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VITAMIN A DEFICIENCY IN PARROTS

Authors:

Abstract

The occurrenoe of stomatitis in three parrots, most probably caused by Vitamin A deficit, had been reported by Z w a r t elsewhere (1978). The diagnosis of avitaminosis A in his report had been based on pathognomic metaplasia of non-squamous epithelia and hyperkeratosis of squamous epithelia of the upper digestive and respiratory tracts. Presented in this paper are data on the vitamin A status of recently imported parrots and of others that died while being with their owners. Also reported are clinioal and histopathological lesions in parrots due to avitaminosis A. Material and methods A oontrol group oonsisted of five animals that had been freshly captured, before they died during the prescribed quarantine period of six weeks. They were analysed for vitamin A levels.
VERHANDLUNGSBERICHT DES XXI INTERNATIONALEN SYMPOSIUMS UEBER DIE ERKANKUNGEN
DER ZOOTIERE MULHOUSE 1979 Akademie Verlag Berlin
47
From State University of Utrecht, Department of Special Animal Pathology
(Head of Department Doz. Dr. P. Z w a r t ), and Central Institute of
Nutrition and Food Researoh (Director Prof. B. K r o l)
VITAMIN A DEFICIENCY IN PARROTS
P. Z w a r t , W. H. P. S c h r e u r s and G. M. D o r r e s t e i n
The occurrenoe of stomatitis in three parrots, most probably caused by
Vitamin A deficit, had been reported by Z w a r t elsewhere (1978). The
diagnosis of avitaminosis A in his report had been based on pathognomic
metaplasia of non-squamous epithelia and hyperkeratosis of squamous epithelia
of the upper digestive and respiratory tracts. Presented in this paper are
data on the vitamin A status of recently imported parrots and of others that
died while being with their owners. Also reported are clinioal and
histopathological lesions in parrots due to avitaminosis A.
Material and methods
A oontrol group oonsisted of five animals that had been freshly captured,
before they died during the prescribed quarantine period of six weeks. They
were analysed for vitamin A levels.
A group of 24 potential patients died in the possesslon of their owners.
Their 11ver-borne vitamin A levels were ana17s6d. Their posterior lingual and
anterior submandibular salivary glands were histologioally examined.
Additional checks were performed on suspicies cases.
Histological tests only were applied to six advanced cases which had been
identified and selected by clinical examinations or post-mortems. All
material earmarked for histological testing was fixed in ten-per-cent neutral
formalin. Paraffin sections were prepared in the usual way and stained with
hemalum and eosin. Posterior lingual and anterior submandibular salivary
glands were examined in all cases.
Liver-born Vitamin A levels were analysed, using the technique of CAR-Price
(Mu1der, 1957).
The feeding schedules that had been used for 20 of the 24 animals were
provided by the owner on request.
Results
Vitamin A levels recorded from the 1ivers of those animals that had died
during quarantine are presented in Table 1. The data are representative of
the range of vitamin A levels normally recorded from recently captured
parrots.
Table 1: Vitamin A levels of parrots that died during quarantine (I.U./gm
liver)
No. Species
Vitamin A
1. Blue-fronted amazon (Amazona aestiva)
706.80
2. Afrioan grey parrot (Psittacus erithacus)
12~.80
3. African grey parrot (Psittacus erithacus)
849.10
4. African grey parrot (Psittacus erithacus)
525.50
5. African grey parrot (Psittacus erithacus)
503.50
Only eight animals of those histologioally examined and tested for their
1iver-borne Vitamin A levels did not exhibit any histological lesion (33.4
per cent). These animals are given in Table 2.
All animals that had died without any histological lesion under the oontrol
of their private owners obviously had daily received greens in their feed
rations, as was seen from the owners' feeding schedules. Some form of
multivitamin preparations with vitamin A in them had been received
additionally by the animals numbered 7, 8, 9, 12, and 13.
-48-
Table 2: Vitamin A levels (I.U./gm 1iver) in parrots that had
been under the control of their owners and not exhibited any
alterations in their salivary glands
No.
Species
Vitamin A
6
Duivenbode’s lory (Chalopsitta
duivenbodei)
7399.20
7
African grey parrot (Psittacus
erithacus)
899.20
8
African grey parrot (Psittacus
erithacus)
767.30
9
Blue-fronted amazon (Amazona aestiva)
589.90
10
Yellow-fronted amazon (Amazona
ochrocephala)
481.20
11
African grey parrot (Psittacus
erithacus)
252.70
12
Chattering lory (Domicella garrula)
136.90
13
Yellow-crested cockatoo (Cacatua
galerita)
30.11
An injection with Vitamin A was given to the Duivenbode’s lory a few days
before death.
One of the African grey parrots (No. 8) suffered from extensive
arteriosclerosis The animal had been in captivity five years, according to
the owner. Daily doses of four drops of an aqueoua Vitamin A-D preparation
(9,000 I.U./ml) were insti11ed tbrough the last three weeks of life. That
treatment may have been equivalent to daily Vitamin A intakes of 250 I.U. and
led to a rise of the vitamin A level in the 11ver.
The chattering lory had been received from a larger 001leot10n of 10r1es.
These animals had received soft food w1th 18,750 I.U. of vitamin A in one
1itre.
The yellow-crested cockatoo had received in its drinking water two drops of
an oily vitamin A-D preparation with 15,000 I.U. of vitamin A in one
milli1itre, which, however, failed to provide an. an effeotive uptake of
vitamin A.
Another African grey parrot (No. 7) and the yellow-fronted amazon (No. 10)
had been with their owners a few days only. Their vitamin A status was
comparable to that of an1mals in quarantine.
The blue-fronted amazon (No. 9) and the African grey parrot (No. 11) are
believed to have had the benefits of the reserves at the moment of capture.
The histological lesions recorded from posterior lingual and anterior
submandibular salivary glands were graded according to Konstantinov (1972).
Stage I: Diagnosis of lesions in animals with metaplasia restricted to the
epithelium of the major excretory duct of one or more salivary glands (listed
in Table 3);
Stage II: Metaplasia more generalised, though normal areas still present
(listed in Table 4);
Stage III: Metaplasia has fully affected the sa11vary glands in totality
(listed in Table 5).
Table 3:Vitamin A levels (I.U./gm 1iver) in parrots with Stage I metaplas1a
in salivary glands
No.
Species
Vitamin-A
14
Blue and yellow macaw (Ara ararauna)
13.70
l'
Yellow-crested cockatoo (Cacatua galerita)
7.90
16
Blue and yellow macaw (Ara ararauna)
7.70
17
Cockatoo (Cacatua sp. indet.)
5.80
18
Blue and yellow macaw (Ara ararauna)
2.80
19
Pink cockatoo (Cacatua leadbeateri)
1.60
Table 4:Vitamin A levels (I.U./gm 11ver) in parrots with Stage II metaplasia
in salivary glands
No. Species Vitamin-A
20 Slender-bi11ed cockatoo (Cacatua tenuirostris) 47.60
21 Bodinus amazon (Amazona festiva bodini) 22.10
22 African grey parrot (Psittacus erithacus) 4.60
The slender-bi11ed cockatoo had been given salad or endive twice a week and
carrots three times a week. The greens were eaten very well. The African grey
parrot (No. 22), With 4.60 I.U. of vitamin A/gm 1iver, had been with its
owner during five years. The animal had received some drops of a vitamin A-D
preparation once a week.
49
Table 5: Vitamin A levels (I.U./gm 1iver) in parrots with stage III
metaplasia
No.
Species
Vitamin-A
23
White cockatoo (Cacatua sulphurea)
7.00
24
White cockatoo (Cacatua sulphurea)
1.40
25
Thickbilled parrot (Rhynchopsitta pachyrhyncha)
26
Parrot (Spec. indet.)
0,90
27
Bodinus amazon (Amazona festiva bodini)
0,70
28
Grand eclectus (Lorius r. roratus)
0,40
29
African grey parrot (Psittacus erithacus)
0,40
Vitamin A deficit to an extend by which a parrot usually w111 be unable to
retain the normal morphological structure of epithelia of its salivary glands
obviously appears to occur, when the liver-born vitamin A level drops below
50 I.U./gm liver tissue. Severe vitamin A deficit, resulting in metaplasia of
all epithelial lining of the salivary glands, wi11 develop, when vitamin A
levels in the liver drop below 2.0 I.U./gm.
With reference to those parrots listed in Tables 2, 3, 4, and 5 it appears
that 66.6 per cent of the 24 animals had developed vitamin A deficits to the
extend of morphological changes. Consistent correlations were found to exist
between liver-born vitamin A levels, on the one hand, and histological
changes, on the other.
Clinical manifestations of vitamin A deficit in parrots
More specific clinical symptoms of vitamin A deficit were recorded only from
advanced cases. Some of the birds had difficulties in dehusking and
swallowing seeds, which revealed severe lesions to posterior salivary glands.
Visual inspection revealed the presence of symmetrically placed whitish
swel1ings at the tongue base. The posterior salivary glands were packed with
desquamated cornified cells, the origin of those swellings. It was that
whitish matter, that actually showed through the overlying epithelium of the
tongue. The tracheal opening was of irregular appearance because of the
presence of small whitish pustules which had originated from metaplastic
mucous glands. Irregular whitish foci, sometimes, occurred under the
epithelium along the cleft in the hard palate, because the palatine salivary
glands were overfi1led with cornified matter.
There may be bacterial (staphylococci) or mycotic (Candida albicans)
infections which may affect deficient epithelia of the upper digestive and
respiratory tracts, as reported earlier (Z w a r t , 1978), and lead to the
development of stomatitis, gingivitis, tracheitis, and oesophagitis. External
nares were plugged only in occasional instances, when cornified cells of
metaplastic epithe1ia in the nasal cavity had undergone desquamation. The
conditon of that material was caseous situated deep in the nasal cavity but
hardened following evaporation of water when in oontact with air.
Symmetrical outbulgings, dorsally of the eyes, were recorded from an African
grey parrot (Psittacus erithacus) and a yellow-fronted amazon (Amazona
ochrocephala) as a result of extensive metaplasia of lacrimal glands.
Outbulg1ngs were also recorded ventrally of the eyes of the same two animals
and attributed to fi11ing of the nasal sinuses with a mixture of desquamated
cornified cells and heterophilic granulocytes. Distinctly circumscribed round
swellings were observed between the caudal parts of the mandibles due to
extreme packing and di1atation of the submandibular glands. Those swellings
first were thought to be abscesses. Yet, no inflammatory reaction was
palpated from the immediate surrounding. On incision, the swellings produced
a friable whitish mass, occasionally mixed with some mucus. Fresh
preparations were made by adding some water for microscopic examination. The
cornified cells then were identified as very thin, iso1ated, flattened cells
of somewhat irregular shape, with remnants of nuclei sti11 present in some of
them.
Histopathological aspects related to vitamin A deficit in parrots
The existence of stratification in the epithelium of the tongue, oral cavity,
and oesophagus suggested the presence of hyperkeratosis with thickening of
the stratum corneum and desquamation
50
of cornfied oe11s. Absence of stratifioat1on in epithelia suggested the
presence of metaplasia, with the epithelia being transformed into squamous,
stratified keratinising epithelium. The posterior lingual salivary glands,
anterior submandibular salivary glands, and tracheal mucous membranes, in a
more advanced stage, were the most common sites of metaplasia. The membranes
of nasal sinuses and lacrimal glands were less often affected. Metaplaaia of
ureteral epithelia was observed only once in a yellow-headed amazon (Amazona
ochrocephala oratrix). It had been caused by ureter clogging with desquamated
cornified cells and urate and resulted in irregular ureter distension.
The most charaoter1stic lesions were exhibited by the posterior lingual
sal1vary glands and, therefore, wil1 be described in greater detail.
In Stage I, a thin layer of squamous epithelium reached from the opening down
the major excretory duct. No changes were recordable from deeper regions of
the gland.
In Stage II, metaplas1a developed in the major excretory duct, with isolated
is1ands occurring also on the intertubular septa of the glands. Metaplasia
seemed to occur preferentially in more central areas of the glands in this
stage. Some of the acinic septa turned atrophic and simplified the glandular
structure.
The complete posterior 1ingua1 gland eventual1y became invo1ved in Stage III.
Metap1as1a now extended to the very periphery of the gland. The delicate
septa in the acini had comp1ete1y turned atrophic. The acini now have been
transformed into rounded sacs coated with a thick layer of cornifying
epithelium and fi11ed with desquamated keratinised cells.
Disoussion
According to Konstantinov's proposition (1972), histo1og1cal lesions
assoc1ated with vitamin A deficit in chickens can be graded into three
stages. The same subdivision was applied by the authors to their parrots.
Stages I (minimum) and II (moderate) were found to have been not distinctly
separate in their corre1ations w1th l1ver-borne vitamin A levels. It,
therefore, was considered appropriate to use only two grades to classify
histologica11y established lesions in parrots. Konstantinov's stages I and II
could be put together to give one distinct relat1onsh1p with the vitamin A
level in the 11ver. An unamb1guous correspondence to the clinical picture is
another advantage. Subclinical avitaminosis A in parrots may be related to a
oombinat1on of stages I and II, according to Konstantinov, and to liver-born
vitamin A levels between 50 and 2 I.U./gm 1iver tissue.
Subclinical avitaminosis A was recorded by the authors of this paper from
nine in 24 animals (37.5%).
Severe avitaminosis A with clinically detectable symptoms was found to
develop, when liverborn vitamin A levels dropped below 2 I.U./gm liver
tissue. Suoh severe forms were recorded from seven cases (29.25%).
Avitaminosis A, therefore, appears to be one of the most common causes of
sub-optimum health status in parrots. In poultry avitaminosis A oauses marked
decrease in egg production ( S h e r w o o d and F r a p s, 1932). The
speculative assumption is tempt1ng that minimal reproduction, known among
parrot, may be related partly to the poor vitamin A status of these birds.
The data presented in Tables 1 and 2 are likely to support the conclus1on
that a vitamin A level of 500 I.U./gm 1iver tissue or more might be
acceptable as a physiological level.
Many parrots are imported at young age. The proposed level of 500 I.U./gm
liver would be in agreement with levels recorded from three young wood
pigeons (Columba palumbus) ( S t a m, 1965). These were 582, 541, and 903
I.U. Other values were 3,552 I.U., recorded from an adult wood pigeon, as
well as 2,634, 1,800, and 666 I.U. which were recorded from tbree sparrows
(Passer domesticus).
The data presented are likely to suggest that parrots, just as other birds,
are able to store vitamin A in the liver. However, fairly high doses and
strict regimes wi11 be necessary to aohieve levels oomparable to those
recorded from recently imported parrots.
Feeding should be the preferential route for vitamin A supply. Addit1onal
vitamins and minerals can then be given at the same time. The seed mixtures
for parrots should contain higher percentages of sma11 seeds and not more
than l5 per ccent of sunflower seed. In addition these, rations should
51
oontain feed concentrates with vitamin A amounts of not less than 50,OOO
I.U./kg. Experience so far accumulated is likely to suggest that the strongly
pronounoed feeding habits of parrots can be changed by feeding restricted
amounts of seeds through about 14 day., such as 10 gm per day for one Afrioan
grey parrot. During the same period, concentrate is offered in a separate
feeding trough ad libitum in a quantity of about 20 per cent of the given
bird's daily feed intake. All feed items have to be weighed carefully to keep
the feeding system restricted and thus to maintain the regime as a whole.
This system also wi11 prevent the bird from selecting preferred seeds.
Additional titbits, suoh as greens and branches, should be given, provided
that the basic feed is made up of 80 per cent seeds and 20 per cent
vitaminised and minera1ised concentrate which should contain some 22 per cent
of protein.
Summary:
Vitamin A Deficiency in Parrots
The occurrence of av1tam1nos1s A in parrots was stud1ed by analys1s of liver-
born vitamin A levels. Values between 500 and 1,200 I.U./gm liver were
recorded from recently imported animals and oons1dered to be acceptable.
Levels between 50 and 2 I.U./gm l1ver coino1ded with subclinical avitaminosis
A and focal metaplas1a of epithe11um in the posterior sa1ivary glands of the
tongue. Levels below 2 I.U./gm liver we re found to be correlated with
severe, extensive metaplasia of epithe1ia with clinically detectable
symptoms. Accumulations of desquamated cornified cells occurred in salivary
glands and less often 1n lacrimal glands and nasal sinuses, as well. They
appeared as whitish circumscribed swel11ngs. The development of avitaminosis
A may be prevented by offering feed concentrate with 50,000 I.U. of vitamin A
per kilogram of feed. This should account for 20 per cent of the da1ly feed
intake. Restriction of seed quantit1es, however, is a prerequis1te.
Zusammenfassung;:
Vitamin A-Mangel bei Papa8eien
Duroh Analysen der Lebern wurde d1e Avitaminosis-A bei Papage1en untersuoht.
Der normale Gehalt bei frisoh import1erten Tieren betrug 500 - 1200 i.E. pro
Gramm Lebergewebe. Be1 einem Gehalt zwisohen 50 und 2 I.E. pro Gramm Leber
entwickelte sich eine subklinische Avitaminose-A, charakterisiert durch
lokale Metaplasien des Epithels in den hinteren lingualen Speicheldrüsen. Ein
Gehalt von weniger als 2 I.E. Vitamin-A ging mit klinisch sichtbaren
Erscheinungen in Form von Hyperkeratosen und desquamierten Epithelzellen in
den Speicheldrüsen sowie in geringerem Umfang in den Tränendrüsen und
Nasensinus einher. Diese Anhäufungen von weißlichem Material verursachten
siohtbare, umschriebene, blaß gefärbte Schwellungen. Als Vorbeuge wird ein 20
%iger Zusatz von Konzentratfutter mit 50.000 I.E. Vitamin-A pro kg zur
Tagesfutterration vorgeschlagen. Dementsprechend muß die Körnerration
verringert werden.
sumé:
Carence de vitamine A chez des perroquets
L'analyse du foie a permis de découvrir les causes de l'avitaminose A chez
des perroquets. La teneur normale d'animaux nouvellement importés était de
500 à 1200 de u.i. par gramme de tissue patique. En cas d'une teneur
occillant entre 50 et 2 u.i. par gramme de foie s'est développée une
avitaminose A subclinique, caractérisée par des métaplasies de l'épithélium
aux glandes salivaires linguales postérieure. Une teneur de moins de 2 u.i.
de vitamine A allait de pair avec des manifestations cliniques visibles sous
forme d'hyperkératose et de cellules épithéliales tuméfiées aux glandes
salivaires et moins manifestement aux glandes lacrymales et au sinus nasale
Ces entassements d'une matière blanchâtre ont provoqué des tuméfactiöns
visibles, cernées et pâ1es. L'auteur propose comme mesure préventive
d'ajouter à l'affouragement journalier 20 % de concentré avee 50 000 d'u.i.
de vitamine A par kilo ce qui implique la nécessité de réduire la ration de
grains.
52
Literature:
KONSTANTINOV, A. (1972): A oontribution to the pathomorphology of vitamin A
deficiency in chickens. Zbl. Vet. Med. A 19, 407-416.
MULDER, F. J. (1957): Het isoleren van de onverzeepbare rest bij het bepalen
van in vet oplosbare vitaminen. Amsterdam: Vet.med. Diss.
SHERWOOD, R. M. and G. S. FRAPS (1932): The quantities of vitamin A required
by pullets for maintenance and for egg production. Tex. Agr. Exper. Sta.
Bull., 468.
STAM, J. W. E. (1965): Een onderzoek naar de vitamine A behoefte bij de duif.
Diss Utrecht.
ZWART, P. (1978): Vitamin A-Mangel und Stomatitis bei Papageien. Prakt.
Tierarzt, 121-123.
Address of author: Doz. Dr .P. Zwart, Biltstraat 172 Utrecht (Netherlands)
... Most psittaciformes of private owners are fed exclusively on seeds. The patient under consideration has lived for a considerabie time on a diet that was definitely deficient in both vitamin A and calcium and/or vitamin D. Squamous metaplasia of salivary gland epithelium occurs if the vitamin A content in the liver is less than 50 I.U per gram (ZWART et al., 1979). It is known that depletion of vitamin A reserves in the liver takes about one year. ...
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The findings are presented of a number of investigations, recorded elsewhere, carried out by the author and showing that in vitamin A deficiency in chickens, in addition to the metaplastic changes known so far in the conjunctiva and in the epithelium of the apper digestive and respiratory tracts, metaplastic processes also occur in other parts of the bird. As a result of this the appearance is observed of a stratified squamous, keratinizing epithelium, both in the surface epithelium and the follicles of the bursa of Fabricius and in the surface epithelium and the glands of the cloaca, in the epithelium of the vagina of the oviduct, the ureters, the collecting tubules of the kidneys, as well as in the epithelium of the parathyroid glands. The metaplastic changes in the epithelium of the ureters leads to the partial or complete obstruction of the urate outflow toward the cloaca, which may be the immediate cause of the occurrence of uratic diathesis (gout) in chickens in cases of vitamin A deficiency. On the basis of the established pathological pattern the lesions observed in the glands of the oesophagus and the oral mucosa in A avitaminosis in chickens are divided into three stages: (1) the onset of the disease; (2) more advanced form of deficiency; and (3) very marked deficiency, the time interval between the stages being about two weeks.
Het isoleren van de onverzeepbare rest bij het bepalen van in vet oplosbare vitaminen
  • F J Mulder
MULDER, F. J. (1957): Het isoleren van de onverzeepbare rest bij het bepalen van in vet oplosbare vitaminen. Amsterdam: Vet.med. Diss.
The quantities of vitamin A required by pullets for maintenance and for egg production
  • R M Sherwood
  • G S Fraps
SHERWOOD, R. M. and G. S. FRAPS (1932): The quantities of vitamin A required by pullets for maintenance and for egg production. Tex. Agr. Exper. Sta. Bull., 468.
Vitamin A-Mangel und Stomatitis bei Papageien
ZWART, P. (1978): Vitamin A-Mangel und Stomatitis bei Papageien. Prakt. Tierarzt, 121-123.
Een onderzoek naar de vitamine A behoefte bij de duif
  • J W E Stam
STAM, J. W. E. (1965): Een onderzoek naar de vitamine A behoefte bij de duif. Diss Utrecht.
  • P Zwart
ZWART, P. (1978): Vitamin A-Mangel und Stomatitis bei Papageien. Prakt. Tierarzt, 121-123.