Ocular lesions associated with dissemination of type 2 herpes simplex virus from skin infection in newborn rabbits.

The subcutaneous inoculation of the backs of New Zealand white rabbits 17 to 34 hr old with 10(3) 50% tissue culture infection dose (TCID50) of type 2 herpes simplex virus (HSV-2) induced cutaneous lesions within 24 hr, foci of disseminated infection in many organs (including the eye) on day 3 and thereafter, and the death of the animals on day 5 with infection of the central nervous system. Infectious HSV-2 could be isolated from the mononuclear cells and plasma of the peripheral blood, indicating the active role of both elements in the dissemination of the virus. Infectious HSV was also recovered from the corresponding sensory ganglia of the skin lesion (the cervicothoracic ganglia) as early as 2 days after the subcutaneous inoculation of the virus. About 40% of the animals developed ocular consisting of retinal folds with or without degenerative changes, Iritis and choroiditis also developed in some eyes. Infectious HSV-2 could be isolated from 33% of the eyes on days 4 and 5. Thus the newborn rabbit may serve as a suitable experimental animal for the study of HSV-2-induced chorioretinitis in the human newborn.

Acyclovir therapy of neonatal herpes simplex virus type 2 infections in rabbits.

New Zealand white rabbits less than 30 h old were inoculated subcutaneously with 10(3) 50% tissue culture infectious doses of type 2 herpes simplex virus. The animals were randomly assigned to a treatment schedule of daily intraperitoneal injections of acyclovir, beginning on the day of virus inoculation for 6 or 12 days, on post-inoculation day 1 for 6 days, or on post-inoculation day 2 for 6 days. The acyclovir was given in doses of 50 mg/kg of body weight per day. Similarly infected animals receiving daily intraperitoneal injection of Eagle minimum essential medium served as controls. All of the control animals died on day 4 or 5 after inoculation. At death they exhibited severe skin lesions, viremia, and dissemination of virus in various visceral organs and spinal as well as trigeminal ganglia. In contrast, animals treated with acyclovir failed to develop significant skin lesions, and death did not occur while treatment continued. Termination of treatment after 6 days resulted in late-onset fatal disease and virus isolation from the brain in many rabbits regardless of the treatment schedule. No such late fatality was observed and no virus could be detected from the brain when treatment was initiated on the day of virus inoculation and continued for 12 consecutive days. With respect to all of the variables studied, treatment for 12 days beginning on the day of virus inoculation was most effective.