Jan. 12, 2000 MANHATTAN -- Saving the life of a dog with Canine Streptococcal Toxic Shock Syndrome requires quick action by the pet owner and awareness of the disease by the attending veterinarian.
That's the word from Dr. Brad Fenwick, Kansas State University veterinarian who has been studying the disease since he first observed it among racing greyhounds. Little is known about transmission or prevention.
"Typically, dogs that develop Canine Streptococcal Toxic Shock Syndrome are healthy prior to being found very sick only a few hours later," Fenwick said. "The course of the disease from initial recognition of disease to death can be as short as six hours. Typically, infected dogs are found lying down, on their side, either too weak to move or experiencing rigidity with mild convulsions. At an early stage vomiting may occur. The dog also may have rapid, uncontrolled fine muscle twitches."
Fenwick said a consistent and important clinical finding is a very high temperature -- greater than 105 degrees F. Treatment at this point with injectable antibiotics, clindamycin or crystalline penicillin-G, is important in order to increase the likelihood of recovery.
As the disease progresses a deep, nonproductive cough typical of pulmonary edema develops. The dog may soon experience spontaneous hemorrhaging including coughing up blood, bleeding from the nose, severe bruising of the skin, and in some cases bloody diarrhea. At this point, antibiotics and even aggressive shock therapy are generally not sufficient to save these dogs. Fenwick said the mortality rate is 70-80 percent for dogs that are not treated quickly and appropriately.
When owners and their veterinarians catch the disease in its early stages, the chances for a recovery are significantly improved, he said.
Although he said the cause may be new strains of Streptococci, Fenwick does not believe Canine Streptococcal Toxic Shock Syndrome is a brand new disease, but rather that it has been misdiagnosed in the past. Cases have been confirmed from as early as 1979.
"It looks very similar to a poisoning -- similar to what can happen when a dog gets into rat poison. It's more of a toxicosis than many other bacterial infections," he said. And although he believes it is more common than once thought -- that cases have been occurring unrecognized for many years, he said it is still relatively uncommon.
"We think it is fairly rare," Fenwick said, "maybe one case in every 50,000 dogs, but that is just a guess, because we do not keep death certificates on dogs, nor do we have reportable statistics on dog deaths. Many veterinarians have never seen a case. Others learn more about it and then recall cases they have had in the past and wonder if a specific case might have been Canine Streptococcal Toxic Shock Syndrome."
Fenwick said some misinformation is being circulated about the syndrome. He said there is no evidence that the disease can be transmitted from dog to dog, from humans to dogs, or from dogs to humans. The human version of the disease first emerged about 10 years ago. Among the victims was Muppet creator Jim Henson. Rapid onset, high fever, hypotension and shock are prominent characteristics of Streptococcal Toxic Shock Syndrome in humans and dogs.
Fenwick does not recommend that dog owners make any changes in their routine to try to prevent the disease.
"There is no justification to do anything differently," he said. "We have no evidence that dog show conditions, crowding, sharing crates or bowls, or stress is a cause of this disease. People should not panic and change what they are doing. There is no reason to stop showing or participating in performance sports."
Also, although Fenwick is conducting research on the disease, dog owners should not expect to see a vaccine for it. The disease is caused by a toxin -- Toxic Shock Toxin -- that is a super-antigen, which short-circuits the immune system. If a vaccine with a super-antigen is injected into an individual, it wouldn't be effective. Fenwick explained that it is the same reason people can get food poisoning over and over again -- the body can't produce an effective immunity against these toxins.
A tissue sample is required to confirm the diagnosis of Canine Streptococcal Toxic Shock Syndrome. If you or your veterinarian have questions, or if you think your dog may have the disease, contact Dr. Brad Fenwick, Kansas State University College of Veterinary Medicine, at (785) 532-4412, or e-mail: email@example.com. Fenwick would like information on any dog who may have or have had Canine Streptococcal Toxic Shock Syndrome, surviving or not. Contact him regarding cultures and tissue samples he needs and where to send them.
Prepared by Cheryl May. For more information contact Fenwick at (785) 532-4412.
"Canine Streptococcal Toxic Shock Syndrome" - Fact sheet
Brad Fenwick D.V.M., M.S., Ph.D., DACVM
Department of Diagnostic Medicine / Pathobiology
College of Veterinary Medicine
Kansas State University
Streptococci are a family of gram-positive bacteria which cause either localized or systemic infections in humans and animals. While some strains rarely cause disease and are often considered to be commensal inhabitants of the skin and mucosal surfaces (oral, nasal, intestinal), other strains are capable of causing life-threatening primary infections. In dogs, Streptococci are known for their ability to occasionally cause septicemia in puppies and a range of localized diseases in adults.
Approximately 10 years ago, new strains of Streptococci (Group A, beta-hemolytic) emerged as the cause of a previously unrecognized disease in humans. The clinical disease became known as Streptococcal Toxic Shock Syndrome (STSS) because it closely mimics the better known "Toxic Shock" in women caused by toxin producing strains of Staphylococci. Rapid onset, high fever, hypotension and shock are prominent characteristics of STSS in humans. At approximately the same time, a number of unusual cases of necrotizing fasciitis (NF) caused by Streptococci were also reported in humans. This syndrome relates to a very aggressive and rapidly advancing infection of subcutaneous tissues with extensive tissue destruction and high mortality rates.
In 1996, Miller and Prescott reported on a series of seven dogs from southern Ontario that had severe systemic disease and shock associated with infection with b-hemolytic Streptococci canis (Group G). In four of these dogs the infection was associated with necrotizing fasciitis. As a result of surgical debridement, supportive medical care, and treatment with antibiotics, all of these dogs survived. In contrast, all three dogs with streptococcal shock without necrotizing fasciitis died or were euthanized within 48 hours. The lungs were considered the primary site of infections in two of these dogs as their clinical signs were related to respiratory distress and shock. Historically, similar disease outbreaks have been reported by Garnett et al (1982) in a group of research dogs, in captive coyotes by Gates and Green in 1979, and in racing Greyhounds in 1981 by Sundberg et al. More recently, multiple outbreaks of fatal STSS occurred in racing Greyhounds in 1992 and again in January/February of 1999. Additional cases have recently been reported in other dog breeds and has become a concern for owners of dogs housed in large groups or participating in shows or performance events. Like in humans, the reason for the emergence/re-emergence of canine STSS/NF is unclear and very little is known about transmission or prevention.
Typically, dogs that develop STSS are healthy prior to being found very sick only a few hours later. The course of the disease of initial recognition of disease to death can be as short as 6 hours. Typically, infected dogs are found in lateral recumbence, either being too weak to move or experiencing rigidity with mild convulsions. At an early stage vomiting may occur. Rapid, uncontrolled fine muscle fasciculations are often noted. A consistent and important clinical finding is a very high temperature (greater than 105 degrees F). Treatment at this point with injectable antibiotics (clindamycin or crystalline penicillin-G) is important in order to increase the likelihood of recovery. As the disease progresses a deep, nonproductive cough typical of pulmonary edema develops. Rapidly, spontaneous hemorrhaging typical of disseminated intravascular coagulation develops which is associated with coughing up blood, bleeding from the nose, severe bruising of the skin, and in some cases bloody diarrhea. Profound hypotension and toxic cardiomyopathy may develop. At this point, antibiotics and even with aggressive shock therapy are generally not sufficient to save these dogs.
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