ABSTRACT
Five- to six-month-old specific-pathogen-free cats were exposed to cobra venom factor (CVF) alone (4 cats), Rickard feline leukemia virus (FeLV; 9 cats), or CVF and FeLV (6 cats). Host-virus relationships were evaluated by monitoring the development of viremia, production of antibody against feline oncornavirus-associated cell membrane antigen, and amount of circulating immune complexes (CIC). Exposure to CVF induced complement depletion, which lasted 8 to 15 days. However, complement depletion did not promote the development of persistent viremia nor alter the production of antibody to feline oncornavirus-associated cell membrane antigen or CIC. Results indicated that the complement system did not protect cats during their initial exposure to FeLV and that an intact complement system was not necessary for the development of antibody against feline oncornavirus-associated antigen or for the formation of CIC.
Subject(s)
Complement System Proteins/immunology , Elapid Venoms/pharmacology , Leukemia, Experimental/immunology , Animals , Cats , Leukemia Virus, FelineABSTRACT
A total of 3 cases of acute lead poisoning in calves was confirmed by atomic absorption spectrophotometric analysis of biological samples, presence of an acute lead exposure source, clinical signs of impaired vision in one case and eosinophilic meningoencephalitis in another case. One of two other calves which died approximately 2 months earlier had nervous signs and it is likely that they also had lead poisoning. Dams of two of the cases did not have elevated lead levels. Municipal sewage sludge had been applied to most fields on the farm during the preceding 5 year period. There had been approximately a doubling of the lead content in the soil; however, the foodstuffs produced on the farm had low lead concentrations. The extremely high lead levels in the abomasal contents and feces of calves eliminated sludge as the source of the lead in this acute poisoning episode. The contents of oil filters, accessible to calves but not to adult cattle, had lead levels as high as 26,922 micrograms/g and was the most likely lead source responsible for this lead intoxication. It appears that the manifestation of eosinophilic meningoencephalitis in lead poisoning cases may occur in young calves as well as in cows and in acute as well as in chronic intoxications.
Subject(s)
Cattle Diseases/chemically induced , Eosinophilia/veterinary , Lead Poisoning/veterinary , Meningoencephalitis/veterinary , Sewage/adverse effects , Soil Pollutants/poisoning , Acute Disease , Animal Feed/analysis , Animals , Brain/pathology , Cattle , Cattle Diseases/pathology , Eosinophilia/chemically induced , Eosinophilia/pathology , Lead Poisoning/pathology , Meningoencephalitis/chemically induced , Meningoencephalitis/pathology , Metals/analysis , Soil/analysis , Water Supply/analysisABSTRACT
The role of the complement system in containment of feline leukemia virus infection was studied by cobra venom factor treatment of feline leukemia virus-immune cats. One to three weeks after cobra venom factor treatment, an increase in viral antigen in marrow myelomonocytic cells and circulating immune complexes was noted. Prevention of reactivation of feline leukemia virus infection may in part depend on an intact complement system.
Subject(s)
Elapid Venoms/pharmacology , Leukemia, Experimental/immunology , Animals , Antigen-Antibody Complex/analysis , Cats , Complement System Proteins/physiology , Leukemia Virus, FelineABSTRACT
A microscale ELISA immune complex assay which utilized a solid phase C1q and a Protein A-peroxidase enzyme conjugate is described. This ELISA was used to detect and quantitate circulating immune complexes (CIC) during the initial feline leukemia virus infection. Significant increases in CIC were seen in the cats which were transiently infected at weeks three through eight after viral exposure. A persistent elevation in CIC was observed in the one cat which developed a persistent viremia. The addition of EDTA to the serum strongly interfered with this assay.
Subject(s)
Antigen-Antibody Complex/analysis , Enzyme-Linked Immunosorbent Assay , Immunoenzyme Techniques , Preleukemia/immunology , Animals , Cats , Complement Activating Enzymes , Complement C1q , Leukemia Virus, Feline , Leukemia, Experimental/immunology , Staphylococcal Protein A , Time Factors , Viremia/immunologyABSTRACT
A comparison was made of the binding of radiolabeled heat aggregated cat immunoglobulin G (125I-ACG) to Raji cells using normal or heat-inactivated cat or human serum. The binding with normal or heated cat serum, as well as heated human serum were essentially identical. The binding using normal human serum was 2.5- to 3-fold greater than observed with heated human serum. These results suggest that feline complement associated with 125I-ACG does not bind to Raji cells via complement receptors, but only by receptors for the Fc portion of IgG. Human serum and 125I-ACG can bind to both Fc and complement receptors on Raji cells.
