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Neisseria subflava as a cause of bacteremia
dollars. Hiring less skilled persons to perform the less technical procedures or hiring generalists to obtain better overall staff utilization may have to be part of the answer. "Flexible scheduling" may be still another strategy. Some people, especially younger ones, find that time off during slow periods in the middle of the day is more attractive than money or job security. Another way to cut costs is to perform fewer tests and fewer kinds of tests. In some cases clinicians may be oyertesting and the laboratory will have to show them how fewer tests will provide the essential information; for example, ordering a BUN rather than a chemistry screen, or a "betastrep" screen rather than a full flora throat culture. The laboratory director will be asked to help evaluate whether test utilization is appropriate and effective. Since data from the DRG system will permit tracking of individual physicians' ordering patterns and costs by diagnosis, laboratories will have an important role in educating the physician to be a cost-effective user of laboratory services. Under the PPS, the laboratory will have to consider the cost of performing a test in-house as opposed to sending it to a commercial laboratory. Some community hospitals have already contracted out their work to private laboratories. Increased competitive bidding by such independent laboratories will lower their charges to
hospitals. We may also need to consider sharing our workload with other hospitals; for example, we'll do tests A, B, and C, whereas you will do tests D, E, and F. Group purchasing for certain supplies will become more attractive under PPS. The tight market that DRGs will create will also put pressure on vendors to " m a k e a better deal" whether it be for purchase of an instrument, a reagent rental agreement, or for supplies. Quality control and proficiency testing are expensive, and we may even have to look at these sacred cows to determine whether we can reduce costs in this area and still maintain quality. Finally, DRGs will force laboratory professionals to improve management at every level. Because of the fixed payment per DRG, the laboratory will become just another cost center and no longer enjoy the benefits of being a revenue center. Although the total effect of DRGs will not have a full impact on us for several years, there is real concern that prolonged trimming of costs will compromise the ability of the laboratory to provide quality care. When we are asked to provide new services we may first have to get rid of some old procedures, ones that are not sensitive and don't provide as much diagnostic information as others: for example, performing protein electrophoresis rather than protein assays. If you don't take DRGs seriously
now and evaluate what changes you might make, you run the risk of seriously compromising patient care in the future. No doubt a number of unpleasant prospects are in store for us, but it makes more sense to view this new challenge as an opportunity to improve the laboratory. In the health care field we often find that tough changes are best accomplished by using a third party (in this case, DRGs) as the bad guy. Using this ploy we can get various groups in the hospital to sit down and agree on what might be some exciting improvements to our services. In addition to the factors discussed, forecasting, marketing, and continuing education will become important. We'll have to make it our business to be informed, to know the language of administrators, to understand their problems in keeping the institution running under reimbursement constraints, and be willing resource people for helping to make the difficult decisions about restructuring laboratory services for maximum cost-effectiveness.
Additional Reading Becker, B. L. 1983. Learning to live with DRGs: The New Jersey experience. MLO 15:35-41. Becket, B. L. 1984. The impact of DRGs on New Jersey labs. MLO 16:30-41.
Case Report
Neisseria subflava as a C a u s e of B a c t e r e m i a Donald N. Wright, Ph.D. Microbiology Department Brigham Young University Provo, Utah 84602 Francis Liu, M.D. Department of lnternal Medicine Veterans Administration Medical Center Salt Lake City, Utah 84132
A recent brief review of Neisseria other than N. menb2gitidis and N. gonorrheae suggests that these organisms have been reported variously as etio-
58
0196-4399/84/$0.00 + 02.00
logic agents, commensals, and questionable pathogenic agents. The problem usually associated with assessing a pathogenic role for these organisms is their ubiquitous presence in normal human hosts and the concomitant isolation of other flora that may be the etiologic agent of a disease process (I, 2). We rel~ort here a documented case of Neisseria subflava sepsis. A 63-year-old male with a five-year history of an IgG class multiple my-
eloma was admitted with the acute onset of fever to 105°F. The patient was hypotensive (82/40) and had a pulse rate of 118. Admission laboratory data showed a white count of 800/ mm 3 and severe thrombocytopenia (20,000 platelets/l~l). A chest X-ray showed a patchy infiltrate in the right upper and lower lobes and in the left lower lobe. He was thought to be septic and was placed in intensive care. The patient had received multiple doses of chemotherapy and was asplenic. He had completed a Cytoxan, vincristine, and prednisone reg-
Clinical Microbiology Newsletter
Table 1 Characterization of Neisseria subflava Characteristic
Reaction of N. subflava
Oxidase Growth on nutrient agar Hemolysis Pigment Fermentation of: Fructose (~lucose Lactose Maltose Sucrose
+ + (22°C) Yellow (yellow-green)
imen five days earlier, with the last of the prednisone taken on the day before admission. Three sets of blood cultures (six bottles) were drawn on admission and the patient ,~).~s started on a combination of piperacillin and amikacin therapy. All six blood culture bottles were positive for N. subflava (characterized as indicated in Table 1). The isolate was susceptible to both beta-lactam and aminoglycoside antibiotics, erythromycin, trimethoprim/sulfamethoxazole, chloramphenicol, and rifampin. Of the 20 antimicrobials tested it was resistant only to vancomycin. Subsequent blood cultures were negative and remained negative throughout the hospital course. The patient's clinical condition improved dramatically and he was transferred from intensive care
Variable + + Variable
Reaction of lsolate
+ + (22°C) Yellow + + + +
on day 4 of his hospitalization. However, as a result of the severity of his underlying disease he expired on the tenth hospital day.
accompanying the patient's underlying disease and his recent chemotherapy undoubtedly predisposed him to infection with an organism of low-level virulence. No literature references are available for the use of many currently available antimicrobials in the treatment of disease caused by Neisseria other than N. meningitidis and N. gonorrheae. However, the rapid response of this patient to two recently available antibiotics and the broad in vitro susceptibility pattern of the isolate suggest that appropriate empiric therapy for such infections may be readily available.
Neisseria subflava is a commensal with very limited virulence properties. This organism has previously been reported as a cause of human infection (1, 3, 4). Except for isolates from endocarditis (4) and meningitis (5), however, the role of this organism in disease pathogenesis is questionable. In the case reported here, the successful repeated isolation of N. subflava alone from the blood of a septic patient strongly supports the concept that it was a primary pathogen. The marked decrease in measurable host defense mechanisms
References 1. Carpenter, C. M. 1943. Isolation of Neisseria tiara from the genitourinary tract of three patients. Am. J. Public Health 33:135-136. 2. Herbert, D. A., and J. Ruskin. 1981. Are the "nonpathogenie" Neisseria pat]aogenic? Am. J. Clin. Pathol. 75:739-743. 3. Lewin, R. A., and W. T. Huges. 1966. Neisseria subflava as a cause of meningitis and septicemia in children. J. Am. Med. Assoc. 195:821-823. 4. Major, R. H., and E. W. Johnson. 1945. Neisseria perflava endoearditis recovery. J. Am. Med. Assoc. 127:1051 - 1052. 5. Sophian, L. H. 1944. A case of acute meningitis caused by Neisseria perflava. Am. J. Med. Sci. 207:376-378.
G. The group C streptococci include Streptococcus equishnilis, S. zooepidemicus, S. equi, and S. dysgalactiae. Human group C streptococcal infections are usually caused by S. equisimilis. The group F streptococci include two colonial types, one markedly hemolytic referred to as S. anginosus and a minute hemolytic type called S. tnhzttttts. Both produce tiny colonies. The group G streptococci contain a large colony type that has not been named, but at times is called S. canis, and a minute colony,type referred to as S. anginosus (Type I, group G). The pathogenesis of groups C, F, and G streptococci is not generally known. These organisms have been
reported to cause a wide variety of disease states including meningitis, bacteremia, endocarditis, empyema, abscesses, and puerperal infections. It appears that these organisms are now being isolated more frequently from pathologic processes. It is not known whether this represents a real increase or an increase in the awareness of the organisms. The wide variety of specific typing sera now available probably has contributed to increased reporting of individual groups rather than just "beta-hemolytic streptococci, not group A . " The role of groups C , F, and G in pharyngitis is not understood and needs elucidation. Several outbreaks of pharyngitis caused by
Comment
Question and Answer Q: As a microbiologist working hi a clinical laboratory, I often isolate heavy amounts of beta-hemolytic streptococci that are susceptible to 23.75 mcg sulfamethoxazolell.25 mcg trimethoprim and resistant to O.04-ttnit bacitracin. Are these nongroup A streptococci considered pathogens? Robert G. Busch
Microbiologist Coon Rapids Medical Center Coon Rapids, Minnesota 55433 A: Beta-hemolytic streptococci susceptible to sulfamethoxazole/trimethoprim and resistant to bacitracin usually belong to Lancefield groups C, F, or
© 1984 by Elsevier Science Publishing Co., Inc.
01964399/84/$0.00 + 02.00
59
hospitals. We may also need to consider sharing our workload with other hospitals; for example, we'll do tests A, B, and C, whereas you will do tests D, E, and F. Group purchasing for certain supplies will become more attractive under PPS. The tight market that DRGs will create will also put pressure on vendors to " m a k e a better deal" whether it be for purchase of an instrument, a reagent rental agreement, or for supplies. Quality control and proficiency testing are expensive, and we may even have to look at these sacred cows to determine whether we can reduce costs in this area and still maintain quality. Finally, DRGs will force laboratory professionals to improve management at every level. Because of the fixed payment per DRG, the laboratory will become just another cost center and no longer enjoy the benefits of being a revenue center. Although the total effect of DRGs will not have a full impact on us for several years, there is real concern that prolonged trimming of costs will compromise the ability of the laboratory to provide quality care. When we are asked to provide new services we may first have to get rid of some old procedures, ones that are not sensitive and don't provide as much diagnostic information as others: for example, performing protein electrophoresis rather than protein assays. If you don't take DRGs seriously
now and evaluate what changes you might make, you run the risk of seriously compromising patient care in the future. No doubt a number of unpleasant prospects are in store for us, but it makes more sense to view this new challenge as an opportunity to improve the laboratory. In the health care field we often find that tough changes are best accomplished by using a third party (in this case, DRGs) as the bad guy. Using this ploy we can get various groups in the hospital to sit down and agree on what might be some exciting improvements to our services. In addition to the factors discussed, forecasting, marketing, and continuing education will become important. We'll have to make it our business to be informed, to know the language of administrators, to understand their problems in keeping the institution running under reimbursement constraints, and be willing resource people for helping to make the difficult decisions about restructuring laboratory services for maximum cost-effectiveness.
Additional Reading Becker, B. L. 1983. Learning to live with DRGs: The New Jersey experience. MLO 15:35-41. Becket, B. L. 1984. The impact of DRGs on New Jersey labs. MLO 16:30-41.
Case Report
Neisseria subflava as a C a u s e of B a c t e r e m i a Donald N. Wright, Ph.D. Microbiology Department Brigham Young University Provo, Utah 84602 Francis Liu, M.D. Department of lnternal Medicine Veterans Administration Medical Center Salt Lake City, Utah 84132
A recent brief review of Neisseria other than N. menb2gitidis and N. gonorrheae suggests that these organisms have been reported variously as etio-
58
0196-4399/84/$0.00 + 02.00
logic agents, commensals, and questionable pathogenic agents. The problem usually associated with assessing a pathogenic role for these organisms is their ubiquitous presence in normal human hosts and the concomitant isolation of other flora that may be the etiologic agent of a disease process (I, 2). We rel~ort here a documented case of Neisseria subflava sepsis. A 63-year-old male with a five-year history of an IgG class multiple my-
eloma was admitted with the acute onset of fever to 105°F. The patient was hypotensive (82/40) and had a pulse rate of 118. Admission laboratory data showed a white count of 800/ mm 3 and severe thrombocytopenia (20,000 platelets/l~l). A chest X-ray showed a patchy infiltrate in the right upper and lower lobes and in the left lower lobe. He was thought to be septic and was placed in intensive care. The patient had received multiple doses of chemotherapy and was asplenic. He had completed a Cytoxan, vincristine, and prednisone reg-
Clinical Microbiology Newsletter
Table 1 Characterization of Neisseria subflava Characteristic
Reaction of N. subflava
Oxidase Growth on nutrient agar Hemolysis Pigment Fermentation of: Fructose (~lucose Lactose Maltose Sucrose
+ + (22°C) Yellow (yellow-green)
imen five days earlier, with the last of the prednisone taken on the day before admission. Three sets of blood cultures (six bottles) were drawn on admission and the patient ,~).~s started on a combination of piperacillin and amikacin therapy. All six blood culture bottles were positive for N. subflava (characterized as indicated in Table 1). The isolate was susceptible to both beta-lactam and aminoglycoside antibiotics, erythromycin, trimethoprim/sulfamethoxazole, chloramphenicol, and rifampin. Of the 20 antimicrobials tested it was resistant only to vancomycin. Subsequent blood cultures were negative and remained negative throughout the hospital course. The patient's clinical condition improved dramatically and he was transferred from intensive care
Variable + + Variable
Reaction of lsolate
+ + (22°C) Yellow + + + +
on day 4 of his hospitalization. However, as a result of the severity of his underlying disease he expired on the tenth hospital day.
accompanying the patient's underlying disease and his recent chemotherapy undoubtedly predisposed him to infection with an organism of low-level virulence. No literature references are available for the use of many currently available antimicrobials in the treatment of disease caused by Neisseria other than N. meningitidis and N. gonorrheae. However, the rapid response of this patient to two recently available antibiotics and the broad in vitro susceptibility pattern of the isolate suggest that appropriate empiric therapy for such infections may be readily available.
Neisseria subflava is a commensal with very limited virulence properties. This organism has previously been reported as a cause of human infection (1, 3, 4). Except for isolates from endocarditis (4) and meningitis (5), however, the role of this organism in disease pathogenesis is questionable. In the case reported here, the successful repeated isolation of N. subflava alone from the blood of a septic patient strongly supports the concept that it was a primary pathogen. The marked decrease in measurable host defense mechanisms
References 1. Carpenter, C. M. 1943. Isolation of Neisseria tiara from the genitourinary tract of three patients. Am. J. Public Health 33:135-136. 2. Herbert, D. A., and J. Ruskin. 1981. Are the "nonpathogenie" Neisseria pat]aogenic? Am. J. Clin. Pathol. 75:739-743. 3. Lewin, R. A., and W. T. Huges. 1966. Neisseria subflava as a cause of meningitis and septicemia in children. J. Am. Med. Assoc. 195:821-823. 4. Major, R. H., and E. W. Johnson. 1945. Neisseria perflava endoearditis recovery. J. Am. Med. Assoc. 127:1051 - 1052. 5. Sophian, L. H. 1944. A case of acute meningitis caused by Neisseria perflava. Am. J. Med. Sci. 207:376-378.
G. The group C streptococci include Streptococcus equishnilis, S. zooepidemicus, S. equi, and S. dysgalactiae. Human group C streptococcal infections are usually caused by S. equisimilis. The group F streptococci include two colonial types, one markedly hemolytic referred to as S. anginosus and a minute hemolytic type called S. tnhzttttts. Both produce tiny colonies. The group G streptococci contain a large colony type that has not been named, but at times is called S. canis, and a minute colony,type referred to as S. anginosus (Type I, group G). The pathogenesis of groups C, F, and G streptococci is not generally known. These organisms have been
reported to cause a wide variety of disease states including meningitis, bacteremia, endocarditis, empyema, abscesses, and puerperal infections. It appears that these organisms are now being isolated more frequently from pathologic processes. It is not known whether this represents a real increase or an increase in the awareness of the organisms. The wide variety of specific typing sera now available probably has contributed to increased reporting of individual groups rather than just "beta-hemolytic streptococci, not group A . " The role of groups C , F, and G in pharyngitis is not understood and needs elucidation. Several outbreaks of pharyngitis caused by
Comment
Question and Answer Q: As a microbiologist working hi a clinical laboratory, I often isolate heavy amounts of beta-hemolytic streptococci that are susceptible to 23.75 mcg sulfamethoxazolell.25 mcg trimethoprim and resistant to O.04-ttnit bacitracin. Are these nongroup A streptococci considered pathogens? Robert G. Busch
Microbiologist Coon Rapids Medical Center Coon Rapids, Minnesota 55433 A: Beta-hemolytic streptococci susceptible to sulfamethoxazole/trimethoprim and resistant to bacitracin usually belong to Lancefield groups C, F, or
© 1984 by Elsevier Science Publishing Co., Inc.
01964399/84/$0.00 + 02.00
59