Le « schizocoque » est une bactérie imaginée pour ironiser sur les théories bactériennes de la schizophrénie (SCZ). Au début du xx^e siècle les toxines occupaient une place importante, bactériennes et extérieures d’une part, molécules de l’auto-intoxication digestive produites par des bactéries intestinales d’autre part. La théorie de l’infection focale supposait des toxines circulantes provenant d’infections cachées. Dans les années 1920, ce concept a conduit Henry A. Cotton à laisser une trace scandaleuse dans l’histoire de la psychiatrie, en faisant opérer des centaines de malades pour rien, causant une mortalité considérable. Dans les années 1950, Walter L. Bruetsch était connu pour ses travaux sur les psychoses post-rhumatisme articulaire aigu qui ressemblaient peu à la SCZ. Henri Baruk avait, durant les années 1930, décrit des « psychoses colibacillaires » et postulé un effet catatonigène d’une toxine neurotrope d’Escherichia coli. Dans les années 1950, le Soviétique Georgy Yurevitch Malis s’opposa, surtout pour des raisons politiques, aux théories endogènes de la SCZ, génétiques ou liées à l’auto-intoxication, privilégiant une cause infectieuse externe. En 1951, il fut le premier à faire des recherches sur les virus, suivi par les Morozov qui visualisèrent un virus sans prouver son rôle étiologique. Malis nous fait remonter aux « encéphalites psychotiques chroniques » décrites par Marchand et Courtois dans les années 1930, mais récusait l’assimilation SCZ-encéphalite. La découverte des virus lents et des séquelles des virus neurotropes durant la grossesse conduisit Torrey et Peterson à s’intéresser aux « schizovirus » dans les années 1970. Évoquant les psychoses post-grippales de Karl Menninger (années 1920), ils nous rappellent les « psychoses toxi-infectieuses » de Maurice Dide en 1905–1906. Les bactéries réapparaissent depuis quelques années dans la théorie d’une modification du microbiote intestinal (dysbiose) causant un syndrome inflammatoire chronique de bas grade.

“Schizococcus” is a bacterium invented to mock the old research on a bacterial etiology of schizophrenia (SCZ). The term appeared in the 1960s, under the pen of the American sociologist August B. Hollingshead, around the time when these bacterial theories fell into disuse. At the beginning of the 20th century, the causal theories of mental illnesses gave a large part to the question of toxins. Bacterial toxins from external contamination on the one hand, molecules of digestive auto-intoxication resulting from the accumulation of toxic molecules produced by intestinal bacteria in the event of an obstacle to transit on the other (Charles Bouchard). Under the impetus of Emmanuel Régis, French psychiatry attributed an important place to these models, particularly in mental confusion, close to dementia praecox. The theory of focal infection was popular among the Anglo-Saxons, based on the idea of hidden infections without infectious symptoms but with circulating toxins. The American Henry A. Cotton popularized this concept, leaving a scandalous mark in the history of psychiatry because of a large-scale medical fraud. In the 1920s, relying on often indirect clues of the presence of sometimes commensal bacteria in the dental, ENT, genital and intestinal spheres, he operated on hundreds of patients for nothing. Although he caused considerable mortality, without any net benefit, he remained unpunished until the end of his career. In the 1950s, the American Walter L. Bruetsch was known for his work on the organic causes of psychoses. He had especially explored psychic disorders following rheumatic fever which nevertheless bore little resemblance to SCZ. His work had little impact in France, unlike that of Henri Baruk. The latter, who very quickly became versed in experimental methods and opposed psychoanalysis, had, during the 1930s, coined the term “colibacillary psychoses” and postulated a catatonic effect of a neurotropic toxin of Escherichia coli. Catatonia is now considered a syndrome transcending diagnostic categories. In fact, colibacillary psychoses did not convince psychiatrists. In the 1950s, the Soviet psychiatrist Georgy Yurevitch Malis opposed, mainly for political reasons, the endogenous theories of SCZ, genetic or linked to auto-intoxication, favoring an external infectious cause. His work on streptococci having led to disappointing results in the early 1950s, he was the first to conduct active, immunological research on viruses. He was followed shortly after by the Morozovs who visually identified a virus without proving its etiological role. Malis takes us back to the work of the French psychiatrists Marchand and Courtois on “chronic psychotic encephalitis” in the 1930s, while rejecting that SCZ is a form of encephalitis. In Western countries, the discovery of slow viruses and data suggesting the etiological role of neurotropic viruses during the prenatal period led Torrey and Peterson to take an interest in “schizoviruses” in the 1970s. Recalling the post-influenza psychoses of the American Karl Menninger (1920s), they made us rediscover the bacterial “toxic-infectious psychoses” of the Frenchman Maurice Dide in 1905–1906, which the latter subsequently left by the wayside. This partial review leaves aside the work of William Ford Robertson, Edward C. Rosenow, Vito Maria Buscaino. Bacteria, which had been in the background for some time now, have gradually reappeared over the past dozen years with the theory of a modification of the intestinal microbiota (dysbiosis) causing a chronic low-grade inflammatory syndrome. From possible causes, microorganisms have become additional risk factors.