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8/13/2019 P Anormalidades BS

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GENETICABNORMALITIES IN BROWN SWISS CATTLE

The following four abnormalities found in Brown Swisscattle have been determined to be inherited characteristicscaused by simple recessive genes and declared to beundesirable genetic recessive factors: Weaver (BovineProgressive Degenerative Myeloencephalopathy), SMA(Spinal Muscular Atrophy), Spiderleg (Syndrome of

Arachnomelia and Arthrogryposis [SAA]) and SpinalDysmyelination (SDM). These abnormalities occur as a resultof defects in the genetic code which have been passed on tooffspring as recessives. There is no danger of other animals"catching" them. Recessives can only be passed on throughgenetic inheritance and can only be controlled through carefulbreeding management.

Weaver

Bovine Progressive Degenerative Myelo-encephalopathy(myelodestruction of the spinal cord, encephalopathy changes inthe brain) causes a noticeable weaving gait of the affectedanimal, and this brought about the nickname "Weaver". Dr.Horst Leipold of Kansas State University initially suspected asthe original cause to be a genetic mutation in a Brown Swissmating in the 1920's or 1930's. Prevalence of this recessivewas compounded by inbreeding and the early use of artificialinsemination.

There are four basic criteria used for clinical diagnosis.Pathological examination of the brain and spinal cord is theonly means of verification.

The onset of bilateral (both sides) hind leg

weakness and ataxia (inability to coordinatemovements) normally between six to eighteenmonths of age (around puberty).

Deficient proprioceptive reflexes (nerve impulsesfrom brain not received by muscles in hind legs),but normal motor and sensory reflexes with noother neurological abnormality. (In other words,the animal can't seem to find its hind legs).

Absence of clinically significant skeletal or muscularabnormality.

Adherence to familial relationship (common to abreed). (So far, this has only been found in BrownSwiss.)

What to Look For: Symptoms generally appear from 6 to months of age. Symptoms are caused fromdegeneration of nerve passages in the spinalcord and brain which prevent the transfer onerve impulses from the brain to the legmuscles. Any deterioration of the central

nervous system is permanent and irreversiblSymptoms include:

!Lack of coordination!Hind legs seem to be overstepping too high!Front legs are held far apart to maintain balance!When standing, the animal sways slightly!Hind feet are close together and may cross!Animal often tries to stand against something!Staggering and/or swaying, an erratic gait!Stumbling and falling, especially when excited!Loss of control of pelvic limbs

The animal eventually suffers from malnutrition, so muscleatrophy (wasting away) is apparent. It usually takes up to twor three years to die. During this time, the animal should nobe kept on concrete as it could fall unexpectedly. It is best tkeep the animal in an open lot or on dirt. When the animalcan no longer eat or drink, it should be put down by aveterinarian.

To have an animal clinically verified as a Weaver, the spinalcord and cerebellum (intact) must be obtained as soon aspossible after death and forwarded to an approved laboratorto have the tissue analyzed before it deteriorates.Degeneration of the spinal cord is most evident in thethoracic (chest) area. This spinal cerebellar degeneration iscomparable to Lou Gehrig's disease in humans.

Pictures 1-3 show a Weaver-affected animal

1 Hind feet close or cross while front feet are apart


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Male Weaver carriers through DNA testing:Blessing Cline B Wayne ET (W*) 189420Blessing Cline B Wisdom ET(W*) 189421Blessing Coll Abstract ET (W*) 193925Blessing Collect Accord ET(W*) 193922Cal-Ticino Prediction (W*) 189742Fabs PR An Educate ET (W*) 186370Fabs PR An Elijah (W*) 187604Viking Valley Guiliano ET (W*) 195606Heilinger Babaray Norman (W*) 194575

Hilltop Acres JT Jaguar ET(W*) 192608Forest Lawn Matt Jerry ET (W*) 190144Harts Matthew Raider ET (W*) 192031IW Garbro Preston Nomad ET(W*) 190815Johann Las Vegas (W*) 183920R Hart C B Brad ET (W*) 186966Shen-Val Jubilat Styleman (W*) 184474V B Riedland Marty ET (W*) 193687Viking Valley Garth Twin (W*) 188671Vinra Ensign Hamlet (W*) 191445

Male Weaver carriers through affected offspring:Ash Hollow Tammys Target (W)(M) 1743Autumn Sun of Lees Hill (W) 1079Blessing Johny Customade ET(W) 1826Bridge View Mod Heritage ET(W) 1768Creek Cove Dapper Milestone (W) 1732CMT Notable Renegade (W) 1793H Brigeen Elegant Lou (W) 1757Hermit Haven S D J Sunshine (W) 1670

Holler Hill Taffys Dynamite (W) 1817Idyl Wild BB Flair ET (W) 1832Johann Johnny D (TN) (W) 1722Johann Proud Matthew (W) (M) 1715Meadow View Matt Alex (W) 1830Mile Away Medallion (W) 1815Mort Modern Click (W) 1751Norvic Jason Notable (W)(A) 1599Pope Hilltop JD Cavalier ET(W) 1827Rolling View Modern Stretch(W) 1564Sunny View Prestige (W) 1782Tarafona Dapper Janson (W) 1727

Trout Run Brigadier Twin (W) 1826Tuolumne Touchstone (W) 1830Twin Oaks Jordan (W) 1759Ventures ESP Babaray (W) 1755Ventures Sunny Bruce (W) 1506West Lawn Dorset Improvr(M)(W) 1601Willow Wells Double D J (W) 1701

SMA

Spinal Muscular Atrophy is a condition very easy to miss sinaffected animals usually die of a secondary illness. Most cashave been reported since the mid-1980's. SMA is similar to

Vitamin E or Selenium deficiency and some SMA calves aremistakenly thought to be Weavers. When there is noimprovement with treatment for white muscle disease, SMAseems likely. SMA affects the nervous system characterizedby skeletal muscle atrophy, decreased spinal reflexes, andmotor weakness.

The onset of SMA occurs in a calf's first few weeks of life,usually between three to six weeks of age. In the earliestobserved stages, the calves show loss of strength and balancin the rear legs. They appear to be healthy except for theirstumbling and eventual inability to stand. Though well-fed

and alert, SMA calves will become weaker and lose flesh.

What to look for: SMA symptoms generallyappear from three to six weeks of age. There ino cure for this condition. Symptoms include:!Loss of balance in rear legs!Difficulty in standing!Calves lie with front legs outstretched!Wasting away of muscle mass!Eventual inability to stand!Labored breathing

2 Animal sways or weav es as if intoxicated

3 Animal eventually falls in advanced stages


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4 Shows calf in typical position with front legsoutstretched and upright on sternum

5 Shows weakness of hind legs and wastingaway of muscle mass

As the condition progresses, SMA calves develop motorproblems in the front end. They typically show signs oflabored breathing. At this point, the chest muscles havebegun to atrophy. Once the calf can no longer get up, deathusually occurs within a couple of days. Usually the cause ofdeath is pneumonia by six to eight weeks of age. Theassociation may wish to have the brain and spinal column ofthe affected animal sent to an approved laboratory for clinicalconfirmation.

Pictures 4-5 show an SMA-affected calf

Male SMA carriers through DNA marker testing:Bell-Manor TA Top Rox ET (M*) 191398CAOD Emer Plin Link *TW (M*) 194816Gor Plin Monte *TW (M*) 193244

Horseshoe Hill Pilt Kegger(M*) 197438North Star Bud ET (M*) 198530Old Mill Supremo ET (M*) 197840R Hart Protein Preview (M*) 190739Rolling View Jet Colby ET (M*) 190480Sun-Made Garbro Prstige ET(M*) 193852Top Acres Jet Pilot ET (M*) 191611

Male SMA carriers through affected offspring or DNAgene testing:Alfa Creek Jolt Heratio ET (M) 1974Ash Hollow Tammys Target (W) (M) 1743Aytola Tit Reggiano (M) 1950Chestnut Lane Happy Singer (M) 1780Crows Nest Progression ET (M) 1915Cutting Edge Hawkeye ET (M) 681120Fashion Star Frosty ET (M) 1971

Forest Lawn Jargon ET (M) 1821Forest Lawn Jason ET (M) 1821Forest Lawn Mat Jesse ET*TW(M) 1893Forest Lawn Simon Jetway ET(M) 1853Fox Trail Anchorman (M) 1786Goose Creek Jericho ET (M) 1981Haakes Ilas Evilo Ichabd*TW(M) 1755Hilltop Acres Z Jingo (M) 681033Johann Evilo Rocket (M) 1717Johann Lottery ET (M) 1843Johann Lucifer ET (M) 1831Johann Proud Larry ET (M) 18282Johann Proud Matthew (W) (M) 1715

Johann Stylish (M) 1726Ka Wa Westley (M) 1770Kruses Jetway Flashback ET (M) 1909Lyndale Patrick Eric ET (M) 1888Meadow View Destiny (M) 1186Mort Patrick Tom ET (M) 1875Nakota Destiny Dapper (M) 1484North Star Cale (M) 1965Old Mill JP Sting ET (M) 4702101Old Mill JW Snickstyle ET (M) 1990Onword Vet ET (M) 1992R Hart Cartoon ET (M) 1920R Hart CD Chairman ET (M) 1869

R Hart Christians Pride ET (M) 1912R Hart CJ Jasper ET (M) 1907R Hart CJ Jemstone ET (M) 1903R Hart Connies Precise ET (M) 1926R Hart Ensign Perfecta (M) 1934R Hart Jetway Ice (M) 1907R Hart KC Cedric (M) 1903R Hart PR Crosscut ET (M) 1897Rainbow Hills Zeus Zane ET (M) 1992Red Brae Ace Zenith (M) 1957Red Brae Prelude Zeus (M) 1938Rolling View Compason ET*TW(M) 1889Rolling View Conway ET (M) 1917

Rolling View Cooper ET (M) 1917Roseledge SS BMLL Snappy ET(M) 1989SCF Starbuck Jesse ET (M) 1972Sun-Made Trek ET (M) 1911T-N-T Meadows Zeus Mclovin (M) 6580449To-Bran Col Snowman ET (M) 1984Top Acres M Jet Global ET (M) 1916Top Acres Roll Mead Baerga (M) 1893Top Acres TJR Proctor ET (M) 1922Tuolumne Patrick (M) 1815West Lawn Dorset Improvr(M)(W) 1601West Lawn Stretch Improver (M) 1631White Cloud Doreen Delegate(M) 1469


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7Calf has absence of limb movement and support.

6Animal shows lateral position, opisthotonos,and extended limbs.

8 Calf shows almost normal appearancewhen placed in sternal position.

SDM

Spinal Dysmyelination is a relatively new abnormality found inBrown Swiss cattle. First diagnosed in Germany in 1993, thisdefect has some similarities with SMA, but appears to be adifferent abnormality. While it also affects calves, SDMseems to have a quicker onset time than SMA. While SMAcalves show symptoms from 2 to 12 weeks after birth, SDMshows its affects immediately upon birth of the calf. The calf

cannot stand at all after birth, and it will have spasticmovement in its rear legs although they seem normalotherwise. SDM is also believed to be passed on as a geneticrecessive. This means that two carriers must be mated for thecondition to occur and then it will occur only once in everyfour offspring.

What to look for:SDM symptoms generallyappear at birth. There is no cure for thiscondition. Symptoms include

!Inability to stand immediately after birth!Spastic rear legs

!Calf otherwise alert

As more information is available on SDM, we will keep youupdated additional characteristics of this genetic abnormality.

Pictures 6-8 show SDM-affected calf

Male SDM carriers through affected offspring:Ka Wa Balison (D) 1724Tateys Elegant Loadstar (D) 1724White Cloud Jasons Elegant(D) 1485

Spiderleg

Syndrome of Arachnomelia and Arthrogryposis (SAA), is duto an inherited neuromuscular dysfunction early in gestationCalves are born with both muscular and skeletal deformity.Although only a few cases have been confirmed in the UniteStates, there have been many cases in Europe stemming fromthe use of one bull family's genetics.

What to look for: Affected animals are self-evident. Symptoms include:

!Spiderleg affected calves are usually stillborn or die duringbirth, although some live for a few hours!Legs are abnormally long and thin and are curved or broke

and bent grotesquely!Joints may be hypermobile or frozen (requiring fetaldissection in the uterus to aid in birth)!Fragile bones No te : Spontaneous fractures duringbirth could result in injuries to the dam's uterus andgenital passage.!Small and underdeveloped muscles

!Short, crooked or taut, overstretched tendons!Short skull with dent in the frontal bone!Short lower jaw!Defects in vertebral column (twists)!Large blood vessel aneurysms


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9A newborn Brown Swiss calf afflicted with Spiderleg

10X-ray of hind leg of Brown Swisscalf with Spiderleg

11Stillborn Spiderleg-affected calf

1298-day old Spiderleg-affected fetus

Pictures 9-12 show Spiderleg-affected calves & fetuses

Note arrowsindicating

fractures in long

bones of leg

Male Spiderleg carriers through affected offspring:Betta Vue DQ ET (A) 1802Norvic Jason Notable (W)(A) 1599Norvic Lilasons Beautician(A) 1387Norvic Lilasons Lonance (A) 1396Preabla Pete Rose Amaranto (A) 1957

Shelburne Quality (A) 1521Top Acres Modern Genesis TN(A) 1763Tuolumne Winslow (A) 1767

Reporting Abnormalities

In order to maintain a breed relatively free of undesirablegenetic factors and to provide valuable information formaking breeding decisions, it is recommended that everyBrown Swiss breeder report the occurrence of any abnormalanimal to the National Association office at Beloit, Wisconsi(608) 365-4474. The following guidelines are established for

such reporting:

A. All animals should be reported to the Brown Swiss officeby telephone as soon as they are discovered. Please beprepared to provide as much of the following information aspossible:!A description of the animal and its abnormality

!Identification of the animal, such as registrationnumber and name, tattoo number, etc.!Date of birth!Sire and dam registration number and name!Whether or not the animal itself and its sire and dam

are alive

B. Based on the information received in the original report,the Brown Swiss office may request that blood samples beobtained from the abnormal animal and the sire and dam.These blood samples will be sent to an approved serologylaboratory for parentage verification. The fees for suchparentage verification will be paid by the National BrownSwiss Association.

C. Based on the information received in this initial report, thBrown Swiss Association may request that such abnormalanimals be sent to an approved laboratory for examinationand verification of the abnormality.


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Declaration of Known Carriers

A registered Brown Swiss animal which has met any of thefollowing conditions shall be declared a known carrier of thatgenetic defect.

1. One first-generation offspring must be diagnosed by anapproved laboratory as abnormal because of a recognizedundesirable defect. A second first-generation offspring mustbe inspected by an Association authorized person and verified

to be typical of the undesirable defect. Both affected first-generation offspring must have their parentage verified at alaboratory approved for parentage verification.

2. Three first-generation offspring must be diagnosed by anapproved laboratory as abnormal because of the geneticdefect.3. Tested positive by a BSCBA approved DNA gene test.

A statement will be published in the Brown Swiss Bulletinupon declaration of animals as known carriers. Periodically, alist of known carrier sires will be published in the BrownSwiss Bulletin and published on the association website.

A registered Brown Swiss animal that has completed anapproved testing program for a specified recessive factor andhas been determined to be a probable carrier or non-carrier ofthat genetic recessive at the established confidence level shallbe so declared.

A registered Brown Swiss animal that has been declared to bea carrier for a specified recessive factor as designated by aforeign Brown Swiss Association and meeting the conditionsabove shall be declared a known carrier of that genetic defect.

Designation of Abnormality Carrier Status

Suffixes are a means to inform breeders of the current statusof animals as known carriers or tested probable carriers ornon-carriers of genetic abnormalities. Such animals shall beidentified as follows:

A. An animal confirmed through diagnosis by an approvedlaboratory as abnormal due to an inherited undesirable geneticrecessive factor or the DNA gene test.

1. Confirmed Weaver designated as (CW)2. Confirmed SMA designated as (CM)3. Confirmed Spiderleg designated as (CA)4. Confirmed SDM designated as (CD)

B. Known carriers of undesirable genetic recessive factors1. Known Weaver Carrier designated as (W)2. Known SMA Carrier designated as (M)3. Known Spiderleg Carrier designated as (A)4. Known SDM Carrier designated as (D)

C. An animal determined through an approved marker testingprogram to be a probable carrier at a confidence level of 90%or above

1. Weaver Tested Carrier designated as (W*)2. SMA Tested Carrier designated as (M*)3. Spiderleg Tested Carrier designated as (A*)4. SDM Tested Carrier designated as (D*)

D. An animal determined through an approved testingprogram to be a probable non-carrier at a confidence level o90% or above or the DNA gene test.

1. Tested Non-Carrier for Weaver designated as *TW2. Tested Non-Carrier for SMA designated as *TM3. Tested Non-Carrier for Spiderleg designated as *TA4. Tested Non-Carrier for SDM designated as *TD

Note: Suffixes enclosed in parentheses indicate animal as acarrier or affected with the abnormality. Suffixes withoutparentheses indicate a non-carrier animal.Suffixes with an asterisk indicate the results from an approvemarker testing program at a confidence level of 90% orabove. Suffixes without an asterisk indicate the informationfrom diagnosis of affected animals.

Ethics

The Association considers it an unethical practice to offer fosale a registered Brown Swiss animal, semen from an animalor an embryo from a parent which has been determinedthrough an approved testing program to be a probable carrie

or is a known carrier of an undesirable genetic recessivefactor, unless such fact is made known to the potential buyerIdentifying such an animal in the pedigree or stating such facin advertising such animal, semen, or embryo for sale shall bdeemed as sufficient notice.

Genetics

It is possible for a genetic recessive to be present for manygenerations without being detected. Due to ET flushing,many cows are having increased numbers of offspring andlabeling of the dams is also important.

Animals on the known carrier list still have a place in somebreeding programs. Wholesale elimination of carriers is notpractical. The decision of whether or not to use a knowncarrier sire depends on whether the benefits to be gainedoutweigh the possible consequences of getting carrier oraffected offspring from such a mating. Through carefulbreeding, the number of affected animals can be controlled;and through the use of non-carrier sires, the practical effect othe abnormality can be eliminated over a period of time.

Keeping breeders informed of the genetic nature of recessivand how to breed around them is the key to control of anyabnormality in a breed. Making use of genetic and specific

pedigree information to make wise breeding choices isessential not only to individual progressive breedingmanagement but also to breed progress as a whole.

Cows have 30 pairs of chromosomes which carry all of thecow's genes. Half of an individual animal's genetic material(30 chromosomes) is received from each parent. Each parenthen is only transmitting half of their own genetic material toan offspring. "The luck of the draw" can mean the differencbetween a carrier or non-carrier of a genetic recessive. Usingblue and brown eyes as an example, brown eyes are adominant factor over blue eyes (a recessive factor). If one


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