134 Syphilis

Syphilis or, more properly, venereal syphilis is a chronic communicable disease, which, until the ac­quired immunodeficiency syndrome emerged in the early 1980s, was the most serious and dreaded of the so-called sexually transmitted diseases (STD) - formerly, venereal diseases (VD).

Syphilis develops naturally through three clinical stages (primary, secondary, and tertiary or late), each separated by a Subclinical period. Of the sub- clinical periods, the one between the secondary and tertiary stages (latent syphilis) is the most pro­nounced. Clinical manifestations of syphilis are ex­tremely protean, and capable, at the tertiary stage, of affecting any system of the human body.

Syphilis took its name from Girolamo Fracastoro’s well-known poem, Syphilis, siυe morbus gallicus (1530), in which the Italian humanist-physician in­vented this phrase to name the disease then known all over Europe as morbus gallicus. However, the term syphilis did not become widely used until the late eighteenth century, and that usage was vague and applied to many other symptoms besides those of venereal syphilis until the development of the germ theory in the late nineteenth and early twenti­eth centuries.

Distribution and Incidence

Unlike human nonvenereal treponematoses (pinta, yaws, and endemic syphilis), venereal syphilis has managed to establish a worldwide distribution, al­though its incidence patterns are somewhat differ­ent in developed and developing countries.

The incidence of syphilis, for example, has continu­ously declined in the Western world since the 1860s, although major wars have momentarily interrupted this trend. After the Second World War, late and congenital syphilis almost disappeared, mainly as a result of public health measures and penicillin. Since the 1950s, however, both primary and secon­dary syphilis have steadily increased (nearly 29,000 cases in the United States in 1984) with its peak incidence in the 15- to 34-year age group. A strik­ingly high male/female ratio (2.6:1 in the United States in 1983) is due to a considerable incidence of syphilis in male homosexuals. In 1980, 58 percent of all syphilitic men in England were homosexuals as were 50 percent in the United States (Csonka 1987; Holmes and Lukehart 1987).

In developing countries, syphilis continues to be a widespread disease, although interpretative prob­lems of serologic tests for syphilis make it difficult to estimate the numbers of infected people in those regions. Syphilis is increasing in areas where yaws was previously endemic, such as tropical and equato­rial America and Africa, and Southeast Asia. In­fected prostitutes seem to play an important role in the spread of syphilis in these areas, most noticeably in the Far East. The risk of congenital syphilis con­tinues to be considerable in many developing coun­tries, resulting in fetal wastage, neonatal mortality, and infant morbidity (WHO 1986; Csonka 1987).

Etiology and Epidemiology

Although syphilis is transferred predominantly by sexual contact, it may also be transmitted in nonsex- ual ways, such as by close contact with either an open lesion of early syphilis or infected fomites, by

Table VIII. 134.1. Etiology, epidemiology, and clinical manifestations of the human treponematoses

“Because the nonvenereal treponematoses are usually acquired in childhood, and because treponemal bacteremia ceases with time, only in adult-onset venereal syphilis is there any likelihood of a mother giving birth to an infected child.

infection of an unborn infant in utero, and by trans­fusions of infected blood.

As noted above, T. pallidum, the causal agent of syphilis, is a member of the order Spirochetales. This order of bacteria includes three genera patho­genic for humans and several other animals: (1) Borrelia, responsible for Vincent’s angina (Borrelia recurrentis), relapsing fever (Borrelia υincentii), and Lyme disease (Borrelia burgdorferi)-, (2) Leptospira, which causes human leptospirosis; and (3) Trepo­nema, responsible for a group of diseases known as treponematoses (Holmes and Lukehart 1987).

The Treponema genus includes several pathogenic species and subspecies responsible for four different human diseases: (1) pinta, a Central and South American disease, which affects the skin, caused by Treponema carateum; (2) yaws, a disease of skin and bones occurring in rural populations of the humid tropics, caused by Treponema pallidum subspecies pertenue; (3) endemic syphilis, similar to yaws, but found only in warm, arid climates, and caused by T. pallidum subspecies endemicum; and (4) venereal syphilis, which has no climatic restrictions and may affect any tissue of the body including internal or­gans, and is caused by T. pallidum subspecies pal­lidum. These and other major features concerning the human treponematoses are indicated in Table VΠI.134.1. Surprisingly, in spite of the differenti­ated (both clinically and epidemiologically) disease entities they produce, these four treponemes cannot be morphologically distinguished from one another. Moreover, they elicit the same immunologic reac­tions, and are all susceptible to penicillin (Hackett 1963; Perine et al. 1984; Csonka 1987).

Almost from the time of Columbus’s arrival in America, but particularly from the European En­lightenment, the uncertain geographic and histori­cal origins of syphilis have been the object of schol­arly controversy (Guerra 1987).

For E. H. Hudson, the most outstanding defender of Unitarian theory, there is only one treponema- tosis, although it assumes different clinical patterns under different epidemiological conditions. Thus, the changing physical and sociocultural environ­ment of human beings has caused treponematosis to change into one or another of those four different clinical syndromes already mentioned: pinta, yaws, endemic syphilis, and syphilis. From the Unitarian viewpoint, then, it does not make sense to talk about transmission of syphilis from the New World to the Old, or vice versa (Hudson 1965).

By contrast, C. J. Hackett, the main upholder of nonunitarian theory, maintains that the clinical va­riety of human treponematoses is probably due to mutational changes in the treponemal strains them­selves. His thesis is that successive mutations have been responsible for the different human treponema­toses starting from a lost ancestral animal trepo­nematosis. The earliest of the treponematoses seems to have been pinta, which might have extended from Africa and Asia into America about 15,000 B.C.; that is, during the last part of the last glaciation and before the subsequent melting of the polar icecaps that formed the Bering Strait.

By about 10,000 B.C., a warm humid environment caused either the pinta treponemes themselves (hy­pothesis A) or the lost ancestral animal treponemes (hypothesis B) to mutate in Afro-Asia, bringing forth yaws, a disease that extended through Africa, Southeast Asia, and eventually Australia and the Pacific islands, but that did not reach the Americas.

Around 7000 B.C., in the warm arid climates that developed after the last glaciation, another muta­tion occurred, this time from yaws to endemic syphi­lis. The latter appeared in northern and Saharan Africa, southwestern and central Asia, and central Australia, whereas yaws itself remained unchanged in the warm and more humid climates.

Finally, about 3000 B.C., the development of large

Figure VΠI.134.1. Two hypotheses as to the possible evo­lution of the organisms responsible for human treponema­toses (according to C. J. Hackett 1963, 25). [From C. J. Hackett. 1963. On the origin of the human treponema­toses (pinta, yaws, endemic syphilis, and venereal syphi­lis). Bulletin of the World Health Organization 29: 7-41.]

urban areas and the increasing use of clothing in the eastern Mediterranean and southwestern Asia be­came selective agents for still another mutation as syphilis changed from a nonvenereal disease of rural children (endemic syphilis) to a venereal disease of urban adults (venereal syphilis). According to Hack­ett, at any rate, by the first century B.C., as Figure VIII. 134.1 indicates, syphilis had spread throughout the Mediterranean. He suggests, however, that this early venereal syphilis was a “mild” form of the disease, which may explain why there is no evidence of the illness in Europe before the end of the fif­teenth century, when a new successful treponeme mutation - probably favored by environmental and social conditions in congested European cities at that time - gave rise to a far more serious disease. Initially extremely virulent, this form of syphilis is supposed to have become progressively less destruc­tive from around the 1530s onward (Hackett 1963). As will be discussed below, however, still other schol­ars trace the sudden epidemic of venereal syphilis to the post-Columbian importation of an American parasite to Europe, and thence to Asia and Africa.

Immunology

There is no natural immunity to infection by patho­genic treponemes. However, “only about 50 percent of the named contacts of primary and secondary syphi­lis become infected,” and 25 percent after a single exposure. The chance of infection is influenced - in undefined proportions - by sexual and hygienic prac­tices, inoculum size, environmental and body tem­perature, and other factors.

Acquired immunity is related to inoculum size and duration of infection prior to treatment. In­tradermal inoculation of T. pallidum usually causes primary lesions and serologic response in those who have previously been treated for early syphilis. By contrast, it produces no symptoms or responses in those with untreated latent syphilis, or in those pre­viously treated for late latent (more than 1 year’s duration) syphilis (Holmes and Lukehart 1987).

Clinical Manifestations and Pathology

When William Osler asserted that “who knows syphilis, knows medicine,” he was doing no more than stressing the extreme clinical variety of this disease, which is capable of affecting any system of the human body. As noted previously, the natural course of venereal syphilis includes three consecu­tive clinical stages, each stage separated by a latent period with no visible signs of infection (Perine et al. 1984; Csonka 1987; Holmes and Lukehart 1987).

Primary Syphilis

T. pallidum penetrates intact mucous membranes and abraded skin. After an incubation period rang­ing from 2 to 6 weeks (average 3 weeks), the primary lesion — the chancre - appears at the site of entry, it is a single, small, and painless ulcer with undurated edges, usually appearing in the genitalia (penis, vulva, labia, cervix) and, less frequently, in other regions such as the anus, mouth, buttocks, and fin­gers. Chancres of the penis and vulva are usually accompanied by moderate bilateral enlargement of inguinal lymph nodes. The chancre heals spontane­ously over a period of 2 to 6 weeks.

Secondary Syphilis

In most patients, after a brief latent period (6 to 8 weeks), there is a secondary clinical stage character­ized by the appearance of disseminated lesions on the skin and in the internal organs. In women, these lesions are often the first overt clinical sign of syphi­lis. Secondary lesions consist of a symmetrical, evolu­tive, and painless rash, very variable in appearance and localization, and usually accompanied by fever, malaise, aches in the bones (often worse at night), and generalized enlargement of lymph nodes. After a few weeks - generally 2 to 6 - secondary lesions and symptoms spontaneously disappear. In 25 per­cent of untreated patients, however, there is a recur­rence of secondary lesions during the first 2 years of infection.

Tertiary or Late Syphilis

The tertiary stage develops only in about one-third of untreated cases, and only after another latent period lasting from 1 to 20 years, or even longer. This stage is characterized by progressively destruc­tive lesions of the skin and mucous membranes, bones, and internal organs. The most typical lesion is the gumma, a small rubbery tumor that is a be­nign manifestation of tertiary syphilis, which can develop in any part of the body.

Particularly serious forms of late syphilis involve the cardiovascular and central nervous systems. Cardiovascular syphilis may cause aneurism of the thoracic aorta, and dilatation of the aortic valve. Neurosyphilis includes a loss of positional sense and sensation (tabes dorsalis, locomotor ataxia) or a form of insanity (general paresis [GPI], dementia paralytica).

As a result of the introduction of antibiotic ther­apy, tertiary syphilis has almost disappeared. Thus the most reliable information available on it today has been provided by two major studies on the course of untreated syphilis, the Oslo Study (1891-1951) and the Tuskegee Study (1932-72). The former sur­veyed retrospectively a group of nearly 2,000 pa­tients with primary and secondary syphilis diag­nosed clinically before immunologic tests came into use. The latter studied prospectively 431 black men with seropositive latent syphilis of 3 or more years’ duration, who were deliberately kept untreated. Be­cause of the ethical issues raised by this racist experi­ment, the Tuskegee Study has been crucial in formu­lating the present guidelines concerning medical ex­perimentation on humans (Jones 1981; Holmes and Lukehart 1987).

Congenital Syphilis

The risk of congenital syphilis to the fetus is high during the first 2 years after the mother has ac­quired the infection. An infected fetus may die dur­ing pregnancy, be stillborn, or be bom prematurely. Secondary-type lesions are present at birth or ap­pear within the first 6 months of life (Perine et al. 1984; Csonka 1987; Holmes and Lukehart 1987).

History and Geography

Medical historiography has in the past usually iden­tified the disease known today as venereal syphilis with the morbus gallicus that was mentioned for the first time in European medical and lay writings of the late fifteenth century. Indeed, nineteenth- and twentieth-century medical historians, in looking at past medical and lay descriptions of morbus gallicus, have systematically practiced a retrospective diagno­sis of syphilis.

According to them, the history of syphilis began with the eruption of morbus gallicus in Europe in the 1490s, and can be traced throughout the centu­ries until today, although neither its geographic ori­gins nor the precise date of its appearance has been established. Since the European Enlightenment, both of these questions have been the object of a continuous - and often tart - controversy between the defenders of an American origin of syphilis and those who have claimed that syphilis did exist in the Old World long before Columbus arrived in the New World. The most varied documental proofs (medical and lay writings, iconography) and - increasingly since the late nineteenth century - material proofs (paleopathological remains) have been wielded in this debate. It is an unfinished debate, however, for in claiming that present-day venereal syphilis was already known and had been described under sev­eral names before or after the Europeans’ arrival in America, historians have produced the kind of con­tradictory conclusions that serve only to keep it alive (Guerra 1978; Wood 1978).

A second way of approaching the history of syphi­lis has already been referred to in the section on the etiology and epidemiology of syphilis. This approach lies in studying the disease and the germ responsi­ble for it in the broad biological and epidemiological context of the development of human treponema- toses, and integrates results provided by both paleo­pathological and historicoepidemiological studies. A result of this approach has been some attractive and promising hypotheses on the history of syphilis, but at the moment, no definitive conclusions have

Figure VIIL 134.2. Infectious diseases considered as a dy­namic triangular interaction among host, parasite, and environment (according to E. H. Hudson, 1958, 8-9.) (Adapted from E. H. Hudson. 1958. Non-Venereal syphi­lis. Edinburgh-London.)

been reached (Hackett 1963; Hudson 1965; Wood 1978).

Given these circumstances, a third approach seems appropriate, which actually deals with the history of the concept of syphilis, rather than with the history of the disease itself. This third way renounces retrospec­tive diagnosis of syphilis and insists on the need to contemplate the disease entity called syphilis within the strict historicocultural context in which it occurs, and from which it receives its true significance. Put plainly, every disease entity is an intellectual con­struction that is peculiar to some form of medicine; and every form of medicine is nothing but a historical variable in any human community. Thus the disease entity known today as venereal syphilis can be con­ceived of, at this point, as a paradigmatic example as was demonstrated by a Polish microbiologist, Ludwik Fleck, in the mid-1930s in a monograph in which there has been renewed interest since the late 1970s (Fleck 1979).

Furthermore, in looking at what we call infectious diseases, we must distinguish between what may be termed disease entities and the diseases themselves. As disease entities, infectious illnesses assumed their present shape only in late nineteenth- and early twentieth-century Western medicine as a re­sult of the development of germ theory. But as dis­eases in themselves they have existed for a long time.

Infectious diseases, moreover, cannot be regarded ontologically as natural beings in the same way as the microbiological agents that cause them can be regarded (Reznek 1987). Rather, as Hudson (1958) has demonstrated, in the case of human treponema- toses, they should be considered the result of a dy­namic interaction among host, parasite, and environ­ment, as portrayed in Figure VΠI. 134.2. Moreover, any such interaction that has occurred in the past can neither be reproduced under experimental condi­tions, nor be easily reconstructed historically.

To be precise, venereal syphilis took shape in West­ern scientific medicine only as a result of deep changes, both intellectual and social, during the sec­ond half of the nineteenth and the first decade of the twentieth century; foremost among these changes was the formulation of germ theory. Yet an exhaus­tive bibliographical survey on venereal diseases done by J. K. Proksch in 1889-1900 makes clear that the term syphilis, though invented by Fracastoro in the sixteenth century, did not become widely used until the late eighteenth or early nineteenth century. So, it may be anachronistic to refer to as syphjlis either the disease entity that we call “venereal syphilis” before the late nineteenth or early twentieth century, or a disease entity named “syphilis” before the late eigh­teenth or early nineteenth century.

Let us now consider the origins, emergence, and development of the concept of syphilis. Our depar­ture point will be the disease entity that began to be called morbus gallicus in late fifteenth-century Eu­rope. Although for the above-mentioned reasons we cannot agree with those who have identified morbus gallicus with syphilis, it is obvious that the former may well be considered the earliest identifiable con­ceptual ancestor of the disease entity that we now call venereal syphilis (Fleck 1979).

1400—1600

Morbus gallicus is the name that soon became domi­nant in designating a disease generally considered as new in Europe of the 1490s. It was perceived as an incurable and loathsome disease consisting of se­vere aches in the bones, and of sores usually begin­ning in the genitals, but eventually covering most or all of the body. Contemporary medical and lay evi­dence concurred in including it among the numerous calamities (floods, earthquakes, epidemics, famines, wars) that Europeans - especially Italians - suffered at the end of the fifteenth century.

Italian sources show us that the “French Pox” spread in Italy during the period 1494-5, after the clash between the armies of France and Spain over the question of the kingdom of Naples. The notoriety the phrase morbus gallicus soon achieved all over Italy was closely associated with the tragic conse­quences of the impact of the French invasion on the fragile Italian political equilibrium. Similarly, the prompt acceptance in early sixteenth-century Italy of the theory of an American origin for morbus gal­licus may be explained by the fact that Spaniards were regarded as the newest barbari Stranieri to devastate Italy. The great prestige of Renaissance Italy and its cultural hegemony throughout Europe were important factors, among others, in ensuring the rapid popularization of both the term morbus gallicus and the theory of its American origin.

Through the sixteenth century, the phrase “French Pox” achieved in Europe and overseas an overwhelm­ing dominance over any other names for the disease, not only in the medical academic world, but also at popular levels. Only French physicians - those na­tive to or settled in France - seem, understandably, to have rejected this name, and put forth others. For example, in 1552 Thierry de Hery of Paris suggested maladie venerienne or grosse υairolle; in 1553 Auger Ferrier of Toulouse proposed pudendagra or lues his­panica; in 1560 Antoine Chaumette of Paris put forth the denomination morbus υenereus; and in 1563 Leo­nardo Botallo, also of Paris, used the term lues venerea, as did Jean Fernel in posthumous publica­tion in 1579.

1600-1750

During the seventeenth century this new term, lues venerea (venereal disease), was adopted all over Eu­rope, sharing an ex aequo leadership with that of morbus gallicus. In eighteenth-century Europe the term “lues venerea” eventually superseded that of morbus gallicus, and the use of the latter declined dramatically.

Two points may be raised about the expression lues venerea. First, the adjective “venerea” stresses the direct relationship existing between the French Pox and the pleasures of Venus and, thus, the individ­ual responsibility of those who contract the disease. Applied to the morbus gallicus, this adjective seems to have appeared for the first time in 1527 in a work by French physician Jacques de Bethencourt, enti­tled Nova poenitentialis Quadragesima, nec non Purgatorium in Morbum Gallicum sive Venereum. Both the title and contents of this book evoke the climate of religious exaltation and of moral rearma­ment present in Reformation Europe (Temkin 1977). The second point has to do with the name “lues,” which underscores the perception of the disease, at that time, as a contagious and calamitous one from a physical, and even from a moral, viewpoint.

A good example of the dominance exerted by the expression “lues venerea” on eighteenth-century Eu­ropean university medicine is offered to us by an influential work of the French royal physician Jean Astruc, De Morbis Veneris, published in 1736, which was reissued many times and translated into a great

number of European languages before the end of the nineteenth century. The work argues that the lues venerea was caused by a unique and specific virus venereum. It treats the particular morbi venerei as species making up the genus Lues venerea, and it differentiates between lues venerea incipiens and con­firmata. The first was composed of different morbi venerei (gonorrhea, hernia venerea, bubones ven­erei, caries pudendorum, and porri, among others); whereas the second, the lues venerea confirmata, also called morbus venereus universalis, comprised numerous complaints affecting the whole human body. Among these were morbi genitalium, vitia cutis, morbi oris et narium, dolores venerei, morbi ossium, tumores, glandulosi et lymphatici, oculorum morbi, morbi aurium, and Iesiones functionum.

1750-1850

Whether venereal disease was caused by an ani­mated contagion or by a chemical poison, until the mid-eighteenth century almost every intellectual stream in European academic medicine seems to have defended the unity of lues venerea on the basis of a unique and specific virus venereum. How­ever, after 1750 the concept of lues venerea began to be challenged as a result of nosographic and nosological efforts made by Enlightenment patholo­gists, who (with the support of clinical observations, anatomopathological analyses, and inoculation ex­periments) began to question whether lues venerea was a single disease entity after all. The result of this challenge was the progressive disappearance of the expression lues venerea from the literature. And although it did not entirely disappear until the nineteenth century, it was increasingly replaced by the plural expression morbi venerei (venereal dis­eases), which began to be used at the beginning of the eighteenth century. At about the same time, specific denominations given to each one of the “morbi venerei” (chancre, gonorrhea, bubo, and syphilis, among others) started to appear with in­creasing frequency. From the early nineteenth cen­tury, the number of medical works specifically de­voted to certain among these diseases - mainly to gonorrhea and syphilis - began to proliferate.

Let us look in more detail at how the concept of lues venerea was destroyed during the period 1750-1850, while keeping in mind that it was during this period that specialized hospitals emerged, including those for the treatment of venereal disease and that dermatovenerology was bom as a medical specialty. Enlightenment controversies over lues venerea came to concentrate mostly on whether the Mennorrhagic discharge - usually called gonorrhea - happening in many venereal patients, constituted a disease entity different from lues venerea, or (as thought before), was just a peculiar clinical form or stage of lues venerea (Flegel 1974). The beginning of this process of disease differentiation, which, roughly speaking, took place in Europe and North America throughout the century 1750—1850, may be found in the influen­tial work by Giovanni Battista Morgagni, De Sedibus et Causis Morborum per Anatomen Indagatis, pub­lished in Venice in 1761. He found at autopsy that venereal patients with Hennorrhagic discharge and no evidence of chancre rarely had hidden in the geni­tal passages the expected chancre, which was sup­posed to provoke the discharge in the first place.

During the following decades, numerous physi­cians argued the single or dual nature of lues venerea, resorting to anatomoclinical observations and to autoinoculative and heteroinoculative experi­ments with pus from venereal lesions. This contro­versy did not end until the 1830s in part, at least, because there was tremendous ambiguity in the use of terms referring to venereal complaints. Although terms like syphilis, maladie(s) syphilitique(s), and so forth spread rapidly in the European medical liter­ature during the first two decades of the nineteenth century, the term syphilis became almost dominant after the 1820s. The word nonetheless continued to appear in some works as an alternative term or one complementary to that of “venereal diseases.”

The controversy, however, over whether venereal disease was a single disease entity or more than one illness was brought to an end in the late 1830s. During this period the French venereologist Phi­lippe Ricord had developed a vast clinical and experi­mental program at the Paris Hopital du Midi, includ­ing both the systematic use of the uterine speculum and numerous (more than 2,500) autoinoculative ex­periments with pus from venereal patients. In 1838 he presented his results and conclusions in Traite pratique sur les maladies υeneriennes, ou recherches critiques et experimentales sur Vinoculation appli- quee a Vetude de ces maladies. These experiments, asserted Ricord, had permitted him to demonstrate the existence of the so-called virus Syphilitique, so that chancre and Hennorrhagia could be definitely separated. Moreover the expectations had also al­lowed him to distinguish the primary lesions of verole from those that are not primary, and primary symptoms from secondary symptoms. As a result, Ricord proposed the division of syphilis symptoms into primary, successive, secondary, transitional, and tertiary.

1850—1950

During the second half of the nineteenth and the beginning of the twentieth century, Ricord’s concept of syphilis was gradually reshaped, as other disease entities recognized today as sexually transmitted diseases (gonorrhea, chancroid, lymphogranuloma venereum, genital herpes, venereal warts, and oth­ers) were emerging. If most of these new disease entities were first shaped according to anatomoclini- cal criteria, each one of them (syphilis included) eventually got its definitive “identity card” when the relevant germ causing it was isolated.

Gonorrhea and chancroid are two illustrative ex­amples in this respect. Ricord, who definitely sepa­rated chancre and blennorrhagia, asserted that the latter might be the result of local irritation, exces­sive sexual intercourse, or excessive sexual excite­ment. The present clinical picture of gonorrhea was completed only in 1879, when Albert Neisser discov­ered the germ responsible for it, which he called gonococcus. On the other hand, chancroid or soft sore (ulcus molle) emerged as a disease entity in 1852, when a pupil of Ricord, Leon Bassereau, demon­strated that the two kinds of luetic chancre - one hard, painless, and unique; the other soft, painful, and frequently multiple - resulted from exposure to a like lesion. In addition, the latter was autoinocula- ble. Almost 40 years later, in 1889, August Ducrey identified the bacillum responsible for it (Kamp- meier 1984).

As for the concept of syphilis, it developed and changed profoundly during the second half of the nineteenth century as the disease became a major research area in Western scientific medicine. Per­haps the person who contributed most to the develop­ment of the concept of syphilis during this period was the French venereologist Jean-Alfred Foumier. It was Foumier who propounded the concept of la­tency in both acquired and congenital syphilis, defi­nitely established the relationship between syphilis and so-called parasyphilitic affections (mainly tabes dorsalis and general paresis of the insane), and be­gan a social campaign against the disease.

But the discovery of the germ responsible for syphi­lis did not occur until 1905, when Fritz Schaudinn and Erich Hoffmann isolated it in serum from a lesion of secondary syphilis. In 1906 the collective work of August von Wassermann, Albert Neisser, Carl Bmck, and others made possible the invention, in Germany, of the first serologic procedure for the diagnosis of syphilis. This was the complement­fixation test, which soon became well known as the Wassermann Reaction (WR). In the following years, T. pallidum was also found in lesions of tertiary syphilis, verifying Fournier’s theory. Karl Reuter, for example, in 1906 found the germ in the wall of a syphilitic aorta, whereas Hideyo Noguchi in 1913 proved its presence in brain tissue from paretics (Quetel 1986).

By way of conclusion it should be emphasized that, as has been the case with many other disease en­tities, a crisis of a disease entity concept based upon its specific biological cause (Lafn-Entralgo 1982) has also ensnared venereal syphilis. In 1935, whereas most bacteriologists and pathologists still claimed specificity of a causal microorganism to be the defini­tive nosographic criterion for an infectious disease, Fleck lucidly insisted upon the essential incomplete­ness of the concept of syphilis (Fleck 1979).

Time has confirmed Fleck’s insight. Put plainly, it should be obvious from the foregoing that Western medicine has had enormous difficulties in establish­ing scientific criteria that delimit precisely the so- called venereal syphilis from the remaining human treponematoses (Hackett 1963; Hudson 1965; Perine et al. 1984).

Jon Arrizabalaga

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