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The genus Phlebovirus (order Bunyavirales, family Phenuiviridae) consists of 66 species according to the International Committee on Taxonomy of Viruses (1). Phleboviruses are globally distributed and can be transmitted by [...]

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging and mostly fatal tickborne zoonosis in eastern Asia. The causative agent is Dabie bandavirus, of the family Phenuiviridae and genus Bandavirus, [...]

Human ehrlichiosis is a tickborne infectious disease caused by Ehrlichia sp. that has primarily been detected in the United States. Common clinical manifestations of human ehrlichiosis are fever, headache, myalgia, [...]

Determining the etiologic causes of febrile illness in tropical settings provides public health and local community benefits. In the context of a decline in malaria cases in many parts of [...]

Author(s): Dayu Lin Author Affiliations: How stress can cause a fever You are about to take the stage to speak in front of a large audience. As you wait, your [...], Psychological stress can trigger physiological responses, including an increase in body temperature. A neural circuit that underlies this stress-induced heat response has been identified. A neuronal pathway that governs stress-induced hyperthermia.

The article discusses the case of a 35-year-old woman brought to hospital with fever, abdominal pain and hypotension three days after undergoing elective cesarean section. The diagnosis and management of Group A streptococcal infection causing necrotizing fasciitis of the abdominal wall and vulva and streptococcal toxic shock syndrome are described.

As with other forms of psychological stress, conditioned fear causes an increase in body temperature. The mechanisms underlying this stress-induced hyperthermia are not well understood, but previous research suggests that nonshivering thermogenesis might contribute, as it does during cold exposure. The major source of nonshivering thermogenesis in the rat is brown adipose tissue (BAT), and the largest BAT deposit in that species is in the interscapular area just below the skin. BAT is also under sympathetic control via [beta]-adrenoceptors. If BAT contributes to fear-induced hyperthermia, then the interscapular skin should warm up faster than other skin areas, and this response should be suppressed by the [beta]-adrenoceptor antagonist, propranolol. We tested this noninvasively by infrared thermography. In conscious rats, 30 min of contextual fear caused hyperthermia (as indicated by a + 1.5[degrees]C increase in lumbar back skin temperature) and increased the difference in temperature between interscapular and lumbar back skin (TiScap - TBack) by + 1[degrees]C. Propranolol (10 mg/kg ip) completely abolished this hyperthermia; however, the TiScap-TBack increase was not reduced. In contrast, exposure to cold air (4[degrees]C) induced a +2.7[degrees]C increase in TiScap-TBack, which was reduced to +1[degrees]C after propranolol. The results show that conditioned fear-induced hyperthermia is of nonshivering origin and mediated by [beta]-adrenoceptors, but interscapular BAT does not contribute to it and does not appear to be activated, either. stress hyperthermia; thermoregulation; tail skin; freezing; sympathetic responses

Parasitic infection with Plasmodium falciparum is responsible for the most severe form of human malaria in which patients suffer from periodic fever. It is well established that during intra-erythrocytic maturation of the parasite in the red blood cell (RBC), the RBC becomes significantly more cytoadhesive and less deformable; these and other biochemical factors together with human host factors such as compromised immune status are important contributors to the disease pathology. There is currently substantial interest in understanding the loss of RBC deformability due to P. falciparum infection, but few results are available concerning effects of febrile conditions or parasitization on RBC membrane rheology. Here, for the first time, we report rheology of the single, isolated RBC with and without P. falciparum merozoite invasion, spanning a range from room temperature to febrile conditions (41[degrees]C), over all the stages of parasite maturation. As expected, stiffness increased with parasite maturation. Surprisingly, however, stiffness increased acutely with temperature on a scale of minutes, particularly in late trophozoite and schizont stages. This acute stiffening in late falciparum stages may contribute to fever-dependent pathological consequences in the microcirculation. deformability; magnetic twisting cytometry; malaria; fever; environmental stress

Acute starvation attenuates the fever response to pathogens in several mammalian species. The under-lying mechanisms responsible for this effect are not fully understood but may involve a compromised immune and/or thermoregulatory function, both of which are prerequisites for fever generation. In the present study, we addressed whether the impaired innate immune response contributes to the reported attenuation of the fever response in fasted rats during LPS-induced inflammation. Animals fasted for 48 h exhibited a significant and progressive hypothermia prior to drug treatment. An intraperitoneal injection of LPS (100 [micro]g/kg) resulted in a significantly attenuated fever in the fasted animals compared with the fed counterparts. This attenuation was accompanied by the diminution in the concentration of some [TNF and IL-1 receptor antagonist (RA)] but not all (IL-1[beta] and IL-6) of the plasma cytokines normally elevated in association with the fever response. Nevertheless, fasting had no effect on the LPS-induced inflammatory responses at the level of the brain, as assessed by mRNA expressions of inhibitory factor(I)-KB, suppressor of cytokine signaling (SOCS3), IL-1[beta], cyclooxygenase (COX)-2, and microsomal PGE synthase (mPGES)-1 in the hypothalamus, as well as by [PGE.sub.2] elevations in the cerebrospinal fluid. In contrast, fasting significantly attenuated the fever response to central [PGE.sub.2] injection. These results show that fasting does not alter the febrigenic signaling from the periphery to the brain important for central PG[E.sub.2] synthesis but does affect thermoregulatory mechanisms downstream of and/or independent of central PG[E.sub.2] action. thermoregulation; acute starvation; cyclooxygenase; hypothermia

Interleukin (IL)-6 is an important humoral mediator of fever following infection and inflammation and satisfies a number of criteria for a circulating pyrogen. However, evidence supporting such a role is diminished by the moderate or even absent ability of the recombinant protein to induce fever and activate the cyclooxygenase-2 (COX-2) pathway in the brain, a prerequisite step in the initiation and maintenance of fever. In the present study, we investigated the role of endogenous circulating IL-6 in a rodent model of localized inflammation, by neutralizing its action using a specific antiserum (IL-6AS). Rats were injected with LPS (100 [micro]g/kg) or saline into a preformed air pouch in combination with an intraperitoneal injection of either normal sheep serum or IL-6AS (1.8 ml/rat). LPS induced a febrile response, which was accompanied by a significant rise in plasma IL-6 and nuclear STAT3 translocation in endothelial cells throughout the brain 2 h after treatment, including areas surrounding the sensory circumventricular organs and the median preoptic area (MnPO), important regions in mediating fever. These responses were abolished in the presence of the IL-6AS, which also significantly inhibited the LPS-induced up-regulation of mRNA expression or immunoreactivity (IR) of the inducible form of COX, the rate-limiting enzyme for [PGE.sub.2]-synthesis. Interestingly, nuclear signal transducer and activator of transcription (STAT)3-positive cells colocalized with COX-2-IR, signifying that IL-6-activated cells are directly involved in [PGE.sub.2] production. These observations suggest that IL-6 is an important circulating pyrogen that activates the COX-2-pathway in cerebral microvasculature, most likely through a STAT3-dependent pathway. local inflammation; cytokines; nuclear factor-[kappa]B; prostaglandins; circumventricular organs

A 58-year-old man suffering from sacral ulcer was admitted to the hospital for chemotherapy to treat acute myeloid leukemia. After the chemotherapy he developed fever, which was not reducing inspite of the various anti microbial medicines that were given, but slowly his condition improved and he was discharged.

Byline: B. Circiumaru (1), G. Baldock (2), J. Cohen (1) Keywords: Key words Fever; Infection; Intensive care; Post-operative Abstract: Objective: To determine the epidemiology of fever on the intensive care unit (ICU). Design: Prospective, observational study. Setting: Nine-bed general ICU in a 500-bed tertiary care inner city institution. Patients: 100 consecutive admissions of 93 patients over a 4-month period between July and October 1996. Interventions: All patients were seen and examined by one investigator within 24 h of ICU admission. Patients were followed up on a daily basis throughout their ICU stay, and all clinical and laboratory data were recorded during the admission. Measurements and results: Fever (core temperature aY= 38.4 degC) was present in 70 % of admissions, and it was caused by infective and non-infective processes in approximately equal number. Most fevers occurred early in the course of the admission, within the first 1--2 days, and most lasted less than 5 days. The median Acute Physiology and Chronic Health Evaluation (APACHE) II score was 15 ( +- 0.6). The 70 episodes associated with fever at any time were associated with a significantly higher APACHE II score on admission than the afebrile episodes (15.8 +- 6.1 vs 12.1 +- 6.7, p = 0.04). The most common cause of non-infective fever was in the group designated post-operative fever (n = 34). All the patients in the post-operative fever group were febrile on day 0 or day 1 their mean admission APACHE score was 12.4 ( +- 4.4) compared to 15.9 ( +- 7.1) for the remaining patients (p = 0.01). Fever alone was not associated with a higher mortality: 26/70 (37 %) of febrile patients died, compared to 8/30 (27 %) of afebrile patients, ([chi] .sup.2 = 1.23, p = 0.38). Prolonged fever ( > 5 days) occurred in 16 patients. In 13 cases, fever was due to infection, and in the remaining 3 both infective and non-infective processes occurred concurrently. The mortality in the group with prolonged fever was 62.5 % (10/16) compared to 29.6 % (16/54) in patients with fever of less than 5 days' duration, a highly significant difference (p < 0.0001). Conclusions: Fever is a common event on the intensive care unit. It usually occurs early in the course, is frequently non-infective and is often benign. Prolonged fever is associated with a poor outcome. Post-operative fever is a well-recognised but poorly defined syndrome which requires further study. Author Affiliation: (1) Department of Infectious Diseases, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road., London W12 0NN, UK Tel.: + 44 (181) 383 3243 Fax: + 44 (181) 383 3394 email: jcohen@rpms.ac.uk, GB (2) Department of Anaesthesia, Imperial College School of Medicine, Hammersmith Hospital, London, UK, GB Article note: Received: 29 December 1998 Final revision received: 16 March 1999 Accepted: 14 April 1999

A man who had gradually lost the ability to sweat over most of his body was diagnosed with chronic idiopathic anhidrosis. Anhidrosis means a long-term problem with the ability to sweat of unknown origin. The inability to sweat had caused him to run high fevers during exercise and to become heat intolerant. The natural thermal regulation of the body was disrupted. Other neural and skin diseases were ruled out by the absence of other symptoms. Nerve biopsy confirmed that the small unmyelinated nerve fibers that were responsible for initiating sweat production in response to rise in body temperature were abnormal.

The recommendations of the Advisory Committee on Immunization Practices (ACIP) with respect to the use of seasonal influenza vaccine (Afluria) manufactured by CSL Biotherapies for the 2010-11 influenza season in the United States are discussed. Many agencies will be closely monitoring the safety of seasonal influenza vaccines during 2010-11, as 2010 seasonal influenza vaccine is associated with increased reports of fever and febrile seizures in young children.

In the present work, some biological effects of the AC magnetic field exposure after magnetoliposome sample treatment were investigated through micronucleus assay and blood and peritoneum cytometry. Data showed that after 5 min exposure AC magnetic field might induce inflammatory reactions, genotoxicity, and cytotoxicity. We conclude that under our experimental conditions magnetohyperthermia experiments may be safely conducted by 3-min AC magnetic field exposure. Index Terms--Alternating magnetic field, cytometry, hyperthermia, inflammation, magnetoliposome, micronucleus.