CHAPTER 115 Klebsiella 1541
C H A P T E R
Klebsiella
115 Randall G. Fisher
Klebsiella is a genus of Enterobacteriaceae, a frequent cause
of nosocomial pediatric infection. Classically described by
Friedländer38 as a cause of pneumonia, Klebsiella can cause infec-
tions of the urinary tract, lung, and central venous catheters in
high-risk newborns and immunocompromised older children.18
BACTERIOLOGY
Klebsiella organisms were named for Edwin Klebs, the noted
German bacteriologist.86 Distinguishing features of Klebsiella spp.
include the absence of motility and the presence of a polysac-
charide capsule that gives rise to large mucoid colonies on solid
media. The organisms are oxidase-negative and citrate-positive;
they ferment inositol and hydrolyze urea but do not produce
ornithine decarboxylase or hydrogen sulfide. Acetoin and 2,3-
butanediol predominate over acidic end-products during sugar
fermentation (positive result on the Voges-Proskauer test). Four
species of Klebsiella commonly are agreed on by microbiologists:
Klebsiella pneumoniae (the most common human pathogen), Kleb-
siella oxytoca (a less common human pathogen), Klebsiella terrigena,
and Klebsiella planticola. Previously, K. planticola was recovered
almost exclusively from soil and aquatic environments; reports
now suggest that this organism may be a relatively common
neonatal pathogen in some parts of the world.92,113 K. planticola
may express virulence factors similar to those of K. pneumoniae.93
Organisms are defined serologically by their capsular poly-
saccharide (K antigens) and lipopolysaccharide (O antigens).
Significant cross-reactivity exists between the capsule of some
pneumococci (e.g., 19F) and Klebsiella.68 The reader is referred to
a review by Podschun and Ullman95 for a detailed description of
Klebsiella spp.
EPIDEMIOLOGY
Friedländer38 proposed that K. pneumoniae was the most common
cause of community-acquired pneumonia, an observation that
was refuted by Fraenkel’s36 observations on pneumococcal pneu-
monia. K. pneumoniae accounts for less than 10 percent of hospi-
talized cases of pneumonia in adults.20 Klebsiella spp. now are in
greatest evidence as opportunistic nosocomial pathogens of the
urinary tract, respiratory tract, biliary tract, and bloodstream. In
one survey of the Centers for Disease Control and Prevention,
the infection rate of nosocomial K. pneumoniae was 16.7 infections
per 10,000 patients discharged.54 Hand-carriage generally is
regarded as the common mode of transmission.42 Environmental
sources of Klebsiella spp. include contaminated blood-pressure
monitoring equipment,98 ventilator traps,42 dialysate,64 ultrasound
coupling gel,40 dextrose solution,66 and hand disinfectant.101 The
emergence of plasmid-mediated, β-lactamase resistance can be
responsible for the rapid spread of resistant organisms to suscep-
tible patients in intensive care units (ICUs).10,12 Outbreaks may
be complex; patient-to-patient transmission of epidemic strains
containing different plasmids may be interspersed with sporadic,
nonepidemic Klebsiella infections.12 Klebsiella spp. are second only
to Escherichia coli as causes of sepsis,41 with the highest rates of
infection being reported from larger hospitals affiliated with
medical schools.
Klebsiella spp. commonly are highlighted as pathogens of
debilitated adults and alcoholics,60 but by 1985, nearly 50 percent
of reported outbreaks of Klebsiella were in neonatal ICUs.54
Outbreaks in newborns continue to occur frequently world-
wide.2,7,24,30,49,90,100 Most outbreaks in newborns have been
associated with K. pneumoniae infection, but scattered outbreaks
of K. oxytoca infection in nurseries also have been reported.6,112 A
high percentage of infants in ICUs may become colonized with
hospital strains of Klebsiella.46 In one longitudinal study in which
weekly rectal swabs were cultured, 80 (22%) of 368 neonates in
an ICU harbored extended-spectrum β-lactamase (ESBL)–
producing Klebsiella spp.15 Infecting organisms have been isolated
from care providers and from mothers of colonized infants.24 One
report described an outbreak among newborns associated with
infestation of a neonatal unit by cockroaches colonized with
infecting Klebsiella strains.25 Klebsiella may spread from newborn
units to adult units; interhospital and international spread of
resistant strains has been described.23,30,106
Ribotyping, pulsed field gel electrophoresis, and DNA ampli-
fication techniques have proven valuable in characterizing Kleb-
siella strains associated with outbreaks.70,108 Different ribotypes
that share plasmids conferring antibiotic resistance can be respon-
sible for pediatric infections in a particular institution.12 Strains
expressing ESBL may become endemic and may present a
complex and diverse pattern of production of enzymes with resis-
tance to β-lactamase inhibitors.31,35 Although broad-spectrum
resistance to β-lactams and carbapenems72 has been described,
some longitudinal studies have shown that the frequency of
ESBLs in K. pneumoniae isolates is decreasing.103
PATHOPHYSIOLOGY
Pneumonias caused by Klebsiella most commonly arise from colo-
nization of the upper respiratory tract, followed by aspiration of
organisms to the lower respiratory tract. Some degree of gram-
negative oropharyngeal colonization is a normal finding in new-
borns. The oropharynx of nearly one third of healthy newborns
is colonized by gram-negative rods, including Klebsiella, by the
time infants reach 1 month of age; colonization rates generally
are lower in breast-fed infants.9 Antibiotic pressure in high-risk
newborns and older children has been observed to promote over-
growth of Klebsiella.11,105 Enteric organisms are recovered less
frequently from the oropharynx of healthy older children and
adults; oral colonization with gram-negative rods is increased
during illness,57 after postoperative viral infections,56,97 and in
debilitated adults.73 Increased adherence of gram-negative rods
to oropharyngeal cells contributes to increased colonization.56
Elastase made by polymorphonuclear cells contributes to such
colonization by reducing the fibronectin coating of sugar recep-
tors.27 The capsule plays an initial role in interactions of epithelial
cells but is not required for an adhesin interaction with the cell
surface.34 Adherence properties may be affected by plasmid
content29 and may be transferred between E. coli and K.
pneumoniae.53
In animal models of sepsis, capsular polysaccharide (K anti-
gens) is a virulence factor; monoclonal antibodies to the K anti-
gens reduce the severity of illness in mice.67 In a mouse model of
urinary tract infection, the K antigens seemed to be more impor-
tant in infection than was the lipopolysaccharide (O antigens),
and clinical strains deficient in lipopolysaccharide retained viru-
lence by resistance of capsule to complement.3,19 In one series of
adult patients, capsular type K2 frequently was associated with