There is a fair bit of either confusion or misinformation re the origin of TH and PHA - so here are the facts (Whitlock et al Heritable bovine fetal abnormalities Theriogenology 70 (2008) 535–549)
The Tibial hemimelia syndrome was first described in 1951 in Scotland in the Galloway breed of cattle [62]. This lethal condition is characterized by multiple congenital skeletal deformities, most notably shortened absent tibia, abdominal hernia, cryptorchidism, failed Mu¨llerian duct development, hirsutism, and improper neural tube closure, resulting in meningocele (Fig. 11). Calves are born dead or die shortly after birth. The Scottish Galloway Association used test breeding and pregnancy termination to identify carriers and eliminate the autosomal recessive defect from Galloway breeding stock [63].
The syndrome was first described in the USA in 1974 [64], and subsequently in a case report of a female Simmental calf with arthrogryposis, ventral abdominal hernia, tibial hemimelia and the nonunion of Mu¨llerian ducts, with the suggestion that it might be a genetic disorder [65]. A decade later, TH was identified in six genetically related registered Shorthorn calves, three from the USA, and three from Canada [66]. Although the skeletal abnormalities varied, the combination of tibial hemimelia, abdominal hernia and meningocele was felt to be strikingly similar to the condition previously described and determined to be inherited as autosomal recessive.
It is interesting that the phenotype of the heterozygote (straight hind limbs and long shaggy hair coat) was considered desirable in the show ring and frequent use of popular sires lead to excessive inbreeding and increased allele frequency due to selective pressure. The occurrence of affected calves was increasingly noted after 2000. The mutation was traced to the Irish bull Deerpark Improver (ASA # 3,684,142; born 1972), one of a few direct imports to North America. Improver was used extensively in the U.S. in the 1970s, as there are 635 direct progeny registered with the American Shorthorn Association. The defective gene has been shown to be aristaless-like homeobox 4 (ALX4), a major regulator of hind limb formation (J. Beever, personal communication). The Improver deletion removes approximately one-third of the ALX4 gene, including the upstream regulatory sequence and involves approximately 46,000 base pairs. After identification of the Improver deletion, it was noted that although the parentage of some TH calves was DNA-verified, some parents did not test positive for the Improver deletion. Additional studies revealed that the bull TKA Outcast (ASA # 4,046,304; born 2001) possessed a larger deletion of 450,000 base pairs that overlapped the Improver deletion, and removed four genes, including ALX4. The Outcast deletion is rare and affected calves sired by Outcast were ‘‘compound heterozygotes’’ (heterozygous with the Improver mutation on one chromosome and the Outcast mutation on the other). Although ‘‘heterozygous’’, these calves were affected like those homozygous for the Improver deletion. The frequency of the Outcast mutation is so low, and the magnitude of the deletion so much larger, that it is unlikely that there have been any TH calves homozygous for the Outcast deletion. Because samples from the Scottish Galloway cattle are unavailable for testing, it is unclear whether the Improver or Outcast deletions in Shorthorns originated from the Galloway breed or are different mutations.
The popularity of the TH phenotype has led to extensive use of carrier bulls in the club calf and show cattle arena. A substantial number of cattle registered with the Shorthorn, Maine Anjou, Chianina breed Associations, as well as crossbred or composite cattle, are known to carry the defective gene. In 2004, more than half of the top 10 sires for number of Shorthorn registrations were putative carriers. In 2005, 21 of 24 black composite AI sires offered by a single vendor were verified as carriers.
In a 2007 sire directory of popular ‘‘club calf sires’’, one-third of bulls were TH carriers, including clones and sons of a popular TH carrier bull. Of the 10 most popular Shorthorn AI sires for 2006 calves, three were carriers for both TH and PHA and one was a carrier of TH (Shorthorn Country, April 2007).
PHA
Originally PHA calves were identified as Maine- Anjou, Shorthorn or their crosses. The apparent link was three popular bulls: two registered Maine-Anjou bulls (Draft Pick, born 1989; AMAA # 165,744 and Stinger, born 1985; AMAA # 111,205) and a bull registered with the American Chianina Association (Payback, born 1992; ACA # 232,907). Subsequent genetic testing suggested a common ancestor of the three bulls. Because Draft Pick had the most complete pedigree and the largest number of samples available, an informative pedigree was developed and used to identify the defective gene (J Beever personal communication). In that regard, PHA is the result of a single mis-sense mutation common to Draft Pick, Stinger, and Payback, and identified in modern Shorthorn, Maine Anjou, and composite cattle. Draft Pick’s maternal great grand sire, Paramount (AMAA # 77; born 1973), a full-bood Maine-Anjou bull exported from England to Canada, was a PHA carrier. Due to incomplete or inaccurate pedigrees or inability to obtain samples from older full-blood Maine-Anjou cattle, the origin of the mutation in Stinger and Payback has not been positively identified. Molecular markers surrounding the gene suggest the French import Dalton (AMAA # 15; born 1970) as a common source for Stinger and Payback.
In the USA, the Maine-Anjou breed is considered the origin of PHA. In registered Maine-Anjou cattle, Draft Pick is primarily responsible for the widespread dispersion of the mutation, whereas in registered Shorthorn cattle, Stinger is considered primarily responsible. Paramount is also found in the pedigrees of some registered Shorthorn cattle. One registered halfblood Simmental bull, the son of a Stinger cow, has been identified as a PHA carrier. In crossbred, composite or ‘‘club calf’’ cattle, the origin of the defect cannot always be determined.
Heterozygous PHA carriers have a ‘‘normal’’ phenotype and can be identified only by genetic testing. Following identification of the gene in late 2006, over 40 popular Maine-Anjou, Shorthorn, and ‘‘club calf’’ sires were identified as PHA carriers.
Interestingly, several of the most popular Shorthorn bulls are carrier for both TH and PHA. A syndrome similar to PHA was identified in Dexter cattle in 2006 when Windsor et al reported three cases of PHA in the Dexter breed [37]. The cows were related and the inheritance was felt to be autosomal recessive. Although the mutation in the Dexter breed involves the same gene as the condition seen in Maine cattle, it is not the identical defect. The Maine-Anjou mutation was a simple point mutation, whereas the Dexter mutation was an 84 base pair deletion involving the same exon as the Maine mutation.
Contrary to what Mark said Stinger is NOT a TH carrier.
Although DeBull may not have been tested for TH, (he is PHA free) it is believed that Heat Seeker got the TH mutation from his dam BC Tex Shorthorn 23 an Improver daughter
There are multiple double carriers including but not limited to
Donnie
Wild Card
Silver Bullet
Moody Blues
The Bookie
Lights Out
Mindale’s Teddy Bear 305
Bad Moon Rising
XRay Vision
AHL Double Stuff 306
AR SU LU Kool 1007
4D Double Vision
MCF Warhorse
and of course this doesn't really answer the original question 
