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Although limited data are available about the epidemiology and transmission of K. kingae, the organism most likely is transmitted through respiratory secretions and saliva. In one study of an Israeli day care center, the monthly prevalence of K. kingae colonization ranged from 6% to 35%, and approximately 70% of children were colonized at some point during the 11-month study period. No invasive disease was observed (9). Subtyping by PFGE, immunoblotting, and ribotyping of the isolates demonstrated that children were colonized continuously, or intermittently with different subtypes over weeks to months. Two distinct subtypes with temporal clustering represented approximately 75% of the isolates (10). In comparison, a cohort of epidemiologically unrelated cases showed substantially more subtype variability (10). These findings suggest person-to-person transmission within the facility.
Although limited data are available about the epidemiology and transmission of K. kingae, the organism most likely is transmitted through respiratory secretions and saliva. In one study of an Israeli day care center, the monthly prevalence of K. kingae colonization ranged from 6% to 35%, and approximately 70% of children were colonized at some point during the 11-month study period. No invasive disease was observed (9). Subtyping by PFGE, immunoblotting, and ribotyping of the isolates demonstrated that children were colonized continuously, or intermittently with different subtypes over weeks to months. Two distinct subtypes with temporal clustering represented approximately 75% of the isolates (10). In comparison, a cohort of epidemiologically unrelated cases showed substantially more subtype variability (10). These findings suggest person-to-person transmission within the facility.
==References==
1. Goutzmanis JJ, Gonis G, Gilbert GL. Kingella kingae infection in children: ten cases and a review of the literature. Pediatr Infect Dis J 1991;10:677--83.
2. Yagupsky P, Dagan R. Kingella kingae: an emerging cause of invasive infections in young children. Clin Infect Dis 1997;24:860--6.
3. Yagupsky P, Press J. Arthritis following stomatitis in a sixteen-month-old child. Pediatr Infect Dis J 2003;22:273--4, 276--7.
4. Amir J, Yagupsky P. Invasive Kingella kingae infection associated with stomatitis in children. Pediatr Infect Dis J 1998;17:757--8.
5. Yagupsky P, Bar-Ziv Y, Howard CB, Dagan R. Epidemiology, etiology, and clinical features of septic arthritis in children younger than 24 months. Arch Pediatr Adolesc Med 1995;149:537--40.
6. Moylett EH, Rossman SN, Epps HR, Demmler GJ. Importance of Kingella kingae as a pediatric pathogen in the United States. Pediatr Infect Dis J 2000;19:263--5.
7. Yagupsky P, Peled N, Katz O. Epidemiological features of invasive Kingella kingae infections and respiratory carriage of the organism. J Clin Micro 2002;40:4180--4.
8. Yagupsky P, Dagan R, Howard CB, Einhorn M, Kassis I, Simu A. Clinical features and epidemiology of invasive Kingella kingae infections in southern Israel. Pediatrics 1993;92:800--4.
9. Yagupsky P, Dagan R, Prajgrod F, Merires M. Respiratory carriage of Kingella kingae among healthy children. Pediatr Infect Dis J 1995;14:673--8.
10. Slonim A, Walker ES, Mishori E, Porat N, Dagan R, Yagupsky P. Person-to-person transmission of Kingella kingae among day care center attendees. J Infect Dis 1998;178:1843--6.

Revision as of 08:24, 9 January 2009

Kingella kingae is a fastidious gram-negative coccobacillus that colonizes the respiratory and oropharyngeal tract in children. K. kingae occasionally causes invasive disease, primarily osteomyelitis/septic arthritis in young children, bacteremia in infants, and endocarditis in school-aged children and adults (1--8). Although diagnosis of this organism frequently is missed, invasive disease is uncommon. Only sporadic, non-epidemiologically linked cases have been reported.

K. kingae constitutes part of the normal respiratory flora in children but can cause isolated cases of invasive disease, primarily osteomyelitis/septic arthritis (65%--75% of cases) in young children and bacteremia (20%--30% of cases) in infants (1,2,7,8). The majority of children who have invasive disease are previously healthy without immunosuppressive conditions; >90% are aged <2 years (1,2,5-8).

Invasive disease is associated frequently with concomitant or precedent URI or stomatitis (3,4); disrupted respiratory or buccal mucosa might facilitate bacterial invasion and hematogenous dissemination. Biting might be an alternative means of introducing oropharyngeal pathogens into the bloodstream.

The presence of K. kingae is difficult to detect without immediate clinical suspicion. Gram stain of synovial fluid shows WBCs but frequently is negative for organisms. Recovery of the organism in culture is difficult because of its fastidious nature, and might require laboratories to hold culture plates for up to 7 days. For cases described in this report, cultures were held longer than routine laboratory protocol recommends (usually 3 days) because an atypical organism was suspected. Studies of cases in Israel indicate that 40%--50% of culture-negative septic arthritis cases in children aged <2 years might be attributable to K. kingae (5,8). Inoculating synovial fluid or bony exudates directly into blood-culture bottles with a continuous monitoring system increases the rate of K. kingae recovery substantially, compared with direct plating of specimens on solid media (5,8). The increased awareness and enhanced capability of laboratories to isolate this organism might lead to an observed increase in incidence of K. kingae invasive disease.

Although limited data are available about the epidemiology and transmission of K. kingae, the organism most likely is transmitted through respiratory secretions and saliva. In one study of an Israeli day care center, the monthly prevalence of K. kingae colonization ranged from 6% to 35%, and approximately 70% of children were colonized at some point during the 11-month study period. No invasive disease was observed (9). Subtyping by PFGE, immunoblotting, and ribotyping of the isolates demonstrated that children were colonized continuously, or intermittently with different subtypes over weeks to months. Two distinct subtypes with temporal clustering represented approximately 75% of the isolates (10). In comparison, a cohort of epidemiologically unrelated cases showed substantially more subtype variability (10). These findings suggest person-to-person transmission within the facility.

References

1. Goutzmanis JJ, Gonis G, Gilbert GL. Kingella kingae infection in children: ten cases and a review of the literature. Pediatr Infect Dis J 1991;10:677--83.

2. Yagupsky P, Dagan R. Kingella kingae: an emerging cause of invasive infections in young children. Clin Infect Dis 1997;24:860--6.

3. Yagupsky P, Press J. Arthritis following stomatitis in a sixteen-month-old child. Pediatr Infect Dis J 2003;22:273--4, 276--7.

4. Amir J, Yagupsky P. Invasive Kingella kingae infection associated with stomatitis in children. Pediatr Infect Dis J 1998;17:757--8.

5. Yagupsky P, Bar-Ziv Y, Howard CB, Dagan R. Epidemiology, etiology, and clinical features of septic arthritis in children younger than 24 months. Arch Pediatr Adolesc Med 1995;149:537--40.

6. Moylett EH, Rossman SN, Epps HR, Demmler GJ. Importance of Kingella kingae as a pediatric pathogen in the United States. Pediatr Infect Dis J 2000;19:263--5.

7. Yagupsky P, Peled N, Katz O. Epidemiological features of invasive Kingella kingae infections and respiratory carriage of the organism. J Clin Micro 2002;40:4180--4.

8. Yagupsky P, Dagan R, Howard CB, Einhorn M, Kassis I, Simu A. Clinical features and epidemiology of invasive Kingella kingae infections in southern Israel. Pediatrics 1993;92:800--4.

9. Yagupsky P, Dagan R, Prajgrod F, Merires M. Respiratory carriage of Kingella kingae among healthy children. Pediatr Infect Dis J 1995;14:673--8.

10. Slonim A, Walker ES, Mishori E, Porat N, Dagan R, Yagupsky P. Person-to-person transmission of Kingella kingae among day care center attendees. J Infect Dis 1998;178:1843--6.