Infectious Diseases, 2015; 47: 101–103
CASE REPORT
Streptococcal toxic shock syndrome complicating a peritonsillar abscess
MATHILDE AALLING & TEJS EHLERS KLUG Infect Dis Downloaded from informahealthcare.com by Yale Dermatologic Surgery on 07/26/15 For personal use only.
From the Department of Otorhinolaryngology, Head and Neck Surgery, Aarhus University Hospital, Aarhus, Denmark
Abstract A 68-year-old man was admitted to hospital in an acute confusional state with a 2-week history of fever, influenza-like illness and sore throat. He quickly developed coagulation disturbances, hypotension and renal function impairment. Despite broad-spectrum antibiotic therapy, he deteriorated. Group A streptococcus (GAS) was recovered from blood cultures, which gave the diagnosis streptococcal toxic shock syndrome (STSS). A computed tomography scan showed a right-sided peritonsillar abscess (PTA). Acute tonsillectomy was carried out and the patient recovered. STSS complicating PTA has not previously been described in the literature, but GAS is a common pathogen in PTA. Clinicians should be aware that STSS can develop secondary to tonsillar infections and that abscess development should be suspected in STSS patients who do not respond to antibiotic treatment.
Keywords: Group A streptococcus, peritonsillar abscess, streptococcal toxic shock syndrome
Introduction Group A streptococcus (GAS) is a frequent pathogen in mild infections most often located to the throat and the skin. In some cases the infection becomes invasive with associated high morbidity and mortality. The mean annual incidence rate of invasive GAS disease is 2.8/100 000 population in Europe [1]. Streptococcal toxic shock syndrome (STSS) comprises approximately 13% of these cases, with a reported mortality rate of 44% [1]. STSS is caused by an excessive cytokine response to streptococcal superantigens and is characterized by septic shock, multi-organ failure, skin rash and, in some cases, necrotizing fasciitis (NF) [2].
Case report A previously healthy 68-year-old man was admitted to hospital in an acute confusional state with a 2-week history of fever, influenza-like illness and sore throat. Physical examination revealed high fever (41.6°C), light pharyngeal redness without signs of peritonsillar abscess formation (trismus, peritonsillar swelling
and induration), and a reddish rash on the face and chest. Initial laboratory testing showed elevated C-reactive protein, elevated white blood cell count, reduced renal function and coagulation disturbances (Table I). Cerebrospinal fluid, chest X-ray, urine samples and echocardiography were normal. Despite fluid resuscitation and treatment with ceftriaxone and benzylpenicillin, the patient developed septic shock during the first day of admission and was transferred to the intensive care unit. The antibiotic regimen was expanded to include metronidazole and ciprofloxacin, but he deteriorated and therapy with vasopressors and haemodialysis was required. A computed tomography (CT) scan of the head, neck, thorax and abdomen revealed a low attenuation area of 10 ⫻ 10 mm in the right tonsillar region (Figure 1). Acute bilateral tonsillectomy with drainage of a peritonsillar abscess (PTA) was done. There were no signs of tissue necrosis. GAS was recovered from all four blood culture bottles. Yeast was grown from abscess pus culture (obtained after antibiotic treatment was initiated). The patient received one dose of intravenous immunoglobulin (IVIG) (80 g) and therapy was changed to meropenem and clindamycin.
Correspondence: Mathilde Aalling, Department of Otorhinolaryngology, Head and Neck Surgery, Aarhus University Hospital, Nørrebrogade 44, 8000 Aarhus C, Denmark. Tel: ⫹ 45 7846 3344. Fax: ⫹ 45 7846 3180. E-mail: [email protected] (Received 31 July 2014 ; accepted 25 August 2014 ) ISSN 2374-4235 print/ISSN 2374-4243 online © 2014 Informa Healthcare DOI: 10.3109/00365548.2014.961543
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M. Aalling & T. E. Klug Table I. Clinical and biochemical findings during the first 3 days of admission.
Parameter
Infect Dis Downloaded from informahealthcare.com by Yale Dermatologic Surgery on 07/26/15 For personal use only.
Temperature (°C) Systolic blood pressure (mmHg) Heart rate (per min) C-reactive protein (mg/l) Leukocytes (⫻ 109/l) Creatinine (μmol/l) INR APTT (s) D-dimer (mg/l) Fibrinogen (μmol/l) Platelets (⫻ 109/l)
At time of admission
24 h after admission
32 h after surgery
Reference levels
41.6 112 102 217 28.2 212 1.5 39 6.4 17.5 267
40.6 82 124 329 43.6 278 1.8 44 ⬎ 20 18.7 254
38.8 75a 100 261 16.3 410 1.4 48 4.2 15.4 179
35–38 90–140 50–100 ⬍8 3.5–10 60–105 ⬍ 1.2 25–38 ⬍ 0.5 5.5–12 145–350
APTT, activated partial thromboplastin time; INR, international normalized ratio. aMean arterial pressure.
During the following days the patient’s condition improved steadily and 3 weeks later he was discharged. At clinical follow-up 2 months after discharge, he was feeling well and renal function was normal.
Discussion The current case of STSS complicating PTA is the first described in the literature. Previously, a few cases of pharyngitis associated with STSS have been described [3,4]. In these cases surgical debridement was performed but no abscess formation was reported.
STSS is primarily seen secondary to skin and soft tissue infections after minor traumas or surgical procedures [5,6]. However, in 5–35% of cases the primary site of infection is not identified [1,4]. The recommended treatment for STSS is high dose β-lactam antibiotics in combination with clindamycin [7]. Although the effect is controversial, IVIG is often administered to neutralize streptococcal superantigens [8]. Surgical intervention is performed in cases with development of an abscess or NF. Supportive care depends on the type and degree of organ dysfunction and can include mechanical ventilation, haemodialysis and administration of vasopressors and blood products. PTA is a relatively common complication of acute tonsillitis, with an annual incidence rate of 41/100 000 population [9]. The major pathogens are Fusobacterium necrophorum and GAS, which are both sensitive to penicillin [10]. Other rare complications of PTA are parapharyngeal abscess, Lemierre’s syndrome and NF. The case presented here demonstrates that a tonsillar focus should be considered in patients with STSS and other invasive GAS infections. Moreover, abscess development, which requires timely surgical intervention, should be suspected in patients who do not respond to antibiotic treatment. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
Figure 1. CT scan of the head showing a right-sided peritonsillar abscess (black arrow).
[1] Lamagni TL, Darenberg J, Luca-Harari B, Siljander T, Efstratiou A, Henriques-Normark B, et al. Epidemiology of severe Streptococcus pyogenes disease in Europe. J Clin Microbiol 2008;46:2359–67.
Streptococcal toxic shock syndrome
Infect Dis Downloaded from informahealthcare.com by Yale Dermatologic Surgery on 07/26/15 For personal use only.
[2] The Working Group on Severe Streptococcal Infections. Defining the group A streptococcal toxic shock syndrome. Rationale and consensus definition. JAMA 1993;269:390–1. [3] Wood TF, Potter MA, Jonasson O. Streptococcal toxic shocklike syndrome. The importance of surgical intervention. Ann Surg 1993;217:109–14. [4] Stevens DL, Tanner MH, Winship J, Swarts R, Ries KM, Schlievert PM, et al. Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A. N Engl J Med 1989;321:1–7. [5] Svensson N, Oberg S, Henriques B, Holm S, Källenius G, Romanus V, et al. Invasive group A streptococcal infections in Sweden in 1994 and 1995: epidemiology and clinical spectrum. Scand J Infect Dis 2000;32:609–14. [6] Wong CJ, Stevens DL. Serious group a streptococcal infections. Med Clin North Am 2013;97:721–36.
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[7] Zimbelman J, Palmer A, Todd J. Improved outcome of clindamycin compared with beta-lactam antibiotic treatment for invasive Streptococcus pyogenes infection. Pediatr Infect Dis J 1999;18:1096–100. [8] Darenberg J, Ihendyane N, Sjölin J, Aufwerber E, Haidl S, Follin P, et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial. Clin Infect Dis 2003; 37:333–40. [9] Ehlers Klug T, Rusan M, Fuursted K, Ovesen T. Fusobacterium necrophorum: most prevalent pathogen in peritonsillar abscess in Denmark. Clin Infect Dis 2009; 49:1467–72. [10] Klug TE, Henriksen JJ, Fuursted K, Ovesen T. Significant pathogens in peritonsillar abscesses. Eur J Clin Microbiol Infect Dis 2010;30:619–27.
CASE REPORT
Streptococcal toxic shock syndrome complicating a peritonsillar abscess
MATHILDE AALLING & TEJS EHLERS KLUG Infect Dis Downloaded from informahealthcare.com by Yale Dermatologic Surgery on 07/26/15 For personal use only.
From the Department of Otorhinolaryngology, Head and Neck Surgery, Aarhus University Hospital, Aarhus, Denmark
Abstract A 68-year-old man was admitted to hospital in an acute confusional state with a 2-week history of fever, influenza-like illness and sore throat. He quickly developed coagulation disturbances, hypotension and renal function impairment. Despite broad-spectrum antibiotic therapy, he deteriorated. Group A streptococcus (GAS) was recovered from blood cultures, which gave the diagnosis streptococcal toxic shock syndrome (STSS). A computed tomography scan showed a right-sided peritonsillar abscess (PTA). Acute tonsillectomy was carried out and the patient recovered. STSS complicating PTA has not previously been described in the literature, but GAS is a common pathogen in PTA. Clinicians should be aware that STSS can develop secondary to tonsillar infections and that abscess development should be suspected in STSS patients who do not respond to antibiotic treatment.
Keywords: Group A streptococcus, peritonsillar abscess, streptococcal toxic shock syndrome
Introduction Group A streptococcus (GAS) is a frequent pathogen in mild infections most often located to the throat and the skin. In some cases the infection becomes invasive with associated high morbidity and mortality. The mean annual incidence rate of invasive GAS disease is 2.8/100 000 population in Europe [1]. Streptococcal toxic shock syndrome (STSS) comprises approximately 13% of these cases, with a reported mortality rate of 44% [1]. STSS is caused by an excessive cytokine response to streptococcal superantigens and is characterized by septic shock, multi-organ failure, skin rash and, in some cases, necrotizing fasciitis (NF) [2].
Case report A previously healthy 68-year-old man was admitted to hospital in an acute confusional state with a 2-week history of fever, influenza-like illness and sore throat. Physical examination revealed high fever (41.6°C), light pharyngeal redness without signs of peritonsillar abscess formation (trismus, peritonsillar swelling
and induration), and a reddish rash on the face and chest. Initial laboratory testing showed elevated C-reactive protein, elevated white blood cell count, reduced renal function and coagulation disturbances (Table I). Cerebrospinal fluid, chest X-ray, urine samples and echocardiography were normal. Despite fluid resuscitation and treatment with ceftriaxone and benzylpenicillin, the patient developed septic shock during the first day of admission and was transferred to the intensive care unit. The antibiotic regimen was expanded to include metronidazole and ciprofloxacin, but he deteriorated and therapy with vasopressors and haemodialysis was required. A computed tomography (CT) scan of the head, neck, thorax and abdomen revealed a low attenuation area of 10 ⫻ 10 mm in the right tonsillar region (Figure 1). Acute bilateral tonsillectomy with drainage of a peritonsillar abscess (PTA) was done. There were no signs of tissue necrosis. GAS was recovered from all four blood culture bottles. Yeast was grown from abscess pus culture (obtained after antibiotic treatment was initiated). The patient received one dose of intravenous immunoglobulin (IVIG) (80 g) and therapy was changed to meropenem and clindamycin.
Correspondence: Mathilde Aalling, Department of Otorhinolaryngology, Head and Neck Surgery, Aarhus University Hospital, Nørrebrogade 44, 8000 Aarhus C, Denmark. Tel: ⫹ 45 7846 3344. Fax: ⫹ 45 7846 3180. E-mail: [email protected] (Received 31 July 2014 ; accepted 25 August 2014 ) ISSN 2374-4235 print/ISSN 2374-4243 online © 2014 Informa Healthcare DOI: 10.3109/00365548.2014.961543
102
M. Aalling & T. E. Klug Table I. Clinical and biochemical findings during the first 3 days of admission.
Parameter
Infect Dis Downloaded from informahealthcare.com by Yale Dermatologic Surgery on 07/26/15 For personal use only.
Temperature (°C) Systolic blood pressure (mmHg) Heart rate (per min) C-reactive protein (mg/l) Leukocytes (⫻ 109/l) Creatinine (μmol/l) INR APTT (s) D-dimer (mg/l) Fibrinogen (μmol/l) Platelets (⫻ 109/l)
At time of admission
24 h after admission
32 h after surgery
Reference levels
41.6 112 102 217 28.2 212 1.5 39 6.4 17.5 267
40.6 82 124 329 43.6 278 1.8 44 ⬎ 20 18.7 254
38.8 75a 100 261 16.3 410 1.4 48 4.2 15.4 179
35–38 90–140 50–100 ⬍8 3.5–10 60–105 ⬍ 1.2 25–38 ⬍ 0.5 5.5–12 145–350
APTT, activated partial thromboplastin time; INR, international normalized ratio. aMean arterial pressure.
During the following days the patient’s condition improved steadily and 3 weeks later he was discharged. At clinical follow-up 2 months after discharge, he was feeling well and renal function was normal.
Discussion The current case of STSS complicating PTA is the first described in the literature. Previously, a few cases of pharyngitis associated with STSS have been described [3,4]. In these cases surgical debridement was performed but no abscess formation was reported.
STSS is primarily seen secondary to skin and soft tissue infections after minor traumas or surgical procedures [5,6]. However, in 5–35% of cases the primary site of infection is not identified [1,4]. The recommended treatment for STSS is high dose β-lactam antibiotics in combination with clindamycin [7]. Although the effect is controversial, IVIG is often administered to neutralize streptococcal superantigens [8]. Surgical intervention is performed in cases with development of an abscess or NF. Supportive care depends on the type and degree of organ dysfunction and can include mechanical ventilation, haemodialysis and administration of vasopressors and blood products. PTA is a relatively common complication of acute tonsillitis, with an annual incidence rate of 41/100 000 population [9]. The major pathogens are Fusobacterium necrophorum and GAS, which are both sensitive to penicillin [10]. Other rare complications of PTA are parapharyngeal abscess, Lemierre’s syndrome and NF. The case presented here demonstrates that a tonsillar focus should be considered in patients with STSS and other invasive GAS infections. Moreover, abscess development, which requires timely surgical intervention, should be suspected in patients who do not respond to antibiotic treatment. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
Figure 1. CT scan of the head showing a right-sided peritonsillar abscess (black arrow).
[1] Lamagni TL, Darenberg J, Luca-Harari B, Siljander T, Efstratiou A, Henriques-Normark B, et al. Epidemiology of severe Streptococcus pyogenes disease in Europe. J Clin Microbiol 2008;46:2359–67.
Streptococcal toxic shock syndrome
Infect Dis Downloaded from informahealthcare.com by Yale Dermatologic Surgery on 07/26/15 For personal use only.
[2] The Working Group on Severe Streptococcal Infections. Defining the group A streptococcal toxic shock syndrome. Rationale and consensus definition. JAMA 1993;269:390–1. [3] Wood TF, Potter MA, Jonasson O. Streptococcal toxic shocklike syndrome. The importance of surgical intervention. Ann Surg 1993;217:109–14. [4] Stevens DL, Tanner MH, Winship J, Swarts R, Ries KM, Schlievert PM, et al. Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A. N Engl J Med 1989;321:1–7. [5] Svensson N, Oberg S, Henriques B, Holm S, Källenius G, Romanus V, et al. Invasive group A streptococcal infections in Sweden in 1994 and 1995: epidemiology and clinical spectrum. Scand J Infect Dis 2000;32:609–14. [6] Wong CJ, Stevens DL. Serious group a streptococcal infections. Med Clin North Am 2013;97:721–36.
103
[7] Zimbelman J, Palmer A, Todd J. Improved outcome of clindamycin compared with beta-lactam antibiotic treatment for invasive Streptococcus pyogenes infection. Pediatr Infect Dis J 1999;18:1096–100. [8] Darenberg J, Ihendyane N, Sjölin J, Aufwerber E, Haidl S, Follin P, et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial. Clin Infect Dis 2003; 37:333–40. [9] Ehlers Klug T, Rusan M, Fuursted K, Ovesen T. Fusobacterium necrophorum: most prevalent pathogen in peritonsillar abscess in Denmark. Clin Infect Dis 2009; 49:1467–72. [10] Klug TE, Henriksen JJ, Fuursted K, Ovesen T. Significant pathogens in peritonsillar abscesses. Eur J Clin Microbiol Infect Dis 2010;30:619–27.
