The wormy horse

The number of larvae in the mucosa depends, of course, on how many cyathostomin L₃ there were on the pastures being grazed. Seasonal fluctuations in pasture larval counts follow the same general pattern as that seen in the epidemiology of ruminant PGE (see Figure 6.18), with large numbers accumulating during the summer and autumn. Cyathostomin L₃ (see Figure 9.1) survive average winters relatively well but they die when temperatures rise in spring.

When horses are allowed to express natural behavioural patterns, they defecate onto some parts of a field (the ‘roughs’) while other areas (the ‘lawns’) are reserved for grazing. This provides some natural protection from parasitism. If overstocked, horses are forced to eat the highly contaminated grass as well.

As horses remain vulnerable to parasitism throughout their lives, they have by tradition been wormed at regular intervals to keep them healthy, but this has inevitably given rise to resistance problems. Only three types of anthelmintic are currently available for broad-spectrum worm control in horses – benzimidazoles (BZDs), macrocyclic lactones (MLs) and pyrantel. It is therefore of paramount importance that control schemes should comply with best practice for maintaining the usefulness of those anthelmintics still effective on a property (by applying the principles outlined under ‘Ovine PGE’ in Section 8.2.1). Some options for horse owners are discussed in the next section.

Larval cyathostominosis

Diagnosis is difficult as faecal egg-counts give no information on larval development. Large numbers of small (4–8 mm) red L₄ may be passed in faeces or be seen adhering to the clinician’s glove after rectal examination. Haematology will show hyperglobulinaemia (mainly IgE), hypoalbuminaemia and leukocytosis. At autopsy, enormous numbers of EL₄ can be seen as brown flecks in the inflamed and oedematous luminal mucosa of the caecum and colon (see Figure 9.2).

Larval cyathostominosis is an unpredictable disease which can destroy valuable or well-loved horses with little warning. Arrested larvae protected within their nodules are insusceptible to most anthelmintics and so the most effective way to prevent this disease is to ensure that EL₃ do not accumulate in the mucosa. Thus, the primary objective of worm control programmes must be to maintain pasture contamination within safe limits.

One useful way of doing this is by mechanical removal of faecal material from paddocks at intervals of no more than a week. Although labour intensive, this approach has the twin advantages of reducing the number of worming treatments needed during the year and increasing the amount of palatable grass, allowing better utilisation of the pasture.

Anthelmintic usage can be further reduced by performing faecal egg-counts at intervals. This determines when the overall faecal egg-output reaches a level justifying intervention and identifies which individuals have high egg-counts and should be treated. Those with low egg-counts contribute little to pasture contamination and their worm-burdens can therefore be left in refugia (see Section 1.6.3).

The cyathostomin population in a horse comprises five distinct developmental stages with different anthelmintic susceptibilities. These are:

1. Within the mucosa: arrested third-stage larvae (EL₃); developing (late) third-stage larvae (LL₃); early fourth-stage larvae (EL₄) (see Figure 9.3).
   
2. Within the intestinal lumen: late fourth-stage larvae (L₄) and adults.

Some anthelmintics such as pyrantel are active mainly against luminal forms. Others, such as fenbendazole at normal dose-rates, will kill luminal forms and the more advanced mucosal larvae. The macrocyclic lactones impact earlier larvae as well, but to different degrees depending on the compound and conditions of use. Fenbendazole when given daily for at least five consecutive days also has good effect against earlier larvae. The clinical relevance of this information has two facets:

1. Egg reappearance period: when given to healthy horses, anthelmintics will suppress faecal egg-output for different lengths of time depending upon how many mucosal life-cycle stages are killed (see Figure 9.4). The ‘ERP’ for different products varies from around 5–14 weeks and is an important factor in determining treatment intervals. The first sign of an impending resistance problem is often a shortening of the ERP.
   
2. Choice of anthelmintic: for treating clinical cases of larval cyathostominosis or for protecting ‘high risk’ horses (e.g. those that have grazed heavily contaminated pasture) it is, of course, imperative to choose an anthelmintic that kills as many mucosal larval stages as possible.

Other parasitic infections

Small intestine

Strongyloides infections are generally asymptomatic and high faecal egg-counts can be recorded from healthy foals. Alternative causes of diarrhoea should be investigated before Strongyloides is judged to be the culprit. Parascaris usually does no more than contribute to the ‘wormy horse’ syndrome although blockage, and even perforation, of the small intestine is possible in heavy infections on account of its impressive size, up to 50 cm long (see Figure 9.5).

The eggs of Strongyloides (see Figure 7.2) and Parascaris are easily detected and identified in faecal samples, the latter being similar to Ascaris eggs (see Figure 8.28). T. axei produces typical strongyle ova. These can be differentiated from those of the cyathostomins and Strongylus spp. by faecal culture as T. axei L₃ lack the long filamentous tail characteristic of the others (see Figure 9.1). Spiruroid eggs have a characteristic appearance (see Figure 7.21) but are rarely seen on faecal examination.

Horses have just one significant coccidian species, E. leuckarti. This produces large subepithelial gametocytes at the tips of intestinal villi, which become disrupted, stunted and oedematous (see Figure 9.6). The nucleus of the swollen host cell is pushed to one side, giving a ‘signet ring’ appearance. The clinical significance of E. leuckarti infection is uncertain, but it is sometimes associated with intermittent diarrhoea in foals. The oocysts are unlike those of other Eimeria species in that they are much larger (80 μm long) and dark brown in colour (see Figure 9.7). They are ovoid with a distinct ‘gap’ (the micropyle) at the narrow end. E. leuckarti is often overlooked in routine diagnosis as the oocysts are heavy structures that do not rise in commonly used flotation fluids.

Lungworm

In contrast to horses, infected donkeys rarely show clinical signs but often shed eggs (see Table 9.3). They can therefore act as asymptomatic carriers and it is prudent to check that donkeys are free of lungworm before allowing horses onto pastures that they have grazed. The D. arnfieldi life-cycle can, however, continue in horses in the absence of donkeys.

Verminous endarteritis

Equine piroplasmosis

Fly worry

Flies can worry horses in a number of ways. The nonbiting muscid flies that cluster round the eyes, lips, genitalia and open wounds to sponge-feed on secretions and exudates are an obvious annoyance. They disturb grazing and induce head shaking, tail switching and other protective behaviours. Biting flies inflict different degrees of discomfort. The stabbing action of the stable fly, Stomoxys, provokes irritable reactions such as stamping. But most painful are the rasping bites of the tabanids (horse flies). These can elicit sudden alarm that may result in a rider becoming unseated. The simuliids (blackflies) are much smaller but attack in persistent swarms and can cause considerable distress, especially those species that crawl into the nose or ear (see Figure 9.8). All the flies so far mentioned are transient visitors but Hippobosca, once it has found a host, adopts a parasitic lifestyle and remains on the thin skin of the upper hindquarters until it is ready to give birth to the fully grown larva it has been nurturing. Other flies feeding on horses include midges, phlebotomine sandflies and mosquitoes. The bot fly, Gasterophilus, does not bite but upsets horses by hovering nearby and darting in to deposit eggs onto hairs.

Many ectoparasites have specific predilection sites (see Figure 9.9). Some species of Culicoides, for example, feed along the line of the mane and tail, while other species attack the ventral midline or other parts of the body. As well as the physical damage they cause, biting flies can induce allergic reactions in some horses. Self-trauma may follow and lesions can become secondarily infected and attract myiasis flies such as calliphorine blowflies or screwworms. Flies also transmit skin pathogens such as the nematode parasites Habronema and Parafilaria.

Equine seasonal allergic dermatitis

Lesions occur initially on the skin of the forelock, mane and tail-head (see Figure 9.10), but can progress along the spine and may, in very severe cases, affect other parts of the body surface. The itching provokes vigorous rubbing and hair loss. The skin becomes thickened, corrugated and scaly. There may be secondary infection if the skin becomes broken. The lesions resolve in the winter (or the dry season in the tropics if midges are not biting).

Management of the condition falls into three parts (although desperate owners often attempt alternative strategies that are not evidence-based):

1. Decrease exposure: by stabling affected horses during periods of greatest midge activity, i.e. from late afternoon through early morning. Fine mesh screens may be necessary over ventilation gaps. While grazing, vulnerable parts of the body can be covered with light blankets etc. (see Figure 9.11).
   
2. Repel midges: insect repellents, such as some pyrethroids, can have beneficial effects if used according to label recommendations, but results are sometimes disappointing.
   
3. Supportive therapy: aimed at moderating immune responses and promoting healing.

Lice, mange and ticks

Lice

Louse infestations generally become apparent in winter causing horses to lose their ‘bloom’. Hair loss may follow from licking, biting and rubbing (see Figure 9.12). Horses have a sucking louse, which favours areas of the body with long coarse hair, but heavy infestations may spread over the body (see Figure 9.13). There is also a chewing louse which prefers finer hair cover. Lice and their nits (eggs) are not always obvious but can often be found by parting the hair. The chewing louse, however, will try to move out of sight. Nits are cemented onto the hairs (see Figure 2.24) and can be distinguished from bot eggs which are larger and held in place with a clasp.

Mites

Body mange (caused by a Psoroptes species) and sarcoptic mange are severe equine conditions but both are becoming rare in the modern world. Demodex is uncommon and benign, so leg mange (chorioptic mange) is now the most troublesome mite infestation (see Figure 9.14). Papules, crusty lesions and hair-loss appear on the lower limbs of heavier breeds, particularly if this site is cloaked with long hair (‘heavily feathered’).

For diagnosis, a wooden spatula is adequate for taking scrapings and is preferred to a scalpel blade (in case the horse kicks). Mites can sometimes be captured on sticky tape. Opportunistic blood-sucking mites, such as the poultry red mite or trombiculid larvae, can also be detected in this way. Finally in this category, horses occasionally become infested with the rabbit ear-mite (a Psoroptes species) which induces head-shaking.

Nematode conditions

Cutaneous and ocular habronemosis

Although only sporadic in occurrence, cases of cutaneous habronemosis in horses are difficult to manage. Infective larvae of Habronema or Draschia after deposition by feeding muscids can survive in an open wound for prolonged periods. Their presence prevents the wound from healing (see Figure 9.15). As this condition is initiated by fly activity, it is seasonal in occurrence and known as ‘summer sores’. Larvae deposited around the eye can cause a swelling of the third eyelid or median canthus. Diagnosis is based on history and appearance, but biopsy may be necessary to exclude other possible causes.

Dourine

Clinical signs are nonspecific and highly variable depending on the virulence of the strain, the condition of the horse and stress factors. The only pathognomonic sign is the presence of raised 2–10 cm diameter plaques on the skin (see Figure 9.16), but these are transitory and do not always occur. Oedema of the genitalia spreads to the ventral abdomen and mammary gland or scrotum (see Figure 9.17). This may be followed by conjunctivitis, facial paralysis, progressive weakness, emaciation, incoordination and death (see Figure 9.18).

Serology is used for diagnosis as demonstration of the parasite is extremely difficult. The most widely used method is the complement fixation test although false positives may occasionally occur. In endemic areas, dourine is controlled by using artificial insemination or by ensuring that only seronegative animals are used for breeding. If a case is suspected all venereal contacts must be traced and isolated until their infection-status can be determined.

Equine protozoal myeloencephalitis

Spirocercosis

Dogs will, if opportunity arises, eat beetles and small vertebrates. In tropical and subtropic climates, some of these act as intermediate and paratenic hosts for Spirocerca lupi (see Figure 7.23). Infection is therefore common but fortunately mostly asymptomatic. Large oesophageal lesions (see Figure 9.19) may hinder the passage of food or induce persistent vomiting. Red 3–8 cm long worms are sometimes regurgitated. Faecal egg-counts are of limited value as S. lupi eggs are not passed in the early developmental stages of the disease and, in any event, are similar to those of the stomach spiruroids. Endoscopy or radiography, possibly aided by a barium meal, may confirm diagnosis. Neoplastic transformation of the lesion or sudden death due to rupture of an aortic aneurism are occasional sequelae.

Toxocarosis

Heavy infestations of Toxocara canis can easily accrue in young puppies if appropriate precautions are not taken. Most of the worms will have been derived from the dam by transplacental transfer (see Figure 7.9). Affected puppies fail to thrive, have a dull coat and a distended abdomen (‘pot-belly’). They may have diarrhoea and ascarid worms are often seen in faeces or vomit (see Figure 9.20). More serious signs of intestinal dysfunction may occur in severe cases. Respiratory signs and nasal discharge are indicative of continuing larval migration. Faecal examination will register high egg-counts after the pups are about two weeks of age. The adult worm population is expelled spontaneously after about six weeks but in the meantime growth and development can be affected, with stunting or even death in the worst cases.

Although disease can be prevented by using a single anthelmintic treatment prior to the expected onset of clinical signs, this empirical approach does little to reduce the overall faecal egg-output of an infected litter. There are several reasons for this:

1. large numbers of eggs can be shed before infection becomes obvious;
   
2. reinfection occurs during suckling and later by ingestion of embryonated eggs from the environment;
   
3. few canine anthelmintics kill ascarid life-cycle stages migrating through the body at the time of treatment.

If egg-production is not eliminated completely, environmental contamination will continue and bitches will accumulate more somatic larvae. The clinical problem is thereby perpetuated for future litters. To break this cycle, a routine worming programme must be initiated when puppies are two weeks old with treatments repeated every two weeks. A longer dosing interval is possible if the chosen anthelmintic has good activity against migrating larvae. Nursing bitches should also be treated. This is because a relaxation of their immunity at this time sometimes allows the establishment of T. canis in the intestine. A scrupulous level of kennel hygiene is needed. This is particularly important as few commonly used disinfectants are capable of killing the thick-walled Toxocara eggs.

Transmission of T. cati from the queen to her offspring occurs only via the transmammary route and so associated events occur rather later in the life of kittens than they do in puppies.

Toxocara is not usually a clinical issue in older dogs as adult worm burdens are generally small or absent. Nevertheless, eggs shed by dogs with patent infections into gardens and public places can constitute a potential zoonotic hazard (see Section 9.3.2). Adult dogs should therefore be wormed if they have positive egg-counts. At the time of writing, no routine treatments are licensed for killing somatic larvae in bitches and special anthelmintic therapies (e.g. multidose fenbendazole) are required to prevent transplacental and transmammary transmission.

Other helminth infections

Protozoan infections

A number of protozoan infections can cause diarrhoea, especially in younger animals, but Giardia is probably the commonest of these. It is also the most difficult to diagnose. Trophozoites and cysts are shed intermittently and so repeat faecal samples over 3–5 days increase chances of detection. Microscopy requires patience as the organisms are often few in number. They are also small (see Figure 9.21) and easily confused with pollen grains and yeasts. The cysts are relatively heavy objects and so concentration techniques using high density flotation fluids have to be employed (although sugar solutions are not appropriate as they cause Giardia to collapse). Commercially available coproantigen tests are easier to use and generally reliable. Some BZD compounds are effective against this protozoan and provide an alternative to the older drugs used for this purpose. Although many routes of infection exist, contaminated water is a common source.

Cryptosporidium oocysts are even smaller than Giardia, but are often present in large numbers in clinically affected animals. They show up clearly on Ziehl-Neelsen stained faecal smears (see Figure 8.5) and immunodiagnostic tests are also available. There is still no completely effective treatment and so reliance has to be placed on strict hygiene and supportive therapy.

Dogs and cats can each harbour several host specific Isospora species. High oocyst counts often occur in apparently healthy animals and so the pathogenicity of these infections is uncertain. Isospora oocysts at 20–40 μm, are much larger than those of the tissue cyst-forming coccidia that also occur in canine and feline faeces.

Lungworms

The presence of Oslerus nodules close to the bifurcation of the trachea in dogs may provoke a chronic dry cough which can be stimulated by gently pinching the throat. Eggs and larvae can sometimes be found in sputum (see Figure 9.22) or larvae in faeces, but they are often few in number and difficult to recover. In such cases, diagnosis is best confirmed by endoscopy. Transmission occurs directly from dam to pup and clinical cases are therefore often linked to particular breeding kennels. Aelurostrongylus is rarely a problem in cats unless there is an underlying immunodeficiency.

Angiostrongylosis

Although commonly known as the canine lungworm, Angiostrongylus vasorum actually resides in the pulmonary artery and right side of the heart. The alternative name of ‘French heartworm’ is perhaps more accurate but leads to confusion with canine heartworm disease caused by Dirofilaria immitis. Use of the technical term, angiostrongylosis is therefore preferable.

Clinical presentation is very variable as there are at least two disease processes developing simultaneously:

1. Release of anticoagulant factors: These worm secretions make affected dogs prone to bruising and internal haemorrhage. Clinical consequences will, of course, depend on where the internal bleeding occurs but include subcutaneous haematoma and epistaxis (nose-bleed). Neurological signs result if there is haemorrhage into the brain or spinal cord (see Figure 9.23).
   
2. Lung damage: A microinjury is caused every time an A. vasorum egg is caught in a lung capillary and the hatched larva migrates to the air passages. Damage accumulates leading eventually to exercise intolerance and coughing, followed by lethargy, weakness, dyspnoea and, in extreme cases, right-sided heart failure.

The highly motile first-stage larvae are usually easy to find in the faeces of infected dogs (see Figure 9.24) but cases can be missed. Earlier efforts to develop an immunological test were thwarted by cross-reactions with other pathogens, but recent developments suggest that a more reliable test may soon become available. Haematology will often show a thrombocytopaenia (reduced platelet count), prolonged clotting times and sometimes anaemia.

Historically, angiostrongylosis was confined to defined endemic areas, but the condition is spreading as dogs travel greater distances with their owners. Control is difficult as foxes act as a reservoir host and the molluscan intermediate hosts are plentiful in all but the driest localities. Moxidectin is effective against larval and adult A. vasorum and can be used to protect dogs at high risk.

Canine heartworm disease

In some parts of the world, diagnosis is still dependent on parasite detection. This can be achieved by finding motile microfilariae (mf) during microscopic examination of a wet blood film. Greater sensitivity can be obtained by forcing blood through a micropore filter to capture the mf, which can then be fixed and stained. Alternatively, the RBCs can be lysed with 2% formalin and the mf (see Figure 9.25) concentrated by centrifugation – this is known as Knott’s test. Whichever method is used the mf of D. immitis have to be distinguished from those of less pathogenic filarial parasites such as Dipetalonema (see Table 9.9).

Experience in endemic areas shows that mf cannot be demonstrated in the blood of up to 40% of infected dogs. This happens if:

1. infection comprises only immature worms: therefore, no mf-producing females;
   
2. only one adult worm present: so fertilisation cannot take place;
   
3. adult worms all the same sex: again, fertilisation cannot occur;
   
4. mf succumbing to immune attack: this happens in about 15% of infected dogs;
   
5. inadequate chemotherapy: this can sterilise female worms without killing them.

Consequently, other approaches such as immunodiagnostic techniques are preferred where they are available and affordable. There are a number of commercial kits employing different methodologies (see Figure 9.26). Antigen-detection is generally the most reliable as antibody-detection systems sometimes give false positives. Even so, heartworm antigen tests will not give an accurate result on every occasion as they are based on a glycoprotein originating from the female reproductive tract. Hence they will not detect all-male infections, nor will they pick up immature infections until about one month prior to patency. This antigen also lingers in the blood for some 10–12 weeks after worms have been expelled by chemotherapy.

Treatment can be hazardous as dying worms up to 30 cm long will be swept into the lungs and trapped as emboli (see Figure 9.27). This can cause coughing, haemoptysis (expectorating blood) and an exacerbation of cardiac and pulmonary signs. This can be serious or fatal in a dog already weakened by its clinical condition. A comprehensive physical examination, radiography (see Figure 9.28), echocardiology, an electrocardiogram and a full clinical pathology profile are therefore required to establish the degree of heart failure and organ dysfunction. This will determine the treatment strategy (e.g. whether hospitalisation is necessary) and prognosis. Symptomatic supportive therapy is essential in advanced cases.

The use of chemotherapeutic drugs in HWD has three distinct objectives requiring different approaches, although these can be combined in some cases:

1. Adulticidal: drugs are used to kill adult worms slowly. In this way, the body is able to deal with the pulmonary emboli one by one, increasing the chances of a favourable outcome.
   
2. Microfilaricidal: not all drugs are active against both adults and mf. It may be an advantage in some circumstances to delay microfilaricidal treatment until the risk of embolism from adulticidal therapy has receded. Some dogs develop a hypersensitivity to dead microfilariae indicated by lethargy, retching, tachycardia and circulatory collapse.
   
3. Prevention (prophylaxis): this relies on the fact that migrating D. immitis larvae are very sensitive to ML anthelmintics and can be killed by very small doses given at appropriate intervals (usually monthly). Microfilaraemic dogs should be cleared of infection before the start of a prophylactic programme.

It can be appreciated from the preceding paragraphs that the treatment and prevention of HWD is a complex topic and sophisticated protocols have been developed to assist veterinarians. These, however, are the domain of specialist texts on veterinary cardiology.

Extra information box 9.1