In rats, infection altered the mitogenic responses of T cells, reduced severity of adjuvant arthritis, and decreased antibody response to sheep erythrocytes (Garlinghouse and Van Hoosier, 1978).

Mice naturally infected with SV have been found to have increased natural killer cell mediated cytotoxicity (Clark et al., 1979), and increased cytotoxic lymphocyte responses after stimulation with SV-coated syngeneic cells (Finberg et al., 1980).

SV infection altered isograft rejection in mice (Streilein, et al., 1981).

SV infection altered host responses to transplantable tumors (Wheelock, 1966, 1967; Collins and Parker, 1972; Matsuya et al., 1978; Takeyama et al., 1979).

Previous or concurrent infection in mice may increase or decrease neoplastic response to respiratory carcinogens (Nettesheim et al., 1974, 1981; Parker, 1980; Peck et al., 1983; Hall et al., 1985).

SV infection delayed wound healing in mice (Kenyon, 1983).

Athymic (nulnu) mice (Ueda et al., 1977b; Iwasaki, 1978; Iwai et al., 1979) and nude (rnulrnu) rats (Carthew and Sparrow, 1980c) had increased susceptibility and developed chronic lung disease when infected with SV.

Cyclophosphamide increased clinical and pathological severity of SV infection in mice (Robinson et al., 1969; Blandford, 1975; Anderson et al., 1980).

SV infection can cause deaths and retarded growth of young mice (Parker and Reynolds, 1968; Bhatt and Jonas, 1974) and rats (Makino et al., 1972).

Very high, particularly in long term studies.

1937: Nelson (1937a,b,c) described the proximal airway disease called "infectious catarrh" in mice and attributed it to "coccobacilliform bodies" (later identified as M. pulmonis).

1937: Klieneberger and Steabben (1937) described pulmonary "bronchiectasis" in rats, and subsequently (Klieneberger and Steabben, 1940) recognized the association of their "L3" organism (later identified as M. pulmonis) with this lesion.

1957: Nelson (1957) advanced the term "chronic respiratory disease" and proposed that it was due to two agents: M. pulmonis which caused "infectious catarrh" (proximal airway disease), and "enzootic bronchiectasis virus" alleged to cause the bronchopulmonary (distal airway) disease. (This putative virus still has not been identified.)

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)