462 BARBARA SMITH

REFERENCES BUTLER, M., AND LEACH, R. H. . EATON, M. D . . . . . . . . LAUGHTON,NANCY . . . . . MACPHERSON, I. . . . . . . PEASE, PHYLLIS . . . . . . PEASE, MLIS, AND LAUGHTON,

NANCY ,, ,,

ROGERS, K. B., AND HESLOP, W. . SHEDDEN, W. I. H., AND COLE, B. C. STIM, T. B., GRACE, J. T., JR, AND

MOORE, G. E.

1964. 1965. 1963. This Journal, 85, 413. 1966. 1965. 1962. Ibid., 27, 383.

J . Gen. Microbiol., 34, 285. A . Rev. Microbiol., 19, 379.

J. Cell Sci., 1, 145. J. Gen. Microbiol., 41, 299.

1965. Zbid., 41, 293. 1947-48. J. Clin. Path., 1, 315. 1966. Nature, Lond., 210, 868. 1963. Bact. Proc., 22, 134.

THE MYENTERIC PLEXUS IN CHAGAS’ DISEASE

BARBARA SMITH Department of Pathology, St Bartholomew’s Hospital, London

PLATES CXLII AND CXLIII

K~BERLE (1963) has shown that the megacolon associated with South American trypanosomiasis (infection with Trypanosoma cruzi) has a marked diminution in the number of neurones in Auerbach’s plexus. The myenteric plexus has not been widely studied pathologically, and as there appears to be a fairly specific destruction of ganglion cells in this condition, histological appearances could serve as a reference pattern for other varieties of megacolon in which the pathogenesis is not so clear.

MATERIAL AND METHODS

Two specimens of sigmoid colon, both removed surgically, were available; both showed gross enlargement (one, case A, 25 cm. long by 18 cm. circumference, the other, case B, 22 cm. long by 16 cm. circumference). The muscle coats were thickened and the mucosal surface was smooth without haustration.

Eight paraffin and eight frozen blocks were taken from each specimen. The paraffin blocks were cut perpendicular to the surface in the usual way. The frozen blocks were cut parallel to the plexus by placing a flat piece of gut wall, mucosal surface down, on the tissue holder of the microtome as described previously in a study of Hirschsprung’s disease (Smith, 1967). In this way the plexus is shown flat in the plane of section and it is possible to demonstrate its anatomy both in normal and in pathological cases by silver impregnation.

RESULTS

Paraffin sections of these two cases showed in case A a few remaining ganglion cells and some infiltration of the circular muscle with chronic inflammatory cells. Case B showed no ganglion cells in any section and no inflammatory cells were seen. The muscle coats were thickened but the mucosa was normal. There was no evidence of ischaemia such as might have been produced by a partial volvulus.

SMITH PLATE CXLII

MYENTERIC PLEXUS IN CHAGAS’ DISEASE

FIG. ].-The myenteric plexus in the rabbit. It shows groups of ganglion cells joined by small trunks. Branches, often containing only a single axon, are given off to the muscle coats on either side. Cholinesterase technique. X 55.

FIG. 2.-The myenteric plexus in the normal human adult. Only a small part can be seen in a photograph as the axons pass out of the plane of focus, but the pattern is the same as in the rabbit. Schofield’s silver impregnation method. X 90.

MYENTERIC PLEXUS IN CHAGAS’ DISEASE

PLATE CXLIII

FIG. 3.-The myenteric plexus in case A. The pattern remains, but there are fewer axons and no ganglion cells visible. Schofield. ~90.

FIG. 4.-A single wandering fibre in the inner muscle coat in case A. This continued for a considerable distance with a number of bends, quite unlike the normal short straight muscular branches. Schofield. x 550.

MYENTERIC PLEXUS IN CHAGAS DISEASE 463

In the normal large gut the anatomy of the myenteric plexus is very regular in spite of its complexity. It consists of groups of neurones joined by branches con- taining a small number of rather widely spaced straight axons and at an angle to these axons, branches, usually consisting of only a single fibre, supply the two muscle coats (figs. 1 and 2).

Silver impregnations (Schofield, 1960) confirmed that in both cases there was considerable reduction in the number of ganglion cells. A 100p section cut parallel to the gut wall may show up to two hundred times the amount of plexus seen in a 5p paraffin section cut the other way, so that a few remaining neurones may not be seen in the latter. In the areas in which the ganglion cells were absent, there was in some no plexus either, but in others anatomically normal plexus with a reduced number of axons and no neurones was seen (fig. 3). An additional feature was the presence of fine long regenerating fibres, which were single and followed no anatomical pattern, but wandered in and out of the muscle coats for very consider- able distances (fig. 4). Retraction balls, which are sometimes seen in gut distended behind an obstruction, were not observed.

DISCUSSION The features seen in these cases are explicable on the grounds of neurotoxic

damage by the parasite, which destroys many ganglion cells together with their axons. Since the neuronal destruction is not complete, parts of the plexus, which are derived from intact cells above and below, remain. It is also possible that some of the fibres are extrinsic. The presence of fine wandering regenerating fibres occurs in skeletal muscle in response to partial denervation. It is an attempt on the part of the remaining neurones to supply the deficit and these fibres, lacking end-plates, may wander well away from the motor point. The same process is probably occurring in the gut wall.

The changes in the myenteric plexus in acquired idiopathic megacolon have not been described. If there is ganglion cell fall-out in this condition, comparison with the pathology of Chagas’ disease might help to elucidate the mechanism of the impaired function.

SUMMARY The megacolon of Chagas’ disease shows reduction of axons and neurones in

the myenteric plexus, with evidence of regeneration in the form of long fine single nerve fibres.

I am grateful to Mr Ferreira-Santos of S o Paolo for the gift of the material. Mr P. Crocker took the photographs.

REFERENCES K~BERLE, F. . . . . . . . 1963. Gut, 4, 399. SMITH, BARBARA . . . . . . 1967. Ibid., 8,308. SCHOFIELD, G. C. . . . . , . 1960. Brain, 83,490.