Avian Diseases Flashcards
What causes lead toxicosis? What species are most affected?
(AKA: lead poisoning, plumbism)
ingestion of lead from pellets, sinkers, mine waste, paint pigments, etc.
ALL - not just birds
Why are birds more susceptible to lead toxicosis?
- low pH in the gizzard (typically due to grains) increases lead availability
- stones in the gizzard grind down lead do it remains in there longer
What 2 species of birds tend to get lead toxicosis more frequently?
- WATERFOWL: ducks, geese, swans, and loons eat things at the bottom of lakes (sinkers)
- RAPTORS: bald eagles and scavengers eat carcasses with lead pellets left in them
What are the 4 steps to the pathogenesis of lead toxicosis?
- lead is ingested (rarely can be inhaled or transcutaneously absorbed)
- lead travels in the blood attached to RBC membranes and albumin
- remains ubiquitous with long-term deposition in bone, liver, kidney, and fat, and can cross the BBB (neurotropism)
- excreted in bile urine, milk, and exfoliated skin
In what 2 ways does lead toxicosis affect red blood cells?
- inhibits hemoglobin synthesis enzymes causing microcytic hypochromic anemia
- lead inhibits nucleotidase, causing erythrocyte fragility and exacerbating the anemia
What nervous system and vascular lesions does lead toxicosis cause?
NERVOUS: disrupts metabolism of neurons and astrocytes
VASCULAR: disrupts metabolism of endothelium, causing ischemia and/or hemorrhage
What are the 5 most common clinical signs of lead toxicosis?
- reluctance to fly or weakness when flying
- unsteady gait (ataxia)
- flaccid neck - CANADA GEESE
- wings held in “roof shape” or drooping - DUCKS, GEESE, SWANS, LOONS
- bile-stained feathers and feces around cloaca (due to turnover of RBC)
Lead toxicosis, wing:
“roof-shaped”
drooping
What are 3 common gross findings with lead toxicosis? What is most common with chronic cases?
- bile-stained feathers and feces around cloaca
- impacted food in the upper GI tract +/- gastric ulceration
- lead fragments in gizzard - not always present
emaciation + facial edema in Canada geese = small dose not enough to kill, long-term
How can lead fragments be differentiated from other metals in the gizzard?
magnet - will not be picked up with iron and aluminum will
Lead toxicosis, upper GI tract:
food impaction
Lead toxicosis, gizzard:
lead fragments
Lead toxicosis, radiograph:
sinker, common loon
Lead toxicosis, radiograph:
shot gun pellet
Lead toxicosis, bald eagle:
white head = 5 years old
- acute, in good body condition
Lead toxicosis, bald eagle gross findings:
ovary should be smooth
Lead toxicosis, gross finding:
rough pattern
How does lead toxicosis affect the kidney in acute cases? Chronic?
ACUTE: tubuloepithelial degeneration and necrosis with the PCT most affected with IN inclusions that can be acid-fast (Ziehl Nielsen) stained due to lead being bound to nuclear proteins
CHRONIC: nephropathy, fibrosis
In what 3 ways are blood vessels most commonly affected by lead toxicosis?
- fibrinoid necrosis of the wall
- hemorrhage
- secondary ischemic or hemorrhagic lesions
Lead toxicosis, kidney
Lead toxicosis, heart:
bright pink walls = fibrin deposition
Lead toxicosis, intestinal vessels:
fibrin deposition + necrotic cells
How is lead toxicosis diagnosed antemortem? Post mortem?
AM = lead levels in blood
PM = lead levels in liver, kidney, and bone
What birds are most susceptible to lead levels in their blood and organs?
(usually there is no lead in blood at all)
- waterfowl are the most susceptible at lower levels
- raptors
How is lead toxicosis controlled?
regulations on lead shots and sinkers
Why is it unlikely for lead toxicosis to be zoonotic? How are humans most likely to get it?
most of the lead will be in the liver, kidney, and bone, not muscle
the same way birds do - eating lead pellets or fragments in game meat
What are the 3 types of gout?
- RENAL - kidney; urolithiasis, nephrosis, caged layer nephritis
- VISCERAL - other tissues
- ARTICULAR - joints
What is gout?
accumulation of urate crystals in renal tubules and/or other tissues (specifically, serosal and synovial surfaces)
What is the main cause of gout?
impaired excretion of uric acid/urate salts by the kidneys due to severe….
- dehydration
- renal disease
- post-renal obstruction
- nephrotoxic drugs or plant toxins
- nephropathogenic viral infections
- overproduction of uric acid in high-protein diets
- defects in enzymes of uric acid metabolism
What species of birds are affected by gout?
ALL
How do the 3 types of gout compare due to severity?
ACUTE = renal/visceral with little to no inflammation
CHRONIC = articular associated with granulomatous inflammation
What are the 6 steps to gout pathogenesis?
- hyperuricemia
- precipitation of monosodium urate crystals (tophi) on renal tubules, visceral surfaces, and synovial surfaces
- attempted phagocytosis of tophi by macrophages
- tissue damage
- inflammatory reaction
- development of chronic inflammation +/- fibrosis
What are the most common clinical signs of the 3 types of gout?
ACUTE RENAL/VISCERAL = little to no signs with possible progressive weakness before death
ARTICULAR = difficulty flying and perching, rigid and inflamed feet
What are the main gross findings of renal, visceral, and articular gout?
RENAL = enlarged kidneys with patchy or streaky appearance; ureters are dilated and filled with grey-white concretions (urate calculi)
VISCERAL = white-gray chalky patches on serous membrane, especially in the pericardium and hepatic capsule and mesentery/peritoneum
ARTICULAR = swollen jionts and tendon sheaths filled with chalky white deposits, ruptured synovial membrane and overlying skin
Visceral gout:
white, chalky patches on heart
Visceral gout:
white, chalky, gritty pericardial sac
Articular gout:
swollen joints
What is pathognomonic of gout? How does this compare based on severeity?
tophi - clusters of sharp needle-shaped (acicular) birefringent crystals radiating from the center
- peracute = tophi only
- acute = tophi with tissue necrosis and histiocytic (macrophage) inflammation
- subacute/chronic = tophi surrounding by heterophilic and granulomatous lesions
Why are tophi crystals often not birefringent on histology slides?
tissue degradation during formalin fixation and processing
Gout, kidney:
tophus in lumen with some heterophils
Gout, kidney:
heterophils, macrophages
Gout, tophi:
degeneration and necrosis makes tophus not as well-fixed
Chronic gout, kidney:
G = normal tubule
P = necrotic tubule
Visceral gout:
liver
Visceral gout:
spleen
How is gout diagnosed? How is this confirmed?
gross chalky material and histological appearance of tophi
confirm the tophi are urate crystals by fixing in alcohol and staining with GMS and Von Kossa stains for calcium
How should samples with tophi for gout diagnosis not be treated?
do not fix in formalin - urate crystals are water-soluble, so they will disappear during routine fixation
In what 3 ways can gout be controlled?
- lower protein in diet, keep birds hydrated, avoid nephrotoxic plants
- avoid nephrotoxic drugs
- treat viral infections
What causes infectious laryngotracheitis in birds? What is another name for this disease?
avian alphaherpesvirus, Gallid herpesvirus type 1 (dsDNA virus)
fowl diptheria - necrotic epithelium accumulates in tubular organ, forming a pseudomembrane
What species are most affected by infectious laryngotracheitis? What 2 other groups are affected?
galliforms - clinical disease in domestic chickens
- pheasants, peafowl, turkeys - less common
- anseriforms (ducks, geese) - carriers
How is infectious laryngotracheitis spread?
acute, highly contagious - contact with infectious aerosols by inhalation, conjunctival contact, or ingestion
How does infectious laryngotracheitis spread once in the body? What does this cause?
cell-to-cell spread by syncytial cell formation without viremia
severe necrosis to tracheal mucosa
What determines recovery from infectious laryngotracheitis? What tends to happen upon recovery?
cellular immune response - cytotoxic T cells
may become carriers for life caused by the virus remaining latent in the trigeminal nerve ganglion + immunosuppression can lead to reactivation
What are the 3 main clinical signs of infectious laryngotracheitis?
- high morbidity with moderate to high mortality
- respiratory distress - coughing, sneezing, head shaking, GASPING FOR AIR
- expectoration of bloody/mucous exudate
What are the 3 main gross findings in cases of infectious laryngotracheitis?
- tracheal mucosal necrosis and hemorrhage
- occlusive pseudomembrane, fibrinonecrotic and hemorrhagic - casts/plugs fill tracheal lumen
- mild cases = sinusitis, conjunctivitis, seromucous exudate
Infectious laryngotracheitis:
tracheal mucosal necrosis and hemorrhage
Infectious laryngotracheitis, mild case:
conjunctivitis
What are the 4 main histopathological findings with infectious laryngotracheitis?
- tracheal mucosal necrosis with fibrinonecrotic pseudomembrane
- syncytial cell formation with IN inclusion bodies at the early stages of disease
- mucosal ulceration, mixed inflammation, squamous metaplasia
- may affect bronchi and air sacs
Infectious laryngotracheitis:
- no glands or normal epithelium present
- mononuclear (lymphocyte) inflammation
- pseudomembrane to the left with fibrin, RBC, and degeneration
Infectious laryngotracheitis:
IN inclusion bodies, Cowdry type A
- circle = normal
How is infectious laryngotracheitis diagnosed? What is not helpful?
- clinical signs, gross lesions, histopathology
- PCR, IFA, IHC, EM, viral isolation
SEROLOGY - can’t distinguish real infection from vaccine-induced antibodies
In what 2 ways if infectious laryngotracheitis controlled?
- vaccination (first avian disease for which an effective vaccine was developed)
- hygiene measures - some transmission through fomites, quarantine
Is infectious laryngotracheitis zoonotic?
NO, not at all - herpesviruses are species specific
