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Systemic Pathology I > Avian Diseases > Flashcards

Avian Diseases Flashcards

1
Q

What causes lead toxicosis? What species are most affected?

A

(AKA: lead poisoning, plumbism)
ingestion of lead from pellets, sinkers, mine waste, paint pigments, etc.

ALL - not just birds

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2
Q

Why are birds more susceptible to lead toxicosis?

A
  • 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
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3
Q

What 2 species of birds tend to get lead toxicosis more frequently?

A
  1. WATERFOWL: ducks, geese, swans, and loons eat things at the bottom of lakes (sinkers)
  2. RAPTORS: bald eagles and scavengers eat carcasses with lead pellets left in them
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4
Q

What are the 4 steps to the pathogenesis of lead toxicosis?

A
  1. lead is ingested (rarely can be inhaled or transcutaneously absorbed)
  2. lead travels in the blood attached to RBC membranes and albumin
  3. remains ubiquitous with long-term deposition in bone, liver, kidney, and fat, and can cross the BBB (neurotropism)
  4. excreted in bile urine, milk, and exfoliated skin
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5
Q

In what 2 ways does lead toxicosis affect red blood cells?

A
  1. inhibits hemoglobin synthesis enzymes causing microcytic hypochromic anemia
  2. lead inhibits nucleotidase, causing erythrocyte fragility and exacerbating the anemia
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6
Q

What nervous system and vascular lesions does lead toxicosis cause?

A

NERVOUS: disrupts metabolism of neurons and astrocytes

VASCULAR: disrupts metabolism of endothelium, causing ischemia and/or hemorrhage

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7
Q

What are the 5 most common clinical signs of lead toxicosis?

A
  1. reluctance to fly or weakness when flying
  2. unsteady gait (ataxia)
  3. flaccid neck - CANADA GEESE
  4. wings held in “roof shape” or drooping - DUCKS, GEESE, SWANS, LOONS
  5. bile-stained feathers and feces around cloaca (due to turnover of RBC)
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8
Q

Lead toxicosis, wing:

A

“roof-shaped”
drooping

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9
Q

What are 3 common gross findings with lead toxicosis? What is most common with chronic cases?

A
  1. bile-stained feathers and feces around cloaca
  2. impacted food in the upper GI tract +/- gastric ulceration
  3. lead fragments in gizzard - not always present

emaciation + facial edema in Canada geese = small dose not enough to kill, long-term

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10
Q

How can lead fragments be differentiated from other metals in the gizzard?

A

magnet - will not be picked up with iron and aluminum will

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11
Q

Lead toxicosis, upper GI tract:

A

food impaction

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12
Q

Lead toxicosis, gizzard:

A

lead fragments

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13
Q

Lead toxicosis, radiograph:

A

sinker, common loon

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14
Q

Lead toxicosis, radiograph:

A

shot gun pellet

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15
Q

Lead toxicosis, bald eagle:

A

white head = 5 years old
- acute, in good body condition

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16
Q

Lead toxicosis, bald eagle gross findings:

A

ovary should be smooth

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17
Q

Lead toxicosis, gross finding:

A

rough pattern

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18
Q

How does lead toxicosis affect the kidney in acute cases? Chronic?

A

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

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19
Q

In what 3 ways are blood vessels most commonly affected by lead toxicosis?

A
  1. fibrinoid necrosis of the wall
  2. hemorrhage
  3. secondary ischemic or hemorrhagic lesions
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20
Q

Lead toxicosis, kidney

A
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21
Q

Lead toxicosis, heart:

A

bright pink walls = fibrin deposition

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22
Q

Lead toxicosis, intestinal vessels:

A

fibrin deposition + necrotic cells

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23
Q

How is lead toxicosis diagnosed antemortem? Post mortem?

A

AM = lead levels in blood

PM = lead levels in liver, kidney, and bone

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24
Q

What birds are most susceptible to lead levels in their blood and organs?

A

(usually there is no lead in blood at all)
- waterfowl are the most susceptible at lower levels
- raptors

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25
Q

How is lead toxicosis controlled?

A

regulations on lead shots and sinkers

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26
Q

Why is it unlikely for lead toxicosis to be zoonotic? How are humans most likely to get it?

A

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

27
Q

What are the 3 types of gout?

A
  1. RENAL - kidney; urolithiasis, nephrosis, caged layer nephritis
  2. VISCERAL - other tissues
  3. ARTICULAR - joints
28
Q

What is gout?

A

accumulation of urate crystals in renal tubules and/or other tissues (specifically, serosal and synovial surfaces)

29
Q

What is the main cause of gout?

A

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

30
Q

What species of birds are affected by gout?

A

ALL

31
Q

How do the 3 types of gout compare due to severity?

A

ACUTE = renal/visceral with little to no inflammation

CHRONIC = articular associated with granulomatous inflammation

32
Q

What are the 6 steps to gout pathogenesis?

A
  1. hyperuricemia
  2. precipitation of monosodium urate crystals (tophi) on renal tubules, visceral surfaces, and synovial surfaces
  3. attempted phagocytosis of tophi by macrophages
  4. tissue damage
  5. inflammatory reaction
  6. development of chronic inflammation +/- fibrosis
33
Q

What are the most common clinical signs of the 3 types of gout?

A

ACUTE RENAL/VISCERAL = little to no signs with possible progressive weakness before death

ARTICULAR = difficulty flying and perching, rigid and inflamed feet

34
Q

What are the main gross findings of renal, visceral, and articular gout?

A

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

35
Q

Visceral gout:

A

white, chalky patches on heart

36
Q

Visceral gout:

A

white, chalky, gritty pericardial sac

37
Q

Articular gout:

A

swollen joints

38
Q

What is pathognomonic of gout? How does this compare based on severeity?

A

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
39
Q

Why are tophi crystals often not birefringent on histology slides?

A

tissue degradation during formalin fixation and processing

40
Q

Gout, kidney:

A

tophus in lumen with some heterophils

41
Q

Gout, kidney:

A

heterophils, macrophages

42
Q

Gout, tophi:

A

degeneration and necrosis makes tophus not as well-fixed

43
Q

Chronic gout, kidney:

A

G = normal tubule

P = necrotic tubule

44
Q

Visceral gout:

A

liver

45
Q

Visceral gout:

A

spleen

46
Q

How is gout diagnosed? How is this confirmed?

A

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

47
Q

How should samples with tophi for gout diagnosis not be treated?

A

do not fix in formalin - urate crystals are water-soluble, so they will disappear during routine fixation

48
Q

In what 3 ways can gout be controlled?

A
  1. lower protein in diet, keep birds hydrated, avoid nephrotoxic plants
  2. avoid nephrotoxic drugs
  3. treat viral infections
49
Q

What causes infectious laryngotracheitis in birds? What is another name for this disease?

A

avian alphaherpesvirus, Gallid herpesvirus type 1 (dsDNA virus)

fowl diptheria - necrotic epithelium accumulates in tubular organ, forming a pseudomembrane

50
Q

What species are most affected by infectious laryngotracheitis? What 2 other groups are affected?

A

galliforms - clinical disease in domestic chickens

  • pheasants, peafowl, turkeys - less common
  • anseriforms (ducks, geese) - carriers
51
Q

How is infectious laryngotracheitis spread?

A

acute, highly contagious - contact with infectious aerosols by inhalation, conjunctival contact, or ingestion

52
Q

How does infectious laryngotracheitis spread once in the body? What does this cause?

A

cell-to-cell spread by syncytial cell formation without viremia

severe necrosis to tracheal mucosa

53
Q

What determines recovery from infectious laryngotracheitis? What tends to happen upon recovery?

A

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

54
Q

What are the 3 main clinical signs of infectious laryngotracheitis?

A
  1. high morbidity with moderate to high mortality
  2. respiratory distress - coughing, sneezing, head shaking, GASPING FOR AIR
  3. expectoration of bloody/mucous exudate
55
Q

What are the 3 main gross findings in cases of infectious laryngotracheitis?

A
  1. tracheal mucosal necrosis and hemorrhage
  2. occlusive pseudomembrane, fibrinonecrotic and hemorrhagic - casts/plugs fill tracheal lumen
  3. mild cases = sinusitis, conjunctivitis, seromucous exudate
56
Q

Infectious laryngotracheitis:

A

tracheal mucosal necrosis and hemorrhage

57
Q

Infectious laryngotracheitis, mild case:

A

conjunctivitis

58
Q

What are the 4 main histopathological findings with infectious laryngotracheitis?

A
  1. tracheal mucosal necrosis with fibrinonecrotic pseudomembrane
  2. syncytial cell formation with IN inclusion bodies at the early stages of disease
  3. mucosal ulceration, mixed inflammation, squamous metaplasia
  4. may affect bronchi and air sacs
59
Q

Infectious laryngotracheitis:

A
  • no glands or normal epithelium present
  • mononuclear (lymphocyte) inflammation
  • pseudomembrane to the left with fibrin, RBC, and degeneration
60
Q

Infectious laryngotracheitis:

A

IN inclusion bodies, Cowdry type A
- circle = normal

61
Q

How is infectious laryngotracheitis diagnosed? What is not helpful?

A
  • clinical signs, gross lesions, histopathology
  • PCR, IFA, IHC, EM, viral isolation

SEROLOGY - can’t distinguish real infection from vaccine-induced antibodies

62
Q

In what 2 ways if infectious laryngotracheitis controlled?

A
  1. vaccination (first avian disease for which an effective vaccine was developed)
  2. hygiene measures - some transmission through fomites, quarantine
63
Q

Is infectious laryngotracheitis zoonotic?

A

NO, not at all - herpesviruses are species specific

Systemic Pathology I (25 decks)

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