After preliminary trials, the detailed changes in the concentration of specific circulating and local antibodies were followed in 15 volunteers inoculated with coronavirus 229E. Ten of them, who had significantly lower concentrations of pre-existing antibody than the rest, became infected and eight of these developed colds. A limited investigation of circulating lymphocyte populations showed some lymphocytopenia in infected volunteers. In this group, antibody concentrations started to increase 1 week after inoculation and reached a maximum about 1 week later. Thereafter antibody titres slowly declined. Although concentrations were still slightly raised 1 year later, this did not always prevent reinfection when volunteers were then challenged with the homologous virus. However, the period of virus shedding was shorter than before and none developed a cold. All of the uninfected group were infected on re-challenge although they also appeared to show some resistance to disease and in the extent of infection. These results are discussed with reference to natural infections with coronavirus and with other infections, such as rhinovirus infections.
Infection of normal individuals with human parvovirus (B19) results in a mild disease (erythema infectiosum) but gives rise to aplastic crises in patients with chronic hemolytic anemias. The effects of this disease on hemopoiesis were investigated following intranasal inoculation of the virus into three volunteers. A typical disease ensued with a viremia peaking at 9 d. Marrow morphology 6 d after inoculation appeared normal but at 10 d there was a severe loss of erythroid precursors followed by a 1-2-g drop in hemoglobin, and an increase in serum immunoreactive erythropoietin. Erythroid burst-forming units (BFU-E) from the peripheral blood were considerably reduced, starting at the time of viremia and persisting for 4-8 d depending on the individual. Granulocyte-macrophage colony-forming units (CFU-GM) were also affected but the loss started 2 d later. Both CFU-GM and BFU-E showed a sharp overshoot at recovery. In the marrow, BFU-E and CFU-E were reduced at 6 and 10 d in the individual having the longest period of peripheral progenitor loss. In contrast, there was an increase in BFU-E and CFU-E in the subject with least change in peripheral progenitors. In the third subject, with an intermediate picture, there was a loss at 6 d but an increase at 10 d of erythroid progenitors. It is suggested that the architecture of the marrow might partially isolate progenitors from high titers of virus in the serum and individual variation in this respect might give the results observed.
We report a case of meningitis caused by inadvertent introduction of bacteria following spinal anaesthesia for Caesarean section. The technique of performing the spinal anaesthesia is reviewed. Meningitis may occur, although very rarely, despite meticulous aseptic techniques. It is vital that meningitis should be considered in the differential diagnoses of post-spinal headache when patients present with headaches, pyrexia and meningism in the postoperative or postpartum period.
Blood was collected from 684 healthy volunteers and examined for total and differential white blood cell (WBC) counts. A subgroup also was tested for numbers of T cells, B cells, and CD4 and CD8 subsets. Smoking status and alcohol consumption were determined by means of questionnaire, and smoking status was verified with serum cotinine concentration. High smoking rate was associated with increases in all counts. Former smokers abstinent less than 5 years still demonstrated elevated counts, whereas those abstinent more than 5 years had WBC counts comparable to It has been reported for some time that smoking influences the peripheral blood leukocyte count. Studies in both the United Kingdom 1 and France 2 found that mean total white blood cell (WBC) count was 30% higher in smokers than in nonsmokers. Leukocyte counts in ex-smokers, however, were similar to those in nonsmokers. The French study also found that those who inhaled had higher counts than those who smoked similar amounts without inhaling. Other studies have shown that, although smoking was associated with a higher WBC count, consumption of up to three alcoholic drinks a day was not.3 Nevertheless, there has been much interest in the effect of alcohol excess on WBC count and function, because alcoholic those in persons who were never smokers. Compared with levels in those who had never smoked, total WBC counts were 27% higher in current smokers and 14% higher in former smokers who were abstinent for less than 5 years. Lymphocyte counts were 9% higher in those consuming more than one alcoholic drink per day than in those consuming less alcohol, but drinking was not associated with other cell populations. ( Impaired WBC function has been recorded in alcoholic patients 5 ; however, data on WBC count in persons who regularly consume modest amounts of alcohol are few. Furthermore, recent evidence indicates that for nonsmokers (but not smokers), temperate drinking is associated with increased resistance to experimentally induced upper respiratory tract infections. 6 We studied the peripheral WBC count in 684 healthy volunteers and related it to the amount they smoked and drank. We confirmed earlier findings, and extend this work by providing data on how long smoking-associated elevation in cell count persists after persons stop smoking. We also provide data on the potential role of social drinking on WBC count, differential counts, and lymphocyte subsets. MATERIALS AND METHODS SubjectsTwo hundred eighty-three men and 401 women volunteered to take part in studies at the Common Cold Unit, Salisbury, England. They were screened by means of medical history, routine clinical examination, and laboratory tests as part of the regular admission procedures of the Unit.7 Pregnant women were excluded from the study. Mean age of the study subjects was 33 years (±10.4 SD). All studies were approved by the Harrow District Ethical Committee.
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