All issues > Volume 29(12); 1986

Original Article

J Korean Pediatr Soc. 1986;29(12):1295-1308. Published online December 31, 1986.

Experimental Diphtheritic Myocarditis with Special Reference to Ultrastructural Changes.

Hyo Seop Ahn¹

¹Department of Pediatrics, college of medicine, Seoul, National University,Korea.

Abstract

Myocardiopathy following diphtheria infection is one of the most serious and fatal complications, but its nature of the lesion remained in controversy, and even ultrastructural understanding on the direct effect of diphtheria toxin has not been clarified. The purpose of this experiment is to illustrate the full morphological spectrum of subclinical or EKG free diphtheritic myocardial injuries by administration of small (sublethal) amount of diphtheria toxin to New Zealand white rabbits. Animals were divided into 2 groups with subcutaneous injection of 0.4 MLD/kg and 1.2 MLD/kg of diphtheria toxin respectively, and their myocardial injuries were subsequently investigated with a period of 1,3,5,10,20,30 and 50 days under the light and electron microscopies. 1) The myocardiopathy was represented by both degenerative and inflammatory processes in myocardial fibers, regardless its extents of histological severity, and so was in healthy myocardium by light microscopy. 2) By small dose administration, patchy loss of cross striation, focal myocytolysis and fatty changes started to appear 24 hours after injection, and they persisted till the 50th day. Myocardial edema and congestion followed the similar sequence, but seemed regressed slowly. 3) Similar myocardial changes were appreciated in the large dose administration. 4) Inflammatory exudative changes as a tissue reaction against the degenerated myocardial fibers appeared from the first day, but tended to diminish by the 30th day in the small dose group, whereas in the large dose group cell infiltration persisted. 5) Ultrastructural changes appeared from the myocardial fibers adjacent to the interstitial capillaries, being characterized by disruption of mitochondria and vesicular dilatation of ER; irregular contraction, disintegration and dissolution of myofibrils were subsequent associations together with fatty degeneration and lysosomal increase. Reduced glycogen granules and detachment of ribosome followed thereafter. 6) Presence of fibrin thrombi in a few animals suggested the development of disseminated intravascular coagulopathy. With the above findings, it is assumed that subclinical myocardial damage induced by diphtheria toxin manifests with both degenerative and inflammatory processes as a consequence of mitochondrial and endoplasmic reticular damages, and persists for a period of time.

Keywords :Diphtheria;Myocarditis; Ultrastructural change