TOXIC SHOCK SYNDROME DUE TO RESISTANT GROUP A STREPTOCOCCUS IN THE SETTING OF INFLUENZA B COINFECTION
Abstract Number: 675
A healthy 48-year-old male presented to the emergency department with fever, joint pain, fatigue, malaise, and oliguria. One week prior he had been seen at an urgent care clinic for fevers, chills, nasal congestion, and sore throat and was formally diagnosed with influenza B and strep pharyngitis. At that office visit he was prescribed Oseltamivir and Azithromycin, due to a childhood penicillin allergy. On admission, his exam was remarkable for a temperature of 101.1, HR of 106, BP of 95/60, multiple painful, erythematous joints, and desquamation his left hand and forearm. Labs revealed a white blood cell count of 22.6, platelet count of 54, elevated INR and D-dimer, and acute renal failure with a Creatinine of 4.08. Patient was admitted to the ICU for mechanical ventilation and vasopressor support. Blood cultures, surgical cultures of affected joints, and a throat swab all revealed Streptococcus pyogenes with resistance to macrolides. The diagnosis of Strep Toxic Shock Syndrome was made and patient was successfully treated with Cefazolin, high dose Clindamycin, surgical debridement, and supportive care measures.
Discussion: Toxic shock syndrome is a potentially fatal complication of Group A strep infections. Many virulence factors play a role in the development of invasive Group A strep infections, one of which is the M protein, a cell wall bound protein that helps the organism to prevent opsonization and phagocytosis. The M protein is coded for by the emm gene. One particular type, the emm1 type, is associated with higher rates of both macrolide resistance and invasive Group A strep infections. For this reason, the treatment of choice for strep pharyngitis is oral penicillin or an aminopenicillin, however, due to a documented penicillin allergy, our patient had been given Azithromycin. He was later found to be infected with a macrolide-resistant organism. Our patient was also found to be coinfected with the influenza B virus, another factor that has been shown to have a link to increased virulence and higher rates of invasive Group A Strep infections due to effects of the virus on the host immune system, primarily on neuraminidase-mediated increase in bacterial adhesion.
Conclusions: When effectively treated, strep pharyngitis is typically an uncomplicated disease. However, this case serves to show clinicians how resistant subtypes and viral coinfections can attribute to the virulence of Group A Streptococcus, making it a significant and oftentimes complex organism capable of causing devasting disease. It also suggests that increasing knowledge of the molecular basis of Group A Streptococcus will help clinicians to effectively risk stratify patients and choose appropriate therapies.
To cite this abstract:
TOXIC SHOCK SYNDROME DUE TO RESISTANT GROUP A STREPTOCOCCUS IN THE SETTING OF INFLUENZA B COINFECTION.
Abstract published at Hospital Medicine 2017, May 1-4, 2017; Las Vegas, Nev..
Journal of Hospital Medicine Volume 12 Suppl 2.
May 30th 2020.