Bacillus anthracis can cause an acute bacterial disease in most warm-blooded animals, including swine and man.
In swine, anthrax is relatively rare except when large numbers of anthrax organisms are ingested. Although anthrax occurs throughout the world, incidence in swine in the United States is low. Anthrax in grazing animals other than swine tends to occur in certain geographic areas and to be seasonal. This may not be true of swine.
Although there are many old reports on anthrax in species other than swine, most reports on the disease in swine have occurred since 1952-53. At that time a major epidemic occurred in several Midwestern states. The outbreak was caused by imported, contaminated bone meal used in preparing feed for swine. The feed was widely distributed before anthrax was finally diagnosed.
In 1989-90 an outbreak lasting over 14 weeks in a 500-sow operation was reported. Reports on this outbreak serve to emphasize the great difficulties and expense in depopulating, cleaning and disinfecting a large contaminated confinement facility or slaughterhouse.
Anthrax is caused by Bacillus anthracis, a large, aerobic, Gram-positive rod. The organism is easy to culture and nonhemolytic colonies appear on blood agar in 12-18 hours. Colonies have irregular borders and are sticky when touched by a bacteriologic loop. Under suitable aerobic conditions, spores are formed and are quite resistant to heat, desiccation and many disinfectants. Spores can persist in favorable soils for over 15 years.
In tissue the organisms have a well-developed capsule and grow in short chains. They have square ends where in contact with others of the same chain but may be rounded on free ends.
Decaying, anthrax-infected carcasses and their fluids contaminate the soil where resistant spores are then formed. Most grazing animals ingest the spores while grazing over contaminated soil. Swine, however, are rather resistant to anthrax and seldom are infected while grazing. Infection of swine usually occurs when they have fed on an anthrax-infected carcass or when feeds containing large numbers of spores are fed to them. The source in contaminated feeds is the animal source component, e.g. bone meal, tankage or meat scraps.
During infection the anthrax bacilli produce a complex exotoxin. A lethal factor in the exotoxin is responsible for the death of experimental animals and, presumably, of swine. Lethal factor causes depression of the central nervous system (CNS) and has a harmful effect on mitochondria.
Invasion of the anthrax bacilli usually is through defects in the pharyngeal mucosa or the tonsils. Invasion often is followed by lymphangitis and localization of B. anthracis in tonsils and/or cervical lymph nodes. Alternatively, there can be focal or multifocal localization in the intestine followed by spread to one or more mesenteric lymph nodes. Localizations tend to be necrotizing. Frequently both pharyngeal and intestinal lesions develop. There seldom is a septicemic form of anthrax in swine except, perhaps, in young pigs.
Sudden, unexpected deaths may be the first signs of anthrax following a highly variable incubation phase (one to 20 days). Signs depend upon the site of localization of lesions. Three forms of anthrax, based on site of localization, are termed pharyngeal anthrax, intestinal anthrax, and septicemic anthrax. Swine with pharyngeal anthrax, the most common form, show marked cervical swelling and dyspnea; they may die from suffocation. Other signs include fever, depression, and inappetence, perhaps vomiting.
Swine with intestinal anthrax have similar signs except that cervical edema and dyspnea may not be apparent. Also, there may be bloody feces. Both pharyngeal and intestinal forms can occur in the same animal. Swine are fairly resistant to anthrax and spontaneous recovery from cases with localized lesions is not unusual. Septicemic cases have a short course and may result in sudden death.
A necropsy should not be performed on any animal suspected of having died from anthrax; spores will be formed when the carcass is opened and will persist at the site. Necropsy also will expose humans to anthrax.
In anthrax-infected cadavers, rigor mortis may be weak or absent and the blood may fail to clot. Many animals have no visible external lesions other than, perhaps, pharyngeal swelling. Animals with pharyngeal anthrax, opened inadvertently, usually have a gelatinous cervical edema and markedly enlarged, hemorrhagic, cervical lymph nodes. Tonsils often are covered with fibrinous exudate. There may be a marked pharyngitis. In chronic cases, necrotic lesions in nodes or tonsils may be grayish yellow and circumscribed; often these (signs) are seen in recovering animals.
Swine with intestinal anthrax usually have peritonitis with excessive, bloody peritoneal fluid. Fibrin may be present in the fluid and overlay the serosa of affected segments of intestine. The mesentery attached to affected intestine is edematous and may contain reddened streaks around the vasculature. There are focal or multi-focal areas of severe, often diphtheritic, enteritis. Regional lymph nodes draining the area are enlarged and reddened. Animals with intestinal anthrax often have pharyngeal lesions.
In septicemic anthrax, more likely in small pigs, carcasses appear pale and dehydrated. There is bloodstained peritoneal fluid and scattered petechiation.
Although bacteremia and septicemia are unusual in swine with anthrax, it is advisable to take a peripheral blood sample aseptically for smears and culture. Smears can be fixed in Zenker’s solution and stained with polychrome methylene blue. Anthrax bacilli will appear as long, square-ended, blue rods with a pinkish capsule. Alternatively, smears can be stained with Gram stain. The large Gram-positive, rod-shaped organisms have a “boxcar” appearance that is presumptive but not definitive, of anthrax. Sometimes it may be necessary to biopsy or excise an affected lymph node for culture, using sterile technique. Any necessary cut on a suspected cadaver should be disinfected or plugged with a mass of cotton saturated with 10% formaldehyde.
B. anthracis can be cultured on blood agar and identified from colonies that soon develop. If in doubt about identity of the colony, or if the culture is not pure, it may be possible to purify the culture and confirm the diagnosis by scarifying and inoculating the footpad of a laboratory mouse or guinea pig. They will develop anthrax and the bacillus can then be isolated in pure culture from the laboratory animal. Anthrax must be differentiated from pharyngeal malignant edema, acute erysipelas and CSF.
All cultures, contaminated materials, disposable equipment and infected experimental animals and their feces should be incinerated. Any known or suspected areas of contamination should be disinfected. Ten percent fresh sodium hydroxide, 5% formaldehyde, and 2% glutaraldehyde are among the better disinfectants for B. anthracis.
An attenuated live vaccine against anthrax has been used for prevention in some species but is seldom used for swine since they have enough natural resistance to withstand considerable exposure. Limited experience seems to indicate the vaccine could be used to advantage if necessary. Prevention in swine is usually by avoidance of heavy exposure that might occur through ingestion of anthrax-infected carcasses or contaminated feeds. Laws now exist that prevent importation of raw bone meal. Some states have laws that regulate the use of animal origin products in feeds.
Treatment of infected animals can be effective if given early. Both penicillin and oxytetracycline have been used effectively.