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PubMed1994

Microbial products and cytokines in sleep and fever regulation.

Excessive sleepiness and fever are constitutional symptoms associated with systemic infection. Although fevers have been investigated for many years, sleep responses to infectious challenge have only recently been investigated. Inoculation of animals with bacterial, viral, protozoan and fungal organisms result in complex sleep responses dependent upon the microbial agent and route of administration. The general pattern is characterized by an initial robust increase in non-rapid eye movement sleep (NREMS) followed by a period of NREMS inhibition. REMS is inhibited after infectious challenge. The sleep responses are accompanied by fever but the two responses are, in part, independent from each other. Sleep responses, like fevers, may be beneficial to host defense although this area is relatively uninvestigated. Microbial products likely responsible for sleep and fever responses include bacterial muramyl peptides and endotoxin, and viral double stranded RNA. These microbial products induce sleep and fever responses in animal models. The exact mechanism of how these structurally diverse microbial products elicit sleep and fever remain unknown; however these substances share the ability to induce cytokine production. Cytokines such as interleukin-1 (IL-1), tumor necrosis factor, acidic fibroblast growth factor (FGF), and interferon-alpha (IFN-alpha) are somnogenic whether given directly into brain or intravenously. Other cytokines lack somnogenic activity, e.g., IL-2, IL-6, IFN beta and basic FGF. The somnogenic actions of cytokines probably involve growth hormone-releasing hormone (GHRH) and nitric oxide. Anti-GHRH or inhibition of NO production inhibits normal sleep and inhibits IL-1-induced sleep. In conclusion, cytokines are likely key mediators of fever and sleep responses to infection. The microbial-cytokine altered sleep likely results from an amplification of physiological sleep mechanisms which include cytokines, several neuropeptides and neurotransmitters such as nitric oxide.

Animals↗

PubMed2005

Fever and hypothermia in systemic inflammation: recent discoveries and revisions.

Systemic inflammation is accompanied by changes in body temperature, either fever or hypothermia. Over the past decade, the rat and mouse have become the predominant animal models, and new species-specific tools (recombinant antibodies and other proteins) and genetic manipulations have been applied to study fever and hypothermia. Remarkable progress has been achieved. It has been established that the same inflammatory agent can induce either fever or hypothermia, depending on several factors. It has also been established that experimental fevers are generally polyphasic, and that different mechanisms underlie different febrile phases. Signaling mechanisms of the most common pyrogen used, bacterial lipopolysaccharide (LPS), have been found to involve the Toll-like receptor 4. The roles of cytokines (such as interleukins-1beta and 6 and tumor necrosis factor-alpha) have been further detailed, and new early mediators (e.g., complement factor 5a and platelet-activating factor) have been proposed. Our understanding of how peripheral inflammatory messengers cross the blood-brain barrier (BBB) has changed. The view that the organum vasculosum of the lamina terminalis is the major port of entry for pyrogenic cytokines has lost its dominant position. The vagal theory has emerged and then fallen. Consensus has been reached that the BBB is not a divider preventing signal transduction, but rather the transducer itself. In the endothelial and perivascular cells of the BBB, upstream signaling molecules (e.g., pro-inflammatory cytokines) are switched to a downstream mediator, prostaglandin (PG) E2. An indispensable role of PGE2 in the febrile response to LPS has been demonstrated in studies with targeted disruption of genes encoding either PGE2-synthesizing enzymes or PGE2 receptors. The PGE2-synthesizing enzymes include numerous phospholipases (PL) A2, cyclooxygenases (COX)-1 and 2, and several newly discovered terminal PGE synthases (PGES). It has been realized that the "physiological," low-scale production of PGE2 and the accelerated synthesis of PGE2 in inflammation are catalyzed by different sets of these enzymes. The "inflammatory" set includes several isoforms of PLA2 and inducible isoforms of COX (COX-2) and microsomal (m) PGES (mPGES-1). The PGE2 receptors are multiple; one of them, EP3 is likely to be a primary "fever receptor." The effector pathways of fever start from EP3-bearing preoptic neurons. These neurons have been found to project to the raphe pallidus, where premotor sympathetic neurons driving thermogenesis in the brown fat and skin vaso-constriction are located. The rapid progress in our understanding of how thermoeffectors are controlled has revealed the inadequacy of set point-based definitions of thermoregulatory responses. New definitions (offered in this review) are based on the idea of balance of active and passive processes and use the term balance point. Inflammatory signaling and thermoeffector pathways involved in fever and hypothermia are modulated by neuropeptides and peptide hormones. Roles for several "new" peptides (e.g., leptin and orexins) have been proposed. Roles for several "old" peptides (e.g., arginine vasopressin, angiotensin II, and cholecystokinin) have been detailed or revised. New pharmacological tools to treat fevers (i.e., selective inhibitors of COX-2) have been rapidly introduced into clinical practice, but have not become magic bullets and appeared to have severe side effects. Several new targets for antipyretic therapy, including mPGES-1, have been identified.

Animals↗

PubMed2003

Prevalence of markers of Q fever exposure in the Kimberley, Western Australia.

Although a large pastoral industry exists in the Kimberley region of Western Australia, there is no previously published information about the prevalence of immune markers for Q fever exposure in this region's population. This paper identifies the prevalence of, and factors associated with, positive immune markers of Q fever, and reports the uptake of Q fever vaccination by eligible subjects in the Kimberley region of Western Australia. Data regarding Q fever risk-factors were obtained using a standard questionnaire. Immunity and previous exposure to Q fever were assessed using both serology and a skin test, in accordance with accepted protocol. Fifty-nine subjects underwent Q fever pre-vaccination testing. The prevalence of a positive skin and/or blood test, indicating past exposure was 66 per cent (95% CI 52%-78%). After controlling for age and having lived on a farm at any time, employment in the pastoral industry was the only factor significantly associated with being skin and/or blood test positive (OR=24.6, 95% CI 3.0-204). Acceptance of vaccination was high, with 75 per cent of eligible subjects undergoing vaccination. The high prevalence of immune markers for Q fever in the Kimberley in this sample indicates that the disease is present in the region, despite the last recorded case being in 1986. Ensuring that Q fever vaccination is readily accessible to pastoralists, abattoir workers and other at-risk groups is a challenge that needs to be met by these industries and health services of the region.

Adult↗

PubMed2006

National surveillance and the epidemiology of human Q fever in the United States, 1978-2004.

Although Q fever is considered enzootic in the United States, surveillance for human Q fever has been historically limited. From 1978 through 1999, 436 cases (average = 20 per year) of human Q fever were reported. After Q fever became nationally reportable in 1999, 255 human Q fever cases (average = 51 per year) were reported with illness onset during 2000 through 2004. The median age of cases was 51 years, and most cases were male (77%). The average annual incidence of Q fever was 0.28 cases per million persons, and was highest in persons 50-59 years of age (0.39 cases per million). State-specific incidence ranged from a high of 2.40 cases per million persons in Wyoming, to 0 cases in some states. Since Q fever became reportable, case reports have increased by more than 250%. Surveillance for Q fever is essential to establish the distribution and magnitude of disease and to complement U.S. bioterrorism preparedness activities.

Adolescent↗

PubMed1999

Unexplained fever-analysis of 233 cases in a referral hospital.

A study was conducted to analyse the causes of fever of unknown origin (FUO) in a teaching hospital in central India. Study subjects consisted of 233 patients having FUO admitted in the medical ward. Specific causes of FUO were identified in 73.4% cases. The commonest causes (46.4%) were of infectious diseases origin foremost being enteric fever (29.6%) followed by malaria (9.0%) and tuberculous fever (5.2%). Chloroquine responsive fever accounted for 26% cases of FUO. Enteric fever were seen more commonly in younger adults less than 50 years, tuberculous fever presented usually after four weeks of onset of symptoms and more in elderly patients aged 50 years or more. Intermittent type of fever was more commonly recorded in infectious diseases. Approach to causes of FUO should be focused primarily on infectious diseases followed by other specific investigations. Empirical treatment of cases having intermittent fever with chloroquine seems justifiable even in absence of malarial parasite in peripheral blood smear.

Adult↗

PubMed2001

[Yellow fever epidemiology in Brazil].

We have carried out a meticulous time-space-analysis of the incidence of yellow fever in humans in Brazil from 1954 to 1972 and especially from 1973 to 1999. This study has added to our knowledge of the epidemiology of yellow fever and enabled us to redefine epidemiological zones and determine their geographical limits. The endemic area is located within the Amazon basin; here cases are scattered and generally limited in number. However, there are also "foci of endemic emergence" within this area, where cases are less rare, although occurrence remains irregular. The epidemic area is for the most part situated outside the Amazon basin, to the north east and particularly to the south. It has been divided into two parts according to whether the occurrence of yellow fever is cyclic or sporadic. The epidemics, which are all sylvatic, follow either a circular path (in the forest area) or a linear path (in forest-galleries of the savannah area). The study of the development of the 3 main epidemics (1972-74; 1979-82; 1986-92) in the cyclic emergence area showed that, on each occasion, the yellow fever virus appeared at a particularly active outbreak site located in the "serra dos Carajás", and from there, it followed the courses of the Tocantins and Araguaia rivers upstream, moving southwards during the "pre-epidemic phase" which may be visible due to the occurrence of a few cases, or may remain invisible. Subsequently the virus reached the emergence area, where it appeared in the form of epidemics. In this zone, it also followed privileged south-western pathways, moving from one hydraulic basin to another along the upstream courses of the rivers. Almost exactly the same pathways have been identified for each of the 3 epidemics studied. The distances travelled by the virus over a period of one year--when it goes rapidly--can reach several hundred kilometers. On the other hand, it may be stationary for a period of one or two consecutive years, occasionally three, remaining present in the area but infecting humans only rarely if at all. The virus occasionally leaves the cyclic emergence area and appears in the sporadic emergence area to the east, in the states of Bahia, Minas Gerais and São Paulo, and, as a consequence, moving onto other hydraulic basins. The small river basins in Maranhão and NorthWest states, as well as in the northern part of the state of Roraima also form part of the sporadic emergence area. The epidemics that occur here are directly linked to the endemic area and are only preceded by sometimes indiscernible epizootics and can consequently not be foreseen. Again the virus appears to use privileged pathways to reach the sporadic emergence areas where human and monkey populations are generally only partially immunised against yellow fever and where contact with mosquitoes is intense despite the fact it is limited in space and time, being restricted to the often narrow strip of trees along the water courses. Other routes used by the virus may be the Madeira, Xingu and Tapajós rivers, the scene of outbreaks observed in the state of Rondônia and in the north of Mato Grosso, where ongoing environmental changes are likely to result in an increasing number of outbreaks in the coming years. Since the discovery of the sylvatic cycle of yellow fever in 1933, not only the extent of the epidemiological areas has changed, but also their limits. Ecological modifications that are currently taking place in the Amazon basin, which is an endemic reservoir of the virus, will inevitably facilitate an increase the contact between humans and vectors. While more and more urban areas harbour populations of Aedes aegypti, the domestic and urban vector of yellow fever, it is particularly important to try to protect human populations living in emergence zones and epidemic areas and thus to prevent the arrival of the virus in towns via humans with viremia--in other words the much feared urbanisation of yellow fever in Brazil.

Aedes↗

PubMedDate not supplied

Neonatal herpes simplex virus infection presenting with fever alone.

OBJECTIVE: Unlike bacterial infections, herpes simplex virus (HSV) infections are rarely considered as the diagnosis in neonates less than 1 month of age who present with fever alone. We wanted to determine the proportion of neonates with HSV who presented with fever alone and to compare that with the proportion of neonates with bacterial infection who presented with fever alone over the same period of time at our institution. STUDY DESIGN/METHODS: We retrospectively reviewed all neonatal medical records from March 1995 to February 1997 with a discharge diagnosis of HSV infection and all laboratory reports of a positive assay for HSV. We reviewed the medical records of neonates with a discharge diagnosis of bacterial infection over the same period of time. We excluded neonates who were afebrile, whose fever source was evident on physical examination, or who were immunocompromised. RESULTS: Eighteen neonates were diagnosed with an HSV infection over the 2-year period. One presented with fever alone. Twenty-seven of 113 neonates who presented with fever alone had a bacterial infection; 2 of these babies had meningitis. CONCLUSION: The proportion of neonates with HSV infection who presented with fever alone was comparable to that of neonates with bacterial meningitis who presented with fever alone at our institution. Testing and empirically treating for HSV infection might be warranted in febrile neonates with negative bacterial cultures.

Bacteremia↗

PubMed2001

Antibody response to 17D yellow fever vaccine in Ghanaian infants.

OBJECTIVES: To assess the seroresponses to yellow fever vaccination at 6 and 9 months of age; assess any possible adverse effects of immunization with the 17D yellow fever vaccine in infants, particularly at 6 months of age. METHODS: Four hundred and twenty infants who had completed BCG, OPV and DPT immunizations were randomized to receive yellow fever immunization at either 6 or 9 months. A single dose of 0.5 ml of the reconstituted vaccine was administered to each infant by subcutaneous injection. To determine the yellow fever antibody levels of the infants, each donated 1 ml whole blood prior to immunization and 3 months post-immunization. Each serum sample was titred on Vero cells against the vaccine virus. FINDINGS: The most common adverse reactions reported were fever, cough, diarrhoea and mild reactions at the inoculation site. The incidences of adverse reactions were not statistically different in both groups. None of the pre-immunization sera in both age groups had detectable yellow fever antibodies. Infants immunized at 6 months recorded seroconversion of 98.6% and those immunized at 9 months recorded 98% seroconversion. The GMT of their antibodies were 158.5 and 129.8, respectively. CONCLUSIONS: The results indicate that seroresponses to yellow fever immunization at 6 and 9 months as determined by seroconversion and GMTs of antibodies are similar. The findings of good seroresponses at 6 months without significant adverse effects would suggest that the 17D yellow fever vaccine could be recommended for use in children at 6 months in outbreak situations or in high risk endemic areas.

Antibodies, Viral↗

PubMedDate not supplied

[Fever of unknown origin. Presentation of 180 pediatric cases].

Fever of unknown origin (FUO) is a frequent disorder in pediatric age. FUO is defined as the presence of fever over 38.4 centigrades in a patient for more than three weeks in which the etiology remains undetermined. From 30.736 consecutive admittances into our hospital, 180 patients with FUO were detected, and studied in a systematized way and according to a predetermined protocol. FUO was commonly found in children under six years of age. Our patients presented fever from three weeks to six and a half years of evolution; however, in the vast majority of the cases (n = 115) fever had a three weeks course. Several symptoms and physical manifestations other than fever were observed in our patients but they were widely variable and nonspecific. Infectious diseases were the commonest etiological factor encountered; among them, thyroid fever, and urinary tract infections were the most frequent infectious disorder found; in four children fever was associated to ampicillin administration; in 19 patients, fever was no demonstrated. A large number of laboratory investigations were done in the diagnosis of neoplastic diseases. We think that the study of a patient with FUO requires of a systematized approach.

Adolescent↗

PubMed1992

Spontaneous splenic rupture complicating acute Q fever.

Q fever is usually a self-limited febrile illness that involves the lungs and the liver. Acute complications are rare. We present the case of a 30-yr-old patient with spontaneous splenic rupture during the course of acute Q fever infection. He was admitted to the hospital with high temperature and the radiological signs of an atypical pneumonia. Forty-eight hours after admission, he developed shock. Because of free intraabdominal liquid, a laparatomy was performed that revealed a tear in the enlarged spleen. A splenectomy was performed. The diagnosis of Q fever was established by a significant titer increase in complement fixation test and IgM-ELISA. Serological investigations into the patient's surroundings revealed evidence of Q fever infection in 10 additional persons. Q fever should be taken into account as a possible differential diagnosis in patients with unexplained febrile illness and symptoms of pneumonia. The acute course of Q fever infection can be complicated by splenic rupture. The diagnosis of an acute infection with Coxiella burnetii often requires serologic testing of a second serum sample obtained at least 10 days after the onset of symptoms. Q fever should be ruled out in cases of unexplained splenic rupture particularly in Q fever endemic areas.

Adult↗

PubMedDate not supplied

[West African tick-borne relapsing fever].

West African tick-borne relapsing fever is an endemic disease due to Borrelia crocidurae. The tick Alectorobius sonrai is the only known vector of this bacterium. Several species of rodents and insectivores may be reservoir for this spirochete. The geographic distribution of Borrelia crocidurae is not well known. The zone where the presence of the vector has been recorded is situated in Sahelian regions, from Mauritania and northern Senegal up to Chad. In Senegal, it has been shown that the persistence of drought is responsible for a considerable spread of tick-borne relapsing fever to the south. Few epidemiological data are available about West African tick-borne relapsing fever. In Senegal, epidemiological investigations indicate that Borrelia crocidurae is a major cause of morbidity (annual incidence rate of 5.1%). The relapsing nature of tick-borne borreliosis depends on Borrelia's antigenic variability. Except relapsing febrile episodes, this illness presents no pathognomonic signs. Borrelia crocidurae relapsing fever is generally benignant but neurologic or ocular complications can occur. The diagnosis of tick-borne relapsing fever is made by demonstrating the presence of Borrelia in peripheral blood in thick smear, by intraperitoneal inoculation of mice or more recently with quantitative buffy coat method (QBC test). The best treatment for relapsing fever is tetracycline or doxycycline. When tetracyclines are contraindicated, the alternative is erythromycin. In neurologic complications, the effective treatment is intravenous penicillin G or ceftriaxone. West African tick-borne relapsing fever must be systematically mentioned in case of fever in a patient returning from the endemic area.

Africa, Western↗

PubMed2004

Q fever in children in Greece.

The aim of this study was to investigate the incidence, epidemiology, and clinical manifestations of Q fever among hospitalized children in Greece. During a two-year period, 1,200 children with various clinical manifestations were prospectively tested for Coxiella burnetii infection by indirect immunofluorescence. Acute Q fever was diagnosed in eight (0.67%) patients. No chronic case of infection was detected. Multivariate analysis showed that children 11-14 years old and children reporting consumption of cheese from rural areas were at increased risk for this illness. Clinical manifestations of acute Q fever were pneumonia (two patients), meningitis (two), prolonged fever (two), hepatitis (one), and hemolytic-uremic syndrome (one). Q fever accounted for 2.9% of the cases with prolonged fever, 1.2% of the cases of meningitis, and 0.5% of the cases of pneumonia. Fever and headache were the most common symptoms at presentation. Our study indicates that Q fever is a rare cause of hospitalization during childhood.

Adolescent↗

PubMed2004

The global burden of typhoid fever.

OBJECTIVE: To use new data to make a revised estimate of the global burden of typhoid fever, an accurate understanding of which is necessary to guide public health decisions for disease control and prevention efforts. METHODS: Population-based studies using confirmation by blood culture of typhoid fever cases were sought by computer search of the multilingual scientific literature. Where there were no eligible studies, data were extrapolated from neighbouring countries and regions. Age-incidence curves were used to model rates measured among narrow age cohorts to the general population. One-way sensitivity analysis was performed to explore the sensitivity of the estimate to the assumptions. The burden of paratyphoid fever was derived by a proportional method. FINDINGS: A total of 22 eligible studies were identified. Regions with high incidence of typhoid fever (>100/100,000 cases/year) include south-central Asia and south-eastAsia. Regions of medium incidence (10-100/100,000 cases/year) include the rest of Asia, Africa, Latin America and the Caribbean, and Oceania, except for Australia and New Zealand. Europe, North America, and the rest of the developed world have low incidence of typhoid fever (<10/100,000 cases/year). We estimate that typhoid fever caused 21,650,974 illnesses and 216,510 deaths during 2000 and that paratyphoid fever caused 5,412,744 illnesses. CONCLUSION: New data and improved understanding of typhoid fever epidemiology enabled us to refine the global typhoid burden estimate, which remains considerable. More detailed incidence studies in selected countries and regions, particularly Africa, are needed to further improve the estimate.

Adolescent↗

PubMed1992

The significance of fever following cholecystectomy.

BACKGROUND: Family physicians are often called upon to evaluate a patient with fever that occurs following a surgical procedure. While fever is a common postoperative event, it can have various prognostic implications. METHODS: The incidence and significance of postoperative fever was studied in a relatively healthy group of patients who had undergone cholecystectomy. Risk factors for infection as well as the incidence of infection were recorded. RESULTS: The overall rate of infection was 5.7%. In comparing the epidemiologic, operative, and laboratory data of patients with fever with those without fever, the only statistical difference noted was a greater incidence of fever in men (P less than .01). As the sole diagnostic criterion for determining the presence of infection, fever was of little value. Other clinical findings proved to be more discriminating markers for infection. CONCLUSIONS: Postoperative fever in a cholecystectomy patient by itself is not suggestive of infection. Clinical findings remain the primary diagnostic guide to distinguishing those patients who require further evaluation.

Adult↗

PubMed2005

Fever control in septic shock: beneficial or harmful?

The beneficial effects of interventions to control fever in sepsis are controversial. We investigated whether the use of acetaminophen and external cooling is beneficial to control fever in septic shock. We studied 24 fasted, anesthetized, invasively monitored, mechanically ventilated female sheep (27.0 +/- 4.6 kg) that received 0.5 g/kg body weight of feces into the abdominal cavity to induce sepsis. Ringer's lactate (RL) was titrated to maintain pulmonary artery occlusion pressure (PAOP) at baseline levels throughout the experimental period. During the 2 h after the surgical operation, animals were placed in the hypothermia group if their temperature fell below 36.0 degrees C; the other animals were randomized to three groups: high fever (T > 39.0 degrees C), mild fever (37.5 degrees C < T < 38.5 degrees C), and normothermia (36.0 degrees C < T < 37.0 degrees C). The administration of 25 mg/kg acetaminophen every 4 to 6 h combined with external cooling (ice pad) was used to control core temperature in these three groups. The PaO2/FiO2 ratio was higher and blood lactate concentration was lower in the high fever than in the other groups (P < 0.01 and 0.05, respectively). Survival time was longer in the high fever group (25.2 +/- 3.0 h) than in the mild fever (17.7 +/- 3.5 h), normothermia (16.0 +/- 1.9 h), and hypothermia (18.5 +/- 2.5 h) groups (P < 0.05 for all). Plasma heat shock protein (HSP) 70 levels were higher in the two fever groups than in the other groups (P < 0.05). In this clinically relevant septic shock model, the febrile response thus resulted in better respiratory function, lower blood lactate concentration, and prolonged survival time. Antipyretic interventions including acetaminophen and external cooling were associated with lower circulating HSP70 levels. These data challenge the temperature control practices often used routinely in acutely ill patients.

Acetaminophen↗

PubMed2005

[Countermeasure against viral hemorrhagic fever at the border in Japan].

Human have struggled against many infectious diseases such as cholera, plague, dysentery and yellow fever for a long time. And we have spent a lot of energy to control these infectious diseases and developed various tool for them. One of these efforts was Quarantine system that was established in 14th century in Europe. But during recent days, we are suffering from newly emerged diseases. These new infectious diseases are zoonosis and most of them are serious and highly infectious. Viral hemorrhagic fever such as Ebola hemorrhagic fever, Marburg hemorrhagic fever and Lassa fever are typical these emerging serious diseases, and these outbreak always have occurred in Africa and neighboring countries. Fortunately we have never experienced any case, but as these diseases are so serious, we are so nervous diseases entering in Japan. Against these serious diseases, in Japan, Quarantine Station are doing screening examination at airport and port by questionnaire and measuring body temperature, because these viral hemorrhagic fever patients show high fever. If people were suspected viral hemorrhagic fever at Quarantine Station at the border, they will be leaded to hospital for further examination and treatment as soon as possible.

Animals↗

PubMed2006

Predictors of serious bacterial infection in children aged 3 to 36 months with fever without source.

INTRODUCTION: Children commonly present with fever without source yet there is no reliable and consistent method of identifying those at risk of serious bacterial infection. In this study, we sought to identify predictors of serious bacterial infection in children aged between three to 36 months with fever without source. METHODS: Inpatient records of all children aged three to 36 months admitted from the Emergency Department of Singapore's main paediatric hospital between October 2001 to February 2002 with International Classification of Diseases (ninth revision) diagnosis codes 038 (septicaemia), 079 (viral fever), or 780 (pyrexia of unknown origin), were retrieved and reviewed. Patients identified as having fever without source were enrolled. RESULTS: Of 86 enrolled children, 17 (19.8 percent) had serious bacterial infection. Duration of fever and white blood cell count were found to be significant predictors. Children with white blood cell count equal to or greater than 16,000/cubic mm had 6.9 times (95 percent confidence interval [CI] is 1.7 to 28.4) increased risk of serious bacterial infection, while children with fever of duration exceeding three days before presentation had 3.8 times (95 percent CI is 1.1 to 13.1) increased risk of serious bacterial infection. A combination of white blood cell count less than 16,000/cubic mm and duration of fever three days or less had a negative predictive value of 1.0 (95 percent CI is 0.88 to 1.0) and a sensitivity of 1.0 (95 percent CI is 0.82 to 1.0). CONCLUSION: The two identified predictors offer an estimate of the risk of serious bacterial infection in children aged three to 36 months with fever without source.

Bacterial Infections↗

PubMed1991

[Fever. A guideline in the development of medical thinking].

Fever being one of the best known symptoms, and appearing so frequently that it is often assimilated to "illness", has brought us to try and find out what "fever" means in a general way; in other words, we examined its medical and scientific concept throughout the centuries. In the course of primitive and archaic periods, fever, as well as diseases, was placed in the supernatural sphere and was reserved to magico-religious practices. Hippocrates will change this method by devoting himself to meticulous clinical observation, considering fever as a sign of illness, and by characterizing the different types of fever. When considering the mechanisms of its appearance, he will stick to the theory of "body-humors" and the "theories of numbers." Galenos will adapt that theory to Aristotle's philosophy and, doing so, he made it last for several centuries. The Renaissance will place critical thinking higher than slavish acceptance of theories, but it will not start any revolution in the appreciation of fevers. The possibility of contagion is mentioned, but the latter will only be well established by Pasteur and Koch. The breakthrough of microscopy into pathology will have to wait for Virchow. Thermometry will have to wait two centuries between Santorio and Wunderlich. The fever-concept will stay vague until experimental physiology and medicine will acquire their vested rights owing to Magendie and Bernard. They will moreover be followed by the microbiological era. The breakthrough will be the consequence of experimental proofs of the existence of a temperature-centre located in the hypothalamus and the pre-optic area. The discovery of endogenous as well as exogenous pyrogens has contributed to the creation of rational models which cover nearly completely the problem of body-temperature and fever. This long way did not progress as a regularly favourable evolution but, now and again, appeared figureheads who allowed us to approach the truth nearer and nearer.

Fever↗