Heat-related illnesses and deaths--Missouri, 1998, and United States, 1979-1996.
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Although heat-related illness and death are readily preventable, exposure to extremely high temperatures caused an annual average of 381 deaths in the United States during 1979-1996. Basic behavioral and environmental precautions are essential to preventing adverse health outcomes associated with sustained periods of hot weather (daytime heat index of > or = 105 F [> or = 40.6 C] and a nighttime minimum temperature of 80 F [26.7 C] persisting for at least 48 hours). This report describes four heat-related deaths that occurred in Missouri during 1998, summarizes heat-related deaths in the United States during 1979-1996, describes risk factors associated with heat-related illness and death, especially in susceptible populations (young and elderly, chronically ill, and disabled persons), and recommends preventive measures. (+info)
A retrospective examination of sporozoite- and trophozoite-induced infections with Plasmodium falciparum: development of parasitologic and clinical immunity during primary infection.
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A retrospective analysis was made of the parasitologic and fever records of 318 patients who had been infected with the El Limon, Santee Cooper, or McLendon strains of Plasmodium falciparum for treatment of neurosyphilis between 1940 and 1963 to determine the development of parasitologic and clinical immunity during primary infection. The presence of fever > or = 101 degrees F and > or = 104 degrees F, asexual parasite counts > or = 1,000 and > or = 10,000/microl, and gametocyte counts > or = 100/microl and > or = 1,000/microl are presented. The frequency of fever (number of patients with fever/number of patients remaining in study) for the first 100 days of patent parasitemia, the frequency of parasite counts > or = 1,000 and > or = 10,000/microl during the first 100 days of patent parasitemia, and the frequency of gametocyte counts > or = 100 and > or = 1,000/microl during the first 100 days of patent parasitemia are presented for 4 groups of patients: 1) sporozoite-induced and 2) trophozoite-induced infections requiring treatment during their primary attack, and 3) sporozoite-induced and 4) trophozoite-induced infections not requiring treatment during the primary attack. For each sporozoite-induced infection, the route of inoculation (bites or syringe), the species of mosquito used, the number of mosquito glands or bites, the intensity of salivary gland infection, and the length of the prepatent period are recorded. Prepatent periods for 109 sporozoite-induced infections ranged from 6 to 28 days. Patients with parasitologic or clinical findings that required suppressive, but non-curative treatment, during the primary attack had higher frequency of fever, parasitemia, and gametocytemia than patients not so treated. Fever was concentrated in the first 2 weeks of patent parasitemia although instances of fever were reported >100 days after infection. High-density parasitemia was also concentrated early in the infection; instances of parasite counts > or = 10,000/microl occurred > 75 days after infection. In conclusion, immunity to infection with P. falciparum was shown to develop rapidly. Following primary infection, clinical and parasitologic immunity was evident within 2-3 weeks following the detection of parasites in the peripheral circulation. (+info)
A retrospective examination of secondary sporozoite- and trophozoite-induced infections with Plasmodium falciparum: development of parasitologic and clinical immunity following secondary infection.
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A retrospective study was made of clinical records to determine parasitemia and episodes of fever of 59 patients reinfected with Plasmodium falciparum for treatment of neurosyphilis, which was considered standard medical care at the time. Records were collected at the National Institutes of Health laboratories in Columbia, South Carolina and Milledgeville, Georgia during the period 1940 to 1963. Nineteen patients were infected via the bites of Anopheles albimanus, An. quadrimaculatus, or An. freeborni mosquitoes; the median prepatent period was 11.5 days. It was evident that clinical immunity, as measured by the frequency of fever, particularly high intensity fever (> or = 104 degrees F), was increased following reinfection. The parasitologic immunity, as measured by the frequency of asexual parasite counts and gametocyte counts, was also evident. In general, in secondary infections with homologous and/or heterologous strains of P. falciparum, fever episodes > or = 101 degrees F and > or = 104 degrees F were reduced in number, parasitemia was reduced, and gametocyte production was reduced. However, despite long courses of parasitemia during their primary infections, most patients developed fever and, in some cases, high-density parasitemia and gametocytemia following reinfection. The intensity of the secondary response did not appear to be associated with the length of the previous course of parasitemia. In addition, current infection with heterologous strain parasites did not prevent the development of fever or higher density parasite counts following imposition of the new strain of parasite. (+info)
A retrospective examination of sporozoite- and trophozoite-induced infections with Plasmodium falciparum in patients previously infected with heterologous species of Plasmodium: effect on development of parasitologic and clinical immunity.
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A retrospective examination was made to determine parasitemia and episodes of fever in 97 patients, previously infected with Plasmodium malariae, P. ovale, and/or P. vivax, who were reinfected with P. falciparum for treatment of neurosyphilis, the standard treatment at the time. Data were collected at the National Institutes of Health laboratories in Columbia, South Carolina and Milledgeville, Georgia during the period 1940 to 1963. Results were compared with observations recorded for patients following primary infection with P. falciparum. The mean daily percentage of patients with fever > or = 101 degrees F during the first 20 days of primary infection with P. falciparum was 42.4; the percentage with fever > or = 104 degrees F was 19.9%. Those previously infected with P. ovale, P. vivax, and P. malariae had mean daily percentages of fever > or = 101 degrees F and > or = 104 degrees F of 39.1% and 14.8%, 39.1% and 19.4%, and 28.4%, and 11.3%, respectively. Previous infection with P. ovale or P. vivax had little, if any, effect on subsequent clinical malaria due to P. falciparum, whereas infection with P. malariae resulted in reduced frequencies of fever. A similar comparison was made for parasite counts > or = 1,000/microl and > 10,000/microl. The percentages for 268 patients during the first 20 days of primary infection with P. falciparum parasite counts > or = 1,000/microl and > or = 10,000/microl were 58.2% and 29.9%, respectively. Those previously infected with P. ovale, P. vivax, and P. malariae had mean daily percentages of parasitemia > or = 1,000/microl and > or = 10,000/microl of 58.0% and 24.3%, 57.3% and 31.1%, and 45.9% and 19.0%, respectively. Previous infection with P. malariae resulted in a reduction in the frequency of high-density parasitemia (> or = 10,000/microl) as well as an asexual parasite count > or = 1,000/microl. These results suggest that P. falciparum and P. malariae share common antigens that are able to induce parasitologic and clinical protection when infection with P. falciparum follows that with P. malariae. The results did not suggest that protection to P. falciparum is provided by previous infection with P. ovale or P. vivax. (+info)
Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia.
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We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (VO(2 max)) 4.7 +/- 0. 4 l/min (mean +/- SE)] cycled for 30 min in the heat (35 degrees C) in the upright and in the supine positions (VO(2) 2.93 +/- 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (T(es)) was 37. 8-38.0 degrees C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (T(es) = 38. 7-38.8 degrees C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 +/- 6 ml, 3.0 +/- 0.7 l/min, 6 +/- 2 mmHg, 22 +/- 8%, 14 +/- 2 beats/min, and 50-96%, respectively; all P < 0. 05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 +/- 2 vs. 9 +/- 1%) and the reductions in SV (13 +/- 4 vs. 21 +/- 3%) and cardiac output (8 +/- 3 vs. 14 +/- 3%) (all P < 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure. (+info)
Suppression of PGE(2) fever at near term: reduced thermogenesis but not enhanced vasopressin antipyresis.
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Fevers are known to be suppressed near term in the mother, but the mechanism responsible for this phenomenon is not understood. We tested the hypothesis that the suppression of fever at term is a result of enhanced vasopressin-induced antipyresis. Effects of intracerebroventricular prostaglandin E(2) (PGE(2)) were examined in rats at gestational days 16-17 and 19-20 (near term) and days 1-2 postpartum. PGE(2) (50 ng) elevated body and interscapular brown adipose tissue (iBAT) temperatures and increased sympathetic nerve activity to the iBAT. PGE(2)-induced changes in iBAT temperature and nerve activity, as well as in rectal temperature, were reduced or eliminated near term, and responses were recovered in the postpartum period. Blood pressure and heart rate changes induced by central PGE(2) were also decreased at near term. Coinfusion of Manning compound, a V(1) vasopressin receptor antagonist, with PGE(2) throughout the peripartum period did not reverse the suppressed iBAT temperature and nerve activity or body temperature responses to PGE(2). Microdialysis experiments revealed unchanged terminal release of vasopressin in the ventral septal area after PGE(2) infusion in either pregnant or parturient rats. These results suggest that fever reduction at near term is not associated with enhanced vasopressin antipyresis, but may be a result of reduced sympathetic tone and in particular a reduced sympathetic drive to the iBAT. This finding may reflect a generalized reduction in autonomic output around the time of parturition. (+info)
Carbon monoxide as a novel mediator of the febrile response in the central nervous system.
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Heme oxygenase catalyzes the metabolism of heme to biliverdin, free iron, and carbon monoxide (CO), which has been shown to be an important neuromodulatory agent. Recently, it has been demonstrated that lipopolysaccharide (LPS) can induce the enzyme heme oxygenase in glial cells. Therefore, the present study was designed to test the hypothesis that central CO plays a role in LPS-induced fever. Colonic body temperature (T(b)) was measured in awake, unrestrained rats (basal T(b) = 36.8 +/- 0.2 degrees C). Intracerebroventricular injection of zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG; 75 nmol), a heme oxygenase inhibitor, caused no significant change in T(b), indicating that the central heme oxygenase pathway plays no tonic role in T(b) under the experimental conditions used. Intraperitoneal injections of LPS (50-100 microgram/kg) evoked dose-dependent increases in T(b). Intracerebroventricular injection of ZnDPBG in febrile rats attenuated LPS-induced fever (thermal index with ZnDPBG = 1.1 +/- 0. 2 degrees C, thermal index with vehicle = 2.3 +/- 0.4 degrees C), suggesting that the central heme oxygenase pathway plays a role in fever generation. The antipyretic effect of ZnDPBG could be reversed by intracerebroventricular administration of heme-lysinate or CO-saturated saline. Collectively, our data indicate that CO arising from heme oxygenase may play an important role in fever generation by acting on the central nervous system. (+info)
Clinical algorithm for malaria during low and high transmission seasons.
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OBJECTIVES: To assess the proportion of children with febrile disease who suffer from malaria and to identify clinical signs and symptoms that predict malaria during low and high transmission seasons. STUDY DESIGN: 2490 children aged 2 to 59 months presenting to a health centre in rural Ethiopia with fever had their history documented and the following investigations: clinical examination, diagnosis, haemoglobin measurement, and a blood smear for malaria parasites. Clinical findings were related to the presence of malaria parasitaemia. RESULTS: Malaria contributed to 5.9% of all febrile cases from January to April and to 30.3% during the rest of the year. Prediction of malaria was improved by simple combinations of a few signs and symptoms. Fever with a history of previous malarial attack or absence of cough or a finding of pallor gave a sensitivity of 83% in the high risk season and 75% in the low risk season, with corresponding specificities of 51% and 60%; fever with a previous malaria attack or pallor or splenomegaly had sensitivities of 80% and 69% and specificities of 65% and 81% in high and low risk settings, respectively. CONCLUSION: Better clinical definitions are possible for low malaria settings when microscopic examination cannot be done. Health workers should be trained to detect pallor and splenomegaly because these two signs improve the specificity for malaria. (+info)