Etiology and Epidemiology

Although syphilis is transferred predominantly by sexual contact, it may also be transmitted in nonsexual 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

Venereal syphilis

Endemic syphilis

Yaws

Pinta

Organism

T. pallidum

T. pallidum endemicum

T. pertenue

T. carateum

Occurrence

Sporadic, urban

Endemic, rural

Endemic, rural

Endemic, rural

Geographic

Worldwide

Southwest Asia, sub-

Africa, Southeast Asia,

Central and South

distribution

Saharan regions of Africa, Bosnia

Western Pacific, South America, Caribbean

America, Mexico

Climate in which the

All types

Arid, warm

Humid, warm

Semiarid, warm

disease mostly occurs

Age group with peak in

18-30

2-10

2-10

15-30

cidence (years)

Transmissibility

High

High

High

Low

Reservoir of infection

Adults

Children 2—15 years

Children 2-15 years

Cases with long

old; contacts in home,

old; contacts in home,

standing skin

school and village; la

school and village; la

lesions

tent cases capable of

tent cases capable of

becoming active

becoming active

Mode of transmission

Sexual,

Household contacts:

Skin-to-skin; ? insect

Skin-to-skin; ? in

transplacental"

mouth-to-mouth or via drinking, eating utensils

vector

sect vector

Usual age

Adult

Early childhood

Early childhood

Adolescent

Primary lesion

Cutaneous ulcer

Rarely seen

Framboise (raspberry),

Nonulcerating

(chancre)

or "mother yaw"

papule with satellites

Secondary lesion

Mucocutaneous; oc

Florid mucocutaneous le

Cutaneous papulo

Pintides

casional periostitis

sions (mucous patch, split papule, condyloma latum); osteoperiostitis

squamous lesions; osteoperiostitis

Tertiary lesion

Gumma, cardiovas

Destructive cutaneous

Destructive cutaneous

Dyschromic,

cular, and CNS lues

osteoarticular gummas

osteoarticular gummas

achromic macules

"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.

Sources: Adapted from Perine et al. (1984, 2); Perine (1987, 650).

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 vincentii), 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 VIII.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). Since the 1950s, however, the rise of molecular biology has pushed anthropologists and historical epidemiologists to frame this problem progressively in terms of the evolutionary origins of all the human treponema-toses. At present, two major theories - the unitarian and the nonunitarian - contend with each other in providing an explanation for the surprising similarities of the human treponematoses.

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

HYPOTHESIS A

"Commensal" "Saprophyte"

HYPOTHESIS B

Figure VIII.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.]

HYPOTHESIS A

"Commensal" "Saprophyte"

HYPOTHESIS B

Figure VIII.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.

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