Penicillin Therapy in Acute Bacterial Endocarditis

Dolphin, Annette; Cruickshank, R

doi:10.1136/bmj.1.4408.897

Cited by 25 publications

(4 citation statements)

References 1 publication

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“…were associated with childbirth and abortion, and most of these were cases of endocarditis. Only five cases of meningitis were recorded; none was stated to be in a neonate, but the clinical information (present series) * Colebrook and Purdie, 1937;Fry, 1938;Brown, 1939;Hill and Butler, 1940;Rosenthal and Stone, 1940;Koletzky, 1941;Ramsay and Gillespie, 1941;Rantz and Keefer, 1941;Rantz, 1942;Rantz and Kirby, 1942;Gaustadt, 1942;Wheeler andFoley, 1943. tDawson, Hobby andLipman, 1944;Dolphin and Cruickshank, 1945;Loewe and Alture-Weber, 1946;Roemer and Grun, 1949;Kahler andAicher, 1952. TNyhan andFousek, 1958;de Moor, 1960;Hood et al, 1961;Wahl et al, 1962;Mannik, Baringer and Stokes, 1962;Keitel et al, 1962;Eickhoff et al, 1964;Bret and Durieux, 1965;Sicherman, 1965;Etienne, Curioni and Laplane, 1965;Reinarz and Sanford, 1965;Hall, 1965;Lazarus, Sellers and Marine, 1965;Kexel, 1965;Kexel and Schonbaum, 1965;Winterbauer et al, 1966;Maher and Irwin, 1966;Butter and de Moor, 1967;Canet et al, 1967;Lafaix et al, 1968;Kvittingen, 1968;<...>…”

Section: Discussionmentioning

confidence: 99%

Neonatal streptococcal infections

Parker

1977

Postgraduate Medical Journal

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Summary Most serious neonatal streptococcal infections are caused by group-B streptococci. The pattern of serious group-B neonatal disease in Britain resembles that described in other countries; both "early-onset" and "late-onset" forms are seen, but reliable incidence rates have not yet been determined. Serological-type III strains predominate in neonatal meningitis in Britain, but not so markedly as in some parts of the U.S.A. A deficiency of group-II strains in meningitis is, however, apparent in both countries. Present information about the carriage of group-B streptococci suggests that antibiotic prophylaxis administered to mothers or infants is unlikely to reduce greatly the frequency of "early-onset" disease. The continuous presence of a suitable chemical disinfectant in the vagina during labour might be more effective. Insufficient is known about the epidemiology of "late-onset" neonatal disease for rational preventive measures to be designed. More information is required about the postnatal acquisition of group-B streptococci by neonates and its sources, and about passive transfer of type-specific antibody from the mother to her child.

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Section: Discussionmentioning

confidence: 99%

Neonatal streptococcal infections

Parker

1977

Postgraduate Medical Journal

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“…A number of gaps remain in our knowledge of Candida –host interactions, and these gaps require further research. In addition to VT‐1161, which was previously mentioned, the beta‐glucan synthase inhibitor Ibrexafungerp (formerly SCY‐078) is a promising candidate, 191 particularly in patients with chronic RVVC who have not responded adequately to fluconazole maintenance therapy 72,241‐243 . There are also new formulations that exist for vaginal application, including the combination of clotrimazole with the non‐steroidal analgesic diclofenac (ProF‐001, phase 3).…”

Section: Future Researchmentioning

confidence: 99%

“…In addition to VT-1161, which was previously mentioned, the beta-glucan synthase inhibitor Ibrexafungerp (formerly SCY-078) is a promising candidate, 191 particularly in patients with chronic RVVC who have not responded adequately to fluconazole maintenance therapy. 72,[241][242][243] There are also new formulations that exist for vaginal application, 1).…”

Section: Future Re S E Archmentioning

confidence: 99%

Guideline: Vulvovaginal candidosis (AWMF 015/072, level S2k)

Farr

Effendy

Tirri

et al. 2021

Mycoses

146

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Approximately 70‐75% of women will have vulvovaginal candidosis (VVC) at least once in their lifetime. In premenopausal, pregnant, asymptomatic and healthy women and women with acute VVC, Candida albicans is the predominant species. The diagnosis of VVC should be based on clinical symptoms and microscopic detection of pseudohyphae. Symptoms alone do not allow reliable differentiation of the causes of vaginitis. In recurrent or complicated cases, diagnostics should involve fungal culture with species identification. Serological determination of antibody titres has no role in VVC. Before the induction of therapy, VVC should always be medically confirmed. Acute VVC can be treated with local imidazoles, polyenes or ciclopirox olamine, using vaginal tablets, ovules or creams. Triazoles can also be prescribed orally, together with antifungal creams, for the treatment of the vulva. Commonly available antimycotics are generally well tolerated, and the different regimens show similarly good results. Antiseptics are potentially effective but act against the physiological vaginal flora. Neither a woman with asymptomatic colonisation nor an asymptomatic sexual partner should be treated. Women with chronic recurrent Candida albicans vulvovaginitis should undergo dose‐reducing maintenance therapy with oral triazoles. Unnecessary antimycotic therapies should always be avoided, and non‐albicans vaginitis should be treated with alternative antifungal agents. In the last 6 weeks of pregnancy, women should receive antifungal treatment to reduce the risk of vertical transmission, oral thrush and diaper dermatitis of the newborn. Local treatment is preferred during pregnancy.

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“…The use of standard protocols prepared in expectation of future urgent needs would help. So too would wider adoption of adaptive trial protocols, such as platform trials,14 which allow the evaluation of several treatments at once and permit interim analyses after which treatments may be discarded or introduced.…”

Section: Better Evidence Fastermentioning

confidence: 99%