Hemagglutination and hemagglutination inhibition of turkey red blood cells with Mycoplasma hyopneumoniae

The ability of Mycoplasma hyopneumoniae to agglutinate RBC was evaluated to develop an in vitro cytadsorption assay. Using swine RBC in a microtitration hemagglutination test, no agglutination or partial agglutination was detected. Comparison of RBC from various other species indicated that improved hemagglutination was obtained with RBC from turkeys. This hemagglutination was detected only when mycoplasma cells used in the assay had been frozen and thawed, heated at 50 C for 30 minutes, or treated with trypsin. Treatment of RBC with trypsin or neuraminidase enhanced hemagglutination. Possible surface lectin activity in M hyopneumoniae was evaluated by use of carbohydrates in a blocking assay; hemagglutination was not inhibited by any of 13 carbohydrates evaluated. Mycoplasma hyopneumoniae convalescent porcine serum and monoclonal antibodies against 2 M hyopneumoniae immunogens of molecular weights of 64,000 and 41,000 inhibited hemagglutination.     

Chicken anemia agent in the United States: isolation of the virus and detection of antibody in broiler breeder flocks

Chicken anemia agent (CAA) was isolated from broiler chickens in Texas with a blue wing or anemia dermatitis-like syndrome. Specific-pathogen-free chicks inoculated with field material developed anemia, and CAA was isolated in MDCC-MSB1 cells from bone marrow and lymphoid tissue from inoculated chicks. One isolate, designated EF88/78/276, was further characterized. Infectivity of EF88/78/276 was resistant to treatment with chloroform and with heat at 70 C for 5 minutes. EF88/78/276 was indistinguishable from the Cux-1 and Gifu-1 isolates of CAA by cross-neutralization tests. Almost all 1-day-old susceptible chicks inoculated intramuscularly with EF88/78/276 developed anemia, but contact-infected chicks did not. Antibody to CAA was detected in broiler breeder flocks from Texas, the Delmarva peninsula, and Alabama.     

Ionophores alter hepatic concentrations of intermediary carbohydrate metabolites in steers

The effects of ionophores on liver weight and function were determined in finishing steers (n = 24; avg weight 440 kg). Steers were group-fed one of three treatments (control, lasalocid or monensin at 33 mg/kg feed) for 46 d prior to slaughter. Three days prior to slaughter, blood was collected for the determination of serum Ca and Mg. At slaughter, the liver was removed, weighed, sampled, frozen in liquid nitrogen and subsequently analyzed for concentrations of carbohydrate metabolites and minerals. Liver weight (5.9 kg) was unaffected by treatment. Serum and hepatic Ca and Mg were not affected by ionophore treatment. Hepatic glycogen levels in steers fed ionophores were unaffected by treatment. Fructose 1,6-bisphosphate was 21% lower (P less than .10) in hepatic tissue of steers fed ionophores, whereas dihydroxyacetone phosphate was 15 to 37% greater in hepatic tissue of steers fed monensin (P less than .20) or lasalocid (P less than .10). Glyceraldehyde 3-phosphate was elevated more extensively by lasalocid than by monensin with increases of 72 (P less than .05) and 132% (P less than .001), respectively, over controls. Glycerol 3-phosphate levels were 37% (P less than .05) and 12% (NS) greater with these ionophores. Hepatic levels of pyruvate were elevated 12 (NS) to 36% (P less than .17) for monensin and lasalocid. Fructose 2,6-bisphosphate levels were 25% lower (P less than .25) in hepatic tissue of steers fed ionophores than in hepatic tissue from control steers. Other metabolites of carbohydrate metabolism in hepatic tissue were not altered appreciably. Changes in levels of intermediary metabolites of carbohydrate metabolism suggest alterations in hepatic carbohydrate metabolism favoring gluconeogenesis in steers fed ionophores.     

Food aversion learning: ability of lambs to distinguish safe from harmful foods

We studied the ability of lambs to select safe foods in the presence of harmful foods. In a series of feeding experiments, 3- to 6-mo-old lambs were offered a choice between 1) a familiar, safe and a novel, harmful food, 2) a novel, safe and a novel, harmful food and 3) a familiar, harmful and a novel, safe food. All harmful foods were palatable feeds that had been treated with lithium chloride (LiCl), a non-lethal gastrointestinal poison. When lambs ingested a meal composed of a novel food containing LiCl and a familiar, safe food, lambs subsequently avoided the novel food. Lambs avoided the novel food even when the familiar food contained LiCl. The response of lambs varied when lambs were given a choice between a novel, safe food and a novel food containing LiCl. Lambs either avoided the novel food containing LiCl and ingested the safe food or they limited their intake of both novel foods. Their response was dependent on the novelty of the food containing LiCl. When a novel, palatable food contained 2% LiCl, lambs always ate some of the food, even after experiencing illness from ingesting it. Lambs experienced with foods containing LiCl displayed greater food neophobia than lambs naive to LiCl-treated foods. Thus, novelty was the major criterion that lambs used to associate foods with gastrointestinal illness.     

P‐33 Poxvirus infection in two cats

A 3‐year‐old Burmese cat was presented with a history of nonresolving crusted and papular lesions of the face and prior treatment with prednisolone. Skin biopsies revealed typical pox lesions with hyperplasia and ulceration of the epidermis and eosinophilic cytoplasmic inclusion bodies in the epidermal cells. In the upper dermis there was prominent diffuse mast cell infiltration and mild neutrophilic and eosinophilic inflammation. Rare cytoplasmic inclusion bodies were also present in swollen endothelial cells of dermal venules, which showed no other degenerative changes. Histological diagnosis was confirmed by electron microscopic evidence of pox virus particles in inclusion bodies of epidermal cells. The lesions resolved within 6 weeks with systemic antibiotic therapy and supportive care. A 2‐year‐old domestic short‐haired cat was presented with multiple disseminated papular and ulcerative pox lesions with central eschar over the entire body. Histologically, large epidermal inclusion bodies (up to 6 μm in diameter) were present. Widespread haemorrhage and vascular wall necrosis was visible in the dermis and subcutis. Some subcutaneous vessels showed neutrophilic vasculitis. In addition to diffuse dermal neutrophilic and eosinophilic inflammation, a lymphohistiocytic panniculitis was also present. The cat died as a result of massive haemorrhage and lymphedema, despite supportive care. Funding: Self‐funded.     

Effect of endocytic and metabolic inhibitors on the internalization and intracellular growth of Brucella abortus in Vero cells.

Uptake, transfer to rough endoplasmic reticulum, and intracellular growth of Brucella abortus were studied in Vero cells treated with endocytic and metabolic inhibitors. Infection of Vero cells was suppressed when inhibitors of energy metabolism (iodoacetate, dinitrophenol), receptor-mediated endocytosis (monodansylcadaverine, amantadine, methylamine), or endosomal acidification (chloroquine, ammonium chloride, monensin) were added to the inoculum. Inhibition was not observed when these drugs were added after the inoculation period. Infection of Vero cells by B abortus was inhibited by dibutyryl-cyclic adenosine monophosphate and Vibrio cholerae enterotoxin, but was stimulated by dibutyryl-cyclic guanosine monophosphate and escherichia coli heat-stable enterotoxin a. Uptake of B abortus by Vero cells was not prevented by colchicine, but was abolished by cytochalasin B. Uptake of heat-killed B abortus and noninvasive E coli was similar to that of viable brucellae. Intracellular growth of B abortus was not affected by cycloheximide. Results indicate that: B abortus may be internalized by a receptor-mediated phagocytic process; transfer of B abortus from phagosomes to rough endoplasmic reticulum may require endosomal acidification; and replication of B abortus within the rough endoplasmic reticulum may not depend on protein synthesis by the host cell.