tuberculosis(redirected from Pulmonary consumption)
Also found in: Dictionary, Thesaurus, Medical.
Related to Pulmonary consumption: primary tuberculosis, Koch's Disease
tuberculosis(TB), contagious, wasting disease caused by any of several mycobacteria. The most common form of the disease is tuberculosis of the lungs (pulmonary consumption, or phthisis), but the intestines, bones and joints, the skin, and the genitourinary, lymphatic, and nervous systems may also be affected.
There are three major types of tubercle bacilli that affect humans. The human type (Mycobacterium tuberculosis), first identified in 1882 by Robert KochKoch, Robert
, 1843–1910, German bacteriologist. He studied at Göttingen under Jacob Henle. As a country practitioner in Wollstein, Posen (now Wolsztyn, Poland), he devoted much time to microscopic studies of bacteria, for which he devised not only a method of
..... Click the link for more information. , is spread by people themselves. It is the most common one. The bovine type (M. bovis) is spread by infected cattle but is no longer a threat in areas where pasteurization of milk and the health of cattle are strictly supervised. The avian type (M. avis) is carried by infected birds but can occur in humans. The tubercle bacillus can live for a considerable period of time in air or dust. The most common means of acquiring the disease is by inhalation of respiratory droplets.
Course of the Disease
Tuberculosis of the lungs usually results in no or minimal symptoms in its early stages. In most persons the primary infection is contained by the body's immune system, and the lesion, called a tubercle, becomes calcified. In many the infection is permanently arrested. In others the disease may break out again and become active years later, usually when the body's immune defenses are low. Untreated, the infection can progress until large areas of the lung and other organs are destroyed. Symptoms of the disease include cough, sputum, bleeding from the lungs, fever, night sweats, loss of weight, and weakness.
The incidence of tuberculosis of the lungs, the "white plague" that formerly affected millions of people, declined in the United States from the 1950s until 1984; sanatoriums were closed and routine screening was abandoned. Then, between 1984 and 1992, the incidence increased by 20%, chiefly because of immigration from countries where it is common and because of AIDSAIDS
or acquired immunodeficiency syndrome,
fatal disease caused by a rapidly mutating retrovirus that attacks the immune system and leaves the victim vulnerable to infections, malignancies, and neurological disorders. It was first recognized as a disease in 1981.
..... Click the link for more information. , which leaves people particularly vulnerable to the disease. Renewed efforts at control and advances in treatment have been rewarded with incidence declines each year, amounting to a total decline of 31% from 1992 to 1998.
Worldwide the outlook has been far less encouraging. In 1993 the World Health Organization (WHO) declared TB a global health emergency. Approximately one third of the world's population is infected; an estimated 1.3 million died in 2012, making tuberculosis one of the most deadly infectious diseases. The vast majority of new cases occur in sub-Saharan Africa. Spread of TB is especially rapid in areas with poor public health services and crowded living conditions. In homeless shelters and prisons, crowded conditions and inadequate treatment often go together. Areas where living conditions are disrupted by wars, famine, and natural disasters also are heavily affected.
Especially alarming has been the spread of drug-resistant strains of TB. By the late 1990s scientific experts and international health officials warned that drug-resistant strains were spreading faster than had been anticipated. Bacteria can survive and become drug resistant in patients whose treatment is not properly monitored and seen to completion. Multidrug resistant (MDR) TB strains are resistant to two or more of the commonly prescribed first-line drugs, while extensively drug resistant (XDR) strains are also resistant to three or classes of the more toxic second-line drugs. Some believe that unless major new treatment strategies are initiated in source countries, drug-resistant TB will eventually become epidemic even in areas with good control programs, such as Europe and America. In 2011, WHO estimated that there were more than 80,000 cases, many of them undiagnosed, of drug-resistant TB in Europe.
Diagnosis and Treatment
Diagnosis is made by a tuberculin skin test. It can be confirmed by X raysX ray,
invisible, highly penetrating electromagnetic radiation of much shorter wavelength (higher frequency) than visible light. The wavelength range for X rays is from about 10−8 m to about 10−11
..... Click the link for more information. of the chest and sputum examination. Ideally, treatment begins after a skin test signals exposure but before active disease has developed. The treatment of choice for prevention and for active cases is the antimicrobial drug isoniazidisoniazid
, drug used to treat tuberculosis. Also known as isonicotinic acid hydrazide, isoniazid is the most effective antituberculosis drug currently available. The drug inhibits or kills the tubercle bacilli that cause the disease.
..... Click the link for more information. (INH), available since 1956. In infected individuals it now is usually used in combination with other antituberculosis drugs such as rifampin, pyrazinamide, and ethambutol. Bedaquiline is used to treat multidrug resistant and extensively drug resistant TB.
Tuberculosis drugs have to be taken regularly, typically for 6 to 12 months. Many patients abandon their treatment when they feel better; similarly, preventive treatment is often abandoned because of the inconvenience. Such noncompliance is believed to be the main reason for the upsurge in drug-resistant strains of the TB bacilli, many of which are resistant to more than one drug. Drug-resistant TB is difficult to treat and has a much higher death rate; extensively resistant TB is especially worrisome because it can be essentially untreatable.
The combination drug rifater (rifampin, isoniazid, and pyrazinamide) has simplified drug administration. Directly observed treatment, where health-care workers watch patients take each dose of medicine, has proved effective in eliminating the problem of noncompliance in the United States, but monitoring has been less effective in many other parts of the world.
Prevention of Tuberculosis
Preventive measures include strict standards for ventilation, air filtration, and isolation methods in hospitals, medical and dental offices, nursing homes, and prisons. If someone is believed to have been in contact with another person who has TB, preventive antibiotic treatment may have to be given. Infected persons need to be identified as soon as possible so that they can be isolated from others and treated.
An antituberculosis vaccine, bacille Calmette-Guérin, or BCG vaccine, was developed in France in 1908. Although there is conflicting evidence as to its efficacy (it appears to be effective in 50% of those vaccinated), it is given to over 80% of the world's children, mostly in countries where TB is common; it is not generally given in the United States. Federal health officials in the United States have stated (1999) that a new vaccine is essential to TB prevention. It is hoped that the determination of the complete DNA (genome) sequence of Mycobacterium tuberculosis, achieved in 1998, will hasten the development of an effective vaccine.
See R. Dubos, The White Plague (1955); S. A. Waksman, The Conquest of Tuberculosis (1964).
An infectious disease caused by the bacillus Mycobacterium tuberculosis. It is primarily an infection of the lungs, but any organ system is susceptible, so its manifestations may be varied. Effective therapy and methods of control and prevention of tuberculosis have been developed, but the disease remains a major cause of mortality and morbidity throughout the world. The treatment of tuberculosis has been complicated by the emergence of drug-resistant organisms, including multiple-drug-resistant tuberculosis, especially in those with HIV infection. See Acquired immune deficiency syndrome (AIDS)
Mycobacterium tuberculosis is transmitted by airborne droplet nuclei produced when an individual with active disease coughs, speaks, or sneezes. When inhaled, the droplet nuclei reach the alveoli of the lung. In susceptible individuals the organisms may then multiply and spread through lymphatics to the lymph nodes, and through the bloodstream to other sites such as the lung apices, bone marrow, kidneys, and meninges.
The development of acquired immunity in 2 to 10 weeks results in a halt to bacterial multiplication. Lesions heal and the individual remains asymptomatic. Such an individual is said to have tuberculous infection without disease, and will show a positive tuberculin test. The risk of developing active disease with clinical symptoms and positive cultures for the tubercle bacillus diminishes with time and may never occur, but is a lifelong risk. Only 5% of individuals with tuberculous infection progress to active disease. Progression occurs mainly in the first 2 years after infection; household contacts and the newly infected are thus at risk.
Many of the symptoms of tuberculosis, whether pulmonary disease or extrapulmonary disease, are nonspecific. Fatigue or tiredness, weight loss, fever, and loss of appetite may be present for months. A fever of unknown origin may be the sole indication of tuberculosis, or an individual may have an acute influenzalike illness. Erythema nodosum, a skin lesion, is occasionally associated with the disease.
The lung is the most common location for a focus of infection to flare into active disease with the acceleration of the growth of organisms. There may be complaints of cough, which can produce sputum containing mucus, pus- and, rarely, blood. Listening to the lungs may disclose rales or crackles and signs of pleural effusion (the escape of fluid into the lungs) or consolidation if present. In many, especially those with small infiltration, the physical examination of the chest reveals no abnormalities.
Miliary tuberculosis is a variant that results from the blood-borne dissemination of a great number of organisms resulting in the simultaneous seeding of many organ systems. The meninges, liver, bone marrow, spleen, and genitourinary system are usually involved. The term miliary refers to the lung lesions being the size of millet seeds (about 0.08 in. or 2 mm). These lung lesions are present bilaterally. Symptoms are variable.
Extrapulmonary tuberculosis is much less common than pulmonary disease. However, in individuals with AIDS, extrapulmonary tuberculosis predominates, particularly with lymph node involvement. Fluid in the lungs and lung lesions are other common manifestations of tuberculosis in AIDS. The lung is the portal of entry, and an extrapulmonary focus, seeded at the time of infection, breaks down with disease occurring.
Development of renal tuberculosis can result in symptoms of burning on urination, and blood and white cells in the urine; or the individual may be asymptomatic. The symptoms of tuberculous meningitis are nonspecific, with acute or chronic fever, headache, irritability, and malaise.
A tuberculous pleural effusion can occur without obvious lung involvement. Fever and chest pain upon breathing are common symptoms.
Bone and joint involvement results in pain and fever at the joint site. The most common complaint is a chronic arthritis usually localized to one joint. Osteomyelitis is also usually present.
Pericardial inflammation with fluid accumulation or constriction of the heart chambers secondary to pericardial scarring are two other forms of extrapulmonary disease.
The principal methods of diagnosis for pulmonary tuberculosis are the tuberculin skin test (an intracutaneous injection of purified protein derivative tuberculin is performed, and the injection site examined for reactivity), sputum smear and culture, and the chest x-ray. Culture and biopsy are important in making the diagnosis in extrapulmonary disease.
A combination of two or more drugs is used in the initial therapy of tuberculous disease. Drug combinations are used to lessen the chance of drug-resistant organisms surviving. The preferred treatment regimen for both pulmonary and extrapulmonary tuberculosis is a 6-month regimen of the antibiotics isoniazid, rifampin, and pyrazinamide given for 2 months, followed by isoniazid and rifampin for 4 months. Because of the problem of drug-resistant cases, ethambutol can be included in the initial regimen until the results of drug susceptibility studies are known. Once treatment is started, improvement occurs in almost all individuals. Any treatment failure or individual relapse is usually due to drug-resistant organisms. See Drug resistance
The community control of tuberculosis depends on the reporting of all new suspected cases so case contacts can be evaluated and treated appropriately as indicated. Individual compliance with medication is essential. Furthermore, measures to enhance compliance, such as directly observed therapy, may be necessary. See Mycobacterial diseases
an infectious disease of animals and man that tends to be chronic and that causes inflammatory changes, often in the form of small tubercles located mainly in the lungs and lymph nodes.
Tuberculosis of man is the concern of the medical discipline known as phthisiology. Descriptions of tuberculosis symptoms are found in ancient Egyptian papyri and Indian manuscripts, in the works of Hippocrates and other physicians, and in the writings of ancient priests and classical poets. Traces of tuberculosis have been found in Egyptian mummies dating from 3000 to 2000 B.C.. Avicenna (tenth-llth centuries A.D.) noted the extensive occurrence of the disease.
In 17th- and 18th-century London, mortality from tuberculosis reached 700 to 870 per 100,000 inhabitants annually. The rates were comparable in Hamburg, Stockholm, and other large European cities, where tuberculosis accounted for approximately 20 to 40 percent of all deaths. In prerevolutionary Russia, mortality from tuberculosis in Moscow and St. Petersburg was 467 and 607 per 100,000 inhabitants, respectively (1881). Factory workers were particularly susceptible to “the cellar-dweller disease, ” as tuberculosis was called. The mortality from tuberculosis among St. Petersburg workers from 1910 to 1916 was three to five times higher than among the city’s more well-to-do population. A sharp increase in the incidence and mortality rates of tuberculosis occurred everywhere during socioeconomic crises and wars.
The incidence of tuberculosis, as well as its morbidity and mortality, have declined in the economically developed countries owing to improved living conditions and sanitation and the use of effective measures of prevention and treatment. However, the extent of the decline varies from country to country and among different age, sex, and social groups within the same country. For example, the incidence of tuberculosis per 100,000 population in 1969–70 was 60.3 in the German Democratic Republic (GDR), 71.9 in France, 81.5 in the Federal Republic of Germany (FRG), and 199.0 in Japan. The mortality per 100,000 population in 1970 was 5.4 in the GDR, 8.2 in France, 15.3 in Japan, 36 in Hong Kong, and 82 in the Philippines.
In the USA, the incidence and mortality rates of tuberculosis among Negroes, Indians, Puerto Ricans, and other nonwhite groups are three to four times higher than among whites. Among whites, the rates are highest for unskilled laborers and low-salaried employees. In France, the mortality from tuberculosis is three to five times higher among miners, sailors, and fishermen than among persons engaged in the professions, highly paid government employees, and industrial managers. In Paris, the risk of contracting tuberculosis is 25 times higher for immigrant workers from Portugal and Yugoslavia than for native Parisians, and 30 to 50 times higher for Africans (1969–70). Incidence and mortality are high among New Zealand aborigines and among Australian aborigines relocated to regions in the northern and western parts of the country, where living conditions are unfavorable.
No statistics on the incidence and mortality rates for tuberculosis existed in many developing countries of Africa, Asia, and Latin America by the mid-1970’s. Medical examinations of the inhabitants of some areas of these countries have been conducted by personnel of the World Health Organization (WHO) since 1951. The results of these examinations have revealed a high incidence of all forms of tuberculosis, including severe and progressive forms. In India alone, according to approximate calculations, 7 to 10 million persons have bacillary pulmonary tuberculosis. According to WHO estimates, tuberculosis holds third or fourth place among the main causes of death in many developing countries, as compared to eighth or ninth place in economically developed countries.
In the USSR, all the indexes of tuberculosis, especially among children and adolescents, have declined sharply owing to the higher standard of living and the implementation of measures of prevention and treatment on a nationwide scale. In 1972, the incidence and mortality rates of tuberculosis in the USSR had declined by a factor of two as compared to the 1960 levels. Disability from the disease had declined by a factor of almost five. The USSR exhibits a pattern typical of economically developed countries: the sharpest decline in the indexes of tuberculosis was observed in children, adolescents, and young adults, and more among females than among males. The age differences result from the use of the antituberculosis vaccine BCG, of preventive drugs, and of other preventive measures among children and adolescents. The sex differences are caused by the lower incidence among women of such harmful habits as alcohol abuse and smoking.
Mechanisms of infection and pathogenesis. Long before the Common Era, it was believed that tuberculosis was an infectious disease, but it was not until 1865 that the French physician J. A. Villemin proved that it is caused by an infectious agent. In 1882, R. Koch discovered the causative agent, the tubercle bacillus—a sometimes granular bacillus in the shape of a straight or slightly bent rod 1.5–3 micrometers long. The bacillus occurs in filtrable and atypical forms. L-shaped forms have been isolated; these have partly or completely lost their cell wall but are capable of reproducing and, under favorable conditions, of reverting to the classical tubercle bacillus.
All forms of the bacillus are tuberculosis mycobacteria and occur in human, bovine, and avian varieties. The human variety, Mycobacterium tuberculosis var. hominis, infects mainly man. The bovine variety, M. tuberculosis var. bovis, is pathogenic for man as well, but more commonly infects animals. The avian variety, M. avium, infects mainly poultry. In cases of pulmonary tuberculosis in which the causative agent can be isolated, the human variety of the bacillus is found in the sputum and other excretions in 90 to 95 percent of the cases; the bovine variety is found in the remaining 5 to 10 percent of the cases. The bovine variety is somewhat more common in nonpulmonary tuberculosis. The frequency of infection in man by the bovine or avian variety depends on the extent of the infection among domestic animals and poultry, and on the prevailing sanitary conditions.
Tuberculosis is transmitted mainly by airborne droplets of sputum and saliva containing mycobacteria; the droplets are discharged when an infected person coughs, sneezes, or laughs. The bacteria are disseminated with these droplets to a distance of 0.5–1.5 m, remaining in the air about 30 to 60 minutes, and enter the lungs of nearby persons. Droplets of sputum may also remain on the clothing and underwear of an infected person, or on the floor, furniture, rugs, and walls. The droplets dry up, but the mycobacteria they contain are highly resistant to environmental factors and remain viable for a long time. When infected clothing is shaken, the surrounding air may become contaminated with minute particles of dried sputum if the room is not thoroughly cleaned.
Mycobacteria may also enter the body when a person drinks raw infected milk or eats incompletely cooked meat, as well as through a scratch on the skin, for example, when a dairymaid milks a cow with an infected udder. Important factors in all modes of infection are the duration of contact with the source of infection, and the number of bacilli entering the body—that is, the extent of the infection. If the contact is brief, tuberculosis is less likely to develop; it occurs far more often after prolonged, close contact with an infected person who discharges mycobacte-ria-containing sputum without following rules of personal hygiene. Drug-resistant mycobacteria develop in the body of an infected person after incorrect and irregular treatment with modern antituberculotic agents, and these mycobacteria may infect individuals who come in contact with him.
Tuberculosis results only rarely from infection. The great majority of infected persons do not develop the disease, owing to the activity of the body’s defense mechanisms. The body’s innate resistance to tuberculosis is reinforced by specific immunity acquired after vaccination with BCG or after recovery from a mild case of the disease. Factors favoring the development of tuberculosis include extensive and repeated infection, as well as low resistance caused by insufficient high-quality animal proteins and vitamins, in particular, vitamin C. Other contributing factors are unfavorable working conditions and occupational hazards, especially the inhaling of dust containing large amounts of suicide and fluorine. A person is more susceptible if he has had, or is presently suffering from, diabetes mellitus, chronic bronchitis, or alcoholism. Age is also an important factor: young children, who have insufficiently developed immunity mechanisms, are particularly susceptible, as are adolescents, whose nervous and endocrine systems are unstable during puberty. Also susceptible are the middle-aged and the elderly, who often suffer from functional impairment of various organs.
Tuberculosis is marked by the formation of single or multiple small tubercles or of larger foci and inflammatory areas, both at the site where the mycobacteria penetrate and in the organs and tissues to which the mycobacteria are conveyed by the blood and lymph or during inhalation. Under the influence of bacterial toxins, these tissue elements undergo caseous degeneration, and, owing to the influence of the enzymes formed by leukocytes, the tissue elements partially or completely liquefy. If the body’s resistance is adequate, the tubercles or foci are sometimes resorbed. A connective-tissue capsule that is separate from the surrounding tissue generally forms around the tubercles or foci, which may scar over completely and be deposited in caseous masses of calcium salts, sometimes with ossification of the focus. Under unfavorable conditions, caverns may form.
The mycobacteria pass from the cavern in the lungs through the bronchi to other areas of the lung tissue; if sputum is swallowed, they may be conveyed to the intestine. The mycobacteria may also penetrate the mucous membrane of the larynx and pharynx, where they help form new foci. Both the mycobacteria and other bacilli such as streptococci and staphylococci multiply in the cavern, aggravating the patient’s condition. Similar changes take place in other organs where mycobacteria find conditions favorable for reproduction and cause tuberculosis of the pleura, lymph nodes, eyes, bones, kidneys, and meninges. Generalized forms of the disease with simultaneous or successive involvement of many systems of the body are rare.
Tuberculosis is also marked by the rapid development of connective tissue in the lungs, liver, spleen, myocardium, and kidneys. Consequently, many patients die not of the underlying disease but of its complications or of concurrent diseases. However, even widespread and cavernous tuberculosis is curable if treated promptly and correctly. The tubercles, foci, and caverns in the lungs and other organs then undergo scarring, and the exúdate in the pleura, abdominal cavity, and meninges is resorbed.
Symptoms. The symptoms of tuberculosis are varied. Some appear soon after infection; this is the case with primary tuberculosis, whose course depends on the extent of the infection and of the individual’s resistance, and on age and living conditions. In children, the changes in the internal organs are sometimes so slight that they cannot be detected even by a thorough examination. The infection (tuberculosis intoxication) is manifested only by a positive skin reaction to tuberculin, followed by such symptoms as elevated body temperature, night sweats, insomnia, loss of appetite, fatigability, tearfulness, and irritability. This form of tuberculosis has become increasingly rare, and is now uncommon among adolescents and adults.
Symptoms of bronchadenitis, or involvement of the endotho-racic lymph nodes, generally occur after primary infection. The course of bronchadenitis is relatively benign since the foci formed in the lymph nodes are generally small. More severe forms of bronchadenitis develop in young children and are accompanied by a dry, hacking cough and sometimes by labored breathing. In primary infection, individual (and occasionally multiple) small tubercles or relatively large foci form in the lungs at the site where the mycobacteria entered, chiefly from the endothoracic lymph nodes. A primary tuberculosis complex is diagnosed from the presence of a single focus in a lung and the involvement of the endothoracic lymph nodes. The infection may spread from the lungs and lymph nodes to the pleura, resulting in tuberculous pleurisy, which is often the first clinical manifestation of tuberculosis.
Mycobacteria may also enter the cervical, axillary, subman-dibular, and inguinal lymph nodes, which then enlarge and become tender and immobile. The skin over the lymph nodes gradually becomes thin and inflamed. As the disease progresses, the lymph nodes liquefy, and the pus formed in them flows to the surface; over a lengthy period of time it is discharged through fistulas that scar over after healing. If the mycobacteria settle mainly in the lymph nodes of the abdominal cavity, the inflammation involves not only these nodes but the peritoneum (tuberculous peritonitis), the omentum, and the intestine. Symptoms include severe spasmodic abdominal pain, diarrhea alternating with constipation, distension of the intestine, poor appetite, and loss of weight. The infection may reach the bones and joints, causing symptoms of intoxication as well as local manifestations. Tuberculosis of the joints is marked by limited mobility and pain during movement. If the spine is affected, symptoms of spondylitis are also present.
In tuberculosis of the kidneys and bladder, urination is frequent and painful, and there are dull pains in the lumbus. If meningitis occurs, symptoms include severe persistent headaches, vomiting unrelated to food intake, convulsions, and unconsciousness. Timely treatment can prevent death, which was once inevitable, and result in a complete cure.
Tuberculosis of the skin is marked by the formation of tubercles and nodules, or of fairly large nodes and indurations in the subcutaneous tissue. These often appear on the extremities, face, chest, and buttocks, and sometimes ulcerate. Lupus vulgaris is a rare disfiguring form of tuberculosis. When tuberculosis affects the eyes, the symptoms are reddening and edema of the mucous membrane, and the formation of phlyctenae. Symptoms of tuberculosis of the vascular membrane of the eye are the formation of tubercles, photophobia, loss of visual acuity, and sometimes blindness.
The commonest form of tuberculosis is pulmonary tuberculosis, which results chiefly from reinfection of former foci and scars in the lungs and lymph nodes where the infection is dormant. When the body’s resistance is low, the mycobacteria begin to multiply rapidly and to release toxins, causing active tuberculosis. Pulmonary tuberculosis may also be caused by repeated infection, especially after close, prolonged contact with an infected person. Such secondary pulmonary tuberculosis generally begins with the formation of individual small foci, mainly in the upper lobes of the lungs (focal tuberculosis), or with fairly large inflammatory foci differing in shape and size (infiltrative tuberculosis). Disseminated tuberculosis, or acute miliary tuberculosis, in which the foci are disseminated throughout the lungs, is less common.
In pulmonary tuberculosis, symptoms are sometimes slow to manifest themselves, but most patients experience a lowered sense of well-being, night sweats, elevated body temperature, and loss of appetite and of capacity for work. The disease is often accompanied by a dry cough, and occasionally by the discharge of mucopurulent sputum that often contains mycobacteria. The symptoms are more pronounced when lung tissue decomposes and a cavern forms. This occurs in acute tuberculosis and in acute fibroid tuberculosis, in which there may be pulmonary hemorrhage or the expectoration of blood or of blood-stained sputum (hemoptysis). Mycobacteria are generally found in the sputum. The disease may be manifested by dry pleurisy or by pleurisy accompanied by an accumulation of exúdate in the pleural cavity.
Pulmonary tuberculosis is diagnosed mainly by photo-fluorography, a type of roentgenography that is used for testing large numbers of people. Photofluorography can detect tuberculosis when the disease is latent or when it resembles influenza, chronic bronchitis, or chronic pneumonia.
Pulmonary tuberculosis affects persons of all ages, particularly the elderly, and even persons over 90 years of age. Generally, however, the disease begins in youth or middle age and progresses slowly, sometimes for ten to 20 years or more, mainly because of delayed and inadequate treatment. Acute and severe forms that involve the larynx, intestine, and other organs are becoming increasingly rare, owing to a number of factors: improved living conditions, early detection, and highly effective methods of prevention and treatment.
Treatment. The use of isoniazid, streptomycin, and other anti-tuberculotics is an important element in the treatment of tuberculosis. By acting on the enzymes, proteins, and other biochemical constituents of mycobacteria, these drugs suppress the metabolism’and reproduction of the causative agent and decrease the amount of toxins discharged. Two or three antituberculotics are generally taken simultaneously for nine to 18 months or more, depending on the patient’s ability to tolerate the drugs and on the mycobacteria’s resistance to the drugs. The daily dose is often taken at one time; later, the drugs are taken two or three times a week. Vitamins B1, B6, and C, desensitizing agents, and cortico-steroid hormones are used to prevent or eliminate allergic, toxic, or metabolic side effects or their combinations.
Chemotherapy is combined with other methods of treatment to restore the body’s normal physiological state and increase its resistance to infection. It is imperative for the patient to stay in a sanatorium and make use of natural therapeutic factors. Of great importance are proper diet, rest or physical conditioning, and hardening, that is, development of the body’s resistance. A stay in a climatic health resort, for example, in the southern Crimea, is prescribed for some patients. Tuberculin is sometimes administered together with tuberculostatics. Artificial pneumothorax and other types of collapse therapy, widely used before antibacterial agents were known, are occasionally used.
When the patient cannot be cured by antituberculotics and other agents, the affected parts of the lungs are removed surgically. Surgery is also performed for tuberculosis of the bones, kidneys, and appendages of the sex organs. Chemotherapy is used in operative cases and is continued for a long time after the operation. Early treatment cures the great majority of patients with pulmonary tuberculosis. When the prescribed regimen is followed and tuberculostatics are taken regularly for 12 to 15 months, the discharge of bacteria ceases in 90 to 98 percent of the patients in whom pulmonary tuberculosis is detected at an early stage; caverns in the lungs heal in 80 to 90 percent of such patients. Many children, adolescents, and adults now recover from tuberculosis of the bones and kidneys and from meningitis. Consequently, mortality from tuberculosis has greatly declined.
Prevention. Tuberculosis is prevented by state-supported and community programs, including the construction of apartment buildings and public facilities, improved sanitation at places of work, environmental protection, and the raising of the population’s economic and cultural level. Resistance to tuberculosis is increased by such measures as physical culture, hardening, hiking, sports, and proper hygienic conditions for children in nurseries, children’s homes, and schools. To prevent infection within a family, family members with the disease should have separate rooms or live in separate apartments.
Other means of preventing tuberculosis include raising the educational level and increasing the observance of proper sanitation among the population, teaching patients to observe the rules of personal hygiene, hospitalizing infected persons, and removing infected persons from work in children’s institutions and enterprises involving contact with food. Veterinary measures include the disinfection of milk and other food products, and the isolation and slaughter of diseased cattle.
Vaccination with BCG is used for the specific prevention of tuberculosis. In the USSR, all newborns are vaccinated, and all persons are revaccinated up to the age of 30. A positive reaction to the Mantoux test indicates immunity, which lasts for three to five years and then gradually declines. If tuberculosis does not develop during this time, vaccination is repeated. Vaccination with BCG prevents the disease in almost 80 percent of cases and mitigates its course in the remaining-20 percent. Isoniazid, sometimes combined with para-aminosalicyclic acid, is administered daily, generally for a two- to three-month period twice a year, to children, adolescents, and adults in close contact with patients who discharge mycobacteria. These drugs are also administered to other high-risk individuals, including those exhibiting a positive reaction to the tuberculin test, a pronounced reaction to the Mantoux test, or nonactive tuberculous changes in the lungs.
The timely detection of tuberculosis is an important preventive measure. It is achieved by administering the tuberculin test to young children, as well as by testing children over 12 years of age by means of photofluorography at least once every two years, and yearly in Moscow and some other cities. All urban and rural dwellers should be examined regularly in this way. More frequent examinations (yearly or twice yearly) are advisable for hospital and clinical personnel, workers in children’s institutions, students and school personnel, transport workers, barbers and hairdressers, persons who handle food, industrial workers exposed to dust and harmful gases, and persons who come in contact with tuberculosis patients. Persons who have recovered from tuberculosis, but who have traces of latent forms of tuberculosis in their lungs, should be examined at least once a year.
Special working arrangements for individuals and groups help prevent exacerbations of tuberculosis and maintain the work capacity of affected persons. If patients cannot return to their former jobs and need to be requalified, they are taught new skills with the aid of all types of therapy in workshops organized in clinics and sanatoriums in many cities of the USSR. Special work sanatoriums also exist for agricultural workers. Some tuberculosis sanatoriums in the GDR, Poland, Hungary, Italy, the FRG, and other countries have been converted to work rehabilitation centers for pulmonary tuberculosis patients.
Efforts to control tuberculosis in the USSR involve the cooperation of public health, educational, and welfare agencies, trade unions, large industrial enterprises and kolkhozes, public health committees of councils of workers’ deputies, the Red Cross, and the Red Crescent. The most important control functions are carried out by specialized medical institutions and their clinics, and such subdivisions as hospitals, preventoria, and rehabilitation workshops. As of 1972, the USSR had more than 5,500 tuberculosis sanatoriums and divisions or consulting rooms in polyclinics, as well as 261,000 hospital beds. More than 23,500 specialists in tuberculosis and other diseases were employed in these medical facilities. Medical care of patients of all ages and with all forms of tuberculosis is free in the USSR.
REFERENCESRubinshtein, G. R. Differentsial’naia diagnostika zabolevanii legkikh, vols. 1–2. Moscow, 1949–50.
Krasnobaev, T. P. Kostno-sustavnoi tuberkulez u detei, 2nd ed. Moscow, 1950.
Ravich-Shcherbo, V. A. Tuberkulez legkikh u vzroslykh. Moscow, 1953.
Einis, V. L. Tuberkulez: Klinika, profilaktika i léchenle. Moscow, 1961.
Rabukhin, A. E. Tuberkulez organov dykhaniia u vzroslykh. Moscow, 1963.
Rabukhin, A. E. Khimioterapiia bol’nykh tuberkulezom. Moscow, 1970.
Pokhitonova, M. P. Klinika, léchenle i profilaktika tuberkuleza u detei, 5th ed. Moscow, 1965.
Shebanov, F. V. Tuberkulez. Moscow, 1969.
Rukovodstvo po tuberkulezu organov dykhaniia. Edited by S. M. Kniazhetskii. Leningrad, 1972.
Lotte, A., and S. Perdrizet. “Morbidité par tuberculose en France et dans d’autres pays Européens, ” Bulletin de l’Institut national de la santé et de la recherche médicale, l’INSERM, 1971, vol. 26, no. 2, pp. 601–742.
Edwards, L., F. Acquaviva, and T. Livescay. “Identification of Tuberculosis Infected.” American Review of Respiratory Diseases, 1973, vol. 108, no. 6, pp. 1334–39.
The source of the causative agent is infected animals that discharge bacteria together with feces, sputum, or milk, and occasionally with urine or sperm. The disease is transmitted in feed, water, manure, and litter and by grooming implements that have been contaminated by infected excretions. The causative agent survives for a long time in barnyards, poultry yards, ranges, pastures, and watering places. The animals become infected by inhaling the causative agent with airborne droplets or ingesting it with food, generally when they are confined in stalls or pens in congested conditions, improperly fed, and overworked.
Tuberculosis in animals is chronic but may be acute in young animals after extensive infection. The symptoms are highly varied and appear several months or even years after infection. In cattle, the symptoms of pulmonary tuberculosis include a cough and elevated body temperature; the symptoms in intestinal tuberculosis are diarrhea and the presence of mucus, pus, and blood in the feces. Involvement of the uterus and ovaries results in miscarriages and sterility. The lymph nodes typically become enlarged. As the disease develops, the animals lose their appetite and become emaciated; their eyes become sunken and their hair luster-less. Affected animals tire easily and become stooped.
Tuberculosis in swine is generally asymptomatic; if pronounced, the lymph nodes enlarge, a cough develops, and the animals become emaciated. Hens infected with tuberculosis are listless, become rapidly emaciated, and cease laying eggs. Tuberculosis in dogs affects the lungs, intestine, bones, and joints.
Tuberculosis in animals is diagnosed by means of clinical, pathological, allergy, and laboratory tests. Application of the tuberculin test is of major importance. The treatment of tuberculosis in animals is economically unjustified. The disease is prevented and controlled by protecting disease-free farms against the causative agent, examining animals regularly in order to detect the disease promptly, slaughtering diseased animals and segregating unaffected young animals, carrying out coordinated sanitary measures to eradicate the causative agent, and protecting humans from infection. The animals on all farms are examined and given the tuberculin test yearly in order to detect those with the disease. Farms on which tuberculosis is found are placed under quarantine. The diseased animals are slaughtered, and the remaining animals examined by means of the tuberculin test. The farms are then stocked with animals from disease-free farms. Milk from animals with a positive tuberculin reaction is disinfected by boiling and used on the same farm. Eggs from infected flocks are used mainly in the baking industry.
REFERENCERotov, V. I., P. I. Kokurichev, and P. E. Savchenko. Tuberkulezsel’skokhoziaistvennykh zhivotnykh. Kiev, 1973.
any of several bacterial plant diseases characterized by the formation of rough protuberances, or tubercles, on the affected organs. Cavities filled with bacteria develop inside the tubercles; the bacteria are the causative agents of the disease. Tuberculosis attacks the sugar beet, olive, oleander, and ash.
The causative agent of the disease in sugar beets is Xantho-monas beticola. The growths form on the edible roots. The disease occurs in many countries where the sugar beet is a major crop. Usually only a few plants are affected, and, therefore, economic losses are minor. Control measures include proper crop rotation and destruction of diseased roots during harvesting.
In the olive the disease is caused by Pseudomonas savastanoi and is manifested by the formation of walnut-sized swellings on the branches, leaves, and roots. Diseased branches do not grow or bear fruit; sometimes the trees die. Epiphytotics are especially harmful in plant nurseries. The disease is spread by wind and rain, as well as by the olive fruit fly. It occurs mainly in Greece, Italy, and France. In the USSR the disease is an object of external quarantine. Control measures include obtaining healthy planting and grafting material and pruning and destroying diseased branches.
Tuberculosis of the oleander is caused by Pseudomonas savastanoi v. nerii. Galls form on the branches, leaves, and inflorescences. The disease is known in Italy, Spain, France, southern Africa, Australia, the USA, the USSR, and other countries. The causative agent of the disease in ash is Pseudomonas savastanoi v. fraxini. The knots develop on trunks and branches. The disease is observed in France, Italy, the Federal Republic of Germany, the German Democratic Republic, Great Britain, Australia, and the USSR. Control measures for tuberculosis of oleander and ash are the same as for tuberculosis of olive.
REFERENCESBakterial’nye bolezni rastenii, 2nd ed. Moscow, 1960.
Slovar’-spravochnik fitopatologa, 2nd ed. Edited by P. N. Golovin. Leningrad, 1967.
Zhuravlev, I. I., and D. V. Sokolov. Lesnaiafitopatologiia. Moscow, 1969.
N. P. IASHNOVA