Equine enteric coronavirus in a Canterbury pony

EQUINE ENTERIC CORONAVIRUS

IN A CANTERBURY PONY

A case study by JoAnna Faircloth, formerly of Canterbury Equine Clinic, covers the signs, diagnosis and treatment of equine coronavirus in a gelded pony.

INTRODUCTION

Horses who present with cases of anorexia and concurrent pyrexia without mild signs of abdominal discomfort have been annually documented during the cooler months in Canterbury. These cases have largely been described as mild and self-limiting, and have typically resolved without definitive diagnoses. In recent years these cases have been the topic of discussion, and horses with these conditions are now routinely tested in the Canterbury region to screen for equine coronavirus.

CASE HISTORY

In July 2019 a 16-year-old, mixed-breed gelded pony was attended to in the field for sudden onset of inappetence and lethargy. The pony had participated in a local competition three days before presentation and a dentist had performed a routine dental check without sedation approximately two days later. There was no recent history of antimicrobial or antiinflammatory administration. The owner had not noted any signs of abdominal discomfort, and all manure in the vicinity was well formed.

CLINICAL FINDINGS

On presentation the pony was dull and standing off on his own, facing away from feed but was in ideal condition (body condition score 4/9). An examination detected a heart rate of 50 beats per minute, a temperature of 39.6˚C and very decreased gastrointestinal sounds. Other findings were unremarkable. The pony was subsequently isolated from other horses on the property and administered a 0.5mg/kg dose of flunixin IV, and blood was collected for screening.

Notable bloodwork abnormalities included profound leukopenia of 2.1 x 109/L with a left shift and lymphopenia indicating severe, acute inflammatory demand. A very mild hypomagnesaemia and hypochloraemia were also noted. All other results of the initial blood sample were unremarkable.

On being told of the bloodwork findings, the owner revealed that the pony had since stretched out as if to urinate three times, flank watched twice, and been standing close to the water trough. Haematological findings and emerging signs of abdominal discomfort placed impending colitis in the top differential diagnoses. The owner was left to administer flunixin oral paste and an electrolyte paste while monitoring the pony overnight.

Approximately 48 hours after the original presentation, the pony developed profound ataxia despite improvements in other clinical signs (heart rate of 46 beats per minute, temperature 36.9˚C). Although no diarrhoea had yet been noted, a faecal culture swab was taken and sent to SVS Laboratories for processing. An intravenous bolus of 8L Hartmann’s solution was commenced while new bloodwork was processed. A nasogastric tube was passed but no net reflux was obtained, and 250ml of lactulose was administered along with 6L of water with electrolytes. Dimethyl sulfoxide was administered intravenously (1.0g/kg every 24 hours).

The second blood sample indicated persistent leukopenia, moderately increased alkaline phosphatase and electrolyte derangements (all mildly to moderately decreased), despite adequate hydration parameters and no outward fluid losses through diarrhoea or reflux. The ataxia was suspected to have been caused by hyperammonaemia secondary to disruption of the gastrointestinal mucosal barrier, although severe or sudden electrolyte derangements can also be responsible for encephalopathic signs.

Unfortunately, hyperammonaemia could not be confirmed in this case as the test for blood ammonia level was unavailable on the weekend. The ataxia improved slowly and resolved within 30 hours of initiating fluid therapy of twice-daily IV boluses of 8L Hartmann’s solution per 400kg bodyweight and oral lactulose. The pony’s mucous membranes became injected with a brick-red appearance in the third and fourth days of treatment. The owner noted two small piles of manure that were cow pat consistency in the pony’s pen; this was the only evidence of non-formed manure during the case management.

Supportive care consisting of sucralfate (20mg/kg orally, three times a day), lactulose (100ml orally, two to three times a day), oral flunixin paste (0.5mg/kg every 12 hours) and oral electrolyte paste (15ml every 12 hours) was continued for three days, with decreasing amounts of intravenous fluids supplemented with electrolytes as needed and bolused once or twice daily as dictated by daily blood results. The pony also received metronidazole (20mg/kg orally, every 12 hours) for the first three

days of treatment, due to the original findings of profound leukopenia and development of clinical signs congruent with hyperammonaemia. Due to a lack of available isolation facilities, the pony was managed in the field.

DIAGNOSIS

The faecal polymerase chain reaction (PCR) result was positive for equine coronavirus (ECoV). Other enteric pathogens such as Salmonella spp., Clostridium difficile and C. perfringens were not detected in the sample. Clinical signs in this case can be closely compared to moderate-to-severe cases of ECoV reported overseas.

CONTINUED TREATMENT AND FOLLOW-UP

On receipt of the faecal PCR result supporting ECoV diagnosis, and

CLINICAL SIGNS IN THIS CASE CAN BE CLOSELY COMPARED

TO MODERATE-TOSEVERE CASES OF ECOV REPORTED OVERSEAS.

confirmation of an improved leukogram on the fourth day of treatment, antimicrobial therapy was discontinued. By the sixth day of treatment the pony’s vital signs and appetite had returned to normal and bloodwork findings were unremarkable. All medications were discontinued aside from sucralfate, which was continued orally every 12 hours for another seven days after resolution of clinical signs. The pony was given two months of reduced exercise before returning to ridden work, and has since competed successfully (see image above).

DISCUSSION

The most common clinical signs in documented cases of ECoV include pyrexia, inappetence and lethargy, as seen in the early stages of this case (Nemoto et al., 2014; Pusterla et al., 2018; Berryhill et al., 2019). Haematological findings often, but not always, include lymphopenia and neutropenia (Berryhill et al., 2019). Primary clinical signs may be quickly followed by enteric signs such as colic, transient diarrhoea or loose manure and, rarely, more severe clinical presentations associated with loss of barrier function

in the intestinal mucosa (Pusterla et al., 2018; Mattei, et al., 2020).

While the clinical morbidity of ECoV has been documented to reach up to 83%, mortality is low (Pusterla et al., 2018). The route of transmission for ECoV is faecal-oral (Mattei et al., 2020; Pusterla et al., 2018; Fielding et al., 2015). Most cases are mild and self-limiting, but a proportion require intensive care with supportive treatments (Goodrich et al., 2020).

ECoV is more frequently diagnosed during winter months and is thought to survive for longer in cooler temperatures (Pusterla et al., 2018). However, some cases have been documented in warmer seasons (Mattei et al., 2020). Faecal samples from two horses with anorexia, pyrexia and mildly loose manure tested positive for ECoV in Canterbury in March 2020, while ambient temperatures were still reaching 20–22˚C daily, possibly demonstrating the adaptability of this virus in New Zealand.

Antibiotics are rarely necessary or effective for the treatment of viral enteric disease. In the case described here, the suspected breakdown in gastrointestinal mucosal barrier and concurrent, profound leukopenia led to the decision to treat with metronidazole while awaiting culture results. Metronidazole has been shown to be effective in decreasing the enteric production of ammonia and has anti-inflammatory properties (Orsini and Divers, 2008).

Dimethyl sulfoxide was administered intravenously due its reported antiinflammatory and reactive oxygen radical scavenging properties that may reduce cellular damage (Sprayberry and Robinson, 2008). Lactulose (non-absorbable disaccharide) was administered in an effort to achieve ionisation and reduce the absorption of ammonia into the bloodstream (Sprayberry and Robinson, 2008). The progression of ECoV infection to necrotising enteritis, septicaemia, endotoxaemia and hyperammonaemiaassociated encephalopathy, as was suspected in this case, has been reported but is uncommon (Pusterla et al., 2018; Berryhill et al., 2019).

ECoV PCR testing is currently available in several laboratories in New Zealand. The timing of faecal swabbing for PCR is important, as faecal shedding is often delayed until 24 hours after pyrexia is evident (Nemoto et al., 2014). ECoV has been historically detected in faeces for three to 11 days after the onset of clinical signs. This has been used to guide the duration of isolation and biosecurity measures (Fielding et al., 2015).

In this case the owner was advised to maintain the pony’s isolation from other equids and continue biosecurity measures for 21 days after the resolution of clinical signs. However, in recent studies, beta coronavirus has been detected by PCR in faeces of asymptomatic carriers up to 25 days after initial detection during outbreak surveillance testing (Goodrich et al., 2020). The role of asymptomatic carriers in perpetuating outbreaks of ECoV, and the ability of humans to act as fomites in transfers of the virus may have been previously underestimated and deserves consideration when approaching cases of suspected ECoV.

As with all infectious and contagious diseases, biosecurity recommendations should be aimed at reducing the spread of an agent throughout the affected premises and on to other properties. Current recommendations pertinent to the control of ECoV transmission emphasise the need to: use footbaths and personal protective equipment; clean with disinfectants any shared facilities and transportation vehicles; allocate equipment for the collection and disposal of manure and bedding from cases; and, ideally, test other equids on the property to identify asymptomatic shedders (Pusterla et al., 2018; Goodrich et al., 2020).

Equine coronavirus should be included as a differential for cases of anorexia, lethargy and pyrexia in adult horses in New Zealand, as isolated cases or as clusters of cases. Most cases resolve quickly with minimal supportive care, but infected individuals can continue to shed the virus in faeces for several weeks after clinical resolution. Testing suspected cases via faecal swabs could provide more insights into the prevalence of this disease in New Zealand and help to reduce the occurrence of outbreaks.

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Orsini JA, Divers TJ. Equine Emergencies: Treatment and Procedures. 3rd Edtn. P 246. Saunders, St Louis, Missouri, USA. 2008

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ACKNOWLEDGEMENTS The author would like to acknowledge Harriet Bell and Shaan Mocke, who helped with treating the pony. This article was originally published in the June 2020 issue of the Equine Veterinary Practitioner and has been edited for publication in VetScript. Access to all Equine Veterinary Practitioner articles can be obtained by joining the New Zealand Equine Veterinary Association at www.nzva.org.nz/members/

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