Pyogenic tenosynovitis (PTS) is a closed-space infection of a tendon sheath.1,2 In the upper and lower extremities, tendon sheath infections mostly occur after a penetrating trauma such as cuts, bites, or stings. Although PTS often occurs in the fingers tendons, any tendon’s sheath can be affected by PTS.1,3 Another possible route of infection is contiguous spread from adjacent soft tissue or hematogenous spread during a systemic infection.2 Blood supply of the tendon sheath is poor, and, thus, the immune system defense mechanisms are ineffective in this environment. Therefore, once microorganisms have penetrated the tendon sheath, they proliferate using the synovial fluid as a nutrient source.1 In adults, the most common pathogens causing PTS are Staphylococcus aureus, β-hemolytic Streptococcus, Pasteurella multocida (from animal bites) and Eikinella corrodens (from human bites).3 In 2004, a case of tenosynovitis caused by Kingella kingae was mentioned for the first time in a brief report published by the Infectious Diseases Society of America Emerging Infections Network.4 Almost 10 years later, the first case of PTS affecting a finger’s flexor tendon sheath in an infant was published.5 Today, K. kingae is a well-documented cause of osteoarticular infections (OAI) in children younger than 4 years of age. However, it is rarely suspected as the causative microorganism of PTS in the pediatric population. The purpose of this article is to present a series of 11 cases of PTS in infants highlighting the role of K. kingae as a possible causative agent of PTS.
MATERIALS AND METHODS
After approval from the Children Hospital Review Board (CE 14-102R), we retrospectively reviewed the medical charts of all children admitted to our institution for suspected PTS between January 2007 and December 2016. Charts were screened for patient demographics (sex and age at admission), location(s) of PTS, body temperature, results of laboratory studies, results of bacteriologic investigations, surgical procedures performed, length of antibiotic treatment and complications. Clinical examination and laboratory evaluation (peripheral white blood cell counts, platelet counts, C-reactive protein levels, erythrocyte sedimentation rate and blood cultures) results were obtained (Table 1). When the fingers were affected, the clinical diagnosis was based on the 4 Kanavel signs: tenderness along the tendon sheath, digital swelling, a semiflexed digital position and pain on extension of the digit. When other anatomical areas were affected, the clinical diagnosis relied only on tenderness along the tendon sheath and pain when stretching the affected tendons.
The diagnosis of PTS was further supported by pathognomonic findings on ultrasonography or on magnetic resonance imaging. Confirmation of the diagnosis was obtained by synovial sheath aspiration or by a tissue biopsy of the infected site. The samples were sent to the laboratory for Gram staining and were immediately inoculated on Columbia blood agar, Centers for Disease Control anaerobe 5% sheep blood agar and chocolate agar and in brain–heart broth. A broad-range polymerase chain reaction (PCR) amplification of 16S rRNA and a specific real-time PCR amplification of the K. kingae genes rtxA and rtxB were used for bacterial identification when cultures were sterile. Starting in September 2009, in all children between 6 months and 4 years of age admitted for a musculoskeletal infection, an oropharyngeal swab was taken to culture K. kingae. In severe PTS, tendon sheath irrigation was performed using multiple small incisions. Empiric intravenous antibiotic therapy was started at the discretion of the attending physician. The duration and mode of administration of the antibiotic treatment were adjusted with regard to the patient’s age and the causative organism.
Charts of 11 children (7 boys and 4 girls) admitted for PTS were reviewed. The mean patient age was 15 ± 5.3 months, with age ranging from 8 to 22 months. The median duration from the onset of symptoms to the diagnosis of PTS was 3 days (standard deviation, 2.8 days). Three patients were febrile (T ≥ 38°C) at admission. Infections were localized in the hand in 6 patients, in the wrist in 1 patient and in the ankle in the remaining 4 patients. The white blood cell count was normal in 36% of children, with a mean of 15.2 ± 4 per mm3 (range: 11.1–24.7/mm3). The C-reactive protein levels were normal (≤10 mg/L) in 18% of patients at the time of admission and averaged 39.9 ± 33 mg/L. Erythrocyte sedimentation rate was available for 54% of the patients and was slightly elevated in all patients (25–48 mm/h). The platelet count was elevated in 63% of the patients.
One of the 7 blood cultures taken during initial work-up was positive, identifying infection with Corynebacterium. In 1 case, K. kingae was identified by PCR using a peripheral blood sample. In 5 children, diagnostic biopsies or needle tendon sheath aspirations were performed. Culture of the obtained tendon sheath liquid was negative for microorganisms, but PCR assays were positive for K. kingae. Oropharyngeal swabs were collected from 7 children and were used for real-time PCR assays specific for K. kingae. These assays showed positive results for all the 7 patients. Identification of the microorganism was thus possible in these 7 patients (63.6%); the most commonly identified causative pathogens of PTS in our study were K. kingae (6 patients) and Corynebacterium (1 patient). Despite negative blood tests, K. kingae was highly suspected in 3 patients on the basis of the result of the oropharyngeal PCR assay. In 3 patients, biologic data were indicative of a K. kingae infection even if oropharyngeal PCR was not performed. The mean antibiotic duration was 21.1 ± 5.1 days, with 4.5 ± 1.3 days of intravenous treatment followed by 16.6 ± 5.4 days of oral treatment. One child required a second joint irrigation 5 days after the primary surgery in the absence of clinical improvement. No late complications were reported.
PTS is an uncommon infection in children,2,3 and, thus, only case reports on this condition are found in the literature.3,6 Tenosynovitis most commonly results from the introduction of bacteria into the tendon sheath through a small penetrating wound such as that made by the point of a needle or thorn, especially on hands.1,3 However, PTS may also result from a contiguous spread from infected adjacent soft tissue or by hematogenous diffusion.2 The bacteriologic profile of PTS in adults is well established and shows a predominance of S. aureus and β-hemolytic Streptococcus as the primary causative pathogens.
The present study focuses on the bacteriologic profile of PTS in infants and provides evidence that PTS in young children is frequently caused by a different pathogen, namely, K. kingae. In children younger than 4 years of age, K. kingae has already been recognized as one of the primary causative pathogens for osteoarticular infections. It is well known that this pathogen is quite difficult to culture and that blood cultures for this pathogen are frequently negative. PCR assays specific for K. kingae have significantly improved the diagnosis of infection with this pathogen. A recent study demonstrated that the presence of K kingae RTX toxin genes in the oropharynx was strongly associated with OAI caused by the same pathogen, whereas its absence excluded a K. kingae OAI.7 Although we could identify the causative pathogen in only 7 of 11 patients, K. kingae was the predominant pathogen. In 1 additional patient, a throat swab was positive for K. kingae; this led us to conclude that tenosynovitis in this patient was probably caused by K. kingae. PTS caused by S. aureus and β-hemolytic Streptococcus show a clear clinical picture with the presence of some or all of Kanavel signs, whereas laboratory parameters are often in the normal range or are only slightly elevated.
Infections caused by K. kingae are often characterized by a mild-to-moderate clinical and biologic inflammatory response.8 The platelet count is one of the few laboratory parameters that show an increase regularly in patients with K. kingae infection, and, thus, an increased platelet count in osteoarticular or musculocutaneous infections in a young child should prompt a physician to actively search for K. kingae as the causative pathogen. PTS caused by S. aureus or beta-hemolytic Streptococcus requires rapid diagnosis and surgical care to prevent the spread of infection, adhesion formation in the tendon sheaths and tendon necrosis,2,9,10 and a delay in diagnosis can result in a worse prognosis.9,10 There are, however, few data on the treatment of K. kingae infections of the tendon sheaths. The pathogen responds well to antibiotic treatment, and tissue destruction as seen with other more aggressive pathogens is rare. Thus, in the presence of mild clinical symptoms, an antibiotic treatment can be initiated without a surgical irrigation of the tendon sheath. However, as increased pressure in the tendon sheath can compromise vascular supply of the tendons, we believe that in cases of significant swelling, tendon sheath irrigation remains the gold standard of treatment.
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