Abortion, perinatal and early postnatal Problems in Cows and/or Calves
Phil Rogers MRCVS
Grange Research Centre, Dunsany, Co. Meath, Ireland
| best blood samples | calf losses | abortion/foetal mummification | stillbirth | dwarf calves | weak calves / neonatal or early postnatal death | low immunity/poor thrive in young calves | low immunity in cows | lazy calving | retained placenta | remedial actions in problems around calving | dry cow supplements | calf supplements | trace element drench | drench warnings |
Many factors apart from mineral imbalances (infection, toxins, poisons, maternal effects etc) may cause these problems.
Prepartum blood samples are best to investigate periparturient and early postnatal problems: Calved cows on rations high in minerals usually have much higher blood mineral levels, especially of Cu, Se (GPx) and I, than unsupplemented cows in late pregnancy. Thus, postpartum bloods may mislead; they can over-estimate the mineral status prepartum.
CALF LOSSES: Calves can die in-utero, at birth, or in the days or weeks after birth. "Acceptable losses" for abortion, stillbirth and neonatal calf deaths are 2, 3 and 2% respectively, or a total calf mortality of up to 7%. Teagasc investigation of farmer-complaints is unlikely to reduce losses significantly if total calf loss is <7%.
ABORTION/FOETAL MUMMIFICATION can be due to INFECTION in pregnancy (bacterial (Leptospira, Salmonella, B. licheniformis, Haemophilus, Brucella, Campylobacter (Vibrio), Chlamydia, A. pyogenes, Trichomonas, Listeria etc), viral (BVD/IBR etc), protozoal (Neospora etc), fungal (Aspergillus, Mortierella, Mucor etc)); TOXINS in pregnancy (plant, fungal, microbial, algal, chemical (Se, I, F etc) etc); SEVERE TRACE-ELEMENT/VITAMIN IMBALANCE in pregnancy (Cu, Se, I, Vit A and E etc); INTERCURRENT DISEASE (fever, Babesia etc) and TRAUMA (lumbosacral or abdominal, seldom a herd problem).
All abortions should be notified to the DVO. Has RVL been involved ? Has the vet/RVL identified specific causes? What was done to exclude infection, intercurrent disease, toxins, trauma or dystocia as possible causes ?
STILLBIRTH arises due to the same factors as cause abortion (previous paragraph); also DYSTOCIA (especially in heifers(1); poor supervision of parturition; relative foetal oversize; malpresentation; pelvic abnormalities; double-muscles/bull effect; hypocalcaemia; hypomagnesaemia; severe trace-element deficiency). FAT-COW SYNDROME (cows overfat at calving) can also be associated with high calf mortality at calving.
Is body score too high/too low at calving? Is supervision of calving OK? Is dystocia a problem? Pelvic anomalies? Is the incidence of the problem greater in heifers than in cows? Is the problem related to a specific bull? See Note below.
(1)Dystocia/stillbirth in heifers is more prevalent than in cows. Dairy and Continental X heifers should be at least 340 and 360 kg respectively at mating. Use easy-calving bulls. Ensure that in-calf heifers get DRY-COW MINERAL for 6 weeks precalving and ensure good calving technique and supervision.
DWARFISM, SMALL CALVES can arise due to the same factors as cause stillbirth. Severe deficiency of I, Cu or Se can cause the birth of small weak calves. Severe Mn deficiency is a specific cause of dwarfism, with chondrodystrophy, joint laxity, superior brachygnathism and domed foreheads. This is very rare in Ireland. Inherited dwarfism can arise in certain breeds and lines. "Bulldog-calf" (Dexter syndrome) is also inherited. Bovine inherited spinal muscular atrophy also occurs in certain breeds and lines. It manifests as a progressive ataxia, weakness, muscle atrophy and recumbency in calves 0-2 weeks old. Some calves may be stillborn. The main lesion is degeneration of the ventral horn neurons of the spinal cord.
WEAK CALVES, NEONATAL or EARLY POSTNATAL DEATH and ILLTHRIFT IN YOUNG CALVES can arise due to the same factors as cause abortion, stillbirth or dwarfism. It can arise also due to NEONATAL INFECTION (pneumonia, septicaemia, scour, etc), sometimes with poor quality colostrum. The causes (apart from specific pathogens) may lie in faulty nutrition of the dam, inadequate feeding or quality of colostrum, poor hygiene, poor calf nutrition, poor ventilation or uncomfortable calf housing.
LOW IMMUNITY/POOR THRIVE IN YOUNG CALVES: Inadequate feeding- or quality of- colostrum is a primary cause of low immunity in calves. However, foetal infections (BVD etc) and deficiency of trace-elements and Vitamin E in late pregnancy can compromise the immune system of the neonate. This may increase susceptibility to scour, pneumonia, navel-ill, joint-ill etc.
If lab tests confirm a deficiency in dry cows, supplementation of the affected group of neonates with the relevant trace elements and vitamins can quickly verify the clinical significance of the deficiency. Alternatively, drench the affected group of neonates with the relevant mineral(s). See drench formula, enclosed. If minerals are involved, a definite response should occur quickly. If a response is obtained, ensure that all dams in late pregnancy get a good Dry-Cow mineral for at least 1 month pre-calving in future. Ensure that the young calves get 4 litres of good colostrum in the first 6 hours and a good mineral supplement also in the following weeks.
LOW IMMUNITY IN COWS: Stress and Fatty Liver Syndrome can compromise the immune system of cows, as can deficiency of trace-elements and Vitamin E in late pregnancy and/or in the days and weeks postpartum. This can lead to increased susceptibility to mastitis, metritis and other infections.
If lab tests confirm a deficiency pre- and/or post- partum, supplementation of the affected group with increased amounts of the relevant trace-elements (especially Se, I and Zn) and vitamins (especially Vit E) can quickly verify the clinical significance of the deficiency. If minerals are involved, a definite response should occur within 3-6 weeks. If a response is obtained, ensure that, in future, all dams get a good Dry-Cow mineral for the last month prepartum and a good supply of Lactation Minerals postpartum (via the concentrate ration, or sprinkled on easy-feed forage).
LAZY CALVING (prolonged calving, slow calving, "no push, no effort") can be a serious problem in some herds. The national incidence is unknown, but seems to be increasing since 1990 or so. Deficiency of Se & I and subclinical hypocalcaemia were causes in some herds. A therapeutic dose of Ca borogluconate s/c can verify if latter is involved. If calving occurs quickly thereafter, subclinical hypocalcaemia is probably the prime cause. Weakness, dystocia and Fat-Cow syndrome may be involved in some cases. Some outbreaks remained unsolved.
RETAINED FOETAL MEMBRANES: RFM is defined as placental retention >12 hours. The longer the retention interval (up to 7 days), the more likely are secondary effects of RFM. Background incidence is +4%. The incidence in individual affected herds can be 4-100%. Herd investigation is warranted if incidence is >8%. Age, season and sire had no consistent effects on RFM. Though heifers have more calving problems than multiparous cows, parity per se is a debatable risk factor in RFM. Some authors report higher incidence in heifers and very old cows; others report lower incidence in heifers.
The main causes are: drug-induction of calving; twinning or multiple births (especially with male calves); dystocia (especially in heifers; also in cows with large male calves); abortion; infection (leptospirosis, Q-fever (C. burnetii)); short gestations (<275 days, as in summer calvings); poor management (short dry period (<30 days); confinement without exercise, especially in tie-in stalls; stress; poor supervision/expertise at calving; removing the calf at birth); poor prepartum nutrition (under- or over- feeding; Fat Cow/fatty liver syndrome; hypoglycaemia; thyroid disorders; deficiency of Se & I + Cu, Mg, b-carotene; subclinical hypocalcaemia + hypomagnesaemia at calving). Other causal factors include high milk potential; oxidative stress and inadequate dietary antioxidants or exposure to high levels of linolenic acid, or toxic pro-oxidants prepartum.
Many RFM cases develop delayed utero-cervical involution (still open >6 weeks); endometritis, pyometra and repeat breeders; infertility, ovarian dysfunction and cysts (delay in onset of 1st pp oestrus by 5-60 days (delayed cyclicity, and non-detected oestrus (NDO)); delay in the number of days open and calving interval by 8-40 days; delay in the service period by 10-70 days; a fall of 7-17% points in pregnancy rate); left displacement of the abomasum; mastitis; ketosis; lameness; abortion; lowered current and 305-day milk yield.
Methods used to treat RFM include: manual removal (controversial and has risks); i/m injection of 50 mg propranolol hydrochloride (Uterotonic-Polfa) + 1 g cimetidine (Tagamet) (very good results claimed but in a very small trial); oxytocin + ergometrine maleate i/m + a combination of antibiotics (better results than manual removal); oxytocin or an analogue alone (mediocre results); oxytocin + cloprostenol (slightly better results). Some authors advise no intervention in RFM unless the cow is clinically ill.
REMEDIAL ACTIONS IN PROBLEMS AROUND CALVING TIME include:
MINERAL SUPPLEMENTATION OF COWS IN LATE PREGNANCY
If I deficiency alone is involved, supplement with 60 mg I/cow/d for 4-6 weeks prepartum. This can be done via 1.2 ml 5% tincture of I/cow/d or 2 ml of 4% potassium iodide solution/cow/d (via the water supply). An alternative is 5% tincture of I (9 ml/cow/week), sprayed or painted on the thin skin of the pocket of the flank fold once/week for 4-6 weeks prepartum. Oil-based I injections are not recommended.
If Se deficiency alone is involved, s/c injection of 50 mg Se (as Na selenite or selenate), given 3-4 weeks prepartum may suffice. Cows which do not calve within 6 weeks should be re-treated, as soluble Se has short-lived effect (max. 6 weeks). Alternatively, give a half dose of Deposel (250 mg Se as Ba selenate), which should protect for 4-6 months.
If Cu deficiency alone is involved, an oral CuO capsule (20-25 g), given 3-4 weeks prepartum may suffice. Although s/c injection of Cu-EDTA (100 mg Cu) is useful, avoid Cu injections if possible - it can lead to abscesses and reduce meat quality. Repeat the treatment for cows which do not calve within 6 weeks.
MINERAL SUPPLEMENTS FOR CALVES BORN TO DEFICIENT DAMS: A drystock mineral mix can be fed in the concentrate feed, or can be dosed weekly with trace-elements, as in the cattle drench formula (see enclosed notes on cattle minerals).
A TRACE ELEMENT DRENCH FOR COWS, CATTLE AND CALVES: As an alternative to feeding trace elements in mineral mixes, the following may be used in small herds, preferably dosed at 1-2 week intervals:
Weight to mix (g)
sodium selenite (30.0% Se)
Include copper sulphate ONLY on specific veterinary advice. Add distilled water to 30 litres. Shake until ingredients are fully dissolved. In practice, depending on the specific deficiencies identified on the farm, only 1-3 of the ingredients are used together. The unwanted ingredients are omitted from the formulation.
|LABEL THE DRENCH
DOSE: CLINICAL CASES OR CALVES OF DEFICIENT DAMS: 17 ml/100 kg LW once/week.
THE USE OF PERIODIC DRENCHES OF TRACE ELEMENTS
SHAKE CONTAINER WELL between every few doses. Many drenches, especially those combining anthelmintics and trace elements, are not solutions: they are colloidal suspensions. If the container is not shaken frequently during use, de-mixing of the colloidal suspension can cause sedimentation of trace elements. The upper layer of the suspension may contain low concentrations of trace elements and the lower layer may contain toxic levels. Animals dosed from the upper layer may get too little supplement. Those drenched from the lower layer can die of acute poisoning within 1-3 days of drenching.
DRENCHING TECHNIQUE: Drenching can be dangerous. Consider other methods of supplementation before drenching. Inhalation of part of the drench can kill stock, cause shock, or lung damage. Drench carefully at the correct dose. Avoid damage to the back of the throat. Avoid drenching too fast.
COPPER POISONING (see Web article): If they inhale part of the drench, or if the dose is too high, cattle can die after Cu drenches. N.B. Unweaned calves are easily poisoned with copper; they absorb Cu more efficiently than weaned calves and adult cattle. Unweaned calves should not get Cu in drenches unless Cu deficiency has been confirmed by a veterinary surgeon by a herd blood test and/or on clinical/postmortem findings. If they need a Cu supplement, dosing with oral Cu oxide (CuO) capsules or Cu-containing glass boluses is safer than drenching Cu compounds. Unweaned calves could get one 4-8 g CuO bolus in a gelatin capsule at 2-4 weeks of age(2).
SELENIUM POISONING (see Web article): Under EU Feed Regulations, total Se intake by cattle should not exceed 0.57 mg Se/kg total feed DM.
Endemic Se poisoning occurs in a few localised areas in Ireland, due to toxic Se levels in soil and herbage. Do not use high-Se supplements within 5 miles of known Se-toxic areas without veterinary confirmation of Se deficiency in the herd.
(2)A dose of 8 g CuO/100 kg LW/year usually is recommended in adults. Two doses/year at 4 g/100 kg LW each time gives longer protection than 8 g/100 kg LW given at one time. Especially on high-Mo farms, severely Cu-deficient herds may need 16-20 g CuO/100 kg LW/year but 4-5 doses/year at 4 g/100 kg LW each time gives longer protection than the whole dose given at one time.
Note: CuO capsules can be used safely during the breeding season, but Cu injection is not advisable at that time.