Failure of a single dose amoxycillin as prophylaxis against endocarditis.
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Biomedical subjects
Publications and source records attributed to D C Shanson.
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Four fatal and two non-fatal cases of pneumonia caused by Pneumocystis carinii and one case of co-trimoxazole-responsive interstitial pneumonia, all in homosexual patients with the acquired immune deficiency syndrome, are described. The lack of clinical signs in the chest and of abnormal radiological findings at presentation in three of the six patients with P. carinii infection, the rapidly progressive course of the disease, as well as the need for early diagnosis and treatment are stressed. The possibility of chemoprophylaxis against P. carinii is discussed.
In 1982 only two cases of acquired immune deficiency syndrome (AIDS) and one case of persistent generalized lymphadenopathy (PGL) were diagnosed at St Stephen's hospital in central London. By 31 July 1985, the numbers of cases with these conditions had increased to 41 and 185 respectively and a total of approximately 400 patients had been recognized as having HTLV III infection. A large increase in the numbers of cases of AIDS was noted between July 1984 and July 1985. Over 80 patients with HTLV III infection were admitted to hospital and had surgery or other invasive procedures carried out. Approximately 3000 blood samples from HTLV III antibody positive patients were processed by the pathology department--mainly by the microbiology and haematology laboratories. Hospital and laboratory staff observed hepatitis B precautions. In spite of regular contact with patients with HTLV III infection and their samples, serological studies on 150 hospital staff showed no evidence of spread of HTLV III from patients to staff.
Erythromycin stearate, 1.5 g, was effective in reducing the prevalence of streptococcal bacteraemia following dental extraction when administered orally under supervision 1 h before extraction. Blood samples were collected from adult patients for culture and erythromycin assay 1 to 2 min after the dental procedure. High dilution techniques involving the use of 1 litre bottles of broth were used to inactivate erythromycin present in blood cultures. Viridans streptococci were isolated from 6 of 40 patients receiving erythromycin (15%) compared with 18 of 42 control patients (43%). The mean serum erythromycin concentration at the time of extraction was 3.7 mg/l for 34 patients receiving erythromycin who had negative blood cultures compared with 1.8 mg/l for the six patients given erythromycin who had viridans streptococci isolated from the blood. Both the 1.5 g erythromycin stearate and placebo oral doses were well tolerated in a double blind comparative study which included 109 adult dental patients.
Fastidious anaerobe broth and brain-heart infusion cysteine broth supplemented with 'Panmede' (a papain digest of ox liver) 2.5% supported the recovery of five Streptobacillus moniliformis strains from simulated blood cultures. Other media tested in parallel--brain heart infusion cysteine broth without 'Panmede' and Brewer's thioglycollate broth--were unreliable. Sodium polyanethol sulphonate (Liquoid) 0.05%, inhibited five isolates of S. moniliformis, including isolates from patients with Haverhill Fever. Occasionally, Liquoid 0.025% was also inhibitory and a heavy inoculum of one strain, NCTC11194, was completely inhibited by Liquoid 0.012% in simulated nutrient-broth blood cultures. These results suggest that the choice of media included in each blood-culture set is critical for the optimal isolation of S. moniliformis. Brain-heart infusion cysteine broth supplemented with 'Panmede', or commercially available fastidious anaerobe broth, without Liquoid, is recommended.
Brain heart infusion cysteine broth, with and without Panmede (a papain digest of ox liver) and Fastidious Anaerobe Broth, with and without Liquoid, were compared by inoculating the broths with blood collected from each of 51 patients, 2 min after dental extraction. Bacteraemia caused by viridans streptococci or oral non-sporing anaerobes or both was detected in 39 patients (76%). Detection of bacteraemia caused by viridans streptococci and anaerobes was more rapidly achieved by the addition of Panmede to brain heart infusion broth. Significantly more cases of bacteraemia caused by viridans streptococci were detected by use of the Panmede-containing medium than by use of Fastidious Anaerobe Broth after incubation of the broths for only 1 day. Use of brain heart infusion cysteine broth with and without Panmede, and Fastidious Anaerobe Broth permitted detection of bacteraemia caused by viridans streptococci in 26, 11 and 22 patients respectively during incubation for 2 weeks. Bacteraemia caused by anaerobes was detected by use of these three media in 24, 13 and 23 patients respectively. The addition of Liquoid to Fastidious Anaerobe Broth had no significant effect on the detection of bacteraemia caused by viridans streptococci or anaerobes. The Panmede-containing blood-culture medium should be a useful anaerobic broth in the investigation of patients with suspected endocarditis, because viridans streptococci are also rapidly detected.
Serum fluorescent streptococcal antibody tests were carried out on 71 patients with clinically suspected infective endocarditis, and a final diagnosis of endocarditis was obtained in 46 patients. A serological diagnosis of streptococcal endocarditis was obtained in 10 patients who had persistently negative blood cultures, as fluorescent streptococcal antibody titres equal to or greater than 400 were detected against at least one of four strains of streptococci used as heterologous antigens. There were no false positive fluorescent antibody results with heterologous antigens during tests on 29 patients who had either non-streptococcal endocarditis, a final diagnosis other than endocarditis, or streptococcal sepsis not associated with endocarditis. A negative result with the heterologous antibody test could not, however, exclude a diagnosis of streptococcal endocarditis as six of 11 patients with endocarditis due to Streptococcus viridans or Str bovis confirmed on blood culture had serum fluorescent antibody titres less than 400 against all the heterologous streptococcal antigens tested. Homologous fluorescent streptococcal antibody titres equal to or greater than 400, using the patient's own blood culture isolate as the antigen, were found in the serum samples of 14 of 15 patients with endocarditis caused by viridans streptococci, three patients with enterococcal endocarditis, two patients with endocarditis caused by Str pneumoniae, and one patient with Str bovis endocarditis. In contrast, all five patients who had clinically insignificant streptococcal bacteraemias had serum fluorescent homologous antibody titres of only 100 or less. These results showed that the homologous serum fluorescent streptococcal antibody test could help to decide the clinical importance of a streptococcus which is initially isolated from only one or two of a number of inoculated blood culture bottles.
To detect streptococcal bacteraemia in patients undergoing dental extraction blood cultures containing glucose broth with 0.05% sodium polyanethol sulphonate (Liquoid) were compared with identical cultures without Liquoid.
A single supervised oral dose of amoxycillin 3 g combined with clavulanic acid 125 mg as a suspension (Augmentin 3.125G) plus probenecid 1 g, cured 97 of 100 assessable patients who had uncomplicated anogenital gonorrhoea. Thirteen of the 100 patients were infected with penicillinase producing strains of Neisseria gonorrhoeae (PPNG) and 11 (85%) of these patients were cured, including one infected with a PPNG strain that was also resistant to spectinomycin. Another group of 93 assessable patients was treated with ampicillin 3 g plus probenecid 1 g, and only 85 (91%) patients were cured. Of the eight treatment failures in this group, five were found to be infected with PPNG strains. In a second study 144 assessable patients were treated with amoxycillin 3 g combined with clavulanic acid 250 mg, (Augmentin 3.250G) plus probenecid 1 g, and a 97% cure rate was again obtained. Five of seven (71%) patients infected with PPNG strains were cured. Although both Augmentin regimens were effective for treating gonorrhoea caused by PPNG and non-PPNG strains, side effects were noted in more patients treated with 250 mg clavulanic acid (24%) than with 125 mg clavulanic acid (5%). In addition, a similar cure rate was obtained in the three primary sites of infection, the urethra, cervix, and rectum.
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An outbreak of methicillin- and gentamicin-resistant Staphylococcus aureus infections started in a university hospital after a patient, who was not known to be colonized, was admitted. During a 3-month period 15 surgical or geriatric patients and five staff were found to be infected or colonized by the epidemic strain in five surgical/orthopaedic wards, a geriatric ward, the intensive care unit and the isolation unit. Difficulties in controlling the outbreak arose when two patients who initially had negative bacteriological screening results were returned to general wards. Both patients were subsequently shown to be colonized and caused outbreaks which led to the further closure of two general wards. There was strong circumstantial evidence to suggest that physiotherapy staff were involved with the spread of the epidemic strain. Control of the outbreak was achieved by more strict isolation of 'negative' patient contacts as well as colonized/infected patients and increasing the level of staffing on the separate isolation unit.
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2000 persons in the UK were examined serologically for antibodies to human T-lymphotropic virus type III (HTLV-III). Sera reacting in a membrane immunofluorescence assay (IFA) to HTLV-III were also positive when tested against cells infected with lymphadenopathy virus (LAV-1), and cross-adsorption tests indicated that these retroviruses are probably identical. A competitive radioimmunoassay (RIA), which was wholly concordant with IFA, was used to screen the sera. 30/31 patients with the acquired immunodeficiency syndrome (AIDS) were seropositive, as were 89% patients with persistent generalised lymphadenopathy (PGL), 17% symptomless homosexual men, 34% haemophiliacs receiving pooled clotting factors, and 1.5% intravenous drug abusers. None of more than 1000 unselected blood donors was seropositive. These data confirm the close association between HTLV-III and AIDS and PGL and show that infection with HTLV-III is also prevalent in the populations in whom these syndromes are most likely to develop. However, it would be unwise to presume that AIDS will necessarily develop in seropositive subjects.
Between 1980 and 1984 28 homosexual men who had had ano-genital intercourse with patients with either acquired immunodeficiency syndrome (AIDS) or persistent generalised lymphadenopathy (PGL) were followed up. The pattern of the sexual links indicated that within this group there were two clusters, one consisting of 7 men and the other of 13.17 of the 28 contacts became ill with either AIDS or PGL; among those in the clusters, 4 died of AIDS and 11 had PGL, and of the rest 2 had PGL. 16 of the 19 men in the clusters who were tested for HTLV-III antibodies were seropositive, as were 7 of those not in the clusters. 111 men attending a genitourinary medicine clinic who had not had known contact with either AIDS or PGL patients and who were being screened for syphilis served as controls. Of these, 19/86 who were homosexual and 0/25 who were heterosexual were positive for HTLV-III antibodies. None of the 4 who died of AIDS had had contact with each other. The 2 in the first cluster seemed to have been linked by a symptomless HTLV-III-negative man, who was also probably the link between the two clusters, while in the second cluster the chief "carrier" seemed to be a seropositive man in whom PGL developed. These findings are consistent with the hypothesis that HTLV-III is the sexually transmitted causative agent of AIDS and PGL.
Antibodies reacting selectively with human T-cell leukaemia virus type I (HTLV-I) were detected in approximately 5% patients with extended lymphadenopathy syndrome (ELAS) and in less than 1% of unselected homosexual patients and drug abusers. None of 22 patients with acquired immunodeficiency syndrome (AIDS) had HTLV-I antibodies and neither did 85 haemophiliacs and 940 blood donors. 3 out of 113 drug addicts had high titres of antibodies to human T-cell leukaemia virus type II (HTLV-II). A T-cell line was derived from 1 of the seropositive ELAS patients. This line was found to be infected with, and releasing, HTLV-I. Infection by HTLV-I and HTLV-II retroviruses thus occurs more frequently in ELAS patients and drug addicts than in the UK population as a whole, but the low prevalence of these infections in ELAS and AIDS patients indicates that these two strains of lymphotropic retroviruses have no aetiological role in ELAS and AIDS.
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Serum concentrations of amoxycillin were significantly higher with probenecid than without probenecid for up to 18 h after administration of a single 3 g oral dose of amoxycillin. At 12 to 16 h after this dose the mean serum amoxycillin concentrations exceeded the expected minimum bactericidal concentrations of amoxycillin for viridans streptococci when probenecid was given together with amoxycillin. The concurrent oral administration of probenecid with amoxycillin is discussed for the prophylaxis of endocarditis in susceptible patients who require dental procedures under general anaesthesia.