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Malaria infection due to Plasmodium falciparum has been widely recognized as associated with important adverse consequences in pregnant women, particularly in areas of high transmission. Although strategies using antimalarial drugs for prevention had been recommended, even by the late 1980s, few studies had been carried out to examine the efficacy of these prevention efforts. The objectives of the Mangochi Malaria Research Project investigation were to determine the comparative efficacy of regimens containing chloroquine (CQ) or mefloquine (MQ) antimalarial treatment and chemoprophylaxis in an area of CQ-resistant P. falciparum on the following outcomes: 1) the frequency of placental malaria infection; 2) the frequency of low birth weight; 3) the frequency of prematurity or intrauterine growth retardation; 4) the frequency of maternal fever illness and severe anemia; and 5) the likelihood of infant acquisition of malaria infection. Although the investigation was not designed to evaluate the role of antimalarial chemoprophylaxis and treatment on infant mortality reduction, because babies born to study women were scheduled to be followed for up to two years of life, the study allowed for an examination of mortality and morbidity in this population. The sample size was insufficient to provide more than descriptive analysis of mortality and morbidity in the fetal, perinatal, neonatal, postneonatal, and infant time intervals. The study design allowed for the evaluation of two additional aspects of maternal and infant health: other determinants of the above-listed outcomes in addition to malaria prevention (e.g., maternal age, gravidity, socioeconomic status, infection with human immunodeficiency virus or syphilis) and reported cause-specific mortality in the fetal-to-infant intervals. The study design included 22 months of enrollment of pregnant women at their first antenatal clinic visit from four clinic sites in Mangochi District, Malawi, with assignment to one of four antimalarial regimens and prospective follow-up through pregnancy, at delivery, and during infancy. All drug dosing was performed under supervision by the study team, making this an evaluation of intervention efficacy (excluding the role of patient compliance).
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PMID:Objectives and methodology in a study of malaria treatment and prevention in pregnancy in rural Malawi: The Mangochi Malaria Research Project. 870 43

Developing nations in sub-Saharan Africa experience childhood mortality rates that are much higher than any other region of the world. In a rural Malawian community we investigated risk factors for deaths occurring during the neonatal (birth-28 days), postneonatal (29-365 days), infant (birth-365 days), and second-year (366-730 days) periods among a cohort of 3,724 infants monitored from birth. The neonatal mortality rate in this cohort was 48.6 per 1,000 live births (LB); the postneonatal mortality rate was 108.7/1,000 LB. The overall infant mortality rate was 157.3 deaths/1,000 LB and the mortality rate for the first two years of life was 223.7 deaths/1,000 LB. The predominate risk factors for neonatal deaths identified in multivariate analysis were low (hazard ratio [HR] = 2.3) and very low birth weight (HR = 12.7), first pregnancy (HR = 1.8) and maternal syphilis infection (HR = 2.4). Maternal infection with human immunodeficiency virus (HIV) (HR = 1.5) predominated for postneonatal deaths. Low (HR = 1.4) and very low (HR = 5.0) birth weight, first pregnancy (HR = 1.6), maternal HIV infection (HR = 2.4), and the combination of low education and low socioeconomic status (SES) of the mother (HR = 2.0) were the most important factors during the infant period. Maternal HIV infection (HR = 3.3) and the combination of low education and low SES of the mother (HR = 2.6) were the predominate risk factors for mortality occurring during the second year. Factors that were significant in univariate analysis but not significant in the final multivariate models included prematurity, previous adverse reproductive outcome, dying during high malaria transmission season, and being born at home. Interventions to prevent maternal HIV infection and low birth weight and treatment of syphilis infection would have a great impact on reducing early childhood deaths. Improving the delivery of health care and education to women during their first pregnancy and to the most socially disadvantaged women may also help reduce the burden of early childhood mortality in communities such as the one studied in Malawi.
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PMID:Rates and risk factors for mortality during the first two years of life in rural Malawi. 870 44

The chemokine superfamily is composed of at least 20 different leukocyte chemoattractants that act by binding to a family of G protein-coupled receptors. Leukocyte subtypes respond preferentially to unique but overlapping subsets of chemokines as determined by the receptor distribution, yet the receptors appear to signal through a common Gi-type G protein. Since chemokines appear to play major roles in inflammatory pathology, their receptors may be good targets for developing leukocyte selective anti-inflammatory drugs. Two chemokine receptors, CC CKRS and ONCC, function pathologically as cell entry factors respectively for human immunodeficiency virus 1, the cause of AIDS, and Plasmodium vivax, the major cause of malaria.
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PMID:Chemokine receptors: structure, function and role in microbial pathogenesis. 886 54

Although it has not been definitely proven that the severity of malaria is associated to human immunodeficiency virus (HIV) we know that infection through Plasmodium falciparum can favor a rapid evolution of the HIV infection. Besides, association of malaria with HIV/AIDS from a clinical point of view can be clinically severe in the face of the occurrence of other microorganisms or neoplasias, which worsens the evolution and prognosis of the affected patients. The concurrence of HIV with Plasmodium in malaria endemic zones is a possibility which should always be taken into consideration, since transmission is related to risk factors caused by people's behavior which are not always promptly revealed and/or identified. The authors report one case of brain malaria infection by Plasmodium vivax and Plasmodium falciparum in a patient with AIDS. They describe the clinical evolution and therapy.
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PMID:[Cerebral malaria and AIDS: case report]. 898 95

The current status and future prospects of vaccines for adults are discussed. For every child in America who dies of a vaccine-preventable disease, about 400 adults die of such a disease. Evidence of the merit of influenza vaccination continues to accumulate, yet < 30% of high-risk people younger than 65 have been vaccinated. Use of pneumococcal vaccine lags behind that of influenza vaccine. Serious discrepancies in immunization levels exist among different segments of U.S. adult society. A vaccination status assessment is now recommended for everyone reaching the age of 50. New vaccines are available to prevent varicella, hepatitis A, and typhoid fever. There are now two formulations of hepatitis A virus vaccine; adult users of these vaccines include travelers, people relocating to areas with poor sanitation, military personnel, laboratory workers, and hemophiliacs. New rabies vaccines may be the next vaccines to be used primarily in adults. Vaccines against pertussis, Lyme disease, cholera, herpes simplex, malaria, other infectious diseases, and cancer are in various stages of development. For health care personnel in areas where there is a strong likelihood of Mycobacterium tuberculosis transmission and infection, BCG vaccination is recommended. The risk of immunization to a person infected with the human immunodeficiency virus is likely outweighed by the protection offered against other health threats. Health systems should select tetanus-diphtheria toxoids adsorbed for their formularies for immunizing adults, not monovalent tetanus toxoid. Vaccines are available to prevent a growing list of infectious diseases but are underused in adults.
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PMID:Status and future of vaccines for adults. 904 59

Chimeric simian/human immunodeficiency virus (SHIV) consists of the env, vpu, tat, and rev genes of human immunodeficiency virus type 1 (HIV-1) on a background of simian immunodeficiency virus (SIV). We derived a SHIV that caused CD4+ cell loss and AIDS in pig-tailed macaques (S. V. Joag, Z. Li, L. Foresman, E. B. Stephens, L. J. Zhao, I. Adany, D. M. Pinson, H. M. McClure, and O. Narayan, J. Virol. 70:3189-3197, 1996) and used a cell-free stock of this virus (SHIV(KU-1)) to inoculate macaques by the intravaginal route. Macaques developed high virus burdens and severe loss of CD4+ cells within 1 month, even when inoculated with only a single animal infectious dose of the virus by the intravaginal route. The infection was characterized by a burst of virus replication that peaked during the first week following intravenous inoculation and a week later in the intravaginally inoculated animals. Intravaginally inoculated animals died within 6 months, with CD4+ counts of <30/microl in peripheral blood, anemia, weight loss, and opportunistic infections (malaria, toxoplasmosis, cryptosporidiosis, and Pneumocystis carinii pneumonia). To evaluate the kinetics of virus spread, we inoculated macaques intravaginally and euthanized them after 2, 4, 7, and 15 days postinoculation. In situ hybridization and immunocytochemistry revealed cells expressing viral RNA and protein in the vagina, uterus, and pelvic and mesenteric lymph nodes in the macaque euthanized on day 2. By day 4, virus-infected cells had disseminated to the spleen and thymus, and by day 15, global elimination of CD4+ T cells was in full progress. Kinetics of viral replication and CD4+ loss were similar in an animal inoculated with pathogenic SHIV orally. This provides a sexual-transmission model of human AIDS that can be used to study the pathogenesis of mucosal infection and to evaluate the efficacy of vaccines and drugs directed against HIV-1.
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PMID:Animal model of mucosally transmitted human immunodeficiency virus type 1 disease: intravaginal and oral deposition of simian/human immunodeficiency virus in macaques results in systemic infection, elimination of CD4+ T cells, and AIDS. 909 79

Approaches to improve the efficacy of the current (killed) influenza virus vaccines include the generation of cold-adapted and genetically engineered influenza viruses containing specific attenuating mutations. It is hoped that these genetically altered viruses, in which the hemagglutinin and neuraminidase genes from circulating strains have been incorporated by reassortment, can be used as safe live influenza virus vaccines to induce a long-lasting protective immune response in humans. In addition, genetically engineered influenza viruses may provide a means for expressing foreign antigens. Immunization of mice with recombinant influenza and vaccinia viruses expressing specific antigens of Plasmodium yoelii resulted in a dramatic protective immune response against malaria in this model. Mice immunized with recombinant influenza viruses expressing human immunodeficiency virus (HIV) epitopes generated long-lasting HIV-specific serum antibodies and secretory IgA in the secretory nasal, vaginal, and intestinal mucosa. These results suggest that genetically engineered influenza viruses may be developed for use as live virus vaccines against influenza as well as other diseases.
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PMID:Development of novel influenza virus vaccines and vectors. 924 Jun 94

Emerging and reemerging infections are attracting greater attention from the public health and medical communities. Pathologists and other physicians are increasingly aware of the importance of the subspecialty of infectious disease pathology as a tool for diagnosis, surveillance, and research of emerging infections. In this communication, we describe the role that infectious disease pathologists have played during the last 2 years in broadening our understanding of selected emerging infections, including such examples as new variant Creutzfeldt-Jakob disease and bovine spongiform encephalopathy, leptospirosis, microsporidiosis, Ebola hemorrhagic fever, and cyclosporiasis. The significance of providing pathology services, especially the autopsy, to patients with potentially hazardous communicable diseases is discussed with the supposition that it is unethical to exclude or withhold health care from a patient based on his or her underlying disease or on risk factors for acquiring a disease. The increasing occurrence of infectious diseases imported into the United States and other nations, including human immunodeficiency virus-1 group O, dengue fever, tuberculosis, malaria, diphtheria and cholera in immigrants and travelers, and Ebola virus in nonhuman primates, emphasizes the necessity for pathologists of having competence with infectious disease pathology. It is critical that new generations of pathologists not only be trained in the subspecialty of infectious disease pathology, but that they also be willing participants in the diagnosis and investigation of infectious diseases. The lack of training programs for infectious disease pathologists, as well as the deficiency in infectious disease pathology support for ongoing and future epidemiologic investigations and research, has led to the broadening of pathology services and initiation of a dedicated section of Infectious Disease Pathology at one of the nation's premier public health institutions, the Centers for Disease Control and Prevention in Atlanta, Ga. Together with preexisting groups of medical and veterinary infectious disease pathologists at universities, the Armed Forces Institute of Pathology, the US Army Medical Research Institute of Infectious Diseases, and the National Institutes of Health, this new program will significantly strengthen the capability of the United States to respond to future challenges of emerging and reemerging infections, both in this country and abroad.
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PMID:Emerging and reemerging infections. Progress and challenges in the subspecialty of infectious disease pathology. 927 4

Each year, approximately 100,000 refugees are resettled to the United States. Before resettlement, these refugees undergo medical screening to identify inadmissable conditions (e.g., infectious tuberculosis and human immunodeficiency virus [HIV] infection) among individual refugees. This report describes the implementation and results of an enhanced refugee medical assessment strategy among Barawan Somali refugees in Kenya during July 1997. This strategy employs population-based screening for parasitic infections. The findings indicate that, among these refugees, the prevalences of malaria and intestinal parasites were sufficient to warrant pre-embarkation therapy to improve the health of both individuals and the total refugee population. This therapy also may prevent local transmission of parasitic infections in the resettlement communities in the United States.
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PMID:Enhanced medical assessment strategy for Barawan Somali refugees--Kenya, 1997. 943 15

Because malaria-stimulated cytokine production may have deleterious effects on human immunodeficiency virus type 1 (HIV-1) replication, the effects of Plasmodium falciparum antigens on HIV-1 replication were studied. Stimulation with malarial antigens significantly enhanced HIV-1 replication of HIV-1LAV and primary HIV-1 isolates (subtype A) in CD8-depleted peripheral blood mononuclear cells from naive donors. The malarial antigen-induced activation of HIV-1 was due to cellular activation as judged by the expression of cell activation markers and proliferative responses. While malarial antigen stimulation increased expression of tumor necrosis factor (TNF-alpha) and interleukin-6 (IL-6), only monoclonal antibodies (MAbs) to TNF-alpha inhibited malarial antigen-induced HIV-1 replication, whereas MAb to IL-6 had no effect. Malarial antigen increased HIV-1 replication by increasing viral mRNA expression and by activating long terminal repeat-directed viral transcription. These data suggest that P. falciparum infection can modulate HIV-1 pathogenesis by activating lymphocytes and stimulating viral replication through the production of cytokines.
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PMID:Plasmodium falciparum antigen-induced human immunodeficiency virus type 1 replication is mediated through induction of tumor necrosis factor-alpha. 946 33


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