{"id":1317711,"date":"2022-07-01T12:00:40","date_gmt":"2022-07-01T10:00:40","guid":{"rendered":"https:\/\/staging.laboklin.com\/int\/en\/?p=1317711"},"modified":"2025-07-29T11:29:10","modified_gmt":"2025-07-29T09:29:10","slug":"equine-parvovirus-an-update-on-the-aetiology-of-acute-serum-hepatitis","status":"publish","type":"post","link":"https:\/\/laboklin.com\/en\/equine-parvovirus-an-update-on-the-aetiology-of-acute-serum-hepatitis\/","title":{"rendered":"Equine parvovirus \u2013 an update on the aetiology of acute serum hepatitis"},"content":{"rendered":"

[vc_row][vc_column width=”2\/3″][vc_column_text]Hepatic diseases are quite common in equids. In addition to poisonous plants, toxins, parasitoses and neoplasms, they can also be caused by bacterial or viral infectious agents. Many aetiologies have already been studied sufficiently, but the cause of the disease known as Theiler\u2019s disease or serum hepatitis has remained largely unexplained for over a century. Since 2012, research has focused on the following four viruses as possible causes of hepatopathies: equine hepacivirus (EqHV), equine pegivirus 1 (EPgV), Theiler\u2019s disease-associated virus (TDAV) and equine parvovirus-hepatitis virus (EqPV-H). EqHV<\/strong>, a flavivirus that was first detected in equine serum in 2012, can cause both an acute and a chronic persistent course of infection. It is not yet known whether infection with EqHV, which is thought to show liver tropism, always leads to clinical signs.<\/p>\n

So far, no affinity to hepatic tissue has been confirmed for EPgV<\/strong>, but performance losses have been described. TDAV<\/strong> was given its name by mistake after an outbreak in 2013 with signs of acute hepatitis. Once it was detected that TDAV did not cause the outbreak but only occurred as a co-infection together with equine parvovirus, it was renamed as equine pegivirus 2.<\/p>\n

The equine parvovirus hepatitis virus (EqPV-H)<\/strong>, which, thanks to Thomas Divers\u2019 team, has now been identified as the cause of Theiler\u2019s disease, will be discussed in more detail below.<\/p>\n

EqPV-H is a single-stranded, non-enveloped DNA virus that belongs to the genus Copiparvovirus. The highest viral load of EqPV-H is found in the liver, which indicates hepatotropism.<\/p>\n

So far, two different modes of transmission<\/strong> are assumed:
\nOne is the administration of products made from horse serum containing equine parvovirus. These include tetanus antitoxin, botulinum antitoxin, stem cell preparations and equine plasma products in general.<\/p>\n

On the other hand, EqPV-H outbreaks also occur in horses that have not received a biological preparation in the past. In this case, transmission between horses or spread by insects is assumed, but this is currently still being researched.<\/p>\n

Clinical signs <\/strong>of EqPV-H infection occur about 4 \u2013 10 weeks after the administration of a biological product infected with the virus. The course of the disease ranges from asymptomatic to fulminant liver failure. Acute hepatitis is characterised by lethargic behaviour with accompanying anorexia and icteric mucous membranes (Figure 1). Some of the infected horses show neurological signs, such as manic behaviour, head pressing and also ataxic movement, as a result of hepatic encephalopathy. Moreover, colic, recumbency (Figure 2) and death within 72 hours have been described.<\/p>\n

In addition to a detailed clinical history and a thorough general examination, the diagnostic work-up<\/strong> of patients with liver disease also includes a blood test.<\/p>\n

The following laboratory parameters<\/strong> may indicate acute liver dysfunction in infected horses:<\/p>\n

The activity of the liver-specific enzymes gamma-glutamyl transferase (\u03b3-GT) and glutamate dehydrogenase (GLDH) is usually increased in serum. However, the extent of the increase does not correlate with the functional abnormalities. While \u03b3-GT is mainly located in the membrane structures of the bile duct system, GLDH is bound to the mitochondria of the hepatocytes. Both enzymes have a half-life of about 3 days. Alkaline phosphatase (AP) is found in the mitochondria of many organs, so it should not be interpreted as a liver-specific parameter. Aspartate aminotransferase is also not liver-specific as it can also be found in muscle cells and its activity increases with muscle damage. In addition, horses may also have increased levels of bile acid. Hepatocytes synthesise bile acids from cholesterol. They are continuously secreted into the duodenum where they help to digest fats. In hepatopathy, bile acids accumulate and their increase can be measured in the blood. Bile acid values above 12 \u00b5mol\/l are considered an early diagnostic marker for functional liver failure. Neurotoxic ammonia, which is produced during protein digestion, also increases in the blood in case of liver dysfunction (resulting in hepatoencephalic syndrome). However, a laboratory-diagnostic determination of the ammonia level is only possible if the sample material reaches the laboratory quickly (within 30 minutes), which makes it difficult to use in practice. If hyperbilirubinaemia is present, it is advisable to classify it more precisely as conjugated and unconjugated bilirubin in order to narrow down the cause of jaundice (pre-hepatic, hepatic, post-hepatic). Albumin is low in about 18% of horses with liver failure, whereas globulins are elevated in about 64% of horses. Table 1 summarises the relevant laboratory parameters for the work-up of patients with liver disease.<\/p>\n

An ultrasound scan of the liver from both sides of the body and a liver biopsy complete the diagnosis of hepatic disease.[\/vc_column_text][\/vc_column][vc_column width=”1\/3″][vc_column_text]<\/p>\n\n\t\t\t