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

Plasmodium falciparum (human malaria) infections are characterized by the attachment of erythrocytes infected with mature stage parasites to endothelial cells lining the post-capillary venules, a phenomenon known as sequestration. In the human body, the microvessels of the heart, lungs, kidneys, small intestine, and liver are the principal sites of sequestration. Sequestered cells that clog the brain capillaries may reduce blood flow sufficiently so that there is confusion, lethargy, and unarousable coma--cerebral malaria. This review considers what is known about the molecular characteristics of the surface proteins, that is, the red cell receptors and the endothelial cell ligands, involved in sequestration. Recent work from our laboratory on the characterization of the adhesive proteins on the surface of the P falciparum-infected red cell, and the ligands to which they bind on human brain endothelial cells is also discussed. Finally, consideration is given to the multifactor processes involved in sequestration and cerebral malaria, as well as the possible role of 'anti-adhesion therapy' in the management of severe malaria.
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PMID:Membrane proteins involved in the adherence of Plasmodium falciparum-infected erythrocytes to the endothelium. 159 38

We compared placebo and dexamethasone (initial dose, 3 mg/kg; total, 11.4 mg/kg per 48 h) in a double-blind trial involving 10 stuporous and 28 comatose patients with cerebral malaria. Patients were 18 mo to 42 y of age (geometric mean, 10.2 y), and the 19 patients in each group were comparable on admission. All patients received intravenous quinine therapy. Four patients (21%) in each group died. There were no significant differences between the placebo- and dexamethasone-treated groups in time until patients became afebrile (median, 51 vs. 19 h), the level of consciousness became normal (mean, 80 vs. 83 h), or parasitemia was cleared (mean, 2.1 vs. 3.4 d) or in the incidence of complications. Coma or hyperparasitemia (greater than or equal to 5% of erythrocytes parasitized) at the time of admission and hypoglycemia at any time during hospitalization were significantly correlated with a fatal outcome, which was not improved by using dexamethasone. We conclude that high-dose dexamethasone is not indicated for treating cerebral malaria.
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PMID:High-dose dexamethasone in quinine-treated patients with cerebral malaria: a double-blind, placebo-controlled trial. 304 74

Mice infected with Plasmodium berghei, P. chabaudi, or P. yoelii became lethargic and ceased to display normal antimosquito behavior. Periods of reduced defensiveness corresponded with maximum mosquito engorgement and with periods of maximum gametocyte infectivity to mosquitoes. Increased feeding success of mosquitoes during periods of peak gametocyte infectivity may be important to the natural maintenance of these malaria parasites.
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PMID:Malaria renders mice susceptible to mosquito feeding when gametocytes are most infective. 633 90

Acute clinical malaria caused by Plasmodium inui was diagnosed in an adult female cynomolgus monkey (Macaca fascicularis) 4 years after importation into the United States. Stress and immunosuppression associated with experimentation completed 2 weeks earlier may have contributed to the development of severe clinical disease. Clinical findings included severe regenerative anemia, hepatosplenomegaly, weakness, lethargy, weight loss, and anorexia. The infection was treated and successfully eliminated with chloroquine hydrochloride administered intramuscularly at a dose of 5 mg/kg base given at 0, 6, 24, 48, and 72 hours. Treatment also included a blood transfusion and intensive supportive care.
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PMID:Acute clinical malaria (Plasmodium inui) in a cynomolgus monkey (Macaca fascicularis). 683 80

George Carmichael Low, like so many early pioneers of Tropical Medicine, had his origin(s) in Scotland. Following a distinguished undergraduate (and early postgraduate) career, he joined Dr Patrick Manson at the newly established London School of Tropical Medicine in 1899. His first major contribution to the specialty (in 1900) was to demonstrate filariae in the proboscis sheath of mosquitoes which had been infected with Filaria bancrofti in Australia, using a technique recently learned in Heidelberg and Vienna. Shortly afterwards, he led an expedition to the Roman Campagna; this established beyond doubt mosquito-transmission of Plasmodium vivax infection to Homo sapiens. In 1901-1902, Low undertook a demanding tour of the Caribbean where he made important contributions to the understanding of the filariases, and assisted in malaria eradication. In 1902 he led a small team (the Royal Society's first sleeping sickness expedition) to investigate the 'negro lethargy' which had emerged in epidemic proportions on the northern shores of Lake Victoria in East Africa. This expedition narrowly failed to establish the aetiological agent (Trypanosoma sp.) of this disease. Following his return to London, Low became superintendent of the Albert Dock Hospital and from then onwards devoted most of his career to the London School of Tropical Medicine and the Hospital for Tropical Diseases (where he became senior physician). He wrote extensively, in addition to his clinical, teaching and administrative commitments. Perhaps Low's major contribution, however, was in establishing the Society (later Royal) of Tropical Medicine and Hygiene in 1907, with Mr (later Sir) James Cantlie.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Royal Society of Tropical Medicine and Hygiene meeting at Manson House, London, 10 December 1992. George Carmichael Low FRCP: twelfth president of the Society and underrated pioneer of tropical medicine. 824 57

BACKGROUND Salicylates continue to be marketed and to be used in developing countries as over-the-counter (OTC) antipyretics in children, whereas in developed countries they are no longer used in children because of safety concerns. The presenting signs of salicylate poisoning, especially chronic (repeated administration of therapeutic or excessive doses for longer than 12 h), can include metabolic acidosis, hypoglycaemia, lethargy, and coma and fits. These signs are also common in severe malaria in African children. Admission of two probable cases of chronic salicylate poisoning prompted us to look for other cases among children presenting to our hospital in Kenya, apparently with severe malaria. METHODS All children admitted to Kilifi District Hospital between July and September, 1994, who had a positive blood film for Plasmodium falciparum, and one or more of coma, prostration, or respiratory distress were eligible. As well as routine tests for malaria and routine biochemistry, salicylate concentrations were measured. Management of children (aged 6 months to 10 years) in the community was assessed by a cross-sectional survey of 463 households and by interviews with mothers 2 days after they had bought OTC drugs for a child with fever. FINDINGS Data were available for 143 of 154 children with initial primary diagnoses of severe malaria. 129 (90 percent) had detectable (>l mg/dL) salicylate. Six of these had salicylate concentrations of 20 mg/dL or higher. All six had neurological impairment and metabolic acidosis and four were, or became, hypoglycaemic. OTC drugs were the first-line treatment in 188 (74 percent) of 254 fever episodes during the 2 weeks before the cross-sectional survey. Of 250 mothers who bought drugs for a febrile child, 236 (94 percent) bought a preparation containing salicylates and 50 (21 percent) gave a dose higher than the manufacturer's recommended maximum. INTERPRETATION These cases suggest that in some children salicylate poisoning may cause or contribute to the development of metabolic acidosis and hypoglycaemia, complications of severe malaria associated with high mortality.
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PMID:Chronic salicylate poisoning and severe malaria. 865 7

A total of 1,885 blood and stool samples of four main protozoan parasitic infections were retrospectively reviewed from January, 2000 to April, 2004. Eleven of the 1,350 stool samples were shown positive for Cryptosporidium and Giardia infections; one of the 5 cases was clinically diagnosed as gastrointestinal cryptosporidiosis, while 6 cases were giardiasis. In patients with giardiasis, children were among the high-risk groups, making up 66.7% of these patients. The common presenting signs and symptoms were: diarrhea (83.3%), loss of appetite (83.3%), lethargy (83.3%), fever (66.7%), nausea/vomiting (50.0%), abdominal pain (16.7%), dehydration (16.7%) and rigor and chills (16.7%). Metronidazole was the drug of choice and was given to all symptomatic patients (83.3%). For the blood samples, 28 of the 92 peripheral smears for Plasmodium spp infection were diagnosed as malaria. The age range was from 4 to 57, with a median of 32.5 years. The sex ratio (M:F) was 3.6:1, while the age group of 30-44 years was the most commonly affected in both sexes. The majority of patients were foreigners (60.7%) and non-professional (39%). Plasmodium vivax (71%) infection was the most common pathogen found in these patients, along with a history of traveling to an endemic area of malaria (31%). The predominant presenting signs and symptoms were: fever (27%), rigor and chills (24%), nausea/vomiting (15%) and headache (8%). Chloroquine and primaquine was the most common anti-malarial regimen used (78.6%) in these patients. The seroprevalence of toxoplasmosis in different groups was 258/443 (58%): seropositive for IgG 143 (32.3%); IgM 67 (15%); and IgG + IgM 48 (10.8%). The age range was from 1 to 85, with a mean of 34 (+/- SD 16.6) years. The predominant age group was 21 to 40 years (126; 28.4%). The sex ratio (M:F) was 1.2:1. Subjects were predominantly male (142; 32%) and the Malay (117; 26.4%). Of these, 32 cases were clinically diagnosed with ocular toxoplasmosis. The range of age was from 10 to 56 years with a mean of 30.5 (+/- SD 12.05) years. The sex ratio (M:F) was 1:1.7. The majority were in the age group of 21 to 40 years, female (20; 62.5%), and Malay (17; 53%). They were also single (16; 50%), unemployed (12; 37%), and resided outside Kuala Lumpur (21; 65.6%). The more common clinical presentations were blurring of vision (25; 78%), floaters (10; 31%) and pain in the eye (7; 22%). We found that funduscopic examination (100%) and seropositivity for anti-Toxoplasma antibodies (93.7%) were the main reasons for investigation. Choroidoretinitis was the most common clinical diagnosis (69%), while clindamycin was the most frequently used antimicrobial in all cases. Among HIV-infected patients, 10 cases were diagnosed as AIDS-related toxoplasmic encephalitis (TE) (9 were active and 1 had relapse TE). In addition, 1 case was confirmed as congenital toxoplasmosis.
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PMID:Parasitic infections in Malaysia: changing and challenges. 1643 80

A neuronal storage disease affecting 5 captive Humboldt penguins is described. One bird died after 3 days of lethargy and anorexia. The 4 remaining birds died after a slowly progressing course of disease with signs that included lethargy, weakness, and neurologic dysfunction. Neurologic signs included dysphagia and ataxia. Gross lesions in the first animal to die consisted of hepatosplenomegaly indicative of avian malaria, which was confirmed histologically. The 4 remaining animals were mildly to moderately emaciated. Moderate to marked vacuolation of the neuronal perikarya was observed in Purkinje cells, neurons of the brainstem nuclei, and motorneurons of the spinal cord in all birds. By electron microscopy the vacuoles represented multilayered concentric lamellar structures. These findings were indicative of sphingolipidosis. All animals had been prophylactically treated for avian malaria, aspergillosis, and possible bacterial infections with chloroquine, itraconazole, and enrofloxacin. Circumstantial evidence implicates chloroquine therapy as the possible cause of the storage disease.
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PMID:Neuronal storage disease in a group of captive Humboldt penguins (Spheniscus humboldti). 1709 67

An adult male white eared-pheasant (Crossoptilon crossoptilon) at a Japanese zoo exhibited lethargy and emaciation. Microscopic examination of a blood smear revealed a haemosporidian parasitic infection. Based on the morphological characteristics and molecular analysis of the parasite, it was identified as Plasmodium (Bennettinia) juxtanucleare. This is the first report of P. juxtanucleare infection in bird species belonging to the genus Crossoptilon. Caution against avian malaria infection is required for the conservation of endangered bird species in zoos.
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PMID:Plasmodium (Bennettinia) juxtanucleare infection in a captive white eared-pheasant (Crossoptilon crossoptilon) at a Japanese zoo. 1831 84

Introduced mosquito-borne avian disease is a major limiting factor in the recovery and restoration of native Hawaiian forest birds. Annual epizootics of avian pox (Avipoxvirus) and avian malaria (Plasmodium relictum) likely led to the extinction of some species and continue to impact populations of susceptible Hawaiian honeycreepers (Drepanidinae). The introduction of a novel pathogen, such as West Nile virus (WNV), could result in further population declines and extinctions. During September and October 2004, we infected Hawai'i' Amakihi (Hemignathus virens) with a North American isolate of WNV by needle inoculation and mosquito bite to observe susceptibility, mortality, and illness in this endemic passerine, and to determine the vector competence of the co-occurring, introduced mosquito Culex quinquefasciatus. All experimentally infected Hawai'i ;Amakihi became viremic, with a mean titer >10(5) plaque-forming units (PFU)/ml, and they experienced clinical signs ranging from anorexia and lethargy to ataxia. The fatality rate among needle-inoculated Hawai'i' Amakihi (n=16) was 31.3%, but mortality in free-ranging birds is likely to increase due to predation, starvation, thermal stress, and concomitant infections of avian malaria and pox. Surviving Hawai'i' Amakihi seem to clear WNV from the peripheral blood by 7-10 days postinfection (DPI), and neutralizing antibodies were detected from 9 to 46 DPI. In transmission trials, Hawaiian Cx. quinquefasciatus proved to be a competent vector and Hawai'i Amakihi an adequate amplification host of WNV, suggesting that epizootic WNV could readily become an additional limiting factor of some native Hawaiian bird populations.
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PMID:Experimental infection of Hawai'i 'Amakihi (hemignathus virens) with West Nile virus and competence of a co-occurring vector, culex quinquefasciatus: potential impacts on endemic Hawaiian avifauna. 1939 35


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