 Wysłany: Pon 14:59, 14 Mar 2011 Temat postu: _9066 laboratory diagnosis of falciparum malaria |
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| Falciparum malaria laboratory diagnosis
Send. Method to dry in the blood drops on filter paper, eluted antibody saline ingredients, add in monkeys infected with Plasmodium falciparum antigen tablets, washing tablets (light) after the addition of anti IgG conjugate fluorescence staining, fluorescence microscopy after washing inspection, the fluorescence response of cells as positive, and Jing-fold dilution of blood titer observed. 2. Dot enzyme (Dotimmunoassay, DIA) to take the soluble antigen of Plasmodium falciparum, drop in the nitrocellulose membrane, plus serum and after washing the membrane coupled with anti-human IgG conjugate, and finally adding chromogenic substrate as positive. 3. Staphylococcal protein A enzyme-linked immunosorbent assay (SPA-ELIS'A) soluble P. falciparum antigen obtained by reaction plate, add serum, washer SPA after the addition of a conjugate, washer after the chromogenic substrate were added positive. 4. Yan-free red blood cell enzyme-linked Assay (ce11 an E}, LIsA) crossing with P. falciparum erythrocyte suspension was plate, after incubation, plate washer, then add together after suffering washer anti-human lgG conjugate, Washer added the end pieces, choose to use, improved and enhanced. Complications of falciparum malaria in the First Affiliated Hospital, Third Military Medical University, and other types of malaria compared to the complications of falciparum malaria is more common and more severe disease, some patients with complications of falciparum malaria is the leading major cause of death. Therefore, it is necessary to familiar with its various complications, for proper control. Now common complications are described below. First, dark urine fever is an acute falciparum malaria sudden intravascular hemolysis. Disease has been rare in recent years than in the past. The mechanism has been considered an autoimmune response caused by Plasmodium infection, and later considered a congenital red cell glucose 6-phosphate dehydrogenase A (G-6 one PD) deficiency or other red cell enzyme deficiency, and malaria infection, malaria drugs (such as quinine and primaquine morpholine) or other drugs is their incentive. Also be found in G-6-PD normal and renal failure in patients with severe falciparum malaria, its causes are unknown. General acute onset, seen in falciparum malaria attack was, or a few days after the attack. When onset of chills, fever malaise, abdominal pain, headache, vomiting, liver and spleen increased fast left, progressive anemia and jaundice; feces volume plummeted, showing color of soy sauce (dark urine), developing a large number of hemoglobin from and a self-protein, casts, epithelial cells; light who only see black and show a transient, severe acute renal failure in addition, hypotension, confusion, convulsions, coma and put to death. Which is the cause of acute renal failure in patients with dark urine fever is an important cause of death. = Acute renal failure more common in adult patients with falciparum malaria. Its pathogenesis is the first of two t cross the blood rheological changes. Can be caused by several factors: by the red cells and capillary endothelial cells and small veins end units, reduced by the deformation of red cells,timberland portugal, red blood cell viscosity reduction,ghd piastre, and acute phase protein induced from the increased plasma viscosity increased, all contribute to blood viscosity degree of increased microcirculation sense of stasis followed by Plasmodium falciparum, s stained non-specific effect: low blood passenger volume, disseminated intravascular coagulation (DIC), intravascular hemolysis, catecholamine effect, endotoxemia and yellow pox , also play a role. According to different pathogenesis of renal failure can be divided into pre-renal nature. Which is more common in severe falciparum malaria such as cerebral malaria and jaundice associated with the patients. After onset of fever occurred in the first leopard 4 ~ 7d, showed into the character of oliguria and anuria (individual as much, serum urea nitrogen and creatinine increased. May be complicated by hypoglycemia, jaundice, hypertension and pulmonary edema. Acute renal Activity fu dried by dialysis treatment, mortality fell from 3O lO. more clamor mortality is still high when the officer involved, including pulmonary swimming more than half of patients who died amidships. Third, low blood Mo Lai rumors in recent years, the new emphasis by the jackals. more common in patients with falciparum malaria in pregnant women, children, the use of quinine and quinidine treatment and patients with severe falciparum malaria. which, with severe falciparum malaria in pregnant women treated with quinine and quinidine occurs when the rate of hypoglycemia 5O. the mechanism of low blood sugar is not evil f} 5 Jing Chu, probably due to the use of blood glucose and malaria parasite (mainly quinine) on the stimulation of islet cell population, causing an increase in insulin secretion caused by the recent discovery of hypoglycemia associated with falciparum malaria neoplasms in serum necrosis factor (TNF) was significantly higher than other patients, and has proved able to inhibit TNF thorn gluconeogenesis, it may be associated with the occurrence of low blood sugar. falciparum malaria may typically hypoglycemia, often without sweating and pupil dilation,p90x workout schedule, common symptoms of anxiety, shortness of breath, chills, tachycardia and oliguria and so on. severe cases, bizarre behavior, faintness,tory burch outlet, unconsciousness, coma and body grams and so on. As P. falciparum itself has a variety of serious symptoms, Therefore, hypoglycemia is often the clinicians ignored. IV, pulmonary edema is a rare serious complications of malignant smallpox dark, more common in falciparum malaria in low immunity,tory burch shoes, high parasite, need. q, sweet hai ~ Mu-Su Tsai ago. yu embroidery pick vinegar deleted hoe., |
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