Anthrax is a serious zoonotic disease that can affect most mammals and several species of birds, but is particularly important in herbivores. This disease is caused by a spore-forming bacterium, Bacillus anthracis. Anthrax spores are extremely resistant to inactivation by heat or chemicals, and can survive in the environment for decades. Susceptibility to clinical disease varies, with domesticated and wild ruminants most susceptible, horses somewhat less susceptible, and omnivores and carnivores relatively resistant.
B. anthracis is derived from the Greek word for coal, anthrakis, because in its cutaneous form it causes black, coal-like lesions. B. anthracis is an aerobic, grampositive, endospore-forming Bacillus species that is encapsulated, non-motile, and non-hemolytic.
B. anthracis is a member of the Bacillus cereus group, which also contains B. cereus and Bacillus thuringiensis. These three organisms are very closely related. Based on genetic analysis, some authors consider them to be a single species; however, this idea is controversial. Plasmids closely related to pX01 and/or pX02 have recently been found in a few B. cereus isolates that caused anthrax-like diseases in people, chimpanzees or gorillas.
The natural reservoir for B. anthracis is soil, and the predominant hosts are herbivores (cattle, sheep, goats, horses, pigs, and others) that acquire infection from consuming contaminated soil or feed. Anthrax spores can persist in soil for years and are resistant to drying, heat, ultraviolet light, gamma radiation, and some disinfectants.5 Anthrax in animals is endemic in many areas of the world and anthrax outbreaks in animals occur sporadically in the United States.
Anthrax as a Biological Weapon
Anthrax was successfully used as a biological weapon in the United States in October 2001. Cases resulted from direct or indirect exposure to mail that was deliberately contaminated with anthrax spores. In total, 22 cases were identified, 11 with inhalational (five fatal) and 11 with cutaneous anthrax (seven confirmed, four suspected).
Several countries have had anthrax weaponization programs in the past, including the United States. In 1979 an outbreak of anthrax in the Soviet Union resulted from accidental release of anthrax spores from a facility producing weaponized anthrax. Of 77 reported human cases, all but two were inhalational, and there was an 86% fatality rate.
Experts believe that an aerosol release of weapons-grade spores is the most likely mechanism for use of anthrax as a biological weapon in the future. Anthrax spores could also be used to deliberately contaminate food and water. Spores remain stable in water for several days and are not destroyed by pasteurization.
Naturally acquired human anthrax infection generally results from contact with infected animals, or occupational exposure to infected or contaminated animal products. The incidence of the natural disease depends on the level of exposure to affected animals. Reported animal: human case ratios in a country or region reflect the economic conditions, quality of surveillance, social traditions, dietary behaviour, etc. in that country or region. In contrast to animals, age- or sex-related bias is generally not apparent in humans, though males generally have higher occupational risk rates in many countries.
Mode of transmission
Anthrax is generally a zoonotic disease. Humans become infected through contact with infected animals and animal products through several mechanisms:
• Contact with infected animal tissues (e.g., veterinarians, animal handlers, meat processors, and other processes that involve animal hides, hair, and bones) or contaminated soil
• Ingestion of contaminated, undercooked meat from infected animals
• Inhalation of infectious aerosols (e.g., those generated during processing of animal products, such as tanning hides, processing wool or bone) Person-to-person transmission of B. anthracis does not occur with gastrointestinal (GI) or inhalational anthrax, but has been reported rarely with cutaneous anthrax
Inhalational anthrax is caused by inhalation of spores that reach the alveoli, undergo phagocytosis and travel to regional lymph nodes. The spores then germinate to become bacterial cells, which multiply in the lymphatic system and cause lymphadenitis of the mediastinal and peribronchial lymph nodes.
The bacteria release toxins that cause hemorrhage, edema, and necrosis. Bacteria entering the bloodstream lead to septicemia, septic shock, and death. Systemic infection following inhalational anthrax is almost always fatal.
In cutaneous anthrax, spores or bacilli are introduced through cuts or breaks in the skin. Spores germinate at the site of contact and release toxins, causing development of a lesion and edema. Organisms may be carried to regional lymph nodes and cause painful lymphadenopathy and lymphangitis. Septicemic complications of cutaneous anthrax occur in 10-20% of untreated cases
Pediatric considerations: A case of cutaneous anthrax occurred in a 7-month old during the anthrax attack of 2001. This case was difficult to recognize and rapidly progressed to severe systemic illness despite timely antibiotic treatment.
Clinical features included a painless draining lesion with edema that developed into an eschar, fever, leukocytosis, severe microangiopathic hemolytic anemia, renal failure, and coagulopathy
Gastrointestinal (GI) anthrax results from ingestion of B. anthracis bacteria, such as may be found in poorly cooked meat from infected animals. The incubation period for GI anthrax is 1-7 days. Two clinical presentations have been described: intestinal and oropharyngeal.
With intestinal anthrax, intestinal lesions occur in the ileum or cecum and are followed by regional lymphadenopathy. Symptoms of intestinal anthrax are initially nonspecific and include low-grade fever, malaise, nausea, vomiting, anorexia and fever. As disease progresses, abdominal pain, hematemesis, and bloody diarrhea develop.
The patient may present with findings of an acute abdomen. After 2-4 days, ascites develop and abdominal pain lessens. Hematogenous spread with resultant septicemia can occur. Mesenteric adenopathy on CT scan is likely, and mediastinal widening on CXR is possible
In oropharyngeal anthrax, a mucosal ulcer occurs initially in the mouth or throat, associated with fever, throat pain, and dysphasia. This is followed by cervical edema and regional lymphadenopathy. Ulcers may become necrotic with development of a white patch covering the ulcer. Swelling can become severe enough to affect breathing. Hematogenous spread, septicemia, and meningitis can occur.
Anthrax meningitis can occur as a complication of cutaneous, inhalational, or GI anthrax, but is most commonly seen with inhalational anthrax (up to 50%). Patients may or may not present with symptoms of the primary site of infection. In addition to typical symptoms of bacterial meningitis, anthrax meningitis may involve hemorrhage or meningoencephalitis.
Case fatality with anthrax meningitis is greater than 90%. Even one case of anthrax meningitis should alert public health authorities to identify the source of exposure and investigate the possibility of bioterrorism
Anthrax and Pregnant Women
Maternal and perinatel complications are not completely understood, because anthrax infection during pregnancy is rare. Preterm delivery may be one of the major complications
Natural strains of B. anthracis are usually susceptible to several antibiotics; most but not all natural strains are susceptible to penicillin. Some strains, particularly those used in bioterrorist attacks, may be resistant to penicillin. For this reason, the U.S. Centers for Disease Control and Prevention (CDC) recommends other antibiotics as the initial treatment, particularly for systemic disease, until antibiotic susceptibility has been determined. Antibiotics are effective only against the vegetative stage of B. anthracis, and not against spores.
Treatment is continued for at least 60 days in inhalational anthrax, as spores may be able to remain dormant in the lungs and germinate during that time. Supportive therapy may also be necessary, particularly for the inhalational and gastrointestinal forms. Effective treatment depends on early recognition of the symptoms: treatment for cutaneous anthrax is usually effective, but the inhalational and gastrointestinal forms are difficult to recognize early and the mortality rates are higher.