€¦ · Web viewNotes – Lecture 16 – Sheep Health: Key concepts, economic impact, bacterial and viral disease. Notes – Lecture 16 – Sheep Health: Key concepts, economic

Lecture 16: Sheep health: Key concepts, economic impact, bacterial and viral diseases

Steve Walkden-Brown and Brown Besier

Learning ObjectivesOn completion of this topic you should be able to:

describe the major disease challenges faced by sheep during their lifecycle and the reasons why these challenges occur when they do

discuss the impact of disease on sheep productivity and underlying mechanisms for this describe and the most important bacterial and viral diseases of sheep and their control.

Key terms and conceptsEpidemiology, pathogenesis, resistance, resilience, life cycles, risk factors, preventive, strategic, tactical and curative disease control, integrated parasite management

Introduction to the topicDisease is one of the major environmental factors, like nutrition or climate, which markedly influences the efficiency of sheep production for wool or meat. This lecture introduces you to the major disease challenges facing sheep and the mechanisms by which they influence sheep productivity and welfare. The lecture will then briefly some important viral and bacterial diseases of sheep.

16.1 A framework for understanding health and diseaseSeveral key concepts underpin our understanding of all disease and these are necessary tools for a consideration of disease in any species.

a) Health and disease form a continuum and the boundary between a healthy, or an unhealthy (and thus diseased) animal or flock is not distinct.

b) Disease may be infectious (caused by other living organisms or transmissible agents) or non-infectious (caused by physical or chemical agents, deficiencies, genetic or immune system disorders). Both are important in the sheep industry, but infectious disease, primarily parasitic, predominates.

c) Disease causation is almost invariably multi-factorial and an understanding of the many risk factors contributing to disease spread and expression is essential to properly controlling disease. There is often one factor that must be present for disease to occur (eg. a causative organism, or a specific toxin or deficiency) but the presence of this factor on its own without other risk factors is rarely sufficient to induce disease. To control disease one or more of the whole range of risk factors for the disease may be targeted. When several factors are targeted we are moving into the area of integrated management of disease. The risk factors for disease are commonly grouped as follows:

Host factors such as genotype, nutritional status, immune status, age, sex, physiological status

Environmental factors such as temperature, rainfall, pasture quantity/quality, presence or absence of toxicities or deficiencies, air quality etc.

Pathogen factors such as virulence, reproductive potential, ability to spread, host range, requirement for intermediate hosts, ability to survive in the environment etc.

d) The effects of disease may be clinical (ie visually obvious) or more importantly sub-clinical (not visually obvious). Increasingly clinical disease is well controlled and the focus is on limiting the adverse effects of sub-clinical disease.

e) There are many ways of classifying approaches to controlling disease but most disease control strategies fall into one of the following broad categories:

Curative. Aimed at controlling clinical disease. Animals are only treated when clinically ill so sub-clinical disease is not controlled. An extreme form of curative control is salvage, which is aimed at preventing mortality not disease. An example of this is treating sheep for worms when scouring or anaemia is present.

WOOL412/512 Sheep Production 16-1© 2013 The Australian Wool Education Trust licensee for educational activities University of New England

Notes – Lecture 16 – Sheep Health: Key concepts, economic impact, bacterial and viral disease

Tactical. Aimed at intervening to control disease when certain risk factors arise, or when disease monitoring indicates that intervention is worthwhile in the short term. This is usually well before the onset of clinical disease and so offers some level of control of sub-clinical disease. An example of this is treating sheep for worms in response to worm egg count monitoring results.

Strategic. Strategic control is a longer-term approach based upon fixed interventions at key times or points based on a deep understanding of the disease and its behaviour. It generally controls both clinical and sub-clinical disease. An example of this would be the giving of a routine summer worm treatment in Mediterranean climate environments in Australia, or the provision of a weaning or pre-lambing treatment in most of Australia.

Preventive. The occurrence of some diseases can be totally prevented by disease control measures including exclusion with quarantine, vaccination, supplementation to overcome a deficiency and in-feed or in-water chemical control. An example of this is the use of the 5-in-1 vaccine to control the major clostridial diseases of sheep.

7.2 Major disease syndromes in sheepThe life of sheep is dominated by two key cycles, the life cycle from birth through development, maturity, senescence and death, and the annual female reproductive cycle from mating through conception, foetal development parturition and lactation. As sheep move through these cycles both the incidence and type of disease they encounter varies widely as shown in Table 16.1. Clearly these differences are due mostly to host factors operating on disease incidence. It should be noted that there are marked regional differences in the importance of these syndromes, signifying the importance of environmental factors on disease incidence. The presence of severe deficiency (eg. P, Se, Co, Cu) and toxicity problems (plant, fungal, inorganic) can also limit sheep production in some locations.

Table 16.1: Summary of major threats to sheep health in Australia for different classes (Walkden-Brown and Besier 2006).

Class of stock Main disease threats Reason

Suckling lambs Starvation, mismothering and exposure syndrome (SME)

Small size, adaptation to extrauterine life.

Predators Small size, lack of evasive skillsPost weaned lambs

Weaner ill-thrift syndrome Adaptation to roughage diet, loss of maternal nutrition and immunity, high nutrient demands, susceptibility to parasitism

Helminth infections (roundworms, flukes)

Lack of immunity

Mineral and nutritional deficiencies

High requirements for growth

Blowfly strike High incidence of scours and fleece rot – different 1st fleece

Adult sheep Blowfly strike No vaccine or significant immunity development

Lice No vaccine or significant immunity development

Roundworm infection Weak or intermittent immunityFootrot (regional) Only weak immunity developsLiver fluke infection (regional) No vaccine or significant immunityOvine Johne’s disease (regional)

Long incubation period

Reproducing females

Pregnancy toxaemia (twin lamb disease)

Nutrient demands of large or twin foetuses where nutrition is poor

Hypocalcaemia High calcium requirement in milkDystocia/metritis/mastitis Complications of giving birthHelminth infections (roundworms, flukes)

Periparturient loss of immunity

16.3 Impact of diseaseDisease has effects at the molecular, cellular, individual animal and population levels and these effects result in economic impact at the farm, state, national and international levels.

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Economic impact of diseaseThe Food and Agriculture Organisation (FAO) has estimated that disease costs between 15 and 40% of the farm gate value of animal production worldwide, with the impact depending on the quality of animal husbandry and veterinary services available. The economic impact of disease at an enterprise or industry level is comprised of one or more of the following components.

a) Loss of productionThis may be due to reduced quantity of animal product produced due to animal deaths, reduced productivity or reduced rate of genetic gain. The latter arises from reduced reproductive rates and survival rates, resulting in fewer animals to select from. This results in reduced selection intensity. Loss of production may also be due to reduced quality of animal product. Wool is produced by specialised skin organs (wool follicles), and so the quality of wool is highly susceptible to diseases that affect the skin. Thus lice infection, blowfly strike and various forms of dermatitis (skin inflammation) reduce the quality of the wool produced independently of effects on quantity. Examples include reduced staple strength, stained wool and cotting. However, effects on wool quality are not restricted to diseases of the skin. Because wool is largely composed of protein, any generalised disease which impairs the availability of protein to wool follicles can affect wool growth. If effects are sudden and large, staple strength can be significantly reduced (eg blowfly strike).

b) Costs of controlMany diseases of sheep are quite well controlled by vaccines, chemicals, preventive surgery and other management strategies, but these usually have a cost to them. These costs, including labour, must be included when calculating the impact of the disease on the enterprise. Table 16.2 presents some formal estimates of the cost of the major sheep diseases to the Australian sheep industry. Costs are broken down into loss of production and costs of control. Note that the three most important diseases of sheep are parasitic. Note that the distribution of costs between costs of control and production loss varies widely between diseases. Given that the gross farm gate value of Australian sheep production is approximately $4 billion, these four disease syndromes alone are estimated to cost some 21% of this value.

Table 16.2: Cost ($m) of the major endemic diseases of sheep in Australia (Sackett et al. 2006).

Disease Cost of control ($m) Production loss ($m) Total

Internal parasites 59 310 369

Flystrike 197 83 280

Lice 83 40 123

Post-weaning deaths

-23 113 90

Total 316 546 862

c) Loss of market opportunityAlthough not reflected in the formal estimates of disease cost in Table 16.2, effects on market access can be an important impact of disease. Disease status can influence the ability of the producer to trade in livestock or their products. At one extreme an outbreak of exotic disease such as foot and mouth disease may preclude any trade in sheep or their products. More common examples are stud breeders who are unable to fully exploit markets for their rams because they have notifiable diseases such as Ovine Johne's disease, ovine footrot, ovine brucellosis or body louse infestation. Conversely, producers who are free of these diseases and/or whose properties are free of anthelmintic-resistant worms may be constrained in their purchases of stock to stock from properties with a similar status. For example this may reduce the options for stock trading to take advantage of seasonal pasture abundance.

Disease mechanisms resulting in loss of production in sheepDisease, either clinical or sub-clinical, may be local or systemic (generalised) in its effects or may involve both. Localised disease is normally manifest by clear dysfunction of one or more organ systems (eg. gastrointestinal tract, lungs, musculo-skeletal system, nervous system) whereas systemic disease is associated with generalised signs such as depression, fever and altered behaviour.



Mechanisms in localised diseaseThe ways in which localised disease can impact adversely on the productivity of wool sheep include:

a) Impaired organ system function. For example: Skin - Wool follicle and skin function. Direct effects on wool Gut - Digestion/absorption, reduced feed intake Liver - Reduced synthesis of plasma protein, impaired excretory function Nervous system - Abnormal behaviour, reduced feed intake Musculoskeletal system - Impaired mobility.

b) Direct loss of nutrients Loss of plasma and gut proteins in inflammatory disease of the gut (eg. parasitic disease) and

kidney Direct loss of blood by blood sucking parasites (eg. Barber's pole worm) or haemorrhage (eg

liver fluke).

c) Metabolic costs of repair Repair or replacement of damaged tissues Metabolic cost of mounting an immune response Energy costs of recycling protein through the gut (eg. internal parasites).

Mechanisms in generalised (systemic) diseaseGeneralised disease is characterised by generalised responses by the immune system and the hypothalamo-pituitary-adrenal axis (the "stress" response). Often these responses contribute significantly to the disease syndrome.

a) Effects of the immune responseThe immune response is involved in combating infectious disease. It is a stereotyped response to tissue damage or invasion which later becomes specific and targeted. Important components of a generalised immune response include:

Inflammation. This results in increased blood flow, and decreased capillary wall integrity leading to movement of plasma and leucocytes (white blood cells) from the blood to the tissues or body cavities.

Increased leucocyte numbers. These are key effector cells of the immune system and numbers increase to combat infection.

Production of cytokines by immune system cells. Cytokines are the intercellular messengers of immune system cells and they regulate the immune response. Whether cytokines have direct effects on wool follicles is unknown, but in humans interleukins 1α and 6 have all been shown to exhibit a potent inhibitory effect on the hair growth cycle, so effects on wool cannot be ruled out.

Fever. Inflammatory cytokines such as interleukin-1 (IL-1), tumour necrosis factor α (TNFα), and interleukin-6 (IL-6) are important in generating a febrile response in the host. Studies have shown that components of the immune system function optimally at temperatures slightly higher than body temperature and this is probably the reason fever has evolved. However, fever has a suppressive effect on feed intake which can exacerbate some disease conditions.

Antibody production. One effector arm of the immune response is based upon the production of specific binding proteins called antibodies or immunoglobulins. These bind to invading organisms or their products, inactivating them or facilitating their destruction. Normally antibody production does not have an adverse effect on productivity but in the case of allergic reactions this is not so. The intense itching felt by sheep infested with body lice (Bovicola ovis) is due to a hypersensitivity (allergic) reaction to antigens in the saliva and secretory products of the lice, in part mediated by IgE. It is the itching that results in loss of wool from the fleece and reduction in quality of the remaining wool. Without the itch, it would be a fairly benign infection.



While the immune response protects against infectious disease, there can be adverse consequences for the host. Colditz (2008) identified six potential costs of mounting an immune response to gastrointestinal worm infections. These arise from

(i) increased metabolic activity;(ii) reduced nutrient availability due to anorexia; (iiij altered priorities for nutrient utilization; (iv) change in size and turnover of pools of immune cells and proteins;(v) immunopathologv from inappropriate or excessive immune activation. vi) The genetic cost which arises from a change in the capacity of offspring to express production and life-history traits following selection for resistance.

Indeed the cost of mounting an immune response to worm infection is the subject of considerable current interest and debate, with the work of Greer and colleagues (2005; 2008a; 2008b) indicating a significant improvement in performance of sheep infected with scour worms when their immune response is suppressed, despite harbouring much higher worm burdens. Some of the pro’s and con’s of this for the host are reviewed by Williams (2011).

Blowfly strike, another important disease of sheep, is characterised by a massive systemic response. The initial skin lesion is widened by successive waves of larvae (maggots) causing physical damage to the skin with their mouthparts and also digesting it away with secreted proteases. The wound becomes rapidly infected with bacteria from the skin and the environment and these, coupled with extensive tissue damage and foreign secretory products of the fly larvae induce a marked systemic response characterised by pain, fever and anorexia (loss of appetite). Colditz et al. (2005) investigated the role of anorexia in mediating the effects of blowfly strike on wool growth. Groups of 18 month old wethers were either uninfected (Control), infected daily for 8 days with 500 1st instar larvae of Lucilia cuprina (Flystruck) or uninfected but pair fed with flystruck sheep so that feed intake was the same as struck sheep (Pair fed). Flystruck and Control groups were fed ad libitum. The effects of flystrike on body temperature, IL-6 concentrations and feed intake are illustrated in Figures 16.1, 16.2 and 16.3 respectively.

Figure 16.1: Rectal temperature (mean ± SEM) before and during flystrike. The Struck group were infected on days 0-7. (* P<0.05) (Colditz et al. 2005).



Figure 16.2: Plasma IL-6 (mean ± SEM) before and during flystrike (as above) (Colditz et al. 2005).

Figure 16.3: Feed intake (mean ± SEM) of 2 weeks before and 6 weeks after initiation of the flystrike treatment (as above) (Colditz et al. 2005).

Clearly flystrike led to elevated IL-6 concentrations and a high fever resulting in a marked reduction in voluntary feed intake. Blowfly strike is associated with marked reductions in staple strength across the whole of the fleece indicating a systemic effect. In extreme cases there is a complete break in the wool and the whole fleece may be shed. In the study described above, depression in feed intake associated with flystrike accounted for 25% of the observed effects on staple strength and 55% of the reduction in wool growth over the 6 weeks during and after the flystrike. This means that factors other than reduced feed intake play an important role in mediating the effects.

b) Effects of the stress responseComponents of the stress response that may contribute to the adverse effects of disease on wool production and quality are discussed below.



Altered behaviour. Stress may influence a wide spectrum of behaviours, directly or indirectly. If these result in reduced feed intake wool growth is reduced and the catabolic effects of the stress hormones are exacerbated.

Elevated glucocorticoid production. Elevated secretion of glucocorticoids is a response to more chronic types of stress. In sheep, the active glucocorticoid is cortisol, produced by the adrenal cortex. As can be seen from Figure 16.4, cortisol levels can be dramatically elevated in systemic disease such as blowfly strike. Low concentrations of cortisol are required for normal wool growth. High concentrations of cortisol or its synthetic analogues depress wool growth (Figure 16.5). Very high doses can cause complete cessation of wool growth (follicle shutdown). Concentrations need to be elevated for at least 24hr to depress wool growth. Thus short sharp stressors are not sufficient to cause a break in the wool. At least part of this effect is direct (demonstrated by in vitro effects) and is not due to changes in metabolite concentrations induced by glucocorticoids. Some data suggests that cortisol can affect linear wool growth without affecting fibre diameter.

Figure 16.4: Plasma cortisol concentrations (mean ± SEM) before and during flystrike. The Struck group were infected on days 0-7. (* P<0.05) (Colditz et al. 2005).

Elevated catecholamine production. Elevated secretion of catecholamines (adrenaline and noradrenaline) from the adrenal medulla occurs in response to acute stress. Catecholamines also act as neurotransmitters involved in both the central and autonomic nervous systems, influencing blood flow (especially to the skin) and heart beat. Thus they can have a direct effect on wool growth by constricting the supply of circulating nutrients available to the wool follicle. These direct effects on wool growth are relatively short lived.

Increased sympathetic tone. This can also form part of the stress response. It induces vasoconstriction in peripheral tissues and vasodilation in central tissues. It is difficult to differentiate these responses from those arising from increased catecholamine secretion.



Figure 16.5: Effect of increasing doses of cortisone acetate on wool growth in adrenalectomised sheep. Controls received 0.25 mg/kg of cortisone acetate and 0.05 mg/kg of deoxycorticosterone per day (Ferguson 1965).

Effects of disease on the efficiency of feed utilisation for productionAny factor which limits the exogenous supply of nutrients, or impedes digestion and absorption of nutrients, will impact on sheep productivity by reducing the supply of circulating nutrients available. Likewise, any factor which induces a loss of circulating nutrients will impact negatively on sheep production. Subclinical disease presents very much like malnutrition, due largely to suppression of appetite (i.e. reduced feed intake) and a decrease in the efficiency of feed utilisation. Clearly, by providing more food, production and survival may be maintained but at the cost of efficiency. This is increasing the resilience of the animal. If feed intake is suppressed, it may be feed quality that needs to be improved, or there may be a need to by-pass the voluntary ingestion system and supply nutrients parenterally, such as occurs when treating pregnancy toxaemia.

Specific effects of disease on wool productionSevere acute disease episodes tend to disrupt homeostasis severely and thus have marked effects of short duration. For wool growth this means that overall effects on fleece weight and mean fibre diameter are small due to the short duration (days, weeks) of the effect on the wool follicle. However, if the magnitude of the effect is large (eg. severe flystrike) the abrupt reduction in wool follicle activity can result in a short term narrowing of the fibre across the whole fleece which results in reduced staple strength or in extreme cases, shedding of the fleece.

In chronic disease wool growth tends to be depressed over long periods resulting in reductions in fleece weights and mean fibre diameter. Effects on staple strength tend to be less marked.

The major diseases affecting wool production in sheep are parasitic. Their effects on wool are summarised below and in Table 7.3.

Blowfly strike - An acute disease of the skin. Direct effects include: 2-8% reduction in wool production (up to 30% during 40 days following fly strike); up to 2% of the clip classified as stained, cotted or dead wool; staple strength may be reduced appreciably; the entire fleece may be shed in severe strikes. Most of the cost is in control

Body lice - A chronic disease of the skin. The itching and rubbing that results also results in wool loss from the fleece (10-30%) as well as cotting and staining (orange/yellow) of the remaining wool. Yield may be reduced by 3-5% in absolute terms. Most of the cost is in control

Helminthiasis (worm infection) - A chronic gut disease with appetite depression as a major feature (severe infections can halve feed intake). It is mainly a problem in young sheep up to 18 months of age. Lambs are affected most, followed by reproducing ewes and then wethers. Effects on production include: 10-30% reduction in greasy fleece weight; 0.5-2 µm reduction in mean fibre diameter; reduced staple length; staple strength may be reduced depending on severity of the severity of worm burden

Bacterial diseases such as footrot (even benign forms) and cheesy gland also cause significant reductions in wool growth while dermatophilus (lumpy wool) and fleece rot affect wool quality.

Table 16.3: Overview of the effects of key diseases on wool production (GFW-Greasy fleece weight, MFD-Mean fibre diameter, SL-Staple length, SS-Staple strength) (Walkden-Brown and Besier 2006).


Notes – Lecture 16 – Sheep Health: Key concepts, economic impact, bacterial and viral diseaseDisease Effects on Wool Traits Other

GFW Yield MFD SL SS

Fly strike ↓+ ↓+ ↓+++ Stain, Cotting

Lice ↓++ ↓++ Stain, Cotting

Helminthiasis ↓+++ ↓+++ ↓++ ↓+

Bacterial DiseaseAcute ↓+ ↓+ ↓+ ↓++

Chronic ↓++ ↓+ ↓+ ↓+

16.4 Viral diseases of sheepThere is only one significant viral disease of sheep in Australia (contagious ecthyma, orf or scabby mouth) with some other viruses of minor importance and a number of important viral diseases that are exotic to Australia.

Contagious ecthyma (orf or scabby mouth) is a common viral disease of sheep and goats in Australia caused by a parapoxvirus. It is a highly contagious, zoonotic, viral skin disease that affects sheep, goats and some other domesticated and wild ruminants. The virus, which survives well in the environment, gains entry through damaged skin, particularly in the lips and interdigital skin, often after eating coarse feed, or thistles, or in the case of the feet, after prolonged exposure to wet pasture. All ages can be affected, but as infection produces strong immunity, the disease is commonly seen in young animals, usually in explosive outbreaks. The virus causes scabby, painful lesions in all sites, but predominantly the mouth, where it interferes with suckling and feeding, or the feet, which may result in lameness or blowfly strike. The udder may also be affected. The disease can transmit to humans, although this is not common. Treatment is generally unrewarding. Outbreaks of this condition on livestock carrier ships carrying sheep to the Middle East have led to rejection of sheep and significant welfare and economic issues. A live attenuated vaccine is available for control or homemade vaccines may be used in the face of an outbreak. The vaccine is applied to a scratch on the inner thigh or foreleg skin where a scab forms but is basically harmless.

Other viral diseases of sheep

Hairy shaker disease (Border disease) is caused by a Flavivirus closely related to the bovine pestivirus/Bovine virus diarrhaoea virus. It causes foetal death and abnormalities in lambs of ewes exposed to it during the first 10 weeks of pregnancy. There are no control measures.

Bluetongue is a major insect-transmitted disease of sheep and goats in the tropical and subtropical regions of the world. Cattle and buffalo can also be infected but tend not to show clinical signs. Eight strains of bluetongue virus occur in Australia (there are 24 worldwide), but they have only been isolated from cattle and insects, and no clinical disease occurs in Australian sheep.

16.4 Bacterial diseases of sheepUnlike for viruses, there are many significant bacterial infections of sheep. Nevertheless, these are less important overall, than the major parasitic diseases caused by multicelled parasites. Brief descriptions of key bacterial diseases are provided below.

Bacterial infections in young lambs are quite common and generally cause one of the following: Septicaemia. Lambs are depressed, have a fever and die rapidly. Mostly associated with

inadequate colostrum intake. Bacterial scours (diarrhoea). This is relatively rare in suckling lambs, but can cause serious

problems in post-weaned lambs. The main causative bacteria are Yersinia and Campylobacter, and treatment is with antibiotics – requiring veterinary diagnosis.

Navel ill. Localised infection around the navel. Can spread to other organs Arthritis. Commonly follows non-fatal septicaemia, or infections at marking time. Bacteria settle

out in the joints which are poorly vascularised, and therefore sequestered somewhat from the



immune system. They set up a chronic joint infection which is responsive to antibiotics only if treated very early. Otherwise cull affected animals. Prevent by good marking hygiene.

Clostridial diseasesThe genus Clostridium comprises rod-shaped gram-positive obligate anaerobes capable of producing endospores which survive for long periods in the environment. The vegetative forms of the bacteria can produce potent exotoxins which are amongst the most potent toxins known. Many of the clostridia are normal gut inhabitants and spores, which are shed in the faeces and are widespread, are the main means of infection. Under the right conditions (anaerobic) spores germinate and bacteria multiply and produce toxins in the gut (enterotoxamia), in wounds (tetanus, malignant oedema), in damaged liver tissue (Black disease) or in muscle (Blackleg). The toxins are responsible for the clinical signs of each disease and as they are proteins, the vaccines which we use to control these diseases are directed against the toxin, not the bacteria producing it. The vaccines are therefore toxoids. The 5 major clostridial diseases of sheep are summarized below. All are well controlled by administration of a 5-in-1 multivalent toxoid vaccine, usually at lamb marking with a booster 4-6 weeks later and an annual booster given pre-lambing. Up to marking time lambs should be protected against these diseases by passive immunity obtained via colostrum. However, if ewes did not receive booster vaccinations in late pregnancy, or a lamb received a marginal dose of colostrum, they disease may occur.

Tetanus caused by Cl. tetani is a highly fatal disease seen in lambs within 3 weeks of marking. Affected lambs show rigidity of the limbs and body, tremors and pricked ears and restricted jaw movements. Sudden sounds or movements can trigger convulsions and affected lambs usually die within 3-4 days of signs becoming evident.

Malignant oedema or gas gangrene caused mainly by Cl. septicum is a highly fatal disease mainly of sheep and mainly due to lack of, or failure vaccination. It is a wound infection characterised by swelling, dark discoloration, bloodstained discharge and gas production. Affected sheep become dull, lie down and generally die 24-48 hours after signs are first observed. Infectious typically follow man made wounds or crow pick, lambing injury or dog bites. Treatment may be attempted if the condition is caught early.

Black disease caused by Cl. novyi Type B is a highly fatal disease of sheep of all ages following liver damage caused by immature liver fluke. The livers of normal sheep generally carry spores of Cl. novyi Type B which is widespread – it is the liver fluke injury which triggers the disease. Sheep are generally found dead and putrefy fast. Pale coloured necrotic areas on the liver, and liver damage and immature flukes may be seen on post mortem.

Blackleg caused by Cl. chauvoei is a highly fatal disease seen in sheep of all ages generally when vaccination has not occurred or has failed. Wounds or muscle can be affected and animals develop a high fever, dark discoloration of the area with gas production and die within a few hours of the first clinical signs. More common in cattle.

Enterotoxaemia or Pulpy Kidney caused by Cl. perfringens Type D is a highly fatal disease, generally of lambs growing rapidly on lush feed or sheep of any age being grain fed. It mainly occurs when vaccination has not occurred or has failed. Most sheep are simply found dead with death occurring within 24 hrs of signs. Signs include dullness, convulsions and frothing at the mouth. Diagnosis is difficult and post mortem findings often unremarkable.

Bacterial hoof infectionsLameness in sheep is often associated with bacterial infections and it is important to differentiate between following disease syndromes.

Footrot caused by Dichelobacter nodosus is a notifiable highly contagious disease of sheep of all ages. It is characterised by seasonal occurrence (warm wet periods), many sheep being affected, multiple hooves affected on individual sheep, and severe lameness and hoof lesions including underrunning of the hoof horn and fly strike. There is a wide spectrum of virulence/severity. The disease must be reported and each state has its own control program. Control is difficult. There is vaccine which can assist with control, but which does not completely eliminate the disease.

Ovine interdigial dermatitis is caused by Fusiformis necrophorus and initially looks like footrot with a scald between the claws and multiple sheep and feet affected, although any lameness is mild. Also it does not go on to develop the severe underrunning observed with footrot. Control is via footbathing or waiting for paddocks to dry out.

Foot abscess is also initiated by Fusiformis necrophorus. This is a non-contagious hoof infection generally affecting a few sheep in one foot only. Sheep are typically heavy and conditions wet and muddy. Toe abscess is seen in the front feet and entry is gained via a crack in the hoof. Heel abscess is mostly seen in the hind feet of heavy sheep and entry is via the

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interdigital skin. Pus accumulates in the abscess causing intense pain and severe lameness. Sometimes the pus breaks out relieving the pain. Treatment is generally by drainage via hoof paring, together with antibiotics.

Pinkeye (infectious keratoconjunctivitis, contagious opthalmia)This is a highly contagious eye infection caused by Mycoplasma conjunctivae. Note that the organisms causing pinkeye in cattle, sheep and goats all differ. The condition is favoured by dry dusty conditions and flies, which help spread the organism. Outbreaks are most common in weaners and feedlot sheep. The infection is very painful, sheep lose condition and some may be permanently blinded. Treatment is mainly with topical antibiotics (ointments are best), but repeat treatments need to be made and the value assessed against the stress and dust associated with mustering for treatment.

Cheesy Gland (Caseous lymphadenitis or CLA)This is a very common but slow developing infection of lymph nodes caused by Corynebacterium pseudotuberculosis. Infected sheep show few visible signs although performance is reduced by around 5% and occasional burst glands may be observed, especially in front of the shoulder. The disease shows up mostly in the abattoir where “cheesy” abscesses of lymph nodes in a range of tissues are found, with condemnation of affected areas. This mostly seen in older mutton sheep. The disease is thought to be transmitted during shearing and dipping and is best controlled by vaccination. The 6-in-1 vaccine covers the main clostridial diseases plus cheesy gland.

Mycoplasma ovis infection (previously Eperythrozoonosis)M. ovis infects red blood cells causing anaemia, jaundice, loss of production and death in severe cases. It is a common infection, particularly in high rainfall areas. It affects all ages of sheep but severe infections are mainly seen in weaners. The organism is spread by infected blood cells, so mosquitoes and stock management procedures that induce bleeding are the main causes of spread. Treatment with antibiotics is effective but expensive and control is mainly via good marking hygiene and reducing stress on weaned sheep.

Ovine brucellosisThis is a venereal disease (spread by mating) caused by Brucella ovis. It is largely a disease of the ram testicle and epididymis with few effects on ewes. British breeds are thought to be more susceptible. The acute disease causes swelling and warmth of the testis which progresses to fibrosis (hardening) of the testis and enlargement and hardening of the tail of the epididymis, with associated loss of fertility. There is no effective treatment and the aim is generally to eradicate the disease from affected properties using a blood test with culling of affected rams. Most states have brucellosis accreditation programs. Properties free of the disease need to buy rams or semen from accredited free sources.

Ovine Johne’s disease (OJD)This is another slow developing disease, caused by a sheep specific strain of Mycobacterium paratuberculosis. It is a chronic wasting disease, mainly of older sheep with no effective treatment. The disease has a relatively limited distribution with high prevalence areas restricted to central southern NSW and the eastern half of Victoria. It is generally transmitted by movement of stock. Diagnosis on an individual sheep basis is inaccurate, so testing and control is herd based. OJD has been the subject of major control programs, originally aimed at eradication. The current aim is to manage the disease using market assurance programs, risk assessment and declaration on the Animal Health Statement together with individual property disease management plans. These may include the use of a vaccine.

Readings There are no prescribed readings for this lecture. Students are advised to access and read papers that interest them in the references section.

References



Besier, B., Jacobson, C., Woodgate, R. and Bell, K. (2010). Sheep Health. In “International Sheep and Wool Handbook” (ed. D.J. Cottle) Nottingham University Press, Nottingham.

Brightling, A. 2006, Livestock Diseases in Australia, C.H. Jerram & Associates, Mt. Waverley Victoria, pp. 388

Brightling, A. 2006, ‘Vaccination’, in Livestock Diseases in Australia, C.H. Jerram & Associates, Mt. Waverley Victoria, pp. 31-34.

Brightling, A. 2006, ‘Worm control – sheep’, in Livestock Diseases in Australia, C.H. Jerram & Associates, Mt. Waverley Victoria, pp. 1-11.

Broadmeadow, M., Gibson, J.E., Dimmock, C.K., Thomas, R.J. and O'Sullivan, B.M. 1983, ‘The pathogenesis of flystrike in sheep’, Sheep Blowfly and Flystrike in Sheep, (Ed. Raadsma, H.W.), University of NSW, Sydney, NSW Department of Primary Industries, Orange, NSW, pp. 327-332

Colditz IG, Walkden-Brown SW, Daly BL, Crook BJ (2005) Some physiological responses associated with reduced wool growth during blowfly strike in Merino sheep. Australian Veterinary Journal 83(11), 695-699.

Colditz IG (2008) Six costs of immunity to gastrointestinal nematode infections. Parasite Immunology 30(2), 63-70.

Edwards, C.M., al-Saigh, M.N.R., Williams, G.L.I. and Chamberlain, A.G. 1976, ‘Effect of liver fluke on wool production in Welsh Mountain Sheep’, Veterinary Record, vol. 98, pp. 372.

Ferguson, K.A., Wallace, A.L.C. and Lindner, H.R. 1965, ‘Hormonal regulation of wool growth’, Biology of the skin and hair growth. Proceedings of a symposium held at Canberra, Australia, August 1964 (Eds. Lyne, A.G. and Short, B.F.), Angus and Robertson, Sydney.

Greer AW, Stankiewicz M, Jay NP, McAnulty RW, Sykes AR (2005) The effect of concurrent corticosteroid induced immuno-suppression and infection with the intestinal parasite Trichostrongylus colubriformis on food intake and utilization in both immunologically naïve and competent sheep. Animal Science 80, 89-99.

Greer AW (2008) Trade-offs and benefits: implications of promoting a strong immunity to gastrointestinal parasites in sheep. Parasite Immunology 30(2), 123-132.

Greer AW, Huntley JF, Mackellar A, McAnulty RW, Jay NP, Green RS, Stankiewicz M, Sykes AR (2008) The effect of corticosteroid treatment on local immune responses, intake and performance in lambs infected with Teladorsagia circumcincta. International Journal for Parasitology 38(14), 1717-1728.

Johnstone, I.L., Darvill, F.M., Bowen, F.L., Butler, R.W., Smart, K.E. and Pearson, I.G. 1979, ‘The effect of four schemes of parasite control on production in Merino wether weaners in two environments’, Australian Journal of Experimental Agriculture and Animal Husbandry, vol. 19, pp. 303-311.

Lipson, M. and Bacon-Hall, R.E. 1976, ‘Some effects of various parasite populations in sheep on the processing performance of wool’, Wool Technology and Sheep Breeding, vol. 23, pp. 18-20.

Sackett D, Holmes P, Abbott K, Jephcott S, Barber M (2006) Assessing the economic cost of endemic disease on the profitability of Australian beef cattle and sheep producers. Final Report of Project AHW.087. Meat and Livestock Australia, Sydney.

Steel, J.W. and Symons, L.E.A. 1979, ‘Current ideas on the mechanisms by which gastrointestinal helminths influence the rate of wool growth’, in Physiological and environmental limitations to wool growth, (Eds. Black, J.L. and Reis, P.J.), University of New England Publishing Unit, Armidale, pp. 311-325.

Williams AR (2011) Immune-mediated pathology of nematode infection in sheep - is immunity beneficial to the animal? Parasitology 138(05), 547-556.

Useful references for veterinary terms are medical or veterinary dictionaries. A useful veterinary dictionary which may be in your library is:

Blood, D.C. and Studdart, V.P. 1988, Ballière's Comprehensive Veterinary Dictionary. Ballière Tindall, Sydney. pp. 1123. It has 52,000 entries!

16-12 _______________________________________________WOOL412/512 Sheep Production© 2013 The Australian Wool Education Trust licensee for educational activities University of New England

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