Schmallenberg Virus Infection

Shamonda-like Virus

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Changed on: 22.01.2019
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A then unknown orthobunyavirus was detected by the Friedrich Loeffler Institute (FLI Federal Research Institute for Animal Health) in Germany in November 2011 for the first time, in connection with an increased occurrence of high-fever diarrhoea infections (> 40 °C) with a general decrease in the wellbeing of the animals and decline in milk production of up to 50 % in cattle livestock from North Rhine-Westphalia. Genome analyses carried out by the FLI showed the virus had a high conformity with the Simbu serogroup (Shamonda, Akabane virus). The isolate was named “Schmallenberg virus” (Shamonda-like virus).

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A then unknown orthobunyavirus was detected by the Friedrich Loeffler Institute (FLI Federal Research Institute for Animal Health) in Germany in November 2011 for the first time, in connection with an increased occurrence of high-fever diarrhoea infections (> 40 °C) with a general decrease in the wellbeing of the animals and decline in milk production of up to 50 % in cattle livestock from North Rhine-Westphalia. Genome analyses carried out by the FLI showed the virus had a high conformity with the Simbu serogroup (Shamonda, Akabane virus). The isolate was named “Schmallenberg virus” (Shamonda-like virus).

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Transmission

The virus is transmitted similar to bluetongue disease via mosquitoes (biting midges) as vectors. The vectors for bluetongue disease are mainly found in the genus Culicoides spp. Some Culicoides spp. species are now also suspected of being vectors for the Schmallenberg virus in Europe.

Given the fact that arthropods are integral to the spreading the virus, the spread of the disease is likely to be bound to the seasonal activity of mosquitoes – similar to bluetongue that has been detected in Europe since 2006.

Symptoms

Orthobunyavirus infections are often mild, but may also cause the following symptoms:

  • higher inner body temperature (> 40 °C) 
  • reduced general wellbeing and loss of Appetite 
  • medium to severe diarrhoea 
  • significant decline in milk production (up to 50 %)

The virus can also get past the placental barrier and infect the foetus causing embryopathies, depending on when the animal is infected during pregnancy. The affects are described under Akabane disease and other related orthobunyavirus infections as follows (PFEFFER, M. 2011):
Females give birth to very weak animals that show various neural defects in the motor or sensory system (infection of the mother within the first third of pregnancy).

The birth of arthrogrypotic animals when the mother is infected during the second third of pregnancy: polymyelitis causes the loss of spinal motoneurons, which fixes the extremities in an unphysiological position. Additionally, an unphysiological position of the head (torticollis) and body position (kyphosis, scoliosis) can be observed.

Premature births and/or miscarriages

Deformed calves, lambs or kids (hydrocephalus, microencephalus).

Surveillance

The first evidence of SBV antibodies in an Austrian animal was found in mid-September 2012. Comprehensive tests that were carried out immediately showed a rapid spread of the infection.
A total of 186 miscarriages, 181 of which were in cattle, tested negative for the SBV genome via RT-qPCR between May and December 2013. However, evidence of one single SBV genome was found as part of the private examination of a goat with subsequent seroconversion in 2013.

A screening for SBV antibodies in cattle was carried out in autumn 2013 to examine the epidemiologic situation in 2013, the first year after the almost nationwide initial infection of Austrian cattle livestock in 2012, together with the blood serological monitoring for the bluetongue virus (BTV).

The blood samples were taken in line with the BTV sample taking plan from cattle that had been on Alpine pastures in summer 2013 from four regions in equal distribution. About 50 % were young animals between the ages 6 to 12 months, the second half were adult animals. This was done to reach 2 objectives:

  1. Create an overview of new infections in 2013 by examining young animals that had not been born at the time of the very first infection in 2012 and that had a high probability of being protected from infection via the colostrum and maternal antibodies of 2012.
  2. Create an overview of the seroprevalence of SBV antibodies in the group of adult animals and, thus, productive cattle one year after the almost nationwide first infection. 
  3. A very high level of antibody prevalence of 88 % could be detected in the group of adult animals in 2013, but only in 13 % of young animals. An increase in the share of SBV naïve animals in cattle livestock must be expected in the future. Evidence of the presence of only one SBV genome was found in the new infection period in 2013. This could change should the number of SBV antibody negative animals rise.

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