No abstract

Squirrel monkeys (Saimiri sciureus) inoculated intratracheally with 10(4.2)-10(8.2) egg median infectious doses (EID50) of type A influenza virus (H3N2) responded with clinical illness including such signs as fever, sneezing or coughing, coryza, and increased respiratory rates. Necropsy studies performed six days after inoculation revealed bronchopneumonia in addition to a mild tracheitis. Squirrel monkeys given 10(5)-6 x 10(8) colony-forming units (cfu) of Streptococcus pneumoniae intratracheally died four to six days later after developing severe illness characterized by fever, bacteremia, lethargy, anorexia, coughing, labored breathing, and bronchopneumonia. Monkeys given 770 cfu of S. pneumoniae responded with less severe symptoms and survived. Four squirrel monkeys inoculated with 10(8.2) EID50 of virus and then 102 hr later with 770 cfu of S. pneumoniae developed severe disease; three of the four animals died within 40 hr. At necropsy these monkeys had more extensive and severe bronchopneumonia than was seen in monkeys infected with either organism alone.

Three chemotherapeutic drugs active against type A influenza virus (amantadine, rimantadine, and ribavirin) were tested as therapeutic agents against established infections with influenza virus in mice. The drugs were administered intraperitoneally or as aerosols either from 6 hr to four days or from three to seven days after infection. Small-particle aerosols were administered continuously 24 hr per day. Continuous dissemination of aerosols was superior to intraperitoneal administration, as evidenced by higher survival rates at 21 days. Rimantadine, amantadine, and ribavirin were effective when treatment was delayed for three days. Ribavirin was the most efficacious if therapy was initiated as an aerosol 6 hr after infection. In contrast to amantadine, ribavirin given in samll-particle aerosols at 6 hr prevented the development of pneumonia and decreased titers of virus in lung.

No abstract

The phagocytosis and subsequent degradation of phase I and II Coxiella burnetii by macrophages obtained from immune and nonimmune guinea pigs were compared. Phase I rickettsiae were more resistant to phagocytosis than were phase II organisms. There was no significant difference in the percentage of phagocytosis of either phase of rickettsiae by macrophages from immune or nonimmune animals. After ingestion, phase I and II organisms pretreated with normal serum multiplied and destroyed normal macrophages as well as macrophages obtained from guinea pigs immunized with phase II rickettsiae. In contrast, only phase I organisms were degraded by macrophages from phase I-immunized animals in the presence of normal serum. Immune serum rendered rickettsiae more susceptible to phagocytosis and also potentiated the destruction of organisms by all types of macrophages. The specificity of macrophages from phase I animals to degrade only phase I rickettsiae was demonstrated by the ability of Rickettsia rickettsii to replicate in these macrophages.