Transmissible gastroenteritis in neonatal dogs: experimental intestinal infection with transmissible gastroenteritis virus.

Fourteen neonatal dogs (4 through 11 days of age) were exposed orally to the Purdue strain of transmissible gastroenteritis (TGE) virus, and six dogs of similar age were noninoculated controls. Clinical signs of enteric disease did not develop. Both exposed and control dogs had normal fecal passages and appetite throughout the experiment. Jejunal epithelium from dogs euthanatized at 12, 24, 48, and 96 hours and at 10 days after exposure did not exhibit morphologic alterations detectable by light microscopy. Electron microscopic examination indicated that jejunal epithelial cells contained TGE viral particles as early as 12 hours after dogs were exposed. There were no apparent morphologic alterations or signs of desquamation of virus-infected cells, however. Results of pig transmission studies indicated that viable TGE virus was in jejunal tissue of the dogs as early as 12 hours and as late as 10 days after exposure to the virus.     

Prolactin and colibacillus-induced fluid transport in ligated intestinal segments.

Two experiments, using the ligated intestinal segment technique, were conducted to determine whether the pituitary hormone prolactin (PRL) could reduce Escherichia coli-induced fluid loss into the small intestine of 2- to 3-week-old pigs. Inoculation of 10(6) to 10(8) enteropathogenic E coli organisms into ligated jejunal segments caused a significant accumulation of luminal fluid within 12 hours. In the first experiment, intraluminal inoculation with 0.5 mg of ovine PRL along with the bacteria did not have any effect on fluid accumulation. Systemic IV treatment of the animals with 1.0 mg of ovine PRL at 3-hour intervals, beginning either immediately after or 9 to 10 hours before intestinal ligation, did not significantly (P less than 0.05) reduce fluid accumulation as compared with control animals. In the second experiment, IM administration of 100 microgram of thyrotropin-releasing hormone (TRH) at 3-hour intervals, beginning 6 hours before intestinal ligation, significantly (P less than 0.05) increased circulating PRL concentrations, as measured by radioimmunoassay. However, TRH treatment did not reduce the accumulation of luminal fluid in E coli-inoculated segments.     

Replication of turkey herpesvirus and Marek's disease virus in chick embryo skin organ culture.

Turkey herpesvirus (HVT) and an attenuated Marek's disease virus (MDV) replicated in organ cultures of chick embryo skin as assessed by immunofluorescence and/or electron microscopy. HVT-specific immunofluorescent antigen was detected in the feather follicle epithelium (FFE) and in the surface layer of the skin epidermis. Electron microscopy of infected explants revealed herpes-type cytopathology. Immature particles of both viruses appeared first in the nucleus. Oval or horseshoe-shaped non-enveloped particles of HVT and enveloped virions of MDV were seen in the cytoplasm of some transitional cells. The difference in the ability of HVT and MDV to form an envelope was believed to account for the difference in their transmissibility in chickens. The results indicated that HVT replicated in the FFE and in the epidermis of the skin. However, attempts to localise the site(s) of MDV replication by electron microscopy were unsuccessful.     

Plasma concentration of sulphadimethoxine in pigs after multiple dosing and during injections of Escherichia coli endotoxin

The effect of endotoxin induced fever on the steady state concentration of sulphadimethoxine in pigs has been studied.Sulphadimethoxine 20 mg/kg b.wt. was injected at 9 a.m. in an ear vein each day for eleven days. From day 6 until the end of the experiment, endotoxin fromEscherichia coli 1.5 g/kg b.wt. was injected at 9 a.m. and at 3 p.m. The plasma concentration versus time curves were calculated by means of a computer program, assuming a two-compartment model. During the endotoxin injections the plasma concentrations were simulated and compared with those calculated.It was not possible to show any clinically significant changes in pharmacokinetics of sulphadimethoxine after the start of endotoxin injections.