7. sheep health · 2017-07-10 · 7.1 a framework for understanding health and disease several key...

7 - 1 – WOOL412/512 Sheep Production ©2009 The Australian Wool Education Trust licensee for educational activities University of New England

7. Sheep Health

Steve Walkden-Brown and Brown Besier

Learning Objectives On 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 quantify the impact and discuss the management of disease caused by

internal and external parasites of sheep

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

Introduction to the topic Disease 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 consider internal and external parasitic disease of sheep in considerable detail.

7.1 A framework for understanding health and disease Several 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

• Tactical. Aimed at intervening to control disease when certain risk factors arise, or when disease monitoring indicates that intervention is worthwhile. This is usually well before the onset of clinical disease and so offers some level of control of sub-clinical disease

• Strategic. Strategic control is 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

• 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.

7.2 Major disease syndromes in sheep The 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 7.1. 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 7.1 Summary of major threats to sheep health in Australia for different classes. Source: 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 skills Post 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 Adult sheep Blowfly strike No vaccine or significant immunity

development Lice No vaccine or significant immunity

development Roundworm infection Weak or intermittent immunity Footrot (regional) Only weak immunity develops Liver fluke infection (regional) No vaccine or significant immunity Ovine Johne’s disease

(regional) Long incubation period

Reproducing females

Pregnancy toxaemia (twin lamb disease)

Nutrient demands of twin foetuses

Hypocalcaemia High calcium requirement in milk Dystocia/metritis/mastitis Complications of giving birth Helminth infections

(roundworms, flukes) Periparturient loss of immunity


7.3 Impact of disease Disease 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 disease The 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 production This 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 control Many 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 7.2 presents some formal estimates of the cost of the major sheep diseases to the Australian sheep industry. There are no more recent authoritative estimates, although Australian Wool Innovation is planning to commission another study. Costs are broken down into loss of production and costs of control. Note that the three most important diseases of sheep are parasitic and this is why this module will concentrate on parasitic disease in sheep. 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 $4 billion, these four diseases alone cost some 16% of this value. Table 7.2 Cost of the major endemic diseases of sheep in Australia. Source: Sackett et al (2006) Disease Cost of control ($M) Production loss ($M) Total ($M)

Blowfly strike1 130 31 161

Body lice1 114 55 169

Worms1 81 141 222

Footrot2 63 18 81

Total 388 245 633 1McLeod, R. S. (1995) 2Collins, D. (1992)


c) Loss of market opportunity Although not reflected in the formal estimates of disease cost in Table 7.2, 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, 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.

Did you know?

An epidemic of ovine Johne's disease (paratuberculosis) has been slowly spreading in Australia since its initial identification in the Central Tablelands of NSW in 1980. The lives of many sheep producers, particularly stud owners, have been thrown into turmoil by the trading restrictions imposed on producers once they test positive to the disease. At 30 June, 2003, 631 flocks were classified as Infected with a further 2,446 flocks (3.0 % of Australian flocks) under investigation as either Suspect or Under Surveillance flocks. There have been a total of 1,872 flocks (2.3% of Australian flocks) detected as Infected since 1980. For more information go to http://www.agric.nsw.gov.au/reader/ojd

Disease mechanisms resulting in loss of production in sheep Disease, both 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 disease The 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) disease Generalised 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 response The 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.

One of the important diseases of sheep that is characterised by a massive systemic response is blowfly strike. 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). A recent study investigated the role of anorexia in mediating the effects of blowfly strike on wool growth (Walkden-Brown et al., 2000). 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 7.1, 7.2 and 7.3 respectively.


Figure 7.1 Rectal temperature (mean ± SEM) before and during flystrike. The Struck group were infected on days 0-7. (* P<0.05). Source: Walkden-Brown et al. (2000).

Day of infection

1 3 5 7 9 11 13 15

Temperature (

oC)

38

39

40

41Control StruckPair-fed*

* * * * * * * *

Figure 7.2 Plasma IL-6 (mean ± SEM) before and during flystrike (as above). Source: Walkden-Brown et al. (2000).


Figure 7.3 Feed intake (mean ± SEM) of 2 weeks before and 6 weeks after initiation of the flystrike treatment (as above). Source: Walkden-Brown et al. (2000).

Week

-1 0 1 2 3 4 5 6

Daily feed intake (g/kgB

W0.75

)

20

30

40

50

60

70

80

Control StruckPair-fed

* *

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 response Components 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 7.4, 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 7.5). 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 7.4 Plasma cortisol concentrations (mean ± SEM) before and during flystrike. The Struck group were infected on days 0-7. (* P<0.05). Source: Walkden-Brown et al. (2000).

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 7.5 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. Source: Ferguson (1965).

Effects of disease on the efficiency of feed utilisation for production Any 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 production Severe 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 7.3. Overview of the effects of key diseases on wool production (GFW-Greasy fleece weight, MFD-Mean fibre diameter, SL-Staple length, SS-Staple strength). Source: 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 Disease Acute ↓+ ↓+ ↓+ ↓++

Chronic ↓++ ↓+ ↓+ ↓+


7.4 Internal parasites The major disease problems of the Australian sheep industry are parasitic in nature (Table 7.1). This is typical of grazing industries where parasites that spend part of their lifecycle in the environment prove difficult to control, particularly during the environmental phases of the lifecycle. Classification of major gastro-intestinal parasites of sheep Of the internal parasites of sheep the vast majority inhabit the gastro-intestinal tract. Lungworm infection can be important locally but is not a major disease under Australian conditions and will not be considered further. Nasal bot infection with the larvae of the fly Oestrus ovis is widespread and discomfiting but appears not to have major effects on productivity. Apart from coccidiosis, a disease caused by a protozoan parasite, all of the major gastro-intestinal parasites of sheep are helminths (“worms”) and the rest of this topic will focus on these. Gastro-intestinal helminthiasis (also called helminthosis) is the single biggest disease problem of sheep in Australia. Of the helminths the nematodes (roundworms) are most widely distributed and by far the most important of the helminth parasites (Figure 7.6). Liver fluke is also an important parasite, but has a much more restricted distribution. Tapeworms are common and spectacular for their size, but appear to have few adverse effects on productivity.

Figure 7.6 Broad classification of the major helminth parasites of sheep. Source: Walkden-Brown and Besier (2006).

Gastro-intestinal nematode infection This 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. Species and life cycle Table 7.4 lists the common species in Australian sheep. 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.

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.

Ostertagia spp. (also known as Teladorsagia spp. Small Brown Stomach worm). The mature worm lives deep in the crypts of the abomasum. This is a parasite of cool/cold wet regions.

Roundworms(Nematodes)• Haemonchus contortus• Trichostrongylus spp.• Ostertagia circumcincta• Numerous other spp.• Lungworms

Flukes(Trematodes)• Fasciola hepatica

Tapeworms(Cestodes)• Monezia spp.

Helminths (Worms)


The life cycle is very similar for these species and involves phases in the host animal (parasitic) and in the environment (Figure 7.7). 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 lay eggs which pass out in the faeces of the host. Once the eggs hatch, the larvae undergo three stages of development (without multiplication), with the L3 stage being the infective stage. The L1 and L2 larvae live on bacteria and fluids in the faeces of soil but the infective L3 larvae are encased in a protective sheath and cannot feed until ingested by a host. 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 a 16 day period.

Table 7.4 Common gastrointestinal nematodes of sheep in Australia and their prevalence in the different rainfall zones. Source: Walkden-Brown and Besier (2006).

Specific name Common name Location Egg production*

Rainfall zone

Summer Winter

Haemonchus contortus Barber's Pole worm Abomasum 5,000-10,000 +++ +

Trichostrongylus spp. Black Scour worm Small intestine 100-200 +++ +++

Ostertagia circumcincta Small Brown Stomach worm Abomasum 100-200 ++ +++

Nematodirus spp. Thin Necked Intestinal worm Small intestine 50 ++ ++

Oesophagostomum spp. Large Bowel worm/Nodule worm Large intestine 5,000-12,000 ++ ++

Chabertia spp. Large Mouthed Bowel worm Large intestine ? + +++

Trichuris spp. Whip worm Large intestine ?

*Daily egg production by a single adult female worm

Figure 7.7 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. Source: Walkden-Brown and Besier (2006).


In Nematodirus, the L1 to L3 development occurs within the egg making it particularly resistant to adverse environmental conditions. In Trichuris, the eggs hatch once they are eaten by the host. The duration of the lifecycle varies widely, depending on environmental conditions and worm species. But under optimum conditions it can be as short as 3 weeks from egg to egg (16 days in the host and 5 days in the environment). When environmental conditions are unfavourable some L4 larvae enter into hypobiosis (arrested development) in the wall of the gut and remain in this state, only resuming development when conditions improve. Factors affecting distribution and prevalence (epidemiology) Environmental factors These largely determine the distribution of parasites as shown in Table 7.4 and their prevalence on pasture during the year as shown in Figure 7.8.

• Temperature. An air temperature of >10°C is required for larval development of most species and >15°C for Haemonchus. Rate of development and the speed of the lifecycle increases with increasing temperature. Very high temperatures are lethal, but the effects of high temperatures are mainly mediated by increased desiccation

• Moisture. Desiccation is the major cause of losses in the environment. Eggs, L1 and L2 are most affected. Approximately 50mm soaking rain/month with favourable temperatures is required to maintain development. Under hot summer conditions up to 125mm/month may be required.

The most favourable combinations of temperature and moisture are often found in during spring and Autumn although summer rainfall areas have a summer problem with Haemonchus (Figure 7.8). Figure 7.8 Typical larval distribution patterns on Australian sheep pastures in the winter

and summer rainfall zones. Source: Brightling, (1994).

Parasite factors

• Egg production. This varies greatly between species (Table 7.4) and to some extent is largely a function of adult parasite size. High levels of egg production allow rapid build up in parasite numbers and explosive outbreaks of disease to occur (eg. Haemonchus)

• Pathogenicity of adult worms. Haemonchus adults are approximately 6-8 times more pathogenic than Ostertagia, Nematodirus and Trichostrongylus adults and L4 larvae

• Resistance to cold and desiccation. Haemonchus eggs and larvae are most susceptible to desiccation, Trichostrongylus and Nematodirus most resistant. Similarly, Haemonchus and Oesophagostomum columbianum eggs and larvae are most susceptible to cold, with Ostertagia and some Trichostrongylus species most resistant


• Anthelmintic resistance. This is a very serious and growing problem! It widespread for the levamisole (“clear drench”) and benzimidazole (“white drench”) groups and closantel, and is increasing rapidly with the macrocyclic lactones (“oily drench” or “mectins”).

Host factors

• Immunity. Sheep develop acquired or “age immunity” as they grow. Young sheep in the first 18 months of life are the most susceptible to infection. Immunity is influenced by:

- Worm species. Haemonchus induces less immunity than the other species and remains a threat to adult sheep

- Degree of challenge. Immunity requires exposure to infection - Host genotype. There is within and between breed variation in resistance to

helminth infection. The heritability of faecal worm egg count is approximately 0.25

- Physiological state. Immunity is almost totally lost during late pregnancy and lactation. This leads to a “peri parturient rise” in faecal egg counts.

• Host nutrition. This affects both resistance to infection (numbers of worms in the host) and resilience (ability to continue to produce for a given number of worms)

• Stocking rate/grazing management. This has profound effects on the level of pasture contamination with eggs and infective L3 larvae (see section on control).

Clinical signs The major clinical signs of nematode infection in sheep are: ill-thrift in young stock, anaemia and scouring (diarrhoea). All nematode worm species induce ill-thrift and most induce scouring. Few are associated with anaemia, the major species being Haemonchus contortus (Table 7.5). Scouring and ill-thrift can also be caused by other factors other than worm burdens and for this reason, are very poor indicators of infection. Also, by the time these clinical symptoms are evident, substantial sub-clinical losses will already have occurred. Infection with Trichostrongylus spp. is often (but not always) associated with dark green to black scours. This provides a suitable environment for the development of larvae of the sheep blowfly (i.e. breech strike). Severe infection with Haemonchus can result in the accumulation of fluid under the lower jaw, known as “bottle jaw”, due to the loss of protein from plasma. Table 7.5 Main clinical signs and severity associated with different worm species. Source: Walkden-Brown and Besier (2006).

Genus Anaemia Scouring Ill thrift Haemonchus +++ - +++ b Trichostrongylus - +++ +++ Ostertagia - +++ +++ Nematodirus - ++ ++ Oesphogostomum - +a +++ Chabertia - ++ a ++ Trichuris - ++ a +++

a Faeces may contain mucus or blood b Can kill adult sheep

Pathogenesis (pathophysiology) of infection The mechanisms by which nematode infection brings about the observed loss of production and clinical signs are as follows:


Reduced feed intake This is one of the most important pathophysiological consequences of worm infection. In the case of Ostertagia, reduced feed intake accounts for 60-70% of the effect of the parasite on the host. The associated rise in plasma gastrin concentrations has been implicated as a cause of appetite suppression. Increasing the level of infection with Trichostrongylus colubriformis induces reductions in feed intake, especially in young sheep (Figure 7.9). However, note that as the infection progresses, the animals develop immunity and feed intake can return to normal values. Pair feeding studies indicate other factors apart from reduced feed intake are involved, including altered protein metabolism.

Figure 7.9 Mean daily feed intake for groups of 4 lambs continuously infected with 0, 900, 3,000 or 30,000 infective larvae of Trichostrongylus colubriformis per week.

Source: Steel and Symons (1979).

Altered protein metabolism This is also very important and results in reduced nitrogen retention as a consequence of:

• Loss of plasma and erythrocytes leading to hypoproteinaemia and anaemia. Losses may be due to direct blood sucking (eg. Haemonchus, or as a result of inflammation of the gut (other species). Much of these losses is re-digested and absorbed but this is an energy inefficient process

• Increased production and loss of mucus and epithelial cells. These are high in cysteine and methionine (important for wool production) and are poorly re-absorbed.

Maldigestion and malabsorption These do not appear to be very important due to the capacity of the gut to compensate for damaged sites by using uninfected regions.

Effects on wool production Research over the years has shown that, depending on severity, worm infection has the following overall effects:

• Wool production - 10-30% reduction in annual wool production in young stock depending on level of infection. Reduction of 5-20% in mature sheep. Short term reductions can be up to 70%

• Yield - Unaffected • Mean fibre diameter - Reduced by 0.5-2µm • Staple length - Reduced • Staple strength - Unchanged or reduced • Processing losses - Increased losses during carding and combing.

Figures 7.10 to 7.12 below show the effects on productivity of four parasite control treatments at two locations, Armidale (summer rainfall) and Hamilton, Victoria (Winter rainfall). The experiment was conducted with 100 weaner wethers per treatment set-stocked at 12.4 per hectare at Armidale and 16 per hectare at Hamilton. The treatments were:


Salvage - (Most wormy). Treat individual animals only to prevent death (58+10 = 68 individual animal treatments) Curative - Treat animals when clinical signs present (4 thiabendazole + 1 rafoxanide = 5 drenches) Preventive - Traditional practice, include rafoxanide (5+5 = 10 drenches) Suppressive - (Least wormy). Monthly thiabendazole plus rafoxanide in Armidale November-April (11 + 5=16 drenches). Figure 7.10 Effect of different worm control programs from 5-7 months of age on fleece

weight at first shearing in Merino wethers. Source: Johnstone et al. (1979).

Figure 7.11 Effect of different worm control programs from 5-7 months of age on mean

fibre diameter at first shearing in Merino wethers. Source: Johnstone et al. (1979).

Figure 7.12 Effect of different worm control programs from 5-7 months of age in Merino

wethers on some processing characteristics of the first fleece. Source: Lipson and Bacon-Hall (1979).


Diagnosis A provisional diagnosis may be made on the basis of clinical signs (ill thrift, scours, anaemia) and history of treatment and climatic conditions. However the diagnosis is confirmed with 2 following steps.

• Worm egg count (WEC). This is the number of nematode eggs per gram of faeces. However, the three major species (Haemonchus, Trichostrongylus and Ostertagia) all produce eggs of similar size and shape, making it difficult to identify the prevalent species

• A larval culture (hatching the eggs) and differentiation (identification of species on the basis of the L3 morphology) is required to correctly identify the species present and enable sound interpretation of WEC as the species differ in egg production. Trichostrongylus and Ostertagia produce similar numbers of eggs, such that where they are the major species present, WEC provides a useful guide to total number of worms present. But when Haemonchus is present, WEC can be extremely high even though only a small number of adult worms are present. This species produces up to 50 times more eggs per adult female than the other two. WEC in excess of 3000 eggs per gram is indicative of infection with Haemonchus.

Post-mortem examination of the gastrointestinal tract enables species identification and total worm counts. This allows both immature and mature worms to be counted and provides an accurate measure of worm burden. However, this method is laborious and not suitable for routine farm monitoring for worm control.

• Haemonchus (Barber’s Pole Worm) is up to 40 mm long and 4 mm wide. They are visible in the abomasum during post-mortem inspection. The worm is characterised by the red (blood-filled) digestive tract spiralling along a white egg-filled oviduct (in the case of females) giving rise to the parasite’s common name

• Trichostrongylus (Black Scour Worm) is light brown in colour, up to 8 mm long and 1 mm wide. It is a so called “hair worm” and is almost impossible to see while in the intestine. It must washed from gut contents and stained appropriately to be identified

• Ostertagia (Small Brown Stomach Worm) is light brown in colour, up to 10 mm long and 1 mm wide. As it is another hair worm it is hard to see without proper processing of gut contents.

Control Control has relied traditionally on chemical (anthelmintic) treatment supplemented with grazing management. Anthelmintics represent the major strategy employed in controlling nematode infection. A range of anthelmintics exist on the market, including both narrow- (species specific) and broad- (control a number of species) spectrum drenches. The broad-spectrum drenches are normally effective against Haemonchus, Trichostrongylus, Ostertagia and Nematodirus, and include white drenches (benzimidazole group), clear drenches (levamisole group) and oily drenches or “mectins” (macrocyclic lactones). Anthelmintics may be administered orally via drenching or intra-rumenally via sustained release devices.

There are four broad approaches to the use of anthelmintics.

• The curative approach involves treatment only when clinical signs are apparent. It is not economical to use this approach due to the large losses in production that can be incurred

• The tactical approach bases the decision to treat on weather conditions favourable for the parasite or if monitoring of WEC indicates that a drench should be given

• The strategic approach entails giving a fixed number of treatments at specified times to delay the seasonal build up in numbers. It is based on detailed epidemiological understanding of the disease in a given area. Examples include the WormKill, DrenchPlan, WormBuster programs in different regions


• The suppressive approach uses anthelmintics in a blanket fashion in an attempt to suppress the disease. This was used widely in the 1960s and 1970s following the introduction of highly effective broad spectrum anthelmintics but it is expensive and results in rapid selection for anthelmintic resistance and so is not widely used any more.

Grazing management is largely based upon placing the most susceptible stock on the pastures least contaminated with worm larvae. Typically this involves putting lambing ewes and freshly weaned lambs onto “clean” pastures. Producing relatively clean pastures is easier said than done however. Methods include:

• Use of sown pastures or crop residues • Prior grazing by resistant animals which “mop up” infective larvae but prevent them

from developing into adults. This may involve: - Prior grazing with cattle. Very effective - Prior grazing with older wethers - Prior grazing with animals carrying an effective sustained release capsule. However the use of sustained release capsules favours the development of anthelmintic resistance.

• The spelling of pastures to reduce the population of infective larvae has been demonstrated to be highly effective in tropical regions as larvae deplete their energy reserves much more quickly (5-9 weeks) in these conditions. Remember that L3 cannot feed due to their protective sheath so will always eventually die if not ingested. In cooler temperate regions, rotational grazing has been less successful, but there is strong evidence emerging in the Northern Tablelands of NSW that short duration long interval rotational grazing (“cell grazing”) is highly effective at reducing infections with H. contortus. These systems involve grazing paddocks heavily for short periods (1-4 days) with long rest periods (60-120 days) between grazings.

Newer approaches to control The growing problem of anthelmintic resistance is driving research into a range of newer control measures that can be integrated with anthelmintic usage and grazing management into more effective integrated control programs that are effective in controlling worms while also slowing the rate of development of anthelmintic resistance. Some of these newer approaches include:

• 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

• Strategic use of Nutrition. The provision of protein supplements to young stock or periparturient ewes can be used to increase the resistance and resilience of stock to infection, giving lower worm egg counts and sub-clinical losses. However the economics of this need to be carefully evaluated as feeding for worm control alone is rarely economic. However, when coupled with increased productivity economic responses can be obtained

• Biological Control of the free-living larval stage holds considerable potential. The most promising candidate is Duddingtonia flagrans, a net-trapping, nematode-destroying fungus. These nematophagous fungi normally feed on a range of free-living soil nematodes. It has been shown that the fungal spores can survive passage through the gastrointestinal tract, significantly reducing the number of infective larvae that develop in the faeces and the level of contamination of pastures. The aim is to achieve reductions in clinical and sub-clinical diseases while also stimulating development of acquired immunity in young stock

• Vaccination. Despite the ability of sheep to develop strong natural immunity to worms, effective vaccination is still a long way off despite much research work. The only commercial nematode vaccine developed to date has been against lungworm in cattle. One problem is the relatively short nature of induced immunity against roundworms

• Wormboss. A decision support tool developed by the Sheep CRC is now available on the web. See Project 1.4.5 on the Sheep CRC Website.


Liver fluke (fasciola hepatica) infection Fasciola hepatica and its life cycle Liver fluke occurs mainly in the higher rainfall areas of SE Australia, encompassing a wide range of climatic types from the Mediterranean-type environment of western Victoria to the sub-tropical south-east coast of Queensland (Figure 7.13). It is also found in irrigation areas. The distribution of liver fluke coincides with the distribution of Lymnaea tomentosa, the intermediate snail host. The main habitats of this snail include temporary springs, billabongs and swamps. Large lakes and rivers are unsuitable habitats. It is highly prolific and can spread rapidly when climatic and physical conditions are suitable. For snail identification see http:///www.agric.nsw.gov.au/reader/ 7912.

The life cycle of the liver fluke is complex, requiring a freshwater snail for part of the cycle. Mature fluke are found in the bile ducts of the liver of the host animal. The eggs produced are passed down the duct, into the small intestine and passed out with faeces. The eggs hatch in up to 3 weeks under warm moist conditions (spring and summer), but may take up to 3 months in winter. The larvae, known as miracidia, then infect the host snail (which is usually Lymnea tomentosa, the mud snail). Without this host, the larvae cannot develop. The larvae remain in the snail for up to 12 weeks, multiplying into several hundred second stage larvae known as cercariae, which are passed into the water. A single miracidium may yield over 1000 cercariae. These larvae form cysts (metacercariae) and adhere to pasture plants. Infection occurs when the sheep ingest the cysts while grazing. The cysts dissolve in the gastrointestinal tract of the host, releasing immature fluke. These burrow into the intestinal wall and migrate to the liver. Burrowing through the liver to the bile ducts may take up to 6 weeks. They develop to maturity in 6-7 weeks. The minimum period for whole lifecycle is 4-5 months. Liver fluke are flat and leaf-like in shape, and grey to brown in colour. They measure 1-2 cm in length when mature.

Figure 7.13 The distribution of Fasciola hepatica in Australia. Source: Barger et al. (1978).

Disease syndromes, clinical signs and effects Liver fluke is a very serious pathogen of sheep and cattle. It is a long-lived blood-sucking parasite found in the bile ducts of the liver. No immunity to this parasite develops in sheep so it is found in all age classes, but adult cattle do develop effective immunity. There are four different diseases associated with liver fluke.

• Acute liver fluke is caused by severe damage to liver 5-6 weeks after ingestion of metacercariae. It is due to immature fluke burrowing into liver tissues. Affected sheep become dull, weak, lose appetite and may die within 24-48 hours of clinical signs appearing


• Chronic liver fluke is caused by liver damage arising from mature flukes in the bile ducts and a lesser number burrowing into liver tissue over a period of weeks or months. Affected sheep lose weight slowly and weaken, become anaemic (characterised by pale membranes in mouth and eyes) and may develop “bottle jaw”. Affected sheep look severely “wormy” but do not respond to normal worm drenches that are ineffective against fluke

• Sub-clinical liver fluke occurs when the numbers of fluke are low. Affected sheep show depressed productivity in terms of growth, wool production and reproduction

• Black disease occurs when the larvae migrate through the liver, stimulating Clostridium novyi spores to germinate and multiply. It is characterised by sudden death.

Liver fluke infection results in loss of protein from the host due to the loss of blood and plasma in the bile ducts. Wool growth can be significantly reduced with as few as 25 adult flukes present. Fleece weights are typically reduced by 10-40% (Figure 7.14) indicating that sub-clinical losses can be appreciable.

Figure 7.14 Reduction in greasy fleece weights following infection with 100, 500 and 1000 metacercariae. Source: Edwards et al. (1976).

Diagnosis and treatment Immature fluke cause damage to the liver but do not produce eggs. Thus acute liver fluke disease can occur before eggs appear in the faeces. A range of blood tests are available to assess liver damage but they do not indicate the cause of the damage. Diagnosis of acute liver fluke is based on post-mortem examination. Chronic liver fluke can be diagnosed by worm egg count, as the eggs have a characteristic shape. Post-mortem examination is also used in diagnosis of this disease. Lymnea tomentosa can also be identified by its characteristic cone-shaped shell and clockwise spiral when viewed from the apex. There are a number of anthelmintics available which have action against liver fluke, but they vary in the level of control provided over each stage of the parasite. For example, Triclabendazole (Fasinex®) is the most effective control over all stages of liver fluke, whereas Closantel (Seponver®) or Nitroxynil (Trodax®) are effective against mature fluke and immature fluke 6 weeks after entering the liver. Other treatments such as Albendazole (Valbazen®) or Oxyclosanide (Nilzan®) are only effective for controlling adult fluke and have no action against immatures.


Control A fluke control program has three components:

• Strategic drenching to reduce pasture contamination and to reduce liver damage. Drenching in autumn through to early winter removes fluke before they mature and produce eggs. Drenching with Fasinex® at the end of February, mid-May and end of July effectively eliminates pasture contamination

• Grazing management. As cattle build up stronger immunity to liver fluke and are less affected by acute liver fluke than sheep, grazing affected pastures with adult cattle in summer is one strategy for reducing contamination. Fencing off highly contaminated areas is another common strategy

• Snail control. Chemical control of the snail is not economically feasible as the snail breeds prolifically. Eradication involves destruction of their habitat, requiring drainage of the area. This may not be feasible for water conservation reasons.

7.5 External parasites While the single most important sheep disease problem in Australia is gastro-intestinal worm infection, the external parasites, sheep blowfly and body louse are also major multi-million dollar problems for the industry. Furthermore, unlike the worm problem, these problems are found throughout the industry and are not restricted to the higher rainfall areas. As is illustrated in Figure 7.15 there are other external parasites of sheep such as nasal bots, sheep ked (perhaps now extinct in Australia), sucking lice and mites that are less important than blowflies and biting lice, but which nonetheless can cause severe problems on individual properties. Figure 7.15 Classification of the main groups of external parasites of sheep in Australia.

The most important groups are identified with an asterisk. Source: Walkden-Brown and Besier (2006).

Blowfly strike (cutaneous myiasis) This 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. Up to 3 million sheep are estimated to die from blowfly strike each year, depending on seasonal conditions.

Class Insecta3 pairs of legs, distinct head,thorax and abdomen, one pairof antennae

Class Arachnida4 pairs of legs,cephalothorax andabdomen, no antennae

Phylum Arthropoda

Mites (Acarina)- Itchmite

Flies (Diptera) Lice (Phthiraptera)- Blowfly * - Biting * - Primary - Sucking - Secondary- Nasal bot- Sheep ked


The sheep blowfly and its life cycle 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 foreleg (Figure 7.16). Its maggots are characterised by a smooth body. Flystrike initiated by L. cuprina may resolve after a few days or it may be complicated by secondary strike or bacterial infections. Existing strike sites may be struck again by L. cuprina or secondary blowflies (such as Chrysomyia rufifaces, the hairy maggot blowfly) making existing wounds much worse. Secondary blowflies breed in decaying carrion and other material and are unable to initiate flystrike on their own. They tend to be larger and rounder than L. cuprina and have a variety of colours.

Figure 7.16 The major primary (Lucilia cuprina) and secondary (Chrsomya ruffifacies) blowflies of sheep in Australia. Source: Levot (1999).

Figure 7.17 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.

Larvae pass through 3 larval instars in 4-6 days. The first instar requires a liquid protein meal but cannot damage the skin as they have no mouth hooks. Hence, the requirement for damaged or inflamed skin. The second instar has hooked mouth parts and also secretes proteolytic enzymes so is capable of physically and chemically damaging the skin. Larval products such as proteases cause an intense immune response and set up a bacterial dermatitis that can lead to severe systemic disease characterised by toxaemia and septicaemia (“blood poisoning”). Mature larvae drop off at night after 4-6 days of feeding on the host and pupate in the soil. The pupal stage lasts only 3-7 days in summer but development is arrested by low temperatures and the fly usually over-winters in the pre-pupal stage. Adult flies can emerge as early as 7 days after dropping off the sheep. Thus the minimum time to complete the lifecycle is around 2 weeks. As with most parasitic lifecycles, in cooler weather the duration of the lifecycle is greatly extended.


Figure 7.17 The lifecycle of Lucilia cuprina, the Australian sheep blowfly. Source: Levot (1999).

Types of blowfly strike There 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 (Figure 7.18), 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.

Figure 7.18 Sheep with fly strike of the body (body strike). Source: Agnote, Simpson (1990).


Effects of fly strike on wool production The effect of flystrike on wool production depends on the severity and frequency of strikes. Annual fleece weight may be reduced by up to 8% while up to 2% of the clip may be classified as stained, cotted or dead wool. Figure 7.19 shows that individual fibre growth rate declined by around 17% by the end of an experimental infection period. However, there was an on-going reduction in growth rate after cessation of infection, with up to 27% reduction in growth rate during the post-infection period. The short term effects on wool follicle function tend to have greater effects on staple strength than overall wool growth as can be seen in Figure 7.20 in which moderate flystrike more than halved staple strength. The actual mechanisms underlying these effects on wool growth are not fully defined, in particular the roles of stress hormones, reduced feed intake and potential role of cytokines, along with their interaction. However, recent work at UNE indicates that reduced feed intake accounts for only some 25% of the effects on staple strength and about 55% of the overall effects on wool growth (Walkden-Brown et al., 2000).

Figure 7.19 Reduction in wool growth associated with fly strike (500 larvae/day for 8 days) as determined by autoradiography. Source: Broadmeadow et al. (1983).

Figure 7.20 Staple strength (± SEM) in Control Merino wethers and those infected with 500 L. cuprina larvae daily for 8 days (Struck) or uninfected sheep pair fed with the

struck animals (Pair fed). Two of the 5 sheep in the struck group had fleeces too tender to measure (“rotten”) so data for these animals is excluded.

Source: Walkden-Brown et al. (2000).


Factors affecting the incidence of flystrike The occurrence of fly strike is influenced by a range of environmental (temperature, rainfall, wind) and host (genotype, phenotype, presence of dermatitis) factors. Environmental factors The major environmental factors affecting the incidence of flystrike are:

• Temperature – Flies are active at air temperatures between 17 and 35°C while soil temperatures between 13 and 30°C are optimal for pupal development. High summer temperatures induce larval mortality

• Rainfall - Both soil and fleece moisture are required. Humidity >70% is required for egg hatching

• Wind - Moderate wind speeds (5-30 km per hour) are ideal. Flies are less active during totally still conditions or strong winds

• Carrion - This allows maintenance of fly populations, although Lucilia is less efficient when using carrion instead of the host sheep. In carrion it is generally out-competed by secondary blowflies.

These environmental factors lead to a seasonal distribution in fly activity, with a peak in late spring, and a smaller peak in autumn in the southern areas but with sustained activity throughout summer in northern regions. Host factors 1 – Damaged skin The presence of liquid protein on skin is an absolute requirement for first instar larvae. Thus flies will strike wounds, sites of infection (eg. footrot) and dermatitis-affected areas. Fleece rot is the major predisposing factor for body strike. It is a bacterial dermatitis caused by Pseudomonas aeruginosa but is not a contagious disease, as the organism is present on the skin of all sheep. The enzyme phospholipase C is a virulence determinant for P. aeruginosa, producing a dermonecrotic toxin. When the fleece is wet to skin level for around 1 week there is rapid build up in the population size of the organism and dermatitis develops. Other Pseudomonas species and other organisms participate in the dermatitis but P. aeruginosa produces inhibitory compounds, thus becoming dominant. A pigment (pyocyanin) also results from this bacterial activity, changing from blue-green to brown over time. This is referred to as bacterial stain which, although partly scourable, attracts penalties. P. aeruginosa, also produces a specific blowfly-attracting odour making it the major predisposing factor in body strike.

Fleece rot is mainly seen in young sheep. However, predisposing factors to fleece rot in all classes of sheep include open fleeces with fringed staple tips, high suint content, low wax content and high diameter variation. Producers in high rainfall areas commonly cull young stock showing evidence of fleece rot (Figure 7.21). Medium and strong woolled Merinos are much more susceptible to fleece rot than finewool strains.

Lumpy wool, also referred to as dermatophilosis or dermo, is a bacterial dermatitis caused by the bacterium Dermatophilus congolensis. Unlike P. aeruginosa, this organism is not a normal inhabitant of the sheep skin and so lumpy wool is a true contagious disease. The disease is characterised by crusty scab formation and yellow discoloration in the fleece while infection of the lower legs causes strawberry footrot. It spreads from sheep to sheep by contact when sheep are wet or via contaminated dipping fluid. Although it can be readily controlled (antibacterials in dipping fluid, don’t yard wet sheep) and treated (antibiotics), when present it acts as a predisposing factor to body strike.


Figure 7.21 Inspection sites for examining sheep for fleece rot susceptibility. Source: Murray and Mortimer (2001).

The skin scald associated with urine or faecal wetting is another form of dermatitis and predisposes to breech and pizzle strike. 2 – Phenotype There are a number of phenotypic factors influencing the degree of susceptibility of the individual to flystrike. Some of these have a genetic basis.

• The length of wool is critical, with the incidence of body strike being rare when there is less than 4 months wool carried by the animal. Short wool allows the fleece to dry quickly, preventing development of fleece rot. Thus the timing of annual shearing is an important control measure

• Fleece structure or type is also important, relating to the wetting and drying potential of the fleece environment (see fleece rot section)

• Conformation problems such as “devil’s grip” impede the ability of regions of the fleece to dry, while other attributes such as a wrinkly breech impede the breech area from drying, thus facilitating breech strike

• The use of the Mules operation and docking of the tails to the third joint can reduce the incidence of breech strike by up to 90%. These are routine management operations for replacement sheep in Australia

• Close-set horns in rams can also predispose the animal to poll strike. 3 – Genotype The genotype of the host influences the incidence of body strike. Figure 7.22 shows clear differences between the Merino strains in their susceptibility to both fleece rot and body strike, showing how the incidence of each disease is related. In general, fine wool genotypes are more resistant to both diseases than broader wool genotypes. There is also within-flock genetic variation in resistance to fleece rot (heritability of around 0.35) that can be exploited to increase resistance to body strike. There are also breed differences in susceptibility to body strike, with British breeds being more resistant than Merinos.


Figure 7.22 Differences in susceptibility to fleece rot and body strike within and between strains of Merino. Source: Atkins and McGuirk, (1979).

Strategies for controlling fly strike Strategies for controlling blowfly strike can involve modification of the host or the environment. Conventional control measures

• Permanent modification of host phenotype. A number of conventional control strategies are aimed at modifying the host phenotype permanently to reduce the incidence of breech strike in all sheep (mulesing and tail docking) and pizzle strike in wethers (pizzle dropping)

• 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

• 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 and the extent to which resistance has developed:

- Organophosphates (eg. Diazinon, propetamphos). Used to control blowfly and lice via jetting, dipping or backline treatment. Resistance is widespread and is manifest by a reduced duration of protection, now typically down to around 4 weeks from 12 weeks originally. Residue issue with longwool treatments. - Insect growth regulators (eg. cyromazine, dicyclanil) and insect development inhibitors (eg. diflubenzuron, triflumuron) act by inhibiting larval transitions in development. Used to control blowfly and lice via jetting, dipping, backline or spray on treatment. Resistance in flies has been reported for diflubenzuron. Residues can be an issue with long wool treatments.

- Macrocyclic lactones (eg. ivermectin). Used to control blowfly and lice by jetting. Can be suitable for long wool treatments (6-12 weeks withholding) and no resistance reported to date.

- Spinosyns (eg. Spinosad) are a relatively new class of insecticide. They are suitable for long wool treatments for control of blowfly and lice. They have no withholding period and no resistance has been reported. They provide a relatively short duration of protection (4-6 weeks).


• Genetic selection. This exploits genetic variation in susceptibility to body strike via selection for resistance to fleece rot. It is used quite widely in high rainfall areas, based on culling of any animals showing signs of severe fleece rot or body strike

• Monitoring or manipulating the environment. 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 provide a useful strategy for controlling adult fly numbers in some areas

• 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 measures Potential control measures that have been tried or considered include:

• Vaccination. There are two approaches, both of which are experimental at present. Firstly vaccinate against fly antigens such as peritrophic membrane antigens in the gut of the fly (hidden antigen approach) or secondly 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

• 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 shows 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.

Body louse infection (bovicola ovis) The sheep body louse Bovicola ovis is an obligate parasite of sheep that can also infect goats for a short period. It feeds on the stratum corneum of the skin, causing irritation and a hypersensitivity reaction. This itchiness is the root problem with this disease. B. ovis is present in all states of Australia with 35-70% of properties being affected. It is a major disease of the wool industry costing an estimated $169 million per annum, primarily in the form of costs of control (McLeod, 1995).


Lifecycle All stages of the lifecycle occur on the sheep. Adult females lay 2 eggs every 3 days. These eggs are attached to wool fibre 6-12 mm from the skin and hatch in 10 days (Figure 7.23). Eggs attached to fibre removed from the host, do not hatch. After hatching, the nymphs pass through 3 stages lasting 7, 5 and 9 days respectively. The pre-oviposition period in the female is 3-4 days. The minimum time required to complete the lifecycle is 34 days. Under good conditions it takes 4-5 months for a light infestation (0.3 lice per sq. cm) to develop into a heavy infestation (30 lice per sq. cm). As lice can only survive for 1-2 days off the host, transmission of the parasite is by direct contact between sheep.

Figure 7.23 Life cycle of Bovicola ovis. Source: Joshua (2001).

Effects on wool production Lice infestation causes a reduction in greasy fleece weight ranging from 15-30% depending on the severity of the infestation. The main mechanism is irritation (due to local immune system hypersensitivity responses) causing rubbing and biting of the fleece by the host, leading to loss of fibre. Yield also tends to be reduced by up to 5% (absolute units) while cotting and discolouration results in increased classing of fleeces into cast lines. Fibre length and fibre diameter are unaffected.


Table 7.6 Effects of different levels of lice infestation on wool production and processing performance. Source: Wilkinson et. al. (1982).

abc Means within rows not sharing a common letter in the superscript are significantly different (P<0.05).

The data in Table 7.6 presented above were collected over three years. The light infestation treatment commenced with around 100 lice per sheep while the heavy infestation commenced with around 1000 lice per sheep. While there was a relationship between severity of infestation and wool production, it is also worth noting that processing losses (carding and combing) also increased as severity increased. From the producer’s viewpoint, the lice infestation equated to a loss of $0.72 to $1.92 per lousy sheep. From the processor’s viewpoint, this equated to a loss of $21 -$32 per 100 kg wool processed into top. Factors affecting the incidence and severity of lice infestation Environmental factors

• Temperature - B. Ovis is very sensitive to changes in temperature. Its optimum temperature is 37°C. Below 37°C egg production ceases while above 39°C egg production reduced. 45°C for 18 hr causes death irrespective of humidity

• Moisture - Lice are susceptible to drowning on a wet skin. Up to 90% of adults can drown during a thunderstorm. Eggs fail to hatch at a relative humidity of 90%.

Host factors

• Shearing removes most of the eggs, 30-50% of the adults and exposes the remainder to high skin temperatures. Summer skin temperatures in shorn sheep are often in the range 45-55°C

• Wool cover affects lice survival through effects on skin temperature. Less cover allows greater penetration of solar radiation and greater variation in skin temperatures. The longer the staple the better for lice.

Due to temperature and shearing effects there is a marked seasonal variation in numbers. Few lice are found after shearing, numbers remain low over summer, then increase from autumn through winter until the next shearing. Increases in numbers can be interrupted by soaking thunderstorms.

GFW (kg)

CFW (kg)

MFD (um)

Scouring yield (%)

Card loss (%)

Noil (%)

Top and noil yield (%)

Fibre length in top (cm)

None

5.1a

3.4a

24.9a

66.8a

9.8a

4.1a

60.5a

8.3a

Light

4.9ab

3.1ab

24.7a

63.0b

12.3b

4.8b

55.7b

7.7b

Heavy

4.5b

2.8c

25.0a

62.6b

13.3b

5.4c

53.3b

7.2b

Level of infestationVariable


3.4 Control measures B. ovis is theoretically easy to eradicate from farms, but this has never been achieved on a state scale. In theory (and practice) eradication can be achieved by a single effective treatment to all sheep, as lice do not survive well off the host. Control is based solely upon chemical treatment of all animals with organophosphates (dip, spray or jet), synthetic pyrethroids (backline, dip, spray or jet), insect growth regulators or development inhibitors (IGRs, IDIs, backline, dip , jet), macrocyclic lactones (jet) or spinosyn (dip, jet). It should be noted that IGRs and IDIs act only at the transitions during the lifecycle and have no effects on adult lice. Thus it can take up to 5 months for sheep to be completely free of lice after treatments with these chemicals. In terms of effectiveness, off shears treatments (backline, dip or spray) are more effective than short wool treatments (dip or spray), which in turn are more effective than long wool treatments (dip or jet). This reliance on chemical treatments raises issues of chemical residues and resistance. Withholding periods to shearing must be strictly observed. Short wool treatments are not only more effective, but they use less chemical and allow longer for it to break down prior to shearing so are preferable from a residue management point of view. Prevention of re-infestation is a major aspect of control. This requires good boundary fencing and care when purchasing new stock. Readings The following readings are available on CD:

1. Various 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.

2. Besier, R.B. Management of helminth parasites of sheep in Australia (2004), proceedings 355: Sheep Medicine (Course, May, 2004) (Port Graduate Foundation in Vet Science, University of Sydney) Chapter 10, pp 129-172.

3. Brightling, A. 1994, ‘Worm control – sheep’, in Stock Diseases, Inkata Press, Melbourne, pp. 1-11.

4. Brightling, A. 1994, ‘Vaccination’, in Stock Diseases, Inkata Press, Melbourne, pp. 17-21.

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Summary Summary Slides are available on CD Disease is a critical factor in determining the profitability of sheep production enterprises. Disease affects profitability by causing loss of production, increasing costs of control and causing loss of markets. The major diseases affecting sheep in Australia are blowfly strike, body lice, helminthiasis, and bacterial diseases such as footrot and cheesy gland. There are numerous measures which can be implemented to prevent and/or control disease which range from grazing management to chemical controls to permanent modification of the host (eg mulesing).

References 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. 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.

Brightling, A. 1994, Stock Diseases, Inkata Press, Melbourne, pp. 328 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

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

Collins, D. 1992, ‘Costs to the Australian sheep industry of major endemic diseases’, Rural Lands Protection Board District Veterinarians Annual Conference, Orange, NSW, NSW Department of Primary Industries, Orange, NSW, pp. 107-113.

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.

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.

Joshua, E. 2001, Sheep lice, Agfact A3.9.31, NSW Department of Primary Industries, Orange, NSW.

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.

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.

Glossary of terms

Acute disease disease with rapid onset, resolution or death in a matter of hours or days

Anaemia abnormally low numbers of red blood cells (erythrocytes) or haemoglobin concentration in the blood

Anorexia lack or loss of appetite for food. "Inappetence" is used interchangeably

Anthelmintic chemical administered to host animals to kill or suppress "worms" (ie. roundworms, tapeworms, flukes)

Antibiotic chemical, based on natural compounds, administered to host animals to kill or suppress bacteria

Antibody protein produced by cells of the host immune system which binds to antigens on the surface of invading organisms. This binding may kill or inhibit the organism. Antibody circulates in the blood and can also be found in the tissues and some body secretions eg. milk. There are 4 major classes of antibody, IgM, IgG, IgE and IgA. Antibody production is one of the major immune-mediated body defences. Antibody-mediated immunity is also known as humoral immunity. Antibody belongs to a class of proteins known as Immunoglobulins

Antigen substance (usually a protein) capable of initiating a specific immune response. Invading organisms have antigens on their surface and often in their secretory products which are recognised by the host immune system. Antibody is directed against specific antigens

Catecholamine group of amines which act as neurotransmitters and hormones, and have a sympathomimetic action. They include adrenaline, noradrenaline and dopamine. They are important mediators of stress responses

Chronic disease disease that persists for some time, generally more than a week, but up to years

Clinical disease disease that can be readily ascertained from abnormalities detected by the five senses

Clinical signs the observable signs of disease. Roughly equivalent to the term "symptoms" used in human medicine

Control of disease the whole spectrum of activities used to limit the effects of disease. These may range from the imposition of quarantine measures, through to treatment of clinical disease

Cytokine chemical messenger produced by cells of the immune system for the purposes of cell-cell communication. They play a pivotal role in determining the type and magnitude of immune response mounted

Diagnosis the process that enables the specific disease or disease syndrome affecting an animal or group of animals to be determined. An important part of this process is the differential diagnosis, in which the signs observed are compared with those of a range of possible disease syndromes followed by a process of elimination


Epidemiology the study of the frequency, distribution and determinants of disease in animal populations. Clinical medicine is the study and practice of disease control in individual animals or small groups of animals, while epidemiology is the study and practice of disease control in populations

Fever abnormally high body temperature. Often due to generalised infection or toxaemia. It is caused by cytokines produced by cells of the immune system

Genotype genetic make up of an animal. As opposed to phenotype which is the physical or outward make up of an animal

Glucocorticoid group of hormones secreted by the adrenal cortex which elevate blood glucose levels amongst their many actions. They are secreted at elevated rates during chronic stress and are also anti-inflammatory. They include cortisol, corticosterone and cortisone

Helminth parasitic worm. Roundworm, tapeworm or fluke

Helminthiasis disease caused by helminths. Also called helminthosis

Hypobiosis arrested development. Lifecycle pauses at some stage, usually in the host, until conditions become favourable for the lifecycle to resume

Hypoproteinaemia deficiency of protein in the blood. Commonly associated with gastrointestinal helminthiasis

Immunity resistance to disease due to the specific action of the immune system. Different from the broader term resistance to disease which may involve both immune and non-immune defences

Infection invasion of the body by another living organism

Infectious disease disease caused by infection

Inflammation stereotyped protective response of the immune system to tissue injury or invasion. The cardinal signs of inflammation are redness, heat, swelling and pain

Larval culture and differentiation

the most common genera of roundworm affecting ruminants can not be differentiated by observing the worm eggs. The eggs need to be cultured in the faeces for a week or so, and the 3rd stage infective larvae can then be differentiated by a skilled operator. Full interpretation of a WEC (worm egg count) requires larval culture and differentiation to determine the species or genus of worm involved

Leucocyte "White blood cell". Nucleated cells of myeloid and lymphoid origin circulating in blood. Form part of the immune system and move between blood and the tissues. Examples include lymphocytes, monocytes, neutrophils, eosinophils and basophils

Myiasis invasion of tissue by larvae of flies

Non-infectious disease

disease caused by factors and agents other than living organisms

Parasite in broad terms the same as a pathogen (see below). In practice it tends to refer to larger eukaryotic pathogens (eg protozoa and multi-celled animals). These are the province of parasitology, while the smaller organisms are the province of microbiology. The two disciplines overlap with the protozoa, which both study

Pathogen a disease-causing organism


Pathogenesis the mechanisms by which disease is induced in the host animal

Pathogenicity the severity of the disease caused by the particular organism. Also known as virulence

Phenotype physical or outward make up of an animal, as opposed to the genetic make up of an animal. Phenotype is a function of genotype and all the environmental factors that operated on the organism from conception

Plasma liquid portion of blood after cells have been removed by centrifugation. Requires the addition of an anticoagulant to prevent the blood clotting

Resilience ability of an animal to perform despite the presence of disease organisms (eg worms)

Resistance ability of an animal to resist colonisation by a disease organism (eg. worms)

Serum liquid portion of blood remaining after allowing blood to clot and removing the clot

Sub-clinical disease

disease processes that are not readily detectable with the five senses at a clinical examination. Often the most economically-important form of disease

Systemic disease disease which is generalised throughout the body. Generally spread via the bloodstream

Vaccination controlled exposure of animals to antigen or antibody to prevent disease. Based upon activating or enlisting the immune system to combat disease

Voluntary feed intake

the feed intake of animals with unrestricted access to feed

Worm egg count the number of worm eggs per unit of host faeces usually. Normally in eggs per gram of faeces (epg). Widely known as faecal egg count (FEC), but worm egg count is the more correct term

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!

7. sheep health · 2017-07-10 · 7.1 a framework for understanding health and disease several key...

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