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In this paper we propose the hypothesis that pathogen-induced host defense responses result in altered host behaviors and enhanced predation. In particular we examine the effects of the acute phase response (whose effects include fever, reduced activity and malaise) on antipredatory behavior in bullfrog (Rana catesbeiana) tadpoles. This host response is associated with the preliminary stages of infection with many pathogens yet its behavioral effects have received little attention. Bullfrog tadpoles were injected with alcohol-killed bacteria to induce a response to infection and their ability to detect and avoid capture by predatory salamanders (Taricha granulosa) was explored. We predicted that acute phase responses increase tadpole vulnerability to predation by influencing thermoregulatory behavior and their ability to detect, and avoid capture by, salamanders. We found that the sterotypical effects of the acute phase response can lead to increased predation. Malaise affected the refuge seeking behavior of the tadpoles in the presence of salamanders. We suggest that for tadpoles provided with refuges, altered behaviors are a liability. This endogenous response may afford some parasites a potential pathway to their next host.

A method for the determination of cyanate concentration in blood plasma over the range I to 1000 pM is presented. Cyanate present in the dried residue of acetone-deproteinized plasma is converted to a chromophoric thiocarbamyl derivative by addition of pH 3.0-buffered thionitrobenzoic acid. The derivative is then analyzed by reversed-phase high-performance liquid chromatography with detection at 3 I3 nm, near the absorption maximum. Carbamyl thionitrobenzoic acid peak height is quantified by comparison to a standard curve made by analysis of plasma samples to which known quantities of cyanate have been added. This technique is sensitive and linear with respect to cyanate concentration, and is faster than other reported methods; sample analysis and column regeneration are accomplished within 20 min. cyanate; carbamyl thionitrobenzoic acid: high-performance liquid chromatography.

Uremic patients tend to have a lower than normal deep-body temperature. In addition, there is a clinical impression that uremic patients are also more thermolabile than healthy people; that is, in a warm environment, body temperature tends to be higher, and in a cold environment, body temperature tends to be lower than in healthy subjects. To test the hypothesis that uremia results in enhanced thermolability, nonoperated control (NO), nephrectomized (NX), and sham-nephrectomized (SHAM) rabbits were subjected to mild cold (5 degrees C) and heat (30 degrees C) stresses. At 48 hours postsurgery, the core temperature of NX rabbits was significantly lower than that of the NO or SHAM rabbits (P less than .01). Exposure to 5 degrees C resulted in a significant fall in body temperature of the NX (from 39.1 degrees C to 38.3 degrees C; P less than .05) rabbits compared to the NO rabbits. There was a tendency for body temperature of the SHAM rabbits to fall, and as a result, there was no significant difference in the change in body temperature between the SHAM and NX rabbits. Exposure to 30 degrees C resulted in virtually no change in the core temperature of the NO or SHAM rabbits, but did result in a significant rise in core temperature of the NX rabbits (P less than .02 and P less than .01 for respective comparisons), as well as a significant increase in mortality rate (P less than .02). Based on these data, we conclude that anephric animals are more thermolabile, and are less able to tolerate exposure to a warm environment, than are normal animals.

A coorelation has been observed between increased blood ketones and the tolerance of mice to hypoxia (4-5% oxygen). In previous studies fasted mice, alloxan diabetic mice and mice given 1,3-butanediol were found to be ketotic and to have increased tolerance to hypoxia. We attempted to induce a similar increased hypoxic tolerance by direct elevation of blood ketones with IV and IP beta-hydroxybutyrate (BHB). No increase in hypoxic tolerance was observed with BHB alone. Inasmuch as fasting and alloxan diabetes are both associated with elevated blood glucagon (G), hypoxic tolerance tests were made 30 min after G alone or a combination of G plus BHB. The mice given G alone or BHB alone had hypoxic survival times not different from saline controls. The mice given G plus BHB had increased survival times that could not be explained on the basis of a G mediated alteration in blood BHB.

The regulation of body temperature is often conceptualized as a negative feedback control system complete with afferent limb, integrating area and effector limb. Most vertebrates regulate body temperature and these animals have been classified into two groups - ectotherms and endotherms. Ectotherms rely largely on behavioural responses to raise or lower their body temperature. Among the vertebrates, most fishes, amphibians and reptiles are ectotherms. Endotherms rely to a large extent on physiological responses to raise or lower their body temperature. Often this includes increasing or decreasing metabolic heat production. Birds and mammals are endotherms. The distinction between endotherms and ectotherms, however, is not absolute. For example, a large percentage of the thermoregulatory effector responses of endotherms is behavioural modifications designed to avoid extremes in temperature. This is why most desert animals are nocturnal, or in cold climates many animals either migrate to warmer climates, avoid the intense cold by burrowing under the snow or hibernate. The result of these numerous thermoregulatory effector responses is that the deep-body temperature of both endotherms and ectotherms is regulated around a hypothetical thermoregulatory set-point.

Polymyxin B is often added to in vitro samples to 'ensure' that endotoxin activity is removed. We present data, from the standard rabbit pyrogen test and the Limulus amebocyte lysate assay, that polymyxin B bound to a gel support will bind some, but not all, endotoxin. These data, in conjunction with previously published data by Morrison and Curry (1979), indicate that those studies that have relied on polymyxin B to inactivate endotoxin must be re-evaluated.