Injury to the hamstring muscle complex (HMC) is extremely common in the athletic community. Anatomical and functional aspects of the HMC predispose it to injury, including the fact that the muscles cross two joints and undergo eccentric contraction during the gait cycle. Injury most commonly occurs at the muscle tendon junction but may occur anywhere between the origin and insertion. Complete hamstring avulsions require early surgical repair. The principal indication for imaging is in a triage role to rule out or confirm proximal hamstring avulsion. Acute onset and chronic posterior thigh and buttock pain may relate to pathology at the hamstring origin or muscle tendon junction that can be readily defined on magnetic resonance imaging or, less frequently, ultrasound. Some cases of buttock and thigh pain may relate to spinal pathology. In the elite athlete there is an increasing emphasis on optimizing the rehabilitation process after hamstring injury, to minimize the absence from sports and improve the final outcome. Imaging has a role in confirming the site of injury and characterizing its extent, providing some prognostic information and helping plan treatment. There is increasing interest in the use of growth factors to accelerate healing after muscle and tendon injury. Animal studies have demonstrated clear benefits in terms of accelerated healing. There are various methods of delivery of the growth factors, all involving the release of growth factors from platelets. These include plasma rich in platelets and autologous blood. Clinical studies in humans are very limited at this stage but are promising. At present the World Anti-Doping Authority bans the intramuscular administration of these agents. Other percutaneous injection therapies include the use of Actovegin and Traumeel S and antifibrotic agents.
BackgroundStrains of Dirofilaria immitis suspected of lack of efficacy (LOE) to macrocyclic lactone (ML) preventive drugs have been increasingly reported in dogs by practicing veterinarians since 2005 in the Lower Mississippi Delta region. If proven, and not controlled in the early stages, the emergence of ML drug resistance threatens to become a widespread problem in the US that may limit the effectiveness of current preventive drug treatment methods.MethodsTo validate practice reports, a statewide survey of Louisiana veterinarians was done to define the extent of the problem and identify focal ‘hotspots’ of reported ML LOEs using Geographic Information Systems (GIS) methods. The present study then utilized microfilariae (Mf) from two canine field cases from different state locations that fit criteria for a high index of suspicion of LOE against heartworms by ML drugs. Blood containing Mf from the canine field cases was used to infect and produce L3 in Aedes aegypti for experimental infection of two groups of dogs, each of which contained two laboratory dogs, one treated with prophylactic ivermectin (12 μg/kg) monthly for 6 months at twice the label dose (6 μg/kg), and one untreated control.ResultsBoth treated and untreated dogs from Group I and Group II developed patent D. immitis infections by 218 DPI and 189 DPI, respectively, as evidenced by a positive occult heartworm antigen test and microfilaremia by the Knott’s test. Mf counts gradually increased post-patency in test and control dogs. Infective larvae raised from microfilariae from the treated Group I dog were used to successfully establish a second generation isolate, confirming heritability of resistance in the face of a monthly ivermectin challenge dose of 24 μg/kg, given monthly for 3 months.ConclusionsThese experimental infection studies provide in vivo evidence of the existence of ML drug resistance in dogs infected by D. immitis L3 from suspect field LOE cases in the Lower Mississippi Delta. Results encourage further work on mechanisms underlying the emergence of ML resistance in D. immitis and development of evidence-based resistance management strategies for heartworm preventives in order to extend the useful life of current drugs.
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