Fatal Case of Toxic Shock-Like Syndrome Due to Group C Streptococcus Associated with Superantigen Exotoxin

Abstract

Group C streptococci have been reported to cause invasive disease similar to that classically associated with group A streptococcus (GAS). We describe a fatal case of toxic shock-like syndrome due to Streptococcus equi subsp. zooepidemicus. The causative organism did not possess any known GAS superantigen exotoxin genes but did show evidence of superantigen production. CASE REPORTA 63-year-old man developed left thigh pain and swelling while on an airplane flight. Two hours later, he developed fever, rigors, and a rapidly progressing skin rash on his trunk and limbs. Two days earlier, after presenting with vertigo and vomiting, he had received an intramuscular injection of prochlorperazine into the left thigh for presumed acute labyrinthitis.Treatment was commenced for presumed meningococcal sepsis with intravenous (i.v.) benzylpenicillin and ceftriaxone at his local hospital. A cranial computerized tomography scan showed no abnormalities. He was intubated for a reduced conscious state and transferred to the intensive care unit at our institution.Examination revealed a temperature 39.5°C, a pulse of 120/ min, a blood pressure of 100/60 mmHg, and a confluent erythematous skin rash on his trunk and limbs, with petechiae on his legs. His left thigh was tender, swollen, and erythematous. Hypotension developed requiring inotropic support, and there were no other clinical features of toxic shock syndrome (TSS).Initial investigations revealed a leukocyte count of 5.1 ϫ 10 9 /liter (61% neutrophils, 18% band neutrophils) and a platelet count of 25 ϫ 10 9 /liter; the blood film showed neutrophilia with a left shift and toxic granulations. The C-reactive protein level was 239 mg/liter (normal range, Ͻ5 mg/liter). Serum urea was 12.8 mmol/liter (normal range, 2.5 to 9.6 mmol/liter), creatinine was 194 mol/liter (normal range, 40 to 120 mol/ liter), calcium was 1.84 mmol/liter (normal range, 2.2 to 2.6 mmol/liter), and lactate was 9. An ultrasound scan revealed generalized edema of the anterolateral musculature of the left thigh with no abscess. At operation, there was marked subcutaneous and muscle edema but no obvious necrosis. Biopsies demonstrated muscle necrosis and gram-positive cocci. Treatment was continued for presumed group A streptococcus-associated soft-tissue infection and TSS with benzylpenicillin and clindamycin plus i.v. immunoglobulin (IVIG) at 1.5 g/kg.Postoperatively, he had a persistent fever exceeding 40°C and developed progressive multisystem organ failure. Repeat hemoglobin was 7.9 g/dl, leukocytes were 26.0 ϫ 10 9 /liter, and platelets were 14 ϫ 10 9 /liter. He had circulatory failure, requiring high-dose i.v. adrenaline and noradrenaline infusions, and ventricular tachycardia, requiring cardioversion. A transthoracic echocardiogram revealed severe global hypokinesis with no evidence of endocarditis. Respiratory failure developed with increasing hypoxia and ventilatory requirements. Chest radiograph revealed bilateral diffuse pulmonary alveolar opacities. Anuric renal failure (serum creatinine, 402 m...

Clonal Relationships between Invasive and Noninvasive Lancefield Group C and G Streptococci and emm -Specific Differences in Invasiveness

“…More recently, an increasing number of reports described the association with streptococcal syndromes typically caused by Streptococcus pyogenes (Lancefield group A streptococcus [GAS]), such as streptococcal toxic shock syndrome (STSS) (16,19) and acute rheumatic fever (15). Despite differences in the disease burden attributable to each of these organisms, GGS, GCS, and GAS are closely related genetically and share several virulence factors (9,12).…”

Coinfected cases with equine herpesvirus type 1, 4 and Streptococcus equi subsp. zooepidemicus in throughbred horse

“…S. zooepidemicus may be found in the nasopharynx, tonsils, respiratory tract, and on the genital mucous membrane of healthy horses. It is an important cause of respiratory tract infections in foals and young horses, and associated with uterine infections in mares (Anzai et al, 2002;Korman et al, 2004). Damage from Herpesvirus infection to the protective respiratory mucosal barrier predisposes affected horses to opportunistic bacterial infections.…”

Lesson of the month 2: Toxic shock syndrome

“…Clindamycin also suppresses lipopolysaccharideinduced monocyte synthesis of TNF-α. 16 Intravenous immunoglobulin (IVIG) therapy reduces T cell production of pro-infl ammatory cytokines, and signifi cantly increases the plasma neutralising activity against superantigens, thereby resulting in improved survival in many TSS studies. 16,17 IVIG therapy has also demonstrated an anti-TSST-1 effect and signifi cantly improved survival in cases of S aureus TSS.…”

“…16 Intravenous immunoglobulin (IVIG) therapy reduces T cell production of pro-infl ammatory cytokines, and signifi cantly increases the plasma neutralising activity against superantigens, thereby resulting in improved survival in many TSS studies. 16,17 IVIG therapy has also demonstrated an anti-TSST-1 effect and signifi cantly improved survival in cases of S aureus TSS. 18 Identifi cation of potentially implicated foreign bodiesespecially tampons, surgical drainage and irrigation or excision of infected sites such as implants or necrotizing fasciitis -is of high priority, and input from surgical teams can be essential.…”