Johnson K P, Hillman J D
Arch Oral Biol. 1982;27(6):513-6. doi: 10.1016/0003-9969(82)90093-0.
Prior establishment of a lactate dehydrogenase (LDH)-deficient mutant of Streptococcus mutans in the mouths of rats caused a 10-10,000-fold increase in the minimal infectious dose for persistent colonization by wild-type strains of this organism. The finding that LDH-deficient mutants can render their host relatively resistant to infection by decay-causing strains of Strep. mutans while being much less pathogenic themselves, lends support to their prospective usefulness as effector strains in the replacement therapy of dental caries.
先前在大鼠口腔中建立变形链球菌乳酸脱氢酶(LDH)缺陷型突变体,导致该生物体野生型菌株持续定植的最小感染剂量增加了10至10000倍。LDH缺陷型突变体可使宿主对变形链球菌致龋菌株的感染具有相对抗性,而其自身致病性则低得多,这一发现支持了它们作为龋齿替代治疗中效应菌株的潜在用途。