COVID-19 and animal contagion: Part Two …beware of the bovine coronavirus infections

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By Dr Tony Monda

THE need to fight animal diseases at a global level led to the creation of the Office International des Epizooties (OIE), through an international Agreement signed on January 25 1924.  

In May 2003, the Office became the World Organisation for Animal Health but kept its historical acronym OIE. 

The OIE is an inter-governmental organisation responsible for improving animal health worldwide.  It is recognised by the World Trade Organization (WTO) as a reference organisation for standards relating to animal health and zoonoses.

As of 2018, the OIE had a total of 182 member-countries, regional and sub-regional offices on every continent and maintains permanent relations with nearly 75 other international and regional organisations.

The Agreement on the Application of Sanitary and Phytosanitary Measures (SPS Agreement) encourages the members of the WTO to base their sanitary measures on international standards, guidelines and recommendations.

In cattle, bovine coronavirus infections are associated with three distinct clinical syndromes:  calf diarrhoea, winter dysentery (hemorrhagic diarrhoea) in adult cattle and respiratory infections in cattle of various ages, including the bovine respiratory disease complex (shipping fever) in feedlot cattle. 

Coronaviruses were first reported in the US in 1973, as a cause of diarrhoea in calves; since then, they have been recognised worldwide in association with the three clinical syndromes. 

The economic impact of respiratory disease and calf diarrhoea cannot be underestimated.

Although many coronaviruses have restricted host ranges, beta coronaviruses such as bovine and SARS coronaviruses can infect other animal species – including wildlife. Bovine coronavirus is closely related to the human coronavirus OC43 that causes the common cold; indeed, OC43 has been proposed to represent prior zoonotic transmission of bovine coronavirus. 

Bovine coronavirus has also been shown to infect dogs sub-clinically and to infect turkey poults, leading to fecal virus shedding, diarrhea, seroconversion and transmission to contact controls. 

Genetically and/or antigenic related bovine coronavirus variants have been isolated from dogs with respiratory disease, humans with diarrhoea, and captive or wild ruminants with intestinal disease similar to winter dysentery of cattle and has also been linked to enteric disease in South American camelids.  

Interestingly, the human enteric coronavirus and wild ruminant coronaviruses both infected and caused diarrhoea in experimentally exposed gnotobiotic calves, and the inoculated calves were subsequently immune to infection by bovine coronavirus.

Despite the different disease syndromes and apparent interspecies transmission of bovine coronavirus and its variants, only a single serotype of bovine coronavirus is recognised; there is little sequence diversity between the wild ruminant coronaviruses and coronaviruses associated with the different disease syndromes in cattle. 

Coronavirus-induced diarrhoea commonly occurs in calves under three weeks after the decline of passively acquired antibodies, but disease can occur in calves up to three months of age.  The severity of diarrhea and dehydration depends on the infecting dose as well as the age and immune status of the calf.  Calf coronavirus diarrhoea is often seasonal, being more common in winter, in part, because of the increased stability of the virus in the cold.

Bovine coronavirus has also been implicated as a cause of winter dysentery, a sporadic, acute enteric disease of adult cattle worldwide that is especially prevalent during winter months.  Winter dysentery is characterised by explosive, often bloody diarrhoea.  

This is accompanied by decreased milk production, depression, anorexia and recurrent respiratory symptoms.  Morbidity rates range from 20 to 100 percent in affected herds, but mortality rates are usually low (one to two percent). 

The anorexia and depression in dairy cattle with winter dysentery may explain the rapid and sometimes prolonged decrease in milk production; while the cause of the acute and often voluminous bloody diarrhea in some cattle is unexplained.

A similar winter dysentery syndrome, associated with bovine coronaviruses variants, occurs in captive and wild ruminants. This suggests that sharing common grazing areas with cattle could be a reservoir for coronavirus strains transmissible to cattle, or vice versa. 

Bovine coronavirus also causes mild respiratory disease (coughing, rhinitis) or pneumonia in two-six-month-old calves.  An epidemiologic study of calves from birth to 20 weeks of age confirmed both fecal and nasal shedding of coronavirus, with diarrhoea prominent on initial infection.  

The calves subsequently shed virus intermittently via the respiratory route, with or without signs of disease, suggesting that long-term mucosal immunity in the upper respiratory tract is ineffective in mediating virus clearance. 

As a consequence, coronavirus may recycle among cattle of all ages and regardless of their immune status, with sporadic nasal or fecal shedding from individual animals.  Alternatively, new virus strains may be introduced when cattle from different sources are mixed, or from cohabiting wild ruminants.

Since 1993, bovine coronavirus has been singled out as a progressive cause of the bovine respiratory disease (shipping fever) complex. 

Both respiratory and enteric shedding of bovine coronavirus are common in affected feedlot cattle, peaking shortly after arrival at feedlots. 

In fact, since its discovery, bovine coronavirus has frequently been identified in the lungs of feedlot cattle that died with bovine respiratory disease complex.  

Most feedlot cattle also seroconvert to bovine coronavirus within three weeks of arrival.  

Importantly, studies suggest that cattle arriving at feedlots with high serum titers of bovine coronavirus antibody were less likely to shed virus or to develop shipping fever. 

This observation suggests a role for serum antibodies in protection, or as an indicator of recent infection and active immunity.

Dr Tony Monda holds a PhD and DBA (Doctorate in Business Administration) He is a writer, lecturer and a specialist Post-Colonial Scholar. He is currently carrying out veterinary epidemiology research in Zimbabwe: tonym.MONDA@gmail.com

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