Microflora of plaque in rats following infection with an LDH-deficient mutant of Streptococcus rattus.
Microflora of plaque in rats following infection with an LDH-deficient mutant of Streptococcus rattus.
复制标题
感染大鼠链球菌 LDH 缺陷突变体后菌斑的微生物区系。
DOI：
10.1159/000261211
复制
发表时间：
1989
期刊：
影响因子：
4.2
通讯作者：
Hillman,JD
中科院分区：
文献类型：
--
作者：
Stashenko,KP;Hillman,JD
Lactate dehydrogenase (LDH)-deficient mutants of mutans streptococci have been extensively charac terized to determine their usefulness as effector strains in the replacement therapy of dental caries [for re view, Hillman and Socransky, 1987], Several studies have shown them to be virtually noncariogenic both in vitro and in gnotobiotic and conventional rats [Hillman, 1978; Johnson et al., 1980], Also, once col onized by the mutant, the teeth of conventional rats show greatly increased resistance to infection by wildtype strains of mutans streptococci [Johnson and Hill man, 1982], Ideally, replacement therapy for the pre vention of a particular disease should not signifi cantly alter the composition of the microflora asso ciated with the treated tissues. To do so might increase the susceptibility of the host to other, potentially more hazardous diseases [Bohnoff et al., 1954], With regard to most phenotypic properties, LDH-deficient mut ants of mutans streptococci resemble closely their wild-type parents [Hillman, 1978] and, thus, would not be expected to alter the composition of the normal plaque flora. However, the mutants have been shown to metabolize glucose to yield substantially more eth anol and acetoin than their parents [Hillman et al., 1987], The mutants have also been found to produce somewhat greater amounts of plaque than their par ents when grown in the presence of sucrose [Hillman, 1978], The following study was designed to determine whether these phenotypic changes (and others that may be currently unrecognized) cause the mutant to affect the ecology of dental plaque. Nine Sprague-Dawley rats were purchased from the Charles RiverBreeding Laboratories (Wilmington, Mass). The ani mals were separated into three groups and housed sep arately in metal wire cages. They were maintained on diet 2000 [Keyes and Jordan, 1964] containing 56%(w/w) sucrose throughout the experiment. Three swab samples of plaque and saliva were taken at daily intervals from each animal and streaked onto Mitis-Salivarius agar (Difco) containing bacitracin [Gold et al., 1973] to verify the absence of indigenous strains of mutans streptococci. At 21 days of age, animals in group 1 were infected with the Streptococcus rattus parent strain, BHT-2 [resistant to 1mg/ml streptomy cin; Hillman, 1978], by pipetting 0.1 ml of an over night, Todd-Hewitt broth (Difco) culture into their oral cavities. Animals in group 2 were treated with 0.1-ml samples of a culture of a spontaneous LDH-deficient mutant of strain BHT-2 called JH145 that has been previously characterized [Johnson et al., 1980], Animals in group 3 were treated with sterile Todd-Hewitt broth. Oral swab samples taken at monthly intervals and streaked on glucose tetrazolium medium [Hillman, 1978] containing 1 mg/ml streptomycin were used to verify the continued pres ence of the infecting strains throughout the experi ment. Visual examination of colonies of the mutant arising on this medium also confirmed that the fre quency of its reversion to wild-type was below the limits of detection (ie,< 1%). Six months following infection, the animals were killed using hyperbaric carbon dioxide. The maxillary and mandibular mo lars from the left side of each animal were scored for incidence and severity of carious lesions using the
