Anthrax


Anthrax is an infection caused by the bacterium Bacillus anthracis or Bacillus cereus biovar anthracis. Infection typically occurs by contact with the skin, inhalation, or intestinal absorption. Symptom onset occurs between one day and two months after the infection is contracted. The skin form presents with a small blister with surrounding swelling that often turns into a painless ulcer with a black center. The inhalation form presents with fever, chest pain, and shortness of breath. The intestinal form presents with diarrhea, abdominal pains, nausea, and vomiting.
According to the U.S. Centers for Disease Control and Prevention, the first clinical descriptions of cutaneous anthrax were given by Maret in 1752 and Fournier in 1769. Before that, anthrax had been described only in historical accounts. The German scientist Robert Koch was the first to identify Bacillus anthracis as the bacterium that causes anthrax.
Anthrax is spread by contact with the bacterium's spores, which often appear in infectious animal products. Contact includes inhalation, eating, or through an area of broken skin. It does not typically spread directly between people. Risk factors include people who work with animals or animal products, and military personnel. Diagnosis can be confirmed by finding antibodies or the toxin in the blood or by the culture of a sample from the infected site.
The anthrax vaccine is recommended for people at high risk of infection. Immunizing animals against anthrax is recommended in areas where previous infections have occurred. A two-month course of antibiotics such as ciprofloxacin, levofloxacin and doxycycline after exposure can also prevent infection. If infection occurs, treatment is with antibiotics and possibly antitoxin. The type and number of antibiotics used depend on the type of infection. An antitoxin is recommended for those with widespread infection.
A rare disease, human anthrax is most common in Africa and central and southern Asia. It occurs more regularly in Southern Europe than elsewhere on the continent and is uncommon in Northern Europe and North America. Globally, at least 2,000 cases occur a year, with about two cases a year in the United States. Skin infections represent more than 95% of cases. Without treatment the risk of death from skin anthrax is 23.7%. For intestinal infection the risk of death is 25 to 75%, while respiratory anthrax has a mortality of 50 to 80%, even with treatment. Until the 20th century anthrax infections killed hundreds of thousands of people and animals each year. In herbivorous animals infection occurs when they eat or breathe in the spores while grazing. Humans may become infected by killing and/or eating infected animals.
Several countries and non-state groups have developed anthrax as a weapon. It has been used in biowarfare and bioterrorism since 1916. Likely delivery methods of weaponized anthrax include aerial dispersal or dispersal through livestock. In World War II, it was developed and used by the Empire of Japan's Unit 731 against China, and researched by a British plan against Nazi Germany. The Soviet, United States, and Iraqi biological weapons program developed weaponized strains. In 1975, the Biological Weapons Convention prohibited the "development, production and stockpiling" of biological weapons. It has since been used in bioterrorism, including the 2001 anthrax attacks in the United States and an incident in 1993 by the Aum Shinrikyo group in Japan.

Etymology

The English name comes from anthrax, the Greek word for coal, possibly having Egyptian etymology, because of the characteristic black skin lesions people with a cutaneous anthrax infection develop. The central black eschar surrounded by vivid red skin has long been recognised as typical of the disease. The first recorded use of the word "anthrax" in English is in a 1398 translation of Bartholomaeus Anglicus's work De proprietatibus rerum.
Anthrax was historically known by a wide variety of names, indicating its symptoms, location, and groups considered most vulnerable to infection. They include Siberian plague, Cumberland disease, charbon, splenic fever, malignant edema, woolsorter's disease and la maladie de Bradford.

Signs and symptoms

Skin

Cutaneous anthrax, also known as hide-porter's disease, is when anthrax occurs on the skin. It is the most common and least dangerous form. Cutaneous anthrax presents as a boil-like skin lesion that eventually forms an ulcer with a black center. The black eschar often shows up as a large, painless, necrotic ulcer at the site of infection. In general, cutaneous infections form within the site of spore penetration two to five days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections normally do not cause pain. Nearby lymph nodes may become infected, reddened, swollen, and painful. A scab forms over the lesion soon, and falls off in a few weeks. Complete recovery may take longer. Cutaneous anthrax is typically caused when B. anthracis spores enter through cuts on the skin. This form is found most commonly when humans handle infected animals and/or animal products.

Injection

In December 2009, an outbreak of anthrax occurred among injecting heroin users in the Glasgow and Stirling areas of Scotland, resulting in 14 deaths. It was the first documented non-occupational human anthrax outbreak in the UK since 1960. The source of the anthrax is believed to have been dilution of the heroin with bone meal in Afghanistan. Injected anthrax may have symptoms similar to cutaneous anthrax, with the exception of black areas, and may also cause infection deep into the muscle and spread faster. This can make it harder to recognise and treat.

Lungs

Inhalation anthrax usually develops within a week after exposure, but may take up to 2 months. During the first few days of illness, most people have fever, chills, and fatigue. These symptoms may be accompanied by cough, shortness of breath, chest pain, and nausea or vomiting, making inhalation anthrax difficult to distinguish from influenza and community-acquired pneumonia. This is often described as the prodromal period.
Over the next day or so, shortness of breath, cough, and chest pain become more common, and complaints not involving the chest such as nausea, vomiting, altered mental status, sweats, and headache develop in one-third or more of people. Upper respiratory tract symptoms occur in only a quarter of people, and muscle pains are rare. Altered mental status or shortness of breath generally brings people to healthcare and marks the fulminant phase of illness.
It infects the lymph nodes in the chest first, rather than the lungs themselves, a condition called hemorrhagic mediastinitis, causing bloody fluid to accumulate in the chest cavity, thereby causing shortness of breath. The second stage occurs when the infection spreads from the lymph nodes to the lungs. Symptoms of the second stage develop suddenly within hours or days after the first stage. Symptoms include high fever, extreme shortness of breath, shock, and rapid death within 48 hours in fatal cases.

Gastrointestinal

infection is most often caused by consuming anthrax-infected meat and is characterized by diarrhea, potentially with blood, abdominal pains, acute inflammation of the intestinal tract, and loss of appetite. Occasional vomiting of blood can occur. Lesions have been found in the intestines and in the mouth and throat. After the bacterium invades the gastrointestinal system, it spreads to the bloodstream and throughout the body, while continuing to make toxins.

Cause

Bacteria

Bacillus anthracis is a rod-shaped, Gram-positive, facultative anaerobe bacterium about 1 by 9 μm in size. It was shown to cause disease by Robert Koch in 1876 when he took a blood sample from an infected cow, isolated the bacteria, and put them into a mouse. The bacterium normally rests in spore form in the soil, and can survive for decades in this state. Herbivores are often infected while grazing, especially when eating rough, irritant, or spiky vegetation; the vegetation has been hypothesized to cause wounds within the gastrointestinal tract, permitting entry of the bacterial spores into the tissues. Once ingested or placed in an open wound, the bacteria begin multiplying inside the animal or human and typically kill the host within a few days or weeks. The spores germinate at the site of entry into the tissues and then spread by the circulation to the lymphatics, where the bacteria multiply.
The production of two powerful exotoxins and lethal toxin by the bacteria causes death. Veterinarians can often tell a possible anthrax-induced death by its sudden occurrence and the dark, nonclotting blood that oozes from the body orifices. Most anthrax bacteria inside the body after death are outcompeted and destroyed by anaerobic bacteria within minutes to hours post mortem, but anthrax vegetative bacteria that escape the body via oozing blood or opening the carcass may form hardy spores. These vegetative bacteria are not contagious. One spore forms per vegetative bacterium. The triggers for spore formation are not known, but oxygen tension and lack of nutrients may play roles. Once formed, these spores are very hard to eradicate.
The infection of herbivores by inhalation normally begins with inhaled spores being transported through the air passages into the tiny air sacs in the lungs. The spores are then picked up by scavenger cells in the lungs and transported through small vessels to the lymph nodes in the central chest cavity. Damage caused by the anthrax spores and bacilli to the central chest cavity can cause chest pain and difficulty breathing. Once in the lymph nodes, the spores germinate into active bacilli that multiply and eventually burst the macrophages, releasing many more bacilli into the bloodstream to be transferred to the entire body. Once in the bloodstream, these bacilli release three proteins: lethal factor, edema factor, and protective antigen. The three are not toxic by themselves, but their combination is incredibly lethal to humans. Protective antigen combines with these other two factors to form lethal toxin and edema toxin, respectively. These toxins are the primary agents of tissue destruction, bleeding, and death of the host. If antibiotics are administered too late, even if the antibiotics eradicate the bacteria, some hosts still die of toxemia because the toxins produced by the bacilli remain in their systems at lethal dose levels.