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Conversion of Pseudomonas aeruginosa to the phenotype characteristic of strains from patients with cystic fibrosis
55 Infectious Diseases Newsletter 9(7) July 1990 complicating Streptococcus milleri endocarditis. Postgrad Med J 59:250-253, 1983. Ball LC, Parker MT: The cultural and biochemical characters of Streptococcus milleri swains isolated from human sources. J Hyg (Cambridge) 82:63-78, 1979. Bateman NT, Eykyn SJ, Phillips I: Pyogenic liver abscess caused by Streptococcus milleri. Lancet 1:657-659, 1975. Blayney AW, Frootko NJ, Mitchell RG: Complications of sinusitis caused by Streptococcus milleri. J Laryngol Otol 98:895-899, 1984. Colman G, Williams REO: Taxonomy of some human viridans streptococci. In: Wannamaker LW, Matsen JM (eds): Streptococci and Streptococcal Diseases: Recognition, Understanding and Management. New York, Academic Press, pp. 281-299, 1972. Duma RJ, Weinberg AN, Medrek TF, et
al: Streptococcal infections. A bacteriologic and clinical study of streptococcal bacteremia. Medicine 48:87-127, 1969. Facklam RR: Physiological differentiation of viridans streptococci. J Clin Microbiol 5:184-201, 1975. Gossling, J: Occurrence and pathogenicity of the Streptococcus milleri group. Rev Infect Dis 10:257-285, 1988. Guthof O: Ueber pathogene "vergriiende streptokokken" Streptokokken Befunde bein dentogenen Abszessen und Infiltraten im Bereich der MundhOhle. Zentralblatt fur Bakteriologie, Parasitenkunde, Infektionskrankheiten und Hygiene. 1. Abteilung. Originale 166:553-564, 1965.
Mejare B, Edwardsson S: Streptococcus milleri (Guthof); an indigenous organism of the human oral cavity. Arch Oral Biol 20:757-762, 1975.
Highet AS, Warren RE, Staughton RCD, et al: Streptococcus milleri causing treatable infection in perineal hidradenitis suppurativa. Br J Dermatol 103:375-382, 1980.
Shlaes DM, Lemer PI, Wolinsky F, et al: Infections due to Lancefield group F and related streptococci (S. milleri, S. anginosus). Medicine 60:197-207, 1981.
Murray HW, Gross KC, Massur H, et al: Serious infections caused by Streptococcus railleri. Am J Med 64: 759-764, 1978. Poole PM, Wilson G: Occurrence and cultural features of Streptococcus milleri in various body sites. J Clin Pathol 32:764-768, 1970. Poole PM, Wilson G: Streptococcus milleri in the appendix. J Clin Pathol 30:937-942, 1977.
C O M M E N T S ON C U R R E N T P U B L I C A T I O N S Stead WW, Senner JW, Reddick WT,
et al: Racial differences in susceptibility to infection by Mycobacterium tuberculosis. N Engl J Med 322:422-427, 1990. Although the prevalence of tuberculosis among blacks is known to be about twice that among whites, this phenomenon is usually ascribed to social factors such as crowding and poverty. This study used a data base of more than 53,000 residents of racially integrated nursing homes in Arkansas in order to investigate whether the difference in prevalence of tuberculosis could be due in part to racial differences in susceptibility to Mycobacterium tuberculosis infection. The study found that under the same social conditions, blacks are apparently infected more readily by M. tuberculosis than whites. On repeat skin testing of tuberculin-negative nursing home residents, 13.8% of the blacks and only 7.2% of the whites had evidence of new infection. This difference was seen regardless of the race of the source patient. There was no racial difference in the percentage of residents who, in the absence of
therapy, were later found to have clinical tuberculosis. These unexpected findings are supported by data from three outbreaks of tuberculosis in two prisons that showed that blacks have about twice the relative risk of whites of becoming infected with M. tuberculosis.
dioidomycosis. In summary, this observation may offer methods to enhance preinfection defense mechanisms to prevent the implantation of tubercle bacilli. The use of bacille Calmette-Gu6rin vaccine might be one such method. CWS
Comment Clearly, there appears to be a racial difference in infectibility of M. tuberculosis. One wonders about the high prevalence of tuberculosis among American Indians. The mechanism of this difference is speculative. In vitro work (unpublished) has demonstrated that macrophages from blacks permit significantly more replication of M. tuberculosis than those from whites (P < .001). There are well-recognized racial differences in the immune defenses against two other infections, malaria and coccidioidomycosis. In one of these, malaria, the mechanism appears to involve differences in red blood cell membranes. In the other, coccidioidomycosis, there is no explanation. A difference in macrophage function would be an attractive answer for this phenomenon in cocci-
[]
© 1990 Elsevier Science Publishing Co., Inc. 0278-2316/90/$0.00 + 2.20
Speert DP, Farmer SW, Campbell ME, et al: Conversion of Pseudomonas aeruginosa to the phenotype
characteristic of strains from patients with cystic fibrosis. J Clin Microbiol 28:188-194, 1990. Patients with cystic fibrosis are known to frequently be infected and/or colonized with mucoid strains of Pseudomonas aeruginosa. This study investigated the reason for this phenomenon by subjecting nonmucoid clinical strains of P. aeruginosa to prolonged growth under conditions of suboptimal nutrition. The nonmucoid strains subjected to suboptimal growth conditions became mucoid. Thus, the
56 Infectious Diseases Newsletter 9(7) July 1990 mucoid strains seen in cystic fibrosis patients may represent a phenotype of P. aeruginosa arising as a consequence of nutrition limitation.
Comment Mucoid strains of P. aeruginosa are commonly found in patients with cystic fibrosis. The presence of such strains is a problem clinically as the exopolysaccharide appears to be a penetration barrier for aminoglycosides. This study presents compelling evidence that these mucoid strains arise from nonmucoid strains that are nutritionally deprived. This explanation is, in part, supported by the observation that similar mucoid strains of P. aeruginosa are also found in other forms of chronic bronchopulmonary disease and in chronic urinary tract disease. Possibly the polysaccharide can serve as a source of nutrition (or source of necessary cations) for these isolates. Phenotypic
Aims and Scope The InJe~tious Diseases Newsletter seeks to provide concise reports of the current state of knowledge and practice in infectious diseases. Diverse sources arc tapped. the primary consideration being the relevance of the information that is gained. The intended audience includes physicians, nurses, and laboratory personnel who participate in the diagnosis, treatment, and prevention of infectious diseases. Such broad dissemination is warranted by the essential, yet interdependent, nature of the efforts of those health care providers whose concern is patients with infectious diseases.
modulation is a well-recognized means of allowing bacteria to survive in hostile environments; mucoid strains of P. aeruginosa appear to be yet another example of such phenotypic adaptation. CWS
[]
and liver biopsy for determining the cause of fever of undetermined origin in 12 patients with serologic evidence of human immunodeficiency virus infection. Mycobacterial infection was found in 8 of the 12 patients (Mycobacterium tuberculosis in 3 and Mycobacterium avium in 5). Mycobacteria were isolated from the blood of six of these eight patients. Acidfast organisms or granulomas were seen in four bone marrow and six liver specimens.
Prego V, Glatt AE, Roy V, et al:
Comparative yield of blood culture for fungi and mycobacteria, liver biopsy, and bone marrow biopsy in the diagnosis of fever of undetermined origin in human immunodeficiency virus-infected patients. Arch Intern Med 150:333-336, 1990. This study prospectively compared the diagnostic yield of mycobacterial blood cultures, bone marrow biopsy,
Comment This study indicates that in patients infected with HIV, fever of undetermined origin is commonly associated with mycobacterial infection. An aggressive approach using mycobacteriat blood cultures followed by the timely use of both liver and bone marrow biopsy will provide the optimal chance for diagnosis. CWS
General Information Infectious Diseases Newsletter is published monthly by Elsevier Science Publishing Co., Inc., 655 Avenue of the Americas, New York, New York 10010. Please see inside front cover for subscription information. This newsletter has been registered with the Copyright Clearance Center Inc. Consent is given for copying of articles for personal or internal use, or for the personal or internal use of specific clients. This consent is given on the condition that the copier pay through the Center the per-page fee stated in the code on each page for copying beyond that permitted by the US Copyright Law. If no code appears on an article, the author has not given broad consent to copy and permission to copy must be obtained directly from the author. This consent does not extend to other kinds of copying, such as for general distribution, resale, advertising and promotional purposes, or for creating new collective works. Address orders, changes of address, and claims for missing issues to Journals Fulfillment Department, Elsevier Science Publishing Co., Inc., 655 Avenue of the Americas, New York, New York 10010. Claims for missing issues can be honored only up to three months for domestic addresses and six months for foreign addresses. Duplicate copies will not be sent to replace those undelivered because of failure to notify Elsevier of change of address. Address editorial correspondence to Charles W. Stratton, MD, Director of Clinical Microbiology, Department of Pathology, Vanderbilt University Medical Center, C3321 Medical Center North, Nashville, TN 37232.
Infectious Diseases Newsletter is included in BIOS1S. © 1990 Elsevier Science Publishing Co., Inc. 0278-2316/90/$0.00 ~ 2.20
al: Streptococcal infections. A bacteriologic and clinical study of streptococcal bacteremia. Medicine 48:87-127, 1969. Facklam RR: Physiological differentiation of viridans streptococci. J Clin Microbiol 5:184-201, 1975. Gossling, J: Occurrence and pathogenicity of the Streptococcus milleri group. Rev Infect Dis 10:257-285, 1988. Guthof O: Ueber pathogene "vergriiende streptokokken" Streptokokken Befunde bein dentogenen Abszessen und Infiltraten im Bereich der MundhOhle. Zentralblatt fur Bakteriologie, Parasitenkunde, Infektionskrankheiten und Hygiene. 1. Abteilung. Originale 166:553-564, 1965.
Mejare B, Edwardsson S: Streptococcus milleri (Guthof); an indigenous organism of the human oral cavity. Arch Oral Biol 20:757-762, 1975.
Highet AS, Warren RE, Staughton RCD, et al: Streptococcus milleri causing treatable infection in perineal hidradenitis suppurativa. Br J Dermatol 103:375-382, 1980.
Shlaes DM, Lemer PI, Wolinsky F, et al: Infections due to Lancefield group F and related streptococci (S. milleri, S. anginosus). Medicine 60:197-207, 1981.
Murray HW, Gross KC, Massur H, et al: Serious infections caused by Streptococcus railleri. Am J Med 64: 759-764, 1978. Poole PM, Wilson G: Occurrence and cultural features of Streptococcus milleri in various body sites. J Clin Pathol 32:764-768, 1970. Poole PM, Wilson G: Streptococcus milleri in the appendix. J Clin Pathol 30:937-942, 1977.
C O M M E N T S ON C U R R E N T P U B L I C A T I O N S Stead WW, Senner JW, Reddick WT,
et al: Racial differences in susceptibility to infection by Mycobacterium tuberculosis. N Engl J Med 322:422-427, 1990. Although the prevalence of tuberculosis among blacks is known to be about twice that among whites, this phenomenon is usually ascribed to social factors such as crowding and poverty. This study used a data base of more than 53,000 residents of racially integrated nursing homes in Arkansas in order to investigate whether the difference in prevalence of tuberculosis could be due in part to racial differences in susceptibility to Mycobacterium tuberculosis infection. The study found that under the same social conditions, blacks are apparently infected more readily by M. tuberculosis than whites. On repeat skin testing of tuberculin-negative nursing home residents, 13.8% of the blacks and only 7.2% of the whites had evidence of new infection. This difference was seen regardless of the race of the source patient. There was no racial difference in the percentage of residents who, in the absence of
therapy, were later found to have clinical tuberculosis. These unexpected findings are supported by data from three outbreaks of tuberculosis in two prisons that showed that blacks have about twice the relative risk of whites of becoming infected with M. tuberculosis.
dioidomycosis. In summary, this observation may offer methods to enhance preinfection defense mechanisms to prevent the implantation of tubercle bacilli. The use of bacille Calmette-Gu6rin vaccine might be one such method. CWS
Comment Clearly, there appears to be a racial difference in infectibility of M. tuberculosis. One wonders about the high prevalence of tuberculosis among American Indians. The mechanism of this difference is speculative. In vitro work (unpublished) has demonstrated that macrophages from blacks permit significantly more replication of M. tuberculosis than those from whites (P < .001). There are well-recognized racial differences in the immune defenses against two other infections, malaria and coccidioidomycosis. In one of these, malaria, the mechanism appears to involve differences in red blood cell membranes. In the other, coccidioidomycosis, there is no explanation. A difference in macrophage function would be an attractive answer for this phenomenon in cocci-
[]
© 1990 Elsevier Science Publishing Co., Inc. 0278-2316/90/$0.00 + 2.20
Speert DP, Farmer SW, Campbell ME, et al: Conversion of Pseudomonas aeruginosa to the phenotype
characteristic of strains from patients with cystic fibrosis. J Clin Microbiol 28:188-194, 1990. Patients with cystic fibrosis are known to frequently be infected and/or colonized with mucoid strains of Pseudomonas aeruginosa. This study investigated the reason for this phenomenon by subjecting nonmucoid clinical strains of P. aeruginosa to prolonged growth under conditions of suboptimal nutrition. The nonmucoid strains subjected to suboptimal growth conditions became mucoid. Thus, the
56 Infectious Diseases Newsletter 9(7) July 1990 mucoid strains seen in cystic fibrosis patients may represent a phenotype of P. aeruginosa arising as a consequence of nutrition limitation.
Comment Mucoid strains of P. aeruginosa are commonly found in patients with cystic fibrosis. The presence of such strains is a problem clinically as the exopolysaccharide appears to be a penetration barrier for aminoglycosides. This study presents compelling evidence that these mucoid strains arise from nonmucoid strains that are nutritionally deprived. This explanation is, in part, supported by the observation that similar mucoid strains of P. aeruginosa are also found in other forms of chronic bronchopulmonary disease and in chronic urinary tract disease. Possibly the polysaccharide can serve as a source of nutrition (or source of necessary cations) for these isolates. Phenotypic
Aims and Scope The InJe~tious Diseases Newsletter seeks to provide concise reports of the current state of knowledge and practice in infectious diseases. Diverse sources arc tapped. the primary consideration being the relevance of the information that is gained. The intended audience includes physicians, nurses, and laboratory personnel who participate in the diagnosis, treatment, and prevention of infectious diseases. Such broad dissemination is warranted by the essential, yet interdependent, nature of the efforts of those health care providers whose concern is patients with infectious diseases.
modulation is a well-recognized means of allowing bacteria to survive in hostile environments; mucoid strains of P. aeruginosa appear to be yet another example of such phenotypic adaptation. CWS
[]
and liver biopsy for determining the cause of fever of undetermined origin in 12 patients with serologic evidence of human immunodeficiency virus infection. Mycobacterial infection was found in 8 of the 12 patients (Mycobacterium tuberculosis in 3 and Mycobacterium avium in 5). Mycobacteria were isolated from the blood of six of these eight patients. Acidfast organisms or granulomas were seen in four bone marrow and six liver specimens.
Prego V, Glatt AE, Roy V, et al:
Comparative yield of blood culture for fungi and mycobacteria, liver biopsy, and bone marrow biopsy in the diagnosis of fever of undetermined origin in human immunodeficiency virus-infected patients. Arch Intern Med 150:333-336, 1990. This study prospectively compared the diagnostic yield of mycobacterial blood cultures, bone marrow biopsy,
Comment This study indicates that in patients infected with HIV, fever of undetermined origin is commonly associated with mycobacterial infection. An aggressive approach using mycobacteriat blood cultures followed by the timely use of both liver and bone marrow biopsy will provide the optimal chance for diagnosis. CWS
General Information Infectious Diseases Newsletter is published monthly by Elsevier Science Publishing Co., Inc., 655 Avenue of the Americas, New York, New York 10010. Please see inside front cover for subscription information. This newsletter has been registered with the Copyright Clearance Center Inc. Consent is given for copying of articles for personal or internal use, or for the personal or internal use of specific clients. This consent is given on the condition that the copier pay through the Center the per-page fee stated in the code on each page for copying beyond that permitted by the US Copyright Law. If no code appears on an article, the author has not given broad consent to copy and permission to copy must be obtained directly from the author. This consent does not extend to other kinds of copying, such as for general distribution, resale, advertising and promotional purposes, or for creating new collective works. Address orders, changes of address, and claims for missing issues to Journals Fulfillment Department, Elsevier Science Publishing Co., Inc., 655 Avenue of the Americas, New York, New York 10010. Claims for missing issues can be honored only up to three months for domestic addresses and six months for foreign addresses. Duplicate copies will not be sent to replace those undelivered because of failure to notify Elsevier of change of address. Address editorial correspondence to Charles W. Stratton, MD, Director of Clinical Microbiology, Department of Pathology, Vanderbilt University Medical Center, C3321 Medical Center North, Nashville, TN 37232.
Infectious Diseases Newsletter is included in BIOS1S. © 1990 Elsevier Science Publishing Co., Inc. 0278-2316/90/$0.00 ~ 2.20