Aggregation of platelets by Fusobacterium necrophorum

Abstract

Broth cultures and washed cells of 13 of 24 bovine isolates of Fusobacterium necrophorum aggregated human platelets in platelet-rich plasma. The cell-free culture fluid was inactive. Bacteria stored at 4°C in saline remained active for at least 3 months, but they did not release activity into the storage solution. Aggregation typically began within 1 min after the addition of 103 bacteria to 103 platelets and was complete within 5.5 min. Assays for cytosolic lactic dehydrogenase revealed that platelet lysis did not occur. The release of ['4C]serotonin from platelets preincubated with this amine accompanied aggregation, indicating that this was a typical aggregation-degranulation reaction. Platelet aggregation was inhibited by EDTA (88% at 2.0 mM), aspirin (75% inhibition at 1.0 mM), and quinacrine (80% inhibition at 0.25 mM). Thus the reaction was an ion-dependent, cyclooxygenase-sensitive event. Gel-filtered platelets were less sensitive to aggregation than were platelets in plasma, but this sensitivity was fully restored by the addition of plasma and partially restored with fibrinogen. Biotyping of the cultures revealed that none of the avirulent, B-type strains of F. necrophorum could aggregate platelets, whereas 13 of 16 virulent A type strains were positive. These results suggest that platelet aggregation by F. necrophorum is related to the virulence of this organism.

Platelet Aggregation Induced by Strains of Various Species of Coagulase‐Negative Staphylococci

“…As noted above, inhibitory activity of Y. USUI ET AL ASA and quinacrine was slight in most species of CNS used, indicating that the arachidonate pathway was not a major route in cases of CNS. Serotonin release, which is considered to be one of the markers for platelet aggregation, has been reported to occur during platelet aggregation by various species of bacteria (8,9,20,31,32,34,36) as well as several agonists (14). As noted above, serotonin was released by the interactions between 10 species of CNS having ability to induce platelet aggregation and rabbit platelets.…”

“…4). By heat treatment at 100 C for 10 min, the potentials of platelet aggregation of S. epidermidis, S. simulans, and S. hyicus were decreased in 65.6% (Pc 0.05), 61.4% 0.05) and 70.9% (P<0.05) compared to those of the controls, respec- (20), group B streptococci (34,36), Viridans group streptococci (31,32), F. necrophorum (9), and H. capsulatum (8) were reported to be inhibited with the addition of arachidonate pathway inhibitors such as ASA, indomethacin, or quinacrine, while those by L. monocytogenes (7), A. .fumigatus (29), C. albicans (30) were not.…”

Lemierre syndrome: Study of 11 cases and literature review

“…16 In addition, platelet aggregation is considered as a virulence property of Fusobacterium necrophorum that causes thrombocytopenia, disseminated intravascular coagulation, fibrin deposition, and other coagulative effects. 25 All these factors contribute to infection spread in the parapharyngeal space by direct contamination or through lymphatics. Finally, extension occurs to the cervical region resulting in thrombosis of the IJV or one of its tributaries.…”

The changing pattern of fusobacterium infections in humans: recent experience with fusobacterium bacteraemia

“…Twelve patients presented with a haemostasis disorder associated with both F. nucleatum and F. necrophorum. This may reflect a non-specific haemostasis disorder, although F. necrophorum has been shown to display platelet-aggregating activity [10]. This has not been demonstrated for F. nucleatum.…”