LIBIDO

Mounting and thrusting behavior, sniffing the urogenital region, and exhibiting the flehman response are common behaviors of adult bucks. As in sheep, during the nonbreeding season (in the Northern Hemisphere, autumn is the breeding season), it may be difficult to obtain an ejaculate with an artificial vagina or the buck may be very slow to serve a doe in heat.¹ Out of the breeding season the buck may rest his head on the doe’s hindquarters but fail to align himself with the longitudinal axis of the doe.² With the onset of the breeding season, bucks properly align, and mounting, thrusting, and ejaculation occur.

One of the most common reasons for a buck to come to the end of his breeding career is arthritis. Painful hips, stifles, or hocks cause reluctance or inability to mount. If several bucks are run together with does, a dominant but arthritic male may prevent breeding by another fertile buck. Lame bucks also tend to lose body condition because they do not get up to eat as much as they should. The cause of lameness may be trauma (degenerative) or infectious. Bucks with degenerative arthritis, which is often caused by congenitally poor conformation, or with other anatomic defects, should not be used for breeding.

Infectious causes of arthritis may result from caprine arthritis encephalitis (CAE) virus. With the CAE virus, the clinical disease is more common in some families than in others, suggesting an inherited susceptibility to effects of the virus. Research has shown that clinical CAE is associated with certain histocompatibility antigens, again suggesting a hereditary component.³ Transmission of CAE infection by breeding appears to occur infrequently, if at all.⁴ Detection of antibodies against CAE virus at the Washington Animal Disease Diagnostic Laboratory is performed with the use of a kinetic enzyme-linked immunosorbent assay. The antigen used in this assay is prepared from purified CAE virus with a technique designed to enhance the dominant antigens against which goats infected with CAE develop antibodies.⁵

INTERSEXES

Abnormal sexual differentiation leading to the intersex condition is relatively common in goats. It is more prevalent in dairy goats of the Saanen, Toggenburg, and Alpine breeds than in any other breeds of animals.⁶ Intersexes exhibit phenotypic variations ranging from nearly normal females to nearly normal males. Generally they are female-like at birth, but as they reach the age of sexual maturity, they become larger than normal females, with a masculine head and erect hair on their neck. They exhibit small teats and a bulbous clitoris or a shortened penis. At puberty the clitoris becomes enlarged enough to be externally visible.⁷

The intersex acts like a female at birth but later, usually at puberty, starts to butt like a buck and become aggressive toward other goats and people. These animals also develop the odor characteristic of bucks. A majority of intersexes show pronounced male libido in the presence of a doe. Some of the more female-like intersexes lactate.⁶ Intersexes are named with reference to the gonads they carry. The term “true hermaphrodite” is used to distinguish an animal that carries both gonads from those that carry either one or the other type of gonads (pseudohermaphrodites). Male pseudohermaphrodites have testes and female pseudohermaphrodites have ovaries. Most intersexes, however, have testes. Usually the testes are abdominal or they may be partially or totally descended (Fig. 66-1). The principal hormone produced by the gonads in caprine intersexes is usually testosterone.⁶ Intersexes are frequently seen in polled dairy goats. The most accepted hypothesis is that hermaphroditism and horned traits are controlled by recessive genes and that these two loci are close to each other on the same chromosome (linked). The polled condition is the result of a mutation at the horn locus. The polled trait (P) is dominant to the horned trait (p) and appears together with hermaphroditism (h) in PPhh or Pphh goats because the two loci are linked.⁸ Therefore, intersexes will be seen mainly among polled goats and only rarely among horned animals (pp) because of the occasional crossing over between the two loci, which results in a pphh genotype. Cytogenetic evaluations of caprine intersexes clearly show that most polled intersexes are karyotypically female (XX) and the breeding histories of the parents indicate that intersexes are homozygous for the polled trait.⁹ The presence of male gonads in these homozygous polled (PP) intersexes of XX makeup suggests that they are sex-reversed females. In the female caprine fetus, which is homozygous for the polled gene, two doses of the P gene divert the process of sexual differentiation toward the male despite the presence of two X chromosomes.¹⁰

Fig. 66-1 Hermaphrodite goat, on its dorsum, showing testes, vulva, and enlarged clitoris.

Intersex goats have been found to have the H-Y antigen. The H-Y antigen is a male-specific transplantation antigen and is reportedly lower in intersexes than in normal XY males.¹¹ The suggestion has been made that animals of the same genotype and sex may differ in the density of H-Y antigen on their cell surface, which might explain the variability in primary sex determination among goats.

The gene for the polled trait has an impact on the reproduction performance of bucks. Bucks that are homozygous for the polled gene tend to become sterile. Although the testes of these bucks are of normal size and the seminiferous tubules display active spermatogenesis, there are no sperm detectable in the ejaculates because of blockage in the caput epididymidis. These trapped sperm form hard masses of variable size that are palpable near the head of the epididymis. In older bucks, the seminiferous tubules are closed, causing degeneration or rupture, releasing sperm into the interstitium (extravasation), which often leads to sperm granuloma formation.¹² Thus, the homozygous state for the polled gene is disadvantageous to both sexes. In males, it causes poor differentiation of the duct system, resulting in sterility, and in genetic females it causes gonadal reversal leading to masculinization of the gonads and external genitalia.

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