Enterobacteriaceae gram negative facultative anaerobic rods oxidase negative no cytochrome oxidase. Feces E. Serotypes reference laboratory antigens O lipopolysaccharide H flagellar K capsular.
Escherichia coli E. Transmission meat products or sewage-contaminated vegetables Hemorrhagic Bloody dysentery copious diarrhea few leukocytes afebrile hemolytic-uremic syndrome hemolytic anemia thrombocytopenia low platelets kidney failure.
Enterotoxigenic E. Enteropathogenic E. Treatment -gastrointestinal disease fluid replacement antibiotics not used usually unless systemic e. Shigella S. Shigellosis man only "reservoir" mostly young children fecal to oral contact children to adults transmitted by adult food handlers unwashed hands Treating shigellosis manage dehydration patients respond to antibiotics disease duration diminished.
Gram-negative, enteric, rod prokaryote dividing ; causes typhoid fever. TIF bacilli bacillus bacteria bacterial pathogen bacterium division Gram-negative human disease infection prokaryote rod Salmonella typhi typhoid fever enteric bacterial pathogen intestinal tract infection SEM.
Salmonellosis S. Control of salmonellosis Monitoring of food in the US is limited microbiology is difficult. Open navigation menu. Close suggestions Search Search.
User Settings. Skip carousel. Carousel Previous. Carousel Next. What is Scribd? Explore Ebooks. Bestsellers Editors' Picks All Ebooks. Explore Audiobooks. Farmer III, J. Duguid, J. The demonstration of bacterial capsules and slime. Genus Budvicia. Fimbriae and adhesive properties in Klebsiella strains. J Gen Microbiol, 21, — The Salmonella-Arizona Duguid, J. Clin Microbiol News, 6, 63—6. J Pathol Bacteriol, 74, — Fimbriae and haemagglutinating specimens.
J Clin Microbiol, 21, 46— Xenorhabdus luminescens J Pathol Bacteriol, 75, — DNA hybridization group 5 from human clinical specimens. J Clin Duguid, J. Adhesive properties of Microbiol, 27, — In: Beachey, E. Farthing, M. New York: Raven Press. J Pathol Bacteriol, 70, — Fimbriae and nov. J Pathol Bacteriol, 92, — Durham, H.
A simple method for demonstrating the production Fox, G. How close is close: of gas by bacteria. Br Med J, 1, Cold-tolerant fermentative Gram- species identity.
Int J Syst Bacteriol, 42, — J Appl Bacteriol, 22, Freer, J. The anatomy and chemistry of gram- 57— In: Weinbaum, G. Nosocomial bloodstream Microbial toxins, Vol. New York: Academic Press, 67— Clin Infect Gamage, S. Nonpathogenic Escherichia coli Dis, 29, — Infect Immun, 71, Edwards, P. Enterobacteriaceae, 3rd edn. Minneapolis: Burgess Publishing. Gaughran, E. From superstition to science: the history of a Eijkman, C. Trans NY Acad Sci, 31, 3— Centralbl Bakteriol Parasitenkd Gavini, F. Transfer of Enterobacter Infektionskr, 37, — Enterobacteriaceae Subcommittee Report.
Int Bull Bacteriol nov. Int J Syst Bacteriol, 39, — Int Bull Bacteriol Gillespie, W. Biochemical mutants of coliform bacilli in Nomencl Taxon, 4, 47— J Pathol Bacteriol, 64, —7. Int Bull Bacteriol Goebel, W. Colanic acid. Nomencl Taxon, 8, 25— Grant, W. Int Bull Bacteriol Exopolysaccharide colanic acid and its occurrence in the Nomencl Taxon, 13, 69— References 41 Grimont, P.
Enterobacter cancerogenus Kauffmann, F. The principles of Urosevic, Dickey and Zumoff , a senior subjective group differentiation within the Enterobacteriaceae by biochemical synonym of Enterobacter taylorae Farmer et al. Res Microbiol, methods. Int Bull Bacteriol Nomencl Taxon, 6, 29— Koser, S. Utilization of the salts of organic acids by the colon- Grimont, P. Cedecea davisae gen. J Bacteriol, 8, — Correlation of citrate utilization by members of the clinical specimens. Int J Syst Bacteriol, 31, — Immunochemistry of the habitat.
J Bacteriol, 9, 59— J Exp Med, , Koser, S. Further observations on utilization of the salts of — J Bacteriol, 11, — Harber, M. Bacterial adherence. Eur J Clin Microbiol, 4, — Krieg, N. Harden, A. Chemical action of bacillus lactis 1. Evidence for a 2,3,butyleneglycol and acetylmethylcarbinol. Proc R Soc, B77, common hapten associated with endotoxin fractions of E. Proc Soc Exp Biol Med, , —6. Hayashi, T. Complete genome sequence of Kwon, S. Int J Syst Bacteriol, 47, with a laboratory strain K Res Apr 27; Lannigan, R.
Wound isolate of Salmonella Hickman, F. J Clin Microbiol, 31, —8. Hinshaw, L. Handbook of endotoxin. Pathophysiology of Lapage, S. Beta-galactosidase and lactose endotoxin. Amsterdam: Elsevier. J Bacteriol, salmonellae. J Clin Pathol, 17, — Lapage, S. Zoonotic Yersinia enterocolitica infection: host range, Enterobacteriaceae. In: Skinner, F.
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Phylogenetic analysis and Oelschlaeger, T. An understanding of antimicrobial resistance mechanisms is important for the logical treatment of GNB infection, especially since the genes that encode antimicrobial resistance are often mobile and can move between strains and species.
Further, there is a likelihood that species that have not acquired certain resistance genes will do so in the future, since resistance genes are often on mobile elements e.
The recent emergence of the colistin resistance gene mcr-1 on a stable, transferrable plasmid is such an example and extremely concerning since polymyxins polymyxin B and E [colistin] are a last line of defense against strains that produce metallo-carbapenemases e.
Confer resistance to many penicillins and first-generation cephalosporins generation cephalo via beta-lactam ring cleavage. These beta-lactamases are inhibited by beta-lactamase inhibitors e. Confer resistance to the same antimicrobials as BSBL plus third- and sometimes fourth-generation cephalosporins and aztreonam.
These are often present on large, transferrable plasmids with linked or associated resistance to the fluoroquinolones levofloxacin and ciprofloxacin hereafter referred to as FQ , trimethoprim-sulfamethoxazole TMP-sulfa , aminoglycosides, and tetracyclines. Although ESBL containing strains are wide-spread in the United States, international travel, particularly to Asia or the Middle East, increases the likelihood of colonization with these strains. Human acquisition of E.
Oral treatment options for ESBL-containing strains are limited to fosfomycin and nitrofurantoin as the best empirical choices for some types of urinary tract infections. These are primarily chromosomal enzymes present in nearly all strains of Enterobacter, Serratia, Citrobacter, Providencia, Morganella, and Proteus vulgaris at low constitutive steady state levels.
Occasionally, strains of E. High-levels of AmpC production can be induced or stably de-repressed mutants by exposure to beta-lactams e. Cefepime fourth-generation cephalosporin may be an option with source control and exclusion of the concomitant presence of an ESBL. FQs, piperacillin-tazobactam, TMP-SMX, tigecycline, and aminoglycosides, if isolates are susceptible in vitro, although clinical data are limited.
Confer resistance to the same antimicrobials as ESBL plus second-generation cephalo and carbapenems. These often present on large, transferrable plasmids with linked or associated resistance to FQ, TMP-sulfa, aminoglycosides, and tetracyclines. The NDM-1 containing plasmid has a broad host range and contains fourteen, linked antimicrobial resistance genes. These genes are becoming increasing prevalent in Enterobacteriaceae on a worldwide basis, particularly in the Middle East and Asia.
The highest prevalence is in K. Automated susceptibility systems may fail to detect carbapenemases, and ertapenem resistance is the most sensitive marker for these systems. A modified Hodge test or polymerase chain reaction PCR testing are more reliable detection systems. Ceftazidime-avibactam is active in vitro against the serine carbapenemases e.
Tigecycline achieves low urine and blood concentrations, raising concerns for treating bacteremia and urinary tract infection UTI. Clinical studies on these agents are uncontrolled, retrospective, use variable regarding dosing and duration of treatment and often simultaneous administration of other antimicrobials. Enterobacteriaceae-exhibiting plasmid-mediated resistance to polymixin and colistin have now been recovered on 5 continents and will likely result is more widespread infection over time.
Although the majority of E. Prior antimicrobial use, recent or ongoing hospital care, and international travel, especially to the Middle East or Asia, increase the likelihood of MDR-strains. For critically-ill patients, amikacin, carbapenems, and and ceftaz-avibactam are the most reliable empirical agents.
Tigecycline and the polymyxins, with or without a second agent, have been used most frequently for these extremely resistant isolates. For critically-ill patients, amikacin, carbapenems and ceftaz-avi are the most reliable empirical agents.
Combination therapy may be beneficial. NNIS reported that All strains possess AmpC beta-lactamases, which can be inducted by exposure to third-generation cephalosporins. Although resistance to tigecycline remains uncommon, Serratia has a narrow susceptibility window and decreased permeability or efflux may confer resistance. Resistance to second- and third-generation cephalosporins, azreonam, TMP-sulfa is variable but increasing.
In healthy humans, commensal and extra-intestinal pathogenic E. In healthy humans, E. By contrast, in hospitalized patients and, to a lesser degree, in residents of long-term-care facilities LTCF , the Enterobacteriaceae emerge as the dominant flora of the oropharynx and skin, which, in turn, leads to an increased incidence of pneumonia and soft-tissue infections by these GNB in these settings.
Serratia and Enterobacter infection may rarely be acquired through a variety of infusates, including medications and blood products. Edwardsiella infections are acquired through freshwater and marine environment exposures and are most common in Southeast Asia. Antimicrobial use, co-morbidities, and extended length of hospital stay are associated with increased colonization with these GNB.
The incidence of infection with these GNB is increasing due to an aging population and increasing antimicrobial resistances. Antimicrobial stewardship programs should be implemented to minimize the development of antimicrobial resistance. Inanimate objects e. Room dedicated instruments for patients on contact precautions are reasonable. Avoiding or minimizing the duration of use of indwelling devices, such as intravascular and urinary catheters and endotracheal tubes, decreases the risk of infection.
When indwelling devices are required, an appropriate protocol should be used for placement, and certain infection control measures may decrease the incidence of subsequent infection and protocols for daily use, evaluation, and removal as soon as possible should be implemented. Presently, there are no vaccines available for the prevention of infection due to Enterobacteriaceae except Salmonella typhi, which is not discussed here.
Prophylaxis should not routinely be used to prevent infection because of the Enterobacteriaceae, except for select patient groups e. Increasing data support the implementation of universal decolonization to prevent infection in ICU patients.
The innate immune system is the critical first line of defense in protecting against infections due to Enterobacteriaceae. Innate immunity e. PAMP are recognized by host defense signaling systems, termed pattern or pathogen recognition receptors PRR , which initiate the innate host defense response. If host tissue damage ensues, these signaling systems are further activated by host-derived motifs e.
Pre-existing antibodies facilitate bacterial clearance and prevent or control infection. However, if the host is immunologically naive, in the absence of antimicrobial treatment, outcome is often decided by the effectiveness of initial innate response. Subsequent activation of the clonal, pathogen-specific adaptive response e.
Therefore, deficiencies or dysfunction of the components of these systems increases the risk and severity of infection. Examples include:. Any cause of neutropenia or neutrophil dysfunction e. Complement dysfunction or deficiency particularly C3, C1qrs, C4, and C2 for encapsulated bacteria and C5,6,7 attack complex. Urinary catheter, endotracheal tube, and skin breaks e.
Splenic dysfunction or splenectomy filters pathogens opsonized with antibodies or complement from the blood has been associated with over-whelming infection due to various pathogens, particularly encapsulated bacterial pathogens. Although S. Hepatic macrophage dysfunction, a decrease in complement production, and portal hypertension have been implicated as contributing causes of spontaneous bacterial peritonitis in cirrhotics.
TLR5 polymorphism results in susceptibility to recurrent cystitis nearly all cases of which are due to E. By contrast to gram-positive pathogens, metastatic spread of the Enterobacteriaceae to bone, joints, and native heart valves is uncommon and, even then, usually requires a predisposing condition, such as:.
A physically abnormal heart value may enable the development of the rare circumstance of native valve endocarditis due to Enterobacteriaceae. An exception to this general rule appears to be a new hypervirulent variant of K. The cell-mediated immune response is generally unimportant in directly protecting against extracellular pathogens excepting its role in antibody development , such as the Enterobacteriaceae, since this host defense requires the recognition of HLA receptors, which are not present on bacteria.
Given the extracellular location of these pathogen and the importance of the innate host response histologically:. The Enterobacteriaceae are capable of producing gas with growth; therefore, gas may be seen at the site of infection, and this usually reflects a severe infection e. The Enterobacteriaceae discussed here cause extra-intestinal infection except Edwardsiella, which can cause extra- and intra-intestinal infection, and perhaps a toxin-producing variant of Klebsiella.
Infections involve nearly every extra-intestinal anatomic site and organ, and new infectious syndromes are emerging e. ExPEC and Klebsiella are the most virulent, being able to cause infection in healthy hosts and cause the majority of infections.
Therefore, a knowledge of clinical presentations combined with predicted antimicrobial resistance will enable optimal early management decisions to be made. The more common clinical syndromes seen with each pathogen are listed below in decreasing order of likelihood along with a few clinical caveats. Commensal E.
Since nearly everyone is colonized with ExPEC, entry, not acquisition is generally the limiting step for infection. This is the most common cause of severe sepsis and septic shock.
Bacteremia can arise from any site of infection. One-half of bacteremias arise in the community, and one-half arise in the hospital. The increasing number of ESBL and carbapenemase-producing ExPEC isolates is concerning, and, given their innate virulence, it is reasonable to anticipate that the incidence of nosocomial ExPEC infections may increase, since antimicrobial resistance is a critical enabler of infection in that setting.
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