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Biomedical subjects

J K Baird

Publications and source records attributed to J K Baird.

At least 37 records · Page 2Linked to original sources
PubMed1998

Age-dependent susceptibility to severe disease with primary exposure to Plasmodium falciparum.

This study investigated the incidence of severe disease following primary exposure to Plasmodium falciparum by nonimmune children and adults in Irian Jaya, Indonesia. Four months after arrival, the cross-sectional prevalence of P. falciparum was 72%, and the monthly cumulative incidence of clinical diagnoses of malaria was 81%. Delirium or unconsciousness prompted evacuation to the hospital. Records of emergency evacuation of persons with a clinical diagnosis of malaria revealed an incidence density among adults (>15 years) of 1.34 events/person-year in the third month, whereas the rate in children remained stable at approximately 0.25 events/person-year (relative risk = 4.51, 95% confidence interval [CI] = 1.94-11). Through the first 6 months of exposure, 23.2% of adults were evacuated to the hospital with a diagnosis of malaria compared with 8.6% of children (relative risk = 2.7, 95% CI = 1.9-3.8). In this population with relatively few infants or people of advanced age, the risk of severe disease following primary exposure to P. falciparum increased with age.

Adolescent↗
PubMed1998

Chloroquine-resistant Plasmodium vivax in transmigration settlements of West Kalimantan, Indonesia.

Malariometric surveys were conducted during July 1996 in native Dayak villages and predominantly Javanese transmigration settlements in Ketapang district of West Kalimantan, Indonesia. Malaria prevalence ranged from 0.9% to 2.7% in Dayak villages and from 1% to 20% in the transmigration settlements. Plasmodium falciparum accounted for 67% of the cases among Dayaks but P. vivax was dominant among transmigrants, accounting for more than 72% of the infections. Chloroquine sensitivity/resistance was assessed by 28-day in vivo testing of uncomplicated malaria infections and measurement of chloroquine blood levels in cases where parasitemias reappeared within the 28-day test period. Resistance was based on the appearance of asexual parasites against chloroquine plus desethylchloroquine levels exceeding the minimally effective whole blood concentrations proposed for sensitive parasite strains (P. vivax, 100 ng/ml; P. falciparum, 200 ng/ml). All parasitemias cleared initially within four days of beginning supervised chloroquine therapy (25 mg base/kg over a 48-hr period), but asexual parasites reappeared within 28 days in 27 of 52 P. vivax and three of 12 P. falciparum cases. Chloroquine blood levels at the time of recurrent parasitemias revealed resistance in 12 of the 27 P. vivax cases and in one of the three P. falciparum cases. Genotypes of nine of the 12 recurrent P. vivax isolates matched with their primary isolates and ruled out reinfection. These findings establish the presence of chloroquine-resistant P. vivax on the island of Borneo. The pattern of malaria and the high frequency of chloroquine resistance by P. vivax at the West Kalimantan location may relate to demographic, ecologic, agricultural, and socioeconomic changes associated with transmigration.

Adolescent↗
PubMed1997

Electrophoretic mobility and zeta potential of lysozyme crystals.

Using free-solution capillary electrophoresis, the electrophoretic mobility of micro m-sized lysozyme crystals in their growth solution at 283 K, 1.5%(w/v) NaC1, and over a range of pH values between 3.59 and 5.70 has been measured. Under these conditions, the mobility is independent of crystal size, while the calculated zeta potential increases from +8 to +24 mV as the pH decreases. Since the pH dependence of the zeta potential mirrors the pH dependence of charge on the free molecule, as determined by acid titration, it is concluded that the charge on the crystal is a result of H(+) adsorption from solution.

Journal Article↗
PubMed1997

The age-specific prevalence of Plasmodium falciparum in migrants to Irian Jaya is not attributable to agglutinating antibody repertoire.

Previous observations have shown that individuals migrating from a malaria free area to a malaria endemic region in North Eastern Irian Jaya quickly acquire anti-parasite immunity, in an age-dependent manner. Sera from migrants and long-term residents in this area were examined for their ability to agglutinate a range of Plasmodium falciparum isolates and to disrupt erythrocyte rosettes. Antibody responses to merozoite surface protein 2 (MSP2) and ring-infected erythrocyte surface antigen (RESA) were also determined. The range of isolates agglutinated by sera from the migrants approached that seen in long-term residents. No difference was found between migrant adults and children in the range of agglutinating antibody, size of agglutinates, nor disruption of rosettes. Anti-MSP2 and anti-RESA antibodies were the only factors examined which showed a correlation with age. We conclude that although antibody to parasite neoantigens expressed on the surface of infected erythrocytes may play a role in the acquisition of immunity, the humoral response to other P. falciparum antigens is more likely to account for the age-dependent prevalence of parasitaemia observed.

Adult↗
PubMed1997

Halofantrine and primaquine for radical cure of malaria in Irian Jaya, Indonesia.

The combination of halofantrine and primaquine therapies was calculated as a regimen for achieving radical curve of falciparum or vivax malaria in Irian Jaya, Indonesia, and compared with combined chloroquine and primaquine therapies. The patients who volunteered for the study [adult, male, Indonesian immigrants with no previous exposure to endemic malaria, normal glucose-6-phosphate dehydrogenase (G6PD) activity, uncomplicated malaria illness, no prior use of antimalarials, and parasitaemias of 0.001%-1.1%] were randomized to receive either halofantrine (24 mg base/kg bodyweight, in three equal doses over 12 h) or chloroquine (25 mg base/kg bodyweight over 48 h, in doses of 10, 10 and 5 mg base/kg at 24-h intervals). Each patient also received concurrent daily primaquine (0.5 mg base/kg bodyweight) for 14 days followed by the same dose on alternate days to day 28. A recurrent parasitaemia during the 28 days of follow-up constituted drug failure. Of the 40 cases of falciparum malaria and 26 cases of vivax malaria treated with halofantrine-primaquine, none had a recurrent parasitaemia (100% efficacy). In contrast, 20 of 30 patients with falciparum malaria and three of 27 with vivax malaria had recurrent parasitaemias after chloroquine-primaquine, giving efficacies of 33% and 89%, respectively. Halofantrine-primaquine was significantly more effective than chloroquine-primaquine against falciparum malaria (P < 0.001) but was similarly efficacious against vivax malaria (P = 0.23). On average, fever associated with falciparum or vivax malaria cleared 17 h faster with halofantrine-primaquine (P < 0.01) although there were no significant differences (P > 0.4) in parasite-clearance times between the two regimens. The halofantrine-primaquine regimen was also associated with a more rapid and significant decline in malaria-related physical complaints.

Adult↗
PubMed1997

Malaria in a nonimmune population after extended chloroquine or primaquine prophylaxis.

Extended chemoprophylaxis against endemic malaria raises concern with regard to susceptibility after ceasing use of the drug. In this study, we measured attack rates of malaria among adult men for 28 weeks after they ended one year of prophylaxis using either weekly chloroquine (5 mg base/kg, n = 20), daily primaquine (0.5 mg base/kg, n = 30), or a placebo of primaquine (n = 41). The 28-week incidence densities, times to parasitemia, parasite densities, and symptoms of primary post-prophylaxis infections were not significantly different among the former primaquine, chloroquine, and placebo groups. However, the incidence of Plasmodium falciparum infection in the post-chloroquine group was significantly greater than in the post-primaquine group during the first (P = 0.03) and second (P = 0.02) months post-prophylaxis. Six of 10 primary P. falciparum and three of 10 P. vivax infections occurred in the former chloroquine group within one month after ending prophylaxis and the mean time to infection was 30-35 days. In contrast, only one P. falciparum and no P. vivax infections occurred during the first month after ending primaquine prophylaxis. The mean time to first parasitemia by either species of malaria parasite in this group was 72-77 days. There was no indication that daily use of primaquine for one year placed subjects at greater risk of malaria infection or to more severe clinical symptoms of malaria than subjects who had taken placebo or chloroquine, despite the potential for some degree of immunity to have been acquired in these latter two groups during the year-long prophylaxis period. The results do suggest that chloroquine suppressed P.falciparum infections until drug levels decreased, and that primaquine had effectively prevented the establishment of liver-stage parasites.

Antimalarials↗
PubMed1997

Survey of in vivo sensitivity to chloroquine by Plasmodium falciparum and P. vivax in Lombok, Indonesia.

A malariometric survey was conducted in 14 villages of Sekotong district, in Lombok, Indonesia during October 1994. Point prevalence of malaria ranged from 0% to 15% in the surveyed villages, averaging 6% overall, and Plasmodium falciparum accounted for 63% of the infections. Forty-nine patients with uncomplicated malaria and parasite counts ranging from 40 to 10,800 asexual forms/microliter were enrolled in a 28-day in vivo test of chloroquine sensitivity. All subjects received a supervised therapeutic regimen of chloroquine (25 mg base/kg over a 48-hr period) and parasitemia and symptoms were closely monitored for 28 days. Asexual parasites were eliminated within four days in the 29 P. falciparum and 20 P. vivax study patients enrolled. The cumulative incidence of therapeutic failure (recurrent symptomatic parasitemia) among P. falciparum cases at days 7, 14, and 28 was 7%, 10%, and 14% (4 of 29), respectively. However in all four cases, parasitemias recurred against chloroquine blood levels below the minimally effective concentration (MEC) of 200 ng/ml and do not confirm chloroquine resistance. All 20 P. vivax parasitemias were sensitive to chloroquine and the blood remained clear, with the exception of one case in which an asymptomatic parasitemia appeared on day 28. Parasitemias by P. falciparum and P. vivax that were observed before supervised therapy, but in the presence of whole blood chloroquine above normally suppressive MEC levels, suggest resistance to suppressive or prophylactic regimens of chloroquine.

Adolescent↗
PubMed1997

Whole blood chloroquine concentrations with Plasmodium vivax infection in Irian Jaya, Indonesia.

Whole blood concentrations of self-administered chloroquine (CQ) and its metabolite desethylchloroquine (DCQ) were measured in 168 patients with microscopically confirmed infection by Plasmodium vivax in northeastern Irian Jaya, Indonesia. The study consisted of both survey and passive case detection in four separate villages between 1992 and 1994. The subjects were Javanese people 4-51 years old who had lived in the Arso region for up to two years. The sum of CQ and DCQ ranged from 0 to 8,342 ng/ml of whole blood, and 122 subjects (73%) had > or = 100 ng/ml of CQ plus DCQ, the estimated minimally effective concentration (MEC) in whole blood against chloroquine-sensitive P. vivax. Among 56 subjects reporting to a clinic with symptoms of malaria, 53 (95%) had ordinarily effective levels of chloroquine in blood. Among 109 largely asymptomatic malaria patients found by survey case detection, 69 (63%) had chloroquine blood levels greater than the MEC. Virtually all clinical and most subclinical vivax malaria in this region occurs despite ordinarily effective levels of chloroquine in blood.

Adolescent↗
PubMed1997

Diagnosis of resistance to chloroquine by Plasmodium vivax: timing of recurrence and whole blood chloroquine levels.

To develop criteria for the diagnosis of resistance to chloroquine using an in vivo test, we examined published records of early clinical trials of quinine and chloroquine against Plasmodium vivax. These data established the timing of relapse by tropical P. vivax relative to therapy by these drugs. The first relapse occurred 17 days after initiating and three days after terminating quinine therapy. The median day of relapse was day 23, and 59% of the patients had relapsed by day 30 (n = 333). In contrast, no relapse occurred until day 36 following chloroquine treatment (n = 256). Data from our laboratory may help explain this difference; among 91 Indonesian patients with malaria, the mean whole blood levels of chloroquine (CQ) and desethylchloroquine (DCQ) were 141 ng/ml (95% confidence interval = 115-167) on day 28 after initiating standard therapy (25 mg base/kg in three doses over a 48-hr period). This exceeds the estimated minimal effective concentration of chloroquine (100 ng/ml of whole blood). Thus, chloroquine lingering in the blood for at least 28 days after starting standard therapy was sufficient to eliminate or at least suppress chloroquine-sensitive tropical P. vivax. We conclude that a parasitemia by P. vivax recurring in the 28 days after full compliance to standard chloroquine therapy demonstrates resistance. If the recurrence appears before day 16, it is almost certainly a recrudescence and between days 17 and 28 it may be either a recrudescence or a relapse by chloroquine-resistant parasites. Recurrences beyond day 28 could be relapse by chloroquine-sensitive P. vivax.

Animals↗
PubMed1997

In vivo resistance to chloroquine by Plasmodium vivax and Plasmodium falciparum at Nabire, Irian Jaya, Indonesia.

A survey of resistance to chloroquine by Plasmodium vivax and P. falciparum was conducted during May 1995 at three mesoendemic villages 30 km southeast of Nabire, near the central northern coast of Irian Jaya, Indonesia. The prevalence of malaria at Urusumu (n = 157), Margajaya (n = 573), and Topo (n = 199) was 18%. 9%, and 9%, respectively, with spleen rates among children of 79%, 10%, and 27%. Infected patients among those screened formed a study population of 64 subjects eligible for a 28-day in vivo test of resistance to chloroquine. Sixty-three patients successfully completed the test; 45 males and 18 females 1-60 years of age, of whom 29 were Javanese transmigrants of five years residence in Irian Jaya and 34 were native to Irian Jaya. The seven-day day cumulative incidence of therapeutic failure for P. vivax and P. falciparum was 15% (n = 34) and 30% (n = 37). The 14- and 28-day estimates of cumulative incidence were 45% and 64% for P. vivax and 58% and 89% for P. falciparum. Almost all recurrences appeared in the face of ordinarily effective levels of chloroquine and its major metabolite, desethylchloroquine, in whole blood (> or = 100 ng/ml). Four infections by P. malariae in subjects enrolled in this study cleared by day 2 and none reappeared within 28 days. Chloroquine no longer provides effective therapy for falciparum or vivax malaria along the northern coast of Irian Jaya, Indonesia.

Adolescent↗
PubMed1996

The rate of water equilibration in vapor-diffusion crystallizations: dependence on the distance from the droplet to the reservoir.

The rate of water equilibration in hanging-drop vapor-diffusion experiments was studied as a function of the distance separating the hanging drop from the surface of the reservoir solution. Hanging drops of 1.00 M NaCl were allowed to partially equilibrate with reservoirs of 2.00 M NaCl at room temperature. Over the range of droplet-reservoir distances examined, 7.6-119.4 mm, the larger the distance that separated the droplet and reservoir, the slower the droplet equilibrated with the reservoir. The variation of the rate of equilibration with droplet-reservoir distance was non-linear; the rate was most sensitive to variations in the droplet-reservoir separation at short separations. A mathematical model of the equilibration kinetics was developed that fits the experimental data. The model is based on the assumption that the rate-limiting step in vapor-diffusion equilibration is transit of water across the vapor space. A simple device to vary the rate of water equilibration, and thereby optimize macromolecular crystal growth conditions, is described.

Journal Article↗
PubMed1996

Lymphocyte proliferative response and subset profiles during extended periods of chloroquine or primaquine prophylaxis.

Immune suppression and disturbances of normal leukocyte populations are side effects attributed to many antimalarial drugs and were concerns during a recent year-long placebo-controlled trial that compared daily primaquine (0.5 mg of base per kg of body weight per day) with weekly chloroquine (300 mg of base one time per week) for malaria prophylaxis. The study took place in Irian Jaya, Indonesia, from July 1994 to August 1995 and enrolled 129 Javanese men with normal glucose-6-phosphate dehydrogenase function. Tests for lymphocyte function and subset composition were conducted blindly on a cross-section of subjects during weeks 10 (n = 42) and 48 (n = 72) of supervised prophylaxis. Lymphocyte function, measured as the proliferative response of peripheral blood mononuclear cells to a panel of mitogens (pokeweed mitogen, phytohemagglutinin, and concanavalin A) and antigens (purified protein derivative of Mycobacterium tuberculosis and Clostridium tetani toxoid) and expressed as a stimulation index, allowed for statistical comparison between groups and sampling times. The lymphocyte subset composition for each group and time point was based on flow cytometry profiling, and the results were expressed as the mean percentages of CD3 (total T cells), CD19 (total B cells), CD4+ (T-helper and inducer cells), and CD8+ (T suppressor and cytotoxic cells), CD3/CD16+ CD56 (natural killer cells), CD3/anti-HLA-DR (activated T cells) cells and the CD4+/CD8+ ratios. Lymphocyte stimulation indices were statistically comparable among the placebo, primaquine, and chloroquine groups at both time points, although the primaquine group was distinguished by having repeatedly greater proportions of subjects with high ( > 3.0) stimulation indices. The lymphocyte subset profiles of these groups at both time points were also similar and undistorted relative to those of healthy reference populations matched for age, sex, and ethnicity. The results provide quantitative support for the safety of daily primaquine prophylaxis.

Adult↗
PubMed1996

A focus of endemic malaria in central Java.

This report describes one of the few remaining foci of endemic malaria on the island of Java, the Kokap subdistrict, near the Southcentral coast. Kokap was hypoendemic in June 1994 with prevalence of parasitemia at 0.98% (n = 10,606 of 40,246 residents). Plasmodium vivax comprised 63% of infections and P. falciparum all others. The incidence of indigenous infection during 1993 was 48 cases/1,000 person-years (p-yr), and it was relatively uniform among age groups (38 to 53/1,000 p-yr). Nine deaths due to malaria had been recorded in the past three years (8.3 deaths per 100,000 p-yr); the case fatality rate was 0.17%. Subdistricts adjoining Kokap to the north, east, and south reported incidence rates of < 2 cases/1,000 p-yr. To the west, Purworejo District had a high case incidence (11 cases/1,000 p-yr) but other districts to the west did not (< 1.2 cases/1,000 p-yr). The highest case incidence village area within Kokap (169 cases/1,000 p-yr) bordered the district of Purworejo to the west. Endemic malaria in Kokap and Purworejo coincided with where steep hills and narrow valleys dominated the terrain.

Adolescent↗
PubMed1995

Randomised placebo-controlled trial of primaquine for prophylaxis of falciparum and vivax malaria.

Drug resistance has made malaria prevention difficult and the new agents are too expensive for widespread use. Primaquine, an established drug for treatment, is potentially useful for prevention. Malaria prophylaxis with primaquine was evaluated in Irian Jaya during one year in Javanese men who were not deficient in glucose-6-phosphate dehydrogenase (G-6-PD). 126 volunteers were randomised to receive 0.5 mg/kg primaquine base or placebo daily (double-blinded), or 300 mg chloroquine base weekly (open). The protective efficacy of primaquine relative to placebo was 94.5% (95% confidence interval 57-99) for Plasmodium falciparum and 90.4% (95% CI 58-98) for P vivax. Attack rates for either parasite did not differ significantly between the chloroquine and placebo groups. Incidence density of physical complaints not associated with parasitaemia was low (17-18 complaints/person-year) and was about the same in all groups except for cough, which was increased in the primaquine group. Complete blood counts were normal and no evidence of hepatic or renal dysfunction was found with primaquine. However, at 50 weeks the primaquine group had a mean methaemoglobin of 5.8% (range 1.4-13%), which declined by half within 7 days of ending prophylaxis. When used daily for one year by men with normal G-6-PD activity, primaquine was well tolerated and effective for prevention of malaria.

Adolescent↗
PubMed1995

Host age as a determinant of naturally acquired immunity to Plasmodium falciparum.

The usual course of infection by Plasmodium falciparum among adults who lack a history of exposure to endemic malaria is fulminant. The infection in adults living with hyper- to holoendemic malaria is chronic and benign. Naturally acquired immunity to falciparum malaria is the basis of this difference. Confusion surrounds an essential question regarding this process: What is its rate of onset? Opinions vary because of disagreement over the relationships between exposure to infection, antigenic polymorphism and naturally acquired immunity. In this review, Kevin Baird discusses these relationships against a backdrop of host age as a determinant of naturally acquired immunity to falciparum malaria.

Journal Article↗
PubMed1995

Treatment of chloroquine-resistant Plasmodium vivax with chloroquine and primaquine or halofantrine.

Optimal therapy for infection by chloroquine-resistant Plasmodium vivax has not been established. From 1992 to 1994 during three separate studies, 147 Javanese residents of Irian Jaya infected by P. vivax were treated with either chloroquine (25 mg of base/kg during 3 days or 10 mg of base/kg in one dose) plus primaquine (10 mg/kg during 28 days or 2.5 mg/kg during 3 days) (n = 78), chloroquine plus placebo (n = 50), or halofantrine (24 mg base/kg in 12 h; n = 19). There was no difference in tolerance to or side effects of any of the regimens. Within 14 days of starting therapy, therapeutic failure among these patients was 44% for chloroquine, 5% for chloroquine plus primaquine (P < .001), and 0 for halofantrine (P < .001). After 28 days, therapeutic failure was 78%, 15%, and 6%, respectively. Thus, chloroquine plus primaquine in combination and halofantrine alone are effective therapies for chloroquine-resistant P. vivax.

Adolescent↗
PubMed1995

Primaquine for prophylaxis against malaria among nonimmune transmigrants in Irian Jaya, Indonesia.

A comparison of primaquine versus chloroquine for prophylaxis among nonimmune transmigrants from Java and Bali in the hyperendemic Arso region of Irian Jaya, Indonesia was conducted. Forty-five subjects received 0.5 mg of primaquine base/kg of body weight every other day, and 54 people in the same village received weekly 5 mg of chloroquine base/kg for 16-19 weeks beginning in December 1992. Plasmodium falciparum accounted for 18 of 30 infections with chloroquine, and four of five infections among subjects receiving primaquine. Plasmodium vivax was found in 12 people taking chloroquine but in just one person taking primaquine. The risk of malaria among people taking chloroquine relative to that among subjects taking primaquine was 3.96 (P = 0.014) for P. falciparum and 10.56 (P = 0.012) for P. vivax. Primaquine was better tolerated than chloroquine. The minimal protective efficacy for primaquine prophylaxis was 74% against P. falciparum and 90% against P. vivax among nonimmune children and adults living in Irian Jaya. These findings require confirmation with randomized, double-blinded, and placebo-controlled trials.

Adolescent↗