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.

Protozoan Disease

Black Head ( Histomonosis, Enterohepatitis)

Cause

It is caused by a protozoan parasite Histomonas meleagridis.

Transmission

Infected water, feed or droppings play a role in transmission of the protozoa (direct transmission). The infected eggs of the caecal worm Heterakis gallinarum is also responsible for  the transmission (indirect transmission).

Species affected

It affects both the chickens, turkeys and peafowl. But the young chickens are more susceptible

Clinical signs and lesions

There is depression, ruffled feathers and yellowish diarhhoea.  The turkeys have dark head parts so the disease is known as black head. Mortality is higher, particularly in young turkey but the mortality is lower in young chickens. The infection can be also be seen in older birds.

Upon postmortem examination, liver has circular necrotic areas with a crater like centre and the caeca has cheesy cores.

Diagnosis

It can be diagnosed on the basis of clinical signs and postmortem findings

Treatment

The protozoan drugs can be given in starter and grower feeds for turkeys. The incidence of the disease can be minimized by growing turkeys on wire and indoors. The caecal worms should be eliminated and strict hygiene should be maintained.

Coccidiosis is complex disease of intestinal tract caused by an intracellular protozoan parasite.

Etiology

Eimeria is responsible for coccidiosis which is intracellular protozoan parasite of intestinal tract. The economically important species are E. acervulina, E. maxima, E. tenella, E. necatrix and E. brunette

Transmission

Intake of fecal contaminated food is the mode of transmission. The feces containing sporulatedEimeriaoocyst transmits the disease.

Incubation period of ceacalcoccidiosis is 5-6 days and intestinal coccidiosis is 5 days. Coccidiosis is most commonly seen in chickens between 3-6 weeks of afe although can be seen in all ages if not exposed withcoccidapreviously.young ones are more reversly affected.

Cecal coccidiosis

This is most common coccidiosis caused by E. tenella. This form is characterized by profuse haemorrhage due to rupture of blood vessel. Formation of cecal core can be observed at necropsy of dead birds.

Intestinal coccidiosis

E. necatrix, E. acervulina, E. mevati and E. maxima are mostly responsible for such kind of infection. Sudden death occurs at 5-7 days due to post infection. Infection leads to congestion of mucous membrane and hemorrhage. Wall of intestine becomes thick.

Rectal coccidiosis

E. brunette is mostly involved in causation of this form which is characterized by lossening of wall coming out of mucous casts in droppings.

Of the seven disease producing species E. tenella, E. necatrix, E. brunette are most harmful and cause high mortality and morbidity. E. maxima and E. acervulina are moderately harmful, E. nitis, and E. preaecox are least harmful.

E. maxima, E. acervulina, and E. mitiscauses causse non haemorraghiccoccidiosis and E. tenella , E. necatrix, and E. brunette causes haemorrhagiccoccidiosis.

Clinical findings

Affected birds are apathic, dull depressed and lethargic. They pass loos dropping which may contain mucous. Some droopings may be stained with blood. Severely affected ones die and other show clinical symptoms. They are also dehydrated anemic with ruffled feather.

Lesions

Inflammation and profuse haemorrhage of intestinal tract, thickening of intestinal mucosa are found. Profuse haemorraghe in caeca in cecalcoccidiosis .haemorrhagic foci are visible on mucous membrane and caecal core are found. Ladder like haemorrahage may be seen in rectum in recalhaemorrhage .

Diagnosis

Clinical symptoms and lesions are indicative but finding of oocyst in feces is confirmatory .

Occyst of different species of coccidian are seen at following sites.

Coccidian Site Oocyst
 E. tenella Caeca Broad and ovoid, no micropyle, residuum
 E. necatrix Middle portion of SI Long, oval, thin wall
 E.acervulina Upper 1/3rd of SI Ovoid, micropyle, residuum
 E.maxima Middle and post 1/3rdof SI Ovoidbilayered, yellowish large
 E.bruneti Lower 1/3rdof SI Oval, residuum, micropyle
 E. imitis Anterior ½ of SI Subspherical smooth walled

Differential diagnosis

Intestinal coccidiosis should be differentially diagnosed with necrotic enteritis.

Treatment

Sulphonamide or combination of diaverdin andsulphaquinoxaline is effective in treating coccidiosis. It is treated in specific pattern – 3 days medicated water, 2 days plain water and 2 days medicated water. Vit.A and K supplement is necessary for early recovery.

Prevention and control

Use of anti coccidial drugs on prophlctic dose controls coccidiosis. They are used on rotational and shuttle programme. Shuttle programme is the use of one anticoccidial in the starter and other in grower ration. Rotational programme is to make changes in the use of anticoccidial drugs. It is necessary to maintain good hygiene and sanitation , prevent access of infected dropping to the non-infected birds and keep older birds away from chicks, since older are carrier.  Also avoid moisture and humidity in litters by frequent turning of litter to keep the litter dry to reduce the sporulation of the oocyst.

Parasitic Diseases

Ectoparasites

The primary effects of lice on their hosts are the irritations they cause. The birds become restless and do not feed or sleep well. They may injure themselves or damage their feathers by pecking or scratching areas irritated by lice. Body weight and egg production may drop.

All lice infecting poultry and birds are the chewing type. Mites may be confused with lice, but mites suck blood. In general, each species of lice is confined to a particular kind of poultry, although some may pass from one kind to another when birds are closely associated. Chickens usually are infested with one or more of seven different species; turkeys have three common species.

All species of poultry lice have certain common habits. All live continuously on feathered hosts and soon die if removed. The eggs are attached to the feathers. Young lice resemble adults except in color and size. Lice differ in preferred locations on the host, and these preferences have given rise to the common names applied to various species.

In general, the incubation period of lice eggs is four to seven days, and development of the lice between hatching and the adult stage requires about twenty-one days. Mating takes place on the fowl, and egg laying begins two to three days after lice mature. The number of eggs probably ranges from fifty to three-hundred per female louse.

Head Louse (Cuclotogaster heterographa)

These are found mainly on the head, although it occurs occasionally on the neck and elsewhere. It usually is located near the skin in the down or at the base of the feathers on the top and back of the head and beneath the beak. In fact, the head of the louse often is found so close to the skin that poultrymen may think it is attached to the skin or is sucking blood. Although it does not suck blood, the head louse is very irritating and ranks first among lice as a pest of young chickens and turkeys. Heavily infested chicks soon become droopy and weak and may die before they are a month old. When the chickens become fairly well feathered, head lice decrease but may increase again when the fowls reach maturity.

This louse is oblong, grayish and about 1/10-inch long. The pearly-white eggs are attached singly to the down or at the base of the small feathers on the head. They hatch within five days into minute, pale, translucent lice resembling adults in shape.

Body Louse (Menacanthus stramineus)

These chickens prefers to stay on the skin rather than on the feathers. It chooses parts of the body that are not densely feathered, such as the area below the vent. In heavy infestations, it may be found on the breast, under the wings and on other parts of the body, including the head.

When the feathers are parted, straw-colored body lice may be seen running rapidly on the skin in search of cover. Eggs are deposited in clusters near the base of small feathers, particularly below the vent, or in young fowls, frequently on the head or throat. Eggs hatch in about a week and lice reach maturity within twenty days.

This is the most common louse infesting grown chickens. When present in large numbers, the skin is irritated greatly and scabs may result, especially below the vent.

Shaft Louse or small body louse (Menopon gallinae)

These are similar in appearance to the body louse, but smaller. It has a habit of resting on the body feather shafts of chickens where it may be seen running rapidly toward the body when feathers are parted suddenly. Sometimes as many as a dozen lice may be seen scurrying down a feather shaft.

Since the shaft louse apparently feeds on parts of the feathers, it is found in limited numbers on turkeys, guinea fowl and ducks kept in close association with chickens. It does not infest young birds until they become well feathered.

The same control measures used to eliminate mite populations is effective for treating lice. It is more important to apply the insecticides directly to the bird’s body rather than the premises.

All classes of poultry are susceptible to mites, some of which are blood-suckers, while others burrow into the skin or live on or in the feathers. Others occur in the air passages and in the lungs, liver and other internal organs. Poultry mites cause retarded growth, reduced egg production, lowered vitality, damaged plumage and even death. Much of the injury, consisting of constant irritation and loss of blood, is not apparent without careful examination.

Common Chicken Mite (Dermanyssus gallinae)

This is the most common mite found on all types of poultry. It is a blood-sucker, and when present in large numbers, loss of blood and irritation may be sufficient to cause anemia. Egg production is seriously reduced.

This mite feeds at night, and usually remains hidden in cracks and crevices during the day. It attacks birds at night while they are on the roost. In heavy infestations, some mites may remain on the birds during the day. About a day after feeding, the female lays eggs in cracks and crevices of the house. The eggs hatch and the mites develop into adults within about a week. During cold weather, the cycle is slower. A poultry house remains infested four to five months after birds are removed.

Since the mite feeds on wild birds, these birds may be responsible for spreading infestations. However, it is more likely that spread of the mite is promoted by using contaminated coops. Human carriers are also important. Since these mites do not stay on the birds during the day, apply treatments to houses and equipment as well as the birds.

Scaly-Leg Mite (Knemidocoptes mutans)

These mites lives under the scales on feet and legs of poultry. It also may attach to the comb and wattles. It causes a thickening of scales on the feet and legs that gives the impression that the scales are protruding directly outward, rather that laying flat on the limb. It spends its entire life cycle on the birds and spreads mainly by direct contact.

The Depluming Mite (Knemidocoptes laevis, variety gallinae)

These mites causes severe irritation by burrowing into the skin near the bases of feathers and frequently causes feathers to be pulled out or broken. The mite is barely visible to the naked eye and can be found in follicles at the base of the feathers. The mites crawl around the birds at times, spreading from bird to bird.

The most effective treatment for all mite species is a regular inspection and spraying program of both the birds and their premises. An appropriate solution of permethrin, when sprayed on the birds, will eliminate all mites that infest the bird. The spraying of all facilities will ensure that any mites hiding in cracks and crevices will be destroyed. The treatment should be repeated on a one to two month schedule or whenever populations of the mites are detected.

The Fowl Tick (Argas persicus) may be a serious parasite of poultry if it becomes numerous in poultry houses or on poultry ranges. The tick is a blood-sucker, and when present in large numbers it results in weakened birds, reduced egg production, emaciation and even death. The fowl tick is found throughout most of the South and is extremely hardy. Ticks have been kept alive without food for more than three years. The ticks will feed on all fowl.

Fowl ticks spend most of their lives in cracks and hiding places, emerging at night to take a blood meal. Mating takes place in the hiding areas. A few days after feeding, the female lays a batch of eggs. In warm weather the eggs hatch within fourteen days. In cold weather they may take up to three months to hatch. Larvae that hatch from the eggs crawl around until they find a host fowl. They remain attached to the birds for three to ten days. After leaving the birds they find hiding places and molt before seeking another blood meal. This is followed by additional moltings and blood meals.

Ticks are difficult to eradicate and methods employed must be performed carefully. It is not necessary to treat the birds, but houses and surrounding areas must be treated thoroughly.

Control of External Parasites

There are many insecticides available to help control external poultry parasites. The most effective broad spectrum insecticide is permethrin. Permethrin has a significant residual activity, thus making it ideal for treating facilities and equipment. At reduced concentrations it can be applied to the bird. Follow all manufacturers recommendations when using all insecticides.

Endoparasites

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Tapeworms/cestodes

Tapeworms or cestodes are ribbon-shaped, flattened worms composed of numerous segments or division. These parasites vary in size from very small to several inches in length. The head or anterior end is much smaller than the rest of the body. A portion of the intestine may be opened and placed in water to assist in finding the tapeworms.

Tapeworm infections can be controlled by regular treatment of the bird with fenbendazole or leviamisole. Tapeworms are most readily controlled by preventing the birds from eating the infected intermediate host.

Syngamus trachea (synonyms:Forked-worm, Red worm) 

It’s the round red worm which causes open mouth breathing, a characteristic symptoms of infected bird. Heavily infected birds usually emit a grunting sound because of the difficulty in breathing and many die from suffocation. The worms can easily block the trachea, so they are particularly harmful to young birds.

The gapeworm is sometimes designated as the “red-worm”; or “forked-worm” because of its red color and because the male and female are joined in permanent copulation. They appear like the letter Y. The female is the larger of the two and is one-fourth to one inch in length.

Theses posses simple and indirect lifecycle.The female worm lays eggs in the trachea, the eggs are coughed up, swallowed, and pass out in the droppings. Within eight to fourteen day the eggs are embryonate and are infective when eaten by birds or earthworms. The earthworm, snails and slugs serve as primary intermediate hosts for the gapeworm. Gapeworms in infected earthworms remain viable for four and a half years while those in snails and slugs remain infective for one year. After being consumed by the bird, gapeworm larvae hatch in the intestine and migrate from the intestine to the trachea and lungs.

Febendazole Is the drug to control the gape worm infestation in puolty flock.

1. Ascarids (Large Intestinal Roundworms)

Ascaridia Galli is one of the most common roundworm of poultry. Adult worms are about one and a half to three inches long and about the size of an ordinary pencil lead. Thus, they are easily visible with the naked eye. Droopiness, emaciation and diarrhea are most commonly seen in heavily infected birds. The primary damage is reduced efficiency of feed utilization, but death has been observed in severe infections.

Chickens of three to four months of age show resistance to infection. Specimens of this parasite are found occasionally in eggs. The worm apparently wanders from the intestine up the oviduct and is included in the egg contents as the egg in being formed.

The life cycle of this parasite is simple and direct. Females lay thick heavy-shelled eggs in the intestine that pass in the feces. A small embryo develops in the egg but does not hatch immediately. The larvae in the egg reach infective stage within two to three weeks. Disinfectants and other cleaning agents do not kill eggs under farm conditions. Birds become infected by eating eggs that have reached the infective stage.

Drugs available are only effective to remove the adult parasite. The immature form probably produces the most severe damage. The treatment of choice is piperazine.

The parasite can be controlled by strict sanitation, Segregate birds by age groups, with particular care applied to sanitation of young birds.

2. Cecal Worms(Heterakis gallinae)

This parasite (Heterakis gallinae) is found in the ceca of chickens, turkeys and other birds and apparently does not possess serious affect to health of bird. . Its main importance is that it has been incriminated as a vector of Histomonas meleagridis, the agent that causes blackhead disease. This protozoan parasite apparently is carried in the caecal worm egg and is transmitted from birds to birds through this egg.

The life cycle of this parasite is simple and direct. Females lay thick heavy-shelled eggs in the intestine that pass in the feces. A small embryo develops in the egg but does not hatch immediately. The larvae in the egg reach infective stage within two to three weeks

Febendazole is the drug of choice for the treatment of this parasitic worm.

Metabolic Disease

Ascities is a metabolic disease of poultry associated with inadequate supplies of oxygen, poor ventilation and physiology usually casing pulmonary vasoconstriction. This disease has a complex etiology and is predisposed by the reduced ventilation, high altitude and respiratory disease. Morbidity and mortality ranges around 1-5% and 1-2% respectively.

Clinical signs and symptoms:

  • Sudden deaths in rapidly developing birds.
  • Poor development.
  • Progressive weakness and abdominal distension.
  • Recumbency.
  • Dyspnoea.
  • Possibly cyanosis.

Lesions:

  • Liver enlargement.
  • Spleen small.
  • Ascites.
  • Pericardial effusion.
  • Microscopic – cartilage nodules increased in lung.
  • Thickening of right-side myocardium.
  • Dilation of the ventricle.
  • Thickening of atrioventricular valve.
  • General venous congestion.
  • Severe muscle congestion.
  • Lungs and intestines congested.

Diagnosis:

Diagnosis depends majorly upon the history, clinical findings in correlation to the lesion observed. A cardiac specific protein (Troponin T) may be measured in the blood. This may offer the ability to identify genetic predisposition. Differentiate from broiler Sudden Death Syndrome and bacterial endocarditis.

Treatment:

Improve ventilation, vitamin C supplement , reduce the ration protein ratio. Etc

Prevention:

Improving ventilation, and control over the respiratory disease.

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Fungal Diseases

Aspergillus fumigatus is primarily responsible for it

Transmission

Inhalation of fungal spores from contaminated litter or feed play a role in transmission.

Species affected

The susceptibility is high in young chickens than older ones. It can infect a wide range of species including turkey poults, pheasants, quails, ducklings and goslings.

Clinical signs

Depression, thirsty behavior, gasping and rapid behavior can be noticed. Yellow-white pin head sized lesions are common gross lesions in lungs and airsacs. But there be small yellow-green granular fungus growth in the entire body cavities. Mortality varies from 5 to 50%.

Diagnosis

The fungus can be identified microscopically from the lesion samples from respiratory passage, airsacs or abdominal cavity. Sometimes, it can be seen grossly as well. The confirmation is done by isolation and identification from the above lesions.

Treatment and Control

The strict hygiene and quality litter are most for its prevention. These are quite important in breeders and hatchery where antifungal disinfectants and appropriate disinfection procedures can be useful. But the treatment is not specifically available for disease once the birds get infection. Removal and destruction of the infected birds is the best way to manage the disease

Candidiasis, mycotic diseases of the digestive tract of various avian species, including chickens, turkeys, and quail caused by Candida albicans.

 It’s more likely to develop after use of therapeutic levels of various antibiotics or when using unsanitary drinking facilities.

Lesions are mostly confined in the crop and consist of thickened mucosa and whitish, raised pseudo membranes. The same lesions may be seen in the mouth and esophagus. Occasionally, shallow ulcers and sloughing of necrotic epithelium may be present. Listlessness and in appetence may be the only signs.

 A presumptive diagnosis may be made on observation of gross lesions. Diagnosis can be confirmed by demonstrating tissue invasion histologically and by culture of the organism. However, culture alone is not diagnostic of disease, because the yeast-like fungus is commonly isolated from clinically normal birds. Young chicks and poults are most susceptible.

Improving sanitation and minimizing antibiotic use in poultry help reduce the incidence of candidiasis. Candidiasis can be treated or prevented with copper sulfate at 1:2,000 dilution in the drinking water, but its effectiveness is controversial.

Bacterial Disease

Avian chlamydiosis is characterized by respiratory, digestive, or systemic infection. Infections are cosmopolitan in distribution and have been identified in at least 460 avian species.Among them poultry, turkeys, ducks, and pigeons are most often affected.  The disease is a significant cause of economic loss and human exposure in many parts of the world.

Etiology

Chlamydia psittaci, formerly renamed Chlamydophila psittaci, is an obligate intracellular bacterium.

Transmission:

Transmission is by the fecal-oral route or by inhalation. Airborne particles and dust spread the organism. Persistence of C psittaci in the nasal glands of chronically infected birds may be an important source of organisms.

Clinical Findings

Clinical signs and symptoms are variable depends upon the virulence of the organism, infectious dose, stress factors, and susceptibility of the bird species; asymptomatic infections are common.

Nasal and ocular discharge, conjunctivitis, sinusitis, green to yellow-green droppings, fever, inactivity, ruffled feathers, weakness, inappetence, and weight loss can be seen in clinically affected birds.

Lesions:

Serofibrinous polyserositis (airsacculitis, pericarditis, perihepatitis, peritonitis), pneumonia, hepatomegaly, and splenomegaly are most often observed. Multiple tan to white to yellow foci and/or petechial hemorrhages can be seen in the liver and spleen. Lesions are usually absent in latently infected birds, even though C psittaci is often being shed.

Diagnosis

Due to difference in the clinical presentations and common occurrence of latently infected carriers, no single diagnostic test can reliably determine infection.

The combination of a serologic and an antigen detection test, especially PCR, or culture, is a practical diagnostic scheme to confirm chlamydiosis. Serologic methods include direct and modified direct complement fixation, elementary body agglutination, antibody ELISA, and indirect immunofluorescence. The elementary body agglutination test detects IgM and is useful to determine recent infection. The complement fixation methods are more sensitive than agglutination methods. High antibody titers may persist after treatment and complicate evaluation of subsequent tests.

Antigen detection methods include immunohistochemistry (eg, immunofluorescence, immunoperoxidase), ELISA, and PCR. ELISA kits developed for detection ofChlamydia trachomatis in people are available commercially and are relatively inexpensive. The organism can also be identified in impression smears of affected tissues (eg, liver, spleen, and lung). Chlamydiae stain purple with Giemsa and red with Macchiavello and Gimenez stains.

Treatment

Avian chlamydiosis is a reportable zoonotic disease. Treatment prevents mortality and shedding but cannot be relied on to eliminate latent infection; shedding may recur. Tetracyclines (chlortetracycline, oxytetracycline, doxycycline) are the antibiotics of choice. Drug resistance to tetracyclines is rare, but reduced sensitivity requiring higher dosages is becoming more common. When tetracyclines are administered orally, additional sources of dietary calcium (eg, mineral block, supplement, cuttle bone) should be reduced to minimize interference with drug absorption.

Doxycycline is the current drug of choice, because it is better absorbed, has less affinity for calcium, better tissue distribution, and a longer half-life than other tetracyclines.

Zoonotic Risk

Avian chlamydiosis is a zoonotic disease that can affect people after exposure to aerosolized organisms shed from the digestive or respiratory tracts of infected live or dead birds or by direct contact with infected birds or tissues.

Some individuals, especially pregnant women and those with impaired immunity, are more susceptible than others. The illness in people is usually respiratory and varies from flu-like symptoms to systemic disease with pneumonia and possibly endocarditis and encephalitis.

Listeriosis is caused by the bacterium Listeria monocytogenes. Although many species of birds, including chickens are susceptible to infection but clinical disease in birds is rare.

Etiology

Caused bya gram-positive, non-spore forming, facultative intracellular, rod-shaped bacterium Listeria monocytogenes . Transmission occurs via ingestion, inhalation, or wound contamination.

Clinical Findings

Clinical signs are not specific in septicemic form but include depression, lethargy, and sudden death. In the encephalitic form, torticollis, leg paddling, opsisthotonos, paresis and paralysis lateral recumbency, ataxia, have been seen.

Lesions:

In septicemic form of listeriosis, extensive degeneration and necrosis of the myocardium along with splenomegaly, necrotic foci in the liver, and pericarditis.

 In the encephalitic form, no gross lesions are seen in the brain, but histopathologic lesions are remarkable and include disseminated microabscesses, extensive fibrinous thrombosis.

Diagnosis

Diagnosis is confirmed by immunohistochemistry to demonstrate L monocytogenes in the tissues or by isolation of the organism, usually from the liver and/or spleen in the septicemic form and brain in the encephalitic form.

Treatment and Prevention

Antibiotics may be used successfully to treat the septicemic form of the disease. In vitro, L monocytogenes is susceptible to penicillin, tetracycline, erythromycin, gentamicin, and trimethoprim-sulfamethoxazole. Treatment of the encephalitic form is usually unsuccessful. Prevention should focus on identifying and eliminating potential sources of infection.

Zoonotic Risk

Listeriosis is a serious zoonotic disease. L monocytogenes is recognized as an important food-borne pathogen in people and is of great concern to the public and poultry industry.

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Campylobacteriosis is a significant enterocolitis of people frequently acquired through consumption of undercooked poultry meat contaminated with Campylobacter jejuni. It is the leading bacterial cause of sporadic enteritis in developed countries. Some strains of C jejuni have been reported to cause enteritis and death in newly hatched chicks and poults

Cause:

C jejuni is the predominant species associated with food borne infection derived from poultry. C coli and C lari can also be recovered from the intestinal tract of poultry and have also been implicated in foodborne infection.

Once C jejuni has been introduced into the environment, rapid transmission within the flock occurs, with subsequent colonization of a high proportion of exposed breeders, commercial-meat, or laying-strain poultry. Some strains of Campylobacter can be transmitted vertically, either on the surface of eggs or by trans-ovarian transmission. It has been isolated from the reproductive tracts of hens and roosters.

Clinical Findings and Lesions

Most chicks display no lesions associated with Campylobacter infection. Frequently observed lesions are distention of the jejunum, Disseminated hemorrhagic enteritis, Focal hepatic necrosis.

Microscopic lesions of infected chicks include edema of the mucosa of the ileum and cecum with C jejuni in the brush border of enterocytes. Mononuclear infiltration of the submucosa and villous atrophy occur, with intraluminal accumulation of mucus, erythrocytes, and mononuclear and polymorphonuclear cells.

Diagnosis

Campylobacter can be cultured on many different selective media, but commonly available formulations contain Brucella agar base and bovine blood with as many as seven antibiotics that inhibit overgrowth of Enterobacteriaceae. They also can be cultured on blood agar by selective filtration.

Control and Prevention

Because C jejuni is not found as a specific pathogen under commercial conditions, treatment of poultry flocks is not a consideration. If C jejuni is considered a problem in companion bird aviaries or in exotic species, Antibiotics such as erythromycin can be administered in drinking water. Fluoroquinolones and erythromycins are the classes of antimicrobials used to treat people for campylobacteriosis. Sanition is the key for prevention.

It is a very important wide spread bacterial disease causing great economic loss in the poultry industry. It affects the birds of different age group.

Cause

It is caused by various strains of Escherichia coli.There are various strains which are abundantly present in the environment but all are not pathogenic.Based on antigenic structure are O antigen(154 serotypes),K antigen(88),H antigen(49) and all together 292 serotypes Most common serotypes in poultry are O1,O2,O35 and O78 andin human O157. It is estimated that 15% of the intestinal coliforms are potentially pathogenic. Infection can be primary or secondary after primary host defense damage (eg respiratory viral infections, Mycoplasma infections, parasites, wounds, nutrition).

Transmission

E. coli are normal intestinal inhabitants and are shed via  feces. Egg transmission (via egg surface contamination) is also common and can lead to high chick mortality.The water and droopings are the main source of spread of the disease. Infected cage and incubator act as constant source of infections. Contaminated feed is the frequent source of transmission.

Clinical Signs

Colisepeticemia:Acute infection day to week chicks,characterized by bronchopneumonia,pasty vent with diarrhea,mortality upto 60%.Enteritis:More common in young than adults usually diarrhea.Coligranoloma(Hajares Disease),Omphalitis (Mushy Chick disease), Egg Peritonitis, Arthiritis, Panopthalmitis, Pericarditis

Diagnosis

Isolation and identification of organism, clinical signs with characteristics postmortem lesion(plastic membrane in liver surface,pericardial sac,air sac,pericarditis)

Treatment

Antibiotics based on antibiotic sensitivity test. Drugs like furaltadone,neomycin & doxycyline, chloramphenicol, ampicillin, enrofloxacin, gentamicin and kanamycin have been found to be sensitive.

Control

Biosecurity, proper hatchery management, use of pellet feed,use of probiotics, acidification of gut e.g.citric and fumaric acid @0.5% feed .E.coli vaccination and vaccination against primary causes like respiratory viruses, coccidiosis, IBD, CAV.

It’s a bacterial disease caused by Erysipelothrix rhusiopathiae. This causative organism infect wild rang of birds Disease form is most commonly seen as septicemia but urticarial and endocardial forms also exist.

Erysipelas in poultry is seen worldwide and, although considered a sporadic disease, endemic areas exist.

Etiology:

E rhusiopathiae is a facultative, anaerobic bacterium. Two additional genomic species have been described: E tonsillarum, and most recently E inopinata, but neither is considered pathogenic for poultry. The organism is small, non-acid fast, nonmotile, does not form spores, and produces no known toxins. There is no flagellum, but a capsule has been demonstrated.

Epidemiology

Erysipelas occurs sporadically in poultry of all ages. It is ubiquitous in nature and found where nitrogenous substances decompose.

In nonvaccinated flocks, morbidity and mortality rates may reach 40%–50%, but mortality is usually <15%. In vaccinated flocks, some birds may be depressed for a short period and recover. Mortality in vaccinated and nonvaccinated poultry is influenced by the virulence of the organism.

Clinical Findings:

– Droopy, with an unsteady gait

– Cutaneous lesions and swollen hocks

– Decrease in Egg production and conjunctival edema can be seen in organic, cage-free flocks.

– Egg production may drop markedly

Lesions

Gross lesions such as peritonitis, pericarditis, petechiation of the heart, catarrhal exudate in the GI tract, and degeneration of fat associated with the thigh and heart may be noted. Vascular damage and fibrin thrombi are common findings on microscopic examination.

Diagnosis

A presumptive diagnosis can be based on an impression smear of the liver or spleen or on a smear of cardiac blood or bone marrow that shows gram-positive, slender, pleomorphic rods. Bone marrow is the tissue of choice in partially decomposed specimens. Isolation and identification of E rhusiopathiae is necessary for definitive diagnosis. Identification can be made by fluorescent antibody staining and PCR

Treatment

The antibiotic of choice is a rapid-acting penicillin such as potassium or sodium penicillin. As soon as a presumptive diagnosis is made, penicillin should be administered IM at 22,000 U/kg body wt, simultaneously with a full dose of erysipelas bacterin.

Vaccination will control erysipelas. Both inactivated and live vaccines are available for use in turkeys; only vaccines approved for use in turkeys should be used.

Fowl Cholera ( Avian Cholera, Pasteurellosis, Avian Haemorrhagic Septicaemia)

Cause

Pasteurella mulotocida, a gram negative bacterium that casuses fowl cholera

Transmission

It takes place by ingestion of contaminated feed or water. It is not transmitted vertically through eggs. The flies and red mite act like carriers while the rodents (rats and mice) can contaminate the feed and water.

Species affected

It can affect turkeys, chickens, ducks, geese, etc.

Clinical signs and lesions

There is depression and decrease in appetite in the birds. There is fall in egg production by 5-15%. In case of acute infection, there is bluish combs and wattles while there is swollen wattles in chronic infection. Mortality is higher in acute infection than chronic infection.

The lesions in acute phase include vascular changes in abdominal viscera, haemorrhages, liver swollen with focal necrosis, flaccid and haemorrhagic ovaries and ruptured yolks. The lesions in chronic phase include localized infections in conjunctiva and facial odema. The lesions can also be seen in infection in middle ear which causes torticollis and infection in meninges.

Diagnosis

It is diagnosed on the basis of clinical signs. Virus can be isolated from the affected internal organs.

Treatment and Control

It is treated by use of antibiotics after antibiotic sensitivity test. The proper management of hygiene and control of rodents are to applied for prevention. The live and inactivated vaccines can be given in the endemic areas.

Disease is characterized by rapid onset of acute mortality.  Birds succumbing to the infection have necrosis of the skin and subcutaneous tissue, usually involving the breast, abdomen, wing, or thigh.

Etiology:

It’s the disease of turkeys and chickens caused by Clostridium septicumC perfringens type A, and Staphylococcus aureus, either singly or in combination.

Clinical Findings

clinical findings are generally includes  depression, incoordination, inappetence, leg weakness, ataxia, and high fever.

Lesions:

Gross lesions consist of dark reddish purple to green, weepy areas of the skin. Affected areas usually include abdomen, breast, wings, or legs. Areas of affected dermis and subcutis are characterized by extensive blood-tinged edema, with or without gas (crepitus). Infection may extend into underlying musculature, which may be discolored and contain edema and gas.

Diagnosis

Tentative diagnosis is based on the history, lesions and clinical findings. Diagnostic confirmation is based on the presence of lesions and isolation of the causative agent(s) from affected tissue.

Treatment and Control

Total cleanout and disinfection of affected houses has reduced or eliminated gangrenous dermatitis infection on farms with historical problems. Salting of floors has also reduced bacterial challenge in subsequent flocks.

Gangrenous dermatitis can be treated effectively with administration of many broad-spectrum and gram-positive antibiotics. Water acidifiers have been used in cases to reduce, but not eliminate, mortality where mortality rates are low or antibiotic efficacy has been poor.

It is an acute respiratory disease of chicken caused by gram negative bacterium Haemophilus  paragalinarum. Three serotypes (A,B,C) have been reported among them serotype B is confined only to certain geographical areas.It occurs in growing chicks and layers.Great economic loss is due to increased culls and marked decrease in egg production 10-40%.Economical impact of IC in multi-stage farm is enormous.

Transmission

Transmit from bird to bird through air borne,farm to farm by contaminated feed,water,equipments and personnels,transport cages and truck.

Clinical signs and lesions

Signs are like CRD,the most prominent features of disease are facial edema,swollen wattles,cyanosis with cherry exudates in sinus,drop in egg production upto 10-40% sometimes total loss. Morbidity is very high, mortality is variable,but can reach in same flock ,a percentage as high as 20-30%.Acute catarrhal-fibrinous rhinitis and sinusitis are the specific lesions, Mouth and nostril have peculiar fowl odour.

Diagnosis

Diagnosis can be done on the basis of rapid spread of the disease and characteristic clinal signs but conformation can only be done by the isolation. In field condition Gram’s staining of the nasal or infraorbital exudates  revealing bipolarly stained gram negative organism will be very helpful. Besides these above method serological test like haemaggluination test, haemagglutination Inhibition test and dot blotting test are reliable method for diagnosis.

Treatment

Potentiated sulphonamide is a combination of choice.Treatment of the disease done effectively by administering antibiotics like amoxicillin, macrolides,erythromycin, tetracyclines &quinolones in drinking water.

Prevention and control

Bio-security and proper disinfection are most important.Since there is the problem of carrier bird among the treated the affected bird should be depopulated and equipment and premises be disinfected properly and kept vacant for 30-60 days before reuse.There should be adequate flock density and regular ,timely vaccination of the bird against the infectious coryza.

Necrotic Enteritis is an acute enterotoxemia. The disease primarily affects broiler chiken ( 2-5 weeks old) and turkeys (7- 12 weesk old) raised on litter but can also affect commercial layer pullets raised in cages.

Etiology

It is caused by gram positive obligatory anaerobic bacteria Clostridium perfringes, C. pergringens type A and type c are associated with necrotic enteritis in poultry. Toxins produced by the bacteria cause damage to the small intestine, liver lesions and mortality.

Transmission

 C. perfringes is a nearly ubiquitous bacteria readily found in soil, dust, feces feed and used poultry litter. It is a normal inhabitant of the intestine of healthy chickens. It causes necrotic enteritis if there is alternation in intestinal microflora or damage to intestinal mucos due to Coccidiosis, Mycotoxcosis, Salmonellosis.

Clinical symptoms

The disease is mostly characterized by sudden increase in mortality with severely depressed and anorectic birds. However birds reluctant to move and diarrhea may also be seen.

Lesions

Lesion are found in small intestine which may be ballooned, friable, and contain a foul smelling, brown fluid. The mucosa is often referred to as a Turkish towel appearance as it is covered with a tan to yellow pseudomembrane.

Diagnosis

History, clinical sign and lesions help in diagnosis. Isolation of large numbers of C. perfringes from intestinal contents confirms the diagnosis. Differential media specially designated for isolation of C. perfringens  can be used.

NE must be deferentially diagnosed with Intestinal Coccidiosis and Ulcerative Enteritis.

Treatment and control

It is essential to prevent the coccidiosis as coccidial damage is mainly responsible for NE. Avoiding drastic changes in feed and minimizing level of fishmeal, wheat, barley or rye in feed helps in prevention.

Antibiotic are given through drinking water for treating NE. bacitracin and Lincomycin are commonly used. The medicated drinking water should be the sole source of water.

It’s acute febrile bacterial disease that affects wide range of birds.

Etiology:

The causal organism, Borrelia anserina, is an actively motile spirochete, ~0.2–0.3 μm × 8–20 μm, and consists of 5–8 loosely arranged coils. Cultivation in vitro is difficult. Borrelia will grow on Barbour-Stoenner-Kelly medium but loses virulence after 12 passages.

Generally, an infected Argas tick can transmit the bacteria at every feeding and maintains the infection throughout larval, nymphal, and adult stages. The ticks also transmit the infection transovarially.

Clinical Findings

Signs include listlessness, depression, somnolence, moderate to marked shivering, and increased thirst. Ruffled feathers, anemia, and pale combs can be noticed as well, and in appetence can lead to reduced weight. Young birds are affected more severely than older ones. Egg production in layers or breeders may be reduced by 5%–10%, with a higher number of small eggs.

Lesions:

The spleen is enlarged, with petechial or ecchymotic hemorrhages, appearing dark or mottled. However, a contrasting situation may be seen in Mongolian pheasants, in which the spleen is reported to be small and pale. Occasionally, the liver may be swollen and contain focal areas of necrosis. Kidneys may be enlarged and pale. Green, catarrhal enteritis is common.

Diagnosis

Diagnosis depends on demonstration of Borrelia in the blood, either as actively motile during darkfield microscopy, as stained spirochetes in Giemsa-stained blood smears, or by PCR. In young birds, theBorrelia may reach vast numbers per oil-immersion field and persist for several days. Older birds usually have low numbers of Borrelia that are detected only with difficulty, or not at all, and that persist for only 1–2 days. Increased numbers of immature RBCs are noticed due to the anemia. Silver staining can be used to demonstrate the bacteria in tissues.

Treatment and Control

Several antibacterial agents are effective. The most widely used are penicillin derivatives, but streptomycins, tetracycline and tylosin is also effective.

Control must be directed against the biologic vector. Argas ticks are notable for their long lifespan, ability to survive for extended periods without a blood meal, efficiency in transmitting the spirochete, and ability to remain securely hidden in cracks and crevices often beyond the effective reach of pesticides. Accordingly, control is difficult. A combination of tick eradication and immunization is the most effective means of control.

 

Staphylococcosis is a bacterial disease that can affect a wide range of avian species, including poultry, and is seen worldwide. Economic losses may result from decreased weight gain, decreased egg production, lameness, mortality, and condemnation at slaughter.

Etiology

Caused by gram positive bacteria staphylococcus aureus. S aureus is a gram-positive, catalase-positive, coccoid bacterium that appears in grape-like clusters on stained smears. Staphylococcus toxins can enhance the pathogenicity of a strain.

Clinical Findings

Common clinical finding includes ruffled feathers and reluctant to walk, Depression, swollen joints in chronic cases along with gangrenous dermatitis.

Lesions:

Common lesion includes osteomylitis and fragile bones, femoral head necrosis, arthritis and synovitis. In most of the cases dark moist areas under skin is observed.

In addition, septicemia can result in green livers or livers with multifocal necrosis and/or granulomas. In acute infections, a sudden increase in mortality may be noted.

Diagnosis

Although some lesions may be suggestive of a Staphylococcus infection, diagnosis is confirmed by isolation and identification of causative organism.

Treatment and Prevention

Antibiotics used to treat Staphylococcus infections include penicillin, erythromycin, lincomycin, and spectinomycin. Proper management to prevent injury and immune compromised poultry helps prevent staphylococcosis. Beak and toe trimming procedures in young chickens and turkeys could result in a staphylococcal septicemia.

It’s a bacterial disease caused by gram positive streptococcus species.

Etiology

Streptococci are non spore forming, non-motile, gram-positive, catalase-negative coccoid bacteria that occur singly, in pairs, or in short chains when observed on stained smears.

 Transmission is via oral or aerosol routes as well as through skin injuries.

Clinical Findings

Streptococcal infections show septicemia, depression, lethargy, ruffled feathers, pale comb and wattles. In affected layers, egg production may drop by 15%. Acute fibrino-purulent conjunctivitis has been noted in infections caused by other Streptococcus spp.

Lesions:

Lesions in the acute septicemic form include splenomegaly, hepatomegaly (with or without reddish tan to white multifocal necrotic foci), and enlarged kidneys, congestion of subcutaneous tissue with or without sero-sanguinous fluid. Omphalitis in chicks. Blood stained feathers around the mouth and head due to blood from the oral cavity have been reported occasionally.

Chronic streptococcal infections result in arthritis and/or tenosynovitis, osteomyelitis, pericarditis, myocarditis ,salpingitis and valvular endocarditis. Lesions on the heart valves appear as small yellowish white or tan raised areas on the valvular surface.

Diagnosis

Diagnosis is made on the basis of history, clinical signs, and lesions. Isolation of Streptococcus spp from lesions confirms the diagnosis. Streptococci can be cultured easily on blood agar.

Treatment and Control

Antibiotics, including penicillin, erythromycin, novobiocin, oxytetracycline, chlortetracycline, and tetracycline, have been used to treat acute and sub acute infections.

Vaccination Methods in Poultry.

INDIVIDUAL BIRD APPLICATION METHODS OF POULTRY VACCINATION

Subcutaneous injection: Marek’s Disease vaccine in the hatchery. Inactivated vaccines such as Newcastle Disease Virus, Infectious Bronchitis Virus, Reovirus and Infectious Bursal Disease Virus may be given to Breeder Hens at housing by subcutaneous injection into the back of the mid-neck region.

Conjunctival sac installation: (eyedrop) Newcastle Disease, Infectious Bronchitis, Infectious Laryngotracheitis vaccines. One hand holds the head, thumb pressing the lower eyelid down, deposit one drop into the eye, said to be faster operation than transnasal drop.

Wing-web puncture: Fowl Pox (pigeon pox), and Avian Encephalomyelitis, Fowl Cholera chickens. Use double-prong sewing machine needle (supplied by vaccine manufacturer), dip into vaccine before each stab, spread the wing to expose the underside (up), stab through, do not touch feather with needles, avoid vessels. For fowl pox, examine for “take” 6-10 days post, swelling followed by scab formation. Revaccinate non-reactor flock. To vaccinate turkeys, puncture the loose skin between the thigh and abdomen.

Feather follicle inoculation: Fowl pox vaccine in turkeys. Remove 2-3 feather follicles over the thigh, brush against the opening of the follicle with vaccine-dipped brush (supplied) or the vaccine may be sprayed on the area with a sprayer, hold the tip 2?-3? away. Examine for “take” 6-10 days post.

Intramuscular injection: Vaccines (Infectious Bursal Disease, Newcastle Disease, Mycoplasma gallisepticum Fowl Cholera, Infectious Bronchitis, Reovirus) alone or in combination are used in Breeder birds usually just before housing. IM injection is in the pectoral muscles, using continuous flow, automatic syringe.

Embryo Injection: Vaccines (Marek’s Disease, Infectious Bursal Disease, Newcastle Disease or Infectious Bronchitis) are injected into 18 day old embryonating eggs with an automated machine.

METHODS OF POULTRY VACCINATION  FLOCK APPLICATION

Aerosol: Infectious Bronchitis vaccine, Newcastle Disease vaccine, and Laryngotracheitis vaccine. Day or night, house closed sufficiently to prevent cross drafts, use sprayer recommended by vaccine manufacturer, minimum spraying time 3-4 minutes, do not open the house for 15 minutes. Protect worker with goggles and face mask. Now also done in a spray cabinet at day one in hatchery for administering Newcastle-Bronchitis and Infectious Bursal Disease.

Water Administration: Newcastle disease, Infectious Bronchitis, (or the two combined), Avian Encephalomyelitis, Infectious Bursal Disease and Infectious Laryngotracheitis vaccines. Waterer with plastic bottom or glass container best, free of sanitizer in water or container, withhold water one hour in hot weather, or longer in cold weather, vaccine in cold water, and provide enough water space so that 2/3 birds of the flock can drink at one time. Add 0.1% powdered skim milk as stabilizer. All vaccine should be consumed within 45 minutes.

METHODS OF DRUG ADMINISTRATION TO DISEASED POULTRY FLOCKS

Commonly used drugs include – antibiotics, anticoccidial, antihistomonals and growth promotants

In Feed: Often used in preventive or long-term medication. Must be done when mixing feed and requires planning so that delivery and storage on the farm does not delay treatment. Requires no additional work at the farm.

In Drinking Water: Must be done at the farm and requires supervision. Compared to feed administration there is no delay in administration or withdrawal, prompt absorption and convenient to use. Birds may continue to drink when sick and “off feed”.

Topical Spray or Dust: (for Ectoparasites)

Egg Dipping: Must be done at the hatchery under controlled conditions. Usually results in reduced hatchability or fertility (e.g. antibiotics to control egg transmissible diseases such as mycoplasma).

Individual Bird Injection: Expensive labor use and time consuming, but sometimes necessary in severe disease or when drug of choice is non-absorbable (e.g. antibiotics).

Note: Some drugs or antibiotics require pre slaughter withdrawal time or are not permitted for use in laying birds.