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Splenectomy of the fetal lamb early in development as a model for congenital asplenia
Author(s) -
King Karen J.,
Mccullagh Peter
Publication year - 2001
Publication title -
anz journal of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.426
H-Index - 70
eISSN - 1445-2197
pISSN - 1445-1433
DOI - 10.1046/j.1440-1622.2001.02001.x
Subject(s) - splenectomy , asplenia , spleen , medicine , fetus , gestation , in utero , pregnancy , physiology , immunology , biology , genetics
Background : The liability to overwhelming infection of children lacking a spleen either as a result of its congenital absence or because of splenectomy, has been frequently documented. Although there have been numerous studies of the consequences of experimental splenectomy in postnatal animals, this is the first study of the effects of this operation in early fetal life. Methods : A technique is described for microsurgical removal of the spleen from fetal lambs approximately one‐third of the way through gestation, when the fetus is approximately the size of a mouse. Lambs that had been splenectomized in utero were submitted to haematological examination in postnatal life and were challenged with pneumococcal polysaccharide to test their immunological competence. Results : Lambs in which splenectomy had been performed close to the gestational age of initiation of the splenic contribution to differentiation of immune and haemopoietic systems, exhibited insignificant deviations from normality in postnatal life. Conclusion : Provided the spleen is removed from the fetal lamb sufficiently early in gestation, it is possible for other lymphoid tissues to compensate for most of the deficiencies that would be anticipated in animals lacking a spleen. In this experiment, splenectomy was performed at approximately the developmental stage equivalent to that at which the spontaneous interruption of development that leads to human congenital asplenia occurs. The absence of major postnatal abnormalities observed in these lambs reinforces the significance of the associated abnormalities in the development of the clinical deficits observed in children with spontaneous asplenia.