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

A 38-day-old infant had fever, jaundice, hepatosplenomegaly, and a hemolytic anemia. A peripheral blood smear demonstrated intraerythrocytic malarial parasites identified as Plasmodium vivax. Maternal and infant sera contained antibodies to this species. A directed history revealed the mother had suffered several febrile illnesses in Mexico during her pregnancy. Malaria had not been diagnosed nor was it considered at the time of her delivery at this hospital. Review of this and six other cases of congenital malaria reported in this country since 1950 indicates clinical manifestations seldom appear before 3 weeks of age. Although these signs are more frequently associated with other transplacental infections, their occurrence in an infant whose mother is from or who has traveled in an endemic area should prompt consideration of the diagnosis of congenital malaria.
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PMID:Congenital malaria: a rare cause of splenomegaly and anemia in an American infant. 32 10

Since 1974 an epidemic of tertian malaria has been spreading around the Adana and Tarsus townships in southern Turkey, with a peak incidence of 115 500 cases in 1977. A further increase is to be expected because the insect vectors have become resistant to insecticides. Since 1975 eleven children and three adults have been treated for P. vivax malaria. They had all stayed in the epidemic area during the transmission season which lasts from July to October. Because of a long primary latent period seven patients only developed first manifestations of the disease six to nine months after leaving Turkey. The classical malarial paroxysms were missing during the first weeks of the primary attack. Several children had a febrile illness over weeks with headache, vomiting, abdominal pain, hepatosplenomegaly, high blood-sedimentation rate and severe haemolytic anaemia, so that appendicitis or septicaemia had been suspected. Tetracyclines and trimethroprimsulphamethoxazole were able to suppress the disease without preventing relapses.
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PMID:[Tertian malaria in children and adults from an epidemic region in southern Turkey (author's transl)]. 36 41

Rat-adapted Plasmodium chabaudi caused a syndrome characterized by hemolytic anemia, splenomegaly, and glomerulonephritis. All rats recovered and appeared normal after 4 weeks despite persistence of proteinuria. Serologic studies on the malarious rats revealed that the infection was associated with a soluble antigen which was present concurrently with antibody in plasma, in material eluted from blood cells, in extracts of kidney tissues, and in the urine. This antigen appeared to be identical with one extracted from P. chabaudi parasites and did not cross-react with antigens of Plasmodium gallinaceum. Tests for the cold-active hemagglutin (CAH) and the globulin associated serum antigen (SA) previously associated with acute malaria, revealed that CAH, but not SA, was present. From these observations it is suggested that soluble complexes of the parasite antigen and its antibody may have been causal in this syndrome.
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PMID:Experimental infection with Plasmodium chabaudi in rats: antigen and antibody associated with anemia and glomerulonephritis of acute infection. 59 39

Two weeks after leaving Nigeria for temperate zones and a few hours after giving birth to twins, a nigerian mother suffered an acute attack of malaria due to Plasmodium falciparum accompanied by cerebral, renal and hematolgical complications. Both infants were apparently healthy at birth, and no parasites were found on peripheral blood smears. Both placentas were macroscopically normal. At two months of age the second infant, a boy, developed non-febrile hemolytic anemia due to Plasmodium falciparum. The clinical picture and pathogenic mechanisms of perinatal malaria are discussed. Possible protection of the twin sister by partial glucose-6-phosphate dehydrogenase deficiency is considered.
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PMID:[Perinatal transmission of Plasmodium falciparum malaria]. 76 66

A survey of cold haemagglutinin using the normal and tyrpsinized group O red blood cells was performed in 101 normal individuals, 139 individuals with Plasmodium falciparum malaria, 115 individuals with various infections other than malaria and 46 cases of auto-immune haemolytic anaemia. A marked reduction in the incidence of cold haemagglutinin reacting with the normal group O red blood cell was observed in cases of P. falciparum with parasitaemia higher than 100 000/mm3. Although this was also found in other infections, the proposed mechanism seems to be different. Neither remarkable changes in the incidence of cold haemagglutinin reacting with trypsinized red blood cell not the rise of the titres of agglutination in both types of the red blood cells could be detected in P. falciparum malarial cases. The findings are somewhat unexpected and the possible causes are discussed.
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PMID:A marked reduction in the incidence of cold haemagglutinin in Plasmodium falciparum malaria. 79 45

Those who live in areas where Malaria is endemic, acquire immunity by continuous contact. This immunity cannot be acquired during a short holiday. Children in endemic areas acquire a more severe form of malaria during the period of developing immunity and more often suffer complications like acute hemolytic anemia and, in the case of plasmodium falciparum infection, cerebral malaria. This is a report of 39 cases of cerebral malaria which corresponds to an acute encephslopathy with high temperatures, generalized tonic-clonic spasms and unconsciousness. All children were between 6 months and 5 years old. Cerebral malaria at higher ages is rarely seen in Malawi. But its frequency depends on the intensity of endemic infection and the geographic distribution of the types of malaria. 11 (29%) of the 39 children died. Treatment was with chloroquine against which there was no resistance in East Africa for falciparum infections and with plasmaexpanders. In 1 case permanent neurologic changes a spastic cerebral paresis, were seen. Unconsciousness lasting more than 36 hours appears to be a bad prognostic sign. The CSF is clear and normal except for an occasional rise in protein never higher than 90 mg%.
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PMID:[Malaria in children, with special reference to cerebral malaria (author's transl)]. 110 Aug 97

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzymopathy. Because its gene locus is on the X-chromosome it is more common in males than females in all populations. Prevalence rates vary from 62% among Kurdish Jews to the very low rates (0.1% or less in Japan, for example), which are compatible with sporadic cases arising from spontaneous mutations. However, there is at least one population in which G6PD deficiency has not been found, namely the indigenous (Amerindian) population of America. Approximately 400 variants have been described. Despite the clinical burden imposed by this enzymopathy, polymorphic frequencies have been reached in many populations. There is abundant epidemiological evidence that this has happened because of a biological advantage conferred on heterozygotes in falciparum malaria endemic areas. This advantage may apply to quartan malaria as well. Clinical severity varies, from the rare chronic nonspherocytic haemolytic anaemia to progressively milder forms like the Mediterranean and A- types. The other clinical syndromes, i.e. neonatal jaundice and haemolysis caused by infections, foods, drugs and chemicals, are not always predictable. This is because only a fraction of such enzymopathic persons develop these syndromes after exposure to the relevant stimulus. Modern techniques of molecular biology may elucidate why this is so. There is some emerging evidence that the genetic burden or survival value associated with G6PD deficiency may be relevant not only in tropical and infectious diseases, but also in their chemotherapy (e.g. malaria) as well as in the control of a long-recognized environmental pollutant such as lead.
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PMID:Glucose-6-phosphate dehydrogenase deficiency. 151 Nov 80

Mutations producing beta-thalassemia reach individual gene frequencies greater than .01 in malarial-endemic regions because beta-thalassemia trait individuals have increased genetic fitness over that of normal individuals. Exon 3 of the beta-globin gene has been relatively spared as a site of common beta-thalassemia mutations. Frameshifts caused by the loss of a single nucleotide and nonsense mutations produce beta-thalassemia trait when they occur in exons 1 and 2. In contrast, they usually produce chronic hemolytic anemia when present in exon 3. Certain missense mutations in exon 3 produce unstable globins and thalassemia intermedia with hemolysis in heterozygotes. Here we report two new mutations in exon 3 of the beta-globin gene. One is a single nucleotide deletion in codon 109 in a 78-year-old Lithuanian with chronic hemolytic anemia and features of thalassemia. It leads to an abnormal globin (beta Manhattan) that is elongated to 156 amino acids. The second is a CAG-CGG missense mutation at codon 127 that causes a Gln----Pro substitution (beta Houston) and a thalassemia intermedia with hemolysis in three generations of a British-American family. Although the clinical phenotypes of these two patients differed little, differences in globin-synthetic ratios were significant, presumably reflecting differences in the ability of each abnormal beta-globin to form alpha beta dimers. The paucity of high-frequency exon 3 mutations and their worldwide distribution is likely attributable to their phenotypic severity and loss of increased genetic fitness vis-a-vis malaria.
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PMID:Dominant thalassemia-like phenotypes associated with mutations in exon 3 of the beta-globin gene. 158 46

Thalassemia has been considered a recessive, autosomic, hereditary disease, characterized by microcytic, hypochromic, hemolytic anemia, which occurs as the consequence of a defect in the synthesis of the globin chains, the two most frequent types are thalassemias a and b, which in their most severe forms are known as Hydrops Fetalis and Major Thalassemia. The patients who bear thalassemia are concentrated to those places on earth where malaria is endemic, including the Mediterranean region, Northern Africa, The Middle East, India, China and Southern Asia. The simple Heterozygotic states in both types of thalassemia are more benign and may go unnoticed or confused with iron deficiency.
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PMID:[Molecular aspects of alpha dn beta thalassemias]. 166 26

Forty cases of hemolysis (drop of hematocrit greater than 12%/12 h) were retrospectively analyzed for hyperamylasemia and pancreatic complications. In 15 subjects the serum amylase level was greater than 360 U/l, i.e., three times the normal range, in ten the amylase level exceeded 900 U/l. Excluding patients in circulatory shock and/or hepatic coma, acute pancreatitis as defined by an elevation of serum amylase and clinical signs (epigastric pain) was present in four, with additional ultrasound findings (pancreatic swelling) and/or laparatomy/postmortem findings in a further six subjects (total ten patients = 25%) with various causes of hemolysis: autoimmune hemolysis 2, microangiopathic hemolytic anemia 2, toxicemia, G-6-PDH deficiency, septic abortion, malaria, Wilson's disease, and hypophosphatemia, one case each. In all subjects acute renal failure and in seven an activation of intravascular coagulation was seen. Three patients died (33% vs 47% of all hyperamylasemic patients and 46% of the whole group), but none of the deaths was attributed to pancreatitis. Pancreatic postmortem findings were diffuse edema and patchy parenchymal necrosis in two cases and petechial bleeding in one case. We conclude that acute pancreatitis is a complication of massive hemolysis, occurring at a prevalence of above 20%. It may progress from diffuse edema and inflammation to focal necrosis, rarely if ever to gross hemorrhage, and does not contribute to the high mortality of massive hemolysis. Back pain in hemolysis might originate from the pancreas rather than from the kidneys.
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PMID:Pancreatitis in acute hemolysis. 171 92


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