Serratia

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Background

Serratia species are opportunistic gram-negative bacteria classified in the tribe Klebsielleae and the large family Enterobacteriaceae. Serratia are widespread in the environment, but are not a common component of the human fecal flora.[1]

Serratia marcescens is the primary pathogenic species of Serratia.[2] Rare reports have described disease resulting from infection with Serratia plymuthica,[3] Serratia liquefaciens,[4] Serratia rubidaea,[5] Serratia odorifera, and Serratia fonticola.[6]

Some strains of S marcescens are capable of producing a pigment called prodigiosin, which ranges in color from dark red to pale pink, depending on the age of the colonies. The chemical structure of prodigiosin has been unveiled.[7] Serratia are capable of thriving in diverse environments, including water, soil, and the digestive tracts of various animals.[8] S marcescens has a predilection for growth on starchy foodstuffs, where the pigmented colonies are easily mistaken for drops of blood.

In 1819, Bartolomeo Bizio, a pharmacist from Padua, Italy, discovered and named S marcescens when he identified the bacterium as the cause of a miraculous bloody discoloration in a cornmeal mush called polenta. Bizio named Serratia in honor of an Italian physicist named Serrati, who invented the steamboat, and Bizio chose marcescens (from the Latin word for decaying) because the bloody pigment was found to deteriorate quickly.[9]

Since 1906, physicians have used S marcescens as a biological marker for studying the transmission of microorganisms because, until the 1950s, this bacterium was generally considered a harmless saprophyte. Only since the 1960s has S marcescens been recognized as an opportunistic pathogen in humans.[10]

Derivatives of prodigiosin have recently been found to have immunosuppressive properties and antitumor activity in vivo[11, 12] and are also currently being considered as a candidate treatment for Chagas disease.[13]

Pathophysiology

It appears that at least some Serratia isolates interfere with macrophage function or viability.[14] In the hospital, Serratia species tend to colonize the respiratory and urinary tracts, rather than the gastrointestinal tract, in adults.

Serratia infection is responsible for about 2% of nosocomial infections of the bloodstream, lower respiratory tract, urinary tract, surgical wounds, and skin and soft tissues in adult patients. An outbreak of S marcescens bloodstream infections was identified in patients receiving contaminated bags of parenteral nutrition.[15] Outbreaks of S marcescens meningitis, wound infections, and arthritis have occurred in pediatric wards.

Serratia infection has caused endocarditis and osteomyelitis in people addicted to heroin.

Cases of Serratia septic arthritis have been reported in patients receiving intra-articular injections, individuals with joint trauma, and patients with intravascular devices or who are undergoing intravascular procedures.

An outbreak of meningitis caused by S marcescens in patients who had undergone spinal anaesthesia for caesarean section has been ascribed to contaminated medications used for this purpose.[16]

Epidemiology

Frequency

United States

Serratia species are responsible for 1.4% of nosocomial bloodstream infections.

International

The yearly incidence of Serratia bacteremia is 1.03 per 100,000 population, with 47% of episodes having their onset in the community.[17]

The prevalence of Serratia species as a cause of nosocomial infections is diminishing, but these bacteria are still able to cause hospital outbreaks, especially in intensive care units.

In the University Hospital of Heraklion, Crete, S marcescens was isolated in 65 (84.4%) of 77 patients with Serratia infection; the remaining 12 patients had infection with a nonmarcescens Serratia species. The most frequently observed infections were respiratory tract infection (32.5%) and keratitis/endophthalmitis (20.8%).[18]

Mortality/Morbidity

In a population-based study of Serratia bacteremia, the 7-day and 6-month mortality rates were 5% and 37%, respectively.[17]

Serratia meningitis and Serratia endocarditis carry a high mortality rate.

Serratia species cause less than 6% of cases of hospital-acquired bacterial pneumonia.[19]

S marcescens causes 11% of burn-related surgical wound infections.[20]

Sex

Most (68%) episodes of Serratia bacteremia occur in males.[17]

Age

Outbreaks of Serratia infection occur in neonates and infants. In adults, most Serratia infections are isolated, but occasional nosocomial outbreaks occur.

History

Sepsis

Patients with Serratia sepsis may present with fever, chills, shock, and respiratory distress.

Urinary tract infection

Approximately 30-50% of patients with Serratia urinary tract infections are asymptomatic. Symptoms may include fever, frequent urination, dysuria, pyuria, or pain upon urination.

In 90% of cases, patients have a history of recent surgery or instrumentation of the urinary tract.

Important risk factors for with Serratia urinary tract infections include diabetes mellitus, urinary tract obstruction, and renal failure.

Respiratory tract infection

Patients with Serratia respiratory tract infection are usually are colonized with Serratia species after instrumentation (eg, ventilation, bronchoscopy), especially those with chronic obstructive pulmonary disease.

Serratia pneumonia may develop, but this is rare. Patients with pneumonia may have fever, chills, productive cough (sometimes with pseudohemoptysis[21, 22] ), hypotension, dyspnea, and/or chest pain.

Meningitis or cerebral abscess

Serratia meningitis or cerebral abscesses may develop in premature children and neonates with prior sepsis. Patients who have experienced head trauma or have undergone neurosurgery,[23] lumbar puncture, or even epidural injections are at risk of developing meningitis or cerebral abscess.

The symptoms are those of gram-negative meningitis (eg, headache, fever, vomiting, stupor, coma).

Intra-abdominal infections

Patients with Serratia intra-abdominal infections may present with biliary drainage, hepatic abscess, pancreatic abscess, and peritoneal exudate. Serratia peritonitis can complicate peritoneal dialysis.[24]

Osteomyelitis and arthritis

Serratia osteomyelitis and arthritis may develop following hematogenous spread in persons who are addicted to intravenous drugs or may be caused exogenously by surgery, open trauma, or intra-articular injection. S marcescens osteomyelitis is a common presentation of chronic granulomatous disease in infancy.[25]

Endocarditis

Patients with Serratia endocarditis may present with fever, petechiae, and, occasionally, embolic complications (eg, stroke, arterial emboli).

Ocular infections

Patients with Serratia ocular infections present with keratitis or endophthalmitis.

Soft-tissue infections

Patients with Serratia soft-tissue infections may have surgical scars, cellulitis, phlebitis, or skin infections.

Otitis media

Patients with Serratia otitis media present with earaches, hearing loss, and ear discharge.

Parotitis

Serratia parotitis is rare.

Physical

Pink hypopyon in the absence of hyphema may suggest S marcescens endophthalmitis.[26]

Breast milk can turn pink with Serratia postpartum mastitis.[27, 28]

Causes

Sepsis or bacteremia

The main risk factor for Serratia sepsis/bacteremia is hospitalization. Placement of intravenous, intraperitoneal, or urinary catheters and prior instrumentation of the respiratory tract have been identified as risk factors among inpatients.

Other risk factors include cardiac valve replacement, transfusions, and the use of contaminated intravenous infusions. An outbreak of bacteremia was caused by pooling the residual contents of preservative-free epoetin vials for later use. Another outbreak was traced to tampering with an infused narcotic by a hospital employee.[29] A multistate outbreak of S marcescens bloodstream infection was linked to contaminated intravenous magnesium sulfate distributed in the United States by a compounding pharmacy.[30]

Contamination of a faucet resulted in 2 cases of bacteremia during an outbreak of 10 S marcescens infections in an intensive care unit.[31]

Urinary tract infection

Ninety percent of patients with Serratia urinary tract infection have a history of recent surgery or instrumentation of the urinary tract.

Important risk factors include diabetes mellitus, urinary tract obstruction, and renal failure.

Respiratory tract infection

Serratia respiratory tract infection may develop after instrumentation (eg, ventilation, bronchoscopy), especially in patients with chronic obstructive pulmonary disease. During an outbreak of S marcescens infections traced to a contaminated faucet (including consumption of tap water from the faucet) in an intensive care unit, 9 patients developed respiratory tract infection (8 developed septic bronchitis; 1 developed empyema), while another 9 patients developed only S marcescens colonization of the respiratory tract.[31]

Meningitis and cerebral abscess

Serratia meningitis or cerebral abscess may develop in premature children and neonates with prior sepsis. Serratia meningitis may also develop in adults who have experienced head trauma or have undergone neurosurgery, epidural injection, or lumbar puncture.

Osteomyelitis and arthritis

Osteomyelitis or arthritis can be hematogenous in people addicted to intravenous drugs, or can be caused exogenously by surgery, open trauma, or intraarticular injection.

Endocarditis

Although Serratia endocarditis tends to appear in intravenous drug abusers, it usually involves aortic or mitral valves.[32]

Ocular infections

Serratia infection frequently causes nonulcerating bacterial keratitis, which is associated with wearing rigid or soft contact lenses.[33]

Serratia endophthalmitis usually occurs after eye surgery.

Parotitis

Bacterial parotitis may develop in individuals with prior sialectasia.

Cutaneous infections

Poorly healing skin ulcers in combination with S marcescens infections at multiple sites are typical in young adults with chronic granulomatous disease.[25] Dermal abscesses and skin ulcers in the legs have appeared after a toe-web infection.[34]

Laboratory Studies

See the list below:

Imaging Studies

Perform chest radiography in patients with suspected pneumonia or with respiratory distress.

Abdominal ultrasonography or CT scanning is used to rule out obstructive hydronephrosis or intra-abdominal abscesses (eg, hepatic, pancreatic).

Transthoracic or transesophageal echocardiography may reveal valvular vegetations and valvular or paravalvular regurgitation.

Perform spinal CT scanning or MRI if spondylitis is suspected.

Procedures

Lumbar puncture should be performed in all patients with suspected meningitis. Signs of increased intracranial pressure (focal neurologic abnormalities, seizure, altered mental status) should prompt evaluation with CT scanning prior to puncture to exclude cerebral abscess or mass lesion.

Medical Care

Antibiotic therapy is the primary treatment in most patients with Serratia infection. Home therapy is an option in patients who are clinically stable.

Surgical Care

Purulent collections (abscesses) may require drainage.

Consultations

Consult a cardiac surgeon if considering valve replacement in patients with infective endocarditis.

In a possible nosocomial outbreak of Serratia infection, strain typing may assist the epidemiologic investigation.

Medication Summary

S marcescens is naturally resistant to ampicillin, macrolides, and first-generation cephalosporins. In Taiwan, 92% of the strains are resistant to cefotaxime, but 99% are still susceptible to ceftazidime. Extended spectrum beta-lactamases are produced by most S marcescens strains.[35] International data on antimicrobial susceptibility of Serratia and other nosocomial isolates have been published.[36, 37]

Serratia infections should be treated with an aminoglycoside plus an antipseudomonal beta-lactam, as the single use of a beta-lactam can select for resistant strains. Most strains are susceptible to amikacin, but reports indicate increasing resistance to gentamicin and tobramycin. Quinolones also are highly active against most strains.

Cefepime or broad-spectrum beta-lactam/beta-lactamase inhibitor combinations may be a reasonable option for the treatment of infections with Serratia strains that produce AmpC beta-lactamase.[38, 81]

Definitive therapy should be based on the results of susceptibility testing because multiresistant strains are common.

Levofloxacin (Levaquin)

Clinical Context:  For pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Cefepime (Maxipime)

Clinical Context:  Fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitter ion; rapidly penetrates gram-negative cells. Best beta-lactam for IM administration. Poor capacity to cross blood-brain barrier precludes use for treatment of meningitis.

Ertapenem (Invanz)

Clinical Context:  Bactericidal activity results from inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. Stable against hydrolysis by various beta-lactamases including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases. Hydrolyzed by metallo-beta-lactamases.

Amikacin

Clinical Context:  Preferred aminoglycoside. Usually synergistic with antipseudomonal beta-lactams. Use both in combination, pending results of susceptibility testing. For gram-negative bacterial coverage of infections resistant to gentamicin and tobramycin. Effective against Pseudomonas aeruginosa. Irreversibly binds to 30S subunit of bacterial ribosomes. Blocks recognition step in protein synthesis. Causes bacterial growth inhibition.

Aztreonam (Azactam)

Clinical Context:  Usually synergistic with amikacin. Use both in combination, pending results of susceptibility testing. A monobactam that inhibits cell wall synthesis during bacterial growth. Active against gram-negative bacilli.

Meropenem (Merrem IV)

Clinical Context:  Preferred therapy for Serratia meningitis. Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has increased activity against gram-negative bacteria and slightly decreased activity against staphylococci and streptococci compared to imipenem.

Imipenem-cilastatin (Primaxin)

Clinical Context:  Carbapenem is used for treatment of multiple-organism infections in which other agents do not have wide-spectrum therapeutic activity or are contraindicated because of potential toxicity. Comparable in activity to meropenem.

Ciprofloxacin (Cipro)

Clinical Context:  Greatest anti-P aeruginosa activity among the quinolones. May be particularly useful for isolates resistant to the aminoglycosides.

Ticarcillin/clavulanate (Timentin)

Clinical Context:  Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active growth. Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive organisms, most gram-negative organisms, and most anaerobes. Contains 4.7-5.0 mEq of Na+/g.

Piperacillin/tazobactam (Zosyn)

Clinical Context:  This drug combination consists of an antipseudomonal penicillin plus a beta-lactamase inhibitor. It inhibits the biosynthesis of cell wall mucopeptide and is effective during the active multiplication stage.

Ceftazidime/avibactam (Avycaz)

Clinical Context:  Ceftazidime/avibactam has shown showed potent in vitro activity when used against enterobacteriacae with inducible AmpC beta-lactamases, including Serratia marcescens.

Ceftolozane/tazobactam (Zerbaxa)

Clinical Context:  Inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins. This results in the inhibition of the final transpeptidation step of peptidoglycan synthesis in bacterial cell walls, thus inhibiting cell wall biosynthesis.

Amoxicillin/clavulanate (Augmentin, Augmentin ES-600, Augmentin XR)

Clinical Context:  Amoxicillin is a third-generation aminopenicillin. Combined with the beta-lactam clavulanic acid, it is less susceptible to degradation by beta-lactamases produced by microorganisms. For children older than 3 months, base the dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in the 250-mg tablet (250/125) versus the 250-mg chewable tablet (250/62.5), do not use the 250-mg tablet until the child weighs more than 40 kg.

Class Summary

Empiric antimicrobial therapy should cover all likely pathogens in the context of the clinical setting.

Further Inpatient Care

Remove or change catheters suspected of being contaminated with Serratia bacteria.

Deterrence/Prevention

Avoid reusing single-use vials, and reject possibly contaminated intravenous fluids.

Avoid using soaps or disinfectants that may be contaminated.

Avoid using tap water for administration of medication orally or via a nasogastric tube in critically ill patients.[31]

Use disposable ECG leads.

Emphasize standard precautions. Hospital employees should wash their hands[39] before and after contact with patients. The most common mechanism of Serratia transmission in nosocomial outbreaks is through soiled hands. Long-term carriage of an epidemic strain of S marcescens on the hands of a health care worker has been described.[40]

Intravenous lines should be removed as soon as possible.

Prognosis

Severe Serratia infection (bacteremia) carries a mortality rate of 26%. Among survivors, the prognosis for complete recovery is good.

S marcescens endophthalmitis carries a poor prognosis in terms of maintaining vision.

What are Serratia species?What is the pathophysiology of Serratia infection?What is the incidence of Serratia infection in the US?What are the mortality rates for Serratia infections?How does the incidence of Serratia bacteremia vary by sex?Which age group is at highest risk for Serratia infection?What are the signs and symptoms of Serratia sepsis?What are the signs and symptoms of Serratia urinary tract infection (UTI)?What are the signs and symptoms of Serratia respiratory tract infection?What are the signs and symptoms of Serratia meningitis or cerebral abscess?What are the signs and symptoms of Serratia intra-abdominal infections?Which history is characteristic of Serratia osteomyelitis and arthritis?What are the signs and symptoms of Serratia endocarditis?What are the signs and symptoms of Serratia ocular infections?What are the signs and symptoms of Serratia soft-tissue infections?What are the signs and symptoms of Serratia otitis media?How common is Serratia parotitis?Which physical findings suggest Serratia infection?What are the risk factors for Serratia sepsis or bacteremia?What are the risk factors for Serratia urinary tract infection (UTI)?What are the risk factors for Serratia respiratory tract infection?What is the risk factors for Serratia meningitis and cerebral abscess?What is the risk factors for Serratia osteomyelitis and arthritis?What is the risk factors for Serratia endocarditis?What is the risk factors for Serratia ocular infections?What is the risk factors for Serratia parotitis?What is the risk factors for Serratia cutaneous infections?What are the differential diagnoses for Serratia?Which lab studies are performed in the workup of Serratia infection?What is the role of imaging studies in the workup of Serratia infection?What is the role of lumbar puncture in the workup of Serratia infection?What is the medical treatment for Serratia infection?When is surgery indicated in the treatment of Serratia infection?Which specialist consultations are beneficial in the treatment of Serratia infection?Which medications are used in the treatment of Serratia infection?Which medications in the drug class Antibiotics are used in the treatment of Serratia?What should be included in inpatient care for Serratia infection?How is Serratia infection prevented?What is the prognosis of severe Serratia infection?

Author

Antonette B Climaco, MD, Attending Physician, Division of Infectious Diseases, Department of Medicine, Albert Einstein Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Prithiv J Prasad, MBBS, Resident Physician, Department of Internal Medicine, Albert Einstein Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Disclosure: Nothing to disclose.

Additional Contributors

Basilio J Anía, MD, Associate Professor of Infectious Diseases, Universidad de Las Palmas de Gran Canaria; Consultant in Internal Medicine, Hospital Universitario Dr. Negrín, Spain

Disclosure: Nothing to disclose.

Thomas E Herchline, MD, Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Consultant, Public Health, Dayton and Montgomery County (Ohio) Tuberculosis Clinic

Disclosure: Nothing to disclose.

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