Birds 2 Flashcards
Disease investigations what is an important aspect and how to determine
Definition of problem - Comparison to breed standards/targets ○ 1% first week mortality ○ Mortality breeders - 1% per month ○ Broilers now about 3.5% per batch
If mortality is a feature of disease what to do
POST-MORTEMS
Define biosecruity and 3 ways this is upheld
Biosecurity is the prevention or control of contact of pathogens with animal populations
Basics
1. All in all out
○ Easy as day old chick is independent -> can separate
○ Need some time when the whole site is empty in each cycle
2. Single age sites
○ Stops build-up of challenge to later flocks
○ Stop the spread from non-susceptible to susceptible flocks
3. Single purpose sites
○ Only one part of the process
○ Slaughter house isn’t with breeders or growers
Define management and what need to keep in mind
- It is the control and adjustment of the environment, nutrition or any other factor by the keeper of the animal.
○ It is also the failure to adjust these conditions. - The failure to decide a parameter of the environment to the detriment of the animal is a profound welfare issue
- By domesticating animals we invented management.
NEED TO - Freedom from hunger, thirst, disease and pain and able to express normal behavioural patterns.
What adjustments are important with management and which vets involved with
• Stock type ○ Males and females • Equipment • Housing • Food quantity • Food quality • Water quality • Lighting • Ventilation • Temperature • Humidity • Stocking density • Biosecurity • Vaccination and medication programme - vets largest impact
Beck what is normal in parrots, diseases and what cause
- Parrots -> upper beck curved over the lower beck
○ NOT normal in chickens - Beck upper or lower may overgrow -> need to be worn down naturally
○ Hepatic diseases and mites can cause overgrowth - Change in texture of the beck -> Psittacine beck and feather disease
- Trauma, pulling of the bird while grasping onto objects or just bird fighting with each other -> Not necessary need to euthanise, can grow back the beck
Beck trimming what used for, how occur and issues
- Reduce the effects of feather pecking/cannibalistic behaviour
- Hot blade, laser
○ Painful due to exposure of nerve fibres - Painful to eat after the procedure -> deepen the feed tough so doesn’t have to
- Can get post-infection leading to mortality
○ Infection can move into blood vessels of the beck -> localise to joints -> Can lead to osteomyelitis -> die of septicaemia
Oropharynx what are some important lesions and main disease in pigeons, what if see lesion
- Trauma/toxins -> foreign bodies such as fish hooks, trauma from crop tubing, burns - necrosis, chemicals
- Trichomoniasis (canker)
- If see lesions - TAKE A SMEAR
Trichomoniasis (canker) what birds common in, age and how transmitted
• Common in pigeons in small numbers
• Most common in young post-fledgling altricial(when first hatch reliant totally on parents) birds
○ Pigeons, Magpies, Budgies. Raptors
• Transmitted via feeding of young birds, possible sexual behaviour of regurgitation
○ Raptors possibly get infected via prey of infected pigeons
Trichomoniasis (canker) predisposing factors, signs and lesions
• Predisposing factors ○ Immunosuppression diseases - circovirus ○ Stress (overcrowding) ○ Intercurrent disease • Signs ○ Hypersalivation/regurgitation/vomiting ○ Poor growth ○ Severe form - systemic and death • Lesions ○ Diptheretic oral lesions § Thickening oesophagus/crop wall
Trichomoniasis (canker) treatment and control
• Treatment ○ Easily treated with § Ronidazole, emtryl (don't over medicate as can be toxic) - Control ○ Predisposing factors ○ Maximize host resistance ○ Source of infection-> Could be the water supply -> clean this out often ○ Strategic medication § Parents § Fledgelings
List some differential diagnosis other than trichomoniasis for budgies, pigeons and raptors
- Budgies ○ Goitre and other obstructions causing regurgitation ○ Behavioral regurgitation ○ “Megabacteriosis” - a yeast ○ Crop mycosis (regurgitation and lesions) ○ Vitamin A deficiency - Pigeons ○ Herpesvirus ○ Pox - Raptors ○ Helminthiasis ○ Pox
Stomatitis in gallinacious birds (chickens, turkeys) what is not likely and what is likely
- Trichomoniasis is very rare - NOT THIS ONE
- Pox
- ILT (infectious Laryngotracheitis virus)
Oesophagus and crop when change in what species, variation and what can be found within folds how significant
- EXCEPT in pigeons in breeding season -> crop produces nutritional regurgitate (crop milk) to feed the babies
○ Increase in gland production - Crop size and shape varies between species, generally lots of folds and therefore flexible
○ Parasites can be found within the folds
§ Contracaecum in fish eating birds -> generally not causing an issue
Humans can be an intermediate host -> severe enteritis and abdominal pain
What are the 2 main diseases of the oesophagus and crop
1) herpes virus
2) crop mycosis (canidiasis, thursh)
herpes virus what lead to and lesions
- Polyuria -> pale kidneys
- Diptherial membranes down oesophagus
- Inclusion bodies found in histology
Crop mycosis cause, predisposing factors and lesions
- Overgrowth of Candida albicans -> opportunistic pathogens
- Predisposing factors
○ Crop dysfunction -> stasis, impaction, diseases
○ Suppression of normal bacterial flora
○ Poor hygiene - Lesions -> Thickening of alimentary and digestive tract especially in the crop, crop can be flaccid, filled with mucoid fluid content
Crop mycosis diagnosis, treatment and control
- Diagnosis -> Gram stain to find the budding yeasts via smears/scraping
- Treatment -> Antifungal agents -> Imidazole, Nystatin, Amphotericin
- Control -> involved correction/avoidance of predisposing factors
Proventriculus function and clinical signs when diseased
- Producing hydrochloric acid and pepsin
- Generally non-specific clinical signs in disease -> just looking sick -> fluffed up, bottom of the cage
○ May see vomiting -> vomit/seeds ends up on the back of the head, shake their head
○ May see dilation of the proventriculus
Gizzard function
- Grinding action to break down food (seeds)
- No obvious demarcation between gizzard and proventriculus in some birds like penguins
- Produces cuticle that protects the mucosa of the wall against the grinding action
What injury results in issues or both the proventiculus and gizzard
- Foreign bodies/impaction
○ Coarse indigestible food, grass, straw etc.
○ Special issue in young ostriches with over-consumption of sand/gravel leading to impaction
○ Consumption of mature grass can result in tangled mass can form rope leading to intestinal intussusception
What are the 3 main diseases that cause enlargement of the proventriculus
1) Proventricular Dilation Syndrome (neuropathic gastric dilation, myenteric ganglioneuritis)
2) Megabacteriosis - Avian Gastric Yeast
3) Parasites - nematodes (Tetrameres, Contracaecum)
Proventricular Dilation Syndrome (neuropathic gastric dilation, myenteric ganglioneuritis) what cause, where found, signs, diagnosis and treatment
○ Viral disease
○ Not found too often in Australia mainly in quarantine facilities -> not exotic but not common
○ Signs: anorexia, weight loss, wasting, regurgitation, myelitis - ataxia, treatment
○ Diagnosis: radiography - contrast studies
○ Treatment: supportive: affected birds often die despite treatment
Megabacteriosis - Avian Gastric Yeast what birds most susceptible, cause, signs, diagnosis and treatment/control
○ Budgies/canaries and finches particularly susceptible
§ Finches need special nutrition as omnivores -> maggots, insects help decrease susceptibility
○ Generally occurs with other diseases -> possibly a secondary disease to coccidiosis
§ Predisposing factors -> stress, viral infection, nutrition
○ Signs - weight loss, weakness, high morbidity, some mortality, regurgitation
○ Diagnosis - presence of the yeast rods via faecal smear, also can do via histopathology of proventriculus
§ Found in the proventricular glands
○ Treatment/control
§ Amphotericin B (human or bird version) for a few days
§ Acidify drinking water
§ Balanced diet -> finches as above
§ Probiotics -> not cheap
What parasites are important in the proventriculus what birds common in and significance
○ Tetrameres common in pigeons
○ Contracaecum -> common in fish eating birds
○ In small number not large issues but in large numbers can lead to large amount of ulceration
§ Perforation of the stomach, peritonitis
List the 3 main diseases of the gizzard
1) gizzard impaction - Enlargement of the gizzard due to engorgement or feed or consuming something it shouldn’t eat
2) heavy metal toxicities
3) gizzard parasitism
Heavy metal toxicities what results from and diagnosis
○ Ingestion of lead, zinc, others ○ Diagnosis § X-ray - radiopaque material in left side of the GIT § Blood lead § Serum chemistry □ delta ALAD ↓ □ haeme synthesis □ protoporphyrin □ Anaemia
Heavy metal toxicities in waterfowl what form occurs and treatment
§ Chronic form more common due to low exposure via environmental contamination -> ingestion into gizzard and absorption
□ Enlargement of the gizzard, cannot grind the food and pass through the rest of the GI tract
□ Impaction of the alimentary system
§ Treatment - removal of the source
Heavy metal toxicities in parrots what form, clinical signs and diagnosis
§ Generally ingest via metal coating objects/cages –> Acute form
§ Clinical signs
□ Sudden death, blood in droppings, depression, polyuria, neurological signs (convulsions), dehydration
§ Diagnosis
□ Lesions -> acute nephrosis, lead particles within histopathology
□ History -> just got new toys, cage etc.
□ Response to treatment
□ Blood chemistry
□ Radiography
Heavy metal toxicities 6 treatments options and controls
○ Treatment
1. Remove the source
2. Chelation therapy - Ca EDTA (IM or Oral)
3. Laxative
4. Activated charcoal - hard to give if cannot pass food down to lower alimentary tract
5. Surgery? -> if severely ill may not be the best option
6. Supportive therapy -> vitamins, fluids
○ Control
§ Exclude access
§ Good-quality wire
§ Weathered wire
§ Treatment of wire
Gizzard parasitism in finches what are the main ones
○ Finches
§ Thickening of the coiling of the gizzard
§ Examples
□ Acuaria (also common in chickens)
® Spiuroid helminths, intermediate hosts of insects and beetles
® Signs - weight loss, poor growth and death
® Control - removal of intermediate hosts -> difficult in outdoor aviaries
□ Candidiasis
Viral enteritis what is the most common one, also called, cause, signs and results
○ Also called: malabsorption syndrome, runting/stunting syndrome, infectious stunting, pale bird syndrome, helicopter feathering
○ Unsure the exact viral cause
○ Signs - undigested droppings, reduced growth despite good appetite, poor plumage
○ Results in - Malabsorption -> undigested food found in the colon
§ Something affecting digestion and absorption
□ Shortened villi, shallow crypts and damaged cells
Pancreas also damaged
Viral enteritis clinical signs
- Diarrhoea
- Undigested faeces
- Blood in faeces
- Severe cases -> fatality
What are the 5 main bacterial enteritis
1) salmonellosis
2) campylobacterosis
3) necrotic enteritis
4) ulcerative enteritis (quail disease)
5) avian tuberculosis
Necrotic enteritis what caused by how occurs, what common in and clinical signs
○ Caused by Clostridium perfringens type A and C
§ Live in the intestinal tract anyway -> need predisposing factors to cause disease
□ Change in diet -> from juvenile to grower hen
□ Other diseases such as coccidiosis
○ Common in broilers but can affect a large amount of bird species
○ Clinical signs
§ Subclinical - reduced growth rate
§ Clinical -> death, diarrhoea, blood in faeces
§ Lesions -> oedematous organs, enlarged livers, necrosis/thickening of villi of intestinal mucosa
Necrotic diagnosis, treatment and control
○ Diagnosis
§ Take a smear
§ Look under slide
§ Gram stain -> shouldn’t see lots of gram positive bacilli in normal chickens
§ Histopathology -> bacteria clustered on top of villi, necrosis of the villi (not the deeper layer of mucosa)/thickened
○ Treatment
§ Antibiotics -> readily work against -> Neomycin
○ Control
§ Gradual introduction of new ration
§ Prevention of coccidiosis
§ Avoid feeding wild birds -> lorikeets die from eating feed they shouldn’t
Ulcerative enteritis (quail disease) what species, caused by, clinical signs, treatment and control
○ Multiple species affected
○ Caused by Clostridium colinum
○ Clinical signs
§ High mortality, acutely sick, depressed
§ Lesions -> wide spread necrosis throughout whole length of GIT tract (whole width of the mucosa is affected), deep penetration -> peritonitis
○ Treatment
§ Antibiotics
○ Control
§ Reduce predisposing factors
□ Reduce stocking density, wire floors, control coccidiosis
Avian tuberculosis caused by, transmission, does it affect lungs and zoonoses?
○ Caused by Mycobacterium avium - environmental inhabitant excreted in faeces -> chronic condition
§ Therefore can see in most birds however not commercial as don’t live long enough
○ Faecal-oral infection via contaminated dropping or carcasses
○ BUT doesn’t affect the lungs - no respiratory involvement
○ POTENTIALLY ZOONOTIC -> generally immunocompromised people -> REPORTABLE CONDITION
avian tuberculosis clinical signs and diagnosis
○ Clinical signs
§ High mortality, vents stained with dark coloured droppings (diarrhoea)
§ Lesions -> cheesy exudate attached to cloaca, throughout intestinal tract, liver
○ Diagnosis
§ Lesions at post-mortem
§ Take a smear
§ look under slide with acid fast staining -> chickens will see lots of mycobacteria, other birds not necessarily
§ Culture via special medium -> takes 4 weeks to grow
Avian tuberculosis treatment and control
○ Treatment
§ Long term not usually warranted
○ Control
§ Separate from source of infection - outside or carrier bird (need to quarantine)
§ In commercial farms -> removal of birds before 1-2 years old as chronic condition
§ Remove/treat the soil?? -> CAN BE INFECTIVE FOR UP TO 10 YEARS
□ Treat soil with lime, and put more soil on-top and monitor
What are the 3 main parasitic enteritis
1) ascaridiasis
2) intestinal capillariasis
3) intestinal cestodiasis (tapeworms)
Ascaridiasis how common, does it cause disease, lifecycle and clinical signs
○ Most common parasite found in birds
○ In some birds species doesn’t cause disease (chickens - less susceptible), others it does (galahs, parrots)
○ Direct lifecycle -> faecal-oral route, cycle takes 30-50days
○ Clinical signs
§ Species dependent
□ Parrots -> high burden can get mortality due to intestinal blockage
□ Chickens -> subclinical -> reduced weight gain and egg production
Ascaridiasis diagnosis, treatment and control
○ Diagnosis
§ Faecal-flotation -> eggs - large thick wall, generally lots of eggs found
§ Post-mortem -> worm within the GI tract -> dilated intestines
○ Treatment
§ Species dependent
□ In parrots with high burden if treat worms will die and may cause blockage -> death of parrot BUT NEED TO TREAT
□ Backyard chickens -> if low burdens chickens may be resistant so may not need to treat
§ Levamisole (Avitrol), Flubendazole, Piperazine
○ Control
§ Break faecal-oral route -> wire floor, hygiene
§ Moisture content prevention -> need for eggs to hatch
§ Quarantine
§ Periodic medication
□ Initially treat every month then can push out the treatments (depends on the bird and parasite)
Intestinal capillariasis lifecycle, clinical signs, diagnosis, treatment/control
○ Direct or indirect lifecycle via earthworms
○ Clinical signs
§ Mucoid enteritis, diarrhoea, poor growth/condition
○ Diagnosis
§ Faecal float
□ Not highly prolific so if see eggs - TREAT
Treatment/control
§ Generally same as ascarids
§ However treatment intervals smaller -> Smaller prepatent period- 20-26 days
Intestinal cestodiasis (tapeworms) life cycle, clinical signs, diagnosis, treatment and control
○ Large variation in sizes (microscopic or up to 1m) and host species
○ Life cycle -> need an intermediate host (slugs, snails, ants, earthworms) IMPORTANT IN CONTROL
§ Eggs already embryonated -> 6 striations within -> characteristic
○ Clinical signs - mild/moderate enteritis, weight loss, poor condition
○ Diagnosis - seeing segments and eggs in faeces
○ Treatment
§ Praziquantel (Avitrol Plus)
○ Control
§ Periodic treatment
§ Elimination of secondary host
Coccidiosis what caused by and clinical signs
○ Caused by Eimeria - E. maxima common, mixed infections common
○ Clinical signs - diarrhoea (some blood tinged), thickened intestinal tract
§ Severe infection - can lead to death
§ Subclinical infection - mainly decrease in production
§ Severity influenced by:
□ Host factors
® Birds species
◊ Can be fatal in parrots
◊ Turkeys and chickens relatively resistant
® Immune status -> acquired immunity with age
□ Parasite factors
® Dose and species (depends on where they are found, intestinal lining not fatal but further down can damage blood vessels -> can lead to haemorrhages)
Coccidiosis diagnosis
○ Diagnosis
§ Smear of the mucosa (not the contents of GIT) on slide with cover slip and spread out to thin layer
□ If keep slide moist will remain viable for others to look at (put in fridge)
§ Determine stage of disease, where in the intestinal tract and characteristic lesions
List 4 species of coccidiosis what clinical signs, location and cause
1) E. acervulina - subclinical, proximal intestinal tract (epithelial) causing mucosal thickening - bundles of oocysts seen in smear
2) E. maxima -> clinical, middle part of intestinal tract (sub-epithelial), leads to orange discolouration of GIT contents, large oocysts
3) E. necratrix -> mortality, same area as maxima however causes very severe dilation/haemorrhage (lamina propria)
□ Cannot see oocysts in smear instead see schizont -> schizont causes the disease
4) E. tenella -> mortality, distal intestinal tract (lamina propria), both sexual and asexual within, haemorrhages generally related to schizonts
What is the main species of coccidia for budgies and pigeons
○ Species for budgies
§ E. dunsingi - very similar to E. necratrix - haemorrhagic - high mortality
○ Species for pigeons
§ E. labbeana - like E. acervulina - mucoid enteritis mainly, occasional mortality
Coccidia treatment
§ Important to look at both aspects of the lifecycle
§ Depends on the species
□ Chickens -> large numbers then medicate - medicate in the water if large numbers affected - 3 days on, 3 days off
□ Budgies -> always medicate if detect
□ Pigeons -> depends on if pet or racing pigeons
§ Moisture control -> oocysts don’t like dry environment
§ Anticoccidials - Sulfaquinoxaline, Amprolium (coccivet), Toltrazuril (baycox), Trimethoprim
□ Resistance is a consideration
□ Route of medication
□ Dose
□ Residues - for chicken - withholding period
□ Toxicity
® Species -> dose for one species isn’t for others
® Combination with other drugs can lead to worsened side effects - ionophores
Coccidia treatment
§ Environment!!!
□ Moisture control (ventilation, leakage, etc)
□ Hygiene (litter management, wire/slat floor, etc)
§ Periodic medication
§ Vaccines
1. Total prevention wanted
□ Broilers -> no time to develop immunity
□ Commercial pullets
□ Parrots -> medicate
□ Racing pigeons
2. Controlled exposure
□ Commercial breeders - allow to develop immunity
□ Pigeons
□ How works?
® Continuous use of coccidiostats at sub-therapeutic dose
® OR just give vaccines
Atoxoplasma in passerines how detected and what leads to
○ Not easily detected in droppings/ facecal flotations -> just histopathology
○ Has extra-intestinal life stages not just causing enteritis
§ Thickened intestinal tract
○ Resistant to treatment
What are 4 main causes of renal disease, pre-renal and post-renal conditions
- Renal disease ○ Toxic? ○ Infectious? ○ Metabolic? ○ Tumours? - Pre-renal conditions ○ Water deprivation? - Post-renal conditions ○ Obstruction? ○ Ureter(s) ○ Cloaca ○ Pelvic canal
Avian renal system what type of nephrons, what are 2 main things kidneys are associated with and describe the renal portal system
- Two types of nephrons -> reptilian and mammalian type
- Kidneys associated with:
○ Sciatic nerve -> lesions on kidney may result in paresis of limb on same side
○ Abdominal air sac -> diseases of air sac may extend into the kidney - Renal portal system- valves associated with external iliac vein and vena cava therefore medication directed into vena cava may go into the renal circulation and excreted via kidneys before entering the body
List the 4 main signs of renal disease
1) polyuria - physiologic as well, diet or stress related, if persistence than renal
2) discolouration of the urine/urate
3) gout
4) presence of uric acid crystal within tissues especially kidney - cytology or histopath, irritation
Discolouration of urine/urate what occurs with and the types of gout
Discoloration of the urine/urate
○ Also occurs with
§ Food items
§ Medication
§ Anorexia
§ Liver diseases
Gout - Uric acid retention
○ Visceral gout -> deposition of urates on epicardium, peritoneum especially over liver capsule, usually associated with acute renal failure
○ Articular gout -> deposition of urates on joints and synovial sheaths, usually associated with chronic renal failure but sometimes in the absence of obvious renal disease -> lameness, swelling
○ Renal gout -> acute inflammation associated with uric acid crystals in interstitial tissues of kidneys
what are the 2 main toxins that lead to renal disease and metabolic causes
1. Toxic ○ Medications - VETERINARIANS FAULT § Diclofenac § Antibiotics (aminoglycosides) § Excess Vit D/Ca ○ Heavy metal toxicity § Generally lead to haematuria, haemoglobinuria, porphyrinuria 2. Metabolic - may be associated with fatty liver, renal amyloidosis
What infectious and tumours may lead to renal disease
- Infectious
○ Viral (IBV (infectious bronchitis virus), APV)
○ Bacterial
§ septicaemic diseases
§ ascending infections of ureter - “pyelonephritis” - Tumours
○ Adenocarcinoma
§ One of the most common tumors of budgie especially in older budgies
§ Generally affects one kidney while the other kidney compensates
§ Generally not too many clinical signs just generally paralysis -> perching on one leg
□ Lameness due to pressure on sciatic nerve
Marek’s disease or leucosis sarcoma virus may go metastatic
which ovary and oviduct grows
A -> left ovary -> only ovary that grows
B -> left oviduct -> only oviduct
List and describe the 6 parts of the reproductive system
- Ovary – yolk production
- Infundibulum – fertilisation site and inner albumin layer and chalaza – 15mins
- Magnum – bulk of albumin (egg white) – 180 mins
- Isthmus – extra protein in albumin and shell membranes - 73 mins
- Uterus (shell gland) – ‘plumping’ w/ water and shell formation – 1200 minutes (20h)
- Vagina -> close to keep oviduct sterile, until lay then relax and open
What are the 4 main factors that affect ovarian activity
- Light - need at least 12 hours of daylight
- Moisture
- Nutritional factors
○ Calcium - Stress and disease
What occurs with follicles in stressed animals
- Degeneration of the follicles
- Release of follicle into abdomen
- Can result in sterile inflammatory response to the egg yolk
○ Non-infectious Peritonitis
Not very severe unless bacteria contamination
What are the 2 main diseases of the ovary and 6 of the oviduct
1) oophoritis
2) tumours
OVIDUCT
1. cytsotic right oviduct
2. generation of oviduct
3. salpingitis
4. tumours of the oviduct
5. egg drop syndrome
6. egg binding
Oophoritis what is it, types and cause and results
- Oophoritis - inflammation of the ovary
○ Sterile or non-sterile
○ Bacteria results in changes in the egg and yolk - atrophy, discoloration, thinning
Tumours of the ovary what are important ones
○ Metastatic § MD § LL ○ Primary § Ovary Adenocarcinoma □ Distended abdomen □ Yellow coloured fluid running out of abdominal cavity □ Can lead to peritoneal lymphatic blockage -> ascites -> distended abdomen
Degeneration of the oviduct effects and caused by
○ Effects - depends on the part of the oviduct it affects
§ Magnum -> produces the albumin -> effect now runny albumin
§ Can result in eggshell thickness/quality decrease
○ Caused by - nutrition, toxic effects, infectious diseases such as infectious bronchitis
Salpingitis causes and tumours of the oviduct
inflammation of oviduct
○ IBV - infectious bronchitis virus
○ NDV - new castle disease virus - very nasty - stop exports for 6 months .
- Bacterial -> salmonella, E. coli, mycoplasma gallisepticum
TUMOURS
- Oviductal adenoma/adenocarcinomas - spread transcoelomicly - firm white, cream plaques and can invade lymphatics -> ascites
- Looks like ovarian adenocarcinomas
Egg drop syndrome cause, transmission, signs, differential and prevention
- Cause - EDS virus - hemagglutinating adenovirus
○ Commonly associated with waterfowl -> infection through the water - Transmission
○ Vertical -> from infected breeder stock
○ Horizontal
§ Between shed-mates
§ Water fowl -> water with contaminated faeces from water fowl - Signs - production drops, wrinkly eggs, discoloured
- Differential diagnosis (IB, ND, heat stress)
○ Differentiate with PCR or serology - Prevention
○ EDSV- free parents
○ Vaccination -> 13-16 weeks of age generally occurs
○ Get water from non-contaminated areas without water fowls
§ Can add chlorine to water to kill the virus
Egg binding cause, signs and diagnosis
- Aetiology ○ Hypocalcemia ○ obesity - Signs ○ weakness ○ depression ○ abdominal distention, wide stance ○ sudden death - Diagnosis ○ Palpation ○ X-ray
egg binding what are the 7 treatment options
- Warm environment - try this first for a few hours
- Calcium (50-100mg/kg IM) +/- Oxytocin
- Manual assistance
- lubricate cloaca
- Position the egg transrostral
- Ovocentesis
- Surgical intervention
What are the 6 functions of the feather
- Display
- Insulation
- Waterproofing
- Protection
○ Against trauma while fighting - Sensory function
- Flight
What is different about bird skin
- Skin is very thin and loose
- No sebaceous glands within
○ Pudenal gland on the back of the tail -> provides the oil that they rub on their feathers
What are blood feather, how to prevent and what not useful for
- Immature feathers with the pulp cavity exposed and their calamus is filled with highly vascular connective tissue
- Broken/damaged blood feathers bleed profusely
- Haemostasis should be done by removal of entire calamus from feather follicle
- Are NOT useful for histological examination
What are the 5 main causes of feather loss
1) normal/seasonal loss of feathers - moulting
2) congenital
3) nutritional
4) feather peacking
5) infectious
- psittacine beak and feather disease
- budgerigar fledgling disease
- polymaviruses in other psittacine
Moulting what are the 2 ways this occurs and types within
1) Natural
□ Cyclic
® For some species
® Annual - loss all their feathers yearly - penguins
® Biennial
□ Continuous/progression -> chickens, parrots
2) Induced - false moulting -> complete deprivement of nutrition and water for a few days -> 3-4 weeks to loss their feathers and grow some more
□ No longer legal to do in chickens this way
What are the 3 main types of congenital issues that result in feather loss
§ Feather dusters
§ Strobe feathers -> feathers don’t come out of the sheath properly
§ Feather cysts -> feathers can’t come out of the skin -> surgical removal skin over the feather to let them escape, problem is that occurs next moulting -> don’t breed from these birds
What is the main nutritional condition that results in feather loss
○ Clubbed down -> feather down doesn’t come out of the sheath
§ Common in commercial flocks in very low numbers, if getting high than issue
§ Vitamin B2 deficiencies
Feather pecking clinical signs and predisposing factors
○ Clinical signs § Feather loss around the body - front of neck, legs □ Not on the head and tail -> harder to reach ○ Predisposing factors § Overcrowding § Light intensity § Nutritional deficiencies □ Protein and sodium deficiency
Feather pecking causes and treatment
○ Causes
§ Pruritis
§ Systemic disease
§ Boredom
§ Psychosis
□ Sexual frustration
□ Change of environment - introduction of a new pet
○ Treatment
§ The underlying cause -> anti-boredom devices such as twigs and plants to chew on
§ Can use a collar around the bird to prevent self-trauma
Psittacine beck and feather disease which birds most susceptible and lesions/clinical signs
§ Cockatiels less susceptible -> can be carrier animals
Lesions/clinical signs
□ Feathers not growing at all or growing like blood feathers - mainly head, wings and hip (generally first)
® Follicles were destroyed
□ Atrophy of the lymphoid tissues
□ Secondary infections common
□ Cannot clean themselves so look dirty
□ Beck abnormal - malformed and easy to break
Psittacine beck and feather disease cause transmission and treatment
§ Cause - circovirus - hardy virus that survives well in the environment
§ Transmission
□ Horizontal transmission - from faeces, crop, wash, feather dust
Vertical transmission - from parent to progeny
§ Treatment
□ Supportive therapy - Keep the bird warm, give blanket, protection from sun and skint trauma
□ Treatment for secondary infections should be considered
□ No vaccine in Australia
Psittacine beak and feather disease 3 main diagnosis
- Histopathology - microscopic lesions including inclusion bodies
® Caecal histopathology - PCR - screen a large number of birds, can use feather, blood or faecal material
® Not cheap - HI (antibodies) and HA (antigens) test - blood test - can determine the quantity of the virus and assess the immunologic response to the virus
® HI- HA- → not exposed
® HI+ HA+ → active carrier/recovered birds
® HI + HA- → exposed & recovered
® HI- HA+ → Peracute/chronic infection & carrier - unlikely to recover
Budgerigar fledgling disease what other birds occur in, cause and lesions
§ Can occur in other species such as lorikeets (possible another strain)
§ Cause - polyomavirus infection
§ Lesions/clinical signs
□ Short tail feathers - cannot fly -> generally called “runners” or “bullets”
□ Can look similar to PBFD
□ Kills embryo before they hatch -> decreased viability of chicks
Budgerigar fledgling disease transmissin, diagnosis and prevention
§ Transmission □ Vertical and horizontal - like PBFD □ Carriers - continuous vs intermittent shedding ® All secretion and feather dust § Diagnosis □ Histopathology - of major organs ® Lots of inclusion bodies -> larger and paler than PBFD □ PCR - via cloacal swabs, serum, tissues § Prevention □ Quarantine if important! □ Hygiene □ Isolation □ Vaccination -> north America
Polyomaviruses in other psittacine (BFDV-3) what are the clinical signs
§ Inapparent infection § Poor feathering § Immunosuppression* § CNS signs § Sudden death § Weigh loss § Anorexia § Bleeding
What is the main viral dermatitis cause, transmission and clinical signs
- Poxvirus infection
○ Minimum cross species transmission besides pigeon pox into chickens
○ Canary pox -> generally die via secondary infections
○ Clinical signs
§ Skin form - Cause cutaneous papilloma’s affecting head, neck, commissures of the mouth, feed and preen gland
§ Diphtheritic form - involves diptheretic lesions in oral/pharyngeal mucosae
○ Transmission
§ Sheds from infected skin
§ Cannot penetrate intact skin -> need a vector
□ mosquitoes and mites
Poxvirus infection lesions, diagnosis, treatment and control
○ Lesions
§ Vacuoles -> eosinophilic inclusion bodies within
○ Diagnosis
§ PCR -> specific for different pox viruses
○ Treatment
§ Antibiotics - prevent the secondary infection that generally kills the birds
§ Vaccination
○ Control
§ Insect control
§ Vaccination -> via wing web or feather follicles (mimic the insect bites)
□ Attenuated chicken pox
□ Pigeon pox -> can infect chickens but doesn’t cause disease -> GOOD VACCINE FOR CHICKENS
□ Canary pox
What are 2 causes of bacterial dermatitis
- Staphylococcus
2. Clostridium perfingens -> gangrenous dermatitis
What are the 3 main external parasites of birds and the types within
1) mites
1. knemidocoptes species
2. dermanyssus - red mite
3. ornithonyssus - northern fowl mite
2) ticks - argas persicus
3) lice
Knemidocoptes clinical signs in different bird species, diagnosis and treatment
§ Clinical signs
□ Scaly leg disease -> in chickens
□ In budgies leads to scaly face/scaly leg
□ Canaries and finches leads to tassel foot
§ Diagnosis
□ DEEP scrapings -> visualisation of the adult or immature mites
® Can get so deep done to the bone
§ Treatment
□ Easily treatable
□ Beware of withholding periods for commercial chickens
1) Malathion spray/dust
2) Ivermectin medications -> on the skin surface -
3) Moxidectin -> can be used in birds
Dermanyssus and ornithonyssus what are important about them and significance
○ Red mite - Dermanyssus § Doesn't live on the birds all the time -> at night-time on the birds, during day in the coop □ Can survive long periods off the host § ZOONOTIC -> can cause irritation § Medicate birds as well as the environment ○ Northern fowl mite - ornithonyssus § Always lives on the birds ○ Significance for all mites □ Dermatitis □ Anaemia - in large infestations □ Transmission of blood-borne pathogens
What are important ticks and lice
Ticks - mainly argas persicus - suck blood of the chickens -> anaemia, ill-thrift and possible death in young birds
○ Nocturnal feeding habits so detection mainly at night-time
Lice - generally host specific, entire lifecycle on the host - cannot last 7 days without
○ Heavy infestations -> reduced egg production, irritation, unkempt plumage
Treatment for lice and mites and flies
Lice and mites
○ Pyrethroids (permethrin)
○ Azamethiphos (Alfacron, Novartis Pty Ltd)
○ Organophosphates (malathion/maladison wash/dip/spray), beware of registration and withholding period
Flies
○ Larvadex (cyromazine) -> feed to the chickens and leaves through faeces where flies ingest
List the 12 main septicaemic diseases
- Chlamydiosis
- Pasteurellosis
- Yersiniosis
- Ornithobacterium
- Staphylococcosis
- Erysipelas
- Spirochaetosis
- Colibacillosis
- Anatipestifer
- Miscellaneous bacteria
- Avian influenza
- Duck viral enteritis
clinical signs for septicaemic diseases what are the 4 forms
Peracute form is associated with deaths, sometimes without gross lesions - cyanosis of the comb
Acute form involves in sick-bird look, increasing mortality, enlarged congested liver and spleen, petechial haemorrhages on serosal surfaces and foci of necrosis (pin point/pinhead) in liver
Sub-acute form is associated with abscessation/granuloma formation in viscera and air sac inflammation, serositis (peritonitis, pericarditis, etc).
Chronic form involves in abscess/granuloma formation, arthritis, synovitis, ophthalmitis, meningitis, etc..
Erysipelas cause, what most susceptible, zoonoses? and signs/lesions
Cause - Erysipelothrix rhusiopathiae
- Turkeys are susceptible
- ZOONOTIC - swelling of the limbs -> painful
○ If suspect use protective gloves
Signs/lesions
- Acute: sudden death, congested viscera, haemorrhages and fibrin exudates on epicardium with swollen liver/spleen
- Subacute/chronic: debilitation, poor condition, lameness/arthritis and endocarditis
Erysipelas transmission
Transmission
- Persists in the environment -> route of entry through skin trauma
○ Fighting, poor husbandry, overcrowding, artificial insemination
§ 12-20 weeks of age most common due to increased
○ FREERANGE CHICKENS -> generally more susceptible
- Pigs and sheep can shed it
Erysipelas diagnosis, treatment and control
Diagnosis
- History of raising sheep/pigs in same location
- Cutaneous trauma lesions are suggestive
- Isolation and identification of the organism
Treatment
- Penicillin injections together with vaccination (bacterin - takes a few weeks for immunisation to occur -> don’t do if about to go to abattoir)
Control
- Hygiene, prevention of trauma and vaccination
Pasteurellosis (fowl cholera) cause and transmission
Cause - Pasteurella multocida
- More commonly affects mature in birds although young birds may also be affected
- Many species are susceptible
Transmission
- Infected birds remain as carriers and can transmit to susceptible birds
○ Latent infection can be broken via stresses such as overcrowding
- Other animals -> pigs, dogs, cats, rabbits and humans
- Wild birds -> especially important in FREERANGE systems
Pasteurellosis signs and lesions
Signs
- Peracute/acute deaths
Lesions
- Acute/Peracute form lesions of septicaemic diseases
○ Large congested liver/spleen - haemorrhaging on serosal surfaces, foci of necrosis on liver (above images)
- Subacute/chronic form lesions of septicaemic diseases
○ Localised lesions such as sinusitis, arthritis, synovitis
Pasteurellosis diagnosis, treatment and control
Diagnosis
- Organism demonstrated as gram negative bipolar coccobacilli impression smear of affected tissue/blood - gram stain
- Conformation via culture - in order to help with making a vaccine
Treatment
- A range of antibiotics - beware of resistance
Control
- Eliminate contact with carrier birds/mammals - feral birds, rodents
- Practice “all in, all out” management
- Inactivated vaccines - some don’t include serotype P. multocida
