Seroepidemiology of Toxoplasma gondii among pregnant women in different parts of Sweden.

Surveys of pregnant women in four areas of Sweden in 1987-88, reveal a significant trend for decrease in Toxoplasma seroprevalence from Gotland island (26%, n = 467) in the south through Orebro county (18%, n = 1413) and Stockholm area (18%, n = 939), to Northern Sweden (12%, n = 837). No within area differences were observed between samples from rural and urban localities. Quantitative antibody data indicate marginally higher levels in the north than in the south, and a significant declining trend by age only in Orebro county. Incidence models are used to describe age-seroprevalence profiles for each area, using different assumptions about age- and time-specific infection rates, and to estimate the risk of maternal infection at the time of the survey. It is shown that the patterns of seroprevalence with age in Orebro county and Northern Sweden, but not Gotland island or Stockholm, strongly implicate time-dependent changes in Toxoplasma incidence, consistent with a declining incidence in the past which has possibly been reversed in recent years. The estimates of Toxoplasma incidence and risk of maternal toxoplasmosis are strongly dependent upon the underlying assumption of temporal change in incidence, with wide ranges in the predicted values. These studies demonstrate the difficulties in interpretation of horizontal cross-sectional data and the need for longitudinal studies of age-prevalence and seroconversion in the determination of the true risk of maternal toxoplasmosis.

Modelling toxoplasma incidence from longitudinal seroprevalence in Stockholm, Sweden.

Age-stratified data on toxoplasma seroprevalence in pregnant women in Stockholm, Sweden for the years 1969, 1979 and 1987 provide the basis for an analysis of temporal patterns of Toxoplasma gondii infection, and estimation of the risk of maternal toxoplasmosis, in this population. A catalytic infection model, in which the rate or force of infection is assumed to be a function of time (and not, as is more usual, age), was employed to describe the observed changes in levels of toxoplasma seropositivity. A range of simple incidence functions (up to 3 parameters) were fitted using a method of maximum likelihood. The data were significantly better described by a linear or an exponential decay in the rate of infection through time compared with a constant level. More complex incidence functions gave no better data description. Thus, whilst there is strong evidence for declining incidence in Stockholm over the past 4-5 decades, the data do not allow discrimination between different possibilities for the nature of this decline. Based on these modelling results, best estimates of the force of infection in 1987 acting on susceptible women are within the range 0 to 0.0045/susceptible/year (95% confidence limits), yielding a possible risk of maternal toxoplasmosis of between 0 and 2.7 cases/1000 pregnancies. These values are shown to be significantly lower than estimates based upon an assumption of temporal stability in toxoplasma incidence, which may be of practical significance to public health policy.

Low seroprevalence of Toxoplasma gondii antibodies in a Tanzanian village.

The prevalence of antibodies against Toxoplasma gondii was studied in the population of Nyamisati village in Tanzania using the direct agglutination test, indirect immunofluorescence test, and immunosorbent agglutination test. All positive sera were positive by both direct agglutination and indirect immunofluorescence tests and were confirmed by the dye test. The seropositivity was confirmed by immunoblotting showing a distinct 32 kDa band in all the seropositive samples. The seropositivity rate was 4% (19/450) among the subjects of Nyamisati origin and 47% (15/32) among immigrants from other areas of Tanzania. Most of the infections appeared to have occurred between 5 and 15 years of age. The generally low transmission in this mainly Muslim village appeared to be related to sparse consumption of contaminated food and low prevalence of oocysts due to scarcity of felines.

Longitudinal study of seroreactivities to Pf155/RESA and its repetitive sequences in small children from a holoendemic area of Liberia.

The seroreactivities to Pf155/RESA antigen and to three oligopeptides (EENV)2, EENVEHDA and K(DDEHVEEPTVA)2, which constitute repeat subunits of the RESA molecule, were investigated between 1980 and 1986 in two cohorts of children (n = 114) with and without monthly chemosuppression (pulsed reduction of parasite load) against malaria from six months to five years of age during development of protective immunity. Serum samples were collected first at half-yearly and then yearly intervals. Positive immunofluorescence against Pf155/RESA (EMIF) was only found in 24% of the samples. The children with chemosuppression were more often seropositive (30%) than the non prophylactic children (17%). This was in contrast to the seroreactivity against crude parasitic antigens which was highest in the non prophylactic children. In these children, there was a general decrease of EMIF titres around two years of age. Immunosuppression by chronic parasitaemia may be suggested as a reason for this. ELISA seroreactivity was found against one, two or three oligopeptides in all children with high EMIF titres (greater than 250) although (EENV)2 appeared to best correlate (92%) with the EMIF seropositivity. While EMIF seropositivity only showed partial correlation to immunoprotection against patent parasitaemia in the non prophylactic children, the individual profiles of the seroreactivities to the different specific epitopes of the Pf155/RESA molecule and their relevance with regards to protective immunity to malaria need to be investigated further.

The affinity of (-)-propranolol for beta 1- and beta 2-adrenoceptors of human heart. Differential antagonism of the positive inotropic effects and adenylate cyclase stimulation by (-)-noradrenaline and (-)-adrenaline.

An appraisal of the affinity of (-)-propranolol was made for beta-adrenoceptors of isolated heart preparations and myocardial membrane particles from patients undergoing open heart surgery. In order to eliminate possible distorting influences of neuronal and extraneuronal uptakes of catecholamines on the affinity estimates for (-)-propranolol, isolated tissues were pretreated once with 5 or 10 mumol/l phenoxybenzamine for 2 h. Phenoxybenzamine caused potentiation of the positive inotropic effects of (-)-noradrenaline and (-)-adrenaline but not of (-)-isoprenaline; potentiation was more pronounced in atrial than in ventricular preparations. Potentiation was greater for (-)-noradrenaline than for (-)-adrenaline. It is concluded that the concentration of physiological catecholamines at the human heart beta-adrenoceptors is limited by neuronal capture but not by extraneuronal uptake. The antagonism of the positive inotropic effects of (-)-adrenaline and (-)-noradrenaline by (-)-propranolol was simple competitive in left ventricular myocardium of patients with mitral lesion. The effects of (-)-adrenaline and (-)-noradrenaline were antagonized to similar extent by (-)-propranolol. An equilibrium dissociation constant KB (-log mol/l) of 8.6 was estimated for (-)-propranolol. In atrial preparations the inotropic effects of (-)-adrenaline were antagonized significantly more by (-)-propranolol than those of (-)-noradrenaline. KB-Values (-log mol/l) of 8.9 [against (-)-adrenaline] and 8.5 [against (-)-noradrenaline] were estimated for (-)-propranolol. Concentration-effect curves for the stimulation of adenylate cyclase of both atrium and ventricle were biphasic for (-)-noradrenaline and monophasic for (-)-adrenaline. The high-sensitivity and low-sensitivity components of (-)-noradrenaline comprised 1/3 and 2/3, respectively, of maximum cyclase stimulation. As expected from beta 1-adrenoceptors, the high-sensitivity component of the curve for (-)-noradrenaline was selectively antagonized by (-)-bisoprolol; as expected from beta 2-adrenoceptors, the low-sensitivity component was selectively antagonized by ICI 118,551. (-)-Propranolol antagonized the effects of (-)-noradrenaline mediated by beta 2-adrenoceptors 2 to 3 times more potently than the effects mediated by beta 1-adrenoceptors. (-)-Propranolol competed with 3H-(-)-bupranolol for binding to left ventricular beta-adrenoceptors. An equilibrium dissociation constant (-log mol/l) of 8.6 was estimated for (-)-propranolol.(ABSTRACT TRUNCATED AT 400 WORDS)