Modern-day parasite control is made up of a range of factors. Historically, anthelmintics were relied upon heavily. However, with the emergence of increasing evidence of resistance, a more integrated framework of management practices is needed, for example, in grazing management, genetics and nutrition. Anthelmintic use at housing is still the cornerstone of control, due to the low risk of re-infection once cattle are away from pasture. Anthelmintic resistance is already widely reported in sheep with more reports emerging of resistance in cattle (Baiak et al, 2018). Efforts to reduce and target the use of these drugs, should be the focus over the next few years. Knowledge of the parasite populations present on a farm, as well as of levels of pasture contamination and immunity levels, is key to tailoring parasite control plans for individual farms.
Available drugs
The Agriculture and Horticulture Development Board's (AHDB) (2020) parasite control guide provides all anthelmintic preparations currently available for cattle. Anthelmintic classes available include the following:
- Benzimidazoles
- Levamisols
- Macrocyclic lactones (MLs)
- Flukicides and combination products including flukicides.
Ideally, animals should be treated on the basis of herd-level diagnostics, e.g. for fluke, faecal egg counts (FECs) and enzyme-linked immunosorbent assay (ELISA) serology. However, there are limitations with some of these including potential false-negative results depending on what stage of infection cattle are sampled at. More oft en, producers will use a blanket anthelmintic treatment as, without diagnostics, it is impossible to differentiate between prepatent and patently infected animals.
Use of treatments at housing
A treatment at housing aft er the summer grazing season is both therapeutic and strategic; it will remove any nematode or trematode parasite burdens acquired during the grazing season, including Ostertagia ostertagi, Dictyocaulus viviparus and Fasciola hepatica. These burdens will cause production losses through the winter if left unchecked and contribute to poor growth rates and feed efficiency (Fox et al, 1989; Forbes et al, 2000). Chronic infections can become established with O. ostertagi encysting in the gut wall and F. hepatica causing chronic infections in the liver with some able to survive for years (Control Of Worms Sustainably (COWS), 2013). The treatment is strategic as there is minimal risk of new infections post treatment. The lifecycle of nematodes will be stopped through the housing period and the few eggs that are passed from surviving worms that develop to larvae are unlikely to be ingested. This ensures that cattle are shedding minimal fluke eggs, worm eggs or lungworm larvae at the following spring turnout and these animals do not contaminate the pasture.
For lungworm, as well as causing clinical disease, it is reasonable to predict that the tissue damage post infection could predispose cattle to secondary pneumonia infections, despite limited evidence, which is always an increased risk during housing periods. Ectoparasites can also cause productivity losses and both mites (e.g. Chorioptes bovis) and lice (e.g. Bovicola bovis) are more prevalent in the winter due to thick coats and a lack of ultraviolet (UV) light. They live permanently on the animal but populations rise during the winter; a treatment at housing can eliminate this.
From a management perspective, treating animals once they are housed is also more efficient and less time-consuming as it is convenient once animals are nearby to handling facilities.
Parasitic gastroenteritis
Two most common species of gastrointestinal tract nematodes seen in the UK are O. ostertagi and Cooperia oncophora (COWS, 2014a). Primarily seen in the first grazing season, if cattle are weaned at turnout, burdens will peak mid-summer; if suckling beef calves are not weaned until late summer, infectious burdens will peak in early autumn. In warm summers with adequate rainfall (temperature and moisture are essential for larvae development on pasture), the average prepatent period is 3 weeks. The prepatent period is defined as the time interval between cattle in-gesting infective larvae and the development and maturation of adult parasites that produce eggs. Immunity is developed quickly for C. oncophora but less so in O. ostertagi. Parasitic gastroenteritis (PGE) should still be on any differential list for scouring adult cattle (Bellet et al, 2016) and they need to be taken into account when planning housing treatments. Nematodes are generally host-specific and species infecting sheep have the most documented resistance towards them (Kamaludeen et al, 2019) and there are recent reports into resistance seen in cattle (Baiak et al, 2018). When using anthelmintic treatments through the grazing season, it is important to use targeted treatments (Berk et al, 2017), ideally based on daily live weight gains at 0.75 kg/day (Höglund et al, 2009; Jackson et al, 2017). This strategy involves weighing animals regularly and leaving well-grown ‘resilient’ animals untreated, maintaining a susceptible inrefugia population. Using a treatment at housing will help to reduce the larvae that encyst over winter in the gut wall, and that cause the O. ostertagi type II syndrome. It is important to remember that MLs are the only anthelmintic to have consistent efficacy against encysted larvae (Williams et al, 1997); oxfendazole benzimidazoles are highly variable and levamisole has no action at all. Targeted treatment strategies are efficient; however, if lungworm infection is also present on the same pasture, care must be taken with targeted treatments, so as to not withhold treatment from animals at risk.
Grazing management is key as larvae can survive on pasture for up to a year (COWS, 2014b), as well as over winter. Therefore, rotating turnout pastures, using silage aftermath and rotating grazing with sheep, are all strategies to reduce pasture challenge to cattle and help reduce reliance on anthelmintics.
Liver fluke and rumen fluke
The most common species of trematode seen in the UK is F. hepatica (Salimi-Bejestani et al, 2005); it is not host-specific and affects both sheep and cattle. The lifecycle relies on the intermediate host, the snail (Galba truncatula), and is thus highly dependent on the weather (COWS, 2013). Both the life stages of snails and fluke — miracidium and cercaria — need moisture and warmth to develop and move on the pasture. The lifecycle can take up to 12 weeks, so infection levels take time to build up, peak infection tends to be late summer and disease is then seen during the autumn/early winter. A hot dry summer will mean a small late peak of infection.
There is little evidence that cattle can develop immunity to fluke and can be repeatedly infected. Fluke can also survive in the liver for a long period of time, without causing obvious clinical signs, but being a source of infection (COWS, 2013). On endemically-infected farms, treatments are used at strategic times of the year. Treatment at housing is commonly carried out and helps to reduce chronic fasciolosis infection over the winter; chronic infection can cause a reduction in growth rates, milk yield and reproduction (Forbes et al, 2015). It has also been seen to affect immune responses to Mycobacterium bovis (Howell and Williams, 2020), potentially impacting routine surveillance testing.
Due to the slow progress of the disease, it can take up to 8–12 weeks for fluke to mature, and only a few flukicides treat both immature and juvenile fluke. This needs to be taken into account when designing a fluke treatment strategy at housing. Options include:
- Leave treatment until 10–12 weeks post housing and treat with an adult-only treatment. However, this risks production losses as immature fluke cause considerable damage to the liver's structure during maturation and migration to bile ducts
- Blanket treat at housing with a triclabendazole drench that covers all life stages. However, there is documented resistance to triclabendazole in sheep (Fairweather, 2011; Hanna et al, 2015). Due to not being host-specific, this means the risk is transferable to cattle (Sargison, 2012). To avoid blanket treatment with triclabendazole, treatment could be targeted using diagnostics, including ELISA antibodies or FECs. There are however limitations that need to be considered with both of these. FECs only show presence of adult fluke; if the animal is in the pre-patent stage, eggs will not be seen up until 10–12 weeks. Eggs are also sometimes shed intermittently. Antibodies can detect infection down to 2 weeks but can persist after a treatment so a positive result may not mean a current infection
- Treat once at housing and then repeat at 10–12 weeks with an adult-only drench. This will cover any immature fluke missed at the first treatment. On account of the double drenching, there is of course an increased cost associated with this option.
Withdrawal periods of flukicides need to be considered in dairy herds. There are only two products licensed for lactating dairy cows and both only treat adults (albendazole and oxyclozanide). If a triclabendazole product is needed, Fasinex is licensed, but only 50 days from calving so needs to be used at drying off (Elanco UK, 2020). Other products containing triclabendazole with similar profiles are also available. Care must be taken with accurate calving dates. Therefore, herd-level treatment is difficult in all-year-round calving herds.
Pasture management is also advisable but, practically, it is difficult to stop cow exposure to snail habitats. Fencing high-risk areas of fields or avoiding wet grazing, improvement of drainage to particularly wet pasture or even use of natural snail predators have been tried (Hull, 2017).
Rumen fluke
Calicophoron daubneyi, known as rumen fluke, has been increasingly diagnosed in the UK and Ireland over the last 5 years (Toolan et al, 2015). Its lifecycle is very similar to that of liver fluke. The immature rumen fluke mainly cause clinical disease, poor thrift and diarrhoea, with adult rumen fluke relatively harmless once in the rumen. It is usually diagnosed either post mortem or through a positive FEC result and a negative F. hepatica ELISA antibody result, as the eggs look very similar to those of F. hepatica with no response to the usual flukicides. Rumen fluke can occur alongside liver fluke; however, the only flukicide known to work in the UK on rumen fluke is oxyclozanide. If treating a co-infection, immature liver fluke must be taken into account, as well as that oxyclozanide use is off-license for rumen fluke.
Lungworm
D. viviparus, known as lungworm or ‘husk’, is a type of nematode that targets the lungs (COWS, 2014c). Commonly seen in young-stock during their first grazing season in the UK and increasingly in adult cattle (Morgan, 2020). Adult worms live in the bronchi, and cause bronchitis and secondary pneumonia after aspiration of in-flammatory exudate, eggs and larvae. Infection causes irreversible damage to lung tissue, which will have a lifelong impact on productivity (Mejía et al, 2011; Perri et al, 2011; Dank et al, 2015).
First season grazing youngstock with no immunity are the most susceptible when grazing in permanent pastures previously grazed by infected cattle. When turned out in the spring, any arrested larvae on the pasture will resume their development; if pastures are not rotated, clinical disease can be seen once infection levels have risen by the second- or third-worm generation (approximately 2 or 3 months). Carrier animals are thought to be the most important and reliable contributors to the year-to-year survival of D. viviparus (McLeonard and Van Dijk, 2017).
Primary and secondary levels of immunity are developed; the primary will wane after 6 months, with no constant low-level exposure (i.e. over the winter during housing). Animals having lost their primary immunity can succumb to ‘reinfection’ syndrome on subsequent turnout (McLeonard and Van Dijk, 2017). Performing serological tests on stock at housing is a sensible precaution for ensuring the previous grazing season has allowed adequate immunity to develop. However, it is important to remember that primary immunity may have waned by spring turnout.
The prepatent period is highly dependent on weather; sporadic outbreaks can be seen after warm and wet summers. If weather conditions are suitable, larvae will develop on the pasture quickly and outbreaks of disease will occur throughout the grazing season; therefore, treatment is needed promptly. Strategic treatment at housing can also help break the cycle if infection is picked up later in the season. Options for control include the following:
- Anthelmintics — all three classes discussed will target D. viviparus. Currently, there is little resistance reported in D. viviparus populations (McLeonard and Van Dijk, 2017). Levamisole was historically used because of its mechanism of only paralysing adult worms, allowing the body to rid itself of them and avoid the more severe immune response caused by killing the parasites. However, MLs have a slower onset and do not elicit such a severe reaction. MLs and levamisole are effective against more of the developmental stages of the parasite. This is important, as if larvae are left, it allows animals to become carriers and a recurrence of disease may be seen. The persistent activity of MLs means that following treatment, subsequent reinfection is avoided if cattle have to remain on infected pastures. If using to treat clinically infected animals, prognosis depends on stage of infection and level of adult worm burden; care must be taken during application to reduce stress. Non-steroidal anti-inflammatories should be given to reduce any inflammation reaction post treatment
- Strategic dosing of anthelmintics to avoid infection through the summer can be used — it is important that the first treatment is given at or within 3 weeks of turnout. This allows some exposure to larvae, but it is unlikely that there will be high enough burdens to stimulate immunity development that early in the season. Alternatively, leaving youngstock unexposed at the end of the grazing period once a long-acting drug has waned does the same thing. This system is high-use for anthelmintics and although there is not much resistance documented in lungworm, other gastrointestinal nematodes are also being exposed on each treatment, creating a selection pressure for resistance in those species simultaneously. If consistent long-acting anthelmintic treatments are used during the first grazing season, it has been documented in some evidence that these animals can still mount a primary immune response to larvae (Taylor et al, 2000; Ploeger, 2002)
- Alternatively, vaccination can be used — however, it has to be given past 8 weeks of age, two doses a month apart, and 2 weeks has to pass before turnout to allow the antibodies to develop. In all-year-round calving herds, this is impractical during summer months if weaned youngstock are turned out. Therefore, a combination of vaccination and anthelmintics can be used
- Last, a leave-and-monitor approach could be used — however, this obviously runs the risk of clinical disease. Grazing rotations can be used to reduce larvae transmission although, again, dependent on weather; if wet and over 22°C, larvae can develop in 4 days on pasture. Larvae can survive on pasture for a long time and over winter; on farms where the disease is endemic, it is hard to avoid exposure completely.
Ectoparasites
Ectoparasites can also cause weight loss or reduced weight gain as a result of pruritus (COWS, 2014d). Both mites, such as C. bovis and lice such as B. bovis, are more prevalent in the winter owing to thick coats and a lack of UV light. C. bovis mites are susceptible to MLs that are topically administered as they are on the skin's surface. Other species including Psoroptes ovis and Sarcoptes scabiei are susceptible to injectables. Lice are susceptible to pyrethroid pour-ons and either pour-on or injectable MLs.
Conclusions
Housing is the most responsible time to use treatment for endoparasites and ectoparasites to reduce the risk of anthelmintic resistance. There is a low risk of contribution of any resistant isolates surviving and being ingested while cattle are inside.
Knowledge of what parasites are endemic on individual farms is vital. PGE is ubiquitous through the UK so a certain level can be expected on most UK permanent pastures. Lungworm and liver fluke are more farm-specific and, in particular, liver fluke need a certain type of environment. Knowing whether these parasites are present and need to be targeted for treatment will affect anthelmintic use.
A recent meta-analysis from Baiak et al (2018) described emerging resistance in cattle to several anthelmintics, predominately in South America, but including several reports in EU countries. Therefore, it is still prudent to strive to use anthelmintics in a more targeted fashion, to try to reduce the risk of resistance developing to them in the future. Strategies to reduce pasture challenge involve pasture rotations, use of diagnostics and targeted treatments to individuals, and should be prioritised if possible.
KEY POINTS
- Treatment at housing is used to remove endoparasite burdens acquired during the grazing season.
- The risk of re-infection post treatment and development of resistant populations over the winter are low when animals are treated once housed.
- Treatments should be farm specific and given in response to known parasite history of a farm or after adequate herd level diagnostics.
- Anthelmintic resistance is increasingly being reported in cattle, a more integrated approach is needed including grazing management strategies and targeted treatments.