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| INFECTIOUS DISEASES
I. INTRODUCTION Agricultural workers are at increased risk of contracting certain infectious diseases because of regular contact with domestic livestock, poultry, and their environments. For many of these diseases, infected animals appear to be healthy while harboring infectious agents that are capable of infecting humans. These "zoonotic diseases" can be transmitted to humans from live animals, their carcasses or by-products (wool, bone, hides), or the environment they contaminate. Thus farmers and ranchers, slaughterhouse workers, animal transporters, persons who process animal products, and veterinarians all constitute high risk groups for certain zoonoses. Many of the zoonotic infections are not considered to be major human health hazards today. Like other infectious diseases, zoonoses have decreased in importance relative to chronic illnesses. Some (such as bovine tuberculosis) have been dramatically reduced in animal populations in developed nations, and thus are quite rare in humans. Some (such as swine influenza and tularemia) have been more significant hazards in the past, and may increase in importance if the strains of infecting agent increase in virulence. Some (such as histoplasmosis) commonly are subclinical infections. Other zoonoses are probably more common than usually thought, but rarely are properly diagnosed or reported. Zoonoses such as Newcastle disease that can create generalized febrile illness may easily be dismissed by patients and physicians as "the flu." Lack of physician awareness, inadequate diagnostic support, and poorly functioning reporting systems undoubtedly minimize the reported rates of zoonotic disease. Regardless of disease rates, an understanding of the occupational nature of these zoonoses, including the source of an infecting agent and mechanisms of its transmission to humans, is crucial for such diseases as hydatidosis and tularemia which can be fatal if not properly diagnosed and treated. An understanding of many of the zoonoses that are influenza-like when infections are mild can help a physician explain and attack an outbreak of "the flu" in an agricultural industry. Diagnosis of all zoonotic diseases will be greatly improved if physicians routinely draw blood for any febrile illness. This can be spun down and the serum frozen and held for later comparison with convalescent serum, when an illness does not resolve promptly. Only a limited number of the over 150 known zoonoses are considered to be a significant occupational threat to the respiratory systems of agricultural workers in this country. These eight zoonoses either produce systemic illness with major respiratory involvement, or their effects are focussed primarily on the respiratory tract. For most, the lungs are the primary site of entrance of the infectious agent. The eight zoonoses are summarized in Table 1, and are discussed in detail in the remainder of this unit. One additional zoonosis, brucellosis, should be mentioned. This severe systemic, septicemic, febrile illness is not characterized by major respiratory involvement, but can be contracted by packing house workers through inhalation. Most cases among packing house workers may be contracted via aerosols'. In swine and beef packing houses, cases are most common in workers on the killing floor who eviscerate animals and work with warm tissues; however, anyone working in the premises, including janitors and truck drivers who have no contact with animal tissues, can contract brucellosis through aerosols. As more packing houses are built in very small rural communities, the incidence of brucellosis among rural inhabitants is likely to increase. Rural physicians should be aware of the potential for this disease among rural inhabitants, including farmers, who may be working seasonally or part-time in local packing plants. Table 1 Agricultural Infectious Diseases Affecting the Respiratory System Bovine tuberculosis Causation:
ingestion (or inhalation) of Mycobacterivm bovis from
milk, milk products (or inhalation of droplet nuclei from
cattle or other animals)
Population at Risk:
dairy cattle workers, persons ingesting raw milk
Agricultural Activities Resulting in Infection:
any handling of infected animals, especially stabled
animals (resulting in pulmonary TB)
Infection in Humans:
identical to tuberculosis from M. tuberculosis
Prevention:
control of disease in cattle, pasteurize milk
Histoplasmosis Causation:
inhalation of Histoplasma capsulatum spores from
environment where this fungus has grown (bird or bat
feces-enriched soil)
Population at Risk:
farmers, other persons frequenting old buildings where
birds have congregated
Agricultural Activities Resulting in Infection:
any activities aerosolizing dusts from soil or from bird
or bat feces in bird or bat roosts, for example razing
old chicken coops
Infection in Humans:
usually asymptomatic; primary lesions usually in lungs.
4 clinical forms:
ש acute pulmonary, influenza-like-cough, chest pains,
dyspnea, fever, weight loss, hemoptysis,
spontaneous resolution; most common form
ש acute disseminated, hepatosplenomegaly, fever,
prostration, resembles miliary TB, often fatal
ש chronic pulmonary, resembles pulmonary TB
ש chronic disseminated, varied presentation, often
fatal
Prevention:
when working in potentially contaminated enclosures,
spray soil with water and wear dust mask; decontaminate
infected areas
Hydatidosis Causation:
ingestion of cestode eggs (Echinococcus granulosus) from
hands, food, water contaminated by infected dog feces
Population at Risk:
sheepherders in western U.S.; Eskimos
Agricultural Activities Resulting in Infection:
caring for sheep, contact with dogs eating sheep (or
moose) viscera
Infection in Humans:
cysts, possibly growing to great size in lungs, liver (or
elsewhere), producing deformities or pressure, rupturing,
causing death
Prevention:
control dogs' feeding on sheep (or moose) viscera;
careful slaughter of sheep; good personal hygiene
Newcastle disease Causation:
inhalation or contamination of conjunctiva with N.D.
virus from live vaccines, infected birds, their
excrements, carcasses
Population at Risk:
poultry vaccinators, farmers slaughterhouse workers, lab
workers
Agricultural Activities Resulting in Infection:
administering live vaccines, working with live or dead
animals
Infection in Humans:
conjunctivitis; generalized febrile illness with
spontaneous and rapid recovery
Prevention:
prevent disease in poultry; use full face mask respirator
when administering aerosol vaccines
Ornithosis Causation:
primarily through inhalation of Chlamydia psittaci from
infected birds, their carcasses, secretions, contaminated
environments
Population at Risk:
primarily persons owning or handling types of parrots or
pigeons, and turkey processing plant workers-potentially
poultry farmers, others handling poultry
Agricultural Activities Resulting in Infection:
working in turkey processing plant especially
eviscerating birds, any work with poultry, especially
birds that are stressed or crowded
Infection in Humans:
systemic illness with lungs most prominently involved;
great variety of clinical courses from mild influenza-
like infection to acute fulminating pneumonia
Prevention:
control disease in birds, disinfect potentially
contaminated environments, mechanically process poultry
carcasses, regulate importation of birds
Q Fever Causation:
inhalation of Coxiella bumetii (rickettsia) from sheep,
cattle, goats, environment
Population at Risk:
sheep ranchers, dairy workers, slaughterhouse workers,
veterinarians; workers in meat, animal by-product,
transportation industries; lab workers
Agricultural Activities Resulting in Infection:
working with infected placentas, reproductive discharges,
carcasses, by-products of cattle, sheep, goats,
especially assisting in birth process
Infection in Humans:
acute systemic illness: recurrent fever, chills,
sweating, headache, myalgia, malaise, anorexia, nausea,
slow resolution, relapse and chronic infection possible;
pneumonitis in half of patients: dry cough, chest pain,
crepitant rales, lesions on x-ray
Prevention:
limit environmental contamination (burn or bury
placentas, fetal discharges, soiled bedding of infected
animals), pasteurize milk; vaccinate cattle and high risk
groups
Swine influenza Causation:
inhalation of swine influenza virus
Population at Risk:
anyone in direct contact with swine or swine products
Agricultural Activities Resulting in Infection:
handling, working around swine or swine products
Infection in Humans:
influenza (mild or subclinical)
Prevention:
control measures unnecessary, barring evolution of more
virulent strain capable of human-to-human transmission
Tularemia Causation:
ingestion, inhalation, skin or conjunctival inoculation
of Francisella tularensis (bacterium) from numerous
animal species, contaminated environment or insect bites,
contaminated food or water
Population at Risk:
farmers, sheep ranchers, hunters, anyone frequenting
endemic natural environment
Agricultural Activities Resulting in Infection:
contact with sheep and dogs during outbreak (handling
animals, wool, shearing sheep, working in contaminated
environment); contact with contaminated natural
environment
Infection in Humans:
low grade to overwhelming infection
Clinical forms:
ש ulceroglandular (from inoculation of lesions)
generalized febrile illness
ש primary pulmonary (from inhalation), pneumonia or
systemic illness
ש oculoglandular (from inoculation of conjunctiva)
ש typhoidal (from ingestion)
Prevention:
control infection in domestic animals, avoid potentially
infected wild animals and contaminated environments
II. HISTOPLASMOSIS The Infecting Agent Histoplasmosis is caused by inhalation of airborne spores of the fungus, Histoplasma capsulatum. The disease is not contagious, and cannot be contracted from infected animals. The fungus proliferates in old dry bird and bat manure and in soil enriched with feces of gregarious birds (chickens, pigeons, blackbirds, and the like), or feces of bats. Roosting places (old chicken coops, belfrys, attics, caves, barns, silos) are prime habitats for fungal growth. Found around the world, endemic regions in the United States are concentrated in the Missouri, Mississippi, and Ohio River valleys. When are people infected by H. capsulatum? Infection typically results during activities that disturb soil and aerosolize spore-contaminated dusts, especially when razing old chicken coops or barns, cleaning or tearing down other rural buildings, bulldozing and excavating, and visiting bat-inhabited caves. (See Fig. 1) Because of association of H. capsulatum with farm buildings, the disease is frequently found in farmers. However, infection can occur even from casual exposure to fungal spores, such as when a person passes an infested belfry during a downwind. Outbreaks can occur among any families, workers, or other groups exposed to a single focus of infected soil. Bird and bat feces-enriched soil or dust within any enclosed structure should be suspect. Infection also has been found among domestic dogs and, less commonly, in other domestic and wild animals including cattle, sheep, horses, cats, bats, rats, and skunks, but cannot be transmitted from these to other animals. How common is infection with H. capsulatum? In endemic areas, infection rates are high: skin tests for sensitivity to histoplasmin indicate that as much as 80% of these populations has been infected, with prevalence rates increasing from birth to 30 years of age 2; a half million new cases have been estimated to occur in the U.S. annually3. However, 90 to 95% of these cases are asymptomatic, and severe disease is rare. Infection In Humans Many persons in endemic areas demonstrate a positive skin reaction to histoplasmin, and radiological exams sometimes reveal calcified foci from past infection. Most of these were subclinical or mild, undiagnosed cases. Clinical cases vary in severity. Although the primary lesions occur in the lungs, four clinical forms have been differentiated. Following an incubation period of 5 to 18 (most commonly 10) days, acute, pulmonary histoplasmosis may manifest as a flu-like illness, with nonproductive cough, chest pains, and dyspnea. (See Fig. 2) Fever, nightsweats, weight loss, and hemoptysis are evident in more serious cases. This form, which is more common than the other clinical forms, often resolves spontaneously within a day to several weeks, although pulmonary calcifications may remain. Occasionally these cases progress to acute, disseminated histoplasmosis, most commonly in infants and young children, and demonstrate hepatosplenomegaly, septic type fever, and prostration. The course and lesions resemble miliary tuberculosis. Without therapy, such disseminated cases are usually fata.. Chronic pulmonary histoplasmosis, most common in persons over 40, is clinically similar to pulmonary tuberculosis. The disease progresses over months to years, with periods of quiescence. Resolution sometimes occurs spontaneously. Chronic disseminated histoplasmosis occurs rarely in persons with a compromised immune system. Illness varies depending on the location of the fungus, and can include pneumonia, hepatitis, meningitis, endocarditis, and the like. Most frequent in adults, disease may progress over weeks to years, often is fatal, and is extremely refractory to treatment. Diagnosis Histoplasmosis must be differentiated from tuberculosis, influenza, pneumonia, neoplasia, and other mycotic infections. Diagnosis typically is made on the basis of serological tests for serum antibodies, including immunodiffusion and complement-fixation tests. Serological tests for blastomycosis and coccidioidomycosis should be done simultaneously. Diagnosis is confirmed through isolation and identification of H. capsulatum in culture and through detection of fungal cells in clinical materials. Special stains are recommended for detection of the small fungal cells in smears of pus, blood, or sputum, or in histological sections of liver, Iymph nodes, lung, or other tissues. Immunofluorescence techniques also are useful. Positive skin tests to histoplasmin are of limited diagnostic use since they often indicate previous asymptomatic infection. Treatment Treatment is supportive except in more serious cases, when amphotericin B (Fungizone) is the drug of choice. A new oral drug, ketaconizole, may become the drug of choice. Prevention Whenever working in old chicken coops or other possibly contaminated enclosed areas where dusts may become aerosolized, a dust mask should be worn. Soil can be sprayed with water to avoid aerosolization of dust and spores, or may be decontaminated by spraying with a solution of three percent formalin. Caution should be taken when spraying formalin in an enclosure, since it is irritating and can be allergenic. The formalin should dry and buildings should be ventilated before they are used. III. ORNITHOSIS The Infecting Agent Ornithosis is caused by Chlamydia psittaci, an intracellu!ar parasite that (like other chlamydiae) is distinguished from bacteria, viruses, and rickettsiae by reproductive, morphological, and structural traits. Numerous wild and domestic avian species around the world are primary hosts for C. psittaci, with well over 100 species potentially infected. Members of the parrot family are the most frequent hosts. Other potentially infected birds include domestic fowl (turkeys, ducks, geese; typically not chickens), pigeons, starlings, seashore birds, pheasants, and other pleasure and show birds. Infection increases among birds that are crowded or under stress, such as parrot species during importation and turkeys raised in crowded conditions. Poor sanitation and inadequate ventilation of bird quarters promote spread of the agent. Infection in birds is most commonly inapparent or latent, and may remain so for years. Thus, birds that appear healthy may shed the agent and transmit infection. Infected birds can contaminate the environment by shedding C. psittaci in feces and nasal secretions. C. psittaci remains viable in the environment after drying; aerosolized dust can cause infection for extended time periods. Examples of potentially contaminated environments include poultry lots and buildings, other farm buildings where wild birds may congregate such as haylofts, poultry processing or rendering plants, and pet shops. When are people infected with C. psittaci? Humans are incidental hosts of C. psittaci. Persons are infected most commonly by inhaling contaminated air--air, usually in an enclosed space, with aerosolized dusts contaminated with infectious agents (such as dusts from dried fecal material). Infection also can occur from direct contact with infected or dead birds, their feathers, feces, or nasal secretions. Although rare, infection can be transmitted through bird bite, from person to person (especially from seriously ill people with paroxysmal cough), or in laboratories. Both latently and clinically ill birds can transmit infection. However, when under stress, latently infected birds become actively infected and rapidly spread disease by shedding greatly increased numbers of chlamydia. Humans are not infected through handling or ingestion of infected meat. In the United States, infection is contracted most often from members of the parrot family or pigeons. Turkey processing plant workers, especially those who eviscerate birds, experience large outbreaks at irregular intervals. ~See Fig. 3) Anyone having contact with fowl or domestic birds is potentially at risk, including poultry husbandrymen, workers in bird processing or rendering plants, pigeon fanciers, pet shop employees, bird dealers or breeders, pet bird owners or caretakers, exporters of parrot family members, zoo workers, and veterinarians. Even very minor contact with birds or a contaminated environment can cause infection; one in five infected persons recalls no bird contact whatsoever. How common is infection with C. psittaci? Ornithosis is a reportable disease, with 40 to 60 cases reported annually in the U.S. However, a reliable estimate of the number of human cases is not available, because many influenza-like cases go undiagnosed and unreported. Also, serological tests have shown that the majority of human cases are subclinical. The disease's threat as a major public health hazard has been dramatically decreased through bird importation regulations and antibiotic treatment of infection in birds. In recent years, most cases are sporadic, although outbreaks among households with infected pet birds or turkey processing plant employees do still occur. Infection in Humans Infection with C. psittaci produces systemic illness, with lungs being both the portal of entry and the organ system most prominently involved. Following an incubation period of one to two weeks or longer, any of a variety of clinical courses may commence, from asymptomatic cases to acute fulminating pneumonia. Infection is rare but possible in children and most severe in older persons. Mild infection resembles a common respiratory disease or mild influenza, with temperature returning to normal within a week. Onset may be insidious, but cases usually present suddenly, with very high fever, chills, severe headache, photophobia, anorexia, malaise, and painful myalgias and arthralgias. Sore throat or cough (usually dry, but sometimes producing mucopurulent sputum) and chest pain may be present. Pulse is slow in relation to temperature. Pulmonary involvement often is greater than physical findings would indicate. Radiographs reveal soft, patchy infiltrates in the lower lung fields, typically progressing to a bronchopneumonia with extensive consolidation. However, x-rays are variable, and may reveal atelectatic, miliary, or nodular patterns. Auscultation of the thorax may be normal or may reveal moist rales over the lower lung fields. Cases are most severe in patients over 50. Hepatosplenomegaly, vomiting, diarrhea, constipation, myocarditis with chronic valvular dysfunction, hepatitis, insomnia, disorientation, depression, or delirium may be present. Dyspnea and cyanosis reflect extensive pulmonary involvement. Encephalitis or meningitis may appear in terminal cases. Death results from pulmonary collapse and toxemia. Treatment with antibiotics has reduced the case-fatality rate from between 20 and 40% to 1%. Both relapse and later reinfection are possible. Diagnosis Physician awareness of the disease and familiarity with its clinical signs are crucial. Ornithosis should always be suspected in cases of pneumonic illness where there has been any history of recent contact with birds, especially diseased or dead birds. Physicians treating patients employed in a poultry processing plant should suspect ornithosis with any pneumonic illness. It may be helpful to contact the USDA veterinarian about earlier meat inspection records. Even if there is no history of contact with birds, ornithosis should be suspected for any pneumonic illness with persistent high fever, severe headache, myalgia, and pulse-temperature dissociation; splenomegaly is another helpful finding in cases where it is present. Ornithosis must be differentiated from typhoid fever, influenza, brucellosis, Legionnaire's disease, infectious mononucleosis, Q fever, Mycoplasma infections, tularemia, tuberculosis, and other pneumonias. Hemograms are of little diagnostic value, although there may be a modest leukopenia or leukocytosis or anemia. Radiographs may be variable, as described in the previous section. Examination of suspected birds by trained veterinary personnel may prove helpful in human diagnosis. Laboratory confirmation involves serology or isolation. A four-fold increase in acute and convalescent serum samples, using the complement-fixation test for C. psittaci, indicates ornithosis; a single titer of 1:16 in a patient with compatible illness is presumptive evidence of ornithosis. Isolation from sputum, blood, or postmortem tissues can be made in mice, eggs, or tissue culture. Contact the local or state health department, or the Virology Division, Bureau of Laboratories, Center for Disease Control, Atlanta, Georgia. Isolation is hazardous to laboratory personnel and may be difficult, especially if antibiotic treatment is in course. Cases of ornithosis must be reported to a public health authority. Treatment Ornithosis is treated with tetracycline, given ten days to two weeks after the temperature returns to normal to prevent relapse. Improvement if usually noted in 48 to 72 hours, but may require up to a month. Although person-to-person transmission is rare, it is prudent to minimize contact especially with coughing patients. Cases should be traced to their source, and proper precautions taken (see the next section). Prevention Prevention depends on education of persons at risk, focussed on stopping the chain of infection through prevention or early detection of cases in birds. Although the disease cannot be eradicated, it can be kept under control in birds through good sanitation and management techniques that decrease stress and the spread of chlamydiae. These techniques include proper feeding, avoiding prolonged transportation with little food or water, avoiding overcrowding or other stresses, using a running water source rather than stagnant and potentially contaminated water, and, if disease is suspected, repeated serological testing and treatment of the flock. Any birds with a suspected infection must be transported immediately, following proper techniques, to a competent laboratory for diagnosis. Infected birds must be destroyed or treated with antibiotics added to feed. Tetracycline usually eliminates infection in psittacine birds, especially if fed for 45 days. Similar treatment of poultry is of variable efficacy. Ideally, detection occurs before actively infected birds shed high numbers of chlamydia and greatly contaminate the environment. Contaminated farm premises must be quarantined, cleaned, and disinfected with a phenolic compound. Breeding stock must be carefully checked, and farms or pet shops where ornithosis has occurred kept under surveillance. Infected turkeys in particular may show minimal or no antemortem signs, only to demonstrate characteristic lesions at slaughter. Thus, poultry processing plant workers, especially inspectors, need to be constantly aware of possible infection. If infection is detected, if should be traced to its source, the infected flock treated or destroyed, and farm quarters disinfected. Spread of infection can be decreased by mechanical evisceration and defeathering of poultry, and frequent disinfection of the plant. If feeding of subtherapeutic antibiotics to poultry is restricted, ornithosis may increase in the poultry industry. Importation regulations involving quarantine and prophylactic use of antibiotics have decreased spread of ornithosis through imported pet birds. Optimally, high risk personnel should be serologically monitored. No vaccines are available for these workers. IV. Q FEVER The Infecting Agent Q fever is caused by Coxiella burnetii, a rickettsia with several distinctive traits including a strong resistance to physical and chemical agents. This rickettsia has a world-wide distribution, with many species of wild and domestic animals (including fowl), ticks, and other ectoparasites potentially harboring infection. Widespread outbreaks among animals occur in nature. Although infection in domestic animals remains inapparent, C. burnetii becomes localized in the mammary glands and placental tissues, and is shed in large numbers during parturition with the placenta, amniotic fluid, and in milk. Animals may become carriers, shedding the agent for prolonged time periods. Since the rickettsia is highly resistant to heat, desiccation, and other external factors, it survives for months in a contaminated environment and can be transported long distances in contaminated products or as an aerosol. When are people infected by C. buMetii? Most cases of Q fever are contracted through inhalation by persons having occupational contact with infected placentas and reproductive discharges, infected carcasses, and by-products (hides, fleeces, bones) of cattle, sheep, and goats, or dusts from straw or soil in stables where infected animals have given birth. Persons assisting an infected animal giving birth are exposed to very large numbers of rickettsiae. (See Fig. 4) Occupational risk groups include sheep ranchers, slaughterhouse workers, dairy workers, veterinarians, and workers in meat processing, hide, fat rendering, fertilizer, and animal transportation industries. Laboratory workers handling live C. burnetii also constitute a high risk group. Infection through ingestion of milk containing C. burnetii, human infection from wild animals or their ectoparasites, and human-to-human transmission are thought to be possible but very rare. Casual contact with a contaminated environment (such as traveling through a contaminated rural region) may result in infection. How common is infection with C. buMetii? Although infection in animals is widespread, with a majority of dairy cattle in the United States harboring the rickettsia, few clinical cases are diagnosed among humans. The vast majority of human infections are asymptomatic (as are most cases among infected livestock), and a large number of cases remain undiagnosed because of inability to culture the rickettsia and the disease's varied manifestations. Human cases often appear as sporadic outbreaks, corresponding to animals' seasons of birth (when among animal husbandry workers), or to the processing of an infected load of animals (when among those who slaughter livestock or process their by-products). Infection in Humans After an incubation period of two to four weeks, Q fever presents suddenly, most commonly as an acute systemic illness with fever, chills, profuse sweating, severe frontal headache, myalgia, general malaise, anorexia, and sometimes nausea or vomiting. The fever is recurrent, usually lasting 9 to 14 days, but sometimes as long as three months. About half of the patients exhibit respiratory symptoms, including a dry cough, chest pain, or crepitant rales. A percentage of these demonstrate lung lesions on x-ray. Hepatitis is commonly present, but usually not severe enough to cause jaundice. There is much variation in severity and duration. The disease resolves slowly, typically over five to 14 days (if untreated), but possibly requiring up to eight weeks, with a convalescence lasting months and possibly with relapse. Infection is more severe and longer lasting among older persons. Occasionally, Q fever may take a chronic form manifest as subacute endocarditis, most commonly affecting the aortic valve. This may appear as long as a year after acute illness, and often is fatal unless treated. Diagnosis Examination of patients presenting with Q fever may reveal conjunctival suffusion, a slightly inflamed pharynx, and an enlarged liver or spleen. Chest films of persons demonstrating respiratory involvement may reveal lung lesions, usually discrete densities in the middle and lower zones of the lungs. Unlike other rickettsial diseases, rash is absent. Diagnosis is confirmed by specific serologic tests, most commonly a demonstration of a fourfold rise in titer in acute and convalescent sera using the complement-fixation test. More sensitive agglutination tests are available in some laboratories. Although isolation of C. buMetii from body fluids or tissues also is diagnostic, this is not used often because of danger to laboratory personnel. Because of its varied manifestations, Q fever is suggestive of numerous other diseases including influenza, mononucleosis, brucellosis, or typhoid fever (when there is no specific organ involvement); viral pneumonia, Mycoplasma infections, or ornithosis (when there is respiratory involvement); or various forms of hepatitis, leptospirosis, toxoplasmosis, or hepatic abscess (when there is liver involvement). Treatment Tetracycline (or chloramphenicol) administered orally and continued for several days after a patient is afebrile, with reinstatement in the case of relapse, is recommended for treatment of Q fever. However, Q fever is not as responsive to antibiotics as are other rickettsial diseases. The mortality rate for acute Q fever is less than one percent. Patients with subacute endocarditis have a high mortality rate, which can be lowered dramatically with very long-term antibiotic therapy, coupled with valve replacement when necessary. Prevention Control of Q fever depends upon limiting the environmental contamination produced by infected livestock. In particular, placentas and fetal discharges, along with soiled straw or other bedding, should be collected and burned or buried. Cattle also can be vaccinated. Control of the disease in livestock usually cannot be justified unless a severe public health problem arises. Workers constituting high risk groups (such as laboratory workers working with C. burnetii) can be vaccinated. The vaccine, however, often induces skin abscess and should not be administered to sensitized persons. Because milk has been implicated as a source of infection, all milk should be pasteurized. V. BOVINE TUBERCULOSIS Although the primary host of Mycobacterium bovis is cattle, this bacterium can infect a large number of mammalian species including humans. Disease is transmitted among cattle typically through inhalation (resulting in pulmonary tuberculosis), but disease resulting from ingestion of the bacterium also is possible. Infection of cattle or other domestic animals can result in severe economic losses. Human infection with M. bovis is still a public health concern in areas where disease in cattle is not control1ed. This form of tuberculosis remains common in the developing world, especially where milk is not pasteurized or where cattle are stabled. In most of the developed world, where eradication programs and pasteurization of milk are routine, this form of tuberculosis is nearly eradicated among both animals and humans. Although a severe health problem in the United States in the early twentieth century, most human cases today are among older people who were exposed in their youth. Because the disease is not completely eradicated, new cases are seen occasionally. Either cattle or other wild or domestic animal species may infect humans, who are accidental hosts for the bacterium. Earlier in the century, human infection occurred primarily through ingestion of unpasteurized milk or milk products, resulting in extrapulmonary tuberculosis. New cases seen today primarily result from inhalation of droplet nuclei, resulting in pulmonary tuberculosis among farmers or other agricultural workers handling infected animals. Human to human transmission is possible but exceptional. Humans can infect cattle with M. bovis, and have been known to reinfect clean herds. M. bovis is closely related to M. tuberculosis, the human tuberculosis agent, and pulmonary infections from the two bacteria are clinically and radiologically identical. Persons infected with M. bovis have a positive skin reaction to PPD-S. Diagnosis depends on isolation and typing of the agent, including distinguishing any isolate from BCG. Prevention of bovine tuberculosis depends upon repeated testing and eradication of all infected cattle, accompanied by pasteurization of all milk. Once a herd has been repeatedly tested and all positive animals have been eradicated, the herd can be certified as TB-free. Other farm animals (dogs, cats, swine, and the like) in contact with infected cattle also should be tested. Persons with a high risk of infection can be vaccinated with BCG. Bovine tuberculosis is notifiable in most states. The atypical mycobacterium, M. avium, also can infect humans and produce a pulmonary disease resembling tuberculosis. The bacterium's primary host is birds, both wild and domestic. Infection of humans is rare in the Midwest, but common in the southeastern United States. Most cases are occupational, contracted either by dust inhalation from chicken coops or through ingestion. Human infection is difficult to diagnose since it can result in cross reactions that interfere with the routine skin test for M. tuberculosis. Treatment is extremely difficult, and should be conducted under direction of a specialist. Eradication of the disease among chickens requires drastic measures, since the agent may persist in contaminated manure and soil. VI. HYDATIDOSIS Hydatidosis (also called unilocular hydatid disease and echinococcosis) results from infection with the larval stage of the cestode Echinococcus granulosus. These tapeworms normally complete their life cycle in domestic or wild canines (hosts for the adults) and herbivores including sheep, cattle, swine, or moose (hosts for the larval stages). Eggs in feces of canines are ingested from contaminated grass or water by herbivores. These eggs hatch and migrate through intestinal walls to various organs, where they encyst. Later ingestion of the cysts by canines leads to reinfection and completes the tapeworm's life cycle. (See Fig. 5) Human infection in the continental United States is rare, but has occurred in sheep-growing regions of western states, where the tapeworm is propagated by dogs and sheep. Humans unwittingly ingest the eggs in food or water contaminated by infected dog feces, or through hand-to-mouth transfer from dogs or feces-contaminated objects. Infections have been reported among native Americans and Rocky Mountain sheepherders; a fair number of cases have been found in Eskimos, due to the tapeworm's propagation by dogs and domestic caribou. Humans do not harbor the adult worm, and human-to-human transmission does not occur. Cysts in humans occur primarily in liver and lungs, although any organ can be affected. The slow growing, strongly encapsulated cysts may take years to produce clinical symptoms, or may remain asymptomatic, to be found at autopsy or during surgery or radiography performed for other reasons. On the other hand, cysts can attain great size (to 10 cm. diameter) and produce severe to fatal responses by producing physical deformities, by placing pressure on vital organs, by rupturing (producing anaphylactic shock and pulmonary edema, arterial embolisms, or seeding to other organs), or by causing bone necrosis or central nervous system disorders. Cysts in the lungs may be asymptomatic or may produce pain, dry cough, hemotysis, vomiting (when cysts have ruptured), or deformation of the thorax. Hydatidosis in humans is detected by radiography or surgery, with serological tests or (when cysts have ruptured) examination of body discharges for cyst contents aiding in diagnosis. Surgical removal is the only treatment. Hydatidosis is best prevented by interrupting the tapeworm's life cycle through eliminating dogs' feeding on viscera of sheep or other intermediate hosts. Sheep should be butchered under controlled conditions, with incineration or deep burial of their entrails. In endemic areas, the number of dogs should be reduced, and those remaining should be regularly treated for tapeworms. Public education on the causes and dangers of this disease is important; residents should understand the importance of controlling dogs and their feeding habits, of careful slaughter of sheep, and of personal hygiene. Hydatidosis caused by infection with E. multilocularis (also called alveolar hydatid disease) is similar to unilocular hydatid disease except for a few key points. In humans, these cysts are found primarily in the liver, but can occur in lungs or other organs. The cysts are not restricted by a strong membrane, and therefore they can invade surrounding tissues and also metastasize. Thus, this disease often is fatal. It has been found in north-central states and Alaska, where it is maintained primarily by foxes and small rodents, although wolves, domestic dogs, and cats also can harbor the mature tapeworms. Thus, this is not considered to be an occupational hazard of sheep growers or other agricultural workers. VII. NEWCASTLE DISEASE Newcastle disease, resulting from infection with an RNA virus of the paramyxovirus group, is found in fowl throughout the world. One of the most important diseases of domestic fowl, it causes high mortality rates and significant economic losses. Although not common among humans, it occurs primarily among persons who administer vaccines to poultry and laboratory workers but also is seen in poultry farmers and slaughterhouse workers. The virus is transmitted by diseased birds or their excrements, by poultry products, by live vaccines, and by virus cultures in laboratories. Humans become infected either through inhalation or through contamination of conjunctiva, such as when infected body fluids are splashed, sprayed, or rubbed by contaminated hands into eyes. Use of live vaccines applied as aerosols permits mass vaccination; thus this technique is used in modern poultry industries with large concentrations of birds. (See Fig. 6) Such vaccination permits human infection both through exposure of the conjunctiva and inhalation. Human disease most commonly appears as mild to severe conjunctivitis. However, inhalation of aerosols of the virus results in a generalized febrile influenza-like infection, lasting three to four days. Recovery is spontaneous, without sequelae. Due to the mild and self-limiting nature of most infections, they may go undiagnosed and without medical attention. Subclinical infections also are common, as demonstrated by high titers found among poultry slaughterhouse workers. Definitive diagnosis depends on isolating the virus from conjunctival or nasopharyngeal secretions, saliva, or urine. Treatment is symptomatic. The chief control measure is prevention of the disease in poultry, through good hygiene and routine vaccination. Persons administering aerosol vaccines must wear respirators (full face masks) that protect eyes, nose, and mouth from exposure. Persons working with vaccines, infected birds, or virus cultures should take steps to avoid formation of aerosols, and exposure of eyes by contaminated hands. VIII. SWINE INFLUENZA Transmission of influenza from farm animals to humans became a widespread concern in 1976, when a new human influenza A virus (A/New Jersey/76) was identified in Fort Dix army recruits. This virus proved to be related antigenically to the virus that had caused many millions of deaths in the 1918-19 pandemic, and since then has been circulating among swine. Fears that the new swine-like virus would create an equally devastating pandemic resulted in a massive nation-wide vaccination effort. However, the appearance of the virus was an isolated event. Although over 500 persons at Fort Dix were shown to be serologically positive, evidence of communicability of this influenza from person to person was never found elsewhere. The influenza virus first appeared among swine in 1918, when it hypothetically was contracted from humans suffering from the "Spanish flu." This virus appeared to have become less virulent, until it disappeared from the human population in the 1920's. It continues to circulate among swine, where outbreaks typically recur annually. No changes in virulence or distribution have been recognized. The virus retains a low virulence for humans. Although a few human deaths have been attributed to swinelike viruses, severe disease resulting from a swine-like virus is extremely rare, and (except for Fort Dix cases) has resulted only from direct contact with swine. However, persons regularly in contact with swine (veterinarians, hog producers, abattoir workers) have an above-normal rate of antibody to the swine influenza virus. Mammalian reservoirs of Group A influenza viruses (including horses and fowl as well as swine) may act as sources of new human sub-types, perhaps by recombination with human strains. Although never proven, this may have been the source of the Fort Dix cases, which differed from other swine-like viruses infecting humans by being somewhat more virulent and also capable of transmission from person to person. Some speculate that a major pandemic resulting from antigenic shift in a swine-like virus may yet occur. Swine influenza could be considered an occupational hazard of agricultural workers or others in frequent contact with swine or swine products. However, the vast majority of all human cases appear to be mild or subclinical. IX. TULAREMIA Tularemia, caused by infection with the bacterium Francisella (Pasteurella) tularensis, infects a large number of vertebrates and invertebrates throughout North America, the USSR, continental Europe, and Japan. Normally, the disease circulates among wild animals; domestic animals and humans become accidental hosts when they enter areas where infection prevails. Tularemia has been identified in sheep, goats, swine, cattle, horses, cats, and dogs. Humans become infected either directly from infected animals or from a contaminated environment in any of a number of ways: through tick or insect bites, skin inoculation (through scratches or knife cuts), splashing contaminated water onto the conjunctiva (or rubbing the conjunctiva with contaminated hands), ingesting contaminated water or improperly cooked meat of dead animals, or inhalation of contaminated dusts. The North American animals most commonly affecting humans are wild rabbits, sheep, horses, beaver, muskrat, microtine rodents, ticks, and deer flies. Both hunters and farmers are considered to be risk groups, with farmers risking infection both because of their contact with the natural environment (and potentially contaminated water or infected ticks or biting insects), and because of their contact with sheep and dogs. In western states, sheep become chronically infected causing degenerative illness of moderate economic significance. Sheep farmers and shearers are infected by inhalation of aerosols of the desiccated organism from the animals, their wool, contaminated hay, grain, feces, or soil; by skin inoculation with blood, tissues, or excreta of infected sheep; or by rubbing their eyes after handling or shearing sick animals. Human cases usually are sporadic, and the number of human infections in the United States has decreased dramatically since 1950. Illness can range from low grade to overwhelming infection. Following an incubation period of two to ten days, illness commences rapidly, with undulant fever, chills, asthenia, myalgia, cephalagia, and vomiting. If untreated, the disease resolves over three to five weeks, with a lengthy convalescence. Systemic infection occurs with tularemia regardless of the route of invasion and clinical presentation. Over three quarters of all cases are ulceroglandular, resulting from inoculation of a local lesion, which may develop into a necrotic ulcer with swelling of regional lymph nodes. A less common but more serious form of importance to farm workers is primary pulmonary, due to inhalation of aerosols, producing pneumonia in one or both lungs. In addition, about one-third of all patients develop bronchopneumonia irrespective of the portal of entry. Other forms of tularemia include the oculoglandular form (from inoculation of conjunctiva), and the typhoidal form (from ingesting contaminated food or water). The typhoidal and pulmonary forms are most severe, with fatality rates of over 50% prior to the era of antibiotics. Today, with prompt administration of streptomycin (or, when necessary, tetracycline or chloramphenicol), the mortality rate and recovery period for all forms have dropped dramatically. Prevention of tularemia involves controlling infection among domestic animals (e.g., through treating sheep with acaricides and antibiotics during outbreaks) and avoidance of potentially infected wild animals or contaminated environments in endemic areas. Techniques to do so include properly cooking wild rabbit meat, not drinking untreated water from ponds, streams, and the like in endemic areas, and avoiding arthropod bites through use of repellents and protective clothes. High risk personnel can be immunized. תתתתתתתתתתתתתתתתתתתתThe National Dairy Database (1992)תתתתתתתתתתתתתתתתתתתת תתתתתתתתתתתתתתתתתתתתת\NDB\OCCSAFE\TEXT2\OF201000.TXTתתתתתתתתתתתתתתתתתתתתתת %f TITLE;INFECTIOUS DISEASES |
