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Veterinary Dermatology 2005, 16, 39 46

Adult-onset hair loss in Chesapeake Bay retrievers: a clinical and


histological study

Blackwell Publishing, Ltd.

R. CERUNDOLO*, E. A. MAULDIN, M. H. GOLDSCHMIDT, S. L. BEYERLEIN,


K. R. REFSAL and J. W. OLIVER
*Department of Clinical Studies and Department of Pathobiology, University of Pennsylvania, Philadelphia, USA
Endocrine Section, Diagnostic Center for Population and Animal Health, Michigan State University, Lansing, USA
Clinical Endocrinology Service, University of Tennessee, Knoxville, USA
(Received 20 July 2004; accepted 21 September 2004)

Abstract Ten Chesapeake Bay retriever (CBRS) dogs with hair loss were recruited in collaboration with the
American Chesapeake Club. All dogs had nonpruritic, noninflammatory, regionalized hair loss affecting the same
areas of the body in male and female dogs. Hormonal investigations showed increased adrenal and sex steroid
concentration in seven cases. Histopathology revealed follicular hyperkeratosis and plugging, follicular atrophy,
and occasional melanin clumping with malformed hair shafts. This study suggests that hair loss in CBRS is a
breed syndrome in which young adult dogs have hair loss characterized by unusual histological features and
abnormal steroid production. A familial predisposition seems likely and selective breeding might reduce the
occurrence of this condition.

IN TRO D U CT I ON
Adult-onset, nonpruritic, symmetrical or generalized
hair loss in dogs is commonly caused by endocrine disorders such as hyperadrenocorticism, hypothyroidism,
and hyperestrogenism due to testicular Sertoli cell
tumour. In some breeds such as Nordic breeds, miniature poodle and water spaniel dogs, there is an adultonset form of hair loss in which the pathogenesis is still
not completely clear.13 Both male and female dogs,
neutered or intact, are affected. Symmetrical hair loss
develops around the neck, and over the trunk, flanks,
caudal thighs and/or perineum. Apart from the coat
changes, the dogs seem to be healthy and the results of
routine adrenocortical and thyroid function tests have
been reported to be normal.
In the last few years, CBR breeders have started to
recognize coat disorders characterized by areas of hair
loss affecting the axillae, latero-ventral thorax, flanks,
ventrum, dorsum, rump and/or the caudal part of the
thighs in both male and female dogs.
The purpose of this study was to describe in detail
the clinical aspects of hair loss in CBRS, to evaluate
their hormonal status, and to review the histopathology of the skin from affected and unaffected areas from
dogs. The dogs were those recruited for the study and
those available from the archives of the Dermato-

pathology Service of the University of Pennsylvania


(DS-UPENN) and the Dermatopathology Specialty
Service of the University of Texas Veterinary Medical
Center (DSS-UTVMC). Pedigree data relating to
affected dogs were also collected and analysed.

M AT E R IA L S A N D M E T H O D S
Epidemiological survey
In September 2002, the American Chesapeake Club
(ACC) was contacted regarding the occurrence of hair
loss in this breed. Owners and breeders of CBRS with
nonpruritic, regionalized hair loss were solicited by a
letter published in the ACC Newsletter and also sent by
the ACC List Server. The respondents reporting dogs
with this pattern of hair loss were invited to participate
in a clinical study by either coming to the MJ Ryan
Veterinary Hospital of the University of Pennsylvania
(MJR-VHUP) or going to their local veterinarian. In
each case, the veterinarian and owner received a copy
of the protocol of the tests to be carried out, and the
veterinarian was mailed a package including 1 dose of
adrenocorticotrophic hormone (ACTH) and tubes for
storing the blood and skin specimens. They were asked
to send back the samples with ice packs and to send the
parcel containing the samples by courier.

Clinical study
This study was presented as a free communication at the Fifth World
Congress of Veterinary Dermatology Vienna, Austria, August 25
28, 2004.
Correspondence: R. Cerundolo, Department of Clinical Studies,
School of Veterinary Medicine, University of Pennsylvania, 3900
Delancey Street, Philadelphia PA 19104, USA. E-mail:
cerundol@vet.upenn.edu
2005 European Society of Veterinary Dermatology

Four of the 10 cases were examined at MJR-VHUP


and a general and dermatological examination was
performed. Routine dermatological investigations (skin
scrapings, coat brushings for fleas and trichogram) and
fungal culture were undertaken in these cases. Six of
the 10 cases were examined by the referring veterinarians
39

40

R Cerundolo et al.

(three of these dogs were seen by three Board-certified


dermatologists). Intact bitches were examined during
diestrus, roughly 2 months after their oestrus cycle.

Blood investigations
Blood was collected by jugular venipuncture for
routine haematological and biochemical investigations.
Two aliquots of the serum were stored at 20 C for
hormonal assay. One was sent to Michigan State University for a thyroid panel to measure: total thyroxine
(T4), total triiodothyronine (T3), free T4 by equilibrium dialysis (fT4 ED), free T3 (fT3), T4 and T3
autoantibody (T4AA, T3AA), thyroid stimulating hormone (TSH), and thyroglobulin autoantibody (TgAA);
insulin-like growth factor 1 (IGF1) was also measured.
The second half of the serum was sent to the University
of Tennessee for a sex-hormone panel to measure the
hormone basal concentration. A second blood sample
was collected 1 hour after intravenous administration
of 0.25 mg dog1 of tetracosactrin acetate (Synacthen;
Alliance Pharmaceuticals Ltd., Chippenham, Wilts, UK).
The hormones measured in both samples included cortisol, 17-hydroxyprogesterone (17-OHP), androstenedione, estradiol, progesterone and testosterone.
The source of reagents, as well as assay procedures
and suitability for use in canine serum, has previously
been reported for all thyroid-related tests, with the
exception of fT3. Validation data for T4 and TSH,4
T3,5 fT4 ED,6 T4AA and T3AA,7 and TgAA8 have
been described. Free T3 was measured using a directserum analogue-based radioimmunoassay kit (Clinical
Assays Gammacoat Free T3 125I RIA Kit, DiaSorin
Inc., Stillwater, MN, USA). The manufacturers protocol for the assay was followed with the exception that
the incubation of antibody-coated tubes containing
radioligand and sample was extended to 3 h in a 37 Cwater bath. The manufacturer of the kit described
antibody specificity of 100% cross-reactivity with triiodothyronine and less than 0.02% cross-reactivity with
all other iodothyronines evaluated. The analytic sensitivity of the assay, defined as the concentration of fT3
at 90% specific binding, was 1.1 pmol L1 (10 assays).
In direct-serum analogue-based assays of free thyroid
hormones, there are equilibrium reactions between the
hormone measured, endogenous binding proteins, and
the assay antibody. As a result, assessment of recovery
and dilutional parallelism is not applicable as in a
standard radioimmunoassay. For canine serum pools
of fT3 concentrations of 2.5 and 13.8 pmol L1, respective intra-assay coefficients of variation (CV) were 0.064
and 0.059 and respective interassay CV were 0.138 and
0.051 (n = 10 replicates).
Insulin-like growth factor 1 (IGF1) was measured in
canine serum samples with a commercially available
radioimmunoassay kit (IGF-1 Insulin-like growth
factor by extraction, Nichols Institute Diagnostics,
San Clemente, CA, USA). An acid-ethanol solution
consisting of 12.5% 2 N HCl/87.5% absolute ethanol
(% by volume) was prepared following the manufacturers instructions. Extraction of sera and radio-

immunoassays were performed with reagent volumes


and incubation times specified in the manufacturers
protocol. The manufacturer of the kit described essentially no antibody cross-reactivity with other peptide
hormones including growth hormone, thyrotropin,
luteinizing hormone, prolactin, porcine insulin and
proinsulin, or insulin-like growth factor II. The sensitivity of the assay, defined as the concentration of
IGF1 at 90% specific binding, was 2.1 nmol L1 (mean
of 10 assays). When IGF1 was added to each of two
extracted samples at amounts of 19, 36 and 75 nmol L1,
the average rates of recovery in the assay were 77%,
80% and 85%, respectively. A canine serum sample
with measured concentration of 118 nmol L1 was
diluted at rates of 50%, 25% and 12.5% with reagent
phosphate buffer prior to extraction. When the results
were corrected for dilution, 105%, 130% and 100%
recovery of the expected value was obtained for the
respective dilutions. Intra-assay repeatability was
assessed with three pools of canine sera assembled to
have lower (17 nmol L1), mid-range (51 nmol L1),
and high (118 nmol L1) concentrations. The respective intra-assay coefficients of variation for 10
extracted samples of each pool were 0.118, 0.053, and
0.068. In 10 assay runs, the interassay CV of the same
serum pools were 0.254, 0.131 and 0.160, respectively.
The sex-hormone panel hormones were measured
using human kits that have been previously validated
for the dog.9,10 The sensitivity of the hormone assay is:
testosterone (0.04 ng mL1); androstenedione (0.05 ng
mL1); 17-OHP (0.08 ng mL1); progesterone (0.03 ng mL1);
estradiol (7.2 pg mL1); cortisol (0.2 g/dL). Normal
reference range for the two laboratories is given in
Table 1.

Urine investigations
Owners were also asked to collect morning urine
samples on 10 consecutive days. For this purpose, the
owners were provided with 10 polypropylene tubes in a
package with ice packs, to be sent back to MJR-VHUP
by courier. In each sample, the corticoid/creatinine
ratio (UCCR) was determined according to a procedure described,11 and the average of the 10 ratios was
subsequently calculated for each dog.

Histopathology
Three or four 6-mm punch biopsy specimens of skin
were collected under local anaesthesia using 2%
lidocaine from eight CBRs. Specimens were obtained
from one or more areas with hair loss on the flanks,
rump and thigh. One specimen, to serve as a control,
was collected in each case from a clinically normal
area, which was most often the dorsal thorax. Specimens were fixed in 10% neutral buffered formalin and
transferred to the DS-UPENN for processing and
examination. These were bisected vertically, along the
line of the hair where possible, and paraffin sections
that had been stained with haematoxylin and eosin
were prepared from one half of each sample using
standard histological methods. All sections were

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 39 46

Hair loss in Chesapeake Bay retrievers

41

Table 1. Clinical sites of hair loss in affected dogs included in this study
Cases

Age (years)

Sex

Ventrolateral thorax

Axillae

Flanks

Abdomen

Thighs

Rump

1
2
3
4
5
6
7
8
9
10

2
6
2
2
4
3
3
3
2
1 1 /2

F
NM
NM
F
NM
F
NF
NF
F
F

v
x
v
x
v
x
v
v
v
x

v
x
v
v
v
x
v
x
x
x

x
v
v
v
v
v
v
v
v
v

v
x
x
v
v
x
v
x
x
x

v
v
v
v
v
x
v
v
x
x

x
x
x
x
x
x
x
v
v
x

v, affected area; x, nonaffected area.

Figure 1. Extensive hair loss affecting the lateral side of the body (a), the rump (b) and the thighs (c).

initially examined blind (i.e. without prior knowledge of the condition or site of the skin sampled).
Results were subsequently reviewed in relation to the
clinical findings. Three of the dogs had already been
biopsied by board-certified dermatologists. Skin sections from 11 additional cases were identified from
the archives of the DS-UPENN (six cases) and the
DSS-UTVMC (five cases). These cases were selected
through a computer search using keywords Chesapeake Bay retriever and noninflammatory alopecia
in conjunction with compatible historical and clinical
findings.

Pedigree analysis
Four-generation pedigrees of six dogs were available.

RESU LTS
Responses from the ACC members were high and 24
owners of affected dogs agreed to collaborate. Due to
funding restraints, only the first 10 people who replied
were contacted and their dogs recruited. Four were
examined at MJR-VHUP, while six dogs were seen and
sampled by the local veterinarians. There were seven
female dogs (two of which had been spayed) and three
neutered male dogs. Nine of the dogs were between 1.5
and 4 years of age (median 2.5 years); only dog 2 was
6 years old but hair loss had started 2 years previously.

In dog 4 hair loss had started at 5 months of age, and


in dog 5 hair loss had started at 2 years of age soon
after castration.
Dog 5 had previously been treated for 2 years with
melatonin without showing hair re-growth. Dogs 3 and
8 had had several episodes of superficial pyoderma,
which had resolved with antibiotic therapy but no hair
re-growth had occurred following the resolution of the
pyoderma.

Clinical findings in dogs with coat disorders


General physical examination revealed no significant
findings. Dermatological examination revealed various
patterns of hair loss ranging from sparse hair to complete baldness in various sites such as the axillae (dogs
1, 36, 7), ventrum (1, 4, 5, 7), flanks (210), rump (8,
9), latero-ventral thorax (1, 3, 5, 79), or the thighs (1
5, 7, 8) (Fig. 1a,b,c; Table 1). No differences in the
location of hair loss were seen in this group of dogs
between sexes. The owner of dog 10 felt that hair loss
was more prominent during the oestrus cycle, with subsequent poor hair re-growth.

Laboratory investigations
Routine haematological and biochemical investigations gave values that were within normal limits in all
cases (data not shown).
Hormonal assays showed normal thyroid hormone
concentrations in all dogs except for dog 4 which had

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 3946

42

R Cerundolo et al.

Table 2. Clinical details, cortisol/creatinine ratio and thyroid panel results of the affected dogs included in this study

Cases

Age
(years)

Sex

NM

NM

NM

7
8

3
3

NF
NF

10

1.5

Reference range

Urine
C/C ratio
mean
710
7.8
69
7.3
612
8.8
810
8.6
1013
11.2
69
7.8
ND
68
6.57
612
9.6
56
5.7
824

TSH
mU I1

TgAA

T4
nmol L1

T3
nmol L1

FT4 ED
pmol L1

FT3
pmol L1

T4AA

T3AA

IGF 1
nmol L1

13

93

93

0.5*

4.3*

13

29.5

28

105

34

1.2

14

3.5*

13

11.8

13

89

35

1.5

15

8.2

38.3

38

270

26

0.2*

15

5.3

45

30

20

71

55

0.2*

12

6.7

33

17

75

34

1.0

18

5.5

41.3

ND
59

ND
1.8

ND
22

ND
6.5

ND
5

ND
1

ND
53.1

ND
11

ND
76

16

53

55

1.0

28

8.3

ND

13

32

33

1.1

19

10.8

ND

1567

1.02.5

037

< 200%

642

4.512

< 20%

< 10%

5 45

*Values are below the reference range. Values above the reference range are in bold; M, intact male dog; NM, neutered male dog; F, intact female
dog; NF, neutered female dog.

slightly increased concentrations of T3AA, TSH and


TgAA. Normal IGF1 concentrations were seen in all
cases except for dog 8 (Table 2). The sex-hormone
panel found slightly increased cortisol concentration
pre-ACTH in dogs 2, 5 and 10 and post-ACTH in dog
2; increased 17-OHP concentrations pre-ACTH in
dogs 1, 2, 4 and 10, and post-ACTH in dogs 1, 4 and 7;
increased androstenedione concentration pre-ACTH
in two neutered male dogs (nos. 2, 3) and one female
dog (no. 1) and post-ACTH in one female dog (no. 1)
and one neutered male (dog 2); slightly increased oestrogen concentration pre- and post-ACTH in one
female dog (no. 1) and one neutered male dog (no. 3);
increased progesterone concentration pre-ACTH in
three neutered male dogs (nos. 2, 3, 5) and two female
dogs (nos. 1, 10), and post-ACTH in one neutered male
dog (no. 2), one neutered female dog (no. 7) and one
female dog (no. 10) (Table 3). The testosterone concentrations were within the reference range although most
results for this hormone were below assay sensitivity.
The UCCRs were within the normal range in all
dogs.

Histopathological findings
A total of 53 skin biopsy specimens from 14 CBRs submitted at the DS-UPENN and from five CBRs submitted at the DSS-UTVMC were examined. Eight 6-mm
biopsies from clinically normal sites were received from
eight CBRs in the clinical study. Two biopsy specimens
from two dogs were unavailable for review. These cases
had been interpreted by a board-certified veterinary
pathologist with expertise in dermatopathology, and
had similar histological findings as in our cases. These
cases were selected by the description of the pattern of
hair loss mentioned in the history submitted with the
skin samples, and were suggestive of this condition. Of

the 14 dogs, 13 had mild to moderate nonscarring


alopecia in affected sites. Follicular infundibula were
dilated and distended with keratin. The hyperkeratosis
extended into secondary follicles and sebaceous glands
ducts, producing an abnormally globose shape to the
infundibular region (Fig. 2a). Atrophy of primary and
secondary follicles was evident, but secondary follicles
were more severely affected. Some follicles were miniaturized. Distended infundibula contained small,
contorted hair shafts with irregular melanin clumping
and loss of corticomedullary distinction (eight dogs)
(Fig. 2a,b). Changes were the same in all sites (except
normal skin). Flame follicles were seen in dog 8 only.
Sebaceous glands were consistently normal to hyperplastic in relation to the body site sampled. Dog 2 had
multifocal folliculitis in one of the initial biopsies. A
repeat biopsy from a noninflammed alopecic area
revealed pronounced infundibular hyperkeratosis, similar but less severe than the remaining cases.

Follow-up
The owners of two dogs (1 and 4) had their bitches
spayed after the first examination. In both dogs no hair
re-growth was evident 5 and 6 months, respectively,
after spaying.

Pedigree analysis
Analysis of six pedigrees of affected dogs revealed
common ancestors in both the sire and the dam line of
all dogs except dog 9.

D ISC U S S IO N
This study is the first to describe the clinical findings,
hormonal status and histopathology of a noninflammatory

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 39 46

0.46 22.1
0.02 0.42
0.03 0.1
0.02 0.45

43

*Values are below the reference range. Values above the reference range are in bold; M, intact male dog; NM, neutered male dog; F, intact female dog; NF, neutered female dog.

0.1926.3
0.01 0.24
0.01 0.1
0.01 0.32
0.55 1.70
0.221.45
0.33 4.33
0.101.50
0.02 0.4
0.01 0.17
0.03 2.16
0.01 0.49
30.0 65.6
23.3 69.4
31.8 63.1
27.9 69.2
6.8 79.2
2.4 29.0
3.8 42.1
2.739.7
2.1 42.6
0.13.6
1.9 11.9
0.15.7
Reference range

M
NM
F
NF

2.5 56.7
2.0 56.5
4.0 59.9
2.158.8

70.8 108.5
70.6 151.2
66.7174.8
65.0 174.6

0.06 0.84
0.01 0.22
0.05 0.69
0.01 0.07

0.372.87
0.25 2.63
0.68 4.44
0.40 1.62

30.5 66.6
23.1 65.1
31.5 65.4
30.8 69.9

Post
Pre

0.03
0.03
0.02
0.03
0.04
0.03
0.03
0.03
0.01
0.03

Post

4.1
1.96
1.11
3.29
1.03
2.23
1.75
0.96
1.50
5.71

Pre

2.7
0.37
0.23
0.27
0.53
0.08
0.05
0.01
0.08
3.36
77.4
56.6
73.9
40.2
47
60.4
26.1*
56.9
61.2
57.7
77.2
54.6
72.2
41.4
47.4
61.8
22*
57.1
56.1
60.2
43.0
66.2
15.5
27.5
12.7
35.6
20.7
17
13.4
18.7
14.9
12.4
5.4
4.4
12.8
4.3
2.7
0.6
2.3
8.8
4.75
2.12
0.78
11.5
2.23
3.04
1.98
0.83
1.46
3.81

Post
Pre
Post
Pre
Post

1.04
0.41
0.20
0.76
0.81
0.14
0.08
0.06
0.12
1.15

Pre
Post

124.5
157.5
133
103.4
105.1
109.9
95
72.5
113.8
64.3
47.8
68.8
37.9
15.4
68.0
8.8
11.4
7.4
14.5
66.9

Pre

2
6
2
2
4
3
3
3
2
1.5
1
2
3
4
5
6
7
8
9
10

Sex
Age
(years)
Cases

F
NM
NM
F
NM
F
NF
NF
F
F

Testosterone
ng mL1
Progesterone
ng mL1
Estradiol
pg mL1
Androstenedione
ng mL1
17-OHP
ng mL1
Cortisol
ng mL1

Table 3. Clinical details, adrenal and sex steroid results of the affected dogs included in this study

0.03
0.03
0.02
0.04
0.04
0.05
0.03
0.03
0.02*
0.04

Hair loss in Chesapeake Bay retrievers

Figure 2. (a) Note the pronounced distension of follicular


infundibula by marked orthokeratotic hyperkeratosis.
Bar = 400 m. (b) Higher magnification of (a). Dystrophic hair
shafts with abnormal melanin clumping. Bar = 200 m.

alopecic disorder unique to Chesapeake Bay retrievers.


This disorder has generated a great deal of confusion
among breeders and veterinary practitioners for many
years. Many cases were misdiagnosed as hypothyroidism and failed to respond to hormonal replacement therapy.
The most common presentation in our dogs was
thinning to complete hair loss on the axillae, flanks,
abdomen and caudal thighs. Most cases had no accompanying inflammation. This pattern of hair loss is similar to that seen in cyclic flank alopecia, canine pattern
baldness and greyhound bald thigh syndrome.12,13 The
dogs were otherwise healthy and the hair loss did not
respond to hair growth stimulants (thyroxine, melatonin). Furthermore, the hair growth and loss did not
appear to cycle.
The term follicular dysplasia has been reported in
many breeds but the term is loosely applied to both
disorders of hair cycling (e.g. canine recurrent flank
alopecia),14,15 as well as true anagen-based structural
defects in hair shaft production (e.g. colour dilution
alopecia, black hair follicular dysplasia).16,17 The
Chesapeake Bay retriever has previously been cited as

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 3946

44

R Cerundolo et al.

a breed predisposed to follicular dysplasia but not


further defined.12
Clinically, our cases differ from canine recurrent alopecia in that (1) the alopecia is always multifocal (not
confined to the flank area) with a unique distribution and
(2) the hair growth does not cycle with the seasons of the
year. Histologically, our cases had a spectrum of changes
and some were very similar, if not identical, to recurrent
flank alopecia. Common changes were pronounced
infundibular hyperkeratosis with misshapen telogen
follicles. Some cases had twisted hair shafts and clumped
melanin. Further histological analysis is needed to
determine if this is a true dysplastic syndrome or a disorder of hair cycling. We believe the latter is more likely.
The symmetrical loss of hair on the caudal thighs
and axillae is somewhat similar to canine pattern baldness. This disorder has three distinct clinical forms, as
described by Scott et al.12 Unlike the pattern baldness
reported in dachshunds, our dogs did not have any
gender predilection. Clinically, none of our dogs had
pinnal or facial (preauricular) involvement. Histologically, in canine pattern baldness there is moderate to
severe size decrease (miniaturization) of the hair follicles they are both shorter and thinner than normal,
and the residual hair shafts are also thin. The most
common finding in our study, however, was infundibular hyperkeratosis. There was a subtle decrease in
follicular size in some biopsies compared with control
sites; however, because morphometric examination of
follicular anatomy in cases of pattern baldness and
greyhound bald thigh syndrome has not been performed, strict comparisons are difficult. No distinct
histopathological differences were seen between the
flank and the dorsal specimens when compared with
those from the thighs; however, only three biopsies
from the thigh area were reviewed.
Superficial pyoderma is a common finding in
dogs with hyperkeratosis of the follicular infundibula,
which predisposes to bacterial colonization. The presence
of previous episodes of pyoderma in two dogs in this
study may have contributed to the hair loss. However,
when treated, normal coat condition was not achieved.
In this study, we evaluated the function of the
thyroid and adrenal glands, and sex hormone status.
Growth hormone (GH) production was evaluated by
measuring the IGF1 concentration and found to be
normal in all dogs, thus a central growth hormone deficiency was unlikely. Adult-onset hyposomatotropism
or GH responsive alopecia has been reported previously in a few cases,18 but it is now believed that true
hyposomatotropism in adult dogs leading to alopecia
is rare and that syndrome is now commonly named
Alopecia X. The hair re-growth following GH supplementation was probably only an additional stimulus to
the function of the hair follicle. A further study
sampling nonaffected CBRs should be carried out to
compare the results.
The level of various hormones was measured in a
specialized endocrine veterinary laboratory to assess
thyroid function. This allowed us to rule out hypothy-

roidism in all our cases. One dog (no. 4) had elevated


TgAA and T3 autoantibody results, suggesting that this
dog has a risk of becoming hypothyroid in the future
but at the time of the study it was unlikely that the hair
loss in this case was related to an abnormal thyroid
function. It has been reported that the CBR breed has
higher prevalence of thyroid hormone autoantibodies,7,19
and the owner has therefore been advised to have the
thyroid tests repeated in future for this dog.
Three neutered male dogs (2, 3, 4) and four female
dogs (1, 4, 7, 10) one of which was neutered (dog 7)
had increased adrenal and sex steroid concentrations.
Three female dogs (nos. 6, 8, 9) one of which was neutered had normal hormone concentrations despite
presenting a similar pattern of hair loss to the other
dogs. These hormonal findings resemble the adrenal
and sex hormone abnormalities reported in Irish water
spaniels.1 Two of the five intact female dogs (1, 10) had
an increased concentration of progesterone and dog
no. 1 had an increased concentration of androstenedione. Although the blood tests were carried out more
than 2 months after the oestrus cycle (according to the
owner), it cannot be ruled out that their high concentrations were the result of the diestrus phase of their
cycle. The cyclic episodes of hair loss in one bitch might
support a cause and effect relationship between oestrus
and alopecia but a larger number of affected intact
bitches need to be studied to confirm this.
The number of affected male dogs (intact and neutered) was insufficient to demonstrate a correlation
between hair loss and male sex hormones. In contrast
to human male pattern alopecia, where castration is
associated with hair re-growth,20 castration in dog 5
seems to have coincided with hair loss. It is unlikely
that testosterone plays a role in this syndrome. The
presence of the hormonal receptors in the affected and
unaffected skin in these dogs should be investigated to
further evaluate this hypothesis.
The results of the haematology and biochemistry
tests were not indicative of classic hyperadrenocorticism or of a sex-hormone-related condition in alopecic
CBRs. Furthermore, there have been no clinical signs
at the time of the first examination and during the
1-year follow-up indicative of these conditions. A
low-dose dexamethasone suppression test could have
helped to further assess the pituitary-adrenal axis but
this was considered unnecessary as the UCCRs were
within normal values in all dogs. This rules out a
hyperadrenocorticism-like syndrome affecting the
cortisol pathway as reported in Pomeranians and
miniature poodles.2 The adrenal function and the sex
steroid concentrations in healthy intact and neutered
CBRs should be evaluated to statistically compare the
data of the affected dogs of this study.
Although only four-generation pedigrees were
available and considering that this is a small breed
population, there is evidence suggesting a familial predisposition. The genetic basis of this disease and the
mode of inheritance need to be further elucidated to
eliminate this condition from the breed.

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 39 46

Hair loss in Chesapeake Bay retrievers


The pattern of hair loss seen in CBRs has both of the
clinical features seen in dogs with follicular dysplasia
and pattern baldness. The histology of the affected skin
of CBRs is similar and, in same cases, identical to
CRFA but the history and the clinical features are
markedly different. This syndrome resembles the one
in the Irish water spaniel, where a multifactorial cause
of hair loss was found, as previously described by one
of the authors (RC).1 Interestingly, in the early 1900s
an Irish water spaniel was bred to a Chesapeake Bay
dog. Their progeny, highly valuable as hunting dogs,
has generated many of the modern CBRs.21 It is possible that the genetic contribution from that single Irish
water spaniel, which might have been a carrier of the
syndrome previously reported, played a role in producing affected CBRs.

6.

7.

8.

9.

10.

ACKN OWLEDGE ME NT S
The authors are grateful to the veterinarians Drs D.
Gram, M. Guise, R. Mowday, M. Stankovics, E. Robinson, E. Rothstein, T. Tapp and N. Schoulberg for
their help in sampling most of the affected dogs. We are
also grateful to Dr Kelly Credille for providing copies
of the skin sections from the archive of the Dermatopathology Specialty Service of the University of Texas
Veterinary Medical Center (DSS-UTVMC). We would
like to thank the owners of affected dogs and the members of the American Chesapeake Club for their collaboration, and in particular Ms Baldwin for helping to
gather information on the CBR history. This study was
sponsored by the University of Pennsylvania, Departmental Research Grant.

11.

12.

13.

14.

15.

REFEREN CE S
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1. Cerundolo R, Lloyd DH, McNeil PE et al. An analysis
of factors underlying hypotrichosis and/or alopecia in
Irish water spaniels in the United Kingdom. Veterinary
Dermatology 2000; 11: 10722.
2. Cerundolo R, Lloyd DH, Mol JA et al. Alopecia X in
Pomeranians and miniature poodles is associated with
abnormal pituitary-adrenal function. Journal of Veterinary Internal Medicine in press.
3. Schmeitzel LP. Alopecia X of Nordic breeds. In: Proceedings 15th Annual Members Meeting AAVD and
ACVD. Maui, Hawaii, 1999: 1317.
4. Paradis M, Sauve F, Charest J et al. Effects of moderate
to severe osteoarthritis on canine thyroid function.
Canadian Veterinary Journal 2003; 44: 40712.
5. Panciera DL, MacEwen EG, Atkins CE et al. Thyroid
function tests in euthyroid dogs treated with 1-thyroxine.

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Daminet S, Paradis M, Refsal KR et al. Short term influence of prednisone and phenobarbital on thyroid function in euthyroid dogs. Canadian Veterinary Journal
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Nachreiner RF, Refsal KR, Graham PA et al. Prevalence
of autoantibodies to thyroglobulin in dogs with nonthyroidal illness. American Journal of Veterinary Research
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Frank LA, Hnilica KA, Rohrbach BW et al. Retrospective evaluation of sex hormones and steroid hormone
intermediates in dogs with alopecia. Veterinary Dermatology 2003; 4: 917.
Frank LA, Rohrbach BW, Bailey EM et al. Steroid hormone concentration profiles in healthy intact and neutered dogs before and after cosyntropin administration.
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Randolph JF, Toomey J, Center SA et al. Use of the
urine cortisol-to-creatinine ratio for monitoring dogs
with pituitary-dependent hyperadrenocorticism during
induction treatment with mitotane (o,pDDD). American Journal of Veterinary Research 1998; 59: 25861.
Scott DW, Miller WH, Griffin GE. Congenital and
hereditary defect. In: Muller and Kirks Small Animal
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Miller MA, Dunstan RW. Seasonal flank alopecia in boxer
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Roperto F, Cerundolo R, Restucci B et al. Colour dilution alopecia (CDA) in ten Yorkshire terriers. Veterinary
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Miller WH, Scott DW. Follicular dysplasia of the Portuguese water dog. Veterinary Dermatology 1995; 6: 6774.
Bell AG, Jones BR, Scott MF. Growth hormone responsive dermatosis in three dogs. New Zealand Veterinary
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Rsum Dix Chesapeake Bay retriever (CBR) prsentant une chute de poils ont t slectionns en collaboration avec le American Chesapeake Club. Tous les chiens prsentaient une perte de poils non prurigineuse, non
inflammatoire, localise, touchant les mmes zones chez les mles et chez les femelles. Les tudes hormonales ont
montr une augmentation des concentrations des hormones sexuelles surrnaliennes dans sept cas. Lexamen
2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 3946

46

R Cerundolo et al.
histopathologique a montr une hyperkratose folliculaire et une atrophie associe des bouchons de kratine,
parfois associs des aggrgats de mlanine dans des poils malforms. Cette tude suggre que la chute de poils
dans la CBR est un syndrome dans lequel une anomalie de la production de stroides est prsente. Une prdisposition familiale semble probable et une reproduction slective pourrait diminuer lincidence de cette maladie.

Resumen Se seleccionaron diez perros Retriever de Chesapeake Bay (CBR) con prdida de pelo, en colaboracin con el Club Americano del Chesapeake. Todos los perros mostraban una prdida de pelo no-prurtica,
no-inflamatoria, regionalizada, afectando las mismas zonas corporales en machos y hembras. Las investigaciones
hormonales mostraron concentraciones elevadas de esteroides adrenales y gonadales en siete casos. La histopatologa revel una hiperqueratosis y obturacin folicular, atrofia folicular, y agregados ocasionales de melanina
con pelos malformados. Este estudio sugiere que la prdida de pelo en el CBR es un sndrome de la raza en el
que los perros adultos jvenes padecen una prdida de pelo caracterizada por caractersticas histolgicas inusuales y produccin anormal de esteroides. Parece probable una predisposicin familiar y la cra seleccionada
podra reducir la incidencia de esta enfermedad.

Zusammenfassung 10 Chesapeake Bay Retriever (CBR) mit Haarverlust wurden in Zusammenarbeit mit
dem American Chesapeake Club rekrutiert. Alle Hunde hatten nicht juckenden, nicht entzndlichen, regionalen
Haarausfall, der sich bei mnnlichen und weiblichen Tieren auf die gleichen Krperregionen erstreckte. Hormonuntersuchungen zeigten bei sieben Fllen erhhte adrenale und Geschlechts-Hormonkonzentrationen. Die
Histopathologie zeigte follikulre Hyperkeratose und Anschoppung, follikulre Atrophie und gelegentliche Melaninverklumpung in malformierten Haarschften. Diese Studie lt vermuten, dass Haarausfall in CBR eine
Rasseerkrankung ist, bei denen junge erwachsene Hunde Haarausfall haben, der durch unbliche histologische
Eigenschaften und anormale Steroidproduktion charakterisiert ist. Eine familire Prdisposition erscheint wahrscheinlich und selektives Zchten mag das Auftreten dieser Erkrankung reduzieren.

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 39 46