This report describes the first isolation and partial characterization of a herpesvirus from the harbor seal (Phoca vitulina). The virus was isolated during a disease outbreak in a group of young seals nursed in a seal orphanage in The Netherlands. Almost half of the seals died with symptoms of acute pneumonia and focal hepatitis and the virus was isolated of organs of most of the dead animals. Seven out of ten seals of which paired serum samples were obtained showed seroconversion in a virus neutralization test during this outbreak. The virus was tentatively characterized as a herpesvirus (seal herpesvirus: SeHV or phocid herpesvirus 1) on the basis of its characteristic morphology in electron microscopy, buoyant density in sucrose, sensitivity to ether and heat treatment and its antigenic relationship with other probable members of the Alphaherpesvirinae subfamily. The virus caused cytopathic changes within 24 hours after inoculation in seal kidney cells, consisting of a focal rounding of cells and syncytium formation. No cytopathic changes were observed in the cells of nine other mammalian species tested.

Recently morbilliviruses were isolated from harbour seals (Phoca vitulina) in North West Europe (phocid distemper virus-1: PDV-1) and from Baikal seals (Phoca sibirica) in Siberia (phocid distemper virus-2: PDV-2) during outbreaks of severe disease which resembled distemper in dogs. PDV-1 and PDV-2 were passaged in SPF dogs, in which they caused distemper-like disease symptoms, and were subsequently passaged in Vero cells in which they caused cytopathic changes. PDV-1, PDV-2, and canine distemper virus (CDV) were compared with respect to their biological, morphological, physical, protein chemical, and antigenic properties. It was concluded that PDV-1 should be considered a newly recognized member of the genus Morbillivirus, whereas PDV-2 proved to be quite similar if not identical to CDV.

During a recent disease outbreak among harbour seals (Phoca vitulina) in the North and Baltic seas, more than 17,000 animals have died. The clinical symptoms and pathological findings were similar to those of distemper in dogs. Based on a seroepizootiological study, using a canine distemper virus (CDV) neutralization assay, it was shown that CDV or a closely related morbillivirus (phocid distemper virus-PDV) was the primary cause of the disease. The virus was isolated in cell culture from the organs of dead seals and characterized as a morbillivirus by serology (immunofluorescence neutralization and enzyme-linked immunosorbent assays) and by negative contrast electron microscopy. Experimental infection of SPF dogs resulted in the development of mild clinical signs of distemper and CDV-neutralizing antibodies. The disease was reproduced in seals by experimental inoculation of organ material from animals that had died during the outbreak. However, seals that had been vaccinated with experimental inactivated CDV vaccines were protected against this challenge. This fulfilled the last of Koch's postulates, confirming that the morbillivirus isolated from the seal organs, was the primary cause of the disease outbreak. The recent demonstration of the presence of a similar virus in Lake Baikal seals (Phoca sibirica), which infected these Siberian seals 1 year before the northwestern European seals were infected, raises new questions about the origin of this infectious disease in pinnipeds.

The encapsulation of Trichinella spiralis larvae in host striated muscle was studied.Capsule formation starts at 13 days post-infection. Between days 20–50 p.i. the largest increase in capsule formation was observed. The capsule is exclusively, or almost exclusively, formed from and by the infected muscle fibre, as might be concluded from the presence of the sarcolemmal basal lamina surrounding the capsule substance during the initial stages of capsule formation. A collagen nature of the capsule cannot be excluded.

Intravesical administration of Bacillus Calmette-Guérin (BCG) has been shown to be effective in the treatment of patients with superficial bladder cancer. For a better understanding of the mechanism of this antitumor activity, scanning and transmission electron microscope (SEM, TEM) studies were carried out to investigate morphological aspects of the interaction of BCG with the bladder wall in vivo and in vitro. Adherence of BCG to the bladder wall in vivo was studied 1 and 24 h after single or multiple (6x) BCG instillations in intact and in electrocauterized guinea pig bladders. Despite extensive search with SEM for its presence, virtually no BCG was found on the intact urothelium, and BCG was only occasionally observed in the coagulation lesions. SEM and TEM studies revealed adherence and phagocytosis of BCG by the T24 human bladder carcinoma cell line in vitro. Time sequence studies on the phagocytosis and fate of BCG showed that T24 cells are capable of progressively degrading the mycobacteria in phagolysosomes. However, BCG did not alter MHC class II antigen expression on T24 cells in vitro. In contrast, 54 urine sediments and bladder washings of 11 bladder cancer patients, taken prior to or after several intravesical BCG instillations, failed to demonstrate urothelial (tumor) cells showing evidence of BCG phagocytosis (682 cells screened by TEM), while BCG was phagocytized avidly by leukocytes. These data suggest that a direct interaction of BCG with urothelial bladder cells in vivo can be called in question.