Blue-tongue in Sheep

Blue tongue virus is a member of the genus Orbivirus and family Reoviridae. It is transmitted by Culicoides midges. In Africa, it is transmitted by Culicoides imicola. It causes disease in ruminants, with sheep being the most susceptible.  Goats are affected occasionally, and cattle rarely. In sheep, it may result in significant morbidity and variable mortality. Symptoms include erosions and ulceration on mucous membranes, lameness as a result of coronary band inflammation and necrosis, and dyspnea. Affected sheep may loose their wool after infection, and occasionally they may slough their hooves.  

Wild ruminants are infected by the virus, but do not show symptoms. In Africa, some large carnivores have antibodies to bluetongue. The virus was first recognised in South Africa and has since been found in Africa, Europe, the Middle East, Australia, the South Pacific, North and South America and parts of Asia. Geographic distribution is limited by the distribution of the Culicoides midges. Twenty four serotypes have been identified world-wide. Serotypes identified by the Onderstepoort Veterinary Institute in recent years are as follows:  
a). 2008 and 2009 =  1;3;4;6;8;16;18;24
b). 2009 and 2010 =  1;3;4;6

The main vectors are various species of biting Culicoides midges. Ticks or sheep keds may be mechanical vectors and the disease may be spread on veterinary equipment. Cattle are the preferred hosts of many Culicoides species. They develop a prolonged viraemia and often amplify the virus, therefore playing a major role in transmission of the virus.
Infected animals remain infectious to the insect vector for several weeks. The incubation period in sheep is between 5 and 10 days. Cattle show viraemia at 4 days post-infection. They rarely develop symptoms.

Clinical signs seen in sheep include fever, depression, salivation, dyspnea and panting. The lips, ears  and eyelids may be swollen and hyperaemic. Dyspnea and panting may be seen. The tongue is often very swollen, may be cyanotic and protrude from the mouth. The mouth often has erosions and ulcerations on mucous membranes. This may be sufficiently severe to lead to necrosis and sloughing of mucous membranes. Hooves are often painful and the coronary band hyperaemic, leading to lameness. Such animals should not be moved long distances, as this may contribute to sloughing of hooves. Abortions may occur, or so-called dummy lambs may be born to affected ewes. Other signs may be seen, such as torticollis, pneumonia and conjunctivitis.  Some sheep may shed their wool three to four weeks after recovery. Severity of disease and death rate is influenced by the strain of virus.

At post mortem, the following signs may be seen:
Oedema of face and ears
Crusty nasal exudate
Hyperaemia of coronary bands
Petechia, erosions and ulcers on  tongue and dental pad and rest of oral cavity.
Necrotic or cyanotic oral cavity
Trachea may be hyperaemic with foam.
Hydrothorax  is seen occasionally
The heart may have petechiae, ecchymoses and necrotic foci.
The reticulum and omasum may show hyperaemia and erosions.
Characteristically haemorrhage is seen at the base of the pulmonary artery.
Oedema may be seen in intermuscular fascial planes and skeletal muscles may have focal haemorrhages or necrosis.

Cattle rarely show symptoms, although clinical signs have been seen and have included nasal discharge, swelling of head and neck, conjunctivitis, swelling and ulceration of the mouth, swollen teats, lethargy and salivation.

Clinical diagnosis is based on symptoms and insect activity. In cattle the disease must be confirmed by laboratory testing. Differential diagnoses include vesicular stomatitis, foot-and-mouth disease, rinderpest, photosensitivity due to plant poisoning, malignant catarrhal fever, infectious bovine rhinotracheitis, bovine virus diarrhoea, foot rot, oestrus ovis infection.

Laboratory diagnosis includes PCR. This allows for rapid diagnosis and can identify the serogroup and serotype.  Several EDTA blood samples should be collected from several live febrile animals as early in the course of disease as possible.  
Serology may also be used for diagnosis. Competitive ELISA identifies IgG antibodies and will be be positive from 7 to 14 days onwards. These antibodies are persistent. Complement fixation test is positive as early as 1 to 2 days after symptoms appear and measures IgM antibodies. These antibodies start to disappear by 7 days. (Personal communication: Dr. Alison Lubisi).
Serum neutralisation tests will identify the serotype involved.

Control is based on control of the insect vector. Peak populations of Culicoides occur in late summer and autumn.  Synthetic pyrethroids or organophosphates are effective against Culicoides. Housing animals from late afternoon to early morning reduces the risk of infection. Animals should also be kept away from low-lying areas near open water.
Although the virus does not affect horses, Culicoides will feed on them and breed in manure piles, so this should be considered in control of an outbreak.
A freeze dried polyvalent live attenuated  vaccine is available in South Africa.  The vaccine is given as a series of three separate injections with different serotypes of bluetongue virus in each bottle. The vaccine will only stimulate immunity to all serotypes after a number of annual innoculations.
(See vaccine insert for full instructions. )

Nitrate Poisoning in Livestock

Significant Stock Losses caused by drought feeding.

Last week two farms suffered significant livestock losses. Deaths were caused by drought feeding of millet silage in one case and millet hay in the other. Approximately 10% of cattle died apparently overnight after being fed the millet products.
Laboratory tests confirmed that the cause was nitrate/nitrite poisoning in both cases.
Nitrates in fodder are converted to nitrites in the rumen. Nitrates in stored fodder can also be converted to nitrites when plant materials heat up or are attacked by bacteria or fungi. Normal levels of nitrite are converted to ammonia in the rumen by bacterial action. However excessive levels of nitrate or nitrite are poisonous.

Certain soil and environmental conditions facilitate nitrate uptake and accumulation by plants, eg.:

Use of nitrogen containing fertilizers
Low soil sulfur and molybdenum
Areas where stock have congregated and urinated and defecated (stock yards)
Drought
Cloudy or cold weather
Herbicide application, esp 2.4-D
Wilting
Plant species
Stage of maturity of plant
Part of plant

Young plants have higher nitrate concentrations and most plant nitrate is located in the bottom third of the stalk.
Hays made from cereal crops, especially those grown under drought conditions and cut while "sappy" can develop toxic nitrite levels when they heat up.
Hays contain almost the same level of nitrate as the parent crop. Silage normally contains significantly less due to the fermentation process.

Sheep are less susceptible to nitrite poisoning than cattle, but can also be affected.
Stressed animals in poor health or poor condition are more susceptible and hunggry animals are more likely to eat large amounts.

The risk of poisoning can be reduced by
Having feeds and forages analysed for nitrate levels.
Gradually introducing any new feeds by feeding small amounts frequently and diluting with known safe feeds.
Cattle can become acclimatized to relatively high levels of nitrate this way.
Frequent observation of stock, especially when changing food or grazing.
Don't overstock.
Prevent hungry stock from grazing on high risk fodder.
Do not graze high nitrate pastures for 7 days after rainfall, cloudy weather, frosts or high temperatures causing wilting.
Do not harvest pastures under these conditions either.
Graze these pastures during sunny afternoons above 15 degrees Celsius and remove livestock at night.
Never feed mouldy hay.
Harvest crops close to maturity and raise the cutter head selectively to avoid the bottom part of the stalk.

Keep in mind that rapidly growing weeds after rainfall may also contain excessive levels of nitrate as well as cyanide (prussic acid).