Pathology: Systemic - Avian Disease Flashcards
Lead toxicosis
1. AKA _____ poisoning, ________
2. CAUSE: ingestion of ____
3. Species affected: ____ (not just ____)
lead, plumbism, lead, ALL, birds
Lead toxicosis
1. CAUSE: ingestion of ___
- ______ & _____ (main)
- _____ waste
- ___ pigments, etc.
Pellets, sinkers, Mine, Paint
What can be seen in this image? What does this cause?
Lead toxicosis
lead pellets
What can be seen in this image? What does this cause?
Lead toxicosis
Pellets and sinkers
Mistaken for pebbles –> ingested by animals
Lead toxicosis
- Low pH increases ___ availability
- e.g. __ + ____ = _____ toxicity
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
Lead toxicosis species main avian species affected?
- Waterfowl: Ducks, geese, swans, loons (eating stuff from bottom of lakes)
- Raptors (particularly scavengers)
- Bald eagles, other eagle sps
- water birds, upland gamebirds
- Others (other waterfowl)
- Loons
______, _______, and ______ are more commonly reported with lead poisoning.
Ducks, geese, swans
Lead toxicosis pathogenesis
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
Mechanisms of pathogenicity
- Attaches to membrane of RBC
- Hemoglobin synthesis (anemia due to reduced RBC and problem with O2 transport)
- Goes through BBB and target and kills neurons and astrocytes. Directly toxic to endothelial cells –> fibrinoid necrosis of the wall of BVs.
- 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
Lead toxicosis: Clinical signs
- Reluctance to fly or weakness when flying
- Unsteady gait (ataxia) (more typical with neurotropism)
- Flaccid neck (goose can walk and try to fly but can not lift its neck).
- Canada geese - Wings held in ‘roof shape’ or drooping
- Ducks, geese, swans, loons - 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
What can be seen in this image?
Wings held in ‘roof shape’ or drooping
Ducks, geese, swans, loons, etc.
What can be seen in this image?
Wings held in ‘roof shape’ or drooping
Ducks, geese, swans, loons, etc
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 _____
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
What can be seen in this image? What condition is this animal suffering from?
Bile-stained feathers (& feces) around cloaca
What can be seen in this image? What condition is this animal suffering from?
Emaciation, if chronic lead poisoning
What can be seen in this image? What condition is this animal suffering from?
Impacted food in upper GI tract
What can be seen in this image? What condition is this animal suffering from?
- Lead fragments in gizzard – not always present
- Pb vs other metals (Fe, Al) – magnet
What can be seen in this image? What condition is this animal suffering from?
If not doing necropsy or have live bird, do Xray because can see lead (metal).
What can be seen in this image? What condition is this animal suffering from?
- Lead fragments in gizzard – not always present
- Pb vs other metals (Fe, Al) – magnet
What can be seen in this image? What condition is this animal suffering from?
Mature bald eagle = white head
Takes 5 years to get white head.
Good BDS b/c fat in subcutis, well deveoped pectoral muscle
What can be seen in this image? What condition is this animal suffering from?
Female bird
Ovaries
Kidneys with lead poisoning, or other diseases that cause damage to tubules look like a brain.
What can be seen in this image? What condition is this animal suffering from?
Cut open kidney
- 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: _______ & ______ - Blood vessels
- Fibrinoid necrosis of the ____
- _______
- Secondary _____ or _______ lesions
Tubuloepithelial, necrosis, Proximal, fibrinoid, hemorrhage, nephropathy, fibrosis, wall, Hemorrhage, ischemic, hemorrhagic
What can be seen in this image? What condition is this animal suffering from?
Lead toxicosis - Kidney
normal tubule
Inclusion bodies are little purple circles
Ziehl Nielson stain to highlight more.
What can be seen in this image? What condition is this animal suffering from?
What can be seen in this image? What condition is this animal suffering from?
Myocardium
Lead toxicosis vessels - heart
What can be seen in this image? What condition is this animal suffering from?
What can be seen in this image? What condition is this animal suffering from?
Fibrinoid necrosis in walls of BV
Lead toxicosis: Antemortem and Postmoretm diagnosis?
- Antemortem:
- Pb level in blood - Post-mortem
- Pb level in liver, kidney, bone
* Need species-specific values for Pb levels
Please explain what is shown in the diagram below.
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.
Please explain what is shown in the diagram below.
Waterfowl = die with lower levels of lead then in pigeons
Lead toxicosis: Control
- Lead shot & lead sinkers
- Regulations are country and state-specific
Is Lead toxicosis a zoonotic disease?
- Possible ‘zoonosis’ but unlikely
- Most Pb in liver, kidney & bone, not muscle - H more likely to get lead toxicosis the same way birds do:
- Eating lead pellets or fragments in game meat
H = humans
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
Multiple, Kidney, visceral, articular
What is gout?
- 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
Describe the typical presentation of Gout
- Renal / Visceral gout is usually acute
- Often with little to no inflammation - Articular gout is usually chronic
- Associated with granulomatous inflammation
Gout: Pathogenesis
- Hyperuricemia - uric acid in blood
- Precipitation of monosodium urate crystals (called tophi as in starburst shape of crystals) on
- Renal tubules
- Visceral surfaces
- Synovial surfaces - Phagocytosis of tophi by MQ (attempts, at least; not usually successful but still try )
- Tissue damage (renal tubular epithelial necrosis)
- Inflammatory reaction
- Development of chronic inflammation +/- fibrosis
Gout: Clinical signs
1. Acute renal / visceral form
2. Articular form
- Little to no clinical signs, - May exhibit progressive weakness before death
- Difficulty flying and perching; rigid & inflamed (swollen & hot) feet
Renal gout gross findings
- _____________ kidneys, ______ or ________ appearance
- Ureters ______ & filled with ____-___ concretions = urate _____
Enlarged, patchy, streaky, dilated, grey-white, calculi
Visceral gout gross findings
______-______, _______ patches on serous membrane, particularly in the _________ & _______ capsule – also ________ & ________
White, gray, chalky, Pericardium, hepatic, mesentery, peritoneum
Articular gout gross findings
__________ joints & ________ sheaths filled with ________ ________ deposits
_________ of synovial membrane & overlying _____ is possible
Swollen, tendon, chalky white, Rupture, skin
What can be seen in this image? What condition is this animal suffering from?
Visceral gout
White-gray chalky patches on serous membrane, particularly in:
What can be seen in this image? What condition is this animal suffering from?
Visceral gout
White-gray chalky patches on serous membrane, particularly in:
Pericardium & hepatic capsule – also mesentery & peritoneum
What can be seen in this image? What condition is this animal suffering from?
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.
- _____ 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.
Tophi, sharp, needle, acicular, center, basophilic, colorless, tophi, necrosis, heterophilic, granulomatous, birefringent, degradation
What can be seen in this image? What condition is this animal suffering from?
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
What can be seen in this image? What condition is this animal suffering from?
Gout.
What can be seen in this image? What condition is this animal suffering from?
When not fixed well, see degeneration and ?
What can be seen in this image? What condition is this animal suffering from?
Necrotic tubule.
Normal on left, and necrotic tubule with cellular cast on right.
What can be seen in this image? What condition is this animal suffering from?
Visceral gout = everywhere. Not just on surface, but also within tissue.
Gout, iver
What can be seen in this image? What condition is this animal suffering from?
gout, liver
What can be seen in this image? What condition is this animal suffering from?
gout, spleen
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
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 ?
Gout: control
- Prevention of causative factors
- Diet / hydration / nephrotoxic plants
- Nephrotoxic drugs
- Viral infections
Wild birds = usually problem with kidney that gives you gout
Is gout a zoonotic disease?
No
Infectious laryngotracheitis
1. CAUSE: ?
- Species affected?
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
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
Acute, contagious, aerosols, respiratory
- Inhalation (upper respiratory mucosae)
- Conjunctival contact
- Ingestion
viremia, Syncytial, Giant, epithelium
tracheal, cellular, life, trigeminal, Immunosuppression
Infectious laryngotracheitis: clinical signs
- Outbreaks may be:
- Highly pathogenic form (epizootic)
- Lowly pathogenic form (endemic) - High morbidity (50-70%) and moderate to high mortality (10-20%)
- Respiratory distress
- Coughing / sneezing / head shaking – gasping for air
- Expectoration of bloody / mucous exudate
What can be seen in this image? What condition is this animal suffering from?
Clinical signs: mostly respiraotry distress; birds are gasping for air. Cough out or sneeze out bloody mucous material
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
epizootic, endemic, morbidity, mortality, distress, Coughing, head, gasping, bloody, mucous
Infectious laryngotracheitis: gross findings
- Tracheal mucosal necrosis and hemorrhage
- Occlusive pseudomembranes, fibrinonecrotic & hemorrhagic
- Casts or plugs fill tracheal lumen - Mild cases: sinusitis, conjunctivitis, seromucous exudate
What can be seen in this image? What condition is this animal suffering from?
What can be seen in this image? What condition is this animal suffering from?
IFT
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 _______ & _____ ______
Tracheal, Fibrinonecrotic, Syncytial, IN, A, clear, halo, Early, ulceration, inflammation, squamous, bronchi, air sacs
What can be seen in this image? What condition is this animal suffering from?
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.
What can be seen in this image? What condition is this animal suffering from?
Necrotic material and hemorrhage here.
This is the pseudomembrane. Fibrin, RBCs, pobably some bacteria too. mostly degenerated epithelial cells
What can be seen in this image? What condition is this animal suffering from?
Synctial cell formation
What can be seen in this image? What condition is this animal suffering from?
Syncytial cell formation
IN inclusion bodies, Cowdry type A
Normal = 1 or 2 nuclei (top right)
Infectious laryngotracheitis: Diagnosis
- Characteristic clinical signs, gross lesions & histopathology
+ - PCR (to confirm), IFA, IHC, EM, virus isolation
- 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.
Infectious laryngotracheitis: Control
- Vaccination
- First avian disease for which an effective vaccine was developed
- Economically important disease - Hygiene measures
- Some transmission may be through fomites
- quarantine, if have sick birds = do not use same materials.
Infectious laryngotracheitis: zoonosis?
no
Marek’s disease
1. CAUSE: ?
2. Species affected: ?
- 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
- Chickens mostly
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).
young, days, dust, 1, condition, Lymphoproliferative, leukosis, neoplastic, oncogenic, chickens, turkeys
Marek’s disease: pathogenesis
Describe the phases of pathogenesis.
- Phase 1 – early cell-to-cell infection
- Phase 2 – latent infection
- Phase 3 – feather follicle shedding
- Phase 4 – proliferative (lymphoma) phase
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 & _______
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
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?
neurolymphomatosis, CNS, Paralysis, Sciatic, Brachial, Torticollis, star gazing, vagus, intercostal
Classic Marek’s disease = neurolymphomatosis
Paralysis, depending on what nerve is most affected
Sciatic nerve – legs
Classic Marek’s disease = neurolymphomatosis
Paralysis, depending on what nerve is most affected
Sciatic nerve – legs
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.
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
Ocular lymphomatosis
LQ infiltration of iris w/loss of pigmentation = ‘grey eye’
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.
Cutaneous Marek’s disease
Enlarged feather follicles/nodules
Erythematous legs - ‘Alabama redleg’
Photo: Dr Jean Sander, MSD Manual
Cutaneous Marek’s disease
Enlarged feather follicles/nodules
Erythematous legs
Cutaneous Marek’s disease
Enlarged feather follicles/nodules
Erythematous legs
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, B, demyelination, paralysis, C, paralysis, B, cuffing, microgliosis, endotheliosis, plumper, pleomorphic, T, B, IHC, iris, pigmentation, perifolliculitis, LQ, PL, lymphomatous, follicles, perivascular, sometimes
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!
Cutaneous Marek’s disease
-Lymphomatous lesions:
Perivascular and within the wall of BV. Characteristic of Marek’s
Cutaneous Marek’s disease
Lymphomatous lesions:
Perivascular
Purple grey = clusters of lymphocyte around and within BVs
Cutaneous Marek’s disease
Lymphomatous lesions:
Perivascular
endotheliosis*
MQ, plasma cells present too
Marek’s disease: diagnosis
- Clinical signs
- Gross lesions
- Virus isolation
- IFA, viral neutralization, PCR, IHC
No the differences between the two
Should be less than 4 weeks old, not greater than.
Marek’s
disease:
control
Vaccine – 1 day old chicks
Marek’s
disease:
zoonosis
Not at all
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]
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.
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-____
Chickens, most other birds, waterfowl & psittacines, less, Velogenic, 1
Newcastle disease
- Pathogenicity depends on the strain of ?
- ICPI (?) _______ method
OR
- __ protein sequence (penetration of host cell membrane) _____ method
APMV-1, intracerebral pathogenicity index, Older, F, Newer
What are the strains of APMV-1?
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
Ingestion, inhalation, feces, respiratory
secretions/excretions, IMPORTANT, Fomites, feces, shells, Vertical, upper, intestine, hematogenous, RBC, HN, spleen, BM, CNS, 2, shed
Focus on the velogenic strains
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?
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
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: ?
Acutely, all, 50, 90, decrease, thinning, no, difficulty, wheezing, gurgling,
prostration, tremors, torticollis (stargazing), paralysis, opisthotonus, death
NVND (Neutrotrophic Velogenic Newcastle Disease)
Torticollis (stargazing), opisthotonus
NVND (Neutrotrophic Velogenic Newcastle Disease)
Torticollis (stargazing), opisthotonus
NVND (Neutrotrophic Velogenic Newcastle Disease)
Torticollis (stargazing), opisthotonus
What can be seen in the image below?
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
Newcastle disease: histopathology
1. VVND
- __________ gastroenteritis
- Hemorrhages in junctions of: ?
- ______ necrosis
2. NVND
- ______ (interstitial)
and/or
- _________: non-suppurative, with LQ perivascular _____, _________ & ________ _____ (IN & IC) Viscerotrophic
Necrotizing, esophagus, proventriculus, gizzard, GALT, Pneumonia, Encephalitis, cuffing, endotheliosis, inclusion bodies
Gliosis – tricky to see without normal control
b/c birds normally have a lot of glial cells in their brain.
Necrosis & degeneration (moth-eaten look of neuropil)
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.
Spheroids
Spheroids
Neuronal necrosis (red = dead)
Polygonal shape, large nucleus, etc.
Neuronal inclusion bodies: IN & IC
Neuronal inclusion bodies: IN & IC
Neuronal inclusion bodies: IN & IC
Neuronal inclusion bodies: IN & IC
Paramyxo virus and herpes virus inclusions are usually pink
Neuronal inclusion bodies: IN & IC
New castle disease diagnosis:
For OIE
Virus _______ & ____
qPCR ____ panel
Other tests:
_________ – only for unvaccinated flocks
IHC
______________ strips (Li et al., 2019)
isolation, qPCR, VSL, Hemaglutination, Immunochromatographic
Newcastle disease: control
- Vaccines
- Live-attenuated (in water, aerosol, eye/nose droplets, beak dipping)
- Virus shedding for about 2 weeks
- Some Inactivated (injected) available, but not as effective - Hygiene / biosecurity
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)
Bornavirus disease
1. CAUSE: Avian ___________ (ABV)
- _____ __NA virus w/ _______ replication
- ___ species
- Aka:
bornavirus, ss, R, nuclear, 8
- Macaw wasting disease
- Psittacine Proventricular Dilatation Disease (PPDD)
- Proventricular Dilatation Disease (PDD) Mainly called this
- Neuropathic gastric dilatation (NGD)
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:
Progressive, Worldwide, psittacines, Psittacines, canaries, finches, Canada geese
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
autonomic, upper, middle, brain, ganglia
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
loss, Crop, dilatation, Regurgitation, Undigested, Starvation, CNS, predator
- Flaccidity & dilation of portion(s) of GI tract
- Proventriculus, ventriculus & crop are most affected
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
Emaciation, Flaccidity, dilation, Proventriculus, ventriculus, crop, Lack, undigested, GI, Cardiomegaly, hydropericardium
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.
- Myenteric plexuses, ganglia, & peripheral nerves
- Brain, spinal cord
- Heart, adrenal, less
demyelination, cuffs, Purkinje
See lesions in brain, digestive tract
brain
brain
perivascular lymphocytic inflammation
Perivascular cuffs of LQ (fewer MQ & PL) – neuritis
Perivascular cuffs of LQ (fewer MQ & PL) – neuritis
LQ (fewer MQ & PL) inflammation – ganglioneuritis
LQ (fewer MQ & PL) inflammation – ganglioneuritis
What can be seen in the image below?
Bornavirus Antemortem:
Plucked feathers – ______ for virus
______ signs & _____ findings
_____ & ______ glands – less characteristic
Histopathology + IHC
Bornavirus Antemortem:
Plucked feathers – qPCR for virus
Clinical signs & gross findings
Heart & adrenal glands – less characteristic
Histopathology + IHC
Bornavirus disease: zoonosis?
Not at all
When you see chicken, think?
Marek’s
When you see Cockatiel?
Borna
When you see ?
Borna
Salmonellosis in wild birds is caused by?
CAUSE: Salmonella enterica (S. typhimurium –most common)
- Gram (-) rod
- Worldwide distribution
Salmonellosis affects which species?
- Species affected: all (avian & mammalian)
- ‘Songbirds’ or ‘Garden birds’ in most cases – many species
__________, along with _______ birds, are the species _______ affected and the most likely to be found ____ or _____ due to Salmonellosis infection.
Songbirds, aquatic, most, sick, dead
Name the poster child of Salmonellosis.
Pine siskin in NA
- Common redpoll (Canada
Pine siskin
- can be found @ bird feeders
Common redpoll
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 _______.
Fecal, oral, feeders, congregation, fecal, more, Long, environment, days, weeks, no, intestine, environment, Vertical, songbirds, upper, crop, esophagus, enteritis
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
tame, weak, feeders, up, dead
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).
inflammation, fibrinonecrotizing, multifocal, coalescing, acute, subacute
esophagus, crop, Fibrinonecrotic, -, Heterophilic, granulomatous, Emaciation
necrosis, inflammation
Ovoid shape structure = crop. Lumen looks like it is full of seeds, it is full of necrotic tissue.
Yellow fibrinonecrotic material = plaques
Very characteristic of salmenollosis
Salmonellosis in songbird.
Crop is full of necrotic material.
Round, pale nodules on right side. Microscopically you would see gram - rods. Granulomatous inflammation.
Salmonellosis, in songbirds:
diagnosis
- Signalment + ______ lesions + ___________ + __________:
- ______ swab / _____ tissue
Sample from _____ or _______ is better b/c crop is usually contaminated with other bacteria.
- 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.
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.
contact, crowding, BIRD FEEDERS
Salmonellosis, in songbirds:
zoonosis?
- Yes, very much so
- And not just humans… Cats can get infected with salmonella as well.
Numbers of feral cats in the
U.S. were estimated at ? in 2000.
73 million
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.
Mycoplasmosis, in wild birds
(NA) is caused by?
CAUSE: Mycoplasma gallisepticum
– finch strain
Mycoplasma is a Bacterial organism w/o a _____ _______ ( ________-side-up egg colonies)
- _________ self-replicating prokaryote
Aka:
- _______ respiratory disease, infectious ________, house finch ___________
- Occurrence: North America
cell wall, sunny, Smallest, Chronic, sinusitis, conjunctivitis
Mycoplasma
Species affected: House finch (Carpodacus mexicanus)
Aka: Haemorhous mexicanus
Other finch species (less so)
Species affected by Mycoplasma:
1. House finch (Carpodacus mexicanus)
2. West / East pop
‘40s “Hollywood finch”
Wash. DC, 1993-94
1st outbreak
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
Project FeederWatch
- Ask people to submit photos of wild birds at feeders.
- Asked people to report birds that looked sick.
What condition do you think that this house finch has?
Mycoplasmosis most likely.
House finch with bulging eyes.
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
Direct, ocular, sinusoidal, horizontal, finches, gallisepticum, ocular, nasal, apical
ciliary, innate, out, cytotoxic, inflammatory, LQ, PL, thick
Mycoplasmosis: clinical signs
Swollen eyelids (conjunctivitis & blepharitis)
Blindness
Serous exudate (caseous exudate if secondary bacterial infection)
Die from either Emaciation and/or Predation
What condition is this animal suffering from?
Mycoplasmosis
Swollen eyelids (conjunctivitis & blepharitis)
Blindness
Serous exudate
Emaciation and/or Predation
What condition is this animal suffering from?
Swollen eyelids (conjunctivitis & blepharitis)
Blindness
Serous exudate
Emaciation and/or Predation
Third eyelid is also veyr swollen
Purple dots = lymphocytes and plasma cells. in submucosa and LP
Conjunctivitis & blepharitis & sinusitis, lymphoplasmacytic,
focally extensive, subacute, marked to severe
Mycoplasma on surface of epithelium
Conjunctivitis & blepharitis & sinusitis, lymphoplasmacytic,
focally extensive, subacute, marked to severe
Mycoplasmosis: diagnosis
- _____ or ____
- Can also do Culture, but mycoplasma is VERY ______ (too many other organisms)
Rely mostly on history, clincial signs, IHC, PCR
PCR, qPCR, difficult
Mycoplasmosis:
control
1. Reduce ______ /_____
2. Bird _____
- Type of feeder may be important
- Should we just not feed birds?
contact, crowding, Feeders
Mycoplasmosis: zoonosis
- None (for the finch strain…or any, really)
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)
gallinae, Protozoan, trophozoites, mobile
What parasite can be seen here?
Trichomonas gallinae
Trichomoniasis, wild birds
Species affected?
Doves & pigeons (usually carriers)
Raptors (falcons and halks)
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.
Ever since 2009, circulating in finches in eastern canada and in europe.
Trich is a ________ disease. Depending on when birds nest is when you see first birds affected.
summer
Purple finches nest _______, in late ____, where american gold finches, is late ____
earlier, june, july
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
milk, feeders / water baths, Regurgitated, regurgitated,
Oral cavity, esophagus/crop
Cranial bones; in finches, trich enters cranial bones of head
Binary fission
Due to regurgitation, things stick to feathers around beak.
Weakness, fluffed feathers, loss of predator response
Regurgitation
Crusty material around beak
Emaciation Photo: S&D Wilson
Weakness, fluffed feathers, loss of predator response
Regurgitation
Crusty material around beak
Emaciation Photo: S&D Wilson
Esophagus in small birds is very thin,This one of very chunky.
Caseous material (cankers) in lumen of esophagus/crop/mouth
Thickened esophageal/ingluvial wall
Kankers = chunks of necrotic white material in mouth
Esophagitis/ingluvitis/stomatitis, necrotizing & hyperplastic
(proliferative(, focally extensive to diffuse, subacute to chronic,
severe; occasional osteomyelitis and/or hepatic necrosis
Intralesional protozoans
Whitish lesion on side = trichomoiasis
Sometimes enter bone, especially of mandible.
Trichomoiasis: diagnosis
Signalment + Season (mid to late summer)
+
Gross lesions, histopathology
Trichomonad detection by:
Direct smear
Culture
PCR
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.
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.
Trichomoiasis:
zoonosis
None at all
