Heparin therapy in meningococcal septicaemia

Hunter, John

doi:10.1136/adc.48.3.233

Cited by 11 publications

(7 citation statements)

References 13 publications

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“…In this context it is tempting to speculate about the effect of heparin treatment of patients with meningococcal sepsis in terms of protection of N . meningitidis against complement 55 – 57 . However, any inhibitory effect of heparin on the complement system would not be relevant to survival of the bacteria, which are rapidly killed upon the immediate administration of antibiotics to the patients.…”

Section: Discussionmentioning

confidence: 99%

Anticoagulants impact on innate immune responses and bacterial survival in whole blood models of Neisseria meningitidis infection

Strobel¹,

Johswich²

2018

Sci Rep

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Neisseria meningitidis (meningococcus) causes invasive diseases such as meningitis or septicaemia. Ex vivo infection of human whole blood is a valuable tool to study meningococcal virulence factors and the host innate immune responses. In order to consider effects of cellular mediators, the coagulation cascade must be inhibited to avoid clotting. There is considerable variation in the anticoagulants used among studies of N. meningitidis whole blood infections, featuring citrate, heparin or derivatives of hirudin, a polypeptide from leech saliva. Here, we compare the influence of these three different anticoagulants, and additionally Mg/EGTA, on host innate immune responses as well as on viability of N. meningitidis strains isolated from healthy carriers and disease cases, reflecting different sequence types and capsule phenotypes. We found that the anticoagulants significantly impact on cellular responses and, strain-dependently, also on bacterial survival. Hirudin does not inhibit complement and is therefore superior over the other anticoagulants; indeed hirudin-plasma most closely reflects the characteristics of serum during N. meningitidis infection. We further demonstrate the impact of heparin on complement activation on N. meningitidis and its consequences on meningococcal survival in immune sera, which appears to be independent of the heparin binding antigens Opc and NHBA.

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Section: Discussionmentioning

confidence: 99%

Anticoagulants impact on innate immune responses and bacterial survival in whole blood models of Neisseria meningitidis infection

Strobel¹,

Johswich²

2018

Sci Rep

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Section: Case Reportmentioning

confidence: 99%

“…The clinical picture on admission was that of meningococcal septicaemia with an unfavourable prognosis, since (a) petechiae appeared 6 hours before admission, (b) CSF contained 12 white cells, and (c) white blood count was 7000/mm3 (Stiehm and Damrosch, 1966;Hunter, 1973). Disseminated intravascular coagulation was suspected on clinical grounds and was substantiated by the low platelet count and prolonged prothrombin time.…”

Section: Case Reportmentioning

confidence: 99%

Heparin therapy in meningococcal septicaemia.

Smith¹

1973

Archives of Disease in Childhood

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“…The anti-infective effect of HP was later confirmed in vivo in a rabbit model of skin infection (3). Later studies in the 1970’s examining the anti-infective effects of HP showed that this highly sulfated GAG also inhibits the initial attachment of other pathogens to host cells, such as Neisseria meningitides (4) and Chlamydia trachomatis (5). …”

Section: Introductionmentioning

confidence: 99%

Glycosaminoglycans and infection

2016

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Glycosaminoglycans (GAGs) are complex linear polysaccharides expressed in intracellular compartments, at the cell surface, and in the extracellular environment where they interact with various molecules to regulate many cellular processes implicated in health and disease. Subversion of GAGs is a pathogenic strategy shared by a wide variety of microbial pathogens, including viruses, bacteria, parasites, and fungi. Pathogens use GAGs at virtually every major portals of entry to promote their attachment and invasion of host cells, movement from one cell to another, and to protect themselves from immune attack. Pathogens co-opt fundamental activities of GAGs to accomplish these tasks. This ingenious strategy to subvert essential activities of GAGs likely prevented host organisms from deleting or inactivating these mechanisms during their evolution. The goal of this review is to provide a mechanistic overview of our current understanding of how microbes subvert GAGs at major steps of pathogenesis, using select GAG-pathogen interactions as representative examples.

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Heparin therapy in meningococcal septicaemia

Cited by 11 publications

References 13 publications

Anticoagulants impact on innate immune responses and bacterial survival in whole blood models of Neisseria meningitidis infection

Anticoagulants impact on innate immune responses and bacterial survival in whole blood models of Neisseria meningitidis infection

Heparin therapy in meningococcal septicaemia.

Glycosaminoglycans and infection

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