A condition seen worldwide in chickens, turkeys and ducks due to bacterial infection of the navel and yolk sac of newly hatched chicks as a result of contamination before healing of the navel. Disease occurs after an incubation period of 1-3 days. Various bacteria may be involved, especially E .coli, Staphylococci, Proteus, Pseudomonas. Morbidity is 1-10% and mortality is high in affected chicks. It is seen where there is poor breeder farm nest hygiene, use of floor eggs, inadequate hatchery hygiene or poor incubation conditions, for example poor hygiene of hatching eggs, ‘bangers’, and poor hygiene of setters, hatchers or chick boxes. Inadequate incubation conditions resulting in excessive water retention and slowly-healing navels and ‘tags’ of yolk at the navel on hatching also contribute to the problem.

Signs

• Dejection.
• Closed eyes.
• Loss of appetite.
• Diarrhoea.
• Vent pasting.
• Swollen abdomen.

Post-mortem lesions

• Enlarged yolk sac with congestion.
• Abnormal yolk sac contents (colour, consistency) that vary according to the bacteria involved.

Diagnosis

A presumptive diagnosis is based on the age and typical lesions. Confirmation is by isolation and identification of the bacteria involved in the internal lesions. Differentiate from incubation problems resulting in weak chicks.

Treatment

Antibiotics in accordance with sensitivity may be beneficial in the acute stages, however the prognosis for chicks showing obvious signs is poor; most will die before 7 days of age.

Prevention

Prevention is based on a good programme of hygiene and sanitation from the nest through to the chick box (e.g. clean nests, frequent collection, sanitation of eggs, exclusion of severely soiled eggs, separate incubation of floor eggs etc. There should be routine sanitation monitoring of the hatchery. Multivitamins in the first few days may generally boost ability to fight off mild infections.

A spectrum of diseases of chickens and turkeys, occasionally ducklings and other birds, seen worldwide, characterised by oxidation of various tissues and caused by Vitamin E deficiency. The problem is associated with feed rancidity typically in diets with high fat. Encephalomalacia and exudative diathesis tends to be seen in young birds of 1-5 weeks of age. Muscular dystrophy is seen more frequently in older and mature birds.

Signs

• Imbalance.
• Staggering.
• Uncontrolled movements.
• Falling over.
• Paralysis.
• Ventral oedema.
• Green wings.

Post-mortem lesions

• Swollen cerebellum with areas of congestion.
• Haemorrhage.
• Necrosis.
• Blood-stained or greenish subcutaneous oedema.
• Steatitis.
• White streaks in muscle.

Diagnosis

Signs, lesions, feed rancidity, histopathology, response to medication. Differentiate from Encephalomyelitis, toxicities, necrotic dermatitis.

Treatment

Vitamin E and/or selenium in feed and/or water. Broad-spectrum antibiotics where there are extensive skin lesions.

Prevention

Proper levels of vitamin E, selenium, antioxidant, good quality raw materials.

The B complex vitamins are water soluble and not stored to any significant extent in the body. They act in a broad range of metabolic pathways. Simple deficiency is now rare as diets are usually well supplemented. However, because a continuous supply is required, damage to the intestine or increased demand for some reason may have an effect. Most will reduce productivity, including growth in the young animal, and egg production in the layer. The embryo is particularly dependent on having adequate supplies of vitamins deposited in the egg. Vitamin deficiencies are especially prone to cause problems of hatchability. See the separate discussion under Chondrodystrophy and Fatty Liver and Kidney Syndrome.

Signs

These may be summarised:

• Perosis
• Curled Toe Paralysis
• Paralysis/’Stargazing’
• Dermatitis/Scaly Skin
• Mouth Lesions
• Conjunctivitis
• Anaemia
• Fatty Liver and Kidney Syndrome
• Poor Feathering
• Loose feathers
• Hatchability problems
• Embryo with clubbed down

• Thiamine (B₁)
• Riboflavin (B₂)
• Pantothenic acid
• Pyridoxine (B₆)
• Niacin
• Folic Acid
• Cyanocobalmin (B₁₂)
• Biotin

Post-mortem lesions

• Usually the gross lesions are non-specific.
• Some deficiencies induce characteristic microscopic effects.

Diagnosis

Signs, exclusion of specific diseases, response to supplementation. If it is suspected that the vitamin premix may not have been included in the ration (or included at too low a level) it may be appropriate (faster, less expensive) to analyse feed for a marker substance such as manganese rather than testing for vitamin levels.

Treatment

If a specific vitamin deficiency is suspected, drinking water supplementation with that vitamin is ideal and usually results in a rapid response in birds that are still drinking. Good quality multivitamin solutions are beneficial in the supportive care of a range of problems characterised by reduced feed intake. The balance of vitamins present should be similar to the daily nutritional requirement of the stock concerned.

Prevention

Adequate supplementation of the feed with all required vitamins in levels which both support normal productivity but also have enough overage to deal with the increased demands that often occur during periods of disease challenge.

Vitamin A deficiency is occasionally seen in chickens and turkeys (insufficient vitamin A during 1-7 weeks of age). As in the case of other nutritional deficiencies, classic signs of deficiency are very rare in commercial poultry fed complete diets.

Signs

• Poor growth.
• Poor feathering.
• Nasal and ocular discharge.
• Drowsiness.
• Pale comb and wattles.
• Eyelids stuck shut with thick exudate.

Post-mortem lesions

• Eyelids inflamed and adhered.
• Excessive urates in kidneys and ureters.
• Pustules in mouth and pharynx.
• Microscopically – squamous metaplasia of epithelia.

Diagnosis

Signs, lesions, feed formulation. Differentiate from Infectious coryza, chronic fowl cholera, infectious sinusitis etc.

Treatment

Vitamin A in drinking water.

Prevention

Supplementation of diet with vitamin A, antioxidant, good quality raw materials.

Visceral gout is the deposition of white urates, which are normally excreted as a white cap on well formed faeces, in various tissues. Urates are also often deposited in joints and in the kidney. This condition can occur as an individual problem at any age. Outbreaks are seen in young chicks in the first week of life (baby chick nephropathy) or in flocks suffering kidney damage, or reduced water intake. All poultry species are susceptible. The kidney damage can arise from infection with certain strains of Infectious Bronchtiis virus, exposure to some mycotoxins or inadequate water intake (often because the birds have not adapated to a new type of drinker). Baby Chick Nephropathy can be due to inappropriate egg storage conditions, excessive water loss during incubation or during chick holding/transport, or inadequate water intake during the first few days of life. Very low humidity in brooding will also increase the likelihood of this problem. The timing of mortality is a reasonable guide as to the source of the problem. In Pekin/mallard ducks the condition is almost always due to inadequate water intake, whereas in muscovy ducks it is seen in breeders allowed to continue laying for over 24 weeks without a rest.

Signs

• Depression.
• Low feed intake and growth.

Post-mortem lesions

• Chalky white deposits on pericardium, liver, air sacs, peritoneum.
• Similar deposits may be present in joints and are usually present in the kidney.

Diagnosis

Lesions.

Treatment

This is based on correcting any management errors and encouraging water intake. Avoid any intentional or unintentional restriction in water intake. Sodium bicarbonate at 1g/litre water is mildly diuretic, however it could be counter-productive if water intake is in any way restricted.

Prevention

Careful monitoring of the conditions of hatching egg storage and incubation with a view to achieving a standard egg weight loss profile. Humidification of holding rooms and chick transporters may also be beneficial. Humidifiers in chick brooding areas are being used increasingly, especially where whole house hot air brooders are in use. Ample supplies of drinkers should be available and filled with water at house temperature prior to the arrival of the chicks.

Viral Arthritis is the classic, but by no means the only, manifestation of reovirus infection of chickens; at least 5 sero-types of virus occur. Morbidity is high but mortality is usually low. Transmission is by faecal contamination, and good both laterally and vertically. Birds remain carriers for over 250 days. The virus is resistant to heat, ether, chloroform, pH and environmental factors. Reoviruses vary markedly in pathogenicity and the tissue damaged. Some can cause other disease syndromes such as early chick mortality and malabsorption syndrome. Some strains have shown severe systemic disease including pericarditis in chickens. Others have caused immunosuppression by damaging the cloacal bursa in ducks.

Signs

• Lameness.
• Low mobility.
• Poor growth.
• Inflammation at hock.
• Swelling of tendon sheaths.
• Unthriftiness.
• Rupture of gastrocnemius tendons.

Post-mortem lesions

• Swelling and inflammation of digital flexor and metatarsal extensor tendon sheaths.
• Foot pad swelling.
• Articular cartilages may be ulcerated.
• Haemorrhage in tissues.
• Fibrosis in chronic cases.

Diagnosis

Diagnosis may be based on the history, lesions, IFA and rising antibody titre. Isolation may be readily achieved in CE yolk sac and CAM and also cell cultures (CE kidney or liver cells). Serology may be by DID, FAT or Elisa. ‘Silent’ infections (not associated with obvious disease) are common. Differentiate from mycoplasmosis, salmonellosis, Marek’s, Pasteurella, erysipelas.

Treatment

None.

Prevention

Vaccination is ideally carried out by administering a live vaccine in rear followed by an inactivated vaccine prior to coming into lay. Most vaccines are based on strain 11/33. Rear birds in all-in/all-out production systems.

An insidious onset disease of chickens caused by Vibrio bacteria. Morbidity is low. Transmission is by faecal contamination, birds remaining carriers for months, and disease is precipitated by stress. The infective agent is rather resistant to environment and disinfectants.

Signs

• Dejection.
• Diarrhoea.
• Loss of condition.
• Inappetance.
• Pale comb and wattles.
• Scaly comb.
• Jaundice.
• Drop in production/weight gain.

Post-mortem lesions

• Focal hepatic necrosis in 10% of affected. Foci often stellate, or there may be a cauliflower-like ‘spotty liver’.
• Haematocysts under capsule.
• Swelling of organs.
• Catarrhal enteritis.

Diagnosis

History, lesions, isolation of infective agent from bile. Differentiate from leukosis, histomonosis, ulcerative enteritis, fowl cholera, and typhoid.

Treatment

Erythromycin, fluoroquinolones.

Prevention

Hygiene, depopulate, obtain birds free of disease, contain stressors.

Ulcerative Enteritis is an acute, highly contagious disease of chickens and quail caused by the bacterium Clostridium colinum and characterised by ulcers of the intestines and caecae. It can start suddenly and cause high mortality: 100% in quail and 10% in chickens. Turkeys, game birds and pigeons may also be affected. The condition occurs worldwide. The route of infection is oral and transmission is from faeces of sick or carrier birds or via flies. The bacterium resists boiling for 3 minutes. Predisposing factors include Coccidiosis (especially E. necatrix, E. tenella, and E. brunetti), IBDV and overcrowding.

Signs

• Listlessness.
• Retracted neck.
• Drooping wings.
• Partially closed eyes.
• Ruffled feathers.
• Diarrhoea.
• Anaemia.
• Watery white faeces (quail).

Post-mortem lesions

• Deep ulcers throughout intestine, but mainly ileum and caecae, which may coalesce and may be round or lenticular.
• Pale yellow membranes,.
• Peritonitis (if ulcers penetrate).
• Blood in intestine.
• Necrotic foci in liver.

Diagnosis

A presumptive diagnosis may be made on history and lesions. Confirmation is on absence of other diseases and isolation of Cl. colinum in anaerobic conditions (the agent is often present in pure culture in liver). Differentiate from histomonosis (‘Blackhead’), necrotic enteritis, coccidiosis, salmonellosis, trichomoniasis.

Treatment

Streptomycin (44 gm/100 litres water), Bacitracin, Tetracyclines, penicillin (50-100 ppm in feed), amoxycillin, multivitamins. Response to treatment should occur in 48 to 96 hours. Treat for coccidiosis if this is a factor.

Prevention

Infection-free birds, all-in/all-out production, low level antibiotics as per treatment, possibly probiotics.

A complex condition seen in chickens and turkeys. Morbidity is 1-20% and mortality is low. Factors involved may include genetics, nutrition, environment and high growth rate.

Signs

• Lameness.
• Distortion at hock.
• Valgus/varus.
• Various angulations of leg.
• Gastrocnemius tendon may slip.

Post-mortem lesions

• Linear twisting of growth of long bones.
• Changed angulation of tibial condyles; intertarsal angulation up to 10% is physiological, greater than 20% is abnormal.

Diagnosis

Symptoms, lesions. Differentiate from perosis, arthritis and synovitis.

Treatment

None.

Prevention

Selection for good conformation in primary breeding. Adoption of optimal nutrition and growth patterns for the economic objectives of the production system.

An infection of turkeys caused by an unidentified virus. Morbidity varies, mortality is 1-25%. Transmission may be by direct or indirect contact and possibly vertical. Birds remain carriers for up to 16 days.

Signs

• Signs are usually subclinical.
• Depression and sporadic deaths in birds in good condition.

Post-mortem lesions

• Grey foci (c. 1 mm) coalescing.
• Congestion.
• Focal haemorrhage.
• Bile staining.
• Grey to pink foci in the pancreas.
• Microscopically – no inclusion bodies.

Diagnosis

Isolation in CE, lesions pathognomonic. Differentiate from histomonosis, bacterial and fungal infections.

Treatment

None; with good management many birds recover.

Prevention

Good sanitation and management.