DEPARTMENT OF PATHOLOGY
The Johns Hopkins Medical Institutions


Vol. 20, No. 49
THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Tuesday, December 4, 2001

A. Provided by Karen Fujii, Division of Outbreak Investigation, Maryland Department of Health and Mental Hygiene.

3 outbreaks were reported to DHMH during MMWR week 48 (November 25 - December 1, 2001):

1 outbreak of foodborne gastroenteritis at a restaurant (Prince George's Co.)
1 outbreak of folliculitis at a private home (Harford Co.)
1 outbreak of foodborne gastroenteritis at a private home (Wicomico Co.)
B. The Johns Hopkins Hospital, Department of Pathology.  Information provided by Rob Law, M.D.

Case Description

A 66 year old white male presented to his PMD with acute onset sensorineural hearing loss. Imaging revealed a left-sided acoustic tumor, no evidence of increased intracranial pressure. Resection of an acoustic neuroma was performed without complications. Approximately four days postoperatively, the patient experienced fever and lethargy. Imaging revealed ventriculomegaly and subependymal fluid. A intraventricular catheter was placed. Altered mental status and fevers persisted, and the patient became ventilator dependent. Culture of CSF revealed Serratia marcescens.

Serratia marcescens

Organism: Serratia marcescens is an opportunistic gram-negative bacteria classified in the large family Enterobacteriaceae. S. marcescens is the only pathogenic species, although rare reports of infection with S. plymuthica, liquefaciens, rubidaea, and odifera exist.

Epidemiology. Since the early 1900’s, physicians have used S. marcescens to study transmission of microorganisms, as it was assumed to be a harmless saprophyte. In the hospital, Serratia tends to colonize the respiratory and urinary tracts of adults, rather than the GI tract. Serratia is responsible for 1.4% of nosocomial septicemia. It is also responsible for 2% of lower respiratory, urinary tract, and surgical wound infections. Serratia can be a cause of meningitis, especially after surgical intervention. Also reported is endocarditis and osteomyelitis in heroin addicts. Crude mortality for Serratia septicemia is 26%, while the mortality for meningitis and endocarditis is very high.

Diagnosis. Diagnosis is established by culture of the organism. Serratia species grow well on enriched media (e.g., blood agar) at 35-37o C. They are non-lactose fermenters and are motile. Serratia species produce extracellular DNase at 25 o C and gelatinase at 22 o C. They elaborate lipase and are resistant to colistin, ampicillin and cephalothin. These properties are unique to Serratia, but not all Enterobacteriaceae. Not all S. marcescens organisms produce the typical red pigment prodigiosin. S. rubidaea and S. plymuthica elaborate the same water-insoluble compound or a very similar one. Epidemiologic differentiation of S. marcescens can be achieved by biotyping based primarily on carbon sources or by pulsed-field gel electrophoresis.

Management. Antibiotic therapy is the primary treatment, although purulent collections may require drainage. Therapy would include an antipseudomonal beta-lactam plus an aminoglycoside. Most strains are amikacin susceptible, but reports of resistance to gentamicin and tobramycin are increasing. Quinolones are highly active against most strains. Definitive therapy rests on susceptibility testing.

References:
1. Arnon, Stephen S. Textbook of Pediatric Infectious Disease, fourth edition, Feigin and Cherry, eds. 1998.
2. Koneman et. al. Color Atlas and Textbook of Diagnostic Microbiology, 5th Edition, Lippincott-Raven, Philadelphia, 1997.

3. Mandell, GL, Bennet, JE, and Dolin R: Principle and Practice of Inf. Dis. Fifth Edition (1999), Churchill Livingstone Inc., PA. 2903-15.


Help | Feedback | Pathology Home | Previous Menu | Tool Box* | Search
Copyright © 2001 THE JOHNS HOPKINS UNIVERSITY