Introduction

Classification

Taxonomy

• Phylum: firmicutes.
• Class: bacilli.
• Order: bacillales.
• Family: bacillaceae.
• Genus: bacillus.
• Species: anthracis.

Etymology

• Bacillus from Latin meaning ‘small-rod’.
• Anthracis is derived from the Greek word for coal because of the characteristic black skin lesions caused by infection with the bacteria.

Active Forms

Resting Forms

Clinical Effects

Epidemiology

Habitat

• Survives best in calcium rich soils with a pH of above 6.1.
• Can also survive on contaminated wool and hair.

Transmission

• Anthrax is not believed to spread from animal-to-animal at any level of significance.
• Grazing animals usually become infected when they ingest or inhale sufficient quantities of B. anthracis spores from the soil (derived from dead animals). They can also become infected via abrasions on the skin.
• Infection can also occur when an animal is bitten by a Fly Flies (Tabanus/Stomoxys spp.) which has fed on an infected animal or carcass. Flies are believed to cause explosive outbreaks where multiple animals become infected. Non-biting blowflys have also been implicated.
• Following death vegetative B. anthracis cells are discharged from the carcass and sporulation is induced by the oxygen content of air. This allows the transmission cycle to begin again.

Pathological effects

• Anthrax is an acute/peracute disease. Chronic infections are rare and unusual.
• Capsule is a polypeptide composed of poly-ᵞ-D-glutamic acid which allows the bacteria to escape host defenses such as phagocytosis by macrophages.
• Anthrax toxin is made up of 3 components:
  • Edema factor.
  • Lethal factor.
  • Protective antigen (PA).
• Individually these 3 components lack any effect on the host organism but together they result in the specific disease characteristics of anthrax.
• Edema factor is an adenylate cyclase which causes increased levels of cyclical adenosine monophosphate (AMP) within cells.  This causes a change in membrane permeability and results in fluid accumulation within cells, which presents as edema.
• Lethal factor is a zinc metalloprotease which causes death of macrophages and neutrophils as well as epithelial and endothelial cells. This presents as necrotic lesions within the infected animal.
• Protective antigen has no pathogenic effect; but instead has a structural role in binding lethal factor and edema factor together.
• In herbivores, anthrax commonly presents as an acute septicemia with a high fatality rate, often accompanied by hemorrhagic lymphadenitis.
• Typical clinical signs include fever, depression, respiratory distress and convulsions; however in the majority of cases death occurs prior to the presentation of any of the above signs, often within 24-48 hours after infection.
• Ruminants are believed to be the most susceptible mammalia group.
• Incubation period in ruminants is normally 3-5 days (1-14 days is possible).
• Following death carcasses appear bloated (due to edema) putrefy rapidly and do not show signs of rigor mortis.
• Post-mortem necrotic lesions can be observed within the mesenteric lymph nodes, spleen, liver, epicardium and endocardium.

Control

Control via chemotherapies

• Due to the rapid onset of the disease treatment is seldom possible; however B. anthracis is sensitive to Penicillin Penicillin and many other antibiotics.

Control via environment

• The primary route of transmission is through the environment, but this can be reduced by ensuring that any affected animals are not moved and steps are taken to prevent spillage of blood and other body fluids from carcasses.
• Suspected carcasses should be disposed of by incineration only. Carcasses should not be opened as this will expose the bacteria to oxygen which is the trigger for formation of spores.
• Disinfection of premises and equipment should be undertaken using an approved Defra approved disinfectant.
• Premises should be quarantined.
• Insect and rodent control is required.

Vaccination

• If an outbreak of anthrax is confirmed, a vaccine (live, non-encapsulated, spore former held in suspension) can be used to protect animals which may become exposed.

Diagnosis

Further Reading

Publications

Refereed Papers

• Recent references from PubMed and VetMedResource.
• Muller J, Gwozdz J, Hodgeman R, Ainsworth C, Kluver P, Czarnecki J, Warner S & Fegan M (2015) Diagnostic performance characteristics of a rapid field test for anthrax in cattle. Prev Vet Med 120 (3-4), 277-82 PubMed.
• Beyer W & Turnbull P C (2009) Anthrax in animals. Mol Aspects Med (6), 481-9 PubMed.
• Ndiva Mongoh M, Dyer N W, Stoltenow C L, Hearne R & Khaitsa M L (2008) A review of management practices for the control of anthrax in animals: the 2005 anthrax epizootic in North Dakota--case study. Zoonoses Public Health 55 (6), 279-90 PubMed.
• Ndiva Mongoh M, Hearne R & Khaitsa M L (2008) Private and public economic incentives for the control of animal diseases: the case of anthrax in livestock. Transbound Emerg Dis 55 (8), 319-28 PubMed.
• Siamudaala V M, Bwalya J M, Munang'andu H M, Sinyangwe P G, Banda F, Mweene A S, Takada A & Kida H (2006) Ecology and epidemiology of anthrax in cattle and humans in Zambia. Jpn J Vet Res 54 (1), 15-23 PubMed.
• Hugh-Jones M E & de Vos V (2002) Anthrax and wildlife. Rev Sci Tech 21 (2), 359-83 PubMed.

Other sources of information

• Waine K, Busin V & Strugnell B (2019) Getting the Most out of On-Farm Post-Mortems: A Guide for Veterinary Surgeons. AHDB, UK. Website: https://ahdb.org.uk.

Organisation(s)

• OIE (World Organisation for Animal Health).