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PubMed2006

Clinical features of fever associated with poor outcome in severe pediatric traumatic brain injury.

We describe the incidence and etiology of fever and the relationship between fever characteristics and outcome in children with severe traumatic brain injury (TBI). We conducted a retrospective study of children <14 years and with Glasgow Coma Scale (GCS) score of <9 admitted to a level I pediatric trauma center intensive care unit (PICU) between 1998 and 2003. We examined whether fever characteristics were associated with poor outcome (hospital discharge GCS score <13 and discharge disposition of either death or discharge to a skilled nursing facility). PICU length of stay (LOS) and hospital LOS were also examined. Data are presented as means and medians (SD), and P < 0.05 reflects significance. Ninety-three records were reviewed. Patients were 5.7 (SD 4.1) years old, 70% were male, and the average admission GCS score was 5. Mortality rate was 14%. Forty-eight (52%) patients had fever, and 23 (48%) of those patients had infectious fever. Each additional febrile episode was associated with a twofold higher risk of patients having a hospital discharge GCS score of <13 (odds ratio 2.4, 95% confidence interval 1.2-5.0) and having a 0.4-day longer PICU LOS (P < 0.001). Patients with infectious fever had a 0.9-day longer PICU LOS (P < 0.001). Patients with any fever in the PICU had an increased HLOS (0.9 days; P < 0.001). Our data suggest that in severe pediatric TBI, both fever and infection were common, and both were associated with longer LOS. Patients with higher fever burden had poor hospital discharge GCS score.

Adolescent↗
PubMed2004

Parents' beliefs and practices regarding childhood fever: a study of a multiethnic and socioeconomically diverse sample of parents.

OBJECTIVE: To examine childhood fever beliefs and practices in a multiethnic, multiracial, and socioeconomically diverse sample. DESIGN: Cross-sectional survey. PARTICIPANTS: Parents of children attending a hospital clinic, neighborhood health center, and a private practice. RESULTS: Two hundred seventy-four parents were interviewed; 45% were Latino; 15%, African-American; 25%, white; and 14%, other (excluded from further analysis, leaving a final sample size of 235). Latinos (11%) and African-Americans (7%) were more likely than whites (0%) to have no thermometers (P < 0.006). Only 42% of parents knew the correct temperature for fever. Greater proportions of Latinos (55%) and African-Americans (44%) take their child to the emergency department for fever than whites (21%; P < 0.001 and P = 0.02, respectively). Multivariate analyses revealed that parents who had not graduated from high school had 5 times the odds of not using a thermometer to check for fever and triple the odds of not asking a health care provider for fever advice, and parents of uninsured children were 5 times less likely to bring their febrile child to the emergency department. Low-income parents significantly more often used the emergency department and remedies other than antipyretics for their febrile children. Latino parents were more likely to believe that certain Latino folk illnesses cause fever, and African-American parents had triple the odds of not knowing the correct temperature for fever. CONCLUSIONS: Parents' beliefs and practices regarding childhood fever vary by race, ethnicity, sociodemographics, and the child's insurance coverage. Educating parents about fever, improving access to health insurance and primary care, and ensuring that families have thermometers may enhance appropriate use of health services and improve outcomes for febrile children.

Adolescent↗
PubMed1979

Effects of central administation of probenecid on fevers produced by leukocytic pyrogen and PGE2 in the rabbit.

1. Single intracerebroventricular (I.C.V.) injections of probenecid (PBCD, 0.125--0.5 mg) enhanced and prolonged fever caused by I.V. administration of leukocytic pyrogen (LP) in rabbits resting in neutral (23 degrees C), cold (10 degrees C) and hot (30 degrees C) environments. Similar effects were produced by single I.C.V. injections of PBCD given before PGE2 (0.5 microgram) was injected I.C.V. in the three ambient temperatures. 2. Fever produced by IV. LP was also prolonged by infusion and by multiple injections of PBCD. 3. PBCD given I.P. (100 mg/kg) enhanced and prolonged fever caused by I.V. injection of Salmonella typhosa endotoxin. 4. Hyperthermia produced by I.C.V. PGE2 was not augmented by subsequent PBCD infusion. However, pre-treatment with PBCD followed by PGE2 injection and PBCD infusion caused hyperthermia that was very high and prolonged, and, in some cases, lethal. 5. Acetaminophen (2 mg, I.C.V.) and indomethacin (10 mg/kg, I.V.) lowered body temperature when given during fever induced by LP and prolonged by PBCD infusion. 6. The concentration of PGE in cerebrospinal fluid (c.s.f.) samples taken from the third or lateral ventricles rose or stabilized during PBCD infusions made during LP fever. However, similar changes in PGE concentration also occurred during control infusions when body temperature was low. 7. We conclude that termination of the actions of both central endogenous pyrogen and centrally administered PGE2, and the subsequent reduction of fevers produced by them, require a PBCD-sensitive facilitated transport system. The reduction of PBCD-prolonged PL fevers by antipyretics which block PGE synthesis suggests that prolongation by PBCD of LP fever is not due to blockade of PGE transport in a subsequent step in fever mediation per se, but is due to inhibition of transport of LP itself, or of other mediators associated with it.

Animals↗
PubMed2004

Malaria, from natural to supernatural: a qualitative study of mothers' reactions to fever (Dienga, Gabon).

OBJECTIVE: Decision making for health care at the household level is a crucial factor for malaria management and control among young children. This study sought to determine exactly how mothers reacted when faced with fever in a child. DESIGN: Qualitative study based on in depth semistructured interviews of mothers and free form discussion with traditional healers (Nganga). SETTING: Village of Dienga, a rural area of Gabon (Central Africa). PARTICIPANTS: 12 mothers and three traditional healers. RESULTS: All mothers thought that fever and malaria were identical. Mothers home treated or went to the village treatment centre, or both, on the last episode of fever, if they judged it to be "natural" fever. However, if fever was thought to be a result of malicious intent, then a Nganga was consulted first. It was believed that strong and above all persistent fever was "supernatural". In this case, traditional treatment was thought to be best. CONCLUSIONS: Results indicate that fever is perceived as a dual condition, with two distinct but non-mutually exclusive aetiologies (either "natural" or from witchcraft). In contrast with what is commonly believed, there seems to be no clear cut distinction between diseases suitable for management by western medicine and diseases to be managed solely by traditional health practitioners. Moreover, these data do not support the commonly held notion that the decision to seek western medicine to treat fever is considered a "last resort". Results strongly imply that some severe cases of fever, being initially considered supernatural, may partially or completely escape medical attention.

Adult↗
PubMed2005

Central endothelin ET(B) receptors mediate IL-1-dependent fever induced by preformed pyrogenic factor and corticotropin-releasing factor in the rat.

Blockade of central endothelin ET(B) receptors inhibits fever induced by LPS in conscious rats. The contribution of ET(B) receptor-mediated mechanisms to fever triggered by intracerebroventricular IL-6, PGE2, PGF(2alpha), corticotropin-releasing factor (CRF), and preformed pyrogenic factor derived from LPS-stimulated macrophages (PFPF) was examined. The influence of natural IL-1 receptor antagonist or soluble TNF receptor I on endothelin (ET)-1-induced fever was also assessed. The selective ET(B) receptor antagonist BQ-788 (3 pmol icv) abolished fever induced by intracerebroventricular ET-1 (1 pmol) or PFPF (200 ng) and reduced that caused by ICV CRF (1 nmol) but not by IL-6 (14.6 pmol), PGE2 (1.4 nmol), or PGF(2alpha) (2 nmol). CRF-induced fever was also attenuated by bosentan (dual ET(A)/ET(B) receptor antagonist; 10 mg/kg iv) but unaffected by BQ-123 (selective ET(A) receptor antagonist; 3 pmol icv). alpha-Helical CRF(9-41) (dual CRF1/CRF2 receptor antagonist; 6.5 nmol icv) attenuated fever induced by CRF but not by ET-1. Human IL-1 receptor antagonist (9.1 pmol) markedly reduced fever to IL-1beta (180 fmol) or ET-1 and attenuated that caused by PFPF or CRF. Murine soluble TNF receptor I (23.8 pmol) reduced fever to TNF-alpha (14.7 pmol) but not to ET-1. The results of the present study suggest that PFPF and CRF recruit the brain ET system to cause ET(B) receptor-mediated IL-1-dependent fever.

Animals↗
PubMed2004

The effects of selective and nonselective cyclooxygenase inhibitors on endothelin-1-induced fever in rats.

It was previously shown that sustained fever can be induced in rats by central injection of endothelin-1 (ET-1). This peptide appears to participate in the mechanism(s) of LPS-induced fever, which is reduced by pretreatments with ET(B) receptor antagonists. In this study, we compared the effects of a nonselective cyclooxygenase (COX) inhibitor, indomethacin, with those of two selective COX-2 inhibitors, celecoxib and lumiracoxib, on ET-1-induced fever in rats. Fever induced in conscious animals by ET-1 (1 pmol icv) or LPS (5 mug/kg iv) was prevented by pretreatments with celecoxib (5 and 10 mg/kg) or lumiracoxib (5 mg/kg) given by oral gavage 1 h before stimuli. Lower doses of celecoxib had partial (2.5 mg/kg) or no effect (1 mg/kg). Indomethacin (2 mg/kg ip) partially inhibited fever induced by LPS but had no effect on ET-1-induced fever. The levels of PGE(2) and PGF(2alpha) in the cerebrospinal fluid (CSF) of pentobarbital sodium-anesthetized rats were significantly increased 3 h after the injection of LPS or ET-1. The latter increase was abolished by celecoxib at all tested doses and by indomethacin. In conclusion, selective COX-2 inhibitors were able to prevent ET-1-induced fever, indicating a role for COX-2 in this phenomenon. However, the fact that reduced CSF PG levels obtained with indomethacin and a low dose of celecoxib are not accompanied by changes in fever induced by ET-1, along with the lack of inhibitory effects of indomethacin on ET-1 fever, suggests that the latter might also involve COX-2-independent mechanisms.

Animals↗
PubMed1997

Attenuation of lipopolysaccharide fever in rats by protein kinase C inhibitors.

The purpose of this study was to assess the effects of inhibitors of protein kinase C (PKC) on lipopolysaccharide (LPS)-induced fever and changes in circulating interleukin-6 (IL-6) levels in freely moving biotelemetered rats. We used PKC inhibitors with different inhibition constants (Ki): H-7 (Ki = 6 microM) and chelerythrine (Chel; Ki = 0.66 microM; a more potent PKC inhibitor). Rats were injected subcutaneously with either 3 or 15 microM/kg of these inhibitors and then 1 h later were injected intraperitoneally with LPS (50 micrograms/kg). Blood samples for IL-6 bioassay were collected 4 h after LPS injection. H-7 at lower doses did not significantly affect fever and LPS-induced elevation of circulating IL-6, whereas at a higher dose (15 microM/kg) H-7 reduced both fever and the increase of IL-6 (analysis of variance, Scheffé's test, P < 0.05). Chel (3 and 15 microM/kg) significantly reduced fever and almost completely inhibited the LPS-induced elevation of plasma IL-6. In separate experiments, we studied the effect of H-7 on antipyresis due to dexamethasone (Dex). Dex at a dose of 0.6 microM/kg given subcutaneously 1 h before LPS partially prevented fever (approximately 55% inhibition) and attenuated the increase of IL-6 (P < 0.05). Simultaneous pretreatment of the rats with Dex and H-7 (3 microM/kg; a dose that did not affect fever and IL-6 elevation) led to a potentiation of the antipyretic effect of Dex, resulting in no fever. H-7 did not potentiate, however, the inhibitory effect of Dex on LPS-induced elevation of circulating IL-6. We conclude that PKC is involved in the regulation of LPS fever and constitutes a rate-limiting factor in modulation of the fever by glucocorticoids.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1998

Role of hypothalamic interleukin-1beta in fever induced by cecal ligation and puncture in rats.

Bacterial endotoxin induces fever by causing the release of interleukin (IL)-1beta into the circulation or the brain. IL-1beta is believed to mediate fever via triggering the production and/or release of IL-6 in the hypothalamus. The present study examined whether IL-1beta and IL-6 in the hypothalamus of the rat are also involved in fever during bacterial sepsis caused by cecal ligation and puncture (CLP). CLP induces fever for 2 days. Polyclonal rabbit antibody against rat IL-1beta (anti-IL-1beta, 2 microg/microl) or control rabbit IgG (2 microg/microl) was unilaterally microinjected into the hypothalamus of rats immediately after or 24 h after CLP or sham-CLP surgery. Anti-IL-1beta injected 24 h after CLP (when fever was already present) or sham-CLP surgery did not affect fever. Microinjection of anti-IL-1beta into the hypothalamus immediately after surgery caused a significant decrease in body temperature during the night after CLP surgery and a 48% reduction of fever on the following day. Although blood plasma levels of IL-6 were significantly elevated 1.5, 6, 24, and 48 h after CLP surgery, there were no differences in IL-6 concentrations in the extracellular fluid of the anterior hypothalamus (collected by push-pull perfusion). These data suggest that fever due to bacterial sepsis is initiated by IL-1beta within the hypothalamus, and this febrile response, unlike endotoxin-induced fever, is not accompanied by elevation in the hypothalamic concentration of IL-6.

Animals↗
PubMed1998

Inhibitors of alternative pathways of arachidonate metabolism differentially affect fever in mice.

Inhibitors of cyclooxygenases prevent fever. The purpose of this study was to test the hypothesis that selective and dual inhibitors of the other enzyme systems of arachidonic acid oxygenation (i.e., lipoxygenase and epoxygenase) affect the time course or magnitude of fever in mice. Swiss Webster mice kept at 30 degreesC ambient temperature were implanted with biotelemeters to monitor body temperature. Fever was induced by intraperitoneal injection of lipopolysaccharide at doses from 10 micrograms/kg to 2.5 mg/kg. Phenidone (20-30 mg/kg ip), a dual lipoxygenase and cyclooxygenase inhibitor, prevented fever in these mice, but esculetin (1-10 mg/kg ip), a selective inhibitor of lipoxygenases, did not affect fever. Intramuscular injection of nordihydroguaiaretic acid (10-20 mg/kg), a dual lipoxygenase and epoxygenase inhibitor, as well as SKF-525A (5 mg/kg ip) and clotrimazole (20 mg/kg im), inhibitors of the cytochrome P-450/epoxygenase pathway, augmented fever in mice. Indomethacin (5 mg/kg ip), an inhibitor of cyclooxygenase, suppressed the exacerbation of fever due to clotrimazole, suggesting that the epoxygenase inhibitor-induced potentiation of fever in mice is a prostaglandin-mediated effect. From this study, we hypothesize that the cytochrome P-450/epoxygenase branch of the arachidonate cascade is involved in antipyresis and in controlling the upper limit of fever.

Animals↗
PubMed2001

Differential inhibition by nimesulide of the early and late phases of intravenous- and intracerebroventricular-LPS-induced fever in guinea pigs.

OBJECTIVES: The findings that inducible cyclooxygenase (COX)-2, but not constitutive COX-1, is upregulated in the brain of conscious rats approximately 1.5 h after intraperitoneal pyrogen administration, that the systemic administration of COX-2 inhibitors abolishes fever, and that COX-2-deficient mice do not develop fever in response to intraperitoneal lipopolysaccharide (LPS) have strongly implicated COX-2 in the mediation of the febrile response. However, the biosynthesis of COX-2 is significantly slower than the onset of the fever produced by intravenously injected LPS. It consequently seems improbable that inducible COX-2 could play a role in the initiation of this febrile response, but a role for COX-1 has not yet been categorically ruled out; or, alternatively, a constitutive isoform of COX-2 could have such a role. We have studied, therefore, the effects of the non-selective COX inhibitor indomethacin, the COX-1-selective inhibitor SC-560, and the COX-2-selective inhibitor nimesulide on the characteristically biphasic fever induced by intravenous LPS in conscious guinea pigs; it has an onset latency of approximately 10 min. METHODS: We injected the inhibitors 30 min before LPS, in various combinations of doses and routes; their respective vehicles were the control solutions. Core temperatures (T(c)) were monitored continuously, and plasma and brain PGE(2) levels were measured before and at 2-hour intervals after LPS administration. RESULTS: Intraperitoneal indomethacin at 10 mg kg(-1) attenuated both phases of intravenous LPS (2 microg kg(-1)) fever, but the first more so than the second; at 50 mg kg(-1), it inhibited the febrile response completely. Intraperitoneal SC-560 (5 mg kg(-1)) did not affect the febrile response to intravenous LPS (2 microg kg(-1)). Intraperitoneal nimesulide (0.3, 1.0, and 3.0 mg kg(-1)) dose dependently attenuated intravenous LPS (0.1 and 2 microg kg(-1)) fever; the second phase of the biphasic T(c) rise was affected significantly more than the first. Intraperitoneal nimesulide also prevented the associated rises in plasma and brain PGE(2) levels. Intracerebroventricular LPS (150 ng kg(-1)) evoked a monophasic fever with a long onset latency ( approximately 30 min); it was accompanied by a rise in brain PGE(2) only, implying that the febrigenic PGE(2) was generated directly in the brain. This response, however, was completely abolished by intraperitoneal nimesulide (3 mg kg(-1)), indicating that nimesulide crosses the blood-brain barrier. Intracerebroventricular nimesulide at 0.3 mg kg(-1) prevented the rise in plasma PGE(2) after intravenous LPS (2 microg kg(-1)) and again attenuated the second febrile peak significantly more than the first. CONCLUSIONS: COX-1 is not involved in intravenous LPS fever production, and COX-2 appears to play a greater role in the late than in the early phase of intravenous LPS fever in guinea pigs. The involvement of a constitutive COX-2 is inferred in the early phase.

Animals↗
PubMed1994

Corticosterone modulates interleukin-evoked fever in the rat.

The role of endogenous corticoids in fever responses caused by recombinant murine interleukin (IL)-1 beta and IL-6 was studied in adult male Wistar rats. Adrenalectomy diminished the development of fever after intracerebroventricular (icv) injection of these ILs and lowered body temperature. Intraperitoneal administration of the same doses of ILs did not produce fever in intact animals or hypothermia in adrenalectomized rats, thus suggesting a central site of action of IL-1 beta and IL-6 in these experiments. Chronic replacement with moderate doses of corticosterone restored the fever response in adrenalectomized animals in response to icv administration of IL-1 beta but only partially reversed the fever caused by IL-6. Adrenalectomized animals acutely treated with corticosterone and thereafter with either IL-1 beta or IL-6 developed fever more rapidly than did chronically corticosterone-treated animals. In intact animals corticosterone blocked the fever response to icv injected IL-1 beta. We propose that in the rat corticosterone acts in a bimodal manner on body temperature; it exerts a permissive central effect on the fever response and limits the production of inflammatory mediators in the brain. Conversely, higher corticosterone doses probably reduce the magnitude of the fever response.

Adrenalectomy↗
PubMed1984

Mechanisms of fever induced by recombinant human interferon.

Since the early trials using human interferon (hIFN) derived from blood leukocytes or cell lines, fever has been a prominent component of IFN therapy. Human protein impurities might account for the fever to cell-derived hIFN, but recombinant hIFN, free of extraneous human proteins, has produced fever in nearly all recipients during clinical trials. Our present studies were carried out to determine the mechanisms of fever due to recombinant hIFN currently being used in humans. Because recombinant hIFN is produced in Escherichia coli, in these experiments we considered contaminating endotoxin as the cause of fever. Polymyxin B, which blocks endotoxin, had no effect on the pyrogenicity of hIFN in rabbits. In addition, hIFN injected into an endotoxin-resistant strain of mice produced fever. The pyrogenicity of hIFN does not appear to involve production of leukocytic pyrogen (LP), since no circulating LP was detected in rabbits during IFN fever. Furthermore, human mononuclear cells incubated with hIFN in vitro at 10(4)-10(6) U/ml did not release LP. However, hIFN stimulated prostaglandin E2 (PGE2) release from rabbit hypothalamic tissue in vitro. Intracerebroventricular injection of hIFN into the awake cat also produced fever and a rise in PGE2 levels in the cerebrospinal fluid; both effects were reversed by treatment with indomethacin. We conclude that the fever of recombinant hIFN is not due to endotoxin but that hIFN is intrinsically pyrogenic by inducing PGE2 in the hypothalamus.

Animals↗
PubMed1992

Precise quantification of fever in childhood bacterial meningitis.

Precise quantity of fever was determined in 191 cases of childhood bacterial meningitis by calculating the areas between the line indicating 37.8 degrees C or 39.5 degrees C temperature and the line connecting all individual temperature values. Temperature measurements were performed rectally one to four times a day throughout the hospitalization. The obtained areas under the curves (AUC), expressed as degree-hours, proved to be a sensitive index for delineating each individual fever pattern and reflected the magnitude of fever more precisely than the traditional fever curves. Children under five had significantly (p less than 0.05) greater AUC than those at five to 15 years; similarly, patients with Haemophilus influenzae meningitis showed greater AUC (i.e., had more fever) than those with meningococcal disease (p less than 0.05). The overall rates of secondary (14%), persistent (16%), and prolonged fever (8%) were virtually identical to previous reports; no drug fever was reported in this study. In cases with prolonged fever, a significantly higher rate (40%) of neurological complications was found compared to those who became afebrile earlier. This method is potentially utilizable in other diseases and conditions where precise measurement of fever is of clinical or scientific relevance.

Adolescent↗
PubMed2000

A prospective study of fever and bacteremia after flexible fiberoptic bronchoscopy in children.

STUDY OBJECTIVES: To assess the incidence of fever and bacteremia after fiberoptic bronchoscopy in immunocompetent children. DESIGN: Prospective study. PATIENTS: Immunocompetent children undergoing fiberoptic bronchoscopy between January 1997 and June 1998. MEASUREMENTS AND RESULTS: Ninety-one children were included in the study. Forty-four children (48%) developed fever within 24 h following bronchoscopy. Bacteremia was not detected in any of the cases at the time of the fever. Children who developed fever were younger than those who remained afebrile (mean age, 2.4 +/- 3.6 years vs 4.2 +/- 3.7 years; p = 0.025). In the fever group, 66% of the bronchoscopies were considered abnormal, compared to 45% in the nonfever group (p = 0.04). Of the fever group, 40.5% of BAL fluid cultures had significant bacterial growth, significantly higher compared to the nonfever group (13.2%; p = 0.006). Of the 80 patients in whom BAL was performed, fever occurred in 52.5% compared to only 18.2% in those who did not have BAL (p = 0.03). BAL fluid content of cell count, lipid-laden macrophages, and interleukin-8 were not significantly different in both groups. In a logistic regression analysis, the significant predictors for developing fever were positive bacterial culture (relative risk, 5.1; 95% confidence interval, 1.6 to 16.4; p = 0.007) and abnormal bronchoscopic findings (relative risk, 3.1, 95% confidence interval, 1.2 to 8.3; p = 0.02). When age < 2 years was included in the model, this factor became highly significant (relative risk, 5.01; 95% confidence interval, 1.83 to 13.75; p < 0.002). CONCLUSIONS: Fever following fiberoptic bronchoscopy is a common event in immunocompetent children and is not associated with bacteremia. Risks to develop this complication are age < 2 years, positive bacterial cultures in BAL fluid, and abnormal bronchoscopic findings.

Bacteremia↗
PubMedDate not supplied

[Yellow fever in the Ribeirão Preto region at the turn of the 19th century: its scientific importance and economic repercussions].

Yellow fever in the Region of Ribeirao Preto at the turn of XIX century: scientific importance and economic repercussion. This historical review describes the bad situation of public health in Brazil during the XIX Century caused by multiple yellow fever outbreaks. The knowledge regarding to yellow fever at that time is also described. A short history is presented of the development of the Region of Ribeirao Preto, located in the Northeast of Sao Paulo State, Brazil, emphasising the actuation of immigrants and pioneer coffee farmers like Luiz Pereira Barreto. Yellow fever outbreaks occurred in the City of Sao Simao in 1896, 1898, and 1902 are described as well as an outbreak in the City of Ribeirao Preto occurring in 1903. It is shown that yellow fever outbreaks were stopped in the 2 cities by Emilio Ribas who led the fight against the transmitting mosquito Aedes aegypti. Emilio Ribas, helped by Adolpho, Lutz and Luiz Pereira Barreto, promoted scientific experiments in order to confirm the vectorial transmission of yellow fever and to annul the supposed importance of other kinds of contagion. The yellow fever outbreaks caused damage to the development of Sao Simao and influenced the transference of the economic pole of the region to the City of Ribeirao Preto. The vector control work done during yellow fever outbreak and the scientific experiments on the transmission of yellow fever were important for the development of medical science and fpublic health in Brazil.

Brazil↗
PubMed2006

Cells that trigger fever.

Bacterial lipopolysaccharide (LPS) is recognized by several receptors, including the toll-like receptor (TLR) 4, on various cells. Among many biological responses to LPS is fever, an often polyphasic rise in body temperature that is thought to be mediated by prostaglandin (PG) E(2). Which receptors on which cells are linked to fever production is unknown. It is also unknown which cells produce PGE(2) that triggers the earliest (first) phase of fever. Two recent studies from our group answer these questions. In the first one, we studied LPS-induced fever in mouse chimeras selectively lacking the TLR4 in hematopoietic or nonhematopoietic cells. We found that the first phase of fever is triggered via the TLR4 on hematopoietic cells. In the second study, we investigated LPS fever in rats. We found that the number of cells expressing cyclooxygenase (COX)-2, a PGE(2)-synthesizing enzyme, surged at the onset of fever in the lung and liver (but not in the brain), and that most of these cells were macrophages. Because LPS-induced PGE(2) production in macrophages is TLR4-dependent, it is tempting to speculate that the TLR4-bearing, bone marrow-derived cells implicated in fever pathogenesis by the first study are the same as the COX-2-positive macrophages identified in the second study. Hence, pulmonary and hepatic macrophages that recognize LPS via the TLR4 and rapidly produce PGE(2) are likely triggers of the fever response.

Animals↗
PubMed2006

Prevalence of pneumococcal bacteremia among children <36 months of age presenting with moderate fever to pediatric emergency rooms of the Metropolitan Region (Santiago), Chile.

Blood culture collection from outpatients < age 36 months with high fever (>40 degrees C, rectal) became a standard of ambulatory care in Emergency Rooms (ERs) of the government Children's Hospitals in Chile's Metropolitan Region (MR) in 1999; thereafter, invasive pneumococcal disease (IPD) incidence doubled over preceding years' estimates limited to hospitalizations. We studied IPD among children with moderate (>39 degrees C but <40 degrees C, rectal) rather than high fever visiting Pediatric ERs. Recruitment ensued Monday to Friday, 1-5 PM, September 1, 2002 through August 31, 2003. Age <36 months; rectal temperature >39 degrees but <40 degrees C; outpatient management; parental consent for hemoculture were inclusion criteria. Thirteen-thousand five hundred seventy-seven children < age 36 months with moderate and 3,214 children with high fever sought ER care. Of 1,134 moderate fever children seen in ERs during the enrollment, parents of 837 consented (73.8%). During these days and hours, 714 children < age 36 months presented with high fever and 651 (91.2%) had a "routine" blood culture. Pneumococcemia was detected among 0.7% with moderate and 1.2% with high fever (6/837 vs 8/651, p > 0.05). Extrapolating these rates to all ER outpatients < age 36 months with moderate and high fever, we estimate the true burden as 95 and 39 cases, respectively. The burden of pediatric IPD in the MR is currently underestimated because bacteremias among ER outpatients with moderate fever are not detected. If blood cultures were systematically collected from outpatients with moderate fever, recorded pediatric IPD burden would rise >2-fold. However, economic and logistical constraints preclude such a practice.

Bacteremia↗
PubMed1999

The prophylaxis of acute rheumatic fever in a pair of monozygotic twins. The public health implications.

Recurrent acute rheumatic fever and rheumatic heart disease can be prevented by antibiotic intervention. We report the case of genetically identical twins, one of whom had overt rheumatic fever, received penicillin prophylaxis and did not have rheumatic heart disease. The other must have had inapparent rheumatic fever, received no chemotherapy prophylaxis and proceeded to develop rheumatic heart disease. A greater clinical and laboratory vigilance is required for the diagnosis of acute rheumatic fever in the asymptomatic identical twin of a patient with rheumatic fever. This case provides further evidence of a genetic predisposition to rheumatic fever and demonstrates the continued value of penicillin in the prophylaxis of acute rheumatic fever. It emphasises the need to maintain the integrity of preventive programmes against rheumatic fever worldwide. Studies which explore the HLA and other genetic linkages with rheumatic fever should be encouraged.

Aspirin↗