REPRODUCTIVE MANAGEMENT OF DAIRY CATTLE

 

REPRODUCTIVE MANAGEMENT :

Reproductive management in dairy cows

Reduced fertility is one of the commonest reasons for vets being called onto dairy farms. In many cases cows presented to vets have obvious problems such as “whites” or ovarian cysts.

However, not every cow failing to hold to service has an obvious problem. A significant number (around 10 to 15%) of cows require four or more inseminations to get pregnant despite apparently cycling normally.

Most of these are indeed “normal” since, assuming no cows are culled after earlier services, then even in a herd with every cow becoming pregnant at a rate of 50% (a good rate for our dairy farms these days) there will be 12.5% of cows presented for a 4th service!

However, in some cases there is an underlying problem reducing the chance of the cow getting pregnant. These may be either cow factors that require ultrasound examination or even other more sophisticated tests e.g. oviduct patency, or the result of a wide range of external factors, such as poor management.

An obvious example is inefficient oestrous detection. On farm, without extensive testing, it is very difficult to distinguish between all these factors, as their only sign is a cow that is apparently normal but hasn’t got pregnant. Such cows get lumped together as having ‘repeat breeding syndrome’.

CARE AND MANAGEMENT OF PREGNANT COW

• Pregnant animals should be watched carefully, particularly during the last stages of pregnancy to avoid abortion due to fights or other physical trauma.
• During early stages of pregnancy, there is no need of special feeding for heifers. The system of feeding and management recommended for heifers before breeding may continue. During last three months of pregnancy when fetal growth is very rapid, a special pregnancy allowance of about 1-2 Kg of concentrate should be offered.
•  Special care should be taken regarding mineral and vitamin deficiencies because they can have a serious adverse effect on the newborn calf. Feeding trace mineralized salt plus recommended amounts of calcium and phosphorus is usually sufficient to avoid these problems. Care must be taken that calcium and phosphorus should not be taken in excessive amounts.
•  During the last few weeks of pregnancy there is a tendency of prolapse of vagina which may be caused by constipation, mineral deficiency and debility. Balanced and laxative rations should be fed to maintain the normal tone of the reproductive tract.
• Some time udder edema occurs before calving. This can be avoided by moderate exercise for a half an hour, two to three times per day. Massaging the udder for a few minutes is also helpful. Use of diuretics and prepartum milking may be helpful in severe cases.
•  Isolate the pregnant animal 8-10 days before the expected date of calving and keep it in a clean well bedded, dry and disinfected maternity pen. The animal should be watched closely as calving time approaches at least every two to three hours.
•  A good calving environment reduces the exposure of cows and newborn calves to infectious disease. A clean and comfortable area that provides cows with good footing minimizes the potential for injuries. Calving areas should be landscaped to allow for adequate drainage. Shade structures are recommended.
•  Calves are usually born without assistance. Any abnormality in their presentation requires immediate attention by a competent person to correct the position of the calf so that it can be delivered. Strict sanitation must be observed during assistance.
•  After removal of calf, milk animal it will help in removal of placenta. Placenta is normally expelled within 2 to 6 hours after calving. If placenta fails to be expelled with 12 hours it is considered retained placenta. In case of retained placenta veterinarian should be called for its removal.
•  After normal birth, the dam is alert and willing to eat and drink within one or two hours of calving. Warm water and some wheat bran should be offered to dam after calving. It is necessary to encourage the dairy animals to rise and to move to the manger for feeding after calving, especially on the day of calving and the first 2 days after calving.
• The animal should be closely watched for health problems after calving. In addition to observing feed intake and milk production, rectal temperature and ketone levels should be monitored daily. Animals having health problems should be identified and treated accordingly, whereas healthy animals can join the general population 3 to 4 days postpartum.

Cystic ovarian degeneration (COD) in cattle

Definition of COD

Traditionally cysts have been defined as anovulatory follicular structures (diameter, >25 mm) that persist for 10 or more days in the absence of a functional corpus luteum and are accompanied by abnormal oestrous behaviour (irregular oestrus intervals, nymphomania or anoestrus). However, recent data using ultrasonography indicate that follicles typically ovulate at 17 mm in diameter, so follicles that persist at 17mm or greater may be considered to be “cystic.”

 

Nymphomanic behaviour                                                                     Follicular cyst

Occurrence and consequences

Cystic ovarian disease in dairy cattle occurs most frequently during the post partum period, 30 to 60 days after calving, when normal ovarian activity usually resumes.

The incidence of COD varies between 5 and 30 %. (Hooijer et al., 2001). Each incidence of ovarian follicular cysts increases the calving interval by 22-64 days.

Cause

Factors predisposing to cystic ovaries include metabolic diseases, negative energy balance, high productivity, retained placenta, dystocia, stress and genetics.

Follicular cysts result from failure of ovulation and luteinization. (Luteinization is the structural and biochemical changes that occur in a follicle after ovulation. Follicular cells that once produced estrogen change into luteal cells of the new corpus luteum (CL) that secrete progesterone. Follicular cysts are blister-like structures, flaccid to the touch.

Luteinized cysts apparently fail to ovulate, but some luteinization occurs. Because of the varying degree of luteinization, luteinized cysts are firmer to the touch than follicular cysts though not as solid as CL.

Cystic CL are CL with a fluid filled center. Several early researchers did not find cystic CL in pregnant cows and reasoned that cystic CL could not support pregnancy. However, Cornell University researchers reported that a CL producing only 100 µg of progesterone can support pregnancy. Therefore, a cystic CL could maintain pregnancy. In the absence of pregnancy, cystic CL regress and are considered nonpathological.

Symptoms

Abnormal estrous behavior patterns are the most noticeable sign of cystic ovarian disease.

This includes persistent oestrus, shortened oestrus intervals or failure to cycle (anoestrus). Anoestrus is by far the most common sign.

Persistent bulling behaviour, or nymphomania, is by far the least common clinical sign associated with cystic ovaries.

 

Sterility hump in cows with chronic cystic ovarian degeneration

Ultra sound scanning of follicular cyst

Treatment

Early, prompt treatment is important as most cysts will not resolve on their own. Modern treatment of cystic ovaries in cattle addresses the underlying factors responsible for the development of the condition.

This could include correction of nutritional and metabolic disorders or hormonal treatment leading to induction of normal follicular turnover and resumption of cyclic ovarian activity.

Progesterone, prostaglandins and gonadotrophin-releasing hormones are the most commonly used products.

Prevention

The causes of ovarian cysts are not fully understood, which means there are no specific prevention regimes. However energy deficiency is a major factor and reducing the depth and length of the period of negative energy balance after calving, will significantly reduce the incidence of cystic ovaries.

 

Early embryonic death

Embryonic mortality is generally defined as loss of the conceptus which occurs during the first 42 days of pregnancy, which is the period from conception to completion of differentiation when organ systems develop.

Approximately 30 percent of all embryos and fetuses will not survive to birth.

About 80 percent of this loss occurs before day 17, 10-15 percent between day 17 and 42 and 5 percent after day 42.

These losses to be much higher in “repeat breeders” those cows and heifers inseminated three or more times.

This has a significant economic impact on dairy herd profitability.

Because of the complex interactions among the various processes involved in establishment and maintenance of pregnancy, no single factor can be identified as the primary cause of embryonic death.

The following are some major factors contributing to this loss:

It is well documented that short term exposure to heat stress several days before and after insemination results in low conception rate or embryonic death. This is due to elevated temperature of the uterine environment. This has been a serious problem affecting reproductive performance this spring and summer.

Chromosomal abnormalities are known to be a cause of embryo mortality. One research summary estimated an average of 10 percent embryos had gross chromosomal abnormalities. Most of these embryos were lost before day 12. Unfortunately, this problem cannot be controlled through management.

Nutritional factors have been shown to contribute to low conception rates resulting from embryonic mortality. Research studies have shown that cows with severe change in body condition score (greater than 1 point loss on a scale of 1 to 5) during the first five weeks postpartum had an extended interval to first service and a very low conception rate compared to herdmates with only a minor or moderate change in body condition.

Whether this is due to an abnormal hormonal situation such as reduced progesterone secretion or ovulation of a defective oocyte has not been determined. Several reports showed that feeding excess crude protein, excess degradable intake protein or low levels of fermentable carbohydrate and the various combinations of these nutrients can cause low conception rates. Such situations can produce excessive levels of ammonia in the blood and uteri of cows.

Some researchers believe this could be toxic to the gametes and the developing embryo. The excess ammonia that is not utilized by the rumen microbes must be converted to urea at a significant energy cost which can further adversely impact conception rate. Mycotoxins and exposure to toxic substances and toxic plants have also been implicated as a cause of embryonic mortality.

Infectious agents can cause uterine infection or directly affect the embryo causing death. The major organisms adversely affecting reproduction are : Corynebacterium pyogenes, Campylobacter fetus (Vibriosis), Haemophilius somnus, Leptospirosis, Neospora and the viruses bovine virus diarrhea (BVD), infectious bovine rhinotracheitis (IBR) and to a lesser extent Ureaplasma and Mycoplasma.

Uterine defense mechanisms including the immune system are critical to maintaining embryonic development. For example, recent reports show that subclinical mastitis and other systemic infections can substantially increase the incidence of early embryo loss. Furthermore, nutritional deficiencies or an environmental challenge can alter uterine immune function. Currently this is a very active area of research.

Hormonal patterns or imbalances associated with embryonic mortality have been identified. The challenge for researchers is to develop synchronization programs and treatments that provide high progesterone, maintain low estrogen, and lead to a highly functional corpus luteum to maintain pregnancy. Dairy producers should continue to keep informed about new systems that will be developed to minimize embryonic loss. However, these systems will not correct problems associated with nutrition, disease, heat stress or postpartum problems that challenge the uterine defense mechanism.

There are management practices that can be implemented to minimize the incidence of embryonic mortality. These include: proper transition cow management and nutrition, effective vaccination, providing a clean environment, minimize heat stress and proper timing of insemination. There is abundant data to support the fact that between 5 percent and 30 percent of the cows inseminated are not in estrus when bred. Not only will this situation result in a low fertilization rate but most likely such cows are inseminated when the uterus is under the influence of progesterone and the immune system is not geared up to combat an infectious agent introduced during insemination.

Mummification of the fetus

          

Mummification of the bovine fetus occurs in cattle of all ages. The condition usually affects single fetuses but may occasionally involve one or both fetuses in twin pregnancies. Bovine fetal mummification occurs in the third to eight month of gestation but most commonly the fourth, fifth and sixth months; if the condition is undiagnosed the mummified fetus will remain in the uterus for months beyond a normal gestation period.

Spontaneous abortion before or near the expected end if gestation are not uncommon. Conditions necessary for the occurrence of fetal mummification include the maintenance of the dead fetus within the uterus by the presence of a normal viable fetus or fetuses or the persistence of the corpus luteum.

Fetal mummification apparently does not occur in the first trimester of gestation because embryonic or fetal death prior to development of the fetal bones usually is followed by absorption or resorbtion of the fetal and placental tissues.

Fetal death the last month or six weeks of gestation will begin fetal mummification may be undiagnosed at parturition and called a stillbirth, especially in multiparous.

Causes of fetal mummification:

The causes of fetal death and mummification in cattle are often the same as causes for fetal and abortion. The cause of fetal mummification is often impossible to determine because the time of fetal death is not known and autolysis and mummification of the fetus and membranes makes determination of the causative agent difficult or impossible:

1- Genetic factors

2- Torsion of umbilical cord or compression of umbilical cord by its passing around a fetal extremity.

3- Infectious causes of fetal death such as V. fetus, molds, Leptospirosis….etc.

Diagnosis of F.M:-

Depending on:

1- Case history.

2- Rectal palpation.

As the fetus mummifies the uterine walls contract and tightly enclose the concepts. The longer the condition exists, the dryer, firmer, and more leather- like tissues of the fetus become.

The uterine walls are fairly thick and no cotyledons are palpable. The uterine artery is small and has no fremitus, uterus may be drawn forward by the weight of the mummified fetus and normal cervical seal may be present, a carful rectal examination will readily reveal the mature of the disease. If the uterus dropped downward out of reach it may be pulled up to the pelvic cavity manually by grasping the cervix or intercornual ligament.

Treatment:

To expel the mummified in the cow the simplest treatment is to administer 50 – 80 mg of estilbestrol or 5 to 8 mg of i.m. The injected estrogen causes contraction of the uterine muscles, relaxation of the cervix, involution of the corpus luteum and results in the expulsion of the fetus. When the fetus is large or mummification occurs at 6 to 8 months of gestation or the cow is small or immature, the genital tract should always be examined within 48 to 72 hours after the injection to make sure dystocia does not occur with secondary infection of the uterus and maceration of the fetus. The use of large doses of potent glucocorticoids to cause the expulsion of mummified fetuses has not been reported.

Removal of the persistent corpus luteum of pregnancy will usually result in estrum and evacuation of the uterus. There is the added danger of trauma and damage to the ovary by the forceful or surgical removal of deeply imbedded corpus luteum of pregnancy. PGF2α 30 mg/ i.m can be used in treatment of fetal mummification.

Following treatment and expulsion of the mummified fetus, most cattle recover promptly since no infection is present to delay recovery. Conception usually occurs within 1 to 3 month.

Any cow with a history of having one mummified calf may have another one at any gestation period; hence the prognosis should always be guarded.

 

Maceration

Macerated fetus in the uterus

Maceration may occur at any stage of gestation and has been observed in all species. When the fertilized ovum or embryo succumbs to bacterial or viral infection or other disease or abnormality early in gestation it is usually absorbed in the uterus or a slight and often insignificant purulent uterine or vaginal discharge may be evident.

The embryo is seldom observed. The interval between estrrual periods may be prolonged if the embryo did not succumb until 20 to 50 days after conception. Early embryonic death and maceration are probably caused by a variety of miscellaneous organisms that may be found in the uterus, and are of common occurrence in cows affected with trichomoniasis or vibriosis.

In the cow fetal maceration that occurs after third month of gestation by which time fetal bones are fairly well developed, may be caused by similar wound – infection bacterial agent. More commonly fetal emphysema and maceration follow fetal death and beginning abortion in the cow in which the cervix dilated but the fetus was not expelled due to a failure of the genital tract to dilate sufficiently or contract normally or because the fetus was dead and in an abnormal position and posture. In rare instances fetal emphysema and maceration may be associated with uterine torsion during gestation. Two factors of open cervix and a dead fetus at body temperature cause a rapid bacterial invasion of the fetus and membranes of organisms already present in the uterus or from the more caudal portions of the reproductive tract, fetal emphysema and maceration follow.

If the bovine fetus is beyond the third month of pregnancy and if the usual expulsive efforts are not observed or are unsuccessful, the fetus develops emphysema in 24 to 48 hours and in 3 to 4 days maceration begins.

Symptoms:

In long standing fetal maceration, the acute emphysematous stage has passed straining is seldom observed and the cervix is usually quite contracted. Generalized symptoms of elevated temperature and pulse and anorexia are usually not present.

There is often a history of chronic, fetid, mucopurulent discharge from the vulva over a period of several weeks or months.

There may be a history of a gradual drop in milk flow and loss of weight.

On rectal examination in the cow, fetal bones may be palpated in the uterus either floating in pus or crepitating with little pus around them. The uterine wall is thick and heavy and the cervix usually large and hard.

Treatment

The prognosis is poor. Treatment in the cow is difficult. If much pus is present, treatment as for Pyometra is indicated and possibly the bones may be passed through the cervix with the pus.

 

 

Pyometra

     

Pyometra is characterised by a progressive accumulation of pus in the uterus and by the persistence of functional luteal tissue in the ovary.

In most cases, pyometra occurs as a sequel to chronic endometritis when, as noted above, as a result of inflammation, the uterus ceases to produce or release the endogenous luteolysin. The corpus luteum of dioestrus persists and, since the genital tract remains under the continuous influence of progesterone, the infection is not eliminated. Because the cervix remains fairly tightly closed the purulent exudate accumulates within the uterine lumen, although occasionally there is a slight purulent discharge. Occasional cases of pyometra occur in the presence of a luteal cyst.

 

The second main cause of pyometra is the death of the fetus, invasion of the uterus by A. Pyogenes and retention of the corpus luteum of pregnancy. This is a relatively infrequent cause of the condition.

 

Thus pyometra usually results from contamination of the uterus during dioestrus, such as occurs after insemination during the luteal phase. Venereal infection with organisms such as

Trichomonas fetus, which cause embryonic death, also causes pyometra.

 

Cows which suffer from pyometra show few or no signs of ill health; the main reason for them being examined is the absence of cyclical activity, or, perhaps, the presence of an intermittent vaginal discharge.

The uterine horns are enlarged and distended, quite often to an unequal degree, owing to incomplete involution of the previously gravid horn or to recent conceptual death.

 

Differentiation of pyometra from a normal pregnancy can sometimes be difficult, but there are a number of distinguishing points:

 

• The uterine wall is thicker than at pregnancy.
• The uterus has a more ‘doughy’ and less vibrant feel.
• It is not possible to ‘slip’ the allantochorion.
• In most cases of pyometra, no uterine caruncles can be palpated. However, when the infection occurred in a non-involuted uterus, involution of the caruncles is delayed and they may remain palpable for quite a long time.
• Transrectal ultrasonography will demonstrate the absence of a fetus and the presence of a ‘speckled’ echotexture of the uterine contents compared with the black anechoic appearance of normal fetal fluids

 

Pyometra associated with T. foetus infection presents features which are different from those previously described. Uterine pus is, as a rule, much more copious and may attain a volume of many litres. It is generally more fluid and is greyishwhite or white. The uterus undergoes much greater distension. The mucus occupying the cervix is moist and slippery, rather than sticky and tenacious, and motile trichomonads can generally be found in it.

 

Treatment

 

The best treatment is the use of PGF2α or its analogues. They result in regression of the corpus luteum, dilatation of the cervix and expulsion of the purulent fluid, with oestrus occurring 3–5 days later.

 

If there is any doubt about the diagnosis of pyometra the cow should be left untreated and re-examined 2 weeks later for evidence of change Provided that the condition is not too longstanding and therapy is instituted quickly, there is a reasonable possibility that the cow will eventually conceive again.

However, long-standing cases are associated with more severe degeneration of the endometrium, reducing chances of reconception.

 

Repeat Breeder cow

To identify repeat breeder cows you need two things: good records and good heat detection. Given what has been said above and that on many farms the efficiency of oestrous detection is less than 60% (i.e. for every 10 cows potentially cycling only 6 are served) it can be seen that this is quite a need!

However if done well they allow the farmer or herdsperson to pick up cows that are cycling normally but not getting pregnant or most importantly those not fitting a normal pattern. Using this information these possible problem animals can be identified quickly, subjected to veterinary examination and a treatment protocol applied. This reduces the potential days open and so saves money.

The exact amount depends on farm circumstances but it more than pays for a regular veterinary visit on most farms.

Good heat detection needs an ability to recognise the signs of heat and time set aside to look carefully for these as in some cases they may not be very obvious. The 3-week calendar can be very useful in pinpointing likely candidates.

Other aids, such as beacons, tail paint pedometers and milk progesterones can also improve heat detection but there is still no really cost effective substitute for the astute observer apart from the bull. Even the latter can be overwhelmed if there are too many cows in season at one time.

Causes:

1. Early Embryonic death:

In this case the retention of CL of pregnancy, which has been terminated early, occurs. This is usually encountered during 90-120 days of gestation where the embryo is too small to be detected when aborted or it may be reabsorbed. This may be a characteristic feature in served cows coming into heat after a period longer than the normal oestrus cycle.

Treatment

• Improved nutrition.
• Suspect for Trichomoniasis and Vibriosis and treat them.
• Inj. receptal 11 days after insemination is known to improve embryo survival.

Anovulation:

Ovum not released from ovary. The animal has normal cycle, normal reproductive tract but fails to conceive.

Causes:

• Inadequate level or absence of L.H.
• Ovaro-bursal adhesion. It may be diagnosed by palpation of matured GF on the ovary more than 48hrs after the end of estrum.

Treatment:

• L.H preparations (HCG- human chorion Ganadrotrophin)- 3000 IU. I/V. when the animal is in heat.
• Inj. Receptal – 5 ml I/m.
• Improved feeding.

Delayed Ovulation:

Ovulation takes place 48-72 hours after the onset of oestrus but the spermatozoa would be dead by then.

Cause:

Due to low level of LH.

Treatment:

As for anovulation.

Preventing repeat breeder cows

Ensure you are serving cows at the correct time. This means that all staff should know the signs of heat. Milk progesterone testing is also useful; cows in a true heat will have very low progesterone.

Ensure insemination techniques are as good as possible. This is particularly important if you use DIY AI. Do not serve cows previously diagnosed as pregnant without doing a cow-side progesterone test to confirm it is has a low progesterone and is not pregnant. If the cow is pregnant AI may cause foetal loss.

Identify and treat cows with whites before starting to serve them.

Don’t start serving too soon after calving. Herds that start early have lower pregnancy rates to service and so more repeat breeder cows.

Minimise stress at service. For example, try and avoid serving around turnout or when you change the diet.

A comprehensive analysis and review of your breeding programme is time well spent in the battle to reduce repeat breeding. Get together with your vet and go through your herd records and present breeding protocols and see if there are not some areas where this important area could be improved.

 

 

Endometritis

 

whitish/ mucopurulent vulval discharge from cow affected with endometritis

• Endometritis is an infection of the uterine endometrium.
• Cattle endometritis is a common condition that is known by the layman as ‘whites’.
• It occurs three weeks or more after calving and should not be confused with the more severe condition of metritis which occurs immediately post-partum.
• The main consequence of endometritis is poor fertility. Therefore it has a major economic impact by increasing calving interval, services per conception and cull rates and by decreasing milk yield.
• It is reported to have an incidence of between ten and fifteen percent in dairy herds (however it is very variable from herd to herd), with the total cost of £160 per case.

Etiology

• The normally sterile uterus is contaminated by environmental microorganisms during parturition or immediately postpartum.
• The main bacteria involved in endometritis is Trueperella pyogenes, however, numerous gram-negative anaerobes may also be involved.
• The presence of this opportunist bacteria can delay return to service and cyclical activity, prevent fertilisation and cause early embryonic death by producing a hostile uterine environment. It is also reported that it increases incidence of ovarian cysts.

Signalment

• Endometritis can occur in any cow post-partum however incidence is increased by the following predisposing factors:
• Retained foetal membranes
• Dystocia
• Caesarian section or assisted calving
• Induced parturition
• Still Birth
• Twins
• Unhygienic calving environment – includes seasonal effect as indoor calving has higher endometritis rates
• Ovarian inactivity
• Parity
• Concurrent disease and nutrition – fatty liver disease and hypocalcaemia are reported to increase endometritis rates.
• Multiple defense mechanisms exist to prevent opportunistic infection of the uterus. The vulva and cervix provide a physical barrier to opportunist bacteria; resident bacteria in the vagina prevents the colonisation of harmful bacteria; involution and caruncle sloughing expel contaminants and tissue debris; a higher pH during oestrus prevent bacterial growth and various immunological mechanisms also act to prevent infection of the uterus. Following parturition endometritis may still occur, especially is one or more of the mentioned predisposing factors is present.

Clinical Signs

• Mucopurulent vaginal discharge should be evident on vaginal exam 21 days or more post-calving. Discharge is relatively odourless (dependant on severity) and whites in colour, hence the name ‘whites’.
• The discharge should not be confused with lochial discharge or vaginitis.
• Rectal palpation should reveal a poorly-involuted, oedematous uterus.
• On an individual or herd level there may be a history of subfertility.

Diagnosis

• Diagnosis should be based on the calving history and clinical signs following vaginal and rectal exam.
• Vets may use a scoring system to categorise the colour and odour of the vaginal discharge which indicates how severe the infection is and whether treatment is necessary.
• Measurements of the uterine and cervical diameter may be included in the scoring system. Definitive diagnosis can only be achieved by endometrial biopsy, however this is rarely indicated.

Treatment

• Greater success is achieved with milder cases of endometritis. Treatments available include antibiotics, hormones and intrauterine antiseptics:
• (1) Antibiotics

Various factors should be considered when selecting an antibiotic for the treatment of endometritis. Criteria for antibiotic:

appropriate efficacy in infected uterine environment

appropriate efficacy against the causal bacteria

no inhibition of natural uterine defense mechanisms

appropriate concentration and duration of action in the infected uterine lumen

little or no milk withdrawal period

cost effective

no detrimental effect on fertility

Generally, a broad spectrum antibiotic, active against Actinobaccillus pyogenes and gram-negative anaerobes should be used. Ideal antibiotics are cephalosporins and oxytetracycline as they match the majority of criteria listed above. Some resistance to oxytetracyclines is reported and additionally some formulations cause irritation to the endometrium, therefore intrauterine cephalosporin should be considered the most effective antibiotic treatment.

Sulphonamides, aminoglycosides, nitrofurazones and penecillins have decreased activity as a result of the uterine environment and bacteria present.

Metranidazole and chloramphenicol should not be used as they are banned from use in food-producing animals.

Some antibiotics are rapidly absorbed and distributed throughout the body, and in these cases it may be of more use to administer them parenterally.

(2) Hormones

Oestrogens: controversial treatment bases on the knowledge that the uterus is more resistant to infection during oestrus. It is not licensed in the EU for use in cattle.

Prostaglandins: PGF2a or analogues can be administered parenterally. They should be considered the treatment of choice if a corpus luteum is present. The administration of prostaglandins removes the inhibitory effect of progesterone on the uterus and induces oestrus, which both of these actions improve the uterine defense mechanisms. They may have an additional beneficial ecbolic effect, aiding clearance of the lumenal contents. There is no milk withdrawal period for prostaglandins, making them ideal for use in dairy cattle.

These are mainly used in chronic cases.

(3) Antiseptics

Chlorhexidine and metakresol sulphonic acid (Lotagen), povidone iodine antiseptic administered intrauterine are reported to be a effective alternative to antibiotic treatment, however few studies have been carried out to confirm this and detrimental effects on fertility are reported.

Prognosis

Prognosis is dependant on the severity of infection and the effectiveness of treatment. Greater success is seen with mild cases of endometritis.

SILENT HEATS (UNOBSERVED AND SUBESTRUS)

Incidence of subestrus in cattle and buffaloes has a wide variation in the frequency (15 – 73%).

The intensity of heat signs in buffaloes is generally lower and also homosexual activity is not pronounced as in cows.

The intensity of expression of estrus is generally affected by housing, floor surface, yield, lameness and number of herd mates in estrus simultaneously.

Summer anestrous is an important condition is buffaloes contributing to infertility in buffaloes. 

Heat stress has a pronounced effect on the estrus behavior of the female animals as heat stress reduces the length and intensity of estrus. Changes caused by heat stress reduce the likelihood of estrus detection.

Heat stress causes increased cortisol secretion and this hormone blocks estradiol-induced sexual behavior. Effect of heat stress on estrous behavior also includes actions independent of the pituitary-adrenal axis reducing the ovarian activity and follicular development. Heat stress causes a reduction in peripheral concentrations of estradiol at estrus.  Moreover reduced physical activity is also probably an adaptive response that limits heat production and reduced estrous behavior.

Heat stress at the beginning on the day of ovulation reduces the diameter and volume of the dominant follicle of the estrous cycle. Secretion of the hormones regulating reproductive tract function is also altered by heat stress. These changes lead to variable changes in steroid hormone concentrations in peripheral blood. This reduced action of steroid hormones on reproductive tract tissue during heat stress eventually impairs uterine and oviductal functions.

Factors responsible for anestrus are environmental stress, endocrine (endogenous opioid peptide, lower insulin concentration, imbalance in hormones such as LH, FSH, prolactin, melatonin and thyroid), nutritional (negative energy balance, micro and macronutrient deficiency), managemental factors such as lactational stress, suckling etc.  A lower level of body weight, total serum protein, blood hemoglobin, blood glucose, blood insulin, inorganic phosphorus, calcium, manganese, iodine, cobalt, copper, iron, cholesterol and vitamin A deficiency also causes anestrus. Anestrus may be diagnosed by per-rectal palpation of reproductive organs and frequent activity of reproductive cycles of buffaloes using ultrasonography.

Anoestrus

Anoestrus is the failure of a cow to cycle and display oestrus (heat). Anoestrus is normal before puberty, during pregnancy and for a short period after calving (postpartum anoestrus, PPA). All cows undergo varying degrees of PPA. On average, 20% of seasonal-calving cows are anoestrus at the start of mating, with extreme cases of over 50% of the herd also being reported.

Incidence of anestrus in buffaloes has been documented in various states as given below:

State	Incidence (%)
Haryana	56-67
Punjab	19.84
West Bengal	50.84
UP	69.40
Gujarat	9.18
Tamilnadu	9.09
Madhya Pradesh	60.83
Andhra Pradesh	30.67
Bihar	44.60
Karnataka	51.00
Andhra Pradesh	56.36

 

Causes

The major causes of PPA in dairy cows are inadequate nutrition (negative energy balance, NEB), late-calving cows and uterine disease. NEB happens when energy intake is lower than output in milk production and maintenance. It is seen as a loss of body condition as body fat is mobilised to meet the energy demands of lactation.

Some degree of NEB is inevitable in nearly all dairy cows in the month after calving. Variation in BCS at calving, weather conditions, pasture availability and supplementary feeds from one year to the next will result in differences in the extent of NEB experienced, and this is reflected in submission rates early in the mating period.

Classification of anoestrus in cattle

Benefiting from the use of ultrasonography and growing knowledge of follicular dynamics in cattle Wiltbank et al. (2002) proposed the following classification of anovulatory status:

Anovulation with follicle growth up to the emergence stage

Cows exhibit very small follicles that are growing only to the emergence phase and do not proceed further.

Fairly common in cattle exposed to poor feeding conditions such as extensive pasture management in tropical zones.

The underlying factor is inadequate FSH stimulation

 

Anovulation with follicle growth up to deviation phase

Follicular growth takes place and proceeds through emergence and deviation but does not lead to ovulation. A frequently reported form of anoestrus. Commonly occurs in the post partum period in lactating dairy and suckled beef cows.

The characteristic signs of this condition are small ovaries, with the absence of a corpus luteum or ovulatory size follicles. The ovaries however show continuing follicular growth in a dynamic wave pattern up to the deviation phase.

The underlying physiological problem is an inhibitory effect of oestradiol on GnRH/LH pulses that does not allow the final growth or oestradiol production by the post deviation dominant follicle.

Pathogenesis of anovulatory status/anoestrus in cattle

Resumption of cyclic activity after calving is influenced by:

• nutrition
• body condition
• suckling
• lactation

• breed
• age
• uterine pathology
• debilitating disease

Fewer than 10% of cows fail to ovulate in most well-managed dairy herds by day 40 post partum. It is well established that poor nutritional status and Negative Energy Balance are responsible for the majority of anoestrus cases in both dairy and beef cattle.

 

 

Treatment of anovulatory/anoestrus conditions in cattle

Treatment is based on:

Improvement in energy status- optimal nutrition during the transition period and during early lactation.

Hormonal treatments- combined with increased energy supplementation or reduced suckling stimulus may also help to stimulate oestrus.

Anovulation with follicle growth up to the emergence stage

In these cases treatments with GnRH usually have no effect, as the follicles on the ovary do not have adequate LH-receptors to respond.

FSH/PMSG treatment combined with improved nutrition can increase follicle growth.

Start with PMSG (Folligon):

– 500-850 iu per cow of bos taurus type and crosses

– 300-350 iu per cow of bos indicus type

Once the follicular growth is increased GnRH (eg. Receptal; 2.5-5ml) can be used to stimulate maturation and ovulation of the dominant follicle.

Do not breed/AI in the first oestrus

Anovulation with follicle growth up to deviation phase

• Ovsynch protocol
  – GnRH stimulation + induction of ovulation.
  Click on thumbnail sketch for protocol.
• Modified Ovsynch protocol– second GnRH replaced by hCG (e.g. Chorulon; 1.500 IU).

Dairy cows can be successfully treated with simple or modified Ovsynch protocol as many anovulatory dairy cows have follicles of sufficient size and ovulatory capacity but do not have an LH surge.

Source: http://www.partners-in-reproduction.com/reproduction-cattle/treatment-anoestrus.asp

 

CULLING OF UNPRODUCTIVE COWS

Culling of Dairy Animals

Dairymen should develop a checklist of culling reasons to use in their decision making process. The following list of 10 questions is one that could be used for each cow before deciding her future in the herd.

Is her yearly production 20 per cent or more below the herd’s rolling average?

Is she a chronic mastitis case? Check this one closely, because a cow with chronic mastitis is producing below her capability and, in addition, could be spreading mastitis to other cows in the herd through the milking equipment.

Will she be dry four months or more? Long dry periods are costly to the dairyman and may indicate the cow has a problem of becoming pregnant, a trait not desired.

Is she a hard milker? Is her udder shape or teat structure such that she is a nuisance to milk?

Does she have a history of calving difficulties or post calving illnesses such as retained placenta, metritis, or milk fever? Cows that cause problems at calving time are not pleasant to have and are costly to keep in the herd.

Does she have an undesirable disposition? Is she a nervous cow or does she kick whenever her udder is touched? These are undesirable traits that should be noted along with production and calving problems.

Is she below the herd’s average body type? Check body confirmation to see if it comes up to specifications for the herd.

Is she a timid cow? With the type of dry lot housing systems most dairymen have today, timid cows usually will not get the amount of feed required to be high producing animals.

Is she an old cow, and is the available barn space needed for freshening heifers? Fresh heifers usually have a higher genetic potential for milk production than older cows, especially if a progressive A.I. program is used in the herd.

A yes answer should probably be given to at least two questions before making the cow a strong candidate for culling. In many cases, though, one reason may be enough justification to base a culling decision.

Besides using a checklist in making culling decisions, other facts should be considered.

First-calf heifers:

In evaluating first calf heifers, consider the size of the heifers. Undersized heifers will probably produce less milk the first lactation because of their size. This situation is an indictment of the dairyman’s heifer feeding program and not necessarily the producing potential of the heifer. So, among possible culls of equal performance, preference should probably be given to the younger, undersized heifer, especially if she improved during her lactation.

Stage of gestation:

Extremely long calving intervals can be costly. With other factors being equal, cows in mid-lactation with several months to go before freshening are better prospects for culling than cows that will freshen sooner and return to peak production sooner.

Mastitis:

Mastitis CMT (California Mastitis Test) scores, somatic cell counts should be checked carefully. Cows with CMT scores of 2, somatic cell counts of 1.2 million or greater, should be culled before other potential culls because they are potential sources of intramammary infections of other cows.

Age:

Other factors being equal, cull older cows before younger cows of comparable relative value. The genetic potential of younger animals should be greater than that of older animals, so keeping the younger cows in the herd longer should be a sound practice.

Past performance:

Given two cows with the same relative value and other factors equal, cull the cow first that has the lowest previous production records. Past performance can be suggestive of future potential. Management errors in the current lactation could adversely affect a cow’s performance.