to be dog-sitting. A total of 37 days after initial lameness was noted, the local District Veterinarian (DV) was contacted and attended the property to provide welfare advice, euthanasia service and to exclude notifiable diseases such as Bovine Spongiform Encephalopathy (BSE). The bull was found to be laterally recumbent with significant generalised muscle weakness and an inability to raise its head. It was also pyrexic, tachycardic, vocalising, and distressed.

The bull was euthanised on welfare grounds. A post-mortem revealed the following abnormalities:

The affected and adjoining vertebrae were excised for laboratory investigation.

Image of bovine post-mortem abomasal ulcerations
Figure 1: Abomasal ulcerations detected on post-mortem. Image credit: Dr Lyndell Stone HLLS
Image of bovine blood sample showing serosanguinous exudate
Figure 2: Serosanguinous exudate from carpus of right limb. Image credit: Dr Lyndell Stone HLLS
Image of bovine post-mortem vertebral abscess
Figure 3: Ventral aspect of T12/L2 showing the granular caseous-purulent material draining from a dorsal tract. Image credit: Dr Lyndell Stone HLLS

Spleen was also collected and submitted for BEF PCR. All other tissues had no gross abnormalities.

Samples were submitted to the NSW DPI Elizabeth Macarthur Agricultural Institute (EMAI). Because BEF was of concern initially, and BEF viral antigen can be detected in spleen for several months post infection, it was a worthy exclusion. The spleen was confirmed to be PCR negative. No bacterial growth was found on aerobic culture of the joint fluid. There was a profuse predominant growth from the spinal abscess material, which was confirmed to be Trueperella pyogenes using MALDI-TOF MS. Serology found no history of Chlamydia infection using a complement fixation test.

The submitted vertebrae (T12-L2) were sectioned longitudinally using a band saw to reveal a locally extensive abscess causing liquefactive, necrotic osteomyelitis of L1, extending into the adjacent intervertebral space common to T13. The dorsal cortical bone of the vertebral body of L1 was markedly thickened and distorted causing narrowing of the vertebral canal and impingement of the spinal cord (Figure 4). The yellow granular, caseous material was noted to be present in a 1-2cm tract that extended into the ventral musculature.

Image of bovine post-mortem vertebral section showing abscess impinging on spinal cord
Figure 4: Transverse section of T12-L2 showing the abscess and osteomyelitis of L1 and adjacent intervetbral space (left is cranial, top of the image is dorsal). The compression of the spinal cord due to remodelling primarily of L1 can clearly be visualised. Image credit: Dr Mark Hazelton EMAI

DISCUSSION

The spinal abscess and associated osteomyelitis with remodelling of L1 is consistent with the history and clinical presentation consisting of lameness, hindlimb ataxia, recumbency, dog-sitting, and pyrexia. Osteomyelitis and bone remodelling are indicative of chronicity consistent with the timeline of illness. Gradual impingement on the spinal cord at T13-L1 fits with the described clinical progression from lameness to hindlimb ataxia. Lesions of the thoracolumbar region (T3-L3) result in paraparesis with hindlimb deficits but normal forelimb function. The noted dog-sitting position combined with periods of recumbency is also consistent with progression of the spinal cord lesion. Slight improvement with penicillin and anti-inflammatories also supports this diagnosis as these treatments would have minimised bacterial growth and relieved pain. To successfully treat osteomyelitis, long courses of antimicrobials are required1, therefore the short course of penicillin would not have been adequate to be curative.

Trueperella pyogenes (formerly Arcanobacterium pyogenes) is a commensal of mucous membranes. It is frequently isolated from purulent lesions, and is commonly associated with metritis, mastitis, and Bovine Respiratory Disease (BRD)1,2. It is generally not considered a primary pathogen and often requires another more virulent pathogen or some kind of trauma to initiate a lesion that T. pyogenes then colonises3. Given the post-mortem did not reveal any other possible sites of primary infection, the source of infection is unknown. The large fibrin clot in the pericardial fluid provides supportive evidence of inflammation. The bull had been fighting prior to onset of clinical signs, so trauma was suspected as an inciting cause3,4. Iatrogenic infection was considered less likely as musculature adjacent to the affected site is not typically used for intramuscular injection and there was no associated abscessation of dorsal musculature.

In young animals, failure of passive transfer is known to predispose them to bacteraemia and subsequent colonisation of vertebrae with T.pyogenes is possible2,3. Although there is an expectation of immunocompetence given the bull’s age, a bacteraemia and subsequent T. pyogenes colonisation of compromised vertebrae may be considered likely, particularly given there was no identified primary source of infection. Given the abomasal ulceration found at post-mortem, it is possible this allowed for bacteraemia. It is unknown whether these were present prior to the bull’s onset of clinical signs or if they may have been caused by protracted illness, acidosis, consumption of mouldy feed/silages or administration of anti-inflammatories1,5. The region experienced intense drought during 2019, depleting pasture levels and requiring supplementary feeding of stock. In animals on a high-concentrate ration, subclinical acidosis can predispose to abomasal ulceration and liver abscessation1. However, the bull was mainly on pasture/silage and the liver was grossly normal. The arthritis of the right carpus is probably due to trauma from repeated attempts to stand whilst recumbent.

The clinical signs associated with BEF are recumbency, neuromuscular pain and lameness, increased nasal and respiratory secretions, anorexia, and significant pyrexia6. Whilst some of these changes were evident initially, as the case progressed the changes become inconsistent with BEF. Typically, clinical signs should only last a short period of time in vaccinated animals, although it is documented that animals in particularly good condition occasionally have more severe clinical signs and a longer duration of illness1,6,7. The bull had been affected and progressively deteriorating during the period of the tentative BEF diagnosis. If the bull was viraemic or had clinical evidence of inflammation at this time is unknown, as no samples were collected or submitted for testing.

As an alternate differential diagnosis to trauma, it was hypothesised that the effects of BEF (vasculitis) may have resulted in sufficient damage for T.pyogenes to colonise tissues such as bone. However, if this were the case one might expect multifocal bacterial abscesses throughout the body as vasculitis is not specific to a tissue type such as bone. BEF can be detected in lymphoid tissue using PCR for several months after infection8. Therefore, the negative BEF PCR on the spleen provides evidence to suggest the bull was not infected with the virus. There is evidence to suggest barbiturate use may affect PCR detection in the spleen, however as these were not used in euthanasia for this bull the result is considered highly likely to be a true-negative9. The spinal abscess alone is sufficient to explain the clinical presentation.

Early veterinary intervention may have provided an opportunity for a more favourable outcome with administration of an extended course of antimicrobials and anti-inflammatories. This case also highlights the importance of conducting a thorough post-mortem examination of the nervous and musculoskeletal systems of any animal experiencing neurological signs, as the abscess could otherwise have been easily missed.

ACKNOWLEDGEMENTS

The authors would like to thank the team at EMAI for their input and advice.

REFERENCES

  1. Smith BP, editor. Large animal internal medicine. Fifth edition. edn. Elsevier Mosby, Saint Louis, Missouri, 2015
  2. Jubb KVF & Kennedy PC. Pathology of Domestic Animals. Elsevier Science & Technology, Saint Louis, UNITED STATES, 1985
  3. Gieling F, Peters S, Erichsen C et al. Bacterial osteomyelitis in veterinary orthopaedics: Pathophysiology, clinical presentation and advances in treatment across multiple species. The Veterinary Journal 2019;250:44-54
  4. Caffaro KA, Hussni CA, Risseti RM et al. Deforming mandibular osteomyelitis in a cow caused by Trueperella pyogenes. Ciencia Rural 2014;44:2035-2038
  5. Hund A & Wittek T. Abomasal ulcers in cattle. Tierärztliche Praxis Ausgabe G: Großtiere - Nutztiere 2017;45:121-128
  6. Walker PJ. Bovine Ephemeral Fever in Australia and the World. In: Fu ZF, editor. The World of Rhabdoviruses. Springer Berlin Heidelberg, Berlin, Heidelberg, 2005:57-80
  7. Uren MF, St. George TD & Murphy GM. Studies on the pathogenesis of bovine ephemeral fever in experimental cattle III. Virological and biochemical data. Veterinary Microbiology 1992;30:297-307
  8. Barigye R, Davis S, Hunt R et al. Post-viraemic detection of bovine ephemeral fever virus by use of autogenous lymphoid tissue-derived bovine primary cell cultures. Australian Veterinary Journal 2017;95:49-52
  9. Pers. Comm., Zoetis. 2020

 


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