Aplasia of a Uterine Horn in Two Syrian Hamsters
(Mesocricetus auratus)
LISA C. HALLIDAY, DVM, RALPH M. BUNTE, DVM, ACVP, AND JAMES E. ARTWOHL, MS, DVM, ACLAM
Abstract _ This report describes aplasia of the left uterine horn in two Syrian hamsters. We discuss the embryologic development
and research implications of this mutation, which is heritable in piebald hamsters.
Aplasia of the left uterine horn was found in two approximately
10-week-old Syrian hamsters (Sasco, Inc., Kingston, NY). These
two animals were among the almost 1500 hamsters whose uterine tubes (oviducts) were collected over a 5-year period for use
in a sperm penetration assay to assess male fertility in humans.
All hamsters arrived at our facility when 6 to 7 weeks of age.
They were conventionally housed in AAALAC-accredited facilities in groups of five in polycarbonate shoebox cages with corncob
bedding (Green Products Co., Conrad, IA) and had free access
to rodent feed (Harlan Teklad 8640-22/5 Rodent Diet; Harlan
Teklad, Madison, WI) and municipal water. The husbandry conditions were consistent with the recommendations of the Guide
for the Care and Use of Laboratory Animals. Monthly monitoring for
serologic evidence of Encephalitozoon cuniculi and viral pathogens,
including Sendai virus, pneumonia virus of mice, lymphocytic
choriomeningitis virus, and reovirus 3, and quarterly assessment
for bacterial pathogens, ectoparasites, and pathogenic endoparasites by the vendor ensured that the animals were free of known
pathogenic organisms.
The animals were allowed to adapt to their new environment
for at least 3 days before experimental manipulation. All hamsters were used in the following project, which was approved by
the Institutional Animal Care and Use Committee of the University of Illinois at Chicago, within 2 months of arrival at the
facility. The hamsters were superovulated by injecting them intraperitoneally with 30 I.U. pregnant mare serum gonadotropin
and 30 I.U. human chorionic gonadotropin 1 day prior to collection of the uterine tubes. Animals were euthanatized with
carbon dioxide prior to harvesting the tissues.
Two hamsters had a thin (1 mm wide) band of pale
whitish-pink tissue rather than the left uterine horn (Figure 1).
The left ovary and uterine tube, the right ovary, uterine tube,
and horn, the vagina, and all other abdominal viscera of these
animals appeared normal on gross examination. Both uterine
tubes were collected for the described assay, and the remainder
of the reproductive tracts of these two hamsters were fixed in
10% formalin for histologic examination.
Cross-sections of the ovaries, the uterine horns, and the vagina were embedded in paraffin, cut in 3-mm sections, and stained
with hematoxylin and eosin. The ovaries, right uterine horn, and
the vagina of both hamsters were normal on histologic examination. The left uterine horn consisted only of smooth muscle
bundles interspersed with bands of fibrous connective tissue,
which were covered by a normal serosa and subserosa (Figure
2). There was no evidence of a lumen, endometrium, or endometrial glands in multiple tissue sections of the left horn. Histology
was not performed on any other organs from these animals.
Malformations of the female reproductive tract have been reported in various species, including swine (1, 2), cattle (2–4),
sheep (5), goats (6), cats (7, 8), rats (9), guinea pigs (10), hamBiologic Resources Laboratory, University of Illinois, Chicago, Illinois
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CONTEMPORARY TOPICS © 1998 by the American Association for Laboratory Animal Science
FIG. 1. Hamster uterus with a fibrous band rather than the left horn.
The right horn, both ovaries, and the vagina were normal.
FIG. 2. Photomicrograph of the abnormal tissue replacing the left uterine horn. Note the smooth muscle bundles interspersed with bands of
fibrous connective tissue. There is no evidence of a lumen or endometrial glands. Hematoxylin and eosin, 50X magnification.
sters (11), and humans (12–16). Abnormalities arise due to defects in the development of the paramesonephric (or Muellerian)
ducts, the embryologic precursors of the female urogenital tracts
(1). These embryologic structures develop into the uterine tubes,
uterus, and upper vagina of adult female mammals (16). The
distal portion of the ducts fuse to form the upper vagina and the
uterine body. In bicornuate species, the proximal portions of
Volume 37, No. 6 / November 1998
the ducts remain separate and form the uterine tubes and horns
(8). Defects in the developmental process can lead to defects
ranging from complete fusion of the ducts, thereby forming a
single uterus, to complete absence of a uterine tube or horn.
Absence of an entire uterine horn has been given the descriptive term uterus unicornis (1). In both hamsters, the left uterine
horn was affected. Similarly, the various renal and uterine defects that occurred in 17 rats, all of which were direct descendents
of three female siblings that were used to establish the breeding
colony, were always present on the left side of the animals (9).
Defects of the urinary system often accompany reproductive
abnormalities because the mesonephric (Wolffian) ducts, which
give rise to the urinary tract, and the paramesonephric ducts
have similar embryologic origins (16). If the development of the
urinary and reproductive systems is halted early during gestation (when the mesonephric and paramesonephric ducts are in
close proximity), absence of a uterine horn and the ipsilateral
kidney and ureter may result. This condition has been reported
in rats (9), guinea pigs (10), hamsters (11), and humans (14).
However, the two hamsters we describe lacked any gross abnormality of the urinary tract.
Aplasia of the left uterine horn has previously been documented only in piebald hamsters. The inbred hamster colony
that gave rise to those animals was established from two piebald
male littermates. The pathogen status of those animals was not
reported. Aplasia of the female urogenital tract appeared to be
associated with the piebald trait to the degree that approximately
25% of the 41 female piebald hamsters necropsied had defects
of the urogenital tract. The defects ranged from complete absence of the uterus and a kidney to aplasia of a portion of one
uterine horn; whether the left side was predominantly affected
was not mentioned. None of the wild-type littermates of the affected piebald animals had aplasia of a uterine horn. However,
of 1000 necropsied hamsters, three unrelated, wild-type animals
(each from a different commercial stock) had some degree of
aplasia (11). The two hamsters in the present report came from
a single commercial vendor that maintains an outbred colony.
Because these two hamsters arrived at the facility nearly a year
apart, the degree of relatedness was probably small and likely
limited to the common origin of all Syrian hamsters in the
United States from one original litter in 1930. In light of the
previous study and our findings, the prevalence of aplasia of
the left uterine horn among wild-type color hamsters is less than
1%. The piebald color and associated urogenital aplasia were
inherited as single recessive traits (11). However, in unrelated,
wild-type color hamsters, urogenital tract defects seem to be
rare mutations that occur during the development of these organ systems in utero.
Animals with aplasia of a uterine horn may have decreased
reproductive performance, because the absence of a uterine horn
reduces the number of implantation sites for embryos. In addition, uterine abnormalities may have a heritable aspect, as has
been shown for humans and rats (9, 13). A practical implication
of this finding is the culling (especially in lines of inbred hamsters) of siblings and other relatives of animals with uterine
defects to avoid propagation of the defect. As far as can be determined from a review of the literature, uterine aplasia cannot
be accurately predicted according to external characteristics in
hamsters of wild-type color. Because the mutation occurs so in-
Volume 37, No. 6 / November 1998
frequently in the normal Syrian hamster population, the significance to production and research colonies is minimal. The defect
might not even be noticed unless frequent necropsies are performed on retired breeders or culled animals.
In summary, aplasia of a uterine horn in Syrian hamsters appears to be a rare mutation that occurs during embryologic
development of the reproductive system. Piebald hamsters have a
high frequency of this aplasia; therefore this abnormality has serious implications in breeding hamsters with this coat color. In
hamsters with wild-type color, uterine horn aplasia does not seem
to affect the reproductive performance of breeding colonies.
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