Atypical Spondylodiscitis

Abstracts

As infecções por Staphylococcus coagulase-negativo correspondem a uma pequena percentagem do total das espondilodiscites piogênicas, estando associados a estados imunocomprometidos. Apresentamos o caso clínico de um homem de 58 anos, com uma espondilodiscite L1-L2, por um micro-organismo bastante atípico, o S. hominis. A resolução da patologia só foi possível após duas cirurgias e terapia com antibióticos específicos.

Staphylococcus; Staphylococcus hominis; Discite

CASE REPORT RELATO DE CASO RELATO DE CASO

Atypical spondylodiscitis

Espondilodiscitis atípica

Pedro Miguel Dantas Costa Marques; António Félix; Bruno Alpoim; Maria Elisa Rodrigues; Pedro Sá; Paulo Gonçalves; Carlos Alves; António Rodrigues

Department of Orthopedics and Traumatology, Unidade Local de Saúde do Alto Minho, Viana do Castelo, Portugal

Correspondence

ABSTRACT

Infections with coagulase-negative Staphylococcus correspond to a small percentage of the total pyogenic spondylodiscitis and are associated with immunocompromised conditions. We present a case of a 58 year old male with a L1-L2 spondylodiscitis by a very atypical microorganism, the S. hominis. Only after two surgeries and specific antibiotic therapy it was possible to eliminate the disease.

Keywords:Staphylococcus, Staphylococcus hominis; Discitis.

RESUMEN

Las infecciones por Staphylococcus coagulasa-negativa corresponden a un pequeño porcentaje del total de las espondilodiscitis piogénicas, estando vinculadas a estados inmunocomprometidos. Presentamos el caso clínico de un hombre, de 58 años de edad, con una espondilodiscitis L1-L2, por un microorganismo muy atípico, el S. hominis. La solución de la patología fue posible solamente después de dos cirugías y de terapia con antibióticos específicos.

Descriptores:Staphylococcus; Staphylococcus hominis; Discitis.

INTRODUCTION

In spondylodiscitis, the main route of infection is hematogenous. Symptoms primarily consists of pain in the spine, inflammation, whether or not it is associated with a fever.¹ It may arise spontaneously (most commonly in pediatric cases), but it is significantly more common to arise accompanied by other infections, malignancy, or collagenosis. Spondylodiscitis often occurs as a complication of sepsis, urinary tract infection, respiratory tract infection, gastrointestinal pathology or even after amygdalectomy.^2-7 The clinical picture is analytically completed with leukocytosis (with neutrophilia), and increased sedimentation velocity (SV) and C-reactive protein (CRP). With regards to imaging, X-ray (XR) provides some information, but complementation by computed tomography (CT) and especially magnetic resonance (MR) allows us to make a diagnosis. Note that the most frequently encountered pathogen is St. aureus and the lumbar spine is most often affected.

CASE

Patient, male, 58 years old, with a history of lung tuberculosis and chronic obstructive pulmonary disease (COPD) treated with corticotherapy, was referred to the emergency room (ER) due to progressive low back pain without radiation or apparent triggering factor that is refractory to medication. After physical examination, only lumbar pain on palpation without associated neurological or systemic changes was observed. Laboratory tests showed increased CRP and SV, and a lytic lesion at L1-L2 was seen in XR. (Figures 1 and 2) We subsequently performed a CT scan of the lumbar spine (Figure 3) followed by MR (Figure 4A-B), and changes consistent with spondylodiscitis were found at the level of the L1-L2 intervertebral disc, in the presence of anterior paravertebral phlegmon at the same level. Given the clinical picture, the patient was admitted to conduct antibiotic therapy and to collect samples for a blood culture.

Due to a fruitless attempt at drainage guided by CT (Figure 5), clinical deterioration (with a 38°C fever) and progressive analytical deterioration, we performed during the first surgical period costotomy, surgical drainage of the anterior paravertebral abscess, L1-L2 discectomy and interbody grafting via an anterior approach, about three weeks after arriving at the ER. Two weeks later, and after having a confirmed negative bacteriological examination and anatomical-pathological examination of the material excised evidencing only nonspecific inflammation, we proceeded to posterior pedicle D12-L3 instrumentation. (Figure 6 A-B) Bacteriological and anatomical-pathological samples were taken again and one St. hominis was isolated only during this last intervention, resistant to penicillin and its derivatives.

The patient underwent directed antibiotic therapy during the rest of the hospitalization, and some improvement of the clinical and analytical picture was observed during this time. The patient was discharged at the end of 2 months after the initial episode, continuing the specific antibiotic treatment (clindamycin + levofloxacin) at home.

After 3 months postoperatively the patient is without complaints of pain or neurological changes, and is afebrile, monitored in external consultation.

DISCUSSION

In spondylodiscitis, as well as in infectious arthritis, the main route of infection is hematogenous, and the principal cause is staph infection in 40-60% of cases, especially Staphylococcus aureus among all species, through the production of the coagulase enzyme. In the past, coagulase-negative staphylococci rarely caused infections of clinical relevance, but the continued use of cardiac and joint catheters and prostheses has led to an increase in its pathogenic capacity, especially in immunocompromised patients. Currently, coagulase-negative staphylococci are responsible for about 3-18% of infectious spondylodiscitis cases;^8-12 this percentage increases to 25-30% in post-surgery cases.^13,14 The most common coagulase-negative subspecies is St. epidermidis (72%) followed by St. lugdunensis (7%).^8-30

Spondylodiscitis by St. hominis is clinically rare. There are few cases described in the literature;³¹ the microorganism is resistant to penicillins and their derivatives. It is associated with immunocompromised states or invasive procedures, but may arise as a result of a contamination of a microbiological examination.

Although the history of tuberculosis in this patient leads one to suppose infection by Mycobacterium tuberculosis, this diagnosis was not confirmed.

It is concluded that a St. hominis infection is very uncommon, and that there is a fundamental need for directed antibiotic therapy.

REFERENCES

• 1. Grammatico L, Besnier JM. Infectious spondylodiscitis Rev Prat. 2007;57(9):970-8.
• 2. Tomic D, Stokic E, Turkolov V, Ivkovic-Lazar T. Fever of unknown origin-a case report of brucellar discitis. Med Pregl. 2007;60(1-2):77-9.
• 3. Abdelmoula MS, Abdelmalek R, Chleyfa K, Bejaoui M, Tebib N, Ben Turkia H, et al. Pulmonary aspergillosis in a child with granulomatous disease. Tunis Med. 2003;81(10):815-920.
• 4. Ribeiro MA, Barouni AS, Augusto CJ, Augusto MV, Lopes MT, Salas CE. PCR identification of Mycobacterium tuberculosis complex in a clinical sample from a  patient with symptoms of tuberculous spondylodiscitis. Braz J Med Biol Res. 2007;40(1):1-4.
• 5. Kowalski TJ, Layton KF, Berbari EF, Steckelberg JM, Huddleston PM, Wald JT, et al. Follow-up MR imaging in patients with pyogenic spine infections: lack of correlation with clinical features. Amer J Neuroradiol. 2007;73(5):670-3.
• 6. Alpantaki K, Papoutsidakis A, Katonis P, Hadjipavlou A. Vertebral osteomyelitis, epidural and psoas abscess after epidural catheter use. Acta Orthop Belg. 2007;28 (4):670-3.
• 7. Curry JM, Cognetti DM, Harrop J, Boon MS, Spiegel JR. Cervical discitis and epidural abscess after tonsillectomy. Laryngoscope. 2007;117(12):2093-6.
• 8. Belzunegui J, Del Val N, Intxausti JJ, De Dios JR, Queiro R, González C, et al. Vertebral osteomyelitis in northern Spain. Report of 62 cases. Clin Exp Rheumatol. 1999;17(4):447-52.
• 9. Stefanovski N, Van Voris LP. Pyogenic vertebral osteomyelitis: report of a series of 23 patients. Contemp Orthop. 1995;31(3):159-64.
• 10. Nolla JM, Ariza J, Gómez-Vaquero C, Fiter J, Bermejo J, Valverde J, et al. Spontaneous pyogenic vertebral osteomyelitis in nondrug users. Semin Arthritis Rheum. 2002;31(4):271-8.
• 11. Patzakis MJ, Rao S, Wilkins J, Moore TM, Harvey PJ. Analysis of 61 cases of vertebral osteomyelitis. Clin Orthop Relat Res. 1991;(264):178-83.
• 12. Carragee EJ. Pyogenic vertebral osteomyelitis. J Bone Joint Surg Am. 1997;79(6):874-80.
• 13. Jiménez-Mejías ME, de Dios Colmenero J, Sánchez-Lora FJ, Palomino-Nicás J, Reguera JM, García de la Heras J, et al. Postoperative spondylodiskitis: etiology, clinical findings, prognosis, and comparison with nonoperative pyogenic spondylodiskitis. Clin Infect Dis. 1999;29(2):339-45.
• 14. Dufour V, Feydy A, Rillardon L, Redondo A, Le Page L, Bert F, et al. Comparative study of postoperative and spontaneous pyogenic spondylodiscitis. Semin Arthritis Rheum. 2005;34(5):766-71.
• 15. Le Moal G, Roblot F, Paccalin M, Sosner P, Burucoa C, Roblot P, et al. Clinical and laboratory characteristics of infective endocarditis when associated with spondylodiscitis. Eur J Clin Microbiol Infect Dis. 2002;21(9):671-5.
• 16. Bucher E, Trampuz A, Donati L, Zimmerli W. Spondylodiscitis associated with bacteraemia due to coagulase-negative staphylococci. Eur J Clin Microbiol Infect Dis. 2000;19(2):118-20.
• 17. Parker MA, Tuazon CU. Cervical osteomyelitis. Infection due to Staphylococcus epidermidis in hemodialysis patients. JAMA. 1978;240(1):50-1.
• 18. Tuazon CU, Miller H. Clinical and microbiologic aspects of serious infections caused by Staphylococcus epidermidis. Scand J Infect Dis. 1983;15(4):347-60.
• 19. Karthigasu KT, Bowman RA, Grove DI. Vertebral osteomyelitis due to Staphylococcus warneri. Ann Rheum Dis. 1986;45(12):1029-30.
• 20. Bryan CS, Parisi JT, Strike DG. Vertebral osteomyelitis due to Staphylococcus warneri attributed to a Hickman catheter. Diagn Microbiol Infect Dis. 1987;8(1):57-9.
• 21. Mündlein E, von Baum H, Geiss HK, Springsklee M, Zeier M, Andrassy K. Life-threatening infection with multiresistant Staphylococcus epidermidis in a patient with end-stage renal disease: cure with chloramphenicol and quinupristin/dalfopristin (RP 59500). Infection. 1997;25(4):252-4.
• 22. De Wit D, Mulla R, Cowie MR, Mason JC, Davies KA. Vertebral osteomyelitis due to Staphylococcus epidermidis. Br J Rheumatol. 1993;32(4):339-41.
• 23. Razonable RR, Lewallen DG, Patel R, Osmon DR. Vertebral osteomyelitis and prosthetic joint infection due to Staphylococcus simulans. Mayo Clin Proc. 2001;76(10):1067-70.
• 24. Greig JM, Wood MJ. Staphylococcus lugdunensis vertebral osteomyelitis. Clin Microbiol Infect. 2003;9(11):1139-41.
• 25. Gosbell I, Gottlieb T, Bradbury R. Native valve endocarditis and vertebral osteomyelitis caused by Staphylococcus epidermidis. Med J Aust. 1992;156(9):662.
• 26. Wood CA, Sewell DL, Strausbaugh LJ. Vertebral osteomyelitis and native valve  endocarditis caused by Staphylococcus warneri. Diagn Microbiol Infect Dis. 1989;12(3):261-3.
• 27. Valero R, Castañeda O, de Francisco AL, Piñera C, Rodrigo E, Arias M. [Clinical suspicion of vertebral osteomielitis: back pain in patients with hemodyalisis by catheter related infection]. Nefrologia. 2004;24(6):583-8.
• 28. Announ N, Mattei JP, Jaoua S, Fenollar F, Sati H, Chagnaud C, et al. Multifocal discitis caused by Staphylococcus warneri. Joint Bone Spine. 2004;71(3):240-2.
• 29. Murdoch DR, Everts RJ, Chambers ST, Cowan IA. Vertebral osteomyelitis due to Staphylococcus lugdunensis. J Clin Microbiol. 1996;34(4):993-4.
• 30. Kragsbjerg P, Bomfim-Loogna J, Törnqvist E, Söderquist B. Development of antimicrobial resistance in Staphylococcus lugdunensis during treatment-report of a case of bacterial arthritis, vertebral osteomyelitis and infective endocarditis. Clin Microbiol Infect. 2000;6(9):496-9.
• 31. Gómez Rodríguez N, Durán Muñoz O. [Pyomyositis, sacroiliitis and spondylodiscitis caused by Staphylococcus hominis in a immunocompetent woman]. An Med Interna. 2006;23(12):582-4.

Publication Dates

• Publication in this collection
  21 Nov 2013
• Date of issue
  2013

History

• Received
  19 May 2013
• Accepted
  20 Aug 2013