16 May 2016
Louise Silk explains the importance of raising awareness among sheep farmers of some conditions that may not be severe enough to present observable symptoms.
Louise Silk
Job Title
flock-of-sheep
A subclinical disease has no clinical manifestations and usually occurs either during the early stages of disease or when a mild form of the disease is present.
As a result, a subclinical disease may be detected using clinicopathological tests, but not by clinical examination.
Subclinical disease is important in sheep as it accounts for a significant proportion of production loss in a flock. Causes range from specific diseases, such as maedi-visna (MV), Johne’s disease and Jaagsiekte, to parasitic infections and nutritional deficiencies. In these cases, clinical disease may be apparent in some individuals in the flock, but a degree of reduced performance will certainly exist.
This article does not profess to be a comprehensive list of all the sheep diseases that may present subclinically; the hope is it will provoke readers to consider not only those diseases presented by the farmer as clinical problems, but also those that may lurk.
Diseases such as MV, Johne’s disease and Jaagsiekte are known as “iceberg diseases” because, typically, a small number of clinical cases exist in a flock, but a much larger proportion of the flock may be subclinically affected.
Johne’s disease is caused by infection with Mycobacterium avium subspecies paratuberculosis. Infection can occur at any life stage via the faeco-oral route, but clinical disease is most likely in those infected very early in life via faecal contamination of the dam’s udder (Figure 1).
Following initial infection, the onset of disease is insidious and the disease is probably widespread in the flock before clinical signs become apparent. Despite showing no clinical signs, the large numbers of subclinically affected animals shed small quantities of bacteria into the environment in faeces and milk.
The rate of disease progression varies depending on the animal’s immune system and the bacterium strain.
Johne’s disease affects the terminal ileum and associated lymph nodes, resulting in malabsorption and protein loss. Despite infection occurring, in many cases, shortly after birth, clinical disease is not usually seen until sheep reach two years to five years old. Even when clinical disease does occur, the symptoms of chronic weight loss or poor body condition, and reduced fleece quality, may go unnoticed for a period of time prior to Johne’s disease being diagnosed. Indeed, in many cases, affected ewes may be culled out of the flock, with no diagnosis made.
As a result, the incidence of this disease in UK flocks is largely unknown and probably underestimated. A small-scale fallen stock survey in 2012 showed an incidence of about 5.6% (Lovatt and Strugnell, 2012).
The effect of this disease on flock productivity is considerable, due to increased culling, and is most significant in flocks that breed their own replacements. Difficulties with diagnosis due to high-test specificity, but low sensitivity in the subclinical phase, make control of this disease difficult. It is also known some animals may pass the bacteria through their gut, but will never succumb to disease, again making diagnosis of subclinical cases a challenge.
Control, therefore, centres on reducing the risk of infection by reducing stocking rates, improving management and ensuring flock immunity is strong through good nutrition.
An aggressive culling policy may help to reduce environmental contamination, as well as remove the offspring of suspect cases. A vaccination is available, but it does not prevent infection, so decisions as to its use must be taken on a case-by-case basis.
Ovine pulmonary adenocarcinoma (OPA) is characterised by contagious tumours of the lungs and is caused by the betaretrovirus, Jaagsiekte sheep retrovirus (JSRV).
The virus infects alveolar cells (Clara cells and type II pneumocytes) and induces neoplastic growth (adenocarcinoma) that replaces normal lung tissue, impairs function and causes the production of excessive quantities of white foaming fluid.
Transmission is predominantly by aerosol, but may also be via colostrum and milk. The incubation period following natural infection can be many months or years. As a result, clinical disease is usually seen in sheep aged three years to four years.
Initial signs include a loss of body condition and some exercise intolerance when gathering. These symptoms may go unnoticed, but the disease progresses to mouth breathing/panting at rest, with frothy fluid flowing freely from both nostrils when the head is lowered – the so-called “wheelbarrow test”.
Unfortunately, diagnosis in the subclinical phase of disease is difficult, due to the low sensitivity of available tests. These tests (PCR blood test) can, however, screen for the presence of infection in a flock, but not to confirm a flock is OPA-free.
Subclinically affected individuals will spread this disease in the flock. Control focuses on regular flock inspection and the removal of suspicious individuals (including not retaining their offspring for breeding), as well as reducing close contact by management changes.
Many flocks will have a culling rate of 5%, or more, as a result of this disease circulating, often unrecognised, in their flocks.
The most common presentation of MV in the UK is as the chronic respiratory disease, maedi (ovine progressive pneumonia).
MV is caused by a lentivirus transmitted predominantly in the milk or colostrum from mother to offspring. This is a significant disease, as it is often identified clinically in a flock when the seroprevalence is about 60%.
Symptoms include progressive exercise intolerance and weight loss, often with an indurative mastitis, causing a flabby udder with diffuse hardening and decreased milk production. As a result, perinatal lamb mortality and poor lamb growth rates may increase in an infected flock, causing significant production loss.
Symptoms rarely become detectable until animals are older than three years, with most commercial ewes being culled prior to the onset of clinical disease. As a result, this disease is more significant in pedigree flocks.
Concurrent infection with diseases, such as Jaagsiekte and pneumonia, are common. Infection can be confirmed using an ELISA blood test and this forms the basis of the MV accreditation scheme. The neurological manifestation of MV is rare in the UK.
Chronic mastitis is a major cause of culling and economic loss in commercial sheep flocks, and develops as a consequence of incomplete resolution of acute mastitis. It is characterised by abscesses in the mammary parenchyma, causing enlargement of the gland, thickened teats and reduced lactation, resulting in poor lamb growth rates.
This condition largely goes unnoticed for most of the year, unless the shepherd is actively checking for it, but can result in significant problems (hungry lambs) at lambing time if affected ewes are not culled prior to mating.
Control should focus on rapid identification and effective treatment of acute mastitis during lactation, as well as identification and removal of chronic cases prebreeding.
Significant deficiencies in the trace elements cobalt, copper, selenium, vitamin E and iodine can cause severe disease in sheep. However, a subclinical disease is seen when deficiencies are more marginal.
Cobalt is a constituent of vitamin B12, which is manufactured by rumen microbes. Cobalt deficiency occurs when low soil cobalt concentrations exist, but the situation may be further complicated by parasitic gastroenteritis, which causes diarrhoea and, therefore, interferes with the absorption of vitamin B12.
Subclinical disease, as a result of low level or marginal deficiencies, is seen as poor daily live weight gains in lambs in late summer and autumn, despite adequate nutrition. These animals also tend to exhibit non-specific immunosuppression with increased susceptibility to clostridial diseases and Pasteurella, sometimes despite vaccination.
A general reduction in body condition scores may be seen in adults, with the potential for associated reduced fertility and poor mothering abilities.
Copper deficiency may be seen where sheep are grazing pastures low in copper, but more often the pastures are high in elements such as iron, molybdenum and sulphur. These elements act synergistically to bind with copper, reducing its bioavailability.
The clinical manifestation of copper deficiency is swayback in lambs, but subclinical disease will be present where levels are more marginal. These may include poor weight gains, poor fleece and increased susceptibility to bacterial infections.
Certain soils are more likely to be deficient in selenium – and a deficiency in the soil leads to pasture and crop deficiencies.
Vitamin E is found in high concentrations in green crops, but levels fall rapidly during a drought. Certain root crops are known to be low in both vitamin E and selenium.
The clinical manifestation of selenium/vitamin E deficiency is white muscle disease in rapidly growing young lambs. Marginal deficiencies may contribute to poor lamb growth rates, as well as early embryonic death and reduced implantation rates in ewes.
Iodine deficiency may be seen in grazing ewes at pasture, as well as ewes fed brassica crops.
Clinically, this disease is identified by the birth of weak lambs with significantly enlarged thyroid glands (goitre). Subclinically, poor embryo survival and increased perinatal mortality will exist in the flock.
Diagnosis of subclinical trace element deficiencies can be complicated and requires a multi-pronged approach, which includes blood testing certain groups of animals in the flock at specific times of the year and monitoring trace element levels in the pastures. In many situations, however, if marginal deficiencies are suspected, a supplement trial may be the most useful way forward.
Supplementary trace elements can be delivered to sheep in many ways to correct deficiencies. These range from bolusing to pasture dressing and it is important to select the most appropriate mode of delivery for the farm.
Gastrointestinal (GI) nematodes cause significant damage to the mucosal lining of the gut, predominantly in growing lambs. This damage reduces the capacity of the gut to absorb nutrients, resulting in reduced daily live weight gains.
Many flocks do not regularly weigh their lambs and, therefore, parasitic infections often go unnoticed until overt clinical signs are seen. By this stage, there has already been significant gut damage, resulting in a considerable check in growth that can never be recovered.
Infection with GI parasites also makes lambs more susceptible to other diseases, such as bacterial pneumonia or coccidiosis. Subclinical GI parasitic infections are responsible for considerable production loss on many sheep farms.
To reduce the potential production losses from subclinical and clinical nematode infections, farmers should be encouraged to carry out regular faecal egg counts and pasture risk assessments. This will help not only to ensure an early diagnosis, but also allow the introduction of management strategies to reduce the exposure of lambs to high larval challenge.
The presence of anthelmintic-resistant nematodes in a worm population on a farm reduces the killing capacity of the anthelmintics.
A large number of UK sheep farmers are still unaware of the resistance status of their farms. A consequence of this is the continued use of less effective anthelmintics, resulting in a higher burden of worms remaining in the lambs, despite treatment, and associated ongoing production losses.
Knowledge of the presence and severity of anthelmintic resistance allows the implementation of a number of strategies (Sustainable Control of Parasites in Sheep principles) to reduce the rate of resistance development and maintain lamb productivity.
The external parasites of particular note when considering subclinical disease are sheep scab and lice.
Lice infestations may be present with very little clinical evidence, but it only takes a sudden weather or husbandry change for the population of lice on an animal to increase rapidly – resulting in significant clinical signs.
Equally, sheep scab mites, Psoroptes ovis, may be present on sheep for many months in very low numbers, prior to the onset of clinical disease.
Sheep with early infestations may show few or no clinical signs, but they will go on to infect the rest of the flock. This is particularly significant when considering flock biosecurity, especially when buying in new sheep.
Sheep scab infections can rapidly become a significant welfare problem, as well as being economically costly.
It is essential to ensure the correct diagnosis is made, when it comes to external parasite infections, and the appropriate treatment is administered correctly, to ensure eradication of the parasite from the flock.
Subclinical disease, affecting both ewes and lambs, causes significant production loss in sheep flocks across the UK. Increasing the awareness among farmers of these conditions will ensure disease is either prevented or detected earlier. This will help to reduce production loss, as well as improve the health and welfare of our national sheep flock.
