You are on page 1of 7
Pediat Inet Dis J BAN ANTE-NS (Copycat 1991 by Willian Wikis Val 10, No.8 Printed in 28, Kingella kingae infection in children: ten cases and a review of the literature J. J, GOUTZMANIS MBBS, FRACP, G. GONIS, BSC (HONS) AND G. L. GILBERT, MD, FRACP, PRCPA In 1960 Blizabeth O. King of Atlanta, GA, detected two beta-hemolytic and saccharolytic strains of Mor- axella and designated them Moraxella n. sp. 1, also termed Group M-1 by the Centers for Disease Control, Aanta.':* Henriksen and Bovre' analyzed nine hu: man isolates from blood, throat, nose and bone (eight, from King's collection). In honor of King’s pioneering work the species was named Moraxella kingii sp. nov. Although it showed many characteristics of the genus Moraxella in morphology, culture characteristics, oxi dase reaction and antibiotic sensitivities, it was re- classified on the basis of genetic dissimilarity and its unique biochemical characteristics (namely lack of catalase, acid production from glucose and maltose) to a new genus, Kingella gen. nov. within the family Neisseriaeceae and thereafter termed Kingella kin- a0 * There have been an increasing number of reports of K. kingae sepsis in recent years,’ " but they may rep- resent recognition of cases previously thought to be caused by Neisseria, Moraxella, Streptococcus ot Hae- pecies, rather than an increased incidence. in remain unrecognized or be dismissed as a contaminant because of its slow fastidious growth in culture.’ It exhibits an unexplained’ tropism for skeletal tissue, endocardium and vascular space" and can cause osteomyelitis, suppurative arthritis, endocarditis and bacteremia (which can mimic men, ingococcemia with rash.'! "(In a recent Centers for Disease Control report'* 58 of 78 isolates of K. kingae were from blood, bone or joint; 75% were from children <6 years old. Less common presentations include meningitis,"” pneumonia," ophthalmic infections in cluding eyelid abscess,'" endophthalmitis (Table ‘Accepted for publication May’, 1991, From the Department uf Microliolngs/tnfectins Disease, Reval Children’s Hospital, Parkville, Vietorin 52, Australi, words Kinsella Kinga, ostenmvelits, suppurative arthritis, endocarditis, endophthalmitin, spondylitis. Address for reprints: G. 1, Gilbert, M.D. Department of Clinical Microbiology, Westmead Hospital, Westmead, N.S, W. 2145, Aus: valli, *'SM Carden, Dd Coville, G. Gonis, and GL. Gilbert, submitted for publication, and paraspinal " head and neck” or presternal*! abscesses) PATIEN1 SAND METHODS. ‘The medical records of 10 patients admitted to the Royal Children’s Hospital (RCH), Melbourne, be. tween 1978 and 1990, in whom K. kingae had been isolated from normally sterile sites (blood, joint or other aspirates and bone biopsy), were reviewed. Specimens were inoculated, as appropriate, into sev- eral media including the Bactec’ blood culture system (Becton Dickinson, Cockeysville, MD), horse blood (incubated in air and anaerobically), MacConkey's agar (incubated in air) and chocolate agar (incubated in 10% CO.) at 35°C. Biochemical characteristics were determined by standard methods.** Acid production from glucose, maltose and lactose was detected using the commercially available RIM" method (Austin Bi- ological, Austin, TX), Antimicrobial susceptibility was, determined by the calibrated dichotomous sensitivity disc diffusion method using Isosensitesit” agar (Ox- oid) with 5% horse blood.” Positive and negative control organisms were used for all biochemical tests. RESULTS Characteristies of K. kingae. Growth of K. kin- ‘ae was enhanced by CO,. All 10 of our isolates showed two beta hemolytic colony types on horse blood agar incubated in air. One was pinpoint, transparent, smooth and convex with a central papilla and a well- defined edge; after 48 hours it was 2 to 3 mm in diameter with a narrow zone of beta hemolysis. The other was a spreading, soft, viscid, homogenous col. ony, 5 to 6 mm in diameter, which corroded or pitted the agar. There was uneven growth of both convex and corroding colonies. Most colonies grew aerobically in the top 5 to 10 mm of agar; in anaerobic subculture growth was slow, producing only faint, spreading cor- roding colonies. ‘The ability to pit agar was most obvious on primary isolation and best maintained by culture under anaerobic conditions. K. kingae grew well in Bactec” media; all but one blood culture isolate were detected after 1 to 3 days incubation, but growth was detected earlier in Bactec” Medium 6A (standard 67 678 TABLE 1. ‘THE PEDIATRIC INFECTIOUS DISEASE JOURNAL Kingella hingae sepsis at Royal Children's Hospital Vol. 10, No. 9, Sept, 1991 197 to 1989 7 Mente pelts wanna WI B® WP er oan Rinses di lesen line are then a conten :ooM = femme WHE AT 0 WE ier nay ston Gt chen ona insets inn spiew HM years Maral vate endned PSie Tram oar Md eulturs, +e itp gmt CHD femoral Tiny 2: or nal valve sega . ‘ tah Toe Bas a 7 oo aunths Spica. gmt rsh, AWHEC so tie: ESI, 0 mm/ 4 pn oan vier ye Da “al chien 4 Ftzxrane Satis tne 2 ey ESI Xr mn hme x ye the ral amin a arr rig ue val mcd FAs stv i Whe 2n i hi ier EMR 2 os ae se, 88 BH 2 kor wah Septieenia wi Wie iim pec ta halos ig ‘Wa elton, +o hae eat {CTS sbeonpinctval = Sheba WHC ESR normal Vetta: ebro Funetival dexamert ites tea PR ad ee ee ee 21 iter ES, 18 sie pen get ci h are + Day 2 aerobic) than in medium 7D (anaerobie medium with: out sodium polyanetholsulfonate). Others have re- ported similar success with the Bactec” system in contrast to conventional blood culture media.” K. kingae is a nonmotile, Gram-negative coccoba cillus that appears in pairs or short chains. All 10 isolates of K. kingae showed characteristic biochemical reactions, namely negative catalase and positive oxi dase reactions, and saccharolytic activity with maltose and glucose but not lactose and sucrose. Urease and indole tests were negative for all strains tested (seven, and six strains tested, respectively). By dise diffusion sensitivity testing it was susceptible to penicillin, chloramphenicol, gentamicin and erythromycin, Because of its colonial morphology and Gram: stained appearance K. kingae is easily confused with other fastidious bacteria which can cause similar clin ical syndromes. It often resists decolorization and can, be confused with hemolytic streptococci: one of our isolates (from a patient with septicemia and a pete chial rash) cross-reacted with commercially available Neisseria meningitidis Group B antiserum (Difco Lab oratories, Detroit, MI); it is easily confused with one of two other catalase-nexative, oxidase-positive Gram. negative coccohacilli, Hikenélla corrodens and Cardio bacterium hominis, both of which can cause endocar ditis and/or septic arthritis Clinical cases. Table 1 summarizes the 10 cases of K. kingae sepsis seen at RCH; Cases 1 and 2 have been reported previously" and case 9, in more detail, is reported elsewhere.* Five patients were male and 5, female, ages between 6 months and 12 years. There were 3 cases of endocarditis, 3 of osteomyelitis, 1 of discitis, 2 of septicemia without endocarditis and 1 of endophthalmitis. The patient with endophthalmitis was an 11- month-old girl. She had an intercurrent rhinovirus respiratory tract infection which may have led to a breach of respiratory tract mucosa and hematogenous spread of K. kingae to the eye. She presented with a subacute onset of unilateral hypopyon. A diagnostic paracentesis was performed and she was treated intra- venously with cefotaxime and various topical (includ- ing subconjunctival) antibioties and steroids. K. kin- ae was isolated from fluid aspirated from the hypo- pyon but conservative therapy was continued because of rapid improvement during the first 24 hours. Intra- venous cefotaxime therapy was continued for 7 days and followed by chloramphenicol orally for 2 weeks. She made a rapid recovery, presumably because treat- ‘ment was commenced early, the organism was suscep- tible to the antibiotics used and of low virulence; steroids were used to suppress the inflammatory re- sponse which in itself causes destruction of tissue.* ‘Two of the three patients with endocarditis (Pa- tients 4 and 10) had preexisting structural heart dis- ease and all had favorable outcomes. Patient 3 had had a febrile illness 18 months previously for which he had been admitted to another hospital; he had had recurrent fever and joint pains since. ‘The provisional diagnosis on the second admission was juvenile theu- matoid arthritis; he had a soft systolic heart murmur, Vol. 10, No. 9, Sept., 1991 which was thought to be innocent, but the possibility of rheumatic fever was considered. A rheumatoid screen was negative and anti-streptolysin O and anti- DNase B titers were normal. K. kingae was isolated from initial blood cultures after 3 days of incubation, Echocardiography revealed a mitral valve vegetation which eventually disappeared with penicillin and gen- tamicin therapy. His clinical course was complicated by a femoral artery embolism and acute reduction in the size of the cardiac vegetation. Patient 4 had been investigated for a cardiac mur mur 2 weeks before admission. Echocardiography showed a patent ductus arteriosus and a mass hetween, the main and left pulmonary arteries which was, thought to be a thrombus. A computerized tomo- graphic scan was scheduled but the patient was ad- mitted to hospital in cardiogenic shock. Two days after admission the patent ductus arteriosus was Ii gated and a large pedunculated vegetation, almost occluding the left pulmonary artery, was excised, Gram-negative coccobacilli were seen on Gram: stained smear and later isolated from the vegetation (and subsequently identified as K. kingae’) Patient 10 was an 18-month-old boy with complex congenital heart disease. He presented with a 3-day history of fever and limp, without objective signs of arthritis or osteomyelitis. K. kingae was isolated from two of three sets of blood cultures and he was assumed to have endocarditis although echocardiogram showed no vegetations. Patients 1, 2 and 7 were typical of others with K. kingae osteomyelitis with prolonged prodromes be tween 7 and 28 days. Patient 6, from the Cook Islands, had a strongly positive tuberculin skin test; chest roentgenogram was normal and the lesion on spinal roentgenogram was not typical of vertebral tubercu- losis, but she was given isoniazid prophylaxis. K. hin- 4gae was isolated from cultures of vertebral disc aspi- rate. Negative culture of bone curettings of the verte- bral lytic lesion was consistent with the histologic findings of chronic osteomyelitis which is typical of K. kingae infection. Cultures for mycobacteria were negative. The patient responded well to intravenous TABLE 2. Septic arthritis ¢ THE PEDIATRIC INFECTIOUS DISEASE 679 JOURNAL followed hy oral amoxicillin but was lost to long term follow-up. Patient 5 was systemically unwell with sepsis and rash. He improved dramatically within 12 hours of receiving intravenous penicillin and chloramphenicol followed by oral chloramphenicol. The rash resembled, that of meningococcemia and the isolate cross-reacted with N. meningitidis Group B antiserum. However, the isolate was subsequently identified as K. kingae. Patients 5 and 8 had septicemia without localizing features. CU K, kingae is an uncommon opportunistic resident of the mucous membranes of the upper respiratory tract.|” Although it was isolated from only 1.1% of 437 cultures of nose and throat swabs," this was believed to be less than the true carriage rate because: some strains grow too slowly to be detected; pitting colonies may have been mistaken for inoculating loop scratches; colonies are sparse and hidden by rapidly growing organisms; and some strains are strict anaer- obes in primary culture. K. kingae does not colonize the skin and is not implicated in traumatic inju- ries" ""; the majority of isolates implicated in disease are from normally sterile sites. Osteoarticular infections. K. kingae osteoartic ular infection was first reported by Davis and Peel," in 3 children (including RCH Cases 1 and 2). More than 85% of reported cases have been in children <4 years old (mean age, 2” years)"; all have been <13, years old (Tables 2 and 3). This is similar to other types of hematogenous osteomyelitis and septic ar- thritis in which the median age incidence is 2 to 5 years."" " Females and males are equally affected in K. kingae infections (Tables 2 and 3) whereas in other bone and joint infections there isa male predominance of >2:1."" Most affected children have no underlying illness.*"-""** Only one case of K. kingae arthritis has been reported in an immunocompromised host: a 4- year-old boy with acute lymphoblastic leukemia." ‘Three of the 10 children at RCH and up to 42% of patients in other studies had preceding oropharyngeal bis (ON AND LITERATURE RE caused by Kingella kina Duration of ESI baal Clte Site Nov Age Range e Ment ; ite Sowa References Hip a Tmt ligan 2 Te ma 7 7 Knee 8 tmnt tyene seeks 2 au : y Ankle 3 'Rtmonte 12 Vly" 2 weeks TW 1 1 Ths ' a t m To eds f i H 680 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL Vol. 10, No. 9, Sept., 1991 Kingella hinge = Nisopharenead Theat Tea Cur Qevm-stgined Duration ot ESIC Sie Nw Apel Sec PM ma Caines vettings Smear Pant References senor ee toa éteaes tier Smurf U1 Lvs 2 nth 2 24.260 Uren u ! Hoan t ma Doe Nee BANS tot H i a aa Taal 2s a 4 2s 2 inflammation, suggesting that bacteria enter the blood. through damaged mucosa.!"" "8% Suppurative arthritis caused by K. kingae isan acute illness with symptoms (limp, erythema and edema) occurring <4 days before diagnosis in 70% of eases (Table 2). Osteomyelitis has a more insidious onset and prolonged course; 16 of 23 (70%) patients had symptoms for 1 week or more before diagnosis (Table 3). By contrast in acute osteomyelitis caused by other bacteria, the mean duration of symptoms hefore ad- mission was 34 days (range, 1 to 14 days)."" Some mild cases of K. kingae osteomyelitis have been dis- missed as minor trauma or occasionally not diagnosed until several weeks after onset of symptoms.’-"' Gen. erally up to 85% of eases of osteomyelitis are initially misdiagnosed compared with 31°F of cases of suppur- ative arthritis." Fever is present on admission in 63% (15 of 24) of patients with K. kingae osteomyelitis and in 85% (16 of 19) of those with septic arthritis (see references in Tables 2 and 3). Absence of fever and Ieukocytosis in children with bone and joint infections is well-recognized but bacterial infection is often not suspected without them."” All cases of joint sepsis caused by K. kingae reported. thus far have been monoarticular: 42% knee, 26°% hip. 16% ankle joints (i.¢.,84"% lower limb, 15 of 19) (Table 2). The femur was involved in 33% (9 of 28) and intervertebral disc and vertebrae in 29% (8 of 28) of cases of osteomyelitis. The lower limbs are more com: monly affected than the upper. Spondylodiscitis occurs in otherwise healthy chil- dren < 10 years of age" and accounts for 2% of childhood osteomyelitis." Trivial trauma and upper respiratory tract infections are common anteced- ents." Minor trauma causes microscopic fractures of epiphyses allowing localization of bacteremia to bone or joint." *' In prepubertal children discitis is presumed to be caused hy hematogenous infection because of the profuse vascular supply from adjacent, vertebral bodies. However, only 33% of cultures of dise space aspirates, blood or bone currettings are positive. Staphylococcus aureus is most commonly iso- lated but various fastidious, slow-growing bacteria including K. kingae have also been implicated." As in other types of bone and joint infection, the peripheral blood leukocyte count is often normal (range, 6.1 to 22.3 X 10"/liter, in 40 cases) but the erythrocyte sedimentation rate (ESR) is usually >20 mm/hour (in >90% of cases; median, 32 mm/hour; range, 18 to 117 mm/hour) (Tables 2 and 3). K. Kingae is usually isolated from the septic focus but may take 2-17 days to become detectable." Joint aspirates were positive in 89% (17 of 19) and bone curettings in 93% (26 of 28) of reported cases. ‘This is a high yield considering that only about 70% of joint aspirates overall, from patients with septic arthritis, are positive."” Bacteria have been detected on Gram- stained smear of bone curettings or joint aspirate, in only 14° of eases (Tables 2 and 3) and often have heen mistaken for Neisseria or Haemophilus spp. Blood cultures are positive in only 5 to 7% of K. kingae osteoarticular infections!“ compared with 40 to 57% when Haemophilus influenzae type b, Streptococcus pneumoniae or S. aureus (up to 90% positive) are involved." *"" "These findings are consistent with the relatively indolent, benign course of K. kingae infections. Imaging yields nonspecific information. Plain radio- graphs show soft tissue swelling and joint effusions in 50% of cases of K. kingae arthritis and lytic lesions and soit tissue swelling or dise space narrowing in up to 95% of patients with osteomyelitis or discitis. Iso tope scans were positive in 13 of 14 cases of K. kingae osteomyelitis (data from references cited in Tables 2 and 3}. Endocarditis. In a Mayo Clinic review 10% of approximately 560 cases of endocarditis were caused by Gram-negative bacteria and of these, 32 (57%) were caused by fastidious coccobacilli, the so-called “HA- CEK™ group: Haemophilus spp., 18; Actinobacillus ac- tinomycetemeomitans, 4; C. hominis, 6; E. corrodens, 2; Kingella spp, 2. Six patients had prosthetic valve involvement and 31 (97%) were cured "The first reported case of K. hingae endocarditis, Vol. 10, No. 9, Sept., 1991 THE PEDIATRIC INFECT! TABLE 4. Endocarditis, 1OUS D ASE JOURNAL 681 caused by Kingella kingae Newry meal ser Ne Site can ‘us Otome Retesonces Anvulemet F one ‘doar Trai Falken Dal cn M years Nearer ends Complex: SD) ta entice dystnetion a Fan yvane Mitel sabe sa veri Mitral salve prota oo rich hemlet, Mo fimmhe Mitral save Ni tert Mucot eure 2 in u A sears ie xsn = Wi F years etic wntic wale Tress ate. Ciert a Mo Wsvats Prontwtieaurticraive AV ental Prd ee M "tyr a me Bh ne ei was in 1964, in a 4-year-boy with a small membranous ventriculoseptal defect. Moraxella n. sp. 1 was isolated from 4 of 12 blood cultures obtained before antibiotic therapy was commenced. He recovered but suffered cardiac failure, tricuspid incompetence requiring valve replacement and pulmonary infarction." Septicemia with or without endocarditis is the most severe form, of K. kingae infection"; only 3 of 19 cases of septi cemia did not have endocarditis.* K. kingae and sim: ilar organisms should be considered in initially cul- ture-negative endocarditis inasmuch as growth may take >5 days." " Related species such as Kingella denitrificans, ™ Kingella indologenes,"" Moraxella la- cunata (previously Moraxella liquefaciens),"’ Moraxella nonliquefaciens,"* Moraxella osloensis, C. hominis and. E. corrodens” can all cause endocarditis but do so less, frequently than K, kingac. Endocarditis caused by K. kingae usually occurs in adults; over 60% of patients are >16 years" (mean, 30 years; range, 1 to 68 years).” °° Three-fourths of patients have had preexisting structural heart defects, ‘Table 4 summarizes the nine previously reported pe- diatric cases of whom four had native valve (three mitral, one tricuspid), two prosthetic valve (aortic) and two nonvalvar endocarditis. At least one-third of patients had intercurrent oropharyngeal inflamma- tion. The history and physical findings in K. kingae endocarditis do not differ from those of the more common streptococcal endocarditis’ except that K. kingae may present with septic shock and about 50% of patients develop significant cardiac failure Full blood examination usually shows an elevated white blood cell count (mean, 15.5 x 10'Vliter; refer- ences in Table 4) with neutrophilia and left shift and the ESR is usually >35 mm/hour. Blood cultures were repeatedly positive (70% of cultures positive if >4 are taken) before antibiotic therapy is started" but may take 5 days or more to produce detectable growth in ordinary media. Despite the excellent response to antibioties."""" K. kingae endocarditis has a high complication rate. Vi bruggen et al." reported a case fatality rate of 16% (n 9); subacute bacterial endocarditis caused by the viridans streptococcus group has a cure rate approach- ing 100%." Among 28 patients 50% developed com- plications, including 25% with cerebral infarction sec- ondary to embolization." A mycotic aneurysm, was reported in a previously well 8-year-old gir! with native mitral valve endocarditis." One of the 3 pa- tients with endocarditis (Patient 3) in our series de veloped a femoral embolism. Other manifestations. Moraxella spp. (particu- larly M. lacunata) have been recognized causes of angular and chronic follicular conjunctivitis since 1896 and nasal carrier rates are up to 44%." Pre sumably a proportion of these isolates were Kingella species. K, kingae has been isolated from an eyelid abs Our case of endophthalmitis in this series is the first to be reported.* Bacterial endophthalmitis is, uncommon in children and only 10% are hematoge- nous; the outcome for vision is usually poor but this patient responded to conservative therapy and had no visual impairment Benign, transient bacteremia occurs infrequently, often with clinical improvement before diagnosis is, made.” Seven cases have heen reported previous- ly"; four were asymptomatic hefore treatment was, started and two were not treated. K. kingae bacteremia can cause a rash simulating meningococcal or dissem- inated gonococeal infeetion (as in Case 8).""""""" One case of lung infection with K. kingae associated with measles pneumonia has been reported." Antibiotic therapy. K. kingae is susceptible to most antibiotics including penicillins, cephalosporins, aminoglycosides, trimethoprim-sulfamethoxazole, tet- racyclines, erythromycin and chloramphenicol." Occasional isolates have shown partial in vitro resist- ance to erythromycin, oxacillin, lincomycin,!* “* trimethoprim,"' ciprofloxacin" and clindamycin.” Like most other Gram-negative bacteria it is resistant to vancomycin. Susceptibility to and successful treat ment with antistaphylococcal penicillins (methicillin, 682, THE PEDIATRIC IN cloxacillin) and cephalosporins (cephalothin, cepha zolin) have been reported.” ‘The reported duration of treatment has varied from 17 days to 3 months for arthritis and from 3 weeks to 6 months for osteomyelitis/discitis caused by K. kingae. ‘The duration of antibiotic treatment for os: teoarticular infections traditionally has been 6 weeks" "hut shorter courses are effective." De Groot et al." recommended intravenous penicillin un- til there is clinical improvement and the ESR has fallen by >20%%, followed by 4 to 6 weeks of treatment, with oral penicillin (150 mg/kg/day) for K. kinga bone/joint sepsis. K. kinyae endocarditis usually responds rapidly to antimicrobial therapy which has heen given for 2 to 7 weeks." "= "" Large doses of penicillin alone for 4 weeks or with an aminoglycoside for the first 2 week. is equally efficacious." *" Claesson et al” cited 7 different courses of antimicrobial therapy in 33 pa. tients: beta-lactams, 57; aminoglycosides, 9; chloram- phenicol, 6: bacitracin, 2: erythromycin, 1; and tri methoprim-sulfamethoxazole, 2. The diversity reflects empirical choices in initially culture-negative endo- carditis. Minimal inhibitory and bactericidal concentrations of penicillin, cephalothin and gentamicin are 0.006, 0.2 and 1.6-3.1 mg/liter, respectively." Peak and trough serum bactericidal titers after 3.3 megaunits of penicillin G and 60 mg of gentamicin intravenously were 1:8192 and 1:512, respectively. Similar results were reported” "with ampicillin and tobramycin High serum bactericidal titers have been reported during treatment with benzylpenicillin (1:128 to Kentamicin (1:512)"*and penicillin V (1:16 CONC! Infections caused by K. kingav, particularly in chil: dren, have been recognized more frequently in recent years. The organism is easily overlooked because of its slow growth and requirement for enriched media. It can be mistaken for other bacteria because of similar clinical manifestations and microscopic and cultural characteristics. It usually causes bone and joint infec- tions in children and endocarditis in adults. The clin- ical course is benign, except’ in endocarditis in which embolization from friable vegetations is relatively common. The subacute course of osteomyelitis. ix shown by the fact that blood cultures are often nega- tive, radiologic changes are apparent on presentation, histology shows chronic inflammation and direct Gram-stained smears of bone currettings are rarely positive. K. kingae infections respond rapidly to treat ment with penicillin, which is the agent of choice. By extrapolation from results of treatment with other types of endocarditis, addition of gentamicin may he USION DISEASE JOURNAL Vol. 10, No. 9, Sept., 1991 beneficial, at least until the minimal inhibitory con centration of the isolate is known, REFERENCES, 1 Henriisen SD, Hovre K, Moraaeila kina sp, nova haemolstic, scharulytie species af the genus Mornsvla, } Gen Microbiol wis sAT7 2 Henriksen SD. Bovre K. Tranater of Morasela kingae Henke sen and Rovre to the genus Kingella gen. nos. in the family Neisseriae. Int. Ses) Bacteriol 1924780. 1. Henriksen SD. Marasrila, Nerserrin, Branhamella and Avine tubarter- Annu Kew Microbiol 19561 88 4. Bare K. Henriksen SD, Jnsson V. Carrection of the specific epithet king i the combinations Meravellakingti Hentiksen anil Rare 1868 and Parucomunas king Jonsson 1970 to Kit ae, Itt Set Hater 19742213007 5, Claesson 1 Falsen K, Kjelhnsan 1, Kingla hinge infections: a review ala presentation of data from 10 Swedish eases, Seand Mnfect Dig 517-2 §, Morrison VA, Wagner KE, Clinical manifestations of Kingella ina inteetins: ease report and review. Rew Inteet Dix sth 17 2 Bosworth’ DE. Kingella (Moravellal kingae infections in chit ren. Amt Dix Child FSR INTO 8. Spahe RC. Septic arthritis due to Morayella species, 4 Peat ISTHACHIO, 9. Toshniwal R, Draghi TC, Kocka FE, etal, Manifestations of Kingelta hinge intections in adults: resemblance to neisserial infections. Digger Microbiol Infect Dis I9AR:i81- 5 WW, De Grout R, Glover D, Clausen C, et al. Bone andl joint infec tions mused hy Ringel kings six cine and review of the Titeratre. Ke: Tnfeet Di 19M 1008-1, wns DC, Gazzard GB. Kinga king septicemia with a clinical presentation reserabling disseminated ginneaceal inter ton, Re Meet P184:289°780-1 12 Redield DC. Oserturt GD, Bacteria, arthritis, and skin lesions dhe to Kingvila linge. Arch Dis Child 1980-40 16h, Renentiaum Lieberman DH, Katz WA, Case report: Moraxella infectious aetheitis frst report ins an adult, Ann Rheum Dis TST 14. Graham DR. Bard JD, ‘Thornsherey C, al Infections caused Dy Morasrlla, Morasella urctheuly Moravelte-lie grime M3 and M-6, and Kinella kruae in the United States, 115% 1980, es Infect Dis 1stnht2- 424 8 15, Waterspiel NA Kinsella kina meningitis with bilateral in frets of the hasal ganglia, Infections 8,1 1:37 . 16, Gremillion DH, Crawiord GE, Measles pneumonia in young adults an analysis of HO eases Amd Med TOSLST UR a, 17, Henriksen SD. Corrading bacteria ton the respiratory tract Acta Pathol Microhiid Seana 189:75:85 14. Danis JM. Peel MAL Osteomyelitis aul septic arthritis eaused tn fara) Clin Patho 19M) 22, AS, Dyke J. Berry D, etal, Paraspinal mist asiiated with intervertebral disk unfection secondary Pediatr Isr 20, Odum 1. Frederiksen W. Kdentitivation and characterization KingelteRingue. Acta Pathol Microbiol Sean HSL SDA 0 Marasela ings 21, Raymond J. Bengeret M, Bangy Fetal bolton of to strains Hof Ringel hingae assaiated with septic arthritis. Clin Mien biol 18862421000 22, Lannette EH, Bales A, Hawusel WA, Teuane JP. eds: Mana clinical energy. ihe An dogs. Washington, DO 18286 rican Society for Micnohi 12 2, Bell SM. "The CDS dist’ method of antibintie sensitivity testing lealibrated dichotomous sensitivity. test). Pathology 19553 Supple 4 21, Clement JL, Berard Cahwac JP. et al Kingella nga ‘stenar hrtis andl osteomyelitis in children, J Pediatr Orthop, ssi) 6 . Powell IM. Septic aethriti easel hy Ring hingea Amv Dis Child tourer 6 26, Solve Hla, Mera J, Bache G, et al, Osteoartbrites et este mvelites a Ringella howe cher Pentants a props de} obser ations ef revue de he iterature, Pediatrie HOM 20 Vol. 10, No. 9, Sept., 1991 2, a M. 2. Lae Patel NI, Moore TT Weise TD, etal. Kinga ings infections arthritis’ case report and review of literature of Kingelfa and Moravela infections, Arthritis Rheum 19SI20557 Gamble JG, Kinsky LA. Kingella kingaw infection in healthy children d Pe p 19H 9 IM, Drere M, etal. Osteourtirites a Kingella hinge. Chie Pediate 19862735062 Gay KM, Lane ‘TW, Keller DC. Septic a Kingella nga. Clin Miceabiol 198307 Shelton MAL Nachtgal MP, Veyve DA, Heendon WA, Riley HD Je. Kingela kingar osteomyelitis: report of two cases in volving the epiphysis, Pediatr Infect Dis 1 16874214 Le CT. Kingela (Moraxella) kingae infections. Am) Dis Chile TBR: 1912 Chanal C, Tiget F, Chapuis P. etal. Spondslits and osteumse: Tie eased hy Kingella kingae in children. J Chin Microbiol Iuesre22407- Verbraguen AM, Hauglustaine D, Schildermans Fetal, Infee tons caused by Kingela hing: report of Tour eases and review SV intect 16 F142 Nottal F, Mersal A, Yaschuk Y, et al. Osteomyelitis dae Kingella hingae infection, Can] Surg 19885412 Rotbart HA, Gelland WM, Glode MP. Case report: Kingella Fingaw osteomyelitis of the clavicle, 1 Pediatr Orthop 1984 4500-2 Woolfrey BF, Lally ICT, Faville RU. Intervertebral disetis caused by Kinsella kingae. Amv 3 Clin Pathol 198688:745-9, Dich VQ. Nelson 4D, Haltlin KC. Osteomyelitis im infants and children a review of IG cases, Am 1 Dis Child 1975,129127% 5 Morrisey RIT, Shore Si Bone and joint sepsis, Pediatr Clin Novth Av» 1986:581551- 64, Anderson JK, Ort ID, Maclean DA, etal, Aeute haematoxenons fsteiti. Arch Dis Child 1980:55853- Menelaus MB, Diseti: inflammation affecting the interverte bal disesin children. J Bone Joint Surg 196646: ‘AD, Graham MH, MacQueen JIC. Intervertebral disk infection in children, J Pediatr 14:70:73 Welkon CJ, Long 88, Fischer MC, Alhurger PD. Pyogenic antbritisin infants and children: a review of 95 cases, Pediat Infect Dis 19865369 76. Nelson JD. The bacterial aetiology and antibiotic management ‘of septic arthsitis in infants and children, Pediatrics 1972 5040740 Geraci JE, Wilton WR, on is S. Bndocarditis due to Gramvnegative bacteria, report nf 56 ceases. May Clin Proc 2.57115 Christensen CE, Emmanoullides GC. Brief recording: bacterial endocarditis due to "Moraxella new species 1.” N Engl ol Med Logrezrsns-a 17. Borstl H, Ruckdesehel (, Lang M, der W. Septicaemia caused hoy Kinga hingar, Bur Clin Microbiol 1984¢1207-9 Racdin JI, Brandsetter RD, Wade MJ, et al. Endocardit resulting from Kingela kinwae, presenting initially as culture negative bacterial endocarditis. Heart Ling 1982:11:552-4 Jenny DB, Letendre PW, Iverson G, Endocarditis due so Kin elle npecies, Rew Infect Dis 1988;10:1065, Goldman TS, Ellner PP, Francke El. etal, Infective endacae itis due to Kingella denitrificans. Ines Medd 08152 ‘THE PEDIATRIC INFECTIOUS 8. Van Bijsterveld OP. Host-parasite relations 7. O'Connor MC, DISEASE JOURNAL 683, Khan JA, Sharp $, Mann KR, et al, Case reports Kingella denitrificans prosthetic endocarditis. Am J Med Set 1986: ia inn RA, Holmes B, Infective endocardi denitrificans Clin Pathol 98437-13847 Sithertaely PM, Laawe JE, Endocarditis dve to Morarella lige fociens. Aech Totern Med 1068122512 Rechard DL, Leftock IL, Tillotson JR. Moravella nanliquifacions. South Med 3 197 Stryker D, Stone W, Savage AM. Renal failure secondary to Moraxella sioenis endocarditis, John Hopkins. Med 1982.150217 9, Zeimis RY, Hanley OQ. Endocarditis, caused by Kinsella kingaes case report and review Lab Med! 1985;16547-50. Adachi R, Hammeriers 0, Richardson H, Infective endocarditis caused by Kingela kungae. Can Med Asse I 80:12: 1087 8 Wolf AH, Ullman KF, Strampter MJ. et al. Kingella kingae endocarditis: report of a case and a review of the literature Heart Lung 1987:16:579-80 re WI, Pooling EU. Acute Kingella kingaw endocarditis wi recurrent cerebral emboli in a child with mitral prolapse. Ann Neurol 1954516889 Odum 1, Jensen KT, Slotsbjerg TD. Endocarditis due t» Kin illo ingar. Kise Clin Microbiol 19842636. Rabin Rl, Wong P, Noonan JA, etal. Kingela hingar encocar- itis in a child with a prosthetic sortie valve and hifureation raft. Am J Dis Chile 19850187084 rant JM, Bortolussi RA, Rox Dl et al. Prosthetic valve Dacterial endacarditis caused by Kingella hingar, Can Medd ‘Assoc 4 19812954067 Giamarellow H, Galanukiy N. Use of intravenous ciprofloxacin in dfficult-to-treat infections, Am Med 1987 92:146-51 Kowalski MS, Harwick IC. Ineidence of Murase conjunc infection. Ara J Ophthalmol 1986:101:487-40, Schwartz B, Harrison LH, Motter 4S, etal. Investigation of uthreak of Morazcila conjunctivitin ata Navajo boarding school. Am J Ophthalmol 1989:107:341 caused by Kinga ps and taxonomic position of Morazella and morphologically related onganisins ‘Am J Opthalmol 19776545, Sperry RE, Burdlich CA, et al. Kingella king Dhacteraemin, Clin Microbiol News! 19891214 Laser AK, Goldman El. Moraxella bacteremia: a report of @ cave resembling gonocoecenia with cutaneous manifestations, Cutis 19782657 9, Miridjanian A. Berret D. Infective endocard aqella irgae: West J Med 197812951446. Freij BI, Kusmiesz H. SI in acute osteomyelitis andl suppurative arthritis, Ary} hild 174TH 2, 'Skouby SO, Knudsen FU. Short communication: Kingolla ki sar osteomyelitis mimicking an eusinophiie granuloma. Acta raediatr Seanad 1982:71:511-2 Kennedy CA. Rosen H. Aingella kingae bacteremia and adult epiglottitis ina geanuloeytopenic host. Ary 3 Med ISR8S5/701- is eased by Mor Serogiannopulous GA, Nelson JD, Duration of antimicrobial therapy for acute suppurative osteuarticular infections. Lancet 7-40

You might also like