Cardiac plexus of dogs experimentally infected with Trypanosoma cruzi: inflammatory lesions and quantitative studies

Abstract

Qualitative and quantitative aspects o f the superficial and profound cardiac plexus o f dogs experimentally infected with The pathogenesis of chagasic cardiopathy has been studied by several authors1211. Many factors seem to be involved: inflammation, autoimmunity, fibrosis and denervation18 19. For example, denervation has an important role in the pathology of the disease but is not always the main factor1314. Based on personal experience, mainly with dogs, although it has been found that chagasic cardiopathy is not counterbalanced in the acute and chronic phases, intense systematic lesions are not observed in the intracardial nervous system, mainly in its numerical reduction11.The aims of this paper are: a) to study the inflammatory phenomena, lesions and parasitism of the superficial and profound cardiac plexus of dogs experimentally infected with Be-62 and Be-78 strains of T. cruzi ', b) to carry out a quantitative study of ganglia and neuron bodies of these plexus in infected and control dogs. maintained in the laboratory, were used. Before inoculation, each animal was examined to exclude the possibility of prior T. cruzi infection. Two groups, each of four dogs, were inoculated intraperitoneally with 2000 blood trypomastigotes/ kg body weight, respectively, with Be-6217 and Be-7810 T. cruzi strains. Both strains were isolated, on different occasions, from Berenice, accepted to be the first known human patient of Chagas' disease6. Inocula were obtained from albino mice in the acute phase of infection and counted according to Brener (1962). Four normal dogs were used as controls. MATERIAL AND METHODSDogs were maintained on an ad libitum diet and observed daily. Parasitemia was assessed according to Brener4. Dogs were sacrificed about the 37th day of infection and necropsied. The atria were removed and fixed in totum in buffered formalin at pH 7.2, dehydrated, cleared and infiltrated with paraffin with the vessels in a basal position. Semi-serial sections (1:10), 4fim thick, were stained with HE and Gomori's thricromic.Ganglia were analysed in each section to determine the following aspects: inflammatory reactions, lesions and parasitism. Inflammation was classified as discreet (+ ), moderate (+ +) or intense (+ 4-+) according to the degree of cellular infiltration. Each ganglion and its neurons (normal and degenerated) were counted systematically. The number of neuron bodies per ganglia of infected dogs were compared with control dogs by Student "t" test.13

Comparison of Trypanosoma cruzi infection in dogs inoculated with blood or metacyclic trypomastigotes of Berenice-62 and Berenice-78 strains via intraperitoneal and conjunctival routes

“…Previous studies, comparing the pathogenicity between MT/CO from Berenice-62 and Berenice-78, showed higher parasitaemia and histopathological lesions in dogs infected with Berenice-78 10 . This strain, when applied intraperitoneally, also provoked more severe acute myocarditis 3 and more chronic lesions than the former 11 .…”

Heart autonomic innervation during the acute phase of experimental American trypanosomiasis in the dog.

“…Fortunately, the parasympathetic cardiac ganglia of dogs killed 37 days after inoculation with the Berenice-78 or Berenice-62 strains have been recently studied. 21 In each animal infected with the Berenice-78 strain, most (63-87%) cardiac ganglia remained free of inflammatory processes. In the great majority of the infiltrated ganglia, the inflammation was classified as discrete.…”

“…Consistent with this finding, histoquantitative studies showed no effect of the infection with either Berenice strain on the number of cardiac ganglia per dog and on the number of neurons per ganglion. 21 Therefore, the rarefaction of the AChE-positive nerve fibers now detected in the atria of the dogs killed near the end of the acute phase may result mainly from local damage of the nerve terminals. The presence of nerve trunks and branches revealed by both histochemical techniques reinforced the occurrence of damage limited to the nerve terminals.…”

Heart rate responses to a muscarinic agonist in rats with experimentally induced acute and subacute chagasic myocarditis

“…Consequently, we cannot rule out the presence or absence of morphological abnormalities of the cardiac parasympathetic neurons. Nonetheless, very recent experimental studies, carried out in different animal species, have found that despite an obvious inflammatory response in the cardiac ganglia, the parasympathetic neurons were preserved from the infective process and their number was not significantly diminished 8,9,11,15,28,39 .…”

“…Early studies showed morphologic abnormalities considered to be specifically and irreversibly caused by Trypanosoma cruzi 26,36 . However, more recent studies have found that, despite an obvious inflammatory response in the cardiac ganglia, the parasympathetic neurons were preserved from the infective process 8,9,15,28 .…”