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The Avian Endocrine System

Conference Paper · April 2008

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 The Avian Endocrine System

Robert E Schmidt DVM PhD DACVP

Drury R Reavill DVM DABVP [Avian] DACVP

Zoo/Exotic Pathology Service

• Pituitary Gland
– Embryology
• Neurohypophysis comes from neuroectoderm of the diencephalic floor. During
development this area evaginates and contacts Rathke’s pouch.
• The adenohypophysis develops from Rathke’s pouch which is an outgrowth of the roof
of the oral cavity.
• The residual lumen of Rathke’s pouch may persist as a separation between anterior and
posterior pituitary.
– Anatomy
• Adenohypophysis-comprised of the pars tuberalis and the larger pars distalis.
– Histologically cells of the pt arranged in cords with occasional acini. Cells of the pd
arranged in cords or follicles that sometimes contain amorphous homogeneous
material. Seven types of secretory cells and chromophobes which are nonsecretory.
• Neurohypophysis-direct extension of hypothalamus. Has median eminence,
infundibulum and neural lobe.
– Function
• Neurohypophysis
– Produces anti-diuretic hormones as in mammals.
– Produces oxytocin which may in part control oviposition.
• Adenohypophysis
– Various portions of the gland secrete luteinizing hormone, follicle stimulation
hormone, thyroid stimulating hormone, growth hormone, adrenocorticotropic
hormone, melanocyte-stimulating hormone and prolactin.

– Clinical laboratory testing

• Many of the hormones of the avian pituitary gland have been isolated, but mostly in
research situations and there are no readily available diagnostic tests.
– Diseases
• Congenital
– Dwarfism has been reported in chickens [sex-linked recessive], pheasants, black-
headed gulls and flycatchers. The cause has not been conclusively determined.
• Undetermined
– Diabetes insipidus has been seen in chickens. The problem/pathogenesis has not
been determined.
Neoplastic
 -- Neoplastic lesions are most commonly seen in budgerigars [<80.0% in our
database] They have also been identified in cockatiels, lovebirds, chickens and
African grey parrots. There may be clinical signs referable to the central nervous
system.
-- The tumors are usually adenomas, but histologic carcinomas have also been seen,
and one in a cockatiel was metastatic to the liver.
-- Adenoma is usually gray or red-brown grossly. They may compress the optic
chiasm. Histologically the cells are large and usually do not contain granules. They
form nests and lobules with minimal stroma. Carcinomas have less well-
differentiated borders and more anaplastic cells histologically.
• Parathyroid Gland
– Embryology
• Derived from 3rd [external parathyroid] and 4th [internal parathyroid] pharyngeal
pouches.
– In birds the internal glands are usually not present.
– Anatomy
• In adult birds there are usually two pair of glands on each side just caudal to the thyroid
glands.
• Grossly tan-yellow.
• Occasionally accessory/external glands seen in several locations, particularly in the
ultimobranchial body.
• Histologically has loose connective tissue capsule and is comprised of cords, sheets and
rosettes of cells. Chief cells more abundant and have clear or lightly eosinophilic
cytoplasm. No oxyphil cells in birds. Note occasional association with thymic tissue.

– Function
• Secrete parathormone as a response to decreased plasma calcium.
• Primary target tissues are bone and kidney.
– Stimulates bone resorption to raise plasma calcium level, and increases renal
tubular resorption of calcium as well as regulating renal production of 1.25-
dihydroxycholecalciferol [vitamin D3].

– Clinical laboratory testing

• No commercial PTH assay.
• Calcium and phosphorous measurement is an indirect way to asses parathyroid gland
function.
– Clinical laboratory testing for calcium and phosphorous may indicate the possibility
of hyperparathyroidism.

– Diseases
• Hyperplasia is the most common condition we have seen, and is the most common
condition reported in the literature. Over 80% of the cases are in psittacine birds, with
African grey parrots being the most commonly diagnosed [37.5%]. Clinically some
 birds may present with fractures or soft bones, but in many cases signs are vague or
nonexistent. We have also identified a parathyroid cyst in a Brotogeris sp. and and
adenomas in a ring-neck parakeet and cockatoo.
– In most birds the hyperplasia is due to nutritional secondary hyperparathyroidism.
This is associated with diets deficient in Ca, P or vitamin D3. Diets with excessive
phosphorous or improper Ca/P ratio can also cause the problem.
– Hyperplastic glands grossly enlarged and yellow-orange. The condition is usually bilateral.
Histologically chief cells enlarge with clear or foamy cytoplasm. These cells form
trabecular structures.
– Adenomas are rare and unilateral. No evidence of functionality has been reported.
• Grossly yellow nodules and histologically the lesion is localized and there is evidence
of capsule formation.

• Thyroid Gland
– Embryology
• Earliest gland to appear.
• Derived from the floor of the pharynx at level of 1st/2nd pharyngeal pouches.
• Originally the thyroid diverticulum that connects to the primitive tongue via the
thyroglossal duct.
– Anatomy
• Paired glands present in the area of the thoracic inlet medial to the jugular vein and
cranial to the carotid artery origin. The glands are red-brown, and should not be
confused with the syringeal muscle [small arrow].
• Histologically the glands are comprised of follicles containing colloid[thyroglobulin]
and lined by a single layer of epithelium.
• Birds do not have C cells in their thyroid glands.
– Function
• Control of thyroid hormone production is via a negative feedback loop regulated by the
hypothalamus and adenohypophysis.
• Under the influence of TSH, cyclic 3', 5' adenosine monophosphate [cAMP] is
activated in thyroid follicular epithelial cells. Increased cAMP leads to increased iodide
trapping from the blood by the follicular cells. As a result follicular colloid is processed
into follicular epithelial cells leading to release of thyroid hormones into the circulation.
Approximately 60% is T4, and 40% T3
• Thyroid hormones control metabolism and development with the actions mediated by
nuclear thyroid hormone receptors that have their highest affinity for T3. In birds, the
development of thermogenic metabolic responses is correlated with the pattern of
thyroid development.
• In precocial birds, thyroid function and its control are well developed during the latter
part of incubation. Hatchlings have metabolic responses to cooling and relatively
mature sensory and locomotor capabilities. In altricial birds, thyroid function has
minimal maturation until after hatch.
– Clinical Laboratory Testing
• The best method of testing the avian thyroid for abnormalities is the administration of
TSH and measuring the serum T4 concentration after a particular time period.
Unfortunately veterinary TSH is no longer on the market, and the test must be done
with an expensive human product.
• The alternative is measurement of T4 only. Since avian T4 is lower than mammalian, the
test must be able to detect lower T4 values. A single low T4 test cannot lead to a
definitive diagnosis of hypothyroidism, and a single normal may not be proof that the
bird is not hypothyroid. The test should be interpreted in association with multiple
factors including clinical signs and other tests.
• Recently a method for using a high-sensitivity radioimmunoassay to measure total
thyroxine concentration was developed. This method was developed using psittacine
birds only. In these birds it will be a way to measure T4 concentrations. Results of the
study indicated that T4 concentrations in blue-fronted Amazon parrots were higher and
more variable than in other species tested.

– Diseases
• Congenital
– Partial persistence of the caudal portion of the thyroglossal duct can lead to cysts
within or adjacent to the thyroid gland.
• Infectious
– Systemic infections rarely, if ever, involve the thyroid. Extension of a localized
infection is possible but also rarely seen.
• Noninfectious
– Both inflammatory and noninflammatory conditions are seen with the latter being
most prevalent. Clinical signs may include lethargy and in some cases non-
inflammatory skin problems with loss of feathers.

• Atrophy/degeneration
– Occasional cases are seen. The cause is usually not determined. Affected glands are
small and dark and have a variable amount of histologic colloid loss and follicular
degeneration. There may be hemorrhage. Parathyroid glands may seem relatively
large.

Hyperplasia
• The most prevalent problem [43.3%] seen is diffuse follicular hyperplasia/hypertrophy
[goiter]. In our experience the condition is most prevalent in blue and gold macaws ,
and may be the only lesion seen at necropsy, or may be found in birds with a variety of
systemic diseases. The cause of the condition in individual cases is usually not
determined. Thyroid glands are bilaterally enlarged and microscopically follicular
epithelial cells are enlarged. Colloid is usually reduced or absent.
• Colloid goiter
Colloid goiter is also seen sporadically. This may be the involutionary stage of
 hyperplasia with grossly enlarged glands that histologically have large colloid-filled
follicles lined by cuboidal or flattened epithelial cells.
The primary cause of goiter in birds has been considered to be iodine deficiency,
but other potential causes include the feeding of goitrogenic substances of plant
origin, and genetically induced biosynthetic problems.

– Inflammatory
• Thyroiditis morphologically similar to that seen in autoimmune thyroiditis of humans,
Beagle dogs and some strains of chickens has been seen in African grey parrots and a
cockatoo. The affected glands may be slightly enlarged and mottled or slightly small,
but the condition is usually not noted grossly. Clinical signs have not been described.
Microscopic lesions consist of variable colloid loss and a lymphocytic infiltrate with
follicle formation. Although morphologically similar to the autoimmune condition of
other species the cause in African Grey Parrots has not been determined.
– Neoplasia
• Both adenoma and carcinoma are seen and are usually unilateral. Adenomas may
resemble hyperplasia grossly and histologically. Carcinomas are usually larger and
more irregular as well as being histologically more anaplastic.

• Secondary lesions.
– Potential secondary effects of hypothyroidism include noninflammatory feather loss,
excessive fat in the skin/subcutis, and histologic atrophy of the epidermis [one cell layer]
as well as hyperkeratosis.

• Ultimobranchial Body
– Embryology
• Pharyngeal derivatives [probably 6th pharyngeal pouch] that migrate free with the
associated parathroid during development.
– Anatomy
• Small [2.0-3.0mm] structures that are slightly irregular and gray-pink in the adult.
• Slightly caudal to the thyroids and there may be some variation in exact location-left
gland is often adherent to the parathroid in chickens.
• Histologically the ultimobranchial body is comprised of cords of ‘C’ cells associated
with nodules or cords of parathyroid cells. Epithelial-lined vesicles with colloid-like
material may be seen.
– Function
• ‘C’ cells secrete calcitonin which blocks calcium transfer from bone to blood.
• Bioassay indicates avian calcitonin levels are much higher than mammalian.
• The physiologic function of calcitonin in birds is in question and there are conflicting
research findings. It may not be involved in skeletal integrity and calcium homeostasis.
– Clinical laboratory testing
 • Calcitonin can be assayed by in vivo or in vitro methods. These are research tools not
readily available.
– Diseases
• Long-term hypocalcemia may lead to hypertrophy with the body being grossly visible.
• Cysts may develop and can be lined by squamous epithelium or ‘C’ cells. The cysts
may be remnants of the thyroglossal duct/tract.

• Carotid/Aortic Bodies
– Embryology
• Associated with vessels derived from aortic arches.
• Belong to the Amine Precursor Uptake Decarboxylation [APUD] system of cells.
• Also called the chromaffin system. Chromaffin cells derived from neuroectoderm of
neural crest.

– Anatomy
• Carotid bodies are paired and usually in contact with the parathyroid gland.
– Small white structures that may be embedded in the parathyroid glands in some
species.
• Aortic body between the aorta and pulmonary artery at base of heart.
– Histology
• Comprised of groups of large cells [type I or glomus cells] surrounded by type II
[sustentacular] cells.
– Glomus cells contain granular vesicles.
– Function
• Help control respiration. There are chemoreceptors that detect low arterial oxygen and
high CO2.

Clinical laboratory testing

– No clinical tests to evaluate function are available.
– Diseases
• Neoplasms are the only reported abnormality. Chemodectomas have been reported in a
duck and a budgerigar, and we have seen them in a pionus and an Amazon parrot.
– The location of the tumor is important in determining the exact type.
• Grossly may be red-brown and lobulated.
• Histologically nests, trabeculae and sheets seen. Some appear more anaplastic.
• No evidence of any biologic activity in few cases seen or reported.

• Adrenal Glands
– Embryology
• Cells arise from two different sources and are actually two distinct glands within a
common capsule.
 • Interrenal cells [analogue of mammalian cortex] are mesodermal derivatives.
• Chromaffin cells [analogue of mammalian medulla] are of neural crest origin and are
related to other chromaffin tissue.

– Anatomy
• Paired yellow structures at cranial pole of kidney.
– In a few species [loon, rhea] they are fused. Some species may have accessory
adrenal tissue.
– Histologically there is no cortex/medulla differentiation. Interrenal cells and chromaffin
cells present throughout the gland.
– Interrenal cells are eosinophilic and granular.
• They contain carotenoids which give the yellow color grossly
– Chromaffin cells are basophilic. Both are arranged in clumps or cords.

– Function
• Interrenal cells primarily secrete corticosterone which increases with stress.
– Elevated concentrations can lead to involution of lymphoid tissue.
• There is also aldosterone production which can be stimulated by low sodium or reduced
blood volume.

– Function
• Chromaffin cells release epinephrine or norepinephrine.
– Epinephrine increase can lead to eggshell abnormalities.
– Epinephrine can stimulate glycogenolysis and lipolysis.
– Norepinephrine is involved in blood pressure maintenance.

– Clinical Laboratory Testing

• RIA measurement of plasma corticosterone a reliable indicator.
• ACTH stimulation tests have been done in psittacine and other birds, but not commonl
available.

– Diseases
• Can become involved in generalized disease processes, both infectious and
noninfectious.
• Non-specific adrenal degeneration makes up 29.23% of cases in our database and
52.63% of these cases are in African grey parrots.
• Other conditions seen include inflammation nodular hyperplasia/hypertrophy and
neoplasia.

– Diseases-Noninflammatory
• Adrenal degeneration-Severe vacuolation of interrenal cells is seen in birds
 [predominantly African grey parrots] that die suddenly. The cause of this change is not
known and ante-mortem tests to confirm possible adrenal failure have not been done.
Glands may appear yellow-gray grossly and there is severe swelling and vacuolation of
interrenal cells histologically.
• Amyloidosis-Sporadic occurrence. May be associated with generalized amyloid
deposition. Affected glands enlarged and pale grossly. Histologically the amyloid is
primarily deposited in sinusoidal walls which are thickened by amorphous ampho-or
basophilic material. Loss of both cell types seen.
• Mineralization
– Usually an incidental finding that may or may not be related to other foci of soft
tissue mineral.
– Generally not noted grossly.
– Typical basophilic appearance histologically with variable tissue destruction.

• Diseases-inflammatory
– Can be secondary to generalized infections, or the result of extension of infection from
another organ/tissue.
• Bacterial, mycobacterial and fungal possible. Severe mycotic air sacculitis with
extension occasionally seen.

– Viral disease
• Polyomavirus infection can lead to karyomegaly and intranuclear inclusion body
formation in the adrenal gland.

• Paramyxovirus inclusions have been seen in the cytoplasm of chromaffin cells.

Minimal necrosis also possible.
• Gross lesion usually not seen.

• Adrenal adenitis-seen in cases of proventricular dilatation disease. Adenitis is 26.86%

of adrenal diagnosis in our database. Grossly the gland may appear minimally
discolored and mottled. The lymphoplasmacytic inflammatory infiltrate is seen in the
chromaffin [adrenal medullary analogue] portion of the gland.

• Diseases-proliferative
– Nodular hypertrophy/hyperplasia.
• Infrequently seen
• Focal area of interrenal cells [cortical analogue] that are enlarged and possibly
proliferative.
– Adrenal neoplasia
• Neoplasia includes interrenal [adrenal cortical analogue] adenoma and carcinoma,
pheochromocytoma and ganglioneuroma. Carcinomas can become quite large and may
metastasize. Lung and liver primary metastatic locations.
 – Poor feathering may be presenting sign.
– Adenomas fairly well differentiated and encapsulated.
– Carcinomas anaplastic with poorly formed trabecular structures.

– Pheochromocytoma and ganglioneuroma less common.

• Grossly not specific.
• Cells of pheochromocytoma are small with minimal cytoplasm. They form nests and
poorly defined trabeculae.
• Ganglioneuromas contain large cells with basophilic cytoplasm that resemble neurons.
The cells are embedded in a ground substance that resembles normal neuropil.

• Islets of Langerhans
– Embryology
• The pancreas is a specialized derivative of the primitive gut endoderm.
• At the foregut/midgut junction the septum transversum generates 2 or 3 pancreatic buds
(dorsal and ventral endoderm) which will fuse to form the pancreas. There is some
discrepancy in the literature as to the number of buds. In the fetal period islet cell
clusters differentiate from pancreatic bud endodermal progenitors. The pancreatic lobes
contain A and B islets in which glucagon and insulin cells, respectively, predominate.
Islets contain somatostatin and pancreatic polypeptide (PP) cells.
• Pancreatic exocrine function begins after birth, while the endocrine function (hormone
release) can be measured from 10 to 15 weeks onward.

– Anatomy
• Grossly usually inapparent.
• Islets randomly scattered throughout the pancreas, with the highest concentration of
endocrine tissue in the splenic lobe.
• At least three types of cells are present in the islets of Langerhans, although some
references only mention two and newer ones consider a possible fourth, in the avian
endocrine pancreas.
– There are A-islets and B-islets, with A & D cells in the A islets and B & D cells in
the B islets. There are no C-cells.
• Islets are groups of pale eosinophilic cells withing the exocrine pancreas. The cells are
polyogonal with pale nuclei and prominent nucleoli. Granules not usually noticeable in
H&E-stained sections.

– Function
• Glucagon islets [A cells]-levels of glucagon in birds may be as much as 10x those of
mammals.
– Major role in lipid [raises levels of free fatty acids], and glucose [raises levels]
homeostasis.
 • Insulin islets [B cells]-level of insulin about 1/10 that in mammals. The mechanism[s]
of action have not been completely worked out.

• Somatostatin [D-cells]-depresses insulin, glucagon and avian pancreatic peptide [APP],

however the exact mechanism of action is not known.
• APP-precise role in metabolism not known, but may be primarily lipogenic. May be in
PP or F cells-possibly a fourth type that exists both in islets and exocrine pancreas.

– Clinical laboratory testing

• Most common test for dysfunction is blood glucose.
• Insulin and glucagon levels can be measured but this is primarily a research tool and
usually not available for routine avian testing.

– Diseases
• Non-specific degeneration of islet cells is the most common condition seen, making up
almost 65% of islet cell lesions in our database. The degeneration usually takes the
form of vacuolation of islet cells with variable cellular loss. Some of these cases have
been associated with clinical diabetes mellitus, but in many clinical signs were
nonspecific or absent.
– Birds with islet cell degeneration may have no or minimal gross pancreatic change.
• Slight mottling may be seen.
• There may be gross liver lesions due to fat accumulation. Histologically remaining islet
cells are vacuolated.
• Hyperplasia of islets accounts for almost 30% of islet cell lesions. Neoplastic disease
has been limited to islet cell carcinoma and is less than 0.6% of cases. Grossly changes
may not be seen.
• The cause of islet cell hyperplasia is not known.
– Limited number of cases have been of A cell [glucagon-producing]
hypertrophy/hyperplasia based on immunochemistry.

• Neoplasia
– Islet cell carcinomas are usually locally infiltrative with replacement of pancreatic
parenchyma.
• Moderately undifferentiated to poorly differentiated cells form trabeculae. Minimal
stroma is seen.

Inflammatory
– Inflammation of the exocrine pancreas can affect islets in
some cases.
– Paramyxovirus and herpesvirus two possible causes. May not lead
to clinical signs associated with islets unless generalized, or may
kill bird before islet- associated functional changes occur.
 • Other Endocrine tissue
– Amine Precursor Uptake, Decarboxylation and storage [APUD] system.
• Disseminated in the GI tract, respiratory tract as well as the thyroid and pancreas.
– Secrete polypeptides and biologically active amines.
– Other than previously mentioned exact function not worked out and diseases only
associated with problems in the particular system where located.
• Pineal Gland
– May have edocrine functions, but not established.
– No disease problems reported.

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