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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.

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.

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.