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利用葡聚糖和明胶微载体建立小鼠金黄色葡萄球菌脓肿实验模型。

Establishment of an experimental model of a Staphylococcus aureus abscess in mice by use of dextran and gelatin microcarriers.

作者信息

Ford C W, Hamel J C, Stapert D, Yancey R J

机构信息

Infectious Diseases Research, Upjohn Company, Kalamazoo, MI 49001.

出版信息

J Med Microbiol. 1989 Apr;28(4):259-66. doi: 10.1099/00222615-28-4-259.

Abstract

Staphylococcus aureus UC 9271 mixed with dextran or gelatin microcarrier beads and injected subcutaneously into mice resulted in the formation of reproducible, sustained abscesses with as few as 2 x 10(3) cfu. Without microcarrier beads, 4 x 10(7) cfu were required to produce an abscess. The abscesses that developed with microcarriers attained a diameter of up to 1.5 cm and persisted for several days before discharging through the skin. The pH of the abscesses fell from 7.1 to 6.6 within 24 h. Histological and microscopic examination of the abscesses revealed an influx of phagocytic cells, mostly polymorphonuclear leucocytes, within 1-2 h after injection. Cell debris accumulated and the abscess became encapsulated 24-48 h after infection. Enzymatic digestion of the abscess contents allowed analysis of the host and bacterial cell populations and treatment with lysostaphin permitted differentiation between phagocytosed and free bacterial populations of S. aureus. Phagocytosed but viable S. aureus comprised c. 50% of the total bacterial population after 24 h; however, by 96 h the phagocytosed population was only 1-5% of the total population, primarily because of an increase in extracellular bacterial numbers. Prevention of abscess formation by antibiotic treatment based upon the minimal inhibitory concentration (MIC) of an antibiotic for S. aureus was not always predictable. Tetracycline did not prevent abscess formation even though it possessed a low MIC for S. aureus; methicillin had a borderline MIC value but was quite active. However, the MIC values were quite predictive of antibiotic cures in a systemic-lethal S. aureus infection in mice.

摘要

将金黄色葡萄球菌UC 9271与葡聚糖或明胶微载体珠混合,然后皮下注射到小鼠体内,结果发现,即使接种低至2×10³cfu也能形成可重复出现的持续性脓肿。若不使用微载体珠,则需要4×10⁷cfu才能产生脓肿。有微载体珠时形成的脓肿直径可达1.5厘米,并持续数天,之后通过皮肤排出。脓肿的pH值在24小时内从7.1降至6.6。对脓肿进行组织学和显微镜检查发现,注射后1 - 2小时内有吞噬细胞大量涌入,其中大多为多形核白细胞。感染后24 - 48小时,细胞碎片开始堆积,脓肿被包裹起来。对脓肿内容物进行酶消化,以便分析宿主细胞和细菌细胞群体,用溶葡萄球菌素处理则可区分被吞噬的和游离的金黄色葡萄球菌群体。24小时后,被吞噬但仍存活的金黄色葡萄球菌约占细菌总数的50%;然而,到96小时时,被吞噬的细菌群体仅占总数的1 - 5%,主要原因是细胞外细菌数量增加。基于抗生素对金黄色葡萄球菌的最低抑菌浓度(MIC)进行抗生素治疗来预防脓肿形成,其效果并非总是可预测的。四环素尽管对金黄色葡萄球菌的MIC较低,但并不能预防脓肿形成;甲氧西林的MIC值处于临界水平,但其活性相当高。然而,MIC值对于小鼠全身性致死性金黄色葡萄球菌感染的抗生素治疗效果具有很好的预测性。

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