Chicken Anemia Virus (CAV) is a worldwide known disease that affects young birds between 12-28 days old. It is caused by Circo Virus which has an 8-10 day incubation period. CAV causes a condition in domestic fowl known as blue-wing disease, infectious anaemia, haemorrhagic syndrome or anaemia dermatitis syndrome. It is seen mostly in broilers.
Infection causes anaemia, bone marrow atrophy, and severe immunosuppression in poultry as the virus affects the production of red blood cells, white blood cells and platelets. Clinical signs are predominantly found in young chicks due to vertical transmission from the breeder hens whose maternal antibodies have not yet formed following exposure. Clinical signs include:
Subclinical infection my cause reduced growth rates and other health problems.
Post mortem examination shows anaemia, subcutaneous and intramuscular haemorrhages and atrophy of the thymus and other lymphoid tissues. Skin overlying subcutaneous haemorrhages, particularly on the wings, may turn blue and break, releasing bloody exudate. Gangrenous dermatitis may result from secondary bacterial skin infection.
Vertical spread of the disease can be controlled by the vaccination of breeding hens with the appropriate vaccines which controls anaemia in the birds; however, immunosuppression may still be evident in the progeny of vaccinated birds. Chicks derive immunity from immune parent stock.
Exposure of pullets to infected litter before egg production will produce protective maternal immunity in the progeny, but risks spreading other diseases to the birds. Culling of infected birds is normally performed in infected commercial flocks. Appropriate hygiene and biosecurity measures should be employed to control the disease.
CAV is extremely resistant to high temperatures and extremes of pH. It is inactivated by formalin fumigation if this is properly carried out.
Subclinical losses in broilers may be controlled by use of live attenuated vaccines in the broilers or inactivated vaccines in the breeders, with subsequent prolongation of the period of protection provided by maternal antibodies.
Zinc is an important essential nutrient that is required in the bird’s diet. Not only is there approx. 200 zinc dependent enzymes in the body but it is also an essential component of both RNA and DNA. It plays a key role in stimulating the immune system and is also vital to the activity of various hormones including growth hormones. A deficiency of zinc in the diet can have a serious impact on poultry production.
The small intestine is where zinc is primarily absorbed. The bioavailability of zinc is affected by the presence of dietary calcium, copper, magnesium, iron and phosphorus which ‘bind’ with the zinc to enable it to be absorbed. In monogastric animals zinc absorption can be decreased due to the presence, for example, of phytate.
Signs of zinc deficiency in young chicks include:
Chicks hatched from zinc-deficient hens are weak and cannot stand, drink or eat. They have accelerated respiratory rates and laboured breathing both of which tend to lead to death of the chick. In major deficiency cases hatched chicks can exhibit grossly impaired skeletal development. Curvature of the spine, shorthand and fused thoracic and lumbar vertebrae can be witnessed and in extreme cases embryos may have missing toes or entire lower limbs. In some cases the eyes may be missing or not developed. In ageing hens zinc deficiency can reduce egg production.
Broilers being fed high bioavailable sources of zinc, such as zinc complexes, have been known to show improvements in gain and feed conversion. In layers shell quality and production are greatly improved. It may be necessary to supplement zinc into the diet if feed ingredients have low zinc content with varying levels of bioavailability.
Zinc is an important essential nutrient that is required in the bird’s diet. It is an essential component of both DNA and RNA enzymes with there also being an additional 200 zinc-dependent enzymes in the body. It is vital to the activity of a variety of hormones including growth hormone and sex hormones and it also plays a key role in stimulating the immune system. Adequate dietary zinc supplementation is critical in poultry production as a deficiency can have a serious impact.
Zinc is primarily absorbed in the small intestine and requires other dietary ingredients to ‘bind’ with it to allow it to be absorbed and to influence the bioavailability of the zinc. Bioavailability is affect by the presence of dietary calcium, magnesium, phosphorus, copper and iron. Zinc absorption though can be decreased in monogastric animals due to the presence, for example, of phytate.
Signs of zinc deficiency in young chicks include:
Although, in ageing hens zinc deficiency can reduce egg production, the most striking effects are seen in developing embryos. Chicks hatched from zinc-deficient hens are weak and cannot stand, eat, or drink. They have laboured breathing and accelerated respiratory rates which worsen when disturbed and often results in the death of the chick.
The major defect seen in hatched chicks is grossly impaired skeletal development. Zinc-deficient embryos show curvature of the spine, and shortened, fused thoracic and lumbar vertebrae. Often toes are missing and, in extreme cases, the embryos have no lower skeleton or limbs. Occasionally the eyes of some embryos are absent or not developed.
Feeding highly bioavailable sources of zinc, such as zinc complexes, to broilers has been known to show improvements in weight gain and feed conversion. It also has positive effects on egg production and shell quality in laying hens. Some feed ingredients can have low zinc content with varying levels of bioavailability so it may be necessary to add zinc to the poultry diet.
The Lesser Mealworm Beetle is the most damaging pest to the poultry industry. It is the most common beetle found in broiler litter. These insects are a vector for a variety of poultry diseases, including Marek’s disease, are intermediate hosts for parasites, can transmit bacterial diseases such as Salmonella spp., and the larvae can cause significant and costly damage to poultry housing. There can also be human health risks associated with close contact and exposure to these beetles.
Poultry have difficulty digesting the beetle and larva. If eaten they are put at risk of ingesting harmful organisms, run the risk of intestinal obstruction and gut lesions and it will detrimentally affect their food conversion rate. Chicks are more likely to be infected by eating the larvae and it can lead to death in younger, weakly chicks.
The Lesser Mealworm is reddish brown is colour with a wide oval shape and is roughly 6 millimetres in length. The beetle is mainly nocturnal and thrives in warm, humid environments thus poultry litter is the ideal habitat for them. They feed on the litter as well as mould and feathers. They can also infest and consume dying birds, especially chicks. The female, which can have a two year life span, can produce up to 2000 eggs in a year and within as little as one week these larvae emerge. The larvae are quite active and mobile and can mature in approximately 40 days in the right environment.
Regular removal of manure and litter from poultry houses will help to control the beetle. Care should be taken with disposal of litter to prevent further spread of the infestation. It can be difficult to monitor and assess the extent of the infestation as adult and larvae make themselves inaccessible by burrowing and also by being nocturnal. Care should be taken to ensure that any infested food is not taken into housing. Physical barriers such as metal proofing structures can restrict the migrating of larva to pupation sites within the fabric of the building or using larvae resistant insulation material. Before repopulating houses cooling to sub-zero temperatures for a number of days will help control residual populations. There are a number of insecticides which can be used in the control of the Lesser Mealworm. It is advisable to consult your veterinary consultant on these products and work out a management system that works best for your situation.
Coccidiosis is a parasite which damages the gut wall of chickens. There are six species of Coccidiosis that are of commercial significance – Eimeria.tenella, E.brunetti, E. necatrix, E. maxima, E. mitis and E. acervulina.
The life cycle of coccidiosis begins with an oocyst which doesn’t become infective until eaten and under optimum humid conditions and this can take as little as 24 hours to occur. Oocysts are difficult to destroy and can survive several years thanks to their thick outer wall which protects them from heat, cold and even common disinfectants. Once eaten by the chicken, chemicals in the digestive tract break down this thick wall and releases the infective form of the coccidiosis. Once released the parasite invades the cells of the lining of the gut and replicates in them. Once replicated the parasites burst out of the cell and invade other cells thus repeating the process. As the parasite is released it destroys the cells lining the gut. More oocysts are produced from the coccidiosis infection which are eventually passed out into the environment via the faeces and can then go onto infect other chickens.
If only a few oocysts are eaten by the bird the damage to the cells is reduced and this can induce an immune response in the bird that then becomes resistant to the infection. However, if a large number of oocysts are eaten a lot more damage is done to a greater number of cells. This is painful and birds will stop eating and will adopt a hunched posture with ruffled feathers.
The gut’s ability to absorb nutrients is severely reduced by the damage to the cells in the gut wall, resulting in diarrhoea and weight loss. Blood can be seen in the droppings of birds in severe cases caused by bleeding within the gut from cell damage. This can also lead to anaemia with is characterised by a pale comb and wattle. Birds can die suddenly in very acute cases. Due to the natural balance of bacteria in the gut being disrupted, harmful bacteria can take over and cross the damaged gut wall causing septicaemia.
Ideally the aim is to ensure that birds are exposed to low levels of coccidiosis so that they can build up immunity but not too much so as to develop symptoms already mentioned. Immunity is not passed from the hen to their chicks and generally chicks will get exposed to coccidiosis within their first few weeks and go on to develop immunity without any clinical signs. General only birds up to 3 months of age tend to suffer from coccidiosis.
There are three components involved in the treatment of this parasite:
To prevent an outbreak the first and most important thing is to ensure that the house is properly cleaned and disinfected especially after a flock leaves. Remove old litter and use a detergent to remove dirt and grease so that disinfectant can work better. Allow to dry so the disinfectant isn’t diluted. Then use a DEFRA-approved anticoccidial disinfectant that is licensed to destroy oocysts.
If you suspect a coccidiosis infection within your flock consult your vet immediately and they will be able to advice you on the best course of action to take. They will also be able to advice you of the correct disinfectants to use and control measures to set in place. A vaccine is available commercially, but administration can be complex and needs the correct environment to work.
Gumboro Disease is a highly contagious and acute viral infection also known as Infectious Bursal Disease (IBD). It is an important poultry disease worldwide, which was first reported in the USA in 1962 and in 1987 in Europe. In 2012 IBD had worldwide distribution.
Generally it is seen only in domestic chickens between 3 and 8 weeks of age depending on maternal antibody levels. It can present as a clinical or subclinical disease, causes mortality of 40%+ and immune suppression resulting in secondary infections. It is shed in the faeces and spreads easily from bird to bird by way of droppings. Infected equipment and clothing are means of transmission between farms.
Chickens and turkeys appear to be natural hosts.
Clinical symptoms are manifested by initial inflammation and enlargement and subsequent atrophy of the bursa. Infected birds are depressed, have ruffled feathers, droopy appearance, unsteady gait, lack of appetite, produce watery white diarrhoea and may be seen pecking at the vent. The feathers around the vent are usually stained with faeces. Morbidity and mortality begins 3 days post infection and the birds that die usually do so as a result of dehydration which causes kidney lesions.
Unfortunately there is no treatment for this disease. Rigorous disinfection is always advised but IBD virus has an ability to resist many disinfectants and environmental factors and therefore disinfection achieves only limited success in contaminated farms after depopulation.
Vaccination of broilers against Gumboro Disease is essential. The vaccine is given via the drinking water at 16 days or at 16 and 22 days, depending on which vaccine used. Early infection and subsequent immunosuppression can be minimised if there are high levels of maternal antibodies during early brooding of chicks in broiler flocks (and in some commercial layer operations). During the growing period breeder flocks should be vaccinated one or more times, first with a live vaccine and again with an inactivated vaccine just before egg production.
The goal of any vaccination program should be to use vaccines that most closely match the antigenic profile of the field viruses. Diagnostic testing can be used to select the most appropriate vaccination program that is suitable for individual farms.
Rickets is a common disease found mainly in young meat birds. The main cause of Rickets is inadequate or poor bone mineralisation. A mineral deficiency of either phosphorous or calcium, an incorrect calcium to phosphorus ratio, or a vitamin D3 deficiency in the young growing birds diet may result in abnormal bone development. Generally rickets is caused by a lack of vitamin D3 in the diet, inadequate potency of the D3 supplement or other factors that reduce the absorption of vitamin D3.
At 10-14 days of age young broilers and turkey poults can exhibit lameness as a symptom of rickets and their bones grow rubbery. Another effect seen is a flattening of the ribcage with beading at the attachment of the vertebrae to the ribs and there can also be enlargement of the ends of the long bones. To determine whether the cause of a rickets problem is due to a deficiency of calcium or vitamin D3, or even an excess of calcium, which prevents efficient phosphorous absorption, an analysis of blood levels is needed. Histology can also be performed to confirm rickets.
Although rickets is mainly seen in young growing birds it can also be seen in laying hens which generally results in reduction of shell quality and can lead to osteoporosis. This disorder can also be known as “ cage layer fatigue” and is caused when calcium is taken from the bones to overcome a dietary deficiency resulting in depletion of the bone structure thus the hen is unable to support her own weight.
Providing adequate levels and potency of vitamin D3 supplements and a correct balance of calcium to available phosphorous is necessary to prevent rickets. Due to the young birds limited ability to digest saturated fats (which may lead to an induced deficiency of calcium) a diet should be formulated to ensure optimal utilisation of all fat-soluble compounds.
Marek’s disease is a highly contagious, tumour-causing virus. It is shed from the feather follicles of infected birds and, when inhaled, crosses into the bloodstream and into the white blood cells that fight infection. It then causes devastating cell damage.
Birds aged between three and six months are most susceptible: it’s a disease unlikely to be seen in older birds. In field conditions, Marek’s disease outbreaks can occur in unvaccinated layers from three weeks old, but most serious cases occur between eight and nine weeks of age. Later outbreaks may occur in broiler breeders, or after moulting.
The virus prevents the cells from functioning and reduces a bird’s ability to fight off infection, leaving it vulnerable to other infections and reducing growth rate. Secondary diseases, such as coccidiosis or bacterial infections, can then take advantage of the dampened-down immune system, again reducing growth and resulting in increased mortality rates.
The virus causes the white blood cells to divide uncontrollably and form tumours. Tumours can occur in the feather follicles, presenting as large numbers of raised areas of the skin. Changes in the appearance of the eye can also indicate Marek’s disease – infected birds have poorly pigmented irises and less well-defined pupils.
Tumours which have reduced growth rates and increased the incidence of diarrhoea – as can be found in the liver, spleen, kidneys and reproductive tract – can be found post mortem. This is referred to as acute form.
Marek’s disease can also present in a classical form. Tumours can also develop in the nervous system, leading to paralysis and abnormal head and neck movements, as well as causing splaying of the legs. These birds are unable to eat and drink and, as there is no cure, the only option is culling the affected birds.
The key to prevention is to eliminate the virus so that young chick’s exposure is minimised. Often older birds are the source of infection. These do not necessarily show clinical signs if they are infected. Prevention tactics are: