The history of these infections as diseases begins with the discovery of the worms and continues with the elaboration of the life cycles. P. westermani was discovered in the lungs of a human by Ringer in 1879 (193), and eggs in the sputum were recognized independently by Manson and Erwin von Baelz in 1880 (175, 193). Manson also suggested that a snail might act as an intermediate host, and a number of Japanese workers, including Koan Nakagawa, Sadamu Yokogawa, Harujiro Kobayashi, and Keinosuke Miyairi, reported on the whole life cycle in the snail Semisulcospira between 1916 and 1922 (105).
The most serious human disease caused by a larval cestode is echinococcosis, or hydatid disease, resulting from accidental infection with larval stages of the canid tapeworm, Echinococcus granulosus, which frequently occurs as an adult in dogs and as a larval cyst in wild and domesticated animals including sheep. The massive bladder-like hydatid cysts, particularly in the liver, were well known in ancient times, and there are references to such cysts in ritually slaughtered animals in the Babylonian Talmud and, in animals slaughtered for food, by Hippocrates in the fourth century BC, Arataeus in the first century AD, and Galen in the second century AD (89, 105). There are also descriptions of hydatid cysts in humans in the Corpus Hippocratorum and in the works of Galen and in later European medical texts, in which they have variously been considered to be sacs of mucus, enlarged glands, distorted blood vessels, lymphatic varices, or accumulations of lymph (89, 144). Francisco Redi in the 17th century was the first to appreciate the parasitic nature of these cysts (136, 223), but credit for the hypothesis that these cysts were the larval stages of tapeworms goes to the German clinician and natural historian Pierre Simon Pallas, who showed this in 1766 (136, 212). It was not until 1853 that Carl von Siebold demonstrated that Echinococcus cysts from sheep gave rise to adult tapeworms when fed to dogs (268), and in 1863 Bernhard Naunyn found adult tapeworms in dogs fed with hydatid cysts from a human (198, 136). There are good accounts of the history of hydatid disease by Foster (89) and Grove (105).
The Times Complete History Of The World Richard Overy Pdf 15
Our scientific understanding of malaria did not begin until the end of the 19th century following the establishment of the germ theory and the birth of microbiology, when it became necessary to discover the cause of the disease that was then threatening many parts of the European empires. The discovery of the malaria parasite and its mode of transmission are among the most exciting events in the history of infectious diseases, and this topic has been reviewed many times, particularly by Bruce-Chwatt (27), Garnham (94), Harrison (112), McGregor (170), Poser and Bruyn (218), and Wenyon (273).
While these developments were taking place, there were increasing numbers of records from virtually all species of mammals and many birds, but the nature of the parasite remained obscure until the life cycle had been worked out. The life cycle of T. gondii is a very complicated one and remained elusive until 1970, when scientists in Britain, Germany, The Netherlands, and the United States independently demonstrated that this parasite was a stage in the life cycle of a common intestinal coccidian of cats. In the most simple form of the life cycle, cats become infected when they swallow oocysts, the resistant infective stages containing sporozoites, which invade and multiply in intestinal cells, where sexual stages are produced, fertilization occurs, and oocysts are produced. However, there is an alternative life cycle. If the oocysts are swallowed by a mouse (or any other nonfeline host), multiplication occurs in the intestinal cells, but instead of sexual stages being produced there follows a disseminated infection during which resistant stages form in the brain and muscle. There is no further development in the mouse, but when the mouse is eaten by a cat, the life cycle reverts to its basic sexual pattern. Humans are infected in the same way as mice if they consume oocysts, but they can also become infected by eating any kind of meat containing the resistant forms. It is therefore not surprising that the life cycle remained elusive until William McPhee Hutchison, working in Glasgow in 1965, showed that the infectious agent was passed in the feces of cats. At the time he thought that it was transmitted with a nematode worm, as happens with the flagellate Histomonas meleagridis and the nematode Heterakis gallinarum in fowl. Hutchison subsequently identified protozoan cysts in the feces as those of a coccidian related to Isospora, a common parasite of cats (125, 126). In the meantime, other groups were following up Hutchison's 1965 observation of the presence of infectious agents in the feces of cats, and Hutchison's incrimination of the isosporan parasite of cats as T. gondii was independently confirmed by Jack Frenkel (90) and Harley Sheffield (241) in the United States, Gerhard Piekarski in Germany (216), and J. P. Overdulve in The Netherlands (210). The discovery of the T. gondii life cycle initiated a massive search for similar phases in the life cycles of other coccidian parasites, with the result that a number of protozoa that had not been properly identified were classified as stages in the life cycle of other poorly understood coccidians and that in many cases transmission depended on a predator-prey relationship (250). Humans are infected with two related parasites, Sarcocystis hominis and S. suihominis, acquired from beef and pork, respectively, and S. lindemanni, whose source is unknown. The early history of our knowledge of Sarcocystis is covered by Wenyon (273), and subsequent discoveries are described by Tadros and Laarman (250). 2ff7e9595c
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