Results Secured by Standard Methods of Treatment in Neurosyphilis

Stokes, John H.; Shaffer, Loren W.

doi:10.1001/jama.1924.02660230020005

Cited by 5 publications

(1 citation statement)

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“…Despite an improved understanding of the relationship between the microbe and the natural history of the disease, treatment of syphilis remained based on administration of mercury by mouth, injection, dermatologic application or exposure to its vapours to purge the humour through salivation or sweating. Understandably, optimism greeted Paul Erlich’s development of the arsenicals salvarsan (1910) and neosalvarsan as potential ‘magic bullets’ against syphilis; however, these treatments still exposed patients to significant risk and still failed to ward off or cure neurosyphilis (Stokes and Shaffer, 1924; Arnold, 1984; Jolliffe, 1993). Patients with neurosyphilis were difficult to manage, ‘became completely demented and unable to care for themselves, dying most often in insane asylums’ (Brown, 2000).…”

Section: The Era Of Great Biological Discoverymentioning

confidence: 99%

Red Blood Cell Polymorphism and Susceptibility to Plasmodium vivax

Zimmerman

Ferreira

Howes

et al. 2013

Advances in Parasitology

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Resistance to Plasmodium vivax blood-stage infection has been widely recognised to result from absence of the Duffy (Fy) blood group from the surface of red blood cells (RBCs) in individuals of African descent. Interestingly, recent studies from different malaria-endemic regions have begun to reveal new perspectives on the association between Duffy gene polymorphism and P. vivax malaria. In Papua New Guinea and the Americas, heterozygous carriers of a Duffy-negative allele are less susceptible to P. vivax infection than Duffy-positive homozygotes. In Brazil, studies show that the Fya antigen, compared to Fyb, is associated with lower binding to the P. vivax Duffy-binding protein and reduced susceptibility to vivax malaria. Additionally, it is interesting that numerous studies have now shown that P. vivax can infect RBCs and cause clinical disease in Duffy-negative people. This suggests that the relationship between P. vivax and the Duffy antigen is more complex than customarily described. Evidence of P. vivax Duffy-independent red cell invasion indicates that the parasite must be evolving alternative red cell invasion pathways. In this chapter, we review the evidence for P. vivax Duffy-dependent and Duffy-independent red cell invasion. We also consider the influence of further host gene polymorphism associated with malaria endemicity on susceptibility to vivax malaria. The interaction between the parasite and the RBC has significant potential to influence the effectiveness of P. vivax-specific vaccines and drug treatments. Ultimately, the relationships between red cell polymorphisms and P. vivax blood-stage infection will influence our estimates on the population at risk and efforts to eliminate vivax malaria.

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Section: The Era Of Great Biological Discoverymentioning

confidence: 99%