Pathology: During the course of larval development there is dilation of infected gastric glands and hyperplasia of the glandular epithelium of both infected and neighbouring glands. The lamina propria is oedematous with infiltration by lymphocytes, plasma cells and eosinophils. Larvae are found in the gastric glands with adults mainly on the surface (Fig. 5.1). During the course of development the hyperplasia causes the formation of pale nodules, which may become confluent in heavy infections, leading to the formation of a thickened, convoluted mucosa. There may be focal or diffusely eroded areas and occasionally ulceration of the glandular mucosa.
Epidemiology: Because of the preparasitic larval requirements, infection is confined to pigs with access to pasture or those kept in straw yards. It is therefore more common in breeding stock, particularly gilts. The free-living larvae are particularly sensitive to desiccation and low temperatures. The epidemiology, at least in temperate zones, is similar to that of Ostertagia in ruminants with seasonal hypobiosis a feature. Adult pigs often act as a reservoir of infection.
Treatment: When Hyostrongylus infection is diagnosed, particularly in breeding stock, it is important to use a drug such as a modern benzimidazole or a macrocyclic lactone, which will remove hypobiotic larvae.
Control: The same principles apply as for the control of parasitic gastroenteritis in ruminants. For example, in temperate areas there should be an annual rotation of pasture with other livestock or crops. The timing of the move to other pastures may be dependent on other farming activities; if it can be delayed until October or later and accompanied by an anthelmintic treatment, then eggs from any worms which survive the treatment are unlikely to develop due to the unfavourable winter temperatures. A second treatment, again using a modern benzimidazole or a macrocyclic lactone is recommended 3–4 weeks later to remove any residual infection. It may be advantageous to treat pregnant pigs before farrowing.
Notes: This parasite is responsible for a chronic gastritis in pigs, particularly gilts and sows.
Ollulanus tricuspis
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description, gross: This is a very small trichostrongyle (0.7–1.0 mm long). Males are 0.7–0.8 mm, and females 0.8–1 mm long.
Description, microscopic: It 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: 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 result in 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 from them to other hosts.
Treatment: Not reported in the pig, although benz- imidazoles or ivermectin should be effective.
Control: This is mainly achieved through the implementation of good hygiene procedures and prevention of contact with cats.
Ascarops strongylina
Synonym: Arduenna strongylina
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Small, slender worms, the males measuring up to 15 mm and the reddish females 22 mm long. They live on the stomach wall under a layer of mucus.
Description, microscopic: A cervical ala is located only on the left side of the body. The wall of the pharynx contains several spiral supports. Eggs are thick-shelled, 34–49 × 20 μm, and are embryonated when passed.
Final hosts: Pig, wild boar
Intermediate hosts: Coprophagous beetles (Aphodius, Onthophagus, Gymnopleurus)
Life cycle: The life cycle of A. strongylina 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 pigs ingest the beetles. The prepatent period is about 4 weeks.
Geographical distribution: Worldwide
Pathogenesis: A. strongylina is not severely pathogenic; the main effect being a catarrhal gastritis, particularly in young animals.
Clinical signs: Clinical signs are usually absent, although, in heavy infections, softening of faeces and inappetence may occur.
Diagnosis: Diagnosis of a particular genus is difficult by faecal examination, but the presence of the small elongate eggs in the faeces of animals showing signs of gastritis will give a tentative indication of spiruroidosis.
Pathology: On postmortem, the gastric mucosa is sometimes reddened and oedematous.
Epidemiology: The epidemiology depends on the presence and abundance of the intermediate beetle hosts. Infection is more prevalent in outdoor pigs at pasture.
Treatment: Treatment has not been considered with this genus.
Control: Not usually required.
Ascarops dentata
Synonym: Arduenna dentata
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Geographical distribution: Malaysia, S.E. Asia.
All other details are essentially similar to A. strongylina
Gnathostoma hispidum
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Thick-bodied worms; the males are 1.5–2.5 cm and the females 2.0–4.5 cm long. The presence of the worms in gastric nodules is sufficient for generic diagnosis.
Description, microscopic: The whole body is covered with spines. The left spicule is longer than the right. Eggs are oval, 72–74 × 39–42 μm with a thin cap at one pole.
Final host: Pig, rarely man
Intermediate hosts: Cyclops spp and related freshwater crustacea
Life cycle: The young worms migrate in the abdominal organs of the host, particularly the liver. 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 develop to L2 before hatching after several days. Crustaceans ingest L2 and development to L3 takes place within about 10 days. The final host is infected by ingestion of the crustacea and further development occurs in the stomach wall, where the deeply embedded worms provoke the growth of fibrous lesions. A second intermediate host is not required with G. hispidum.
Geographical distribution: Europe, Asia, Africa
Pathogenesis: The most obvious effect of gnathostomosis is the presence of fibrous growths on the stomach wall. Ulceration and necrosis of the stomach wall are often present. 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. It occurs erratically in man as a cause of visceral larva migrans.
Clinical signs: Gnathostoma infection is usually inapparent. Severe infections may produce a marked gastritis leading to inappetence and weight loss.
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: Fibrous growths are of variable size, the largest being 3–4 cm in diameter, and are cavitated, amounting to thick-walled cysts containing several worms and fluid.
Epidemiology: It should be noted that the final hosts are also eligible second intermediate hosts, so that, for example, the pig may harbour L3 in its liver and muscles as well as adult worms in its stomach.
Treatment: Treatment has not been fully investigated.
Control: With ubiquity of the first and second intermediate hosts, complete control cannot be achieved, but partial limitation is possible by thorough cooking of all food.
Gnathostoma doloresi
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Geographical distribution: Asia
All other details are essentially similar to G. hispidum
Physocephalus sexalatus
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Small, slender worms; the males measuring about 10–12 mm and the females up to 22 mm long.
Description, microscopic: The wall of the pharynx contains a single spiral support. The cervical papillae are asymmetrically located. Eggs are thick-shelled and are embryonated when passed.
Final hosts: Pig; occasionally rabbit, hare
Intermediate hosts: Coprophagous beetles
Life cycle: The life cycle is typically spiruroid and the prepatent period is about 6 weeks.
Geographical distribution: Widely distributed in many parts of the world
Pathogenesis: The parasites lie on the surface of the stomach wall under a layer of mucus. P. sexalatus is not severely pathogenic, the main effect being a catarrhal gastritis, particularly in young piglets.
Clinical signs: In many infections, obvious clinical signs are absent; in heavy infections, softening of faeces and inappetance may occur.
Diagnosis: As for other spiruroid parasites
Pathology: At necropsy, the gastric mucosa is sometimes reddened and oedematous. The tiny worms can be seen in the mucus covering the gastric mucosa.
Epidemiology: Infection occurs where the intermediate hosts are plentiful. Transmission may also occur through paratenic hosts, such as amphibians or birds.
Treatment: Not reported
Control: Measures that restrict dung beetle populations feeding on pig faeces will be beneficial.
Notes: P. sexalatus is not considered to be of great economic or pathogenic importance.
Simondsia paradoxa
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Small slender worms. The females measure up to about 20 mm in length, and males are 12–15 mm long.
Description, microscopic: Females have large lateral alae and a large ventral and dorsal tooth. The gravid female has a characteristic form, the posterior end of the body being a rounded sac filled with eggs. The male has a spirally coiled tail. Eggs are oval or ellipsoid, 20–29 μm.
Final host: Pig
Intermediate hosts: Beetles
Life cycle: The life cycle is indirect. Eggs are passed in the faeces and ingested by beetles in which they hatch and develop to infective larvae. The parasites continue development when the intermediate host is ingested by a pig. Male worms live on the surface of the gastric mucosa, but the females are found in small cysts in the mucosal crypts with their anterior ends protruding.
Geographical distribution: Predominantly a parasite of tropical and subtropical regions; also occurs in parts of Europe.
Pathogenesis: Simondsia paradoxa is not severely pathogenic, the main effect being a catarrhal gastritis. In addition, there can be some fibrous reaction around the nodules in the stomach wall.
Clinical signs: Infections are usually asymptomatic.
Diagnosis: Diagnosis of a particular genus is difficult by faecal examination, but the presence of the small elongate eggs in the faeces of animals showing signs of gastritis will give a tentative indication of spiruroidosis.
Pathology: Females are present in nodules 6–8 mm in diameter.
Epidemiology: Infection is likely to be more common in outdoor pigs where the intermediate hosts are more abundant.
Treatment: Treatment is generally not considered.
Control: Attempts to control these spiruroids are unlikely to be successful because of the ready availability of the intermediate hosts.
Trichostrongylus axei
Synonym: Trichostrongylus extenuatus
Common name: Stomach hairworm
Predilection site: Stomach
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description, gross: The adults are small, hair-like, light brownish red and difficult to see with the naked eye. Males measure around 3–6 mm and females 4–8 mm in length.
Hosts: Cattle, sheep, goat, deer, horse, donkey, pig and occasionally man
Life cycle: This is typically trichostronylid and is described in detail in Chapter 3 (Sheep and goats).
Geographical distribution: Worldwide
Pathogenesis: T. axei may occasionally be found in the stomach of pigs, but is considered to be of minor importance.
SMALL INTESTINE
Globocephalus urosubulatus
Synonym: Globocephalus longemucronatus
Common name: Pig hookworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Strongyloidea
Description, gross: A very small, stout whitish worm, 0.4–0.8 cm long
Description, microscopic: The mouth opens subdorsally and the buccal capsule is globular but with an absence of chitinous structures in the buccal capsule. The male bursa is well developed and the spicules are slender.
Hosts: Pig, wild boar
Life cycle: The life cycle is direct, either by oral ingestion of L3 larvae or by percutaneous penetration. Larval migration through the heart, lungs, trachea, oesophagus and stomach occurs.
Geographical distribution: North and South America, Europe, Africa and Asia
Pathogenesis: Not known but thought to be generally of little pathological significance, although heavy infections may affect piglets severely.
Clinical signs: Generally asymptomatic, although heavily infected piglets may be anaemic and show weight loss and emaciation.
Diagnosis: Identification of eggs in the faeces, or adult worms found in the small intestine on postmortem.
Pathology: Not described
Epidemiology: Not reported
Treatment: Most modern benzimidazoles and macro- cyclic lactones are likely to be effective.
Control: Frequent removal of faeces and bedding on dry straw or concrete will help reduce the risk of infection.
Ascaris suum
Common name: Large roundworm, white spot
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: A. suum is by far the largest nematode of the pig; the white, rigid females are up to 40.0 cm long and the males up to 25 cm in length, and could only be confused with Macracanthorhyncus where this occurs (Fig. 5.2).
Fig. 5.2 A knot of Ascaris suum recovered from the small intestine of an infected pig.
Description, microscopic: The egg is ovoid and yellowish brown, with a thick shell, the outer layer of which is irregularly mamillated. The egg is larvated when passed in the faeces and the thick multilayered eggshell enables the egg to survive desiccation and freezing in the environment for several years.
Hosts: Pig, wild boar, rarely sheep, cattle, man
Life cycle: The life cycle is direct. Though the pre- parasitic moults occur by about 3 weeks after the egg is passed, a period of maturation is necessary, and the egg is not usually infective until a minimum of four weeks after being passed, even in the optimal temperature range of 22–26°C. The egg is very resistant to temperature extremes, and is viable for more than 4 years. After ingestion, the larvated egg hatches in the small intestine, the L3 larva penetrates the intestinal mucosa and then travels to the liver. The larva then passes in the bloodstream to the lungs and thence to the small intestine via the bronchi, trachea and pharynx. In the intestine the final moult occurs and the young adult worms inhabit the lumen of the small intestine. If the eggs are ingested by an earthworm or dung beetle they will hatch, and the L3 travel to the tissues of these paratenic hosts, where they can remain, fully infective for pigs, for a long period. The prepatent period is between 7 and 9 weeks, and each female worm is capable of producing more than 200 000 eggs per day. Longevity is around 6–9 months.
Geographical distribution: Worldwide
Pathogenesis: The migrating larval stages in large numbers may cause numerous small haemorrhages, emphysema and a transient pneumonia, but it is now recognised that many cases of so-called ‘Ascaris pneumonia’ may be attributable to other infections, or to piglet anaemia. In the liver, the migrating larvae can cause ‘milk spot’ or ‘white spot’ which appears as cloudy whitish spots of up to 1.0 cm in diameter on the surface of the liver, and represents the fibrous repair of inflammatory reactions to the passage of larvae in the livers of previously sensitised pigs (Fig. 5.3). Livers showing ‘milk spot’ lesions may be condemned at meat inspection. The adult worms in the intestine cause little apparent damage to the mucosa, but occasionally, if large numbers are present, there may be obstruction, and rarely a worm may migrate into the bile duct, causing obstructive jaundice and carcase condemnation. Experimental infections have shown that in young pigs the important effect of alimentary ascariosis is economic, with poor feed conversion and slower weight gains, leading to an extension of the fattening period by 6–8 weeks.
Fig. 5.3 Milk spot lesions in the liver associated with Ascaris suum.
Clinical signs: The main effect of the adult worms in pigs is to cause production loss in terms of diminished weight gain. Otherwise, clinical signs are absent except in the occasional case of intestinal or biliary obstruction. Heavy infections may increase the susceptibility of young pigs to other bacterial and viral pathogens. In piglets under 4 months old, larval activity during the pulmonary phase of migration may cause a clinically evident pneumonia, which is usually transient and rapidly resolving. In sheep and cattle exposed to contaminated grazing, there may be acute dyspnoea, tachypnoea and coughing following acute challenge with migrating larvae in the lungs.
Diagnosis: Diagnosis is based on clinical signs, history of disease, and, in infections with the adult worm, on the presence in faeces of the yellow-brown ovoid eggs, with thick mamillated shells. Being dense, the eggs float more readily in saturated solutions of zinc sulphate or magnesium sulphate than in the saturated sodium chloride solution, which is used in most faecal examination techniques. Low counts of A. suum eggs in faeces (<200 epg) may represent false-positives due to the coprophagic activity of pigs. At necropsy, the large worms in the small intestine are easy to recognise.
Pathology: Larval migration induces lesions in the liver and lungs. In the lungs, gross lesions are limited largely to numerous focal haemorrhages scattered over and through the pulmonary parenchyma. There may be some oedema, congestion and alveolar emphysema. Microscopically, there is an eosinophilic bronchiolitis. Bronchioles are surrounded by macrophages and eosinophils, and the bronchiolar wall is infiltrated by eosinophils, which are also present, with necrotic debris, in the lumen. Larvae are usually readily found in tissue sections and may be present in alveoli, alveolar ducts, bronchioles or bronchi, and in more chronic cases, are found within eosinophilic granulomas. Lesions in the liver result in considerable economic loss from condemnation at meat inspection. Haemorrhagic tracks are present near portal areas and throughout lobules, visible through the capsule as pinpoint red areas, sometimes slightly depressed and surrounded by a narrow pale zone. These lesions collapse, healing by fibrosis, which extends around portal tracts and extends out more diffusely emphasising lobular outlines. Granulomatous foci containing giant cells, macrophages and eosinophils may centre on the remnants of larvae trapped and destroyed in the liver. The inflammatory infiltrates in livers of animals exposed to larval ascarids may become severe and diffuse, and this is reflected in the gross appearance of the liver, which has extensive ‘milk spots’ and prominent definition of lobules. The liver is firm, and heavy scars may become confluent, obliterating some lobules and extending out to exaggerate interlobular septa throughout the liver.
The pathogenicity of adult ascarids in the intestine is poorly defined. Heavy infections may obstruct the gut, being visible as rope-like masses through the intestinal wall. Ascarids may occasionally pass to the stomach and be vomited or migrate up the pancreatic or bile ducts. Sometimes biliary obstruction and icterus, or purulent cholangitis, may ensue. Rarely, intestinal perforation occurs. On histology, there may be substantial hypertrophy of the muscularis externa and elongation of the crypts of Lieberkühn, though height of villi is not significantly reduced. Hypertrophy and exhaustion of the goblet-cell population and increased infiltrates of eosinophils and mast cells are also observed in infected intestines.
In sheep, and occasionally cattle, migrating ascarids can cause eosinophilic granulomas and interstitial hepatitis and fibrosis with heavy eosinophilic infiltrates in the livers of sheep grazing contaminated areas. In heavy infections where death ensues, the lungs are moderately consolidated, with alveolar and interstitial emphysema and interlobular oedema. Microscopically, there is thickening of the alveolar septae, and effusion of fluid and macrophages into the alveoli. Larvae present within alveoli and bronchioles provoke an acute bronchiolitis.
Epidemiology: Young suckling piglets can become infected early after birth through the ingestion of embryonated eggs that are attached to the underbelly of the sow. Prevalence of infection is usually highest in pigs of around 3–6 months of age. A partial age immunity operates in pigs from about 4 months of age onwards, and this, coupled with the fact that the worms themselves have a limited life-span of several months, would suggest that the main source of infection is the highly resistant egg on the ground, a common characteristic of the ascaridoids. Hence ‘milk spot’, which is economically very important, since it is a cause of much liver condemnation, presents a continuous problem in some pig establishments. This condition has been widely noted to have a distinct seasonality of occurrence, appearing in greatest incidence in temperate areas during the warm summer months, and almost disappearing when the temperatures of autumn, winter and spring are too low to allow development of eggs to the infective stage. Also earthworms are generally more active and available during the summer months. Sows and boars act as reservoirs of light infection. A. suum may occasionally infect cattle, causing an acute, atypical, interstitial pneumonia, which may prove fatal. In most cases reported the cattle have had access to housing previously occupied by pigs, sometimes several years before, or to land fertilised with pig manure. In lambs, A. suum may also be a cause of clinical pneumonia as well as ‘milk spot’ lesions, resulting in condemnation of livers. In most cases lambs have been grazed on land fertilised with pig manure or slurry, such pasture remaining infective for lambs even after ploughing and cropping. Young adults of A. suum are occasionally found in the small intestine of sheep. There are a few recorded cases of patent A. suum infection in man but cross-infection is not of epidemiological significance.
Treatment: The intestinal stages are susceptible to most of the anthelmintics in current use in pigs, and the majority of these, such as the benzimidazoles, are given in the feed over several days. In cases of suspected Ascaris pneumonia, injectable levamisole and ivermectin may be more convenient. For 3–4 days posttreatment the faeces should be removed from the pens and destroyed, as they often will contain large numbers of eggs and expelled/disintegrating worms.
Control: In the past, elaborate control systems have been designed for ascariosis in pigs, but with the appearance of highly effective anthelmintics these labour-intensive systems are rarely used. The chief problem in control is the great survival capacity of the eggs, but in housed pigs, strict hygiene in feeding and bedding, with frequent hosing/steam cleaning of walls, floors and feeding troughs will limit the risk of infection. Some disinfectants and chemical solutions will limit infectivity. In pigs on free range the problem is greater, and where there is serious ascariosis it may be necessary to discontinue the use of paddocks for several years, since the eggs can survive cultivation. It is good practice to treat in-pig sows at entry to the farrowing pen, and young pigs should receive anthelmintic treatment when purchased or on entry to the finishing house and 8 weeks later; boars should be treated every 3–6 months. Washing of the skin of sows prior to their removal to the farrowing pen should reduce contamination with embryonated eggs.
Notes: The type species, Ascaris lumbricoides, occurs in man, and at one time it was not differentiated from A. suum, so that the pig was thought to present a zoonotic risk for man. With species distinction now possible, A. lumbricoides is accepted as specific for man, and is irrelevant to veterinary medicine.
Strongyloides ransomi
Common name: Threadworm
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Rhabditoidea
Description, gross: Slender, hair-like worms 3.4–4.5 mm 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, 45–55 × 26–35 μm.
Hosts: Pig
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.
Piglets 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. In addition, prenatal infection has been demonstrated experimentally in pigs. The prepatent period is 6–9 days.
Geographical distribution: Worldwide
Pathogenesis: Skin penetration by infective larvae may cause an erythematous reaction. 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 catarrhal enteritis with impairment of digestion and absorption.
Clinical signs: In light infections, animals show no clinical signs. In heavy infections, there is bloody diarrhoea, anaemia and emaciation, and sudden death may occur. During the migratory phase there may be coughing, abdominal pain and vomiting.
Diagnosis: Demonstration of larvated eggs in faeces or the adults in scrapings from the intestine on postmortem is diagnostic.
Pathology: The adult female worms burrow into the intestinal wall and establish in tunnels in the epithelium at the base of the villi in the small intestine, causing an inflammatory response. In large numbers they may cause villous atrophy, with a mixed mononuclear inflammatory cell infiltration of the lamina propria. Crypt epithelium is hyperplastic and there is villous clubbing.
Epidemiology: Strongyloides infective larvae are not ensheathed and are susceptible to extreme climatic conditions. However warmth and moisture favour development and allow the accumulation of large numbers of infective stages. Adult breeding stock may be infected with dormant larvae in their subcutaneous fat. Pregnancy and farrowing appear to stimulate the re-emergence of these larvae, which then may infect piglets via the colostrum. This appears to be the major route of infection in young piglets and, in only 7 days after birth, piglets may be passing eggs in their faeces.
Treatment: Specific control measures for Strongyloides infection are rarely called for. The benzimidazoles and the macrocyclic lactones may be used for the treatment of clinical cases and a single dose of ivermectin 4–16 days prior to farrowing has been shown to suppress larval excretion in the milk of sows.
Control: Strict hygiene and cleaning of pens before farrowing helps limit levels of infection. Treating the sows before farrowing can also help reduce infections in piglets.
Trichinella spiralis
Synonym: Trichina spiralis
Common name: Muscle worm
Predilection site: Small intestine, muscle
Parasite class: Nematoda
Superfamily: Trichuroidea
Description, gross: Because of their short lifespan, the adult worms are rarely found in natural infections. The male is about 1.5 mm and the female 3.5–4.0 mm long.
Description, microscopic: The oesophagus is at least one third of the total body length and the tail in the male has two small cloacal flaps, but no copulatory spicule nor a spicule sheath. In the female, the uterus contains developing larvae. Trichinella infection is most easily identified by the presence of coiled larvae in striated muscle (Fig. 5.4). The cysts are lemon-shaped, 0.3–0.8 × 0.2–0.4 mm in size and often transparent.
Hosts: Pig, rat, man, and most mammals
Life cycle: The life cycle is indirect. The adult parasites and infective larvae (muscle trichinae) are unusual in being present within a single host (i.e. development from larva to adult to larva in a single host). Trichinella does not have a free-living stage. The developing adults lie between the villi of the small intestine. After fertilisation, the males die while the females burrow deeper into the intestinal mucosa. About a week later, they produce L1 which enter the lymphatic vessels and travel via the bloodstream to the skeletal muscles. There, still as L1, they penetrate striated muscle cells where they are encapsulated by the host, grow and assume a characteristic coiled position; the parasitised muscle cell is transformed by microvascularisation into a ‘nurse cell’. This process is complete within about 3–4 weeks, by which time the larvae are infective and may remain so for many years. Development is resumed when muscle, containing the encysted trichinae, is ingested by another host, usually as a result of predation or carrion feeding. The L1 is liberated in the stomach and in the intestine undergoes four moults to become sexually mature within about a week. Patent infections persist for only a few weeks at the most.
Fig. 5.4 Coiled infective larvae of Trichinella spiralis in striated muscle.
Geographical distribution: Worldwide, with the apparent exceptions of Australia, Denmark and Great Britain
Pathogenesis: The adults occur in the glandular crypts of the proximal small intestine and their larvae in the striated muscles; the diaphragmatic, intercostal and masseter muscles and the tongue are considered to be the main predilection sites. Infection in domestic animals is invariably light, and clinical signs do not occur. However, when hundreds of larvae are ingested, as occasionally happens in man and presumably also in predatory animals in the wild, including cats and dogs, the intestinal infection is often associated with catarrhal enteritis and diarrhoea, and 1–2 weeks later the massive larval invasion of the muscles causes acute myositis, fever, eosinophilia and myocarditis. Periorbital oedema and ascites are also common in man, sometimes accompanied by vomiting, diarrhoea, fever and myocarditis. Unless treated with an anthelmintic and anti-inflammatory drugs, such infections may frequently be fatal as a consequence of paralysis of respiratory muscles, but in persons who survive this phase the clinical signs start to abate after 2–3 weeks.
Clinical signs: These are variable and depend on the host and the level of infection. Signs are usually non-specific and resemble those of other diseases, such as diarrhoea, fever, muscular pain, dyspnoea and peripheral eosinophilia. T. spiralis infection in young pigs can induce inappetance, weakness and diarrhoea. Older pigs are generally more tolerant of infection.
Diagnosis: This is not relevant in live domestic animals. At meat inspection, heavy larval infections may occasionally be just seen with the naked eye as tiny greyish white spots. For routine purposes small samples of pig muscle (taken from the preferential predilection sites) of about 1 g are squeezed between glass plates, the apparatus being called a compressorium, and examined for the presence of larvae by direct low-power microscopic examination or projection onto a screen using a trichinoscope. Alternatively, small portions of diaphragm tissue may be digested in pepsin/HCl and the sediment examined microscopically for the presence of larvae. The digestion method is now the preferred approach in most countries as it is less expensive and labour intensive to perform. For mass screening purposes, designed to determine the incidence of trichinellosis in pigs within regions or for some high- volume slaughterhouses, immunodiagnostic tests have been used. Of these, the antibody-detection ELISA or EIA appears to be the test of choice.
Pathology: The adults occur in the glandular crypts of the proximal small intestine where there is little associated pathology. Larvae are found in the striated muscles with the diaphragmatic, intercostals, masseter muscles and the tongue considered to be the main predilection sites. On microscpic examination, the larvae lie in a bulging clear segment of muscle fibre, which may be loosely encircled by eosinophils, lymphocytes, plasma cells and macrophages. In a heavy infection, a large proportion of the muscle fibres in the predilection muscles may be infected with larvae and surrounded by reactive zones. As the cellular reaction subsides, muscle fibres surrounded by the larvae have the appearance of a fibrous capsule. Once larvae become encysted, there is muscle fibre degeneration and mineralisation, which doesn’t appear to affect larval viability, as larvae can survive for up to 20 years.
Epidemiology: It is important to realise that trichinellosis is basically an infection of animals in the wild and that the involvement of man in these circumstances is accidental. The epidemiology of trichinellosis depends on two factors. First, animals may become infected from a wide variety of sources, predation and cannibalism being perhaps the most common. Others include feeding on carrion, since the encapsulated larvae are capable of surviving for several months in decomposing flesh, and the ingestion of fresh faeces from animals with a patent infection. It is also thought that transport hosts, such as crustaceans and fish, feeding on drowned terrestrial animals, may account for infection in some aquatic mammals such as seals.
The second factor is the wide host range of the parasite, infecting various carnivores and omnivorous mammals. In temperate areas rodents, brown bear, badger and wild pig are most commonly involved; in the arctic, polar bear, wolf and fox; in the tropics, lion, leopard, bushpig, hyena, jackal and warthog. In these sylvatic or feral cycles, man and his animals are only occasionally involved. For example, the consumption of polar bear meat may cause infection in Inuit and sledge-dogs, while in Europe the hunting and subsequent ingestion of wild pigs may also produce disease in man and his companion animals.
The domestic or synanthropic cycle in man and the pig is an ‘artificial’ zoonosis largely created by feeding pigs on food waste containing the flesh of infected pigs; more recently, tail biting in pigs has been shown to be a mode of transmission. Rats in piggeries also maintain a secondary cycle, which may on occasions pass to pigs or vice versa from the ingestion of infected flesh or faeces. Infection in man is acquired from the ingestion of raw or inadequately cooked pork or its by-products, such as sausages, ham and salami. It is also important to realise that smoking, drying or curing pork does not necessarily kill larvae in pork products. Horsemeat has increasingly been implicated in the transmission of Trichinella to man.
In areas such as Poland, Germany and the USA, human trichinosis acquired from pork has, until recently, been an important zoonosis. Over the past few decades, prohibition of feeding uncooked food waste to pigs, improved meat inspection and public awareness have greatly diminished the significance of the problem. In Britain, and other countries in Europe, and in the USA the numbers of outbreaks are few and sporadic.
The decreasing prevalence is also reflected in the fact that inapparent infection in man, as shown by the presence of T. spiralis larvae in muscle samples at necropsy, has decreased from 10% to not recorded in Britain, and from 20% to under 5% in the USA over the past 50 years.
Treatment: Although rarely called for in animals, the adult worms and the larvae in muscles are susceptible to several of the benzimidazole anthelmintics, such as in-feed treatment with flubendazole in pigs.
Control: Probably the most important factor in the control of trichinellosis is a legal requirement that swill or waste human food intended for consumption by pigs must be boiled (100°C for 30 minutes). In fact, this practice is mandatory in many countries to limit the potential spread of other diseases, such as foot and mouth disease and swine fever.
Other essential steps include:
Table 5.1 Species of Trichinella.
Notes: The taxonomy of the genus has been controversial until very recently. It is composed of several sibling species, which cannot be differentiated morphologically but molecular typing, and other criteria, have now identified eight species of Trichinella (Table 5.1).
Macracanthorhynchus hirudinaceus
Common name: Thorny-headed worm
Predilection site: Duodenum and proximal small intestine
Parasite class: Acanthocephala
Family: Oligacanthorhynchidae
Description, gross: Adults resemble Ascaris suum, but taper posteriorly. The anterior of the worm possesses a retractable proboscis, which is covered with recurved hooks (Fig. 5.5). The males are up to 10 cm and the females around 60 cm in length and slightly pinkish in colour when fresh. The worms are thick (5–10 mm in width) and the cuticle is transversely wrinkled.
Description, microscopic: There is no alimentary canal. The egg is oval with a thick greyish brown pitted shell and contains the acanthor larva when laid. This larva has a small circle of minute hooks at the anterior.
Definitive hosts: Pig, wild boar, occasionally dog, wild carnivores and man
Fig. 5.5 Head of Macracanthorhynchus hirudinaceus showing the retractible proboscis.
Intermediate hosts: Various dung beetles and water beetles
Life cycle: Adults, attached to the small intestinal mucosa, lay eggs which are passed in the faeces. These are produced in large numbers, are very resistant to extremes of climate and can survive for years in the environment. After ingestion by dung or water beetle larvae, the acanthor develops to the infective cystacanth stage in approximately 3 months. Infection of pigs occurs after ingestion of either infected beetle grubs or adult beetles. The prepatent period is 2–3 months and longevity can be around 1 year.
Geographical distribution: Worldwide, but absent from certain areas, for example parts of western Europe
Pathogenesis: Mild infections are not very pathogenic, but heavy infections may retard growth rates and cause emaciation.
Clinical signs: Low-level infections are usually asymptomatic. Heavy infections may cause inappetence and weight loss.
Diagnosis: This is based on finding the typical eggs in the faeces. At necropsy the worms superficially appear similar to Ascaris suum, but when placed in water the spiny proboscis is protruded, thus aiding differentiation.
Pathology: M. hirudinaceus penetrates deep into the intestinal wall with its proboscis and produces inflammation and may provoke granuloma formation at the site of attachment in the wall of the duodenum and the small intestine. Heavy infections may induce a catarrhal enteritis and, rarely, penetration of the intestinal wall, which can result in a fatal peritonitis.
Epidemiology: Infection is seasonal, being partly dependent on the availability of the intermediate hosts. The eggs are able to remain viable in the environment for several years. Infection tends to be more prevalent in pigs of around 1–2 years of age.
Treatment: Although there is little information on treatment, levamisole and ivermectin are reported to be effective.
Control: Pigs should be prevented from access to the intermediate hosts. In modern management systems this may be easily achieved, but where pigs are kept in small sties the faeces should be regularly removed to reduce the prevalence of the dung beetle intermediate hosts.
Fasciolopsis buski
Predilection site: Small intestine
Parasite class: Trematoda
Family: Fasciolidae
Description, gross: Large, thick, elongate-oval fluke without shoulders, broader posteriorly, and variable in size but usually measuring 30–75 × 8–20 mm. The ventral sucker is situated near the anterior extremity and is much larger than the oral sucker. The cuticle bears spines that are frequently lost.
Description, microscopic: Eggs are brown, thin shelled with an operculum, and measure 125–140 × 70–90 μm.
Final hosts: Pig, dog and man
Intermediate hosts: Flat, spiral-shelled freshwater snails of Planorbis and Segmentina species
Life cycle: The life cycle is similar to F. hepatica. The final host is infected through ingestion of metacercariae that encyst on aquatic plants. The prepatent period is 9–13 weeks.
Geographical distribution: India, Pakistan, southeast Asia and China.
Pathogenesis: The parasite is mainly of importance as a cause of disease in humans. It is located in the small intestine where it can cause severe ulceration of the intestinal mucosa in heavy infections in man. Lesions are less severe in the pig and dog.
Clinical signs: Infection causes abdominal pain, diarrhoea, oedema, ascites and occasionally intestinal obstruction leading to malnutrition and death in humans. Symptoms are less severe in pigs and dogs.
Diagnosis: Diagnosis is confirmed by identification of the eggs in faeces that have to be differentiated from eggs of Fasciola spp.
Pathology: Heavier infections produce ulceration of the intestinal mucosa.
Epidemiology: The intermediate snail hosts feed on certain plants, water calthrop (Trapa natans) and water chestnut (Eliocharis tuberosa), which are cultivated for food and usually fertilised with human faeces. The cercariae encyst on the tubers or nuts of these plants, and cause infection if eaten raw. Pigs also become infected through eating these plants.
Treatment: Albendazole (10 mg/kg) and praziquantel (15 mg/kg) are both effective.
Control: The disease is easily preventable by avoiding raw or uncooked aquatic plants in endemic areas. The introduction of good sanitation facilities limits contamination of local watercourses and ponds.
Notes: F. buski is primarily a parasite of man, but can occur in the pig and dog, which may act as reservoir hosts.
Coccidiosis
Although some ten species of coccidia have been described from pigs, their importance is not clear. Isospora suis is a cause of a naturally occurring severe enteritis in young piglets aged 1–2 weeks. Eimeria debliecki has been described as causing clinical disease and severe pathology; E. polita, E. scabra and E. spinosa cause moderate to mild diarrhoea in piglets.
The source of infection appears to be oocysts produced by the sow during the periparturient period, the piglets becoming initially infected by coprophagia; the second phase of diarrhoea is initiated by reinvasion from tissue stages. Diagnosis of the condition is difficult unless postmortem material is available since clinical signs occur prior to the shedding of oocysts and are very similar to those caused by other pathogens such as rotavirus.
Table 5.2 Predilection sites and prepatent periods of Eimeria species in pigs.
| Species | Predilection site | Prepatent period (days) |
| Isospora suis | Small intestine | 5 |
| Eimeria deblieki | Small intestine | 6–7 |
| E. polita | Small intestine | 7–8 |
| E. scabra | Small and large intestine | 7–11 |
| E. spinosa | Small intestine | 7 |
| E. porci | Small intestine | 5–7 |
| E. neodebliecki | Unknown | 10 |
| E. perminuta | Unknown | ? |
| E. suis | Unknown | 10 |
Diagnosis of coccidial infections is based on history and clinical signs, and in patent infections, on the presence of oocysts of the pathogenic species in the faeces. Oocysts may not be shed during the diarrhoeal phase so faecal counts are not always of value.
Treatment for all species of Eimeria has generally relied on the use of a sulphonamide/trimethoprim product combined with electrolyte and fluid therapy. Treatment with several anticcocidial drugs, such as halofuginone, salinomycin and diclazuril given orally to affected animals, has been reported to be effective, although such treatments may not be licensed or approved in many countries. Control of coccidiosis is based on reducing environmental contamination by improved hygiene. Pens should be kept clean and dry. Ammonia-based disinfectants can be used after thoroughly cleaning farrowing pens by high-pressure hosing or steam disinfection. Overcrowding of piglets and faecal contamination of food and water should be avoided. Prevention can be achieved by the in-feed administration of amprolium to sows during the peri- parturient period, from 1 week prior to farrowing until 3 weeks post farrowing, where such treatments are licensed or approved.
Isospora suis
Predilection site: Small intestine
Parasite class: Sporozoasida
Family: Eimeriidae
Description: Oocysts are spherical to subspherical, 17–25 × 16–22 μm (mean 20.6 × 18.1 μm) and the wall is colourless and thin. There is no micropyle or residuum and when sporulated the oocysts contain two sporocysts each with four sporozoites characteristic of Isospora. The two sporocysts are ellipsoidal, 13–14 × 8–11 μm without a Stieda body but with a sporocyst residuum. The four sporozoites in each sporocyst are sausage-shaped with one pointed end (Fig. 5.6).
Fig. 5.6 Oocysts of Isospora suis.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
