Chlamydia pecorum-Associated Sporadic Ovine Abortion.

Despite previous detection of Chlamydia pecorum in sporadic ovine abortions, published descriptions of naturally occurring infections with fetoplacental lesions are lacking. This report provides the first descriptions of severe necrosuppurative chorionitis with vasculitis, and fetal pyelonephritis and enteritis in late-term abortions of maiden ewes. Chlamydial infection was detected using a Chlamydia genus-specific qPCR (quantitative polymerase chain reaction) on tissue extracts from 3 fetuses. C. pecorum was identified using a targeted qPCR assay, which also determined infectious load within fetal tissues. The presence of viable C. pecorum in fetal samples was confirmed by cell culture. Multilocus sequence typing (MLST) data indicated that the C. pecorum strains from each fetus were identical and of sequence type (ST) 23. Chlamydia sp. immunohistochemistry showed strong positive immunolabeling of fetoplacental lesions. Other infectious abortigenic agents were excluded with specific testing. This report confirms C. pecorum as a likely cause of ovine abortion and provides the first descriptions of associated fetoplacental lesions in naturally infected sheep.

Isolation of antigen-specific, disulphide-rich knob domain peptides from bovine antibodies.

As a novel alternative to established surface display or combinatorial chemistry approaches for the discovery of therapeutic peptides, we present a method for the isolation of small, cysteine-rich domains from bovine antibody ultralong complementarity-determining regions (CDRs). We show for the first time that isolated bovine antibody knob domains can function as autonomous entities by binding antigen outside the confines of the antibody scaffold. This yields antibody fragments so small as to be considered peptides, each stabilised by an intricate, bespoke arrangement of disulphide bonds. For drug discovery, cow immunisations harness the immune system to generate knob domains with affinities in the picomolar to low nanomolar range, orders of magnitude higher than unoptimized peptides from naïve library screening. Using this approach, knob domain peptides that tightly bound Complement component C5 were obtained, at scale, using conventional antibody discovery and peptide purification techniques.

Lead Intoxication in Free-Ranging Bald Eagles ( Haliaeetus leucocephalus).

Lead toxicity due to ingestion of spent ammunition is an ongoing cause of mortality in bald eagles. While gross and histologic lesions of lead intoxication have been described in a few individuals of this species, the prevalence of lesions is underreported. A retrospective study of 93 bald eagles with severe lead intoxication was performed to describe the associated lesions and their prevalence and to compare the lesions with blood, liver, kidney, and/or bone lead concentrations. Gross lesions associated with lead toxicity were most frequent within the heart (51/93 birds) and consisted of multifocal myocardial pallor and rounding of the apex. Within the brain, gross lesions included petechiae or hemorrhagic necrosis (13/93 birds). Histologic lesions compatible with lead toxicity occurred within the heart (76/93 birds), brain (59/93 birds), and eyes (24/87 birds). Lead toxicity in bald eagles is characterized by fibrinoid necrosis of small- to medium-caliber arteries, most commonly affecting the heart, brain, and eyes. Gross and histologic lesions are consistent with ischemia caused by a primary vascular injury. A blood lead concentration of greater than 4 ppm and markedly elevated liver lead concentrations were associated with a greater likelihood of lesions in the heart. Severe lead intoxication is frequently associated with lesions that are histologically detectable in bald eagles. The presence of fibrinoid arterial necrosis and parenchymal degeneration, necrosis, and/or hemorrhage within the heart, brain, and/or eyes is suggestive of lead toxicity in bald eagles and warrants evaluation of liver or bone lead concentrations.