Hæwenhnydele: an Anglo-Saxon Medicinal Plant

Summary

The Old English plant-name, hæwenhnydele, occurs in herbal and medical texts and in glossaries containing translated Latin plant-names. Where it is linked with a Latin name, that name is always Herba Britannica, a cure for scurvy. Some scholars, rather naively assuming that the two names must refer to the same plant, have thought the identity of hæwenhnydele almost obvious, whereas others, knowing the frequently garbled accounts of herbal cures inherited by the Anglo-Saxons, have despaired of ever identifying it. An Anglo-Saxon translator, working on the Old English version of the Latin Pseudo-Apuleius, inherited an account of Herba Britannica which was a confusion of two different plants, compiled from several sources. The information available to him is discussed, in an effort to understand how he made an identification. Evidence such as the synonyms attached to the plant entry, the etymology of hæwenhnydele, and the illustration of the plant is presented. There is also a brief discussion of the two recorded occurrences of the rural plant-name, hawdod, from the 16th and 18th centuries, and whether this name could be cognate with hæwenhnydele. In the Durham Glossary, another name, vihtmeresvyrt, is linked with Herba Britannica and hæwenhnydele. This name is discussed, and found to denote a well-known source of Vitamin C, the cure for scurvy. This paper demonstrates that the attempts of the Anglo-Saxons to identify Herba Britannica, and to link their guesses with real herbal cures, are an impressive rationalisation of an almost nonsensical Latin plant record.     

Are Patients with Erythema Migrans Who Have Leukopenia and/or Thrombocytopenia Coinfected with Anaplasma phagocytophilum or Tick-Borne Encephalitis Virus?

Lyme borreliosis (LB), tick-borne encephalitis (TBE) and human granulocytic anaplasmosis (HGA) are endemic in central part of Slovenia. We tested the hypothesis that patients with erythema migrans (EM) from this region, who have leukopenia and/or thrombocytopenia (typical findings in HGA and in the initial phase of TBE but not in patients with LB) are coinfected with Anaplasma phagocytophilum and/or with TBE virus, i.e. that cytopenia is a result of concomitant HGA or the initial phase of TBE. Comparison of clinical and laboratory findings for 67 patients with EM who disclosed leukopenia/thrombocytopenia with the corresponding results in sex- and age-matched patients with EM and normal blood cell counts revealed no differences. In addition, patients with typical EM and leukopenia and/or thrombocytopenia tested negative for the presence of IgM and IgG antibodies to TBE virus by ELISA as well as for the presence of specific IgG antibodies to A. phagocytophilum antigens by IFA in acute and convalescent serum samples. Thus, none of 67 patients (95% CI: 0 to 5.3%) with typical EM (the presence of this skin lesion attests for early Lyme borreliosis and is the evidence for a recent tick bite) was found to be coinfected with A. phagocytophilum or had a recent primary infection with TBE virus. The findings in the present study indicate that in Slovenia, and probably in other European countries endemic for LB, TBE and HGA, patients with early LB are rarely coinfected with the other tick-transmitted agents.     

Thrombocytopenia in malaria: who cares?

Despite not being a criterion for severe malaria, thrombocytopenia is one of the most common complications of both Plasmodium vivax and Plasmodium falciparum malaria. In a systematic review of the literature, platelet counts under 150,000/mm3 ranged from 24-94% in patients with acute malaria and this frequency was not different between the two major species that affected humans. Minor bleeding is mentioned in case reports of patients with P. vivax infection and may be explained by medullary compensation with the release of mega platelets in the peripheral circulation by megakaryocytes, thus maintaining a good primary haemostasis. The speculated mechanisms leading to thrombocytopenia are: coagulation disturbances, splenomegaly, bone marrow alterations, antibody-mediated platelet destruction, oxidative stress and the role of platelets as cofactors in triggering severe malaria. Data from experimental models are presented and, despite not being rare, there is no clear recommendation on the adequate management of this haematological complication. In most cases, a conservative approach is adopted and platelet counts usually revert to normal ranges a few days after efficacious antimalarial treatment. More studies are needed to specifically clarify if thrombocytopenia is the cause or consequence of the clinical disease spectrum.     

Depletion but Activation of CD56dimCD16+ NK Cells in Acute Infection with Severe Fever with Thrombocytopenia Syndrome Virus

Virologica Sinica - Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease with high mortality (12%–30%). The mechanism by which the SFTS bunyavirus (SFTSV)...