including higher feed efficiency and greater yield of lean meat, although there was a
higher incidence of PSE pork (Leach et al. 1996 ). One production strategy has been to
use a heterozygous boar with non-carrier sows in order to produce approximately
25% offspring with desirable growth performance and carcass attributes while
avoiding losses from stress-related deaths (Ritter et al. 2008 ).
Malignant hyperthermia has been recognised as a syndrome in horses since at
least 1975 (Klein 1975 ), with multiple reports of adverse responses to halothane
anaesthesia and/or succinylcholine (Waldron-Mease et al. 1981 ; Hildebrand and
Howitt 1983 ; Manley et al. 1983 ; Riedesel and Hildebrand 1985 ; Aleman et al.
2005 ). Enhanced responsiveness of biopsied muscle from affected horses to halo-
thane, succinylcholine, and caffeine contracture tested in vitro (used clinically to
test for malignant hyperthermia susceptibility in humans) has also been documen-
ted (Waldron-Mease et al. 1981 ; Klein et al. 1989 ). Reported affected breeds
include Quarter horse, Thoroughbred, Appaloosa, Arabian, and also some pony
breeds (Aleman et al. 2009 ). A missense mutation (c.7369c>g; p.R2454G) in exon
46 of the equineRyR1gene has been identified in two Quarter horses that died as the
result of anaesthesia-induced malignant hyperthermia reaction (Aleman et al. 2004 ;
Fig. 6 ). Sarcoplasmic reticulum preparations from these horses also showed higher
affinity and density of ryanodine receptor binding sites. Interestingly, both horses
were heterozygous for the mutation, suggesting a dominant mode of inheritance,
like humans but unlike pigs. In addition, other clinical manifestations including
non-anaesthetic-induced, exertional and non-exertional rhabdomyolysis, hyperther-
mia and other myopathies were also described in other Quarter horses that were
heterozygous for this mutation (Aleman et al. 2009 ). A recent survey of 225
randomly selected Quarter horses in the US indicated a prevalence of 1.3% for
RyR1c.7369c>g (Nieto and Aleman 2009 ). At present it is not known whether this
same mutation occurs in other equine breeds, or whether other mutations in the
RyR1gene have arisen independently.
Malignant hyperthermia was first reported in dogs in 1973 (Short and Paddleford
1973 ) and there have since been several case reports, although in most instances
there were rarely specific confirmatory tests such as drug re-challenge or muscle
biopsy contraction testing (Leary et al. 1983 ; O’Brien et al. 1983 , 1990 ; Kirmayer
et al. 1984 ; Nelson 1991 ). Canine malignant hyperthermia syndrome lacks some of
the clinical features characteristic in other species, including lactic acidosis and
early onset muscle rigidity, while the most prominent sign in dogs is hypercapnia.
No particular breed sensitivity has been identified, with reported breeds including
Pointer, Greyhound, Labrador retriever, Saint Bernard and Springer Spaniels
(Brunson and Hogan 2004 ). Although at one time it was proposed that Greyhounds
may be more susceptible to malignant hyperthermia (Leary et al. 1983 ), neither
in vivo halothane–succinylcholine challenge nor in vitro muscle biopsy contraction
tests revealed a difference in susceptibility of a randomly selected group of
Greyhounds (n¼7) compared with mixed-breed dogs (n¼6) (Cosgrove et al.
1992 ). A mixed-breed colony of halothane–succinylcholine challenge susceptible
dogs was established and studied for a number of years, yielding insights into the
pathophysiology of this syndrome in humans (Roberts et al. 2001 ). Genetic studies
68 C.M. Mosher and M.H. Court