unvaccinated preschool age children (13). These children are part of largely urban, poor, ethnic minorities who are out of touch with the health care system. In Milwaukee, Wisconsin, an outbreak of measles occurred during the fall, winter and spring of 1989 and 1990 that totaled 1,107 patients, the majority of whom were less than 5 yr old. Of these children, 65% had never been vaccinated even though 83% of them were covered by comprehensive medical insurance (14). The 3 deaths and over 250 hospitalizations (average cost per hospitalization: $9,936) shocked the local medical community. During a Milwaukee outbreak of similar size (but different demographics) in 1980 there were no deaths and a hospitalization rate of only 1%. The most common reason given for hospitalization during the 1989-1990 outbreak was dehydration and need for intravenous fluid replacement. Pneumonia and upper airway disease were also common serious complications. Laryngotracheitis, leading to airway obstruction, was the cause of many transfers to the intensive care unit and was implicated in 2 of the 3 deaths. The measles outbreaks in urban centers in the U.S.: New York, Miami, Chicago, Milwaukee, Dallas, Houston, Los Angeles, and others from 1986 to the present all have similar excessive morbidity and mortality rates just as they have similar case demographics and similar low vaccine coverage rates (15). Measles case-mortality rates in these cities approximate 3 per !,000 (16) which is ten times higher than the expected rate noted in the official Ad-
visory Committee on Immunization Practices (ACIP) Measles Prevention document of 1987 (17). This excessive death toll is likely related both to the young age of those afflicted and to conditions of poverty and marginalization such as pre-existing poor health, crowded living situations, lack of access to health care, and perhaps malnutrition. Vitamin A deficiency is not thought to be prevalent in the U.S. but this is currently under investigation among young children with severe measles in New York. However, the most disquieting aspect of the epidemic to many is the fact that despite the existence of a highly effective, cost-efficient vaccine, our society has failed to deliver it to the population most in need of protection, our youngest children.
References 1. Brenan, J. G. 1984. Measles p. 110114. In G. T. Strickland (ed.), Hunter's tropical medicine, 6th Ed., W.B. Saunders Company, Philadelphia. 2. Aaby, P. 1988. Malnutrition and overcrowding intensive exposure in severe measles infection: review of community studies. Rev. Infect. Dis. 10:478491. 3. Hussey, G. D. and M. Klein. 1990. A randomized, controlled trial of vitamin A in children with severe measles. N. Engl. J, Med, 323:160--164. 4. Rahmathullah, L. et al. 1990. Reduced mortality among children in southern India receiving a small weekly dose of vitamin A. N. Engl. J. Med. 323:929935. 5. Kensch, G. T. 1990. Vitamin A supplements--too good not to be true. N. Engl. J. Med. 323:985-986.
6. Markowitz, L. E. et al. 1990. Immunization of six-month-old infants with different doses of Edmonston-Zagreb and Schwarz measles vaccines. N. Engl. J. Med. 322:580-587. 7. Centers for Disease Control. 1991. Measles--United States, 1990. Morbid. Mortal. Weekly Rep. 40:369-372. 8. Sencer, D. J., H. B. Dull, and A. D. Langmuir. 1967. Epidemiologic basis for eradication of measles in 1967. Pub. Health Rep. 82:253-257. 9. Bloch, A. B. et al. 1985. Health impact of measles vaccination in the United States. Pediatrics. 76:524-532. 10. Hedrich, A. W. 1933. Monthly estimates of the child population "susceptible" to measles, 1900-1931, Baltimore, MD. Am. J. Hyg. 17:613630. 11. Centers for Disease Control. 1989. Measles prevention: Recommendations of the immunization practices advisory committee (ACIP). Morbid. Mortal. Weekly Rep. 38:HI-HI7. 12. White, C. C., J. P. Koplan, and W. A. Orenstein. 1985. Benefits, risks and costs of immunization for measles, mumps and rubella. Am. J. Publ. Health 75:739-744. 13. Markowitz, L. E. et al. 1989. Patterns of transmission in measles outbreaks in the United States, 1985-1986. N. Engl. J. Med. 320:75-80. 14. Schlenker, T. and K. Fessler. 1990. Measles in Milwaukee. Wisc. Med. J. 89:403-407. 15. Centers for Disease Control. 1991. Measles vaccination levels among selected groups of preschool-aged children-United States. Morbid. Mortal. Weekly Rep. 40:37-39. 16. Centers for Disease Control. 1990. Measles in the United States. 17. Centers for Disease Control. 1987. Measles prevention. Morbid. Mortal. Weekly Rep. 36:409--418.
Case Report
Leclercia adecarboxylata Isolated from a Blood Culture Ellen Otani, MT (ASCP) David A. Bruckner, Sc.D. Clinical Microbiology Section Department of Pathology and Laboratory Medicine UCLA Medical Center 171315 Los Angeles, CA 90024-1713
An 8Y2-mo-old boy with a history of gastroschisis (congenital fissure of the abdominal wall) and intestinal atresia (congenital absence or occlusion of a portion of the intestines) presented to the emergency room with a fever of 103°F. He had a jejunojejunostomy soon after birth and was dependent on total parenteral nutrition (TPN). At 3 and 6 mo of age, his jejunojejunostomy was obstructed requiring revi-
sion. He received TPN through a central line catheter at home. The evening prior to admission, he had shaking chills and fever approximately 1 h after receiving TPN. On initial physical examination, the patient was alert, with a pulse of 136, respiratory rate was 34, and blood pressure was 103/71. His central venous catheter site was clean and clear, and his gastrostomy site was slightly
uuull
Clinical Microbiology Newsletter 13:20.1991
© 1991 Elsevier Science Publishing Co., Inc.
0196-4399/91/$0.00 + 02.20
157
erythematous, but nontender and no discharge was noted. Peripheral blood counts revealed a white blood cell count of 12,500/mm 3 with a differential of 67 segmented neutrophils, 15 band forms, 12 lymphocytes, and 6 monocytes. One blood culture was obtained by venipuncture and another was drawn from the central line catheter. The patient was admitted to the hospital with a diagnosis of line sepsis and was started on vancomycin, gentamicin and ceftazidime therapy. After 24 h, the blood culture from the central line catheter grew a lactosepositive, gram-negative bacillus. On 5% sheep blood agar, the colonies were large, flat, shiny, and pigmented yellow. The organism was identified as Leclercia adecarboxylata (previously known as Escherichia adecarboxvlata or Enteric Group 41) by both the API 20E system (Analytab Products, Plainview, N.Y.) and the MicroScan Rapid Neg ID Type 2 Panel (Microscan Division, Baxter Healthcare Corp., West Sacramento, Calif.). This organism was not included in the Vitek Gram-Negative Identification Card database (Vitek Systems, Hazelwood, Mo.), and consequently no acceptable identification was obtained (63% Serratia rubidaea; 17% Klebsiella ozaenae). Identification was confirmed by conventional biochemical testing. The organism was susceptible to amikacin, ampicillin, cefazolin, cefoperazone, ceftazidime, gentamicin, mezlocillin, piperacillin, tobramycin and trimethoprim-sulfamethoxazole by a microdilution MIC method (3). Subsequently, the patient's vancomycin therapy was discontinued, but he continued to receive a full 14-d course of gentamicin and ceftazidime. No growth was obtained from the blood culture drawn by venipuncture before antimicrobial therapy or blood cultures
drawn post therapy, Escherichia adecarboxylata was the name proposed by Leclerc (2) in 1962 for organisms that produced yellow pigment, were indole and methyl redpositive but were negative for acetoin production, citrate utilization, lysine, and ornithine decarboxylase and arginine dihydrolase. More recently, the name Leclercia adecarboxylata has been proposed for this group of organisms (6). Although 80 to 95% of all Enterobacteriaceae isolates seen in the general hospital setting are Escherichia coli, Klebsiella pneumoniae or Proteus mirabilis (1), manufacturers of identification systems have expanded their databases to include many of the rarely isolated members of this family. Most of the strains of L. adecarboxvlata studied by Leclerc were obtained from water, and it was reported by Teramoto and Sakazaki (7) that this organism was frequently isolated from food and environmental sources. The clinical significance of L. adecarbox3,lata is uncertain, but it has been isolated from blood, sputum, urine, stool, and wounds (4, 6). Only 1 to 5 ml of blood samples are usually drawn from children for bacterial culture, because of problems in obtaining large volumes of blood and because this amount may be adequate to detect organisms in pediatric patients (5). In the case described, the only blood culture positive for L. adecarbo.~,lata was drawn from the central line catheter. This could represent bacterial colonization of the catheter rather than septicemia; however, it is possible that the blood culture drawn by venipuncture before antimicrobial therapy was negative because there were not sufficient numbers of bacteria present in the blood. The patient's physicians felt that this organism was
a clinically significant isolate rather than a contaminant: therefore, the patient was given a full course of antimicrobial therapy. Because the patient became afebrile and his WBC count returned to normal the day following the start of antimicrobial therapy, his catheter line was not removed nor replaced. Although the frequency of isolating this organism in a clinical setting is rare, its pathogenic significance should not be overlooked, particularly in immunocompromised patients. Rel~,rences 1. Farmer, J. J. 1II et al. 1985. Biochem ical identification of new species and biogroups of Enterobacteriaceae isolated from clinical specimens. J. Ctin. Microbiol. 21:46-76. 2. Lcclerc, H. 1962. Etude biochimique d'cnterobacteriaceae pigmentdes. Ann. Inst. Pasteur 102:726-741. 3. National Committee R)r Clinical Laboratory Standards, 1983. Standard methods for dilution antimicrobial susceptibility tests for bacteria which grow aerobically. Proposed standard: M7-'I'. National Committee for ClinicaJ Laboratory Standards, Villanova, PA. 4. Richard, C. 1989. Nouvelles Enterobacteriaeeae rencontrtSes cn bactdriologie m~dicale: Moellerella wi,~consensis, Koserelta trabulsii. Leclercia adecarbo.tvlam, Escherichia .[ergusonii, Enterobacter asburiae, Rahnella aquatilis. Ann. Biol. Clin. 47:231-236. 5. Strand, C. L. and J. A. Shuhnan. 1988. Bloodstream infections. Labora tory detection and clinical considerations. Am. Soc. Clinical Pathologists, Chicago. 6. Tamura. K. et al. 1986. Leclercia adecarboxvlata gen. nov.. comb. nov., formerly known as Echerichia adecarboxvlata. Curt. Microbiol. 13:179184. 7. Teramoto, T. and R. Sakazaki. 1984. Taxonomic analysis of so-called coliform organisms isolated from foods and environmental materials/in Japanese), J. Food Hyg. Soc. Jpn. 25:322-328.
Case Report
Urease-Positive Thermophilic
Campylobacter Isolated from Human Blood ] 58
O196-4399:9140.00
+ 02.20
Janet A. Schrader Richard A. Venezia James Tillotson Department of Laboratory Medicine Albany Medical Center Albany. NY 12208 i7 ] 901 Elsevier Science Publishing C o . . Inc
Urease-positive thermophilic Campylobacter (UPTC) strains (C. laridis variant) have been isolated from human feces and appendix, confirming an association with humans (1). The present isolate appears to be ,i ( "hnical Microbi(*log? Ncv,,,Ictter t a:2(L l Oq I