Hypocalcemic Seizures in an African Grey Parrot
Lawrence J. McDonald
Asix-year-old African grey parrot
erithacus erithacus), presumed to be a male
although surgical sexing was not done, was presented
to the hospital on an emergency basis. The presenting
complaint was three seizures in the past three days.
Prior to this presentation the bird had had two other
seizure attacks in the preceding month. The client had
owned this bird for four years, and had not detected
any previous problems. Nine other birds lived in the
home: a female African grey, six Amazon parrots and
two conures. All of these other birds were fine accord-
ing to the owner, and none of them had ever had a
After the seizures at home, the bird returned to
normal within a few minutes. He ate well, had no
regurgitation, diarrhea, cough, or sneeze. The diet con-
sisted of peanuts and sunflower seeds, an assorted seed
mix, fresh vegetables (carrots, lettuce, spinach, and
broccoli), and fresh fruits (apples, oranges, and grapes),
all ad lib. No vitamin or mineral supplementation was
given, and the client remarked that the bird's favorite
food seemed to be peanuts.
The bird was well fleshed (448 grams) and had good
feather, beak and nail quality. No clinical abnormali-
ties could be found. The neurological exam appeared
normal; however, handling the bird was not as difficult
as is usual with African grey parrots. The bird was then
hospitalized, and blood for a routine hematological
profile was obtained from both the hospitalized male
bird and the female African grey parrot that currently
lived in the home (Table 1). Bacterial culture and sen-
sitivity was conducted on a cloacal sample taken from
the subject bird.
Until the clinical pathology results became available,
emergency treatment consisted of 25 mg calcium
gluconate (calcium gluconate injection B.P., Glaxo
Laboratories, Toronto, Ontario) given subcutaneously
in 5 mL physiological saline (sodium chloride injec-
tion U.S.P., Abbott Laboratories, Montreal, Quebec),
distributed in three sites over the pectoral musculature,
and Injacom 100 + B complex (Hoffman LaRoche,
Nutley, New Jersey) 0.06 mL diluted in 1 mL physiol-
ogical saline subcutaneously (equals 6000 IU vitamin
A and 600 IU vitamin D3). The bird was placed in a
hospital cage for observation and was fed a seed mix.
liquid (Syntex Agribusiness,
Mississauga, Ontario) (15 drops in 120 mL water),
calcium (Calcium Sandoz syrup 5 mL = 110 mg,
Sandoz Canada, Dorval, Quebec) (1 mL in 30 mL
water), and WinStress powder (WinStress, Winthrop
Animal Health Products, Aurora, Ontario) (1/8 tsp
in 600 mL water) were added to the bird's drinking
By the following day the bird was eating well, pass-
ing normal stools, and was much stronger and more
aggressive. On reviewing the clinical pathology results
(Table 1), the most probable cause of the seizures
appeared to be hypocalcemia. Subsequently the treat-
ment consisted of the previously discussed oral medica-
tions, with the exception of the spectinomycin oral
liquid because of the resistance ofEnterobacter cloacae
to spectinomycin. Spectinomycin was replaced with
carbenicillin (Geopen 500 mg,
Quebec) 95.5 grams added to 120 mL water with 2 to
3 drops of Sucaryl (cyclamate, Abbott Laboratories,
Montreal, Quebec) added to improve palatability. Oral
medication was chosen rather than parenteral due to
the increasingly fractious nature of the bird. The
patient was discharged from the hospital on the same
dose of Calcium Sandoz, WinStress and carbenicillin
with Sucaryl. Seven days later the bird appeared to be
doing well; however, due to costs the owner declined
to have the blood profile repeated. Carbenicillin was
discontinued at that time, but the client was instructed
to continue with Calcium Sandoz (1 mL in 30 mL
water) and WinStress (1/8 tsp in 600 mL water), both
made up fresh daily and administered for the life of
the bird. The client was also instructed to try to correct
the bird's diet; this involved limiting the consumption
of peanuts and sunflower seeds each day and feeding
a variety of seeds, feeding foods high in calcium, such
as cheese and yogurt, and offering more fresh fruits
Calcium and phosphorus homeostasis is a complex
interaction of hormones (parathyroid hormone (PTH),
calcitonin, and vitamin D3 and its metabolites) and
body organs (bones, gastrointestinal tract, kidney, and
Production of PTH is influenced by two major
regulators: ionized calcium (Ca+ + ) (1,2) and cyclic
3' ,5 '-adenosine monophosphate (cAMP) (2). As
Ca+ + decreases or cAMP increases, the parathyroid
gland produces more PTH. Petrak (1) and Stunkard
(3) also suggest that in poultry PTH and estrogen have
a synergistic effect on ionized calcium levels.
Target organs of PTH are bones, kidney and gastro-
intestinal tract. Under the influence of PTH there is
increased mobilization of calcium from bone into
osteoclastic bone resorption
Parathyroid hormone causes increased renal absorp-
tion of calcium and increased excretion ofphosphorus
by the renal tubular epithelium.
Vitamin D3 can be absorbed from food, and perhaps
made by the action of sunlight on theuropygeal gland
secretions which the bird consumes when preening (4).
Once vitamin D3 (cholecalciferol) is absorbed from the
intestinal tract it is metabolized in the liver andkidney
to two compounds: 1,25 dihydroxycholecalciferoland
24,25 dihydroxycholecalciferol (4,5). Ifhypocalcemia
Can Vet J Volume 29, November 1988
Long Lake Veterinary Hospital, 4508 Wellington Road,
Nanaimo, British Columbia
Reprints will not be available.
occurs, PTH is secreted which increases the synthesis
of 1,25 dihydroxycholecalciferol, which in turn pro-
motes absorption of calcium from the intestinal tract
and mobilization of calcium and phosphorus from the
Calcitonin is produced in the ultimobranchial gland
in birds (4). Its primary action is to oppose the action
of PTH on kidney and bone. If there is a pathological
process in a bird's gastrointestinal tract, parathyroid
gland or bones, a hypocalcemic state can result.
The other obvious cause of hypocalcemia is deficient
intake of calcium and vitamin D3. A deficiency of
vitamin D3 results in hypocalcemia after 14 days, even
if the diet contains 1%o calcium (4). Continued defi-
ciency ultimately results in osteomalacia. The normal
dietary Ca:P ratio should approach 1.5:1 (4,6), which
approximates a diet containing
phosphorus. Most seeds that are eaten by caged birds
are low in calcium (4,6). Peanuts and sunflower seeds
are particularly deleterious to calcium homeostasis, for
not only do they only contain about 20% of the calcium
requirement of a nonlaying bird (3), but they also have
a high fat content. This fat may combine in the gastro-
intestinal tract (3,4) with calcium to form insoluble
soaps (3,4). Both of these situations can lead to nutri-
tional "metabolic bone disease". This term applies to
the compensatory hypersecretion and hyperplasia of
the parathyroid glands in an attempt to maintain
in the African
erithacus erithacus) and the Timneh grey parrot
(Psittacus erithacus timneh) (5,7,8), a hypocalcemic
syndrome has been documented. It is usually seen in
young birds (two- to five-years-old) but has been
reported in a ten-year-old bird. The birds have a
history of fainting or seizures, often initiated by excite-
ment. Blood calcium levels are consistently below
normal (i.e. 6 mg/dL with the normal being 8 to
13 mg/dL) (9), and have been recorded as low as 2 to
4 mg/dL. On histopathology parathyroid glands are
No calcium and 0.7Wo
enlarged and there are severe degenerative changes.
Vacuolation of adrenocortical cells is also present.
Cortical bone sections, however, demonstrate no
calcium loss or thinning as would be expected in a
The authors (5,7) then speculate on possible etiol-
ogies. One theory is that perhapsAfrican grey parrots
cannot mobilize skeletal calcium in the face ofhypo-
calcemia. Perhaps viral damage to the parathyroid
glands is necessary to trigger or enhance this inabil-
ity, for apparently not all African grey parrots mani-
fest this problem. A second theory involves renal func-
tion. This hypothesis assumes a loss of calcium
through the kidney; however, a "trigger" for this
phenomenon is unknown. The third and final hypothesis
is that perhaps the syndrome is entirely dietary, with
the concurrent inability to mobilize skeletal calcium.
Obviously a definitive pathogenesis is lacking, but the
syndrome is frequently seen (7) in these two species
The clinical pathology results raise several major
doubts. First, that the most probable cause of the
seizures was hypocalcemia. Other potential causes of
seizures (6) in birds include hypoglycemia, toxicosis
(lead, mercury), infections, and epilepsy. This bird was
not hypoglycemic. The prompt response to calcium
therapy, together with no recurrence of seizures over
a sixteen month period would tend to rule-out epilep-
sy. The possibility of a concurrent bacteremia must
be considered due to the Enterobacteriaceae cloacal
culture. Enterobacteriaceae frequently cause disease
in pet birds (8), and birds seem prone to develop
bacteremia. Thus, the initiation of the seizures by
infection plus stress, as manifested by the increase in
heterophils and glucose (Table 1), cannot be ruled out.
The female bird, living in the same home and fed the
same diet as the subject bird for four years, did not
manifest hypocalcemia. Perhaps this would introduce
some skepticism as to the hypothesis (5,7) of a virus
damaging the parathyroid gland of the male bird.
Can Vet J Volume 29, November 1988
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Circumstantial evidence would suggest that the male
bird was affected by the African grey parrot hypo-
calcemia syndrome because the female, which was on
the same relatively calcium-deficient diet, did not
Prophylactic measures to prevent the hypocalcemic
seizure syndrome in African grey and Timneh grey par-
rots should include vitamin D3 supplementation and
periodic determinations of blood calcium levels.
A calcium replete diet should obviously be provided;
client counselling in this area is very important. I have
seen three cases in the past year, but this is the only
patient to survive the initial hypocalcemic emergency
situation. Consequently, with all African grey patients,
I now stress client education and provide in-depth diet
sheets in an attempt to avoid a crisis situation.
1. Petrack ML. Diseases of Cage and Aviary Birds. 2nd ed.
Philadelphia: Lea & Febiger, 1982: 485-486.
2. Buckley JC. Pathophysiologic considerations of osteopenia.
Compend Contin Educ Pract Vet 1984; 6: 552-560.
3. Stunkard JA. Diagnosis, Treatment and Husbandry of Pet Birds.
2nd ed. Stunkard Publishing Co., 1984: 10.
4. Petrack ML. Diseases of Cage and Aviary Birds. 2nd ed.
Philadelphia: Lea & Febiger, 1982: 223-228.
5. Rosskopf WJ, Woerpel RM, Monahan-Brennan M. Seizures
induced by hypocalcemia in an African grey parrot associated
with an adrenalopathy and parathyroid hyperplasia. Proc Annu
Meet Assoc Avian Vet 1983: 267-271.
6. Walsh MT. Seizuring in pet birds. Proc Annu Meet Assoc Avian
Vet 1985: 121-128.
7. Rosskopf WJ, Woerpel RW, Lane RA. The hypocalcemic
syndrome in African greys: an updated clinical viewpoint with
current recommendations for treatment. Proc Annu Meet Assoc
Avian Vet 1985: 129-131.
8. Woerpel RW, Rosskopf WJ. Clinical experience with avian
laboratory diagnostics. In: Harrison GJ, ed. Veterinary Clinics
of North America, Small Animal Practice, Caged Bird Medicine.
WB Saunders, 1984: 249-286.
9. California Avian Laboratory. P.O. Box 41809, Sacramento,
Can Vet J Volume 29, November 1988