Some Physiological and Clinical Aspects of Pyrogens

Cooper, K. E.

doi:10.1002/9780470719800.ch1

Cited by 13 publications

(7 citation statements)

References 20 publications

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“…Heart rate was elevated with maximum values 3 days after infection. It has been suggested that there is a good correlation between the increase in heart rate and the rise in body temperature during febrile episodes (Cooper, 1971). In the present experiments, however, we did not find such a correlation between these 2 parameters.…”

Section: Discussioncontrasting

confidence: 56%

Clinical, haematological and blood biochemical changes in goats after experimental infection with tick-borne fever

Miert

Duin

Schotman

et al. 1984

Veterinary Parasitology

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Van Miert, A.S.J.P.A.M., van Duin, C.T.M., Schotman, A.J.H. and Franssen, F.F., 1984. Clinical, haematological and blood biochemical changes in goats after experimental infection with tick-borne fever. Vet. Parasitol., 16: 225--233.Tick-borne fever in goats caused by Ehrlichia (Cytoecetes)phagocytophila was characterised by high fever, dullness, anorexia, tachycardia and a slight to moderate inhibition of rumen motility. The animals developed a gradual decline in the total number of circulating white blood cells. There was a decrease in lymphocytes over a short period, followed by an increase. The number of neutrophils was higher on the 3rd day, causing considerable change in the lymphocyte:neutrophil ratios. The number of eosinophils increased slightly. Serum alkaline phosphatase (ALP) decreased during the febrile episodes, and a marked decline was observed in both plasma zinc and iron concentrations. Furthermore, there was a small hut progressive decrease of haemoglobin and haematocrit values. Circulating endogenous pyrogen]leucoeyte endogenous mediator could not be detected in plasma from febrile goats. Tick-borne fever was passively transmitted to kids with plasma obtained from these febrile animals.

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Section: Discussioncontrasting

confidence: 56%

Clinical, haematological and blood biochemical changes in goats after experimental infection with tick-borne fever

Miert

Duin

Schotman

et al. 1984

Veterinary Parasitology

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“…A few years later in 1949, Beeson proved that granulocytes did produce EP, which he called 'granulocyte pyrogen'; later it was called leukocytic pyrogen (LP) or EP (6,7,21,32). In retrospect, which of the cytokines was the original EP?…”

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confidence: 98%

Pro‐inflammatory cytokines in a ruminant model: Pathophysiological, pharmacological, and therapeutic aspects

Miert

1995

Veterinary Quarterly

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Infection evokes complex changes which are thought to be caused by production and release of pro-inflammatory cytokines such as tumour necrosis factor (TNF-alpha), interferons (INFs), and interleukins (ILs). They regulate local inflammatory reactions, but may also gain access to the circulation and induce systemic effects collectively known as the Acute Phase Response. To improve our understanding of the pathophysiology of pro-inflammatory cytokines in ruminants, studies have been performed with TNF-alpha, IL1-alpha/beta, and IFN-alpha/ gamma as well as with cytokine-inducers in dwarf goats. In relation to therapy, the following aspects may be of interest: a) Cytokine therapy given before or just after microbial challenge induces in vivo antimicrobial activity. Moreover, cytokines potentiate in vivo the antimicrobial activity of antibiotics, b) Cytokines may act as biological response modifiers for enhancing specific immunity to vaccines, and c) Cytokines may affect drug absorption, disposition, and metabolite formation in disease states. Although studies of the actions of corticosteroids, nonsteroidal anti-inflammatory and antipyretic agents, antibodies to endotoxin, TNF-alpha, or IL-1, synthetic E. coli lipid A precursors, hydrazine, isoniazid, chloroquine, polymyxin B, bicyclic imidazoles, hydroxamates, and tyrosine kinase inhibitors in endotoxaemic animals have shed further light on inflammatory processes, clinical studies in this field are urgently required to evaluate their beneficial effect.

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“…It is possible that the death of organisms during JHR simulates this situation. Cooper (1971) has successfully used endotoxin-refractory rabbits to demonstrate the presence of leucocyte pyrogen in samples of plasma which also contained endotoxin.…”

Section: Discussionmentioning

confidence: 99%

“…Sample 1 was most pyrogenic and produced fever starting within 8 min, while samples 2 and 3, which might have been expected to contain more pyrogen, produced less fever and of slower onset. There is ample evidence that the detection and assay of both leucocyte and bacterial pyrogens can be validly performed in the rabbit (Cooper, 1971;Cranston, Rawlins, Luff & Duff, 1971). Statistical methods.…”

Section: Pyrogenicity Of Jhr Plasma In Normal Rabbitsmentioning

confidence: 99%

Studies of the Mechanism of the Jarisch—Herxheimer Reaction in Louse-Borne Relapsing Fever: Evidence for the Presence of Circulating Borrelia Endotoxin

et al. 1972

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1.Certain aspects of the Jarisch-Hemheimer reaction (JHR) after treatment of louse-borne relapsing fever have been studied in nine patients. Peripheral vasoconstriction immediately preceded the chill phase and profound vasodilation accompanied the flush phase.2. From four patients 50-150 ml of blood was taken at the onset of the chill and reinjected intravenously into the same patient the next day. One patient experienced a reaction identical with JHR 40-60 min after reinjection, suggesting that the mediator of JHR was present in that blood. 3.From five patients 40 ml of blood were taken serially throughout JHR and 2-ml samples of plasma, free of cells and spirochaetes, were injected into pairs of normal rabbits. All samples taken while the patients had fever were pyrogenic. After incubation with normal rabbit plasma these samples failed to produce fever in endotoxin-refractory rabbits.4. These results suggest that in the plasma of patients with relapsing fever there is a powerful endotoxin. We were unable to show that the concentration of endotoxin increased during JHR, nor could we demonstrate the presence of leucocyte pyrogen. This failure could be a problem of quantity of plasma used or of an endotoxinrefractory state.5. The bearing of these observations on the mechanism of JHR and the uselessness of cortisol in modifying the reaction are discussed.The reaction which follows the treatment of louse-borne relapsing fever with antibiotics is the most violent example of the Jarisch-Herxheimer reaction (JHR) (Schofield, Talbot, Bryceson & Parry, 1968). The salient features of the reaction are (Bryceson, 1970): 1. A rise and then a fall in body temperature; the rise is accompanied by a chill and the fall by sweating.2. Aggravation of pre-existing lesions and their attendent symptoms and signs; e.g. flaring of the rash in syphilis, acute myocarditis in relapsing fever.3. Characteristic physiological changes which include early vasoconstriction, hyperventilation and rise in blood pressure and cardiac output and later a fall in blood pressure associated with low peripheral resistance. These changes have been described in detail by Warrell(l970) and Warrell, Pope, Parry, Perine & Bryceson (1970).

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Some Physiological and Clinical Aspects of Pyrogens

Cited by 13 publications

References 20 publications

Clinical, haematological and blood biochemical changes in goats after experimental infection with tick-borne fever

Clinical, haematological and blood biochemical changes in goats after experimental infection with tick-borne fever

Pro‐inflammatory cytokines in a ruminant model: Pathophysiological, pharmacological, and therapeutic aspects

Studies of the Mechanism of the Jarisch—Herxheimer Reaction in Louse-Borne Relapsing Fever: Evidence for the Presence of Circulating Borrelia Endotoxin

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