Hypothermia in Experimental Infections: III. The Effect of Hypothermia on Resistance to Experimental Pneumococcus Infection

Muschenheim, Carl; Duerschner, Dorothy Rhoades; Hardy, James D.; Stoll, Alice M.

doi:10.1093/infdis/72.3.187

Cited by 27 publications

(12 citation statements)

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“…In 1909, Strouse described the native resistance of pigeons to S pneumoniae type III due to their higher normal core temperature (approximately 41°C) and found they succumbed to infection when cooled with ice or the antipyretic pyramidon 6. Further experiments in S pneumoniae infected rabbits demonstrated higher mortality rates with external cooling 7 8. In contrast, others demonstrated increased mortality in mice exposed to raised environmental temperatures9 and reduced mortality rates in mice subjected to drug induced hypothermia 10 11.…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, others demonstrated increased mortality in mice exposed to raised environmental temperatures9 and reduced mortality rates in mice subjected to drug induced hypothermia 10 11. However, in rabbits infected with S pneumoniae , a febrile response was associated with improved outcomes 7 12. In human patients, in an early 20th century case series, fever therapy (external radiation) in severe S pneumoniae type 3 meningitis appeared to reduce cerebrospinal fluid bacterial cell counts, but did not prevent mortality 13.…”

Section: Introductionmentioning

confidence: 99%

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Systematic review and meta-analysis of the effects of antipyretic medications on mortality in Streptococcus pneumoniae infections

Jefferies

Weatherall

Young

et al. 2011

Postgraduate Medical Journal

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A twofold increased risk of mortality was found with aspirin treatment in animal models of S pneumoniae infection. No relevant human studies were identified. It is difficult to generalise from animal models to clinical medicine, but based on these findings and the prevalence and severity of S pneumoniae infections worldwide, future study of the effects of antipyretic therapy in S pneumoniae infection in humans is recommended.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Systematic review and meta-analysis of the effects of antipyretic medications on mortality in Streptococcus pneumoniae infections

Jefferies

Weatherall

Young

et al. 2011

Postgraduate Medical Journal

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“…Hypothermia inhibited neutrophil accumulation in models of inflammation outside the CNS (Muschenheim et al, 1943;Svanes, 1964;Janssen et al, 1967;Biggar et al, 1984). Reduction of body temperature by less than 3°C substantially decreased neutrophil accumulation in skin, lung, and peritoneum, whereas a 2°C increase in body temperature augmented inflammation (Thomas and Sousa, 1986).…”

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confidence: 99%

The Effect of Brain Temperature on Acute Inflammation after Traumatic Brain Injury in Rats

Whalen

Carlos²,

Clark³

et al. 1997

Journal of Neurotrauma

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The effect of varying brain temperature on neutrophil accumulation in brain and the expression of E-selectin and intercellular adhesion molecule-1 (ICAM-1) on cerebrovascular endothelium after controlled cortical impact (CCI) was studied in rats. Sprague Dawley rats were anesthetized and subjected to CCI to the left parietal cortex. Ten minutes after CCI, brain temperature was modulated and maintained at 32 degrees C, 37 degrees C, or 39 degrees C (n = 8 per group) for 4 h. Rats were then decapitated and immunohistochemistry on brain sections was performed using monoclonal antibodies (MoAb) that recognize neutrophils (RP-3), ICAM-1 (TM-8, Athena Neurosciences), or MoAb that react with E-selectin (La-Roche). Each of these markers was quantified in 100 x fields. Neutrophil accumulation was also quantified with myeloperoxidase (MPO) assay. Absolute neutrophil count (ANC) was measured in blood samples before and 1 h and 4 h after CCI. Neutrophil accumulation in injured brain was decreased in rats maintained at 32 degrees C vs 39 degrees C (4-fold difference as assessed by immunohistochemistry, p < 0.05; 8-fold difference as assessed by MPO assay, p < 0.05). Peripheral blood ANC was not affected by temperature. E-selectin was induced on cerebrovascular endothelium after CCI (p < 0.05), but was only decreased modestly at 32 degrees C versus 39 degrees C (p = 0.11). ICAM-1 was not upregulated on cerebrovascular endothelium at this early time following CCI. Neutrophil accumulation is directly dependent on brain temperature during the initial 4 h after CCI. This appears to be mediated by mechanisms other than effects of temperature on E-selectin or ICAM-1 expression or systemic ANC.

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“…Increased survival with fever has been demonstrated in animal studies [29,30]. In fact, the majority of studies (14 out of 21 studies) evaluated in one review demonstrated a deleterious effect of lowering body temperature [11].…”

Section: Fever and Clinical Outcomesmentioning

confidence: 99%

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221COX-2 = cyclooxygenase-2; HSF = heat shock factor; HSP = heat shock protein; ICU = intensive care unit; IL = interleukin; NF = nuclear factor; OVLT = organum vasculosum of the laminae terminalis; TNF-α = tumor necrosis factor alpha.Available online http://ccforum.com/content/7/3/221 Fever occurs commonly in hospitalized patients. It is estimated that nosocomial fevers occur in approximately one-third of all medical patients at some time during their hospital stay [1]. In patients admitted to the intensive care unit (ICU) with severe sepsis, the incidence of fever is more than 90% [2]. As there is variation in the incidence of reported fevers, the etiology of fever in critically ill patients is similarly diverse-both infectious and noninfectious etiologies are common [1,3,4].The definition of fever is arbitrary. The mean body temperature (oral) in healthy individuals is approximately 36.8°C (98.2°F), with a range of 35.6°C (96°F) to 38.2°C (100.8°F) and a slight diurnal variation [5]. The Society of Critical Care Medicine and the Infectious Disease Society of America, in a recent consensus statement, suggested that a temperature of above 38.3°C (101°F) should be considered a fever and should prompt a clinical assessment [4].Physician and staff response to fever varies institutionally. Besides evaluating the patient and initiating a workup based on the clinical evaluation, it is common for the patient to receive either pharmacologic or mechanical antipyretic therapy. However, there is little evidence that would support such routine practice. The traditional view, at least in pediatrics, is that an exuberant febrile response is inherently dangerous and can, in the worse case, lead to seizures and brain damage [6]. Adult nonhealthcare workers (i.e. patient family members) also have significant misconceptions regarding the perceived detrimental effects of fever [7]. In this complicated psychosocial setting, it is easy for the physician to merely treat the fever. However, there are costs associated with such therapies. It is estimated that when either paracetamol, icepacks or cooling blankets are used, it can cost one 18-bed ICU between $10,000 and $29,000 per year [8]. Pharmacological means to reduce fever cause renal and hepatic dysfunction in patients who are volume depleted or who have underlying kidney or liver disease [9]. Additionally, there is evidence, at least in animal models, that fever is a beneficial host response to infection [10][11][12]. AbstractFever is a common response to sepsis in critically ill patients. Fever occurs when either exogenous or endogenous pyrogens affect the synthesis of prostaglandin E 2 in the pre-optic nucleus. Prostaglandin E 2 slows the rate of firing of warm sensitive neurons and results in increased body temperature. The febrile response is well preserved across the animal kingdom, and experimental evidence suggests it may be a beneficial response to infection. Fever, however, is commonly treated in critically ill patients, usually with antipyretics, without good data to ...

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Hypothermia in Experimental Infections: III. The Effect of Hypothermia on Resistance to Experimental Pneumococcus Infection

Cited by 27 publications

References 0 publications

Systematic review and meta-analysis of the effects of antipyretic medications on mortality in Streptococcus pneumoniae infections

Systematic review and meta-analysis of the effects of antipyretic medications on mortality in Streptococcus pneumoniae infections

The Effect of Brain Temperature on Acute Inflammation after Traumatic Brain Injury in Rats

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