Spotlight Case Part 1: Oligoarticular Septic Arthritis-A Case of Disseminated Pneumococcal Disease

May 13, 2015

By Jennifer S. Mulliken, M.D.

Peer Reviewed

Case Report

A 45-year-old man with a history of mild intermittent asthma presented with two days of right knee pain and swelling accompanied by subjective fevers, shaking chills, and night sweats. He also reported one day of right calf and left groin pain. The patient denied a history of joint trauma, underlying joint disease, or surgery. There was no history of intravenous drug use, recent travel, or preceding illnesses. He was sexually active with women and reported inconsistent condom use in the past.

On physical examination, the patient was in no distress but was unable to get out of bed due to pain. His heart rate was 107/min and temperature was 101°F. The right knee was erythematous and warm with diffuse swelling and decreased range of motion. He had pitting edema extending from the right foot to the base of the right knee. There was tenderness in the left groin, and movement of the left hip elicited severe pain. Two 4 x 4 centimeter areas of fluctuance were noted over the right medial calf and left sternoclavicular joint. There were no meningeal signs or abnormal findings on pulmonary or cardiac exam.

The white blood cell count was 21,000/mm3 with 86% neutrophils. The erythrocyte sedimentation rate and C-reactive protein were elevated to 126 mm/hr and 261 mg/L, respectively. Labs were otherwise significant for a normocytic anemia (hemoglobin 9.5 g/dL) and serum protein-albumin gap of 5. A polyclonal hypergammaglobulinemia with IgG predominance was noted. A chest radiograph showed bilateral pleural effusions, greater on the right than on the left.

Arthrocentesis of the right knee performed before the initiation of antibiotics revealed purulent synovial fluid with a white blood cell count of 9960/mm3 (88% polymorphonuclear leukocytes). Two sets of joint fluid cultures were positive for Streptococcus pneumoniae. Blood cultures were sterile. Magnetic resonance imaging of the left hip showed a thickened enhancing synovium with surrounding myositis, consistent with a septic joint. Soft tissue abscesses of the right calf and left chest were also noted on imaging. A transthoracic echocardiogram revealed no evidence of vegetations or significant valvular disease. A transesophageal echocardiogram was not performed. The patient was started on intravenous ceftriaxone for disseminated pneumococcal disease. Surgical drainage of the left hip and repeat aspiration of the right knee disclosed significant purulence at both sites, although synovial fluid cultures were negative. On hospital day 3, the patient was found to be HIV positive with a CD4 count of 283 and a viral load of 3070 copies/mL.


Infections of native joints can be caused by a wide range of microorganisms including bacterial, viral, and fungal pathogens. The greatest morbidity is seen in bacterial (or septic) arthritis because of the high potential for rapid and irreversible joint destruction [1]. The majority of infections are monoarticular, with the knee being the most commonly involved joint. Abnormal joint architecture is the most important risk factor for bacterial arthritis, and patients with rheumatoid arthritis are at especially high risk [2]. Other common predisposing factors include chronic systemic diseases, immunosuppressive states, local trauma or surgery, and the presence of a prosthetic joint [3-5].

Bacterial arthritis usually occurs by hematogenous spread. The highly vascular environment of the synovium as well as the absence of a synovial basement membrane allow bacterial pathogens to easily access the synovial space [6]. While certain bacterial toxins and virulence factors directly mediate joint injury, the damage in septic arthritis owes more to the host inflammatory response to the infection than to the infection itself [1]. Within the synovial membrane, bacteria trigger an inflammatory cascade that induces a suppurative proliferative synovitis. This, in turn, can progress to destruction of articular cartilage and subchondral bone loss [7].

By far the most commonly isolated pathogen in native joint septic arthritis is Staphylococcus aureus [3,4,8]. The incidence is highest in patients with rheumatoid arthritis, where S. aureus is reportedly responsible for 75% of cases [9]. Streptococcus species are the next most commonly associated pathogen, and group A streptococci account for the majority of these infections [10,11]. While Streptococcus pneumoniae is a less frequent cause of bacterial arthritis, it has been identified as the underlying pathogen in 6-10% of patients [12,13]. Gram-negative bacilli are isolated in 10-20% of cases, with Pseudomonas aeruginosa and Escherichia coli being the most common causative agents. The highest risk groups for gram-negative septic arthritis are intravenous drug users, patients at extremes of age, and those with underlying immunocompromise [11]. Neisseria gonorrhoeae is an important cause of monoarticular and polyarticular bacterial arthritis among young sexually active individuals; however, the prevalence of gonococcal arthritis has declined significantly in recent decades [1,14].

In the preceding case, the patient presented with oligoarticular pneumococcal septic arthritis involving the right knee and left hip. During his hospitalization he was diagnosed with HIV, an established risk factor for invasive pneumococcal disease [15]. A retrospective study from San Francisco conducted before the era of anti-retroviral therapy (ART) showed that 54.2% of patients with invasive pneumococcal disease were also infected with HIV [16]. The incidence of pneumococcal disease per 100,000 person-years was increased 23-fold in patients with AIDS. In addition, 82.5% of pneumococcal isolates in HIV-infected patients were serotypes included in the pneumococcal polysaccharide vaccine (PPSV23). In 2012 the Advisory Committee on Immunization Practices recommended the sequential administration of both the polysaccharide and conjugate (PPSV13) pneumococcal vaccines to HIV-infected patients. The widespread use of ART as well as increased pneumococcal vaccination efforts have helped reduce disease burden. Nevertheless, HIV remains an important risk factor for pneumococcal disease.

In general, the most common risk factors for pneumococcal joint infections are rheumatoid arthritis and alcoholism, but other predisposing factors include B-cell deficiencies, multiple myeloma, and osteoarthritis [15,17-19]. Large joints are affected more often than small joints, with the knee being the most commonly affected site [20]. Infections of the hip, shoulder, elbow, and ankle have also been reported [14]. Polyarticular infections occur in up to 25% of cases, with worse overall outcomes than in monoarticular infections [17,21]. Although pneumococcal joint infections are relatively uncommon, they are an important cause of bacterial arthritis that must be promptly recognized and treated.

Patients typically present acutely with a severely inflamed joint or joints. As with other causes of bacterial arthritis, systemic symptoms are common, including fever and shaking chills [12,22]. The white blood cell count in the synovial fluid may range from less than 10,000 cells/mm3 to greater than 100,000 cells/mm3 [23]. In one review of 90 patients with pneumococcal septic arthritis, the synovial white blood cell count was greater than 11,000/mm3 in more than 50% of patients. A preceding or concurrent site of pneumococcal infection is found in the majority of cases, with pneumonia and meningitis being the most frequent concomitant infections [16]. Endocarditis has also been reported [12,22]. Bacteremia has been found to occur in greater than 70% of patients – more frequently than in all patients with bacterial arthritis combined [12,17].

Antibiotic therapy is recommended for three to four weeks for uncomplicated infections, with one to two weeks of initial intravenous therapy [12,19]. Most pneumococcal infections are sensitive to penicillin, but third-generation cephalosporins (cefotaxime, ceftriaxone) or vancomycin are reasonable alternatives given increasing rates of antimicrobial resistance in S. pneumoniae [1,24]. Repeat joint aspirations are generally adequate for the initial drainage of infected joints. Surgical drainage is indicated for septic arthritis of the hip, loculated infections, and inadequate response to arthrocentesis or after five to seven days of antibiotics [12,25]. The prognosis for pneumococcal septic arthritis is generally favorable. More than 80% of patients survive the infection, and more than 60% have good functional outcomes [17].

In summary: S. pneumoniae is an uncommon yet well-documented cause of septic arthritis. Symptoms are similar to those of other bacterial arthritides; however, oligoarticular and polyarticular infections are more common when S. pneumoniae is the underlying pathogen. Given the high rate of concomitant infections, pneumonia and meningitis should be ruled out in all patients with pneumococcal septic arthritis. An echocardiogram should strongly be considered to rule out endocarditis. In addition, all patients should be tested for HIV given the association between immunodeficiency and invasive pneumococcal disease. Prognosis is usually favorable with appropriate treatment.

Dr. Jennifer S. Mulliken is a 2nd year resident at NYU Langone Medical Center

Peer reviewed by Howard Leaf, MD, Internal Medicine, NYU Langone Medical Center

Image courtesy of Wikimedia Commons


1. Ohl CA. Infectious arthritis of native joints. In: Mandell GL, Bennet JE, Dolin R, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 7th edition. Philadelphia, PA: Saunders Elsevier, 2009, pp. 1443-1456.

2. Kaandorp CJ, Van Schaardenburg D, Krijnen P, et al. Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum. 1995;38(12):1819-1825.

3. Gupta MN, Sturrock RD, Field M. A prospective 2-year study of 75 patients with adult-onset septic arthritis. Rheumatology (Oxford). 2001;40(1):24-30.

4. Kaandorp CJ, Dinant HJ, van de Laar MA, et al. Incidence and sources of native and prosthetic joint infection: a community based prospective survey. Ann Rheum Dis. 1997;56(8):470-475.

5. Saraux A, Taelman H, Blanche P, et al. HIV infection as a risk factor for septic arthritis. Br J Rheumatol. 1997;36(3):333-337.

6. Goldenberg DL, Reed DI. Bacterial arthritis. N Engl J Med. 1985;312:764-771.

7. Goldenberg DL, Chisholm PL, Rice PA, et al. Experimental models of bacterial arthritis: A microbiologic and histopathologic characterization of the arthritis after the intraarticular injections of Neisseria gonorrhoeae, Staphylococcus aureus, group A streptococci, and Escherichia coli. J Rheumatol 1983;10:5-11.

8. Morgan DS, Fisher D, Merianos A, Currie BJ. An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect. 1996;117(3):423-428.

9. Goldenberg DL. Infectious arthritis complicating rheumatoid arthritis and other chronic rheumatic disorders. Arthritis Rheum. 1989;32(4):496-502.

10. Goldenberg DL. Septic arthritis. Lancet. 1998;351(9097):197-202.

11. Shirtliff ME, Mader JT. Acute septic arthritis. Clin Microbiol Rev. 2002;15(4):527-544.

12. Ross JJ, Saltzman CL, Carling P, Shapiro DS. Pneumococcal septic arthritis: review of 190 cases. Clin Infect Dis. 2003;36(3):319-327.

13. Ryan MJ, Kavanagh R, Wall PG, Hazleman BL. Bacterial joint infections in England and Wales: analysis of bacterial isolates over a four year period. Br J Rheumatol. 1997;36(3):370-373.

14. Bardin T. Gonococcal arthritis. Best Pract Res Clin Rheumatol. 2003;17(2):201-208.

15. Frankel RE, Virata M, Hardalo C, et al. Invasive pneumococcal disease: clinical features, serotypes, and antimicrobial resistance patterns in cases involving patients with and without human immunodeficiency virus infection. Clin Infect Dis. 1996;23(3):577-584.

16. Nuorti JP, Butler JC, Gelling L, et al. Epidemiologic relation between HIV and invasive pneumococcal disease in San Francisco County, California. Ann Intern Med. 2000;132(3):182-190.

17. Raad J, Peacock JE Jr. Septic arthritis in the adult caused by Streptococcus pneumoniae: a report of 4 cases and review of the literature. Semin Arthritis Rheum. 2004;34(2):559-569.

18. Ispahani P, Weston VC, Turner DP, Donald FE. Septic arthritis due to Streptococcus pneumoniae in Nottingham, United Kingdom, 1985-1998. Clin Infect Dis. 1999;29(6):1450-1454.

19. James PA, Thomas MG. Streptococcus pneumoniae septic arthritis in adults. Scand J Infect Dis. 2000;32(5):491-494.

20. Epstein JH, Zimmermann B, Ho G Jr. Polyarticular septic arthritis. J Rheumatol. 1986;13(6):1105-1107.

21. Musher, DM. Streptococcus pneumoniae. In: Mandell GL, Bennet JE, Dolin R, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 7th edition. Philadelphia, PA: Saunders Elsevier, 2009, pp. 2623-2642.

22. Kauffman CA, Watanakunakorn C, Phair JP. Pneumococcal arthritis. J Rheumatol. 1976;3(4):409-419.

23. Baraboutis I, Skoutelis A. Streptococcus pneumoniae septic arthritis in adults. Clin Microbiol Infect. 2004;10(12):1037-1039.

24. Kaplan SL, Mason EO Jr. Management of infections due to antibiotic-resistant Streptococcus pneumoniae. Clin Microbiol Rev. 1998;11(4):628-644.

25. Pioro MH, Mandell BF. Septic arthritis. Rheum Dis Clin North Am. 1997;23(2):239-258.


One comment on “Spotlight Case Part 1: Oligoarticular Septic Arthritis-A Case of Disseminated Pneumococcal Disease

Comments are closed.