Viral Diseases

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Cause

Chicken Anaemia Virus( CAV) of the family Circoviridae is a causative agent of Chicken Infectious Anaemia

Transmission

It is mostly transmitted vertically from the infected breeders. There can be horizontal transmission as well.

Clinical Signs and Lesions

The young chickens upto 3 weeks are susceptible to the virus infection. They exhibit depression, anaemia and retardation in growth. Focal skin lesions can also be seen which may be accompanied with bacterial infection which is known as blue wing disease. Though adult birds may acquire infection, the clinical signs are not seen in them. The postmortem gross lesions are the atrophy of thymus and bonemarrow, and subcutaneous and intramuscular haemorrhages. There is a variation in mortality rates which is generally below 30%.

Diagnosis

The clinical signs and postmortem lesions help in the diagnosis. IFT,VN and ELISA aid in the detection of antibodies in serum.

Treatment and Control

There is no treatment for this disease. Live attenuated CAV vaccines can be used to vaccinate breeders to induce the high and uniform levels of Maternal Derived Antibodies (MDA’s) which will be passed to progeny. Thus, the progeny receives the protection at their young age.

Cause

It is caused by Avian Encephalomyelitis (AE) virus from the Picornaviridae family.

Transmission

It is mostly transmitted vertically through eggs.

Species affected

It mostly affect the chickens. The turkey and pheasants serve as natural hosts.

Clinical signs

The young chickens of age between 1 and 3 weeks are more likely to be affected. The clinical signs are the sitting on hocks, difficulty in movement , falling on sides and trembling of head and neck. The trembling of head and neck can be felt better when the infected birds are held in hand. There is a drop in egg production in infected laying and breeders but it is normal in 2-3 weeks. Decrease in hatchability is also seen. There is high mortality in young chickens which can be upto 75%.

Diagnosis

Clinical signs aid in the diagnosis of Avian Encephalomyelitis. Gross lesions are not seen in this disease. There are typical lesions in brain, proventriculus and pancreas upon histological examination which can help to differentiate from the encephalomalacia resulting from Vitamin E deficiency. Antibodies can be detected in the blood serum of breed flocks in case of infection. The antibodies can also be detected in the hatching eggs.

Treatment and Control

Treatment is not available for AE. Live AE vaccine can be given to breeder pullet and layer pullet before the egg production to prevent the infection. In case of an infection in unvaccinated or inadequately vaccinated flocks, the hatching of eggs can be stopped for several weeks until the adequate immunity is obtained in the flock.

Avian Influenza

Avian Influenza (AI) is a viral disease caused by virus belonging to family Orthomyxoviridae and genus Influenza virus serotype A. The virus is worldwide in distribution. It occurs in many forms form asymptomatic to respiratory disease and a drop in egg production, to systemic disease with mortality rate of up to 100%. Thus, the viral isolates are subdivided into low pathogenic (LP) and high pathogenic (HP). Sometimes strains of some subtype (to date, H5 and H7 can mutate from LP to HP. Highly pathogenic avian influenza is included in the list of disease reported by OIE similarly to Newcastle disease. Influenza A virus is classified into subtypes based on the serological reactions of surface glycoproteins, haemagglutinin (H) and neuraminidase (N). Sixteen H and 9 N antigens have been recognized. Many combinations of H and N antigen in virus subtypes have been reported in domestic and wild birds. Antigenic variations; antigenic shift is more common than antigenic drift have been reported in poultry and fewer in case of mammals.

Epizootiology

Waterfowl is the frequent source of AI virus especially ducks, geese, gulls and other wild birds which are the natural reservoirs. AI virus infection usually causes sporadic or no disease. In the past it has been isolated from domestic integrated commercial poultry, frequently from turkeys and chickens and other domestic birds. Birds from live poultry market system and backyard flocks have higher infection rates. However, outbreaks in commercial poultry have become more frequent last 2 decades. When AI infection occur it spreads rapidly through integrated poultry system from farm to farm causing epizootics of LP or HP AI. This virus is excreted by the respiratory and enteric routes thus, it is transmitted by direct contact among infected and susceptible birds or by indirect contact via aerosol droplets or exposure to virus contaminated fomites, equipment and people. Intraspecies transmission is frequent and easy; interspecies transmission may occur, being ever less frequent as the differences between the phylogenetic classes of the animal increase; but some exceptions have occurred. At present to limited extent H1N1 from swine to turkey in the USA and more recently, H5N1 and H7N7 from poultry to humans, respectively in Asian and The Netherlands. Transmission is generally horizontal and evidences of vertical transmission are lacking. However, the virus has been isolated from intestinal contents of eggs during natural outbreak of disease.

Clinical signs and lesions

Clinical signs are variable depending on the pathotype of the virus and host species, age, concurrent infections and environmental conditions. LPAI virus infection in wild birds are asymptomatic however, in domestic birds it produces mild to severe respiratory symptoms like coughing, sneezing, rales along with malaise, anorexia and diarrhea; in breeders and layers there is decrease in egg production (10-80%). Sometimes high morbidity and mortality is low (3-5%) unless complicated by secondary bacterial infections in young birds.

The common lesions in respiratory tract are catarrhal fibrinous to purulent sinusitis, tracheitis, bronchopneumonia, more or less severe air sacculitis. Also depending on secondary bacterial infections, catarrhal to fibrinous enteritis and oviductitis are observed.

HPAI infection in wild birds and domestic ducks usually produces few or no clinical signs; however, a few cases have been reported with moderate to high mortality. In domestic poultry like turkeys, chickens, guinea fowl and quail, clinical signs varies according to damage induced by viral replication into specific organs and cardiovascular and nervous system. In many cases, disease is fulminating, in the absence of any clear symptom; if birds survive for few days, some may exhibit respiratory and nervous disorders. Respiratory signs are less prominent as compared to LPAI. Drop in egg production is rule. Morbidity and mortality is very high (50-90 to 100%). Edematous, hemorrhagic and necrotic lesions in visceral organs, often including the pancreas and non-feathered skin are seen. Hemorrhages are prominent in epicardium, proventriculus and Payer’s patches. In sudden death, no any gross lesions are seen, only congestion with higher severity are observed.

Diagnosis

Presumptive diagnosis is based on epidemiological and clinical data. A definitive diagnosis is established by direct detection of antigens or DNA of the virus in various specimens like tracheal and cloacal swabs, tissues. Isolation and identification of virus in embryonated eggs is done and diagnosis is confirmed by RT- PCR. Antibodies detection can be done by ELISA, HI, AGP, VN.

Control

Control strategies are mainly based on knowledge of how the virus has been introduced into the farm or an area and how it can spread. Wild birds should be considered the natural reservoirs for primary infection to commercial poultry. Strict application of biosecurity measures is the first line of defense which protects direct and indirect contact with virus. Contaminated poultry manures is major source of virus spread between flocks and farms.

When infection with subtype H5 and H7 is detected, response must be prompt and complete, even resorting to immediate culling or depopulation. As regards prevention by vaccination, inactivated vaccines in oily emulsion has been used, particularly in chicken and turkeys. The effectiveness of vaccines in preventing symptoms and mortality has been well documented. But, there is difficulty in developing the vaccine because there are 16 different H types of AI virus. When and outbreak of AI occurs and the virus subtype is identified, vaccination may be a useful tool, particularly in areas with high population densities, but the preparation of vaccine has to be quite rapid. Vaccination is a valid option in controlling the spread of infection, remarkably reducing the susceptibility of birds to the infection and the amount of viral shedding in the environment. The controlled used of vaccines in cases of LPAI H5 and H7 outbreaks might reduce the possibility of HPAI viral emergencies. But, their use continues to be debated in Europe and North America.

Heterologous vaccine has also been used for the N antigen, applying DIVA (differentiating infected from vaccinated animals) strategy, based on serological tests to highlight different specific anti-N antibodies. The trend seems to be in this direction considering the recent examples of results obtained in certain countries.

The judicious use of vaccine, making it possible to reduce transmission and spread of infection and the susceptibility of birds to the virus would favour eradication of the disease preventing it from being endemic.

Fowl Pox, (synonym: Avian pox or Avian Diptheria)

Fowl pox is a slowly spreading viral infection of chickens and turkeys.

Etiology

It is caused by viruses of the family Poxviridae and genus Avipoxvirus. The foxviruses are large DNA viruses, highly resistant and can survive in dried scabs too.

Transmission

The virus is transmitted either by direct or indirect contact. Mosquitoes and other flying insects are also responsible for disease transmission.

Species affected

Fowl pox is seen mostly in chickens and turkey. Pheasants, pigeons, quail, ducks are rarely affected.

Clinical findings

Fowl pox is characterized by proliferative lesions in the skin that progress slowly to thick scabs and by lesions in upper GI and respiratory tracts. In cutaneous form nodular or wart like lesions, yellow to brown in color appear on comb, wattles, eyelids, legs and other non feathered areas of the skin. In diptheric form, also called as wet pox, the lesions appear on mouth, oesophagus or trachea or larynx. The nodules or patches increase in size and often coalease to form yellow, cheery necrotic diptheric membrane or plug.

Affected birds aredepressed, anorectic and in wet pox, respiratory distress is seen, egg production reduced in case of laying birds, mortality varies, 1-2 % in mild cutaneous form and to over 30% in diptheric form.

Diagnosis

Wart like lesions in the featherless part or yellow cheesy lesions on mucus membrane of the nasal and oral cavities suggest the fowl poox. Histological examination or viral isolation in embryonated chicken eggs confirms the fowl pox.

Differential Diagnosis

Pantothenic acid and biotin deficiency ,vitamin E deficiency, infectious laryngotracheitis and other respiratoiry disease injuries caused by external parasites and canabolism.

Treatment and control

Treatment is not effective so its control is important. Removal of warts and treatment of local lesions with disinfectants can be performed. Vaccination is only means to control fowl pox. Live vaccine is applied by wing web method, using a stick with two grooved needles dipped in vaccine solution. Even in case of outbreak, immediate vaccination can be done to prevent further spread of the infection as it is slow spreading disease. The presence of local swelling at the injection site 7 days after vaccination can be observed for correct vaccination.

Inclusion Body Hepatitis

The serotype 4 of  Inclusion Body Hepatitis (IBH) virus of the Group 1 under Avian Adenovirus genera of Adenoviridae family are reported to cause the Inclusion Body Hepatitis( IBH).  Immunosuppressive diseases like Infectious bursal disease or Infectious Anaemia usually infect the birds simultaneously with this IBH virus.

Transmission

It is mostly transmitted vertically through egg while the horizontal transmission due to contact with droppings is also likely to take place. The virus can not isolated from the droppings of the immuned birds.

Species affected

It can infect chicken, turkey and pheasants

Clinical signs

The susceptible age for chickens is between 5 and 7 weeks. The listness and ruffled feathers are the common signs, and hydropericardium, enlarged and mottled liver with pinpoint necrotic and haemorrhagic spots, pale bone marrow, small spleen and pale kidney are the grossly seen internal lesions on postmortem examination. The gangrenous dermatitis can also be seen if infectious anemia accompany the disease while the bursal atrophy  and immune-suppression are seen in case of Infectious Bursal Disease (IBD). The mortality is high which may be upto 25% in the first 10 days of the disease.

Diagnosis

It can be diagnosed from gross lesions seen on postmortem examination. Intranuclear inclusion bodies can be seen on hepatocytes on histological examination. Virus isolation is equally useful.

Treatment

There is not any treatment for the disease but the secondary bacterial infections can be prevented and controlled by using antibiotics. It is important to provide sufficient immunity against the immunosuppressive diseases.

Control

The breeders can be given a controlled exposure before the onset of the lay by the use of inactivated vaccines to control the disease in endemic areas.

Introduction

Infectious bronchitis is the highly contagious acute and economically & epidemically important viral disease of poultry caused by the corona virus which particularly affect the respiratory tract but also the kidney and reproductive tract. Till the date more than 60 serotypes have been discovered in the fields which complicate the prevention of disease by vaccination.

Epidemiology

Epidemiologically it is very important disease of the chickens spreading all over the world. The virus is transmitted rapidly from bird to bird through airborne route even from farm to farm. The incubation period is 1-3 days. It causes considerable damage to the poultry industry. Chicken and to a lesser extent pheasant are primary natural host other species may at as carrier. All ages are susceptible but disease is more severe in young chicks. Virus is excreted by sneezing & coughing for 10 days but infection can persist for week or even months in kidney and gut being shaded by drooping.

Clinical signs and lesions

In young chicks characteristics respiratory sign appears with gasping, tracheal rales, nasal discharge, occasionally swollen sinuses together with more or less severe depression & poor wt gain. In adult, sign are similar but less severe. Infection in chicks few days old, reported to produce some permanent damage to the oviduct causing reduced future egg production and quality. In laying flock decreased in egg production upto 50%. Mortality depends upon the causative virus strain, immune status, stress and secondary bacterial infection which complicate the course of illness.

PM lesions

Young chicks : Yellow cheesy plug at the tracheal bifurcation. In nephropathogenic infections, swollen kidneys and distended ureters with uretes are found in older birds.Various changes in the oviduct depending upon the time and severity. In case of false layers permanent lesion in oviduct make egg production impossible. Oviduct will be blocked/filled with cystic fluid or never developed into an active oviduct.

Diagnosis

Clinical signs and postmortem lesions in a flock followed by laboratory confirmation based on virus isolation and identification with PCR. Serological test like ELISA &AGD for growth specific and HI&VN for type specific antibodies.

Treatment

There is no specific treatment for infectious bronchitis. Antibiotics are used to control the secondary bacterial infection.

Prevention and Control

It is very difficult to apply the biosecurity measures against IB due to high density of farms in certain area and when multiple ages are present in the same farm.

Effective mean is to restore the vaccination with strain specific or cross protective live vaccines and for layers & breeders the addition of inactivated vaccines at point of lay to induce long lasting systemic immunity.

Introduction

It is widely prevalant, highely feberile, immunosuppresive viral disease of brooding & growing stages of chickens causing significant  morbidity but low mortality. There is initial enlargement of bursa of fabricious followed by atrophy.

Etiology

The disease is caused by the double stranded RNA virus. There are two (classic& variant) serotypes but they cannot be differentiated by commercial ELISA kit. Virus can be isolated from bursal cell culture & propagated in CAM.Thus obtained cell cultured strain shows cytopathic effect.

Succeptible host

Chickens between 2-7 weeks of age  are most succeptible, more than 9 weeks are rarely affected.Both broilers and layers may suffer from the disease,other species of birds are resistant to natural infection.

Mode of transmission

The most common mode of entry in healthy bird is through contaminated feed & water but not by aerosol. The virus is  discharged in the faeces and spread from poultry shed by families. Mosquito also acts as vector of the diseases.

Clinical symptoms

In the subclinical(immunosuppresive) infections which occur in the chicks below 3 weeks of age shows the less obvious clinical manifestations. Bird remain dull & depressed with low mortality. But in case of clinical infection bird shows severe depression ,incordination,watery diarrhoea,soiling of vent &cannibalism problem.There is retard in body growth with concurrent  infections altering the clinical manifestations.Classical spike type of mortality is seen in case of very virulent infectious bursal disease(VVIBD).

PM lesions

There is mild bursal lesions in immunosuppressive form but in case of clinical form marked enlargement of bursa with caseous cheesy mass or with complete hemorrhage specially in case of VVIBD.There may be  congestion & haemorrhage in the pectoral, thigh & leg muscles but patchy haemorrhage present in the junction of gizzard & proventriculous is suggestive for diagnosis.Nephritis with or without urate deposition usually occur in almost all cases but fatty changes & diffused necrosis in liver seen occasionally.The carcass is severly dehydrated in general.

Diagnosis

Diagnosis can be made based on the histry, clinical signs, postmortom lesions,but the disease should be differentially diagnosed with infectious bronchitis,Inclusion body hepatitis, coccidiosis,vitamin A deficiency & visceral gout. Conformatory diagnosis is made by serological test.

Treatment

There is no effective treatment for the infectious bursal disease only symptomatic treatment for liver & kidney disorder.Attempt should be made  to boostup the immunity as it causes the immunosuppression.

Prevention and control

Vaccination should be practiced in the breeder flock during growth &booster dose at the time of laying.Strict insecurity measure should be followed with the provision of separate rearing of broiler & layer.Depopulation should be done for affected birds with proper disposal facility by incineration.


Introduction

It is an acute viral respiratory disease of chicken caused by herpes virus and is characterized by severe production loss due to mortality and decreased egg production.

Etiology

It is caused by the herpesvirus, double stranded DNA virus multiplying specially in the respiratory tract and is the virus without viremia. Only one serotype is known till the date.

Epidemiology

It is worldwide in distribution affecting chickens of all ages but males are more susceptible than female. Sometimes pheasants are also affected but chickens are the natural host.

Mode of transmission

Transmission takes place by direct contact with the clinically affected and subclinical carrier bird or by aerosol or contaminated equipment & personnel.

Clinical signs

In acute form of the disease symptoms like rhinitis, edematous head, gasping and drop in productivity upto 50% with hemorrhagic tracheal exudates which is characteristics symptoms of the acute form. Beside that sub-acute or mild form of the disease often observed with mild respiratory (gasping and coughing) symptoms with decreased productivity. Mortality approximates upto 15 %.The course of the disease varies depending upon the lesions.

Postmortem lesions

Lesions are found throughout the respiratory tract but more distinctly seen in the larynx and trachea. Depending upon the severity, lesions are limited in the upper respiratory tract with haemorrhagic tracheitis consisting blood clot or blood stained mucous but in mild form mucoid  exudates with or without blood clot are seen.

Diagnosis

The disease can be diagnosed by characteristic clinical sign like respiratory distress with bloody nasal discharge are indicative signs of the disease. Characteristics Postmortom lesions are also suggestive for diagnosis but reliable confirmatory result can only be obtained by histopathological tests of tracheal epithelium and isolation of the virus from tracheal exudates.

Treatment

There is no effective treatment for the infectious laryngotracheitis emergency vaccination in early stage of outbreak is the only the effective way to reduce the mortality.

Prevention and control

Effective protection can be achieved by using egg-embryo propagated vaccine administered in drinking water. Strict bio-security measures are only the way to prevent the disease outbreak even in endemic areas.

Cause

Retrovirus is the causative agent of Lymphoid Leucosis

Transmission

There is vertical transmission through eggs. There is chance of  horizontal transmission at young age.

Clinical Signs

It is mainly characterized by visceral tumors which can be seen in the liver, spleen, kidneys and bursa of birds. The birds which are older than 25 weeks are more susceptible to it. There is also the drop in egg production in layer flocks.

Diagnosis

Blood can be tested in the suspected breeders. The virus can be isolated from hatching eggs and cloacal swabs .

The listless, weakening, loss of weight, paleness, wasting and death are the common features of the disease. The lymphoid leucosis of bones of legs and wings is known as osteopetrosis. In such case, there bowing  and thickening of the legs. Blood leucosis is also a form of lymphoid leucosis.

Nervous system is not involved and there is no paralysis. This helps to differentiate it from Marek’s disease.

Treatment and Control

There is not any treatment for the disease. Laboratory detection and eradication of the infected flocks is the best and most effective method for control of the disease.

Newcastle disease (ND) is one among the important disease to be controlled in poultry. The importance lies in its rapid spread with high mortality i.e. 100% and its economic impact due to trading restrictions and embargoes placed where the disease outbreak has occurred. It is listed in OIE (Office International des Epizooties) list of diseases as per its severe nature. The causative virus is Paramyxoviridae serogroup 1 (Avian Paramyxovirus – 1) of family Paramyxoviridae from genus Avulavirus. Only one serotype is known with various pathotypes. Different pathotypes include very virulent (velogenic), medium virulent (mesogenic), mildly virulent (lentogenic) and apathogenic strains. Lentogenic and apathogenic strains are used in vaccine preparation.

Epizootiology

ND virus is highly contagious, horizontally transmitting virus through infected aerosol droplets, nasal discharges and droppings either by ingestion or inhalation affecting over 250 species of birds. Spread of the disease occurs by movement of live birds, by means of contaminated poultry products, people, equipment, feed and water and by aerosol route. Though it is controversial, vertical transmission can occur rarely in newly hatched chicks.

Clinical signs and lesions

ND virus has been divided into five groups or pathotypes on the basis of signs, lesions and tissue tropism viz: 1) viscerotropic velogenic; highly virulent disease with high mortality and typical haemorrhagic and necrotic gastro-intestinal lesions; 2) neurotropic velogenic; respiratory and nervous signs with very high mortality; 3) pneumotropic mesogenic; respiratory and in some cases nervous signs with considerable mortality in young birds but low in adult birds; 4) pneumotropic lentogenic; mild or unapparent infection of the respiratory tract, with no mortality and used for vaccine production; 5) naturally apathogenic; mostly thermo-resistant and use more recently as non-stressing vaccines.

Common signs include respiratory signs as labored breathing, rales and sneezing; greenish diarrhea and twisted neck or torticollis, leg weakness including paralysis. These lesions can all be present at the same time however are not strictly pathogonomonic. There is rapid drop in egg production sometimes may reach upto zero. Also, shell less eggs are common and sometimes thin and discolored shelled eggs are seen. Degenerated ovary is frequently seen with egg peritonitis. Morbidity is 100% and mortality varies according to virulence of virus and immune status of birds and reach upto 80%.

Diagnosis

Tentative diagnosis is made on the basis of typical lesions and signs. Inoculation of suspected samples from trachea and intestinal swabs or tissues in 9-11 days old embryonated eggs, HA and HI tests with allantoic fluid is done for isolation and identification of virus. Recently RT-PCR and nucleotide sequencing which are molecular diagnostic approach has been developed. The mean death time (MDT) in embryonated eggs is used for assessment of pathogenicity of virus, Intracerebral pathogenic index (ICPI) for one-day old chicks and Intravenous pathogenic index (IVPI) for six-week-old SPF chickens are also used for assessment of pathogenicity. These measures and some other molecular properties allow distinct viral profiles and helps in distinguishing virulent and avirulent isolates. Haemagglutination inhibition (HI) and ELISA tests are used for demonstration of antibodies against NDV.

Control of Disease

Vaccination helps to prevent susceptible birds from infection and at the same time it reduces the number of susceptible birds. For the control of the disease various international, national and farm level policies are applied consisting the application of all biosecurity measures directed at preventing the introduction and spread of the virus within the farm and countries. Restrictive measures on movement of birds and their products, quarantine procedures for importation any kind of domestic and wild birds need to be applied. Stamping out of outbreaks of disease, surveys at national and international level is organized and controlled by OIE. Vaccination has been adopted throughout the world except Scandinavia, New Zealand and Switzerland. Most recently in intensive areas of poultry rearing vaccination has been started. Vaccination usually protects birds from consequences of the disease, interfering with the spread of virulent virus, although virulent virus replication and shedding may still occur. Vaccination if well applied acts as barrier to the spread of disease. Live and inactivated vaccines are used.

Live Vaccines

These vaccines are prepared from the infected allantoic fluid of embryonated eggs kept freeze-dried. The virus strains used for vaccines production are fully apathogenic, lentogenic and mesogenic.

Mesogenic strains are used only in countries or areas where ND is endemic with widespread presence of backyard birds and not very intensive rearing. It cause severe post-vaccinal reactions, with some signs of disease thus, it is only used where it is permitted for revaccination intramuscularly after priming with apathogenic or lentogenic vaccine.

Lentogenic strains as Hitchner B1 and La Sota (ICPI 0.2-0.4) which replicate particularly in the mucosa of the respiratory tract inducing post vaccinal reactions and some respiratory signs, particularly in young chicks and in primary vaccination, depending on health status of birds, concurrent bacterial infection like Mycoplasma, E. coli and environmental stress like ammonia, dust, smokes etc. La Sota strain is the most stressing and not recommended  for use by spray as first vaccination.

Apathogenic strains multiplies well in enteric and respiratory tissues like NDV 6/10, Ulster 2C, Queensland V4 isolated from waterfowl and chickens are fully asymptomatic with and ICPI < 0.15. These strains induce no post-vaccination reactions even after fine spray vaccination (droplets < 70-80 microns) and at any age. They can be used with fewer problems in storage even in hot seasons and in tropical regions. Apathogenic and lentogenic strains can be applied by individual treatment like intra nasal or eye drop administration or beak dipping. Vaccination can also be done drinking water application at concentrations carefully calculated to give each bird a sufficient dose of virus with addition of skimmed milk powder (SMP) to fresh drinking water (1-2%). SMP is used to prevent viral inactivation by physical and chemical impurities with no concurrent use of disinfectants. Birds should be withheld for water for 1-2 hours before vaccination depending on the season. Live vaccines are used for mass application by spray or aerosol route as a large number of birds can be treated in very short time. Spray vaccination can be performed in hatchery or on the large scale farms with special consideration to achieve the correct droplet size. Coarse spray of large particles (> 100 microns) do not penetrate deeply in respiratory tract of birds and produces less reactions. The major problem with spray method at one day old chicks is it may result in establishment of infection with vaccinal virus inspite of the maternally derived immunity.

Inactivated Vaccines

These vaccines are produced with allantoic fluids from embryonated eggs, infected with different lentogenic strains, such as La Sota or Ulster 2C, rarely with mesogenic strains (Roakin strain), generally no longer with velogenic strains, inactivated with β-propiolactone or formalin and mixed with mineral oil to form a stable emulsion. One or more additional viral or bacterial antigens may be incorporated into the same emulsion as polyvalent vaccines. This vaccine is administered by intramuscular or subcutaneous injection. These vaccines are usually used in pullets, once or twice before going to egg production. It gives long-lasting immunity. Sometimes it has been used in broilers, at one day old together with live vaccine. This type of practice has been done in endemic areas of disease or in case of very severe epidemics.

(Synonyms: Viral arthritis, Tenosynovitis)

Cause The pathogenic strains like S1133, 1733, 2408, ERS of Avian Reoviruses from the genus Orthoreovirus  cause  viral arthritis or tenosynovitis in broilers

Transmission

It can be transmitted both vertically through  eggs or horizontally through contact with droppings with infected birds.

Species affected

These viruses affect chickens and turkeys. It is common in broiler breeders and broilers. It is rare in layer breeders.

Clinical signs and Lesions

The chickens of age between 2 and 10 weeks manifest the early clinical signs of reluctancy to walk, painful and trembling gait, and swelling of tendons of shanks and part above the hock joint. The feathers on the wings are generally ruffled. There is arthritis/ tenosynovitis in the affected birds. The birds are also unevenly distributed in the flocks. Mortality is also high.

The tendons usually lose their natural color and appear brown. They may be blood-tinged as well. The straw colored fluid is also deposited between the tendons. In case of infection by Maycoplasma synoviae or Staphylococcus, the fluid color may be yellow and creamy. There may be rupture in the tendons. A hard knot may be felt in the tendon above the hock joint in older broiler breeders of 29-30 weeks of age.

Diagnosis

It is diagnosed on basis of clinical signs like swelling and rupture of tendons of shanks and part above hock joint. A definite diagnosis requires the histopathology of the affected tissues or PCR from the affected tissues or virus isolation.

Treatment and Control

There is no effective treatment for Reovirus infection. The preventive medications can be applied against Staphylococcus infections.

Biosecurity, cleaning and disinfection of the farm are important. The most effective and important is the vaccination of the broiler breeders   which helps to check the vertical transmission (via egg) and protection of the progeny through the “maternal derived antibodies” (MDA).

Avian Metapneumovirus Rhinotracheitis  (RT) / Turkey Rhinotracheitis (TRT) / Swollen Head Syndrome (SHS)

Cause

Avian Metapneumovirus having 4 subtypes-   A,B,C and is from viral family Paramyxoviridae.

Transmission

There is horizontal transmission which takes place by direct contact with the infected bird and contaminated person, equipment, feed and water.

Species Affected

It infects the turkey and chicken.

Clinical Signs

The clinical signs of respiratory system like snicking, rales, sneezing, nasal discharge, foamy conjunctivitis, swollen infraorbital and periorbital sinus “swollen head” are the characteristic of the disease. The older birds also exhibit shaking of head and coughing. The fall in egg production upto 70% and poor shell quality are observed in adult laying hens.

There is upto 100% morbidity while the mortality varies from 0.5% to 50%. The wide range of mortality is because it depends on secondary infections like E.coli and IBV and the climatic conditions of farm.

Rhinitis, tracheitis and sinusitis are the common post mortem lesions. There is oedema of head and purulent or caseous subcutaneous exudates in Swollen Head Syndrom. When there is secondary infection of E.coli, there is polyserositis (with fibrinous exudates in abdominal cavity).

Diagnosis

It is based on clinical signs and laboratory tests. Virus can be isolated for identification. The nasal secretions, and tracheal and sinus scrapping can be sample for PCR. VN, ELISA, IFT are the serological tools to detect antibodies.

Treatment

Treatment is not available for this viral infection. However, the secondary bacterial infections can be controlled by application of antibiotics

Prevention

Vaccination with live vaccine is effective for short living birds. The long living birds are to be given the live vaccines and booster doses primed with inactivated vaccines. The vaccination has been proved to be the most effective in preventing the disease.

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