Pathogenic Members of the Intestinal Bacteria Family Enterobacteriaceae

General Concepts

Clinical Manifestations

The genera Escherichia, Klebsiella, Enterobacter, Serratia, and Citrobacter (collectively called the coliform bacilli) and Proteus include overt and opportunistic pathogens responsible for a wide range of infections. Many species are members of the normal abdominal flora. Escherichia coli (E coli) is the most commonly isolated organism in the clinical laboratory.

Enteric Infections: East coli is a major enteric pathogen, peculiarly in developing countries. The principal groups of this organism responsible for enteric disease include the classical enteropathogenic serotypes (EPEC), enterotoxigenic (ETEC), enteroinvasive (EIEC), enterohemorrhagic (EHEC), and enteroggregative (EAEC) strains which are described in detail in Chapter 25.

Nosocomial Infections: Coliform and Proteus bacilli currently crusade 29 pct of nosocomial (hospital-acquired) infections in the United states. In gild of decreasing frequency, the major sites of nosocomial infection are the urinary tract, surgical sites, bloodstream, and pneumonias. This group of nosocomial pathogens are responsible for 46% of urinary tract and 24% of surgical site infections, 17% of the bacteremias, and 30% of the pneumonias. Eastward coli is the premier nosocomial pathogen.

Community-Acquired Infections: E coli is the major cause of urinary tract infections, including prostatitis and pyelonephritis; Proteus, Klebsiella,and Enterobacter species are as well mutual urinary tract pathogens. Proteus mirabilis is the nearly frequent cause of infection-related kidney stones. Klebsiella pneumoniae causes a severe pneumonia; Thou rhinoscleromatis causes rhinoscleroma; and K ozaenae is associated with ozena, an atrophic disease of the nasal mucosa.

Construction, Classification, and Antigenic Types

The coliforms and Proteus are Gram negative bacilli. All genera except Klebsiella are flagellated. Some strains produce capsules. Virulence often depends on the presence of attachment pili (which can be characterized by specific hemagglutinating reactions). Sex activity pili also may exist present. The major classes of antigens used in defining strains are H (flagellar), O (somatic), and K (capsular).

Pathogenesis

E coli enteropathogens have diverse mechanisms for disease production which include different toxins and colonization factors (see Ch. 25 ). Specific serotypes of coliforms and Proteus with particular virulence factors often preferentially infect specific extraintestinal sites. Due east coli bacilli in extraintestinal infections accept soluble and jail cell-bound hemolysins, siderophores, capsules, and adherence pili.

Host Defenses

Coliforms and Proteus species rarely cause extraintestinal disease unless host defenses are compromised. Disruption of the normal intestinal flora past antibiotic therapy may allow resistant nosocomial strains to colonize or overgrow. The peel and mucosae may be breached past affliction, trauma, operation, venous catheterization, tracheal intubation, etc. Immunosuppressive therapy also increases the risk of infection.

Epidemiology

The epidemiology of coliform and Proteus infections involves many reservoirs and modes of manual. The infecting organism may be endogenous or exogenous. Transmission may be direct or indirect; vehicles include hospital nutrient and equipment, intravenous solutions, and the hands of infirmary personnel. Nosocomial strains progressively colonize the intestine and throat with increasing length of hospital stay, resulting in an increased chance of infection.

Diagnosis

The clinical moving-picture show depends on the site of infection; diagnosis relies on culturing the organism and on biochemical and/or serologic identification. A variety of phenotypic (i.e., biotyping, serotyping, antibiograms, bacteriocin and phage typing) and genotypic (i.e., plasmid analysis, RFLP, ribotyping, and PCR) methods are used for epidemiological investigations.

Command

The near constructive style to reduce manual of nosocomial organisms is for all hospital personnel to wash hands meticulously after attending to each patient. Vaccines and hyperimmune sera are not currently available. Various antibiotics are the courage of treatment; drug resistance (frequently multiple) due to conjugative plasmids is a major problem.

Introduction

The Gram-negative bacilli of the genera Escherichia, Klebsiella, Enterobacter, Serratia, Citrobacter,and Proteus(Table 26- 1) are members of the normal abdominal flora of humans and animals and may exist isolated from a diversity of environmental sources. With the exception of Proteus, they are sometimes collectively referred to equally the coliform bacilli because of shared properties, particularly the power of well-nigh species to ferment the saccharide lactose.

Tabular array 26-1

Taxonomy of Selected Coliform Bacilli and Proteus in Human Clinical Specimens.

Many of these microorganisms used to be dismissed as harmless commensals. Today, they are known to be responsible for major health problems worldwide. A limited number of species, including E coli, Chiliad pneumoniae, Enterobacter aerogenes, Enterobacter cloacae, S marcescens,and P mirabilis, are responsible for nigh infections produced by this group of organisms. The increasing incidence of the coliforms, Proteus, and other Gram-negative organisms in diseases reflects in part a better agreement of their pathogenic potential simply more importantly the changing ecology of bacterial disease. The widespread and oftentimes indiscriminate use of antibiotics has created drug-resistant Gram-negative bacilli that readily acquire multiple resistance through transmission of drug resistance plasmids (R factors). Also, evolution of new surgical procedures, health support applied science, and therapeutic regimens has provided new portals of entry and compromised many host defenses.

Clinical Manifestations

Equally opportunistic pathogens, the coliforms and Proteus take advantage of weakened host defenses to colonize and arm-twist a multifariousness of disease states (Fig. 26-one). Together, the many disease syndromes produced past these organisms are among the almost common infections in humans requiring medical intervention.

Figure 26-1

Sites of colonization and extraintestinal disease production by the coliforms and Proteus.

Enteric Infections

The role of Eastward coli equally a major enteric pathogen, especially in developing countries, is discussed in item in Ch. 25.Nevertheless, the different types of E coli associated with enteric infections and which are classified into five groups according to their virulence backdrop are briefly described here: Enteropathogenic (EPEC) serotypes in the past were associated with serious outbreaks of diarrhea in newborn nurseries in the US. They remain an important crusade of acute infantile diarrhea in developing countries. Disease is rare in adults. Enteroinvasive (EIEC) types produce disease resembling shigellosis in adults and children. Enterotoxigenic (ETEC) types are a major cause of traveler's diarrhea, and of infantile diarrhea in developing countries. Enterohemorrhagic East. coli(EHEC) occur largely equally a single serotype (O157:H7) causing sporadic cases and outbreaks of hemorrhagic colitis characterized by encarmine diarrhea. EHEC also may crusade hemolytic uremic syndrome (HUS), an association of hemolytic anemia, thrombocytopenia, and acute renal failure. Enteroaggregative (EAEC) types showroom a characteristic aggregative pattern of adherence and produce persistent gastroenteritis and diarrhea in infants and children in developing countries.

Nosocomial Infections

The etiology of nosocomial infections has markedly changed during past decades. Streptococci were the major nosocomial pathogens in the preantibiotic era. Still, post-obit the introduction and utilize of sulfonamides and penicillin, Staphylococcus aureus became the predominant pathogen in the 1950's. Aerobic gram negative rods gained prominence as nosocomial pathogens with widespread apply of aminoglycosides and get-go generation cephalosporins through the early 1970's. Subsequent widespread employ of broad spectrum cephalosporins was associated with changes in the frequency and etiology of nosocomial infections into the 1980'south with the trend towards certain gram-positive pathogens. For instance, in nosocomial bloodstream infections from 1980 to 1989 marked increases in the incidence of coagulase-negative staphylococci, S. aureus, enterococci, and Candida albicans infections occurred.

The coliforms and Proteus were responsible for 29 percent of nosocomial (hospital-acquired) infections in the United States from 1990 through 1992 based on data from hospitals participating in the National Nosocomial Infections Survey (NNIS) (Table 26-2). Estimates of nosocomial infections in U.s.a. hospitals suggest that about 5 percent of the estimated 40 million annual admissions, or 2 million patients, had at to the lowest degree one nosocomial infection. Thus, the coliforms and Proteus probably are responsible for hospital-acquired infections in approximately 600,000 patients each year. Aside from the enormous toll measured in human life, nosocomial infections prolong the duration of hospitalization by an boilerplate of 4 days and increase the cost of medical intendance by $4.five billion a yr in 1992 dollars.

Table 26-2

Frequency of Selected Pathogens Causing Nosocomial Infections ^a.

The highest numbers of nosocomial infections in the NNIS occur in surgical and medicine services. Among surgical patients, highest rates of nosocomial infections occur with surgery on the breadbasket (21%) and bowel (19%), craniotomies (18%), coronary artery bypass graft procedures (11%) and other cardiac surgery (ten%). High rates besides are observed with burn down (fifteen%) and high-risk nursery patients (14%). In society of decreasing frequency, the major sites of nosocomial infection are the urinary tract, surgical sites, bloodstream, and lower respiratory tracts. The coliforms and Proteus were responsible for 46% of urinary tract and 24% of surgical site infections, 17% of the bacteremias, and 30% of the pneumonias from 1990 through 1992. Escherichia coli, the predominant nosocomial pathogen, is the major cause of infection in the urinary tract and is common in other body sites. Staphylococcus aureus and Pseudomonas aeruginosa are currently the most common pathogens in nosocomial pneumonias, followed by Enterobacter and Klebsiella. Coagulase-negative staphylococci have replaced E coli equally the predominant pathogen in primary bloodstream infections. The major causes of surgical site infections are S aureus, coagulase- negative staphylococci, and enterococci.

Other coliform bacilli and Proteus have been incriminated in various hospital-acquired infections. Klebsiella, Enterobacter,and Serratia species are frequent causes of bacteremia at some medical centers and also are oft involved in infections associated with respiratory tract manipulations, such as tracheostomy and procedures using contaminated inhalation therapy equipment. Klebsiella and Serratia species commonly cause infections post-obit intravenous and urinary catheterization and infections complicating burns. Proteus species ofttimes cause nosocomial infections of the urinary tract, surgical wounds, and lower respiratory tract. Less often, Proteus species cause bacteremia, most ofttimes in elderly patients. A series of nationwide outbreaks of bacteremia (1970 to 1971 and 1973), caused by contaminated commercial fluids for intravenous injections, involved Enterobacter cloacae, Enterobacter agglomerans,and C freundii.

The role of Citrobacter species in man illness is not every bit bully equally that of the other coliforms and Proteus. Citrobacter freundii and C diversus (C koseri) have been isolated predominantly equally superinfecting agents from urinary and respiratory tract infections. Citrobacter septicemia may occur in patients with multiple predisposing factors; Citrobacter species too cause meningitis, septicemia, and pulmonary infections in neonates and immature children. Neonatal meningitis produced past C diversus, while uncommon, is associated with a very high frequency of brain abscesses, death, and mental retardation in survivors. Although E coli and group B streptococci cause near cases of neonatal meningitis, the most common cause of brain abscesses in neonatal meningitis is P mirabilis.

Immunocompromised patients often develop non-hospital-acquired infections with coliforms. For instance, group B streptococci and E coli are responsible for most cases of neonatal meningitis, with the latter accounting for about 40 percent of cases. Infections seen in cancer patients with solid tumors or cancerous blood diseases frequently are caused past E coli, Klebsiella, Serratia,and Enterobacter species. Such infections often accept lethal class. Individuals who are immunosuppressed by therapy (e.g., cancer patients or transplant recipients) or by congenital defects of the allowed system may develop Klebsiella, Enterobacter, and Serratia infections. Many boosted factors such as diabetes, trauma, and chronic lung illness may predispose to infection by coliforms and other microbes.

Community-Acquired Infections

The coliform organisms and Proteus species are major causes of diseases acquired outside the hospital; many of these diseases eventually crave hospitalization. Escherichia coli causes approximately 85 percent of cases of urethrocystitis (infection of the urethra and bladder), about 80 per centum of cases of chronic bacterial prostatitis, and up to xc percent of cases of acute pyelonephritis (inflammation of the renal pelvis and parenchyma). Approximately one half of females have had a urinary tract infection by their late twenties due to E coli from their fecal flora. Proteus, Klebsiella, and Enterobacter species are among the other organisms most frequently involved in urinary tract infections. Proteus, particularly P mirabilis, is believed to exist the nearly common cause of infection-related kidney stones, one of the almost serious complications of unresolved or recurrent bacteriuria.

Klebsiella was first recognized clinically every bit an agent of pneumonia. Klebsiella pneumoniae accounts for a pocket-sized percentage of pneumonia cases; however, extensive damage produced by the organism results in high case fatality rates (up to 90 percentage in untreated patients). Klebsiella rhinoscleromatis is the agent of rhinoscleroma, a chronic destructive granulomatous disease of the respiratory tract that is endemic in Eastern Europe and Cardinal America. Klebsiella ozaenae, a rare crusade of serious infection, is classically associated but with ozena, an atrophy of nasal mucosal membranes with a mucopurulent discharge that tends to dry out into crusts; however, recent studies betoken that the organism may cause various other diseases including infections of the urinary tract, soft tissue, eye ear, and claret.

Distinctive Properties

Structure and Antigens

The generalized construction and antigenic composition of coliform bacilli, as well as of Proteus and other members of the family Enterobacteriaceae, are depicted schematically in Figure 26-2. A more detailed figure of the construction is presented in Affiliate 2. The major antigens of coliforms are referred to equally H, 1000, and O antigens. The coliforms and Proteus are divided into serotypes on the basis of combinations of these antigens; different serotypes may have different virulence backdrop or may preferentially colonize and produce disease in item body habitats. The H antigen determinants are flagellar proteins. Escherichia coli, Enterobacter, Serratia, Citrobacter,and Proteus organisms are peritrichous (i.e., they have flagella that grow from many places on the cell surface). Klebsiella species are nonmotile and nonflagellated and thus have no H antigens.

Figure 26-ii

Construction and antigenic composition of coliforms and Proteus species.

Some strains of coliform and Proteus species take pili (fimbriae). Pili are associated with adhesive backdrop and, in some cases, are correlated with virulence. Different pilial colonization factors by and large are detectable as hemagglutinins that can be distinguished by the type of erythrocyte agglutinated and by the susceptibility of the hemagglutination to inhibition past the saccharide mannose. Sex pili, which have receptors for 'male person' specific bacterial viruses and are genetically adamant by extrachromosomal plasmids, are important in coliform ecology and in the epidemiology of diseases produced by coliforms and Proteus species in that sex pili are involved in genetic transfer past conjugation (e.grand., chromosome-mediated and plasmid-mediated drug resistances or virulence factors).

Major Surface Antigens

One thousand antigens (capsule antigens) are components of the polysaccharide capsules. Certain K antigens (e.thousand., K88 and K99 of Due east coli) are hair-like proteins. The K antigens often cake agglutination past specific O antisera. In the by, 1000 antigens routinely were differentiated into A, L, and B groups on the basis of differences in their lability to heat; nevertheless, these criteria are discipline to difficulties that make the distinction tenuous. Some Citrobacter serotypes produce Vi (virulence) antigen, a K antigen likewise establish in Salmonella typhi. Species of Proteus, Enterobacter,and Serratia apparently take no regular K antigens. Yet, the K antigens are important in the pathogenesis of some coliforms. A lengthened slime layer of variable thickness (the Yard antigen) also may be produced but, unlike the K antigens, it is nonspecific and is serologically cross-reactive among different organisms.

The outer membrane of the bacterial cell wall of these species contains receptors for bacterial viruses and bacteriocins (plasmid-encoded, antibiotic like bactericidal proteins called colicins in E coli that are active against the same or closely related species). The outer membrane also contains lipopolysaccharide (LPS), of which the lipid A portion is endotoxic and the O (somatic) antigen is serotype specific. The serologic specificity of the O antigens is based on differences in sugar components, their linkages, and the presence or absence of substituted acetyl groups. Loss of the O antigen by mutation results in a smooth-to-crude transformation, which oftentimes involves changes in colony type and saline agglutination, as well as loss of virulence . Sure strains of P vulgaris (OX-19, OX-2, and OX-K) produce O antigens that are shared past some rickettsiae. These Proteus strains are used in an agglutination examination (the Weil-Felix test) for serum antibodies produced against rickettsiae of the typhus and spotted fever groups (see Ch. 38).

Toxins

Enterotoxigenic strains of Klebsiella, Enterobacter, Serratia,Citrobacter, and Proteus likewise have been isolated from infants and children with acute gastroenteritis. The enterotoxins of at least some of these organisms are of the heat-labile and rut-stable types and have other backdrop in common with the E coli toxins (see Ch. 25). However, the importance of the coliforms and Proteus, other than Eastward coli, in enteric infections is questionable

Pathogenesis

The process of disease production by coliforms is, in many cases, poorly understood. Product of disease by coliforms or Proteus species in extraintestinal sites often involves specific serotypes of the organisms and special virulence factors. For example, respiratory tract infections by K pneumoniae predominantly involve capsular types 1 and 2, whereas urinary tract infections oft involve types eight, 9, 10, and 24. Similarly, simply a few polysaccharide K antigens (types one, two, iii, 5, 12, and 13) of Due east coli are institute with high frequency in urinary tract and other extraintestinal infections. These observations suggest that different serotypes may have specific pathogenicities. An culling explanation is that such strains may but be the near prevalent types in the normal gut flora.

There is practiced evidence for specific pathogenicity in E coli strains that cause extraintestinal infections (Table 26-3). Approximately 80 percent of E coli isolates involved in neonatal meningitis carry the K1 antigen, a fact owing, at least in function, to the higher resistance to phagocytosis of K1-positive strains. Sure O antigens (O7 and O18) are institute in combination with K1, usually in strains that are isolated from cases of neonatal bacteremia and meningitis and that evidence increased resistance to the bactericidal furnishings of serum complement. Interestingly, the E coli K1 antigen, composed of neuraminic acrid, shows immune cross-reactivity with the group B meningococcal polysaccharide sheathing.

Table 26-three

Virulence Factors of E coli Isolates from Extraintestinal Infections.

Escherichia coli strains isolated from extraintestinal infections oftentimes possess a number of backdrop not normally constitute in random fecal isolates. These include product of soluble and prison cell-bound hemolysins, the colicin V plasmid, product of the siderophores aerobactin and enterochelin, and special pilial antigens for adherence to target cells. The hemolysin kills host cells and makes fe more bachelor by releasing hemoglobin-spring iron from lysed ruby-red cells. To strip iron from the host iron-bounden proteins ( transferrin and lactoferrin), E coli produces siderophores of both the hydroxamate (aerobactin) and phenolate (enterochelin) types. Common or type 1 pili may mediate adherence to float cells; P-pili are virulence factors for strains causing pyelonephritis; S-pili, which recognize O-linked sialo-oligosaccharides of glycophorin A, are associated with meningitis and urinary tract infections. Certain afimbrial adhesions and outer membrane proteins also have been associated with urinary tract infections.

The enzyme urease, produced by Proteus, and to a lesser extent by Klebsiella species, is thought to play a major role in the production of infection-induced urinary stones. Urease hydrolyzes urea to ammonia and carbon dioxide. Alkalinization of the urine by ammonia can cause magnesium phosphate and calcium phosphate to become supersaturated and crystallize out of solution to form, respectively, struvite and apatite stones. Bacteria inside the stones may be refractory to antimicrobial therapy. Large stones may interfere with renal role. The ammonia produced by urease action may also harm the pithelium of the urinary tract.

Except in cases of bacteremia and other systemic infection, there is little testify that endotoxin plays a office in most coliform and Proteus diseases. Humans with coliform bacteremia show many of the typical furnishings of endotoxin, including fever, depletion of complement, release of inflammatory mediators, lactic acidosis, hypotension, vital organ hypoperfusion, irreversible shock, and death.

Host Defenses

It cannot be overemphasized that coliforms (except for E coli in enteric diseases) and Proteus species are unlikely to crusade illness unless the local or generalized host defenses neglect in some way. The normal gastrointestinal flora, which includes Due east coli and, frequently, other coliforms and Proteus species in modest numbers, is important in preventing disease through bacterial competition. Prolonged antibiotic therapy compromises this defense mechanism by reducing susceptible components of the normal flora, permitting nosocomial coliform strains or other bacteria to colonize or overgrow.

The organisms may breach anatomic barriers through 3rd-caste burns, ulcers associated with solid tumors of the skin and mucous membranes, intravenous catheters, and surgical or instrumental procedures on the biliary, gastrointestinal, and genitourinary tracts. The lungs may be violated by instrumentation, as in tracheal intubation, or even by aerosols from contaminated nebulizers or humidifiers, which deport organisms to the terminal alveoli.

Corticosteroid administration, radiotherapy, and the increased steroid levels associated with pregnancy tend to subtract host control over infections (eastward.g., by depressing the immune response). Cytotoxic drugs likewise are immunosuppressive. Cancer-or drug-induced neutropenia is an important predisposing factor in bacteremia. Debilitated tissue or foreign bodies may be a source of organisms and may also shelter the organisms from phagocytes and antimicrobial factors.

The interaction of multiple predisposing factors frequently determines the clinical form and event of coliform or Proteus infection. For instance, the mortality of bacteremia increases progressively when the underlying disease (due east.g., cancer or diabetes) is rated as nonfatal, ultimately fatal (expiry within 5 years), or rapidly fatal (decease within one year). Similarly, coliform and Proteus infections commonly are more severe in the very old and very young.

Epidemiology

The epidemiology of coliform and Proteus infections is complex and involves multiple reservoirs and modes of transmission. Klebsiella, Enterobacter, Serratia, Citrobacter, and Proteus species live in h2o, soil, and occasionally food and, in many cases, form part of the intestinal flora of humans and animals. Escherichia coli is believed not to exist gratuitous living, and its presence in environmental samples is taken equally indicating recent fecal contamination. In fact, water quality is determined by the presence of the rapid lactose fermenting E coli, Klebsiella, and Enterobacter (coliform counts ) and E coli(fecal coliform counts) using special selective media.

Coliform and Proteus organisms causing infection may be exogenous or endogenous. While nigh nosocomial infections appear to arise from endogenous flora, studies of hospitalized adults and infants take shown that the abdominal tract is progressively colonized by nosocomial coliforms with increasing length of hospitalization. Patients being treated with antibiotics, severely sick patients, and (probably) infants are more probable to be colonized, and other sites of colonization such every bit the olfactory organ and pharynx may be important in such patients. Colonized patients have a higher risk of nosocomial infection than patients who are non colonized.

The bacteria may be acquired indirectly via various vehicles or past straight contact . A multifariousness of vehicles have been implicated in the spread of nosocomial pathogens. For example, Klebsiella, Enterobacter, and Serratia species accept all been recovered in large numbers from hospital food, specially salads, with the infirmary kitchen being a chief source . An outbreak of urinary tract infections due to multiply drug-resistant S marcescens was associated with contaminated urine- measuring containers and urinometers. Serious outbreaks or individual cases of bacteremia due to coliforms have been associated with extrinsic contagion of intravenous fluids or caps during manufacture and with extrinsic contamination of intravenous fluids and assistants sets in the hospital environment. Other medical devices and medications take served as vehicles for the spread of nosocomial pathogens. Occasionally, transmission may be via members of the infirmary staff who are colonized with nosocomial pathogens in the rectum or vagina or on the easily; however, passive carriage on the hands of medical personnel constitutes the major fashion of transmission.

Certain backdrop of the coliforms may be important in the epidemiology of hospital-acquired infections. Coliform leaner other than E coli frequently are establish in tap h2o or even distilled or deionized water. They may persist or actively multiply in h2o associated with respiratory therapy or hemodialysis equipment. Klebsiella, Enterobacter, and Serratia species, similar Pseudomonas species, may exhibit increased resistance to antiseptics and disinfectants. The same group of coliforms has a selective ability over other common nosocomial pathogens (including E coli, Proteus species, Pseudomonas aeruginosa,and staphylococci) to proliferate rapidly at room temperature in commercial parenteral fluids containing glucose.

Diagnosis

Because the coliforms and Proteus can cause many types of infection, the clinical symptoms rarely allow a diagnosis. Culturing and laboratory identification are normally required. Selected characteristics that are useful in the differentiation of coliform bacilla and Proteus species found in human clinical specimens are shown in Table 26-4. The organisms have uncomplicated nutritional requirements and abound well on mildly selective media commonly used for members of the Enterobacteriaceae, just not on some moderately and highly selective enteric plating media (Salmonella-Shigella, bismuth sulfite, and brilliant green agar). Extraintestinal specimens such as urine, purulent textile from wounds or abscesses, sputum, and sediment from cerebrospinal fluid should be plated for isolation on blood agar and a differential medium such as MacConkey or eosin-methylene blue agar. The finding of more than than x⁵ organisms/ml in clean voided midstream urine is often taken every bit 'significant bacteriuria.' However, in acutely symptomatic females and with other types of specimens (i.e., those obtained past catheterization or suprapubic aspiration) from either sex activity, a more advisable threshold, particularly in the presence of pus cells and the absenteeism of epithelial cells, might be more than 10^two colonies of a known uropathogen/ml. Because urine is a expert growth medium for many microbes, specimens should be refrigerated (4°C) if transport to the laboratory is delayed longer than xxx minutes, unless a urine send container with preservative is used.

Tabular array 26-4

Differentiation of Coliform Bacilli and Proteus Constitute in Human Clinical Specimens.

Isolation of certain coliforms or Proteus species from fecal specimens may be facilitated by adding a moderately selective medium such as xylose-lysine-desoxycholate (XLD) or Hektoen enteric agar. Use of tetrathionate or selenite goop for enrichment of enterotoxigenic strains from feces is non recommended because both media inhibit diverse genera of coliforms. The strong (Due east coli, K pneumoniae, Enterobacter aerogenes) and occasionally the tedious or weak (Serratia, Citrobacter) lactose-fermenting coliforms produce characteristic pigmented colonies on the enteric plating media. A striking characteristic of Proteus species is their propensity to swarm over the surface of most plating media, making the isolation of other organisms in mixed cultures difficult. The swarming growth appears every bit a speedily spreading thin motion-picture show, sometimes with changing patterns of whirls and bands. Sorbitol MacConkey agar is useful for screening EHEC (commonly E. coli O157:H7) on which sorbitol-negative colonies are nonpigmented and considered suspicious for the organism. Unless the physician specifically requests that the laboratory look for the possibility of Eastward coli as an enteropathogen, tests for pathogenic strains, including toxin assays, serotyping, and serogrouping, will non be done.

In cases of suspected bacteremia, replicate bottles (one cultured aerobically, the other anaerobically) containing 25 to 100 ml of appropriate medium with anticoagulant (east.1000., sodium polyanetholesulfonate) are inoculated with 10-ml portions of blood. Information technology is normally necessary to accept multiple specimens, both before and after antibiotic therapy is started. It is important to take specimens after antibody treatment is started so that therapeutic failure can exist recognized while the bacteremia may still be amendable to more ambitious medical or surgical treatment.

All of the coliforms and Proteus species are Gram negative, facultative anaerobic, non-spore- forming rods that are typically motile, except for Klebsiella, which is nonmotile. The oxidase exam is negative, and nitrates are reduced to nitrites. Proteus species and all coliforms ferment glucose, only fermentation of other carbohydrates varies. Lactose usually is fermented rapidly by Escherichia, Klebsiella and some Enterobacter species and more slowly by Citrobacter and some Serratia species. Proteus, unlike the coliforms, deaminates phenylalanine to phenylpyruvic acrid, and it does non ferment lactose. Typically, Proteus is speedily urease positive. Some species of Klebsiella, Enterobacter, and Serratia produces a positive urease reaction, just they do then more slowly. A bombardment of tests for biochemical properties is required to identify the coliforms and Proteus to the species level. Commercial identification systems are now widely used by most US clinical laboratories and consist of 'kits' or miniaturized biochemical tests which are read manually (e.yard., API-20E and BBL Crystal) or automatically (eastward.thou., Vitek or MicroSCAN).

The coliforms are characterized by corking antigenic diversity caused past various combinations of specific H, K, and O antigens. For case, approximately l H, xc One thousand, and 160 O antigens have been identified among various strains of E coli. In dissimilarity, Klebsiella, with no H antigens, has 10 O antigens and approximately 80 K antigens. Serologic identification of the coliforms and Proteus species, commonly by reference laboratories, is an extremely important epidemiologic tool. Similarly, other phenotying methods including biotyping (biochemical profiles), antibiograms (patterns of resistance to antimicrobal agents), and bacteriocin and phage typing have been widely used in epidemiologic studies, particularly of multiresistant isolates of coliforms and Proteus. Recently, genotyping methods such equally plasmid profiles (determined past agarose gel electrophoresis), RFLP (restriction fragment link polymorphism) of total DNA, pulsed-field gel electrophoresis, targeted assay of Deoxyribonucleic acid polymorphism, ribotype, and arbitrarily primed PCR (polymerase chain reaction) have been used in epidemiological studies. In hospital-acquired infections, for example, the same or a modest number of serologic or plasmid types suggests single sources of infection. The finding of multiple serotypes or plasmid profiles suggests multiple sources of infection or endogenous infections.

Control

Prevention of coliform and Proteus infections, especially those that are infirmary caused, is difficult and possibly incommunicable. Sewage treatment, h2o purification, proper hygiene, and other control methods for enteric pathogens volition reduce the incidence of E coli enteropathogens. However, these command measures are rarely available in less developed regions of the world. Chest-feeding is an effective means of limiting outbreaks of enteropahogens in infants. Aggressive infection command committees in hospitals can exercise much to reduce nosocomial infections through identification and control of predisposing factors, education and training of hospital personnel, and limited microbial surveillance. Except for investigations of potential outbreaks, routine culturing of personnel, patients, and the environment is not warranted. Selective decontamination of the digestive tract with a suitable nonabsorbable antimicrobial regimen may be useful during outbreaks acquired by nosocomial coliforms and Proteus. Meticulous manus washing afterward each patient contact a highly constructive means of reducing the transmission of nosocomial pathogens (Fig. 26-3)is infrequently or poorly performed past some infirmary personnel. In a study conducted in an intensive care unit following an educational campaign on the importance of manus washing, the compliance was 17 percent for physicians, 100 per centum for nurses, 82 percent for respiratory technicians, and 88 percent for diagnostic services personnel.

Figure 26-3

Major routes of manual and prevention of spread of nosocomial pathogens.

Agile or passive immunization against coliforms and Proteus species is non practiced. However, vaccines or hyperimmune sera for the six mutual Gram negative pathogens (Eastward coli, Klebsiella, Enterobacter, Serratia, Pseudomonas aeruginosa,and Proteus) probably would have a major impact on morbidity and bloodshed from nosocomial infections. In a trial, the mortality was reduced markedly in a group of patients with Gram-negative bacteremia who had been given antiserum against a mutant E coli with an exposed lipopolysaccharide cadre.

Ampicillin, sulfonamides, cephalosporins, tetracycline, trimethoprim-sulfamethoxazole, nalidixic acid, ciprotloxacin, and nitrofurantoin have been useful in treating urinary tract infections by coliforms and Proteus species. Gentamicin, amikacin, tobramycin, ticarcillin/clavulate, imipenem, aztreonam, and a variety of third-generation cephalosporins may exist effective for systemic infections; however, laboratory tests for drug susceptibility are essential. For example, resistence of E coli to ampicillin, and showtime generation cephalosporins is increasing rapidly to the extent that they can no longer be considered primary drugs of choice in empirical treatment of urinary tract infections. Likewise, emergence of coliforms with chromosomal or plasmid-encoded extended spectrum B-lactamase action is causing global problems with resistance to third generation cephalosporins. Some coliforms have multiple resistance due to the presence of R plasmids transmissible past conjugation. Conjugative resistance plasmids permit the transfer of resistance genes amongst species and genera that unremarkably do not exchange chromosomal Deoxyribonucleic acid (Ch. 5). In some cases, resolution of the infection may require drainage of abscesses or other surgical intervention.

Measures unremarkably used to control epidemics of antibody resistant Gram-negative bacilli have included: (1) endmost the unit to new admissions until control of the outbreak is underway; (two) reinforcing hand-washing practices; (3) gown and glove isolation, frequently combined with isolation of patients in separate quarters; and (4) restricting the utilise of the antibiotic to which the offending clone is resistant.

References

1. Beck-Sague C, Villarino Eastward, Giuliano D. et al. Infectious diseases and death among nursing home residents: results of surveillance in xiii nursing homes. Infect Control Hosp Epidemiol. 1994;15:494. [PubMed: 7963443]

2. Bergeron MG. Treatment of pyelonephritis in adults. Med Clin North Amer. 1995;79:619. [PubMed: 7752732]

3. Bingen, E: Applications of molecular methods to epidemiologic investigations of nosocomial infections in a pediatric hospital. Infect Control Hosp Epidemiol fifteen, 1994 . [PubMed: 7963442]

4. Bodey, GP, Elting LS, Rodriguez Southward, Hernandez M. Klebsiella bacteremia: a 10-yr review in a cancer institution. Cancer. 1989;64:2368. [PubMed: 2804929]

5. Brun-Buisson C, Legrand, P Can topical and nonabsorbable antimicrobials foreclose cantankerous manual of resistant strains in ICUs? Infect Command Hosp Epdemiol. 1994;fifteen:447. [PubMed: 7963436]

6. Conley JM, Loma S, Ross J. et al. Handwashing practices in an intensive care unit: the effects of an educational program and its relationship to infection rates. Am J Infect Control. 1989;17:330. [PubMed: 2596730]

7. Emori GT, Gaynes RP. An overview of nosocomial infections, including the role of the microbiology laboratory. Clin Microbiol Rev. 1993;6:428. [PMC free article: PMC358296] [PubMed: 8269394]

8. Foxman, B, Zhang L, Palin Thousand. et al. Bacterial virulence characteristics of Escherichia coli isolates from first-time urinary tract infection. Infect Dis. 1995;171:1514. [PubMed: 7769286]

9. Gordon MC, Hankins GDV. Urinary tract infections and pregnancy. Comp Ther. 1989;15:52. [PubMed: 2676334]

10. Johnson JR, Stamm Nosotros. Urinary tract infections in women: diagnosis and treatment. Ann Intern Med. 1989;111:906. [PubMed: 2683922]

11. Horan TC, Culver DH. et al. Nosocomial infections in surgical patients in the U.s.a., January 1986-June 1992. Infect Control Hosp Epidemiol. 1993;14:73. [PubMed: 8440883]

12. Lipsky BA. Urinary tract infections in men: epidemiology, pathophysiology, diagnosis, and treatment. Ann Intern Med. 1989;110:138. [PubMed: 2462391]

13. Marshall JC, Christou NV, Horn R, Meakins JL. The microbiology of multiple organ failure: the proximal alimentary canal as an occult reservoir of pathogens. Arch Surg. 1988;123:309. [PubMed: 3341911]

14. Mobley HLT, Chippendale GR. Hemagglutinin, urease, and hemolysin production by Proteus mirabilis. J Infect Dis. 1990;161:525. [PubMed: 2179424]

15. Morris JG, Lin FYC, Morrison CB. et al. Molecular epidemiology of neonatal meningitis due to Citrobacter diversus: a study of isolates from hospitals in Maryland. J Infect Dis. 1986;154:409. [PubMed: 3734491]

16. Nyström B. Bear on of handwashing on mortality in intensive care: examination of the evidence. Infect Control Hosp Epidemiol. 1994;15:435. [PubMed: 7963433]

17. Saito H, Elting L, Bodey GP, Berky P. Serratia bacteremia: review of 118 cases. Rev Infect Dis. 1989;11:912. [PubMed: 2602776]

18. Schaberg, DR, Culver, DH, Gaynes, RP Major trends in the microbial etiology of nosocomial infection. Amer Med. 1991;91(suppl 3B):72S. [PubMed: 1928195]

19. Stamm, Nosotros Catheter-associated urinary tract infections: epidemiology, pathogenesis, and prevention. Amer Med. 1991;91(suppl 3B):65S. [PubMed: 1928194]

20. Swartz MN. Infirmary-caused infections: diseases with increasingly express therapies. Proc. Natl. Acad. Sci. The states. 1994;91:2420. [PMC free article: PMC43382] [PubMed: 8146133]

21. Toltzis P, Blumer JL. Antibiotic-resistant gram-negative bacteria in the disquisitional care setting. Pediatric Clin North Amer. 1995;42:687. [PubMed: 7761147]

22. van Saene HKF, Nunn AJ. et al. Viewpoint: survival benefit past selective decontamination of the digestive tract (SDD). Infect Control Hosp Epidemiol. 1994;15:443. [PubMed: 7963435]

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Source: https://www.ncbi.nlm.nih.gov/books/NBK8035/

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