Summary The immunoprophylactic capacity of specific immune plasma was evaluated in pony foals infected experimentally with Rhodococcus equi. Immune plasma, produced by repeated parenteral administration of viable R. equi to adult horses, was harvested and frozen. Group I (six control foals) and Group II (six principal foals) received lactated Ringers solution and immune plasma respectively at three and five days of age. R. equi were aerosolised into a caudal lung lobe of all foals at seven days of age. Clinical signs, haematological alterations, immune responses, thoracic radiographs and technetium99m pulmonary perfusion scans were monitored. All foals were destroyed and complete post mortem examinations performed. All foals developed pneumonia as evidenced by clinical, radiographic and perfusion alterations, but the survival rate of principal foals was significantly (P < 0.01) greater than that of control foals. Five control foals developed terminal disease, whereas all principal foals recovered. There was no significant (P>0.05) difference in temperature response, or peripheral blood leucocyte, neutrophil or fibrinogen concentrations between groups. ELISA values for R. equi antibody were significantly (P<0.001) greater in principal foals following treatment, but there was no significant (P>0.05) difference in IgG or IgM concentrations between groups. Results of the haemolysis inhibition assay indicated that equi factor neutralising antibodies were transferred by immune plasma to the principal foals. Post mortem examinations of five control foals destroyed at approximately three weeks post infection because of terminal disease, revealed severe pyogranulomatous pneumonia. One control and all principal foals were either free of lesions or had resolving lesions and/or minimal scar formation at three months post infection. The results of this investigation document the importance of humoral factors in controlling the disease process, and the capacity of humoral immunoprophylaxis to alter the clinical progression of R. equi pneumonia.

Summary The immunoprophylactic capacity of colostrum‐derived Rhodococcus equi antibodies was evaluated in pony foals experimentally infected with R. equi. Six pony mares (Group 1) were injected serially with live R. equi during pregnancy; a further six pony mares were not vaccinated and used as controls All (Group 2) foals were permitted to suck from their dams and the adequacy of IgG, passively transferred via colostrum, was determined by single radial immunodiffusion. The presence and relative value of R. equi specific antibodies were determined by ELISA. Mares vaccinated with R. equi developed significantly (P<0.05) increased R. equi antibody levels, and the principal foals from these mares had specific antibody values that were significantly (P<0.01) higher than control foals. Rhodococcus equi were aerosolised into a caudal lung lobe of all foals at seven days of age. Clinical signs, haematological alterations, immune responses and thoracic radiographs were monitored. Foals were subjected to euthanasia and complete post mortem examinations were performed. All foals developed pneumonia as evidenced by clinical and radiographic signs. The survival rate for Group 1 foals did not differ significantly from that of control foals. Two of the six foals in each group survived the bacterial challenge. Also, there were no significant differences between groups for duration of survival, peak febrile responses, duration of fever, time from infection to onset of fever, or peak concentrations of leucocytes and neutrophils. Post mortem examinations of four foals from each group, destroyed approximately three weeks post infection because of terminal disease, revealed severe pyogranulomatous pneumonia involving primarily the caudal portion of one lung. One control foal had miliary pyogranulomatous lesions in both lungs. Rhodococcus equi was cultured from the pulmonary lesions in these foals. Two principal and two control foals that recovered from the infections had mild pulmonary fibrosis at three months post infection. Rhodococcus equi was not cultured from any of these foals at necropsy. The results of this investigation suggest that passive immunisation of newborn foals, by ingestion of colostrum derived R. equi specific antibodies, does not provide adequate protection against experimental infection with R. equi.

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Summary The immunotherapeutic efficacy of specific immune plasma was evaluated in pony foals infected experimentally with Rhodococcus equi. Viable R. equi were aerosolised into the right caudodorsal lung of 10 foals at seven days of age. Immune plasma, produced by repeated parenteral administration of viable R. equi to an adult donor gelding, was harvested and frozen. Group 1 (4 foals) and Group 2 (6 foals) foals received lactated Ringer's solution and immune plasma, respectively, at seven and nine days post infection. Clinical signs, haematological alterations, immune responses and thoracic radiographs were monitored throughout the study. All foals were destroyed and complete post mortem examinations were performed. All foals developed pneumonia as evidenced by clinical and radiographic alterations. Immune plasma had no significant effect on survival rate, length of survival, temperature response or peripheral blood concentrations of leucocytes, neutrophils or fibrinogen. Enzyme‐linked immunosorbent assay values for R. equi‐specific antibody and serum concentrations of IgG were significantly greater in Group 2 foals following treatment with immune plasma. Post mortem examination of three Group 1 and four Group 2 foals, destroyed because of terminal disease, revealed severe pyogranulomatous pneumonia. The two surviving Group 2 foals were free of gross pulmonary lesions and had minimal microscopic scar formation three months post infection; whereas the one surviving Group 1 foal had a large, encapsulated, caseonecrotic pulmonary mass three months post infection. This study demonstrates that the parenteral administration of R. equi immune plasma to foals seven days after experimental infection with R. equi does not alleviate the clinical signs nor alter the course of disease.

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