KINGELLA
Compiled by: Zenisha Acharya
Central Department of Microbiology
Tribhuvan University, Kirtipur
• Kingella
kingae is a species of Gram-negative facultative anaerobic
β-hemolytic coccobacilli.
• In
the 1960s Elizabeth O. King, working at the U.S. Centers for Disease Control
(CDC) in Atlanta, GA, described a novel bacterial species isolated from human
respiratory secretions, blood, and bone and joint exudates.
• The
organism, initially assigned to the genus Moraxella and designated Moraxella
kingii in honor of King’s seminal research, was later placed in a separate
genus and renamed Kingella kingae.
Taxonomy
• The
genus Kingella belongs to the Neisseriaceae family in the beta subclass
of the Proteobacteria and comprises four recognized species:
- K. denitrificans,
which has been implicated in cases of bacteremia, endocarditis, pleural
empyema, pediatric vaginitis, chorioamnionitis, and granulomatous disease
in AIDS patients.
K. oralis, which is a commensal dweller of the human buccal cavity and is associated with dental plaque and periodontitis.
K. potus, a zoonotic organism recovered from an infected bite
Although K. kingae’s taxonomic place remained uncertain for many years, subsequent analysis of its biochemical profile and fatty acid composition and genotypic studies have led to the conclusion that K. kingae constitutes a separate species, only distantly linked to other Neisseriaceae.
kingella kingae
• Scientific classification
• Domain: Bacteria
• Phylum: Proteobacteria
• Class: Betaproteobacteria
• Order: Neisseriales
• Family: Neisseriaceae
• Genus: Kingella
• Species: K. kingae
• Binomial name
• Kingella kingae
Identification
Kingella kingae appears as pairs or chains of 4 to 8 plump (0.6 to 1by 1
to 3) micrometer coccobacilli.
Kingella kingae cells tend to resist decolorization, and thus the
organism may be erroneously identified as Gram positive, but electron
microscopic examination discloses a characteristic Gram-negative cell wall
structure.
The bacterium is beta-hemolytic, non-motile, and non-spore
forming, exhibits negative catalase, urease, and indole tests with rare exceptions,
has oxidase activity.
Produces acid from glucose and usually from maltose, hydrolyzes indoxyl
phosphate and L-prolyl-beta-naphthylamide, and exhibits positive alkaline and
acid phosphatase reactions.
Basic Characteristics Properties
(Kingella kingae)
10% Bile Negative
(-ve)
Capsule Positive (+ve)
Catalase Negative
(-ve)
Citrate Negative
(-ve)
Coagulase Negative
(-ve)
Gas Negative
(-ve)
Gelatin Hydrolysis Negative (-ve)
Gram Staining Gram-negative
H2S Variable
Hemolysis Positive
(+ve)
Indole Negative
(-ve)
Motility Negative
(-ve)
6% NaCl Negative
(-ve)
Nitrate Reduction Negative
(-ve)
Nitrite Reduction Negative
(-ve)
OF Fermentative
Oxidase Positive (+ve)
Shape Coccobacilli (0.6 to 1 μm
by 1 to 3 μm)
Spore Negative (-ve)
Urease Negative (-ve)
DNase Negative (-ve)
Fructose Negative (-ve)
Galactose Negative (-ve)
Glucose Positive
(+ve)
Glycerol Negative (-ve)
Inositol Negative (-ve)
Lactose Negative (-ve)
Maltose Positive (+ve)
Mannitol Negative (-ve)
Mannose Negative (-ve)
Raffinose Negative (-ve)
Rhamnose Negative (-ve)
Salicin Negative (-ve)
Sorbitol Negative (-ve)
Starch Negative (-ve)
Sucrose Negative (-ve)
Trehalose Negative (-ve)
Xylose Negative (-ve)
Culture
K kingae is a facultative anaerobic bacterium that grows on conventional
Trypticase-soy agar supplemented with 5% hemoglobin (blood agar medium),
chocolate agar, Columbia-based blood agar, and GC-based media.
Similar to the case for other Neisseriaceae, most K. kingae strains can
be recovered on Thayer Martin medium but do not develop on MacConkey or Krigler
agar.
Many isolates show poor growth on the cation-supplemented Mueller-Hinton medium
used to determine the antibiotic susceptibility of the species.
Similar to the case for other bacteria that inhabit the respiratory tract,
growth is improved in a 5% CO2 atmosphere, but only a minute proportion of
isolates are strictly capnophilic.
Growth on solid media is characterized by marked pitting of the agar surface,
which is best seen after removal of the colony.
Kingella kingae
strains produce three different colony types that are associated with the
degree of pilus expression:
a spreading corroding morphology distinguished by a small central colony
encircled by a wide fringe,
a non-spreading /non corroding type consisting of a flat colony surrounded by a
narrow fringe, and a dome-shaped colony with no noticeable fringe.
The first two morphologies are associated with the presence of long fimbriae,
whereas strains growing as domed colonies are non piliated.
The ability to produce the spreading-corroding type of morphology can be
irreversibly lost after repeated subculture.
Cultural characteristics on 5% sheep blood agar(35 degree c/5%co2)
K kingae : small, with a small zone of beta hemolysis; may pit agar
K denitrificans : small, non-hemolytic; frequently pits agar; can grow on a
N gonorrhoeae selective
agar( e.g. Thyer martin agar)
VIRULENCE FACTORS
Pili:
The expression of pili in K. kingae appears to be finely regulated by
three genes (54 gene, pilS, and pilR)
Pili are essential for the adherence of the bacterium to the respiratory
epithelium and synovial layer.
Polysaccharide Capsule
Synthesis of polysaccharide capsules is a convergent evolutionary strategy
shared by many important human pathogens that colonize the upper respiratory
tract.
Capsules are lipid-anchored, outer-membrane-associated, and surface-exposed
structures that confer protection from phagocytosis and complement-mediated
killing. Capsules are crucial virulence factors that enable bacterial survival
on the mucosal surfaces by thwarting the host's defensive response.
Exopolysaccharides and Biofilm Production
Protects the organism from the deleterious effects of the
immune response, desiccation, and antimicrobial drugs. K. kingae
exopolysaccharides facilitate colonization of the pharyngeal epithelium by
inhibiting biofilm production by other organisms competing for the same niche.
It is also plausible that these exopolysaccharides play a role in the
regulation of the periodic release of K. kingae cells from the biofilm
matrix, enabling dissemination of the bacterium by droplet transmission.
RTX Toxin
Kingella kingae RTX toxin is a 100-kDa protein that appears to be
secreted in the extracellular environment in a soluble form, as well as a
component of outer membrane vesicles (OMVs) that are internalized by host's
cells.
Mostly all the invasive K. kingae isolates studied
so far produce RTX toxin, whereas it is
absent in the less virulent K. denitrificans and K. oralis,
suggesting that this bacterial constituent is universally conserved in K.
kingae because it improves colonization fitness by disrupting the
oropharyngeal epithelium. Also RTX toxin enable survival of K. kingae in
the bloodstream and invasion of the skeletal system tissues and therefore have
a disease-promoting effect.
PATHOGENESIS OF DISEASE:
Transmission: spread
person-to-person through respiratory secretions and saliva. Transmission is
more likely in child care settings because young children are more likely to
harbor the bacteria.
Incubation period: People can
spread K kingae if the bacteria are present in their respiratory
secretions. Children younger than four years are more likely to carry the bacteria
without symptoms (colonized) and have higher numbers of bacteria than older
children and adults. Older children and adults are usually colonized for only a
short period.
The pathogenesis of disease caused by K. kingae is
believed to begin with colonization of the posterior pharynx. The process of
colonization involves adherence to respiratory epithelial cells, which is
mediated in vitro at least in part by type IV pili that are composed primarily
of a major pilin subunit called PilA1.
The PilA1 protein shares homology with the major pilin subunit in type IV pili
expressed by other bacterial pathogens, including Pseudomonas aeruginosa
PilA, N meningitidis PilE, and Neisseria gonorrhoeae PilE. In
addition, K. kingae pili contain 2 minor pilus-associated proteins
referred to as PilC1 and PilC2, which seem to play complementary roles and
influence the efficiency of adherence to respiratory epithelial cells. After
colonization of the posterior pharynx, K. kingae invade the epithelium to enter the
bloodstream.
K. kingae produces
a potent extracellular toxin that belongs to the RTX family of toxins and is
capable of lysing epithelial, synovial, and macrophage cells. This toxin
facilitate disruption of the respiratory epithelium.
Once in the bloodstream, it evade a variety of host defense mechanisms. It
produce an extracellular polysaccharide capsule that facilitates resistance to
serum-killing activity and opsonophagocytosis.
CLINICAL PRESENTATION OF K kingae INFECTIONS:
Invasive K. kingae disease usually affects previously healthy children
aged less than 4 years, whereas older children and adults frequently having
predisposing conditions such as failure to thrive , congenital heart disease,
prolonged corticosteroid therapy, primary immunodeficiency, hematological
malignancies, liver cirrhosis, end-stage renal disease, sickle cell anemia,
diabetes mellitus, cardiac valve pathology, systemic lupus erythematosus,
rheumatoid arthritis, renal transplants , solid tumors, or AIDS
Skeletal System Infections
K kingae septic arthritis generally involves large joints such as
the knee, hip, ankle, or shoulder. K kingae osteomyelitis usually
affects the long bones, involvement of the calcaneus, talus, sternum, or
clavicle occur.
Bacteremia
K kingae bacteremia without evidence of endocarditis has been
observed primarily in children. The duration of symptoms before diagnosis
ranges from 1 to 7 days, and the mean maximal fever is 39.0°C
Endocarditis
K kingae is included in the HACEK (Haemophilus species, Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella
species) group of organisms that is collectively responsible for up to 5%
of cases of bacterial endocarditis.
In contrast to other K kingae infections,
endocarditis has been diagnosed primarily in older children and adults. In
approximately one-half of patients the infection affects a native valve. A
predisposing cardiac malformation or rheumatic heart disease is observed.
Typically, the left side of the heart is involved, usually the mitral
valve. In general, fever and acute phase reactants are more elevated in
patients with endocarditis.
Despite the remarkable susceptibility of K kingae to antibiotics,
cardiac failure, septic shock, mycotic aneurisms, pulmonary infarctions,
meningitis, cerebrovascular accidents, and other life threatening complications
are common, and the overall mortality rate is 16%.
Lower Respiratory Tract Infections
K kingae has been isolated from the blood or pleural fluid of previously
healthy and immunocompromised adult and pediatric patients with
epiglottitis, laryngotracheobronchitis, pneumonia, or pyothorax, which suggests
that the organism may cause lower respiratory tract infections.
Soft Tissue Infections :
A diversity of soft tissue infections, including cellulitis , tenosynovitis and
dactylitis, bursitis, and subcutaneous, intramuscular abscesses is caused by
bacteria.
Occult Bacteremia:
Isolation of Kingella kingae from the blood without evidence of
endocarditis or another nidus of infection has been reported repeatedly in
children and exceptionally in adults and this syndrome represents the second
most frequent expression of K. kingae disease in pediatric patients.
Mild to moderate fever is usually recorded, and the mean
leukocyte count frequently is less than 15* 10^9 /liter
Ocular Infections:
palpebral abscess, keratitis, corneal ulcer, endophthalmitis, orbital
cellulitis and periorbital cellulitis are common infection.
Other Infections:
Anecdotal cases of K. kingae pericarditis, peritonitis, urinary tract
infection, and apthous-stomatitis have been also reported in adult patients.
EPIDEMIOLOGY OF INVASIVE K. KINGAE DISEASE:
K kingae colonizes the human tonsills and is rarely isolated from
the nasopharynx.
Colonization does not usually start before the age of 6 months. The carriage
rate gradually increases thereafter, reaching a prevalence rate of 9-12% in the
second year of life, declines in older children, and is close to nil in
adults.The colonized pharyngeal surfaces are the source of infectious fomites
that disseminate the organism between young family members and playmates.
Carriage and transmission are enhanced in daycare center attendance among whom
clusters of invasive K. kingae disease have been
reported, especially in the context of a concomitant upper respiratory viral
infection or stomatitis. It is plausible that increased drooling induced
by buccal ulcers facilitates the dissemination of the bacterium among young
children with poor hygienic habitat.
Invasive K. kingae diseases are almost
limited to young children.
Over 95% of cases occur below the age of 5 years and an annual incidence rate
of 9.4/100,000 infections has been reported in this population group, although
because of the suboptimal culture detection of the organism.
Kingella kingae infections are exceptional in the first 6 months of
age suggesting that maternal antibodies confer protection against both
colonization and disease in early infancy. Most affected young patients are
otherwise healthy, whereas older children and adults often have
immunosuppressing conditions, malignancy, or antecedent cardiac valve
pathology. Although the carriage rate remains remarkably constant along the
year, invasive K. kingae infections are most common during
late fall and early winter, coinciding with the seasonal increase of viral
upper respiratory infection.
DIAGNOSIS
Diagnosis of K kingae infection may be challenging due to the
fastidious nature of the organism in culture. Evaluation of cardiac, bone,
joint tissue, or fluid by PCR is a useful tool for the diagnosis of some cases
of K kingae infection.
Sample: depends on the site of infection
Blood, pleural fluid, bone aspirate
Direct detection method:
Gram’s stain: other than this method there is no direct detection methods
for this bacteria
kingella stain as short plump, coccobacilli with squared-off ends that
may forms chains.
Transportation:
inoculated swabs should be kept at room temperature in Amies or similar
transport medium and promptly sent to the laboratory for further processing
Cultivation
Trypticase-soy agar supplemented with 5% hemoglobin
(blood agar medium), chocolate agar, Columbia-based blood agar, and GC-based
media.
Most K. kingae strains can be recovered on Thayer Martin medium
cultural characteristics and biochemical properties: as mentioned earlier
NOTE: K denitrificans may be mistaken for N.
gonorrhoeae when isolated from Modified Thyer-Martin agar. Nitrate
reduction test is key for differentiating K denitrificans from N
gonorrhoeae, which is nitrate negative.
Detection by Molecular Methods:
In recent years, novel molecular detection assays have
enabled diagnosis of K. kingae infections in patients for whom cultures
of joint exudates on routine media does not reveal the presence of the
bacterium.
The PCR-based strategy has been also implemented in investigations of K.
kingae’s carriage and the relationship between respiratory colonization and
clinical disease.
The RTX toxin is produced by all K. kingae strains examined so far, the
encoding RTX locus genes appear to be appropriate targets for detecting the
organism in the blood, synovial fluid, and solid tissues, as well as in upper
respiratory tract specimens.
Serodiagnosis
This technique is generally not used for laboratory diagnosis of infection
caused by K kingae.
PREVENTION:
Since this organism does not posses threat for human
health, there are no such recommended vaccination or prophylaxis protocols.
Good hand washing and respiratory etiquette are important. Cleaning of toys,
tables, and other surfaces that could be contaminated with respiratory
secretions can help prevent the spread of Kingella kingae and other
germs. During outbreaks in child care centers, antibiotics can be used to
reduce the number of children who are colonized with Kingella kingae and
prevent additional infections. If prescribed antibiotics, take them as
directed.
TREATMENT
Antibiotic Susceptibility K kingae is almost always highly susceptible
to penicillins and cephalosporins, although -lactamase production has been
reported in rare isolates.
With few exceptions, K kingae is also susceptible to
aminoglycosides, macrolides, trimethoprim, sulfamethoxazole, tetracyclines,
chloramphenicol, and fluoroquinolones.
The empirical drug therapy for skeletal infections in children usually consists
of intravenous administration of oxacillin/nafcillin or a second or
third-generation cephalosporin while pending culture results.
In areas in which community-associated methicillin-resistant Staphylococcus
aureus is prevalent, a combination of a beta-lactam antibiotic and vancomycin
is recommended.
REFERENCES
https://www.ndhealth.gov/Disease/Documents/faqs/Kingella.pdf
file:///C:/Users/default.DESKTOP-S673BEP/Documents/medical/Bailey_&_Scott_s_Diagnostic_Microbiology_12th_Edition(1).pdf
https://cmr.asm.org/content/cmr/28/1/54.full.pdf
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