CASE NOTES
Stahylococcus aureus mastitis in a jaundiced ewe
Bruce Watt, Central Tablelands Local Land Service, Bathurst and Patrick Shearer, State Veterinary Diagnostic Laboratory, Menangle
Posted Flock & Herd February 2015
Introduction
Jaundice is seen in a number of important sheep diseases. In the authors' experience marked jaundice is most often seen in cases of hepatopathy (and in particular crystal associated cholangiohepatopathy) and copper poisoning but milder jaundice is also seen in a range of diseases such as Mycoplasma ovis infections. In this case the jaundice is presumed to be due to the elaboration of toxins associated with staphylococcal mastitis as there is no evidence of hepatopathy or copper poisoning.
History
A single first cross of 400 in mob 2 to 7 year old ewes was noticed to be sick on the morning of 12 November 2014, then died shortly afterwards. The property runs 2300 first cross ewes on improved pastures. This mob was running on subterranean clover, cocksfoot, ryegrass pasture and before that had run on pastures that included plantain and chicory. The mob had been drenched with a combination anthelmintic (NAPfix containing naphthalophos 135 g/L, albendazole 25 g/L and abamectin 1 g/L administered at 1ml/5kg, Jurox) and vaccinated with 6:1 in June (pre-lambing). The ewes lambed in July-Aug and had some lambs at foot but some probably including the lamb from this ewe, had recently been weaned.
Necropsy findings
A mature crossbred ewe in fat condition was presented for autopsy. The mucous membranes and sclera were dark yellow. The right side of the udder was markedly swollen. The skin over the gland was purple with a watery red brown discharge. Abdominal fat was dark yellow while the kidneys large and tan coloured. The liver was slightly enlarged with sharp edges and was a uniform dark red in colour.
Figure 1. Affected ewe showing yellow sclera
Figure 2. Yellow omental fat, relatively normal liver and mottled purple lungs
Figure 3. Swollen right mammary gland with yellow/orange oedematous fluid in ventral abdomen.
Laboratory Findings
Bacteriology
A culture of mammary exudate grew abundant colonies of Staphylococcus aureus that was sensitive to all antibiotics tested (Sulphafurazole, Trimethoprim, Tetracycline, Erythromycin, Penicillin, Novobiocin, Cefuroxime, Methicillin and Ampicillin).
Histopathology
The major histopathological findings were an acute, multifocal, severe, suppurative mastitis and an acute, multifocal, severe, suppurative pneumonia, both with numerous intralesional bacterial colonies.
The mammary tissue was multifocally effaced and replaced by abscesses composed of aggregates of degenerate and non-degenerate neutrophils arranged around clusters of cocci. Tubules were multifocally dilated with oedema fluid, neutrophils and clusters of cocci. Ducts contained a purulent exudate, composed of a mixture of degenerate neutrophils, clusters of bacteria, fibrin and haemorrhage. Blood vessels were diffusely congested. Interlobular septae were diffusely expanded with fibrin.
Within the lung, the interstitium was diffusely expanded with moderate numbers of lymphocytes, plasma cells and macrophages, with lesser numbers of neutrophils; protein-rich oedema fluid and haemorrhage. Within the parenchyma were multifocal abscesses composed of many degenerate neutrophils and lesser numbers of macrophages, arranged around clusters of cocci. The lumen of occasional bronchioles contained detached epithelial cells, fibrin and haemorrhage. There were multifocal haemorrhages within the pleura.
Other histopathological findings included a mild periportal infiltrate of lymphocytes and plasma cells within the liver, scattered senescent glomeruli within kidney and a nematode in the ileum.
BIOCHEMISTRY
| Liver | Kidney | |
|---|---|---|
| Normal | 0.23 - 3.67 mmol/kg wet wt | 0.00 - 0.20 mmol/kg wet wt |
| Liver | 0.61 | |
| Kidney | 0.04 |
Discussion
In the absence of significant hepatopathy or evidence of copper poisoning and in the presence of an acute severe staphylococcal mastitis it is presumed that, in this case, the jaundice is due to staphylococcal toxins producing haemolysis. Staphylococci are known to produce haemolysins but that this may not be seen in vivo (Parkinson 2010). In humans, jaundice due to hyperbilirubinaemia as a result of septicaemia is associated with an increased risk of mortality (Watanakunakorn, Chan et al. 1987, Quale, Mandel et al. 1988). This phenomenon appears to be associated with lipoteichoic acid, a constituent of bacterial cells walls. Jaundice associated with S. aureus septicaemia in animals is not well documented and is a rare cause of acute jaundice.
Acknowledgements
Stuart Barber's constructive comments are appreciated.
References
- Parkinson TJ, Vermunt JJ and Malmo J (2010) Diseases of Cattle in Australasia. A comprehensive textbook New Zealand Veterinary Association Foundation for Continuing Education, Wellington, pp 384-388
- Quale JM, Mandel LJ, Bergasa NV and Straus EW (1988) Clinical Significance and Pathogenesis of Hyperbilirubinemia Associated with Staphylococcus aureus Septicemia The American Journal of Medicine 85(5):615-618
- Watanakunakorn C, Chan SJ, Demarco DG and Palmer JA (1987) Staphylococcus aureus bacteremia: Significance of hyperbilirubinemia Scandinavian Journal of Infectious Diseases 19(2):195-203