Bird 3 Flashcards
What are the 3 types of salmonellosis
- Paratyphoid
- Pullorum disease
- Fowl typhoid
Paratyphoid types of salmonella caused by, significance and transmission
Caused by - S. typhimurium, S. enteritidis - A NOTIFIABLE DISEASE Significance - Various species affected - Public health risk - uncooked eggs and egg products and improperly/inadequately cooked poultry meat - high risk Transmission - Horizontal ○ Faces -> egg -> chicken ○ Feed, litter ○ Wild birds ○ Other animals
Paratyphoid types of salmonella signs/lesions, diagnosis and treatment
Signs/lesions
- Reduced hatchability, dead embryos, sick and dead chickens
- Most die without clinical signs
- Congested liver/spleen, pin point foci of necrosis on the liver, retained yolk sac which is caseous
- In chronic - localised in joints - arthritis, ophthalmitis, encephalitis
Diagnosis
- Isolation of salmonella from lesions - whole genome sequencing - THEN NOTIFY
Treatment
- Antibiotics medication but it encourages carrier state (doesn’t eliminate) and encourages drug resistance
Paratyphoid types of salmonella control/prevention 7 strategies
- Regular monitoring of breeder/layer flocks by taking faecal litter swabs and culture and detection programs
- Management to minimise faecal contamination of eggs - reduce floor eggs with adequate nests, clean nests
○ Possible fumigation of eggs with formaldehyde as soon after collection as is possible - Hatchery management to minimise disease spread -> hygiene, fumigation of eggs
- Competitive exclusion via use of “pro-biotics” to establish normal flora
- Feed hygiene in human cooking
- Exclusion of wild birds, rodents and other potential carriers of salmonella from commercial flocks
- Vaccination - live attenuated strains of S. typhimurium distributed into drinking water
Pullorum type of salmonella cause, significance and transmission and signs
Cause - S. pullorum -> mainly affects gallinaceous birds
- Eradicated from commercial poultry industry but still in backyard poultry
- NOTIFIABLE DISEASE IN VICTORIA
Transmission
- Vertical - transovarian
- Horizontal - contaminated food, litter, fomites
Signs
- Embryo mortality and reduced hatchability of infected eggs
- If hatch chickens die within first few weeks of life -> spread disease horizontally - persist in environment
Pullorum type of salmonella lesions, diagnosis and control
Lesions
- Young birds
- acute form involves large congested spleen and liver
- Subclinical/chronic form - focal necrosis/abscessation of liver, heart and other viscera
○ Adult - Oophoritis, arthritis common
Diagnosis
- Isolation of organism from infected tissues
- Rapid whole blood agglutination test to detect antibodies in carrier hens -> then cull
Control
- Eradication with the removal of carrier hens
Fowl typhoid cause what age affect and significance
Cause - S. gallinarum that is serologically related to S. pullorum
- Mainly older birds not young
- SAME AS PULLORUM DISEASE
- Also NOTIFIABLE
Yersiniosis (pseudotuberculosis) cause, birds common in, predisposing factors and transmission
Cause - Yersinia pseudotuberculosis
- Cage, aviary birds, canaries, finches, budgies and other parrots
- Predisposing factors -> stress, overcrowding, climatic stress, breeding season - lowers resistance
Transmission
- Previously infected birds -> chronically/latently infected carrier birds
- Rodents
- Wild birds
Yersiniosis (pseudotuberculosis signs/lesions, diagnosis, treatment and prevention
Signs/lesions
- Acute death -> acutely sick birds or chronic wasting disease
- Acute - large swollen liver and spleen, haemorrhages on serosal surfaces
- Subclinical/chronic -> abscesses of spleen and liver
Diagnosis
- Visualisation of small gram negative rods with impression smear of affect tissue
- Or by culture or histopathology
Treatment
- Antibiotics -> sulphonamides, amoxicillin
Prevention and control
- Rodents
- Concrete floor
- Carriers
- Feed contamination
Staphylococcus cause, when occurs, 2 forms with clinica signs and diagnosis
- S. aureus (Coagulase positive -> ONLY ONE THAT CAUSES DISEASE)
- Opportunistic organism -> immunosuppressed,
Two forms
1. Septicaemic
2. Localised form
○ Arthritis, synovitis, osteomyelitis
§ Concrete hard floors -> breaks in skin -> “bumble foot”
§ Femoral head necrosis
Diagnosis - take a sample and do gram stain and catalyse test (positive ensure that is a disease causing organism)
Spirochaetosis (tick fever) cause, distrubution, transmission and signs/lesions
Cause - borrelia anserina -> main vector is argas persicus (fowl tick)
- Only found in warmer parts of the country (north) due to distribution of vector
Transmission - tick bite or ingestion of infected tick
- Nocturnal feeding
Signs and lesions
- Acute form - anaemia, large congested spleen and liver -> sudden death
- Pericardial clouding
Spirochaetosis (tick fever) diagnosis, treatment and prevention
Diagnosis - for changes in the blood
Treatment - penicillin medication at early part of the disease
Prevention - tick prevention and possible vaccine
Colibacillosis cause, when occurs, predisposing factors and transmission
Cause - E. coli
- Opportunistic pathogen
Predisposing factors - avianpathogenic E.coli - doesn’t need these
- Respiratory pathogens -> CRD
- Environmental factors
- Immunosuppressive conditions
Transmission - faecal oral or with avian pathogenic E.coli could be respiratory
Colibacillosis 2 forms, other conditions it leads to, diagnosis and control
2 forms
1. Acute (colisepticaemia) -> avian pathogenic E.coli
○ Fibrin deposits around the liver and heart
2. Subacute/chronic (localised)
Other conditions
- Can cause arthritis, synovitis, osteomyelitis, spondylitis
Diagnosis
- Need to isolate bacteria and do antibiotic sensitivity as the strain is important for treatment
Control
- Hygiene - as faecal-oral route
- Predisposing factors
- Vaccination - doesn’t have the relevant strains
Avian influenza (fowl plague) what is signifiance and affected species
- EXOTIC TO AUSTRALIA
- OIE list A
- HIGH RISK TO HUMANS -> mainly in Asia where there is close contact between poultry and humans
○ Difficult for H5N1 to be transmitted to people only via contact with secretions of sick/dead birds
○ If infected -> symptoms similar to normal flu however mortality high
§ There are medications that are effective against avian influenza in humans - no vaccine
Affected species - Chicken & turkeys
- Ducks & geese -> don’t show the disease
- Wild & migratory birds (H5N1)
- Cage birds
- Humans -> what makes it dangerous that can be transmitted to humans - H5N1
Avian influenza what are the types and the high risk strain, how does it arise and transmission
Type of virus - TYPE A (birds), B and C ○ Sub-type from TYPE A § Neuraminidase (N): 9 § Haemagglutinin (H): 16 □ HIGH RISK STRAINS -> H5 and H7 - Genomic changes ○ Antigenic drift + antigenic shift results in change in tropism -> different tissues/species - How did it arise? -> we don't know Transmission - Shed in faeces - Horizontal transmission ○ Contact ○ Untreated surface water
Hihgly pathogenic avian influenza characteristics signs and lesions
- Characteristics ○ Usually one type of bird ○ High mortality ○ High morbidity ○ Rapid spread - Signs and lesions ○ Sudden death -> high mortality and morbidity ○ Haemorrhages, cyanosis of the comb
Highly pathogenic avian influenza diagnosis, control and prevention
- Diagnosis - we not involved, department of primary industries
- Control - kill all the animals in the area, strict quarantine measures
- Prevention
○ Vaccination - not used in Australia but is used in America
○ Biosecurity
§ Australia DOES NOT import live chickens or raw chicken products, only cooked chicken and sterilised eggs
□ Only egg products that DO NOT pose a risk of introducing avian influenza are permitted into Australia
® All imported/domestic egg products must be pasteurised
○ Proper cooking of meat/egg -> heat over 70 degrees for 30mins will kill virus
§ 80 degrees over one minute will also kill
What is the main pigment that indicates liver issues
Biliverdin
- Birds have very little biliverdin reductase
- Green pigment
- Accumulation in tissues
What are the main clinical signs of liver disease
- Mainly inapparent/silent
- appear in severe cases
○ Greenish colouration of urates (biliverdinuria): often the most obvious indication of liver failure
§ Due to failure of excretion of biliverdin in bile therefore excreted via kidney
○ Can also get greenish discolouration of the muscle - Usually terminal - convulsions and nerves signs
- Generally non-specific
○ “sick bird look”, weight loss and anorexia
○ distention of abdomen
○ Dyspnoea due to pressure of enlarged liver (extended past the sternum) on the lungs - Jaundice not usually evident
What diagnosic tests to assess liver function in live and dead birds
LIVE 1. serum chemistry 2. radiology 3. biopsy? - not recommended as risk of internal haemorrhage NECROSCOPY 1. gross lesions 2. microbiology 3. histopathology 4. impression smear (gram/giemsa stain)
Serum chemistry when assessing the liver, what are problems, important enzymes and summary
§ Problems
□ Interspecies variation
□ Unavailability of standards - not every species
□ Low specificity/sensitivity – especially enzymes
□ IM injections - increased plasma activity of several enzymes
§ Important chemistry enzymes
1. Aspartate amino transferase (AST, GOT)
® Found also in heart and skeletal muscles the - “leakage” enzyme (do CPK to exclude skeletal issues)
2. Lactate dehydrogenase (LDH)
® Found also in muscles, kidney, bone and RBCs*
® Shorter half-life than AST
3. Glutamate dehydrogenase (GLDH)
® Present also in kidney and brain
4. ALT (GPT) AP and GGT with questionable value
5. Bile acids - quite sensitive - the best
® Increased level correlate well with impaired liver “function”
® Kits have recently become available
§ In summary
□ AST ↑
□ Bile acids ↑
□ LDH ↑
What are the 3 main diseases of the liver
1) fatty ,iver
2) aflatoxicosis
3) hepatitis
1. bacterial
2. fungal
3. viral
4. parasitic
Fatty liver when physiological and when pathological
○ Normal -> physiological
§ Young newly hatched chicks that are reliant on metabolism of yolk - first 2 weeks of life
§ Laying hens active egg production have naturally fatty liver - yolk contains large lipid content and liver is the main producer of this
§ Nutritional -> large amount of calories without proper exercise
□ Is wanted in some restaurants -> force feed high calorie diets
○ Pathological -> due to fatty liver/haemorrhage syndrome and fatty liver/kidney disease
Fatty liver/Haemorrhage Syndrome signs, lesions, causes and control
○ Signs
§ Spontaneous mortalities often in obese hens with lower egg production
○ Lesions
§ Obese carcass, globules of fat in peritoneum, large pale friable liver, intrahepatic haemorrhages
○ Aetiology
§ High-energy diet
§ Little exercise
§ Warm condition
§ Low production
○ Control
Provide balance energy level diet - ensure not overweight
Aflatoxicosis cause, interspecies variation and signs
○ Aspergillus spp
○ Interspecies variation
§ Ducks and turkeys have high sensitivity showing acute hepatic necrosis and high mortality
§ Domestic fowl have lower sensitivity showing chronic hepatitis and low mortality
○ Generally due to moisture and heating/cooling of feed in silo
○ Signs
§ Reduced growth rate, poor productivity and ascites
Bacterial hepatitis cause and lesions
□ Cause -> Salmonella, E. coli, Pasteurella ® Often cause septicaemic conditions □ Lesions ® Pale liver, congested ® Multifocal necrosis ® Fibrosis ® Patchy discolouration
Viral hepatitis list the 7 types
- inclusion body hepatitis
- pscittacine adenoviral hepatitis
- pacheco’s disease
- herpesviruses of pigeons
- duck viral hepatitis
- big liver and spleen disease
- hepatitis-splenomegaly syndrome
Inclusion body hepatitis what caused by, what common in and onset
□ Common in young chickens usually 2-6 weeks old
□ Cause - one of the 12 fowl adenoviruses
® 3 groups that cause this in different species with 12 serotypes
□ Acute onset of mortality occurring over a period of 3 to 4 days (spiking mortality)
® After spiking mortality then goes away generally
Different strains cause different mortality rates
Inclusion body hepatitis lesions, diagnosis and treatment
□ Lesions
® Swollen liver with multiple pale haemorrahgic foci
□ Diagnosis
® Histopathological demonstration of liver with presence of inclusion bodies
® PCR is now available - using high resolution melt (HRM)
□ Treatment
® No treatment although supportive therapy may assist in recovery
® Live vaccine in Australia given to parents -> provide maternal antibodies
} Given the bird the virus but going to die soon anyway
} Don’t have a vaccine for all the strain
® Killed virus in other countries
Pacheco’s disease what caused by, is it in australia, signs and lesions
□ Caused by herpes virus in psittacine birds
□ Exotic disease to Australia
□ Signs
® High mortality, diarrhoea, biliverdinuria, tremors/convulsions
□ Lesions
Hepatic swelling, haemorrhage and necrosis
Histomoniasis (black head) what caused by, where present and transmission
□ Caused by Histomonas meleagridis
® Lives in caecal tubes and migrates to viscera such as the liver
® Fragile organism which doesn’t survive in environment
□ Transmission
® Carrier bird often domestic fowl
® Between birds via caecal worm Heterakis gallinarum by eating the eggs of this worm
Histomoniasis treatment and control
□ Treatment ® Dimetridazole -> cannot use in birds used for human consumption ® Removal of birds from source of infection □ Control ® Control Heterakis (the carrier worm) ® Control earthworms ® Regular medication Concrete/wire floor
List some general clinical signs of nervous system disease
- Ataxia
- Paresis
- Paralysis
- Seizures
- Tremors
- Circling
- Head tilt
- Nystagmus
- Abnormal mentation
What are the 4 main diseases of the brain and 3 of the spinal cord
Brain - Cranial trauma - Nutritional deficiencies - Toxicities - Encephalitides ○ Viral, bacterial, mycotic, parasitic Spinal cord and peripheral nerves - Cord compression syndromes - Nutritional deficiencies - Toxins
Cranial trauma what caused by, associated with and clinical signs
- Caused by panic/hysteria resulting in birds colliding with windows, glass wall
- Can be associated with infarction (acute stroke)
○ Atherosclerosis, yok embolism - Clinical signs
○ Blood in mouth, ear and eye
○ Signs of depression - head tilt, circling, paresis
○ Sudden death
Cranial trauma lesions and treatment
- Lesions ○ Areas of haemorrhaging within the cerebrum -> subcutaneous and tissue ○ Malasia -> softening of the brain - Treatment ○ Supportive treatment ○ Corticosteroids thought to help
What are the 2 main nutritional deficiencies
1) vitamin E deficiency induced encephalomalacia
2) thiamine deficiency (vitamin B1)
Vitamin E deficiency induced encephalomalacia how common, clinical signs, lesions and treatment
○ Not that common anymore due to cheap Vit E supplements
○ “crazy chick disease” and often affects young growing chickens
§ Not before 2 weeks as Vitamin E from yolk sac
○ Clinical signs
§ As neurological signs
○ Lesions
§ Swollen cerebellum, petechial and larger haemorrhages in cerebrum
○ Treatment
§ Required vit E supplementation
Thiamine deficiency (vitamin B1) when generally occurs, clinical signs and treatment
○ Often in pet birds or wild in rehabilitation centres if feed inappropriate diet
○ EG - magpies fed “butchers mince”
○ Clinical signs
§ Walking backwards, head tilt to the ceiling (opisthotonus) “star grazing”, can fall backwards
○ Treatment
§ Highly responsive to thiamine medication -> infection or supplementation in water/diet
