Journals | Policy | Permission

This journal has moved to cii.elmerpub.com Please go to the new site to make submissions

Clinical Infection & Immunity

Case Report

Volume 1, Number 2, December 2016, pages 45-47

Iliopsoas Abscess Caused by Streptococcus pyogenes: A Case Report

Recently, the number of fatal infections caused by the so-called “flesh-eating bacteria” has increased and been brought to the spotlight. Streptococcus pyogenes, Vibrio vulnificus, and Aeromonas hydrophila are well-known causes of fatal infections. Several Streptococcus species, including S. agalactiae, S. pneumoniae, and S. milleri group, are known to cause iliopsoas abscess resulting from bacteremia or direct spread from vertebral osteomyelitis and epidural abscesses. S. pyogenes is a member of the Streptococcaceae family and is a wide-spread human pathogen that can cause several infectious diseases, including pneumonia, pharyngitis, scarlet fever, and glomerulonephritis. However, iliopsoas abscess caused by S. pyogenes has rarely been reported. Here we present a case of iliopsoas abscess caused by S. pyogenes.

A 64-year-old female presented to our hospital with a complaint of severe pain on the left side of her back. She worked in an office. She had no past medical history and had been doing well before the clinical presentation. A week before her arrival, she recollected that she had a sore throat and gastrointestinal symptoms, including nausea, vomiting, and diarrhea. A day before arrival, she experienced severe pain on the left side of her back. At first, she visited an orthopedist and was diagnosed with lumbar disc herniation on the basis of X-ray findings. Although pain-killers were prescribed, the patient’s back pain was not alleviated. Moreover, she developed cyanosis of the mouth and cold extremities. She was then suspected to have gone into shock and was transferred to our hospital.

Upon arrival, the patient was alert and repeatedly complained of severe pain on the left side of her back. Cyanosis of the mouth and extremities was apparent. There were no skin scratches, wounds, or infection in her tonsils and pharynx. Examination of the vital signs showed the following: blood pressure 98/54 mm Hg, heart rate 74 beats/min, body temperature 36.0 °C, and percutaneous oxygen saturation (SpO₂) 96% under atmospheric air. An arterial blood gas analysis revealed metabolic acidosis (pH 7.369, pCO₂ 98.0 mm Hg, pO₂ 22.3 mm Hg, HCO_3^- 12.5 mmol/L, and base excess -10.9 mmol/L). Blood examination revealed moderately elevated liver enzyme levels (aspartate aminotransferase 256 IU/L and alanine transaminase 150 IU/L), renal dysfunction (serum creatinine 2.57 mg/dL and blood urea nitrogen 45.2 mg/dL), moderately elevated lactate dehydrogenase (436 IU/L), severely increased creatinine phosphokinase (8,496 IU/L), severely elevated C-reactive protein levels (29.18 mg/dL), and remarkably elevated procalcitonin levels (96.5 ng/mL). Furthermore, coagulation dysfunction was noted (prothrombin time 65%, international normalized ratio 1.38, fibrin and fibrinogen degradation product 15 μg/mL, and D-dimer 7.10 μg/mL).

Contrast-enhanced computed tomography (CT) scan revealed swelling of the left iliopsoas muscle (Fig. 1a). Her clinical symptoms and imaging findings were indicative of an iliopsoas abscess. The patient was also diagnosed with sepsis-associated multiple organ failure. Immediately after admission to the intensive care unit (ICU), her respiratory condition worsened to SpO₂ 89% under atmospheric air, prompting oxygen inhalation therapy. Systemic blood pressure then dropped to 70 mm Hg, requiring continuous administration of dopamine. Concurrent broad spectrum antibiotics, including vancomycin, sulbactam/ampicillin, and meropenem, were initiated. Thereafter, a dialysis catheter was inserted to initiate hemodialysis, including continuous hemodiafiltration (CHDF) and polymyxin-B direct hemoperfusion (PMX-DHP). Three hours after the initiation of CHDF and PMX-DHP, her blood pressure suddenly dropped further, and she went into cardiac arrest. The administration of several doses of adrenaline, as well as chest compressions, restored her heartbeat. However, several minutes after cardiac restoration, cardiac arrest recurred several times. Eventually, she died 22 h after arrival. Blood culture obtained on arrival revealed the presence of S. pyogenes (Fig. 1b).

Click for large image

Figure 1. (a) Contrast-enhanced computed tomography scan revealed swelling of the left iliopsoas muscle (arrow). (b) Blood culture obtained on arrival revealed the presence of S. pyogenes (Gram staining). (c, d) Microscopic analysis of the left iliopsoas muscle revealed the presence of Streptococcus (c: hematoxylin and eosin staining; d: Giemsa staining).

An autopsy was performed after the consent of her family. Gross examination of the body revealed purple spots across the entire body. The autopsy confirmed iliopsoas abscess on the left side. Microscopic analysis of the left iliopsoas muscle revealed the presence of Streptococcus (Fig. 1c, d). The final diagnosis was necrotizing fasciitis and myositis of the iliopsoas muscle caused by group A β-hemolytic Streptococcus (GAS).

S. pyogenes, a member of the Streptococcaceae family, is a part of the normal flora of the human skin, intestines, and pharynx. It is the only species of Lancefield group A, hence the term GAS is known to be a widespread human pathogen that can cause several infectious diseases, including pneumonia, pharyngitis, tonsillitis, rheumatic fever, scarlet fever, septicemia, and glomerulonephritis. Fatal conditions caused by S. pyogenes include streptococcal toxic shock syndrome (STSS), necrotizing fasciitis, and myositis. A fibrillar layer on the surface of GAS is formed by M and T proteins as a protein antigen, and GAS is classified according to its surface antigen. More than 100 M protein serotypes and approximately 50 T protein serotypes have been discovered. M protein plays an important role in GAS virulence and serves to protect GAS from phagocytosis by polymorphonuclear leukocytes; thus, the survival of GAS in human tissues and fluids depends on its M protein [1]. Muscle abscess in GAS infections may be explained by its aggressive nature of invading soft tissue and muscles, spreading to and invading adjacent tissues, and eventually causing systemic dissemination.

Iliopsoas abscess presents as a triad of limpness, back pain, and fever. Notably, however, only 30% of patients with iliopsoas abscess present with the triad of symptoms [2]. In our patient, severe back pain was the key to detection and correct diagnosis. Patients with iliopsoas abscess generally present with atypical symptoms, including deteriorating consciousness, coma, and appetite loss. Imaging modalities, including CT, magnetic resonance imaging (MRI), and ultrasonography, are crucial for quickly and correctly diagnosing iliopsoas abscess. Iliopsoas abscesses form in either of two ways. One way is through hematological or lymphatic routes from other infection site, and the other is through direct dissemination from organs adjacent to the iliopsoas muscle, including spinal caries, peritoneal cavity, ureter, or colon. Reported causative agents of iliopsoas abscesses include Streptococcus species, and Escherichia coli [3]. Treatments of iliopsoas abscesses include anti-bacterial treatment, and percutaneous and surgical drainage. In our patient, abscess drainage was considered an unsuitable surgical intervention because of the patient’s unstable circulatory and respiratory condition. It is reported that mortality rates of psoas abscess are around 25% [4]; however, in our patient, the rapid deterioration of her condition stemmed from the virulence of S. pyogenes, presenting as a form of purpura fulminans [5].

Few case reports about iliopsoas abscess caused by S. pyogenes have been published. As far as case reports about iliopsoas abscess caused by S. pyogenes are concerned, four articles were obtained [6-9]. In these case reports, iliopsoas abscess was presumably formed through bloodstream infection from the skin or pharynx. In our patient, no specimen was obtained from her throat; however, her history of an upper respiratory infection prior to arrival to the hospital may suggest this as a portal into the bloodstream. Considering the nature of S. pyogenes that it spread rapidly hematogenously or lymphatically, psoas abscess may occur as a result of skin or mucosal infections. In order to save patients infected with S. pyogenes, immediate and intensive treatment, including antibacterial treatment, infection removal, and management of respiratory and circulatory disorders must be provided. Upon arrival, our patient already had septicemia and was in poor general condition; there may not have been any medical options to prevent her condition from further deteriorating. Regrettably, there may have been little chance to save the patient with antibacterial treatment and surgical intervention due to its inherent nature even if iliopsoas abscess in this patient was revealed at an earlier period. With an aging society, the burden of dealing with this kind of infectious disease may increase. Hence, physicians should be more aware of critical and fatal iliopsoas abscess caused by S. pyogenes.

Here we present a critical infectious disease caused by S. pyogenes. Our case may well depict the aggressive nature of S. pyogenes. Little is known about iliopsoas abscess resulting from S. pyogenes infection. This case report may help physicians to recognize the critical infections in psoas abscess probably spread from the superficial infection of the skin or mucosa.

Competing Interests

The authors declare that they have no competing interests.

1. Metzgar D, Zampolli A. The M protein of group A Streptococcus is a key virulence factor and a clinically relevant strain identification marker. Virulence. 2011;2(5):402-412.
   doi pubmed
2. Suzuki K, Yamaguchi T, Iwashita Y, Yokoyama K, Fujioka M, Katayama N, Imai H. Case Series of Iliopsoas Abscesses Treated at a University Hospital in Japan: Epidemiology, Clinical Manifestations, Diagnosis and Treatment. Intern Med. 2015;54(17):2147-2153.
   doi pubmed
3. Ricci MA, Rose FB, Meyer KK. Pyogenic psoas abscess: worldwide variations in etiology. World J Surg. 1986;10(5):834-843.
   doi pubmed
4. Hsieh MS, Huang SC, Loh el W, Tsai CA, Hung YY, Tsan YT, Huang JA, et al. Features and treatment modality of iliopsoas abscess and its outcome: a 6-year hospital-based study. BMC Infect Dis. 2013;13:578.
   doi pubmed
5. Smith OP, White B. Infectious purpura fulminans: diagnosis and treatment. Br J Haematol. 1999;104(2):202-207.
   doi
6. Routier E, Bularca S, Sbidian E, Roujeau JC, Bagot M. [Two cases of psoas abscesses caused by group A beta-haemolytic streptococcal infection with a cutaneous portal of entry]. Ann Dermatol Venereol. 2010;137(5):369-372.
   doi pubmed
7. Lau SK, Woo PC, Yim TC, To AP, Yuen KY. Molecular characterization of a strain of group a streptococcus isolated from a patient with a psoas abscess. J Clin Microbiol. 2003;41(10):4888-4891.
   doi pubmed
8. Viani RM, Bromberg K, Bradley JS. Obturator internus muscle abscess in children: report of seven cases and review. Clin Infect Dis. 1999;28(1):117-122.
   doi pubmed
9. Kamiya Y, Hasegawa T, Takegami Y, Horiba K, Ando S, Torii Y, Kidokoro H, et al. Primary psoas abscess caused by group A streptococcus in a child: Case report with microbiologic findings. J Infect Chemother. 2016;22(12):811-814.
   doi

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Clin Infect Immun is published by Elmer Press Inc.