Effect of immunosuppressive treatment on Eperythrozoon suis infection and porcine peripheral-blood natural-killer-(NK) cell activity.
The effects of immunosuppressive treatment on natural-killer-cell activity and the manifestation of eperythrozoonosis in swine were investigated. After infection with Eperythrozoon suis (E. suis), German Landrace piglets received daily intravenous (i.v.) applications of cyclophosphamide (CY, Endoxan) on 6 consecutive days. A combined immunosuppressive treatment using azathioprine (Imurek), a single application of dexamethasone (Devan), and two injections of anti-asialo GM1 serum (1:50) was performed with a piglet over a period of 9 days. Leucocyte counts, differential blood-cell count, and microhaematocrit and rectal temperature were controlled. Direct microscopic observation of E. suis organisms was performed in Giemsastained blood smears. Immunosuppressive treatment resulted in relative lymphocytosis and transient agranulocytosis. CY and azathioprine therapy caused a temporary increase of E. suis organisms in red blood cells. Natural-killer-(NK) cell activity mediated by nylon-wool non-adherent peripheral-blood mononuclear leucocytes (NAD-PBML) was recorded during and after immunosuppressive treatment of pigs infected with E. suis. Cytotoxic activity of NK cells was consistently reduced after two CY injections and further decreased to 70-100% of the initial NK-mediated tumor cell lysis. NAD-PBML of two E. suis infected animals were monitored for cytotoxicity during CY immunosuppressive treatment and were compared to Percoll density separated NK effector cells derived from the same blood sample. Enhancement of NK-cell activity by density separation of NAD-PBML was not longer possible on days 3 and 4 during CY treatment, indicating a decrease of NK cells in peripheral blood. In vitro, only a high dose of CY (4 microgram/ml) suppressed cytolytic activity of NAD-PBML. Short-term treatment with immunosuppressive agents did not replace splenectomy in inducing clinically apparent eperythrozoonosis.
Büttner
M
M
Institut für Medizinische Mikrobiologie, Infektions- und Seuchenmedizin, München, Deutschland.
Plank
G
G
Heinritzi
K
K
D000818:Animals; D001379:Azathioprine / Q000627:therapeutic use; D003520:Cyclophosphamide / Q000627:therapeutic use*; D003907:Dexamethasone / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D007694:Killer Cells, Natural / Q000502:physiology*; D009175:Mycoplasma Infections / Q000188:drug therapy / Q000276:immunology / Q000662:veterinary*; D013552:Swine; D013553:Swine Diseases / Q000188:drug therapy* / Q000276:immunology
D007166:Immunosuppressive Agents; D003907:Dexamethasone; D003520:Cyclophosphamide; D001379:Azathioprine