Klebsiella oxytoca

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Klebsiella oxytoca
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Gamma
Class:
Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Klebsiella
Species: K. oxytoca
Binomial name
Klebsiella oxytoca
(Flügge 1886)
Lautrop 1956

Klebsiella oxytoca is a Gram-negative, rod-shaped bacterium that is closely related to K.

pneumoniae, from which it is distinguished by being indole-positive; it also has slightly different growth
characteristics in that it is able to grow on melezitose, but not 3-hydroxybutyrate.

Contents

 1 Industrial uses
 2 Clinical significance

 3 References

 4 External links

Industrial uses

K. oxytoca has shown promise in industrial ethanol fuel production.[1] K.oxytoca is characterized by
negative methyl red, positive VP, positive citrate, urea and TSI gas production, is AA, and negative for
TSI sulfide, DNAse, SIM motility and PAD.

K. oxytoca is referenced as being used to produce hydrogen in patents filed by Nanologix, Inc.

Clinical significance

It can cause colitis.[2]

References

1. ^ Dien B, Cotta M, Jeffries T (2003). "Bacteria engineered for fuel ethanol production: current
status". Appl Microbiol Biotechnol 63 (3): 258–66. doi:10.1007/s00253-003-1444-y.
PMID 13680206.
2. ^ Högenauer C, Langner C, Beubler E, et al (December 2006). "Klebsiella oxytoca as a
causative organism of antibiotic-associated hemorrhagic colitis". N. Engl. J. Med. 355 (23):
2418–26. doi:10.1056/NEJMoa054765. PMID 17151365.
http://content.nejm.org/cgi/pmidlookup?view=short&pmid=17151365&promo=ONFLNS19.

 MeSH Klebsiella+oxytoca
 This Proteobacteria-related article is a stub. You can help Wikipedia by expanding it.
Infectious diseases · Bacterial diseases: Proteobacterial G- (primarily A00–A79, 001–041, 080–
109)

Rickettsia typhi (Murine typhus) · Rickettsia prowazekii

Typhus (Epidemic typhus, Brill–Zinsser disease, Flying squirrel
typhus)

Rickettsia rickettsii (Rocky Mountain spotted fever) ·

Rickettsia conorii (Boutonneuse fever) · Rickettsia
japonica (Japanese spotted fever) · Rickettsia sibirica
(North Asian tick typhus) · Rickettsia australis
Tick-
(Queensland tick typhus) · Rickettsia honei (Flinders
Rickettsiaceae/ borne
Island spotted fever) · Rickettsia africae (African tick
(Rickettsioses) bite fever) · Rickettsia parkeri (American tick bite
Spotted fever) · Rickettsia aeschlimannii (Rickettsia
Rickettsiales fever aeschlimannii infection)

Mite- Rickettsia akari (Rickettsialpox) · Orientia

α borne tsutsugamushi (Scrub typhus)

Flea-
Rickettsia felis (Flea-borne spotted fever)
borne

Ehrlichiosis: Anaplasma phagocytophilum (Human granulocytic

anaplasmosis, Anaplasmosis) · Ehrlichia chaffeensis (Human
Anaplasmataceae
monocytic ehrlichiosis) · Ehrlichia ewingii (Ehrlichiosis ewingii
infection)

Brucellaceae Brucella abortus (Brucellosis)

Rhizobiales Bartonellosis: Bartonella henselae (Cat scratch disease) · Bartonella

quintana (Trench fever) · either henselae or quintana (Bacillary
Bartonellaceae
angiomatosis) · Bartonella bacilliformis (Carrion's disease, Verruga
peruana)

M+ Neisseria meningitidis/meningococcus (Meningococcal disease, Waterhouse-

Friderichsen syndrome, Meningoccal septicaemia)
M- Neisseria gonorrhoeae/gonococcus (Gonorrhea)
Neisseriales
ungrouped: Eikenella corrodens/Kingella kingae (HACEK) · Chromobacterium
β violaceum (Chromobacteriosis infection)

Burkholderia pseudomallei (Melioidosis) · Burkholderia mallei (Glanders) ·

Burkholderiales Burkholderia cepacia complex · Bordetella pertussis/Bordetella parapertussis
(Pertussis)

Klebsiella pneumoniae (Rhinoscleroma, Klebsiella pneumonia) ·

Klebsiella granulomatis (Granuloma inguinale) · Klebsiella oxytoca

Enterobacteriales Lac+ Escherichia coli: Enterotoxigenic · Enteroinvasive ·

γ
(OX-) O157:H7/Enterohemorrhagic (Hemolytic-uremic syndrome)

Enterobacter aerogenes/Enterobacter cloacae

 Slow/weakSerratia marcescens (Serratia infection) · Citrobacter

Salmonella enterica (Typhoid fever, Paratyphoid fever,

H2S+
Salmonellosis)

Lac- Shigella dysenteriae/sonnei/flexneri/boydii (Shigellosis, Bacillary

dysentery) · Proteus mirabilis/Proteus vulgaris · Yersinia pestis
H2S-
(Plague/Bubonic plague) · Yersinia enterocolitica · Yersinia
pseudotuberculosis

Haemophilus: H. influenzae (Haemophilus meningitis, Brazilian purpuric fever) ·

H. ducreyi (Chancroid) H. parainfluenzae (HACEK)
Pasteurellales
Pasteurella multocida (Pasteurellosis) · Actinobacillus (Actinobacillosis)

Aggregatibacter actinomycetemcomitans (HACEK)

Legionella pneumophila/Legionella longbeachae (Legionellosis) · Coxiella

Legionellales
burnetii (Q fever)

Thiotrichales Francisella tularensis (Tularemia)

Vibrio cholerae (Cholera) · Vibrio vulnificus · Vibrio parahaemolyticus · Vibrio

Vibrionales
alginolyticus · Plesiomonas shigelloides

Pseudomonas aeruginosa (Pseudomonas infection) · Moraxella catarrhalis ·

Pseudomonadales
Acinetobacter baumannii

Xanthomonadales Stenotrophomonas maltophilia

Cardiobacteriales Cardiobacterium hominis (HACEK)

Aeromonadales Aeromonas hydrophila/Aeromonas veronii (Aeromonas infection)

Campylobacter jejuni (Campylobacteriosis, Guillain-Barré syndrome) ·

ε Campylobacterales Helicobacter pylori (Peptic ulcer, MALT lymphoma) · Helicobacter cinaedi
(Helicobacter cellulitis)

Colitis

From Wikipedia, the free encyclopedia

In medicine, colitis (pl. colitides) refers to an inflammation of the colon and is often used to describe
an inflammation of the large intestine (colon, cecum and rectum).

Colitides may be acute and self-limited or chronic, i.e. persistent, and broadly fit into the category of
digestive diseases.

In a medical context, the label colitis (without qualification) is used if:

1. The etiology of the inflammation in the colon is undetermined; for example, colitis may be
applied to Crohn's disease at a time when the diagnosis has not declared itself.
 2. The context is clear; for example, an individual with ulcerative colitis is talking about their
disease with a physician that knows the diagnosis.

Contents

 1 Signs and symptoms

 2 Work-up

 3 Types

o 3.1 Autoimmune

o 3.2 Idiopathic

o 3.3 Iatrogenic

o 3.4 Vascular disease

o 3.5 Infectious

o 3.6 Unclassifiable colitides

o 3.7 Severity of colitides

 4 Treatment

 5 See also

 6 Notes

 7 External links

Signs and symptoms

The signs and symptoms of colitides are quite variable and dependent on the etiology (or cause) of
the given colitis and factors that modify its course and severity.

Symptoms of colitis may include: abdominal pain, anorexia (loss of appetite), fatigue, diarrhea,
cramping, urgency (tenesmus) and bloating.

Signs may include: abdominal tenderness, weight loss, changes in bowel habits (increased
frequency), fever, bleeding (overt or occult)/bloody stools, diarrhea and distension.

Signs seen on colonoscopy include: colonic mucosal erythema (redness of the inner surface of the
colon), ulcers, bleeding.

Work-up

Symptoms suggestive of colitis are worked-up by obtaining the medical history, a physical
examination and laboratory tests (CBC, electrolytes, stool culture and sensitivity, stool ova and
parasites et cetera). Tests in addition to use may include medical imaging (e.g. abdominal computed
tomography, abdominal X-rays) and an examination with a camera inserted into the rectum
(sigmoidoscopy, colonoscopy).

Types

There are many types of colitides. They are usually classified by the etiology.
Types of colitis include:

Autoimmune

Micrograph showing intestinal crypt branching, a histopathological finding of chronic colitis. H&E stain.
 Inflammatory bowel disease (IBD) - a group of chronic colitides.

Main article: Inflammatory bowel disease

o Ulcerative colitis - a chronic colitis that affects the large intestine.

Main article: Ulcerative colitis

o Crohn's disease - a type of IBD often leads to a colitis.

Main article: Crohn's disease

Idiopathic

 Microscopic colitis - a colitis is diagnosed by microscopic examination of colonic tissue;

macroscopically it is normal appearing.

Main article: Microscopic colitis

o Lymphocytic colitis.

Main article: Lymphocytic colitis

o Collagenous colitis.

Main article: Collagenous colitis

Iatrogenic

 Diversion colitis.

Main article: Diversion colitis

 Chemical colitis.

Main article: Chemical colitis

Vascular disease

 Ischemic colitis.

Main article: Ischemic colitis

Infectious

Micrograph of a colonic pseudomembrane in pseudomembranous colitis, a type of infectious colitis.

 Infectious colitis.
A well-known subtype of infectious colitis is pseudomembranous colitis, which results from infection
by a toxigenic strain of Clostridium difficile (c-diff).[1]

Enterohemorrhagic colitis may be caused by Shiga toxin in Shigella dysenteriae or Shigatoxigenic

group of Escherichia coli (STEC), which includes serotype O157:H7 and other enterohemorrhagic E.
coli.[2]

Parasitic infections can also cause colitis.

Unclassifiable colitides

Indeterminate colitis is a term used for a colitis that has features of both Crohn's disease and
ulcerative colitis.[3] Indeterminate colitis' behaviour is usually closer to ulcerative colitis than Crohn's
disease.[4]

Atypical colitis is a phrase that is occasionally used by physicians for a colitis that does not conform to
criteria for accepted types of colitis. It is not an accepted diagnosis per se and, as such, a colitis that
cannot be definitively classified.

Severity of colitides

Fulminant colitis is any colitis that becomes worse rapidly. In addition to the diarrhea, fever, and
anemia seen in colitis, the patient has severe abdominal pain and presents a clinical picture similar to
that of septicemia, where shock is present. About half of human patients require surgery. In horses,
the fulminant colitis known as colitis X usually results in death within 24 hours.

Irritable bowel syndrome, a separate disease, has been called spastic colitis. This name may lead to
confusion, since colitis is not always a feature of irritable bowel syndrome. Since the etiology of IBS is
currently unknown and possibly multifactorial, there may be some overlap in symptoms between IBS
and the various forms of colitis.

Treatment

How a given colitis is treated is dependent on its etiology, e.g. infectious colitis are usually treated with
antimicrobial agents (e.g. antibiotics), autoimmune mediated colitis are treated with immune
modulators/immune suppressants.

Severe colitis can be life-threatening and may require surgery.

Klebsiella Infections

Author: Obiamiwe Umeh, MBBS, Fellow, Center for AIDS Research and Education, David Geffen
School of Medicine at UCLA
Coauthor(s): Leonard B Berkowitz, MD, Chief, Divisions of Infectious Diseases and HIV/AIDS
Services, Brooklyn Hospital Center; Clinical Assistant Professor, Department of Medicine, State
University of New York at Brooklyn
Contributor Information and Disclosures

Updated: May 15, 2009

 Overview
 Differential Diagnoses & Workup

 Treatment & Medication

 Follow-up
  Multimedia

 References

 Keywords

 Further Reading

Information from Industry

Bacterial RTIs: View S pneumoniae resistance map–Click on your state Consider the growing
problem of antibacterial resistance. What is the S pneumoniae resistance rate in your state? Read
more

Introduction

Background

The genus Klebsiella belongs to the tribe Klebsiellae, a member of the family Enterobacteriaceae. The
organisms are named after Edwin Klebs, a 19th century German microbiologist. Klebsiellae are
nonmotile, rod-shaped, gram-negative bacteria with a prominent polysaccharide capsule. This
capsule encases the entire cell surface, accounts for the large appearance of the organism on gram
stain, and provides resistance against many host defense mechanisms.

Members of the Klebsiella genus typically express 2 types of antigens on their cell surface. The first is
a lipopolysaccharide (O antigen); the other is a capsular polysaccharide (K antigen). Both of these
antigens contribute to pathogenicity. About 77 K antigens and 9 O antigens exist. The structural
variability of these antigens forms the basis for classification into various serotypes. The virulence of
all serotypes appears to be similar.

The genus was originally divided into 3 main species based on biochemical reactions. Today, 7
species with demonstrated similarities in DNA homology are known. These are (1) Klebsiella
pneumoniae, (2) Klebsiella ozaenae, (3) Klebsiella rhinoscleromatis, (4) Klebsiella oxytoca, (5)
Klebsiella planticola, (6) Klebsiella terrigena, and (7) Klebsiella ornithinolytica. K pneumoniae is the
most medically important species of the group. K oxytoca and K rhinoscleromatis have also been
demonstrated in human clinical specimens. In recent years, klebsiellae have become important
pathogens in nosocomial infections.1

This scanning electron micrograph (SEM) reveals some of the ultrastructural morphologic
features of Klebsiella pneumoniae. Courtesy of CDC/Janice Carr.

This scanning electron micrograph (SEM) reveals some of the ultrastructural morphologic
features of Klebsiella pneumoniae. Courtesy of CDC/Janice Carr.

Pathophysiology

Host defense against bacterial invasion depends on phagocytosis by polymorphonuclear granulocytes

and the bactericidal effect of serum, mediated in large part by complement proteins. Both classic-
pathway and alternate-pathway complement activation have been described, but the latter, which
does not require the presence of immunoglobulins directed against bacterial antigens, appears to be
the more active pathway in K pneumoniae infections.

Recent data from preclinical studies suggest a role for neutrophil myeloperoxidase and
lipopolysaccharide-binding protein in host defense against K pneumoniae infection. Neutrophil
myeloperoxidase is thought to mediate oxidative inactivation of elastase, an enzyme implicated in the
pathogenesis of various tissue-destroying diseases. Lipopolysaccharide-binding protein facilitates
transfer of bacterial cell wall components to inflammatory cells. Investigators showed higher rates of
infection in experimental mice deficient in the genes that control expression of these 2 agents.

The bacteria overcome innate host immunity through several means. They possess a polysaccharide
capsule, which is the main determinant of their pathogenicity. The capsule is composed of complex
acidic polysaccharides. Its massive layer protects the bacterium from phagocytosis by
polymorphonuclear granulocytes. In addition, the capsule prevents bacterial death caused by
bactericidal serum factors. This is accomplished mainly by inhibiting the activation or uptake of
complement components, especially C3b. The bacteria also produce multiple adhesins. These may
be fimbrial or nonfimbrial, each with distinct receptor specificity. These help the microorganism to
adhere to host cells, which is critical to the infectious process.

Lipopolysaccharides (LPS) are another bacterial pathogenicity factor. They are able to activate
complement, which causes selective deposition of C3b onto LPS molecules at sites distant from the
bacterial cell membrane. This inhibits the formation of the membrane attack complex (C5b-C9), which
prevents membrane damage and bacterial cell death.

Availability of iron increases host susceptibility to K pneumoniae infection. Bacteria are able to
compete effectively for iron bound to host proteins because of the secretion of high-affinity, low
molecular weight iron chelators known as siderophores. This is necessary because most host iron is
bound to intracellular and extracellular proteins. In order to deprive bacteria of iron, the host also
secretes iron-binding proteins.

Epidemiology

Klebsiellae are ubiquitous in nature. In humans, they may colonize the skin, pharynx, or
gastrointestinal tract. They may also colonize sterile wounds and urine. Carriage rates vary with
different studies. Klebsiellae may be regarded as normal flora in many parts of the colon and intestinal
tract and in the biliary tract. Oropharyngeal carriage has been associated with endotracheal
intubation, impaired host defenses, and antimicrobial use.

K pneumoniae and K oxytoca are the 2 members of this genus responsible for most human infections.
They are opportunistic pathogens found in the environment and in mammalian mucosal surfaces. The
principal pathogenic reservoirs of infection are the gastrointestinal tract of patients and the hands of
hospital personnel. Organisms can spread rapidly, often leading to nosocomial outbreaks.

Infection with Klebsiella organisms occurs in the lungs, where they cause destructive changes.
Necrosis, inflammation, and hemorrhage occur within lung tissue, sometimes producing a thick,
bloody, mucoid sputum described as currant jelly sputum. The illness typically affects middle-aged
and older men with debilitating diseases such as alcoholism, diabetes, or chronic bronchopulmonary
disease. This patient population is believed to have impaired respiratory host defenses. The
organisms gain access after the host aspirates colonizing oropharyngeal microbes into the lower
respiratory tract.

Klebsiellae have also been incriminated in nosocomial infections. Common sites include the urinary
tract, lower respiratory tract, biliary tract, and surgical wound sites. The spectrum of clinical
syndromes includes pneumonia, bacteremia, thrombophlebitis, urinary tract infection (UTI),
cholecystitis, diarrhea, upper respiratory tract infection, wound infection, osteomyelitis, and meningitis.
The presence of invasive devices, contamination of respiratory support equipment, use of urinary
catheters, and use of antibiotics are factors that increase the likelihood of nosocomial infection with
Klebsiella species. Sepsis and septic shock may follow entry of organisms into the blood from a focal
source.

Rhinoscleroma and ozena are 2 other infections caused by Klebsiella species. These diseases are
rare. Rhinoscleroma is a chronic inflammatory process involving the nasopharynx, whereas ozena is a
chronic atrophic rhinitis characterized by necrosis of nasal mucosa and mucopurulent nasal
discharge.
K oxytoca has been implicated in neonatal bacteremia, especially among premature infants and in
neonatal intensive care units. Increasingly, the organism is being isolated from patients with neonatal
septicemia.

Extensive use of broad-spectrum antibiotics in hospitalized patients has led to both increased carriage
of klebsiellae and, subsequently, the development of multidrug-resistant strains that produce
extended-spectrum beta-lactamase (ESBL). These strains are highly virulent, show capsular type
K55, and have an extraordinary ability to spread. Most outbreaks are due to a single clone or single
gene; the bowel is the major site of colonization with infection of the urinary tract, respiratory tract, and
wounds. Bacteremia and significant increased mortality have resulted from infection with these
species.

In addition to prior antibiotic use, risk factors for infection include the presence of an indwelling
catheter, feeding tube, or central venous catheter; poor health status; and treatment in an intensive
care unit or nursing home. Acquisition of these species has become a major problem in most
hospitals because of resistance to multiple antibiotics and potential transfer of plasmids to other
organisms.

Frequency

United States

In some parts of the world, K pneumoniae is an important cause of community-acquired pneumonia in

elderly persons. Studies conducted in Malaysia and Japan estimate the incidence rate in elderly
persons to be 15-40%, which is equal to, if not greater than, that of Haemophilus influenzae.
However, in the United States, these figures are different. Persons with alcoholism are the main
population at risk, and they constitute 66% of people affected by this disease. Mortality rates are as
high as 50% and approach 100% in persons with alcoholism and bacteremia.

Klebsiellae are also important in nosocomial infections among adult and pediatric populations.
Klebsiellae account for approximately 8% of all hospital-acquired infections. In the United States,
depending on the study reviewed, they comprise 3-7% of all nosocomial bacterial infections, placing
them among the top 8 pathogens in hospitals. Klebsiellae cause as many as 14% of cases of primary
bacteremia, second only to Escherichia coli as a cause of gram-negative sepsis. They may affect any
body site, but respiratory infections and UTIs predominate.

Of 145 reported epidemic outbreaks of nosocomial bacteremias during 1983-1991, 13 were attributed
to Klebsiella organisms. The US Centers for Disease Control and Prevention report that Klebsiella
strains were responsible for 3% of all pathogenic epidemic outbreaks.

K oxytoca is among the top 4 pathogens that cause infection in patients in neonatal intensive care
units. It is the second most frequent cause of gram-negative neonatal bacteremia.

International

Outbreaks of neonatal septicemia occur worldwide. Infection with K pneumoniae also has a worldwide
distribution. Infection with K rhinoscleromatis is not common in the United States, although it has a
worldwide distribution and is usually observed in areas of eastern Europe, southern Asia, central
Africa, and Latin America.

Mortality/Morbidity

 Klebsiella pneumonia is a necrotizing process with a predilection for debilitated people. It has
a high mortality rate of approximately 50% even with antimicrobial therapy. The mortality rate
approaches 100% for persons with alcoholism and bacteremia.
 Klebsiella bacteremia and sepsis produce clinical manifestations similar to those caused by
other gram-negative enteric organisms. Morbidity and mortality rates are comparable to those
 for other gram-negative organisms that cause sepsis and septic shock. In neonatal units,
outbreaks caused by ESBL-producing strains present a more serious problem and may be
associated with increased mortality.

Age

 Community-acquired Klebsiella (Friedlãnder) pneumonia is a disease of debilitated middle-

aged and older men with alcoholism.
 Nosocomial infections may affect adults or children, and they occur more frequently in
premature infants, patients in neonatal intensive care units, and hospitalized individuals who
are immunocompromised.

Clinical

History

Klebsiellae cause a variety of clinical syndromes. Common klebsiellae infections in humans include
(1) community-acquired pneumonia, (2) UTI, (3) nosocomial infection, (4) rhinoscleroma and ozena,
and (5) colonization.

 Community-acquired pneumonia
o Lobar pneumonia differs from other pneumonias in that it is associated with
destructive changes in the lungs. It is a very severe illness with a rapid onset and
often-fatal outcome despite early and appropriate antimicrobial treatment.

o Patients typically present with an acute onset of high fever and chills; flulike
symptoms; and productive cough with an abundant, thick, tenacious, and blood-
tinged sputum sometimes called currant jelly sputum.

o An increased tendency exists toward abscess formation, cavitation, empyema, and

pleural adhesions.

o Most pulmonary diseases caused by K pneumoniae are in the form of

bronchopneumonia or bronchitis. These infections are usually hospital-acquired and
have a more subtle presentation.

 Urinary tract infection2

o Klebsiellae UTIs are clinically indistinguishable from UTIs caused by other common
organisms.

o Clinical features include frequency, urgency, dysuria, hesitancy, low back pain, and
suprapubic discomfort. Systemic symptoms such as fever and chills are usually
indicative of a concomitant pyelonephritis or prostatitis.

 Nosocomial infection

o Important manifestations of klebsiellae infection in the hospital setting include UTI,

pneumonia, bacteremia, wound infection, cholecystitis, and catheter-associated
bacteriuria. The presence of invasive devices in hospitalized patients greatly
increases the likelihood of infection. Patients with these infections have similar
presentations to those with infections caused by other organisms.

o Other nosocomial infections in which klebsiellae may also be implicated include

cholangitis, meningitis, endocarditis, and bacterial endophthalmitis. The latter occurs
especially in patients with liver abscesses3 and diabetes. These infectious
presentations are relatively uncommon.

 Rhinoscleroma and ozena

 o K rhinoscleromatis and K ozaenae cause rhinoscleroma and ozena, respectively.
Both are rare in the United States and are associated with upper respiratory infection.

o Rhinoscleroma is a chronic granulomatous infection. Patients present with a purulent

nasal discharge with crusting and nodule formation that leads to respiratory
obstruction. Diagnosis is aided by histology findings and positive results from blood
culture.

o Ozena is a primary atrophic rhinitis that often occurs in elderly persons. Common
symptoms include nasal congestion and a constant nasal bad smell. Patients also
may complain of headache and symptoms attributable to chronic sinusitis. Unlike
rhinoscleroma, nasal congestion is not a prominent feature.

 Colonization

o Differentiating nosocomial colonization from infection presents a formidable challenge

in clinical practice. It is a common problem in patients with indwelling catheters.

o Duration of catheterization is the most important risk factor for the development of
bacteriuria. Keeping catheter systems closed and removing catheters as soon as
possible are ways to prevent development of bacteriuria.

o Most catheter-related UTIs are asymptomatic; the usual complaints of frequency,

urgency, dysuria, hesitancy, low back pain, and suprapubic discomfort typically are
absent. Therefore, demonstration of bacteriuria is necessary to make a diagnosis. A
density of 100,000 colony-forming units per milliliter is usually required to make a
diagnosis. Concomitant presence of pyuria is usually present in patients with
catheter-associated infection as opposed to those with colonization.

o In general, the presence of symptoms in conjunction with bacteriological evidence of

infection helps distinguish infection, in which organisms cause disease, from
colonization, in which organisms coexist without causing harm.

Physical

 Klebsiella pneumonia characteristically affects one of the upper lobes of the lung, although
infection of the lower lobes is not uncommon.
 Examination of patients with community-acquired pneumonia usually reveals unilateral chest
signs, predominantly in the upper lobes. When these signs are observed in a patient such as
described in History, the diagnosis of Klebsiella pneumonia is strongly suggested.

 Clinical signs observed in patients with extrapulmonary disease depend on the organ system
involved. In cases of nosocomial infections, physical examination should include a search for
factors that predispose the individual to the development of such infections. These should
include inspection for the presence and duration of invasive devices, wounds, and burn sites.

Causes

 Host factors that lead to colonization and infection include the following:
o Hospitalization (especially admission to an intensive care unit)

o Immunocompromised states (eg, diabetes, alcoholism)

o Antimicrobial therapy

o Prolonged use of invasive medical devices

 o Inadequate infection control practices

o Severe illness, including major surgery

 The organism gains access to the body either by direct inoculation through breached
epithelial surfaces or following aspiration of oropharyngeal organisms.

Role of Klebsiella oxytoca in antibiotic-associated diarrhea.

Zollner-Schwetz I, Högenauer C, Joainig M, Weberhofer P, Gorkiewicz G, Valentin T,

Hinterleitner TA, Krause R.

Section of Infectious Diseases, Division of Pulmonology, Department of Internal Medicine,

Medical University of Graz, Graz, Austria. ines.schwetz@meduni-graz.at

Abstract

BACKGROUND: Klebsiella oxytoca was recently shown to be the causative agent of

antibiotic-associated hemorrhagic colitis. Because it is unclear whether K. oxytoca also
causes nonhemorrhagic antibiotic-associated diarrhea, our study investigated a possible
association between K. oxytoca and that disorder. METHODS: A total of 371 consecutive
patients were recruited into 4 study groups: (1) group A+D+ (patients who received antibiotics
and experienced diarrhea; n = 107), (2) group A+D- (patients who received antibiotics but did
not experience diarrhea; np93), (3) group A-D+ (patients who experienced acute-onset
diarrhea but did not receive antibiotics; n = 60), and (4) group A-D- (patients without diarrhea
who did not receive antibiotics; n = 111). Stool samples were plated on MacConkey agar and
K. oxytoca was identified using a standard test kit. Clostridium difficile was detected by a toxin
A/B antigen test. K. oxytoca strains were tested for cytotoxicity with use of cell-culture assays.
RESULTS: In 15 of 371 stool samples, K. oxytoca strains were isolated during the study
period. There was no significant difference in the distribution of K. oxytoca among the 4 study
groups. Six of the 15 strains were found to be toxin producing. Three of the toxin-producing
strains caused antibiotic-associated hemorrhagic colitis. No case of nonhemorrhagic
antibiotic-associated diarrhea due to toxin-producing K. oxytoca was detected.
CONCLUSION: K. oxytoca is not the causative agent of nonhemorrhagic antibiotic-associated
diarrhea. This is in contrast to the distinct clinical entity of antibiotic-associated hemorrhagic
colitis. Testing for K. oxytoca is therefore only warranted for patients who experience bloody
diarrhea during antibiotic therapy.

Klebsiella oxytoca (KO) is a bacterium that causes urinary tract infections and septicemia. Klebsiella
oxytoca has a high possibility of antibiotic resistance, making related infections very serious and it's
important to treat them rapidly. Septicemia is the most severe klebsiella oxytoca-caused infection;
fortunately, there are treatments for the infections.

Klebsiella Oxytoca Urinary Tract Infection

1. Klebsiella oxytoca often builds up in the urinary tract and multiplies, causing infection. Urinary
tract infections are serious health risks demonstrating many symptoms: frequent urination,
severe burning in the bladder and urinary tract during urination, fatigue, aches, and pain
(without urination) in the bladder and urinary tract. Untreated infection might lead to kidney
infection and severe fever. Klebsiella oxytoca-caused urinary tract infection is treated via
antibacterial medications. The most common antibiotics used for treatment include
trimethoprim, sulfamethocazole, amoxicillin, and ampicillin. A doctor will first confirm that you
have no medical allergies to these medicines prior to writing a prescription. If klebsiella
ocytoca spreads to the kidneys, treatment becomes complicated. Hospitalization and IV-
administered antibiotics are required. It takes several weeks of antibiotics to remedy a
klebsiella oxytoca kidney infection. Because klebsiella oxytoca is more likely to develop
antibiotic resistance, contact your doctor immediately if you experience any symptoms of a
urinary tract infection.
Klebsiella Oxytoca Septicemia

2. Klebsiella oxytoca is responsible for septicemia. Septicemia is an extremely serious, life-

threatening infection of the blood. Severity increases very quickly; treatment is needed
rapidly. Spiking fevers, chills, rapid breathing and heart rate are early symptoms of
septicemia. Symptoms progress to medical shock and steady fever. Often, the body
decreases its temperature sharply, causing hypothermia. As klebsiella oxytoca travels and
multiplies in the blood stream, mental awareness decreases, blood pressure falls and red
spots on the skin emerge on the skin. If you believe that you have septicemia, contact 911
immediately. You will be treated in the intensive care unit, where antibiotics, plasma and
possible blood transfusions will be administered through an IV.