stools were rejected according to the 3- d criteria. At the same time 51 of 677 stools from children were positive for bacterial enteric pathogens, and all but one had been accepted by the 3-d rule. The one non-compliant positive culture was a Salmonella, but the authors be- lieve this child was a carrier rather than having an active infection. This paper also noted that the presence of fecal leu- kocytes was not a useful predictor for the presence of an enteric pathogen. In fact, 39 of 55 (71%) positive stools would have been missed if fecal lenko- cytes had been used as a screening test. They recommend that the 3-d rule apply to children as well as adults with diar- rhea, and to delete the fecal fetal leuko- cyte screen, a move with which I could not agree more. Why not just flip a coin?

So what have we actually recom- mended after this diarrheal diatribe?

(i) With the exception of unique his- tory, etc., stools from in-patients hospi- talized for more than 3 d should be rejected for P&O exams and bacterial enteric pathogen culture.

(ii) Out-patients are not subject to these current criteria except for how many stools per patient will be exam- ined. We were all taught that three stools over a 4-d period was appropriate for P&O or enteric pathogens. At this time, I prefer to stick with that concept

for out-patients. I do agree with the one stool per in-patient, except in special cir- cumstances, e.g., bloody diarrhea.

(iii) Hemorrhagic Escherichia coli culture is allowable in cases of sudden onset of bloody diarrhea regardless of 3- d rule. This problem is not specifically covered in many of the cited papers (5).

(iv) C. difficile toxin was by far the most common cause of microbial diar- rheal disease in all patient groups (14 to 22%) and the rejection criteria dis- cussed do not apply.

(v) If the stool is to receive a P&O exam, it should get the full examina- tion, i.e., direct, concentrate, and trichrome stain if a direct is not done. Other than cryptosporidia, we have not detected any P&O pathogen with the trichrome stain that we did not observe in either the direct or concentrate (7 years of data). The CAP and other certi- fying agencies need to reevaluate the re- quirement for a trichrome stain on all stools. The yield is zilch but the time and effort expended is not.

(vi) Exam for cryptopoddia should be done on appropriate request as these criteria (<3 d) may not apply to certain patient groups, e.g., HIV positives, leukemics, bone marrow transplants).

(vii) Finally, why are we asked to do a "test of cure" antigen (toxin) assay on formed stools of treated C. difficile pa- fients prior to discharge? The result is

misinformational because the antigen can be detected well after the resolution of the diarrheal problem. Are we treat- ing post-therapy residue and keeping these patients in the hospital because a test is positive in the absence of signs and symptoms?

Discussion is the progenitor of deci- sion and if these opinions create contro- versy and discussion, a good decision can't be far behind. Thank you, Ray Bartlett, for instilling a desire for rele- vance and not just reflexive reaction into our science.

References

1. Koontz, F. P. et al., Abstr. Annu. Meet. Am. Soc. Microbiol. 1988, Abstr. No. C-145, p. 356.

2. Siegel, D. L. et al. 1990. Inappropriate testing for diarrheal diseases in the hos- pital. JAMA 263:979-982.

3. Morris, A. J. et al. 1992. Application of rejection criteria for stool ovum and parasite examinations. J. Clin, Micro- biol. 30:3213-3216.

4. Fan, K. et al. 1993. Application of rejec- tion criteria for stool cultures for bacte- rial enteric pathogens. J. Clin. Microbiol. 31:2233-2235.

5. Kay, B.A. et al. 1994. Too fast food: Bloody diarrhea and death from E. coli 0157:H7. Clin. Microbiol. Newslett. 16:17-19.

Case Report

Baeteremic Pyelonephritis Caused by Sphingomonas paucimobilis

J.M. Ramos M. Cuenca-Estrella J. Esteban R. Fernandez-Roblas F. Soriano Department of Medical Microbiology Fundaci6n Jiradnez D[az 28040-Madrid, Spain

Sphingomonas paucimobilis (for- merly known as Pseudomonas paucimo- bilis and CDC group IlK, biotype 1)

(1-3) is a yellow pigmented, gram-nega- five, oxidase- and catalase-positive, non- fermenting oxidative bacillus with a polar flagellum (3). It has been isolated from water sources, plants, hospital equipment, pharmaceuticals, and human clinical specimens (4). S. paucimobilis also has been implicated in several hu- man infections such as bacteremia, pexi- tonitis in CAPD patients, meningitis, brain abscess, leg ulcer infection, splenic abscess, empyema, diarrheal ill- ness, and suppurative lymphadenitis (5- 7). To the best of our knowledge, two cases of nosocomial urinary tract infec- tion (UTI) caused by this microorgan-

ism have been reported (8, 9). We here one additional case of S. paucimobilis lyrI.

Case R e p o r t A 60-yr-old man with history of bi-

lateral nephrolithiasis was admitted to the hospital because of fever, chills, dy- suria, and a left costoverlebral tender- ness of 6 d duration. An antegrade pyelography by direct puncture was per- formed 15 d before admission for a left hydronephrosis with renal atrophy.

On examination the patient was feb- rile and had tenderness on deep pres- sure in the left costovertebral area. The

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white blood cell count was 16,300/ml (85% neutrophils, 12% lymphoeytes, and 3% monoeytes). Erythrocyte sedi- mentation rate was 58 mm at the first hour. The other hematologic studies, electrolytes, metabolic profile, and liver function tests were normal. Urinary sediment showed 20 leukocytes per high-power field and bacterlauria. An abdominal roentgenogram showed bilat- eral renal stones. ACT scan revealed re- hal atrophy, hydronephrosis of left kidney, and left ureteropelvic junction obstruction secondary to stones. Two blood culture sets and one urine culture were perfcmned at admission. Empiric treatment with IV trimethoprim/sul- famethoxazole (TMP/SMX) (1,600/320 mg/day) was begun, but the patient re- mained febrile despite antimicrobial treatment.

Urine culture was positive on the sec- ond day of incubation for 80,000 CFU/ml of a gram-negative bacillus, subsequently identified as S. paucimobi- lis. The same microorganism also grew in one blood culture set after 3 d of in- cubation. When these microbiological results became available, therapy was switched to gentamicin (240 rag/day). On the sixth day after admission, the pa- tient underwent nephrectomy because of the lack of improvement with antibi- otic therapy, and purulent exudate from the renal pelvis was sent to the microbi- ology department for culture. Direct ex- amination by Gram and Ziehl-Neelsen stains was negative for organisms; but a pure and scant growth ofS. paucimobi- lis was obtained after 5 d incubation; the delayed growth may have been a re- sult of previous treatment with gentami- cin. Antibiotic therapy was prolonged for 15 d until discharge.

The organism grew on sheep blood agar at 37 ° and 30°C, appearing as yel- low pigmented, convex, and smooth colonies. The organism was a glucose nonfermenting gram-negative bacillus that did not grow on McConkey agar. It was positive for oxidase, cat alase, and motility at 220C. ONPG and esculin were hydrolyzed. Reactions for urease (Christensen), citrate (Simmons), ni- Irate reduction, and indole were nega- tive. The API 20 NE (biocode

0463254) and AP120 E (biocode 1001006) (bioM6rieux, Lyon, France) were consistent with S. paucimobilis. A disk diffusion susceptibility test was also performed and showed the organ- ism to be resistant to cefazolin, ce- furoxime, ciprofloxacin, chloramphenicol, and TMP/SMX, sus- ceptible to third-generation cephalospor- ins, ticarcillin, amoxicillin/clavulanic acid, imipenem, and aminoglycosides, and intermediate susceptibility to am- picillin.

Discussion UTI caused by S. paucimobilis are

extremely unusual (5). The two eases previously described (8, 9) involved pa- tients hospitalized with urinary cathe- ters. Because the most likely human source of this microorganism is the di- gestive tract (5), we suspect that these bacteria may colonize the perineal area and catheter systems, leading to UTI. However, our patient did not have an indwelling urethral catheter, thus we propose two possible pathogenic mecha- nisms for developing such infection: (i) S. paucimobilis colonized the digestive tract and endogenous pyelonephritis de- veloped after hematogenous spread, or (ii) S. paucimobilis was directly inocu- lated during pelvis puncture performed 15 d before admission. This microor- ganism has been previously reported as an environmental bacterium in the clini- cal setting (4).

The majority of infectious with this microorganism have been associated with a good prognosis (5, 10). Hitherto, no death has been attributed to this bac- teria. In all cases, appropriate antibiotic therapy has been sufficient to eradicate S. paucimobilis. However, in addition to a UTI, our patient had nephrolithi- asis, and nephrectomy associated with appropriate antimicrobial therapy was necessary to obtain a cure.

The bacteriological identification of this organism is not difficult. Among yellow-pigmented, gram-negative, oxi- dase- and catalase-positive nonferment- ing bacilli, S. paucimobilis can be easily differentiated from Pseudomonas mendocina and P. gladioli by the ab- sence of growth on MacConkey agar,

and from F lavobacterium sp. and Sphin- gobacterium sp. by its motility. It is therefore important that clinical micro- biology laboratories be aware of S. pau- cimobilis as a possible cause of human infection.

References: 1. Yabuuchi, E. et al. 1990. Proposals of

Sphingomonas paucimobilis gen. nov. and comb. nov., Sphingomonas para- paucimobilis sp. nov., Sphingomonas yanoikuyae sp. nov., Sphingomonas ad- hahesiva sp. nov., Sphingomonas capsu- lata comb. nov., and two genospecies of genus Sphingomonas. Microbiol. Im- munol. 34:99-119.

2. Van-Bruggen, A.H. et al. 1993. Classifi- cation of Rhizomonas suberifaciens, an unnamed Rhizomonas species, and Sphingomonas spp. in rRNA superfa- mily IV. Int. J. Syst. Bacteriol. 43:1-7.

3. Holmes, B. et al. 1977. Pseudomonas paucimobilis, a new species isolated from human clinical specimens, the hos- pital environment, and other sources. Int. J. Syst. Bacteriol. 27:133--146.

4. Gilardi, G.L. 1991. Pseudomonas and related genera, p. 429 A.A. 1. In A. Balows et al. (eds.): Manual of clinical microbiology, 5th ed. American Society for Microbiology. Washington, D.C.

5. Reina, J. et al. 1991. Infection with Pseudomonas paucimobilis: report of four cases and review. Rev. Infect. Dis. 13:1072-1076.

6. Decker, C.F., R.E. Hawkins, ~ G.L. Simon. 1992. Infections with Pseudo- monas paucimobilis. Clm. Infect. Dis. 14:783-784.

7. Guglielmetti, P. et al. 1993. Commu- nity-acquired suppurative lymphadeni- tis caused by Pseudomonas paucimobilis. Clin. Microbiol. Newslett. 15:54-56.

8. Crane, E.R., L.C. Tagle, and W.A. Palutke. 1981. Outbreak of Pseudo- monas paucimobilis in an intensive care facility. JAMA. 246:985-987.

9. Sanchis-Bayarri, V. et al. 1993. Con- tribuci6n al estudio de las infecciones por Pseudomonas paucimobilis. Anfilisis de dos casos. Rev. Clin. Esp. 192:65-66.

10. Casadevall, A., L.F. Freundlich, and L. Pirofski. 1992. Septic shock caused by Pseudomonas paucimobilis. Clin. In- fect. Dis. 14:784.

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