ABSTRACT
OBJECTIVE: To determine patterns of fecal shedding of feline coronavirus (FCV) by cats, age at which kittens first began to shed FCV in their feces, and whether there was any relationship between fecal shedding of FCV and serum antibody titers in adult cats or kittens. DESIGN: Prospective observational study. ANIMALS: 15 adult cats and 18 kittens from a single cattery. PROCEDURE: Blood and fecal samples were collected from adult cats every other month for 13 months. Serum FCV antibody titers were measured by use of an indirect immunofluorescence assay. A reverse-transcriptase, nested polymerase chain reaction assay was used to detect FCV in feces. Blood and fecal samples were collected from kittens at approximately 2-week intervals from 3 weeks to 15 weeks of age. RESULTS: Adult cats shed FCV intermittently. All adult cats shed virus in their feces at least once during the year, and 4 of 15 shed virus > 75% of the time. Serum antibody titer was not significantly associated with shedding of FCV. For the kittens, median age at the time FCV was first detected in feces was 67 days (range, 33 to 78 days). All except 1 of the kittens was found to be shedding virus in their feces before or at the time of seroconversion. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that serum FCV antibody titers are not a good indicator of shedding of FCV in the feces. Kittens may shed FCV in their feces before they seroconvert, and all kittens in a cattery in which FCV infection is endemic may be infected before 12 weeks of age.
Subject(s)
Cat Diseases/virology , Coronavirus Infections/veterinary , Coronavirus/isolation & purification , Feces/virology , Animals , Animals, Newborn , Animals, Suckling , Antibodies, Viral/blood , Cat Diseases/prevention & control , Cats , Coronavirus/immunology , Coronavirus/physiology , Coronavirus Infections/prevention & control , Coronavirus Infections/virology , Female , Vaccination/veterinaryABSTRACT
Thirty adult, client-owned dogs were diagnosed with hypothyroidism based on history, physical examination findings, hematologic and biochemical abnormalities, thyrotropin (TSH) response testing, endogenous canine thyrotropin (cTSH) concentration, or both, and total serum thryoxine concentration. All dogs received levothyroxine (L-thyroxine) at an initial dose of 22 micrograms/kg PO sid in either a tablet (13 dogs) or chewable form (17 dogs). Energy expenditure of each dog during apparent rest was estimated with an open-flow indirect calorimetry system by determining the rates of carbon dioxide production and oxygen consumption. Energy expenditure of apparent rest (EE) was lower in untreated hypothyroid dogs compared with reference values for EE. After treatment with L-thyroxine, EE of the hypothyroid dogs was significantly (P < .05) higher than pretreatment values.
Subject(s)
Basal Metabolism/drug effects , Dog Diseases/drug therapy , Hypothyroidism/veterinary , Thyroxine/pharmacology , Animals , Basal Metabolism/physiology , Calorimetry, Indirect/veterinary , Dog Diseases/metabolism , Dogs , Female , Hypothyroidism/drug therapy , Hypothyroidism/metabolism , Male , Oxygen Consumption/drug effects , Oxygen Consumption/physiology , Tablets , Thyroxine/administration & dosage , Thyroxine/therapeutic useABSTRACT
In conclusion, interaction between the immune and endocrine systems is highly complex. Generally, abnormalities of T suppressor cells, a result of HLA antigen genetic abnormalities, result in autoimmunity that causes endocrine gland destruction and hormone deficiency, as seen in lymphocytic thyroiditis of dogs, type I DM, hypoparathyroidism, hypoadrenocorticism, and APS. On the other hand, endocrine deficiency (hypothyroidism, DM) or excess (hyperadrenocorticism) states may cause abnormalities of cell-mediated and antibody-associated immunity, leading to susceptibility to a variety of viral, bacterial, and fungal infections. It is hoped that this article sheds some light on the complex and highly integrated endocrine-immune interactions.
