BOTULISM

BOTULISM

160.Botulism Is An Intoxication Caused By The Toxins Of Clostridium Botulinum. With The Exceptions Of Vultures, Most Birds Are Susceptible. The Clinical Signs Appear Within A Few Hours To Several Days. Flaccid Paresis Of Legs, Wings, Necks And Eyelids Is Observed. The Paresis Is Rapidly Progressing To Paralysis And The Birds Fall Into A Deep Coma With Neck And Head Typically Extended Forward. There Are No Typical Gross Lesions. The Treatment With Selenium, Vitamins A, D And E As Well As With Some Antibiotics As Chlortetracycline, Bacitracin Etc. Could Reduce Mortality Rate.

 

161Spirochaetosis Is A Septicaemic Disease Characterized By Depression, Progressive Paresis, Paralysis And Inflammatory Necrobiotic Changes In Parenchymal Organs And The Gastrointestinal Tract. The Birds Are Depressed, Cyanotic; Greenish Diarrhoea With Considerable Amounts Of Urates Is Observed.

 

162The Transmission Of Spirochaetosis Is Related To The Distribution Of The Fowl Tick Argas Persicus That Is The Reservoir And Main Vector. Hens, Turkeys, Geese, Ducks, Pheasants Etc. From All Ages Are Susceptible. At A Later Stage, Paresis And Paralysis Are Developing, The Birds Become Somnolent And Comatose.

 

163After Removal Of Plumage, The Ticks, Adhered To The Skin, Are Discovered. The Aetiological Agent Is Borrelia Anserina, A Highly Motile Spirochaete With 5-8 Coils. The Organism Is Not Resistant Outside The Host And Could Exist Only In Some Vector.

 

164. A Typical Finding For Spiro¬Chaetosis Is The Enlarged Spleen With Marble-Like Appearance. A. Persicus Remains Infective For Over 430 Days And Transmit Spiro-Chaetes To Its Progeny. Spirochaetes Could Be Identified In Giemsa-Stained Blood Smears. In The Late Stage Of The Disease, Spirochaetes Could Not Be Detected.

 

165The Liver Is Often Enlarged, Mottled With Necroses Of A Various Size And Marginal Infarctions. Usually, Bile-Coloured Mucoid Enteritis Is Observed. The Arsenics As Well As Some Antibiotics Including Tylosin, Tetracycline And Penicillin Are Effective For Treatment Of Infected Birds. The Application Of Vaccines Is Successful, But The Acquired Immunity Is Short And Revaccinations Are Needed.

GANGRENOUS DERMATITIS

GANGRENOUS DERMATITIS

148.149.150.The Gangrenous Dermatitis (GD) Is A Disease Affecting Fattening And Growing Birds, Characterized With Necrotization Of Different Skin Areas And A Severe Cellulitis Of The Subcutaneous Tissue. The Sudden And Quick Increase In Death Rates Is Often The First Signal For The Incidence Of GD. The Affected Birds Die After Less Than 24 H. The Death Rate Is From 1% To 60%. The Lesions Are Dark Red To Blue Green Macerated Skin Areas, Usually Featherless, Beginning Generally From Wings And The Adjacent Areas.

 

151.152.153.. Most Outbreaks Are Encountered In Broilers At The Age Of 4 - 8 Weeks. The Disease Is Also Observed In Stock Layer Hens At The Age Of 6 - 20 Weeks And Broiler Parents At The Age Of 20 Weeks. The Outbreaks Are Frequently Observed In Extremely Wet And Warm Premises. The Gangrenous Dermatitis Affects Birds While Still Alive. In More S Evere Cases, The Gangrene Could Begin And Involve The Skin Of The Head, Neck And The Breast. Affected Skin Is Macerated Or Totally Necrotic, Resulting In Exposure Of Underlying Tissues In A Number Of Cases.

 

154.The GD Agents Are CI. Septicum, CI. Perfringens Type A And Staphylococcus Aureus, Independently Or In Combination. The Associated Infection Is More Severe. The Skin Lesions Are Often Crepitating And Are Detected In The Regions Of Breast, Abdomen, Back Or Wings In Both Alive And Dead Birds.

 

155.Under The Affected Skin, Extensive Haemorrhagic Oedemas With Or Without Gas (Emphysema) Are Discovered. The Clostridia Are Encountered In Soil, Faeces And The Intestinal Content. Staphylococci Usually Inhabit The Skin And Mucous Coats Of Birds

 

156.Underlying Muscles Are Haemorrhagically Infiltrated And Also Could Contain Gas Among The Muscle Fibres. The Increased Susceptibility Of Birds To GD Is Related To Immunodeficiency States Secondary To CIA, IBD, IBH Etc. Other Predisposing Factors Are Aflatoxicoses, The Unbalanced Or Deficient Diet Or Poor Hygiene. The Skin Wounds Are The Entrance Door Of The Infection.

 

157.In Most Cases, No Changes In Viscera Are Observed. Rarely, Gas Bubbles Could Be Found Out In The Liver. The Diagnosis Is Confirmed By Imprint Preparations Or Histological Cross Sections. The Bacterial Agent Could Be Isolated From Cellulitic Zones.

 

158.Single Or Multiple Necroses Are Rarely Seen In The Liver. Prevention - The Factors Leading To Skin Injuries (Cannibalism, Mechanical Traumas Etc.) Should Be Minimized. Successful Approaches Are The Immunoprophylaxis Programmes In Breeder Flocks Aiming At Prevention And Reduction Of Possible Immuno¬Suppressive States.

 

159.Microscopic Lesions Are Characterized By Oedema, Emphysema, Hyperaemia, Haemorrhages And Necroses In The Subcutaneous Tissues. GD Could Be Effectively Treated By Tetracyclines: Doxyxycline Hydrochloride, Erythromycin Thiocyanate, Chlortetracycline And Copper Sulfate In The Water.

 

160.

 

 

 

 

CHOLANGIOHEPATITIS IN BROILER CHICKENS

CHOLANGIOHEPATITIS IN BROILER CHICKENS

125.126.Cholangiohepatitis (CAH) In Broiler Chickens Is Characterized By Inflammatory Proliferative And Dystrophic Necrobiotic Alterations In Bile Ducts And The Liver Parenchyma. Usually, No Clinical Signs Are Observed. The Increased Daily Mortality Is Insignificant, Although In Some Chickens, A Retarded Growth And Dehydration Could Be Present. Pathoanatomically, The Liver Is Enlarged And With Paler Yellow Colour. In Some Cases, Its Surface Has A Characteristic Acinous Appearance And In Others Is Mottled With Multiple Small Greyish-White Or Greenish Foci.

 

127The Walls Of The Gall Bladder Are Thickened, Sometimes Up To 5-6 Cm, And Opaque. The State Is Detected In The Last Phase Of The Fattening Period Or In The Slaughterhouse. It Is Possible To Observe CHA As An Independent Disease Or Associated With Necrotic Enteritis.

 

128A Transverse Cross Section Through The Thickened Gall Bladder Wall

 

129Clostridium Perfringens Is The Aetiological Agent. CAH Is Experimentally Reproduced In Broilers By Ligation Of Bile Ducts And Inoculation With CI. Perfringens. The Gall Bladder Is Filled With A Thick Bile Secretion Or A Dense Matter With A Creamy Colour.

 

130In Some Chickens, The Sub¬Cutaneous Fat And The Body Fat Have An Icteric Tint.

 

131.Histologically, The Liver Lesions Are Detected At A Various Stage Of Development. In The Majority Of Cases, Proliferative Changes In Bile Ducts Are Observed. The Overgrown Bile Ducts Form Granulomatous Struc¬Tures, Surrounded By Fine Reticular Fibres. Centrally, In Some Granulomas, Either Initial Or Advanced Degree Of Necrosis And Weak To Moderate Granulocytic Infiltration Are Observed.

 

132In Many Bile Ducts, A Biliary Stasis Is Present And Within Some, Among The Stagnated Secretion, A Huge Amount Of Microorganisms Are Detected. Pericanalicularly, Coagulation Necroses Are Frequently Noticed. Among Some Of These Foci, Hyalinization Of The Necrotic Masses And Single Microorganisms Are Present. Around The Necroses, A Belt Of Macrophages, Lymphocytes And Granulocytes Is Formed.

 

133. Many Gram-Positive Bacteria Are Detected Among Granulomas, In Bile Ducts’ Lumen And Into The Gall Bladder, Often Accompanied By Inflammatory Lesions. The Mucosa Of Bile Ducts And The Gall Bladder Is Frequently Necrotized And The Wall Is Thickened Because Of Connective Tissue Growth. The Diagnosis Is Based On The Characteristic Gross And Microscopic Lesions. The Prevention Is Similar To That In NE.

 

134. 135.Ulcerative Enteritis (UE) Is Characterized By Inflammatory Ulcerative And Necrotic Changes In Intestinal Mucosa And Dystrophic Necrobiotic Lesions Of The Liver And The Spleen. The Clinical Signs Include A General Malaise, Ruffled Feathers, Diarrhoea And Anaemia. In Many Instances, The Disease Begins With A Sudden Death. Pathoanatomically, Deep Button¬Like Ulcers Are Observed, Mainly In Caeca And Less Frequently, In Some Parts Of The Small Intestine, Usually Visible Through The Wall.

 

136.137.UE Is A Problem In All World Regions With Extensive Poultry Breeding. Young Birds Are Infected More Frequently Although The Disease Is Also Common Among Adult Quails. The Early Lesions Appear Like Yellowish Foci With Haemorrhagic Boundaries That Could Be Seen From Both The Serous And The Mucosal Surfaces.

 

138.The Aetiological Agent Is Clostridium Colinum, A Spore-Forming Organism, Highly Resistant To Chemical Agents And Physical Alterations. The Intestinal Content Is Often Mixed With Blood.

 

139.In Older And Larger Ulcers, The Haemorrhagic Zones Tend To Disappear. The Ulcers Could Have An Irregular Round Or Elongated Shape And Are Covered By Large Necrotic Diphtheritic Membranes.

 

140.Frequently, Adhesive Peritonitis Due To Inflammatory Involvement Of Adjacent Serous Coats Is Observed. Numerous Domestic And Wild Birds (Chickens, Quails, Turkeys, Rock Partridges, Geese, Partridges Etc.) Are Susceptible. The Chickens And The Quails Are The Most Vulnerable Between 4 And 12 Weeks Of Age Where As Turkeys Between 3 And 8 Weeks Of Age.

 

141.Liver, A Variety Of Dystrophic Changes And Necroses With Different Size And Shape Are Detected. Necrotic Foci In Some Cases Are Milliary.

 

142.Sometimes, Liver Necroses Reach 1 - 2 Cm. In Diameter And Are Surrounded By A Haemorrhagic Zone.

 

143.144.In Some Instances, Necrotic Foci Involve Large Parts Of The Liver And Are Infiltrated By Haemorrhages. The Aetiolo¬Gical Agent Is Distributed With The Excreta Of Acutely Ill And Recovered Birds And Persists In Soil For Many Months. The Incubation Period Is 1 - 3 Days. The Death Rate In Chickens Varies From 2% To 10% And In Quails Reaches 100%. The Outbreaks Of UE In Chickens Are Often Associated With Or Come After Coccidioses, CIA, IBD Or Stress Conditions.

 

145.. Most Commonly, Necroses Are Distinguished On The Background Of A Marked Parenchymatous Dystrophy, Affecting Partially Or Totally (Uni- Or Bilaterally) The Liver.

 

146.The Spleen Could Be Enlarged, Hyperaemic, Haemorrhagic And Some¬Times, With Necroses. The Diagnosis Is Based On The Typical Gross Lesions. When Needed, Imprint Preparations Are Made, A Histological Study Is Performed Or Attempts For Isolation And Identification Of The Aetiological Agent Are Made. UE Should Be Differentiated From NE, Coccidiosis And Histomonosis (Typhlo-Hepatitis).

 

147.Some Cases, Haemorrhages With Various Intensities Are Detected In The Mucous Coat Of The Gizzard. Prevention -Separate Housing Of The Different Age Groups Of Birds, Avoiding The Contact With Other Avian Species. The Pre¬Medication Of Forages With Some Antibiotics And Their Rotation Would Prevent The Reproduction Of CI. Colinum. A Good Effect Is Achieved With Oxytetra-Cycline Dihydrate (OTC 50% Premix). UE Could Be Effectively Treated With Doxycycline Hydrochloride, Amoxycillin Etc.

NECROTIC ENTERITIS

NECROTIC ENTERITIS

113.. Necrotic Enteritis (NE) Is An Acute Clostridium Infection Characterized By Severe Necroses Of Intestinal Mucosa. The Disease Begins Suddenly, With A Sharp Increase In Death Rate. A Strong Dehydration Is Observed. The Skin Is Sticked On Or Adhered To Body Musculature And Is Hardly Removed.

 

114.Chickens At The Age Of 25 Weeks Are Usually Affected, NE Is Also Encountered In Hens Particularly Near The Period Of The Beginning Of Egg Laying Or Peak Egg Laying, Most Commonly Associated With Coccidiosis. In Acute Cases, Marked Congestion Of Liver, Responsible For Its Dark Red To Black Appearance, Is Present.

 

115.The Aetiological Agent Is Clostridium Perfringens, Mainly From Type A And More Rarely From Type C. The Produced A And P" Toxins, From C. Perfringens Type A And Type C Respectively, Are Responsible For The Necrosis Of Intestinal Mucosa. The Small Intestine Is Often Distended With Gases And The Necrotic Mucosa Is Visible Through The Wall.

 

116.CI. Perfringens Is Ubiquitous And Normally Reside Into The Intestinal Tract. The Alterations Are Particularly In The Jejunum And The Ileum Because Of Their Higher PH And The Lower Oxygen Content In These Areas. Sometimes, Haemorrhages Are Seen Through The Intestinal Wall.

 

117.The Intestinal Lumen Is Filled With Brownish Watery Content, Mixed With Gas Bubbles.

 

118.Necrotic Mucosa Acquires A Greyish-Creamy Or Greenish Appearance. Sometimes The Mucosa Has A Flannelette Blanket-Like Appearance.

 

119.120.In Some Cases, The Mucosa Has A Linear Pattern Similar To The Bark Of A Tree. The Predisposing Factors Are Injuries Of Intestinal Mucosa By Various Eimeria Species, Migration Of Ascarids, Immuno¬Deficiency States Due To CIA, IBD, MD, High Content Of Wheat Or Fish Meal In The Diet.

 

121In Cases When NE Is Associated With Small Intestinal Coccidioses, Multiple Petechial Haemorrhages Could Be Perceived Through The Wall In Different Areas Along The Small Intestine.

 

112.123.124.Throughout The Simultaneous Occurrence Of NE And Cocci¬Dioses, The Content Of The Lumen Is Bloody, Mixed With Necrotic Detritus And Gas Bubbles. The Diagnosis Is Based On The Distinctive Gross Lesions. When Necessary, A Histological Investigation Is Performed Or Attempts For Isolation Of The Causative Agent. NE Should Be Distinguished From Ulcerative Enteritis And Some Small Intestinal Cocci¬Dioses. The Control Should Be Aimed At Predisposing Factors. An Appropriate Medication Of Feeds Is Recommended. A Good Effect Is Obtained With Oxytetra-Cycline Dihydrate (OTC 50% Premix). NE Could Be Effectively Treated With Doxy-Cycline Hydrochloride, Amoxicillin Etc.

MYCOPLASMA

MYCOPLASMA

99. 100. 101. MG Is Characterized By Respiratory Symptoms And A Prolonged Course Of The Disease. Particularly Susceptible Are Hens And Turkeys At All Ages. The Aetiological Agent Is M. Gallisepticum. In Many Cases However, The Pathogenicity Of The Microorganism Is Enhanced Because Of Its Association With Any Or Some Of The Following Agents: E. Coli, P. Multocida, H. Paragallinarum And IB Or ND Viruses. The Most Characteristic Signs In Adult Flocks Are Tracheal Rales, Nasal Discharge, Coughing, Decreased Egg Production. Most Outbreaks Are In Broiler Chickens Older Than 4 Weeks. The Course Of The Disease Is More Severe During The Winter And In Cases Of Associated Infections. Often, Conjunctivrtes, Facial Skin Oedema And Profuse Tear Secretion Could Be Observed.

 

102. In Turkeys, Unilateral Or Bilateral Swelling Of Periorbital Sinuses, Nasal Discharge And Conjunctivitis Are Observed. The Inflammatory Exudate Is Commonly Fibrinous And Is Detected As Diffuse Accumulation After Removal Of Overlying Skin.

 

103. 104.Most Common Gross Finding Is Aerosacculftes, The Air Sacs Being Filled With Fibrinous Caseous Exudate. The Majority Of Routine Chemical Disinfectants Are Effective Against M.Gallisepticum That Rarely Survives Longer Than A Few Days Away From The Host. The Birds Could Carry The Microorganism And Be Asymptomatic Until The Disease Is Triggered By Stress Factors Such As Change Of The Premise, The Diet Or Weather, Vaccinations Against Or Infections With IB Or ND, Increased Levels Of Dust Or Ammonia.

 

105.In Older Cases, The Content Of Air Sacs Is Dense And Compact. A Vertical Transmission Is Done Through The Eggs Of Some Unapparent Carriers. The Infected Progeny Transmits The Agent Horizontally Via Airborne Route, By Coughing Or Contaminated Forage, Water And Environment.

 

106.Serofibrinous Pneumonias, Usually Bilateral, Are A Frequent Finding.

 

107Often, The Inflammation Involves The Adjacent Serous Coats And Thus, Fibrinous Polyserosites Occur.

 

108Sinusites Are Relatively Rarely Observed In Hens. The Positive Agglutination Tests Of Sera In Several Birds From The Flock Confirm The Diagnosis. MG Should Be Distinguished From Other Respiratory Diseases In Poultry. Pulmonary And Air Sacs Lesions Could Be Mistaken With Similar Findings In E. Coli Septicaemia Or Aspergillus’s. In Turkeys, P. Multocida Pneumonia Should Also Be Considered.

 

109.110.Mycoplasma Synoviae (MS) Infections Could Progress As Either Acute Or A Chronic Systemic Disease With Symptoms Of Arthritis, Synovitis And Bursitis Especially In Hens And Turkeys. The Earliest Signs Are Lameness, Lying Down And Retarded Growth. Often, Oedemas Of Tibiotarsal Joints And The Drumstick Are Observed. The Morbidity And Death Rates Are Moderate, Under 10%. Young Chickens At The Age Of 4-12 Weeks And Turkey Poults At The Age Of 10-12 Weeks Are Susceptible. Synovites Are Encountered All Year Round, But Are Prevalent During Cold Humid Seasons Or When The Litter Is Wet.

 

111.112.Affected Birds Get Progressively Exhausted. When The Joints And Tendon Sheaths Are Open, A Serofibrinous Exudate Is Most Commonly Observed. The Aetiological Agent Is M. Synoviae. The Microorganism Shows A Certain Tropism To Synovial Structures As Joints And Tendon Sheaths. An Important Route Of Dissemination Of The Agent Is The Transovarial Trans¬Mission. The Distribution By A Horizontal Route Via The Respira¬Tory Tract Is Also Possible. The Commonly Used Means Of Diagnostics Is ELISA. MS Infections Should Be Differentiated From Staphylococcal Infections, Reoviral Arthritis And RGT (See RGT).

RIEMERELLA ANATIPESTIFER INFECTIONS

RIEMERELLA ANATIPESTIFER INFECTIONS

82.Riemerella Anatipestifer (RA) Infection Is A Contagious Disease In Domestic Ducks, Turkeys And Other Fowl. It Is Encountered As Acute Or Chronic Septicaemia And Is Characterized With Serous Fibrinous Polyserosites. The Respiratory Tract Could Be Also Affected. The Ducklings At The Age Of 18 Weeks Are Especially Susceptible. Clinically, Sneezing, Cough, Trembling Of The Head And Neck, Ataxia And Greenish Diarrhoea Could Be Present.

 

83. The Most Characteristic Gross Lesion Is The Deposit Of Fibrinous Exudate On The Pericardium, The Liver Capsule Or Air Sacs. The Chronic Lesions Affect The Skin And The Joints. Although A Tentative Diagnosis Could Be Made On The Basis Of Observed Clinical Symptoms And Lesions, It Is Confirmed Upon The Isolation And Identification Of RA. The RA Infection Should Be Distinguished From Septicaemiae Due To P. Multocida, E. Coli, Salmonella Etc. The Treatment With Antibiotics (Flumequine) And Sulfonamides IJrimetoprim, Sulfadiazine) Has A Varying Success.

 

84. 85. Staphylococcus Aureus Infections Are Commonly Seen In Poultry. Usually, Bones, Tendon Sheaths And Joints, Particularly Coxofemoral And Tibiotarsal Joints Are Affected. The Clinical Signs Include Unilateral Or Bilateral Lameness, Reluctance To Move And Lying Down. When The Tibiotarsal Joints Are Affected, Swellings, Fever And Sometimes Necroses Of Overlying Tissues And Purulent Exudation Are Observed.

 

86. 87.As A Sequel To Septicaemia, Osteomyelitis Could Occur. The Lesions Are Usually Detected In The Region Of The Proximal Femur, Where Inflammatory Necrotic Foci In The Bone Marrow And Partial Or Complete Fracture Of The Femoral Head Are Observed.

 

88. The Outcomes Of Skin Injuries Are The Appearance Of Cellulites, Characterized By Extensive Purulent Inflammation Of The Subcutaneous Tissue. Most Staphylococcal Isolates Are Identified As Staphylococcus Aureus, Gram-Positive Cocci, Arranged In Clusters.

 

89. 90. Plantar Abscesses Are A Kind Of Local Purulent Inflammation. They Are Located On The Plantar Surface Or Adjacently To It And Appear Following Puncture Wounds. Staphylococci Are Moderately Resistant To Common Disinfectants. Chlorine-Containing Disinfectants Are Efficient In The Absence Of Organic Matter.

 

91. 92.. Other Local Forms Of Staphylococcosis Are Sternal Bursites. The Sternal Bursa Is Enlarged At A Various Extent Because Of Gathering Of Purulent Substance. Sometimes, The Covering Skin Is Necrotized. The Microorganism Is Widely Distributed In The Environment And Mainly On The Skin. Most Of Staphylococcus Oureus-Induced Lesions Are Associated With Skin Injuries, Debeaking, Finger Cuts. All Categories Of Birds Are Affected. Toxicogenic Strains Are Able To Induce Food Intoxications.

 

93. In A Septicaemic Staphylococcal Infection, Hyperaemia, Enlargement And Various-Degree Coagulation Necroses In The Liver Or The Spleen Are Observed. As Staphylococci Are Ubiquitous, Their Presence Could Not Be Prevented. The Measures Should Be Directed Toward Minimizing The Possibilities For Traumas Of Skin, Respiratory And Intestinal Mucosa.

 

94. A Typical Secondary Infection Is Staphylococcal Gangrenous Dermatitis That Is Usually Resulting From Immunosuppressive Infections (IBD, CIA). Affected Skin Areas Are Dark Red To Blue-Greenish, Moist And Sharply Defined From The Adjacent Healthy Skin.

 

95. Histologically, Staphylococcal Lesions Consist Of Necroses, Bacterial Colonization And Heterophilic Infiltration. The Isolation And Identification Of Staphylococcus Spp. Confirms The Diagnosis. From A Differential Diagnostical Point Of View, Infections With E. Coli, S. Gallinarum, P. Multocida, M. Synoviae And Reoviruses Should Be Considered.

 

96. . Streptococcosis In Poultry Is Encountered As Acute Septicaemia Or Chronic Infections With A Death Rate Between 0.5 And 50%. The Agent That Is Most Commonly Associated With Several Pathological Conditions In Poultry Is 5. Zooepidemicus. The Lesions In Chronic Streptococcal Infections Include Arthrites, Tenosynovites, Myocardites And Valve Endocardites. Endocardites Affect Predominantly Mitral Valves And Less Frequently, Aortal And Tricuspid Valves.

 

97. 98. Other Lesions Related To Endocardites, Are Heart, Liver And Spleen Infarctions. Liver Infarctions Are Usually Peripherally Located On Margins, Have A Pale Creamy Colour And Are Sharply Demarcated. The Penetration Of The Infection Occurs Mainly Via The Oral Or Aerogenic Route, But Could Also Enter Through The Injured Skin, Especially In Battery Cage Layer Hens. The Differential Diagnosis Includes Other Bacterial Septicaemias As Staphylococcosis, Fowl Cholera, E. Coli Infections Etc.