Changes in hypothalamic-pituitary-adrenal axis function, immunity, and glucose during acute Plasmodium relictum infection in house sparrows (Passer domesticus).

Hosts of the same species vary in physiological responses to the same parasite, and some groups of individuals can disproportionately affect disease dynamics; however, the underlying pathophysiology of host-parasite interactions is poorly understood in wildlife. We tested the hypothesis that the hypothalamic-pituitary-adrenal (HPA) axis mediates host resistance and tolerance to avian malaria during the acute phase of infection by evaluating whether individual variation in circulating glucocorticoids predicted resistance to avian malaria in a songbird. We experimentally inoculated wild-caught house sparrows (Passer domesticus) with naturally sourced Plasmodium relictum and quantified baseline and restraint-induced circulating corticosterone, negative feedback ability, cellular and humoral immune function, and baseline and restraint-induced glycemia, prior to and during acute malaria infection. During peak parasitemia, we also evaluated the expression of several liver cytokines that are established pathological hallmarks of malaria in mammals: two pro-inflammatory (IFN-γ and TNF-α) and two anti-inflammatory (IL-10 and TGF-ß). Although most of the host metrics we evaluated were not correlated with host resistance or tolerance to avian malaria, this experiment revealed novel relationships between malarial parasites and the avian immune system that further our understanding of the pathology of malaria infection in birds. Specifically, we found that: (1) TNF-α liver expression was positively correlated with parasitemia; (2) sparrows exhibited an anti-inflammatory profile during malaria infection; and (3) IFN-γ and circulating glucose were associated with several immune parameters, but only in infected sparrows. We also found that, during the acute phase of infection, sparrows increased the strength of corticosterone negative feedback at the level of the pituitary. In the context of our results, we discuss future methodological considerations and aspects of host physiology that may confer resistance to avian malaria, which can help inform conservation and rehabilitation strategies for avifauna at risk.

No, you go first: phenotype and social context affect house sparrow neophobia.

Novel object trials are commonly used to assess aversion to novelty (neophobia), and previous work has shown neophobia can be influenced by the social environment, but whether the altered behaviour persists afterwards (social learning) is largely unknown in wild animals. We assessed house sparrow (Passer domesticus) novel object responses before, during and after being paired with a conspecific of either similar or different behavioural phenotype. During paired trials, animals housed with a similar or more neophobic partner demonstrated an increased aversion to novel objects. This change did not persist a week after unpairing, but neophobia decreased after unpairing in birds previously housed with a less neophobic partner. We also compared novel object responses to non-object control trials to validate our experimental procedure. Our results provide evidence of social learning in a highly successful invasive species, and an interesting asymmetry in the effects of social environment on neophobia behaviour depending on the animal's initial behavioural phenotype.

Efficacy of ivermectin against inhibited larvae of Ostertagia ostertagi.

The efficacy of ivermectin against inhibited early 4th-stage larvae of ostertagia ostertagi and other nematodes of the abomasum and intestinal tract was determined in naturally infected yearling beef cattle. The time when large numbers of inhibited larvae were acquired was determined by monthly slaughter of monitor cattle, beginning in January. In April, 12 animals were removed from pasture and maintained free of further helminth exposure until slaughter (21 days). At 9 days after the cattle were removed from pasture, ivermectin was administered to the principals by subcutaneous injection (200 micrograms/kg); the other 6 animals were given subcutaneous injections of the ivermectin vehicle. both groups were klled and necropsied at 12 days after treatment. Mean numbers of O ostertagi in the 6 controls were: adults, 41,906; developing 4th stage, 73,813; and early 4th stage, 334,965. The mean proportion of early 4th-stage larvae was 73.7%. In the 6 principals (treated with ivermectin), the following reductions were observed: O ostertagi adults, 100%; developing 4th stage, 99.8%; and early 4th stage, 99,9%. Small numbers of dead and degenerated O ostertagi of all developmental stages were recovered from abomasal washings before fixation; few viable worms were recovered.

Mutations within the transmembrane glycoprotein of Mason-Pfizer monkey virus: loss of SU-TM association and effects on infectivity.

We have previously reported that an 11-amino-acid deletion (D33) within the immunosuppressive peptide (ISP) region of the Mason-Pfizer monkey virus transmembrane (TM) glycoprotein, gp22, caused the loss of interaction between TM and the surface (SU) glycoprotein, gp70. This resulted in the secretion of large amounts of biologically active SU glycoprotein, and we postulated that the ISP might represent a point of contact between the two glycoproteins. To further define the amino acids that might be involved in this proposed region of interaction, we have made two neighboring 4-amino-acid deletions within the area defined by the D33 mutation and have carried out saturation mutagenesis on this 8-amino-acid region. We found that one of the smaller deletions (delta D), and two single point mutations (R68S and L72P), gave the same phenotype as the original D33 mutant. These results provide additional support for the hypothesis that this region of the TM glycoprotein is in contact with the SU glycoprotein and is important in maintaining the noncovalent interactions of the glycoproteins that function to hold the complex together.

Isolation of two distinct type I angiotensin II receptor genes.

A rat genomic Southern blot, probed with a type I angiotensin II receptor probe, demonstrated that two highly homologous type I angiotensin II receptors were present. A rat genomic library was subsequently screened and four clones were isolated. From restriction mapping, differential hybridization, polymerase chain reaction amplification and sequence analyses we have determined that there are two unique type I angiotensin II receptor genes. The first of these genes corresponds to the published rat vascular complementary DNA sequence; the second, corresponds to a novel receptor not previously described.