Rift Valley Fever
By Dr Mackie Hobson BSc(Agric),BVSc

Tuesday, 12th August 2014

Should I vaccinate my Angora Goats against Rift Valley Fever (RVF)?

Dr Mackie Hobson (SAMGA Vet)

The question I regularly get asked is: ‘Should I vaccinate my Angora goats against Rift Valley Fever?’

One thing is for sure is that we will get an outbreak of RVF again in the karoo……….the unknown part is just when? One hopes not again on our watch!

Due to the extent of the outbreak during 2010-11 it is very likely that most of our Angora goats would have been naturally exposed to the virus and so became naturally ‘vaccinated’. Over the following years however, our ‘vaccinated’ Angora ewe flocks would have been largely replaced by maiden ewes joining each year and the older ewes being culled.  As the proportion of immune goats declines (now 6 years after the last outbreak) in our flocks, the possibility of an outbreak will increase if the rainfall conditions trigger an explosion of vector numbers in late summer.

We can learn from the past outbreaks to try to help us look into the future.

The three major RVF epidemics in the Karoo (1950–1951, 1973–1976 and 2010–2011) can be identified in the graph below. (Nicolaas J. Pienaar and Peter Thompson of Department of Production Animal Studies, University of Pretoria and Directorate Animal Health,Department of Agriculture, South Africa)

rvf1.png

From the graph, it also becomes evident that after a large epidemic, such as the ones experienced during 1950–1951 and 1973–1976, outbreaks continue to occur for several years after the epidemic when conditions favoured the vectors (mosquitoes).

This would suggest that we need to aware that it is still possible to have more outbreaks over the next few years if we get excessively high rainfall patterns over the later summer months.

Studies in Africa indicated that the RVF virus activity was more likely after cumulative rainfall, rather than heavy precipitation over a short period.

Another aspect of the outbreaks which we can gather is that:

  • Most outbreaks occurred from January onwards,
  • Where outbreaks occurred before January, this often followed outbreaks late during the previous season.

 The number of outbreaks (1951 to 2011) are plotted in the graph below from studies by J. Pienaar and P. Thompson

rvf2.png

From this data it is clear than the Angora farming areas of the Eastern Cape are at high risk of future outbreaks of RVF

RECOMMENDATION

We should be vaccinating our Angora ewe flocks.

 If, as a farmer, you are reluctant to vaccinate your Angora goats then I would suggest you at least vaccinate just your maiden ewes as a once off each year (with the live attenuated RVF vaccine) as they enter your ewe flock and again if above average rainfall occurs. Repeating the vaccine will likely stimulate a better immune response than a single vaccination. Vaccinating at the time of an outbreak with the live RVF vaccine is NOT recommended and may exasperate the situation as a reversion to virulence is a possibility as may have occurred in 2010-11. Only a ‘dead’ vaccine should be used during an outbreak.

 

Angora goats can be vaccinated at any age except kids from vaccinated ewes should not be vaccinated before they are six months old - maternal antibodies may block the vaccine response. Pregnant Angora ewes should not be inoculated with this vaccine as it can cause abortion or foetal malformation. The dose is 1 ml subcutaneously (under the skin)

What happens to the virus between outbreaks?

Several possibilities exist:

  1. Trans-ovarial transmission in certain mosquitoes may occur (Aedes spp) (Linthicum et al. 1985; Pepin et al. 2010). The eggs lay dormant on the edges of pans and hatch when conditions of high rainfall occur. However, the three major epidemics were associated with a different RVF virus lineage (Grobbelaar et al. 2011), indicating that long-term survival of the virus in dormant mosquito eggs is unlikely to have been the main mechanism for virus survival between these epidemics.
  2. Another possibility is the low-level circulation of the virus between animals and mosquitoes, without resulting in clinical signs or severe outbreaks (Pepin et al. 2010).

Serological evidence of low-level circulation of RVF virus in African buffalo has been found in the Kruger National Park and antibodies have been found in several wildlife species.

  1. The transmission of vectors from possible endemic areas, either within South Africa or in neighbouring countries, is also a potential mechanism for initiation of an outbreak

Clinical signs of RVF

On the positive side, Angora goats are thought to be slightly less severely affected than sheep. The disease can be classified into 4 grades depending on severity.

  1. Hyperacute RVF:
  • Up to 100% ewes may abort
  • 80-100% kids under 10 days old may die
  • Kid deaths occur within 12 hours after the fever reaction starts, others may survive longer and die within 12-24 hrs.

 

  1. Acute RVF:
  • 10-60% of kids older than 2 weeks may die.
  • Fever, increased respiratory rate, nasal and eye discharge may occur.
  • Abdominal pain and reluctant to move.
  • The goat often develop a haemorrhagic diarrhoea
  • Deaths 24-48 hours after start fever reaction
  • Signs of jaundice occur in surviving goats

 

  1. Subacute RVF
  • More adult goats
  • Fever reaction (40.5-42C) lasting 1-5 days
  • Abortion
  • Nasal and eye discharge
  • Diarrhoea
  • Weak, lack co-ordination.
  • Jaundice
  • Abortions
  • Death rate (5-20%)

 

  1. Undetected RVF
  • Older or resistant goats
  • Fever and decreased appetite
  • Some abortions

 Post Mortem examination:

  • Haemorrhages occur throughout the carcass, notable on the intestine.
  • Often severe haemorrhagic gastroenteritis
  • Generalised lymphadenopathy (enlarged lymph nodes)
  • Lung oedema and emphysema
  • Haemorrhage from the nose may occur.
  • Liver enlargement, swollen with rounded edges and necrosis.
  • Liver congestion, later a bronze to yellow colour.

rvf3.jpgrvf4.jpg

PHOTO: Prof Coetzer                                PHOTO:  Glyn Davies

 

  • The necrotic changes to the liver induce jaundice .
  • Intestine haemorrhages on the serosal surface and mucosal haemorrhages in the abomasum

rvf5.jpgrvf6.png

Photos Prof Coetzer (University Pretoria)

 

  • Haemorrhages especially on the surfaces of the body cavities, and on the heart, gall bladder, kidneys, bladder and other organs. Bloodstained ascitic fluid may occur..
  • Subcapsular haemorrhages of the spleen
  • The lungs may be congested with oedema and emphysema and subpleural haemorrhages are commonly found. The heart will show subepicardial and endocardial haemorrhages. There is a generalised lymphadenopathy involving the superficial and visceral lymph nodes. These are oedematous with petechial haemorrhages.

SOURCE/REFERENCES

Nicolaas J. Pienaar. Department of Production ,Animal Studies, University of Pretoria, South Africa

,Peter N. Thompson:Directorate Animal Health,Department of Agriculture,Forestry and Fisheries,South Africa

Temporal and spatial history of Rift Valley fever in South Africa: 1950 to 2011

 

Recognizing Rift Valley Fever

  1. Glyn Davies,Consultant, EMPRES/Infectious Diseases Group, FAO, Rome

Vincent Martin,Animal Health Officer,EMPRES/Infectious Diseases Group,FAO, Rome

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