The Pathogenicity of Entamoeba histolytica: Is Heat Stress a Factor?

THE PATHOGENICITY OF ENTAMOEBA HISTOLYTICA: IS HEAT STRESS A FACTOR? HARRY WESSENBERG* Introduction Despite a century of investigation, amoebic dysentery remains one of the most baffling diseases that afflicts mankind. The causative organism , Entamoeba hbtolytica, has a worldwide distribution and infects at least 10 percent of the human population [1], but only about 2 percent suffer symptoms of amoebic dysentery [2]. Why the amoebae become tissue invaders in some hosts and remain commensals in others has never been satisfactorily explained. The life cycle of E. histolytica has been thoroughly understood for 6 decades, and it is basically similar to those of the related amoebae that live in the human intestine. They occupy the deep crevices of the lumen of the large intestine, where they feed on bacteria and multiply by fission. At more or less regular intervals some members ofthe population encyst and are swept out with evacuation of host feces. New hosts are infected by ingesting foods or beverages containing viable cysts. Excystation occurs in the stomach or small intestine, and the emerging amoebae ultimately reach the host large intestine, where they attempt to establish new colonies. The mysterious and sinister aspect of this relationship is that in some hosts E. histolytica stops feeding on bacteria, and these transformed amoebae penetrate into the intestinal mucosa, ingest red blood cells, and increase in size. Destruction of the epithelium and underlying tissues ulcerates the intestinal wall. Some amoebae may enter the circulation and be carried to the liver and other organs, where further tissue destruction results. Such invasion and destruction of host tissues is suicidal for the amoebae, because these reckless invaders do not form cysts and thus leave no progeny to infect new hosts. If the amoebae should kill the host, then all perish together. Among the intestinal amoebae, this aberrant behavior occurs only in E. hhtolytica, and from an evolu- ?Department of Biology, San Francisco Stale University, San Francisco, California 94132. 1 thank Drs. Dorothy Pitelka and William Balamuth for comments and suggestions. 250 I Harry Wessenberg · Entamoeba histolytica tionary point of view one would conclude that invasive amoebae must be self-exterminating. Then one is faced with the paradox that invasive amoebae must always arise from noninvasive amoebae. Current Explanations of Tissue Invasion There are three hypotheses for this peculiar bahavior: (1) differences in virulence of various strains of Entamoeba histolytica; (2) influence of the intestinal bacteria on virulence; and (3) deficiencies in host diet that increase host susceptiblity. Studies on virulence in E. hhtolytica have been based on the premises that virulent strains ought to be tissue invaders, avirulent strains ought to be commensals, and these differences should be inherited consistently . A small nonpathogenic species that in other respects exactly resembles E. hhtolytica has been named E. hartmanni [3]. This species is reported present in many asymptomatic carriers [4-6], but since other symptomless carriers are infected with E. hhtolytica or with both species, the problem of virulence in£. hhtolytica remains unsolved. Much experimental work on the constancy of strain virulence was performed with laboratory animals such as kittens, rats, and guinea pigs, where the disease never corresponds exactly to the human disease, and many infections were induced by unnatural methods. Some of these experiments showed that neither virulence nor size is a constant character in E. histolytica , and size is not constant in E. hartmanni [7-12]. The classic work of Walker and Sellards [13] on experimental human amoebiasis is still an important source of information. They infected male volunteers from Bilibid prison in Manila. In a group of 20 prisoners , 16 were fed gelatin capsules containing stool bacteria and cysts ofE. hhtolytica obtained from asymptomatic carriers; four were fed capsules containing stool bacteria and large trophozoites from active cases of amoebic dysentery. (Cysts are not passed in active cases.) Among the 16 fed cysts, 15 became infected and four developed dysentery; among the four fed trophozoites, three became infected but none developed symptoms. Thus some of the cysts from asymptomatic carriers , when introduced into new hosts, produced amoebae that became invasive, while the invasive trophozoites lost their invasiveness in new hosts. The majority of those infected failed to develop any symptoms of amoebic dysentery. Therefore...