Kingella kingae: An Emerging Pathogen in Young Children

Abstract

Kingella kingae is being recognized increasingly as a common etiology of pediatric osteoarticular infections, bacteremia, and endocarditis, which reflects improved culture methods and use of nucleic acid-amplification techniques in clinical microbiology laboratories. K kingae colonizes the posterior pharynx of young children and is transmitted from child to child through close personal contact. Day care attendance increases the risk for colonization and transmission, and clusters of K kingae infections among day care center attendees have been reported. Key virulence factors in K kingae include type IV pili and a potent RTX toxin. In previously healthy children, >95% of K kingae infections are diagnosed between the ages of 6 and 48 months. Among children with underlying medical conditions, K kingae disease may occur at older ages as well. The clinical presentation of K kingae disease is often subtle and may be associated with normal levels of acute-phase reactants, which underscores the importance of a high index of suspicion. K kingae is usually susceptible to ß-lactam antibiotics, and infections typically respond well to medical treatment, with the exception of cases of endocarditis.

Oropharyngeal Kingella kingae carriage in children: characteristics and correlation with osteoarticular infections

“…After 36 mo, the carriage rate declined, probably due to the maturation of the children's immune system and/or an acquired humeral immunity to K. kingae carriage and invasive infection as a result of previous expositions (15)(16)(17)(18)(19). Our results show marked similarities to a recent study carried out by Amit et al (20) among a large cohort of healthy Israeli children; and previous data (13,16). A recent study by Amit et al (19) confirmed the age of 6-29 mo to be a significant risk factor for K. kingae colonization in two different ethnic groups of Israel.…”

“…kingae has recently emerged as an important cause of OAI in young children (1)(2)(3)13). This organism belongs to the normal commensal flora of the posterior pharynx (14,15), but rarely penetrates the bloodstreams and invades distant organs (6,16).…”

“…Yagupsky et al hypothesize that prevalence of K. kingae could be reduced by exposure to antibiotics during the winter months, since K. kingae is highly sensitive to antibiotics commonly used for respiratory infections (13,25). In our study of asymptomatic carriage, throat swabs were collected only from children without clinical findings of OAI who did not receive any antibiotic treatment in the previous 2 mo.…”

“…If so, OAI could result from the interaction of K. kingae colonization and acute URT infection (8)(9)(10)(11)(12)(13)(14). Recent studies have evidenced associations between viral respiratory diseases (32), such as primary herpetic gingiva-stomatitis (30), hand-foot-mouth disease/herpangina (33) and invasive K. kingae infections.…”

Oropharyngeal Colonization Density of Kingella kingae

“…Similarly to S. pneumoniae, H. influenzae type b or Neisseria meningitidis, K. kingae resides in the mucosal surface and is able to penetrate the bloodstream, disseminate and invade distant organs. [9][10][11] Colonization of the respiratory tracts by these organisms is, therefore, a prerequisite for later invasion. For most of these microoorganisms, such as S. pneumoniae or H. influenzae, [2][3][4][5][6][7] there are evidences that the bacterial load varies in the nasopharynx with the age of subjects, and that higher nasopharynx colonization densities play major roles in the development of invasive infections.…”