en route, quarantined by barrier system at the receiving institution until tested and shown to be free of infection, and subsequently maintained by strict barrier protocol. In addition, all biological materials such as transplantable tumors coming into the institution must be pre-tested and shown to be free of the virus before experimental use (Collins and Parker, 1972; Parker and Richter, 1982).

Once infection has been diagnosed in a facility, prompt elimination of infected subpopulation(s) is essential to prevent spread of the infection to other rodents on the premises. A less effective alternative is to place the infected animals under strict quarantine, remove all young and pregnant females, suspend all breeding, and prevent addition of other susceptible animals for a period of 6-8 weeks until the infection has run its course and the virus has been eliminated naturally. Because of this alternative, cesarean derivation of infected stocks usually is not justified.

Vaccination may prove useful in some situations (Parker, 1980; Eaton et al., 1982). A number of killed vaccines (Fukumi and Takeuchi, 1975; Nedrud et al., 1987; Tsukui et al., 1982), a temperature sensitive mutant strain vaccine (Kimura et al., 1979), and a trypsin-resistant mutant strain vaccine (Tashiro and Homma, 1985; Tashiro et al., 1988) have been tested experimentally. A formalin-killed SV vaccine is available commercially in the United States (Microbiological Associates, Bethesda, Md.).

Experimental infection of mice with SV decreases pulmonary bacterial clearance (Degre and Glasgow, 1968; Degre and Solberg, 1971), probably through a variety of mechanisms including altered phagocytic function. Altered functions in pulmonary macrophages that have been identified include: decreased Fc receptor and non-Fc receptor mediated attachment, decreased Fc receptor and non-Fc receptor mediated ingestion, inhibited phagosome-lysosome fusion, decreased intracellular killing, decreased degradation of ingested bacteria, and decreased lysosomal enzyme content (Jakab, 1981; Jakab and Warr, 1981).

Concurrent SV and M. pulmonis infections are synergistic in mice (Howard et al., 1978; Saito et al., 1981) and rats (Schoeb et al., 1985), causing disease of far greater severity than either alone.

SV infected mice have been reported to have deficiencies in T and B cell function that persist throughout life (Kay, 1978, 1979; Kay et al., 1979). (Unfortunately, these results have not been confirmed by other investigators).

SV infection transiently increased splenic IgM and IgG plaque forming cell responses to sheep red blood cells in mice (Brownstein and Weir, 1987).

SV infection inhibited in vitro mitogenesis of lymphocytes (Wainberg and Israel, 1980; Roberts, 1982).

Front Matter (R1-R12)

I. Principles of Rodent Disease Prevention (1-2)

1. Objectives, Terminology, and Overview of Pathogen Status (3-12)

2. Breeding, Transportation, and Use of Pathogen-Free Rodents (13-16)

3. Barrier Programs (17-20)

4. Health Surveillance Programs (21-28)

II. Individual Disease Agents and Their Effects on Research (29-30)

5. Introduction (31-32)

6. Respiratory System (33-84)

7. Digestive System (85-163)

8. Skin and Joints (164-197)

9. Hemopoietic System (198-221)

10. Central Nervous System (222-230)

11. Genitourinary System (231-235)

12. Multiple Systems (236-256)

III. Indexes to Diagnosis and Research Complications of Infectious Agents (257-258)

Introduction (259-259)

Clinical Signs (260-265)

Pathology (266-274)

Research Complications (275-276)

References (277-386)

Index (387-397)