Clinical signs: Light infections of less than 100 worms may cause poor weight gains and lowered egg production. Heavy infections often induce inappetence and emaciation.
Diagnosis: Because of the non-specific nature of the clinical signs and the fact that, in heavy infections, these may appear before Capillaria eggs are present in the faeces, diagnosis depends on necropsy and careful examination of the oesophagus and crop for the presence of the worms. This may be carried out by microscopic examination of mucosal scrapings squeezed between two glass slides; alternatively the contents should be gently washed through a fine sieve and the retained material resuspended in water and examined against a black background.
Pathology: Presence of the adult worms causes catarrhal inflammation and thickening of the oesophagus and crop wall. Heavy infections may cause diphtheritic inflammation and marked thickening of the wall.
Epidemiology: Young birds are most susceptible to Capillaria infections while adults may serve as carriers. The epidemiology is largely based on the ubiquity of the earthworm intermediate host.
Treatment: Levamisole in the drinking water is highly effective as are a number of benzimidazoles given in the feed. Elevated oral doses of these anthelmintics, administered over several days, also give high efficacy.
Control: Control depends on regular anthelmintic treatment accompanied, if possible, by moving the birds to fresh ground. Scrubbing and heat treatment of affected surfaces is essential as is the provision of fresh litter in chicken houses.
Notes: The taxonomic situation regarding many species of Capillaria is complex and recently it has been split into several genera; the old species names are listed with the new proposed generic names.
Capillaria contorta
See under Crop.
Several spiruroid worms are found in the oesophagus, crop and proventriculus of poultry. The life cycles of these parasites are indirect, involving a range of invertebrate hosts. Infections with these parasites are more common in free-ranging birds. Attempts to control the poultry spiruroids are unlikely to be successful because of the ready availability of the intermediate hosts.
Gongylonema ingluvicola
See under Crop.
Dispharynx nasuta
See under Proventriculus.
Tetrameres americana
See under Proventriculus.
Trichomonas gallinae
Synonym: Cercomonas gallinae, Trichomonas columbae
Common name: Canker, frounce, roup
Predilection site: Oesophagus, crop, proventriculus
Fig. 7.2 Trichomonas gallinae.
Parasite class: Zoomastigophorasida
Family: Trichomonadidae
Description: The body is elongate, ellipsoidal or pyriform, 5–19 × 2–9 μm, with four anterior flagella that arise from the blepharoplast (Fig. 7.2). The undulating membrane does not reach the posterior end of the body and a free posterior flagellum is absent. An accessory filament is present. The axostyle is narrow, protrudes 2–8 μm from the body and its anterior portion is flattened into a spatulate capitulum. There is a crescent-shaped pelta anterior to the axostyle and there is no chromatic ring at its point of emergence. The parabasal body is hook-shaped and has a parabasal filament and the costa is a very fine rod running three quarters the length of the body.
Hosts: Pigeon, turkey, chicken, raptors (hawks, falcons, eagles)
Life cycle: The trichomonads reproduce by longitudinal binary fission. No sexual stages are known and there are no cysts.
Geographical distribution: Worldwide
Pathogenesis: In the turkey and chicken lesions most commonly occur in the crop, oesophagus, pharynx and are uncommon in the mouth.
Clinical signs: Severely affected birds lose weight, stand huddled with ruffled feathers, and may fall over when forced to move. Yellow, necrotic lesions are present in the oesophagus and crop and a greenish fluid containing large numbers of trichomonads may be found in the mouth.
Diagnosis: The clinical signs are pathognomonic and can be confirmed by identifying the characteristic motile trichomonads from samples taken from lesions in the mouth or from fluid.
Pathology: The early lesions in the pharynx, oesophagus and crop are small, whitish to yellowish caseous nodules. These grow in size and may remain circumscribed and separate, or may coalesce to form thick, caseous, necrotic masses that may occlude the lumen. The circumscribed disk-shaped lesions are often described as ‘yellow buttons’. The lesions in the liver, lungs and other organs are solid, yellowish, caseous nodules up to 1 cm or more in diameter.
Epidemiology: Turkeys and chickens are infected through drinking contaminated water, the source of contamination being feral pigeons and other wild birds, which also use the water source. Trichomonads enter the water from the mouths, not the faeces, of the wild birds. T. gallinae has no cysts and is very sensitive to drying, so direct contamination is necessary.
Treatment: Nitroimidazole compounds, such as dimetridazole and metronidazole, are effective, but their availability has declined in many countries through legislative changes and toxicity concerns.
Control: Control in chickens and turkeys, depends on preventing access of wild pigeons to drinking water.
CROP
Gongylonema ingluvicola
Common name: Gullet worm
Predilection site: Crop, oesophagus and occasionally proventriculus
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Long, slender worm. The female worm is 32–55 mm long and the males measure around 18 mm.
Description, microscopic: Easily distinguished microscopically by the presence of longitudinal rows of round or oval, cuticular bosses in the anterior region of the body. The eggs measure approximately 58 × 35 μm.
Final hosts: Chicken, turkey, partridge, pheasant, quail
Intermediate hosts: Cockroaches (Blatella germanica) and beetles of the species Copris minutus
Life cycle: The life cycle is typically spiruroid. Eggs are passed in faeces and, when eaten by an intermediate host, they hatch and develop to the infective stage within about 30 days. Infection of the definitive host is through the ingestion of infected cockroaches. The adult worms live spirally (in a zipper fashion) embedded in the mucosa or submucosa of the crop with their anterior and/or posterior ends protruding into the lumen. The prepatent period is about 8 weeks.
Geographical distribution: North America, Asia, Africa, Australia and Europe
Pathogenesis: The adult parasites are moderately pathogenic, depending on the number of worms embedded in the epithelium.
Clinical signs: Light infections are often asymptomatic. Heavier infections may produce regurgitation.
Diagnosis: Usually an incidental finding on postmortem.
Pathology: Heavy infections in fowl can induce hypertrophy and cornification of the epithelium of the crop.
Gongylonema crami
Predilection site: Crop
Parasite class: Nematode
Superfamily: Spiruroidea
Final host: Chicken
Details are essentially similar to Gongylonema ingluvicola
Trichomonas gallinae
See under Oesophagus.
Capillaria contorta
Synonym: Eucoleus contorta
Predilection site: Oesophagus, crop
Parasite class: Nematoda
Superfamily: Trichuroidea
Description: General description as for other Capillaria species. Males measure around 12–17 mm and females 27–38 mm. Eggs are 48–56 × 21–24 μm.
Final hosts: Chicken, turkey, pheasant, partridge, duck and wild birds
Intermediate hosts: Earthworms.
Life cycle: C. contorta appears to be able to develop both directly and indirectly. In the direct life cycle, the infective L1 develops within the egg in about 3–4 weeks. Infection of the final host is through ingestion of this embryonated infective stage, development to adult worms occurs without a migration phase. In the indirect life cycle, the egg requires to be ingested by an earthworm in which it hatches, the final host being infected by ingestion of the earthworm. The prepatent period is about 3–4 weeks in the final host.
Geographical distribution: Worldwide
Clinical signs: Low infections are frequently asymptomatic, possibly causing some reduction in growth and lower egg production. Severely infected birds often become anaemic, weak and emaciated.
Pathology: Large numbers of worms produce an inflammation varying from catarrhal to diphtheritic.
Epidemiology: Young birds are most susceptible to Capillaria infections while adults may serve as carriers. C. contorta is important since, having a direct life cycle, it occurs indoors in birds kept on deep litter and outdoors in free-range systems, allowing large numbers of infective eggs to accumulate.
Control: Control depends on regular anthelmintic treatment accompanied if possible by moving the birds to fresh ground. Scrubbing and heat treatment of affected surfaces is essential as is the provision of fresh litter in chicken houses.
Details of the pathogenesis, diagnosis and treatment are as for C. annulata.
Capillaria annulata
See under Oesophagus.
PROVENTRICULUS
Tetrameres americana
Synonym: Tropisurus americana
Common name: Globular roundworm
Predilection site: Proventriculus
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: The adults show sexual dimorphism. The males are pale white, slender, and only about 5–6 mm long. The females are bright red and almost spherical, with a diameter of about 3.5–5.0 mm (Fig. 7.3).
Description, microscopic: Males have spiny cuticles and no cordons; females have four longitudinal deep furrows on the surface. Eggs are thick-shelled, 42–50 × 24 μm and embryonated when passed.
Final hosts: Chicken, turkey, duck, geese, grouse, quail, pigeon
Fig. 7.3 Adult female Tetrameres americana.
Intermediate hosts: Cockroaches, grasshoppers and beetles
Life cycle: Eggs are shed with the faeces and hatch when eaten by an intermediate host. The final host becomes infected following ingestion of the intermediate host and the males and females locate in the glands of the proventriculus. Males inhabit the mucosal surface and upper regions of the glands but after mating the males leave the glands and die. The females are embedded deep in the mucosal glands.
Geographical distribution: Commonly occurs in Africa and North America
Pathogenesis: The females in the glands of the proventriculus are bloodsuckers, and can cause anaemia as well as local erosion. Heavy infections may be fatal in chicks, but this genus is usually present only in moderate numbers and is well tolerated. The migration of juvenile stages into the wall of the proventriculus can cause inflammation and thickening.
Clinical signs: Infected fowl may become anaemic and lose condition. Heavy infections, particularly in young chickens, can induce thickening of the proventriculus with oedema and in some instances this can lead to partial blockage of the lumen. Heavy infections can be fatal.
Diagnosis: At necropsy, the female Tetrameres appear as dark red spots when viewed from the serosal surface of the proventriculus.
Pathology: The wall of the proventriculus may be thickened to an extent that the lumen is almost obliterated.
Table 7.1 Species of Tetrameres found in poultry.
Epidemiology: Infection is more common in free-ranging birds.
Tetrameres fissispina
Synonym: Tropisurus fissispina
Predilection site: Proventriculus
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: See T. americana. Males are pale white, slender and 3–6 mm long. The females are bright red, ovoid/spherical, with a diameter varying from around 1.5–6 mm.
Description, microscopic: Males have four longitudinal rows of spines along the median and lateral lines and no cordons; females have four longitudinal deep furrows on the surface. Eggs are thick-shelled, 48–56 × 26–30 μm and embryonated when passed.
Final hosts: Duck, goose, chicken, turkey, pigeon and wild aquatic birds
Intermediate hosts: Aquatic crustaceans, such as Daphnia and Gammarus, grasshoppers, earthworms
Geographical distribution: Most parts of the world
Details of the life cycle, pathogenesis, clinical signs, diagnosis and pathology are as for T. americana.
Tetrameres crami
Predilection site: Proventriculus
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: See T. americana. Males are white, slender and about 4 mm long. The red ovoid/spherical females measure around 2 × 1.5 mm.
Final hosts: Domestic and wild duck
Intermediate hosts: Amphipods such as Gammarus fasciatus and Hyalella knickerbockeri
Geographical distribution: North America
All other details are similar to T. americana.
Several other species of Tetrameres found in poultry are listed in Table 7.1. Details on pathogenicity in the host species are essentially similar to T. americana.
Dispharynx nasuta
Common name: Spiral stomach worm
Synonym: Dispharynx spiralis, Acuaria spiralis
Predilection site: Oesophagus, proventriculus
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: The body is slender and coiled, particularly the posterior of the male. Males measure up to around 8 mm long and the females 10 mm.
Description, microscopic: The cuticle is ornamented with four wavy cordons that recurve anteriorly and do not fuse. The left spicule is slender and the right spicule shorter and oval-shaped. The eggs are thick-shelled, 33–40 × 18–25 μm and embryonated when passed.
Final hosts: Chicken, turkey, pigeon, guinea fowl, grouse, pheasant and other birds
Intermediate hosts: Various isopods such as sowbugs (Porcellio scaber) and pillbugs (Armadillidium vulgare)
Life cycle: Typically spiruroid. The intermediate host ingests embryonated eggs and development to the L3 takes place in the body cavity. When the isopod is consumed by the final host, the worms develop to the final stage in the proventriculus or oesophagus.
Geographical distribution: Asia, Africa and the Americas
Pathogenesis: Mild infections usually provoke only a slight nodular inflammatory reaction in the mucosa with excessive mucus production.
Clinical signs: Most mild infections with Dispharynx are inapparent. Heavily infected young birds can rapidly lose weight, become emaciated and anaemic. Deaths can be high.
Diagnosis: A tentative diagnosis is based on the presence of spiruroid eggs, which are difficult to differentiate. Species identification is usually based on morphological identification of adult worms on postmortem.
Pathology: In severe infections, deep ulcers and hypertrophy can occur in the mucosa of the proventriculus in which the anterior ends of the worms are embedded.
Echinuria uncinata
Synonym: Acuaria uncinata
Predilection site: Oesophagus, proventriculus, gizzard
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: The body is slender and males measure 8–10 mm long and the females 12–18.5 mm.
Description, microscopic: The cuticle is ornamented with four wavy cordons that are non-recurrent and they anastomose in pairs. There are four pairs of pre-cloacal papillae in two groups of two either side, and four pairs of post-cloacal papillae. The left spicule is longer than the right spicule. The eggs are thick-shelled, 37 × 20 μm and embryonated when passed.
Final hosts: Duck, goose, swan and various aquatic birds
Intermediate hosts: Daphnia and Gammarus
Life cycle: Typically spiruroid. Eggs are passed in the faeces and ingested by water fleas in which they hatch and develop to infective larvae. The parasites continue development when the intermediate host is ingested by an aquatic bird.
Geographical distribution: Worldwide
Pathogenesis: The worms can cause an inflammation of the alimentary tract and the formation of caseous nodules. These nodules can be very large in the gizzard and proventriculus and interfere with the passage of food.
Clinical signs: Infected birds may become weak and emaciated and deaths have been reported.
Hystrichis tricolour
Predilection site: Proventriculus, oesophagus
Parasite class: Nematoda
Superfamily: Dioctophymatoidea
Description, gross: Adult female worms measure up to about 4 cm and males 2.5 cm in length.
Description, microscopic: The cephalic area is expanded, and possesses many regularly positioned spines. The eggs are thick-shelled, coated with tubercles and have truncated poles.
Final hosts: Domestic and wild ducks and anatid birds
Intermediate hosts: Oligochaetes (annelids)
Life cycle: This is indirect. Fowl and other birds become parasitised through ingestion of infected oligochaetes. The adult worms are deeply embedded in the mucosa with their caudal and cephalic regions lying within the lumen of the tract. The prepatent period is around 2 weeks.
Geographical distribution: The extent of the distribution is not known but it occurs occasionally in Europe
Pathogenesis: The parasite induces nodule formation (pea-sized tumours) on the wall of the proventriculus and oesophagus. Sometimes these can perforate to the pleural cavity.
Clinical signs: Low infections are usually asymptomatic but heavy burdens can induce emaciation.
Eustrongyloides papillosus
Predilection site: Oesophagus, proventriculus
Parasite class: Nematoda
Superfamily: Dioctophymatoidea
Description, gross: Females measure about 3 cm in length.
Description, microscopic: The male has a bursal cup with a fringed margin. Eggs are 68 × 38 μm.
Final hosts: Duck, goose
Intermediate hosts: Not known, possible oligochaetes
Life cycle: This is not fully known but oligochaetes are likely to be involved as intermediate hosts and various fish as paratenic hosts.
Geographical distribution: Many parts of the world
Pathogenesis: Generally considered to be of low pathogenicity and of little veterinary significance, although the parasites can induce the formation of nodules in the wall of the anterior digestive tract.
Trichomonas gallinae
See under Oesophagus.
For treatment and control, see under Gizzard.
GIZZARD
Several species of gizzard worms are found in ducks and geese. The following applies to all species.
Life cycle: Direct and similar to other strongyles. Infection is via ingestion of L3, or through skin penetration. Eggs passed in the faeces are already embryonated and develop to the L3 in the egg. Ingested larvae penetrate the submucosa of the gizzard. Patency is around 2–3 weeks in geese.
Pathogenesis: Adult birds may not show clinical symptoms but act as carriers. These parasites found in the upper alimentary tract, particularly the gizzard, may cause heavy mortality in goslings, ducklings and other young aquatic fowls. Young goslings and ducklings are particularly susceptible. The worms burrow into the mucosa of the gizzard, cause irritation and ingest blood.
Clinical signs: Young fowl may become inappetent, and show diarrhoea and anaemia. Over time the birds become emaciated, weak and, where heavily infected, fatalities can occur. Often older fowl show few clinical signs but act as reservoirs of infection.
Diagnosis: At necropsy, worms may be recovered from the mucosa of the gizzard following incubation in warm saline for 1–2 hours. Amidostomum spp are the main trichostrongyloids of the gizzard, which possess a buccal capsule.
Pathology: Severe infections induce haemorrhages on the gizzard mucosa, which may be accompanied by catarrhal inflammation. Heavy infections can cause necrosis of the horny lining of the gizzard, forming reddish brown loose folds containing many embedded worms.
Epidemiology: The infective L3 requires adequate moisture, such as pond margins, to survive, as they are very susceptible to desiccation.
Treatment: Treatment with one of the modern benzimidazoles or levamisole, often administered in feed or drinking water, is effective.
Control: Gizzard worm infection may be prevented by ensuring that birds do not run on the same ground each year. It is important to restrict access of wild aquatic fowl to areas where geese are raised.
Amidostomum anseris
Synonym: Amidostomum nodulosum
Common name: Gizzard worm
Predilection site: Gizzard, occasionally proventriculus, oesophagus
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description, gross: The slender adult worms, bright red in colour when fresh, and up to 2.5 cm in length, are easily recognised at necropsy where they predominate in the horny lining of the gizzard. Males measure about 10–17 mm and females 15–25 mm.
Description, microscopic: Characterised by a shallow buccal capsule with three pointed teeth, the middle one being the largest. The male spicules are of equal length and are divided into two branches at the posterior. Eggs are thin-shelled, ellipsoidal and measure around 100 × 60 μm.
Hosts: Domestic and wild goose, duck and other aquatic fowl
Geographical distribution: Worldwide
Amidostomum skrjabini
Common name: Gizzard worm
Predilection site: Gizzard, occasionally proventriculus, oesophagus
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description: Similar to A. anseris in possessing a shallow buccal capsule with small teeth. The hatched L3 require about 5 days in the environment before they are fully infective.
Hosts: Domestic and wild duck
Geographical distribution: Worldwide
Epomidiostomum anatinum
Synonym: Epomidiostomum uncinatum, Strongylus uncinatus, Amidostomum anatinum
Common name: Gizzard worm
Predilection site: Gizzard
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description, gross: The body is filiform with a very fine tapering anterior region and yellowish white in colour. Males measure around 6 mm, and females are approximately 10 mm in length.
Description, microscopic: The mouth is surrounded by four protruding papillae. The cuticle bears two lateral epaulets, the posterior edge of which forms a three-toothed fringe. The dark brown spicules are of equal length and the tip comprises three branches. A gubernaculum is absent. The tail of the female has a conical appendage with a small rounded tip. Eggs measure about 80 × 50 μm.
Hosts: Domestic and wild goose, duck and other aquatic fowl
Geographical distribution: Many parts of the world, especially North America, Africa, Asia and Europe
Notes: A similar species, Epomidiostomum crami, is found in Canada geese (Branta canadensis) and bluewinged geese (Chen coeruleus) in North America.
Epomidiostomum orispinum
Synonym: Strongylus anseris, Strongylus orispinum.
Common name: Gizzard worm
Predilection site: Gizzard and oesophagus
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description, gross: Males measure around 11 mm and females 16 mm in length.
Description, microscopic: The anterior of the worm possesses four posteriorly pointing offshoots and lateral festoons bearing a pair of papillae. Spicules are equal with three shafts pointing distally. The body of the female tapers abruptly, towards the digitate tail.
Hosts: Duck, goose and swan
Geographical distribution: Africa, Europe
Epomidiostomum skrjabini
Common name: Gizzard worm
Predilection site: Gizzard
Parasite class: Nematoda
Superfamily: Trichostrongyloidea
Description, gross: The size of the males and females is similar to that of E. orispinum.
Description, microscopic: The head of the worm possesses a cuticular prominence which is armed with four symmetrical, lateral-pointing spines. There are also two epaulet formations.
The mouth is surrounded by four small spines. The bursa has three lobes, the central lobe being poorly developed. Spicules are equal and the posterior ends are split into three sharp-tipped branches. The anterior ends are blunt. The female tail terminates in a fingerlike appendage, which is bent venterally.
Hosts: Domestic and wild goose
Geographical distribution: Russia
Cheilospirura hamulosa
Synonym: Acuaria hamulosa
Predilection site: Gizzard
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Males measure up to 15 mm and females 30 mm.
Description, microscopic: The worms have four wavy irregular cuticular cordons that extend to more than half the length of the body. The males have four pairs of pre-cloacal and six pairs of post-cloacal papillae, a short flattened spicule on the right and a longer slender spicule on the left side. Eggs are embryonated when passed.
Final hosts: Chicken, turkey
Intermediate hosts: Grasshoppers (Melanoplus), weevils and beetles
Life cycle: Eggs shed in the faeces are ingested by the intermediate host where they develop to the infective stage in about 3 weeks. The final host becomes infected after consuming this intermediate host and the prepatent period is about 3 weeks.
Geographical distribution: Worldwide, in particular Europe, Africa, Asia and the Americas
Pathogenesis: Generally, mild to moderate infections are considered to be of low pathogenicity. In heavy infections, many adult worms penetrate under the keratinised layer of the gizzard where they are found embedded in soft orangy-coloured nodules. The keratinised layer of the gizzard may become necrotic and rupture of the gizzard can occur.
Clinical signs: Mild infections are usually asymptomatic. Severe infections can lead to emaciation, weakness and anaemia.
Diagnosis: This is best achieved through autopsy of an affected chicken, as the eggs of several species of Cheilospirura appear very similar.
Pathology: In mild infections, the worms are noticed only if the horny lining of the gizzard is removed, and are found in soft, yellowish red nodules. In severe cases, the horny lining may be partly destroyed, with the worms found below the necrotic material within the altered musculature of the gizzard.
Other species of spiruroid worms found in the gizzard are considered to be of minor significance.
Histiocephalus laticaudatus
Parasite class: Nematoda
Superfamily: Spiruroidea
Hosts: Chicken
Life cycle: Little is known of the life cycle
Geographical distribution: Europe
Streptocara spp
Parasite class: Nematoda
Superfamily: Spiruroidea
Final hosts: Chicken, turkey, duck, goose
Intermediate hosts: Crustaceans (Daphnia, Gammarus)
SMALL INTESTINE
Ascaridia galli
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: The worms are stout and densely white, the females measuring up to 12.0 cm in length (Fig. 7.4). Ascaridia is by far the largest nematode of poultry.
Description, microscopic: The egg is distinctly oval, with a smooth shell, and cannot easily be distinguished from that of the other common poultry ascaridoid, Heterakis.
Hosts: Chicken, turkey, goose, duck, guinea fowl and a number of wild gallifrom birds
Life cycle: The egg becomes infective at optimal temperatures in a minimum of 3 weeks and the parasitic phase is non-migratory, consisting of a transient histotrophic phase in the intestinal mucosa after which the adult parasites inhabit the lumen of the intestine. The egg is sometimes ingested by earthworms, which may act as transport hosts. Eggs can remain viable for several months under moist cool conditions but are killed by a dry hot environment. The prepatent period ranges from 4–6 weeks in chicks to 8 weeks or more in adult birds. The worms live for about 1 year.
Fig. 7.4 Adult worms of Ascaridia galli.
Geographical distribution: Worldwide
Pathogenesis: Ascaridia is not a highly pathogenic worm, and any effects are usually seen in young birds of around 1–2 months of age, adults appearing relatively unaffected. The main effect is seen during the prepatent phase, when the larvae are in the duodenal/intestinal mucosa. There they cause enteritis, which is usually catarrhal, but in very heavy infections may be haemorrhagic. In moderate infections the adult worms are tolerated without clinical signs, but when considerable numbers are present the large size of these worms may cause intestinal occlusion and death. Nutritional deficiency may predispose birds to the establishment of infection.
Clinical signs: Heavily infected birds may become anaemic and show intermittent diarrhoea, anorexia, later becoming unthrifty and emaciated. This can lead to a decrease in egg production.
Diagnosis: In infections with adult worms, the eggs will be found in faeces, but since it is often difficult to distinguish these from the slightly smaller eggs of Heterakis, confirmation must be made by postmortem examination of a casualty when the large white worms will be found. In the prepatent period, larvae will be found in the intestinal contents and in scrapings of the mucosa.
Pathology: Enteritis or haemorrhagic enteritis may be seen when large numbers of young parasites penetrate the duodenal or jejunal mucosa. The embedded larvae cause haemorrhage and extensive destruction of the glandular epithelium, and proliferation of mucous-secretory cells may result in adhesion of the mucosal villi. Damage to the epithelia may not only be caused by the larvae, but also by the adult worms in the form of pressure atrophy of the villi with occasional necrosis of the mucosal layer. In chronic infections a loss of muscle tonus may be seen, and the intestinal wall may assume a flabby appearance. During the histotropic phase, there is loss of blood, reduced blood sugar and the ureters frequently become distended with urates.
Epidemiology: Adult birds are symptomless carriers, and the reservoir of infection is on the ground, either as free eggs or in earthworm transport hosts. Infection is heaviest in young chicks.
Treatment: Treatment with piperazine salts, levamisole or a benzimidazole, such as flubendazole, mebendazole or fenbendazole, can be administered in the feed (30 ppm over 7 days; 60 ppm over 7 days; 60 ppm over 3 days, respectively). Levamisole is effective at 30 mg/kg given orally, or 300 ppm in the feed.
Control: When birds are reared on a free-range system, and ascaridiosis is a problem, the young birds should, if possible, be segregated and reared on ground previously unused by poultry. Rotation of poultry runs is advisable. Since the nematode may also be a problem in deep litter houses, feeding and watering systems which will limit the contamination of food and water by faeces, should be used.
Ascaridia dissimilis
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: The worms are stout and densely white, and 3–7 cm in length
Description, microscopic: The egg is distinctly oval, with a smooth shell, and 80–95 μm in size.
Hosts: Turkey
Life cycle: The parasitic phase is non-migratory, consisting of a transient histotrophic phase in the intestinal mucosa after which the adult parasites inhabit the lumen of the intestine. The egg is sometimes ingested by earthworms, which may act as transport hosts. The prepatent period is 6 weeks.
Geographical distribution: Presumed worldwide
Pathogenesis: Considered non-pathogenic
Clinical signs: Moderate infections are frequently inapparent
Diagnosis: Adult worms may be found in the intestine on postmortem or the characteristic ascarid eggs may be seen in faeces.
Pathology: No associated pathology
Epidemiology: Adult birds are symptomless carriers, and the reservoir of infection is on the ground, either as free eggs or in earthworm transport hosts.
Treatment: Not usually required, although treatment with piperazine salts, levamisole or a benzimidazole, such as fenbendazole, is effective.
Control: Strict hygiene and feeding and watering systems, which will limit the contamination of food and water by faeces, should be used
Porrocaecum crassum
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: The worms are reddish white in colour with males 12–30 mm and female worms 40–55 mm.
Description, microscopic: The tail of the male is conical and there are no caudal alae. The egg is ellipsoidal, and 110 × 85 μm in size.
Hosts: Domestic and wild duck
Life cycle: Similar to other ascarid species
Geographical distribution: Presumed worldwide
Pathogenesis: Considered non-pathogenic
Contracaecum spiculigerum
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Ascaridoidea
Description, gross: Males worms are 32–45 mm and female worms 24–64 mm.
Description, microscopic: An oesophageal appendix is present. The egg is spherical, and 50–52 μm in size.
Hosts: Duck, goose, swan and other waterfowl
Life cycle: Similar to other ascarid species
Geographical distribution: Presumed worldwide
Pathogenesis: Considered non-pathogenic
Capillaria caudinflata
Synonym: Aonchotheca caudinflata
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Trichuroidea
Description: See C. annulata. Males measure around 6–12 mm and females up to 25 mm. Females have a characteristic vulval appendage.
Final hosts: Chicken, turkey, goose, pigeon and wild birds
Intermediate hosts: Earthworms
Life cycle: The life cycle of this species is indirect.
Geographical distribution: Worldwide.
Pathogenesis: The anterior ends of the worms are embedded in the mucosa. Light infections can produce a catarrhal inflammation; heavy infections may cause a haemorrhagic enteritis with bloody diarrhoea.
Clinical signs: Heavy infections often induce anaemia and the birds become weak and emaciated.
Capillaria bursata
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Trichuroidea
Description, gross: See C. annulata. Males measure around 6–12 mm and females up to 25 mm.
Final hosts: Chicken, turkey, pheasant and wild birds
Intermediate hosts: Earthworms
Life cycle: The life cycle of this species is indirect.
Geographical distribution: Worldwide
Capillaria obsignata
Synonym: Baruscapillaria obsignata, Capillaria columbae
Predilection site: Small intestine
Parasite class: Nematoda
Superfamily: Trichuroidea
Description, gross: See C. annulata. Males measure around 10–12 mm and females up to 15 mm.
Description, microscopic: Eggs are barrel-shaped and colourless, 48–53 × 24 μm in size and have thick shells that are slightly striated with bipolar plugs.
Hosts: Pigeon, chicken, turkey, pheasant and wild birds
Life cycle: This species has a direct life cycle. The infective L1 develops within the egg in about 7–10 days. Infection of the final host is through ingestion of this embryonated infective stage, development to adult worms occurs without a migration phase. The prepatent period is around 3 weeks.
Geographical distribution: Worldwide
Pathogenesis: C. obsignata can be highly pathogenic in chickens and pigeons, leading to mortalities. Birds become listless, emaciated and diarrhoeic.
Epidemiology: Young birds are most susceptible to Capillaria infections while adults may serve as carriers. C. obsignata is important since, having a direct life cycle, it occurs indoors in birds kept on deep litter and outdoors in free-range systems, allowing large numbers of infective eggs to accumulate.
Details of the diagnosis, epidemiology, treatment and control for these species are as for C. annulata.
Hartertia gallinarum
Predilection site: Small intestine, gizzard
Parasite class: Nematoda
Superfamily: Spiruroidea
Description, gross: Slender worms that are exceptionally long for a spiruroid. The males measure up to around 40 mm and the females 110 mm.
Description, microscopic: The gross appearance of the worms closely resembles that of Ascaridia galli; they have two lateral lips, each divided medially into three lobes. The male has lateral alae, ventral cuticular bosses, four pairs of pre-cloacal and two pairs of post-cloacal papillae. The left spicule is barbed and is larger than the blunt-ended right spicule. Eggs are thick-shelled, 45–53 × 27–33 μm and are embryonated when passed.
Final hosts: Chicken, bustards
Intermediate hosts: Termites
Life cycle: Typically spiruroid. Eggs are passed in faeces and, when ingested by a termite, develop to the infective stage in the body cavity. Following ingestion of an infected intermediate host the larvae develop to maturity in the final host in about 3 weeks.
Geographical distribution: Widespread in Europe, Africa and Asia. It is not found in the New World.
Pathogenesis: Infections are rarely fatal, but when large numbers of worms are present there may be inflammation of the intestine.
Clinical signs: Diarrhoea and emaciation may occur, often accompanied by a decrease in egg production.
Diagnosis: Differentiation of eggs in faeces is difficult as they are morphologically similar to those of other poultry spiruroids. Diagnosis is usually confirmed at necropsy.
Treatment: Not reported
Control: Where feasible, removal of termite nests from areas adjacent to runs used for poultry will be beneficial.
Tapeworms
Tapeworms are a feature of poultry which are reared on pasture, infection being acquired through ingestion of infected intermediate hosts, such as beetles, earthworms, ants, grasshoppers or flies. Infection is uncommon in intensive indoor systems as suitable intermediate hosts are usually absent. The most important and pathogenic species is Davainea proglottina which penetrates the duodenal mucosa and in young birds can induce a necrotic haemorrhagic enteritis which can be fatal. Raillientina echinobothrida is also pathogenic, inducing a hyperplastic enteritis and multiple caseous nodules where the scolex attaches to the wall of the intestine. Many other tapeworm species produce only mild symptoms, unless infections are heavy, when loss of productivity may be seen. Effective treatment of avian tapeworms is achieved with praziquantel, flubendazole, mebendazole, febantel or niclosamide. The dose rate and duration of administration varies between species of poultry. Control depends on the treatment of infected birds with a suitable anthelmintic and the destruction or removal of intermediate hosts where possible.
Davainea proglottina
Predilection site: Small intestine, particularly the duodenum
Parasite class: Cestoda
Family: Davaineidae
Description, gross: D. proglottina is a very small cestode up to 3–4 mm long, and unlike Amoebotaenia, usually possesses only four to nine segments (Fig. 7.5). Both the rostellum and suckers bear hooks.
Description, microscopic: The genital pores alternate regularly. Eggs measure about 30–40 μm and are found singly within the parenchymatous capsules in the gravid segment.
Final hosts: Chicken, turkey, pigeon and other gallinaceous birds
Intermediate hosts: Gastropod molluscs such as Agriolimax, Arion, Cepaea and Limax
Life cycle: Gravid proglottids are shed in faeces and eggs are ingested by various gastropod molluscs, in which they develop to the cysticercoid stage after about 3 weeks. Following ingestion of the mollusc by the final host, the cysticercoids develop into adult tapeworms in about 2 weeks.
Fig. 7.5 Davainea proglottina adult.
Geographical distribution: Most parts of the world
Pathogenesis: This is the most pathogenic of the poultry cestodes, the doubly armed scolex penetrating deeply between the duodenal villi. Heavy infections may cause haemorrhagic enteritis, and light infections retarded growth and weakness.
Clinical signs: Moderate infections can lead to reduced weight gain, innapetance and lowered egg production. Large numbers of parasites may induce emaciation, dyspnoea and even be fatal.
Diagnosis: This is best achieved at necropsy through microscopic examination of mucosal scrapings from the duodenum and anterior small intestine. The tapeworm can easily be overlooked due to its minute size.
Pathology: The mucosal membranes are thickened and haemorrhagic with localised patches of necrosis. Fetid mucus may be present.
Epidemiology: Infection can be common in free-range fowl as suitable intermediate hosts are often available. Young birds tend to be more severely affected than older fowl.
Raillientina cesticillus
Synonym: Skrjabinia cesticillus
Predilection site: Small intestine
Parasite class: Cestoda
Family: Davaineidae
Description, gross: A medium-size tapeworm reaching around 10–14 cm in length, but often shorter.
Description, microscopic: The broad scolex is large and the rostellum wide. The unarmed suckers are not prominent and the rostellum is armed with several hundred small hammer-shaped hooks arranged in a double row. The gravid proglottids contain several, thin-walled egg capsules, each housing a single egg. Eggs measure approximately 75 × 90 μm.
Final hosts: Chicken, turkey, guinea fowl
Intermediate hosts: Various genera of beetles, including the families Carabidae, Scarabaeidae, Tenebrionidae, and the meal beetles, Tribolium spp.
Life cycle: Gravid proglottids are passed in faeces and eggs are ingested by various intermediate hosts. The embryo hatches from the egg in the intestine and then changes into a cysticercoid in the body cavity. Following ingestion by the final host the activated cysticercoid attaches to the mucosa of the anterior or mid small intestine. The prepatent period is around 2–3 weeks.
Geographical distribution: Worldwide
Pathogenesis: Heavy infections can induce a catarrhal enteritis.
Clinical signs: Reduction in growth rate. Heavy infection can lead to emaciation and weakness.
Diagnosis: This is best achieved at necropsy through microscopic examination of mucosal scrapings from the small intestine.
Pathology: In heavy infections, the embedded scolices of this parasite can produce caseous nodules in the wall of the small intestine.
Epidemiology: Young birds are usually more susceptible to infection than adults. Infection rates depend on the availability of the intermediate hosts. Beetles are numerous for free-range fowl but some beetles may also breed in litter bedding. Eggs are reasonably resistant to environmental conditions and will survive for several months.
Raillietina echinobothrida
Common name: Nodular tapeworm disease
Predilection site: Small intestine
Parasite class: Cestoda
Family: Davaineidae
Description, gross: Raillietina echinobothrida, which may be up to 25 cm in length, is similar in shape to R. tetragona. The suckers are circular and the rostellum is well endowed with two rows of hooks.
Description, microscopic: The gravid proglottids contain multiple fibrous-walled egg capsules, each housing several eggs. Eggs measure approximately 75 × 95 μm.
Final hosts: Chicken, turkey and other fowl.
Intermediate hosts: Ants of the genera Pheidole and Tetramorium
Life cycle: See R. cesticillus. The prepatent period is around 3 weeks.
Geographical distribution: Worldwide
Pathogenesis: A hyperplastic enteritis may occur at the site of attachment.
Pathology: R. echinobothrida is more pathogenic than either R. cesticillus or R. tetragona. In heavy infections, the embedded scolices of this parasite produce large caseous nodules in the subserous and muscular layers of the wall of the posterior small intestine.
Notes: The lesions in the intestine are similar to those associated with avian tuberculosis.
Raillietina tetragona
Predilection site: Posterior half of small intestine
Parasite class: Cestoda
Family: Davaineidae
Description, gross: A large tapeworm reaching around 20–25 cm in length. The scolex is smaller than that of R. echinobothridia.
Description, microscopic: The oval suckers are armed and the rostellum bears one or two rows of hooks (Fig. 7.6). The gravid proglottids contain multiple fibrous-walled egg capsules, each housing many eggs. Eggs measure approximately 65 × 90 μm. R. tetragona has a larger number of egg capsules in the gravid proglottid than either R. cesticillus or R. echinobothrida.
Final hosts: Chicken, guinea fowl and pigeon
Intermediate hosts: Ants of the genera Pheidole and Tetramorium
Life cycle: See R. cesticillus. The prepatent period is around 2–3 weeks.
Geographical distribution: Worldwide
Pathogenesis: In heavy infections, the embedded scolices of this parasite produce large caseous nodules in the wall of the small intestine
Pathology: R. tetragona is usually less pathogenic than either R. echinobothrida or R. cesticillus.
Cotugnia digonopora
Predilection site: Small intestine
Parasite class: Cestoda
Fig. 7.6 Raillientina tetragona: scolex and proglottids.
Family: Davaineidae
Description, gross: The tapeworm is up to 110 mm long. The suckers are large, unarmed and the proglottids are wider than long.
Description, microscopic: The head is large with a small rudimentary retractile rostellum, which is armed with two rows of small hooklets. Segments possess a double set of genital organs.
Final host: Chicken
Life cycle: The life cycle is unknown.
Geographical distribution: Europe, Asia, Africa
Amoebotaenia sphenoides
Synonym: Amoebotaenia cuneata
Predilection site: Small intestine
Parasite class: Cestoda
Family: Dilepididae
Description, gross: A small tapeworm, up to 4.0 mm long, with up to 20 proglottids. It is roughly triangular in shape, although the last few segments decrease in size.
Description, microscopic: The rostellum bears a single row of 14 hooks.
Final hosts: Chicken
Intermediate hosts: Earthworms, particularly Allolobrophora, Helodrilus, Ocnerodrilus and Pheretina species
Geographical distribution: Most parts of the world
Pathogenesis: Generally considered to be of low pathogenic significance.
Choanotaenia infundibulum
Predilection site: Upper small intestine
Parasite class: Cestoda
Family: Dilepididae
Description, gross: A relatively large tapeworm up to around 20 cm in length and 1.5–3 mm in width. Each segment is wider posteriorly, giving the margin of the tapeworm a ‘saw-edge’ appearance.
Description, microscopic: The rostellum is ringed with about 18 slender hooks. The genital pores alternate regularly. Eggs measure about 45 × 55 μm and possess a long distinctive filament.
Final hosts: Chicken, turkey and several wild game birds
Intermediate hosts: The housefly, Musca domestica, beetles of the genera Aphodius, Calathus, Geotrupes and Tribolium, and grasshoppers
Geographical distribution: Most parts of the world
Metroliasthes lucida
Predilection site: Small intestine
Parasite class: Cestoda
Family: Dilepididae
Description, gross: The tapeworm is about 20 cm long and 1.5 mm wide.
Description, microscopic: The scolex has no rostellum or hooks and the suckers are devoid of spines.
Final hosts: Chicken, turkey
Intermediate hosts: Grasshoppers (Chorthippus, Paroxya, Melanopus)
Geographical distribution: North America, India, Africa
Hymenolepis carioca
Predilection site: Small intestine.
Parasite class: Cestoda
Family: Hymenolepididae
Description, gross: This is a slender thread-like tapeworm, reaching a length of up to 8 cm.
Description, microscopic: The scolex is unarmed.
Final hosts: Chicken, turkey and other fowl
Intermediate hosts: Dung and flour beetles and sometimes Stomoxys spp
Life cycle: The prepatent period is 3–4 weeks.
Geographical distribution: Most parts of the world, common in the USA
Pathogenesis: Usually considered to be of low pathogenicity.
Clinical signs: Large numbers of tapeworms may cause diarrhoea.
Hymenolepis cantaniana
Common name: Branching tapeworm
Predilection site: Small intestine
Parasite class: Cestoda
Family: Hymenolepididae
Description, gross: A slender tapeworm, reaching a length of up to 2 cm.
Final hosts: Chicken, turkey, pheasant, quail and other fowl
Intermediate hosts: Beetles (Scarabeidae)
Life cycle: The prepatent period is 3–4 weeks.
Geographical distribution: Most parts of the world, particularly Europe, Africa and the USA
Hymenolepis lanceolata
Synonym: Drepanidotaenia lanceolatum
Predilection site: Small intestine
Parasite class: Cestoda
Family: Hymenolepididae
Description, gross: This is a slender tapeworm, reaching up to 15–20 cm in length.
Description, microscopic: The proglottids are usually wider than they are long.
Final hosts: Duck and goose
Intermediate hosts: Aquatic copepod crustaceans
Life cycle: The prepatent period is 3–4 weeks.
Geographical distribution: Cosmopolitan
Pathogenesis: Heavy infections can be fatal.
Clinical signs: Large numbers of tapeworms may cause diarrhoea.
Pathology: Moderate to heavy infections can induce a catarrhal enteritis and necrosis of the mucosa.
Fimbriaria fasciolaris
Predilection site: Small intestine
Parasite class: Cestoda
Family: Hymenolepididae
Description, gross: The adult tapeworms measure up to about 4 cm in length by 1.5 mm in width.
Description, microscopic: The scolex possesses a ‘pseudoscolex’ (a folded expansion) for attachment to the host.
Final hosts: Chicken, duck, goose and wild anseriform birds
Intermediate hosts: Copepods (Cyclops and Diaptomus spp)
Intestinal flukes
Intestinal flukes are found in both the small and large intestines. The majority of avian intestinal trematodes parasitise aquatic fowl and birds and are of importance where birds forage in habitats that support the snail intermediate hosts.
Eggs passed in the faeces of infected birds hatch to produce a miracidium, which infects the first intermediate snail host. Subsequently cercariae encyst within the snail or are shed and migrate to infect other snails. Cercariae can also encyst in the kidneys of tadpoles and adult frogs. The final host is parasitised by ingesting the infected second intermediate host. The prepatent period is 1–2 weeks.
Large numbers of flukes can irritate the intestinal mucosa inducing a catarrhal, haemorrhagic enteritis and diarrhoea. Young birds are particularly susceptible to infection, showing progressive emaciation, and mortalities can be high. Various anthelmintics are available for treatment. Praziquantel or flubendazole, administered over several days, are effective in aquatic fowl. Niclosamide (not for geese) and fenbendazole are effective against Echinostomatidae.
Echinoparyphium recurvatum
Predilection site: Small intestine, particularly the duodenum
Parasite class: Trematoda
Family: Echinostomatidae
Description, gross: The fluke is about 4 × 0.7 mm and curved ventrally.
Description, microscopic: Spines are present anterior to the ventral sucker and the head-crown is armed with spines. Eggs measure about 110 × 82 μm.
Final hosts: Duck, goose, chicken and pigeon
Intermediate hosts: 1. Snails, such as Lymnaea spp and Planorbis spp. 2. Frogs, tadpoles, snails, such as Valvata piscinalis and Planorbis albus, freshwater clams and mussels
Geographical distribution: Worldwide, particularly Asia and North Africa
Pathogenesis: Heavy infections may induce weakness, anaemia and emaciation.
Pathology: A catarrhal enteritis is often present and the intestinal mucosa is oedematous.
Hypoderaeum conoideum
Predilection site: Posterior small intestine
Parasite class: Trematoda
Family: Echinostomatidae
Description, gross: The fluke measures around 7–12 mm in length and is up to 2 mm wide. The elongate body possesses spines in the anterior region and tapers towards the posterior.
Description, microscopic: The head-collar is small and armed with about 50 very small spines. Eggs measure about 102 × 65 μm.
Final hosts: Chicken, turkey, duck, goose, swan, pigeon and other aquatic birds
Intermediate hosts: As for E. recurvatum
Geographical distribution: Worldwide
Pathogenesis: Enteritis may occur where large numbers of flukes infect the intestine.
Other worms of the small intestine
Polymorphus boschadis
Synonym: P. minutus, Echinorhynchus polymorphus, Profilicollis
Common name: Thorny-headed worm
Predilection site: Small intestine
Parasite phylum: Acanthocephala
Family: Polymorphidae
Description, gross: Males measure around 3 mm and females up to 10 mm in length and are orange coloured when fresh. The anterior region possesses small spines and the cylindrical body has a constriction along its length, about one third from the head.
Description, microscopic: The proboscis has 16 rows of small hooks, their size increasing anteriorly. The spindle-shaped eggs have a thick middle shell and a thin outer shell, the embryo being slightly orange in colour. Eggs measure around 110 × 20 μm.
Final hosts: Duck, goose, chicken, swan and various wild aquatic birds
Intermediate hosts: Crustacean, Gammarus pulex, fresh water shrimp and sometimes the crayfish Potamobius astacus
Life cycle: The definitive host is infected following ingestion of an intermediate host that contains an infective cystacanth. The adult worm establishes in the posterior small intestine. The prepatent period is 3–4 weeks.
Geographical distribution: Worldwide
Pathogenesis: The worm produces inflammation of the intestinal mucosa and localised haemorrhages, which in heavy infection can induce anaemia.
Diagnosis: Identification of the characteristic eggs in faeces or the adult worms at necropsy.
Pathology: Worms use their armed proboscis to penetrate deep into the mucosa of the intestine and nodules frequently form at the point of attachment. Heavy infections can be fatal.
Filicollis anatis
Common name: Thorny-headed worm
Predilection site: Small intestine
Table 7.2 Intestinal flukes of the family Strigidae.
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