[Follow-up of children with congenital toxoplasmosis].
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Follow-Up Studies↗
Biomedical subjects
B Høgh
Publications and source records attributed to B Høgh.
[Hepatitis B screening of pregnant women and follow-up vaccination of infants with HBsAG positive mothers. A survey from the Hvidovre hospital in 1999].
The aim of this study was to assess the implementation of the recommendations of the Danish National Health Service concerning screening of women from hepatitis B (HB) endemic areas and follow-up vaccination of infants of carrier mothers. We examined all birth notification (n = 836) at Hvidovre Hospital during the first three months of 1999. Among 188 women from HB endemic areas only 134 (71%) women had been screened for HBsAg before delivery. Six women were HBsAg positive one of whom was examined after the delivery. Four out of six infants (67%) received Aunativ and Engerix-B within 12 hours of birth, one infant received Aunativ and Engerix-B at four days of age, the infant born of the mother who was screened after delivery didn't receive either Aunativ or Engerix-B. Three out of the six infants (50%) had received all the scheduled Engerix-B vaccinations. Our results suggest it may be necessary to reconsider the current screening and vaccination procedures to prevent an increase in the number of children becoming chronic HB carriers in Denmark.
Carrier State↗
Atovaquone-proguanil versus chloroquine-proguanil for malaria prophylaxis in non-immune travellers: a randomised, double-blind study. Malarone International Study Team.
BACKGROUND: Chloroquine plus proguanil is widely used for malaria chemoprophylaxis despite low effectiveness in areas where multidrug-resistant malaria occurs. Studies have shown that atovaquone and proguanil hydrochloride is safe and effective for prevention of falciparum malaria in lifelong residents of malaria-endemic countries, but little is known about non-immune travellers. METHODS: In a double-blind equivalence trial, 1083 participants travelling to a malaria-endemic area were randomly assigned to two treatment groups: atovaquone-proguanil plus placebos for chloroquine and proguanil, or chloroquine, proguanil, and placebo for atovaquone-proguanil. Follow-up was by telephone 7 and 60 days after travel and at a clinic at 28 days. Serum samples were tested for antibodies to a malaria circumsporozoite protein. Blood and serum samples of participants with a potential malaria diagnosis were tested in a reference laboratory. FINDINGS: 7 days after travel, at least one adverse event was reported by 311 (61%) of 511 participants who received atovaquone-proguanil and 329 (64%) of 511 who received chloroquine-proguanil. People receiving atovaquone-proguanil had a lower frequency of treatment-related gastrointestinal adverse events (59 [12%] vs 100 [20%], p=0.001), and of treatment-related adverse events of moderate or severe intensity (37 [7%] vs 56 [11%], p=0.05). There were fewer treatment-related adverse events that caused prophylaxis to be discontinued in the atovaquone-proguanil group than in the chloroquine-proguanil group (one [0.2%] vs ten [2%], p=0.015). INTERPRETATION: Overall the two preparations were similarly tolerated. However, significantly fewer adverse gastrointestinal events were observed in the atovaquone-proguanil group in than in the chloroquine-proguanil group.
Adolescent↗
Anopheles arabiensis and An. funestus are equally important vectors of malaria in Matola coastal suburb of Maputo, southern Mozambique.
Transmission characteristics of malaria were studied in Matola, a coastal suburb of Maputo, the capital City, in southern Mozambique, from November 1994 to April 1996. The local climate alternates between cool dry season (May-October) and hot rainy season (November-April) with mean annual rainfall 650-850 mm. Saltmarsh and freshwater pools provide mosquito breeding sites in Matola. Malaria prevalence reached approximately 60% among people living nearest to the main breeding sites of the vectors. Plasmodium falciparum caused 97% of malaria cases, others being P. malariae and P. ovale. Potential malaria vector mosquitoes (Diptera: Culicidae) collected at Matola during daytime indoor-resting (n = 1021) and on human bait at night (n = 5893) comprised 12% Anopheles coustani Laveran (93% biting outdoors), 46% An. funestus Giles (68% biting indoors) and 42% An. gambiae Giles sensu lato (60% biting outdoors). All 215 specimens of An. gambiae s.l. identified genetically were An. arabiensis Patton. Anopheles funestus populations remained stable throughout the year, whereas densities of the An. gambiae complex fluctuated considerably, with An. arabiensis peaking during the rainy season. No concomitant rise in malaria incidence was observed. Human landing indices of An. funestus and An. arabiensis averaged 1.8 and 3.8 per man-night, respectively. Overall Plasmodium sporozoite rates were 2.42+/-1.24% in 2181 An. funestus and 1.11+/-1.25% in 1689 An. arabiensis dissected and examined microscopically. Mean daily survival rates were 0.79 for both vector species. Estimated infective bites/person/year were 15 An. funestus and 12 An. arabiensis. Biting rates were greatest at 2100-24.00 hours for An. funestus (68% endophagic) and 21.00-03.00 hours for An. arabiensis (40% endophagic). The entomological inoculation rate (EIR) declined sharply over very short distances (50% per 90m) away from breeding-sites of the vectors. Consequently, P. falciparum prevalence among Matola residents was halved 350 m within the town. Implications for the protective effectiveness of a 'cordon sanitaire' by residual house-spraying and/or the use of insecticide-treated bednets are discussed.
Animals↗
[New drugs in the treatment of malaria].
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Antimalarials↗
Population studies of the human V kappa A18 gene polymorphism in Caucasians, blacks and Eskimos. New functional alleles and evidence for evolutionary selection of a more restricted antibody repertoire.
Immunoglobulin gene polymorphisms are interesting because they reflect differences in the available antibody repertoire which may affect the susceptibility to specific infections. Until recently, the human V kappa gene, A18, was known as a nonfunctional gene only. In this study, we cloned and sequenced four apparently functional alleles and determined the gene frequencies in three well-defined populations: Danish Caucasians, eastern Greenland Eskimos and Mozambican blacks. The A18b allele that was recently described in Native American Navajos by Atkinson et al. was found in all three populations with gene frequencies of 8%, 45% and 23% in Caucasians, Eskimos and blacks, respectively. Conversely, the frequencies of the nonfunctional A18a allele were 92%, 55% and 57%. Further, three new A18 alleles, c, d, and e were found exclusively in blacks, among whom they had an total frequency of 19%. These data indicate that both the A18a and A18b alleles originated before the diversification of Africans and non-Africans 90,000 years ago, whereas the A18c, A18d and A18e alleles may have a more recent origin. The functionality of the A18b allele was documented by the demonstration of properly rearranged and somatically hypermutated A18b messenger RNA present in the blood lymphocytes of individuals carrying this allele. The expression clearly exceeded that of a known functional V gene, A2, indicating that functional A18 alleles contribute significantly to the available antibody repertoire. In this context, it is surprising that the functional A18b allele apparently has been negatively selected in the Caucasian population, among whom 85% completely lack a functional gene.
Alleles↗
Cloning of the fomA gene, encoding the major outer membrane porin of Fusobacterium nucleatum ATCC10953.
The major outer membrane protein, FomA, of the Gram-negative human oral pathogen Fusobacterium nucleatum functions as a porin and is assumed to act as a receptor protein in coaggregation with other oral pathogenic bacteria such as Streptococcus sanguis and Porphyromonas gingivalis. We describe here the cloning of fomA from F. nucleatum in E. coli. Using pGEM3Zf(+), three recombinant plasmids were carrying parts of the fomA gene, but none of these contained regions upstream of the coding sequence. From these plasmids a clone was constructed which contained the whole fomA gene. The ATCC 10953 fomA gene was cloned under the phosphate limitation-inducible phoE promoter, using a vector derived from pACYC184. The protein was found to be incorporated into the outer membrane of the host in an apparently normal manner, as judged by heat-modifiability, trypsin-accessibility, and accessibility to antibodies to the protein in a whole cell enzyme-linked immunosorbent assay. The cloned FomA was found to exhibit pore-forming activity.
Bacterial Outer Membrane Proteins↗
Clinical and parasitological studies on immunity to Plasmodium falciparum malaria in children.
Malaria remains one of the major health problems in many tropical countries. Plasmodium falciparum is the most common malaria parasite in Africa, and it causes much more severe and progressive illness than any of the other types of malaria parasite. Children living in sub-Saharan Africa are bearing the major burden of the disease and the mortality. Whatever parameter is used to measure the mortality or the morbidity from malaria, the true problem is likely to be underestimated. The pattern of morbidity and mortality depends on the transmission intensity; the more intensity of malaria transmission is increased, the earlier and more confined the age range of symptomatic malaria. The asymptomatic carrier status is common, and 60-80% of the children in highly endemic areas have P. falciparum parasitaemia at any given time. Consequently a case definition based on the mere presence of parasites in the blood is non-informative in terms of measuring morbidity. Recognizing that there are no specific diagnostic clinical parameters for malaria, but that fever is very common, and that morbidity is to some extent dependent on the parasite density, we described using a logistic regression model the probability of being sick from malaria in relation to body temperature and parasite density. Acquired clinical and parasitological immunity develop progressively over several years after repeated exposure to infection. Protection is acquired first against death or severe clinical disease, then against milder clinical attacks, but protection against infection is never complete. Clinical and parasitological immunity develop concomitantly, as demonstrated by relating the parasite densities to measured body temperature. However, the ability to control the disease and parasite density develops earlier than the ability to prevent the parasite infection. The individual immune mechanisms that are responsible for the acquired immunity remain uncertain, but classical transfer experiments with polyvalent gamma globulin from immune donors to non-immune individuals showed that antibodies play an important role. Potential targets for malarial vaccines include antigens on the surface of the sporozoites and the merozoites. Several protein antigens from P. falciparum have been characterized at the molecular level, and most of the characterized antigens have the common characteristic that they are recognized by immune sera from individuals living in malaria endemic areas. Working on the approach that potentially useful targets for protective vaccine development can be identified by correlating the naturally acquired immune responses with defined P. falciparum antigens, we examined antigens from both the sporozoite stage (CS-protein) and the blood stages (Pf155/RESA, GLURP, and MSP1), as well as P. falciparum induced neoantigens on the red blood cell (band-3 neoantigens). The relationship between the immune response to these defined P. falciparum antigens and clinical and parasitological protection was analysed in the individual age groups. The contribution of the antigen-specific immune response was evaluated, and a positive correlation of parasite density or probability of an episode of clinical malaria with antibody response to the individual antigens was identified in defined age groups. This correlation, however, did not span all age groups, and thus overall responses to defined antigens are not considered to be reliable indicators of protection. The findings may contribute to the understanding of immunological and clinical host responses to parasitaemia and to defined P. falciparum antigens. The studies on the impact of asexual stage infection and the human immune response led to studies on specific and non-specific responses to P. falciparum blood-stage parasites and observations on gametocytaemia. We demonstrated that pyrimethamine/sulfadoxine and chloroquine did not induce gametocytogenesis as suggested previously, but preformed gametocytes persisted after
Antigens, Protozoan↗
Antigenicity and immunogenicity of recombinant glutamate-rich protein of Plasmodium falciparum expressed in Escherichia coli.
A recombinant Plasmodium falciparum glutamate-rich protein (GLURP) was produced in Escherichia coli as a nearly full-length protein. In order to map immunodominant regions on GLURP, the nonrepetitive amino-terminal region (R0) as well as the central repeat region (R1) and the carboxy-terminal repeat region (R2) were also produced as separate products. All four purified gene products reacted specifically with serum samples from adults living in an area of Liberia where malaria is holoendemic. It appears that the human immune response against GLURP is primarily directed against the R2 region because 94% of the serum samples reacted with this region in an immunoassay. Antibody reactivity against the R0 region was also observed in 75% of the serum samples, while the R1 region showed only weak antibody-binding activity. When the nearly full-length GLURP molecule was adsorbed to Al(OH)3 it was found to be immunogenic in mice. In these experiments, the antibody response was almost exclusively directed against the R2 region. When anti-GLURP sera were obtained from rabbits immunized with the three regions, R0, R1, and R2, respectively, they recognized in immunoprecipitation experiments authentic GLURP from P. falciparum grown in vitro. These results demonstrate that GLURP produced in E. coli can induce a humoral immune response against GLURP derived from blood-stage parasites.
Amino Acid Sequence↗
Relationship between maternally derived anti-Plasmodium falciparum antibodies and risk of infection and disease in infants living in an area of Liberia, west Africa, in which malaria is highly endemic.
In areas where Plasmodium falciparum is endemic, immunoglobulin G is acquired by the fetus in utero, mainly during the third trimester of pregnancy. The potential protective effect of transferred anti-P. falciparum maternal antibodies was examined in a longitudinal study of 100 infants from birth to 1 year of age. The probability of acquiring a P. falciparum infection and developing an episode of clinical malaria was determined in relation to the P. falciparum-specific antibody level of the infant at birth against P. falciparum schizont antigen or recombinant merozoite surface protein MSP1(19) antigen. The risk of acquiring an episode of clinical malaria increased from birth to 6 months of age, after which it decreased. The overall prevalence of P. falciparum parasitemia was highest (48.9%) in the 6-month-old infants. The age-specific hematocrit value showed the lowest mean value (30.2) from 6 to 9 months, and the spleen rate was the highest (69.8%) at the same age. There was a lower risk of developing an episode of clinical malaria during the first year of life in the infants with high levels of anti-MSP1(19) antibodies at birth. The level of maternally derived overall anti-schizont antigen antibodies did not seem to play a role in the relative risk of developing malaria infection or disease during the first year of life, though the level of specific anti-MSP1(19) antibodies may be associated with protection.
Animals↗
Immunogenicity of the Plasmodium falciparum glutamate-rich protein expressed by vaccinia virus.
The glurp gene of Plasmodium falciparum F32 has been inserted into a vaccinia virus, and the recombinant virus was designated VVG4. Expression of glurp in VVG4-infected Vero cells was analyzed by immunoprecipitation and revealed a primary GLURP product of approximately 220,000 Da; GLURP was detected both intracellularly and in culture supernatants. To study the immunogenicity of vaccinia virus-expressed GLURP, mice were immunized with VVG4 and serum samples were analyzed for antibody reactivity with three polypeptides, covering almost the entire GLURP molecule; these three polypeptides were produced in recombinant form in Escherichia coli. The immune response was primarily directed against a carboxy-terminal repeat region. The mouse anti-GLURP serum recognized authentic GLURP by immunoprecipitation analysis from P. falciparum grown in vitro. These results demonstrate that vaccinia virus-expressed glurp product can induce a humoral immune response against GLURP derived from blood-stage parasites.
Animals↗
Glutamate rich Plasmodium falciparum antigen (GLURP).
We have characterized a glutamate rich Plasmodium falciparum antigen, GLURP, which by immunoassays appears to be present in both the pre-erythrocytic and erythrocytic stages of the vertebrate life cycle. The gene, which is located on chromosome 10, encodes a polypeptide of 1271 residues with a predicted molecular mass of 145 kDa. Rabbit antiserum against a fusion protein expressing the C-terminal end of the molecule detects a protein with a molecular mass of 220 kDa. The sequence includes two hydrophobic regions: one consisting of 23 residues and located by the N-terminus which may act as signal peptide, and the second located at the C-terminus consisting of 33 predominantly hydrophobic residues. Except for these hydrophobic regions the protein is hydrophilic and highly charged. The sequence has two tandem repeats designated as R1 and R2. These regions were found to be conserved in isolates from different geographical areas. High levels of anti-GLURP antibodies have been shown to correlate with low parasite density. The indication of GLURP being present in all stages of the parasite in the human host raises significantly the prospects of the potential of this molecule.
Adult↗
Controlled trial of lambda-cyhalothrin impregnated bed nets and Maloprim chemosuppression to control malaria in children living in a holoendemic area of Sierra Leone, west Africa. Study design and preliminary results.
The effect of lambda-cyhalothrin impregnated bed nets and maloprim/placebo was studied in approximately 1,500 children living in 17 villages in a rural area of Sierra Leone, approximately 150 miles south east of Freetown, 30 miles north of the town of Bo. Villages were selected randomly amongst villages with impregnated bed nets and villages with no nets at all. Within these villages, children with ages ranging between 3 months to 6 years were chosen to receive maloprim or a double-blind distributed placebo fortnightly. In the villages randomised to receive nets, all beds have received nets. Malaria morbidity is estimated from weekly active case detection, and the impact on the Anopheles vector is being estimated by indoor spray catching, exit trap catching, human night landing catches and light trap catches. During the first 8 weeks of the intervention there was a significant reduction in slide positive rates, reported fever rates and children with temperature > or = 37.5 degrees C in the villages with impregnated bed nets.
Animals↗
[Parasitic diseases in patients with impaired immune response. Clinical picture and diagnosis].
Patients with impaired immune system are frequently infected with various parasitic diseases. The clinical picture is characterized by unusual manifestations and frequently severe recurrences of infections which are not normally serious. Some almost parasitic microorganisms produce symptoms exclusively in patients with impaired immune system. Parasitic infections have become increasingly common with the increasing number of patients who live for prolonged periods with impaired immune systems, often as a result of infection with HIV. Among the numerous parasitic infections which are observed in man, there are a few which occur particularly frequently in patients with impaired immune systems. This is a brief review of the clinical pictures and diagnostic options in parasitic disease in individuals with impaired immune system with particular emphasis on infections caused by: Pneumocystis carinii, Toxoplasma gondii, Cryptosporidium ssp., Microspora, Entamoeba histolytica, Leishmania ssp., and Strongyloides stercoralis. In patients with impaired immunity, parasitic infections frequently cause nonspecific symptoms and, on account of the impaired immunity, antibodies to the parasite are not always produced. The diagnosis of these infections is, therefore, based on morphological demonstration of the microorganism concerned, culture, specific antigen or DNA defections.
Acquired Immunodeficiency Syndrome↗
The antibody response to well-defined malaria antigens after acute malaria in individuals living under continuous malaria transmission.
The IgG and IgM antibody responses to the C-terminal 783 amino acids of the P. falciparum glutamate-rich protein, GLURP489-1271, expressed as an E. coli fusion protein, the IgG response to a 18-mer synthetic peptide EDKNEKGQHEIVEVEEIL (GLURP899-916) representing the C-terminal repeats of GLURP, and a synthetic peptide (EENV)6 representing the C-terminal repeats from Pf155/RESA, were investigated longitudinally in 13 children and 7 adults living under conditions of continuous, intense malaria transmission. Some subjects did not recognize the antigens after malaria infection, and in subjects recognizing the antigens, the responses were often short-lived. In adults, the antibody responses to the GLURP489-1271 fusion protein and the (EENV)6 peptide peaked after 2 weeks, and not all individuals responded to all antigens. The antibody response, even against large fragments of conserved antigens, is not uniformly elicited by natural malaria infection in previously primed donors.
Adolescent↗
The effect of splenectomy on immunity to Plasmodium malariae and P. falciparum in a malaria immune donor.
A 55 year old Liberian male was splenectomized after an abdominal trauma. A few days after splenectomy he experienced a pure Plasmodium malariae infection with high fever. He was later followed for 12 months with monthly blood films and temperature measurements, and did never show any signs of clinical malaria. The parasite densities observed during the longitudinal follow after splenectomy did not differ from parasite densities in villagers with intact spleens.
Animals↗
Primary structure and localization of a conserved immunogenic Plasmodium falciparum glutamate rich protein (GLURP) expressed in both the preerythrocytic and erythrocytic stages of the vertebrate life cycle.
A gene coding for a 220-kDa glutamate rich protein (GLURP), an exoantigen of Plasmodium falciparum, was isolated and its nucleotide sequence was determined. The deduced amino acid sequence contains 2 repeat regions. The sequence of one of these was shown to be conserved among geographically dispersed isolates, and a fusion protein containing that sequence was able to stimulate B- and T-cells. Antibodies against GLURP stained erythrocytic stages of the parasite as well as the hepatic stage as detected by electron microscopy.
Amino Acid Sequence↗
Development of immunity against Plasmodium falciparum malaria: clinical and parasitologic immunity cannot be separated.
A total of 1622 individuals of all ages living under conditions of continuous malarial transmission in Liberia were enrolled in a cross-sectional study of parasite rates, positive parasite densities, and body temperatures. The age-specific Plasmodium falciparum-positive parasite densities were greatest at ages 0.5-1.0 year, then slowly declined into adulthood. The age-specific mean body temperature at parasite isodensity showed a steady decline even in the oldest age group. The results do not support the hypothesis that adults have higher body temperatures at a given parasite density than do children with the same parasite density. The age-specific P. falciparum parasite density for specific isotemperatures showed that a subgroup of children in the age group 0.5-1.0 year had low temperatures (less than 36.5 degrees C) despite high parasite densities. This indicates that low body temperature should be investigated further as a possible indicator of serious malaria in young children. Parasitologic and clinical immunity develops concomitantly and cannot be separated. The findings do not support the hypothesis that a special "anti-disease" immunity exists independently of parasitologic immunity.
Adolescent↗