Lymphoproliferative disease virus (LPDV) is an exogenous oncogenic retrovirus that induces lymphoid tumors in some galliform species of birds. Historically, outbreaks of LPDV have been reported from Europe and Israel. Although the virus has previously never been detected in North America, herein we describe the widespread distribution, genetic diversity, pathogenesis, and evolution of LPDV in the United States. Characterization of the provirus genome of the index LPDV case from North America demonstrated an 88% nucleotide identity to the Israeli prototype strain. Although phylogenetic analysis indicated that the majority of viruses fell into a single North American lineage, a small subset of viruses from South Carolina were most closely related to the Israeli prototype. These results suggest that LPDV was transferred between continents to initiate outbreaks of disease. However, the direction (New World to Old World or vice versa), mechanism, and time frame of the transcontinental spread currently remain unknown.

Histopathology of 61 captive American horseshoe crabs (HSCs; Limulus polyphemus) is reviewed. HSC organs evaluated histologically included body wall (chitin, epidermis, dermis, and skeletal muscle), hepatopancreas, gut, gonads, book gills, eyes, heart, brain, and coxal gland. In descending order, lesions were most frequently identified in compound eye, body wall, book gills, hepatopancreas, chitinous gut, nonchitinous gut, heart, and brain; lesions were not observed in coxal gland or gonads. Hemocytes (also called amoebocytes) surrounded infectious agents and occluded ulcers. Large hemocyte aggregates had a central eosinophilic coagulum (ie, hemocyte coagulum). Cutaneous ulceration (34/60 cases), branchitis (29/48 cases), and ophthalmitis (17/20 cases) were common lesions and consistently associated with fungi, which were invasive into subjacent tissues, and/or bacteria, which were usually superficial. Fungal culture was performed in 3 cases and isolated Fusarium spp., although fungal morphology varied and multiple fungal species may have been present. Presumptive green algae were associated with ulceration in 1 case with minimal to no inflammation. Presumptive cyanobacteria were identified within a biofilm overlying the gills in 4 of 48 cases and were not invasive. Multifocal, random hepatopancreatitis was identified in 16 of 57 cases, 10 of which were associated with bacteria. Metacercarial cysts were identified in 25 of 61 cases and associated with minimal to no inflammation. Depleted eosinophilic globules in hepatopancreatic interstitial cells were interpreted as decreased nutritional status in 12 of 57 cases.

Pulmonary hypertension is a well-known though poorly characterized disease in veterinary medicine. In humans, pulmonary veno-occlusive disease (PVOD) is a rare cause of severe pulmonary hypertension with a mean survival time of 2 years without lung transplantation. Eleven adult dogs (5 males, 6 females; median age 10.5 years, representing various breeds) were examined following the development of severe respiratory signs. Lungs of affected animals were evaluated morphologically and with immunohistochemistry for alpha smooth muscle actin, desmin, CD31, CD3, CD20, and CD204. All dogs had pulmonary lesions consistent with PVOD, consisting of occlusive remodeling of small-to medium-sized pulmonary veins, foci of pulmonary capillary hemangiomatosis (PCH), and accumulation of hemosiderophages; 6 of 11 dogs had substantial pulmonary arterial medial and intimal thickening. Ultrastructural examination and immunohistochemistry showed that smooth muscle cells contributed to the venous occlusion. Increased expression of CD31 was evident in regions of PCH indicating increased numbers of endothelial cells in these foci. Spindle cells strongly expressing alpha smooth muscle actin and desmin co-localized with foci of PCH; similar cells were present but less intensely labeled elsewhere in non-PCH alveoli. B cells and macrophages, detected by immunohistochemistry, were not co-localized with the venous lesions of canine PVOD; small numbers of CD3-positive T cells were occasionally in and around the wall of remodeled veins. These findings indicate a condition in dogs with clinically severe respiratory disease and pathologic features resembling human PVOD, including foci of pulmonary venous remodeling and PCH.

Manganese (Mn) is both a ubiquitous essential trace element and a toxic metal if ingested at higher doses. Food is the major source of Mn in human beings and animals. Usually, homeostatic mechanisms limit the intestinal absorption to only 1-5% of the normal dietary intake with less than 1% retained after biliary and intestinal excretion while urinary excretion is fairly low. 2Manganese is required for amino acid, lipid, protein, and carbohydrate metabolism. It also serves as an important cofactor for many enzymes including hexokinase, superoxide dismutase, xanthine oxidase, and pyruvate carboxylase, many of which are localized in mitochondria. 2,23 Manganese is evenly distributed throughout the body. Increased Mn concentrations are mostly found in tissues with both high energy demand and mitochondria such as brain, liver, kidney, pancreas, and bone as well as in highly pigmented tissue. 23 Manganese toxicity has been reported in human beings and in experimental animal models.28 Chronic Mn intoxication (manganism) due to prolonged inhalation of Mn dust or fumes in miners, welders, or battery manufacturers historically causes neurologic disease in the form of a Parkinson'slike bradykinetic-hypertonic syndrome. 2,4,18Long-term parenteral nutrition 9 and chronic Mn exposure through contaminated water have also resulted in neurologic disease in human beings.18 Acute Mn intoxication is rare and has been scarcely reported in the literature. Other human case reports include a patient that developed severe pancreatitis after hemodialysis due to a dialysate contaminated with Mn,24 acute Mn pneumonitis after inhalation of Mn-containing dust or fumes, 11 and acute fatal Mn intoxication after accidental, massive oral ingestion. 22 Experimental, intravenous Mn administration in Beagle dogs resulted in severe hepatotoxicosis and hypotension. 15 Acute enteral Mn intoxication has not been reported in animals.A 5-year-old female spayed Pug dog, weighing 5.8 kg, presented to the University of California-Davis Veterinary Medical Teaching Hospital (Davis, California) emergency service for evaluation of vomiting and ataxia after accidental ingestion of approximately 100 joint supplement tablets. Approximately 6-12 hr prior to presentation, the dog ingested approximately 60 g of glucosamine hydrochloride (10.3 g/kg), 25 g of methylsulfonylmethane (4.3 g/kg), 30 g of sodium chondroitin sulfate (5.2 g/kg), and 500 mg of manganese ascorbate (86 mg/kg).On physical examination, the dog was obtunded with pelvic limb ataxia, in mild hypovolemic shock, and was approximately 5% dehydrated. Other physical exam parameters included mild tachycardia and hypothermia, and the dog continued to vomit multiple times during the physical exam. Venous blood gas and electrolyte analysis showed a mixed metabolic and respiratory acidosis with hyperchloremia (143 mEq/l), hypernatremia (166 mEq/l), and hyperlactatemia (2.9 mmol/l). Initial therapy included intravenous crystalloid fluids, and antinausea and gastroprotectant medications 544316V DIXXX10.1177/1040...