Diseases and other
miscellaneous
conditions
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Emaciation
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

Not a disease itself, but the result of
other conditions such as fractures,
chronic disease, etc.
Accompanied by immuno-compromise
Usually seen in Dec-Feb


First year birds experiencing their first
winter
Mid-winter anemia (Redig)
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How bad can it get?

Keel score of 1 out of 5
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RTHA 650-750 g (Normal > 1100)
GHOW 900-1000 g (Normal > 1300)
Total solids < 1 (we’ve seen 0.2)
PCV < 20 (we’ve seen < 10)
Extreme lethargy, hypothermia
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Keel scores
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Treatment

Rehydration is critical
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LRS IO\SQ\PO route
2 x maintenance
Can use D5W IO
Add B vitamins to fluids
Supplmental heat
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Fluid Therapy
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Daily maintenance = 50 ml\kg\day
Can provide in multiple routes
IO catheter
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Distal ulna
Can maintain for 3 days max
Max bolus = 25 ml\kg
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Fluid Therapy
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Daily maintenance = 50 ml\kg\day
Can generally assume either 5 or
10% dehydration
Replace deficits in 48 hours
Can provide in multiple routes
IO catheter
Distal ulna
 Can maintain for 3 days max
 Max bolus = 25 ml\kg
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
Fluid Therapy

Example

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
900 g bird, 10% dehydrated
Deficit = 900 X 10% = 90
Maintenance = 45 ml\day
Bird needs 90 + 90 = 180 over next 48
hours
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Treatment


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Iron Dextrans 0.1 ml\kg IM q10d x 2
Fenbendazole 50 mg\kg SID x 5 d
Broad-spectrum antibiotics?
Itraconazole 10 mg\kg BID for juvenile
RTHAs
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Feeding

Furless whole mice
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Begin after 18-24 hours
Start slow 10-30 g\kg TID
Ramp up over next three days
Continue aggressive hydration
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Monitor PCV\TP
Formulas
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Useful if regurgitating whole food
Oxbow Carnivore diet
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Prognosis


Generally good if there isn’t a
serious underlying cause.
Recovery is quick
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Bumblefoot
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
Refers to injuries or lesions on the
pads of feet and toes.
Usually husbandry related
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Improper perch size or covering
No perch variability
Poor ground substrate
Can also be secondary to leg
fractures or any other cause of
lameness.
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Bumblefoot

Clinical signs
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Redness, smoothening, loss of
scale
Swelling and visible inflammation
Necrosis and open wounds
Osteomyelitis, sepsis
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Bumblefoot

Grades
1.
2.
3.
4.
5.
Flatten, smooth epithelium. May be
a little pink
Infection of SQ tissue but no gross
swelling
Infected, hot, swollen foot without
involvement of tendons or bone
Involvement of tendon and\or bone
End stage with loss of function.
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Bumblefoot
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Bumblefoot

Treatment
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Pressure relieving bandages such as
ball wraps or corn pads
Topical meds

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Preparation H, Silvidine
CEH Cream – Calendula, Echinacea,
Hypericum
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Bumblefoot
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Treatment (continued)
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Aggressive surgical debridement
Systemic antibiotics (Clavamox + Baytril)
Chlorhexidine soaks
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Wrist wounds
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
Husbandry related due to improper
enclosures
Leads to exposure of carpal
joint\bones.
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Wrist wounds
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Wrist wounds

Treatment
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Daily flushes
Staged surgical
debridements\parial
closure
Protect with telfa
and tegaderm
Prognosis is
surprisingly good
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Barbed-wire injuries
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
Usually Great-Horned Owls
Can cause massive soft tissue trauma
and patagial tendon transection.
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Barbed-wire injuries
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Treatment must be aimed at
protecting the tendon from exposure
and desiccation.
Silvidine cream is helpful
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Barbed-wire injuries
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Barbed-wire injuries
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Barbed-wire injuries
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Tendon anastomosis

Patagial transection was once thought to
be hopeless. A recent case (GHOW
13112) has proven otherwise.
 Freshened edges
 Anastomosis with 6-0 Vicryl
 No PT for 2 weeks then very gradual
increase in extension exercises under
anesthesia for 6-8 weeks.
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Aspergillosis


Very important disease in raptors,
especially juvenile RTHA’s
Fungus: Aspergillus fumigatus
Ubiquitous
Saprophytic
Opportunistic
Infectious
Not contagious
Not zoonotic, but…
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Aspergillosis – acute form


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Inhalation of a large
mass of spores
Tracheal granuloma
Causes voice change,
dyspnea and death
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Aspergillosis – chronic form



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Due to immunosuppression or secondary
to weakened state
Emaciation, anorexia,
depression, anemic
“Ain’t doin’ right”
Granulomas\fungus in air
sacs and lungs
Respiratory signs not seen
until late in disease
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Aspergillosis - diagnosis
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

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CBC
 Total count can be 30,000+
 Monocytosis
Cytology – cotton blue stain
Tracheal culture
Serology
Histopathology
Endoscopy
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Aspergillosis - diagnosis
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Aspergillosis – risk factors
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Damp organic bedding
Poor ventilation
Immuno-suppresion
Stress
Poor nutrition (Vit A deficiency)
Extended antibiotic use
Other illness like lead poisoning
Species: Juvenile RTHA, GOSH, GYRF,
RLHA, GOEA
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Aspergillosis – treatment


Difficult, expensive and long-term
Acute cases
 Place air-sac tube
 Can attempt to remove
granuloma endoscopically or
blindly with suction.
 Intratracheal Amphotericin B
(1 mg\kg TID)
Clinical signs due to
tracheal obstruction
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Aspergillosis – treatment

Chronic cases
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Lower stress
Supportive – fluids, nutrition
Reglan\tube feeding if necessary
Amphotericin B 1.5 mg\kg IV\IO TID x 3 days. Dilute in
D5W (maximum allowable bolus)
Nebulize saline or F10 (1:250 dilution in NaCl) 20
minutes BID x 7 days
Itraconazole (Sporonox) 10 mg\kg BID x 3 months.
Monitor for liver problems (AST,CK)



Compounded products are much cheaper but don’t work (studies
done at NC State)
Broad spectrum antibiotics
Monitor CBC’s, weight
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Aspergillosis - Prevention
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Prophylactic itraconazole 10 mg\kg PO
BID x 21 days (Especially in highlysusceptible species)
Start 1 week before a stressful change
Don’t use organic bedding
Provide good ventilation
Keep birds in good health
Keep stress to a minimum
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West Nile Virus

1999 - first seen in western hemisphere
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Affects many bird species, humans, horses
Mosquito vector, bird is a carrier.
Clinical signs develop 10-12 days post infection.

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Now in most states
Can see all types of neurologic disease
Retinal pathology
Diagnosis


Can shed virus in both oral and cloacal cavities. Oral and
chloacal swabs can be used for both ante- and postmortem
diagnosis.
It is not uncommon to see no gross changes at necropsy
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West Nile Virus



Treatment is purely supportive
Prognosis is poor
Prevention


Vaccine - Fort Dodge for horses
Control mosquito exposure
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Trichomoniasis



Carried by pigeons – called “canker”. Raptors are
infected when eating pigeons. Don’t feed pigeons.
Called “frounce” in falcons
Clinical signs
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

Affects the upper digestive and respiratory tracts
Caseous lesions in oral cavity (under tongue, near choanal
opening) and sinuses.
Diagnosis – PE + cytology
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Trichomoniasis
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


Diagnosis – PE + cytology
[Cytology Picture of kestel?]
DDx include capillaria or
candida.
Treatment – Carnidazole
(Spartrix) 100-200 mg\kg PO
once. May need to repeat in
falcons.
Surgical debridement
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Trichomoniasis


Diagnosis – PE + cytology [Cytology Picture of
kestel?]
Treatment – Carnidazole (Spartrix) 100-200 mg\kg
PO once. May need to repeat in falcons.
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Candidiasis
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
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Caused by Candida albicans
Associated with malnutrition (Vit A deficiency) and
long-term antibiotic use
Will see white necrotic lesions in mouth, pharynx
and crop and it causes with dysphagia and
regurgitation.
Diagnosis based on clinical signs, endoscopy of
crop (may see “Turkish towel” appearance) and
cytology (Gram +, oval, budding yeast)
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Candidiasis

Treatment – Nystatin 300,000 IU\kg PO BID x 10
days. Needs contact time so oral lesions may
require systemic antifungal treatment
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Lead Poisoning
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

Sources: Gunshot, ingestion of
contaminated prey
Note that gunshot embedded in the
musculature will not lead to system
lead levels.
Eagles\Ospreys more likely affected
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Lead Poisoning

Clinical signs
 Can be acute or chronic
 Generalized weakness, anorexia, emaciation
 Regurgitation
 Ataxia, tremors, seizures, paresis, paralysis,
blindness
 Hematuria, hemoglobinuria
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Lead Poisoning


Diagnosis
 Blood lead level > 20 ug\dl
 Radiographs
Treatment
 Supportive
 Stomach gavage, endoscopic removal
 Surgical removal
 CaEDTA 35 mg\kg SQ\IM BID, 4 days on, 3 days
off for 4 weeks
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Other Poisonings

OP toxicity
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SLUD not seen in birds
Pupils not affected in birds
Depression, seizures
Treatment is supportive, atropine,
valium to control seizures
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Other Poisonings

Rodenticide toxicity



Pulmonary hemorrhage and dyspnea
are not commonly seen in birds.
Bleeding from superficial wounds is
more common
Treatment: Vit K1 2.5 mg\kg SQ\IM
BID for 3-4 days, then PO SID for 4
weeks.
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Mycobacterium (Avian TB)

Mycobacterium Avium Complex (MAC)

Generalized, chronic, granulomatous disease
Infection usually by fecal-oral route
Clinical signs
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Chronic emaciation
Dyspnea
SQ granulomas\tubercles
Diarrhea – tubercles in intestine is a common
presentation
Arthritis or tubercle formation in leg muscles?
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Mycobacterium (Avian TB)

Diagnosis

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
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

Leukocytosis with monocytosis
Histology or cytology – Acid fast organisms
Acid fast stain of feces (5 days)
Look for non-staining “ghosts” with Dif-Quick
Culture is very difficult
Treatment


Not recommended due to zoonotic potential
Note that the risk to an immunocompetent person
is low
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Avian Pox
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


Important disease in raptors
Worldwide distribution
Survive in dried scabs and in
environment for years
Three forms – dry, wet and septic
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Avian Pox
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Avian Pox

Cutaneous or dry form



Most common
Spread by biting insects such as
mosquitoes, but not all vectors are
known.
Also mechanical spread by fomites
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Avian Pox

Cutaneous or dry form



Vesicles ->pustules -> scabs on
unfeathered areas of skin around
eyes, mouth, feet.
Can lead to severe scarring
Can be self-limiting?
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Avian Pox

Diptheritic or wet form
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Lesions on mucous membranes in
mouth, pharynx, esophagus, trachea
Vesicles -> ulcers
Probably spread due to aerosol
infection
Can turn into septicemic form
Prognosis is poor.
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Avian Pox

Diagnosis



Clinical signs
EM – characteristic virion size\shape
(bricks)
Treatment is supportive, Vit A
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Avian Pox

Prevention



Pigeonpox and turkepox vaccines
have been used with variable success
Vector control
Prevent spread by fomites and use
quarantine procedures
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Questions?
Dave Scott, DVM
Carolina Raptor Center
P.O. Box 16443
Charlotte, NC 28297
704-875-6521
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