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M Paul

Publications and source records attributed to M Paul.

At least 217 records · Page 12Linked to original sources
PubMed1997

Improving empirical antibiotic treatment: prospective, nonintervention testing of a decision support system.

OBJECTIVES: Develop a problem-orientated and data-based decision support system (DSS) to improve empirical antibiotic treatment, and compare the performance of the system to that of the physician. DESIGN: The DSS was tested in a prospective, noninterventional, comparative cohort study. SETTING: University hospital in Israel. SUBJECTS: Consecutive patients (n = 496) in four departments of internal medicine suspected of harboring a moderate to severe bacterial infection. INTERVENTIONS: None. MAIN OUTCOME MEASURES: The percentage of appropriate empirical antibiotic treatments. RESULTS: Out of 496 patients included in the study, 219 had positive cultures or serological tests. The physicians prescribed inappropriate empirical antibiotic treatment in 91 of 219 patients (42%); whilst the recommendations of the system were inappropriate in 50 patients (23%) (P < 0.05). Superfluous treatment was prescribed in 15% of patients by the physician, and in 11% by the system. Out of the 91 patients given inappropriate treatment by the physician, the DSS advised treatment to which the pathogens were susceptible in 61 patients. The advantage of the DSS over the physician was most evident in multiresistant gram-negative isolates, enterococci and Staphylococcus aureus. Out of the 277 patients with negative cultures, the DSS advised narrower-spectrum antibiotic treatment than prescribed by the physicians in 27% of patients, and broader-spectrum in 13%. CONCLUSION: A problem-orientated, data-based DSS outperformed physicians in the choice of appropriate empirical antibiotic treatment, and recommended less broad-spectrum antibiotics.

Acinetobacter↗
PubMed1997

Ultrastructural changes in parasites induced by nanoparticle-bound pentamidine in a Leishmania major/mouse model.

Drug targeting enhances drug efficacy. This principle was tested in the treatment of an experimental visceral leishmaniasis. Using transmission electron microscopy (TEM) we localized pentamidine-loaded polymethocrylate nanoparticles in the liver of mice infected with Leishmania major and compared the ultrastructural changes in the parasites of these mice when they were treated with bound versus free pentamidine. Between days 13 and 17 after infection, loaded nanoparticles treated group were injected i.v. with 3 doses of 0.17 mg/kg bound pentamidine loaded on 2 x 10(11) nanospheres; control groups received 2 x 10(11) unloaded nanospheres. Drug reference control groups received five doses of 200 mg/kg pentavalent antimony (Glucantime) or three doses of free pentamidine (0.17 mg/kg or 2.28 mg/kg). Mice treated with bound pentamidine displayed a 77% reduction in their parasite burden versus the untreated controls. Nanoparticles were located by TEM inside parasitized Küpffer cells, in the phagolysosomes without entering the Leishmania. The low dose of 0.17 mg/kg bound pentamidine damaged the Leishmania to the same extent as 2.28 mg/kg of free pentamidine (the usual dose in human chemotherapy). In the parasites inside the Küpffer cells, TEM showed a swollen mitochondrian with loss of cristae, destruction or fragmentation of the kinetoplast, loss of ribosomes and destruction of parasite structures except for the subpellicular microtubules. This study therefore shows that a dose of bound pentamidine 13 times smaller than the usual dose of free pentamidine has a similar effect on the parasite.

Animals↗
PubMed1997

Activity of pentamidine-loaded poly (D,L-lactide) nanoparticles against Leishmania infantum in a murine model.

The activity of pentamidine-loaded poly(D,L-lactide) nanoparticles was compared, by determination of median effective doses (ED50), to that of free pentamidine in a murine model of visceral leishmaniasis induced by Leishmania infantum. BALB/c mice were infected intravenously on day O with promastigotes and then treated on days 14, 16, and 18. Groups of 5 mice received either 0.57, 1.14 and 2.28 mg/kg of free pentamidine (expressed in pentamidine base) or 0.055, 0.11, 0.22 and 0.44 mg/kg of pentamidine-loaded nanoparticles. In the control group, 12 mice received normal saline. The liver parasite burden was evaluated using the Stauber method 72 h after the last injection and drug levels in livers and spleens were determined. Bound pentamidine was 3.3 times more active than free drug (ED50 value = 0.32 mg/kg versus 1.05 mg/kg for free drug). Drug levels showed a weak accumulation in hepatic and splenic tissues following bound pentamidine administration. A lack of acute toxicity was noted in all groups treated by bound pentamidine. Results obtained with this biodegradable carrier may be of particular interest as no new major antileishmanial compound is today available.

Animals↗
PubMed1997

Women with one ovary have decreased response to GnRHa/HMG ovulation protocol in IVF but the same pregnancy rate as women with two ovaries.

The study compares the response after gonadotrophin-releasing hormone agonist (GnRHa) and human menopausal gonadotrophin (HMG) stimulation for in-vitro fertilization (IVF) in patients with either one or two ovaries. The study group (group A) included 73 cycles in women who had unilateral oophorectomy before their IVF treatment and the control group (group B) included 988 cycles in women with two ovaries. Tubal disease was the sole cause for infertility in all cases. The two groups were similar in age and parity. The patients with one ovary required more ampoules of HMG (62.9 versus 48.9, P < 0.001), a longer induction period (13.5 versus 12.7, P < 0.01) and had significantly lower oestradiol concentrations on the day of human chorionic gonadotrophin (HCG) administration (5840 versus 6473 pmol/l, P = 0.035). They yielded fewer follicles (11.2 versus 13.1, P = 0.005), fewer oocytes (7.3 versus 9.1, P = 0.006) and produced fewer embryos (4.4 versus 5.1, P < 0.05). There was no difference in fertilization rate (60 compared with 58%), or pregnancy rate (25.8 compared with 27.1% per oocyte retrieval). Women with only one ovary responded less well to GnRH agonist/HMG stimulation than women who had both ovaries but pregnancy outcome was the same in both groups.

Adult↗
PubMed1997

Monotherapy versus beta-lactam-aminoglycoside combination treatment for gram-negative bacteremia: a prospective, observational study.

The aim of the present study was to test whether the combination of a beta-lactam drug plus an aminoglycoside has advantage over monotherapy for severe gram-negative infections. Of 2,124 patients with gram-negative bacteremia surveyed prospectively, 670 were given inappropriate empirical antibiotic treatment and the mortality rate in this group was 34%, whereas the mortality rate was 18% for 1,454 patients given appropriate empirical antibiotic treatment (P = 0.0001). The mortality rates for patients given appropriate empirical antibiotic treatment were 17% for 789 patients given a single beta-lactam drug, 19% for 327 patients given combination treatment, 24% for 249 patients given a single aminoglycoside, and 29% for 89 patients given other antibiotics (P = 0.0001). When patients were stratified according to risk factors for mortality other than antibiotic treatment, combination therapy showed no advantage over treatment with a single beta-lactam drug except for neutropenic patients (odds ratio [OR] for mortality, 0.5; 95% confidence interval [95% CI], 0.2 to 1.3) and patients with Pseudomonas aeruginosa bacteremia (OR, 0.7; 95% CI, 0.3 to 1.8). On multivariable logistic regression analysis including all risk factors for mortality, combination therapy had no advantage over therapy with a single beta-lactam drug. The mortality rate for patients treated with a single appropriate aminoglycoside was higher than that for patients given a beta-lactam drug in all strata except for patients with urinary tract infections. When the results of blood cultures were known, 1,878 patients were available for follow-up. Of these, 816 patients were given a single beta-lactam drug, 442 were given combination treatment, and 193 were given a single aminoglycoside. The mortality rates were 13, 15, and 23%, respectively (P = 0.0001). Both on stratified and on multivariable logistic regression analyses, combination treatment showed a benefit over treatment with a single beta-lactam drug only for neutropenic patients (OR, 0.2; 95% CI, 0.05 to 0.7). In summary, combination treatment showed no advantage over treatment with an appropriate beta-lactam drug in nonneutropenic patients with gram-negative bacteremia.

Adolescent↗
PubMed1997

Activity of a new liposomal formulation of amphotericin B against two strains of Leishmania infantum in a murine model.

The efficacy of a new liposomal formulation of amphotericin B was compared to that of amphotericin B deoxycholate (Fungizone) in a murine model of visceral leishmaniasis induced by Leishmania infantum. Median effective doses (ED50) were determined with two different strains: strain 1 was obtained from an untreated patient, and strain 2 was obtained from a patient who had received 12.5 g of amphotericin B over 3 years. BALB/c mice were infected intravenously on day 0 with promastigotes and then treated on days 14, 16, and 18 (strain 1) or on days 21, 23, and 25 (strain 2) with the liposomal formulation of amphotericin B (five doses were tested for each strain: 0.05, 0.1, 0.5, 0.8, and 3 mg/kg of body weight) or with conventional amphotericin B (four doses were tested for each strain: 0.05, 0.1, 0.5, and 0.8 mg/kg). Mice in the control group received normal saline solution. The liposomal amphotericin B formulation was about three times more active than the conventional drug against both strains. ED50 of the liposomal formulation were 0.054 (strain 1) and 0.194 (strain 2) mg/kg. ED50 of conventional amphotericin B were 0.171 (strain 1) and 0.406 (strain 2) mg/kg. Determination of drug tissular levels, 3 days after the last drug administration, showed a drug accumulation in hepatic and splenic tissues much higher after administration of liposomal amphotericin B than after conventional amphotericin B. A lack of toxicity was noted in all groups treated with the liposomal formulation.

Amphotericin B↗
PubMed1997

Expression of a recombinant preproendothelin-1 gene in arteries stimulates vascular contractility.

Endothelin (ET)-1 is a potent vasoconstrictor peptide that is elevated in cardiovascular diseases. However, the biological function of ET-1 gene expression within arteries in vivo has not been determined. The effects of ET-1 gene expression were investigated using gene-transfer methods on porcine vascular cells in vitro and porcine arteries in vivo. Transfection of vascular cells with a vector encoding for human preproendothelin-1 cDNA (pVR-ppET) resulted in significant increase in active ET-1 levels in culture supernatant compared with nontransfected cells (P < 0.05). This supernatant contracted rat aortic strips at concentrations 10-fold lower than synthetic ET-1 protein, which was inhibited by the ET-A receptor antagonist BQ-123. Transfection of pVR-ppET into pig iliofemoral arteries resulted in an increase in contractile responses to angiotensin I compared with control vessels (P < 0.05), in contrast to serotonin, phenylephrine, synthetic ET-1, and angiotensin II. A mitogenic effect of recombinant ET-1 on intimal cell growth was not observed. These findings demonstrate that expression of a recombinant ET-1 gene in vivo augments vascular contractility due to an increased sensitivity to angiotensin I, suggesting a role for ET-1 in the pathogenesis of cardiovascular diseases.

Angiotensin I↗
PubMed1997

Early induction of angiotensin I-converting enzyme in rat carotid artery after balloon injury.

Several studies have demonstrated the effectiveness of angiotensin I-converting enzyme (ACE) inhibitors in preventing the neointima formation found after denudation of the rat carotid artery by balloon injury. The aim of the present study was to determine the role of ACE in this model and to compare the treatment with the ACE inhibitor ramiprilat with that with the angiotensin II antagonist HR 720. The endothelial layer of the left carotid artery was removed using an inflated balloon catheter. Injured and control vessels were both submitted to histomorphological analysis and DNA content quantification at 2, 4, 6, 8, 12, and 14 days after injury. Evaluation of neointima thickening demonstrated a slow but steady increase of neointima that was significant after day 6 and reached 30% of the lumen in 2 weeks. This was paralleled by an increase in DNA content, which was significant 4 days after injury. ACE mRNA levels were quantified by polymerase chain reaction after reverse transcription. Measurement of ACE mRNA levels revealed a significant upregulation 2 and 8 days after injury, with no significant difference when compared with control tissue at later time points. ACE activity was also significantly enhanced at 2 and 8 days after injury, with no significant difference when compared with control tissue at later time points. In addition, the treatment with ramiprilat was more efficient in reducing neointima formation than that with HR 720. These data underlie the role of ACE in this model of restenosis. The early induction of ACE expression after endothelial injury but before significant changes in the vessel structure suggests that ACE activity might be one of the mechanisms that trigger neointima formation in the rat.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Contractile systolic and diastolic dysfunction in renin-induced hypertensive cardiomyopathy.

The present study investigated whether functional, molecular, and biochemical alterations occurring in chronic heart failure can already be detected in compensated hypertensive cardiac hypertrophy. Force of contraction (isolated papillary muscle strip preparations), sarcoplasmic reticulum (SR) protein and myosin heavy chain isoform expression (Northern and Western blot analysis), myocardial fibrosis (collagen stains, hydroxyproline quantification), myocardial renin mRNA (RT-PCR), and angiotensin II levels and plasma aldosterone concentrations (radioimmunoassay) were studied in hypertrophied myocardium from transgenic rats harboring the mouse Ren-2d gene. Contraction and relaxation velocities of isolated papillary muscle strips were significantly reduced in cardiac hypertrophy. The beta-/alpha-myosin heavy chain ratio was significantly increased in the hypertrophied left ventricles, whereas SR Ca2+-ATPase (SERCA 2a) and phospholamban mRNA and protein levels were significantly decreased. The decrease in SERCA 2a was more pronounced than the decrease in phospholamban levels. There was no increased myocardial fibrosis. Left ventricular myocardial renin mRNA and angiotensin II concentrations, as well as plasma aldosterone levels, were higher in transgenic than in control rats. In hypertensive cardiac hypertrophy, myosin heavy chain isoform shift and reduction of SR protein levels are related to systolic and diastolic dysfunction, respectively. These alterations precede the development of myocardial fibrosis. Increased myocardial renin mRNA and angiotensin II concentrations suggest that an activated tissue renin-angiotensin system might contribute to these alterations. Since the alterations in compensated cardiac hypertrophy apparently precede those in chronic heart failure, they might accelerate the transition from hypertrophy to failure and could therefore be targets for pharmacological interventions.

Angiotensin II↗
PubMed1997

Alpha-adrenergic signal transduction in renin transgenic rats.

The alpha1-adrenoceptor-G protein-phosphoinositide-specific phospholipase C (PLC) signal transduction pathway is assumed to play an important role in the regulation of contractile force and in the pathophysiology of myocardial hypertrophy. In the present study, the components of this pathway were investigated in left ventricles of hearts from hypertensive transgenic rats overexpressing the mouse renin gene [TG(mREN2)27] in comparison to age- and weight-matched Sprague-Dawley control rats. Contractile force was assessed in isolated electrically driven left ventricular papillary muscle strips. Alpha1-adrenoceptor density was measured by radioligand binding using [3H]prazosin, steady state levels of alpha q/11, and G protein beta-subunits by Western blotting. PLC activity was determined by a cell-free assay using exogenous phospholipid vesicles containing [3H]phosphatidylinositol (4,5)-bisphosphate as a substrate. Alpha1-adrenoceptor density was significantly increased (by 80%) in transgenic rats compared with control rats, while the positive inotropic response to the alpha1-adrenoceptor agonist phenylephrine was significantly reduced, suggesting a postreceptor defect in TG(mREN2)27. The expression of alpha q and alpha11 was verified by reverse transcription-polymerase chain reaction, and alpha q/11 steady state protein levels were shown to be similar in transgenic and control rats. Western blotting using a beta-common antibody revealed two bands at approximately 35 and 36 kD. The quantities of both were similar in TG(mREN2)27 compared with those in control rats. In contrast, PLC activity was significantly reduced (by 32%) in transgenic rats. In conclusion, our findings are consistent with a desensitization of the alpha1-adrenergic signal transduction pathway at the level of the effector.

Animals↗
PubMed1997

Design and testing of beta-actin primers for RT-PCR that do not co-amplify processed pseudogenes.

Quantitative reverse transcription polymerase chain reaction (RT-PCR) is being used increasingly as an alternative to Northern blots analysis or RNase protection assays for quantitation of gene expression. To quantify different samples, measurements are often normalized using the expression of so-called "housekeeping" genes, such as cytoplasmic beta-actin or glyceraldehyde-3-phosphate dehydrogenase. This approach can produce false results because the presence of processed pseudogenes in the genome, which are related to some of the commonly used transcripts of housekeeping genes, leads to co-amplification of contaminating genomic DNA. By yielding amplification products of the same or similar size as the reverse-transcribed target, mRNA quantitation of expression is prone to error. In this paper, we report the results of using three sets of beta-actin primers for RT-PCR in the presence and absence of genomic DNA. In addition, we propose two new pairs of oligonucleotide primers that specifically amplify the human and rat beta-actin reverse-transcribed mRNA but not pseudogene sequences. These primers are especially suitable for quantitation of mRNA in small tissue samples (e.g., biopsies), where DNase digestion is not feasible, and therefore DNA contamination cannot be avoided.

Actins↗
PubMed1997

[Use of the ISAGA method in detection of specific IgM, IgA, IgE antibodies in acquired and congenital toxoplasmosis].

Immunocapture assays ISAGA PLUS IgA/IgM (bioMérieux) and IgE ISAGA were used to determine their usefulness in the diagnosis of acquired and congenital toxoplasmosis. Specific IgM, IgA and IgE antibodies were tested in 134 patients, namely pregnant women who seroconverted during gestation (n = 20), children with congenital toxoplasmosis (n = 5), patients with toxoplasmic lymphadenitis (n = 56) and immunocompetent individuals with chronic Toxoplasma gondii infection (n = 53). Altogether 172 sera were examined. Specific IgM antibodies were detected in all sera from pregnant women (100%) with recent T. gondii infection (1-8 weeks after seroconversion), in all patients with toxoplasmic lymphadenopathy (1-3 months after onset of symptoms) and in their control examinations after 2 and 5 months (100%) and also in 35 (66%) out of 53 patients with chronic infection. In infants with congenital toxoplasmosis IgM were found only in one new-born; equivocal results were obtained in 3 children during the asymptomatic serological reactivation in the second year of life. Specific IgA antibodies were present in sera from 15 (75%) out of 20 women seroconverted during pregnancy; in 3 cases the results were equivocal. IgA antibodies were detected in sera from 30 (81.1%) out of 37 patients with toxoplasmic lymphadenitis examined once; in 19 patients examined 3 times IgA antibodies were present in all the cases in the first serological examination performed when clinical symptoms were first observed (100%), in 17 patients after 2 months (89.5%) and in 11 patients after 5 months (57.9%). IgA antibodies were also detected in 21 sera (39.6%) from patients with chronic T. gondii infection. In children with congenital toxoplasmosis IgA antibodies were found in 3 cases during serological reactivation after discontinuation of pyrimethamine-sulfadiazine therapy; in these cases equivocal results of IgM antibodies were present, and positive result of IgE antibodies in one case. Specific IgE antibodies were detected in sera from 17 (85%) out of 20 women with seroconversion and in 18 patients with lymphadenopathy (32.1%); in the last group IgE antibodies were not present in the follow-up examination after 5 months. IgE antibodies were detected only in 5 cases (9.4%) with chronic infection. IgA and IgE antibodies in ISAGA begin to appear about a week later than IgM antibodies: in sera collected between the 2nd and 3rd week after invasion the positive results were obtained in all cases (100%). Therefore, ISAGA PLUS IgA/IgM (bioMérieux) is useful for the diagnosis of recent T. gondii infection especially in women with suspected seroconversion during pregnancy. ISAGA PLUS IgA/IgM is more sensitive than any conventional method routinely used and so far is a specially efficient technique for newborns and infants suspected for congenital infection and/OR IN DIAGNOSING CONGENITAL TOXOPLASMOSIS DURING IMMUNOLOGICAL RECRUDESCENCE. tHIS TEST HAS A LIMITED VALUE IN TOXOPLASMOSIS WITH LYMPHADENOPATHY BY REASON OF POSSIBILITY OF A LONG PERSISTENCE OF iGm and IgA antibodies detected by ISAGA. Detection of specific IgE antibodies using ISAGA technique may be useful for differential diagnosis of acute and chronic phase of T. gondii infection and also in some cases of serological reactivation of congenital toxoplasmosis.

Female↗
PubMed1996

Angiotensin II stimulates proliferation of primary human keratinocytes via a non-AT1, non-AT2 angiotensin receptor.

Angiotensin II is a hormone with long known cardiovascular actions. Recent studies revealed an additional role for angiotensin II in the regulation of cell proliferation. This study was performed to clarify whether skin is a target organ for these novel angiotensin actions. Radioligand binding studies identified a high-affinity angiotensin receptor on human primary keratinocytes in vitro with a Kd of 4.5 nM and a Bmax of 0.12 nM. Competition experiments with losartan and PD 123177 revealed that this receptor was not of the AT1- nor the AT2-subtype. Stimulation of human keratinocytes with angiotensin II (10(-10) to 10(-5) M) led to a dose dependent increase in 3H-thymidine incorporation, indicating that the keratinocyte receptor mediates a mitogenic effect. This effect is comparable at 10(-9) M to stimulation of keratinocytes by EGF (50ng/ml) and FGF (50ng/ml). These results demonstrate for the first time a possible physiological role for angiotensin II in human skin involving the regulation of keratinocyte proliferation.

Angiotensin II↗
PubMed1996

Virus load as a marker of disease progression in HIV-infected children.

The relationship of virus load to clinical disease progression in HIV-infected children remains to be elucidated. In this study, HIV-1 proviral DNA load was determined in peripheral blood mononuclear cells (PBMCs) by the quantitative competitive DNA polymerase chain reaction assay (QC-PCR) in 47 HIV-infected children subdivided by age (group I, < or = 2 years; group II, > or = 5 years), who were further categorized to include 12 rapid progressors (RP, age < or = 2 years, Centers for Disease Control [CDC] defined clinical category C and/or immune category 3, or death before age 2 years) and slow progressors (SP, age > or = 5 years, excluding CDC categories C and/or immune category 3). Significantly higher mean proviral copies/10(3) PBMCs were detected in group I versus group II (75.4 +/- 104.3 and 13.0 +/- 17.8 respectively, p < 0.0001) and in RP (158.0 +/- 118.2) as compared to either SP (11.8 +/- 18.8, p < 0.0001) or other age-matched infected children (20.3 +/- 38.8, p < 0.0001). Thus HIV-infected children appear to have a higher cell-associated virus load early in life, especially in association with rapid disease progression.

Adolescent↗
PubMed1996

Endothelin-1-like immunoreactivity in human atherosclerotic coronary tissue: a detailed analysis of the cellular distribution of endothelin-1.

Endothelin (ET) is a very potent vasoconstrictor peptide, which was originally reported to be produced by endothelial cells and to act locally in a paracrine fashion to regulate vascular tone. Recent studies have demonstrated that endothelin-1 (ET-1) not only is produced by endothelial cells, but is also present in non-endothelial cells of atherosclerotic lesions. The present study was therefore designed to characterize the cell type and distribution of ET-expressing cells in different areas of human atherosclerotic coronary plaques, obtained by directional atherectomy of 30 patients. In addition, ET-1 messenger RNA (mRNA) distribution was studied in human atherosclerotic plaque tissue by in situ hybridization (ISH). The strongest ET-1-like immunoreactivity (ET-1-IR) was present in all cell-rich areas of 27 plaques. In fibrotic areas of 27 tissue samples, ET-1-IR was found in 44 per cent (12/27). ET expression was most prevalent in foamy macrophages (MPs, HAM 56-positive) and myofibroblasts (MFBs, alpha-actin-positive) in the vicinity of necrotic areas with signs of previous intraplaque haemorrhage. By contrast, ET-1-IR was weak and inconsistently found in MPs (11/27; 40 per cent) and MFBs (12/27; 44 per cent) in fibrous areas. Luminal endothelial cells (Ulex europeus agglutinin reaction-positive, UEA) exhibited strong ET-1-IR, whereas endothelial cells of intraplaque microvessels demonstrated inconsistent staining for ET-1. ISH revealed that ET mRNA is produced locally in intimal MPs showing strong ET-1-IR. These findings demonstrate that ET-1 is produced by human MPs, the principal inflammatory cell type in atherosclerosis, suggesting a role for ET-1 in the chronic inflammation associated with complicated atherosclerosis.

Arteriosclerosis↗
PubMed1996

Enterotoxigenic Escherichia coli associated diarrhoea among infants aged less than six months in Calcutta, India.

The role of enterotoxigenic Escherichia coli (ETEC) as etiologic agents of diarrhoea in infants aged less than six months was assessed in a hospital based study in Calcutta, India. Of the 218 cases examined, ETEC strains were isolated from 26 (11.9%) cases. Among these, in 17 cases ETEC was the sole infecting pathogen (p = 0.0085). Of the 26 isolates (each isolate representing a case), 24 were distributed among seven different O:K:H serotypes and two different colonization factor antigens (CFAs) I and II. Two of the remaining isolation were untypable, non-haemagglutinating, and were non-hydrophobic as measured by the salt aggregation test (SAT). Of the 26 ETEC strains detected, 15 (57.7%) produced heat-labile toxin (LT) only, 8 (30.8%) liberated heat-stable toxin (ST) only, and the remaining 3 (11.5%) produced both LT and ST. No ETEC strain was isolated from the 102 age-matched controls included in this study. All the ETEC isolates were multiple drug resistant. The study showed that the diarrhoea due to ETEC was of brief duration, mostly within the range of 3 to 7 days.

Anti-Bacterial Agents↗