POSTPARTUM UTERINE INFECTION IN CATTLE

REVIEW

INTRODUCTION
Postpartum metritis is one of the most economically important disorders in cattle. Prolonged intercalving intervals leads to involuntary culling. Lowered conception rates, increased calving intervals ,Key cause of infertility.

Toxic puerperal metritis

Also called acute septic metritis. Increase in rectal temperature. Depression, anorexia, Fetid watery vulval discharges. Life-threatening if not attended. Metritis involves endometrium, glandular tissue and muscular layer. Endometritis no muscular layer involvemet.

Prevalence of Uterine infections

Varies considerably among studies. Depends on Postpartum period at which infection seen The parity of the cow. General characteristics of the cow. The herd management practice. Prevalence rate is much higher in buffaloes than in cow in India due to- poor hygiene, vaginal stimulation for milk let down ( Phooka ) and wallowing.

Pathogenesis
Uterus of over 90% off all cows become contaminated with range of bacteria not always associated with clinical disease. Infection Adherence of pathogenic organisms to mucosa. Colonization and penetration of epithelium. Release of bacterial toxins leading to establishment of uterine disease.

Pathogenesis Contd..
The development of uterine disease depends on Immune response of the cow. Species and number of bacteria capable of overwhelming the uterine defense mechanism. Mild to sever form occurs in 90% of postpartum cows during 2nd to 4th postpartum weeks.

Contd..
Both Gm +ve and Gm ve aerobes and anaerobes can be isolated from early postpartum uterus. A normal PP uterus resolve infection by Rapid involution of the uterus and cervix. Discharge of uterine content. Mobilization of natural host defenses viz., mucus, antibodies and phagocytic cells.

Host Factors affecting infection

Cows with certain periparturent problems have reduced ability to control uterine infections. Excess stretching of uterus as in hydrops allantois. Traumatization of genital tissues during dystocia. Metabolic disorders, unhygienic calving surroundings and rude management practices. Uterine lochia will be retained beyond normal period act as media for bacterial multiplication.

Non specific bacteria causing uterine infection

Organisms involved are Common livestock environmental contaminants. So the uterine infections are non specific. Archanobacterium pyogenes and Escherichia coli either alone or in combination with Fusobacterium necrophorum and Bacteroides spp. F.necrophorum produce leukotoxin and Bacteroides spp. Produce substances that prevent bacterial phogocytosis. A. pyogenes produce a growth factor for F.necrophorum.

Uterine defense mechanism

Anatomically by the simple or pseudo stratified Columnar epithelium on endometrium. Chemically by mucus secretions from endometrial glands. Immunologically by action of polymorphonuclear inflammatory cells and humoral antibodies.

Uterine defense mechanism contd..

Major anatomical barriers for uterus are The vulva Efficient in preventing faecal contamination of the tubular genitalia. The vestibule guarded by muscular sphincter. The cervix - with series of mucosal lined collagenous rings. Cervical- vaginal mucous can function as physical barrier.

 Estradiol and Progesterone have both opposing and complementary effects on the female genital tract. Estradiol stimulate epethelization of vaginal and endometrial gland . vascularization of the endometrium. Increase cervical and oviductal secretions. Progesterone Endometrial gland differentiation. Enhance uterine gland secretion, reduce cervical mucous production and prevent uterine contractility. Counter influence to estradiol in immune responses.

Role of reproductive Hormones

Role of Estradiol

Maximum Estradiol influence for about one day ( immediately preceding standing estrous) Change in the number of WBC causing neutrophelia and shift to left. Increase blood supply to uterus. Increase quantity and nature of vaginal mucous, which flush out the bacterial contaminats.

Role of estradiol contd..

Uterine production of PGF2 and endometrial leukortiene B4. Prostaglandin F enhance neutrophil chaemotaxis and phagocytic ability. leukotriene B4 enhances chaemotaxis, random migration and ADCC. Immune function of the uterus is found to be up regulated. Uterus is able to prevent infection from developing.

Role of Progesterone
Antagonistic effect to estradiol. Immune function is down regulated during luteal phase. Hence, uterus is capable of supporting a conceptus ( fetal allograft ). These two hormones together orchestrate uterine immune function in the favour of the animal.

Factors affecting uterine defense mechanism

1. Status of the uterus During the periparturent period physiological changes will depress the defense mechanism. Polymorphonuclear killing mechanism is impaired. Uterus is more prone to puerperal infection.

Factors affecting uterine defense mechanism

2. Uterine mucosal immune system Exceptional among mucosal tissue as it got the influence of ovarian steroidal hormones on both humoral and CMI. Influenced by the stage of estrous cycle at which infection takes place. Nature of the antigen, route of sensitization and use of adjuvants will affect.

Factors affecting uterine defense mechanism

3. Therapeutic strategies adopted to treat postpartum disorders. Manual removal of fetal membranes may inhibit uterine leukocyte phagocytic activity. Intrauterine administration of most anitseptics and disinfectants will give the same effect.

Factors affecting uterine defense mechanism

4. Uterine secretion of immunomodulators Release of interleukin by uterine epithelium results in increased secretion of PGE2 & PGF2. Secretion of lactofeffin, isozymes and complemets along with Ig A and Ig G which will protect against potential pathogens. IG A synthesized locally in bovine uterus and Ig G derived from endometrium and peripheral circulations.

Factors affecting uterine defense mechanism

5. Cytokines Interleukin- I is predominantly macrophage derived protein that modulates host defense to uterine infections. Interleukin- 2 is secreted by a subset of T cells and large granular lymphocytes after stimulation with antigen. Most important T- lymphocytes in uterine immunity is type 2, which stimulate a humoral response by releasing cytokines that stimulates B cells to proliferate, differentiate and secrete antigen reaction antibodies.

Diagnosis
1. Clinical signs : Clinical sings vary with the virulence of the causative agent and presence of the factor that predisposes the disease. Abnormal white or whitish yellow mucopurulent malodorous uterine discharges. When complicated by septicemia, toxemia, milk yield is reduced with fever, depression and anorexia. The volume of discharge is variable.

Diagnosis
2. Rectal palpation. 3. Vaginal examination. 4. Bacterial culture. A uterine swab is most accurate means of obtaining the sample. True uterine culture can be taken from the uterus without contamination by extraneous bacteria. 5. Endometrial biopsy. 6. Endometrial cytological examination. 7. Ultrasound.

TREATMENT

Success in the treatment of uterine infection depends upon : Evacuation of the uterine fluids. Susceptibility of the infectious agent to the drug used. Concentration and number of times the drug used. Exposure of entire endometrium to the drug.

TREATMENT
1. Antibiotics : Broad spectrum antibiotic that is active in the presence of organic debris is indiated. Antibiotic should be present in sufficient concentration at the site of infection. The preparation should not inhibit the normal defense mechanism and should be well tolerated.

TREATMENT
2. Hormones : Effective use needs knowledge of both normal reproductive endocrinology and therapeutic properties of the available hormonal preparations. The decrease in progesterone and increase in estrogen concentration associated with luteolysis and follicular growth results in maximal resistance of the uterus to bacterial infections.

Estradiol has been recommended for stimulation of myometrial contraction, phagocytosis and mucus production.