Uterine bacterial contamination compromises uterine functions. Initially, the uterus is contaminated with a wide range of bacteria, but this is not consistently associated with uterine disease. Involution of the genital tract after parturition helps reduce uterine infection. In normal cattle the cervix opens after 1 week. Discharge of lochia persists until 15to 20 days post-partum. The size of uterine horns diminishes rapidly to 3-4 cm by a month post-partum, but uterine involution continues for a further period of 10-20 days post-partum. During the course of uterine involution, the uterus produces ProstaglandinF2á in large quantities which enhances uterine immune functions besides increasing uterine motility to help the uterus resolve uterine infections. Hence, the development of uterine disease depends on the immune response of the animal as well as the species of bacteria and their number. It is not unusual to find bacteria from uterine cultures upto two weeks post-partum and in most cases bacterial elimination is completed by about 5 weeks. Persistence of pathogenic micro-organisms in the uterus leads to uterine disease which is a key cause of infertility in cows and buffaloes postpartum. Presence of pathogenic bacterial infection leads to uterine inflammation, endometrial histological lesions, delay in uterine involution and early embryonic death. Uterine infections or bacterial products also prevent follicular development and ovulation by suppression of LH release. Thus persistence of uterine infections will ultimately increase the length of occurrence of first postpartum estrus and hence increase the interval from parturition to conception (service period). Culling of animals not returning to heat postpartum or exhibiting poor conception rates due to uterine disease is not uncommon. It is therefore imperative to ensure that animals suffering from uterine infections are rapidly treated thus allowing the normal process of involution to be completed which is very essential for the next breeding period to commence.
Several terminologies were coined to uterine infections. It is important to delineate the differences among them. Puerperal mastitis can be defined as a condition occurring early postpartum (within 3 weeks) wherein the uterus becomes abnormally large with a foetid watery brown discharge and the animal suffers from fever, produces less milk and is also associated with a sluggish behavior. An animal that is not systemically ill, but has an enlarged uterus and shows a purulent vaginal discharge within 21 days post-partum is classified as a clinical metritis case. Clinical endometritis is characterized by the presence of purulent (> 50% pus) uterine discharge detectable in the vagina 21 days or more after parturition, or muco-purulent (approximately 50% pus, 50% mucus) discharge detectable in the vaginal after 26 days post-partum. In the absence of clinical endometritis, a cow with subclinical endometritis is defined by >18% neutrophils in uterine cytology samples collected 21-33 days postpartum, or 10% neutrophils at 34 to 47 days. The consequences of endometritis on subsequent fertility are manifold as evident by the significant increase in the service period. It affects on fertility by two ways. As a short term impact, there is extension of calving to conception interval which varies from 12 to 31 days as reported by different workers. Also associated is an increase in the number of services required per conception. Endometritis can cause irreversible changes in the genital tract in long term resulting permanent impairment of fertility. This factor causes higher culling rates with increased replacement costs and loss of freedom to cull for other factors such as low production resulting in higher culling of genetically superior animals. Culling rates from an average of 5 % for the organized herd in general to around 20 % have been recorded due to animals suffering from metritis and endometritis. Although endometritis is often a self limiting disease with recovery occurring after subsequent estrous cycles, early diagnosis and treatment is recommended to avoid exaggeration of the condition leading to adverse effects on future fertility of the animal. Among various methods of diagnosis, rectal palpation of the uterus is probably the most commonly employed method, but it may be the most insensitive and non-specific method available. Examination of the vagina with a speculum, culture of uterine fluids and evaluation of uterine biopsies are the techniques available for diagnosing uterine infections. Among recent techniques available for diagnosis are peripheral blood haptoglobins, serum amyloid-A and increased enzymatic activity of alkaline phosphatase in uterine flushing of buffaloes and by ultrasonography. Most important predisposing factors for postpartum endometritis are dystocia, retained foetal membranes, unsanitary calving condition and ketosis. Ninety five percent buffaloes suffer from uterine infection after dystocia. Eighty seven percent buffaloes having prolapse of genitalia have been reported to suffer uterine infections. It has been reported that 64 % animals with retained fetal membranes developed endometritis. Physical damage caused to the endometrium by manual removal of the fetal membranes may be a predisposing factor for chronic endometritis. Endometritis, unlike metritis does not affect the general health of the animal, although it does have a profound effect on fertility.
Pyometra is defined as the accumulation of purulent material within the lumen of uterus in the presence of a persistent corpus luteum and a closed cervix. Progesterone plays a permissive role in the onset of pyometra, which usually develops coincidentally with luteal function during the postpartum period. It is generally believed that potentially pathogenic bacteria enter the uterus during or after calving. Cows with assisted births and cows in which retained fetal membranes are manually removed are the causes of contamination. In pyometra cases the introduced bacteria reside in the uterus without apparently proliferating into infection until progesterone production either from the developing corpus luteum or adrenals increases and suppresses uterine immune functions. The bacteria are then able to proliferate and produce the signs of infection. Pyometra usually persists until luteolysis, when the immunosuppressive progesterone block is removed and the uterine immune defenses are strong enough to resolve the infection. The annual incidences of uterine infections in postpartum animals range from 10 to 50% in dairy cattle and 20 to 75 % in dairy buffaloes. These are however, rough estimates. The real incidence of uterine infections in dairy animals is not known because detection and diagnosis are often inaccurate and most postpartum animals are not evaluated for signs of uterine infections. Also, uterine infections are not considered contagious such as in the case of brucellosis thus reporting of uterine infections is not considered absolutely essential. No single therapy can guarantee absolute success in treatment of uterine infections.
However, our current day knowledge has yielded a hypothesis that administration of prostaglandin F2á and possibly other eicosanoids such as leukotriene B4 (LTB4) can enhance uterine immune defenses and mitigate the immunosuppressive effects of progesterone. Intramuscular injection of prostaglandin F2á is therefore an efficacious treatment for uterine infections principally in pyometra cases although its efficacy in treatment of other cases of uterine infections is inconsistent. Hence, use of intrauterine antimicrobials (antibiotics) is recommended. However, genuine concerns on the long term effects of antibiotic use and their potential for creating antibiotic resistant strains of bacteria have focused research on developing non-antibiotic methods for enhancing host immunity and preventing or resolving uterine infections.