Poultry Disease Guide:

[mikey]

Amyloidosis

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
A Coronavirus infection of chickens with a morbidity of 50-100% and a mortality 0-25%, depending on secondary infections. Infection is via the conjunctiva or upper respiratory tract with an incubation period of 18-36 hours. The infection spreads rapidly by contact, fomites or aerosol. Some birds/viral strains can be carriers for up to 1 year. The virus, which may survive 4 weeks in premises, is sensitive to solvents, heat (56°C for 15 mins), alkalis, disinfectants (Formal 1% for 3 mins). Poor ventilation and high density are predisposing factors.

Signs

Sudden death.
Muscular shivering.
Otherwise as for standard IB.
Post-mortem lesions

Oedema of pectoral muscles and subcutaneously on abdomen, lesions progress to necrosis and scarring of deep pectorals in convalescence.
In layers the ovules may be intensely congested.
Other lesions of 'classical' IB may be encountered.
Diagnosis
3-5 passages in CE allantoic cavity, HA-, typical lesions, FA, ciliostatic in tracheal organ culture, cell culture (Vero, CK) only after adaptation Serology: HI, Elisa (both group specific), SN (type specific), DID (poor sensitivity, short duration, group specific).

Treatment
Sodium salicylate 1gm/litre (acute phase) where permitted - antibiotics to control secondary colibacillosis (q.v.).

Prevention
Live vaccines of appropriate sero-type and attenuation, possible reactions depending on virulence and particle size.

[mikey]

Anatipestifer Disease, New Duck Syndrome, Duck Sepicaemia

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
An acute or chronic septicaemic disease caused by Riemerella anatipestifer, syn Pasteurella, or Moraxella a. It affects ducks of any age, sometimes turkeys, and may also be isolated from chickens, game birds and wild waterfowl. Mortality is 2-75% in young ducks. Transmission is mainly direct, bird-to-bird, via toenail scratches, especially of the duckling foot, or through respiratory epithelium during respiratory disease. It can also be by faecal contamination of feed, water or the environment where survival of the infectious agent may be prolonged. Adverse environmental conditions and pre-existing disease are predisposing factors.

Signs

Weakness.
Neck tucked in.
Head/neck tremor.
Ataxia.
Disinclined to walk.
Incoordination.
Dyspnoea.
Ocular and/or nasal discharge.
Hyperexcitability
Post-mortem lesions

Perihepatitis without much smell or liver damage.
Pericarditis.
Airsacculitis.
Enlarged liver and spleen.
Occasionally fibrinous meningitis.
Salpingitis
Purulent synovitis.
Chronic arthritis, sometimes with erosions of the joint cartilage.
Diagnosis
Lesions, isolation and identification of organism - blood or chocolate agar in candle jar or 5% CO2. Differentiate from duck viral enteritis, duck viral hepatitis, fowl cholera, colibacillosis, coccidiosis, chlamydiosis.

Treatment
Sulphonamides and potentiated sulphonamides are the products most commonly recommended for drinking water application. Subcutaneous injections of penicillin + dihydrostreptomycin, or streptomycin + dihydrostreptomycin are also highly effective.

Prevention
Good husbandry and hygiene, rigid depopulation and disinfection, adequate protection, 'hardening off', correct house relative humidity, sulphonamides in feed. Inactivated and attenuated vaccines available in some countries. Autogenous bacterins sometimes used.

[mikey]

Arizona infection, Arizonosis

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
Caused by the bacterium Arizona hinshawii, renamed Salmonella Arizonae. It affects turkeys, mainly in North America, and is not present in the UK turkey population. Mortality is 10-50% in young birds, older birds are asymptomatic carriers. Transmission is vertical, transovarian, and also horizontal, through faecal contamination of environment, feed etc, from long-term intestinal carriers, rodents, reptiles.

Signs

Dejection.
Inappetance.
Diarrhoea.
Vent-pasting.
Nervous signs.
Paralysis.
Blindness, cloudiness in eye.
Huddling near heat.
Post-mortem lesions

Enlarged mottled liver.
Unabsorbed yolk sac.
Congestion of duodenum.
Cheesy plugs in intestine or caecum.
Foci in lungs.
Salpingitis.
Ophthalmitis.
Pericarditis.
Perihepatitis.
Diagnosis
Isolation and identification, methods as per Salmonella spp. Differentiate from salmonellosis, coli-septicaemia.

Treatment
Injection of streptomycin, spectinomycin, or gentamycin at the hatchery is used in some countries. Formerly in-feed medication with nitrofurans was also used.

Prevention
Eradicate from breeder population, fumigation of hatching eggs, good nest and hatchery hygiene, inject eggs or poults with antibiotics, monitor sensitivi

[mikey]

Ascites

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
Associated with inadequate supplies of oxygen, poor ventilation and physiology (oxygen demand, may be related to type of stock and strain). Ascites is a disease of broiler chickens occurring worldwide but especially at high altitude. The disease has a complex aetiology and is predisposed by reduced ventilation, high altitude, and respiratory disease. Morbidity is usually 1-5%, mortality 1-2% but can be 30% at high altitude. Pulmonary arterial vasoconstriction appears to be the main mechanism of the condition.

Signs

Sudden deaths in rapidly developing birds.
Poor development.
Progressive weakness and abdominal distension.
Recumbency.
Dyspnoea.
Possibly cyanosis.
Post-mortem lesions

Thickening of right-side myocardium.
Dilation of the ventricle.
Thickening of atrioventricular valve.
General venous congestion.
Severe muscle congestion.
Lungs and intestines congested.
Liver enlargement.
Spleen small.
Ascites.
Pericardial effusion.
Microscopic - cartilage nodules increased in lung.
Diagnosis
Gross pathology is characteristic. 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 (500 ppm) has been reported to be of benefit in South America.

Prevention
Good ventilation (including in incubation and chick transport), avoid any genetic tendency, control respiratory disease.

[mikey]

Avian Encephalomyelitis Egg Drop

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
Avian encephalomyelitis virus infection in laying bird causes inapparent infection or drops in egg production. See Avian Encephalomyelitis, Epidemic tremors for its effect in young birds. It affects chickens, turkeys, quail, pheasants and occurs in most poultry-producing countries. Morbidity 5-60%, mortality none. The means of transmission is unknown but probably by faecal contamination of environment, feed, water etc. with an oral infection route. Virus in faeces may survive 4 weeks or more. Predisposed by immunosuppression.

Signs

Drop in egg production, small (5-10%) and lasting no more than 2 weeks.
In breeders there may be a drop in hatchability of about 5%, and there is serious disease in the progeny (see next section).
Post-mortem lesions

None.
Diagnosis
History, rising titre to AE virus, subsequent disease in progeny if breeders. Serology - The embryo protection test has been used in the past, now Elisa is used more commonly. Differentiate from Infectious Bronchitis, lentogenic Newcastle disease, EDS­76.

Treatment
None.

Prevention
Vaccination of breeders/layers at 9-15 weeks, attenuated or not. Immunity is usually long lasting

[mikey]

Avian Encephalomyelitis, Epidemic Tremors

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
Avian encephalomyelitis is a viral disease of the central nervous system of chickens, pheasants, turkeys, and quail. It has a worldwide distribution. Morbidity 5-60% depending on the immune status of the majority of parents, mortality high. Vertical transmission is very important, transmission occurs over about 1-2 weeks, some lateral. The route of infection is transovarian with an incubation period of 1-7 days; lateral transmission is probably by the oral route, incubation >10 days. Virus in faeces may survive 4 weeks or more.

Signs

Nervous signs.
Dull expression.
Ataxia and sitting on hocks.
Imbalance.
Paralysis.
Tremor of head, neck and wings. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand.
Post-mortem lesions

Gross lesions are mild or absent.
There may be focal white areas in gizzard muscle (inconstant).
A few recovered birds may develop cataracts weeks after infection.
Microscopic - nonpurulent diffuse encephalomyelitis with perivascular cuffing.
Diagnosis
A presumptive diagnosis is based on the history, signs, and lack of significant lesions. Histopathology is usually diagnostic and IFA, and/or viral isolation may be carried out if required. The embryo protection test has been used in the past, now Elisa is used more commonly. Differentiate from Newcastle disease, vitamin deficiency (E, A, riboflavin), toxicities, EE (especially in pheasant in the Americas), Marek's disease, Mycotic Encephalitis, Brain abscess, Enterococcus hirae infection.

Treatment
None.

Prevention
Vaccination of breeders at 9-15 weeks, attenuated or not. Immunity is long lasting.

[mikey]

Avian Influenza-Highly Pathogenic (HPAI), Fowl Plague
Related Products:
GALLIMUNE® FLU H5N9
Trovac AIV H5

Extracted From:

A Pocket Guide to

Poultry Health
and
Disease
 
By Paul McMullin
© 2004

Click Here to
Order Your Copy
Introduction
One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE, the equivalent of the World Health Organisation for animal diseases. This viral disease can cause exceptionally high mortality, especially in turkeys. In addition official control measures disrupt trade in poultry products from affected areas. The cause is a virus, Orthomyxovirus type A, its pathogenicity is variable, and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). Highly pathogenic forms are usually of the H groups 5 and 7 and may now be identified (if H5 or H7) by the presence of a sequence at the haemagglutinin cleavage site that codes for multiple basic amino acids.

The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1.2 . This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. The higher the proportion of the chickens dying or showing signs the higher the IVPI. The virus infects chickens, turkeys, ducks, partridges, pheasants, quail, pigeons, and ostriches. Effectively all birds are considered to be at risk of infection. Apathogenic and mildly pathogenic influenza A viruses occur worldwide.

Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Outbreaks due to HPAI were recorded in the Pennsylvania area, USA, in the years 1983-84. More recently outbreaks have occurred in Australia, Pakistan, Mexico and, from December 1999, in northern Italy. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania, Italy). Because of this, and the high mortality that 'low-path' AI can cause in turkeys, OIE and other bodies are currently examining ways to improve control of LPAI. See current OIE records for up to date information on distribution of HPAI. Morbidity is high but mortality usually relatively low, 5-50%.

The route of infection is probably oral initially, but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Transmission is by direct contact with secretions from infected birds, especially faeces, waterfowl, equipment, clothing, drinking water. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. Avirulent in one species may be virulent in others. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. The virus is moderately resistant, can survive 4 days in water at 22°C, over 30 days at 0°C. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min, by acid pH, by oxidising agent and by formalin and iodine compounds. It can remain viable for long periods in tissues. Infections with other pathogens (e.g. Pasteurella) may increase mortality, even with 'low pathogenicity' strains.

Avian Influenza is a potential zoonosis. It can result in inapparent infection, conjunctivitis or severe pneumonia. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets.

Signs

Sudden death.
Marked loss of appetite, reduced feed consumption.
Cessation of normal flock vocalisation.
Drops in egg production.
Depression.
Coughing.
Nasal and ocular discharge.
Swollen face.
Cyanosis of comb/wattles.
Diarrhoea (often green).
Nervous signs such as paralysis.
Post-mortem lesions

Inflammation of sinuses, trachea, air sacs and conjunctiva.
Ovarian regression or haemorrhage.
Necrosis of skin of comb and wattles.
Subcutaneous oedema of head and neck.
Dehydration.
Muscles congested.
Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract.
Turkey lesions tend to be less marked than those of chickens, while ducks may be symptomless, lesionless carriers of highly pathogenic virus.
Diagnosis
A presumptive diagnosis may be made on history and post­mortem lesions. Confirmation is by viral isolation in chick embryo, HA+, NDV-, DID+. Commercial Elisa test kits are now available. However, as with many such tests occasional false positive reactions can occur. The agar gel precipitation test is non-group-specific and is used to confirm any positives. Differentiate from Newcastle disease, fowl cholera, infectious laryngotracheitis, other respiratory infections, bacterial sinusitis in ducks.

Treatment
None, but good husbandry, nutrition and antibiotics may reduce losses. Eradication by slaughter is usual in chickens and turkeys.

Prevention
Hygiene, quarantine, all-in/all-out production, etc. Minimise contact with wild birds, controlled marketing of recovered birds. Vaccination is not normally recommended because, although it may reduce losses initially, vaccinated birds may remain carriers if exposed to the infection. Vaccines have been used in recent outbreaks in Mexico and Pakistan. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). In outbreaks a regime of slaughter, correct disposal of carcases, cleaning, disinfection, isolation, 21-day interval to re-stocking should be followed. Survivors can be expected to have a high degree of immunity but may harbour virulent virus.

[mikey]

Avian Encephalomyelitis, Epidemic Tremors

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
Avian encephalomyelitis is a viral disease of the central nervous system of chickens, pheasants, turkeys, and quail. It has a worldwide distribution. Morbidity 5-60% depending on the immune status of the majority of parents, mortality high. Vertical transmission is very important, transmission occurs over about 1-2 weeks, some lateral. The route of infection is transovarian with an incubation period of 1-7 days; lateral transmission is probably by the oral route, incubation >10 days. Virus in faeces may survive 4 weeks or more.

Signs

Nervous signs.
Dull expression.
Ataxia and sitting on hocks.
Imbalance.
Paralysis.
Tremor of head, neck and wings. Tremor may be inapparent but is accentuated if chicks are held inverted in the hand.
Post-mortem lesions

Gross lesions are mild or absent.
There may be focal white areas in gizzard muscle (inconstant).
A few recovered birds may develop cataracts weeks after infection.
Microscopic - nonpurulent diffuse encephalomyelitis with perivascular cuffing.
Diagnosis
A presumptive diagnosis is based on the history, signs, and lack of significant lesions. Histopathology is usually diagnostic and IFA, and/or viral isolation may be carried out if required. The embryo protection test has been used in the past, now Elisa is used more commonly. Differentiate from Newcastle disease, vitamin deficiency (E, A, riboflavin), toxicities, EE (especially in pheasant in the Americas), Marek's disease, Mycotic Encephalitis, Brain abscess, Enterococcus hirae infection.

Treatment
None.

Prevention
Vaccination of breeders at 9-15 weeks, attenuated or not. Immunity is long lasting.

[mikey]

Avian Influenza-Highly Pathogenic (HPAI), Fowl Plague
Related Products:
GALLIMUNE® FLU H5N9
Trovac AIV H5

Extracted From:

A Pocket Guide to

Poultry Health
and
Disease
 
By Paul McMullin
© 2004

Click Here to
Order Your Copy
Introduction
One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE, the equivalent of the World Health Organisation for animal diseases. This viral disease can cause exceptionally high mortality, especially in turkeys. In addition official control measures disrupt trade in poultry products from affected areas. The cause is a virus, Orthomyxovirus type A, its pathogenicity is variable, and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). Highly pathogenic forms are usually of the H groups 5 and 7 and may now be identified (if H5 or H7) by the presence of a sequence at the haemagglutinin cleavage site that codes for multiple basic amino acids.

The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1.2 . This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. The higher the proportion of the chickens dying or showing signs the higher the IVPI. The virus infects chickens, turkeys, ducks, partridges, pheasants, quail, pigeons, and ostriches. Effectively all birds are considered to be at risk of infection. Apathogenic and mildly pathogenic influenza A viruses occur worldwide.

Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Outbreaks due to HPAI were recorded in the Pennsylvania area, USA, in the years 1983-84. More recently outbreaks have occurred in Australia, Pakistan, Mexico and, from December 1999, in northern Italy. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania, Italy). Because of this, and the high mortality that 'low-path' AI can cause in turkeys, OIE and other bodies are currently examining ways to improve control of LPAI. See current OIE records for up to date information on distribution of HPAI. Morbidity is high but mortality usually relatively low, 5-50%.

The route of infection is probably oral initially, but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Transmission is by direct contact with secretions from infected birds, especially faeces, waterfowl, equipment, clothing, drinking water. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. Avirulent in one species may be virulent in others. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. The virus is moderately resistant, can survive 4 days in water at 22°C, over 30 days at 0°C. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min, by acid pH, by oxidising agent and by formalin and iodine compounds. It can remain viable for long periods in tissues. Infections with other pathogens (e.g. Pasteurella) may increase mortality, even with 'low pathogenicity' strains.

Avian Influenza is a potential zoonosis. It can result in inapparent infection, conjunctivitis or severe pneumonia. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets.

Signs

Sudden death.
Marked loss of appetite, reduced feed consumption.
Cessation of normal flock vocalisation.
Drops in egg production.
Depression.
Coughing.
Nasal and ocular discharge.
Swollen face.
Cyanosis of comb/wattles.
Diarrhoea (often green).
Nervous signs such as paralysis.
Post-mortem lesions

Inflammation of sinuses, trachea, air sacs and conjunctiva.
Ovarian regression or haemorrhage.
Necrosis of skin of comb and wattles.
Subcutaneous oedema of head and neck.
Dehydration.
Muscles congested.
Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract.
Turkey lesions tend to be less marked than those of chickens, while ducks may be symptomless, lesionless carriers of highly pathogenic virus.
Diagnosis
A presumptive diagnosis may be made on history and post­mortem lesions. Confirmation is by viral isolation in chick embryo, HA+, NDV-, DID+. Commercial Elisa test kits are now available. However, as with many such tests occasional false positive reactions can occur. The agar gel precipitation test is non-group-specific and is used to confirm any positives. Differentiate from Newcastle disease, fowl cholera, infectious laryngotracheitis, other respiratory infections, bacterial sinusitis in ducks.

Treatment
None, but good husbandry, nutrition and antibiotics may reduce losses. Eradication by slaughter is usual in chickens and turkeys.

Prevention
Hygiene, quarantine, all-in/all-out production, etc. Minimise contact with wild birds, controlled marketing of recovered birds. Vaccination is not normally recommended because, although it may reduce losses initially, vaccinated birds may remain carriers if exposed to the infection. Vaccines have been used in recent outbreaks in Mexico and Pakistan. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). In outbreaks a regime of slaughter, correct disposal of carcases, cleaning, disinfection, isolation, 21-day interval to re-stocking should be followed. Survivors can be expected to have a high degree of immunity but may harbour virulent virus.

[mikey]

Avian Leukosis (Serotype J), Myelocytomatosis

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
Caused by an avian retrovirus. This condition has until now been seen only in meat-type chickens, with considerable strain-to-strain variation. It has occured in Europe, North and South America. Morbidity is low, though there is high mortality of affected birds.

Transmission is by congenital infection from antibody-negative females, bleeding and vaccination needles; lateral transmission by faecal-oral route (this declines as the bird ages). The incubation period is 10-20 weeks. Congenitally infected birds tend to remain antibody negative, shed virus and develop tumours. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear.

Signs

Depression.
Emaciation.
Loss of weight.
Persistent low mortality.
Enlargement of abdomen, liver.
Many are asymptomatic.
Post-mortem lesions

Liver enlargement, often with tumour foci.
Splenomegaly and enlarged kidneys also occur.
Most characteristically are chalky white tumours in the bone marrow, particularly of the sternum, ribs, sacral joint.
Microscopic - tumours usually contain well-differentiated myelocytes. Two cell types may be found in the same tumour.
Diagnosis
History, age, lesions, histology, ultimately identification of virus by isolation and/or PCR. Differentiate from Marek's disease, Lymphoid Leukosis.

Treatment
None.

Prevention
Checking of antigen in the albumen is a basis for eradication - most but not all, birds with egg antigen will be antibody negative. 'Shedders' - 80% produce infected chicks, 'non-shedders' - only 3% produced infected chicks. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. There is also evidence that it is slightly more sensitive than conventional testing. Serology - an Elisa test is aviailable to identify antibody positive birds. Prevent/ reduce cross-infection in hatchery and on farm.

Critical hatchery practices:

Separate infected and uninfected lines.
Handle clean lines before infected lines, preferably on separate hatch days and in separate machines.
Separation in vaccination.
Minimise stress.
Farm practices:
Brood and rear lines separately and maintain separate for as long as possible.
Minimise group sizes.
Delay live vaccine challenges.
Avoid migration errors (birds unintentionally moving between pens).

[mikey]

Avian Leukosis, Lymphoid Leukosis, Leukosis/Sarkoma Group

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
A complex of viral diseases with various manifestations such as lymphoid leukosis, myeloblastosis (see Sero-type J), erythroblastosis, osteopetrosis, myxosarcomas, fibrosarcomas, other tumours. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock - egg layers are generally more susceptible to lymphoid leukosis.

Morbidity is low but mortality high. Mortality tends to be chronically higher than normal for a prolonged period. Egg production is somewhat reduced. There may be increased susceptibility to other infectious diseases due to damage to the immune system. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers), lateral transmission is poor but infection may occur by the faecal-oral route, especially in young birds. In lymphoid leukosis the incubation period is about 4-6 months; it may be as short as 6 weeks for some of the other manifestations. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants.

Signs

Depression.
Emaciation.
Loss of weight.
Persistent low mortality.
Enlargement of abdomen, liver or bursa.
Many are asymptomatic.
Post-mortem lesions

Focal grey to white tumours, initially in the bursa, then liver, spleen, kidney etc. Liver may be very large.
Microscopic - cells lymphoplastic
Diagnosis
History, age, lesions, cytology. Differentiate from Marek's disease, coligranuloma.

Treatment
None.

Prevention
Good hygiene, all-in/all-out production, control arthropods, eradication - checking of antigen in the albumen is a basis for eradication (see Sero-type J for details).

 
Figure 9. Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. This was a case of Myelocytoma Avian Leukosis (Sero-type J).

[mikey]

Avian Rhinotracheitis 'Swollen Head Syndrome'

Extracted From:

A Pocket Guide to
Poultry Health
and
Disease
 
By Paul McMullin
© 2004
Click Here to
Order Your Copy
Introduction
A viral disease of chickens, turkeys (see separate summary), guinea fowl and possibly pheasants seen in Europe, Africa, South America and North America. It is caused by a pneumovirus of the Paramyxoviridae family, first isolated from poults in South Africa in 1978. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). There is rapid lateral transmission with infection by aerosol through the respiratory route; vertical transmission is uncertain. As for many infections, fomites can be important in moving infection between farms. The incubation period is 5-7 days, morbidity is 10-100% and mortality can be 1-10%.

Signs

Decreased appetite, weight gain and feed efficiency.
Facial and head swelling (though this can occur in other conditions).
Loss of voice.
Ocular and nasal discharge.
Conjunctivitis.
Snick.
Dyspnoea.
Sinusitis.
Post-mortem lesions

Serous rhinitis and tracheitis, sometimes pus in bronchi. If secondary invasion by E. coli then pneumonia, airsacculitis and perihepatitis.
Congestion, oedema and pus in the air space of the skull occurs in a proportion of affected birds due to secondary bacterial infections.
Diagnosis
Clinical signs, serology, isolation of ciliostatic agent. Differentiate from Infectious Bronchitis, Lentogenic Newcastle disease, low virulence avian influenza, Ornithobacterium rhinotracheale. Serology - Elisa normally used, not all commercial kits are equally sensitive to response to both A and B challenge viruses.

Treatment
Antibiotic not very effective. Control respiratory stressors, chlorination of drinking water, multivitamins.

Prevention
All-in/all-out production, vaccination (degree of cross protection between A and B types remains to be established). Live vaccines can reduce clinical signs and adverse effects, inactivated vaccines may be used in breeders prior to lay.

 
Figure 10. Pus in skull bones. This is a common sequel to avian pneumovirus infection in both chickens and turkeys.