INFECTIOUS ENCEPHALOMYELITIS

INFECTIOUS ENCEPHALOMYELITIS

248.The Infectious Encephalomyelitis (IEM) Is Characterized By Signs Of Ataxia, Progressing To Paralysis, Prostration And Marked Tremor Of The Head And The Neck, And Because Of That, Is Also Called Epidemic Tremor. The Chickens With Prostration Are Usually In Lateral Recumbency.

249.The Tremor Could Be Unapparent, But Is Often Perceptible When The Chicken Is Held Gently With The Hand And Carefully Looked At. The Expression Of The Eye Is Dull. IEM Outbreaks Are Generally Observed In Chickens At The Age Between 8 - 9 And 20 Days. The Morbidity Rate Could Reach 40 - 60%. The Average Death Rate Is About 25%, But Could Be More Than 50%. Gross Lesions Are Not Present.

250.The Histological Lesions Are Specific And With A Diagnostic Value. A Nonpurulent Encephalomyelitis With Marked Perivascular Clusters Is Present. The IEM Virus Is From The Picornaviridae Family. The Previous Studies Placed The Virus In The Enterovirus Genus, But Based On The Most Recent Studies, It Is Provisionally Referred To The Hepatovirus Genus. The Virus Is Found In Faeces Of Infected Chickens And Could Survive There For At Least 4 Weeks. It Is Relatively Highly Resistant To Environmental Conditions.

251.252.. A Particularly Valuable Finding Is The Central Chromatolysis (251) Of Neurons In Segments From The Lumbosacral Widening Of The Spinal Cord And More Rarely, Chromatopyknosis (252). The Infection Occurs In Non-Vaccinated Broiler Breeder Flocks And Its Course Is Subclinical. A Vertical Transmission Of The Infection To Susceptible Birds Is Realized By The Eggs Laid During This Period. At The Same Time, Parents Acquire Immunity And Transmit It To The Next Generations Thus Protecting Them From IEM. So, Clinical Manifestation Of IEM Is Observed In Chickens, Hatched From The Eggs During The 2- Or 3 Week Period After Breeder Flock’s Infection. The Next Generations Are Immune.

253.254.Valuable Diagnostic Findings Are The Dense Lymphoid Clusters In The Muscles Of The Proventriculus And The Gizzard (253) And In The Pancreatic Interstitium (254). The History Of The Disease, The Age Of Onset And The Typical Nervous Signs, Especially The Head Tremor Are Indicative For The Diagnosis That Could Be Finally Confirmed By Histology. IEM Should Be Differentiated From Other Diseases With Nervous Symptoms As Encephalomalacia, Mycotic Encephalites, Toxicoses (Salt, Pesticides). Prevention -Vaccination Of Breeder Flocks With Regard To Ensuring Maxi¬Mum Protection Of Their Offspring. The Chickens From Naturally Infected Flocks Obtain An Adequate Maternal Immunity That Preserves Them From The Disease.

SWOLLEN HEAD SYNDROME

SWOLLEN HEAD SYNDROME

237.238.Swollen Head Syndrome (SHS) Is A Complicated Infection In Broilers And Broiler Breeders, Where The Primary Aetiological Agent Is An Avian Pneumovirus (APV) And The Secondary -Usually E. Coli; It Is Characterized By Respiratory And Nervous Signs. In Broilers Chickens, SHS Is Generally Seen After The 4th Week Of Life. The First Clinical Signs Are Sneezing, Coughing, Rales And Conjunctivites. A Profuse Tear Secretion, Reddened Conjunctivas And A Characteristic Oblong Almond¬Like Shape Of Eyes Are Observed. The Inflammatory Exudate Is Initially Transparent, But Afterwards Becomes Opaque.

 

239.240.Subcutaneous Oedemas In The Head Region, Involving Unilaterally Or Bilaterally The Periorbital Sinuses And The Mandibular Space, Are Emerging. A Seasonal Pattern In The Prevalence With Peaks During Spring And Summer Is Observed.

 

241.242.After Removal Of The Covering Skin, Deposits Of Serofibrinous Exidate Are Observed. APV Is A Virus From The Paramyxoviridae Family. The Pneumovirus Is Present In Respiratory Secretions And Discharges. It Survives For A Long Time In Cold And Wet Environment. E. Coli Follows The APV Infection Of The Upper Respiratory Tract. The Triggered Inflammatory Response Results In Accumulation Of Exudate In The Subcutaneous Tissue. In Many Instances, A Croupous Pneumonia Develops At A Later Stage Consequently To Conta¬Mination With Other Pathogens.

 

243.244.245.SHS In Broiler Breeders Is Usually Encountered Around Or After The Peak Egg Laying Period Only In Female Birds. Unilateral Or Bilateral Swellings Of The Head, Affecting The Periorbital Sinuses, The Mandi¬Bular Space And The Wattles Are Seen. The Conjunctiva And The Mucous Membranes Of Sinuses Are Considered To Be The Entrance Door Of The Infection. A Unique Cytotoxin Has Been Identified In Many E. Coli Isolates In SHS That Could Be Involved In The Pathogenesis Of The Disease. The Inflamed By The Virus Infection Conjunctiva-Associated Lymphoid Tissue Is The Site Where The Bacterium Enters The Subcutaneous Tissue.

 

246. Frequently, Nervous Signs Are Observed In Broiler Breeders (Opisthotonus, Torticolis) Due To Inflammatory Processes In Pneumatic Skull Bones And The Middle Ear.

 

247.In Laying Hens, The Ovaries Are Affected In Many Instances (Sero¬Fibrinous Oophoritis), Resulting In Reduced Egg Production. The Diagnosis Is Based Upon The Distinctive Clinico-Morphological Signs. SHS Should Be Differentiated From Mycoplasma And Pasteurella Infections And The Skin Form Of Aspergillosis. Prevention - Improvement Of The Microclimate Of Premises, Use Of Live And Killed Vaccines.

LARYNGOTRACHEITIS

LARYNGOTRACHEITIS

232.Laryngotracheitis (LT) Is A Viral Infection In Hens, Pheasants And Peacocks Characterized By Catarrhal Haemorrhagic To Fibrinous Inflammation Of The Respiratory Tract. It Is Manifested In Laryngotracheal And Conjunctival Form. In The Laryngotracheal Form, Suffocation, Rales And Cough Are Observed. The Head And The Neck Are Strongly Extended Forward And Upward During Inspiration.

 

233.Mucous Coats Of The Larynx And The Trachea Are Catarrhally Haemorrhagically To Fibrinously Inflamed. Most Outbreaks Are Encountered Between The Age Of 4 And 14 Weeks Although The Disease Affects Fowl Of Any Age. LT Is Caused By A Herpesvirus That Is Relatively Resistant.

 

234.Haemorrhagic Laryngotracheitis. The Morbidity Rate Of LT Reaches 50-70% And The Death Rate: 10-20%. Often, It Goes On As A Complicated Infection After The Involvement Of E. Coli, St. Aureus, M. Gallisepticum Etc.

 

235.In Some Cases, Casts Of Haemorrhagic Or Fibrinous Exudate Are Formed That Could Almost Completely Obturate The Larynx And The Trachea. Source Of The Infection Are Sick And Convalescent Birds, The Latter Being Prolonged Carriers Of The Virus (Up To 1 - 2 Years). With This Regard, A Certain Stationarity Is Observed.

 

236.In The Conjunctival Form Of LT, Wet Eyes, Tear Secretion And Oedema Of Infraorbital Sinuses Are Observed, Especially In A Complicated Infection. The Typical Clinical And Morphological Signs Are Sufficient To Assume The Presence Of LT. The Diagnosis Is Confirmed With The Detection Of Intranuclear Inclusion Bodies In The Trachea Throughout The Histological Study In The Early Stages Of The Disease, Serological Studies (VN, ELISA) Etc. LT Should Be Differentiated From IB, SHS, M. Synoviae Infections Etc. Premises, Contamined With The LT Virus, Should Be Freed, Cleansed, Disinfected And Occupied Again After 5 - 6 Weeks. The Vaccination Of Unaffected Birds And These From Other Premises Of The Infected Farm Could Protect And Stop Subsequent Outbreaks.

INFECTIOUS BRONCHITIS . IB

226.In Chickens Up To The Age Of 4 Weeks, IB Is Manifested By Severe Respiratory Signs (Sneezing, Coughing, And Rales). Rhinites And Conjunctivites, Depression And Crowding Around Heat Sources Are Observed. The Death Rate Could Reach 100%. The Mortality In Young Chickens Is Usually Insignificant Provided That A Secondary Infection With A Different Agent Is Not Occurring. In Such Cases, There Is A Moderate To Severe Inflammatory Cell Infiltration Of Upper Respiratory Tract Mucosa, Resulting In Thickened And More Compact Mucosa.

 

227.228.In Layer Hens Infected With The IB Virus, Oophorites And Dystrophic Necrobiotic Lesions Affecting Primarily The Middle And The Last Thirds Of Oviduct’s Mucous Coat Are Observed. The Consequences Are Drop In Egg Production, Appearance And Increase In The Number Of De¬Formed And Pigmentless Eggs Or Eggs With Soft Shells And Watery Egg White.

 

229.230.231.The Nephrotropic Strains Of The IB Virus Cause Severe Inflammatory And Dystrophic Necrobiotic Damages Of Kidneys: Urolithiasis (229), Interstitial Nephritis (230), Haemorrhages (231) That Considerably Increase The Death Rate. Under Natural Conditions, Only Hens Are Infected. Non-Immune Birds Of All Ages Are Susceptible. The Disease Is Even Seen In Vaccinated Flocks. The Serological Methods (VN, ELISA Etc.) Are Widely Used In The Diagnostics. At Present, PCR Is Used For Rapid Identification Of IB Virus Serotypes. IB Should Be Distinguished From Other Acute Respiratory Disease As ND, Laryngotracheitis And Infectious Coryza. The Vaccination With Live Or Killed Vaccines Is Effective Only If They Contain The Respective Serotype Of The Virus For The Given Region.

ADENOVIRUS GROUP I - ASSOCIATED INFECTIONS

ADENOVIRUS GROUP I - ASSOCIATED INFECTIONS

212.. Necrotic Pancreatitis In Broilers. It Is Characterized By Focal Necroses In The Pancreas.

 

213.Gizzard Erosions In Broilers. They Are Manifested By Erosions Affecting The Cuticle And The Underlying Tissues Of The Gizzard.

 

214.Avian Adenovirus Splenomegaly. Avian Adenovirus Splenomegaly Is Characterized By Enlargement Of The Spleen, Pulmonary Oedema And Congestion. It Is Observed In Broiler Breeders At The Age Of 20-45 Weeks. Its Course Is Peracute Or Acute. The Mortality Could Reach 8 - 9%. The Most Typical Lesions Are Splenomegaly, Mottled Or Marble-Like Appearance Of The Spleen, Oedema Or Hyperaemia Of Lungs.

VIRAL INCLUSION BODY HEPATITIS

VIRAL INCLUSION BODY HEPATITIS

175.176.The Viral Inclusion Body Hepatitis (IBH) Is An Adenovirus Infection Characte¬Rized By Haemorrhages And Dystrophic Necrobiotic Changes In The Liver And Kidneys, Accompanied By Intranuclear Inclusion Bodies. A Characte¬Ristic Macroscopic Lesion Is The Enlarged, Dystrophic Liver With Yellowish Colour And Crumbly Texture.

 

177.178.IBH Outbreaks Are Encountered Primarily In Meat Type Chickens, Most Commonly At The Age Of 3-8 Weeks. IBH Often Occurs As A Secondary Infection To Immunodeficiency Resulting From Other Diseases (IBD, CIA). On The Background Of Dystrophic Liver Changes, Haemorrhages Of Various Intensity And Size Are Outlined, Thus Creating A Variety Of Liver Lesions.

 

179.180.Throughout IBH Outbreaks, Several Serotypes From The 12 Known Avian Adenoviruses (AAVs) Of Group I Are Isolated. The Sick Chickens Cany The Virus In Their Excreta, Kidneys, Tracheal And Nasal Mucosa. The Virus Is Resistant To Many Environmental Factors And Could Be Easily Trans¬Mitted By A Mechanical Route. The Transmission Of Adenoviruses Is Realized Vertically By Breeder Eggs And Horizontally, Via Excreta (Mainly Faeces). In A Number Of Cases, The Dominating Lesion Is The Massive Mottled Or Striated Haemorrhages Of The Liver.

 

181.IBH Is Characterized By A Sudden Onset And A Sharply Increased Death Rate That Reaches Peak Values By The 3rd - 4th Day And Returns Back Within The Normal Range By The 6th - 7th Day. The Total Death Rate Is Usually Under 10% But Sometimes Could Attain 30%. More Rarely, Macro-Scopically Visible Necrotic Foci Could Be Detected In The Liver.

 

182.The Kidneys Are Enlarged, Pale And Mottled With Multiple Haemorrhages.

 

183.Many Instances Of IBH, The Amount Of Pericardial Fluid Is Increased (Hydropericardium).

 

184.185.Clinical Signs Could Be Observed Only Several Hours Prior To Death Occurrence. They Consist In Pale Comb And Wattles, Depression And Apathy. Sometimes, The Skin Is Icteric. Often, Ecchymoses And Striated Haemorrhages In Skeletal Muscles Are Observed.

 

186\186"Microscopically, Extensive Dystrophic Changes And Necroses Of Liver Parenchyma Are Detected. In The Nuclei Of Hepatocytes, Basophilic Or Eosinophilic Inclusion Bodies Are Detected. The Basophilic Inclusion Bodies Are Usually Dense And Occupy The Entire Nuclear Inner Space (Arrow B), Whereas The Eosinophilic Ones Are Round Or Irregularly Shaped And Surrounded By A Light Halo (Arrow E). The Diagnosis Is Based Upon The Typical Gross Lesions And The History Records.A Principal Approach In IBH Diagnostics Is The Histological Investigation That Helps To Detect The Intranuclear Inclusion Bodies. IBH Should Be Distinguished Mainly From IBD And Chicken Infectious Anaemia (CIA). With Regard To IBH Prevention And Control, The Eggs Of Broiler Parent Flocks, Where The Disease Is Consecutively Appearing In The Progeny, Should Not Be Used For Hatching. The Access Of Wild Birds Should Be Prevented As They Are Potential Carriers And Distributors Of The Virus. The Most Important Steps In IBH Prevention Are The Control Of IBD And CIA. There Are Neither Vaccines, Nor An Effective Treatment.

EGG DROP SYNDROME -1976

 

209.210.211The Egg Drop Syndrome - 1976 (EDS 76) Is An Infectious Disease In Layer Hens Manifested By A Quick Drop In Egg Production, Failure To Reach Peak Production, Irregularly Shaped Eggs, Soft-Shelled Or Shell-Less Eggs And Depigmentation. The Aetiological Agent Is An Adenovirus Of Group III. The Horizontal Transmission Occurs Slowly In Battery Systems And Rapidly In Floor Housing Systems. The First Sign Is The Loss Of Egg Pigmentation, Rapidly Followed By The Appearance Of Soft-Shelled, Shell-Less Of Deformed-Shell Eggs. If Defective Eggs Are Discarded, The Remaining Ones Have No Problem With Fertilization And Hatching. The Drop Could Be Sudden Or Prolonged. Usually, It Lasts For 4-10 Weeks And The Egg Production Is Reduced By About 40%. Apart The Inactive Ovaries And Oviduct Atrophy, Other Lesions Are Not Discovered. The Replication Of The Virus In Epithelial Cells Of Oviduct Glands Results In Severe Inflammatory And Dystrophic Changes In The Mucous Coat. The Appearance Of Eggs With Impaired Quality And The Dropped Egg Production Are Suggestive For EDS 76. The Diagnosis Is Supported By Some Serological Studies And Is Confirmed After Isolation And Identification Of The Virus. In Many Instances, No Antibodies Are Detected In Infected Flocks Until Egg Production Approaches Levels Between 50% And Peak Production

Infectious Bursal Disease, IBD, Gumboro

Introduction

A viral disease, seen worldwide, which targets the bursal component of the immune system of chickens. In addition to the direct economic effects of the clinical disease, the damage caused to the immune system interacts with other pathogens to cause significant effects. The age up to which infection can cause serious immunosuppression varies between 14 and 28 days according to the antigen in question. Generally speaking the earlier the damage occurs the more severe the effects. 

The infective agent is a Birnavirus (Birnaviridae), Sero-type 1 only, first identified in the USA in 1962. (Turkeys and ducks show infection only, especially with sero-type 2).

Morbidity is high with a mortality usually 0- 20% but sometimes up to 60%. Signs are most pronounced in birds of 4-6 weeks and White Leghorns are more susceptible than broilers and brown-egg layers. 

The route of infection is usually oral, but may be via the conjunctiva or respiratory tract, with an incubation period of 2-3 days. The disease is highly contagious. Mealworms and litter mites may harbour the virus for 8 weeks, and affected birds excrete large amounts of virus for about 2 weeks post infection. There is no vertical transmission.
The virus is very resistant, persisting for months in houses, faeces etc. Subclinical infection in young chicks results in: deficient immunological response to Newcastle disease, Marek’s disease and Infectious Bronchitis; susceptibility to Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD.

Signs

• Depression.
• Inappetance.
• Unsteady gait.
• Huddling under equipment.
• Vent pecking.
• Diarrhoea with urates in mucus.

Post-mortem lesions

• Oedematous bursa (may be slightly enlarged, normal size or reduced in size depending on the stage), may have haemorrhages, rapidly proceeds to atrophy.
• Haemorrhages in skeletal muscle (especially on thighs).
• Dehydration.
• Swollen kidneys with urates.

Diagnosis

Clinical disease - History, lesions, histopathology. 

Subclinical disease - A history of chicks with very low levels of maternal antibody (Fewer than 80% positive in the immunodifusion test at day old, Elisa vaccination date prediction < 7 days), subsequent diagnosis of ‘immunosuppression diseases’ (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. This may be confirmed by demonstrating severe atrophy of the bursa, especially if present prior to 20 days of age. 

The normal weight of the bursa in broilers is about 0.3% of bodyweight, weights below 0.1% are highly suggestive. Other possible causes of early immunosuppression are severe mycotoxicosis and managment problems leading to severe stress.
Variants: There have been serious problems with early Gumboro disease in chicks with maternal immunity, especially in the Delmarva Peninsula in the USA. IBD viruses have been isolated and shown to have significant but not complete cross-protection. They are all sero-type 1. Serology: antibodies can be detected as early as 4-7 days after infection and these last for life. Tests used are mainly Elisa, (previously SN and DID). Half-life of maternally derived antibodies is 3.5- 4 days. Vaccination date prediction uses sera taken at day old and a mathematical formula to estimate the age when a target titre appropriate to vaccination will occur.
Differentiate clinical disease from: Infectious bronchitis (renal); Cryptosporidiosis of the bursa (rare); Coccidiosis; Haemorrhagic syndrome.

Treatment

No specific treatment is available. Use of a multivitamin supplement and facilitating access to water may help. Antibiotic medication may be indicated if secondary bacterial infection occurs.

Prevention

Vaccination, including passive protection via breeders, vaccination of progeny depending on virulence and age of challenge. In most countries breeders are immunised with a live vaccine at 6-8 weeks of age and then re-vaccinated with an oil-based inactivated vaccine at 18 weeks. A strong immunity follows field challenge. Immunity after a live vaccine can be poor if maternal antibody was still high at the time of vaccination. 

When outbreaks do occur, biosecurity measures may be helpful in limiting the spread between sites, and tracing of contacts may indicate sites on which a more rebust vaccination programme is indicated.

Figure 23. This shows the anatomical relationship between the bursa, the rectum and the vent. This bursa is from an acutely affected broiler. It is en larged, turgid and oedematous.

1.