PROFESSIONAL VERSION

Vulvitis and Vaginitis in Large Animals

ByFabio Lima, DVM, MS, PhD, DACT, University of California, Davis
Reviewed ByAngel Abuelo, DVM, PhD, DABVP, DECBHM, FHEA, MRCVS, Michigan State University, College of Veterinary Medicine
Reviewed/Revised Modified Apr 2026
v3292311

Vulvitis and vaginitis refer to inflammation of the vulva and vaginal mucosa, respectively. Lesions can include edema, hyperemia, erosions, ulceration, necrosis, pustules, or granulomatous changes of the vulva, vestibule, and vagina. Traumatic or irritant causes must be distinguished from infectious causes to treat and prevent vulvitis and vaginitis appropriately.

Vulvitis and vaginitis in livestock comprise a heterogeneous group of inflammatory conditions affecting the external and lower portions of the female reproductive tract:

  • Vulvitis refers to inflammation of the vulva, the external opening of the female reproductive tract.

  • Vaginitis describes inflammation of the vaginal mucosa extending from the cervix to the vestibule.

  • Vestibulitis is inflammation localized to the vestibule, the anatomical region between the vulva and the vagina.

  • Granular venereal disease is a condition most commonly recognized in cattle and characterized by hyperplasia of lymphoid follicles within the vestibular mucosa, producing a distinctive granular or cobblestone appearance.

  • Coital exanthema is an acute venereal viral disease characterized by papules, pustules, and ulcers of the external genitalia, most commonly associated with equine herpesvirus 3.

These disorders range from mild, self-limiting irritation to severe traumatic or infectious processes that compromise animal welfare, reproductive performance, and, in some cases, survival. Lesions can include edema, hyperemia, erosions, ulceration, necrosis, pustules, and granulomatous changes of the vulva, vestibule, and vagina.

Although many cases result in only transient decreases in fertility, accurate etiological diagnosis is essential to guide appropriate treatment, prevent complications, and limit transmission of contagious agents within breeding populations. Clinically, a fundamental distinction must be made between traumatic or irritant causes and infectious etiologies. This distinction informs decisions regarding antimicrobial therapy, surgical intervention, breeding management, and biosecurity.

Traumatic Causes of Vulvitis and Vaginitis in Large Animals

Contusion and hematoma of the vagina caused by trauma during parturition is the most common cause of noninfectious inflammation of the lower reproductive tract. It occurs after parturition in all species but especially in mares and sows. Clinically, hematomas present as large, fluctuant swellings involving the vaginal wall or vulvar lips.

Small, nonexpanding hematomas are best managed conservatively and allowed to resolve spontaneously. Large hematomas should not be incised during the acute phase because premature drainage often results in renewed, uncontrolled hemorrhage. Surgical intervention, if required, is best delayed for 7–10 days to allow the clot to organize.

Occasionally, vaginal hematomas in sows rupture and cause serious hemorrhage. In cases of acute rupture and hemorrhage in sows, ligation of the labial branch of the internal pudendal artery may be necessary to achieve hemostasis.

Necrotic vaginitis, vestibulitis, and vulvitis can follow dystocia in all species. Onset of clinical signs, including an arched back, elevated tail, anorexia, straining and dysuria, vulvar and perivulvar swelling, and sometimes a foul-smelling serous vaginal discharge, occurs within 1–4 days of parturition and can persist for 2–4 weeks. In most cases, only medical treatment is needed. In many cases, antimicrobial prophylaxis is indicated because clostridial or other organisms can proliferate in the affected tissues, resulting in tetanus, blackleg, or other forms of clostridial myositis. Potential sequelae of necrotic vaginitis include perivaginal abscessation, transvaginal adhesions and permanent vaginal strictures.

Vestibular lymphocytic follicles, also referred to as granular venereal disease, granular vulvitis, or granular vulvovaginitis, occur in cows and are characterized by hyperemia and hyperplasia of the lymphoid nodules of the vestibular mucosa. These lesions do not constitute a specific disease; rather, they indicate irritation of the vestibular mucosa. They can be reproduced experimentally by means of topical application of Ureaplasma urealyticum or Mycoplasma spp in goats and cattle.

Infectious Causes of Vulvitis and Vaginitis in Large Animals

Infectious pustular vulvovaginitis of cows is caused by bovine herpesvirus 1 (BHV-1) and is transmitted via natural breeding, nasogenital contact, or insect vectors such as flies. Affected animals exhibit sudden onset of dysuria, frequent tail switching, restlessness, and refusal to breed.

Lesions progress sequentially from vesicles to pustules and ulcers. The presence of small white pustules measuring 1–2 mm on the vestibular mucosa is considered characteristic. Transmission occurs through coitus, nose‑to‑vulva contact, or contaminated obstetrical equipment.

Infectious pustular vulvovaginitis is typically self-limiting, with spontaneous recovery occurring within 10–14 days. Breeding should be discontinued during the active phase to limit spread. As with other herpesviruses, latency is established in neural ganglia, and recrudescence may occur during periods of stress.

Histological lesions consist of necrosis of vestibular and vaginal epithelium, with intranuclear inclusion bodies typical of herpesvirus infection. When the virus is transmitted in the semen, infected bulls can have similar lesions of the penis and prepuce. Intrauterine inoculation of the virus produces necrotizing endometritis and cervicitis.

A disease characterized by vaginitis in cows and epididymitis in bulls occurs sporadically in eastern and southern Africa, where it is referred to as epivag. It is transmitted via natural breeding. In the early stages of infection, cows have severe vaginitis characterized by inflamed, reddish mucosa without ulcers, erosions, or vesicular lesions. A thick, creamy, white to yellow vaginal discharge develops. The infection can spread to the uterus and uterine tubes, and salpingitis and fimbrial adhesions frequently result in permanent infertility. Although epivag has been transmitted experimentally by transfer of exudate from affected animals, the cause is unknown.

Necrotic vulvitis, manifesting as a severe granulomatous and necrotic lesion centered on the ventral commissure of the vulva of cows, sometimes occurs as a disease outbreak. It is associated with several pathogens, particularly the bacterium Porphyromonas levii.

Catarrhal bovine vaginitis has been reported in many countries. Although enteroviruses have been associated with this condition, the cause remains unknown. In areas of the world where bovine tuberculosis remains endemic, affected cows may have primary vaginal lesions resulting from service by infected bulls with genital lesions; however, uterine disease and cervicitis can also occur. In goats, caprine herpesvirus 1 (CapHV-1) may cause ulcerative vulvitis characterized by edema, erosions, and crust formation. The condition can be distinguished clinically from contagious ecthyma by the absence of proliferative, papillomatous scabs typical of parapoxvirus infection.

Ulcerative vulvitis and posthitis, commonly referred to as pizzle rot, occur primarily in sheep and goats and are associated with Corynebacterium renale in conjunction with high‑protein diets. C renale produces urease, which hydrolyzes urinary urea into ammonia. Elevated ammonia concentrations cause severe chemical irritation and necrosis of the vulvar and preputial skin. Management requires immediate dietary modification to reduce protein intake, along with shearing of wool around the vulva to prevent urine retention. Systemic penicillin therapy and topical antimicrobial sprays are commonly employed to control secondary bacterial infection. See also Enzootic Posthitis and Vulvitis and Mange in sheep and goats

Equine coital exanthema is caused by equine herpesvirus 3 (EHV-3). It is an acute disease that occurs after breeding with an infected stallion or via artificial insemination. Although mares rarely show systemic signs, red papules appear in the vaginal and vestibular mucosae 2–10 days after infection. Lesions may extend to the perivulvar skin. The lesions progress rapidly to pustules, then ulcerate, and finally heal, leaving depigmented scars. Stallions show similar lesions on the penis and prepuce. The disease causes discomfort and might prevent breeding but does not specifically impair fertility.

Dourine (covering sickness) is a chronic venereal disease of horses and other equids caused by the parasite Trypanosoma equiperdum. Early clinical signs include edematous swelling of the vulva with secondary vulvovaginitis.

Coital injuries in cattle and horses can occur when large adult bulls or stallions breed with heifers or fillies or relatively small cows or mares, or as a result of improper or forceful manipulation. Minor mucosal abrasions generally heal without intervention. In contrast, full-thickness vaginal tears, particularly those involving the rectovaginal shelf, may result in rectovaginal fistula formation and require surgical reconstruction once acute inflammation has subsided.

Injuries of the vulva and vagina can also be caused by horned cattle.

Key Points

  • Distinguishing traumatic/irritant causes of vulvitis and vaginitis from infectious ones is essential to determine whether antimicrobial therapy, surgical intervention, breeding restriction, or biosecurity measures are warranted.

  • Viral vulvovaginitis typically resolves spontaneously within 2–4 weeks, but sexual rest during the active phase of viral infection prevents herd-level spread and prevents stress-induced recrudescence of latent herpesvirus.

  • While most vulvovaginitides cause only transient reductions in fertility, severe traumatic injuries and chronic bacterial or parasitic conditions can lead to permanent structural damage if not promptly and appropriately managed.

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