Anthrax

Bacillus anthracis was the first bacteria shown to cause disease in 1877. Robert Koch grew the organisms in pure culture. It can form endospores, is a Gram + rod, easily grown, and is similar to Bacillus cereus found in soil habitats around the world. Anthrax is easy to get and culture, deadly, and resistant to environmental damage. However, it is not transmitted p2p, so it’s not the perfect bioweapon. The human LD50 is 8,000 –40,000 spores, so one deep breath at the site of release and you’re a goner.

Anthrax is common in herbivores who become infected after eating spores from soil. Natural outbreaks occur in S. America, Mexico, E. & S. Europe, Asia, Africa, Caribbean, and the Middle East. Humans get it following contact with anthrax-infected animals and products. The disease has been known for 100s of years.

Anthrax can manifest in three forms:

1. Cutaneous Anthrax  most common, 2000 cases reported/yr worldwide. Mortality is about 20% without treatment, with treatment death is rare.

2. GI  from eating undercooked infected meat. People get ulcers in the intestines. There is 25-60% fatality

3. Inhalation  most severe, 90-100% fatality when not treated. The form used as a bioweapon. 18 cases between 1900 – 1978, the majority were textile mill workers exposed to it by infected pelts.

Anthrax is a 2-stage illness:

1. Non-specific flu-like symptoms. This can last hours to days, and makes it hard to diagnose and treat promptly because it seems like it’s just the flu.

2. Sudden fever, dyspnea, sweating, mass lymphoadenopathy, expanded mediastinum (best sign to diagnose anthrax), hemorrhagic meningitis, delirium. This stage takes 3-7 days from onset to death.

Anthrax can be Id’d in the lab by microscopy  Gram stain would show it is a Gram + rod, India ink for the capsule. Look at the colony morphology and it can form spores. The bacteria are nonhemolytic and nonmotile.

1. Spores infect macrophages at the site of infection 

2. Proliferate 

3. Produce virulence factors – LF (lethal toxin), EF (edema toxin), PA (protective antigen) 

4. Local necrosis and edema 

5. Evade immune system with antiphagocytic capsule 

6. Toxemia and bacteremia develop 

7. Tissue destruction and organ failure

The toxins have the classic A-B structure. PA acts as the B fragment and is required for binding and translocating LF and EF into host cells. The capsule and toxins are encoded in the pX01 and pX02 plasmids.

TREATMENT

Early antibiotic treatment is essential. In a contained outbreak use IV antibiotics, but in a mass outbreak oral therapy is better. In severe disease use a combination of 2 antibiotics. Treat for at least 60 days and vaccinate against anthrax before stopping antibiotics. We need to give antibodies for so long because antibioyics only kills germinating cells and not the spores.

PROPHYLAXIS

Once exposed, even if only suspected, people should be treated with antibiotics and 3 doses of vaccine immediately. Pre-exposure prevention is to give vaccines. Soldiers are vaccinated with AVA (Anthrax Vaccine Adsorbed), which is based on the PA of anthrax. The UK vaccine is similar, it is called AVP.

Live vaccines are used to vaccinate livestock and in Russia to immunize people. A recombination PA vaccine is in the works. This would be the PA antigen grown in a different strain so there’s no attachment to the bad toxin.

Decontamination is very hard. It took years to decontaminate an island used for research. 280 tons of formaldehyde and 2000 tons of seawater.

Category: Medicine Notes , Microbiology Notes