Kessler C M, Nussbaum E, Tuazon C U
J Lab Clin Med. 1987 Jun;109(6):647-52.
Platelet-bacterial interactions were examined in vitro by incubating organisms isolated from patients with septicemia with normal platelet-rich plasma. The potency of various species of gram-positive and gram-negative bacteria to induce irreversible platelet aggregation was then determined in an aggregometer. The aggregation curves produced by the bacteria resembled the normal platelet response to collagen and were impeded by the presence of aspirin. Strains of Staphylococcus aureus and Pseudomonas aeruginosa isolated from 25 different patients produced maximum increases in light transmission and irreversible platelet aggregation with relatively rapid mean aggregation times; six of these patients had clinical and laboratory evidence of disseminated intravascular coagulation. In contrast, isolates of alpha streptococcus and Staphylococcus epidermidis induced irreversible platelet aggregation much less commonly and were associated with considerably longer mean aggregation times. None of the latter group of patients had evidence of disseminated intravascular coagulation. Isolates of bacteria from a small number of patients with subacute bacterial endocarditis uniformly induced irreversible platelet aggregation. Addition of paired bacterial isolates to normal platelet-rich plasma demonstrated a synergistic aggregation response. These data suggest that a relative hierarchy exists in bacterial strain potency to induce irreversible platelet aggregation. The rapidity and degree of aggregation in vitro correlated well with the clinical and laboratory evidence for subacute bacterial endocarditis and disseminated intravascular coagulation in vivo. These observations may provide useful adjunctive laboratory information to help establish the diagnosis of subacute bacterial endocarditis, especially in the clinical setting where the classical findings of endocarditis are not obvious during initial presentation.
通过将从败血症患者中分离出的微生物与正常富含血小板的血浆一起孵育，在体外检测血小板与细菌的相互作用。然后在血小板聚集仪中测定各种革兰氏阳性菌和革兰氏阴性菌诱导不可逆血小板聚集的能力。细菌产生的聚集曲线类似于血小板对胶原蛋白的正常反应，并且阿司匹林的存在会抑制这种反应。从25名不同患者中分离出的金黄色葡萄球菌和铜绿假单胞菌菌株使透光率最大增加且产生不可逆的血小板聚集，平均聚集时间相对较快；其中6名患者有弥散性血管内凝血的临床和实验室证据。相比之下，α链球菌和表皮葡萄球菌分离株诱导不可逆血小板聚集的情况要少得多，且平均聚集时间长得多。后一组患者均无弥散性血管内凝血的证据。从少数亚急性细菌性心内膜炎患者中分离出的细菌菌株均能一致地诱导不可逆血小板聚集。将成对的细菌分离株添加到正常富含血小板的血浆中显示出协同聚集反应。这些数据表明，在诱导不可逆血小板聚集的细菌菌株效力方面存在相对等级。体外聚集的速度和程度与体内亚急性细菌性心内膜炎和弥散性血管内凝血的临床和实验室证据密切相关。这些观察结果可能提供有用的辅助实验室信息，以帮助确立亚急性细菌性心内膜炎的诊断，特别是在初次就诊时心内膜炎的典型表现不明显的临床情况下。
