Tetratrichomonas felistomae
Predilection site: Mouth
Parasite class: Zoomastigophorasida
Family: Trichomonadidae
Description: The body is piriform, 6–11 × 3–4 μm, (mean 8 × 3 μm). There are four anterior flagella, which are longer than the body. The undulating membrane extends most of the body length and terminates in a free posterior flagellum and the axostyle extends a considerable distance beyond the body.
Hosts: Cat
Notes: The two species may be synonymous. All other details are as for T. canistomae
OESOPHAGUS
Spirocerca lupi
Synonym: Spirocerca sanguinolenta
Predilection site: Oesophagus, stomach, aorta
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Adult worms are spirally coiled and have a blood-red colour; males are around 30–55 mm, and females 55–80 mm.
Description, microscopic: The lips are trilobed and the pharynx is short. The male tail bears lateral alae, four pairs and one unpaired median pre-cloacal papillae and two pairs of post-cloacal papillae, with a group of minute papillae near the tail tip. Eggs have thick shells, 30–37 × 11–15 μm and are larvated when passed in faeces.
Final hosts: Dog, fox, wild canids and occasionally cat and wild felids
Intermediate hosts: Coprophagous beetles: Scarabeus sacer, Akis, Atenchus, Gymnopleurus, Cauthon spp. Many vertebrates such as rodents, birds, insectivores and reptiles can act as paratenic hosts.
Life cycle: The thick-shelled elongate egg, containing a larva, is passed in the faeces or vomit and does not hatch until ingested by a dung beetle. In this, the intermediate host, the larva develops to the L3 and encysts. Paratenic hosts may also be involved if the dung beetle, in turn, is ingested by any of a variety of other animals including the domestic chicken, wild birds and lizards. In these the L3 becomes encysted in the viscera. On ingestion of the intermediate or paratenic host by the final host the L3 are liberated, penetrate the stomach wall and migrate via the coeliac artery to the thoracic aorta. About 3 months later the majority of larvae cross to the adjacent oesophagus where they provoke the development of granulomas as they develop to the adult stage in a further 3 months. The prepatent period is therefore about 6 months. Eggs, however, may not be found in the faeces of a proportion of animals with adult infections where the granulomas have no openings into the oesophageal lumen.
Geographical distribution: Tropical and subtropical areas
Pathogenesis: The migrating larvae produce haemorrhages, scarring and/or the formation of fibrotic nodules on the internal wall of the aorta, which, if particularly severe, may cause stenosis or even rupture. The oesophageal granulomas, up to 4.0 cm in size, associated with the adult worms, may be responsible for a variety of clinical signs including dysphagia and vomiting arising from oesophageal obstruction and inflammation.
Two further complications are, first, the development of oesophageal osteosarcoma in a small proportion of infected dogs. These may be highly invasive and produce metastases in the lung and other tissues. Secondly, also relatively rare, is the occurrence of spondylosis of the thoracic vertebrae or of hypertrophic pulmonary osteoarthropathy of the long bones. The aetiology of these lesions is unknown. Occasionally S. lupi infection can induce a pyaemic nephritis.
Clinical signs: Despite the potential pathogenicity of this parasite, many infected dogs do not exhibit clinical signs even when extensive aortic lesions and large, often purulent, oesophageal granulomas are present. In some dogs infection will induce persistent vomiting with worms passed in the vomit. In less serious cases there may be difficulty in swallowing or interference with the action of the stomach. Aortic infection is not usually observed until sudden death is caused by rupture.
Diagnosis: The location and appearance of the granulomatous lesions, up to golf-ball size, is usually sufficient for identification. Numerous pink-reddish, stout, spirally coiled worms may be seen on section of the granulomas, but these are difficult to extricate intact since they are coiled and up to 8.0 cm long. Eggs may be found in the faeces or vomit if there are fistulae in the oesophageal granulomas. However, the eggs are similar in appearance to those of other spirurids. Otherwise diagnosis may depend on endoscopy or radiography.
Pathology: The migrating larvae produce characteristic lesions in the wall of the aorta (Fig. 6.2) while the adults are found embedded in granulomatous lesions in the wall of the oesophagus and occasionally the stomach. Aortic lesions include haemorrhage and necrosis with eosinophilic inflammation, intimal roughening with thrombosis, aneurysm with rare aortic rupture, and subintimal and medial mineralisation and heterotopic bone deposition. Spondylosis of the ventral aspects of thoracic vertebrae occurs in some cases with exostoses of the vertebral bodies. Granulomas in the oesophagus contain pleomorphic fibroblasts. In some animals mesencymal neoplasms develop in the wall of the oesophageal granuloma with lesions showing cytological characteristics typical of fibrosarcoma and osteosarcoma, with local tissue invasion and, in many cases, pulmonary metastasis.
Epidemiology: In endemic areas the incidence of infection in dogs is often extremely high, sometimes approaching 100%. Probably this is associated with the many opportunities of acquiring infection from the variety of paratenic hosts.
Fig. 6.2 Fibrotic nodules on the internal wall of the aorta from a dog infected with Spirocerca lupi.
Treatment: Treatment is rarely practical, but levamisole and albendazole have been reported to be of value. Levamisole is given at 5–10 mg/kg as a single dose. Diethylcarbamazine at oral doses of 10 mg/kg twice daily for 10 days may kill adult worms but not larvae.
Control: This is difficult because of the ubiquity of the intermediate and paratenic hosts. Dogs should not be fed uncooked viscera from wild birds or from free-range domestic chickens.
STOMACH
Ollulanus tricuspis
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description, gross: This is a very small trichostrongyle. Males are 0.7–0.8mm, and females 0.8–1 mm long.
Description, microscopic: The worm is identified microscopically by the spiral coil of the head. The male bursa is well developed and the spicules are stout and each is split into two for a considerable distance. The female has a tail with three or four short cusps. The vulva is in the posterior part of the body and there is only one uterus and ovary.
Hosts: Cats, wild felids; occasionally found in pigs, foxes and domestic dogs
Life cycle: The worms are viviparous, the larvae developing to the L3 stage in the uterus of the females. Autoinfection can occur, the shed L3 developing into adult worms on the gastric mucosa in around 4–5 weeks. The whole life cycle may be completed endogenously and transmission, at least in the cat, is thought to be via ingestion of vomit containing the L3. The worms live under a layer of mucus in the stomach wall and the anterior end of the worm is often located within the gastric crypts.
Geographical distribution: Mainly occurs in Europe, North and South America, Australasia and the Middle East.
Pathogenesis: The parasite is considered non-pathogenic in cats. Heavy infections may induce a severe catarrhal gastritis and vomiting. Untreated cats may become emaciated. Little is known of its pathogenicity in other hosts, although a chronic gastritis has been reported in the pig.
Clinical signs: Occasional vomiting and emaciation.
Diagnosis: Diagnosis of ollulanosis is seldom made because of their small size and lack of eggs and larvae in the faeces. Examination of vomit, following an emetic, for the presence of worms is a useful approach. At necropsy, recovery and identification of the very small worms from the gastric mucosa should lead to a diagnosis.
Pathology: The worms lie beneath the mucus on the surface of the stomach, or partly in the gastric glands, and their presence may lead to mucosal lymphoid hyperplasia and elevated numbers of globule leucocytes in the gastric epithelium. Heavy infections cause hyperplasia of the gastric glands causing the stomach mucosa to become convoluted and thrown into folds.
Epidemiology: The parasite is common in some parts of the world, particularly in cat colonies and cats that roam. The parasite can replicate in the stomach without any need for external egg or larval phases and can spread via vomit. The disease spreads mainly among starving stray cats and sometimes stray dogs.
Treatment: Levamisole, ivermectin or repeated doses of oxfendazole at 10 mg/kg twice daily for 5 days are effective.
Control: This is mainly achieved through the implementation of good hygiene procedures.
Spirocerca lupi
See under Oesophagus.
Gnathostoma spinigerum
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Thick-bodied worms, reddish at the front, and greyish posteriorly. The males are 1–2.5 cm and the females up to 3.0 cm long. The presence of the worms in gastric nodules is sufficient for generic diagnosis.
Description, microscopic: Confirmation is easily made with a hand lens when the swollen anterior head bulb covered with transverse rows of 6–11 small hooks will be seen. The head contains four sub-median cavities that each communicate with a cervical sac. The anterior of the body is covered with flat cuticular spines and the ventral caudal region of the male bears small spines and four pairs of large pedunculate papillae as well as several smaller sessile ones. The left spicule is longer than the right. Eggs are oval, greenish, 69 × 37 μm with a thin cap at one pole.
Final hosts: Cat, dog, man, mink, polecat and several wild carnivores
Intermediate hosts: Host 1: Many species of freshwater crustaceans, copepods. Host 2: Small vertebrates including mammals, birds, reptiles, fish and amphibians
Life cycle: The adult worms live in tunnels in the gastric nodules, and the eggs pass from there into the lumen and are dropped into the water in the faeces where they hatch after several days. The crustaceans (first intermediate hosts) ingest L1 and development to L2 takes place. The crustaceans are themselves ingested by vertebrates (second intermediate hosts), such as fish, frogs and reptiles, and development to L3 occurs and the larvae become encysted. The L3 can also encyst in many mammals such as mice, rats and dogs. The final host is infected by ingestion of the vertebrate vector and further development occurs in the stomach wall, where the worms provoke the growth of fibrous lesions.
Geographical distribution: Thailand, Japan, South East Asia, China, Mexico
Pathogenesis: G. spinigerum is the most pathogenic Gnathostoma species, which in cats may cause fatal gastric perforation and peritonitis. In some cases a number of larvae will migrate from the stomach to other organs, most commonly the liver, in which they burrow, leaving necrotic tracks in the parenchyma.
Clinical signs: Gnathostoma infection in the cat may cause acute abdominal signs.
Diagnosis: The infection in the living animal can only be diagnosed by the finding of the greenish, oval eggs, which have a thin cap at one pole, in the faeces. Often, however, eggs are not present in faeces.
Pathology: As in many spiruroid infections, the most obvious effect of gnathostomosis is the presence of fibrous growths on the stomach wall. These growths are of variable size, the largest being 3–4 cm in diameter, and are cavitated, amounting to thick-walled cysts containing worms and fluid. Ulceration and necrosis of the stomach wall are often present.
Epidemiology: Dogs, cats and several species of wild mammals are reservoirs of the parasite. These final hosts become infected primarily through eating infected fish or other animals that serve as paratenic hosts. In humans, the ingestion of raw or inadequately cooked fish is the major source of infection. Human infections also are reported from eating raw or poorly cooked catfish, eels, frogs, chickens, ducks and snakes.
Treatment: Treatment has not been fully investigated.
Control: With the ubiquity of the first and second intermediate hosts complete control cannot be achieved. Ensuring only well cooked fish, eels, or other intermediate hosts, such as snakes, frogs, and poultry, are eaten can prevent infections. Potentially copepod infested water should be boiled or treated.
Notes: Like most spiruroids, Gnathostoma inhabits the upper alimentary tract, occurring in nodules in the stomach wall of omnivores and carnivores. It is exceptional in requiring two intermediate hosts in most species.
When visceral larva migrans due to Gnathostoma occurs in humans, G. spinigerum is the species usually involved, and the commonest source of infection is inadequately cooked domestic poultry and fish acting as second intermediate hosts. Infection is particularly common in southeast Asia, Japan and China but occurs in many other countries. The worms never become fully adult, and the immature forms are most commonly found in nodules in subcutaneous tissues and other organs that appear and disappear irregularly as the parasites wander in various parts of the body. In humans, cutaneous gnathostomiosis can result in pruritic swellings and eosinophilia with occasional abscess formation. Ocular gnathostomiosis is characterised by haemorrhage, uveitis and perforation of the iris. A severe form of infection is central nervous system (CNS) gnathostomiosis, leading to haemorrhage and intracranial necrotic tracks that can be fatal.
Physaloptera praeputialis
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Adult worms are larger than most spiruroids, being stout and resembling ascarids. Males measure 1–45 mm and females 1.5–60 mm.
Description, microscopic: The cuticle in both sexes extends posteriorly as a sheath beyond the end of the body. The lips are simple and bear a set of three flattened, internal teeth and a single conical external tooth. The male bears lateral alae, joined anteriorly across the ventral surface. In the female the vulva is slightly anterior to the midbody. The larvated eggs have a thick clear shell and measure 45–58 μm × 30–42 μm.
Final hosts: Cat and wild felids; occasionally the dog
Intermediate hosts: Beetles, cockroaches, crickets and paratenic hosts
Geographical distribution: China, Africa, North and South America
Life cycle: The life cycle is typically spiruroid. Eggs passed in the faeces of the infected host develop into infective larvae if ingested by coprophagous beetles. The life cycle is completed when cats ingest the intermediate hosts. Various transport hosts may also be involved in transmission of infection. The prepatent period is around 8–10 weeks.
Pathogenesis: The adult worms have small teeth on their large triangular lips, and attach strongly to the gastric mucosa, leaving small ulcers when they move to fresh sites. These feeding sites may continue to bleed. They may cause catarrhal gastritis, with emesis, and in heavy infections blood may appear in the faeces.
Clinical signs: In heavy infections there may be vomiting and some degree of anorexia. The faeces may appear dark in colour. Severely affected animals may lose weight.
Diagnosis: Diagnosis is based on clinical signs and by the finding of the elongate eggs, thickened at either pole, in the faeces or vomit.
Pathology: Presence of the adult worms may cause gastric ulceration and haemorrhage.
Epidemiology: The epidemiology depends on the presence and abundance of the intermediate beetle hosts. Infection is more prevalent in outdoor cats that have access to intermediate hosts or paratenic hosts.
Treatment: Treatment with benzimidazoles over a 5-day period has been reported to be effective. Pyrantel is also effective.
Control: The ubiquity of the insect intermediate hosts means that control is not usually feasible.
Physaloptera rara
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Hosts: Cat
Description, gross: Adult male worms are 2.5–3 cm long and females 3–6 cm.
Description, microscopic: This species differs from P. praeputialis in that there is no sheath over the posterior portion of the body in both sexes. The female vulva is anterior to the middle of the body. Eggs are thick-shelled and ellipsoid, 42–53 × 29–35 μm.
Geographical distribution: North America
Details of the life cycle, pathogenesis, treatment and control are essentially similar to those of P. praeputialis.
Spirura ritypleurites
Predilection site: Stomach, occasionally oesophagus
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Thick, short white worms with the posterior region thicker than the anterior of the worm and twisted in a spiral.
Description, microscopic: The eggs have a thick shell and are embryonated when passed.
Final hosts: Cat, rarely dog, fox
Intermediate hosts: Coprophagous beetles
Life cycle: The life cycle is typically spiruroid. Eggs develop into infective larvae within an intermediate host. Larvae may then be ingested by paratenic hosts, such as rodents and lizards, in which they become encapsulated. Cats become infected by ingesting the insects or their transport hosts.
Geographical distribution: This worm is endemic in parts of southern Europe, Africa and Asia.
Pathogenesis: S. ritypleurites is usually presumed to be non-pathogenic.
Clinical signs: Symptoms of nausea, vomiting and digestive upsets have been reported.
Diagnosis: As for Physaloptera spp
Pathology: No associated pathology reported.
Epidemiology: The epidemiology depends on the presence and abundance of the intermediate beetle hosts. Infection is more prevalent in outdoor cats that have access to intermediate hosts or paratenic hosts.
Treatment: Not usually indicated. Treatment with a benzimidazole over an extended period is likely to be effective.
Control: Prevention is difficult because of the large number of intermediate hosts and paratenic hosts.
Capillaria putorii
Synonym: Aonchotheca putorii
Predilection site: Stomach, small intestine
Parasite class: Nematoda
Superfamily: Trichuroidea
Description, gross: These are thin, filamentous worms, about 1 cm long; males are 5–8 mm and females 9–15 mm.
Description, microscopic: Eggs have broad flat poles and granular unsegmented contents.
Hosts: Cat, dog, mustelids, hedgehog
Life cycle: Cats are thought to become infected by eating infective eggs from soil contaminated by hedgehog faeces.
Geographical distribution: Europe, New Zealand
Pathogenesis and clinical signs: There are few reports on the clinical signs of infection in cats. Infected cats have reported anorexia and intermittent bloody vomitus.
Diagnosis: Identification of the characteristic eggs in faeces
Pathology: There is reported chronic, hyperplastic pyloric gastritis and ulceration around the pylorus associated with the presence of worms with eggs present in the pyloric mucus and in the lumen of the pyloric glands.
Treatment and control: Levamisole, given as two doses of 7.5 mg/kg at 2-week intervals, and ivermectin, at 300 μg/kg, have been reported to be effective.
SMALL INTESTINE
Toxocara canis
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: Toxocara canis is a large white worm up to about 18.0 cm in length; males are around 10 cm, and females up to 18 cm (Fig. 6.3).
Description, microscopic: The adult head is elliptical due to the presence of large cervical alae. The mouth is surrounded by three large lips. There is no buccal capsule and the oesophagus lacks a bulb. The tail of the male has a terminal narrow appendage and caudal alae. Female genital organs extend anteriorly and posteriorly to the vulval region. The egg is dark brown and subglobular, 90 × 75 μm with a thick, pitted shell.
Fig. 6.3 Heavy Toxocara canis infection in the small intestine of a pup.
Hosts: Dog, fox
Life cycle: This species has the most complex life cycle in the superfamily, with four possible modes of infection.
The basic form is typically ascaridoid, the egg containing the L3 being infective, at optimal temperatures, 4 weeks after being passed. After ingestion, and hatching in the small intestine, the larvae travel by the bloodstream via the liver to the lungs, where the second moult occurs, the larvae returning via the trachea to the intestine where the final two moults take place. This form of ascaroid migration occurs regularly only in dogs of up to about 2–3 months old.
In dogs over 3 months of age, the hepatic-tracheal migration occurs less frequently, and at around 4–6 months it has almost ceased and is replaced by somatic migration, followed by hypobiosis. However, some dogs will support hepatic-tracheal migration as adults. Instead of hepatic-tracheal migration, the L3 travel to a wide range of tissues including the liver, lungs, brain, heart and skeletal muscle, and the walls of the alimentary tract.
In the pregnant bitch, prenatal infection occurs, larvae becoming mobilised at about 3 weeks prior to parturition and migrating to the lungs of the fetus where they moult just before birth. In the newborn pup the cycle is completed when the larvae travel to the intestine via the trachea, and the final moults occur. A bitch, once infected, will usually harbour sufficient larvae to infect all her subsequent litters, even if she never again encounters the infection. A few of these mobilised larvae, instead of going to the uterus, complete the normal migration in the bitch, and the resulting adult worms produce a transient but marked increase in faecal Toxocara egg output in the weeks following parturition.
The suckling pup may also be infected by ingestion of L3 in the milk during the first 3 weeks of lactation. There is no migration in the pup following infection by this route. Paratenic hosts such as rodents or birds may ingest the infective eggs, and the L3 travel to their tissues where they remain until eaten by a dog when subsequent development is apparently confined to the gastrointestinal tract.
A final complication is recent evidence that bitches may be reinfected during late pregnancy or lactation, leading directly to transmammary infection of the suckling pups and, once patency is established in the bitch, to contamination of the environment with eggs. The bitch may be reinfected via the ingestion of larval stages from the fresh faeces of puppies through her coprophagic activities.
The known minimum prepatent periods are:
- Direct infection following ingestion of eggs or larvae in a paratentic host: 4–5 weeks
- Prenatal infection: 2–3 weeks
Geographical distribution: Worldwide
Pathogenesis: In moderate infections, the larval migratory phase is accomplished without any apparent damage to the tissues, and the adult worms provoke little reaction in the intestine. In heavy infections the pulmonary phase of larval migration is associated with pneumonia, which is sometimes accompanied by pulmonary oedema; the adult worms cause a mucoid enteritis, there may be partial or complete occlusion of the gut and, in rare cases, perforation with peritonitis or in some instances blockage of the bile duct.
Clinical signs: In mild to moderate infections, there are no clinical signs during the pulmonary phase of larval migration. The adults in the intestine may cause tucked-up abdomen or potbelly, with failure to thrive, and occasional vomiting and diarrhoea. Entire worms are sometimes vomited or passed in the faeces. The signs in heavy infections during larval migration result from pulmonary damage and include coughing, increased respiratory rate and a frothy nasal discharge. Most fatalities from T. canis infection occur during the pulmonary phase, and pups, which have been heavily infected transplacentally may die within a few days of birth. Nervous convulsions have been attributed by some clinicians to toxocariosis, but there is still some disagreement on whether the parasite can be implicated as a cause of these signs.
Diagnosis: Only a tentative diagnosis is possible during the pulmonary phase of heavy infections when the larvae are migrating, and is based on the simultaneous appearance of pneumonic signs in a litter, often within 2 weeks of birth. The eggs in faeces, subglobular and brown with thick, pitted shells, are species-diagnostic. The egg production of the worms is so high that there is no need to use flotation methods, and they are readily found in simple faecal smears to which a drop of water has been added.
T. canis in the dog can be confused only with Toxascaris leonina which is slightly smaller. Differentiation of these two species is difficult, as the only useful character, visible with a hand lens, is the presence of a small finger-like process on the tail of the male T. canis.
Pathology: On postmortem, the animal appears poorly grown, potbellied and cachectic. Large numbers of maturing worms are present in the intestines and sometimes the stomach. Focal haemorrhages may be found in the lungs of puppies with migrating T. canis larvae. Inflammatory foci are often observed in the kidneys as white, elevated spots 1–2 mm in diameter in the cortex beneath the capsule. In section, they are composed of a small focus of macrophages, lymphocytes, plasma cells and a few eosinophils, possibly containing larvae. Occasionally, granulomas may be found in the eye.
Epidemiology: Surveys of T. canis prevalence in dogs have been carried out in most countries and have shown a wide range of infection rates, from 5% to over 80%. The highest rates of prevalence have been recorded in dogs of less than 6 months of age, with the fewest worms in adult animals. Infection induces immunity that results in loss of adult worms.
The widespread distribution and high intensity of infection with T. canis depend essentially on three factors. First, the females are extremely fecund, one worm being able to contribute about 700 eggs to each gram of faeces per day, and egg counts of 15 000 epg are not uncommon in pups. Second, the eggs are highly resistant to climatic extremes, and can survive for years on the ground. Third, there is a constant reservoir of infection in the somatic tissues of the bitch, and larvae in these sites are not susceptible to most anthelmintics.
Treatment: The adult worms are easily removed by anthelmintic treatment. The most popular drug used has been piperazine, although this is being superseded by the benzimidazoles (fenbendazole and mebendazole) and by nitroscanate. Pyrantel and the avermectin, selamectin, are also effective. Although several anthelmintics have activity against larval stages and juvenile worms, none are fully effective at their removal.
A simple and frequently recommended regime for control of toxocariosis in young dogs is as follows. All pups should be dosed at 2 weeks of age, and again 2–3 weeks later, to eliminate prenatally acquired infection. It is also recommended that the bitch should be treated at the same time as the pups. A further dose should be given to the pups at 2 months old, to eliminate any infection acquired from the milk of the dam or from any increase in faecal egg output by the dam in the weeks following whelping. Newly purchased pups should be dosed twice at an interval of 14 days.
Since there are likely to be a few worms present, even in adult dogs, in spite of the diversion of the majority of larvae to the somatic tissues, it is recommended that adult dogs should be treated every 3–6 months throughout their lives.
It has been shown that daily administration of high doses of fenbendazole to the bitch from 3 weeks prepartum to 2 days postpartum has largely eliminated transmammary and prenatal infection of the pups, although residual infection in the tissues of the bitch may persist. This regimen may be useful in breeding kennels.
Control: The main aim is to prevent transmammary and intrauterine transmission of infection using the anthelmintic treatment regimens listed above. Hygienic disposal of dog faeces should be encouraged. Where practical, access of rodents to kennels should be prevented.
Notes: Apart from its veterinary importance, this species is responsible for the most widely recognised form of visceral larva migrans (VLM) in man. Though this term was originally applied to invasion of the visceral tissues of an animal by parasites whose natural hosts were other animals, it has now, in common usage, come to represent this type of invasion in humans alone and, in particular, by the larvae of Toxocara canis, although the larval stages of T. mystax, T. leonina and T. vitulorum (see Chapter 2: Cattle, Small intestine) can be implicated. Its complementary term is cutaneous larva migrans (CLM), for infections by ‘foreign’ larvae, which are limited to the skin.
The global condition occurs most commonly in children, often under 5 years of age, who have had close contact with household pets, or who have frequented areas such as public parks where there is contamination of the ground by infective dog faeces. Surveys of such areas in many countries have almost invariably shown the presence of viable eggs of T. canis in around 10% of soil samples. Despite this high risk of exposure to infection, the reported incidence of clinical cases is small. For example, in 1979 a French survey of the world literature reported that only 430 cases of ocular, and 350 cases of visceral, larva migrans had been recorded. However, it has been suggested that 50–60 clinical cases occur in Britain each year, since many are not recorded.
In many cases, larval invasion is limited to the liver, and may give rise to hepatomegaly and eosinophilia, but on some occasions a larva escapes into the general circulation and arrives in another organ, the most frequently noted being the eye. Here, a granuloma forms around the larva on the retina, often resembling a retinoblastoma. Only in rare cases does the granuloma involve the optic disc, with total loss of vision, and most reports are of partial impairment of vision, with endophthalmitis or granulomatous retinitis. Such cases are currently treated using laser therapy. In a few cases of epilepsy, T. canis infection has been identified serologically, but the significance of the association has yet to be established.
Control of visceral larva migrans is based on the anthelmintic regimen described above, on the safe disposal of dog faeces in houses and gardens, and on the limitation of access by dogs to areas where children play, such as public parks and recreation grounds.
Toxocara mystax
Synonym: Toxocara cati
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: Typical of the superfamily, Toxocara mystax is a large white worm (up to 10 cm in length), often occurring as a mixed infection with the other ascaridoids of cats, such as Toxascaris leonina. Males are 3–6 cm, females 4–10 cm.
Description, microscopic: The tail of the male has a terminal narrow appendage. Differentiation is readily made between Toxocara mystax and Toxascaris leonina on gross examination or with a hand lens, when the cervical alae of the former are seen to have an arrow-head form, with the posterior margins almost at a right angle to the body, whereas those of Toxascaris taper gradually into the body (Fig. 6.4). The male, like that of Toxocara canis, has a small finger-like process at the tip of the tail. The egg, subglobular, 65–75 μm with a thick, pitted shell and almost colourless, is characteristic in cat faeces.
Hosts: Cat
Life cycle: The life cycle of T. mystax is migratory when infection occurs by ingestion of the L2 in the egg, and non-migratory after transmammary infection with L3 or after ingestion of a paratenic host.
Fig. 6.4 Comparison of the anterior region of (a) Toxocara mystax and (b) Toxascaris leonina. The cervical alae of Toxocara mystax are arrow-shaped whereas those of Toxascaris leonina are more slender and less protrusive.
Following ingestion of eggs containing an infective second-stage larva, the larvae enter the stomach wall and then migrate via the liver, lungs and trachea back to the stomach and moult to L3, while L4 occur in the stomach contents, the intestinal wall and bowel contents. Rodent infections also play an important part in the life cycle. In these, larvae remain as second-stage forms but when an infected mouse is eaten by a cat the larvae, liberated by digestion, enter the stomach wall of the cat and develop to L3. As well as mice acting as ‘intermediate hosts’, L2 may be found in the tissues of earthworms, cockroaches, chickens, sheep and other animals fed infective eggs.
Transmammary infection is common throughout lactation and the lactogenic route of transmission is the most important. Prenatal infection does not occur. The prepatent period from egg infection is about 8 weeks.
Geographical distribution: Worldwide
Pathogenesis: Because the majority of infections are acquired either in the milk of the dam, or by ingestion of paratenic hosts, there is no migratory phase so any changes are usually confined to the intestine, showing as potbelly, diarrhoea, poor coat and failure to thrive.
Clinical signs: Unthriftiness, potbelly, diarrhoea
Diagnosis: The subglobular eggs, with thick, pitted shells, are easily recognised in faeces.
Pathology: Larvae developing in the mucosa of the stomach may provoke a mild granulomatous reaction comprising lymphocytes and a few macrophages around the coiled larvae.
Epidemiology: The epidemiology of T. mystax depends largely on a reservoir of larvae in the tissues of the dam, which are mobilised late in pregnancy and excreted in the milk throughout lactation. The paratenic host is also of considerable significance because of the strong hunting instinct in cats. Exposure to the latter route of infection does not occur until kittens begin to hunt for themselves or to share the prey of their dams.
Treatment: Fenbendazole, mebendazole, piperazine and pyrantel are all effective against adult nematodes. The benzimidazole anthelmintics are more effective against larval ascarids.
Control: Since infection is first acquired during suckling, complete control would be based on removal of kittens from the dam and artificial rearing. Good hygiene is essential in catteries. Young kittens should be wormed regularly with an anthelmintic from 4–6 weeks of age at 3-week intervals until 4 months of age and thereafter at regular intervals.
Notes: T. mystax has been reported as a rare cause of visceral larva migrans in man.
Toxocara malayiensis
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: Toxocara malayiensis is a large white worm; males are 5.3–8.5 cm, females 1.1–1.4 cm, morphologically similar to T. canis in dogs.
Description, microscopic: There are three well defined lips, each with a deep median notch lined with denticles: a dorsal lip with two large outer papillae, and two subventral lips each with one outer papilla. Cervical alae arise immediately behind the lips, gradually increasing in width to mid-length, then tapering gradually posteriorly
Hosts: Cat
Life cycle: The life cycle has not been fully described.
Geographical distribution: Malaysia
Diagnosis: The subglobular eggs, with thick-pitted shells are similar to those of T. canis.
Epidemiology: Not described
Treatment and control: Presumed similar to T. mystax.
Details of the pathogenesis, pathology and clinical signs have not been reported.
Toxascaris leonina
Synonym: Toxascaris limbata
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: Males are up to 7 cm long and females up to 10 cm.
Description, microscopic: Adults have an elliptical head due to presence of large cervical alae. Three large lips surround the mouth, there is no buccal capsule and the oesophagus lacks a bulb. The tail of the male is simple. The female genital organs lie behind the level of the vulva. The egg is slightly ovoid, light coloured, 75 × 85 μm with a smooth thick shell, and is characteristic in dog and cat faeces.
Hosts: Dog, cat, fox
Life cycle: The infective stage is the egg containing a second-stage larva or the third-stage larvae present in a mouse intermediate host. Following ingestion and hatching, larvae enter the wall of the intestine and remain for about 2 weeks. No migration of larvae occurs as with other ascarid species. Third-stage larvae appear after about 11 days and moult to L4 about 2–5 weeks post infection. Adult stages appear from about 6 weeks post infection and lie in the lumen of the intestine. The prepatent period is 10–11 weeks.
Geographical distribution: Worldwide
Pathogenesis: Infection with Toxascaris is unlikely to occur in isolation and is more usually accompanied by a Toxocara infection. In puppies and young dogs less than 2 months of age the infection is usually absent as there is no prenatal or lactogenic transmission. Damage is caused predominantly by the adult worms and is determined by the number of worms present in the intestine.
Clinical signs: Unthriftiness, potbelly, diarrhoea
Diagnosis: Toxascaris is almost indistinguishable grossly from Toxocara canis, the only point of difference being the presence of a finger-like process at the tip of the male tail of the latter. In the cat, differentiation from Toxocara mystax is based on the shape of the cervical alae, which are lanceolate in Toxascaris but arrowhead shaped in Toxocara mystax. The characterisitic ovoid, smooth-shelled eggs are easily recognised in the faeces.
Pathology: Pathological effects due to Toxascaris leonina are rarely seen. Heavy infections may cause occlusion of the intestinal lumen and are usually associated with the mixed presence of Toxocara spp.
Epidemiology: Infection normally occurs through the ingestion of the larvated eggs. Larvae of Toxascaris leonina may occur in mice with the third-stage larvae distributed in many tissues. If a dog or cat ingests an infected mouse the larvae are released and develop to maturity in the wall and lumen of the intestine of the final host.
Treatment: Fenbendazole, mebendazole, piperazine and pyrantel are all effective against adult nematodes. The benzimidazole anthelmintics are more effective against larval ascarids.
Control: Ascarid infections in the domestic carnivores invariably include Toxocara, such that the measures recommended for control of the latter will also have an effect on Toxascaris. Since the two main reservoirs of infection are larvae in the prey or eggs on the ground, control has to be based on treatment of worm infection in the host animals, and on adequate hygiene to limit the possibility of acquisition of infection by ingestion of eggs.
Notes: This genus occurs in domestic carnivores, and though common, is of less significance than Toxocara because its parasitic phase is non-migratory.
Ancylostoma caninum
Common name: Canine hookworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ancylostomatoidea
Description, gross: The worms are reddish grey in colour, depending on whether the worm has fed, and are readily recognised on the basis of size, and by their characteristic ‘hook-like’ posture. Males are about 12 mm and females 15–20 mm in length, (much smaller than the common ascarid nematodes, which are also found in the small intestine).
Description, microscopic: The anterior end is bent dorsad and the oral aperture is directed antero-dorsally. The buccal capsule is large with three pairs of marginal teeth and a pair of ventro-lateral teeth and possesses a dorsal gutter (Fig. 6.5). The male bursa is well developed. Eggs are ‘strongylate’ with dissimilar poles, barrel-shaped sidewalls, 56–75 × 34–47 μm and contain two to eight blastomeres.
Hosts: Dog, fox and occasionally man
Life cycle: The life cycle is direct and, given optimal conditions, the eggs may hatch and develop to L3 in as little as 5 days. Infection is by skin penetration or by ingestion, both methods being equally successful. Paratenic hosts can also be important. In percutaneous infection, larvae migrate via the bloodstream to the lungs where they moult to L4 in the bronchi and trachea, and are then swallowed and pass to the small intestine where the final moult occurs. If infection is by ingestion the larvae may either penetrate the buccal mucosa and undergo the pulmonary migration described above or pass directly to the intestine where the adult worms burrow their buccal capsules into the mucosa. Whichever route is taken, the prepatent period is 14–21 days. The worms are prolific egg layers and an infected dog may pass millions of eggs daily for several weeks.
Fig. 6.5 Head of Ancylostoma caninum showing the large buccal capsule containing pairs of teeth.
An important feature of A. caninum infection is that, in susceptible bitches, a proportion of the L3 that reach the lungs migrate to the skeletal muscles where they remain dormant until the bitch is pregnant. They are then reactivated and, still as L3, are passed in the milk of the bitch for a period of about 3 weeks after whelping. Transplacental transmission does not occur.
Geographical distribution: Worldwide in the tropics and warm temperate areas. In other countries it is sometimes seen in dogs imported from endemic regions.
Pathogenesis: This is essentially that of an acute or chronic haemorrhagic anaemia. The disease is most commonly seen in dogs under 1 year old and young pups, infected by the transmammary route, are particularly susceptible due to their low iron reserves. Transmammary infection is often responsible for severe anaemia in litters of young pups in their second or third week of life. Infection of the bitch on a single occasion has been shown to produce transmammary infections in at least three consecutive litters.
Following infection, blood loss starts about the eighth day of infection when the immature adult has developed the toothed buccal capsule, which enables it to grasp plugs of mucosa containing arterioles. Each worm removes about 0.1 ml of blood daily and in heavy infections of several hundred worms pups quickly become profoundly anaemic. In lighter infections, common in older dogs, the anaemia is not so severe, as the marrow response is able to compensate for a variable period. Ultimately however, the dog may become iron deficient and develop a microcytic hypochromic anaemia. In previously sensitised dogs, skin reactions such as moist eczema and ulceration at the sites of percutaneous infection occur especially affecting the interdigital skin.
It appears that dormant L3 in the muscles of both bitches and dogs can recommence migration months or years later to mature in the host’s intestine. Stress, severe illness or repeated large doses of corticosteroids can all precipitate these apparently new infections in dogs, which may perhaps now be resident in a hookworm-free environment. Experimentally, L3 of some strains of A. caninum exposed to chilling before oral administration have been shown to remain in arrested development in the intestinal mucosa for weeks or months. The significance of this observation is still unknown, but it is thought that such larvae may resume development if the adult hookworm population is removed by an anthelmintic or at times of stress, such as lactation.
Clinical signs: In acute infections, there is anaemia and lassitude and occasionally respiratory embarrassment. In suckled pups the anaemia is often severe and is accompanied by diarrhoea, which may contain blood and mucus. Respiratory signs may be due to larval damage in the lungs or to the anoxic effects of anaemia. In more chronic infections, the animal is usually underweight, the coat is poor, and there is loss of appetite and perhaps pica. Inconsistently there are signs of respiratory embarrassment, skin lesions and lameness. The adverse effects of infection on the coat can have an economic impact where foxes are reared for their fur.
Diagnosis: This depends on the clinical signs and history supplemented by haematological and faecal examination. High faecal worm egg counts are valuable confirmation of diagnosis, but it should be noted that suckled pups may show severe clinical signs before eggs are detected in the faeces. The presence of a few hookworm eggs in the faeces, although giving confirmatory evidence of infection, do not necessarily indicate that an ailing dog is suffering from hookworm disease.
Pathology: Animals dying of ancylostomosis are extremely pale and there is often oedema of subcutaneous tissues and mesenteries, and serous effusion into the body cavities attributable to hypoproteinaemia. In chronic infections, cachexia may be evident. If recent exposure to heavy percutaneous infection has occurred there may be dermatitis and numerous focal haemorrhages in the lung parenchyma. The liver is pale and the intestinal contents are mucoid and red in colour. Worms may be seen attached to the mucosa and pinpoint haemorrhagic sites may be scattered over the intestinal surface.
Epidemiology: In endemic areas the disease is most common in dogs under 1 year old. In older animals, the gradual development of age resistance makes clinical disease less likely, particularly in dogs reared in endemic areas, whose age resistance is reinforced by acquired immunity. The epidemiology is primarily associated with the two main sources of infection, transmammary in suckled pups and percutaneous or oral from the environment. An important aspect of transmammary infection is that disease may occur in suckled pups reared in a clean environment and nursed by a bitch which may have been recently treated with an anthelmintic and has a negative faecal egg count. Contamination of the environment is most likely when dogs are exercised on grass or earth runs that retain moisture and also protect larvae from sunlight. On such surfaces larvae may survive for some weeks. In contrast, dry impervious surfaces, particularly if exposed to sunlight, are lethal to larvae within a day or so. Housing is also important and failure to remove soiled bedding, especially if the kennels are damp or have porous or cracked floors, can lead to a massive build-up of infection.
Treatment: Affected dogs should be treated with an anthelmintic, such as mebendazole, fenbendazole, pyrantel or nitroscanate, all of which will kill both adult and developing intestinal stages; several of the macrocyclic lactones have similar activity. If the disease is severe, it is advisable to give parenteral iron and possibly vitamin B12 and to ensure that the dog has a protein-rich diet. Young pups may require a blood transfusion.
Control: A system of regular anthelmintic therapy and hygiene should be adopted. Weaned pups and adult dogs should be treated every 3 months. Pregnant bitches should be dosed at least once during pregnancy with an anthelmintic that has high efficacy against somatic larvae, so as to reduce transmammary infection, and the nursing litters dosed at least twice, at 1–2 weeks of age and again 2 weeks later with a drug specifically recommended for use in pups. This will also help to control ascarid infections. The perinatal transfer of both Ancylostoma and Toxocara larvae may be reduced by the oral administration of fenbendazole daily from 3 weeks before to 2 days after whelping.
Kennel floors should be free of crevices and dry and the bedding should be disposed of daily. Runs should preferably be of tarmac or concrete and kept as clean and dry as possible; faeces should be removed with a shovel before hosing. If an outbreak has occurred, earth runs may be treated with sodium borate, which is lethal to hookworm larvae, but this also kills grass. A second possibility, which is often used in fox farms, is the provision of wire-mesh flooring in the runs.
Notes: A. caninum can occasionally use man as a final host. Although infections do not reach full maturity, they may induce an eosinophilic enteritis.
Ancylostoma braziliense
Common name: Hookworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ancylostomatoidea
Description, gross: As for A. caninum except it is smaller than either A. caninum or A. tubaeforme. In the dog, males measure around 7.5 mm and females 9–10 mm in length.
Description, microscopic: The buccal capsule is deep with two pairs of large dorsal and very small ventral teeth. Eggs are similar to A. caninum, measuring around 75–95 × 41–45 μm.
Hosts: Dog, cat
Life cycle: Similar in many respects to A. caninum, using both oral and percutaneous routes of infection, but transmammary transmission has not been demonstrated. Rodents can act as paratenic hosts. The prepatent period is about 2 weeks in the dog and cat.
Geographical distribution: Tropical and subtropical regions
Pathogenesis: While it may cause a degree of hypoalbuminaemia through an intestinal leak of plasma, it is not a blood sucker and consequently is of little pathogenic significance, causing only mild digestive upsets and occasional diarrhoea. The main importance of A. braziliense is that it is regarded as the primary cause of cutaneous larva migrans (CLM) or ‘creeping eruption’ in man. CLM is characterised by tortuous erythematous inflammatory tracts within the dermis and by severe pruritus, and is caused by infective larvae penetrating the skin and wandering in the dermis. These larvae do not develop, but the skin lesions usually persist for weeks. The severity of the skin lesions relate to the degree of exposure to infective larvae.
Clinical signs: Mild digestive upset and diarrhoea in affected animals. In humans there may be skin erythema and pruritis.
Diagnosis: Worms that have been heat-fixed bend markedly at the position of the vulva. This differs from A. ceylanicum.
Pathology: Infected animals may show oedema of subcutaneous tissues and mesenteries, and serous effusion into the body cavities attributable to hypo-proteinaemia. If recent exposure to heavy percutaneous infection has occurred there may be dermatitis.
Details of the epidemiology, treatment and control are as for A. caninum.
Ancylostoma tubaeforme
Synonym: Strongylus tubaeformis
Common name: Feline hookworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ancylostomatoidea
Description, gross: Almost identical to A. caninum, but slightly smaller, the males measuring around 10 mm and the females 12–15 mm.
Description, microscopic: The buccal capsule is deep with the dorsal gutter ending in a deep notch on the dorsal margin of the buccal capsule, the ventral margin of which bears three teeth on each side. The cuticle is thicker and the deep ‘oesophageal’ teeth slightly larger than in A. caninum. The male bursa is well developed and the spicules are about 50% longer than in A. caninum. Eggs are similar to those of A. caninum and measure about 56–75 × 34–47 μm.
Hosts: Cat
Life cycle: As for A. braziliense. The prepatent period is about 3 weeks.
Geographical distribution: Worldwide
Pathogenesis: A. tubaeforme is generally considered to be of low pathogenicity, although heavy infections may lead to a poor coat, anaemia and reduced growth. A strong immunity often develops to infection.
Ancylostoma ceylanicum
Common name: Hookworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ancylostomatoidea
Description, gross: Almost identical to A. braziliense
Description, microscopic: The cuticular striations are wider than in A. braziliense.
Hosts: Dog, cat, wild felids and man.
Life cycle: Similar to A. braziliense. The prepatent period is about 2 weeks in the dog.
Geographical distribution: Asia (Malaysia, Sri Lanka)
Pathogenesis: Infections are usually subclinical but heavy infections can induce anaemia and diarrhoea.
Diagnosis: The heat-fixed female worms are not bent as occurs with A. braziliense.
Notes: A. ceylanicum can complete its life cycle in man and may cause anaemia and abdominal pain and skin penetration by infective larvae may induce cutaneous lesions.
All other details of these two species are in most respects similar to A. caninum.
Uncinaria stenocephala
Common name: Northern hookworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ancylostomatoidea
Description, gross: A small worm, up to about 1.0 cm long; males are 5–8.5 mm and females 7–12 mm.
Description, microscopic: The adult worms have a large funnel-shaped buccal capsule, which has a pair of chitinous plates, lacks dorsal teeth, but has a pair of sub-ventral teeth at the base (Fig. 6.6). The dorsal cone does not project into the buccal capsule. The male worm has a well developed bursa with a short dorsal lobe and two large and separate lateral lobes and slender spicules. Eggs are ovoidal, 65–80 × 40–50 μm.
Fig. 6.6 Head of Uncinaria stenocephala showing the funnel-shaped buccal capsule and the pair of chitinous plates.
Hosts: Dog, cat, fox other canids and felids. Various mammals can act as paratenic hosts.
Life cycle: Infection with infective L3 by oral infection, without pulmonary migration, is the usual route. Although the infective larvae can penetrate the skin, the infection rarely matures and there is no evidence as yet of transmammary or intrauterine transmission. Carnivores may become infected via the consumption of paratenic hosts, such as infected mice. The prepatent period is about 15 days.
Geographical distribution: Temperate and sub-arctic areas, North America and northern Europe
Pathogenesis: The infection is not uncommon in groups of sporting and working dogs. The adult worms attach to the mucosa. They are not voracious blood-suckers like A. caninum, but hypoalbuminaemia and low-grade anaemia, accompanied by diarrhoea, anorexia and lethargy, have been recorded in heavily infected pups. Probably the most common lesion in dogs made hypersensitive by previous exposure is pedal dermatitis, affecting particularly the interdigital skin.
Clinical signs: Anaemia, diarrhoea, anorexia, lethargy, interdigital dermatitis
Diagnosis: In areas where A. caninum is absent, the clinical signs of the patent infection, together with the demonstration of strongyle eggs in the faeces, is indicative of uncinariosis. Where Ancylostoma is also endemic, differential diagnosis may require larval culture, although the treatment is similar.
Pathology: Severe hookworm infections cause villous fusion and atrophy in the small intestine and an inflammatory response in the lamina propria.
Epidemiology: Evidence suggests that in temperate climates like the UK, the seasonal pattern of infective larvae on paddocks used for greyhounds follows that described for gastrointestinal trichostrongyloids in ruminants with a sharp rise in July and a peak in September, suggesting that development to the L3 is heavily dependent on temperature.
Treatment: Fenbendazole, mebendazole, nitroscanate, piperazine, pyrantel and milbemycin oxime are all active against the northern hookworm.
Control: Regular anthelmintic treatment and good hygiene as outlined for Ancylostoma will control Uncinaria infection. The combination of ivermectin and pyrantel pamoate or a formulation of chewable ivermectin can give high efficacy. The pedal dermatitis responds poorly to symptomatic treatment, but regresses gradually in the absence of reinfection.
Strongyloides stercoralis
Synonym: Strongyloides canis, S. intestinalis, Anguillula stercoralis
Common name: Threadworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Rhabditoidea
Description, gross: Slender, hair-like worms around 1mm long. Only females are parasitic.
Description, microscopic: The long oesophagus may occupy up to one third of the body length and the uterus is intertwined with the intestine, giving the appearance of twisted thread. Unlike other intestinal parasites of similar size the tail has a blunt point. Strongyloides eggs are oval, thin-shelled and small, 50–58 × 30–34 μm. The hatched L1 is passed out in the faeces.
Hosts: Dog, fox, cat, man
Life cycle: Strongyloides is unique among the nematodes of veterinary importance, being capable of both parasitic and free-living reproductive cycles. The parasitic phase is composed entirely of female worms in the small intestine and these produce larvated eggs by parthenogenesis, i.e. development from an unfertilised egg. After hatching, larvae may develop through four larval stages into free-living adult male and female worms and this can be followed by a succession of free-living generations. However under certain conditions, possibly related to temperature and moisture, the L3 can become parasitic, infecting the host by skin penetration or ingestion and migrating via the venous system, the lungs and trachea to develop into adult female worms in the small intestine. In dogs, autoinfection may occur with L1 developing rapidly to L3 in the gut, then penetrating the mucosa of the rectum or perianal skin followed by a pulmonary migration to the gut.
Puppies may acquire infection immediately after birth from the mobilisation of arrested larvae in the tissues of the ventral abdominal wall of the dam, which are subsequently excreted in the milk. The prepatent period is 9 days.
Geographical distribution: Worldwide in warmer climates, Europe (Portugal, France, Poland, Ukraine, Romania, Hungary)
Pathogenesis: Severe infections can occur in dogs, especially in puppies. Mature parasites are found in the duodenum and proximal jejunum and, if present in large numbers, may cause inflammation with oedema and erosion of the epithelium. This results in a catarrhal enteritis with impairment of digestion and absorption.
Table 6.1 Strongyloides species reported in cats.
| Species | Description | Pathogenicity |
| S. planiceps | Parasitic females are 2.4–3.3 mm long (mean, 2.8 mm). The tail of the parasitic female narrows abruptly to a blunt tip and the ovaries have a spiral appearance | Non-pathogenic |
| S. felis (syn S. cati) | Similar to S. planiceps. Parasitic females of S. felis have a long tail narrowing slowly to the tip. Ovaries are straight | Non-pathogenic |
| S. tumefaciens | Parasitic female is about 5 mm long | Found in tumours in the mucosa of the large intestine |
Clinical signs: Bloody diarrhoea, dehydration, sometimes death
Diagnosis: The clinical signs in very young animals, usually within the first few weeks of life, together with the finding of large numbers of the characteristic eggs or larvae in the faeces are suggestive of strongyloidosis.
Pathology: Lesions consist of catarrhal inflammation of the small intestine while in severe infections there may be necrosis and sloughing of the mucosa. Adult worms establish in tunnels in the epithelium at the base of the villi in the small intestine.
Epidemiology: The dog may act as a natural host for this species. Transmission is either by the oral or percutaneous route or by autoinfection. The latter route can lead to cases of persistent strongyloidosis occurring without external reinfection. Unweaned puppies are infected orally from larvae adhering to the teats and with larvae ingested with colostrum. Infection is most commonly seen in the summer when the weather is hot and humid and is frequently a kennel problem.
A strain of Strongyloides stercoralis has become adapted to man and usually occurs in warm climates.
Treatment: In dogs, oral fenbendazole at 10–20 mg/kg daily for 3 days is effective. Ivermectin is effective against adult worms.
Control: Disinfection or replacement of kennels and bedding eliminates the sources of infection.
Notes: S. stercoralis can cause several forms of disease in man:
Three other species of Strongyloides are found in cats (see Table 6.1). Details of the life cycle, diagnosis, treatment and control of these species are as for S. stercoralis.
Trichinella spiralis
See Chapter 5 (Pigs).
Alaria alata
Common name: Intestinal carnivore fluke
Predilection site: Small intestine
Parasite class: Trematoda
Family: Diplostomatidae
Description, gross: Adult flukes are 2–6 mm in length and the flat expanded anterior part is much longer than the posterior cylindrical part.
Description, microscopic: At the anterior lateral corners of the anterior part there are two tentacle-like processes. The suckers are very small and the adhesive organ consists of two long folds with distinct lateral margins. The eggs are large, 98–134 μm × 62–68 μm, operculate and unembryonated.
Final hosts: Dog, cat, fox, mink, wild carnivores and rarely man
Intermediate hosts: 1. Fresh water snails (Planorbis spp). 2. Frogs and toads.
Life cycle: Eggs are passed in the faeces from which miracidia eventually hatch and enter fresh water snails (Planorbis). Sporocysts produce cercariae with bifurcated tails. These leave the snail and infect tadpoles or frogs where the cercariae encyst in the muscles forming mesocercariae. If a frog, snake or mouse eats the tadpole, the mesocercariae become encysted, these animals acting as paratenic hosts. Dogs and foxes may be infected by eating rodents infected with mesocercariae. Once infected the mesocercariae migrate extensively, including passage through the lungs and diaphragm, becoming metacercariae before returning to the small intestine and maturing into flukes. The prepatent period is 1–2 weeks.
Geographical distribution: Eastern Europe
Pathogenesis: Adult fluke attach to the mucous membrane of the small intestine (Fig. 6.7) but cause little harm. However the migratory mesocercariae may cause clinical symptoms. Heavy infections may cause a severe duodenitis and pulmonary damage in dogs and cats. A fatal case has been recorded in man through eating inadequately cooked frogs’ legs; the principal lesions were in the lungs.
Clinical signs: Infection is not usually associated with clinical signs.
Diagnosis: Diagnosis is by identifying the presence of eggs in the faeces.
Pathology: Effects are generally limited to the attachment of flukes to the intestinal mucosa and may include local irritation, erosion and ulceration and the production of excessive intestinal mucus and, rarely, haemorrhagic enteritis.
Epidemiology: Infection is maintained in endemic areas where intermediate hosts are abundant. Transmammary infection has been reported with some species in cats and rodents.
Treatment: Treatment with praziquantel or niclosamide is recommended.
Fig. 6.7 Alaria spp attached to the mucosa of the small intestine.
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