List of twelve major viral diseases of chicken:- 1. Viral Inclusion Body Hepatitis 2. Haemorrhagic Enteritis of Turkeys 3. Egg Drop Syndrome-1976 4. Adenovirus Group I — Associated Infections 5. Infectious Bursal Disease 6. Infectious Bronchitis (IB) 7. Laryngotracheitis 8. Swollen Head Syndrome 9. Infectious Encephalomyeliti 10. Newcastle Disease 11. Fowl Pox 12. Reovirus Infections.
Viral Disease # 1. Viral Inclusion Body Hepatitis:
The viral inclusion body hepatitis (IBH) is an adenovirus infection characterized by haemorrhages and dystrophic necrobiotic changes in the liver and kidneys, accompanied by intranuclear inclusion bodies. A characteristic macroscopic lesion is the enlarged, dystrophic liver with yellowish colour and crumbly texture.
IBH outbreaks are encountered primarily in meat type chickens, most commonly at the age of 3-8 weeks. IBH often occurs as a secondary infection to immunodeficiency resulting from other diseases (IBD, CIA). On the background of dystrophic liver changes, haemorrhages of various intensity and size are outlined, thus creating a variety of liver lesions.
IBH is characterized by a sudden onset and a sharply increased death rate that reaches peak values by the 3rd – 4th day and returns back within the normal range by the 6th-7th day. The total death rate is usually under 10% but sometimes could attain 30%.
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More rarely, macroscopically visible necrotic foci could be detected in the liver. Clinical signs could be observed only several hours prior to death occurrence. They consist in pale comb and wattles, depression and apathy. Sometimes, the skin is icteric. Often, ecchymoses and striated haemorrhages in skeletal muscles are observed.
Microscopically, extensive dystrophic changes and necroses of liver parenchyma are detected. In the nuclei of hepatocytes, basophilic or eosinophilic inclusion bodies are detected. The basophilic inclusion bodies are usually dense and occupy the entire nuclear inner space, whereas the eosinophilic ones are round or irregularly shaped and surrounded by a light halo.
The diagnosis is based upon the typical gross lesions and the history records. A principal approach in IBH diagnostics is the histological investigation that helps to detect the intra-nuclear inclusion bodies.
IBH should be distinguished mainly from IBD and chicken infectious anaemia (CIA). With regard to IBH prevention and control, the eggs of broiler parent flocks, where the disease is consecutively appearing in the progeny, should not be used for hatching.
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The access of wild birds should be prevented as they are potential carriers and distributors of the virus. The most important steps in IBH prevention are the control of IBD and CIA. There are neither vaccines, nor an effective treatment.
Viral Disease # 2. Haemorrhagic Enteritis of Turkeys:
The haemorrhagic enteritis (HE) is an acute viral disease in young turkeys, characterized by a sudden onset of bloody faeces causing high death rate. Blood discharge from the vent (187), fresh blood in faeces or melena (188) could be observed. HE is observed in turkeys at the age of 6-11 weeks but most commonly at the age of 7-9 weeks.
As an exception, HE could be observed in turkeys under 4 weeks of age, presumably due to maternal antibodies. The small intestine, especially the duodenum, has a dark red colour and ramiform blood vessels prominating under the serous coat, and sometimes, haemorrhages are seen through the intestinal wall. The staining of peripheral blood smears reveals a picture, characteristic for septicaemia.
The typical gross lesions and the history of the disease allow making a tentative diagnosis for HE. The histological detection of intranuclear inclusion bodies in the reticuloendothelial cells of the spleen or intestines confirms the diagnosis. For identification of the HEV, the agar gel precipitation method could be used.
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The viral antigen could be detected in fresh or frozen spleen tissue, diluted 1:1 with saline or in sera obtained from diseased turkeys. HE should be distinguished from other cases of severe enteritis in turkeys, acute E. coli septicaemia and some other septicaemic states (streptococcosis, fowl cholera, etc.).
Within weeks after the beginning of the disease, an appropriate antibiotic therapy should be initiated for prevention of secondary E. coli septicaemia. Practically, there is no effective therapy for HE in turkeys.
Viral Disease # 3. Egg Drop Syndrome-1976:
The egg drop syndrome – 1976 (EDS 76) is an infectious disease in layer hens manifested by a quick drop in egg production, failure to reach peak production, irregularly shaped eggs, soft-shelled or shell-less eggs and depigmentation. The aetiological agent is an adenovirus of group III.
The horizontal transmission occurs slowly in battery systems and rapidly in floor housing systems. The first sign is the loss of egg pigmentation, rapidly followed by the appearance of soft- shelled shell-less of deformed-shell eggs.
If defective eggs are discarded, the remaining ones have no problem with fertilization and hatching. The drop could be sudden or prolonged. Usually, it lasts for 4-10 weeks and the egg production is reduced by about 40%. Apart from the inactive ovaries and oviduct atrophy, other lesions are not discovered.
The replication of the virus in epithelial cells of oviduct glands results in severe inflammatory and dystrophic changes in the mucous coat. The appearance of eggs with impaired quality and the dropped egg production are suggestive for EDS 76.
The diagnosis is supported by some serological studies and is confirmed after isolation and identification of the virus. In many instances, no antibodies are detected in infected flocks until egg production approaches levels between 50% and peak production.
Viral Disease # 4. Adenovirus Group I — Associated Infections:
Necrotic pancreatitis and gizzard erosions in broilers. It is characterized by focal necroses in the pancreas. They are manifested by erosions affecting the cuticle and the underlying tissues of the gizzard. Avian adenovirus splenomegaly is characterized by enlargement of the spleen, pulmonary oedema and congestion.
It is observed in broiler breeders at the age of 20-45 weeks. Its course is peracute or acute. The mortality could reach 8-9%. The most typical lesions are splenomegaly, mottled or marble-like appearance of the spleen, oedema or hyperaemia of lungs.
Viral Disease # 5. Infectious Bursal Disease (Gumboro):
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Infectious bursal disease (IBD, Gumboro) is an acute, highly contagious viral infection in chickens manifested by inflammation and subsequent atrophy of the bursa of Fabricius, various degrees of nephroso- nephritis and immunosuppression. Clinically the disease is seen only in chickens older than 3 weeks. The feathers around the vent are usually stained with faeces containing plenty of urates.
The period of most apparent clinical symptoms and high death rate is at the age of 3-6 weeks. IBD could, however, be observed as long as chickens have a functioning bursa (up to the age of 16 weeks). In chickens younger than 3 weeks, IBD could be subclinical, but injured bursa leads to immunosuppression.
Also, diarrhoea, anorexia, depression, ruffled feathers, especially in the region of the head and the neck is present. A natural IBD infection is mostly observed in chickens. In turkeys and ducks it could occur subclinical, without immunosuppression.
Most isolates of the IBD virus in turkeys are serologically different from those in chickens. In premises, once contaminated with the IBD virus, the disease tends to recur, usually as subclinical infection. The dead bodies are dehydrated, often with haemorrhages in the pectoral, thigh and abdominal muscles. The IBD virus belongs to the Birnaviridae family of RNA viruses.
Two serotypes are known to exist, but only serotype 1 is pathogenic. The virus is highly resistant to most disinfectants and environmental conditions. In contaminated premises, it could persist for months and in water, forage and faeces for weeks. The incubation period is short and the first symptoms appear 2-3 days after infection.
The lesions in the bursa of Fabricius are progressive. In the beginning, the bursa is enlarged, oedematous and covered with a gelatinous transudate. IBD virus has a lymphocidic- effect and the most severe injuries are in the lymph follicles of the bursa of Fabricius.
Most commonly, IBD begins as a serous bursitis. The kidneys are affected by a severe urate diathesis. In an acute outbreak and manifestation of the typical clinical signs, the diagnostics is not difficult.
The diagnosis could be confirmed by detection of typical gross lesions throughout a patho-anatomical study. IBD should be differentiated from IBH (inclusion body hepatitis). The application of live vaccines in chickens is a key point in the prevention of IBD and should be related to the levels of maternal antibodies.
Viral Disease # 6. Infectious Bronchitis (IB):
In chickens up to the age of 4 weeks, IB is manifested by severe respiratory signs (sneezing, coughing, and rales). Rhinites and conjunctivitis, depression and crowding around heat sources are observed. The death rate could reach 100%.
The mortality in young chickens is usually insignificant provided that a secondary infection with a different agent is not occurring. In such cases, there is a moderate to severe inflammatory cell infiltration of upper respiratory tract mucosa, resulting in thickened and more compact mucosa.
In layer hens infected with the IB virus, oophorites and dystrophic necrobiotic lesions affecting primarily the middle and the last thirds of oviduct’s mucous coat are observed. The consequences are drop in egg production, appearance and increase in the number of deformed and pigmentless eggs or eggs with soft shells and watery egg white.
The nephrotropic strains of the IB virus cause severe inflammatory and dystrophic necrobiotic damages of kidneys: urolithiasis (229), interstitial nephritis (230), and haemorrhages (231) that considerably increase the death rate. Under natural conditions, only hens are infected. Nonimmune birds of all ages are susceptible. The disease is even seen in vaccinated flocks.
The serological methods (VN, ELISA, etc.) are widely used in the diagnostics. At present, PCR is used for rapid identification of IB virus serotypes. IB should be distinguished from other acute respiratory diseases as ND, laryngotracheitis and infectious coryza. The vaccination with live or killed vaccines is effective only if they contain the respective serotype of the virus for the given region.
Viral Disease # 7. Laryngotracheitis:
Laryngotracheitis (LT) is a viral infection in hens, pheasants and peacocks characterized by catarrhal haemorrhagic to fibrinous inflammation of the respiratory tract. It is manifested in laryngotracheal and conjunctival form. In the laryngotracheal form, suffocation, rales and cough are observed.
The head and the neck are strongly extended forward and upward during inspiration, mucous coats of the larynx and the trachea are catarrhally, haemorrhagically to fibrinously inflamed. Most outbreaks are encountered between the age of 4 and 14 weeks although the disease affects fowl of any age. LT is caused by a herpesvirus that is relatively resistant.
In the conjunctival form of LT, wet eyes, tear secretion and oedema of infra-orbital sinuses are observed, especially in a complicated infection. The typical clinical and morphological signs are sufficient to assume the presence of LT.
The diagnosis is confirmed with the detection of intranuclear inclusion bodies in the trachea throughout the histological study in the early stages of the disease, serological studies (VN, ELISA), etc. LT should be differentiated from IB, SHS, M. synoviae infections, etc.
Premises, contaminated with the LT virus, should be freed, cleansed, disinfected and occupied again after 5-6 weeks. The vaccination of unaffected birds and these from other premises of the infected farm could protect and stop subsequent outbreaks.
Viral Disease # 8. Swollen Head Syndrome:
Swollen head syndrome (SHS) is a complicated infection in broilers and broiler breeders, where the primary aetiological agent is an avian pneumovirus (APV) and the secondary — usually E. coli; it is characterized by respiratory and nervous signs. In broilers chickens, SHS is generally seen after the 4th week of life.
The first clinical signs are sneezing, coughing, rales and conjunctivitis. A profuse tear secretion, reddened conjunctivas and a characteristic oblong almond-like shape of eyes are observed. The inflammatory exudate is initially transparent, but afterwards becomes opaque.
Subcutaneous oedemas in the head region, involving unilaterally or bilaterally the periorbital sinuses and the mandibular space, are emerging. A seasonal pattern in the prevalence with peaks during spring and summer is observed. SHS in broiler breeders is usually encountered around or after the peak egg laying period only in female birds.
Unilateral or bilateral swellings of the head, affecting the periorbital sinuses, the mandibular space and the wattles are seen. The conjunctiva and the mucous membranes of sinuses are considered to be the entrance door of the infection.
A unique cytotoxin has been identified in many E. coli isolates in SHS that could be involved in the pathogenesis of the disease. The inflamed by the virus infection conjunctiva-associated lymphoid tissue is the site where the bacterium enters the subcutaneous tissue.
In laying hens, the ovaries are affected in many instances (serofibrinousoophoritis), resulting in reduced egg production. The diagnosis is based upon the distinctive clinico-morphological signs. SHS should be differentiated from Mycoplasma and Pasteurella infections and the skin form of aspergillosis. Prevention — improvement of the microclimate of premises, use of live and killed vaccines.
Viral Disease # 9. Infectious Encephalomyeliti:
The infectious encephalomyelitis (IEM) is characterized by signs of ataxia, progressing to paralysis, prostration and marked tremor of the head and the neck, and because of that, is also called epidemic tremor. The chickens with prostration are usually in lateral recumbency.
The expression of the eye is dull. IEM outbreaks are generally observed in chickens at the age between 8-9 and 20 days. The morbidity rate could reach 40-60%. The average death rate is about 25%, but could be more than 50%. The history of the disease, the age of onset and the typical nervous signs, especially the head tremor are indicative for the diagnosis that could be finally confirmed by histology.
IEM should be differentiated from other diseases with nervous symptoms as encephalo- malacia, mycoticencephalites, toxicoses (salt, pesticides). The chickens from naturally infected flocks obtain an adequate maternal immunity that preserves them from the disease.
Viral Disease # 10. Newcastle Disease:
The Newcastle disease (ND) is characterized by marked variations in morbidity, death rate, symptoms and lesions. The clinico- morphological signs possess a distinct viscerotropic or neurotropic character. In the viscerotropic form, haemorrhagic diphtheritic lesions of the entire alimentary tract, from the beak to the vent, are present. The haemorrhages of gizzard epithelium are remarkable.
The mucous coat is oedematous, covered with thick mucus and mottled with haemorrhages varying from single to multiple, sometimes gathered at the boundaries with the gizzard or the oesophagus. Typical for this form are the haemorrhagic, necrotic and focal diphtheroid lesions affecting the mucosa of the buccal cavity (259, 260), the stomach and the intestines.
The disease is generally prevalent in hens, more rarely in turkeys, exotic or wild birds. Birds at any age are susceptible.
It is caused by a paramyxovirus. Depending on their pathogenicity, the numerous known strains are classified as lentogenic, mesogenic and velogenic. The vaccines made of lentogenic strains provoke a shorter immunity that requires a revaccination.
The vaccines from mesogenic strains result in a lasting immunity, but could provoke a lethal issue especially in birds without a primary immunity created on the basis of lentogenic vaccinal strains.
Viral Disease # 11. Fowl Pox:
Fowl pox (FP) is a viral disease in hens, turkeys and many other birds, characterized by cutaneous lesions on the feather-less skin and/or diphtheritic lesions of mucous coats of the upper alimentary and respiratory tract.
FP is encountered in either cutaneous or diphtheritic form or in both. In most outbreaks, the cutaneous form is prevailing. The lesions vary according to the stage of development: papules, vesicles, pustules or crusts. The lesions are usually in the region of the head. Lesions around the vent in a pigeon.
FP is caused by an epitheliotropic DNA virus from the Avipox genus, the Poxviridae family. Some virus types (strains) exist: fowl pox virus, turkey pox virus, pigeon pox virus, canary pox virus etc., different in pathogenic and immunogenic aspects.
The viruses are very resistant to environmental factors and could persist for several months. Diphtheritic lesions look like whitish or yellowish plaques that are deposited and grown on the mucous coats of the buccal and nasal cavities, the sinuses, the larynx, the pharynx, the trachea or the oesophagus.
The diagnosis is made upon the typical cutaneous and diphtheritic lesions. The prevention is performed by vaccinations that could be made at any age, if necessary.
Viral Disease # 12. Reovirus Infections:
(i) Viral Arthritis/Tenosynovitis:
The most frequent reovirus-associated disease in poultry is viral arthritis. Clinically it is manifested by lameness and swellings affecting primarily tarsometatarsal joints and the feet. Many infected birds are in a good general condition, but some could be lethargic and exhausted. The mortality is very low.
The infections affect predominantly meat type poultry. In some cases, joint cavities or tendon sheaths contain a small amount of straw-yellow exudate whereas in other the exudate is haemorrhagic or fibrinous.
(ii) Fibrinous Tenosynovitis:
The inflammation of the tendon progresses to a chronic type lesion characterized by tissue fibrosis in the affected area. The aetiological agent is a reovirus, member of the Orthoreovirus genus, Reoviridae family. Several serotypes are identified. For their identification, the agar gel precipitation test could be used. Reoviruses are highly resistant to a number of environmental factors (temperature, pH, etc.).
(iii) Stunting Syndrome in Broilers:
The stunting syndrome in broilers is associated with a reovirus infection but according to some studies, the role of the reovirus is probably secondary. It is characterized by a considerably reduced live weight in affected birds and a various degree of un-uniformity in the flock varying from 5-10% to 40-50%, usually seen after the age of 14 days.
The small intestine is pale, dilated and contain indigested forage. The tentative diagnosis of viral arthritis and stunting syndrome could be made on the basis of symptoms and lesions. The detection of reovirus antibodies via ELISA supports the diagnosis.
Viral arthritis should be differentiated from M. synoviae induced, staphylococcal arthritis and the spontaneous rupture of the tendon of the gastrocnemius muscle. The vaccination of broiler breeder flocks with live or inactivated vaccines protects one-day-old chicks. Infected birds should be removed from the premises. The iodine disinfectants are considered effective for inactivation of agents.