Theriogenology and Veterinary Reproduction Flashcards

A mare presents with a 60-day pregnancy loss confirmed by ultrasound. Histopathology of the placenta reveals necrotizing placentitis with intranuclear inclusion bodies in trophoblast cells. Which pathogen is most likely responsible, and what is the characteristic lesion pattern?

Answer: Equine herpesvirus-1 (EHV-1); focal necrotizing vasculitis with endothelial intranuclear inclusions

EHV-1 causes early embryonic and fetal loss through necrotizing vasculitis. The hallmark is intranuclear inclusion bodies (Cowdry type A) within endothelial cells and trophoblasts, along with focal necrotizing hepatitis in the fetus. EVA causes arteritis without inclusions; Leptospira causes cervical star placentitis without inclusions; nocardioform placentitis produces characteristic mucoid exudate with filamentous bacteria.

During AI in a dairy herd, a bull's frozen semen shows 65% post-thaw progressive motility and normal morphology, yet conception rates remain below 40% after multiple inseminations. Sperm chromatin structure assay (SCSA) reveals a DNA fragmentation index (DFI) of 28%. Which statement best explains this discrepancy and the clinical implication?

Answer: A DFI >25% indicates high sperm DNA damage that impairs embryo development past the maternal-to-embryonic genome transition, despite normal motility

A DFI >25% on SCSA is associated with significantly reduced fertility in cattle despite normal conventional semen parameters. DNA-damaged sperm can fertilize oocytes but embryos fail at or around the maternal-to-embryonic genome activation (MET) — occurring at the 8–16 cell stage in cattle — resulting in early embryonic death. This explains normal motility with poor field fertility. DFI does not impair capacitation or zona penetration directly.

A 4-year-old intact male ferret presents with bilateral symmetric alopecia, muscle wasting, and a palpable abdominal mass. Testosterone levels are markedly elevated. Testicular histology shows large, vacuolated Sertoli cells with disorganized tubular architecture and intratubular calcifications. What is the most likely diagnosis and the pathophysiologic mechanism of the alopecia?

Answer: Sertoli cell tumor; hyperestrogenism from estrogen secretion by neoplastic Sertoli cells causing follicular arrest

Sertoli cell tumors in ferrets (and dogs) frequently produce estrogen, leading to hyperestrogenism. Despite elevated testosterone (which may be co-secreted), the neoplastic Sertoli cells' estrogen production causes bilateral symmetric alopecia by inducing follicular arrest in telogen. Bone marrow suppression (aplastic anemia, thrombocytopenia) is another life-threatening sequela. Vacuolated Sertoli cells with disorganized tubules and calcifications are hallmarks of this tumor type.

In bovine embryo transfer, a donor cow is superovulated with FSH and synchronized with a CIDR + PGF2α protocol. At flush on day 7 post-AI, only 2 transferable embryos and 8 unfertilized ova are recovered. Progesterone levels at flush are 4.2 ng/mL (adequate). Which factor most likely explains the high proportion of unfertilized ova?

Answer: Premature LH surge during FSH treatment causing asynchronous ovulation and oocytes aged beyond the fertile window at AI

In superstimulated donors, endogenous estradiol from multiple large follicles can trigger a premature LH surge before the scheduled AI. This causes some follicles to ovulate and release oocytes that age beyond their fertile window before sperm arrives, resulting in unfertilized ova at flush. This is a major cause of poor embryo yield despite apparent synchrony. The CIDR helps suppress premature surges but is not always fully effective in heavy responders. Polyspermy from zona failure is rare; progesterone was adequate ruling out luteolysis.

A bitch is presented for suspected primary uterine inertia at term. Whelping has not initiated despite confirmed fetal maturity. Serum progesterone is 1.8 ng/mL (baseline <2 ng/mL indicates luteolysis). Calcium gluconate administration fails to stimulate effective contractions. What is the most appropriate next step, and why would oxytocin alone be contraindicated at this point?

Answer: Proceed to cesarean section; oxytocin requires functional myometrial calcium-calmodulin activation, which cannot occur if primary myometrial receptor defects are present, making oxytocin ineffective in true primary inertia

True primary uterine inertia reflects intrinsic myometrial failure unresponsive to normal stimuli. While progesterone withdrawal confirms luteolysis and oxytocin receptors should theoretically be upregulated, a myometrium that fails to respond to calcium (the final common effector of contraction via calmodulin-myosin light chain kinase) will also fail to respond to oxytocin, which works upstream through IP3/DAG-mediated calcium release. Administering oxytocin as an IV bolus risks uterine tetany and fetal asphyxia without producing productive labor. Cesarean section is indicated. Dexamethasone is inappropriate at term; manual extraction without surgical access is traumatic.

A stallion has poor libido and repeated failure to achieve ejaculation during breeding despite physical capability. Ejaculatory dysfunction is confirmed. Rectal examination reveals firm, painful seminal vesicles. Semen culture from the urethral fossa grows a Gram-negative rod. Which diagnosis best fits, and which pharmacologic intervention specifically targets ejaculatory dysfunction in this setting?

Answer: Seminal vesiculitis (Pseudomonas aeruginosa); imipramine combined with xylazine to facilitate ejaculation by enhancing sympathetic emission while reducing pain-mediated inhibition

Seminal vesiculitis in stallions — often caused by Pseudomonas aeruginosa or Klebsiella — causes pain during ejaculation, leading to inhibited or incomplete ejaculation. Imipramine (a tricyclic antidepressant) facilitates ejaculation by enhancing sympathetic nervous system tone (norepinephrine reuptake inhibition → increased smooth muscle contraction during emission phase). Xylazine (alpha-2 agonist) provides analgesia and sedation, reducing the aversive pain response. This combination is a validated pharmacologic approach for ejaculatory dysfunction in stallions with vesiculitis. Prostaglandin E2, bethanechol, and corticosteroids do not address this specific combination of infection-induced pain and sympathetic ejaculatory failure.