530
Kingella kingae Intervertebral Diskitis in an Adult Jacques F. Meis, Robert W. Sauerwein, Inge C. Gyssens, Alphons M. Horrevorts, and Albert van Kampen
From the Departments of Medical Microbiology. General Internal Medicine. and Orthopedics. University Hospital Nijmegen, The Netherlands
Kingella kingae rarely causes infection and is mainly associated with endocarditis and septic arthritis in adults. The organism is also capable of causing intervertebral diskitis in children, but thus far, no reports of this infection occurring in adults have been published. A case of diskitis due to K. kingae in an adult is reported for the first time, and the literature on this infection in children is reviewed.
In the past 17 years, Kingella kingae has been recognized with increasing frequency as a human pathogen [1], particularly in children [2]. We report the case ofa 33-year-old male physician who presented with diskitis due to K. kingae and who responded satisfactorily to therapy with penicillin. The patient had developed lower back pain 2 weeks after recovering from acute infection of the upper respiratory tract. During the course of the next 6 weeks, the pain did not abate and extended to the right knee. There were no physical findings other than pain that followed compression of the left sacroiliac joint, and no abnormal laboratory values were observed. Radiographic findings proved inconclusive, and nonsteroidal antiinflammatory agents were prescribed for management of presumed sacroiliitis. However, 3 months later, the patient's condition appeared to have worsened with local pain around the L-3 and L-4 vertebrae and signs of right psoas muscle irritation in the absence of fever. The erythrocyte sedimentation rate and Creactive protein (CRP) level were both elevated at 50 mm/h and 58 ~g/mL, respectively. Serology for syphilis, Salmonella. and Brucella were negative as were results of a Mantoux test. A periosteal process was now evident radiographically with right-sided bone formation and bridging of the L-3 and L-4 vertebrae and some narrowing of the disk. Computed tomography revealed a paravertebral mass at the same level, and a bone scan with 99Tc showed increased uptake at the L-3 to L-4 vertebral bodies. Magnetic resonance imaging revealed lytic lesions at L-3 to L-4, with narrowing of the disk space. Examination of a needle biopsy specimen obtained from the affected disk space showed polymorphonuclear leukocytes, plasma cells, and macrophages dispersed throughout dystrophic hyaline cartilage. Neither fungi nor acid-fast bacilli were detected, but a few small gram-negative coccoba-
Received 2 January 1992; revised 3 April 1992. Reprints or correspondence: Dr. J. F. Meis, Department of Medical Microbiology. University Hospital Nijmegen, P.O. Box 910 I, 6500 HB Nijmegen. The Netherlands.
Clinical Infectious Diseases 1992;15:530-2 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1503-0019$02.00
cilIary forms were seen. Cultures yielded a moderate number of small, translucent colonies surrounded by {3-hemolysis with marked pitting. The organism elaborated oxidase but not catalase, and a gram-stained preparation confirmed the presence of gram-negative coccobacilli. The microorganism was identified as K. kingae and confirmed by the National Institute ofPublic Health (Bilthoven, The Netherlands). The strain was resistant to clindamycin and vancomycin but exceptionally susceptible to penicillin, for which the MIC was 17 d
Diagnostic procedure Disk aspiration, lumbar puncture* Disk aspiration
Site of infections (disk level) L-4 to L-5
Ampicillin iv (NS); dicloxacillin iv (NS)
T-II to T-12
Methicillin iv (200 rnglkg- d])
Vertebral biopsy
L-2 to L-3
Disk aspiration
T-12 to L-I
5 [8] 1986
12 mo/M
II d
Disk aspiration
L-5 to S-I
6 [9] 1987
36 rno/F
21d
Disk aspiration
L-I to L-2
7-9 [10] 1988
18 mo/M: 24 mol F;60 mo/F
15-60 d (patients not specified)
Disk aspiration for all 3 cases
10 [II] 1991
18 rno/F
7d
Disk aspiration
II [12] 1991
12 y/F
NS
Disk aspiration
L-5 to SI. L-3 to L-4, L-3 to L-4 T-II to T-12. L-I to L-2 L-2 to L-3
12 [PRJ 1992
34y/M
6 mo
Disk aspiration
L-3 to L-4
NOTE. Underlying disease was absent in all cases. NS * Only results of lumbar puncture were positive.
Antibiotic treatment (dosage)
Penicillin po (NS) Cefuroxime iv (NS); phenoxymethyl penicillin po (NS) Nafcillin iv (150 mg/[kg. d]); ampicillin iv (200 mg/[kg· d]) Amoxicillin po (50 mgl[kg· d]); dicloxacillin po (75 mg/ [kg· d]) Moxalactam iv (150 mg/[kg. dj): netilmicin iv (60 mg/d) CefacIor po ( 100 mg/[kg· d]) Cefotaxime iv (100 mgl[kg· d]); netilmicin iv (6.5 mg/[kg· d]) Cephalexin po (80 mgl[kg. d]) Oxacillin or ampicillin plus aminoglycoside iv (patient and dose not specified)
Oxacillin iv (NS); ampicillin iv (NS)
Total duration (w)
Outcome
Comment
Favorable
2
Favorable
NS 26
Favorable
3
Favorable
13
Favorable 8 3 8 2-3 w followed by oral therapy for 6 mo 8
Favorable
Lincomycin resistant
Favorable
Favorable
Clindarnycin, vancomycin resistant
Amoxicillin iv: later amoxicillin po (NS)
NS
Favorable initial response
Unavailable for follow-up, positive PPD. isoniazid prophylaxis
Penicillin G iv (12 X 106 U/d]; continuous infusion probenecid po (500 mg q.i.d.)
3
Favorable
Clindarnycin,
Penicillin V po (2 g q-lh): probenecid po (I g once daily)
9
vancomycin resistant: negative PPD
= not stated; PPD = purified protein derivative; PR = present report.
disease, high fever, or initial radiologic evidence or any other specific sign of infection; however, all experienced pain in the lower back and responded favorably to antibiotic therapy. In addition, there was a clear association with preceding infection of the upper respiratory tract, which is the normal habitat of Kingella [13]. Rather than being a primary pathogen, K. kingae probably exploits mucosal impairment that results from a viral infection, which is the more likely cause. In contrast, adults who
develop infection with K. kingae usually present with endocarditis or septic arthritis, and most have evidence of an underlying disease. The case of infective diskitis in our patient may therefore represent a genuine extension of the pathogenic spectrum of K. kingae. Alternatively, the absence of any previous report of this particular clinical manifestation might simply reflect the lower incidence of both diskitis and K. kingae infection in adults. In vitro antibiotic susceptibility tests are predictive of out-
532
Meis et al.
come for ,B-Iactam agents to which K. kingae infection invariably responds [3]. However, treatment failures have been reported for other agents such as erythromycin, lincomycin, and ciprofloxacin despite susceptibility in vitro [3, 9, II]. The optimal mode and duration of therapy have yet to be defined, although marked symptomatic improvement as well as a return to normal CRP levels can be expected within the first 2 weeks of treatment. However, since bone injury resolves more slowly and shorter treatment might result in relapse, the current practice of giving therapy for 3 months seems prudent. Certainly, initial intravenous treatment followed by oral therapy has been shown to be effective. Acknowledgment The authors thank Dr. J. Peter Donnelly for reviewing the manuscript. References I. Morrison VA, Wagner KF. Clinical manifestations of Kingella kingae infections: case report and review. Rev Infect Dis 1989; II :776-82. 2. De Groot R. Glover D. Clausen C. Smith AL, Wilson CB. Bone and joint infections caused by Kingella kingae: six cases and review of the literature. Rev Infect Dis 1988; 10:998-1004. 3. Graham DR, Band JD, Thornsberry C. Hollis DG, Weaver RE. Infec-
4. 5.
6.
7. 8.
9.
10.
II. 12.
13.
CID 1992; 15 (September)
tions caused by Moraxella. Moraxella urethra/is. Moraxella-like Groups M-5 and M-6, and Kingella kingae in the United States. 1953-1980. Rev Infect Dis 1990;12:423-31. Falsen E. Brorson JE, Enger EA. Moraxella kingii: a rare cause ofosteomyelitis. Z Kinderchir 1977;22: 186-9. Wong AS. Dyke J, Perry D. Anderson DC Paraspinal mass associated with intervertebral disk infection secondary to Moraxella kingii. J Pediatr 1978;92:86-8. Claesson B, Falsen E. Kjellman B. Kingella kingae infections: a review and a presentation of data from 10 Swedish cases. Scand J Infect Dis 1985; 17:233-43. Woolfrey BE Lally RT. Faville RJ. Intervertebral diskitis caused by Kingella kingae. Am J Clin PathoI1986;85:745-9. Raymond J. Bergeret M, Bargy F. Missenard G. Isolation of two strains of Kingella kingae associated with septic arthritis. J Clin Microbiol 1986;24: 1100-1. Chanal C Tiget F. Chapuis P, Campagne D. Jan M. Sirot J. Spondylitis and osteomyelitis caused by Kingella kingae in children. J Clin Microbiol 1987;25:2407-9. Clement JL. Berard J. Cahuzac JP, Gaubert J. Kingella kingae osteoarthritis and osteomyelitis in children. J Pediatr Orthop 1988;8:59-61. Amir J. Shockelford PG. Kingellakingaeintervertebral disk infection. J Clin MicrobioI1991;29: 1083-6. Goutzmanis JJ, Gonis G. Gilbert GL. Kingellakingaeinfection in children: ten cases and a review of the literature. Pediatr Infect Dis J 1991; I0:677-83. Hendriksen SO. Corroding bacteria from the respiratory tract. I. Maraxella kingii. Acta Pathol Microbiol Scand 1969;75:85-90.
Kingella kingae Intervertebral Diskitis in an Adult Jacques F. Meis, Robert W. Sauerwein, Inge C. Gyssens, Alphons M. Horrevorts, and Albert van Kampen
From the Departments of Medical Microbiology. General Internal Medicine. and Orthopedics. University Hospital Nijmegen, The Netherlands
Kingella kingae rarely causes infection and is mainly associated with endocarditis and septic arthritis in adults. The organism is also capable of causing intervertebral diskitis in children, but thus far, no reports of this infection occurring in adults have been published. A case of diskitis due to K. kingae in an adult is reported for the first time, and the literature on this infection in children is reviewed.
In the past 17 years, Kingella kingae has been recognized with increasing frequency as a human pathogen [1], particularly in children [2]. We report the case ofa 33-year-old male physician who presented with diskitis due to K. kingae and who responded satisfactorily to therapy with penicillin. The patient had developed lower back pain 2 weeks after recovering from acute infection of the upper respiratory tract. During the course of the next 6 weeks, the pain did not abate and extended to the right knee. There were no physical findings other than pain that followed compression of the left sacroiliac joint, and no abnormal laboratory values were observed. Radiographic findings proved inconclusive, and nonsteroidal antiinflammatory agents were prescribed for management of presumed sacroiliitis. However, 3 months later, the patient's condition appeared to have worsened with local pain around the L-3 and L-4 vertebrae and signs of right psoas muscle irritation in the absence of fever. The erythrocyte sedimentation rate and Creactive protein (CRP) level were both elevated at 50 mm/h and 58 ~g/mL, respectively. Serology for syphilis, Salmonella. and Brucella were negative as were results of a Mantoux test. A periosteal process was now evident radiographically with right-sided bone formation and bridging of the L-3 and L-4 vertebrae and some narrowing of the disk. Computed tomography revealed a paravertebral mass at the same level, and a bone scan with 99Tc showed increased uptake at the L-3 to L-4 vertebral bodies. Magnetic resonance imaging revealed lytic lesions at L-3 to L-4, with narrowing of the disk space. Examination of a needle biopsy specimen obtained from the affected disk space showed polymorphonuclear leukocytes, plasma cells, and macrophages dispersed throughout dystrophic hyaline cartilage. Neither fungi nor acid-fast bacilli were detected, but a few small gram-negative coccoba-
Received 2 January 1992; revised 3 April 1992. Reprints or correspondence: Dr. J. F. Meis, Department of Medical Microbiology. University Hospital Nijmegen, P.O. Box 910 I, 6500 HB Nijmegen. The Netherlands.
Clinical Infectious Diseases 1992;15:530-2 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1503-0019$02.00
cilIary forms were seen. Cultures yielded a moderate number of small, translucent colonies surrounded by {3-hemolysis with marked pitting. The organism elaborated oxidase but not catalase, and a gram-stained preparation confirmed the presence of gram-negative coccobacilli. The microorganism was identified as K. kingae and confirmed by the National Institute ofPublic Health (Bilthoven, The Netherlands). The strain was resistant to clindamycin and vancomycin but exceptionally susceptible to penicillin, for which the MIC was 17 d
Diagnostic procedure Disk aspiration, lumbar puncture* Disk aspiration
Site of infections (disk level) L-4 to L-5
Ampicillin iv (NS); dicloxacillin iv (NS)
T-II to T-12
Methicillin iv (200 rnglkg- d])
Vertebral biopsy
L-2 to L-3
Disk aspiration
T-12 to L-I
5 [8] 1986
12 mo/M
II d
Disk aspiration
L-5 to S-I
6 [9] 1987
36 rno/F
21d
Disk aspiration
L-I to L-2
7-9 [10] 1988
18 mo/M: 24 mol F;60 mo/F
15-60 d (patients not specified)
Disk aspiration for all 3 cases
10 [II] 1991
18 rno/F
7d
Disk aspiration
II [12] 1991
12 y/F
NS
Disk aspiration
L-5 to SI. L-3 to L-4, L-3 to L-4 T-II to T-12. L-I to L-2 L-2 to L-3
12 [PRJ 1992
34y/M
6 mo
Disk aspiration
L-3 to L-4
NOTE. Underlying disease was absent in all cases. NS * Only results of lumbar puncture were positive.
Antibiotic treatment (dosage)
Penicillin po (NS) Cefuroxime iv (NS); phenoxymethyl penicillin po (NS) Nafcillin iv (150 mg/[kg. d]); ampicillin iv (200 mg/[kg· d]) Amoxicillin po (50 mgl[kg· d]); dicloxacillin po (75 mg/ [kg· d]) Moxalactam iv (150 mg/[kg. dj): netilmicin iv (60 mg/d) CefacIor po ( 100 mg/[kg· d]) Cefotaxime iv (100 mgl[kg· d]); netilmicin iv (6.5 mg/[kg· d]) Cephalexin po (80 mgl[kg. d]) Oxacillin or ampicillin plus aminoglycoside iv (patient and dose not specified)
Oxacillin iv (NS); ampicillin iv (NS)
Total duration (w)
Outcome
Comment
Favorable
2
Favorable
NS 26
Favorable
3
Favorable
13
Favorable 8 3 8 2-3 w followed by oral therapy for 6 mo 8
Favorable
Lincomycin resistant
Favorable
Favorable
Clindarnycin, vancomycin resistant
Amoxicillin iv: later amoxicillin po (NS)
NS
Favorable initial response
Unavailable for follow-up, positive PPD. isoniazid prophylaxis
Penicillin G iv (12 X 106 U/d]; continuous infusion probenecid po (500 mg q.i.d.)
3
Favorable
Clindarnycin,
Penicillin V po (2 g q-lh): probenecid po (I g once daily)
9
vancomycin resistant: negative PPD
= not stated; PPD = purified protein derivative; PR = present report.
disease, high fever, or initial radiologic evidence or any other specific sign of infection; however, all experienced pain in the lower back and responded favorably to antibiotic therapy. In addition, there was a clear association with preceding infection of the upper respiratory tract, which is the normal habitat of Kingella [13]. Rather than being a primary pathogen, K. kingae probably exploits mucosal impairment that results from a viral infection, which is the more likely cause. In contrast, adults who
develop infection with K. kingae usually present with endocarditis or septic arthritis, and most have evidence of an underlying disease. The case of infective diskitis in our patient may therefore represent a genuine extension of the pathogenic spectrum of K. kingae. Alternatively, the absence of any previous report of this particular clinical manifestation might simply reflect the lower incidence of both diskitis and K. kingae infection in adults. In vitro antibiotic susceptibility tests are predictive of out-
532
Meis et al.
come for ,B-Iactam agents to which K. kingae infection invariably responds [3]. However, treatment failures have been reported for other agents such as erythromycin, lincomycin, and ciprofloxacin despite susceptibility in vitro [3, 9, II]. The optimal mode and duration of therapy have yet to be defined, although marked symptomatic improvement as well as a return to normal CRP levels can be expected within the first 2 weeks of treatment. However, since bone injury resolves more slowly and shorter treatment might result in relapse, the current practice of giving therapy for 3 months seems prudent. Certainly, initial intravenous treatment followed by oral therapy has been shown to be effective. Acknowledgment The authors thank Dr. J. Peter Donnelly for reviewing the manuscript. References I. Morrison VA, Wagner KF. Clinical manifestations of Kingella kingae infections: case report and review. Rev Infect Dis 1989; II :776-82. 2. De Groot R. Glover D. Clausen C. Smith AL, Wilson CB. Bone and joint infections caused by Kingella kingae: six cases and review of the literature. Rev Infect Dis 1988; 10:998-1004. 3. Graham DR, Band JD, Thornsberry C. Hollis DG, Weaver RE. Infec-
4. 5.
6.
7. 8.
9.
10.
II. 12.
13.
CID 1992; 15 (September)
tions caused by Moraxella. Moraxella urethra/is. Moraxella-like Groups M-5 and M-6, and Kingella kingae in the United States. 1953-1980. Rev Infect Dis 1990;12:423-31. Falsen E. Brorson JE, Enger EA. Moraxella kingii: a rare cause ofosteomyelitis. Z Kinderchir 1977;22: 186-9. Wong AS. Dyke J, Perry D. Anderson DC Paraspinal mass associated with intervertebral disk infection secondary to Moraxella kingii. J Pediatr 1978;92:86-8. Claesson B, Falsen E. Kjellman B. Kingella kingae infections: a review and a presentation of data from 10 Swedish cases. Scand J Infect Dis 1985; 17:233-43. Woolfrey BE Lally RT. Faville RJ. Intervertebral diskitis caused by Kingella kingae. Am J Clin PathoI1986;85:745-9. Raymond J. Bergeret M, Bargy F. Missenard G. Isolation of two strains of Kingella kingae associated with septic arthritis. J Clin Microbiol 1986;24: 1100-1. Chanal C Tiget F. Chapuis P, Campagne D. Jan M. Sirot J. Spondylitis and osteomyelitis caused by Kingella kingae in children. J Clin Microbiol 1987;25:2407-9. Clement JL. Berard J. Cahuzac JP, Gaubert J. Kingella kingae osteoarthritis and osteomyelitis in children. J Pediatr Orthop 1988;8:59-61. Amir J. Shockelford PG. Kingellakingaeintervertebral disk infection. J Clin MicrobioI1991;29: 1083-6. Goutzmanis JJ, Gonis G. Gilbert GL. Kingellakingaeinfection in children: ten cases and a review of the literature. Pediatr Infect Dis J 1991; I0:677-83. Hendriksen SO. Corroding bacteria from the respiratory tract. I. Maraxella kingii. Acta Pathol Microbiol Scand 1969;75:85-90.
