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Topic 13: Managing Sheep Health

Steve Walkden-Brown and Brown Beisier

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 production diseases of sheep and their control.

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 describe some important diseases of sheep.

13.1 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.

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

WOOL300 Fundamentals of Sheep and Wool Production 13-1© 2014 The Australian Wool Education Trust licensee for educational activities University of New England

Notes – Topic 13 – Managing Sheep Health

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.

13.2 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 13.1. 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 13.1: Summary of major threats to sheep health in Australia for different classes (Walkden-Brown and Besier 2006).

Class of stock Main disease threats ReasonSuckling 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

13.3 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.

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

13-2 WOOL300 Fundamentals of Sheep and Wool Production© 2014 The Australian Wool Education Trust licensee for educational activities University of New England


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 13.2 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 13.2: Cost ($m) of the major endemic diseases of sheep in Australia (Sackett et al. 2006).

Disease Cost of control ($m) Production loss ($m) TotalInternal parasites 59 310 369Flystrike 197 83 280Lice 83 40 123Post-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 17.2, 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).

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 13.4, 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 17.5). 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 13.4: 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 13.5: 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 13.3.

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 13.3: 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).

Disease Effects on Wool Traits Other

GFW Yield MFD SL SS

Fly strike ↓+ ↓+ ↓+++ Stain, Cotting

Lice ↓++ ↓++ Stain, Cotting

Helminthiasis ↓+++ ↓+++ ↓++ ↓+

Bacterial DiseaseAcute ↓+ ↓+ ↓+ ↓++

Chronic ↓++ ↓+ ↓+ ↓+

13.4 Example of diseases of importance for sheep and wool productionThere are many diseases that can impact on sheep and wool production in the ways outlined in the previous sections. These diseases can be classified as bacterial, viral and parasitic (both internal and external) and some examples of each are outlined below. For further information on any of these diseases or other diseases of interest to you there are a number of useful textbooks listed in the References.

Internal parasitesThis is the major disease problem of the sheep industry in all but the low rainfall pastoral areas of Australia. It is a chronic disease, with loss of animal production being a major feature. However, infection can be acute and also fatal, particularly in the case of Barber’s pole worm. The three most important species in Australia are:

Haemonchus contortus (Barber’s Pole worm). The mature worm lives in the abomasum, attaching to the stomach lining and feeding by sucking blood. It thrives in warmer, wetter regions and seasons. This is the major nematode in summer rainfall areas of Australia.

Trichostrongylus spp. (Black Scour worm). The mature worm lives in association with the epithelium of the first 3-4 metres of small intestine, probably living on gut cells and fluids. Several species occur depending on climate, so it is the most widespread of the worms. These worms can handle cooler, dryer conditions better than Haemonchus and are the most universal of the common nematodes. Different species affect different climatic regions. T. colubriformis is the main species in summer rainfall regions while T. virtinus is the main species in winter rainfall areas.

Teladorsagia (or Ostertagia) circumcincta. (Small Brown Stomach worm). The mature worm lives deep in the crypts of the abomasum. This is a cold tolerant parasite of cool/cold wet regions. It is a major sheep nematode in winter rainfall areas.

The life cycle is very similar for these species and involves phases in the host animal (parasitic) and in the environment (free living) (Figure 13.6). This poses a major challenge in control, because while it is relatively easy to target the parasite while it is in the host, the environmental stages of the life cycle are much more difficult to attack. The life cycle is direct, with no intermediate hosts. Sheep become infected with nematodes when feeding on contaminated pastures, consuming infective larvae while grazing. The larvae pass into the gastrointestinal tract where they develop into mature adults. These



adults mate and the females lay eggs which pass out in the faeces of the host. Once the eggs hatch, the larvae undergo three stages of development within the faecal pellet (without multiplication), with the L3 stage being the infective stage. The L1 and L2 larvae live on bacteria and fluids in the faeces but the infective L3 larvae are encased in a protective sheath and cannot feed until ingested by a host. L3 migrate from the faeces onto the pasture and into the soil if there is sufficient moisture and are ingested by sheep from the pasture. Large numbers of eggs, L1 and L2 larvae perish from desiccation and low oxygen tension and typically only 0-5% of eggs develop into infective L3 larvae. Once ingested, L3’s undergo exsheathment and develop into adults over about a 16 day period.

Figure 13.6: Lifecycle of typical gastro-intestinal nematode parasite of sheep. This lifecycle is common to all of the major genera such as Haemonchus, Trichostrongylus and Ostertagia (Walkden-Brown and Besier 2006).

Key features of helminth infections are: These are diseases of high rainfall areas. Larval development and survival are dependent

upon moist conditions. The risk of disease increases with increasing rainfall. Because of the development of immunity with age and exposure, these are mainly diseases

of young stock. However liver fluke and barber's pole worm induce little immunity and may affect adult sheep. Immunity to all helminths is reduced during the peri parturient period.

The main outward signs of infection are diarrhoea or scouring (black scour worm, small brown stomach worm) or anaemia (barber's pole worm and liver fluke). All types cause poor body and wool growth due to disturbances in protein metabolism and this occurs well before obvious signs are present. In general, moderate helminth infections cause 10-30% reductions in body growth and annual wool production in young stock with smaller depressions in older stock.

Control has relied traditionally on chemical (anthelmintic) treatment supplemented with basic grazing management, but has now expanded to include a range of strategies such as breeding for worm resistance and more advanced grazing strategies. These methods can be combined into integrated parasite management (IPM) packages that maintain good worm control but limit the development of anthelmintic resistance (Eg. Kelly et al, 2010).

Strategic application of chemicals (anthelmintics) aimed at breaking the life-cycle and reducing pasture contamination with larvae is the main form of control. Generally this involves targeting worms in the sheep when environmental conditions are least favourable for survival of the environmental phases of the life cycle. Drenching sheep when 95% of worms are in the environment and only 5% in the sheep has little impact on the worm population. Wormboss is a key industry decision support tool and worm control information site developed by the Sheep CRC is available on the web (see: http://www.wool.com/Grow_WormBoss.htm).

Over the last 15 years the use of slow release drench capsules has also increased, particularly in weaners and periparturient ewes. These provide up to 100 days of continuous


http://www.wool.com/Grow_WormBoss.htm


protection and eliminate pasture contamination during this period. However, they speed up the development of anthelminitc resistance.

Grazing management is also important. This may involve spelling or cultivation of pastures, or the use of older immune animals or other species (eg. cattle), to reduce the numbers of infective larvae on pasture. Generally speaking ewes should be drenched and placed onto clean pastures for lambing, and lambs should be drenched and moved onto clean pastures at weaning. Rotating grazing between cattle and sheep causes a dramatic reduction in worm burdens because they do not share the same parasites.

Resistance to anthelmintics is widespread in the helminth population. Development of resistance is slowed by minimising the frequency of drenching, rotating drench types, using narrow spectrum drenches instead of broad spectrum drenches as much as possible, and avoiding the use of capsules. The efficacy of a drenching program can be monitored by measuring FEC (faecal egg counts - counts of worm eggs in sheep faeces).

There is considerable variation in genetic resistance to nematode infection in sheep populations and increasingly selection of worm resistance is being included in sheep selection programs. Breeding for Increased Genetic Resistance by placing greater emphasis on resistance to gastrointestinal nematodes in the breeding objectives. The heritability of WEC is about 0.25. Australian Sheep Breeding Values for WEC are readily available for a range of sires through Sheep Genetics® (Lambplan® and MerinoSelect).

Level of nutrition, particularly protein nutrition also influences resistance to worms, and there is scope for including this in the rationale for supplementing sheep, particularly young sheep.

A potential new method of control is the use of nematophagous (nematode eating) fungi. Vaccination has not been successfully developed to date.

External parasitesBlowfly strike and body lice are the two major external parasites affecting sheep and wool production in Australia. Only blowfly strike will be discussed here.

Blowfly strike is an acute disease caused by the feeding of blowfly larvae on the skin of sheep. The disease generally runs a short course (days to a couple of weeks) of varying severity. It has been estimated that up to 80% of fly strikes are small covert strikes causing minor illness that are not noticed by the producer. On the other hand severe strike can kill sheep in a matter of days. The effect of flystrike on wool production depends on the severity and frequency of strikes and is outlined in Table 13.3.

The primary strike fly is the Australian sheep blowfly Lucilia cuprina which initiates 80-90% of strikes. The fly is about the size and shape of a normal house fly but has a green body and forelegs.Figure 13.7 illustrates the lifecycle of the sheep blowfly. The female requires a protein meal before laying eggs, this being obtained from sources such as faeces and carrion. Over a 2-3 week lifespan, the female lays 2-3 batches of 50-250 eggs in the soiled or wet fleece (as well as carrion), being attracted by putrefactive odours and a “sheep odour”. Note that flies will only lay eggs on wounds or inflamed skin (dermatitis). They will not initiate a strike on normal skin.



Figure 13.7: The lifecycle of Lucilia cuprina, the Australian sheep blowfly (Levot 1999).

Types of blowfly strikeThere are a number of forms of flystrike, each differing in the causal factors and the control methods.

Breech strike - flies strike the breech or tail skin with dermatitis due to wetting with urine and/or diarrhoea (scouring). This is the most common form of blowfly strike

Body strike - flies strike the back or sides of the body, on skin with dermatitis (eg. fleece rot or lumpy wool). This is the second most common form of blowfly strike

Poll strike - flies strike the head on rams at fighting wound sites, or where the horns grow close to the skull creating a microenvironment suitable for strike

Pizzle strike - flies strike the urine-soaked area around the prepuce of males Wound strike - flies strike wounds such as marking, mulesing and shearing cuts, as well as

those associated with footrot, foot scald and scabby mouth.

The occurrence of fly strike is influenced by a range of environmental (temperature, rainfall, wind) and host (genotype, phenotype, presence of dermatitis) factors. Strategies for controlling blowfly strike can involve modification of the host or the environment. As it the case with worm control, integrated parasite management (IPM) approaches, using a range of control strategies in concert are ideal. The FlyBoss® web site contains a wealth of information about blowflies and blowfly control, including decision support tools.

Conventional control measures Permanent modification of host phenotype. to reduce the incidence of breech strike in all

sheep (mulesing and tail docking) and pizzle strike in wethers (pizzle dropping). Although mulesing is being phased out.

Non-permanent modifications of host. These include shearing prior to the main fly period for control of body strike, and crutching of ewes and ringing of wethers and rams prior to fly waves for controlling breech and pizzle strike. As scouring can also facilitate breech strike, controlling parasitic and nutritional scours in stock will reduce the incidence of breech strike. In sheep treated with ivermectin capsules to control worms, the residual ivermectin in faeces, and dags inhibits breech strike establishment (Rugg et al. 1998).

Chemical treatment of the host has been widely used in the control of flystrike via shortwool treatments (dipping by plunge or spray, or backline application) or longwool treatments (jetting by hand or jetting race, backline spray). There are a number of classes of insecticide available for use, varying in their mode and duration of action, the degree to which residues in wool are a problem, whether they control lice or not, and the extent to which resistance has


http://www.flyboss.org.au/


developed. The FlyBoss® tools are an excellent aid to optimising the number and frequency of treatments and the chemicals to use.

Genetic selection. Culling for susceptibility to body strike directly and indirectly on the basis of fleece rot, has been and continues to be widely used in high rainfall areas. Early attempts in the 1970s at breeding easy care Merino’s that did not require mulesing were unsuccessful but with the phasing out of mulesing, genetic selection for resistance to breech strike is now a key strategy for long term blowfly control. SheepGenetics®/MerinoSelect® now offer Australian Sheep Breeding Values (ASBVs) for rams for the following breech traits

o Breech wrinkle scoreo Breech cover scoreo Dag score

Monitoring or manipulating the environment. This is less widely practiced. Modelling studies have shown that fly populations are much more sensitive to factors affecting adult fly mortality than larval mortality, so the main strategy is to target the adult fly. Fly traps containing chemical attractants such as LuciTrap can reduce fly numbers by as much as 50% and may provide some reduction in strikes.

Controlling carrion. The value is uncertain, given that secondary fly maggots out-compete and kill primary fly maggots in carrion. This strategy is unlikely to have a major effect on population size of Lucilia cuprina, although it would reduce the size of secondary fly populations.

Potential additional control measuresPotential control measures that have been tried or considered include:

Vaccination. There are two approaches, both of which are experimental at present. Firstly to vaccinate against fly antigens such as peritrophic membrane antigens in the gut of the fly (hidden antigen approach) or secondly to vaccinate against fleece rot, though this is hampered by the diversity of strains of P. aeruginosa. There is still substantial progress to be made in the development of effective vaccines

Use of controlled release capsules containing ivermectin (eg. Ivomec Maximizer®) to control parasitic scours. In addition to the benefits in reducing scours, sheep that continue to scour are protected by the insecticide action of residual ivermectin in their faeces (Rugg et al. 1998).

Use of bacillus thuringiensis toxins. This organism is a normal inhabitant of the sheep skin and there is scope for use of its toxins as a natural control of flystrike. However, it does not have the same degree of persistence in the fleece as do the chemical treatments

Biological control of adult flies. The microsporidium Octosporea muscaedomesticae and various fungal toxins show some promise but there is still some way to go in the development of these methods as commercial strategies

Releasing sterile males. This relies on the principle that female flies tend to mate once, such that if she mates to a sterile male, no viable eggs will be laid. Males can be sterilised by irradiation. This has been used to eradicate screw worm fly from some areas around the world but is prohibitively expensive to implement

Releasing males with defective genes. This has been used with success on a local scale in Australia but would require an expensive national effort to produce sustained results

Genetic engineering. One approach is to engineer the host or skin bacteria to produce inhibitory products such as chitinase to disrupt the development and activity of insect pests.

Viral diseaseThere 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


http://www.flyboss.org.au/


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.

Bacterial diseaseUnlike 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. Some key bacterial diseases include footrot, clostridial diseases and cheesy gland and are described below.

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.

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.



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.

ReadingsThere are no readings provided however it is recommended that students use the reference list to select papers that may be of interest to them.

Revision Questions1. Describe how the impacts of disease can be classified.

2. What are the economic impacts of disease on the sheep industry?

3. How does disease impact on wool production?

4. What are the major diseases of sheep?

5. Describe one major sheep disease, its impacts on production and how it can be controlled.

ReferencesVarious Authors 2003, in Special issue on Nutrition-Parasite Interactions in Sheep

Australian Journal of Experimental Agriculture, Vol. 43(12). Available at: http://www.publish.sciro.au/nid/73/issue/627.htm. Retrieved Aug 2003.

Arundel, J.H. and Sutherland, A.K.. 1988, Animal Health in Australia Volume 10. Ectoparasitic diseases of sheep cattle goats and horses, Australian Government Publishing Service, Canberra. pp. 178.

Atkins, K.D. and McGuirk, B.J. 1979, ‘Selection of Merino sheep for resistance to fleece rot and body strike’, Wool Technology and Sheep Breeding, vol. 27, pp. 15-19.

Bailey JN, Kahn LP, Walkden-Brown SW (2009a) Availability of gastro-intestinal nematode larvae to sheep following winter contamination of pasture with six nematode species on the northern tablelands of New South Wales. Veterinary Parasitology 160, 89-99.

Bailey JN, Walkden-Brown SW, Kahn LP (2009b) Comparison of strategies to provide lambing paddocks of low gastrointestinal nematode infectivity in a summer rainfall region of Australia. Veterinary Parasitology 161(Issues 3-4, 12 May 2009), 218-231

Barger, I.A., Dash, K.M. and Southcott, W.H. 1978, ‘Epidemiology and control of liver fluke in sheep’, in The epidemiology and control of gastrointestinal parasites of sheep in Australia, (Eds. Donald, A.D. et al.) CSIRO, Melbourne. pp. 65-74.

Besier RB, Love SCJ (2003) Anthelmintic resistance in sheep nematodes in Australia: the need for new approaches. Australian Journal of Experimental Agriculture 13(12), 1383-1391.

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. 1994, Stock Diseases, Inkata Press, Melbourne, pp. 328Brightling, A. 2006, Livestock Diseases in Australia, C.H. Jerram & Associates, Mt. Waverley Victoria,

pp. 388Brightling, 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

Brown DJ, Swan AA, Gill JS (2010) Within- and across-flock genetic relationships for breech flystrike resistance indicator traits. Animal Production Science 50(12), 1060-1068.

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.

Cole, V.G. 1986, Animal Health in Australia Volume 8. Helminth parasites of sheep and cattle, Australian Government Publishing Service, Canberra. pp. 255.

Colvin AF, Walkden-Brown SW, Knox MR, Scott JM (2008) Intensive rotational grazing assists control of gastrointestinal nematodosis of sheep in a cool temperate environment with summer-dominant rainfall. Veterinary Parasitology 153(1-2), 108-120.

Colvin AF, Walkden-Brown SW, Knox MR (2012) Role of host and environment in mediating reduced gastrointestinal nematode infections in sheep due to intensive rotational grazing. Veterinary Parasitology 184, 180-192.

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.

Joshua, E., Junk, G., Levot, G. 2010, Sheep lice, Primefact 483, NSW Department of Primary Industries, Orange, NSW.

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.

Kelly GA, Kahn LP, Walkden-Brown SW (2010) Integrated Parasite Management for sheep reduces the effects of gastrointestinal nematodes on the Northern Tablelands of NSW. Animal Production Science 50, 1043–1052.

Levot, G. 1999, Life Cycle of the sheep blowfly, Agnote DAI-192, first edition, December, NSW Department of Primary Industries, Orange, NSW.

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.

McLeod, R.S. 1995, ‘Costs of major parasites to the Australian livestock industries’, International Journal of Parasitology, vol. 25, pp. 1363-1367.

Murray, W. and Mortimer, S. 2001, Scoring sheep for fleece rot, Agfact A3.3.41, NSW Department of Primary Industries, Orange, NSW, pp. 4.

Niven P, Anderson N, Vizard AL (2002) The integration of grazing management and summer treatments for the control of trichostrongylid infections in Merino weaners. Australian Veterinary Journal 80(9), 559-566.

O'Connor LJ, Walkden-Brown SW, Kahn LP (2006) Ecology of the free-living stages of major trichostrongylid parasites of sheep. Veterinary Parasitology 142, 1-15.

Rugg D, Thompson D, Gogolewski RP, Allerton GR, Barrick RA, Eagleson JS (1998) Efficacy of ivermectin in a controlled-release capsule for the control of breech strike in sheep. Australian Veterinary Journal 76(5), 350-354.



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.

Smith J, Brewer H, Dyall T Heritability and phenotypic correlations for breech strike and breech strike resistance indicators in Merinos. In 'AAABG', 2009, pp. 334-337

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.

Walkden-Brown, S.W., Daly, B.L., Colditz, I.G. and Crook, B.J. 2000, ‘Role of anorexia in mediating effects of blowfly strike on wool’, Asian-Australasian Journal of Animal Science, vol. 13, Supplement July B, pp. 76-79.

Wilkinson, F.C., de Channet, G.C. and Beetson, B.R. 1982, ‘Growth of populations of lice, Damalinia ovis, on sheep and their effects on production and processing performance of wool’, Veterinary Parasitology, vol. 9, pp. 243-252.

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


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