Clinical signs and grazing history are usually sufficient for a presumptive diagnosis to be made. The number of ‘strongyle’ eggs per gram of faeces (e.p.g.) in Type I PGE will be close to or greater than 1000 in at least some members of the group, but low or zero values are common in Type II disease (as many worms are still immature when clinical signs first appear). Blood biochemistry shows reduced serum albumin and raised pepsinogen concentrations (see Figure 6.22). At autopsy, abomasal contents have an unpleasant smell (because pH values approaching neutrality allow bacteria and moulds to flourish). Closer inspection of the mucosa reveals typical small nodules (see Figure 8.1) and the presence of brownish threadlike worms. These may number 40 000 or more.

Practical tip box 8.1

PGE is most likely to occur on dairy farms as calves are weaned early in life and often grazed on permanent pastures at high stocking rates. In contrast, calves in beef suckler systems are grazed with their mothers. As most of the grass is utilised by the cows, there are relatively few calves per unit area. Cows produce large volumes of faeces with few Ostertagia eggs per gram. This has the effect of diluting the high e.p.g. faecal output of the calves and so correspondingly few infective larvae accumulate per kg grass.

Adult cattle are not usually clinically affected by PGE as they will have developed a substantial level of immunity. Nevertheless, abomasal damage can accrue if they graze heavily contaminated pasture and milk-yields may be affected to a small, but economically significant degree. An estimate of the level of herd exposure can be obtained by measuring specific antibody titres in bulk milk samples, but serum pepsinogen concentrations do not provide a reliable indicator as normal values tend to increase with age.

At the time of writing, resistance to anthelmintics has not become a serious problem in cattle nematode populations (although this is no reason for complacency, as will become evident in the ovine PGE section below). Compounds active against adult and immature worms include macrocyclic lactones (MLs – see Section 7.3.2), benzimidazoles (BZDs – see Section 7.3.3) and levamisole (see Section 7.3.1). Ideally calves should be moved to clean pasture after treatment but, if this is not an option, the persistent activity of MLs against incoming L₃ will protect against reinfection for three or more weeks (depending on the compound, formulation and method of administration).

The persistent activity of the MLs can also be utilised to prevent PGE from happening. This approach is based on the knowledge that, in temperate climates, the epidemiology of PGE in set-stocked calves (i.e. those kept on the same pasture all season) follows a stereotyped seasonal pattern (see Figure 6.18). Disease can be avoided in two ways:

1. Metaphylaxis: nature is allowed to take its course but the calves are dosed with an ML shortly before the density of L₃ on the pasture rises to potentially pathogenic levels (see Figure 8.2). The persistent activity of the chosen ML kills ingested larvae before they can cause disease. Some mucosal damage will occur, however, and this may influence growth-rates. On the other hand, the calves are given adequate opportunity to develop an immunity that will protect them in their second grazing season.
   
2. Prophylaxis: calves are treated with an ML early in the grazing season to ensure that worms derived from the ingestion of overwintered larvae are killed before they start to lay eggs. This is beneficial as, because no new eggs are dropped onto the pasture at this time, the subsequent disease-producing wave of infective larvae (the ‘autoinfection peak’) fails to develop (see Figure 8.3). The pasture thereby remains ‘safe’ for the remainder of the year. This system works well if early season treatments are timed correctly and provided no untreated animals are introduced onto the pasture. As with all routine parasite control strategies dependent on a single chemical class, careful management is required to avoid resistance developing in the longer term.

For early season prophylaxis, the first dose of ML is usually given three weeks after spring turnout as this corresponds to the prepatent period (PPP) of Ostertagia. One or two further doses will be needed, depending on the period of persistency (PP) of the chosen ML. The dosing interval is calculated by adding together the PPP and PP as this determines the length of time over which no eggs will be dropped onto the pasture. Conservative values are used to allow for possible biological variation. Thus, one such programme uses three doses of ivermectin administered at 3, 8 and 13 weeks after turnout. To reduce the number of times that calves need to be rounded up for treatment, the first dose of ML can be given at turnout (as, for example, in the doramectin 0, 8 week programme).

To eliminate the need for repeated dosing, intraruminal devices have been developed that continuously or intermittently release an appropriate amount of ML or BZD over a sufficient time-period to ensure prophylactic or metaphylactic protection. Although highly successful, most are no longer sold, partly because of the high cost of manufacture and partly because of a concern that, in some circumstances, recipient calves may not receive adequate antigenic stimulation to ensure immunity by the end of their first grazing season.

With ingenuity, other strategies can be devised for preventing PGE. For example, it is known that overwintered larvae die in the early part of the grazing season (see Figure 6.18). Pastures are therefore safe to use (‘clean’) after hay or silage has been harvested in the spring. Thus, calves that graze initially on contaminated permanent pasture can be treated to remove the worms that have established and then moved onto a harvested field (i.e. onto ‘aftermath’). A potential disadvantage, however, of such ‘dose-and-move’ systems is that any eggs subsequently dropped onto the new pasture will have been derived from worms that survived treatment. This may enhance the prevalence of resistance genes in the parasite population.

Extra information box 8.1

Bovine toxocarosis

Somatic larvae of Toxocara vitulorum in the tissues of cattle and buffalo are activated towards the end of pregnancy. They migrate to the udder and are passed in colostrum for about a week. Adult worms establish in the small intestine of the calf and start to pass eggs at about three weeks of age. By five months, the worms have all been expelled. In the meantime, heavy infections cause enteritis, loss of condition and sometimes intestinal obstruction. Fatalities can occur, especially in buffalo. Losses can be avoided by treating vulnerable calves at 10–16 days of age using an anthelmintic with high efficacy against adult and immature stages.

Bovine fasciolosis

Cattle rarely suffer from acute fasciolosis but the chronic form of the disease does occur. Clinical signs are confined mostly to younger grazing stock as a partial immunity follows initial infection. Affected animals show weight-loss accompanied by anaemia and sometimes submandibular oedema. Subclinical infection is responsible for reduced weight gains in growing animals or depressed milk production in dairy cows. The susceptibility of cattle to certain other diseases (e.g. salmonellosis) is increased and the sensitivity of the tuberculin test (an intradermal test to detect cattle infected with bovine tuberculosis) reduced. This is probably the result of powerful immunomodulatory factors released by Fasciola as part of its defence against host immune attack (see Section 5.6.1).

As bovine disease is associated with the presence of adult flukes (see Figure 8.4), faecal examination for parasite eggs is a useful diagnostic aid. Further evidence of infection is provided by elevated plasma enzyme concentrations indicating liver or bile duct damage, e.g. glutamate dehydrogenase and gamma-glutamyl transpeptidase. Specific antibodies can be assayed in serum or bulk milk samples. Almost all commercially available flukicidal drugs are active against the adult worm, although strict regulation controls their use in animals for milk production.

A recombinant vaccine is being developed for use in cattle but is not commercially available at the time of writing. It exerts its effect by stimulating a range of immune responses not normally occurring in chronically infected animals (including Th1-type responses).

Bovine paramphistomosis

Although paramphistomes are cosmopolitan, disease is associated mostly with warmer, wetter regions, especially those prone to flooding, as these are the conditions most favourable for the aquatic intermediate hosts. Large numbers of migrating immature flukes in the duodenum provoke persistent afebrile foetid diarrhoea. This leads to depression, dehydration, weakness and often death. Grazing history and local knowledge are important factors in reaching a presumptive diagnosis. Faecal egg-counts are not dependable since the causal organisms are immature. Small plump flukes may, however, sometimes be seen in faeces. Treatments have to be selected with care as few anthelmintics are effective against this trematode.

Intestinal protozoan infections

Intestinal protozoa are mainly problematic in young stock. Asymptomatic infections are common. Cryptosporidiosis and coccidiosis are the most frequent clinical conditions, although Giardia can also provoke diarrhoea on occasion.

Cattle harbour numerous Eimeria species. Two, E. bovis and E. zuernii, are recognised as serious pathogens in young calves. A third species, E. alabamensis, sometimes affects older calves at pasture producing a milder diarrhoea and weight loss.

E. bovis and E. zuernii sporozoites invade villi along the ileum. They enter endothelial cells lining the lacteals and develop into giant macroschizonts. The consequent tissue damage provokes blood-stained diarrhoea, which often contains strands of sloughed mucosa. The disease occurs mostly in calves kept in poor conditions but can strike when young stock are newly introduced into a herd or when they are turned out to grass. A high faecal oocyst count (>5000 o.p.g.) is suggestive of a causal relationship, although diarrhoea can start shortly before patency becomes evident. Speciation of oocysts is necessary to determine the proportion attributable to pathogenic species. Control revolves around management of the immediate environment, e.g. by ensuring that susceptible animals are not overcrowded or exposed to stress, by keeping buildings dry and by changing bedding regularly, etc.

Cryptosporidiosis is one of the commonest infections detected in diarrhoeic calves, especially in those 1–2 weeks of age. It is more likely to occur if calves are colostrum-deprived, or if other potential enteropathogens (such as rotavirus, coronavirus or enterotoxigenic Escherichia coli bacteria) are also present on the farm. In faecal smears stained by the Ziehl-Neelsen method, oocysts measuring 4–5 μm appear red against a blue-green background (see Figure 8.5). Few drugs are completely effective against Cryptosporidium, so supportive therapy including fluids and electrolytes are particularly important. Control requires scrupulous hygiene in calf rearing facilities. Calves should receive adequate amounts of colostrum.

Novel and sustainable control methods are being developed for both advanced and low-input farming systems. Selection pressure can be reduced by dosing only the most vulnerable individuals within a flock (see Section 1.6.6). A simple but ingenious and effective method of determining which animals to treat is the FAMACHA^© system. This measures the pinkness of the conjunctival mucosa against a calibrated colour chart to indicate the degree of anaemia being experienced by each individual animal (see Figure 8.6).

In addition to the mainstream anthelmintic groups, the flukicidal drug closantel (see Section 5.7.2) is used in some control programmes as it is effective against blood-sucking nematodes. It has residual activity and prevents reinfection with Haemonchus for a period of four weeks.

A hidden-antigen vaccine (see Section 1.6.5) is being developed but is not commercially available at the time of writing.

Nematodirosis

Nematodirosis is a seasonal disease, occurring in the spring, which affects lambs around 6–10 weeks of age. Sudden onset profuse diarrhoea follows a mass hatch of L₃ from eggs that have overwintered on the pasture (see Figure 6.29). The mortality rate can be high, especially if there is concurrent coccidial infection.

Diagnosis is based primarily on clinical history as death can occur before eggs start to appear in the faeces (i.e. within two weeks of infection). Nematodirus eggs are larger than the usual strongyle ova. Those of the most pathogenic species, N. battus, are characteristically brown-coloured with parallel sides (see Figure 6.28).

As infections are passed from one batch of young lambs via overwintering eggs to the following year’s lamb crop, trouble can be avoided by withholding vulnerable lambs from potentially contaminated pastures during the danger period. If this is not possible, treatments with an anthelmintic active against immature Nematodirus can be given in anticipation of the onset of disease. The precise timing of such interventions is critical and is aided in some countries by disease forecasts based on local meteorological data.

Practical tip box 8.2

Ovine fasciolosis

Liver fluke infection, due to Fasciola hepatica in temperate and F. gigantica in warmer regions, is a common cause of disease and suboptimum productivity wherever there is a wet climate and poorly drained pastures that are not too acid for the intermediate host, the mud snail, Galba (Lymnaea). In contrast to the equivalent bovine disease (discussed earlier in this section), ovine immune responses to Fasciola do not provide any useful protection against disease, so sheep remain susceptible to fasciolosis throughout their lives. Unlike cattle, they can succumb during the migratory phase of the liver fluke life-cycle.

Ovine fasciolosis exhibits as a spectrum of disease manifestations with no clear demarcation between each:

1. acute fasciolosis: a few animals in the flock are found dead each day with few if any warning signs. In temperate zones, most outbreaks occur in the autumn.
   
2. subacute fasciolosis: rapid weight-loss becomes evident over 1–2 weeks, usually during the autumn or early winter. Affected animals have pale mucous membranes and may die. Fluke infection can predispose to Black Disease caused by Clostridium novyi type B.
   
3. chronic fasciolosis: progressive weight-loss extends over weeks or months becoming obvious during the winter or early the following spring. Lethargy and submandibular oedema are other frequent signs (see Figure 8.7).
   
4. subclinical effects: fleece weight and wool-fibre quality are affected even by small fluke burdens. Reproductive performance (as measured by number of lambs born and the growth-rate of unweaned lambs) may be adversely influenced (although this is less well documented). Poor carcase quality and liver condemnations reduce value to the meat industry.

The presence of snail habitats on a farm, together with time of year and prevailing weather patterns, will alert the clinician to the possibility of fasciolosis as an explanation for deaths or poor performance. Other indications include:

1. acute fasciolosis: there is seldom opportunity to examine animals prior to death but at autopsy the liver is enlarged, pale, friable and haemorrhagic (see Figure 5.40). Squeezing slices of liver will reveal large numbers of immature flukes in the parenchyma. These are leaf shaped, pale coloured and lack the ‘shoulders’ typical of adult Fasciola.
   
2. subacute fasciolosis: haematology reveals normochromic anaemia. The liver is enlarged and subcapsular haemorrhages are often present (see Figure 5.41). There will be more than 500 flukes of which about half will be adult.
   
3. chronic fasciolosis: diagnosis is usually confirmed by demonstrating characteristic eggs in faeces (see Figure 5.38), although egg-output can be erratic. A recently introduced coproantigen test promises to provide greater sensitivity and is able to detect the presence of flukes in bile ducts before they start to produce eggs. The anaemia is initially normochromic but later becomes hypochromic; afflicted animals are also hypoalbuminaemic and hyperglobulinaemic. Liver enzyme concentrations in the blood are raised. At autopsy, the liver is small, cirrhotic and distorted, with gross enlargement of bile ducts (see Figure 5.42). Opening these and the gall bladder will reveal more than 250 adult flukes. Their size (2–5 cm) and ‘shoulders’ (see Figure 8.4) differentiate them from Dicrocoelium which may be also found in bile ducts, although usually in animals grazing drier environments.

Practical tip box 8.3

Few flukicides kill all parasitic developmental stages (see Table 8.2). Not all products, therefore, are suitable for controlling outbreaks of acute disease. The anthelmintic with the broadest spectrum of activity against immature and adult F. hepatica is triclabendazole, but resistant strains are beginning to emerge and so alternatives should be used when possible in order to preserve the activity of this clinically valuable product.

The prevention of fasciolosis requires an understanding of the epidemiology of the disease. This is determined by the breeding cycle of the intermediate host and the influence of ambient temperature on the rate of fluke development within both the egg and the snail (see Section 5.6.2). The precise timing of the resulting sequence of events varies with local circumstances and so an example (from Great Britain) is used to illustrate the principles underlying control strategies (see Figure 8.9).

There are two main control objectives:

1. to prevent fluke eggs dropping onto pasture: Most fluke eggs die during the winter. Treating sheep in the late winter or early spring to remove adult flukes will ensure that no new eggs are dropped onto the pasture during the spring and early summer (‘a’ in Figure 8.9). As a result, there will be few miracidia hatching to infect the new generation of snails (‘b’ in Figure 8.9) and this will substantially reduce the numbers of metacercariae appearing on the pasture later in the year (‘d’ in Figure 8.9).
   
2. to protect grazing animals during times of high risk: this applies especially to sheep grazing a snail habitat during the autumn of a year when a ‘bad’ fluke season is forecast (‘d’ in Figure 8.9). In the knowledge that such animals are likely to ingest considerable numbers of metacercariae, treatment with a compound active against immature flukes can be given during the incubation period, i.e. while the flukes are in the liver but before they have grown large enough to cause substantial damage (‘e’ in Figure 8.9). A second treatment may be necessary if stock cannot be moved to safer pasture, the dosing interval depending on the persistency of the drug used.

Historically, molluscicides have been employed to control fasciolosis by eliminating snail populations. Although technically successful, they were not commercially viable. This was due partly to environmental concerns and partly because any snails surviving (e.g. if protected from the spray by thick vegetation) could quickly recolonise available habitat.

An ability to recognise and define the extent of snail habitat on an affected farm allows alternative cost- effective control options to be practised, such as fencing, drainage and the removal of vulnerable stock to safer pastures at times of high risk.

Ovine coccidiosis

Sheep harbour many Eimeria species, some producing macroschizonts visible as white spots in the intestinal mucosa. One nonpathogenic species induces papillomatous growths. Two species, E. ovinoidalis and E. crandalis, are commonly responsible for diarrhoea in lambs of about 6 weeks old.

Ewes act as immune carriers passing small numbers of oocysts which accumulate indoors in poorly managed litter or, outdoors, around feed and water troughs. Early lambs amplify the parasite population exposing later lambs to heavier infection pressure. Twins and triplets are particularly vulnerable. Disease is usually associated with high faecal oocyst counts although death can occur within the two week prepatent period. Outbreaks may be coincident with Nematodirus or Cryptosporidium infections, which can complicate diagnosis and control.