Repeat Breeding Syndrome in Bovine A bovine (cow/uffalo) which exhibits normal or nearly normal oestrous cycles and has been bred thrice or more consistently but has failed to conceives called a repeat breeder. The incidence of repeat breeding in Indiais reported around 5,5 33.33 %incattle and around 6-30 %in buffaloes. The incidences are more in cattle as compared to buffalo. The incidence of repeat breeding was highest among the dairy animals kept by marginal farmersin rural conditions. Repeat breeding lowers down the reproductive efficiency resulting in increased calving interval, loss of milk production, increased cost of treatment and lowered breeding value incurring heavy economic losses to the dairy producers. The repeat breeding affected by multiple factors including management, nutritional and pathological factors. Causes for Repeat Breeding 1. Anatomical Abnormalities 2. Genitalinfections 3. Hormonal Aberrations 4, Nutritional Factors 5. Managemental Factors 1. Anatomi Includes under-developed/aplasia of genitalia, oviduct and cervix defects, kinked cervix and persistent hymen (observed in heifers ‘which have not calved/ conceived till date). ‘+ Under-developed Genitalia: Small size ovaries leading to below optimal levels of hormones producit estrusintensity and causes silent/ subnormal heat. Abnormalities reduced cyclic activity, ‘+ Aplasia of Genitalia: The concition in which ovaries are developed, ovulation occur but ovumisnot able to reach fertilization site due to aplasia of reproductive tract. ‘+ Ovaro-bursal Adhesions: Condition developed between ovary and ovarian bursa due to mishandling of ovary or infusion of large volume of irritating drugs under pressurein uterus. + Kinked Cervix: It can be due to trauma orlacerations caused during calving or Al followed by infection and fibrosis. ‘+ Reproductive Neoplasms: Presence of tumors interferes normal reproductive performance in several ways. 2. Genital infections + Uterineinfections are major cause of economiclossto the dairy animals. ‘+ Incidences of uterine infections are influenced by calving management, farm hygiene, exposure to pathogenic organisms and otherenvironmental stress factors. + Theuterusis normally protected from bacterial contamination by vulva, vestibular sphincter and cervix. + During and immediately after parturition, these mechanical barriers are breached and uterus is contaminated by a variety of pathogenic and non-pathogenic microorganisms. Most of these bacteria are only transient residents and are promptly eliminated by uterine defence mechanism during the puerperium. In some cases, however pathogens persist in the uterus and produce diseases, ‘+ Use of contaminated instruments for insemination and injudicious use of intrauterine medications may lead to endometritis (inflammation of endometrium). + History of dystocia, uterine torsion, macerated foetus, retention of placenta (ROP), prolapse of uterus/vagina and hydroallantois conditions lead to uterine infectionslike metritis, pyometra, vaginitis and cervicitisetc. ‘+ Thesedisturbed and contaminated environment of uterus disturbed the normal process of activity ofsperm and ovum leading to non or improper fertilization reducing conception rates. Major groups of Uterine Infectious bacteri » Coliform bacteria: €. coli, Proteus p.,Enterobactor so. » Incidental bacteria: Streptococci, Staphylococci, Pasturella and Bacillus spp, » Corynebacteria:C. pyogenes (now called Actinomyces pyogenes) > Gram-negative anaerobic bacteria: Bacteriods, Fusobacterium spp. » Gram-positive anaerobie bacteria: Clostridium perfringens, C.sporagenes and other Clostridium spp. » Protozoa: Trichomonas foetusFy Consequences of Uterine Infections ‘a. Metritis: It is a result of severe inflammation involving all layers of uterus (endometrial mucosa, submucosa, muscularis and serosa) b. Endometritis: Endometritisis characterized by inflammation of endometrium extending no deeper than stratum spongiosum. Clinical endometritis: Mucopurulent uterinedischarge Sub-clinical endomettit lear uterine discharge while white side testis positive & Pyometra: Pyometra is characterized by accumulation of purulent exudates of variable amount within the endometrial cavity, persistence of corpus luteum and sometimesnon-estral conditions. 4. Retained foetal membranes (RFM) is definedasrnon-separation of foetal membranes even after twelve hoursof calving. + Primary retention of placenta: The AFM which resuits from lack of detachment of cotyledons from maternal caruncles is called primary retention of placenta ‘+ Secondary retention of placenta: The RFM which results from mechanical difficulty in expelling already detached foetal membranes(e.g. uterine tony) scalled secondary retention of placenta Other possible factors include—prolapse of uterus/vagina, foetal maceration, foetal mummification, hydramnios, hydroallantois ete Detecting Uterine infection- White Side test Itis.a simple and rapid test which can be used to ascertain the grades of infection under field conditions and thereby restricting ‘the unnecessary and indiseriminate use of drugs. Procedure 1 ml of estrual cervical mucus was heated with equal volume of 5 to 10% sodium hydroxide up to boiling point ‘After cooling the intensity of colour changes are evaluated Grade are given as Fig 1 ~ The change in colour of cervical mucus and Ws Interpretative a= CD 0 Nocolour change Normel ) 1 (Woh yetiow colour | Midinfection +) 2 _{__Yelowcolow | ___— Moderate infection) 3 |___ dark Yetlowcolour Severe Infection ) 4 RedaishYetow |‘ Bleed tinged mucus) Hormonal Aberrations Failure of fertilization and early embryonic death are conditions that occur due to abnormality in hormone functions. They occur due todelayed ovulation, anovulatory heat, failure of fertilized ovum implantation, anoestrus, cystic ovarian degeneration, deficiency of energy, excess of oestrogen, deficiency of progesterone, aged ovum or sperm, poor hygiene at the time of calving and Al, poor management and handling of frozen semen, high ambient temperature and humidity et.Vital hormones for reproduction are ~ GnRH, FSH, LH, Progesterone, Estrogen and PGF., ‘GnRH - Gonadotropin Releasing Hormone The initiator and regulator of reproductive function in animals are (GnRH) gonadotrophin releasing hormone, synthesised and released from specialised neurons located in hypothalamus on the lower aspect of brain. Once released, GnRH binds to specific receptors on the gonadotrophic cells of the anterior pituitary gland resulting in synthesis and release of gonadotrophic hormones Follicle stimulating hormone (FSH) and Luteinising hormone (LH). The release of GnRH Is internally controlled by concentration of progesterone from corpus luteum. In luteal phase, high amount of progesterone decreases GnRH secretion from the hypothalamus ie. it has a negative feedback effect on GnRH. In the follicular phase (in absence of progesterone and in presence of high concentrations of oestrogen from pre-ovulatory follicle) oestrogen intially has 2 negative feedback effect (to promote LH storage] followed by positive feedback effect on GaRH, causing prolonged elevated secretion of the pre-ovulatory surges Of LH and FSH. The external regulation of GnRH is controlled by nutritional status of animal, stress, environment etc. FSHand LH—Responsible for Ovulatory Cycle and Ovulation Fig 2- Hormona {equlation in Bovines. FSH in follicular phase, produce more and more oestrogen from follicles of ovary. Once oestrogen reaches threshold, pre-ovulatory centreis turnedon large number of GnRH neurons respond with fll potential) and release large quantities of LH causing ovulation, FSH and LH release is controlled by GnRH from brain and oestrogen from ovary. FSH acts specially on smal follicles to stimulate their growth, LHacts on the mature dominant follicle to cause inal maturation > subsequent ovulation > formation of corpus luteum => stimulate progesterone secretion from corpusluteum. Estrogen Responsible orheat/ signs of estrus > Targettissue is hypothalamus, reproductive tractand mammary gland Estrogen actson CNS and creates desire for mating in females Responsible for secondary sexcharacters > Reproductive tissue depends upon estrogen for growth, e.g uterus, ovary and mammary gland. Estrogen causesgrowth of duct system of mammary gland » _Estrogenhas negative feedback on tonic center of hypothalamus and positive feedback fect on surge (pre-ovulatory) center to control FSH/LH release Progesterone (P,)~Pregnancymaintaining hormone Progesterone hormone dominates in luteal phase of cycle. It reduces basal GnRH amplitude and frequency, prevents behavioural ‘estrus, stops pre-ovulatory LH surge. if ovum s fertilized then it helps in maintaining the pregnancy. For the first 12 days of the bovine oestrous cycle, progesterone inhibits the formation of oestradiol receptors in the uterus, as well as reducing the frequency of LH pulses from the pituitary (thus restricting follicular oestrogen production). After 12" day, the suppressive action of progesterone is lost under the influence of increasing oestrogen concentrations from growing follicles of ovary. Oxytocin receptors are formed in the uterus. Oxytocin secreted by the corpus luteum, can now act by occupying receptors and stimulating the sectetionof prostaglandin alpha PGF.) from the endometrium, es PGF,,-Luteolysis Fig 3: Bovines Estrous Cycle Prostaglandins (PGF.,) inhibit progesterone production and stimulate further release of oxytocin from posterior pituitary which in a postive cascade system, results in more prostaglandin secretion by the uterus, Subsequently, luteolysis occur due to decrease in progesterone concentration. lysis of CL must occur before cow can enter next follicular phase/nextoestruscycle. Oxytocin originates from corpus luteum and PGF,, from uterine endometrial glands. If fertilization do not occur by 13-14 day of eycle then the prostaglandins are released on 17° day of cycle and luteolsis occurs around 18" day of cycle I the animalis pregnant, thereisno luteolyss. Animal emainsin sustained luteal phase because of high progesterone which will decrease GnRH secretion and pregnancyis maintained. ‘Anomalies of Hormones a) CysticOvarlan Degeneration (COD)- Ovaries are said to be cystic when they contain one or more ud filled structures larger than a mature follicle (>2.5.cmin diameter) called ‘cyst, which persistfor more than 10 days and resutin aberrant reproductive functionEtiology * Deficiency of LH secretion duringthe pre-ovulatorystage. * Ovarian eysts may be due to defect within the ovary. The ability of follicles to respond to pre-ovulatory LH surge is dependent tupon the timely formation of LH receptors onits surface during follicular maturation. ifless number of receptors are present on the follicle, it will esultin ovulatory falureaswellas cysticovary. Predisposing Factors + Age: Incidenceis higherin peaklactations, Generally uncommon in first lactation, + Nutrition: Feeding of high protein diets causes higher incidence ofthe disease. + Season:Incidenceis more in winter than in other seasons. + Stress: Ketosis, dystocia, twin births, REM, milk fever etc. * Postpartum Uterine Infections: Endotoxin produced by micro-organisms in the uterus may trigger the PGF,, release, whic! ‘turn stimulates the secretion of cortisol, The elevated cortisol level suppresses the pre-ovulatory release of LH and leads to the development of cyst. Classification: Ovarian cysts have been classified into two parts. + Anovulatory cyst or pathogenic ovarian cystare Follicular cysts and Lutealeysts. ‘+ Ovulatorycyst or non-pathogenic ovarian cystor eysticcorpora lutea | PerstenceinGvary | persistonthe ovary for 10 daysor more pers fora poerged period Thin and Soft Thick and Partly Luteinsed Progesterone Level Never rises 0.5 ng/ml More than 2.5 ng/ml b) Delayedovulation Thereisdelayin ovulation. So, sperminseminated gets aged and animal become cyclic repeat breeder. Diagnosis ofthe condition is ficult, since it requires sequential rectal palpation of ovaries which might itselFinterfere wit the process of ovulation and may cause prematurerupture. €)_ EarlyEmbryonicDeath ‘When embryonicdeath occursand then the cow comesin heat at normal oestrouscyce length (18-22 days) Causes maybe + External factors ike stress, pain, long transportation, malnutrition, season and climatelike summer. + Maternal factors lke progesterone deficiency, uterine infection, embryonic factors lke chromosomal abnormalities and genetic factors 1. Nutritional factors Deficiency of Vitamins and Minerals causes delayed puberty and lowered body weight of animals and repeat breeder condition. The conception of the animal and sexual maturity is correlative to the body weight. Underweight animals always have less chances of conception. Feeding of high protein dit and deficiency of B-Carotene (Vit. A) may be a contributory factor. Animal shouldbe in positive ‘energy balance, Under-feeding of energy can cause delayed ovulation, anovulatory condition and embryonic death. The concentrate feed must contain 2% mineral mixture. Energy deficiency affects the fertility in two ways. First through GnRH system and the second through metabolic regulators of ovarian function. The circulating concentrations of glucose, insulin and insulin like growth factor 1 (IGF-1) are lower in cows that are in negative energy balance than in fully fed animals. The concentration of non-esterfied fatty acids (NEFA) are higher in negatively energy balanced animals. Allo these alter the gonadotrophin secretion affecting follicle development. Important Mineralsfor Reproduction a) Copper(cu)/Cobalt (co) + Copperas significantrolein maintaining the optimum fertiltyin bovines and enhances FSH, LH and estrogen actity. ‘© Copperisa ital componentin many enzyme systemsas cofactors. Cytochrome oxidase Isa cupro-enzyme necessary for electron transport in mitochondria for energy metabolism of ATP dependent biosynthetic reactions is required in the body for red blood cell production, asitis essential for absorption and transportof iron necessary for hemoglobin synthesis ‘+ Plasma copper concentrations of aborting cows are significantly lower than recently calved cows copper deficiency seems to have close lationship with abortion ncatte. ‘* Copper along with Cobalt deficiency delays onset of puberty, repeat breeding, low conception, early embryonic mortality and Increasesincidence of retention of placenta,b) Iron (Fe) ‘© Iron functions in transport of oxygen to tissues, maintenance of oxidative enzyme system and is concerned with ferritin, formation. ‘* The lower level of serum iron results in anaemia, which in turn affects reproduction adversely in form of repeat breeding, requiring increased number of insemination per conception and occasionally leading to abortion, ‘© Lowerlevel plays ole in conception failure, embryonic death and repeat breeding. ) Zine(2n) © Optimum level ofzincis essential to maintain the activity of FSH and LH and thereby facilitate reproductive performance. ‘+ Zinc play an important role in regulating gene expression, consequently impacting wide variety of functions including cell division, cell growth, hormone production, metabolism, appetite control and immune functions. ‘+ Zinc deficiency may lead to reduction in GnRH secretion by hypothalamus and eventually ead to decreased levels of luteinizing hormone and follicular stimulating hormone and arrest of ovulation ‘= Zinc deficiencies have been associated with abortion, fetal mummification, lower birth weight and prolonged labour. 4) Chromium (cr) ‘© Chromium plays an important role in secretion of pregnancy specific proteins from the uterine endometrium which ishelpful in preventing arly embryonicdeath, ‘= Itexertsa sigificantinfluence on follicular maturation and LH release. ‘+ Its deficiency canlead tolower sperm count and decreased fertility which influences foetal growth and development. ‘© Chromium concentrations also have a positive correlation with energy levelsin animals thus assist reproduction. €) lodine(t) + _Itisnormally present in diet asiodide andis necessary for synthesis of thyroid hormone which regulates energy metabolism. ‘+ Thethyroid glandisinvolvedin stimulation of anterior pituitary gonadotrophin secretion. ‘© Iodine deficiency causes goitre and birth of weak, premature or dead calves, ‘+ Iodine deficiency in herds lead to impaired fertility and an abnormally high abortion, incidences of retained placenta and high postpartum genital infections. ‘© There's significant relation between serum protein bound iodine (PB!) and reproduction. Improved reproductive performance was associated with higher PBIand number of services required as wellas time interval between first breeding and conception, ‘© Anovulatory estrus observed in cows maintained on iodine deficient diet is attributed to the thyroid disorders and pituitary function which was reversed by supplementation of iodine. f) Selenium (se) ‘© Seleniumalong with Vitamin €functionas preventive and chain breaking antioxidant and inactivate peroxidise formed duringcell metabolic process ‘© Insub-clinical selenium deficiency, reproductive performance may be reduced with increased number of services needed per conception, higher incidence of mastitis and retained foetal membranes. (this may be due to impaired functioning of neutrophils inselenium.) ‘+ Incidence of cystic ovaries and metritisis significantly reducedin Selenium treated animals. 2) Manganese (Mn) ‘¢ Manganese play role in synthesis of steroidal hormonesas most of reproductive hormones are steroidalinnnature ‘© Manganese deficiency leads to infertility in cows, congenital limb deformity and poor growth rate in calves. ‘© Incidence with its deficiency can cause estrus suppression, silent estrus, irregular estrous cycle, cystic ovary, poor follicular developments with delayed ovulation, increased embryonic mortality and reduced conception rate ‘© Itsoptimum|evels can lead to shortening of postpartum anoestrus and increased conception ratein dairy cows. Important Vitamins for Reproduction bh) Vitamin-A, ‘©The vitamin A deficient dam is characterized by cornification or keratinization of vaginal epithelium and failure to conceive resulting in reduced ovarian steroidogenesis. ‘© Vitamin Also helpsin follicular growth and ovarian functionality, ‘+ Vitamin-A deficiency is associated with reduced reproductive efficiency and result in deleterious effects on pituitary testicular and ovarian functions.1) Vitamin. E Vitamin €actsasalipid-soluble antioxidant within membranes, preventing chain reactive oxidation, Its deficiency results in degeneration of germinal epithelium, fetal death or resorption, degenerative changes in uterus, degeneration of embryo vascular system and anaemia of embryoetc. Animals deficient in Selenium and Vitamin € have suppressed defence against infectious diseases. Leukocytes from animals deficientin Selenium are low in glutathione peroxidase activity and have decreased microbicidal activity. i) Vitamin-D ‘+ Specific effects of Vitamin O deficiency on reproductive function is limited. However, its role in calcium metabolism affects reproduction too, ‘+ Iinfluences time of frst postpartum estrus and calving interval. + Reduced blood calcium may delays uterine involution and increases incidence of dystocia, retained placenta and prolapsed uterus. + Gonadotropin-releasing hormone stimulation of LH release from pituitary cells involves Ca-dependent mechanism, No cAMP Is Involved and LH isnot releasedin absence of calcium or inthe presence of calcium blockingagents, ky Vitamin-H ‘+ Ithasimportant role in production of energy and there by maintain optimum release of hormones. ‘+ Estrus cyclestarts only when sufficient energy isavailabe. + Deficiency of Vitamin- H may be teratogenic to developing foetus. 2, Management Factors Despite having clear cervico-vaginal mucus, anatomically normal genitalia and normal hormonal profiles, several animals become repeater due to bad management. Itinvolves a. Stress oflong distance transportation in high temperature b. Failure todetectheat at propertime ©. Impropersemenstorage 4d. Improper timings of inseminations fe. Faulty Altechniques Treatment 1, Anatomical Abnormalities ‘The treatment of repeat breeders for anatomical reasons is difficult, However, itis seen in various studies that conception rate was achieved in dairy animals suffering from cervical fibrosis or partial obstructions through natural service or artifical insemination (Al) ‘with increased concentration of spermatozoa per straw. 2. Uterineinfections Treatment of Uterine Infection may involve one or allsteps mentioned below, a) Lavaging b)Antibacterial Treatment ©) PGF, Therapy ‘© Lavage of the uterine lumen with large volumes of warm saline (40° - 45° C [104° - 118° Fl) removes accumulated fluid and debris, Uterine lavage has been used as an adjunct to antibiotic, antisepticand plasma treatment. ‘+ Dilute solutions of povidone-iodine (one part povidone-iodine stock solution to 10 to 20 parts saline) have been suggested as being useful in treating fungal endometritis. Povidone-iodine is generally available as a 10% solution with 1% free iodine (10,000 ppm of free iodine), so a dilution of 20: 1 saline-to- povidone iodine yields a flush with 500 ppm offfreeiodine, which should be bactericidal b) Antibacterial Treatment ‘+ Fortreating uterine infectionsan antibacterial must be given against the primary uterine pathogens. ‘+ Intrauterine antibacterial with broad spectrum of activity are preferred due to the direct effect atthe site of infection and minimising the withdrawal periods. ‘+ Treatment of metritis should be directed toward controlling septicaemia. Large doses of broad-spectrum systemic antibiotics are indicated, along with luids and other supportive therapy. ©) PGF, Therapy ‘+ PGF,, therapy may be sufficient in mild cases of endometrtis or used in combination with intrauterine or systemic therapy.+ In cases of chronic bovine endometritis, treatment with PGF., for one or two times at 10 to 14-day intervals decreases the number of days open. + PGF, is the treatment of choice for bovine pyometra. Treatment with PGF,, is followed in 3- 6 days by uterine evacuation in 85% to 90% of treated cows. Response to PGF, treatment may be raised with a second injection of PGF in 6to12hours. After endometrial lesions are allowed to heal for 30 days, fertility isrestoredin most patients. For Intra-Uterine Application (flor: T21.U. 30-60 mi per cow Intea-uterine (Ciprofloxacin 25 mg and Tinidazole 30 mg/ml) for 35 days route Lenovo IU. 30-60 ml per cow (Levofloxacin 20 mg, Ornidazole 25 mg and a~ Tocopherol 5 mg/ml) for 35 days ‘Systemic Antibacterials Cflox power (ciprofloxacin) 45 mi/300 kg bavt for 35 days ily Xyrofur / Xyrofur Tazo (Ceftiofur and Tazobactam)| Catte-?.2 mg/kg bavt Bufflo-2.4 mg/kg b.wt for3-Sdays | IM ‘uinintas (Enrofloxacin) 15 ml/300 kg b.wt dally for 3-5 days wily For Retention of Placenta Ropitas (Intrauterine Herbal bolus for placental removal) 4.Boli Intra-Uterine route ProShe (Herbal Uterine tonic) 100-125 ml bud for 3-5 days Orally 3. Hormonal Aberrations For synchronization of estrus following protocols can be used esha ahtadne apr) “eament iene | oY aera cn mate | anton | pag aS sonny | MEphdematend Progesterone + PGFia nee aaa Sea Repeat breeding, Cystic ovarian degeneration, Delayed ovulation, Improvement of conception 2.5 ~Sml rate and Preventing early embryonic death Gynarich (Buserelin acetate} Corpus luteum regression, Chronic endometritis/ pyometra, Persistent corpus luteum, COD, Luteal ml ‘oyst and Anoestrus Pragma (Cloprostenol) 4, Nutritional Management Nutritional management involves use of vitamins and minerals in adequate quantities. The following therapies are advocated for Therapy | Ingreiets ose Route inf go Minerals nd Vins ome diol nave Vitamin , and 5.10" tava Vitamin 0,€ and Sm IM Baer morgane Phosphorous with ATP 25 reconstituted Novizac ‘stimulators and Bioavailability enhancers solution for two days, IM5. Management Animals should be inseminated at right time. 1. Inseminate buffaloes and indigenous cows (heat period: 12-24 hours) according to A.M-P.M rule i.e. if animal comes in heat in morning then inseminate at same time in the evening and vice versa, 2, Inseminate the exotic/crossbred cows (heat period =24- 36 hours) in mid to late heat. 3. Thin, stringy and clear discharge along with mounting of cow on herd mate is the sign of standing heat and conception rate will be high, Double insemination is recommended for crossbreds. 5. Record keeping is a must as it provides the key to locate the various dairy operations. The records include feeding, breeding, health and reproductive behaviour of animals. Fig 4- Managment of Repeat Breeder with FTAI Comprehensive Management of Repeat Breeders dF ‘Non - Infectious Infectious Hormonal Rotational ‘Nutritonal For Better For improving Deworming Harmony Uterine Health Conception Rates [Flex TIF sprijima Uterine ROP FENTAS XP Involution Management «=» CoNCImax Lenovo /& Gynatich Zenvet | Proshe lpascires Nirofur \NzoMEC NEOzIDE PLUS References Sarasa C5 an Purohit G.N. (206). Repeat bcedngncence, rk factors and diagnos in bulfales. Alon Pace oural of Repraduetion 5: 87-55 ps//mwoeresearchgateet/pubication/281€13673_ Repeat breeding, ncidence_rsk factors. and_dagnoss,n_butfaloes Kumar Rand Singh R (2008). Incidence of repeat breeding in burfloes under rural conditions Indian Jourel of Animal Sciences 791 442-444, hips: researehgate.nepubleaton/287676109 Incidence of repeat_breedingin buffaloes under furl condsons Singh M, Sharma A, Sharma & and Kumar (2027). Repeat Breeding and is Treatment in airy Cattle of Himachal Prades Ina) Review Indion Journal (of rial Reproduction 38( 15, htps:/www researeheate ne ubbeation/ 317778138 AFPFAT BREEDING AND ITS. TREATMENT IN. DAIRY CATTLE (OF HIMIACHAL PRADESH INDIA ~ A REVIEW Kumar and Purohit G (2039), fect of biferent Hormonal Therapies on Day Sof Estrus on Plasma Progesterone Profile and Conception Rates in Repeat Areeding Day Cows. Journal of Animal Heath and Production S(}: 103-106. hos: /uwu.esearchgote net/publcation/330341983 effect of Offerent_ Hormonal Therapies on-ay5.0f Exrus_on Plasma, Progesterone Profle and. Conception Rates in. Repeat Bresing. Onry Cows For suggestions and comments, please write tous TECHNICAL CELL INTAS ANIMAL HEALTH INTAS PHARMACEUTICALS LIMITED, Corporate House, Near Sola Bridge, Sarkhe} Gandhinagar Highway, Thalte, Ahmedabad - 380054. Gujarat. 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