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\n <\/a>\n <\/div><\/p>\nParasitic Gastroenteritis in Ruminants<\/h4>\n
Including: Cooperia onchophora<\/em><\/i>,\u00a0Ostertagia ostertagi,\u00a0Teladorsagia circumcincta,\u00a0Trichostrongylus spp.,\u00a0Haemonchus spp. (Barbers Pole Worm),\u00a0Nematodirus battus<\/em><\/strong><\/p>\n <\/p>\n Factors\u00a0that affect parasite infection in livestock<\/strong><\/p><\/div>\n <\/span><\/p>\n Gastrointestinal nematodes (<\/strong>GI nematodes or <\/strong>gut roundworms) are major contributors to reduced productivity in cattle, sheep and goats all over the world. Parasitic Gastroenteritis (PGE) is the condition caused by large numbers of gastrointestinal nematodes\u00a0 that reside in the gut (abomasum and intestines) of the ruminant host.\u00a0 The clinical signs of PGE\u00a0vary depending on nematode species and abundance.\u00a0PGE is primarily a disease of lambs and first season grazing cattle. The \u00a0most profound effect of parasitism in both sheep and cattle\u00a0is the sub-clinical<\/a><\/span> production losses (i.e., not visually obvious), the true extremity\u00a0of which farmers are unlikely to be aware (Waller and Thamsborg, 2004<\/a>).<\/strong><\/p>\n The main species of GI nematode that are of veterinary importance in temperate climates are:<\/strong><\/p>\n Some species of gut parasite have their own disease page on Farm Health Online as their epidemiology and clinical signs do vary. However, nematode infections are almost always a mixture of species so this page provides a broad overview of GI nematodes in cattle and sheep.<\/strong><\/p>\n Most GI nematodes have a simple direct lifecycle, although there are\u00a0species-specific variability in development rates and predilection site<\/a><\/span>. The lifecycle has two distinct phases; 1) within the host, and 2) the free-living stage where the parasite is developing in the environment. The basic parasitic gut worm lifecycle follows the steps below:<\/p>\n <\/a>*Fecal samples can be collected and the number of eggs can be counted \u2013 this is called a Fecal Egg Count. These can be used to monitor worm burden and make treatment decisions. However FECs do have their limitations especially in cattle.<\/p>\n **Exact predilection site<\/a><\/span> depends on worm species (e.g., abomasum or small intestine)<\/p>\n ***This is where the pathogenesis<\/a><\/span> occurs<\/div>\n<\/div>\n <\/p>\n GI nematode lifecycle<\/strong><\/p><\/div>\n <\/span><\/p>\n <\/a>The development of parasite within the host, or through the free-living stage is dependent on many different risk factors and these can be divided into 3 groups:<\/p>\n Unlike sheep and cattle goats do not<\/u><\/strong> develop age-related immunity.<\/p>\n Age is a risk factor for developing PGE.<\/strong><\/p><\/div>\n <\/span>Young animals in their first grazing season are most susceptible<\/a><\/span> to PGE and then as they reach about 12 \u2013 18 months they often develop strong immunity, although the immune response varies according to the worm species, and levels of exposure to the parasite.<\/p>\n The relative importance of the different GI nematodes differs with host age because of acquired immunity<\/a><\/span>. The immune response to GI nematodes is directed at different stages of the parasite development and is a complex interaction of humoral<\/a><\/span> and cellular immunity<\/a><\/span>.<\/p>\n Normally, a protective host resistance develops against Nematodirus<\/a><\/em> and Cooperia<\/em> within one year. Ostertagia<\/a>, Teladorsagia<\/a><\/em> and Trichostrongylus<\/em> spp. stimulate a slower immune response and are therefore sometimes seen in older stock \u00a0(Vercruysse and Claerebout, 1997<\/a>).<\/p>\n Interestingly a study conducted in Brazil found that animals challenged with Haemonchus placei<\/a><\/em> three times a week for 25 days, then treated, and experimentally infected again with Haemonchus placei<\/a><\/em> on day 35 displayed an intense immune response with low parasite establishment, compared to animals who were only challenged once with Haemonchus placei<\/em><\/a>, demonstrating that the protective immune response to Haemonchus placei<\/a> <\/em>only develops when animals are repeatedly infected with this species (Santos et al<\/em>., 2014<\/a>). However, the same was not seen for Haemonchus contortus<\/a><\/em> and which induces relatively poor acquired immune response (Adams and Beh, 1981<\/a>) even after reinfection (Barger, 1988<\/a>).\u00a0This may explain why Haemonchus<\/em> can also affect (and kill) adult sheep.<\/p>\n A vaccine against Haemonchus contortus<\/em> in sheep, (BarbervaxTM<\/sup>) has recently been developed by the Moredun Research Institute in the UK and is licensed for Australia.<\/p>\n Another more recent study carried out in Sweden reported that calving season is a stronger determinant of worm burden in pasture-fed beef than the level of residual larvae in the field. They suggest this is because adult cows produce large amounts of feces at turnout which significantly contaminates the pasture, and early born calves are more likely to ingest more herbage, leading to higher risk of exposure to parasites (H\u00f6glund et al.<\/em>, 2013<\/a>).<\/p>\n <\/a>Immunity and parasite burden is also influenced by genetics<\/a>, pregnancy<\/a>,\u00a0and nutritional state<\/a>.<\/p>\n Animals that withstand a heavy parasite burden and shed lots of eggs in their feces but continue to grow and perform are known as resilient <\/strong>animals. <\/strong>These animals have the ability to resist the pathogen <\/a><\/span> and grow well regardless of worm burden often coping well without treatment. However, the danger with these animals is they are contaminating the pasture for the less-resilient animals.<\/p>\n Contrastingly, genetically resistant <\/strong>animals are those that are able to tolerate a pathogen by maintaining low worm burdens irrespective of infection pressures because they have enhanced immune responses which prevent adult worms establishing in their gut. The drawback is the strong immune response requires energy and can cause local gut mucosal changes resulting in weight loss and scours, affecting performance. Attempts are being made to identify the genes that encode parasite resistance, with the aim of identifying and selecting animals with superior parasite resistance or \u2013 controversially – even\u00a0being able to develop transgenic animals<\/a><\/span> with genes for parasite resistance, and economically productive traits.<\/p>\n <\/a>The genetic basis of both resilience and resistance is complicated and depends on the fate of the animal as to which best suits a particular farming system. If breeding stock are resistant, they will be slower growing, but not infecting the pasture for their progeny. It could be beneficial for finishing stock to be resilient as they will continue to grow and perform well regardless of worm burden.<\/p>\n According to SCOPS<\/a> (Sustainable Control of Parasites in Sheep), the biggest gains are being made by selecting rams that\u00a0sire ewe breeds. If ewes are genetically resistant, their egg output during the periparturient rise and other times of the year will be lower than that of the average population, resulting in lower exposure of lambs.<\/p>\n In commercial flocks just selecting individuals with low egg counts will not lead to significant genetic progress.<\/p>\n <\/p>\n Ewes play a significant role in pasture contamination around lambing time due to a phenomena called Peri-Parturient Rise (PPR).<\/strong><\/p><\/div>\n <\/span>Peri-parturient rise (PPR) also known as spring rise, or post-parturient rise, is the name given to a large increase in fecal egg counts<\/a>\u00a0that occurs about 2 weeks before birth, and for about 6 week afterwards. It occurs mainly in ewes, goats, sows and to a lesser degree in cattle. It is thought to be due to the relaxation of the immune system in late pregnancy, allowing for parasite infection, or hypobiotic<\/a>\u00a0larvae to mature.<\/p>\n The late stages of pregnancy and lactation in ruminants necessitate an increase in their nutrient requirement. The grass quality around lambing is often poor and the inability of the ewe to meet nutritional requirements exacerbates PPR (Walkden-Brown and Kahn, 2002<\/a>). Fecal egg counts<\/a> during the spring rise are higher in animals bearing twins and triplets, compared to those with singles.<\/p>\n <\/a>PPR is important in parasite survival as the large numbers of eggs passed onto the pasture at the same time as the numbers of new susceptible<\/a><\/span> hosts also increases.<\/p>\n Nutrition availability and PGE can be considered from two angles. The first is linked to the damage caused by parasitic infection inhibiting digestion, and the second is linked to the immune response.<\/p>\n The damage caused by a parasitic infection in the gut will vary depending on larval challenge and worm species, and is influenced by the animal factors<\/a> detailed above. GI nematodes influence nutrient availability in one of two ways, they suppress the hosts appetite reducing feed intake, or the worms damage the gut epithelium<\/a><\/span> increasing the pH, \u00a0which consequently reduces the breakdown and absorption of proteins and other nutrients negatively affecting the feed conversion efficiency.<\/p>\n Experiments using radio-isotopic markers have shown that protein losses into the gastrointestinal tract can be substantial, varying from 20 to 125 g protein per day in Teladorsagia colubriformis<\/em>-infected sheep (Poppi et al<\/em>., 1986<\/a>).<\/p>\n It is fair to assume that in most cases improved nutrition will lead to improved ability to induce an immune response and resist disease, especially with gut parasites. Nutrition of the host impacts how well the immune system responds to larval invasion. Protein in particular is required as it provides the building blocks for antibodies and other molecules. It has been demonstrated that ewes fed a high quality diet, compared to ewes fed a poorer diet have a lower FEC during PPR, and higher levels of antibody and numbers of goblet cells in the small intestine (Beasley et al<\/em>., 2012<\/a>).<\/p>\n Mineral supplementation is thought to help the immune response.\u00a0 Swedish pelt lambs provided with access to a mineral supplement containing elemental copper, had significantly lower fecal eggs counts from multiple nematode species in the later part of the grazing season than those without access the supplement (Waller et al<\/em>., 2004<\/a>).<\/p>\n The supplementation of selenium may improve the humoral immune response and therefore reduce worm burden. This has been recently demonstrated in lambs infected with H. contortus<\/a><\/em> but supplemented with selenium and copper (Fausto et al<\/em>., 2014<\/a>). Also lambs supplemented with Vitamins E had a lower burden of H. contortus<\/a> <\/em>\u00a0(De Wolf et al.<\/em>, 2014<\/a>). However, copper supplementation (Copper Wire Particles) was not shown to have the same benefits in first season grazing steers (Dimander et al.<\/em>, 2003<\/a>).<\/p>\n <\/a>Cobalt is known to play a role in immune functions implying that a deficiency could lead to a greater severity of parasite infection (Paterson and MacPherson, 1990<\/a>). Calves deficient in cobalt and experimentally challenged with O. ostertagi<\/a><\/em> had a higher worm burden and egg output compared to calves sufficient in cobalt (MacPherson et al.<\/em>, 1989<\/a>).<\/p>\n <\/p>\n Sheep abomasum containing\u00a0encysted hypobiotic L4 of Trichostronglus axei. Source:<\/strong> www.vet-parasitology.com\/strongyloida.php<\/a><\/p><\/div>\n <\/span>This is sometimes referred to as arrested development. The infective L3 are ingested by the host where they migrate to tissues and cease to develop until they are re-activated by a stimulus. The nature of this stimulus is still uncertain.<\/p>\n <\/a>Hypobiosis is linked to pregnancy and the\u00a0PPR<\/a>\u00a0 and is significant in terms of parasite survival. In temperate climates the infective L3 usually undergo arrested development over the winter period, then re-activate around spring. Hypobiosis enables the nematodes to survive the winters and re-emerge in spring where they mature to adults and then\u00a0contaminate the pasture with eggs.<\/p>\n Hypobiosis also gives rise to type II ostertagiosis<\/a> and type II teladorsagiosis<\/a>. More about each of these conditions can be found on there respective pages.<\/p>\n The free-living stages of GI nematode development are often overlooked by farmers yet they are imperative to enable parasitic infection. The free living stages can be sub-divided into 2 stages both of which are largely dictated by climate:<\/p>\n Climate influences development and survival of larva on the pasture, and the distribution and migratory behavior during the free-living stages. The main factors are temperature and humidity but also sunlight (UV light) can increase mortality.<\/p>\n <\/p>\n Optimal development conditions for Teladorsagia circumcinta<\/em>, Trichostrongylus<\/em> spp. and Haemonchus contortus<\/em>.<\/strong><\/p><\/div>\n <\/span>Extreme heat and cold are detrimental to development and survival, but are tolerable within certain limits (Morgan and van Dijk, 2012<\/a>). Broadly speaking eggs from the common ruminant GI nematodes found in the UK will develop above a threshold of \u00a039.2-41\u00b0F except for Haemonchus<\/a><\/em> which is 46.4\u00b0F (O\u2019Connor et al.<\/em>, 2006<\/a>). As temperature increases, so does the rate at which the eggs develop into infective L3. Increasing warmth not only accelerates development it also increases the rate of L3 mortality. This is to some extent due to the inability of infective L3 to feed (only the pre-infective stages of L1 and L2 feed), and the increased metabolic demand due to increased temperature causing them to perish quicker at higher temperatures.<\/p>\n Moisture from humidity, rainfall, the soil or the fecal pat is required for L3 development and survival and to enable the L3 to migrate out of the fecal pat but is not needed for onward migration onto grass (van Dijk and Morgan, 2011<\/a>).\u00a0 The effect of rainfall on larval dispersal is also important as a drop may transport larvae as far as 35″\u00a0from the dung pat (Stromberg, 1997<\/a>). Eggs and Larva rarely survive in arid climates.<\/p>\n Under optimal conditions of moisture and temperature Ostertagia ostertagi<\/a> <\/em>will reach the infective stage in about 5-6 days (Stromberg, 1997<\/a>).<\/p>\n Sunlight and UV rays increase L3 mortality (Dijk et al.<\/em>, 2009<\/a>). Desiccation of L3 under lab conditions at 77\u00b0F with continuous exposure to UV and 100% humidity, Nematodirus battus<\/a><\/em> 2.5 days, Teladorsagia circumcincta<\/a><\/em> 3 days, and Haemonchus contortus<\/a><\/em> 5 days. Under natural sunlight more L3 survived, but the L3 in the shade survived twice as long (Dijk et al<\/em>., 2009<\/a>).<\/p>\n All of these climatic factors combined make up the seasonal patterns, hence, most clinical cases of nematode infection occur in growing stock in the second half of the grazing season when there is gradual build-up of infective L3 on the pasture.<\/p>\n A good understanding of what drives parasite biology is needed in order to put together a control strategy that does not solely rely on anthelmintics.<\/p>\n <\/a>Sustainable parasite control strategies require knowledge of seasonal larval availability and the climatic requirements for eggs embryonation and hatching, larval development and survival. Different nematodes have evolved to withstand different climatic factors. For example Teladorsagia circumcinta<\/a><\/em> is very tolerant of cold conditions and able to survive below 41\u00b0F, whereas Haemonchus contortus<\/a><\/em> is sensitive to cold but can however, survive well in hot climates. More information about each of the ruminant GI nematodes of veterinary importance can be found on their individual pages:<\/p>\n Nematode infections are almost always a mixture of species.<\/p>\n The grazing system and pasture management impacts on levels of pasture contamination, and therefore worm burden in stock. Different grazing management strategies can be used to minimize larval challenge by targeting, or avoiding the obligatory free-living stage on the herbage to provide \u2018safer\u2019 pasture for the stock to graze. Click on each link to skip to the relevant sections:<\/p>\n![\"Factors](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/05\/PGE-risk-factors-300x234.png\")
<\/a>Understanding Parasite Biology<\/h3>\n
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The Life Cycle of GI Nematodes<\/h3>\n
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![\"GI](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/05\/PGE-lifecycle-1024x768.jpg\")
<\/a>Factors affecting PGE epidemiology<\/h3>\n
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Animal Factors<\/h3>\n
Age-related Immunity and PGE<\/h3>\n
![\"ayrshire\"](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/04\/ayrshire-300x200.jpg\")
<\/a>Genetics and PGE<\/h3>\n
Pregnancy and PGE<\/h3>\n
![\"Ewes](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/05\/twin-lambs-300x215.jpg\")
<\/a>Nutritional Status and PGE<\/h3>\n
Hypobiosis and PGE<\/h3>\n
![\"Sheep](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/05\/Vet-para-hypobiotic-Tricho-larva-300x265.jpg\")
<\/a>Environmental Factors and Nematode Survival<\/h3>\n
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![\"Optimal](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/05\/PGE-Oconnor-300x191.jpg\")
<\/a>![\"Cattle](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/05\/Cattle-PLC-risk-period-2.jpg\")
<\/a><\/p>\n<\/div>\n![\"Sheep](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/05\/Sheep-PLC-risk-period-300x200.jpg\")
<\/a><\/p>\n<\/div>\n\n
Farm Management Factors and PGE<\/h3>\n