Open Access

Kocuria kristinae septic arthritis associated with infectious endocarditis in a hemodialysis patient with diabetes mellitus: a case report and literature review

  • Taro Horino1Email author,
  • Yoshiko Shimamura1,
  • Koji Ogata1,
  • Kosuke Inoue1 and
  • Yoshio Terada1
Renal Replacement Therapy20162:32

DOI: 10.1186/s41100-016-0041-3

Received: 28 November 2015

Accepted: 8 April 2016

Published: 13 June 2016

Abstract

Background

Kocuria kristinae is an aerobic Gram-positive coccus that is considered ubiquitous and non-pathogenic in healthy individuals. Furthermore, only 27 reports have described cases of critical infections with this microorganism, which is notoriously difficult to identify.

Case presentation

We report the case of a 61-year-old male hemodialysis patient with diabetes mellitus, who developed severe septic arthritis that was associated with infectious endocarditis, which was identified using 18F-fluorodeoxyglucose positron-emission tomography/computed tomography (FDG-PET-CT). K. kristinae was identified in two separate blood cultures. The patient recovered immediately after being treated using piperacillin followed by ampicillin/sulbactam and gentamicin.

Conclusions

To the best of our knowledge, this is the first case of K. kristinae septic arthritis associated with infectious endocarditis in a hemodialysis patient with diabetes mellitus. We suggest that physicians consider the pathogenic potential of K. kristinae, which can cause fatal infections, such as septic arthritis and infectious endocarditis, in immunocompromised patients. FDG-PET-CT is a useful and safe diagnostic tool for determining the cause of inflammatory disease in dialysis patients.

Keywords

Kocuria kristinae Septic arthritis Infectious endocarditis Hemodialysis FDG-PET-CT

Background

In Japan, the number of patients with diabetes is increasing every year, as is the rate of renal replacement therapy (RRT) for treating diabetic nephropathy. Both end-stage renal disease (ESRD) and diabetes mellitus are severe immunocompromised states, and dialysis patients are prone to infectious complications. Furthermore, we believe that patients with diabetes mellitus are predisposed to invasive infections. Therefore, we describe the case of a hemodialysis patient who had a wound infection and bacteremia with Kocuria kristinae, which is a microorganism that is considered non-pathogenic in healthy individuals. In addition, we provide a review of case reports regarding K. kristinae infections in humans.

Case presentation

A 61-year-old male hemodialysis patient with a history of diabetes mellitus and polyarthralgia was referred to our hospital. Two months before the referral, the patient had arthralgia of the right knee, which exhibited swelling, tenderness, and restricted motion. The patient subsequently experienced severe polyarthralgia that involved both shoulders, wrists, hip joints, foot joints, and the left knee joint, as well as rapidly progressing severe lumbago. At the admission, his temperature was 36.6 °C. A physical examination revealed swelling and warmth in all joints that the patient identified as being painful. The laboratory test results are shown in Table 1. A chest radiograph revealed mild cardiomegaly without other remarkable findings. Joint radiographs revealed no deformities. Magnetic resonance imaging (MRI) of the left hip joint revealed high-intensity lesions surrounding the head of the femoral bone on the T2-weighted image (Fig. 1).18F-fluorodeoxyglucose positron-emission tomography/computed tomography (FDG-PET-CT) revealed short segments of increased FDG uptake within the shoulders, wrists, hip joints, knees, and foot joints (Fig. 2). We had performed arthrocentesis at the admission, and an aspiration specimen from the right knee joint yielded grossly purulent material. Synovial fluid white cell counts were 13,200/mm3, with 95 % polymorphonuclear leukocytes and 5 % monomorphonuclear leukocytes. Although the synovial fluid culture was negative, clusters of Gram-positive cocci were isolated from a blood specimen that was taken at the admission. Two blood cultures were both positive for K. kristinae, and these results were confirmed using the Vitek 2 system. The isolate was sensitive to all tested antibiotics (Table 1). We started treatment using intravenous piperacillin (2 g once per day), and the polyarthritis immediately improved. After 14 days of antibiotic treatment, the patient’s C-reactive protein levels were 0.8 mg/dL and the other laboratory data were normalized.
Table 1

Laboratory data at admission

CBC (normal range)

Blood chemistry

Tumor markers

Blood culture

 RBC (400–552)

239 × 104/mm3

 FBS (70–110)

179 mg/dL

 CEA (<3.4)

0.8 ng/mL

Kocuria kristinae

(+)

  Hb (13.2–17.2)

6.9 g/dL

 Alp (104–338)

501 U/L

 CA19-9 (<37)

2.8 U/mL

 Antimicrobial susceptibilities (MIC)

μg/mL

  Ht (40.4–51.1)

21.9 %

 γ-GTP (5–70)

41 U/L

Infection

 

  Penicillin

0.12

 Plt (14.8–33.9)

46.8 × 104/mm3

 t-Bil (0.2–1.2)

0.3 mg/dL

 HBs Ag

(−)

  Oxacillin

≤2.0

 WBC (3.6–9.6)

5.6 × 103/mm3

 d-Bil (0–0.4)

0.0 mg/dL

 HCV Ab

(−)

  Ampicillin

≤0.25

  neu

73.0 %

 ChE (168–470)

123 U/L

 HTLV-I Ab

(−)

  Cefazolin

≤8.0

  lym

8.0 %

 ALT (8–42)

24 U/L

 EBV

 

  Cefotaxime

≤8.0

  mon

13.0 %

 AST (13–33)

37 U/L

  VCA-IgG

×640

  cefepime

≤8.0

  eos

6.0 %

 LDH (119–229)

125 U/L

  VCA-IgM

×<10

  Cefotiam

≤8.0

  bas

0.0 %

 CPK (62–287)

10 U/L

  EBNA

×20

  Cefpirome

≤8.0

  aty-ly

0.0 %

 Crn (0.6–1.1)

10.3 mg/dL

 Mumps

(−)

  Cefozopran

≤8.0

Electrolytes

 

 BUN (8–20)

52 mg/dL

 Herpes zoster

(−)

  Cefmetazole

≤16.0

 Na (136–145)

137 mmol/L

 UA (3.4–7.8)

8.5 mg/dL

 Parvovirus B19

(−)

  Cefdinir

≤1.0

 K (3.4–4.5)

4.4 mmol/L

 Amy (37–125)

71 U/L

 Syphilis

(−)

  Cefditoren

≤1.0

 Cl (100–108)

99 mmol/L

 TG (30–150)

106 mg/dL

 QFT

(−)

  Flomoxef

≤8.0

 Ca (8.7–11.0)

10.2 mg/dL

 H-Chol (>40)

17 mg/dL

 Candida Ab

(−)

  Imipenem/cilastatin

≤4.0

 P (2.5–4.5)

4.7 mg/dL

 L-Chol (<140)

61 mg/dL

 β-d-glucan

(−)

  Meropenem

≤4.0

 Mg (1.8–2.4)

2.5 mg/dL

Serological examinations

 

 Chlamydia trachomatis

 

  Amoxicillin

≤4.0

Proteinogram

 

 CRP (<0.3)

35.5 mg/dL

  IgG

(−)

  Gentamicin

≤4.0

 TP (6.7–8.1)

7.1 g/dL

 SAA (<8.0)

1843.9 mg/mL

  IgA

(−)

  Amikacin

≤16.0

 Alb (3.9–4.9)

2.6 g/dL

 MMP-3 (36.9–121.0)

586.4 ng/mL

 Chlamydia pneumoniae

 

  Arbekacin

≤4.0

 Glb

4.5 g/dL

 CH50 (30–45)

47.0 U/mL

  IgG

(−)

  Erythromycin

≤0.5

  α1

11.2 %

 C3 (65–135)

131.5 mg/dL

  IgA

(−)

  Clarithromycin

≤2.0

  α2

16.6 %

 C4 (13–35)

31.7 mg/dL

Synovial fluid

 

  Clindamycin

≤0.5

  β

10.7 %

 ANA

(−)

 Glossly purulent material

 

  Minocycline

≤4.0

  γ

34.3 %

 ds-DNA Ab

(−)

 WBC

13,200 × 103/mm3

  Linezolid

≤2.0

 IgG (870–1700)

2519 mg/dL

 SSA Ab

(−)

  neu

95.0 %

  Vancomycin

≤2.0

 IgA (110–410)

497 mg/dL

 SSB Ab

(−)

  pla

5.0 %

  Teicoplanin

≤8.0

 IgM (35–220)

87 mg/dL

 RF

(−)

 Crystals

(−)

  Fosfomycin

≤4.0

 M-protein

(−)

 ACPA

(−)

 Culture

(−)

  Levofloxacin

≤1.0

 HbA1c (4.6–6.2)

7.9 %

 MPO-ANCA

(−)

  

  Sulfamethoxazole/trimethoprim

≤2.0

ESR (<20)

>140 mm/h

 PR3-ANCA

(−)

  

  Rifampicin

≤1.0

Abbreviations: CBC complete blood cell count, RBC red blood cell count, Hb hemoglobin, Ht hematocrit, Plt platelet, ESR erythrocyte sedimentation rate, WBC white blood cell count, neu neutrophils, lym lymphocytes, mon monocytes, eoseosinophils, bas basophils, aty-ly atypical lymphocytes, Na sodium, K potassium, Cl chlorine, Ca calcium, P phosphorus, Mg magnesium, TP total protein, Alb albumin, Glb globulin, IgG immunoglobulin G, IgA immunoglobulin A, IgM immunoglobulin M, FBS fasting blood sugar, Alp alkaline phosphatase, γ-GTP γ-glutamyltransferase, t-Bil total bilirubin, d-Bil direct bilirubin, ChE cholinesterase, ALT alanine transaminase, AST aspartate aminotransferase, LDH lactate dehydrogenase, CPK creatine phosphokinase, Crn creatinine, BUN blood urea nitrogen, UA uric acid, Amy amylase, TG triglyceride, H-Chol high-density lipoprotein cholesterol, L-Chol low-density lipoprotein cholesterol, CRP C-reactive protein, SAA serum amyloid A, MMP-3 matrix metalloproteinase-3, CH50 complement activity, C3 complement 3, C4 complement 4, ANA antinuclear antibody, SSA Ab anti-SS-A/Ro antibody,SSB Ab anti-SS-B/La antibody, RF rheumatoid factor, ACPA anti-cyclic citrullinated peptide antibody, MPO-ANCA myeloperoxidase-anti-neutrophil cytoplasmic antibody, PR3-ANCA serine proteinase3-anti-neutrophil cytoplasmic antibody, HBs Ab hepatitis B surface antigen, HCV Ab hepatitis C virus antibody, HTLV-I Ab human T-lymphotropic virus type 1 antibody,pla plasma cell, EBV Epstein-Barr virus, VCA viral capsid antigen, EBNA Epstein-Barr nuclear antigen, QFT QuantiFERON-TB, pla plasma cell

Fig. 1

The magnetic resonance imaging findings. The magnetic resonance findings from the left hip joint reveal high-intensity lesions (white arrows) surrounding the head of the femoral bone in the T2-weighted image (right panel)

Fig. 2

The 18F-fluorodeoxyglucose positron-emission tomography/computed tomography findings. 18F-fluorodeoxyglucose positron-emission tomography/computed tomography reveals short segments of increased fluorodeoxyglucose uptake (white arrows) within the shoulders, wrists, hip joints, knees, and foot joints

Electrocardiography detected no remarkable findings during his clinical course. However, 1 month after the admission, echocardiography detected vegetation on the mitral valve, which was compatible with infectious endocarditis (Fig. 3, right panel), although there had been no findings of vegetation at 2 years before the admission (Fig. 3, left panel). Physical examination after the echocardiography revealed Janeway’s lesions, although we did not detect Osler’s nodes or Roth’s spots. Therefore, we stopped the intravenous piperacillin therapy and started treatment using intravenous ampicillin/sulbactam (1.5 g every other day) and intravenous gentamicin (100 mg every other day). The patient’s clinical course was uneventful, and he was later discharged to our outpatient clinic (Fig. 4).
Fig. 3

The echocardiography findings. (Left panel) Echocardiography reveals no remarkable findings at 2 years before the presentation. (Right panel) Echocardiography at 1 month after the admission reveals mitral valve vegetation

Fig. 4

The patient’s clinical course. PIPC piperacillin, APBC ampicillin, SBT sulbactam, GM gentamicin, Hb hemoglobin, CRP C-reactive protein

Discussion

K. kristinae was first described as Micrococcus kristinae in 1974 and was subsequently classified as Micrococcus spp., which is now separated into Micrococcus, Nesterenkonia, Kytococcus, Dermacoccus, and Kocuria [1, 2]. K. kristinae is a strictly aerobic species that is commonly identified among skin and oral flora [3]. Most physicians consider Micrococcus spp. (including Kocuria) non-pathogenic, and we initially assumed that the blood cultures from the present case were negative for pathogenic bacteria. However, reports of infectious diseases that were caused by this species are gradually being published. The clinical characteristics of the 28 reported cases of K. kristinae infections are summarized in Tables 2 and 3 [416]. Most K. kristinae infections are reported as infections in immunocompromised hosts or patients with underlying malignancy, ESRD requiring dialysis, diabetes mellitus, and prematurity. Although published reports of K. kristinae infections are rare, the prevalence of this infection, especially among immunocompromised hosts, may be underestimated, as most physicians likely do not consider this organism as a pathogen.
Table 2

Demographic data, treatments, and outcomes for 28 patients with Kocuria kristinae infections

Case

Antibiotic regimen

Course (days)

TPN

Outcome

Ref.

Year

1

Meropenem + glycopeptide → ciprofloxacin + clindamycin → catheter removal

NA

NA

Recovery

4

2002

2

Levofloxacin

14

No

Recovery

5

2005

3

Ceftriaxone + ofloxacin

16

NA

Death

6

2008

4

Azithromycin + ceftriaxone + vancomycin + oseltamivir → vancomycin + clindamycin → oxacillin

42

Yes

Recovery

7

2011

5

Vancomycin → teicoplanin → oxacillin

NA

Yes

Recovery

8

2011

6

Piperacillin/tazobactam → ciprofloxacin

NA

Yes

Recovery

8

2011

7

Oxacillin + vancomycin

NA

Yes

Recovery

8

2011

8

Oxacillin

NA

Yes

Recovery

8

2011

9

Tobramycin → cefotaxime + tazobactam → ciprofloxacin + teicoplanin + amoxicillin/clavulanic acid

24

No

Recovery

9

2011

10

Cefazolin + cefepime

14

No

Recovery

10

2011

11

Ceftriaxone + vancomycin

14

Yes

Recovery

11

2012

12

Ceftriaxone + metronidazole → sulbactam/ampicillin + gentamicin

25

No

Death

12

2013

13

No antibiotics

No

No

Unknown

13

2013

14

Dicloxacillin + vancomycin + levofloxacin

21

No

Recovery

14

2014

15

Ceftriaxone + amikacin + cefotaxime

16

No

Recovery

14

2014

16

Vancomycin

10

NA

Recovery

15

2014

17

Vancomycin

7

NA

Recovery

15

2014

18

Levofloxacin

7

NA

Recovery

15

2014

19

Linezolid

14

NA

Recovery

15

2014

20

Vancomycin

5

NA

Recovery

15

2014

21

Vancomycin + ceftazidime

10

Yes

Recovery

16

2015

22

Vancomycin

10

Yes

Recovery

16

2015

23

Vancomycin + ceftazidime

10

Yes

Recovery

16

2015

24

Oxacillin + vancomycin

9

Yes

Recovery

16

2015

25

Vancomycin + cefotaxime

12

Yes

Recovery

16

2015

26

Vancomycin + cefotaxime

10

Yes

Recovery

16

2015

27

Vancomycin + piperacillin/tazobactam

10

No

Recovery

16

2015

28

Piperacillin → ampicillin/sulbactam + gentamicin

30

No

Recovery

Current

2015

TPN total parenteral nutrition, NA not available

Table 3

Clinical, demographic, and bacterial data from 28 patients with Kocuria kristinae infections

Case

Age, year (month)

Sex

Country

Underlying disease

Isolation site

Catheters

Clinical presentation

1

51

F

Italy

Ovarian cancer, chemotherapy

Blood, catheter tip

CVC

Febrile neutropenia, sepsis

2

56

M

Hong Kong

Gallstones

Biliary fluid

No

Acute cholecystitis

3

68

M

France

MDS, acute myelogenous leukemia, tuberculosis, chemotherapy

Blood

CVC

Sepsis

4

29

F

USA

Pregnancy, hyperemesis gravidarum

Blood

CVC

Suppurative thrombosis

5

89

F

Taiwan

Post-resection ischemic bowel status, short bowel syndrome

Blood

CVC

Endocarditis

6

37

F

Taiwan

Gastric cancer

Blood

CVC

Bacteremia

7

2

M

Taiwan

Congenital short bowel syndrome, hypogammaglobulinemia

Blood

CVC

Bacteremia

8

68

F

Taiwan

Gastric cancer

Blood

CVC

Bacteremia

9

78

M

Italy

ESRD on CAPD

Peritoneal fluid

PDC

Peritonitis

10

69

M

China

ESRD on CAPD

Peritoneal fluid

PDC

Peritonitis

11

0 (4.0)

F

Turkey

Prolonged diarrhea, severe failure to thrive

Blood

CVC

Black hairy tongue, fever, bacteremia

12

74

M

Italy

Diabetes mellitus

Blood

No

Foot ulcer, endocarditis, sepsis

13

20

M

India

Urethral stricture

Urine

UC

Malaise

14

20

F

Mexico

ESRD on HD

Blood

CVC

Bacteremia

15

68

M

Mexico

ESRD on CAPD

Peritoneal fluid

PDC

Peritonitis

16

65

M

India

Lung small cell carcinoma

Sputum

NA

Leukocytosis (neutrophillia)

17

65

M

India

Carcinoma soft palate

Sputum

NA

Leukocytosis (neutrophillia)

18

41

F

India

Carcinoma lip and gingival sulcus

Sputum

NA

Leukocytosis (neutrophillia)

19

39

M

India

Squamous cell carcinoma of the buccal mucosa

pus

NA

Leukocytosis (neutrophillia)

20

42

F

India

Ductal carcinoma of the breast

pus

NA

Leukocytosis (neutrophillia)

21

0 (1.4)

M

Taiwan

Prematurity

Blood

CVC

Sepsis

22

0 (0.6)

M

Taiwan

Prematurity

Blood

CVC

Sepsis

23

0 (0.7)

F

Taiwan

Prematurity

Blood

CVC

Sepsis

24

0 (1.1)

F

Taiwan

Prematurity

Blood

CVC

Sepsis

25

0 (0.6)

F

Taiwan

Prematurity

Blood, catheter tip

CVC

Sepsis

26

0 (0.6)

F

Taiwan

Prematurity

Blood, catheter tip

CVC

Sepsis

27

0 (2.5)

F

Taiwan

Leukemia

Blood, catheter tip

CVC

Neutropenic fever

28

61

M

Japan

ESRD on HD, diabetes mellitus

Blood

No

Septic arthritis, endocarditis

Age is presented as year (month)

Abbreviations: ESRD end-stage renal disease, CAPD chronic ambulatory peritoneal dialysis, HD hemodialysis, CVC central venous catheter, PDC peritoneal dialysis catheter, UC urinary catheter

Patients who are receiving RRT often have infectious diseases, although the identification of their causative microorganism(s) and focus of infection are difficult to accurately diagnose. Furthermore, patients who are receiving RRT are frequently immunocompromised and may have atypical infectious organisms that are considered normal bacterial flora in healthy individuals [17]. Among patients who are undergoing RRT, the host’s immunity may be compromised by uremia that interferes with T cell and B cell function, macrophage phagocytosis, and antigen presentation, which can increase the risk of infection [17]. The population of patients with ESRD who receive RRT has been increasing worldwide, and this population included 314,180 Japanese patients in December 2013 [18]. Furthermore, the number of patients with diabetes mellitus is increasing, and diabetic nephropathy has recently become the leading cause (43.8 %) of RRT in Japan [18]. Because ESRD and diabetes mellitus can both lead to an immunocompromised status and increase susceptibility to unusual infections, patients with ESRD and diabetes mellitus are likely very susceptible to uncommon and usually non-pathogenic microorganisms. However, Kocuria spp. infections are rarely reported among patients with diabetes and RRT. We speculate that there are two reasons for this phenomenon. First, most physicians believe that Kocuria spp., Micrococcus spp., and especially K. kristinae are non-pathogenic and might not consider these organisms as potentially causative organisms, despite observing positive culture results. Second, most Kocuria spp. and Micrococcus spp. are sensitive to almost all antibiotics (except ampicillin and erythromycin), and monotherapy often results in good outcomes [19]. In this context, Japanese investigators have reported that the causes of fever of unknown origin (FUO) are infection (27.7 %), non-infectious inflammatory disease (18.4 %), malignancy (10.2 %), other conditions (14.8 %), and unknown causes (28.9 %) [20]. Thus, given the frequency of an unknown cause of FUO, we usually use empirical antibiotics to treat infections of unknown origin until culture results are available. Therefore, it is possible that repeating cultures will not identify the same microorganisms in each culture, as the empirical antibiotics might cure the infection without severe clinical events (e.g., sepsis) before the second sample is collected. Interestingly, infection is the primary cause of death among Japanese patients who are receiving RRT (26.5 %) [19], and it is likely that the number of patients with diabetes and RRT is going to continue increasing. Furthermore, the population of elderly Japanese patients is also increasing, which will likely result in a larger number of immunocompromised hosts. Based on these factors, it is possible that an increasing number of patients may have underlying K. kristinae infection that is not diagnosed until they develop severe complications, such as bacteremia and endocarditis. Therefore, it may be prudent to assess the pathogenic capacity of K. kristinae and any other unusual microorganisms, even if an infection of unknown origin improves after antibiotic monotherapy in patients who are elderly, have diabetes, or are receiving RRT. Moreover, clinicians should not underestimate the importance of a positive culture result for K. kristinae, as patients may experience repeated infections, develop severe infectious complications, and possibly die from this infection.

During recent years, many investigators have reviewed the diagnostic value of FDG-PET-CT. Although FDG was first developed to trace brain metabolism [21], FDG-PET-CT has subsequently been recognized as an early diagnostic tool that has high sensitivity for malignancies, such as melanoma and cervical, lung, breast, gastrointestinal, ovarian, and prostatic cancers [22]. Furthermore, recent studies have found that FDG-PET-CT could detect the existence of inflammatory diseases and determine their severity and extent [23]. Although contrast-enhanced CT and/or MRI are performed for diagnosing and examining malignancies, infections, and autoimmune diseases, the use of contrast agents for these techniques is often contraindicated in patients with severe renal insufficiency, as these agents increase the incidence of their adverse effects. In contrast, FDG-PET-CT is considered safer and simpler for dialysis patients, compared to contrast-enhanced CT or MRI. Therefore, we suggest that FDG-PET-CT should be used for diagnosing and evaluating dialysis patients if the origin of their disease is unclear and that physicians should not delay this diagnostic imaging, which can lead to a poor prognosis.

Conclusions

We report the first case of K. kristinae septic arthritis associated with infectious endocarditis in a chronic hemodialysis patient with diabetes mellitus. We suggest that physicians should consider the pathogenic potential of K. kristinae, as it can cause fatal infections (e.g., septic arthritis and infectious endocarditis) in immunocompromised patients or patients with diabetes and RRT. We also suggest that FDG-PET-CT is a very useful and safe diagnostic tool, which can help identify the focus of inflammatory disorders in dialysis patients.

Consent

Written informed consent was obtained from the patient for publication of this case report and the accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School

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