Concomitant infections are common in nature and often involve parasites. A number of examples of the interactions between protozoa and viruses, protozoa and bacteria, protozoa and other protozoa, protozoa and helminths, helminths and viruses, helminths and bacteria, and helminths and other helminths are described. In mixed infections the burden of one or both the infectious agents may be increased, one or both may be suppressed or one may be increased and the other suppressed. It is now possible to explain many of these interactions in terms of the effects parasites have on the immune system, particularly parasite-induced immunodepression, and the effects of cytokines controlling polarization to the Th " or Th # arms of the immune response. In addition, parasites may be affected, directly or indirectly, by cytokines and other immune effector molecules and parasites may themselves produce factors that affect the cells of the immune system. Parasites are, therefore, affected when they themselves, or other organisms, interact with the immune response and, in particular, the cytokine network. The importance of such interactions is discussed in relation to clinical disease and the development and use of vaccines.

Malaria is caused by infection with protozoan parasites belonging to the genus Plasmodium transmitted by female Anopheles species mosquitoes. Our understanding of the malaria parasites begins in 1880 with the discovery of the parasites in the blood of malaria patients by Alphonse Laveran. The sexual stages in the blood were discovered by William MacCallum in birds infected with a related haematozoan, Haemoproteus columbae, in 1897 and the whole of the transmission cycle in culicine mosquitoes and birds infected with Plasmodium relictum was elucidated by Ronald Ross in 1897. In 1898 the Italian malariologists, Giovanni Battista Grassi, Amico Bignami, Giuseppe Bastianelli, Angelo Celli, Camillo Golgi and Ettore Marchiafava demonstrated conclusively that human malaria was also transmitted by mosquitoes, in this case anophelines. The discovery that malaria parasites developed in the liver before entering the blood stream was made by Henry Shortt and Cyril Garnham in 1948 and the final stage in the life cycle, the presence of dormant stages in the liver, was conclusively demonstrated in 1982 by Wojciech Krotoski. This article traces the main events and stresses the importance of comparative studies in that, apart from the initial discovery of parasites in the blood, every subsequent discovery has been based on studies on non-human malaria parasites and related organisms.

The subkingdom Protozoa now inclues over 65,000 named species, of which over half are fossil and approximately 10,000 are parasitic. Among living species, this includes approximately 250 parasitic and 11,300 free-living sarcodines (of which approximately 4,600 are foraminiferids); approximately 1,8000 parasitic and 5,100 free-living flagellates; approximately 5,600 parasitic "Sporozoa" (including Apicomplexa, Microspora, Myxospora, and Ascetospora); and approximately 2,5000 parasitic and 4,700 free-living ciliates. There are undoubtedly thousands more still unnamed. Seven phyla of PROTOZOA are accepted in this classification--SARCOMASTIGOPHORA, LABYRINTHOMORPHA, APICOMPLEXA, MICROSPORA, ASCETOSPORA, MYXOSPORA, and CILIOPHORA. Diagnoses are given for these and for all higher taxa through suborders, and reporesentative genera of each are named. The present scheme is a considerable revision of the Society's 1964 classification, which was prepared at a time when perhaps 48,000 species had been named. It has been necessitated by the acquisition of a great deal of nex taxonomic information, much of it through electron microscopy. It is hoped that the present classification incorporatesmost of the major changes that will be made for some time, and that it will be used for many years by both protozoologist and non-protozoologists.

Humans are hosts to nearly 300 species of parasitic worms and over 70 species of protozoa, some derived from our primate ancestors and some acquired from the animals we have domesticated or come in contact with during our relatively short history on Earth. Our knowledge of parasitic infections extends into antiquity, and descriptions of parasites and parasitic infections are found in the earliest writings and have been confirmed by the finding of parasites in archaeological material. The systematic study of parasites began with the rejection of the theory of spontaneous generation and the promulgation of the germ theory. Thereafter, the history of human parasitology proceeded along two lines, the discovery of a parasite and its subsequent association with disease and the recognition of a disease and the subsequent discovery that it was caused by a parasite. This review is concerned with the major helminth and protozoan infections of humans: ascariasis, trichinosis, strongyloidiasis, dracunculiasis, lymphatic filariasis, loasis, onchocerciasis, schistosomiasis, cestodiasis, paragonimiasis, clonorchiasis, opisthorchiasis, amoebiasis, giardiasis, African trypanosomiasis, South American trypanosomiasis, leishmaniasis, malaria, toxoplasmosis, cryptosporidiosis, cyclosporiasis, and microsporidiosis

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Mice which had been pre-treated with killedCorynebacterium parvumgiven intravenously or intraperitoneally, but not subcutaneously, were completely resistant ot infection withBabesia microtiorB. rodhaini, and protected from death caused byPlasmodium vinckeiorP. chabaudiinfection. There is evidence that the parasites died within circulating erythrocytes. This occurred much too soon for a specific antibody response to be evoked, and no antibody could be detected by the indirect fluorescent-anitbody technique. Thus it is suggested that a non-secific soluble mediator may play an important role in the protection observed.

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