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Systemic Pathology I > Pathology: Systemic - Avian Disease > Flashcards

Pathology: Systemic - Avian Disease Flashcards

1
Q

Lead toxicosis
1. AKA _____ poisoning, ________
2. CAUSE: ingestion of ____
3. Species affected: ____ (not just ____)

A

lead, plumbism, lead, ALL, birds

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2
Q

Lead toxicosis
1. CAUSE: ingestion of ___
- ______ & _____ (main)
- _____ waste
- ___ pigments, etc.

A

Pellets, sinkers, Mine, Paint

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3
Q

What can be seen in this image? What does this cause?

A

Lead toxicosis
lead pellets

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4
Q

What can be seen in this image? What does this cause?

A

Lead toxicosis
Pellets and sinkers
Mistaken for pebbles –> ingested by animals

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5
Q

Lead toxicosis
- Low pH increases ___ availability
- e.g. __ + ____ = _____ toxicity

A

Pb, Pb, grains, higher

Birds develop lead toxicosis more than mammals because low ph increases lead absobablity
birds that eat grain have a lower ph in gizzard, alllowing lead to be abosrbed more. gizzard is grinding the sinkers or lead pellets —> lead secreted. Lead pellets enver truly go away, stay longer in GI tract –> toxicity

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6
Q

Lead toxicosis species main avian species affected?

A
  1. Waterfowl: Ducks, geese, swans, loons (eating stuff from bottom of lakes)
  2. Raptors (particularly scavengers)
  3. Bald eagles, other eagle sps
    - water birds, upland gamebirds
    - Others (other waterfowl)
    - Loons
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7
Q

______, _______, and ______ are more commonly reported with lead poisoning.

A

Ducks, geese, swans

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8
Q

Lead toxicosis pathogenesis

A

Ingestion to excretion
1. Ingested
- Inhaled, transcutaneous – RARELY
2. Pb travels in blood attached to RBC membranes and albumin
- Ubiquitous, with long-term deposition in bone, liver, kidney, fat (b/c Stays longer in tissues without a lot of turnover- look here at necropsy).
- Neurotropism: likes entering brain, goes into BBB and cause nervous clinical signs.
4. Excreted in bile, urine, milk*, exfoliated skin which become sources of further toxicity to other animals.
- Potential sources of toxicity
* = Mammals

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9
Q

Mechanisms of pathogenicity

A
  1. Attaches to membrane of RBC
  2. Hemoglobin synthesis (anemia due to reduced RBC and problem with O2 transport)
  3. Goes through BBB and target and kills neurons and astrocytes. Directly toxic to endothelial cells –> fibrinoid necrosis of the wall of BVs.
  4. Pb inhibits Hb-synthesis enzymes
    – Microcytic hypochromic anemia
    – Erythrocyte fragility
    – Pb inhibits nucleotidase
    – Exacerbates anemia
    – Nervous system lesions – direct toxicity
    – Pb disrupts metabolism of neurons & astrocytes
    – Vascular lesions – direct toxicity
    – Pb disrupts metabolism of endothelium
    – Ischemia and/or hemorrhages
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10
Q

Lead toxicosis: Clinical signs

A
  1. Reluctance to fly or weakness when flying
  2. Unsteady gait (ataxia) (more typical with neurotropism)
  3. Flaccid neck (goose can walk and try to fly but can not lift its neck).
    - Canada geese
  4. Wings held in ‘roof shape’ or drooping
    - Ducks, geese, swans, loons
  5. Bile-stained feathers (& feces) around cloaca (has to do with turnover of RBC, so more pigment in feces).

none of these are exclusive to lead, but characteritic of lead txicosis

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11
Q

What can be seen in this image?

A

– Wings held in ‘roof shape’ or drooping
– Ducks, geese, swans, loons, etc.

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12
Q

What can be seen in this image?

A

– Wings held in ‘roof shape’ or drooping
– Ducks, geese, swans, loons, etc

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13
Q

Lead toxicosis: Gross findings
1. ______-stained feathers (& ____) around cloaca
2. ________, if chronic lead poisoning
- _____ edema (species?)
3. Impacted food in _____ GI tract +/- gastric _______
4. ____ fragments in gizzard – _____ always present
- Pb vs other metals (Fe, Al) – ______ –> lead will not be picked up with _____

A

Bile, feces, Emaciation, Facial, Canada geese, upper, ulceration, Lead, not, magnet, magnet

Lecture Info: chronic versus acute lead toxicosis: DOSE. When you have a little bit of lead = may develop chronic toxicity because not enough to kill you but causesa taxia, GI disturbacnes, etc. In the case of chronic –> emaciation partially necause can’t seem to eat properly. Acute lead poisoning with whomping dose = death, or absolutely nothing?
* Peracute cases with little to no gross lesions and good body condition; when very very high dose of lead, no lesions just a dead bird

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14
Q

What can be seen in this image? What condition is this animal suffering from?

A

– Bile-stained feathers (& feces) around cloaca

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15
Q

What can be seen in this image? What condition is this animal suffering from?

A

– Emaciation, if chronic lead poisoning

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16
Q

What can be seen in this image? What condition is this animal suffering from?

A

Impacted food in upper GI tract

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17
Q

What can be seen in this image? What condition is this animal suffering from?

A
  • Lead fragments in gizzard – not always present
  • Pb vs other metals (Fe, Al) – magnet
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18
Q

What can be seen in this image? What condition is this animal suffering from?

A

If not doing necropsy or have live bird, do Xray because can see lead (metal).

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19
Q

What can be seen in this image? What condition is this animal suffering from?

A
  • Lead fragments in gizzard – not always present
  • Pb vs other metals (Fe, Al) – magnet
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20
Q

What can be seen in this image? What condition is this animal suffering from?

A

Mature bald eagle = white head
Takes 5 years to get white head.
Good BDS b/c fat in subcutis, well deveoped pectoral muscle

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21
Q

What can be seen in this image? What condition is this animal suffering from?

A

Female bird
Ovaries
Kidneys with lead poisoning, or other diseases that cause damage to tubules look like a brain.

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22
Q

What can be seen in this image? What condition is this animal suffering from?

A

Cut open kidney

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23
Q
  1. Kidney
    - ACUTE: _______________ degeneration &, sometimes, _____
    - _______ convoluted tubules are most affected b/c most first tubules where urine is trying to exit.
    - _______ necrosis of BV, maybe _______
    - IN inclusions (well, maybe) – acid-fast [Pb bound to nuclear proteins]
    - CHRONIC: _______ & ______
  2. Blood vessels
    - Fibrinoid necrosis of the ____
    - _______
    - Secondary _____ or _______ lesions
A

Tubuloepithelial, necrosis, Proximal, fibrinoid, hemorrhage, nephropathy, fibrosis, wall, Hemorrhage, ischemic, hemorrhagic

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24
Q

What can be seen in this image? What condition is this animal suffering from?

A

Lead toxicosis - Kidney
normal tubule
Inclusion bodies are little purple circles
Ziehl Nielson stain to highlight more.

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25
Q

What can be seen in this image? What condition is this animal suffering from?

A
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26
Q

What can be seen in this image? What condition is this animal suffering from?

A

Myocardium
Lead toxicosis vessels - heart

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27
Q

What can be seen in this image? What condition is this animal suffering from?

A
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28
Q

What can be seen in this image? What condition is this animal suffering from?

A

Fibrinoid necrosis in walls of BV

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29
Q

Lead toxicosis: Antemortem and Postmoretm diagnosis?

A
  1. Antemortem:
    - Pb level in blood
  2. Post-mortem
    - Pb level in liver, kidney, bone
    * Need species-specific values for Pb levels
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30
Q

Please explain what is shown in the diagram below.

A

No lead is normally found in organisms. CAN live with low levels of lead = subclinical and love a normal life
Green = some clinical signs
Orange = fatal

Waterfowl at 1/2 parts per million in blood cna die, whereas grouse or pigeons cna tae 10/12 PPM; may have clinical signs but not fatal. SPECIES species.

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31
Q

Please explain what is shown in the diagram below.

A

Waterfowl = die with lower levels of lead then in pigeons

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32
Q

Lead toxicosis: Control

A
  1. Lead shot & lead sinkers
  2. Regulations are country and state-specific
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33
Q

Is Lead toxicosis a zoonotic disease?

A
  1. Possible ‘zoonosis’ but unlikely
    - Most Pb in liver, kidney & bone, not muscle
  2. H more likely to get lead toxicosis the same way birds do:
    - Eating lead pellets or fragments in game meat

H = humans

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34
Q

Gout
- _________ tissues affected
- ______ – renal gout (usually called this if targeting kidneys; ______ gout = other organs, ________ gout = joints)
– When in kidney can also call it? Aka:
– Urolithiasis
– Nephrosis
– Caged layer nephritis
– Other tissues – visceral gout
– Joints – articular gout

can affect kidney, liver, spleen

A

Multiple, Kidney, visceral, articular

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35
Q

What is gout?

A
  1. Accumulation of urate crystals in renal tubules and/or other tissues. Birds excrete uric acid in urine. First place to think of is kidneys, can also deposit in other places.
    Serosal & synovial surfaces, particularly
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36
Q

Describe the typical presentation of Gout

A
  1. Renal / Visceral gout is usually acute
    - Often with little to no inflammation
  2. Articular gout is usually chronic
    - Associated with granulomatous inflammation
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37
Q

Gout: Pathogenesis

A
  1. Hyperuricemia - uric acid in blood
  2. Precipitation of monosodium urate crystals (called tophi as in starburst shape of crystals) on
    - Renal tubules
    - Visceral surfaces
    - Synovial surfaces
  3. Phagocytosis of tophi by MQ (attempts, at least; not usually successful but still try )
  4. Tissue damage (renal tubular epithelial necrosis)
  5. Inflammatory reaction
  6. Development of chronic inflammation +/- fibrosis
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38
Q

Gout: Clinical signs
1. Acute renal / visceral form
2. Articular form

A
    • Little to no clinical signs, - May exhibit progressive weakness before death
    • Difficulty flying and perching; rigid & inflamed (swollen & hot) feet
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39
Q

Renal gout gross findings
- _____________ kidneys, ______ or ________ appearance
- Ureters ______ & filled with ____-___ concretions = urate _____

A

Enlarged, patchy, streaky, dilated, grey-white, calculi

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40
Q

Visceral gout gross findings
______-______, _______ patches on serous membrane, particularly in the _________ & _______ capsule – also ________ & ________

A

White, gray, chalky, Pericardium, hepatic, mesentery, peritoneum

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41
Q

– Articular gout gross findings
– __________ joints & ________ sheaths filled with ________ ________ deposits
–_________ of synovial membrane & overlying _____ is possible

A

Swollen, tendon, chalky white, Rupture, skin

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42
Q

What can be seen in this image? What condition is this animal suffering from?

A

Visceral gout
– White-gray chalky patches on serous membrane, particularly in:

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43
Q

What can be seen in this image? What condition is this animal suffering from?

A

– Visceral gout
– White-gray chalky patches on serous membrane, particularly in:
– Pericardium & hepatic capsule – also mesentery & peritoneum

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44
Q

What can be seen in this image? What condition is this animal suffering from?

A

– Articular gout
– Swollen joints & tendon sheaths filled with chalky white deposits
– Rupture of synovial membrane & overlying skin is possible

Some birds can not perch because of damage to joints. Crystals come out through? that burst.

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45
Q
  • _____ are pathognomonic of gout.
    They are Clusters of _____, _________-shaped (________) birefringent* crystals
    radiating from the ______; either ____________ or _________ (to see colors, need to fix with something other than formalin).
  • In peracute form, _______ are all we see
  • In acute form, tophi are associated with tissue __________ (renal tubulare necrosis, for instance) & histiocytic (MQ) inflammation
  • In subacute & chronic forms, tophi are surrounded by _________ & _________ inflammation
  • Crystals are often not ___________ on histology slides because of tissue ________ during processing.
A

Tophi, sharp, needle, acicular, center, basophilic, colorless, tophi, necrosis, heterophilic, granulomatous, birefringent, degradation

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46
Q

What can be seen in this image? What condition is this animal suffering from?

A

Tubular on right with necrosis and ? i lumen.
Tophi = starbust apearance. A few heterophils around it. Not that acite, a bit chronic b/c inflammation around it

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47
Q

What can be seen in this image? What condition is this animal suffering from?

A

Gout.

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48
Q

What can be seen in this image? What condition is this animal suffering from?

A

When not fixed well, see degeneration and ?

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49
Q

What can be seen in this image? What condition is this animal suffering from?

A

Necrotic tubule.
Normal on left, and necrotic tubule with cellular cast on right.

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50
Q

What can be seen in this image? What condition is this animal suffering from?

A

Visceral gout = everywhere. Not just on surface, but also within tissue.

Gout, iver

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51
Q

What can be seen in this image? What condition is this animal suffering from?

A

gout, liver

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52
Q

What can be seen in this image? What condition is this animal suffering from?

A

gout, spleen

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53
Q

Gout: diagnosis
- Gross (______material) & histologic appearance (______) are enough to diagnose gout
- To confirm that the tophi are urate crystals:
- Do not fix in _______ – urate crystals are ______-soluble so they ___________ during routine fixation, but will remain & exhibit birefringent if fixed in ______.
- Tophi can stain with _____ and ______ _______ stains, for calcium

A

chalky, tophi, formalin, water, disappear, alcohol, GMS, Von Kossa’s

fix in alcohol for?
Fix in formalin = dilutes urates and does not birefringe light

can stain with silver and von kossa for ?

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54
Q

Gout: control

A
  1. Prevention of causative factors
    - Diet / hydration / nephrotoxic plants
    - Nephrotoxic drugs
    - Viral infections

Wild birds = usually problem with kidney that gives you gout

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55
Q

Is gout a zoonotic disease?

A

No

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56
Q

Infectious laryngotracheitis
1. CAUSE: ?

  1. Species affected?
A

Avian alphaherpesvirus, Gallid herpesvirus type 1
- dsDNA virus
- Aka: fowl diphtheria

  • Galliforms – clinical disease in domestic chickens
  • Pheasants, peafowl, turkeys – less commonly affected
  • Anseriforms (ducks & geese) – may be carriers; don’t really develop disease

Necrotic material that eventually closes or completely blocks lumen of trachea –> suffocate to death.

Happened to children with diptheria. Would develop pseudomembranes and suffocate.

chickens are the main target; develop clinical disease and if severe enough die from it

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57
Q

Infectious laryngotracheitis: Pathogenesis
1. _______, highly ___________
2. Infection through contact with infectious _________ (____________ secretions from infected birds) by:?
3. Cell-to-cell spread (no ______)
-_________ cell formation* = ______ cell formation –> from ____________
4. Severe necrosis of ______ mucosa b/c hits epithelial cells and kills them.
5. Recovery depends in large part on _______ immune response
6.If recovered, carriers may develop for ____
- Virus is latent in _______ nerve ganglion
- ____________ may result in disease reactivation

A

Acute, contagious, aerosols, respiratory

  • Inhalation (upper respiratory mucosae)
  • Conjunctival contact
  • Ingestion

viremia, Syncytial, Giant, epithelium

tracheal, cellular, life, trigeminal, Immunosuppression

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58
Q

Infectious laryngotracheitis: clinical signs

A
  1. Outbreaks may be:
    - Highly pathogenic form (epizootic)
    - Lowly pathogenic form (endemic)
  2. High morbidity (50-70%) and moderate to high mortality (10-20%)
  3. Respiratory distress
    - Coughing / sneezing / head shaking – gasping for air
    - Expectoration of bloody / mucous exudate
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59
Q

What can be seen in this image? What condition is this animal suffering from?

A

Clinical signs: mostly respiraotry distress; birds are gasping for air. Cough out or sneeze out bloody mucous material

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60
Q

Infectious laryngotracheitis: clinical signs
–> Outbreaks may be:
- Highly pathogenic form (_________)
- Lowly pathogenic form (_____)
- High ________ (50-70%) and moderate to high ______ (10-20%)
- Respiratory _____
- __________ / sneezing /______ shaking – __________ for air
- Expectoration of _____ /______ exudate

A

epizootic, endemic, morbidity, mortality, distress, Coughing, head, gasping, bloody, mucous

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61
Q

Infectious laryngotracheitis: gross findings

A
  1. Tracheal mucosal necrosis and hemorrhage
  2. Occlusive pseudomembranes, fibrinonecrotic & hemorrhagic
    - Casts or plugs fill tracheal lumen
  3. Mild cases: sinusitis, conjunctivitis, seromucous exudate
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62
Q

What can be seen in this image? What condition is this animal suffering from?

A
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63
Q

What can be seen in this image? What condition is this animal suffering from?

A

IFT

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64
Q

Infectious laryngotracheitis: histopathology
- __________ mucosal necrosis
- ______________ pseudomembrane
- ________ cell formation
- _____________ inclusion bodies, Cowdry type ___ = smaller, inclusion body with a _____ _____ around it.
- _______ stages of disease
- Mucosal __________, mixed ____________, __________ metaplasia
- May also affect _______ & _____ ______

A

Tracheal, Fibrinonecrotic, Syncytial, IN, A, clear, halo, Early, ulceration, inflammation, squamous, bronchi, air sacs

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65
Q

What can be seen in this image? What condition is this animal suffering from?

A

ILT:
histopathology
– Tracheal mucosal necrosis
– Fibrinonecrotic pseudomembrane
– Syncytial cell formation

In middle = submucosa and mucosa. Inflammation on right. What type of inflammatory cells are present? Lymphocytes, plasma cells, MQs.

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66
Q

What can be seen in this image? What condition is this animal suffering from?

A

Necrotic material and hemorrhage here.
This is the pseudomembrane. Fibrin, RBCs, pobably some bacteria too. mostly degenerated epithelial cells

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67
Q

What can be seen in this image? What condition is this animal suffering from?

A

Synctial cell formation

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68
Q

What can be seen in this image? What condition is this animal suffering from?

A

Syncytial cell formation
– IN inclusion bodies, Cowdry type A

Normal = 1 or 2 nuclei (top right)

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69
Q

Infectious laryngotracheitis: Diagnosis

A
  1. Characteristic clinical signs, gross lesions & histopathology
    +
  2. PCR (to confirm), IFA, IHC, EM, virus isolation
  3. Serology – not helpful
    Q?: Why not? When a n animal is vaccinated against the disease you are looking at, can’t distinguish real infection from vaccine-induced AB.
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70
Q

Infectious laryngotracheitis: Control

A
  1. Vaccination
    - First avian disease for which an effective vaccine was developed
    - Economically important disease
  2. Hygiene measures
    - Some transmission may be through fomites
    - quarantine, if have sick birds = do not use same materials.
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71
Q

Infectious laryngotracheitis: zoonosis?

A

no

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72
Q

Marek’s disease
1. CAUSE: ?
2. Species affected: ?

A
  1. Avian alphaherpesvirus, Gallid herpesvirus 2
    - dsDNA virus
    - Aka: Marek’s disease virus, skin leukosis (for some presentations; similar to avian leukosis which is caused by a different virus, so just call it Marek’s)
    • Chickens mostly
      - Quails, turkeys, pheasants, jungle fowl, rarely
      - Worldwide distribution
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73
Q

Marek’s disease: pathogenesis
- Highly infectious, particularly for very _______ chicks (get infected within ____ of hatching)
- Inhalation of Feather ___ (dander) may remain infectious for __ year within dust (__________ dependent)
- ____________ disease, the most common of its kind in chickens (virus stimulates lymphocytes to replicate and turn neoplastic. Uncontrollable proliferation. Most common lymphoproliferative disease in chickens. Avian ________ is another one.
- First ‘________’ disease for which a vaccine was developed.
- Three serotypes that we know of:
- Serotype 1 – ________ (main focus)
- Serotype 2 – common in _________
- Serotype 3 – infects ________
- Other oncogenic virus is Avian Leukosis virus (Retroviridae NOT a herpesvirus).

A

young, days, dust, 1, condition, Lymphoproliferative, leukosis, neoplastic, oncogenic, chickens, turkeys

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74
Q

Marek’s disease: pathogenesis

Describe the phases of pathogenesis.

A
  1. Phase 1 – early cell-to-cell infection
  2. Phase 2 – latent infection
  3. Phase 3 – feather follicle shedding
  4. Phase 4 – proliferative (lymphoma) phase
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75
Q

Marek’s disease: Pathogenesis
1. Phase 1 – ______ cell-to-cell infection
- ________ (or ________) of infective feather ______ (___________ or _______ mucosa)
- Infection of respiratory epithelium & MQ (MQ take virus and take it all over the body –> _______.
- Infection of __ & ___ cells in thymus, bursa, spleen and BM – ____________ = immunosuppression (may get secondary infection with another bacteria or virus due to this).
- May result in _________ infections
2. Phase 2 – _______ infection
- Replication in ____ cells (mainly CD__), less so in __ cells and CD__ T cells
- No _______ clinical signs b/c virus is smoldering and replicating
3. Phase 3 – feather follicle ________
- LQ carry virus to feather ________ epithelium
- Virus _________ in epithelial cells
- Virus shedding in feather _______; Transmission to other birds.
- LQ also carry virus to visceral epithelium ( (3) etc.) & nervous system ( ______ & _____); Lesion severity depends on ____ & host _____
- Mononuclear (LQ, PL, MQ) inflammation
4. Phase 4 – __________ (_________) phase
- Some T cells (CD4, mostly) undergo _____ transformation
- _____________ develop in multiple organs
- Tumors are a mixture of neoplastic ___ cells & reactive ___ cells & _______

A

early, Inhalation, ingestion, dander, respiratory, digestive, viremia, T, B, lymphocytolysis, concurrent, latent, T, 4, B, 8, obvious, shedding, follicle, replication, dander, kidney, pancreas, liver, nerves, CNS, strain, resistance, proliferative, lymphoma, neoplastic, Lymphomas, T, B , MQ

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76
Q

Marek’s disease: clinical signs & gross lesions
1. Classic Marek’s disease is called ______________
- Affected ___ or PNS
- __________, depending on what nerve is most affected
- _______ nerve – paralysis of legs
- ______ nerve – paralysis of wings
- ______ (?)- cervical nerves
- Dilatation of crop & respiratory signs (digestive clinical signs) – ______ & ______ nerves
2. Visceral (Acute) Marek’s disease
- Don’t see neuro clinical signs or mild neuro clinical signs
- Lymphomatous proliferations (tumors) in viscera & skin
3. Ocular lymphomatosis
- LQ infiltration of iris w/loss of pigmentation = ‘grey eye’
- rare
4. Cutaneous Marek’s disease
- Enlarged feather follicles/nodules (virus replicating in feather follicles)
- Erythematous legs
- ‘Alabama redleg’
- lumpy appearance in skin

Can be more than one or just one?

A

neurolymphomatosis, CNS, Paralysis, Sciatic, Brachial, Torticollis, star gazing, vagus, intercostal

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77
Q
A

– Classic Marek’s disease = neurolymphomatosis
– Paralysis, depending on what nerve is most affected
– Sciatic nerve – legs

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78
Q
A

– Classic Marek’s disease = neurolymphomatosis
– Paralysis, depending on what nerve is most affected
– Sciatic nerve – legs

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79
Q
A

Classic Marek’s disease = neurolymphomatosis
– Paralysis, depending on what nerve is most affected
– Sciatic nerve – legs

Difference in thickeness; one on left is thicker due to inflammation on the inside. Can even see it at the root.

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80
Q
A

Visceral (Acute) Marek’s disease
– Lymphomatous proliferations (tumors) in viscera & skin

Lymphproliferative disease = tumors in the liver, bone marrow, spleen, kidney - in any viscera. Nodular lesions distributed through those organs. If you did impressions mear, mostly lymphocyte,a a few MQ plasma cells, but mostly lymphocytes

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81
Q
A

Ocular lymphomatosis
– LQ infiltration of iris w/loss of pigmentation = ‘grey eye’

82
Q
A

Ocular lymphomatosis
– LQ infiltration of iris w/loss of pigmentation = ‘grey eye’
Photo: Dr Jean Sander
USDA Agricultural Research Services

Also constricts the pupil because iris is so inflamed.

83
Q
A

Cutaneous Marek’s disease
– Enlarged feather follicles/nodules
– Erythematous legs - ‘Alabama redleg’
Photo: Dr Jean Sander, MSD Manual

84
Q
A

Cutaneous Marek’s disease
– Enlarged feather follicles/nodules
– Erythematous legs

85
Q
A

Cutaneous Marek’s disease
– Enlarged feather follicles/nodules
– Erythematous legs

86
Q

Marek’s disease: histopathology
1. Classic Marek’s disease = neurolymphomatosis
- PNS: Proliferative (type ____) or inflammatory (type ___) w/ ___________ = ______. Chronic mild (type ___) may occur instead ≠ ______
- CNS: Inflammatory (type __) lesion, perivascular ______, _______, & __________ (________ endothelial cells; may be some proliferation)
2. Visceral (Acute) Marek’s disease
- Lymphoid tumors - mixture of _________ LQ (including malignant __ cells) + reactive __ cells, other T cells, & MQ
- do ___ stain of T cells
3. Ocular lymphomatosis
- LQ infiltration of _____ w/loss of ________
4. Cutaneous Marek’s disease
- Dermatitis (________) w/____ & _____, and/or _________ proliferations (lymphocytes, lymphoblasts, & histiocytes/MQ).
- Lymphomatous lesions:
– Around feather ________ (perifollicular)
– Around blood vessels (________)
- IN inclusions in feather follicle epithelium (__________)

A

A, B, demyelination, paralysis, C, paralysis, B, cuffing, microgliosis, endotheliosis, plumper, pleomorphic, T, B, IHC, iris, pigmentation, perifolliculitis, LQ, PL, lymphomatous, follicles, perivascular, sometimes

87
Q
A

Classic Marek’s disease = neurolymphomatosis
– PNS: Inflammatory lesion (type B, lymphoplasmacytic neuritis)

Lymphocytes are dark purple dots. There should be no lymphocytes in your nerves!

88
Q
A

Cutaneous Marek’s disease
-Lymphomatous lesions:
– Perivascular and within the wall of BV. Characteristic of Marek’s

89
Q
A

– Cutaneous Marek’s disease
– Lymphomatous lesions:
– Perivascular

Purple grey = clusters of lymphocyte around and within BVs

90
Q
A

– Cutaneous Marek’s disease
– Lymphomatous lesions:
– Perivascular
– endotheliosis*

MQ, plasma cells present too

91
Q

Marek’s disease: diagnosis

A
  1. Clinical signs
  2. Gross lesions
  3. Virus isolation
  4. IFA, viral neutralization, PCR, IHC
92
Q

No the differences between the two

A

Should be less than 4 weeks old, not greater than.

93
Q

Marek’s
disease:
control
–

A

Vaccine – 1 day old chicks

94
Q

Marek’s
disease:
zoonosis

A

– Not at all

95
Q

Newcastle disease
- CAUSE:
- genus _________. This is the only one that causes Newcastle disease.
- ___RNA virus
- Aka Newcastle disease virus
- Reportable to OIE only is APMV-__ b/c _______ important.
*NOTE: All other avian paramyxoviruses (Avulavirus sp) cause ________ infection, but not Newcastle disease
- ___-___ (depending on which OIE document you read!) serotypes of Avian Paramyxoviruses
- [semantics, but important]

A

Avian paramyxovirus 1 (aka APMV-1)
Avulavirus, ss, 1, economically, paramyxovirus, 10-12

Crested cormorants are famous for Avian PMV.
Usually not APMV-1, but it can be.

96
Q

Newcastle disease
1. Species affected (by APMV-1):
–__________
– Less susceptible: ?
– Potential reservoirs: ?
– - Usually of _____ virulent strains w/potential to mutate up
2. Worldwide distribution
– _________ (highly pathogenic) strains endemic in Mesoamerica, Asia, Middle East and Africa
3. Pathogenicity depends on the strain of APMV-____

A

Chickens, most other birds, waterfowl & psittacines, less, Velogenic, 1

97
Q

Newcastle disease
- Pathogenicity depends on the strain of ?
- ICPI (?) _______ method
OR
- __ protein sequence (penetration of host cell membrane) _____ method

A

APMV-1, intracerebral pathogenicity index, Older, F, Newer

98
Q

What are the strains of APMV-1?

A
99
Q

Newcastle disease:
pathogenesis
1. Transmission:
- Mostly by _________ or ________ of infected secretions (?) – MOST ________
- _______ (long survival in ____ – think dirty egg _____)
- ________ transmission (some strains; not as important; strain would be very pathogenic so chick would die)
2. Virus replicates in mucosae of ____ respiratory and/or _______
3. Virus spreads by _________ route (1 st viremia)
- Adhered to _____ (probably by ____ glycoprotein)
4. Virus infects ______ & ____
5. Virus spreads hematogenously to ___ and/or other organs (___nd viremia)
6. Virus is _____
- Respiratory secretions/excretions and/or feces

A

Ingestion, inhalation, feces, respiratory
secretions/excretions, IMPORTANT, Fomites, feces, shells, Vertical, upper, intestine, hematogenous, RBC, HN, spleen, BM, CNS, 2, shed

100
Q

Focus on the velogenic strains

A
101
Q

Newcastle disease: clinical signs
1. VVND (Viscerotrophic Velogenic Newcastle Disease)
- ______ lethal, kills chickens of ___ ages
- Flock mortality can reach ____%
- ______, ________, ______ diarrhea, ___________, _______, ______, _______, ______, death

Which signs are less likely?

A

Acutely, all, 100, Weakness, anorexia, green, prostration, tremors, torticollis, paralysis, opisthotonus

tremors, torti, death is less likely b/c that is more likely associated with neuro

102
Q

Newcastle disease: clinical signs
- NVND (Neutrotrophic Velogenic Newcastle Disease)
- also respiratory*
- _____ lethal, kills chickens of __ ages but…
- Flock mortality around _____% of adults and ___ % of young chicks
- Sharp _______ in egg production (30-50%), w/shell _______ OR ___ shell at all
- Weakness, anorexia, etc.
- Respiratory signs*: ________ breathing, _______, _______, [conjunctivitis]
- Nervous signs: ?

A

Acutely, all, 50, 90, decrease, thinning, no, difficulty, wheezing, gurgling,

prostration, tremors, torticollis (stargazing), paralysis, opisthotonus, death

103
Q
A

– NVND (Neutrotrophic Velogenic Newcastle Disease)
– Torticollis (stargazing), opisthotonus

104
Q
A

NVND (Neutrotrophic Velogenic Newcastle Disease)
– Torticollis (stargazing), opisthotonus

105
Q
A

NVND (Neutrotrophic Velogenic Newcastle Disease)
– Torticollis (stargazing), opisthotonus

106
Q

What can be seen in the image below?

A

Newcastle
disease: gross
lesions
– VVND
– Necrotizing gastroenteritis & hemorrhage
– Look at junctions
– NVND
– Pneumonia and/or encephalitis

Junctions between prov and gizzard adn pro and ven

107
Q

Newcastle disease: histopathology
1. VVND
- __________ gastroenteritis
- Hemorrhages in junctions of: ?
- ______ necrosis
2. NVND
- ______ (interstitial)
and/or
- _________: non-suppurative, with LQ perivascular _____, _________ & ________ _____ (IN & IC) Viscerotrophic

A

Necrotizing, esophagus, proventriculus, gizzard, GALT, Pneumonia, Encephalitis, cuffing, endotheliosis, inclusion bodies

108
Q
A

Gliosis – tricky to see without normal control

b/c birds normally have a lot of glial cells in their brain.

109
Q
A

Necrosis & degeneration (moth-eaten look of neuropil)

110
Q
A

Spheroids = swollen axons.
When tbere is demyelination, the myelin is keeping axon tight, so when the cells that make myelin die/degeneration the axon starts to swell whicih is what we see here.

111
Q
A

Spheroids

112
Q
A

Spheroids

113
Q
A

Neuronal necrosis (red = dead)
Polygonal shape, large nucleus, etc.

114
Q
A

Neuronal inclusion bodies: IN & IC

115
Q
A

– Neuronal inclusion bodies: IN & IC

116
Q
A

Neuronal inclusion bodies: IN & IC

117
Q
A

Neuronal inclusion bodies: IN & IC
Paramyxo virus and herpes virus inclusions are usually pink

118
Q
A

Neuronal inclusion bodies: IN & IC

119
Q

New castle disease diagnosis:

– For OIE
– Virus _______ & ____
– qPCR ____ panel
– Other tests:
– _________ – only for unvaccinated flocks
– IHC
–______________ strips (Li et al., 2019)

A

isolation, qPCR, VSL, Hemaglutination, Immunochromatographic

120
Q
A
121
Q

Newcastle disease: control

A
  1. Vaccines
  2. Live-attenuated (in water, aerosol, eye/nose droplets, beak dipping)
    - Virus shedding for about 2 weeks
    - Some Inactivated (injected) available, but not as effective
  3. Hygiene / biosecurity
122
Q

Newcastle disease:
zoonosis
1. Potential zoonosis, albeit rare
- Immunosuppression increases risk
- Veterinarians, processing plant employees, laboratory workers, vaccination crews that come in contact with diseased birds, carcasses or live vaccines
2. Clinical signs in humans:
- Self-limiting conjunctivitis - most common clinical
- Excessive lacrimation, eyelid edema, subconjunctival hemorrhage, unilateral or bilateral reddening
- Occasionally, generalized infection (fever, headache, chills)

A
123
Q

Bornavirus disease
1. CAUSE: Avian ___________ (ABV)
- _____ __NA virus w/ _______ replication
- ___ species
- Aka:

A

bornavirus, ss, R, nuclear, 8

  • Macaw wasting disease
  • Psittacine Proventricular Dilatation Disease (PPDD)
  • Proventricular Dilatation Disease (PDD) Mainly called this
  • Neuropathic gastric dilatation (NGD)
124
Q

Bornavirus disease
- ____________ neurologic disease, often fatal
- First identified in the 1970’s in psittacines (Macaw wasting disease)
- __________ distribution
at least for Captive ___________, not sure about wild species
- Species affected:

A

Progressive, Worldwide, psittacines, Psittacines, canaries, finches, Canada geese

125
Q

Bornavirus disease: pathogenesis
- Targets _________ nerves of _____ & ____ GI. It can go into the _____, but typical lesions associated with damage to ____.
- Esophagus, crop, proventriculus, gizzard, duodenum & Central nervous system (CNS)
Cerebrum, cerebellum, brain stem
- Infection route (postulated)
Trauma/inoculation in skin
Fecal-oral & respiratory
- Migration to nervous ganglia (& CNS – Canada geese)
– Retrograde axonal transport (postulated)
- Neurologic signs associated to disfunction of affected ganglia or CNS
- *Subclinical psittacine carriers are common in North America

A

autonomic, upper, middle, brain, ganglia

126
Q

Bornavirus disease:
clinical signs
1. Weight _____
2. Ganglion dependent:
- ____ stasis
- Proventricular/ventricular ________
- ____________
3. __________ material in feces (maldigestion)
4. ___________
5. +/- ____ signs
- Ataxia, loss of _______ reflex
6. Death

A

loss, Crop, dilatation, Regurgitation, Undigested, Starvation, CNS, predator

127
Q
A
  • Flaccidity & dilation of portion(s) of GI tract
  • Proventriculus, ventriculus & crop are most affected
128
Q

Bornavirus disease: gross
findings
- ___________
- __________ & ________ of portion(s) of GI tract
____________, ___________ & _____ are most affected
- ______ of muscular grinding of seeds – _______ material in feces
- If exclusive CNS involvement, no ___ lesions
- ___________ & _________ may be present

A

Emaciation, Flaccidity, dilation, Proventriculus, ventriculus, crop, Lack, undigested, GI, Cardiomegaly, hydropericardium

129
Q
A
130
Q
A
131
Q

Bornavirus disease: histopathology
- LQ PL infiltrates in:
1. (3)?
2. ____ & _______ ______
3. ______ & _____ glands – ____ characteristic

–> If in CNS: ________ & perivascular ____; _________ cell necrosis
- There are perivascular cuffs in the spinal cord and lymphoplasmacytic infiltrates within associated ganglia and dorsal
nerve roots.

A
  1. Myenteric plexuses, ganglia, & peripheral nerves
  2. Brain, spinal cord
  3. Heart, adrenal, less

demyelination, cuffs, Purkinje

132
Q
A

See lesions in brain, digestive tract

133
Q
A

brain

134
Q
A

brain

135
Q
A

perivascular lymphocytic inflammation

136
Q
A
137
Q
A
138
Q
A

Perivascular cuffs of LQ (fewer MQ & PL) – neuritis

139
Q
A

Perivascular cuffs of LQ (fewer MQ & PL) – neuritis

140
Q
A
141
Q
A
142
Q
A

LQ (fewer MQ & PL) inflammation – ganglioneuritis

143
Q
A

LQ (fewer MQ & PL) inflammation – ganglioneuritis

144
Q

What can be seen in the image below?
Bornavirus Antemortem:
– Plucked feathers – ______ for virus
– ______ signs & _____ findings
– _____ & ______ glands – less characteristic
– Histopathology + IHC

A

Bornavirus Antemortem:
– Plucked feathers – qPCR for virus
– Clinical signs & gross findings
– Heart & adrenal glands – less characteristic
– Histopathology + IHC

145
Q

Bornavirus disease: zoonosis?

A

– Not at all

146
Q

When you see chicken, think?

A

Marek’s

147
Q

When you see Cockatiel?

A

Borna

148
Q

When you see ?

A

Borna

149
Q
A
150
Q

Salmonellosis in wild birds is caused by?

A

CAUSE: Salmonella enterica (S. typhimurium –most common)
- Gram (-) rod
- Worldwide distribution

151
Q

Salmonellosis affects which species?

A
  • Species affected: all (avian & mammalian)
  • ‘Songbirds’ or ‘Garden birds’ in most cases – many species
152
Q

__________, along with _______ birds, are the species _______ affected and the most likely to be found ____ or _____ due to Salmonellosis infection.

A

Songbirds, aquatic, most, sick, dead

153
Q

Name the poster child of Salmonellosis.

A

Pine siskin in NA
- Common redpoll (Canada

154
Q
A

Pine siskin
- can be found @ bird feeders

155
Q
A

Common redpoll

156
Q

Salmonellosis, in songbirds: Pathogenesis
- _____-_____ cycle
- Bird ________: large ___________ of birds –> ____ material on bird seed
- Winter/Spring; birds feed out of bird feeders during this time _____ than other seasons;
- Bacterium can survive ____-term survival in ______ (several ___ and _______ at bird feeder even if ___ birds)
- Carrier state (can live in _________ and shed it into __________).
- ________ transmission (chickens, etc.) not documented in wild birds
- Unusual presentation in _________; This is a digestive system disease, but in this case affects _____ GI (____ and ______); Not the usual _______.

A

Fecal, oral, feeders, congregation, fecal, more, Long, environment, days, weeks, no, intestine, environment, Vertical, songbirds, upper, crop, esophagus, enteritis

157
Q

Salmonellosis, in songbirds:
Clinical signs For songbirds
- Birds are abnormally ______, _____ flight, stay on ________ a lot. Can pick them ___ when they are very sick.
- Found ______ at feeders

A

tame, weak, feeders, up, dead

158
Q

Salmonellosis, in songbirds: Gross findings
–> In songbirds
- Esophagus / crop (esophagitis/ingluvitis (____________ of crop), ___________, ________ to _________, ______ to ________, severe):
- Necrosis of ________ and ____ is main finding.
- ___________ pseudomembrane
- Gram (___) rods
-___________ to ________ inflammation (if earlier on: heterophils, if a few days later: granulomatous).
- ________ (birds are usually sick for long enough that they become this way. Some cases are acute and then in that case their BCS is good).
- Other lesions:
- Foci of _______/_________ in other organs/tissues
- Pectoral muscle, brain, liver
- Arthritis (in some chronic cases, but usually in waterfowl, arthritis occurs).

A

inflammation, fibrinonecrotizing, multifocal, coalescing, acute, subacute

esophagus, crop, Fibrinonecrotic, -, Heterophilic, granulomatous, Emaciation

necrosis, inflammation

159
Q
A

Ovoid shape structure = crop. Lumen looks like it is full of seeds, it is full of necrotic tissue.

160
Q
A

Yellow fibrinonecrotic material = plaques
Very characteristic of salmenollosis

161
Q
A

Salmonellosis in songbird.
Crop is full of necrotic material.

162
Q
A

Round, pale nodules on right side. Microscopically you would see gram - rods. Granulomatous inflammation.

163
Q

Salmonellosis, in songbirds:
diagnosis

  • Signalment + ______ lesions + ___________ + __________:
  • ______ swab / _____ tissue
    Sample from _____ or _______ is better b/c crop is usually contaminated with other bacteria.
A
  • In songbirds
  • Signalment + Gross lesions + Histopathology + Culture:
  • Crop swab / liver tissue
    Sample from liver or spleen is better b/c crop is usually contaminated with other bacteria.
164
Q

Salmonellosis, in songbirds:
control In songbirds
- Reduce _______ / _______
- Reduce _______ ___________
- Type of bird feeders that reduce transmission? Some bird feeders are very messy, there are always a lot of seeds on ground. Platform feeders are also bad because eating and pooping on same platform. Don’t use these feeders.

A

contact, crowding, BIRD FEEDERS

165
Q

Salmonellosis, in songbirds:
zoonosis?

A
  • Yes, very much so
  • And not just humans… Cats can get infected with salmonella as well.
166
Q

Numbers of feral cats in the
U.S. were estimated at ? in 2000.

A

73 million

167
Q

In sweden, a red pole and siskin
Very wet summer so flag seed could not be effected, so bird populations that fed on it exploded. Lot more birds at feeders, a lot more salmonellosis and then a huge outbreak in cats b/c they would eat the birds. Some of these cats died.

A
168
Q

Mycoplasmosis, in wild birds
(NA) is caused by?

A

CAUSE: Mycoplasma gallisepticum
– – finch strain

169
Q

Mycoplasma is a Bacterial organism w/o a _____ _______ ( ________-side-up egg colonies)
- _________ self-replicating prokaryote
Aka:
- _______ respiratory disease, infectious ________, house finch ___________
- Occurrence: North America

A

cell wall, sunny, Smallest, Chronic, sinusitis, conjunctivitis

170
Q
A

Mycoplasma

171
Q
A

Species affected: House finch (Carpodacus mexicanus)
– Aka: Haemorhous mexicanus
– Other finch species (less so)

172
Q

– Species affected by Mycoplasma:
1. House finch (Carpodacus mexicanus)
2. West / East pop

‘40s “Hollywood finch”
Wash. DC, 1993-94
1st outbreak

A

House finches used to just be a western US population. Someone in the 40s brought them to NY and then released them into the wild. Ended up with an eastern population of birds. The one with the first outbreak of mycoplasmosis in winter 93/94 was somewhere in washington DC

173
Q

Project FeederWatch
- Ask people to submit photos of wild birds at feeders.
- Asked people to report birds that looked sick.

A
174
Q

What condition do you think that this house finch has?

A

Mycoplasmosis most likely.
House finch with bulging eyes.

175
Q

Mycoplasmosis: pathogenesis
- ________ contact w/surfaces or droplets (________/_________ secretions) requires close contact
- ________ transmission (secretions on edges of bird feeder holes.
- No vertical transmission in _____
- Mycoplasma ___________ (finch strain)
- Targets _____ & _____/sinusoidal mucosase
- Adhesion to _____ surface of epithelium (conjunctival, nasal, or sinusoidal). Adheres to surface of epithelium, does not really enter tissue.
- Cellular damage/necrosis due to:
1. Inhibition of ______ activity; birds lose that ____ immune defense; can’t move mucus _____.
2. Secretion of _________ substances
- Further tissue damage from _____________ response
- ___ /____ inflammation (lymphocytic and plasmocytic; ____ aggregates in in submucosa or lamina propria of tissues –> swelling. Edema too.
- May become chronic / subclinical–> Carriers

A

Direct, ocular, sinusoidal, horizontal, finches, gallisepticum, ocular, nasal, apical

ciliary, innate, out, cytotoxic, inflammatory, LQ, PL, thick

176
Q

Mycoplasmosis: clinical signs

A

– Swollen eyelids (conjunctivitis & blepharitis)
– Blindness
– Serous exudate (caseous exudate if secondary bacterial infection)
– Die from either Emaciation and/or Predation

177
Q

What condition is this animal suffering from?

A

Mycoplasmosis
– Swollen eyelids (conjunctivitis & blepharitis)
– Blindness
– Serous exudate
– Emaciation and/or Predation

178
Q

What condition is this animal suffering from?

A

– Swollen eyelids (conjunctivitis & blepharitis)
– Blindness
– Serous exudate
– Emaciation and/or Predation

Third eyelid is also veyr swollen

179
Q
A

Purple dots = lymphocytes and plasma cells. in submucosa and LP

180
Q
A

– Conjunctivitis & blepharitis & sinusitis, lymphoplasmacytic,
focally extensive, subacute, marked to severe

181
Q
A

Mycoplasma on surface of epithelium
– Conjunctivitis & blepharitis & sinusitis, lymphoplasmacytic,
focally extensive, subacute, marked to severe

182
Q

Mycoplasmosis: diagnosis
- _____ or ____
- Can also do Culture, but mycoplasma is VERY ______ (too many other organisms)
Rely mostly on history, clincial signs, IHC, PCR

A

PCR, qPCR, difficult

183
Q

Mycoplasmosis:
control
1. Reduce ______ /_____
2. Bird _____
- Type of feeder may be important
- Should we just not feed birds?

A

contact, crowding, Feeders

184
Q

Mycoplasmosis: zoonosis

A
  • None (for the finch strain…or any, really)
185
Q

Trichomoniasis, wild birds
- CAUSE: Trichomonas ________
- _______ parasite – _______
- Flagella & undulating membrane – ____
–> Aka:
- Trichomonosis (that’s the ”proper” name). If you are sick with this parasite, you have trichomonosis.
- Trichomoniasis (older way of referring to it). For parasitic diseases that are not causing harm.
- Cankers = old terms used by falconers(doves & pigeons)
- Frounce (raptors)

A

gallinae, Protozoan, trophozoites, mobile

186
Q

What parasite can be seen here?

A

Trichomonas gallinae

187
Q

Trichomoniasis, wild birds
Species affected?

A

Doves & pigeons (usually carriers)
Raptors (falcons and halks)

188
Q

Classic trichomoniasis
Pigeon or dove is feeding chicks. Chicks get trich in that way, and then transmit it via birds feeders, bath, or eaten by predatory bird. Pigeons and doves are very good at giving trich to their chicks, and other birds are not as good, but why? Trich does not survive well in environment, but survives very well in crop of pigeons and doves. They both produce crop milk, which is fed to their chicks inadvertently. Since early 2000s, trich in finches. First report in England. Almost half population of green finches.

A
189
Q

Ever since 2009, circulating in finches in eastern canada and in europe.

A
190
Q

Trich is a ________ disease. Depending on when birds nest is when you see first birds affected.

A

summer

191
Q

Purple finches nest _______, in late ____, where american gold finches, is late ____

A

earlier, june, july

192
Q

Trichomoiasis: pathogenesis
Most information from doves & pigeons
–> Transmission:
- Crop ____
- Contact with infected surfaces – _______/______ _____
- __________ material – finches tend to do this. Birds next to them are more attracted to ________ feed.
- Tissue tropism of:
– lives in ?
- Replication by ?
– Cause Damage to mucosae (& bones) either b/c of their presence or inflammation they recruit.
– Occasional infection of other organs and cause lesions in Liver

A

milk, feeders / water baths, Regurgitated, regurgitated,

Oral cavity, esophagus/crop
– Cranial bones; in finches, trich enters cranial bones of head

Binary fission

193
Q

Due to regurgitation, things stick to feathers around beak.

A

– Weakness, fluffed feathers, loss of predator response
– Regurgitation
– Crusty material around beak
– Emaciation Photo: S&D Wilson

194
Q
A

– Weakness, fluffed feathers, loss of predator response
– Regurgitation
– Crusty material around beak
– Emaciation Photo: S&D Wilson

195
Q
A

Esophagus in small birds is very thin,This one of very chunky.

196
Q
A

Caseous material (cankers) in lumen of esophagus/crop/mouth
– Thickened esophageal/ingluvial wall

Kankers = chunks of necrotic white material in mouth

197
Q
A

Esophagitis/ingluvitis/stomatitis, necrotizing & hyperplastic
(proliferative(, focally extensive to diffuse, subacute to chronic,
severe; occasional osteomyelitis and/or hepatic necrosis

198
Q
A

Intralesional protozoans

199
Q
A

Whitish lesion on side = trichomoiasis

Sometimes enter bone, especially of mandible.

200
Q

Trichomoiasis: diagnosis
– Signalment + Season (mid to late summer)
+
– Gross lesions, histopathology
– Trichomonad detection by:
– Direct smear
– Culture
– PCR

A

Take swab of esphagus, crop or mouth of birds and put in pouch test (used for cattle but also works for birds).
Grow and see them swimming.
PCR to id species.
Put swab on glass slide with water –> see trich moving.

201
Q

Trichomoiasis:
control
– Prevent overcrowding – eliminate feeders
– At least remove platform ones
– Risk of consuming regurgitated material & contact w/doves

Why are finches getting sick now and never before? Sharing feeders with species that are carriers.

A
202
Q

Trichomoiasis:
zoonosis –

A

None at all

Systemic Pathology I (27 decks)

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