Coccidiosis, Upper Intestinal, E acervulina

Introduction

This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. It is seen in layers and in broilers, both alone and in association with other species of coccidia and is caused by Eimeria acervulina, which is moderately pathogenic. Morbidity is variable and mortality low or absent. Eimeria mivati is currently considered not to be a valid species distinct from E. acervulina.

Signs

• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Poor production.
• Diarrhoea.
• Depigmentation.

Post-mortem lesions

• Thickening, and other lesions, restricted to upper third of small intestine - the duodenum and part of the ileum.
• Petechiae.
• White spots or bands in the mucosa. In severe infections they become confluent and cause sloughing of the mucosa.
• Poor absorption of nutrients/pigments.
• A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. A detailed description is beyond the scope of this book. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. Various publications provide a photographic key to severity of lesion.

Diagnosis

Signs, lesions, microscopic exam of scrapings. Differentiate from necrotic and non-specific enteritis.

Treatment

Toltrazuril, Sulphonamides, Amprolium, in feed or water.

Prevention

Coccidiostats in feed, vaccination by controlled exposure, hygiene. Immunity is quite short lived (about 30 days) in the absence of continued challenge.

Figure 12. Moderate Eimeria acervulina infection (score 2) in chicken duodenum. In milder infections there may be scattered white spots, in severe the entire surface is pale or denuded of epithelium.

Unknown

11:48 AM

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Coccidiosis, Mid-intestinal, E necatrix

Introduction

A highly pathogenic form of coccidiosis, caused by Eimeria necatrix, in which the parasite is present in the small intestine and in the caecum. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds.

Signs

• Reduced feed consumption.
• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Poor production.
• Diarrhoea, blood in faeces.

Post-mortem lesions

• Petechiae and thickening, of middle to posterior third or more of small intestine.
• 'Sausage-like' intestine.
• Severe necrotising enteritis.
• Schizonts seen as white spots through the serosa interspersed with petechiae. Deep scrapings necessary to show large schizonts. Oocyts in caecal scrapings.

Diagnosis

Signs, lesions, microscopic examination of scrapings Differentiate from necrotic enteritis, other types of coccidiosis.

Treatment

Toltrazuril, Sulphonamides, Amprolium, Vitamins A and K in feed or water.

Prevention

Coccidiostats in feed, vaccination, hygiene. This is one of the less immunogenic species, commercial vaccines commonly contain more than one strain of E. maxima.

Figure 14. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). In this case the intestine is thickened and can become ballooned and sausage-like. Haemorrhages and white spots are visible from the outside of the intestine.

Unknown

11:47 AM

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Coccidiosis, Mid-intestinal, E maxima

Introduction

One of the more common forms of coccidiosis in commercial broilers. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. Caused by Eimeria maxima, of moderate to high pathogenicity it is seen worldwide. Morbidity and mortality are variable.

Signs

• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Poor production.
• Blood or pigment in the faeces.
• Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets.

Post-mortem lesions

• Petechiae and thickening of middle third of intestine.
• Poor absorption of nutrients/pigments.
• Mild to severe enteritis, contents often orange in colour, mucosa tends to be pinker than normal.
• This infection is often associated with E. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears.

Diagnosis

Signs, lesions, microscopic examination of scrapings. Differentiate from necrotic enteritis, non-specific enteritis.

Treatment

Sulphonamides, Amprolium, Vitamins A and K in feed or water.

Prevention

Coccidiostats in feed, vaccination, hygiene. This is one of the less immunogenic species, commercial vaccines commonly contain more than one strain of E. maxima.

Figure 13. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). The lesions are subtle compared to other forms of coccidiosis. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside.

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11:47 AM

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Coccidiosis, Kidney

Introduction

A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 3-12 weeks of age, it can also infect Barbary ducks and swans.

Signs

• Depression.
• Weakness.
• Diarrhoea - faeces tend to be whitish.
• Reduced feed intake.

Post-mortem lesions

• Enlarged kidneys.
• Kidneys light grey to greyish pink.
• Tiny white foci and petechiae in the kidneys.

Diagnosis

Lesions, presence of coccidial stages in fresh scrapings of kidney lesions.

Treatment

Controlled trials of treatments have not been published.

Prevention

Good Hygiene.

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11:46 AM

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Coccidiosis, Intestinal, of Ducks and Geese

Introduction

Young ducks and geese may suffer from Eimeria spp infection. In the goose E. anseris is the most important, while in ducks Tyzzeria perniciosa is most pathogenic. Tyzerria has eight sporocysts in each oocyst, compared to four per oocyst for Eimeria. Coccidiosis occurs only very rarely in commercially reared ducks in the UK.

Signs

• Sudden death.
• Depression.
• Blood-stained vent.
• Tucked appearance.

Post-mortem lesions

• Massive haemorrhage in upper small intestine.

Diagnosis

Signs, lesions, microscopic examination of scrapings (usually few or no oocysts, large number of merozoites). Differentiate from Duck viral hepatitis, Duck viral enteritis, anatipestifer.

Treatment

Sulphonamides (e.g. Sulphadimidine 30-600gm/100 birds/day, 3 days on, 2 days off, 3 days on), Amprolium, Vitamins A and K in feed or water.

Prevention

If required coccidiostats could be used in feed, however this is not routinely practised. Hygiene.

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11:45 AM

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Coccidiosis, Ileorectal, E brunetti

Introduction

A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. Of moderate to high pathogenicity, it is found in the terminal ileum, caecum and rectum. Morbidity and mortality are variable.

Signs

• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Poor production.
• Diarrhoea, blood in faeces.

Post-mortem lesions

• Petechiae and thickening of the distal third or more of intestine, extending into caecal tonsils.
• Severe necrotising enteritis.
• Oocysts in caecum and rectum.

Diagnosis

Signs, lesions, microscopic examination of scrapings. Differentiate from ulcerative enteritis, caecal coccidiosis.

Treatment

Toltrazuril, Sulphonamides, Amprolium, Vitamins A and K in feed or water.

Prevention

Coccidiostats in feed, vaccination by controlled exposure, hygiene. This species is not usually included in vaccines for broilers. There is good immunity to the same parasite in recovered birds.

Figure 16. Moderate Eimeria brunetti infection in the terminal ileum and rectum of a chicken. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa.

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11:43 AM

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Coccidiosis, E praecox

Introduction

Infection of chickens with the protozoan parasite Eimeria praecox is spread in exactly the same as that with E. mitis but is practically non-pathogenic.

Signs

• Normally asymptomatic but may cause reduced feed efficiency and reduced weight gain, and predispose to other intestinal conditions.

Post-mortem lesions

• Minimal, but usually excess liquid and mucus in the duodenal loop.
• Severe infection can cause dehydration through excessive fluid loss.
• The cells of the sides of the villi (not tips) are usually parasitised.

Diagnosis

Identification of characteristic slightly ovoid oocysts in the duodenum in the absence of E. acervulina lesions. It has a very short pre-patent period (c. 80 hours).

Treatment

Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis.

Prevention

Normally controlled by anticoccidials in feed. Not usually included in vaccines.

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11:42 AM

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Coccidiosis, E mitis

Introduction

This condition of chickens, seen worldwide, is caused by the protozoan parasite Eimeria mitis, which colonises the small intestine.

The infective agent is found in litter, faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. The disease occurring is proportional to the amount of infective agent ingested.

The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants.

Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature, humidity).

Signs

• Reduced feed conversion efficiency and weight gain. May predispose to wet litter, secondary bacterial enteritis.

Post-mortem lesions

• The lesions are minimal and located in the lower small intestine (ileum) which tends to be pale and flaccid with scattered petechiae.

Diagnosis

Mild lesions, identification of typical small round oocysts and other stages in fresh scrapings from the small intestine.

Treatment

Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis.

Prevention

Normally controlled by anticoccidials in feed. May be included in vaccines.

Unknown

11:42 AM

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Coccidiosis, Caecal, E tenella

Introduction

This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. Morbidity is 10-40% and mortality up to 50%. Transmission as for E. mitis (see above).

Signs

• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Diarrhoea, blood in faeces.
• Production less affected than in some of the other forms of coccidiosis.

Post-mortem lesions

• Petechiae.
• Thickening, ecchymoses, of caecal mucosa.
• Accumulation of varying quantities of blood and caseous necrotic material in the caecum.

Diagnosis

Signs, lesions, microscopic examination of scrapings. Differentiate from ulcerative enteritis, histomonosis.

Treatment

Toltrazuril, Sulphonamides, Amprolium, Vitamins A and K in feed or water.

Prevention

Coccidiostats in feed, vaccination by controlled exposure, hygiene. E. tenella is more common when 'straight' ionophore programmes are used. Shuttle programmes with chemicals in the starter diet usually improve control. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. Vaccines are used mainly in breeders but increasingly in broilers. Recovered birds have good immunity to the same parasite.

Figure 15. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen.

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11:41 AM

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Coccidia of Turkeys

Introduction

Infection of turkeys with Eimeria spp. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. Five species of Eimeria have been identified that cause lesions in turkeys, of which two are associated with significant disease effects. E. meleagrimitis affects the upper small intestine, while E. adenoides affects the caecae and rectum. E. gallopavonis and E. meleagridis affect the lower small intestine rectum and caecae, while E. dispersa is found in the small intestine.

Signs

• Huddling.
• Weight loss.
• Depression.
• Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa.
• Tucked appearance, ruffled feathers.

Post-mortem lesions

• The affected area of intestine shows thickening of the wall and dilation. The contents may be haemorrhagic or be watery with white material shed from the mucosa.

Diagnosis

Signs, lesions, microscopic exam of scrapings (oocysts, gamonts). Differentiate from necrotic enteritis.

Treatment

Toltrazuril, Sulphonamides (e.g. Sulphaquinoxaline), Amprolium.

Prevention

The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers, typically to 12 weeks of age. Diclazuril is also used for this purpose. Dosage levels of ionophores may be critical to efficacy and safety. Exposure of previously unmedicated birds to these compounds can cause toxicity. Salinomycin is toxic for turkeys even at very low doses. Avoid use of tiamulin in ionophore treated birds.

Figure 37. Turkey coccidiosis of the upper small intestine caused by E. meleagrimitis. The intestines are dilated, show some spotty congestion and have abnormal contents due to the sloughed epithelium.

Figure 38. Turkey caecal coccidiosis caused by E. adenoides. The exudate can range from semi-liquid to solid white cores.

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11:40 AM

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Slipped Tendon or Perosis

Introduction

Caused by deficiency of manganese, choline, zinc, either singly or in combination (although deficiencies of pyridoxine, biotin, folic acid, niacin may also be involved).

This condition is seen in chickens, ducks and turkeys. In turkeys it may be an inherited deficiency of galactosamine.

Signs

• Short legs.
• Lameness.
• Distortion of hock.
• Slipping of Achilles tendon (or perosis).
• Malposition of leg distal to hock.
• In embryos parrot beak, shortened bones.

Post-mortem lesions

• Shortening and thickening of long bones.
• Tibia and metatarsus bowed.
• Shallow trochlea.
• Lateral slipping of tendon.

Diagnosis

Lesions, analysis of feed.

Differentiate from twisted leg, infectious synovitis, rickets, infectious arthritis, ruptured ligaments.

Treatment

For flock proceed as for prevention, no value to affected bird.

Prevention

Addition of manganese, choline, vitamins, correct mineral balance.

Unknown

11:39 AM

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Chlamydiosis, Psittacosisof poultry

Introduction

An infection of turkeys, ducks, psittacines, pigeons, man, rarely chickens, caused by Chlamydia psittaci, a bacterium of highly variable pathogenicity. It is a 'Scheduled Disease' rarely diagnosed in UK, but occurring probably worldwide. Morbidity is 50-80%, mortality 5-40%.

It is transmitted by contact, faecal dust and wild bird carriers, especially pigeons and robins. Egg transmission does not occur.

Elementary bodies are highly resistant and can survive in dried faeces for many months.

Iodophores and formaldehyde are effective disinfecting agents, phenolics are less so. Intercurrent salmonellosis and, perhaps, other infections may be predisposing factors.

Signs

• Respiratory signs.
• Greenish-yellow diarrhoea.
• Depression.
• Weakness.
• Inappetance.
• Weight loss.
• Nasal discharge.
• Conjunctivitis.
• Occasional transient ataxia in pigeons.
• Production drops in naive laying flocks

Post-mortem lesions

• Vascular congestion.
• Wasting.
• Fibrinous pericarditis.
• Airsacculitis.
• Perihepatitis.
• Spleen enlarged and congested, may rupture in pigeons.
• Necrotic foci in liver.
• Fibrinous pneumonia.
• Congested lungs and air sacs in the turkey.

Diagnosis

History, signs, lesions. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain, IFA).

Serology: complement fixation, Elisa and gel diffusion.

Differentiate from Duck viral hepatitis, Duck septicaemia.

Treatment

Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter.

Prevention

Biosecurity, exclusion of wild birds.

Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications.

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9:18 AM

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Chicken Anaemia

Introduction

A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA.

Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis, Gumboro, Inclusion body heptatitis etc.) or poor management (e.g. poor litter quality).

Transmission is usually vertical during sero-conversion of a flock in lay, lateral transmission may result in poor productivity in broilers.

The virus is resistant to pH 2, ether, chloroform, heat (70°C for 1 hour, 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. Hypochlorite appears most effective in vitro.

Signs

• Poor growth.
• Pale birds.
• Sudden rise in mortality (usually at 13-16 days of age).
• No clinical signs or effect on egg production or fertility in parent flock during sero-conversion.

Post-mortem lesions

• Pale bone marrow.
• PCV of 5-15% (normal 27-36%).
• Atrophy of thymus and bursa.
• Discoloured liver and kidney.
• Gangrenous dermatitis on feet, legs wings or neck.
• Acute mycotic pneumonia.

Diagnosis

Gross lesions, demonstration of ongoing sero-conversion in parent flock, virus may be isolated in lymphoblastoid cell line (MDCC-MSB1).

Treatment

Good hygiene and management, and control of other diseases as appropriate, may be beneficial. If gangrenous dermatitis is a problem then periodic medication may be required.

Prevention

Live vaccines are available for parents, their degree of attenuation is variable. They should be used at least 6 weeks prior to collecting eggs for incubation. Their use may be restricted to those flocks that have not sero-converted by, say, 15 weeks.

Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines.

Serology: antibodies develop 3-6 weeks after infection, and may be detected by SN, Elisa, or IFA.

Unknown

9:17 AM

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Cellulitis

Introduction

Cellulitis is literally an inflammation of connective tissues. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. However its main importance is as a cause of condemnation in meat poultry, particularly broiler chickens.

In the USA it is called 'Inflammatory Process'. The condition is caused by infection of, often minor, skin wounds by particular strains of E. coli, which can replicate in the tissues.

Signs

• Affected flocks tend to have poorer than average productivity and uniformity, but the affected birds are not readily detectable prior to slaughter.

Post-mortem lesions

• Typically it presents as exudate ranging from liquid and pale cream pus to yellowish solid plaques of caseous material under the skin of the abdomen and/or in the leg. Many affected birds have no other lesions and are reasonably well grown. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds.

Diagnosis

Typical lesions.

Treatment

Treatment would not be possible if the problem is identified at a final depletion. If identified at a thinning there may be time for antibacterial treatment to have some benefit for those birds in the early stages of the problem.

Prevention

Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices, though most of the birds showing toe scrapes will not go on to develop cellulitis.

Unknown

9:16 AM

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Hairworm Infection

Introduction

Nematode parasitic worms of poultry, game birds and pigeons of Capillaria species. C. obsignata in the small intestine, C. contorta in the crop and oesophagus.

The worms are 7-18 mm long, about 0.05 mm wide and hair-like in appearance. Morbidity and mortality are usually low. Infection is by the oral route. Worm eggs take about 20 days to embryonate with an L1 larvae, prepatent period about 21-25 days according to species.

Some species have earthworms as intermediate hosts; some are transmitted direct from bird to bird. Worm eggs in the environment are resistant.

Signs

• Diarrhoea.
• Wasting
• Poor growth.
• Dejection.

Post-mortem lesions

• Enteritis.
• Hairworms in mucosa of crop, small intestine or caecum.

Diagnosis

This may be by a combination of macroscopic examination, seiving intestinal contents, or characteristic worm eggs in faeces in patent infections. Differentiate from other causes of enteritis.

Treatment

Coumphos has been licensed in some markets. Fenbendazole has been shown to have high efficacy - other approved benzimidazoles can be expected also to have activity. Levamisole.

Prevention

Separation of birds from possible transport and intermediate hosts, effective cleaning of houses.

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9:14 AM

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Cannibalism

Introduction

A complex multifactorial behavioural problem of poultry and game birds seen worldwide. Morbidity is usually low but mortality is high among affected birds. Predisposing factors include overcrowding, excessive light intensity or variation (e.g. through shafts of light in the house), high temperatures, nutritional deficiencies, feed form (mash takes longer to consume than pellets), tenosynovitis and other diseases affecting mobility, boredom, and strain of bird.

Signs

• Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 8-12 days old), head, face, wings.
• Feather-pulling.

Post-mortem lesions

• Skin wounding related to particular signs exhibited.
• Generalised anaemia.

Diagnosis

Age, distribution of lesions, anaemia. Differentiate from bacterial dermatitis, post-mortem cannibalism.

Treatment

Correct any husbandry problems. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. Beak trimming may be necessary. If so it should be carried out carefully by trained operators, complying with local regulations and any relevant codes of practice.

Prevention

Proper density and temperature, low light level, control ectoparasites. Provision of a diet that closely matches the nutritional requirements of the stock concerned.

Unknown

9:13 AM

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Candidiasis,Thrush of poultry

Introduction

A disease of the alimentary tract of chickens, turkeys, and sometimes other birds and mammals, characterised by thickening and white plaques on the mucosa, especially in the crop but sometimes in the proventriculus, intestine and cloaca, and associated with gizzard erosion.

The cause is a fungal yeast, Candida albicans and the condition is seen worldwide. Morbidity and mortality are usually low.

The route of infection is normally oral and the organism is often present in healthy animals with disease occurring secondary to stress and poor hygiene. The fungus is resistant to many disinfectants.

Signs

• Dejection.
• Poor appetite.
• Slow growth.
• Diarrhoea, possibly confused or masked by signs of the primary disease.

Post-mortem lesions

• White plaques in mouth, oesophagus, crop, occasionally proventriculus and intestine.
• Raised focal lesions may slough into lumen as caseous material.

Diagnosis

Lesions, histopathology, microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. Colonies of this fungus appear as white to ivory colour, smooth and with a yeasty smell.

Treatment

Nystatin (100 ppm in feed) for 7-10 days, copper sulphate (1 kg/tonne feed) for 5 days, or copper sulphate 1gm/2 litre water for 3 days if approved locally.

Prevention

Avoid excessive use of antibiotics and other stressors. Ensure good hygiene, proprionic acid, sodium or calcium proprionate at 1 kg per tonne continually. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets.

Control of Candida through drinking water is sometimes practised with chlorination (e.g. Chlorox, sodium hypochlorite) at 5 ppm. This is economical and effective. It should be repeated periodically. Take care to provide fresh clean feed and water, uncontaminated by fungi.

Unknown

9:12 AM

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Campylobacter Infection

Introduction

Campylobacter spp. are bacteria that commonly infect a broad range of livestock species, pets and wild animals. In poultry they tend to multiply in large numbers in the hindgut, principally in the caecae. Campylobacters are a significant cause of enteritis in man. Infected poultry are a potential reservoir of this zoonosis.

Campylobacter jejuni is the commonest species found in poultry. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material, biofilm or engulfed by protozoa.

Campylobacter jejuni infection is not currently considered to be pathogenic in poultry though a Campylobacter-like organism is considered to be the cause of 'Vibrionic Hepatitis'.

There are indications that plantar pododermatitis, carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. The reason for this is unclear. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock.

There is an annual cycle with increased risk of infection in the summer months in some countries.

Signs

• None.

Post-mortem lesions

• None.

Diagnosis

Isolation of the organism from caecal contents, cloacal swabs or composite faeces. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. Samples should be tested as quickly as possible after collection.

Treatment

Not required on clinical grounds.

Prevention

In principle, housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. Key aspects of this include effective sanitation of drinking water, sourcing of water from high quality supplies, avoidance of contact with pets and other farmed species, good hand hygiene by stockmen, and changing of overalls and boots on entering bird areas.

In practice the success of this will also depend upon the degree of environmental contamination by the organism. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house.

Many infections are introduced during thinning or other forms of partial depopulation. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings.

Research is ongoing on the development of vaccines, phage treatments and competitive exclusion approaches, as well as processing plant technologies to reduce carcase contamination.

Unknown

9:30 AM

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Calcium Tetany

Introduction

A metabolic disease of chickens, especially broiler parents. Predisposing factors include heat stress with reduced feed intake and panting.

Signs

• Paralysis.
• Death from respiratory and cardiac failure.

Post-mortem lesions

• Cyanosis.
• Congested lungs.
• Active ovary with egg in oviduct.

Diagnosis

This is made on signs, lesions, lack of other significant lesions, and response to treatment. Differentiate from IB 793b, other acute infections and other causes of sudden death.

Treatment

Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water.

Prevention

Keep pullet flocks on low calcium diet until 5% production hen/day, managing birds for maximum uniformity.

Unknown

9:29 AM

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Caecal Worm

Introduction

Heterakis gallinae, nematode parasites of poultry and game birds, are small whitish worms with a pointed tail, up to 1.5 cm in length that occur in the caecum. They are found worldwide. Morbidity is high but it is not associated with mortality. Infection is by the oral route. Earthworms may be transport hosts for eggs, or paratenic hosts with partially developed (L2) larvae. There is an incubation period of 2 weeks for eggs to embryonate, and a four-week prepatent period. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. Heterakis gallinae eggs and larvae are a transport hosts for Histomonas, the cause of Blackhead.

Signs

• None.

Post-mortem lesions

• Inflammation of caecum, possibly with nodule formation.

Diagnosis

Adults can be seen in caecal contents at post-mortem examination.

Treatment

Flubendazole, Levamisole, are effective.

Prevention

Avoiding access to earth and earthworms. Routine anthelmintic treatment.

Figure 11. The life cycle of Heterakis showing the location of adults, an undeveloped egg as found in fresh faeces, and the embryonated egg. The egg may be ingested directly by a chicken, or by an earthworm which is in turn ingested by a chicken.

Unknown

9:28 AM

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