The Genus Serratia

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224 F. Grimont and P.A.D. Grimont CHAPTER 3.3.11 was isolated in fecal samples from seven sparrows and unidentified birds. The study involved 90 wild European birds (Müller et al., 1986). About 40% of trapped wild rodents and shrews carried Serratia strains in their gut without any visible sign of infection upon autopsy. The following animal species were found to carry Serratia spp.: 75/180, Apodemus sylvaticus; 7/23, Microtus arvalis; 3/11, Clethrionomys glareolus; 1 /2, Micromys minutus; (rodents); 7/9, Sorex; and 1 /3, Crocidura (shrews) (P. Giraud, F. Grimont, P.A.D. Grimont, unpublished observations). The S. liquefaciens complex (S. liquefaciens, S. proteamaculans and S. grimesii) represented 73 to 94% of all Serratia isolated from the gut of small mammals and from the soil and plants around traps (Table 1). Serratia in Humans The healthy human being does not often become infected by Serratia, whereas the hospitalized patient is frequently colonized or infected. At present, S. marcescens is the only known nosocomial species of Serratia (Table 1). S. liquefaciens and S. rubidaea are occasionally isolated from clinical specimens, but their pathogenic role is not established. The isolation of other Serratia species is anecdotal (Farmer et al., 1985; Gill et al., 1981). Clinically, Serratia infections do not differ from infections by other opportunistic pathogens (von Graevenitz, 1977): respiratory tract infection and colonization of intubated patients (e.g., Cabrera, 1969; von Graevenitz, 1980); urinary tract infection and colonization of patients with indwelling catheters (e.g., Maki et al., 1973); surgical wound infection or superinfection (e.g., Cabrera, 1969); and septicemia in patients with intravenous catheterization or complicating a local infection (osteomyelitis, ocular or skin infections) (e.g., Altemeier et al., 1969). Meningitis, brain abscesses, and intraabdominal infections are more exceptional. The relationship between a Serratia strain and a patient may be in the form of an ephemeral association (in gut or throat, on hands or skin), a long-term colonization (in gut or urinary tract or on the skin), or a localized or generalized infection. The form of relationship might depend on the species or strain of Serratia, the entry route (ingestion, injection, catheter), an ecologic advantage (antibiotic treatment), or the patient’s physiologic status. Patient factors have been reviewed by von Graevenitz (1977). The localization of a hospital-acquired infection is often determined by the kind of instrumentation or intervention done (i.e., the entry route). The same strain may cause a urinary infection in a urology ward, a bronchial colonization in an intensive care unit, and a wound infection in a surgery unit. Five epidemiological situation models can be described (adapted from Farmer et al., 1976): Model 1: “Endogenous,” nonepidemic infections. Sporadic cases of infection are observed that are associated with different Serratia strains. The strains are often susceptible to several antibiotics. The presence of a Serratia strain in feces is not a sufficient proof of the endogenous origin of the infection (Serratia are probably ingested daily with food). There is no prevention mechanism in this epidemiological model. Model 2: Common source epidemics. A single strain (species, biotype, serotype) is found to colonize or infect several patients. Any type of Serratia can be involved, including pigmented biotypes of S. marcescens or environmental species (e.g., S. liquefaciens, S. grimesii, S. rubidaea). The strain is often susceptible to several antibiotics. An investigation can reveal a common infection source such as a breathing machine (the nebulizer and tubings should be sampled), a batch of perfusion or irrigation fluid, or an antiseptic solution. Identification of the source usually allows efficient control of the epidemic. Model 3: Patient-to-patient spread. The Serratia strain involved is typically a multiresistant member of a nonpigmented biogroup of S. marcescens (biogroups A3, A4, A5/8, or TCT). No common source is found although several secondary sources are possible (sink or sponge in patients’ rooms, high rate of fecal carriage). Disinfection of inanimate sources often has no effect on the endemic state. In fact, the reservoir is usually the infected patient, and spread among patients occurs by transient carriage on the hands of nursing or medical staff. Handling of urinary catheters, wound drains, or tracheal tubes of infected (or colonized) patients contaminates the hands of personnel (Maki et al., 1973; Traub, 1972b). Hasty hand washing in an overbusy ward or in the course of an emergency (for example, (in an intensive care unit) allows the transmission of the strain to uninfected patients. These patients are often immunocompromised, treated preventively with broad spectrum antibiotics and subjected to diverse instrumentation. The situation is typically endemic with epidemic peaks in periods of time when the ward is crowded. Transfer of infected or colonized patients from one ward to another or from one hospital to another often results in the spread of the outbreak to other wards or hospitals. Prevention of this epidemiological model is difficult (and in some countries, hopeless). Proper handwashing should be enforced. Some proposed solutions deal with ward/hospital management (e.g., smaller wards, higher nurse/patient ratio, separation of infected from
CHAPTER 3.3.11 The Genus Serratia 225 noninfected patients, and separation of their respective nurses). Model 4: Colonization of the newborn intestinal tract. Typically, an investigation of a case of Serratia infection leads to the discovery that most newborns are colonized by a red-pigmented, drug-susceptible strain of S. marcescens. A common source can be identified (“sterile” water or oily antiseptic solution used to clean the baby’s skin). Contamination may occur on the first day of life. Multiplication of the strain in soiled diapers may show a red discoloration (reddiaper syndrome). Control of this situation is sometimes difficult due to the size of the reservoir. Newly sterilized solutions are quickly contaminated again. Enforcement of handwashing and frequent sterilization (daily or more) of incriminated solutions may be helpful. Model 5: Pseudoepidemics. A drug-sensitive strain of any Serratia species (e.g., S. liquefaciens) is unreproducibly isolated from several patients who show no sign of infection. Investigation of the plastic material used to “sterilely” collect blood occasionally allows the isolation of the environmental strain that contaminated the system (plastic tubing, EDTA, or citrate solution). The above situations are sometimes mixed or less clear. References to reports fitting with the above models can be found in Farmer et al., 1976; Schaberg et al., 1976; von Graevenitz, 1977, 1980; and Daschner, 1980. Properties Relevant to Pathogenicity in Humans Serratia marcescens is generally an opportunistic pathogen causing infections in immunocompromised patients. Among the possible pathogenicity factors found in Serratia strains are the formation of fimbriae, the production of potent siderophores, the presence of cell wall antigens, the ability to resist to the bactericidal action of serum, and the production of proteases. In practice, each strain of the genus Serratia produces one to three different kinds of fimbrial hemagglutinin (HA) (Old et al., 1983). Five types of fimbriae have been observed in serratiae: Type 1 fimbriae: thick, channelled fimbriae of external diameter 8 nm, associated with a mannose-sensitive hemagglutinin (MS-HA) reacting strongly with untanned fowl or guinea pig erythrocytes. The production of MS-HA is increased by serial, static broth cultures in air at either 20, 30, or 37°C. Production of MS-HA was found to be correlated with the ability of S. marcescens cells to attach to human buccal epithelial cells (Ismail and Som, 1982) or to the human urinary bladder surface (Yamamoto et al., 1985). This type of HA was found to be produced by all (Old et al., 1983) or almost all (Franczek et al., 1986) S. marcescens strains, whether environmental or clinical, and in some strains of other Serratia species, except S. plymuthica and S. fonticola. Type 3 fimbriae: thin, non-channelled fimbriae of external diameter 4–5 nm associated with a mannose-resistant hemagglutinin reacting with tannic acid-treated, but not fresh, oxen erythrocytes (MR/K-HA) (Old et al., 1983). MR/K-HA was found to be produced by almost all strains of all Serratia species studied by Old et al. 1983. However, Franczek et al. 1986 found MR/K-HA was more frequently produced by clinical than by environmental strains of S. marcescens. The MR/K-HA of all Serratia species, except S. rubidaea, were immunologically related. MR/K- HA from S. rubidaea was immunologically related to a Klebsiella MR/K-HA (Old et al., 1983). Thin fimbriae associated with a mannose-resistant hemagglutinin reacting with fowl, guinea pig, and horse erythrocytes (type FGH MR/P- HA). This HA was produced by strains from all species except S. plymuthica, S. odorifera, and S. fonticola (Old et al., 1983). The corresponding fimbriae are immunologically related in the different species. Thin fimbriae associated with a mannoseresistant hemagglutinin reacting with fowl erythrocytes only (type F MR/P-HA). This HA was produced by some S. rubidaea strains and was immunologically unrelated to other hemagglutinins (Old et al., 1983). Thick, channelled fimbriae of external diameter 9–10 nm: associated with a mannose-resistant hemagglutinin reacting with fowl erythrocytes only (type F MR/P-HA). This HA was produced by some S. fonticola strains (Old et al., 1983). Nearly all clinical or environmental S. marcescens strains produce potent siderophore(s) capable of scavenging iron from ethylenediamine di-O-hydroxyphenylacetic acid, a chelator with an association constant for ferric iron of 10 33.9 (Franczek et al., 1986). Serratia strains (S. marcescens and S. liquefaciens were tested) generally produce enterobactin (Reissbrodt and Rabsch, 1988) but only rarely produce aerobactin (Martinez et al., 1987). A novel iron (III) transport system named SFU, was evidenced in a S. marcescens strain. In this system, no siderophore production is involved (Zimmermann et al., 1989). At least two patterns of hemolysis were found to be produced by S. marcescens on horse blood: a clear-cut narrow zone of hemolysis under the colony, evoking the action of a cell-bound hemolysin, and a fuzzier, diffusing zone of hemolysis evoking the production of a soluble hemolysin (Grimont and Grimont, 1978b). The
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The Genus Serratia

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