Anthrax is a rare bacterial disease of horses caused by the sporeforming bacterium Bacillus anthracis.
Anthrax is most common in wild and domestic herbivores (eg, cattle, sheep, goats, camels, antelopes) but can also be seen in horses. Grazing animals may become infected when they ingest sufficient quantities of these spores from the soil. In addition to direct transmission, biting flies may mechanically transmit B anthracis spores from one animal to another.
B anthracis spores have a high affinity for macrophages. After wound inoculation, ingestion, or inhalation, spores infect macrophages, germinate, and proliferate. In cutaneous and GI infection, proliferation can occur at the site of infection and the lymph nodes draining the site of infection. Lethal toxin and edema toxin are produced by B anthracis and respectively cause local necrosis and extensive edema, which is a frequent characteristic of the disease. As the bacteria multiply in the lymph nodes, toxemia progresses and bacteremia may ensue. With the increase in toxin production, the potential for disseminated tissue destruction and organ failure increases. After vegetative bacilli are discharged from an animal following death (by carcass bloating, scavengers, or postmortem examination), the oxygen content of air induces sporulation. Spores are relatively resistant to extremes of temperature, chemical disinfection, and dessication. Necropsy is discouraged because of the potential for vegetative cells to be exposed to air, resulting in large numbers of spores being produced. Because of the rapid pH change following death and decomposition, vegetative cells in an unopened carcass quickly die without sporulating.
Typically, the incubation period is 3-7 days (range 1−14 days). The clinical course ranges from peracute to chronic. The peracute form (common in cattle and sheep) is characterized by sudden onset and a rapidly fatal course. Staggering, dyspnea, trembling, collapse, a few convulsive movements, and death may occur in cattle, sheep, or goats with only a brief evidence of illness.
The disease in horses may be acute. Signs may include fever, chills, severe colic, anorexia, depression, weakness, bloody diarrhea, and swellings of the neck, sternum, lower abdomen, and external genitalia. Death usually occurs within 2-3 days of onset.
Rigor mortis is frequently absent or incomplete. Dark blood may ooze from the mouth, nostrils, and anus with marked bloating and rapid body decomposition. If the carcass is inadvertently opened, septicemic lesions are seen. The blood is dark and thickened and fails to clot readily. Hemorrhages of various sizes are common on the serosal surfaces of the abdomen and thorax as well as on the epicardium and endocardium. Edematous, red-tinged effusions commonly are present under the serosa of various organs, between skeletal muscle groups, and in the subcutis. Hemorrhages frequently occur along the GI tract mucosa, and ulcers, particularly over Peyer’s patches, may be present. An enlarged, dark red or black, soft, semifluid spleen is common. The liver, kidneys, and lymph nodes usually are congested and enlarged. Meningitis may be found if the skull is opened. In pigs with chronic anthrax, the lesions usually are restricted to the tonsils, cervical lymph nodes, and surrounding tissues. The lymphatic tissues of the area are enlarged and are a mottled salmon to brick-red color on cut surface. Diphtheritic membranes or ulcers may be present over the surface of the tonsils. The area around involved lymphatic tissues generally is gelatinous and edematous. A chronic intestinal form involving the mesenteric lymph nodes is also recognized.
A diagnosis based on clinical signs alone is difficult. Confirmatory laboratory examination should be attempted if anthrax is suspected. Because the vegetative cell is not robust and will not survive 3 days in transit, the optimal sample is a cotton swab dipped in the blood and allowed to dry. This results in sporulation and the death of other bacteria and contaminants.
Specific diagnostic tests include bacterial culture, PCR tests, and fluorescent antibody stains to demonstrate the agent in blood films or tissues. Western blot and ELISA tests for antibody detection are available in some reference laboratories. Lacking other tests, fixed blood smears stained with Loeffler’s or MacFadean stains can be used and the capsule visualized; however, it can result in some 20% false positives.
In horses, acute infectious anemia, purpura, colic, lead poisoning, lightning strike, and sunstroke may resemble anthrax.
Anthrax is controlled through vaccination programs, rapid detection and reporting, quarantine, treatment of asymptomatic animals (postexposure prophylaxis), and burning or burial of suspect and confirmed cases. In livestock, anthrax can be controlled largely by annual vaccination of all grazing animals in the endemic area and by implementation of control measures during epizootics. The nonencapsulated Sterne-strain vaccine is used almost universally for livestock immunization. Vaccination should be done 2-4 wk before the season when outbreaks may be expected. Because this is a live vaccine, antibiotics should not be administered within 1 wk of vaccination. Before vaccination of dairy cattle during an outbreak, all of the procedures required by local laws should be reviewed and followed. Human anthrax vaccines currently licensed and used in the USA and Europe are based on filtrates of artificially cultivated B anthracis.
Early treatment and vigorous implementation of a preventive program are essential to reducing losses among livestock. Livestock at risk should be immediately treated with a long-acting antibiotic to stop all potential incubating infections. This is followed by vaccination ~7-10 days after antibiotic treatment. Any animals becoming sick after initial treatment and/or vaccination should be retreated immediately and revaccinated a month later. Simultaneous use of antibiotics and vaccine is inappropriate, as the Sterne vaccine is live. Animals should be moved to another pasture away from where the bodies had lain and any possible soil contamination. Suspected contaminated feed should be immediately removed. Domestic livestock respond well to penicillin if treated in the early stages of the disease.
Oxytetracycline given daily in divided doses also is effective. Other antibacterials, including amoxicillin, chloramphenicol, ciprofloxacin, doxycycline, erythromycin, gentamicin, streptomycin, and sulfonamides also can be used, but their effectiveness in comparison with penicillin and the tetracyclines has not been evaluated under field conditions.
In addition to therapy and immunization, specific control procedures are necessary to contain the disease and prevent its spread. These include the following: 1) notification of the appropriate regulatory officials; 2) rigid enforcement of quarantine (after vaccination, 2 wk before movement off the farm, 6 wk if going to slaughter); 3) prompt disposal of dead animals, manure, bedding, or other contaminated material by cremation (preferable) or deep burial; 4) isolation of sick animals and removal of well animals from the contaminated areas; 5) cleaning and disinfection of stables, pens, milking barns, and equipment used on livestock; 6) use of insect repellents; 7) control of scavengers that feed on animals dead from the disease; and 8) observation of general sanitary procedures by people who handle diseased animals, both for their own safety and to prevent spread of the disease. Contaminated soils are very difficult to completely decontaminate, but formaldehyde will be successful if the level is not excessive. The process generally requires removal of soil.