Scientifur publications

HIGHLIGHTS from the IX International Scientific Congress in Fur Animal Production Halifax 2008

Prepared by Dr. Bruce Hunter, Ontario Veterinary College, University of Guelph

#1: Satellite Symposium on Litter Size and Kit Production

The IX International Scientific Congress in Fur Animal Production began with a special one day long symposium organized by Dr. Bente Hansen (Department of Genetics and Biotechnology, Faculty of Agricultural Sciences, Aarhus University, Denmark). This symposium incorporated 13 invited papers (11 mink and 2 blue fox) from international scientists from multiple disciplines including breeding genetics, nutrition, physiology, animal behaviour and pathology. The trans-disciplinary approach provided an excellent overview of issues and factors that affect litter size and kit production. This report is a quick review of the symposium, summarizing areas that I felt were directly relevant to mink farmers. Each paper is published as an abstract or extended abstract in Scientifur Volume 32(4) 2008.

After significant advances in litter size and mink kit survival during the 1980’s and early 1990’s, litter size per mated female has stagnated since 1995 ¹. This symposium was structured to systematically look at factors that might be responsible for this lack of improvement in productivity. Throughout the symposium the term litter size was based on numbers of live kits at 3 days of age (i.e. whelp number minus mortality in the first 3 days of life).

Physiological constraints to litter size:

It is accepted that the lifetime complement of follicles is present at the birth of the female. In pastel mink the number of healthy antral follicles range from 177-352. These follicles must develop in size to at least 0.7 mm in diameter if they are to ovulate. The annual number of follicles available to ovulate averaged 15/animal and this number is likely influenced by genetics. The number of ovulatory follicles can also be manipulated to some degree by environmental conditions and nutrition, so the number of follicles available to be fertilized is a potential constraint on litter size ².

Ovulation is initiated by the breeding process and occurs 36-48 hr after breeding. If a mink is mated 2 or 3 times, the majority of the kits come from the latter breedings suggesting that the breeding process itself causes expulsion of embryos from the first mating. Therefore your breeding protocol may significantly influence litter size.

Fertilization occurs in the oviduct 50-60 hr after breeding. Not all ova become fertilized and there are generally a number of unfertilized ova still present after breeding suggesting that male fertility may be another important constraint to litter size. On some ranches as many as 15% of the males have reduced sperm counts.

The period from breeding to embryo implantation in the uterus (delayed implantation) is a major period of embryo risk as the embryos are floating freely and unprotected in the uterus. Therefore management efforts to reduce the time-to-implantation is very important. Lighting techniques or (much less frequently) the use of chemicals like pimozide (a dopamine antagonist) are used to promote implantation and reduce the pre-implantation mortality. Nutrition is also very important during the implantation period. Brown female mink fed a higher energy allowance during the implantation period (i.e. above maintenance levels) compared to the pre-implantation period had significantly higher litter size and fewer barren females ⁵. This suggested that increased energy at that critical period resulted in more embryos being implanted. This effect was smaller and not significant in black mink.

Embryos are better protected once they have implanted in the uterus, but post-implantation losses still occur. There was disagreement on whether uterine space is a factor limiting litter size. Litters of 18 have been reported so in some animals this is possible and yet other studies examining uteri after whelp have shown that females with litters larger than 10 tend to have an increased number of kits lost and reabsorbed in the uterus based on the presence of placental scars ¹⁰. Feeding low protein in the gestation period resulted in a small increase in the number of barren females. Toxic insults during the gestation period with substances like polychlorinated biphenyls (PCBs) or antiobiotics that interfere with folic acid synthesis like sulfa drugs or trimethoprim sulfa may cause embryonic loss. There are also a significant number of infectious agents including Campylobacter jejuni (often from unwashed chicken offal), E. coli (often from contaminated water sources), Toxoplasma sp. (from young cats), Listeria sp. and other agents that can cause late term mortality or weak born kits ⁹.

Body weight Selection:

Several scientists documented the inverse relationship between selection for large body size (at grading time) and litter size and kit survival ^3,7. Evidence is now emerging that as the mink industry has selected for larger body size this selection process has inadvertently also selected for lower litter size and increased kit mortality.

The importance of female body condition:

Body condition scoring was shown to be a valuable and critical management tool that can greatly impact both litter size and kit survival. Mink researchers around the world utilize the body condition scoring system developed by Kirsti Rouvenin-Watt and Dean Armstrong (see the CMBA newsletter 2007). Body condition is important throughout the breeding cycle and should be repeatedly evaluated right from grading time through the whelping period. Fat mink and thin mink have more dead kits. Females should be fed so that their body condition improves from February through whelping .. without females becoming fat or overweight. An increasing body condition score from a 2 in late February, 3 in late March and 4 in late April was strongly correlated with the number of live-born kits ⁴.

Body condition was also related to the development of the mammary glands and the milking ability of the females ⁶. Mammary development is closely tied to feeding during the last 3 weeks of gestation and fits well with the concept of having females on an ascending body condition scoring during the last weeks of pregnancy. 80% of mammary gland development occurs during these last 3 weeks. Female mink have on average 8 nipples. Each gland is dynamic and becomes active when the kit sucks. If the kit dies the gland becomes inactive, so that the number of active teats should correspond to the number of nursing kits. Mammary glands can become activated up to 12 days post-whelp which partially accounts for their amazing ability to foster new kits. Restricted feeding in the last 3 weeks of gestation results in decreased gland development. Female milking ability is closely linked to kit growth and survival.

Whelping time and early kit growth:

Video observations of whelping mink demonstrated that the birthing time is correlated to number of live born kits. Long birth times (> 10 hr) resulted in increased kit mortality, while shorter birthing times (< 5.5 hr) resulted in more live kits. Birthing time was correlated to body condition. One study on wild type mink showed birthing times averaging approximately 6.5 hr. Birthing problems contributed to both impaired maternal behaviour and early kit mortality. Lack of access to suitable nesting material had a negative effect on early kit mortality and an artificial nest and/or access to straw for nesting reduced the stress in females ¹¹.

Early kit growth is strongly influenced by the dam and it is possible to select for maternal induced kit growth without negatively affecting the dam’s health. Dams genetically disposed for high weight gain during pregnancy are also genetically disposed to induce early growth in kits ⁷.

There are many causes of early kit mortality. Difficult births (dystocia) are correlated with body condition score and over-weight females. Unsuitable nest box environment may result in chilling and weak kits that fail to nurse. Checking of litters in the first few days will reveal problems such as “pimply” kits (Staphylococcus infections of the neonatal skin glands of the neck and inguinal region) and if caught early, successful treatment can be initiated. There are many bacterial problems associated with feed quality and weaning kits onto solid feed. More is becoming known about viral causes of diarrhea in pre-weaned kits including the identification of important viral pathogens like enteric caliciviruses, corona viruses, reoviruses and astroviruses ⁹.

Some key take home messages:

1. careful genetic selection can improve litter size and kit survival.
2. there is significant physiological potential in mink to increase litter size.
3. evaluation of fertility in males needs a higher priority.
4. selection for large body size to meet market demands may be having a significant effect on litter size and kit survival.
5. careful evaluation of body condition and careful feeding during critical periods of the reproduction cycle will have significant positive effects of kit numbers, kit survival and females milking ability. Female body condition score should increase during pregnancy without the animals becoming obese.
6. fat mink and skinny mink have decreased litter numbers and lower kit survival
7. early kit mortality is influenced by the birthing time. Prolonged birthing times correlate with increased kit loss. Birthing time is influenced by body condition score and other management factors such as a providing a comfortable nest box and bedding material.
8. careful examination of nests boxes during the early post-whelp period may reveal disease issues in kits and early treatment may help prevent a disaster.
9. food quality is critical during all stages of the reproductive cycle and particularly during the gestation and the pre-weaning period.
10. avoid using antimicrobial drugs like sulfonamides or trimethoprim sulfas during the gestation period.

References:

1. Hansen BK. Introduction to workshop “Litter size and kit survival”.
2. Lefèvre P and Murphy BD. Physiological constraints on litter size in mink.
3. Hansen BK and Berg P. Reduced litter size and percent kits alive is a consequence

of selecting for high body weight.

4. Baekgaard, Larsen PF, and Sønderup M. Female body condition and early kit

mortality: a description from practice.

5. Møller SH. Feeding during gestation in relation to litter size in mink.
6. Møller SH. Development of mammary glands in mink
7. Hansen BK and Berg P. Genetics of early kit growth and maternal weight changes

during pregnancy and lactation in mink.

8. Matthiesen CF, Blache D, and Tauson A-H. Protein restriction in utero - influence on

metabolic traits and regulatory hormones.

9. Hunter DB. Review of factors associated with mink kit mortality.
10. Clausen TN and Hamme AS. Placental scars in barren females.
11. Houbak B and Malmkvist. Observations of deliveries in mink: Potential for more

kits.

The use of Oxytocin in mink

Prepared by Dr. Bruce Hunter, Ontario Veterinary College, University of Guelph

Introduction:

Each year as whelping time approaches I get calls asking about the use of oxytocin in mink to help with the birthing process. This short fact sheet will hopefully help answer some of these questions.

Oxytocin is a hormone produced in the brain that has great importance at the time of whelping. It is released from a storage area in the brain after the cervix of the female has been distended as the fetus pushes through the birth canal. At the time of parturition the muscles of the uterus are very sensitive to the effects of oxytocin because of other hormones particularly the high estrogen levels. Oxytocin causes the smooth muscles that line the uterus to contract and is important in regulating the strength and coordination of the uterine contractions during birthing. Oxytocin has much less of an effect 48 or more hours after birthing as the estrogen levels that sensitize the uterus have decreased.

Oxytocin is also released when the nipples of the mammary gland are stimulated as the new born begins sucking on the teat. The teat canal system in the mammary gland also contains smooth muscle, and oxytocin stimulates these muscles to contract, helping to push out the mucus plug at the end of the nipple and initiate the milk flow.

In most mammals oxytocin is also released during breeding and helps the sperm move up the oviduct to meet the released ova, again by causing smooth muscle contraction of the uterus.

Clinical uses of oxytocin in mink:

1. Oxytocin can be used to accelerate the process of labor in mink, but should only be used once labor has begun. If oxytocin is used before the cervix is open and relaxed, the powerful contractions that result could rupture the uterus. It should not be used in early stages of labor or if there is a mal-presented fetus blocking the birth canal.
2. Oxytocin can be used to assist in the evacuation of uterine debris or retained placental material from the uterus. Females that fail to “clean” normally after birthing or that continue to have a bloody or cloudy discharge a couple of days after whelping may be helped by treating with oxytocin.
3. Oxytocin is helpful as an adjunct in the treatment of pyometra (pus in the uterus from infection) and chronic endometritis (uterine infections).Appropriate antibiotic therapy is almost always necessary but the oxytocin may be helpful in causing uterine contractions that help evacuate the infected material from the uterus.
4. Oxytocin has value in helping contract the uterus after replacement of a uterine prolapse. This may help keep the animal from prolapsing the uterus a second time. Concurrent antibiotics are usually required.

5. Oxytocin can be very helpful in initiating lactation and milk let-down in females where weak kits are having trouble sucking. Kits must suck on and stimulate the nipples in order to initiate full milk let-down. If the kits are not able for whatever reason to reach the nipples (either they are weak or the mother is nervous and uncooperative), oxytocin may help in stimulating the milking process resulting in the female becoming more maternal and accepting of the kits.
6. Oxytocin has been used as an adjunct therapy in treating mastitis cases. Oxytocin causes the smooth muscle in the gland to contract helping to expel pus, debris and infection from the gland. Treatment with the appropriate antibiotic is a critical part of the treatment and it is unlikely that oxytocin alone will solve a mastitis problem.

Oxytocin should be used with caution. Inappropriate dosage or using it at the wrong time will be very painful for the animal and ineffective as a treatment. If oxytocin is used 48 hr or more after parturition the uterus will no longer be sensitive to the hormone’s effects. In some cases animals can be pre-treated with estrogen therapy to “re-sensitize” the uterus and mammary glands to the hormone. Be sure to consult with your veterinarian if you believe oxytocin is indicated for use on your mink.

There are no dosages reported for mink in the literature. However, we have successfully used 5-10 International Units (IU) to solve some whelping and milk let-down problems in mink. A similar dose range is recommended for use in cats. Most commercial preparations of oxytocin available in Canada contain 20 IU per mL, so the dose is 0.25 to 0.5 mL per animal. It should be given with a sterile needle and a new (clean) syringe. It can be given under the skin (SQ) or into the muscle (IM). Do not reuse the needle or syringe with other medications. Again be sure to consult with your veterinarian.