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42 Cards in this Set

  • Front
  • Back
Blood of birds
Blood of birds
• Large, nucleated erthrocytes that live only 20-35 days (shorter than mammals
• Nucleated thrombocytes rather than platlets
• Heterophils rather than neutrophils
Feather picking
Feather picking
• Healthy birds groom themselves to keep infestation
• Sick birds will not groom themselves
• Psittacines may self-mutilate due to:
a. skin irritants
b. boredom
c. dietary defciency
d. Psychosis
e. Bacteria, virus, fungi
f. Lack of sleep due to lights being left on
g. Contact w/ strangers, dogs or cats
• Chewed feathers show ramus of feather split longitudinally in an irregular, ragged fashion
• Cardinal signs of self mutilation is feathers on head are normal
Enteritis
Enteritis
1. Coccidiosis
2. Giardiasis
3. Psittacosis/Chlamydiosis
Coccidiosis
Coccidiosis
• Eimeria, Isospora, Doriseilla, Wenyonella, Tyzzeria
• Feces blood tinged and watery; wt loss w/ chronic D+
• Tx Sulfa drugs, Amprollium in water
Cnemidocoptes
Cnemidocoptes
• Cnemidocoptes pilae
• Most frequent and most important ectoparasite of small psittcines
• Scaly face and leg mite
• Starts from the angle of beak and spreads to other areas of head or body
• Overgrown and disfigured beaks are commonly seen – dermatitis
• Characteristic tassle-like appearance on feed – hyperkeratosis
• Recover mites from skin scrapings
• Tx
a. Dichlorvos pest strips
b. Liquid paraffin, petroleum jelly, cortamiton and mesulphan provide good penetration and dissolution of hyperkeratic tissue
c. Apply for three day and repeat in 1 week if necessary
d. Topical tx alone NOT recommnded b/c it is messy and the bird may ingest the medicant while preening its feather
Fractures
Fractures
• Radiographs should always be taken
• Glycogen storage capacity in birds is considerably less than in other spp, so tx w/ IV glucose
• Coaptation splinting in which the wing is bound to the body (wing) or simple tape splints (leg fxs)
• Internal fixation should only be administered when conservative tx fails
• Avian bone is very brittle and most fxs tend to be comminuted
• Pneumatized bones and medullary bones
Sinusitis
Sinusitis
• Will see swelling just above or below the eye
• Supraorbital and infraorbital sinuses
• Initiated by Hypovitaminosis A
Egg binding
Egg binding
• Common problem in cage and aviary birds
• Due to obstruction or impaction of vagina w/ a fully formed egg
• Associated w/ atony or spasms of smooth muscles of the oviduct
• Causes:
a. Obesity
b. Oversized eggs
c. Low blood Ca
d. Poor muscle tone
e. Nervousness
f. Variation in temperature
g. Lack of suitable nesting place
• Signs:
a. Straining
b. Neck seeking
c. Abnormal postures
d. Paresis can occur
e. When examined, egg is usually palable just above the pelvic inlet
• Tx
a. If not tx it can rapidly progress to oviduct or cloacal prolapse
b. Place in warm cage w/ infrared irradiation – often the egg is then expelled
c. Lubricate of the cloacal opening and placing the bird over staming kettles have been tried but with variable success
d. Manipulation can easily be overdone
e. If egg accessible in the vagina, contents can be removed w/ hypodermic syringe and needle; eggshell may collapse or the fragments be taken out piecemeal
f. Laparotomy if egg is farther up the oviduct
g. Ca gluconate – IM rapid expulsion of egg (so may be associated w/ low Ca)
Beak deformities
Beak deformities
• Causes:
a. Budges are often seen w/ overgrown or distorted beaks
b. Trauma to germinal layer
c. Excessive wear caused by climbing metal on cage
d. Metabolic bone dz – overlying beak becomes distorted
• Need regular clipping w/ nail clippers and smooth w/ fine sandpaper
• Dislocation of the jaw is unlikely b/c the bird has double articulation
• Candidiasis – disfiguration and hyperplastic tissue growth (see below)
Persistent egg laying
Persistent egg laying
• Cockatiels,
• Removal of oviduct but not ovary
• Medroxyprogesterone – budges and psittacines
Body thermoregulation
Body thermoregulation
• Hypothermia - Anesthesia and sx – always provide hot water bottle
• Hyperthermia – Ketamine causes postanesthetic hyperactivity
• Cloaca temperature is excellent indicator of high body temp – tx w/ oxygen and IM destrose and alcohol spray
Giardia
Giardia
• Protozoan
• Infection via contaminated feces – poor sanitation and hygient
• Budges are very susceptible
• Chronic D+, wt loss and occasionally death
• Small intestine may be filled w/ semisolid material and contain large number of organisms
• Foamy, foul smelling, yellow brown D+
• Dx:
a. Best method is intestinal scrapings of duodenal loop of freshly killed birds
b. Organism in feces is erratic – only cyst is shed in droppings
• Dimtridazole is tx in water
Crop impaction
Crop impaction
• Causes:
a. Fibrous material may be ingested by galliforms allowed to graze long grass
b. Thread in cage
c. Pigeons ingesting soft nesting material
• Main sign is regugitating movement, often unproductive
• Dx via palpation
• Tx is vegetable or mineral oil, or sx
Candidiasis
Candidiasis
• Candida albicans
• Yeast; ubiquitous in nature and lives as commensals on the skin, mouth, alimentary tract of warm blooded animals and birds
• Signs:
a. unthrifitness
b. listlessness
c. Necrotic pseudomembranous patches over mucosa of tongue, pharynx and crop
d. Mucosa looks like a terry cloth
e. Beak deformities
• Dx – characteristic lesions or KOH
• Tx – Nystatin, adequate Vit A & B
• Amphotericin B used for feather injection
• Unsanitary housing overcrowding and dirty utensils are all factors that contribute to an outbreak
Air sacculitis
Air sacculitis
• Air sacs are thin-walled extensions of the lungs that hold about 80% of the volumetric capacity of the respiratory system
• Subject to Aspergillus fungi and coliform bacteria infection
• Can be present for some time and becomes fairly extensive before outward signs are eveident
• To have effective inhalation therapy to tx the air sacs, the droplet must be less that 5um in diameter
Psittacine Beak and Feather Disease (Dystrophy)
Psittacine Beak and Feather Disease (Dystrophy)
• Circovirus that occurs in wild Australian cockatoos, but is know to be able to infect nearly all species of Psittaciforms
• Abnormal molts and develomment of dystophic feathers, beaks and claws of young psittacines
• Feather dust from affected birds is highly infective
• Signs:
a. Acute overwhelming dz w/ bilaterally symmetrical loss of all actively growing feathers over a few days
b. Chronic dz characterized by repeated replacement of feather and quills by deformed, twisted, dystrophic quills that fail to mature and are shed prematurely
c. Hyperkeratosis of feather sheath and outer layers of beak and claws
d. Rapid loss of heterophils
• Dx - M0 w/ intracytoplasmic includison bodies
• No reliable tx
Hypovitaminosis A
Hypovitaminosis A
• Necessary for growth, vision and epithelial maintenance
• Most common nutritional disorder seen in practice
• All birds w/ respiratory signs should be suspected of being Vit A deficient
• Signs:
a. Small, white, necrotic plaques in mouth and throat
b. Abscesses in mouth
c. Swelling of supraorbital and infraorbital sinuses (above and below the eye)
• Dx and Tx – response to Vit A
• Diets should be supplemented w/ Vit A on a routine basis
Cloacal prolapse
Cloacal prolapse
• Causes:
a. After an egg has been removed sx b/c of impaction
b. After normal egg laying in a weakened oviduct
c. Persisent cloacal prolapse due to a tumor (viral papillomas)
d. Cloacitis
• Prolapse may contain intestine, oviduct, ureter and may lead to obstruction of these organs
• Tx:
a. Purse-string suture around the vent – place exactly at cutaneous mucosal junction or ureters may be trapped and serve supply permanently damaged
b. Two mattress sutures on either side of vent
c. Rmove a wedge of vetn to reduce its circumference – usually used on male bird in dorsal aspect
d. Stainless steel wire sutures around the vent to retain the cloaca
e. Cloacoplexy by suturing the abdominal wall to the cloaca; pushing the cloaca into position using a cotton bud
Psittacosis
Psittacosis
• Caused by various strains of Chlamydia (rickettsia-like organisms)
• Zoonotic
• Signs:
a. Urthriftiness
b. Ocular and nasal discharge
c. Enteritis
d. Post mortem hepatomegaly w/ patchy faint necrosis
e. Mottled enlarged spleen
f. Air saculitis
g. Pericardiits
h. Serosal hemorrhage
• Confirm w/ impression smears from liver – Ziehl Neelsen or Macchiavello stain pink intracytoplasmic inclusion bodies
• Isolate organism from tissue and feces
• Tx via isolatio of sick bird and IM oxytetracycline
• Oral tx or prophylaxsis with chlortetracycline for at least 45 days
• Chlortetracycline is preferred to oxytetracycline b/c the latter has tendency to chelate Cu, Fe and Ca for poorer intestinal absroption.
• Tetracyclines are reported to be anti-Vit B in activity
• Use feeders that are NOT lined w/ Fe, Cu, or Zn b/c they can deactivate the tetracycline
• Do not put in water – medication is unpredictable & require three times the medication which would make it unpalatable
Gout
Gout
• Metabolic disorder characterized by deposition of urates and uric acid crystals in different tissues or organs
• Uric acid is a normal product of nitrogen metabolism (Nitrogen  Enzyme Xanthinoxidase  Xanthine  Uric acid) in the liver and kidney
• Two forms depending on site of deposition
a. Visceral Urate deposition – impaired renal function or urinary tract obstruction
b. Articular – unknown etiology but has high uric acid values
• Clinical signs:
a. Not specific for visceral urate depostition – see light urate dusting on liver and pericardial surface and enlarged, swollen kidney
b. Lameness
c. Reluctanceto fly or perch
d. Rigid, swollen and painful joints
e. Will see whitish yellow centers around joints, ligamens and tendons through the skin later in dz
• Dx
a. Visceral urate depostition only at necropsy
b. Clinical signs for articular gout
c. Murexide test (add nitric acid, evaporate and one drop of ammonia) of aspirated joint material will turn red-purple if positive
• Tx – incurable – symptomatic tx
• Allopurinol – inhibits xanthinoxidase and uric acid synthesis may be given
• Glucocoricosteroids are contraindicated b/c of increased protein catabolism
Egg peritonitis
Egg peritonitis
• Egglike material (may be fibrin) in abdominal cavity due to ectopic ovulation
• Signs are sudden death, depression, abdominal distension, dyspnea or wt loss
• Adhesions are common
• Tx is abdominal irrigation via laparotomy w/ Ab
• Occasionally ova are shed into the abdominal cavity when birds have been disturbed or are handled – this is normal, sterile, and will not show congestion of the peritoneal blood vessels
Nutritional Secondary Hyperparathyroidism
Nutritional Secondary Hyperparathyroidism
• Rickets and osteomalacia from lowered blood calcium
• Decrease of blood Ca stimulated the parathyroid glands to release PTH which stimulates Ca reabsorption in the kidney and urinary loss of Ph
• Signs:
a. PU/PD from phosphaturia
b. ADR
c. Bones can be painful
d. Legs and claws may be inflamed and swollen
e. Muscle spasms, tetany and cardiac disturbances from hypocalcemia
• Dx difficult except in severe cases
• Tx is gluconate solution in large birds exhibiting tetany – monitor HR
Hypocalcemia
Hypocalcemia
• Causes Rickets, osteomalacia and subsequent Nutritional Secondary Hyperparathyroidism
• Rickets
a. Failure of mineralization of osteoid matrix in young, growing birds
b. Due to decr Ca, decr Vit D or severely imbalanced Ca:Ph
c. Vit D is needed to stimulate synthesis of specific Ca binding protein in the intestinal wall
d. Normal Ca:Ph is 1 /12 to 3 : 1
e. Signs include:
S shaped sternum
Softening of vertebra, claws
Ribs that curve inward
Can show neurological signs
f. Dx is clinical signs and history
g. Tx Ca, Vit D supplements and diet improvements
• Osteomalacia
• Osteomalacia
a. Dz of adult birds
b. Characterized by mineral loss in bone when reabsorption exceeds deposition
c. Causes:
Prolonged egg laying w/ insufficient Ca supply
Lack of grit in food – grit in the gizzard is necessary for grinding seeds which contain vitamins and minerals
d. Signs:
More discreet than rickets
Bones become thin soft, painful and fragile and can break spontaneously when bird is handled
e. Dx via history and clinical signs – X ray shows cortice thinning and lowered density and may show fxs w/ minimal callus formation
f. Tx same for rickets
Goiter – thyroid dysplasia
Goiter – thyroid dysplasia
• Hypothroidism caused by iodine deficiency
• Iodine is required for thryoxin synthesis – a deficiency in the diet can result in decreased secretion of hormone
• TSH (thyroid stimulating hormone) from the anterior pituitary is released in increased amounts and the thyroid follicles become hyperplastic (enlarged)
• Signs:
a. Thyroid hormone is needed for metabolism – so systemic disturbances occur w/ lack of T3
b. Lethargiy, poor condition
c. Unable to maintain body temperature
d.  cholesterol
e. Increase in body fat
f. Fatty tumors and fatty liver
g. Slowed HR and RR
h. Dystrophic thyroid can interfere w/ digestive system
i. Labored respiration w/ squeaking noises
• Dx blood thyroxin level (hyperplasia of gland CANNOT be palpated or seen by x ray)
• Tx is iodine or levothyroxine
Trichomoniasis
Trichomoniasis
• Trichomonas gallinae
• Common dz especially in pigeons
• Signs:
a. High mortality in young birds
b. Wet canker – diptheritic lesions in mouth, esophagus, larynx and pharynx
c. Dry caseous necrosis – necrotic lesions in beak, esophagus and crop
• Dx via wet smear of fresh specimens showing irrgular twisting movements of tails
• Tx is Dimetridazole in drinking water for 7 days
Salmonellosis
Salmonellosis
• Most widespread zoonosis in the world
• Salmonella typhimurium is most important in birds
• Birds are common reservoir and progresses non-symptomatically
• Open aviaries and children’s petting zoos can cause human salmonellosis via close contact
• Birds termporaily or persistently carry the dz, and shed the agent in the feces
• Three samples of feces must be found to be clear of Salmonella to rule out carrier state – one sample is not sufficient
Aspergillus
Aspergillus
• Aspergillus flavus – aflatoxin mycotoxin
• Found in cereal grains, peanuts or groundnuts or moldy bread
• Hepatocarcinogenic and affects hepatocyte’s ability to metabolize fats
• Signs:
a. D+
b. Incoordination
c. Depression and anorexia
d. Sudden death
e. Liver shill show hemorrhagic foci, necrosis, cirrhosis and fatty infiltration
• Tx is electrolyte solutions
• Never feed any grain that is spoiled or has fungal contamination
Aspergillosis
Aspergillosis
• Aspergillus fumigatus
• AKA Brooder pneuonia, Pseudotuberculosis, Bronchomycosis, Cytomycosis, Chick fever
• Inhalation of spores or hyphal fragments penetrate bronchial walls and parenchyma where they multiply and branch
• Fungal mycelia combine w/ tissue exudates and block air passages and fill the air sacs
• Seen as yellow, green or blue plaques in the lung & air sacs
• Debilitated, weak and overcrowded birds are most prone to infection
• Signs:
a. Gasping, labored and rapid breathing
b. Anorexia
c. Emaciation
d. Gurgling sounds in trachea due to difficulty in mucus movement
e. D+, ataxia and other nervous system signs
f. Usually fatal w/in a few days on young birds
g. Sudden death
• Dx via detection of plaques and hyphae on KOH
• Tx w/ amphotericin B
Air sac mites
Air sac mites
• Sternostoma tracheacolum
• The complete life cycle is spent on MM of respiratory tract
• Mites penetrate through the tachea into the lungs, air sacs, body cavity and kidneys
• Ulceration caused by sucking blood in the air sacs can resemble tumor masses
• Signs:
a. Dyspnea through an open beak
b. Coughing
c. Sneezing
d. Clicking sounds
e. Nasal discharge
f. Loss of voice
g. Loss of song
h. Loss of feather around the ear
• Dx fiber optic examof trachea, TTW
• Postmortem shows:
a. Tracheitis
b. Air sacculitis
c. Black spots on MM
• Tx Malthion powder dust enclosure for 5 mintues once a week for 4-6 weeks
• Transmission is direct form one bird to another
Lead poisoning
Lead poisoning
• A major differential in botulism
• Limber neck – flaccid paralysis w/ inability to hold neck up
• Exposure to old lead paint, pipes, golf balls, lead shots, batteries
Proventricular dilitation syndrome
Proventricular dilitation syndrome
• AKA Psittacine neuropathic gastric dilatation or Macaw Wasting Dz
• Infectious dz, almost certainly viral origin
• Dx via radiology showing a dilated proventriculus and gizzard (in the central abdomen of the body)
• Present w/ signs of:
a. wt loss, regurgitation; passage of whole seeds
b. May also have neurological signs such as trembling and uncoordination
c. Bird may appear hungry and make pathetic begging for food noises
• Proventriculus may be enlarged, thin walled and filled w/ grit and undigested flood
• Scrape and stain biopsy of crop w/ Gram to show large Gram positive filaments of megabacterial organsism
• Histopath is required to confirm the dz by showing lymphocytic, plasmacytic ganglioneuritis involving the autonomic ganglia at various levels in the gut wall
• Tx is high-fiber, moist diet w/ little seed and TMZ Ab to prevent peritonitis and pneumonia
Seizure disorders
Seizure disorders
• Aflatoxicosis caused by Fusarium trcincum – moldy feed T2 toxin can induce hysteroid seizures
• Seizures in African Grey Parrots – due to Nutritional Secondary hyperparathyroidism and ppt by oxytetraccline
• Newcastle dz – paramyoxovirus can cause twirling syndrome
• Idiopathic epilepsy – petit mal or grand mal; response to Phenobarbitone
Teflon toxicosis
Teflon toxicosis
• If Teflon non-stick cooking utensil dries and overheats can produce toxic fumes
• Post mortem shows intesne red coloration of all tissues particularly the lungs
Renal adenocarcinomas
Renal adenocarcinomas
• Male and female Burdes
• First symptom is Paresis b/c tumor causes pressure to sciatic nerve
• Tumor consists of small nests or masses of vesicular epithelial cells separated by varying amounts of mature or immature fibrous C.T.
• Sx removal is seldom successful
Budgerigar Fledgiling Dz – Polyomavirus
Budgerigar Fledgiling Dz – Polyomavirus
• BFDV-1 is in budges
• BFDV-3 is in parrots
• Nestling budges 1-15 days old
• Signs:
a. Abdominal distension
b. Lack of down feathers on back and abdomen
c. Hydropericardium – enlarged heart
d. Enlarged liver – ascites; liver has multiple white or yellow spons
e. Sudden death
f. ‘Runners’ – cann’t fly; aka French molt
g. GI dz w/ SQ hemorrhages
h. CNS signs
• Dx via DNA probe of blood or cloacal swab from liver or spleen
Cryptococcus
Cryptococcus
• Cryptococcus neoformans
• Potentially a serious and fatal zoonosis
• Common saprophytic yeast found on plant and organic material; often excreted and found in feces I sick birds kept in unsanitary conditons
• Signs:
a. Dyspnea
b. Debility emaciation
c. Non regenerative anemia
d. Genralized necrotizing gelatinous granulomata in viscera
• Impression smears of viscera w/ India ink – thick encapsulated yeast-like organisms
Histoplasmosis
Histoplasmosis
• Histoplasma capsulaturm
• Grows well in bird feces
• Associated w/ soil with accumulation of bird and bat droppings
• Zoonotic infection via inhalation of spores
• May cause respiratory signs and D+ w/ heptatopathy
Pachecho’s Parrot Dz
Pachecho’s Parrot Dz
• Herpes virus
• Asymptomatic carriers in Conures
• Not often dx
• Signs:
a. Sudden death
b. Lethargy, anorexia, D+
c. Bright green viliverdin stained feces and urates
d. Conjunctivitis and tremors to convulsions
e. Post mortem faintly mottled, swollen liver w/ saucer shaped necrotic areas
• Isolation by culture in embryonated eggs
• Eosinophilic intranuclear inclusion bodies in hepatocytes and kidney cells
Newcastle Dz
Newcastle Dz
• AKA Velogenic Viscerotropic Newcastle Dz (VVND);
• Highly contagious paramyxovirus of birds
• World trade in nondomestic birds has caused great alrm in domestic poultry industry for fear that VVND might be introduced into domestic flocks
• Spread via aerosols and feces
• Can adhere to articles of clothing of people moving form one place to another = numerous small outbreaks have occurred in the US from a single distributor
• Signs:
a. No pathognomonic signs or lesions
b. Other viral, bacterial or fungal dzs may mimic ND
c. Yellowish or hemorrhagic D+
d. Coughing, sneezing and dyspnea
e. Pantropic – various visceral organ system malfunctions can occur
f. CNS signs – ataxia, incorrdination or hyperexcitability
g. Torticollis, opisthotonus, tremors, nodding, jerking of head and bilateral paralysis
h. Sudden death
• Reportable
• Necropsy shows no pathognomonic lesions
• Isolate birds, prevent exposure of cage birds to carrier birds
• Bird smuggling is big problem
Encephalomyeloties
Encephalomyeloties
• EEE, WEE, SLE, VEE
• Arbovirues transmitted by biting insects
• Birds may act as important hosts and carriers
• Clinical dz in birds are rare
• May cause CNS signs (paralysis, incoordination, torticollis)
• Virus isolation from brain homgenate
• Togavirus – EEE (60%), WEE (15%), VEE
• Flavivirus – St Louis, West Nile
• Mosquito:
Culiseta melanura – E&W
Aedes, Culex – VEE

• Overwinter in migrating birds, reptiles or snakes

• Horses are sentinel for humans.
• Horses
Important in horses
Horse is dead end host for EEE & WEE
Horse is amplyfying host for VEE
Neurological signs (ataxia, inability to stand, multiple limb paralysis

• Birds
High mortality (don’t pick up dead crow)
Neurological signs
Amplifying host for all dzs
Poultry is ampl host for SLE

• Emu
Emu show bloody D+ w/ EEE & WEE
Is amplyfying host for EEE
Sudden onset

• Signs:
V+
Nuchal rigidity
Nausea
Disorientation
Convulsions

• Prevention/Control:
Repellants
Survellance (sentinel A)
Regional spraying
Larvicides
Removal of containers w/ water
Biological control
Good filtration in pools
Dragon
fly larvae

• Guidelines for necropsy:
No needles or sharp inst
No mechanical saws
Minimize aerosols
Disposable clothes
3 prs of gloves
face shield
disposable mask
Anaphylactic shock
Anaphylactic shock
• Signs:
a. Poor CRT
b. Weak depressed bird w/ rapid, weak peripheral pulse
c. Dehydration
d. Metabolic acidosis – plasma bicarb
e. High uric acid values – common in severely ill patients due to renal failure or accelerated tissue metabolism
f. Hyper or hypokalemia