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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute infections caused by the murine malarial parasite Plasmodium chabaudi adami are resolved by antibody-independent mechanisms of immunity. The fact that athymic nude mice developed high-grade unrelenting malaria and died when infected with this parasite suggested a significant role for T lymphocytes. Using adoptive transfer techniques, we demonstrated that spleen cells from either nonimmune or immune donor BALB/c mice eventually suppressed P. chabaudi adami infections in histocompatible recipient nude mice in a dose-dependent manner. Infections in recipients of "immune" spleen cells were less severe, demonstrating a depressed peak parasitemia and a shortened duration of patent infection, than was observed in recipients of normal spleen cells. Also, when sufficient numbers of immune spleen cells were transferred, the second wave of parasitemia (characteristic of this infection in nonimmune mice) failed to occur. T lymphocytes mediated protection in recipient mice, since T-cell-enriched, but not B-cell-enriched, spleen cell fractions suppressed P. chabaudi adami infections in nude mice. Protection was best achieved with T cells that bore the L3T4 phenotype. Patent parasitemias developed in all recipient mice, suggesting that the grafted cells did not limit parasite growth directly but achieved this end by activating other as yet unidentified inhibiting cell systems.
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PMID:T-cell immunity in murine malaria: adoptive transfer of resistance to Plasmodium chabaudi adami in nude mice with splenic T cells. 308 29

Cell-mediated immunity to malaria may involve macrophages, the monokines that mediate endotoxicity, and reactive oxygen species. Since interferon-gamma activates macrophages to release reactive oxygen species, and tumor necrosis factor-alpha (TNF-alpha) helps both to mediate endotoxicity and to induce leukocytes to secrete reactive oxygen, we monitored the effects of administering recombinant forms of these cytokines on Plasmodium chabaudi adami infections in mice. We also fed infected mice a diet containing 0.75% butylated hydroxyanisole, a scavenger of free radicals. Infections were suppressed by daily i.p. injections of 5 x 10(4) U of recombinant mouse interferon-gamma from day -1 or by recombinant human TNF released from i.p. osmotic pumps at the rate of 6 x 10(3) U/hr. Degenerate intraerythrocytic parasites (crisis forms) were evident much sooner in the course of the suppressed infections, and parasitemias fell correspondingly earlier. The butylated hydroxyanisole diet, in contrast, enhanced the infections. In these mice crisis forms were seen later, and at higher parasitemias, than they normally occur. These observations are consistent with the concept that T cell-dependent, macrophage-derived mediators are central to the type of malarial immunity that kills parasites inside circulating red cells. They also suggest, but do not prove, that both TNF and reactive oxygen species are involved, and that the role of TNF may be more indirect, although no less important, than that of reactive forms of oxygen.
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PMID:Inhibition of murine malaria (Plasmodium chabaudi) in vivo by recombinant interferon-gamma or tumor necrosis factor, and its enhancement by butylated hydroxyanisole. 311 10

Infections caused by parasites are common and not limited to the developing world. The spectrum of interactions between pregnancy and parasite infection ranges from minor discomfort to fetal death and are well illustrated by the problems of toxoplasmosis and malaria.
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PMID:Parasites and pregnancy: the problems of malaria and toxoplasmosis. 328 27

Swiss mice with chronic Trypanosoma brucei infections become refractory to subsequent infection with Babesia microti and B. rodhaini. Infection with B. microti 7 days after T. brucei resulted in an obvious inhibition of the babesia parasitaemias and this inhibition became more profound as the time interval between the infections increased, until at 17-20 days the parasitaemias were totally abolished. Even after intravenous injection of large numbers of parasites parasitaemias were inhibited. Similar inhibition was obtained in BALB/c mice but not in C57BL/6 mice. Mice with established T. brucei infections also showed reduced susceptibility to B. rodhaini. In mice similarly infected with T. brucei and the malaria parasites Plasmodium chabaudi chabaudi and P. c. adami the pre-patent periods were noticeably prolonged but the subsequent parasitaemias were unaffected. Infections with P. yoelii were unaffected. Trypanosoma brucei infections were not affected by the intracellular parasites. Among the mechanisms investigated to explain these findings were changes in red blood cell populations, cross-reacting antigens, the release of toxic factors and the generation of activated oxygen species. None of these could account for the inhibition observed.
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PMID:Interactions between Trypanosoma brucei and Babesia spp. and Plasmodium spp. in mice. 400 Jul 2

Infections of mammalian malaria parasites start when sporozoites from an infected anopheline mosquito are injected into the bloodstream of the host. The sporozoites enter the hepatocytes and become transformed into exoerythrocytic schizonts. Since the discovery of the primate parasite Plasmodium cynomolgi in monkey hepatocytes and the rodent parasite Plasmodium berghei in hamster hepatocytes, the ultrastructure of these stages has been extensively studied both in primate and rodent plasmodia. These observations relate only to the development of the exoerythrocytic schizont 25 h after sporozoite injection until the final maturation (of P. berghei) 50 h post-inoculation. Recently, we have studied the route of entry of sporozoites across the cellular lining of liver sinusoids and invasion of the liver parenchymal cells by using transmission electron microscopy. The results of these studies in combination with other physiological experiments strongly suggested that the sporozoite was initially harboured by the Kupffer cell, from which the parasite escaped into the neighbouring hepatocyte. The migration of sporozoites from liver sinusoids to hepatocytes can be achieved within a few minutes. We present here the first ultrastructural observations on the natural transformation of intrahepatocytic sporozoites into exoerythrocytic forms in vivo, using the rodent malaria parasite P. berghei in a laboratory host, the Brown Norway rat. These observations complete the search for the final link in the life cycle of malaria parasites.
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PMID:Malaria parasites--discovery of the early liver form. 633 45

Malaria and filariasis surveys were carried out as part of a broader general health survey between December, 1982 and May, 1983 in the Ok Tedi region of the Star Mountains, Western Province. Malaria, tropical splenomegaly syndrome (TSS) and anaemia were identified as significant health problems. Malaria slide positivity rates of 64.9% in children 2 to 9 years of age and 19.5% in adults 15 years and older indicate high levels of stable malaria transmission. Infections with Plasmodium falciparum were the most common (75.2%), but P. vivax (17.4%) and P. malariae (7.4%) were also encountered. Palpable splenomegaly occurred in 79.2% of adults and children over two years of age with more than 50% of the enlarged spleens grade III or greater (Hackett). Microfilariae (Wuchereria bancrofti) were present in 34.3% of night blood films, and estimated haemoglobin values were considerably below WHO standards. Data from the surveys provide a baseline against which to monitor changes in health status which might be expected to occur in conjunction with the development of a major mining project in the area.
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PMID:Malaria and filariasis in the Ok Tedi Region of the Star Mountains, Papua New Guinea. 659 55

Malaria manifested during the first few months of life may be result of acquisition during pregnancy, at the time of delivery, or by mosquito bite after birth. Both congenital and perinatal malaria are acquired by the transmission of parasitized maternal erythrocytes across the placenta. An infant is described whose mother was diagnosed to have malaria at six months of gestation. The infant developed intermittent fever at 5 weeks of age and presented with anemia and hepatosplenomegaly at 3 months of age at which time Plasmodium falciparum parasites were found on examination of thick smears of the infant's blood. IgG and IgM antimalarial antibodies were detected in maternal blood, but only IgG antibodies were found in the infant's blood at delivery and at the time of diagnosis. These transplacentally transmitted antibodies may afford transient protection for the infant and thus delay the onset of clinical manifestations. Due to the absence of an exoerythrocytic life cycle in congenitally acquired malaria, chloroquine is the drug of choice for treatment. Infections with chloroquine-resistant strains require multiple drug therapy.
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PMID:Congenital malaria due to Plasmodium falciparum. 700 57

Infections with the Uganda Palo Alto, Malayan Camp-CH/Q, Vietnam Oak Knoll, and Vietnam Smith strains of Plasmodium falciparum in owl monkeys (Aotus trivirgatus griseimembra) with concomitant microfilaremias usually, but not always, followed a more benign course than infections with the same strains in monkeys free of filarial infections. Four distinct microfilariae were identified in systematic examinations of 26 monkeys, 5 with self-limited infections with P. falciparum, 9 with normally benign self-limited infections with P. vivax, and 12 without previous malaria. The microfilariae found included: Dipetalonema (Dipetalonema) gracile, Tetrapetalonema (Tetrapetalonema) barbascalensis, T. (T.) panamensis, and an unidentified species designated "Aotus C." Among 23 monkeys studied completely, 14 were infected with a single species, 4 had double infections, and 5 had triple infections. T. barbascalensis was identified in 16 monkeys, T. panamensis in 11. Although data were very limited, there was a suggestion that infections with P. falciparum were less intense in monkeys infected with T. barbascalensis, either alone or with other filariae, than in subjects infected only with T. panamensis.
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PMID:Courses of infections with Plasmodium falciparum in own monkeys displaying a microfilaremia. 701 Oct 72

The Dielmo project, initiated in 1990, consisted of long-term investigations on host-parasite relationships and the mechanisms of protective immunity in the 247 residents of a Senegalese village in which malaria is holoendemic. Anopheles gambiae s.l. and An. funestus constituted more than 98% of 11,685 anophelines collected and were present all year round. Inoculation rates of Plasmodium falciparum, P. malariae, and P. ovale averaged respectively 0.51, 0.10, and 0.04 infective bites per person per night. During a four-month period of intensive parasitologic and clinical monitoring, Plasmodium falciparum, P. malariae, and P. ovale were observed in 72.0%, 21.1% and 6.0%, respectively, of the 8,539 thick smears examined. Individual longitudinal data revealed that 98.6% of the villagers harbored trophozoites of P. falciparum at least once during the period of the study. Infections by P. malariae and P. ovale were both observed in individuals of all age groups and their cumulative prevalences reached 50.5% and 40.3%, respectively. Malaria was responsible for 162 (60.9%) of 266 febrile episodes; 159 of these attacks were due to P. falciparum, three to P. ovale, and none to P. malariae. The incidence of malaria attacks was 40 times higher in children 0-4 years of age than in adults more than 40 years old. Our findings suggest that sterile immunity and clinical protection are never fully achieved in humans continuously exposed since birth to intense transmission.
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PMID:The Dielmo project: a longitudinal study of natural malaria infection and the mechanisms of protective immunity in a community living in a holoendemic area of Senegal. 807 47

Infections are the leading cause of childhood morbidity and mortality in developing countries. Bronchopneumonia, meningitis and gastroenteritis are the commonest fatal infections encountered in Ibadan. Tuberculous lymphadenitis, bronchopneumonia and meningitis are other frequent causes of death. The predominant sequela of measles is respiratory tract infection. Another important cause of childhood mortality is cerebral malaria. In half of the cases of tetanus no obvious portal of entry can be found. It is advocated that the implementation of immunization schedules should be vigorously pursued to curtail childhood mortality resulting from infection.
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PMID:Childhood infections in Nigeria: an autopsy study. 834 43


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