E-Coli in pen feeding trial weaner

A weaner in a phosphorus pen feeding trial herd was noticed to be slow and swaying at a walk during weekly weighing of the animal group.  The following day, the animal was off food, tucked up and depressed.  A fever, together with nasal discharge and saliva drooling from the mouth were noted, with no visible damage to the nose, mouth or teeth.  The breath smelled strongly of acetone, which is an indicator in ruminants of a negative energy crisis, and consequent formation of emergency energy supplies in the form of ketone bodies.  The animal was treated symptomatically with electrolyte and fluid replacement and an anti-inflammatory injection; blood, throat and nasal swabs and faeces were submitted to Berrimah Veterinary Laboratory.  However, the heifer was found dead the following morning.

On post mortem there was a strong smell of ketones throughout the carcass; ketoacidosis was suspected.  One very small section of small intestine (< 5cm long) was severely inflamed (enteritis) without blockage or visible perforation.  Another section of intestine contained what appeared to be a hair faecolith (also known as a hair concretion – a hard solid mass of hair).  The kidneys and liver were friable to handle, tending to turn “mushy” when sections were cut in preparation for laboratory submission.

Laboratory examination of submitted tissues showed extensive necrosis (tissue death) and ulceration through the range of gastro-intestinal tissues submitted, with abundant bacteria in the walls of the gut tissues.  Interestingly, lesions that were seen under the microscope were not limited to the section of small intestine that was seen to be inflamed with the naked eye. Septic thrombi (infected clots), indicative of widespread infection, were found in the spleen and kidney.  The findings are consistent with severe bacterial enteritis (infection and subsequent changes to absorption through the intestinal wall) with spread of the causative organism throughout the body.

The clinical signs associated with this enteritis are consistent with infection by a subset of E.coli bacteria which produce Shiga toxins, causing severe illness in affected animals.  Cattle are a recognised carrier of this bacteria, which is zoonotic, and a cause of haemorrhagic colitis (bloody diarrhoea) in humans.  E.coli is capable of causing different disease syndromes in cattle, based on the specific toxins and virulence of the infecting strain.  Enterotoxigenic strains typically cause disease in neonatal calves, while enterohaemorrhagic strains are associated with disease in older animals, as in this case.  Disease tends to occur in isolated cases rather than herd outbreaks, as cattle carry the infective organism in the gastro-intestinal flora; a primary cause for the development of overwhelming infection was not identified in this case. No other animals in the pen trial were affected.

Tests on the blood confirmed ketoacidosis, which is likely secondary to the gastro-intestinal disease.  A negative energy state in which ketone bodies are elevated can occur when carbohydrate reserves are depleted; in this case, this is a secondary effect following inappetance and depression. Changes in the liver were consistent with hepatic lipidosis, and are secondary changes consistent with ketoacidosis and severe debilitation.

These findings are interesting, as they highlight the fact that the clinical signs that can be seen (and in this case, smelled), may not in fact be the primary cause of disease or death. The results of laboratory testing also serve to emphasize the need to submit a range of tissue samples in order to reach a diagnosis; in this case, microscopic examination of the gut samples demonstrated severe disease that was not visible to the naked eye and would otherwise be missed.