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    Development of an Abiotrophia Defectiva Infection after TKA

    A 61-year-old male patient presents with sudden onset of intense knee pain 6 years after total knee arthroplasty. A positive alpha-defensin and high synovial CRP levels raise the suspicion of an acute periprosthetic joint infection. Further cultures reveal an extremely rare cause of infection in orthopaedic implants: Abiotrophia defectiva.

    Authors

    Rahul Goel, BA; Asim M. Makhdom, MD, MSc, FRCSC; and Matthew S. Austin, MD

    Disclosures

    The authors have no disclosures relevant to this article.

    Background

    Abiotrophia defectiva was traditionally known as a variant of streptococci with fastidious nutritional growth requirement. [1] It was reclassified to its own species based on 16S rRNA gene sequences, phenotypic features, and the presence of alpha- and beta-galactosidases. [1,2]

    This organism resides in the oral flora and the intestinal and genitourinary tracts, and it has been associated with hematogenous infections such as infective endocarditis, brain abscesses, and otitis media. [3-5]

    Very few case reports have linked this organism to orthopaedic implant infections (Table 1). In 2002, Ince et al [6] documented the first infected total knee arthroplasty (TKA) due to A. defectiva. Cassir et al [7] then published the second report of infected TKA, but with different diagnostic and treatment strategies.

    The prior 2 reports of periprosthetic joint infection (PJI) with this species (Table 1) documented the relative difficulty of diagnosis due to:

    • Long incubation period required to grow A. defectiva
    • Inability of rapid detection systems for either gram-positive rods or streptococci to identify this species
    • Indolent progression of this infection with no clear nidus for entry

    Table 1. Case Reports of PJI Caused by Abiotrophia defectiva

    In both case reports, definitive diagnosis could not be made without the assistance of universal polymerase chain reaction (PCR) testing.

    The aim of this case report is to document the third infected TKA due to A. defectiva and demonstrate our experience with this challenging organism.

    Case Report

    Patient Presentation

    A 61-year-old male patient with a past medical history of dyslipidemia, hypertension, and pseudogout underwent left TKA in 2010 at our institution. He had no issues with the knee for 6 years, then suddenly experienced intense pain in the knee.

    One week later, he presented to our office for evaluation. His range of motion had rapidly decreased to 15 of flexion. He could ambulate without assistance, but he had required a cane for a few days following the onset of symptoms. He denied any recent trauma, history of infection, fever, or chills.

    Physical Exam

    • Height: 73 inches; weight: 195 pounds; BMI: 25.72 kg/m2
    • Temperature: 98.6F; heart rate: 70 beats/minute and regular; respiratory rate: 18 breaths/minute
    • Well-healed incision without signs of local skin infection on the anterior aspect of the left knee
    • Swollen left knee with palpable effusion.
    • Diminished left knee mobility
    • Stability and strength well maintained bilaterally
    • Pain on palpation of the anterior aspect of the left knee

    Laboratory Values

    The patient’s erythrocyte sedimentation rate was 2 mm/hour (normal <20 mm/hour) and the C-reactive protein (CRP) level was 8.32 mg/dL (normal <0.80 mg/dL).

    The initial synovial fluid aspirate showed the following:

    • Alpha-defensin positive with synovial CRP > 60mg/L (concern for infection with positive alpha-defensin and CRP elevated over 1.5mg/L)
    • Synovial white cell count: 27,500 cells/µL (normal <150 cells/µL); neutrophils 71% (normal 0-24%); lymphocytes 4% (normal 0-74%); monocytes 25% (normal 0-69%)
    • Positive for calcium pyrophosphate crystals
    • No organisms seen on Gram stain

    The sample was prepared and cultured in aerobic and anaerobic environments for 14 days. The initial report showed no growth, but enrichment broth culture later was positive for A. defectiva.

    The second synovial fluid aspirate was done 3 days after the first aspiration, and it showed:

    • Synovial white cell count: 37,980 cells/µL; neutrophils 80%, lymphocytes 7%, monocytes 13%
    • Red blood cell count: 2,221 cells/µL
    • Gram-positive coccobacilli seen on Gram smear

    The sample was prepared and cultured in anaerobic and aerobic environments for 14 days; acid-fast culture was done as well and held for 48 days. Aerobic culture was positive for nutritionally deficient streptococcus species.

    Imaging

    Radiographs of the left knee show satisfactory alignment and positioning of components with no evidence of loosening (Figure 1).

    Figure 1. Anterior posterior, lateral, and sunrise views of the left knee taken following the onset of pain and decreased range of motion demonstrate acceptable alignment of components and no signs of loosening.

    Diagnosis

    Based on laboratory values and constellation of symptoms, the patient was suspected to have an acute PJI caused by hematogenous spread of A. defectiva from an unknown source.

    Treatment

    The treatment plan included:

    • Incision and drainage and liner exchange synovectomy
    • Thorough sharp soft tissue debridement
    • Mechanical debridement of the prosthesis with povidone-iodine (Betadine) sponges 14 days following the onset of symptoms

    The patient was seen by our preadmissions personnel and medically optimized for surgery, and on the scheduled day, he  was taken to the operating room for an incision and drainage with exchange of the polyethylene liner.

    Cloudy synovial fluid was extracted on aspiration of the knee joint just prior to the arthrotomy and then sent to the lab for culture. After thorough synovectomy, the polyethylene insert was removed.

    Extensive sharp debridement of the soft tissues was performed, removing all non-viable or grossly infected tissue. Three standard tissue samples were sent for culture.

    Thorough irrigation of the joint space then ensued using the following protocol:

    • 6 liters of lactated Ringer’s solution with bacitracin/polymyxin
    • 1 liter of dilute povidone-iodine in lactated Ringer’s solution
    • 1 liter of lactated Ringer’s solution with bacitracin/polymyxin

    The patient was discharged on 6 weeks of intravenous penicillin G followed by 6 months of antibiotic suppression with oral amoxicillin, as recommended by the infectious disease team.

    Perioperative and Postoperative Work-up

    The 3 cultures taken intraoperatively were tested in the lab. Broth cultures showed the presence of nutritionally deprived streptococci, and Gram smear showed evidence of gram-positive coccobacilli.

    Maxillofacial CT scan showed no evidence of abscesses, and chest x-ray and EKG showed no evidence of cardiac abnormalities. The transthoracic echocardiograph revealed normal wall motion and no valvular vegetation.

    Urinalysis showed normal urine pH, with no blood. It was negative for leukocyte esterase, protein, glucose, ketones, and bilirubin.

    Postoperative Follow-up

    At the 1-month postoperative follow-up, the patient presented with no specific complaints and had made excellent progress.

    Antero-posterior and lateral x-rays of the left knee showed satisfactory position and alignment of the components, with no signs of loosening. Physical examination revealed satisfactory wound healing and range of motion, with active flexion greater than 90.

    At the 3-month postoperative follow-up, the patient again presented with no significant complaints, although he reported that he’d had a short period of left knee pain localized to the medial aspect of the knee at approximately 10 weeks postoperatively. The pain resolved within 1 week.

    He had no symptoms of erythema, warmth, or effusion nor any recent history of infection or fall. Range of motion continued to improve.

    At the 6-month postoperative follow-up, the patient presented with no complaints and satisfactory progression

    Treatment Pearls

    This is the third report of the species A. defectiva responsible for PJI, and it illustrates a more facile diagnosis than was seen in the prior 2 cases published in the literature. Identification of the infecting organism in PJI is crucial for using the most effective antibiotic treatment protocol for optimal eradication of infection.

    The positive alpha-defensin and synovial CRP result from the first synovial fluid aspiration helped to raise our suspicion of PJI, despite negative culture and prior history of pseudogout with calcium pyrophosphate crystals that were found in the first aspirate. Alpha-defensin has been shown to be highly sensitive and specific for PJI. [8,9]

    The positive alpha-defensin test and high synovial CRP level from the first aspiration led to a second joint fluid aspiration, with the culture and Gram stain identifying A. defectiva as the infecting organism before the broth result came back from the first aspiration.

    Although our patient had no complaints at his postoperative follow-up visits, long-term follow-up is required to ensure the infection has been eradicated.

    Author Information

    Rahul Goel, BA; Asim M. Makhdom, MD, MSc, FRCSC; and Matthew S. Austin, MD, are from The Rothman Institute, Philadelphia, Pennsylvania.

    Adult Reconstruction Section Editor, The Rothman Institute Grand Rounds

    Antonia F. Chen, MD, MBA

    References

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    2. Ohara-Nemoto Y, Tajika S, Sasaki M, Kaneko M. Identification of Abiotrophia adiacens and Abiotrophia defectiva by 16S rRNA gene PCR and restriction fragment length polymorphism analysis. Journal of clinical microbiology. 1997;35(10):2458-2463.
    3. Bouvet A. Human endocarditis due to nutritionally variant streptococci: streptococcus adjacens and Streptococcus defectivus. European heart journal. 1995;16 Suppl B:24-27.
    4. Cerceo E, Christie JD, Nachamkin I, Lautenbach E. Central nervous system infections due to Abiotrophia and Granulicatella species: an emerging challenge? Diagnostic microbiology and infectious disease. 2004;48(3):161-165.
    5. Frenkel A, Hirsch W. Spontaneous development of L forms of streptococci requiring secretions of other bacteria or sulphydryl compounds for normal growth. Nature. 1961;191:728-730.
    6. Ince A, Tiemer B, Gille J, Boos C, Russlies M. Total knee arthroplasty infection due to Abiotrophia defectiva. J Med Microbiol. 2002;51(10):899-902.
    7. Cassir N, Grillo JC, Argenson JN, Drancourt M, Levy PY. Abiotrophia defectiva knee prosthesis infection: A case report. Journal of medical case reports. 2011;5:438.
    8. Deirmengian C, Kardos K, Kilmartin P, Cameron A, Schiller K, Parvizi J. Diagnosing Periprosthetic Joint Infection: Has the Era of the Biomarker Arrived? Clinical orthopaedics and related research. 2014;472(11):3254-3262.
    9. Deirmengian C, Kardos K, Kilmartin P, Cameron A, Schiller K, Parvizi J. Combined measurement of synovial fluid alpha-Defensin and C-reactive protein levels: highly accurate for diagnosing periprosthetic joint infection. The Journal of bone and joint surgery. American volume. 2014;96(17):1439-1445.