It is often thought that analytic philosophy arises, at least in part, from a reaction against Hegel, or against philosophy inspired by Hegel. To some extent this is correct. The philosophy of Bertrand Russell and G.E. Moore in the first decade or so of this century, which was enormously influential for subsequent analytic philosophy, was developed in conscious reaction to idealist views that owed much to Hegel. This fact, however, does not settle the question of the influence of Hegel, either on Russell and Moore or on analytic philosophy more generally; all that it does is to give us a way of posing the question. And the question is a complex one. Besides the general difficulties involved in tracing the influence of a view as complex as Hegel's, there is also a particular problem arising from the relation between Kant and Hegel.

Favism is an acute hemolytic reaction triggered by exposure either to fava beans (Vicia faba) or to certain drugs (e.g., sulfa-based antibiotics and the antimalarial primaquine) in people with an inherited deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD). In favism, the patient can suffer from destruction of red blood cells, severe anemia, and possibly death. There are two necessary conditions for the disease: (1) genetic inheritance of the “Mediterranean” variant of the abnormal gene trait for G6PD deficiency; and (2) ingestion of fava beans, usually fresh, or exposure to some drugs. The bean is a dietary staple in areas where favism is reported. Only an estimated 20 percent of those with the genetic trait for G6PD are likely to experience episodes of favism. Under modern medical conditions the hemolytic anemia caused by favism is only rarely fatal. Strong evidence suggests that both the gene for G6PD deficiency and the cultural practice of fava bean consumption are evolutionarily adaptive traits that protect against death from all types of malaria. Favism, then, could be described as a negative outcome of the interaction of the positive adaptive qualities of both the gene and the bean.

Distribution and Incidence

Favism is found primarily in the Mediterranean and Middle East regions where fava beans are a staple food and the Mediterranean variant of G6PD deficiency gene is relatively common. Mark Belsey (1973) reports that it is frequently encountered in Greece, Sardinia, Italy, Cyprus, Egypt, Lebanon, Israel, Iran, Iraq, Algeria, and Bulgaria, and is particularly common among Sephardic Jews.

Tetany is a symptom complex characterized by painful and prolonged contractions of the (generally smooth) muscles. These often appear as convulsions and are usually triggered by hypocalcemia. Adult varieties of the condition that result from calcium or magnesium deficiencies include maternal tetany, parathyroid tetany, osteomalacic tetany, and magnesium tetany. Alkalosis can also produce tetany. Examples include gastric tetany and hyperventilation tetany, following a lengthy period of forced inspiration and expiration. Another form of the disease – grass tetany caused by magnesium deficiency – is found in cattle. Despite these many forms, however, the disease occurs chiefly in infants (neonatal tetany) and young children (infantile tetany) in whom it is normally associated with rickets. It affects males far more than females and, in the absence of proper treatment, frequently proves deadly.

Distribution and Incidence

Because tetany has so often been confused with tetanus, very few data are available on the geographic distribution of the disease. It probably occurs worldwide in the temperate zones, with the highest frequency of neonatal tetany among bottle-fed, black, and prematurely born infants. An abundance of year-round sunshine and, hence, vitamin D may have the effect of reducing the incidence of infantile tetany in the tropics. The incidence of neonatal tetany recorded at New York Hospital between 1940 and 1958 was between 1 per 500 and 1 per 700 births.

The “Black Death” is the name given by modern historians to the great pandemic of plague that ravaged parts of Asia, the Middle East, North Africa, and Europe in the middle of the fourteenth century. Contemporaries knew it by many names, including the “Great Pestilence,” the “Great Mortality,” and the “Universal Plague.” This epidemic was the first and most devastating of the second known cycle of widespread human plague, which recurred in waves, sometimes of great severity, through the eighteenth century. Some of the later and milder “plagues” in this period seem to have also involved other diseases, including influenza, smallpox, and dysentery. Nonetheless almost all historians agree, on the basis of contemporary descriptions of its symptoms, that the Black Death should be identified as a massive epidemic of plague, a disease of rodents, caused by the bacillus Yersinia pestis, that can in the case of massive epizootics be transmitted to human beings by fleas. Although the Black Death manifested itself most commonly as bubonic plague, it also appeared at various times and places in its primary pneumonic and septicemic forms.

History and Geography

The geographic origins and full extent of the Black Death are still unclear. The earliest indisputable evidence locates it in 1346 in the cities of the Kipchak Khanate of the Golden Horde, north and west of the Caspian Sea. Until recently, most historians have claimed, based on Arabic sources, that the epidemic originated somewhere to the east of the Caspian, in eastern Mongolia or Yunnan or Tibet, where plague is enzootic in various populations of wild rodents.

Scurvy is a deficiency disease, arising from a lack of vitamin C (ascorbic acid) in the diet. It occurs most characteristically in the absence of fresh fruit and vegetables, but can still be avoided when these are not consumed if the diet is rich in uncooked meat as in the case of Eskimos (heat destroys the vitamin). Scurvy does not appear in a regularly recognizable way in the ancient medical literature, and its name is not classical but, rather, derived from the north European vernaculars of the Renaissance. It was, for example, schverbaujck in Dutch and scorbuck in Danish, and Latinized in 1541 by Johannes Echthius, a Dutch physician living in Cologne, as scorbutus. In the slave trade it was often called the mal de Luanda.

Etiology, Epidemiology, and Distribution

Human beings, like guinea pigs and monkeys but unlike many other animals, do not synthesize vitamin C. No doubt this reflects a period of evolution in a vitamin C–rich environment; and, with the expansion of the species to all parts of the Earth, less generous climates have inevitably taken a toll due to scurvy. The disease occurs where economic, social, or climatic factors prevent access to an appropriate diet, and frequently has appeared under circumstances where diets are circumscribed, including long sea voyages, during military operations, in prisons, with the failure of crops, and during the Gold Rush. In the modern period, infantile scurvy has been a problem, for example, in Canada during the decades 1945–65, where it occurred mostly among the lower socioeconomic groups.

The larval stages of three tapeworms of the genus Echinococcus can cause severe disease in humans. All three normally become adults in the intestines of dogs or other canids. Eggs are passed in the feces and, if ingested by a herbivore, develop in the liver or other organs into a saclike container of larvae, the hydatid cyst. Carnivores become infected by eating cysts with the flesh of the herbivore. Echinococcus granulosus, which commonly has a sheep–dog cycle, but which may also infect goats, cattle, swine, and camels, is the most likely to infect human beings. Human echinococcosis occurs primarily in sheeprearing areas. Dogs ingest cysts in the offal of dead sheep and pass eggs in their feces. Humans acquire the eggs from a dog’s fur or from contaminated food or water. Cysts holding 2 or more liters of fluid and larvae can grow for years in the liver, lungs, brain, or other organs and exert enough mechanical pressure to cause grave or fatal consequences. Rupture of a cyst by trauma or surgery releases daughter cysts, which may grow elsewhere in the victim; the hydatid fluid can cause fatal anaphylactic shock. Hydatid cysts in humans and animals have been known since Roman times, but, as was true for the other tapeworms, the relationship between the larval cyst and the adult worm was not suspected until the eighteenth century. E. granulosus was described as a separate species in 1850, and its life cycle was worked out with feeding experiments in 1863.

Amebiasis is an infection of the colon caused by a parasitic protozoan, the ameba Entamoeba histolytica. Several species of ameba inhabit the large intestine. Most are harmless commensals or minor parasites, usually causing little or no clinical damage. The closely related species Entamoeba coli and Entamoeba hartmanni are commensals, and infection with E. histolytica is also often asymptomatic. E. histolytica is probably a species complex, with a number of morphologically similar forms with varying degrees of invasiveness. E. hartmanni, formerly believed to be a “small race” of E. histolytica, is now recognized as a separate nonpathogenic species. Pathogenic amebas cause light to severe intestinal damage (amebic dysentery) and sometimes spread to the liver, lungs, brain, and other organs.

Etiology

The parasite exists in two forms during its life cycle. Active adults, trophozoites, multiply in the lumen of the colon. They frequently live there harmlessly, feeding on the contents of the intestine. Some strains are generally commensal; others are highly pathogenic. Under conditions of stress, lowered host resistance, or when a particularly pathogenic strain is involved, amebas invade the intestinal wall and cause abscesses. As they pass lower into the large intestine, the drier environment stimulates them to form a cyst wall. The original cell nucleus divides twice, producing four daughter nuclei. nuclei. Cysts are passed with the feces and are infective when swallowed. Excystation takes place in the small intestine, and the young trophozoites, four from each cyst, are carried in the fecal stream to the large intestine. When dysentery occurs, trophozoites are swept out too rapidly to encyst. Even though huge numbers of amebas may be passed, they die quickly and are not infective.

Pica is usually described as a pathological craving for nonfoods, although it can mean a craving for substances generally accepted to be food as well. Medical science has long been interested in this disorder, for although it does not constitute a disease, it is often a symptom of disease and frequently is associated with nutritional deficiencies, especially those connected with minerals. In addition, psychiatry and psychology find that pica is often connected with mental problems, including those of retardation. Anthropologists study it as a cultural phenomenon, since it has been associated with some religions and also perhaps because the use of nonfoods is indicative of food shortages in the distant past.

The word “pica” comes from the Latin for “magpie,” a bird that eats practically anything. The term was first used by Ambroisé Pare in the 1500s, although references to pica consumption can be found in many ancient and medieval writings. M. H. Boezo, in his 1638 work De Pica, was the first to draw a distinction between “pica,” which he believed was an appetite for “absurd things,” and which was common in both men and women, and “malacia,” which referred to a voracious desire for normal food substances. He observed that the latter occurred most often in pregnant women, and believed the cause was a mental alteration caused by the pregnancy.

Tetanus is an acute disease caused by the production of a neurotoxin, tetanospasmin, by a bacterium, Clostridium tetani, when the spores of the organism enter a wound, and develop into the toxin-producing vegetative form. The case-fatality rate averages 50 percent in adults and is higher in neonates (especially those in developing nations) and in patients over 60 years of age.

Etiology and Epidemiology

C. tetani is an obligate anerobe, a spore-forming, gram-positive motile rod. The terminal spore caused the organism to be called the “drumstick” rod. The protein toxin, tetanospasmin, blocks acetylcholine release at the motor end-plates. The toxin travels up the nerve trunks, as well as fixing directly on nerve cells. The spinal cord is the primary target organ, with chromatolysis of the motor neurons and inhibition inhibition of antagonists accounting for the spasm and rigidity that characterize the disease. Toxin fixation to central nervous system neurons may lead to seizures; involvement of the sympathetic nervous system may evoke vascular irregularities.

Humans may be considered accidental interveners in the life cycle of the organism, which is a soil saprophyte and a harmless inhabitant of the intestines of many herbivores. The organism requires a wound to invade mammals. Traumatic, surgical, dental, umbilical, burn, and cosmetic wounds are the most common causes of infection in humans. “Skin popping” of addictive drugs, insect bites, and nonmedical abortions are less common causes of infection. As an obligate anaerobe, the organism can reproduce and produce toxin only when local oxidation-reduction processes reduce tissue oxygen to near zero; deep, infected wounds are thus ideal culture media.

Infections of the middle ear and mastoid encompass a spectrum of potentially serious medical conditions and sequelae. Decreased hearing from ear infections may have a lifelong impact on speech, learning, and social and vocational development, causing these conditions to remain a major health concern. Because of the anatomic relationship of the middle ear and mastoid to the middle and posterior cranial compartments, life-threatening complications may occur.

Classification

Inflammatory diseases of the middle ear and mastoid are categorized according to the underlying disease process and location:

1. Acute suppurative otitis media (AOM) is characterized by obstruction of the eustachian tube, allowing the retention and suppuration of retained secretions. AOM is the medical term associated with, most commonly, the acute ear infection of childhood. Generally the course of this infection is self-limited, with or without medical treatment, and the retained infected secretions are discharged through either the eustachian tube or a ruptured tympanic membrane.

Acute coalescent mastoiditis can result from failure of these processes to evacuate the abscess. Coalescence of disease within the mastoid leads to pus under pressure and ultimately dissolution of surrounding bone. This condition may require urgent surgical evacuation because the infection is capable of spreading to local and regional structures.

3. Otitis media with effusion (OME) is an inflammatory condition of the middle ear in which serous or mucoid fluid accumulates. Both AOM and OME are precursor conditions to tympanic membrane retractions and perforations. Ongoing eustachian tube dysfunction predisposes to persistent retained secretions in the ear and recurrent acute attacks of otitis media. A small percentage of these patients develop a chronic tympanic membrane perforation which, in most cases, allows eventual aeration of the middle ear and mastoid air-cell spaces and resolution of the underlying disease process.

4. …

Anemia, an insufficiency of red blood cells (RBC) and hemoglobin for oxygen-carrying needs, results from a variety of disease processes, some of which must have existed since ancient times. It was defined in quantitative terms in the mid-nineteenth century, but before that the evidence of anemia is found in the descriptions of pallor or in the occurrence of diseases that we now know cause anemia. For example, lead poisoning decreases RBC production and was apparently widespread in Rome. Intestinal parasites cause iron deficiency anemia and were known to exist in ancient times. Parasites found in paleopathological specimens include Ascaris lumbricoides, Trichiuris trichiuria, and various species of Taenia (ovis, globosa, solium, and saginata), all of which can cause intestinal blood loss and anemia. Diphyllobothrium latum, which leads to malabsorption of vitamin B12 and a megaloblastic anemia, has been found in mummies in Prussia and Peru.

Congenital abnormalities in RBC metabolism, including glucose 6-phosphate dehydrogenase (G6PD) deficiency and various forms of thalassemia and sickle-cell disease, were probably present also in ancient times. Thalassemia protects against malaria, and the incidence of the relatively mild, heterozygotic form of thalassemia (thalassemia minor) probably increased in the Mediterranean region after the appearance of falciparum malaria, the most fatal form of the disease.

The history of disease in modern South Asia has been dominated by epidemic diseases. Smallpox, cholera, and malaria, along with plague and influenza, figured prominently among the leading causes of sickness and mortality in the region for much of the period from the eighteenth to the mid-twentieth centuries. The recent decline or disappearance of several of these diseases has correspondingly resulted in a marked fall in overall levels of mortality.

Although the statistics are unreliable in detail (with perhaps a quarter or more of all deaths passing unrecorded), the broad trend is clear. From a peak mortality of nearly 50 deaths per 1,000 inhabitants in British India in the late nineteenth and early twentieth centuries, mortality rates were roughly halved by the 1950s, declining from 42.6 per 1,000 in 1901–10 and 48.6 in 1911–20, to 36.3 in 1921–30, 31.2 in 1931–40, and 27.4 in 1941–50 and 22.8 in 1951–60. In 1966–70, the figure was 15.3 per 1,000. The fall in infant mortality over the same period further confirms this trend. From an annual average of 212 deaths per 1,000 live births between 1911 and 1920, infant mortality in India fell to 176 in 1921–30, 168 in 1931–40, 148 in 1941–50, and 113 in 1966–70 (Davis 1951; Chandrasekhar 1972).

Mortality Levels

The reasons underlying this fall in mortality (and the earlier high levels of mortality) have been much debated. Kingsley Davis (1951) argued that India became “the home of great epidemics” only during the period of British rule (1757–1947), when it was “exposed to foreign contact for the first time on such a great scale.“

Anorexia nervosa is a psychophysiological disorder especially prevalent among young women and is characterized by prolonged refusal to eat or to maintain normal body weight, an intense fear of becoming obese, a disturbed body image in which the emaciated patient feels overweight, and the absence of any physical illness that would account for extreme weight loss. The term anorexia is actually a misnomer, because genuine loss of appetite is rare, and usually does not occur until late in the illness. In reality, most anorectics are obsessed with food and constantly struggle to deny natural hunger.

Clinical Manifestations and Pathology

In anorexia nervosa, normal dieting escalates into a preoccupation with being thin, profound changes in eating patterns, and a weight loss of at least 25 percent of the original body weight. Weight loss is usually accomplished by a severe restriction of caloric intake, with patients subsisting on fewer than 600 calories per day. Contemporary anorectics may couple fasting with self-induced vomiting, use of laxatives and diuretics, and strenuous exercise.

The most consistent medical consequences of anorexia nervosa are amenorrhea (ceasing or irregularity of menstruation) and estrogen deficiency. In most cases amenorrhea follows weight loss, but it is not unusual for amenorrhea to appear before noticeable weight loss has occurred. The decrease in estrogens causes many anorectics to develop osteoporosis, a loss of bone density that is usually seen only in postmenopausal women (Garfinkel and Garner 1982).

Glomerulonephritis, an immunologic disease of the kidneys, affects the glomerulus. This structure, a cluster of capillaries, is the filter in the functioning unit of the kidney, the nephron. Inflammation, initiated by immune complexes (defined below), injures the glomerulus. Often the disease is acute, but it may be silent and completely undetected until signs and symptoms of chronic kidney failure prompt a biopsy, leading to diagnosis. Alternatively, this silent disease may prove fatal, and the diagnosis is made at autopsy.

The urine-secreting structure (nephron) (Figure VIII.60.1) consists of the glomerulus and its tubular system. Each glomerulus consists of a tangle of interconnecting capillaries branching between two tiny arteries (arterioles). A glomerular cross section shows these capillary loops (Figure VIII.60.2). The glomerulus is a blood filter that controls passage of molecules through the basement membrane, depending on their size and charge. Normally red blood cells and albumin are not permitted to pass through the membrane. The tubules reabsorb, secrete, synthesize, and excrete solutes and metabolites, thereby maintaining physiological equilibrium.

This article will deal only with poststreptococcal glomerulonephritis. This disease, described by Richard Bright in the early part of the nineteenth century, still bears his name. Other forms of glomerulonephritis, which he also described, and the glomerular diseases termed glomerulopathies, seen in diabetes or amyloidosis, are not discussed.

Distribution and Incidence

Glomerulonephritis occurs worldwide. The disease was seen frequently in Europe during the eighteenth and nineteenth centuries as a complication of scarlet fever during epidemics. Today glomerulonephritis occurs sporadically. Several epidemics have occurred since the 1950s in the United States, Trinidad, and Venezuela.

Osteoporosis is defined as a proportional decrease of both bone mineral and bone matrix, leading to fracture after minimal trauma. It differs from osteomalacia in which there is a normal amount of bone matrix (osteoid) but decreased mineralization. There are two clinical syndromes of osteoporosis. Type I, or postmenopausal osteoporosis, occurs in women aged 51 to 75; it involves primarily trabecular bone loss, and presents as vertebral crush fractures or fracture of the distal radius. Type II, or senile osteoporosis, occurs in both men and women, particularly after the age of 60; it involves trabecular and cortical bone loss, and more commonly presents with hip and vertebral wedge fractures. Postmenopausal osteoporosis is associated with decreased serum levels of parathyroid hormone and a secondary decrease in activation of vitamin D, whereas senile osteoporosis is associated with a primary decrease in activation of vitamin D and increased parathyroid hormone.

Osteoporosis is an enormous public health problem, responsible for at least 1.2 million fractures in the United States each year. Fractures of the vertebral bodies and hip comprise the majority, and the complications of hip fracture are fatal in 12 to 20 percent of cases. Nearly 30 percent require long-term nursing home care. The direct and indirect costs of osteoporosis in the United States are estimated at over 8 billion in 1989 dollars annually.

The existence of a hereditary tendency to excessive bleeding was recognized in the second century A.D. by Rabbi Judah, who exempted from circumcision the son of a woman whose earlier sons had bled to death after this rite. But only in this century has expanding knowledge of the physiology of hemostasis – the arrest of bleeding – made evident the diverse nature of inherited bleeding disorders. In addition, only recently has it been recognized that a tendency to thrombosis might likewise be due to an inherited hemostatic defect.

Physiology of Hemostasis

The mechanisms by which blood loss in mammals is stopped after vascular disruption are complex. Small vascular injuries are sealed by platelets that adhere to the site of damage, where they attract other circulating platelets, so as to form an occlusive aggregate or plug that can close small gaps. Larger defects in vessel walls are occluded by coagulation of blood – that is, by its transformation from a fluid to a gel-like state. Uncontrolled bleeding and its antithesis, thrombosis (the formation of a clot within a blood vessel), are important pathogenetic factors for human disease, including a large variety of hereditary disorders.

The basic structure of both the occlusive clots that halt blood loss and pathological intravascular clots (or thrombi). is a meshwork of fibrous protein (fibrin) that entraps blood cells. Plato and Aristotle both described the fibers found in shed blood. When the blood vessel wall is disrupted, whether by trauma or disease, a soluble plasma protein, fibrinogen (factor I), is transformed into the insoluble strand of fibrin.

Relapsing fever is a disease characterized by the occurrence of one or more relapses after the primary febrile paroxysm has subsided. Various types of relapsing fever are caused by blood parasites of the Borrelia group. There are two chief forms of the disease: the endemic, transmitted to humans by various ticks of the genus Ornithodoros, and maintained among a variety of rodents; and the epidemic, caused by a parasitic spirochete, Borrelia recurrentis, which is transmitted by human head and body lice. B. recurrentis is less virulent than the tick-borne forms. Under favorable conditions, mortality is about 5 percent, but in times of distress, as in war or famine, it can reach 60 to 70 percent.

It is also known as famine fever and tick fever, and in the past as yellow fever, because of associated jaundice. The term “relapsing fever” was first used by David Craigie of Edinburgh in 1843. The disease was often, and frequently is still, confused with malaria and typhus, whose symptoms are similar.

Etiology and Epidemiology

Tick-borne relapsing fever is normally contained within the relationship between tick and rodent host; human beings become affected only when they accidentally become involved in that relationship. For example, if human shelters such as log cabins attract rodents, they may in turn become tick habitats. Transmission of relapsing fever is through the infected saliva or coxal fluid of the tick, making it essentially a disease of locality. In the case of louse-borne relapsing fever, the only reservoir of B. recurrentis is human beings, despite the fact that the disease is spread by lice, either in the bite, or by contact with the body fluids of the louse through scratching.

Rubella (German measles; 3-day measles) is a common, acute, viral infectious disease, principally of children and young adults, with worldwide distribution frequently characterized clinically as a mild rash illness. Inapparent infection is common and may occur in as many as half of infections. Rubella has special significance when a pregnant woman contracts the disease in early pregnancy because fetal infection can ensue and result in developmental abnormalities known as the congenital rubella syndrome (CRS). Rubella is a vaccine-preventable disease, but the vaccine is not yet widely used on a global basis.

Etiology and Epidemiology

Rubella is caused by the rubella virus, which is in he genus Rubivirus of the family Togaviridae. Rubella virus is 50 to 60 nanometers in diameter and contains a single-stranded RNA genome.

Rubella is a highly contagious disease transmitted by contact of susceptible individuals with the nose and throat secretions of infected persons, primarily by droplet spread. Infection also occurs by direct contact, by indirect contact through freshly soiled articles, and by airborne transmission. There is no reservoir for rubella other than human beings, which means that a continuous chain of susceptible contacts is necessary to sustain transmission. The period of communicability is from about 1 week before rash onset to at least 4 days after. There is no carrier state except for infants with congenital rubella, who may shed virus for many months after birth. Rubella’s incubation period from time of exposure to onset of rash is 16 to 18 days, with a range of 14 to 23 days.

In the inscriptions that record the divinations of Shang dynasty China (eighteenth to eleventh centuries B.C.), we find a number of diagnostic queries like this: “Divining this tooth affliction. Should we hold a festival for Fuyi?” Fuyi refers to a Shang ancestor, and the concern about a propitiatory festival reflects the belief, frequently voiced in the oracles, that sickness arises from the anger and envy of ancestors toward their descendants (Hu 1944; Miyashita 1959). If the welfare of the dead depended on the rituals of the living, the resentments of the dead were something to which the living remained ceaselessly vulnerable.

Disease thus first appears in China embodied in dangerous others, as a menace from without. After the Shang dynasty, the focus of concern would broaden and shift from disgruntled ancestors to parasites and poisons, demons and witchcraft spells. But whomever or whatever the Chinese accused of inspiring sickness, the defining feature of the earliest conceptions of disease was their independence from a conception of the body. In other words, the peculiarities of an individual’s somatic condition were no more relevant to understanding a fever or a toothache than they were for explaining why one’s crops were destroyed in a storm. The fact that an affliction happened to attack the body was incidental. The vengeful spirits that brought sickness could just as easily have inflicted drought and famine.

This accounts in part for why a collection of cures such as the Wushier bing fang (Recipes for fifty-two ailments) of the late third century B.C. tells us so much, on the one hand, about noxious demons and the techniques for exorcizing them and teaches us so little, on the other hand, about the afflicted body itself (Harper 1982).

This form of pneumonia is caused by Pneumocystis carinii, a protozoan of uncertain taxonomic status in the class Sporozoa. An extracellular parasite of the lungs of humans, dogs, rodents, and other mammals, the organism occurs worldwide. It appears to be of low virulence and almost never causes disease except in weak or immunosuppressed individuals. P. carinii was discovered in guinea pigs in 1909, but human disease was first recognized in the 1940s in malnourished and premature infants. Patients suffering from leukemia, Hodgkin’s disease, and other immunosuppressive diseases, or organ transplant recipients and other patients whose treatment requires suppression of the immune system, are also vulnerable to infection. In the early 1980s, pneumocystis pneumonia achieved prominence as the most common opportunistic infection afflicting patients with acquired immune deficiency syndrome (AIDS). Over half of all AIDS victims suffer from this form of pneumonia, and it frequently is the proximate cause of death.

Transmission is usually by airborne droplets, although transplacental passage resulting in fetal death has been reported. Latent infection may be common, with clinical disease and droplet transmission developing only in weakened hosts. The parasite damages the alveolar walls and induces an abundant foamy exudate and fibrosis. Death results from asphyxiation due to the exudate. Although initial response to chemical therapy is common, treatment is difficult because of side effects of the drugs and the debilitated state of the patients.