AIDS is a difficult health issue which mainly concerns medicine, hospitals and public health policies. But the epidemic also concerns the political system. The definition of the nature of risk and of the rank it should occupy amongst the different risks society may be facing is a political task. A new problem and its possible consequences can be evaluated in many different ways. Different social groups will develop various conceptions of the problem according to their position in society and of the danger it may present for them and for society as a whole. Therefore, negotiation is needed between different possible perceptions of the problem and a large consensus is necessary to make the choice legitimate. Priorities as defined will automatically legitimate certain actors and certain means to deal with the problem and exclude others which are considered as irrelevant. The AIDS epidemic offers an excellent case for studying these strategic moments of problem definition and consensus building which shape public policies from their very beginning.

International comparison is of particular interest here, because every country faces a similar problem. But as no legitimate knowledge pre-existed to interpret the new epidemic when it occurred and the threat it might represent to society, problem definition and policy construction largely depended on the characteristics of national policy systems, institutional networks and decision making processes in health policies.

There appear to have been some radical changes in British drug policy since the advent of AIDS. Since the discovery of the HIV virus among British drug users at the end of 1985, the pace of policy change has been rapid. Two major reports on AIDS and Drug Misuse have followed, together with £17 million for the development of drug services. At least a hundred needle exchanges offering new for used syringes are the most tangible public expression of new developments, underlining the view that the danger of the spread of AIDS from drug users into the general population is a greater threat to the nation's health than the dangers of drug misuse itself. British drug policy and in particular the visible manifestation of a harm-minimisation approach in the form of needle exchanges, has attracted world-wide attention. Some commentators have as a result argued that AIDS has changed the direction of British drug policy. ‘The only instance of AIDS overriding established policy objectives has been in the field of drugs… The Government had abandoned its previous stance of augmenting its restrictive and punitive policies on drugs now that AIDS had come to be seen as the greater danger.’ Others have been more cautious. Gerry Stimson comments: ‘these new ideas appear as a distinct break with earlier ones, but as with many conceptual and practical changes, the possibilities are inherent in earlier ideas and work.

Introduction: Genesis and Development of a Scientific Fact revisited

‘If one wants to study scientific facts’, explained the bacteriologist and philosopher of science Ludwik Fleck in 1935 in the introduction of his book Genesis and Development of a Scientific Fact – today viewed as a pioneering study in the sociology of scientific knowledge – ‘a medical fact, the importance and applicability of which cannot be denied, is particularly suitable, because it also appears to be very rewarding historically and phenomenologically. I have therefore selected one of the best established medical facts: the fact that the so-called Wassermann reaction is related to syphilis.’

Fleck's choice of the Wassermann reaction was motivated by two reasons. One was the central role of this test in the development and the present structure of his own scientific specialty – serology. The other was the observation that the most famous serological reaction was based on the use of a non-specific antigen and was thus squarely in contradiction with fundamental principles of immunology and serology. These principles had been summed up in 1910 by Wassermann's collaborator Julius Citron. The fundamental law of immunology, Citron explained, is that ‘every true antibody is specific and that all nonspecific substances are not antibodies. The law of specificity is the precondition of immunodiagnostic.’ This particularity of the Wassermann reaction was central to Fleck's argument that additional, sociologically based explanations are needed to account for the genesis and rapid diffusion of this test.

Carrión’s disease is an infectious disease caused by a microorganism of the genus Bartonella. Two species have been described, the bacilliformis type and the verrugiformis type. These bacteria are parasites of human red blood and histiocytic cells. The bacilliformis type produces two stages of the disease, a febrile acute hemolytic anemia known as “Oroya fever,” followed by a granulomatous mucocutaneous eruption known as “Verruga Peruana.” The verrugiformis type produces only the verrucose stage.

Etiology and Epidemiology

B.bacilliformis are pleomorphic bacteria, well stained with the Romanovsky stain. In the red blood cells and in the histiocytic cells, the bartonella assumes a rodlike (bacillus) or coccoid shape, 1 to 3 microns in size (Figure VIII.22.1). The electron microscope shows the flagella of the bartonella. It grows well in liquid and in semisolid blood media. The human bartonella is closely related to the nimal bacteria Hemobartonella, Eperythrozoon, and Grahamella.

In 1913 Charles Townsend identified the sandfly Phlebotomus verrucarum as the insect vector of the disease. The female is the only transmitter, and the transmission occurs during the night. Carrión’s disease is a rural disease, and, like yellow fever, it does not need a human reservoir because the bartonella lives in the small animals in the area.

Immunology (Experimental Transmission) Between 1948 and 1950, the author and collaborators conducted a series of experimental transmission on human volunteers. Thirty healthy men were inoculated with parasitic blood through subcutaneous, intramuscular, and intravenous routes. None of the volunteers developed the disease, and the blood culture remained negative after more than 120 days.

The members of genus Treponeme, family Treponemataceae, and order Spirochaetales consist of Treponeme pallidum (first described in 1905), which causes syphilis and nonvenereal syphilis; Treponeme pertenue (first described in 1905), which is responsible for yaws; and Treponeme carateum (first described in 1938), which produces pinta. Or at least this is the way that most medical texts would have it. It may be, however, that the three pathogens in question are actually only one, for although they produce different pathological processes, the pathogens themselves are virtually indistinguishable under the microscope, and the diseases they cause respond to the same treatment. The origin of this infamous family and the relationship of its members to one another have been topics of considerable and very interesting debate since the 1970s, largely because such questions bear directly on the centuries-old debate of whether the Americans bestowed syphilis on the rest of the world.

Many agree that the treponemes probably evolved from microorganisms that originally parasitized decaying organic matter, and which later – perhaps hundreds of thousands of years ago – came to specialize in human hosts, but probably only after first parasitizing another animal host (Wood 1978). There is little disagreement that the first treponemes to parasitize humans did so by entering their bodies through traumatized skin and were subsequently passed on to other humans by skin-to-skin transmission. Real disagreement begins, however, over questions of where the first humans were infected, and the identity of the disease they were infected with.

Black and brown lung are the names given by workers in the coal and textile industries, respectively, and by some physicians and public officials, to symptoms of respiratory distress associated with dusty work. Most physicians and epidemiologists have, however, preferred to categorize these symptoms as they relate to findings at autopsy and studies of pulmonary function and to name their appearance in particular patients as, respectively, coal workers’ pneumoconiosis and byssinosis. The terms “black lung” and “brown lung” are historical legacies of intense negotiations about the causes of respiratory distress and mortality among workers in the coal and textile industries of Europe and North America, especially since the nineteenth century. (For the conventional medical definitions of the pathology subsumed under the terms black lung and brown lung, see the extensive bibliographies in papers by Fox and Stone [1981] and Corn [1980]).

History and Geography

For many centuries, medical observers, and workers and their employers, have recognized respiratory distress and its consequences as an occupational hazard among underground miners and employees of industries that generate considerable dust (notably refineries, foundries, and the manufacturing of cotton, flax, and hemp). Pliny described the inhalation of “fatal dust” in the first century. In the sixteenth century, Agricola observed that miners, physicians, and engineers were aware of shortness of breath and premature death. In the early nineteenth century, pathologists observed that some miners in Scotland had black lesions on the lung at autopsy. The term pneumoconiosis appears to have been invented in 1867. Brown lung seems to have been named by analogy with black lung, apparently in the 1960s.

Nonvenereal syphilis has apparently occurred in many forms and places, and one interpretation of this phenomenon is that venereal syphilis can revert to nonvenereal transmission. Others see it as a discrete disease with its own etiologic epidemiology. The most common and enduring form of the disease is called bejel; it occurs in the arid regions of North Africa, the Middle East, and the eastern Mediterranean, and seems to have antedated venereal syphilis as a disease entity by a considerable period of time. It is one of the endemic treponematoses caused by spirochetes, bacteria belonging to the genus Treponema. Other diseases in this group are yaws and pinta. Like yaws, bejel is essentially a disease of children, although those who escape the illness as children are likely to acquire it as adults, often from their own children. Its specific cause seems to be Treponema pallidum, the same agent as that of syphilis, although it may be a treponema intermediary between T. pallidum and Treponema pertenue, the agent of yaws. Although treponemal disease has been transferred experimentally to animals, humans appear to be the only natural reservoir.

Etiology, Epidemiology, and Clinical Manifestations

Because the treponemas that cause yaws, nonvenereal syphilis, pinta (an American disease), and syphilis are morphologically and serologically indistinguishable, it is believed that at least the Old World diseases may represent an evolutionary continuum running from south to north. Yaws, thought to be the oldest, spreads by skin-to-skin contact and flourishes in the hot and moist regions of Africa south of the Sahara where individuals have historically worn little clothing.

Islamic and Indian medicine originated in distinct cultural traditions but have been in close contact for many centuries. The terms Islamic and Indian as they refer to medicine do not describe static, idealized, or monolithic systems that can be categorized by referring to the medical texts of a distant golden age. Medical practices in Islamic and Indian cultures were, as elsewhere, eclectic and pluralistic, evolving in response to complex influences that varied according to time and place. This essay briefly traces the origins and the major components of the two traditions and compares and contrasts their institutional responses to the challenges of modern times.

Islamic medicine is based largely on the Greek medical knowledge of later antiquity and is more properly called Greco-Islamic or Galenic-Islamic medicine, reflecting the influence of Galen, whose works dominated medical learning in the eastern Hellenic world. At the time of the Muslim conquests of the seventh century A.D., the major centers of Greek medical learning in the eastern Mediterranean were flourishing.

Because of theological constraints, Greek Orthodox scholars were more interested in the Greek sciences, which included medicine and philosophy, than in literature, historiography, and other humanistic subjects. The Muslim conquerors recognized the excellence of Greek learning, and the Umayyid and Abbasid caliphs subsequently sponsored the translation of a large portion of the available scholarly works into Syriac and Arabic (Ullmann 1978).

The term croup is used in an inclusive way to identify several different respiratory illnesses of children manifested by varying degrees of inspiratory stridor, cough, and hoarseness due to upper-airway obstruction. Classically croup was a manifestation of diphtheria. In the twentieth century, many other infectious causes of croup syndromes are recognized, and in addition, similar illnesses can be caused by noninfectious processes.

A classification of crouplike illnesses is presented in Table VIII.30.1. Although long-term obstruction in the glottic and subglottic regions can lead to chronic illnesses, croup syndromes are described here as acute self-limited or fatal illnesses. Most cases of croup today are either laryngotracheitis or spasmodic croup.

Etiology

Acute epiglottitis (inflammation of the epiglottis) is virtually always caused by Haemophilus influenzae type B; rare cases have been due to Streptococcus pneumoniae and Staphylococcus aureus. Laryngitis is usually due to the common respiratory viral agents, the most important of which are adenoviruses and influenza viruses.

Laryngotracheitis and spasmodic croup are common illnesses in children and are due to viruses or Mycoplasma pneumoniae. The most important agent is parainfluenza virus type 1. This virus, as well as parainfluenza type 2 and influenza A and B viruses, results in outbreaks of disease. In areas of the world where diphtheria toxoid immunization is not carried out, laryngotracheitis is also caused by Corynebacterium diphtheria.

Laryngotracheobronchitis and laryngotracheobronchiopneumonitis are frequently caused by the same viruses that cause laryngotracheitis. These two illnesses are caused also by S. aureus, Streptococcus pyogenes, S. pneumoniae, and H. influenzae.

Leprosy occurs naturally only in humans and is caused by infection with Mycobacterium leprae. Known also in the twentieth century as “Hansen’s disease,” after the Norwegian microbiologist A. G. H. Hansen who first isolated the microorganism in 1873, true leprosy is a chronic, debilitating, and disfiguring infection. However, the long history of disease attributed to leprosy undoubtedly includes a broad range of skin and systemic afflictions that only resembled leprosy symptoms.

The leprosy bacillus multiplies quite slowly, usually in the sheaths of peripheral nerves. Losing sensation in discrete, patchy areas of the skin is often the earliest, but ignored, symptom of infection. Lacking adequate innervation, the affected dermis can be damaged without evoking a pain response as, for example, by a burn or a cut. Repair of the tissue is then hindered by poor regulation of local blood supply. Hence, secondary infection and inflammation of an involved area are common, leading to scarring and callusing of surviving tissues. This long process can result in the loss of fingers, toes, nasal tissue, or other parts of the body frequently exposed to the elements. A “bear claw” foot or hand becomes one of the characteristically maiming and stigmatizing features of the leper. Involvement of the nasal cartilage and vocal cords, common sites for the organism’s growth, leads to profound disfiguration of the center of the face and also to the raspy, honking voice described in some historical accounts of true leprosy.

Cystic fibrosis, also called fibrocystic disease of the pancreas, and mucoviscidosis, is a genetically determined disease of infants, children, and young adults. Most of its many manifestations result from the abnormally viscous mucus, which interferes with pulmonary function, and the insufficient production of pancreatic digestive enzymes, which causes nutritional deficiencies and developmental retardation.

Etiology

Among Caucasians, cystic fibrosis (CF) is the most common fatal disease having an autosomal recessive inheritance. Despite the primary involvement of several organs, the disease is caused by a single defective gene that is located on chromosome 7 and is carried by about 4 percent of the Caucasian population. Its expression is similar in both sexes.

Clinical Manifestations

CF manifests itself at birth in about 8 percent of cases through mechanical obstruction of the small intestine by the secretion of abnormally viscous mucus (meconium ileus). Symptoms of insufficient secretion of exocrine (noninsulin) digestive enzymes by the pancreas appear during the first year of life in 90 percent of cases. The development of such symptoms indicates that pancreatic function is less than 10 percent of normal; and the more severe the deficiency of pancreatic enzymes, the more severe the fecal excretion of undigested fat, usually as diarrhea. As much as 80 percent of dietary fat may be lost, thus partially explaining malnutrition. Loss of undigested nutrients can be corrected only partially by treatment with pancreatic enzyme tablets. Pulmonary disease is responsible for most of the debility and mortality. Onset occurs in the first 2 years of life in at least 75 percent of cases, and by the age of 6 years in most of the remaining cases.

Pneumonia is an acute inflammatory condition of lung parenchyma (lung tissue excluding the airways) caused by a variety of infectious agents and toxins and favored by aspects of the environment and/or the general physical status of the patient. The term “pneumonia” is derived from the Greek word περιπλευμονιη meaning “condition about the lung”; the word refers to a clinicopathological state that arises in several different yet specific disease patterns. All of these are characterized by some degree of fever, cough, chest pain, and difficulty in breathing. Technically speaking, pneumonitis, which means “inflammation of the lung,” is a synonym for pneumonia, but the former is usually reserved for benign, localized, and sometimes chronic inflammation without major toxemia (generalized effects). Many modifiers and eponyms are applied to the term pneumonia to reflect the cause (e.g., embolic pneumonia) or the localization (e.g., pleuro- or broncho pneumonia). The classic form is lobar pneumonia, an infectious but not particularly contagious condition usually localized to part or all of one of the five lobes of the lungs, and caused by a pneumococcus, the gram-positive organism Streptococcus pneumoniae (formerly called Diplococcus pneumoniae). Untreated lobar pneumonia has a mortality of about 30 percent, but the advent of antibiotic treatment has improved survival rates.

Several other pathogens (bacterial, viral, fungal, and parasitic) are recognized causative agents. The extent of the pulmonary involvement; the onset, pattern, and duration of symptoms; as well as the mortality rate depend on both the causative organism and precipitating factors. Chemical irritation, environmental exposure to noxious substances, or hypersensitivity can occasionally cause pneumonia.

History

In 1967, a disease outbreak occurred in a laboratory in Marburg, Germany, where the kidneys of cercopithecoid (Green African; vervet) monkeys were being taken out for preparation of cell cultures. Twenty-seven laboratory workers (including a worker in Yugoslavia) fell ill with a grave illness, and seven died. There were four secondary cases in total (including the wife of an infected laboratory worker in Yugoslavia secondarily infected by sexual intercourse), but none fatal. Early suspicions focused on yellow fever, but this was soon ruled out (Casals 1971). In due course, a virus was isolated and found to be quite distinct from any other known viruses. Electron micrographs revealed a virus with bizarre morphology of a type never seen before (Peters, Muller, and Slenckza 1971). Pictures taken resembled photographs of a bowl of spaghetti. The agent was named Marburg virus and the disease Marburg disease. Strict monkey quarantines were initiated. No further cases were seen in laboratory workers.

An intensive and extensive series of field studies were initiated in East Africa, which had been the monkeys’ homeland (Henderson et al. 1971; Hennessen 1971; Kalter 1971). No virus recoveries were made from any of the monkeys examined. In later years, serologic studies involving humans and primates, and also rodents, have been carried out in many regions, as can be seen in Table VIII.86.1.

The first Marburg cases seen in Africa occurred in February of 1975. A young Australian couple touring in Rhodesia (Zimbabwe) became ill by the time they got to South Africa. They were admitted to a major hospital in Johannesburg where the young man died and the young lady recovered. A nurse tending them also sickened and recovered.

Scrofula can be denned only historically. That is, scrofula is a term about which there was some measure of consensus in the past, but one that has now been largely superseded by terms that indicate some form of tuberculosis. It must be emphasized, however, that scrofula is not simply an old name for what we call tuberculosis. Our ontology of disease centers on the tubercle bacillus, and we would commit a grave historical error if we assume that with its aid we can know what was actually there in old discussions of scrofula. To understand these old discussions, we need to know how and why the old picture of scrofula was put together. The distribution of scrofula, as we shall see below, has much more to do with the religious and political convictions of those who saw it than with physical geography or economic conditions or other circumstances normally considered conducive to diseases. Likewise in regard to its clinical manifestations, we may note, first, that this term itself implies an underlying entity that becomes manifest. But, second, scrofula, historically, was its collection of symptoms and signs. What we need to understand is what went into that collection, and why.

History and Geography

“Scrophula,” like “scurvy” and “syphilis,” is not a term that was used by the ancients. Whereas there may be special reasons why the latter two were unknown (a distribution to the north of the ancient Mediterranean and a possible Columbian origin, respectively), there seems to be no reason to suspect that scrofula was a new disease.

Osteoarthritis (OA) is the most common rheumatic disorder afflicting humankind and vertebrates in general. The most common alternative terms, osteoarthrosis and degenerative joint disease, are used because of divergent concepts of the nature and cause of the disorder. One school maintains that OA is a family of systemic inflammatory disorders with similar clinical and pathological end results. Another supports the use of the term “osteoarthrosis” because inflammation is not present. Still another uses the term “degenerative joint disease” because it is held that aging and “wear and tear” are responsible for its occurrence.

William Heberden, an eighteenth-century English physician, gained immortality by describing what we now term Heberden’s nodes, a common heritable form of osteoarthritis, especially common in women. In his Commentaries, he writes:

“What are those little hard knots, about the size of a small pea, which are frequently seen upon the fingers, particularly a little below the top, near the joint? They have no connection with the gout, being found in persons who never had it: They continue for life; and being hardly ever attended with pain, or disposed to become sores, are rather unsightly, than inconvenient, though they must be some little hindrance to the free use of the fingers”. (Heberden 1802)

Modern research provides new data for a comprehensive definition encompassing clinical, biochemical, and anatomic features (Denko 1989). OA is a multifactorial systemic inflammatory disorder with clinical symptoms of pain and stiffness in movable joints, showing radiographic evidence of cartilage loss and bony overgrowth. overgrowth. The anatomic changes – cartilage loss and a kind of bony overgrowth and spurs – may occur physiologically without clinical symptoms.

Dengue is an acute febrile disease caused by infection with a group B arbovirus of four serotypes, transmitted by the bite of infected Aedes aegypti and Aedes albopictus mosquitoes. Endemic throughout the tropics and subtropics, uncomplicated dengue is rarely fatal, although return to normal health after an attack may take several weeks. It does not always have a benign course, however, and can be complicated by hemorrhagic manifestations (hemorrhagic dengue) and circulatory collapse (dengue shock syndrome) with a potentially fatal outcome unless facilities are available for the urgent medical treatment of those affected.

Typical uncomplicated dengue has an incubation period of 3 to 15 days and is characterized by abrupt onset of chills, headache, lumbar backache, and severe prostration. Body temperature rises rapidly, perhaps reaching as high as 40°C; bradycardia (slow heart rate) and hypotension (low blood pressure) accompany the high fever. Conjunctival injection, lymph node enlargement, and a pale, pink rash, especially noticeable on the face, are usually present during this first phase of the disease. In classical dengue, the fever lasts for 48 to 96 hours initially, subsides for 24 hours or so, and then returns (saddleback fever), although the peak of temperature is usually lower in the second phase than in the first. A characteristic red rash appears in the second phase, usually covering the trunk and extremities, but sparing the face. The fever, rash, and headache, together with the other pains, are known as the dengue triad. The acute illness ends in 8 to 10 days, and one attack confers immunity to the particular dengue subtype.

Pre-Columbian Peoples

The natural environment of the continent of South America is overwhelmingly diverse and thus has posed special problems of physiological adaptation to its indigenous populations, as well as later to European, African, and Asian intruders. Indeed, because of the harsh environments of much of the continent, there are but few places in which people can flourish without great effort and skillful labor. In much of the continent’s vast interior, even communication and transportation would be impossible without the river systems of the Amazon and the Paraná– Paraguay along with the smaller rivers of Colombia and Venezuela, the Magdalena and the Orinoco, and the Sāo Francisco of northeastern Brazil.

One of the most formidable environments is that of the Andes Mountains, which range from western Venezuela to the tip of the continent, with snow-capped peaks at more than 20,000 feet in altitude and with populations perched at 10,000 and 13,000 feet. At such altitudes, scarcity of oxygen has led to physiological adaptations in the bodies of the indigenous peoples of Peru and Bolivia that permit them to perform hard physical labor in the thin air.

The Andes break the westerly movement of rainfall from the Amazon basin, and rain falls in profusion on the eastern slopes, where lush tropical forests shelter the people of the Upper Amazon from outside invaders. On the opposite side of the Andes, a lack of rainfall creates the semiarid coastal lowlands intersected by small rivers flowing through the desert to the ocean.

Rocky Mountain spotted fever is a severe, acute, rickettsial disease transmitted by ticks and limited to the Western Hemisphere. Its major symptoms are similar to those of epidemic typhus, but its rash covers the entire body, including the face, the palms of the hands, and the soles of the feet. Between 20 and 25 percent of untreated victims die, making Rocky Mountain spotted fever the most severe rickettsial infection in the Americas. First identified in the Rocky Mountain region of the United States, this place name has never been dislodged, even though it is inaccurate and even misleading.

Etiology and Epidemiology

The severity with which Rocky Mountain spotted fever treats its victims underscores its natural existence as an infection of ticks and their mammalian hosts. The microbial cause of the disease, Rickettsia rickettsii, normally inhabits ixodid, or hard shell, ticks, apparently causing little harm to the host. Although small mammals are susceptible to a mild infection with R. rickettsii an may transmit it to uninfected ticks, the principal means by which the organism is maintained in nature is from one generation to the next in the eggs of the female tick.

The epidemiology of Rocky Mountain spotted fever is linked to areas favorable for the habitation of the vector ticks. The Rocky Mountain wood tick, Dermacentor andersoni, and the American dog tick, Dermacentor variabilis, are the most common vectors in the United States, although the Lone Star tick, Amblyomma americanum, also transmits the disease in the south central and southeastern parts of the United States.

The nature and role of public health are constantly changing, and its definition has been a major preoccupation of public health leaders in the twentieth century. Essentially, public health is and always has been community action undertaken to avoid disease and other threats to the health and welfare of individuals and the community at large. The precise form that this action takes depends on what the community perceives as dangers to health, the structure of government, the existing medical knowledge, and a variety of social and cultural factors. From the beginning, communities, consciously or not, have recognized a correlation between filth and sickness, and a measure of personal and community hygiene characterized even the earliest societies.

By the eighteenth century, personal and community hygiene were becoming institutionalized. A wide variety of local regulations governed the food markets, the baking of bread, the slaughtering of animals, and the sale of meat and fish. These regulations were motivated by a concern for the poor, a desire for food of a reasonable quality, and commercial considerations. Bread was always a staple of the poor, and regulations in the Western world invariably set the weight, price, and quality of loaves. For economic reasons, merchants shipping food abroad promoted regulations on meat and grains in order to protect their markets and save themselves from dishonest competition.