A practical and evidence based approach to neonatal lamb diseases

Joseph W Angell BVSc MSc DipLSHTM PhD MRCVS

Wern Veterinary Surgeons and University of Liverpool,Unit 11,Lon Parcwr Industrial Estate,Ruthin.LL15 1NJ

joseph@wernvets.co.uk

Introduction

The mortality and morbidity of neonatal lambs is a cause of poor welfare for affected cases and results in the reduced production and economic profitability of farms. Worldwide, on average, approximately 15% of lambs die in the neonatal period with this rate remaining unchanged for the past 40 years (Dwyer and others 2016). Following birth, the neonate enters a new and hostile environment compared to that in utero and in particular must meet the challenge presented by infectious organisms which very rapidly become important causes of mortality for neonatal lambs.

In recent surveys, infectious disease accounted for 10% of neonatal deaths in Wales, UK (HCC 2011) and 36% in Norway (Holmoy and others 2016), with both surveys reporting the majority of deaths within 48 hours of birth. These data suggest that roughly half of all lamb deaths occur within the first two days, either during lambing or in the period shortly after, and so this a key period to focus on in terms of prevention and intervention. In the Welsh study, a further 11% of the losses occurred in the period directly after this, from 2 to 14 days after birth.

In a study carried out in 1997 (Binns and others 2002), veterinary undergraduate students were recruited to complete a questionnaire whilst on their lambing placement as part of their studies. Data were collected for many variables including flock management variables, such as farm type and size, housing, nutrition etc. as well as the individual practices at lambing such as navel treatments, tail docking and castration, administration of colostrum etc. The authors were specifically interested in lamb mortality as an outcome and in 1997 the mean overall mortality risk was 10.0%. This was split such that 4% were still-births and roughly 3% were classed as perinatal deaths and 3% post-natal deaths; the vast majority of

deaths occur shortly after birth. This corroborates well the data provided by HCC/AHDB Beef and Lamb.

Primary hypothermia/hypoglycaemia

Most lambs will generally survive if they are of average birth weight (4-5kg), kept warm and receive adequate colostrum.

Those lambs that have undergone a protracted parturition, compression of the umbilical cord or mild trauma to the central nervous system can suffer from a short term hypoxaemia. This is usually reversible, however these lambs may initially find it more difficult to maintain an adequate body temperature, and they may be slower and less persistent in searching for and finding the teat and then less persistent in feeding. This can then result in a secondary hypothermia and/or a hypoglycaemia, which if not dealt with can result in death. These effects may be compounded for lambs born to ewes that have suffered more than others during the parturition process, for example those that have incurred some soft tissue damage, have undergone some surgery etc., and so they may be less able to be the attentive mothers they could be. This can have a knock on effect to the lamb for example if it is not dried off quickly enough or if the ewe wants to be recumbent when the lamb wants to feed.

Primary hypothermia obviously occurs as a result of lambs becoming too cold. A normal lamb temperature is 39-40°C, and anything below 39°C can be classed as hypothermia.

This can result from a number of risk factors in isolation or more commonly in combination. Failure to receive adequate colostrum – therefore reducing the energy of the lamb and its ability to generate its own heat may be more likely with younger ewes that are inexperienced mothers and may produce smaller volumes of colostrum and milk for litters with multiple lambs. Lambs have some brown fat reserves which will help to provide some heat, but colostrum will provide a more ready source of energy. Numerous studies have shown reduced survival with lambs of smaller than average birth weight. For example, Christley and others (2003) demonstrated strong associations between low birth weight and reduced lamb survival, as well as low serum-immunoglobulin – an indication of failure of passive transfer.

Young lambs often tend to cope very well with cold dry weather, provided there is not deep snow on the ground. However, wet weather may seriously affect young lambs due to the increased exposure reducing their ability to maintain an adequate core body temperature. The provision of suitable shelter or the use of cheap disposable plastic lamb jackets can make a dramatic difference to ameliorating this risk.

Colostrum

In the first 24 hours following birth, the lamb needs to receive roughly about 1 litre of colostrum. This is not only for the establishment of good passive immunity, but also for its energy requirements including keeping warm.

Cheap commercial stomach tubes can be used to help supplement lambs with colostrum. The lambs’ own ewe colostrum is always best, if it can be milked from the ewe. Failing this, colostrum milked from another ewe can also be used although there is the risk of transmission of infectious disease for example Johnes or Maedi Visna, which could be more of a problem in flocks breeding replacement ewes and rams.

Goat and cow colostrum can be used as substitutes, however care is needed that goat colostrum comes from Caprine Arthritis Encephalitis free herds. Cow colostrum is less energy dense than ewe colostrum and in some cases can lead to an immunological reaction resulting in a potentially fatal anaemia at about 10-14 days of age. It is worth identifying donor cows free of the factor that leads to this reaction, although the assay is not widely available. Affected lambs may be treated by blood transfusion and the use of corticosteroids and antibiotics.

There are numerous commercial colostrum substitutes available, however these are lower in energy and antibodies compared to ewe colostrum but they may provide a suitable alternative when ewe colostrum is unavailable.

After a few hours and a failure to feed, brown fat reserves can be exhausted. Warming a hypothermic lamb at this point can lead to hypoglycaemic seizures so supplementation with an energy source is necessary. If the lamb is able to hold its head up and suck a finger, it may be possible to stomach tube some warm colostrum, however if it is unable to do this it may regurgitate any fed milk, inhale it and die. Intraperitoneal injection with a 20% glucose solution (10 ml/kg body weight) prior to warming can provide a suitable energy source followed by feeding once the lamb has been revived. The needle is inserted at 45 degrees just to one side of the navel.

It is important to not carry out intra peritoneal injections for lambs with watery mouth disease as the needle can easily puncture the distended abomasal wall leading to leakage and peritonitis. Prevention of hypothermia relies on ensuring that pregnant ewes are well fed, that there is sufficient shelter, dystocia problems are avoided and that there is sufficient skilled labour to monitor and manage the feeding of lambs in those first few hours.

Watery mouth disease

Watery mouth, slavery mouth or slavers are colloquial terms for a disease of unknown aetiology of neonatal lambs, and indeed there is some debate if it actually exists at all. However, a survey done in 1991 suggested that in intensively farmed sheep it can account for up to a quarter of all neonatal deaths, and together with this it is cited as the biggest reason for the widespread prophylactic and metaphylactic use of antibiotics in large numbers of flocks. In an unpublished survey of 887 flocks approximately two thirds of farms were using prophylactic or metaphylactic antibiotics to control or prevent watery mouth, and these findings suggest that whilst there is not much published literature on the scale of this specific problem it is likely to be a major issue not always in terms of disease but certainly in terms of the large scale use of antibiotics together with the inherent associated costs.

Watery mouth usually affects young lambs at about 12 to 72 hours of age. In a study of 102 lambs in 1985 80% of cases occurred within the first 72 hours (Eales and others 1986). The lambs initially present as dull and unwilling to suck and normothermic, and then this is followed by the appearance of the ‘watery mouth’ which is saliva drooling from the muzzle. Often there is also abomasal tympany and gentle shaking of these lambs can sometimes produce a splashing sound and hence the colloquialisation ‘rattle belly’. Scouring is unusual but is possible and often constipation or retained meconium may be present. Untreated cases often die within 24 hours showing a terminal hypoglycaemia, hypothermia and lacticacidaemia. Essentially the lamb uses up its reserves, runs out of glucose and then develops a metabolic acidosis leading to death. In a field study of 11 flocks by Eales and others (1986), morbidity was reported to be up to 24% of lambs born and mortality of affected cases up to 83%. In addition, a bacteraemia was found in 38%. In a study by Collins and others (1985) they observed that mortality was worse with age of onset – those aged more than 48 hours old when infected being less likely to recover than those infected earlier.

At post mortem, few abnormalities have been recorded. Most notably the abomasum may be distended with gas, and full of saliva and clots of milk. In a pathological study of 38 cases Gilmour and others (1985) reported inflammatory changes throughout the gastrointestinal tract with enteritis present in 25 out of the 38 cases (66%) and retained meconium in 12 of the cases – 32%. They also reported that in 20 lambs examined six hours prior to post mortem, only 3 had a bacteraemia (that is 15%), but at the time of post mortem 18 had developed a bacteraemia (90%). In all the cultures, no pathogenic species were identified, and rotavirus was only identified in the gut contents of one lamb. Obviously this is a small sample so the exact proportions may not be accurate for all populations, but it shows that these findings may be present in some cases.

The cause of the clinical signs is due to an endotoxaemia possibly due to the death of large numbers of gram negative bacteria. In an experimental study, purified cultures of non-

pathogenic E.coli, were given orally to colostrum deprived lambs fed only glucose and water, followed by ultra heat treated (UHT) milk (Hodgson and others 1989). Control animals were assigned to the same feeding regime but were not inoculated with the E.coli cultures. All the infected lambs developed clinical signs of watery mouth, starting with dullness, followed by excessive salivation followed by a cessation of feeding and then death. The biochemical results were also consistent with those seen in in clinical cases and are consistent with those seen in other experimental studies on endotoxic shock, for example a terminal hypoglycaemia, a terminal lactic acidaemia and leucopenia. Therefore, as such there is no known specific causal agent – no known specific bacteria or virus that may be responsible for causing this disease. It may be that there is a specific pathogen that just has not been found yet, or it may simply be a case of too great a volume of ‘ordinary’ bacteria overwhelming the resources of the lamb.

Normal lambs given colostrum have been shown to have reductions in abomasal tone and motility compared to older lambs and this may be a response to feeding, and the adjustment of the gut in the first few hours and days of life. However, on top of this, cases of watery mouth appear to have an increase in the delay in abomasal emptying and this has been associated in several studies, having been observed in studies of clinical cases (Collins and others 1985) and also confirmed in an experimental study comparing 34 cases with 68 healthy controls (Eales and others 1985). In this second study, contrast radiography with barium sulphate was used to compare the rate of abomasal emptying. Abomasal emptying was significantly slower in the lambs affected by watery mouth aged 24-48 hours than in healthy lambs of the same age.

Based on all this work the following aetiopathogenic hypothesis has been suggested: the abomasal contents of the newborn lamb is relatively neutral and the gut has relatively reduced motility which may allow the survival and growth of bacteria – especially in the absence of colostrum. This may also be compounded by the effects of any bacterial endotoxin. The normal pinocytotic mechanisms, which exist for the first 24 hours of life to transport large molecules from the gut into the systemic circulation, may allow access to the systemic circulation by bacteria. Lysis en-masse of gram negative bacteria may lead to large volumes of endotoxin resulting in an endotoxaemia, the clinical signs observed and subsequent death. Remember though that this is a hypothesis and has not been proven, but the available evidence seems to point to this for now.

Risk factors for watery mouth include increased litter size, triplets being more at risk compared to twins and potentially lamb size with smaller lambs reported to be slightly more at risk – although this difference was not observed in cases when compared to their healthy twin. Lambs born to ewes of poor body condition were also more at risk. Incidence rates vary from year to year which may suggest that combinations of environmental and management factors may be important.

It has been suggested that these factors combined may lead to a reduced colostrum intake increasing the risk of watery mouth. However, although it might seem logical to consider that adequate colostrum intake would reduce the risk of watery mouth particularly if there is a bacterial origin of disease two studies have shown no association with colostrum derived IgG in serum. Whether IgA is an important component remains to be seen.

Watery mouth has also been reported to be more common in lambs born to housed ewes and it is hypothesised that the wet and insanitary conditions lead to an increased risk of ingesting bacteria by the lamb.

Treatment protocols have been aimed at targeting the perceived aetiopathogenesis. One regime reported by Eales and others (1986) included administering antibiotics enterally using a neomycin and streptomycin preparation and parenterally with amoxicillin injection, administering glucose electrolyte solution by stomach tube and not feeding milk to the lamb but leaving it to suck the ewe if and when it recovered. This was successful in 80 out of 90 clinical cases. In a further study by Scott and Gessert (1996), lambs were given amoxicillin with clavulanic acid injection, together with intravenous flunixin and an oral rehydration solution. This protocol was successful in 21 out of 23 cases.

Given the current thinking about the aetiopathogenesis, prevention and control strategies and advice follow logical interventions based on this, but as such there are few controlled investigations of interventions. It is important to promote adequate volumes of good quality colostrum, and supplying this by stomach tube early if sucking dies not occur, particularly for triplets. In addition, good hygiene practices reducing the exposure to infection by ensuring clean and dry bedding and cleaning and disinfecting lambing pens between occupants may also help.

Currently many farms may use prophylactic or metaphylactic antibiotics given to lambs as soon as possible after birth, or used for the second half of lambing when maintaining adequate hygiene of the lambing pens and facilities becomes more difficult. The idea is that E.coli multiplication is suppressed within the gut lumen reducing the risk of a severe bacteraemia and a mass lysis resulting in an endotoxaemia. However given the current opinion around antibiotic use this is (rightly) likely to be come under increasing pressure. Two studies have looked at this in a controlled way.

Eales and others (1986) showed that a neomycin and streptomycin combination was effective at reducing the incidence of watery mouth, as was oral amoxicllin when compared to lambs given no treatment. However, whilst lower incidence rates were observed in treated animals, mortality was relatively higher in cases that became affected despite treatment. In a second study by Hodgson and others (1999), lambs’ exposure to potential pathogens was provided by allowing exposure in a natural environment. Lambs were prevented from sucking their ewes initially. Then three groups were compared. In Group 1 lambs were given just ewe milk replacer as a control group at 2 hours old and these suffered

a high incidence of mortality, with clinical signs and biochemical parameters consistent with watery mouth. In comparison there were no deaths due to watery mouth for a second group of lambs given stored colostrum at 2 hours old and also for a third group of lambs given ewe milk replacer and spectinomycin orally at 2 hours old.

There have been a couple of studies looking at metoclopromide used prophylactively as a preventative, however the results appear equivocal with some positive and some negative effects and some where no difference was observed when compared to placebo. There is also some anecdotal evidence of the use of E.coli vaccines given to ewes prior to birth, although there is no experimental evidence to substantiate this.

Lamb dysentery

Lamb dysentery is caused by the beta and epsilon toxins of the bacteria Clostridium perfringens type B. Affected lambs are usually less than 2 weeks old but it is most common in lambs aged 1-3 days. Many cases are simply found dead, due to the rapid progression of the disease. Others may show abdominal pain, may refuse to suckle, become recumbent, and in some cases have watery, often haemorrhagic diarrhoea. However in many cases the progression is so rapid that the faeces appear normal. On post mortem, classically large areas of the small intestine appear dark red, with ulceration of the mucosa and serosa and sometimes perforation. There can be blood stained peritoneal fluid and the liver may be pale and friable.

Small intestinal contents can be analysed for the beta and epison toxins, and the Clostridium perfringens bacteria can be cultured. These findings can help support the diagnosis. Control can be provided through the use of clostridial vaccines given to ewes. Antibodies to the clostridial toxins are then transferred via the colostrum to the lamb. These vaccines are in general very effective, provided they are used properly, the lambs receive sufficient colostrum and the colostrum is of sufficient quality.

Enterotoxigenic E. coli

Enterotoxigenic E. coli or ETEC is not a common cause of disease. However, when it occurs it can cause severe morbidity and mortality due to rapid spread of disease where lambs are crowded together. ETECs have the K99 and/or F41 antigens and these allow them to attach to the intestinal mucosa, they then produce a toxin which leads to an increase in secretion from the intestinal mucosa resulting in a secretory diarrhoea. This results in the production of profuse volumes of watery brown diarrhoea, and death can occur rapidly unless fluid therapy is instigated promptly.

Diagnosis can be made through faecal culture and subsequent typing for K99 and F41 fimbrial antigens. Control and prevention, as ever, is through good hygiene practices, ensuring that adequate colostrum of sufficient quality is supplied early for all lambs and the isolation of any lambs with diarrhoea. This can be difficult in practice due to the high levels of disease seen in affected flocks. Treatment with oral antibiotics may help and most enterotoxigenic strains are sensitive to the commonly used oral antibiotics containing neomycin or spectinomycin. There is currently no licensed vaccine for use in sheep available in the UK, although vaccines have been used to aid prevention in future years.

Cryptosporidium parvum

The protozoan parasite Cryptosporidium parvum may persist in the environment for long periods of time. It is rarely implicated alone however ingestion of sufficient numbers of oocysts can lead to disease, so it is more of a problem in heavily contaminated environments, and if there are other stressors e.g. other infections etc. The parasite causes villous atrophy of the distal small intestine which leads to malabsorption, secondary fermentation and diarrhoea. There is no specific treatment and anticoccidial agents are not effective, so treatment focuses on supportive fluid therapy and treating concurrent disease. Remember also the parasite is not specifies specific and can be zoonotic!

Drunken lamb syndrome/Lamb D-Lactic Acidosis Syndrome

Drunken lamb syndrome is a fatal disease of unknown aetiology and has been associated with clinical and pathological signs of nephrosis for many years. Due to these factors, in the literature it may be referred to as lamb nephrosis, and now more recently lamb D-lactic acidosis syndrome (Angell and others 2013a).

There has not been a widespread survey to find out the extent of this disease in the UK or further afield, but it would tend to affect individual farms sporadically. Some farms tend to get cases each year but the number of cases may vary from year to year with some years worse than others.

Affected lambs tend to fall into two groups. The classical drunken lambs, which tend to be seen at around 7-10 days of age, and then later cases which may occur at around 1-2 months old. Clinically lambs tend to be ataxic (drunken) and depressed. Observations in the field, also show that lambs stop sucking their mothers and as the disease progresses become recumbent finally resulting in death (Angell and others 2013a).

Later cases are often thin and diarrhoeic and die after about one week, and they can be observed drinking excessively. These later cases have been associated with a concurrent nematodirosis and or coccidiosis.

For the early cases, blood biochemistry can be variable depending on when in the course of the disease blood samples are taken. Typical results are reported to be raised blood urea, raised creatinine and decreased bicarbonate. Potassium and chloride can also be elevated. In Angell and others (2013a), 10 cases were examined in detail biochemically, microbiologically and also by post mortem. Several lambs with the early drunken lamb syndrome showed normal blood urea and creatinine concentrations despite being confirmed as having nephrosis on post mortem. Bicarbonate concentrations were consistently low, and in addition D-lactate was also shown to be consistently high. D-lactate, is lactic acid, but it is the D optical isomer. In mammals, the L-optical isomer is produced during anaerobic respiration and is the cause of the familiar burning sensation when sprinting. D-lactate is produced solely from microbial anaerobic respiration and so has to come from microbial fermentation somewhere. In addition to the biochemical abnormalities, on post mortem, all lambs were investigated histopathologically for changes in the intestine and in the kidney. A few lambs showed mild intestinal changes including villous atrophy, but all the lambs showed histpathological changes in the kidney consistent with nephrosis. This included a toxic tubular necrosis and the degenerative tubules filled with hyaline casts, however the basement membrane of these damaged tubules remained intact suggesting that recovery and regeneration of the damaged tubules could be possible.

There is a similar syndrome of young calves where there is a severe metabolic acidosis with minimal or no dehydration and often without signs of diarrhoea (Kasari and Naylor 1984). These calves are ataxic, incoordinated and appear drunk, progressing to recumbency and death. In these calves D-lactate has been shown to be the cause of the clinical signs seen.

In lambs, because of the consistently elevated D-lactate, and the consistently low bicarbonate concentrations, the name lamb D-lactic acidosis syndrome was suggested to describe the disease more precisely and it has then been hypothesised that as in calves, the clinical signs are as a result of the metabolic acidosis characterised by D-lactate, and the D-lactate is produced from microbial fermentation.

As result the following pathophysiological hypothesis has been suggested: gut ‘pathogens’ enter the neonatal gut; these then damage the intestinal lining sub-clinically leading to villous atrophy; as a consequence the normal microbial flora is disrupted as a consequence of a relatively increased gut transit time, leading to an abnormal bacterial fermentation further on for example in the colon.; as a result of this abnormal fermentation, D-lactic acid is produced by the bacteria which crosses over in to the blood stream; the D-lactate then affects the brain causing the clinical signs seen (although this has only been proven experimentally in calves) (Lorenz and others 2005); the D-lactic acidosis may also lead to the toxic tubular necrosis seen, and then the other biochemical abnormalities may occur as a result of this kidney damage. Because of this theory, it was proposed that the D-lactate could be targeted therapeutically, and in addition because the basement membrane of the

damaged kidney tubules appeared to be intact, it could be possible to keep lambs alive long enough for this to repair and the lambs to recover.

As a result, lambs with clinical signs consistent with lamb D-lactic acidosis syndrome were treated with oral sodium bicarbonate, in an attempt to redress the balance, reduce the acidosis and eliminate the clinical signs seen. It was then hoped that lambs would continue to suck from their mothers and thus give time for the kidneys to recover. In that study (Angell and others 2013b) all the lambs made a full clinical recovery. They all tended to make a rapid recovery within a few hours of treatment and returned to suck their mothers. They then tended to show reduced growth for about 1 week and in some cases developed diarrhoea for a few days before recovering and then thriving with the rest of the group.

The treatment used was a 1 molar solution of sodium bicarbonate given orally by stomach tube. This was made up using 400ml of tap water, in which was mixed 35g of sodium bicarbonate; 50 ml of this solution was then given by stomach tube. In the study, two lambs were bled on three occasions to determine the response rate of the bicarbonate and D-lactate concentrations. This showed that lambs could take 24 hours to respond biochemically, and so it was considered unnecessary to give further doses of the sodium bicarbonate solution to lambs that were slower to respond clinically. Anecdotally, oral rehydration solutions containing bicarbonate precursors have been successful, however, they tend to yield much lower concentrations of active bicarbonate in the blood and may have no effect in the colon as they need to be metabolised by the liver first.

Currently it is not possible to measure D-lactate commercially in the UK, however bicarbonate can be measured using a blood gas machine or a harleco apparatus (where available). In this study, low bicarbonate and elevated D-lactate were reasonably well correlated, and so bicarbonate could be used a proxy diagnostic indicator together with the clinical signs to aid in diagnosis, although many farmers with recurrent problems year on year will be quite good at identifying clinical cases based on age and the clinical signs seen.

The precise cause of lamb D-lactic acidosis syndrome is still unknown, however it is reported to occur more towards the end of lambing, and has been shown to be more likely in lambs with smaller birth weights (Angell and others 2013a). As usual, ensuring lambs receive good quality and sufficient colostrum may help reduce the risk too by helping the lamb deal with any ingested pathogens.

Salivary abomasum disease

Salivary abomasum disease (SAD) is a relatively recently reported disease of lambs and kids aged 3-17 days old (Christodoulopoulos 2008; Christodoulopoulos and others 2013). Clincial signs include lethargy, absence of sucking and hind leg weakness, increasing abdominal distension, dehydration and frequently lying down close to a water trough. Without

treatment the condition progresses to lateral recumbency with abdominal pain, bruxism and death. There is no profuse salivation at any stage of the disease, unlike watery mouth.

At post mortem, the abomasum is usually distended with gas, there is lots of saliva together with the digesta. There has also been reported to be multiple small abomasal haemorrhages with blood clots on the serosal and mucosal surfaces. In Christodoulopoulos and others (2013) (in Greece), abomasal bloat was found in 70% of cases, excess saliva in 43% and abomasal haemorrhages in 93%. In addition nephrosis was observed in 21% of cases. They also cultured E.coli from the abomasal fluid of 16% of the cases and noted a low abomasal pH in many of the cases. They concluded that the low abomasal pH and anecdotally reported successful treatment with oral sodium bicarbonate may imply that a metabolic acidosis results from the pathological changes, but as yet this has not been published.

Joint ill

Joint ill, or infectious polyarthritis is where one or more joints become infected in young lambs and is usually seen in lambs aged 2-3 weeks, but can be seen much earlier and in lambs as young as 5 days of age. It is characterised by a sudden onset lameness, and often specific joints are swollen. Single or multiple joints may be affected, and any joint can be affected but often joints of the limbs and spine are noticed most easily. The affected joints may be swollen and hot and fine needle aspiration or post mortem examination can reveal frank pus. Some lambs recover well whilst others fail to respond to treatment with antibiotics and NSAIDs or corticosteroids. Often treatment needs to be for an extended period of several days for recovery to occur.

In Watkins and Sharp (1998) cases submitted to veterinary investigation centres in England and Wales were investigated. In total there were 242 cases of arthritis in lambs investigated bacteriologically. Some were submitted as whole carcasses and some were investigated as joint aspirations only. Of the 242 cases investigated, bacteria were cultured from 212 (88%). Many different species of bacteria were cultured, but of these 212, 169 (70%) yielded Streptococcus dysgalactiae.

The specific transmission routes of Strep dysgalactiae subsp dysgalactiae (SDD) are unknown, however theories include access via the mouth or through breaks in the skin, for example navels and where castration or tail rings are applied. In Watkins and Sharp (1998), the presence of omphalitis or navel ill was considered where whole lambs had been submitted instead of joint aspirations. So of the 170 carcasses with joint ill, 16 % also had omphalitis. Currently Strep dysgalactiae subsp dysgalactiae is considered as a possible important cause of joint ill, although understanding of the risk factors and specific treatment protocols is still currently limited.

The sources of infection are unknown, but recently a study was carried out between 2008 and 2010 to try and investigate possible sources (Rutherford and others 2014). The authors visited 14 flocks during an outbreak or in the lambing period in the year following an outbreak and investigated different possible sources of infection including the ewes and the environment. They were unable to detect SDD in the majority of samples and were only able to culture it from 1% of the cases, but this may have been due to the sampling sites chosen and the difficulties associated in sampling live animals. They did however show that SDD could be cultured from the vagina from a small number of ewes, and also that the pathogen could survive on straw for extended periods of time – up to 6 weeks. This means that it may be possible for a small number of ewes to contaminate the environment and for the bacteria to survive in lambing pens and sheds particularly on straw and possibly become a source of infection to young lambs. However, this has definitely not been proven conclusively and is more a working hypothesis currently. Another source of infection could be milk from ewes in some cases, and SDD has been isolated from a small number of ewe milk samples. It is possible the bacteria can enter via the tonsils and become blood borne via that route.

Recommendations currently focus on trying to improve lambing hygiene, including wearing gloves during lambing in order to limit the risk of direct spread from ewe to lamb, but the efficacy of these methods is unknown. Treatment options currently carried out by farmers were investigated in another small study by the same authors (Rutherford and others 2015), and they also looked at antimicrobial resistance profiles from 25 samples of SDD cultured from clinical cases. All 25 showed resistance to tetracycline's and one sample was resistant to penicillin. Currently treatment of cases with a penicillin based antibiotic would be best practice but investigation of refractory cases or non-responders might be necessary in case resistance is a problem on particular farms. Non-responsive cases or refractory cases should be culled on welfare grounds.

Navel ill

Omphalophlebitis or navel ill can occur as a result of incorrect dressing of the navel, and/or a failure for it to dry out quickly enough such that the navel becomes colonised with opportunistic bacteria. These can multiply and ascend the navel to cause various sequelae such as navel abscessation, but they can also affect other body cavities and organs and can result in serious conditions including peritonitis, septicaemia and therefore result in death.

The specific condition hepatic necrobacillosis requires colonisation of the navel and then subsequent ascending infection to the liver specifically with Fusobacterium necrophorum. These bacteria then cause multiple abscesses in the liver which appear characteristically as white spots in the liver.

Prevention is simple and can be readily achieved. As ever, good hygiene practices will reduce the contamination of the navel at birth and subsequently. Good colostrum quality and sufficient volumes ensure the lamb has sufficient antibodies to deal with some level of infection. Using strong veterinary iodine will help disinfect the navel as well as aid in desiccation; however it is often totally or partially removed by the ewe licking the lamb clean and dry after birth so repeated applications after 2-4 hours are recommended to ensure adequate efficacy. Some farmers use antibiotic sprays but these are narrower spectrum compared to disinfectants and far more expensive comparatively.

Iodine deficiency

Iodine deficiency is relatively uncommon in the UK, although it can occur in lambs born to ewes grazing pasture that has begun to grow early, or pastures or crops containing chemicals known as thyiocyanates. These thiocyancates act to block the uptake of inorganic iodine by the thyroid gland.

The clinical presentation can appear as a late abortion, or with week lambs born with an enlarged thyroid gland or goitre. In severe cases the lambs can be born with very little fleece, and this of course makes them more at risk of primary hypothermia. Goitre may not always be present and iodine deficiency can cause significant losses perinatally with very few clinical signs.

In New Zealand the prevalence has been higher in flocks fed on brassicas that have high levels of goitrogens.

On post mortem sometimes an enlarged thyroid gland is evident. Weighing the gland and calculating the ratio of the gland weight to the live weight of lamb can help indicate whether enlargement is significant or not. If the gland is greater than 0.4 g per kg of the live weight of the lamb then it is considered enlarged. Comparing the thyroid and body weights of 15 lambs can provide a reasonable indication of whether this is a flock problem or a one off in an individual lamb. Histopathology can be used to aid determination of specific thyroid abnormalities. Supplementation in subsequent years may or may not be required depending if grazing patterns vary and how predictable the environmental conditions are likely to be. Supplementation can be achieved successfully with injections of iodised oil or through oral dosing during latter pregnancy. Ruminal boluses containing iodine selenium and cobalt are available, but whilst they will provide sufficient iodine supplementation, supplementation with cobalt and selenium may not be necessary and thus their use could prove expensive and unnecessary on some farms.

In lambs born alive with a clinical goitre as a result of iodine deficiency, successful treatment can be given using oral potassium iodide at a dose of 20mg per lamb.

Copper deficiency

Copper deficiency can occur in lambs as a result of the ewes grazing soils either primarily low in copper or where copper antagonists are present. Minerals such as iron, molybdenum and sulphur can all serve to reduce the amount of copper ingested by ewes resulting in a copper deficiency. In addition, pasture management practices such as lime application can also result in a reduced bioavailability of copper. This occurs because as the pH is raised this makes molybdenum more available. Sheep fed on kale can have reduced copper absorption due to the high sulphur content of the kale. Ingestion of large quantities of soil can lead to copper deficiency through associated high iron intakes.

Copper is required for many important enzyme systems in the body and therefore reduction can cause a variety of clinical disease syndromes. However, the most obvious clinical sign of copper deficiency is usually swayback in young lambs. In these cases the lamb is incordinated and can have difficulty walking and finding the teats of the ewe. Differentiating this from spinal abscessation can be difficult. Other signs may also be seen in affected lambs including in some cases a fine head tremor which can increase during feeding or other activities, osteoporosis which may result in bone fractures, tendon abnormalities which can be seen as stiffness of the limbs, and changes in the wool such as depigmentation and reduced quality.

Diagnosis of swayback in the lamb can be difficult in the live lamb but can be based on the clinical signs seen. Confirmation can be made by histopathology of the brain and spinal cord and by determining the concentration of copper in the liver. Concentrations below 80 mg/kg are considered low. Unfortunately there is no adequate treatment for clinical cases of swayback in neonates and so affected lambs are euthanized.

There is no straight forward approach to supplementing ewes with copper and the very real risk of causing copper toxicity should always be borne in mind. When considering supplementation it is important to consider the prevalence of clinical cases of lambs with swayback – that is how big a problem it is causing each year and the breed affected – some breeds are much more susceptible to copper deficiency than others for example the Scottish Black face breed don’t retain copper as efficiently as the Texel for example. In addition one needs to consider the use of supplementary feeds. Copper is well absorbed from low fibre feeds such as cereals, but poorly absorbed from pasture. Finally the risk of copper deficiency can vary between different geographical areas so knowledge of the particular area and soil need to be taken into account too. Liver samples from ewes are the most useful animal based copper measurement, indicating the historic long term bioavailability of copper to the ewes. This can be done at the abattoir, using a liver biopsy punch in liver animals or in post mortem cases.

If supplementation is considered necessary after considering these factors then there are various options available. Injections with chelated copper can provide adequate supplementation for a few months over specific critical periods. Mineralised drenches can be given but care needs to be taken to ensure safe amounts are given to avoid toxicity. Because of this, the amount of copper supplied by a drench is quite low and can only provide a short term benefit, so repeated strategic dosing may be necessary. Some farmers use mineral supplements, but the copper concentrations in these tend to be quite low. This is intentional as it is impossible to control the amount of a supplement ingested by each sheep and so there is a risk of copper toxicity in sheep consuming large amounts. They can also be quite an expensive approach to supplementing copper. Copper capsules and copper boluses can be used. These release copper over a longer period of time in small amounts allowing the liver to absorb the copper over a long period of time with a much lower risk of toxicity. Because of the risk of toxicity it is not recommended to provide more than one source of copper supplementation.

White muscle disease

White muscle disease is caused by a deficiency in vitamin E and selenium during pregnancy. Selenium deficiency is present in many soils resulting in pastures low in selenium. It is also associated with the feeding of some root crops and cereals. This results in the degeneration and poor development of the skeletal and cardiac musculature, resulting in still births or live weak lambs.

Clinically affected lambs may struggle to stand and have difficulty sucking due to skeletal weakness and also the weakness of the pharyngeal muscles. As a result lambs can starve and then die from hypothermia. Disease can be confirmed on post mortem by histopathological examination of the cardiac musculature. The disease is now uncommon due to the widespread awareness and understanding and the subsequent prevention through the supplementation of ewes. Treatment can be instigated using potassium selenate: 0.75-1.5 mg and vitamin E: 34-68 mg. Disease can be prevented by supplementation at least 6 weeks before lambing.

Congenital malformations

There are numerous examples of genetic malformations that occur apparently at random on many UK farms. They are all usually of low incidence and put down to being just one of those things. Some congenital malformations are inherited for example congenital entropion and Dandy Walker malformation which is sometimes seen after the introduction of a new ram. These can sometimes be reduced in future years through the careful identification of the associated ram.

Atresia ani

Atresia ani occurs sporadically from time to time. It results in the congenital failure of the anus to form or sometimes the rectum and/or the terminal colon as well. In Dennis and Leipold (1972) (USA), 42 out of 64 cases of atresia ani (65%) had some other defect, and most commonly – accounting for nearly half of these multi defect lambs - the additional defect involved the urogenital system. Additional defects included for example cleft scrotum, tail defects, hypospadia, cryptorchidism etc.

In Dennis (1979), of 401 malformed lambs examined over 3 years, the urogenital system was involved in 92 cases (23%). Of these 92 lambs with a urogenital defect, 35 also had atresia ani (23%). Therefore, there may be some association between the genetic defects that lead to the occurrence of atresia ani and other urogenital problems and so in practice it is wise when dealing with a case of atresia ani to also investigate the possibility of other concurrent defects, urogenital ones probably being the most likely.

It can be easy for farmers not to notice cases for a few days, and they may be initially alerted by swelling of the abdomen. At post mortem in untreated cases, there is often mega-colon present. In Dennis (1979), in the vast majority of those cases the blind end of the rectum was separated by 0.25-0.5 cm of subcutaneous tissue. Therefore, cases in which this is the case, surgical intervention creating an opening in the skin under local anaesthesia and suturing it open can result in a satisfactory outcome in many cases.

References

ANGELL, J. W., JONES, G., GROVE-WHITE, D. H., JONES, E., HIGGINS, R. J. & OTTER, A. (2013a) A prospective on farm cohort study investigating the epidemiology and pathophysiology of drunken lamb syndrome. Veterinary Record 172, 154ANGELL, J. W., JONES, G. L., VOIGT, K. & GROVE-WHITE, D. H. (2013b) Successful correction of D-lactic acid neurotoxicity (drunken lamb syndrome) by bolus administration of oral sodium bicarbonate. Veterinary Record 173, 193BINNS, S. H., COX, I. J., RIZVI, S. & GREEN, L. E. (2002) Risk factors for lamb mortality on UK sheep farms. Prev Vet Med 52, 287-303CHRISTLEY, R. M., MORGAN, K. L., PARKIN, T. D. & FRENCH, N. P. (2003) Factors related to the risk of neonatal mortality, birth-weight and serum immunoglobulin concentration in lambs in the UK. Prev Vet Med 57, 209-226CHRISTODOULOPOULOS, G. (2008) Salivary abomasum disease in young lambs. Veterinary Record 162, 732CHRISTODOULOPOULOS, G., SCOTT, P. R., JEHL, N., FILIOUSSIS, G. & SMITH, S. H. (2013) Clinical, microbiological and histological findings in lambs affected by 'salivary abomasum disease'. Veterinary Record 172, 100COLLINS, R. O., EALES, F. A. & SMALL, J. (1985) Observations on watery mouth in newborn lambs. British Veterinary Journal 141, 135-140DENNIS, S. M. (1979) Urogenital defects in sheep. Vet Rec 105, 344-347DENNIS, S. M. & LEIPOLD, H. W. (1972) Atresia ani in sheep. Vet Rec 91, 219-222DWYER, C. M., CONINGTON, J., CORBIERE, F., HOLMOY, I. H., MURI, K., NOWAK, R., ROOKE, J., VIPOND, J. & GAUTIER, J.-M. (2016) Invited review: Improving neonatal survival in small ruminants: science into practice. Animal 10, 449-459EALES, F. A., SMALL, J., GILMOUR, J. S., DONACHIE, W., FITZSIMONS, J. & DINGWALL, W. S. (1986) A field study of watery mouth: clinical, epidemiological, biochemical, haematological and bacteriological observations. Veterinary Record 119, 543-547EALES, F. A., SMALL, J., MURRAY, L. & MCBEAN, A. (1985) Abomasal size and emptying time in healthy lambs and in lambs affected by watery mouth. Veterinary Record 117, 332-335GILMOUR, J. S., DONACHIE, W. & EALES, F. A. (1985) Pathological and microbiological findings in 38 lambs with watery mouth. Veterinary Record 117, 335-337HCC (2011) Making Every Lamb Count. Hybu Cig Cymru/Meat Promotion Wales. pp 2-3HODGSON, J. C., BREBNER, J. & MCKENDRICK, I. J. (1999) Efficacy of a single dose of oral antibiotic given within two hours of birth in preventing watery mouth disease and illthrift in colostrum-deficient lambs. Veterinary Record 145, 67-71HODGSON, J. C., KING, T. J., HAY, L. A. & ELSTON, D. A. (1989) Biochemical and haematological evidence of endotoxic shock in gnotobiotic lambs with watery mouth disease. Res Vet Sci 47, 119-124HOLMOY, I. H., WAAGE, S., GRANQUIST, E. G., L'ABEE-LUND, T. M., ERSDAL, C., HEKTOEN, L. & SORBY, R. (2016) Early neonatal lamb mortality: postmortem findings. Animal, 1-11KASARI, T. R. & NAYLOR, J. M. (1984) Metabolic acidosis without clinical signs of dehydration in young calves. Can Vet J 25, 394-399LORENZ, I., GENTILE, A. & KLEE, W. (2005) Investigations of D-lactate metabolism and the clinical signs of D-lactataemia in calves. Vet Rec 156, 412-415RUTHERFORD, S. J., JECKEL, S. & RIDLER, A. (2015) Characteristics of sheep flocks affected by Streptococcus dysgalactiae arthritis. Vet Rec 176, 435RUTHERFORD, S. J., RYCROFT, A. N. & RIDLER, A. L. (2014) Sources of Streptococcus dysgalactiae in English and Welsh sheep flocks affected by infectious arthritis (joint ill). Vet Rec 174, 579SCOTT, P. R. & GESSERT, M. E. (1996) Watery mouth disease in lambs: biochemical parameters before and after treatment. Veterinary Record 139, 117-118WATKINS, G. H. & SHARP, M. W. (1998) Bacteria isolated from arthritic and omphalatic lesions in lambs in England and Wales. Vet J 156, 235-238