Introduction

The Bacillaceae are gram-positive rods to filaments that form endospores, and grow in the presence of oxygen (aerobic). With the exception of B. anthracis, they are usually motile and resistant to penicillin. Bacillus species are ubiquitous in soil and plants (exception B. anthracis). The animal pathogens belong to the Bacillus cereus cluster and consist of Bacillus anthracis the agent of anthrax;  B. cereus and B. cytotoxicus which causes gastroenteritis in humans (fried rice disease) and dogs and mastitis in cows; and B. thuringensis which is a butterfly and moth pathogen.

Only anthrax and Bacillus anthracis will be dealt with in any detail in this chapter.

Taxonomy of Bacillus and Paenibacillus

The phylogenetic tree of Bacillus and Paenibacillus is shown below in lilac. I very rarely will ask direct questions on the genetic relatedness of bacteria. However, related bacteria show similarities in appearance, source, hardiness and pathogenicity.

Useful Bacillus species

Included in the Bacillaceae are bacteria that are used for: 1) biological control – probiotics (they compete with Salmonella and Campylobacter), 2) as a source of antibiotics (the polypeptides such as polymixin B from Bacillus subtilis), 3) nitrogen fixers, and 4) as an indicator of effective sterilization (Geobacillus stereathermophilus).

American foulbrood

Related to Bacillus, is Paenibacillus larvae, the causative agent of American foulbrood a contagious bacterial disease of honeybees. The endospores of this bacterium are highly resistant and difficult to remove from bee-keeping equipment. P. larvae infects the bee larvae causing them to turn brown and die. Classic signs of foulbrood include the honey comb centres appearing dark (lost or sunken caps) and the contents brown and sticky. This Notifiable Disease is present in all States of Australia. Thus control involves the destruction of infected hives after the removal of the honey. In January 2023 USA approved the first bee vaccine placed in royal jelly and fed to the queen that protects her offspring from American foulbrood.

For more information refer to American foulbrood (This disease will be taught by Dr Jenny Elliman)

anthrax

introduction

Anthrax is a peracute, acute or subacute disease of domestic and wild mammals and humans (zoonosis) caused by the gram-positive bacillus, Bacillus anthracis. Domestic and wild herbivores are most susceptible, equids (horses, mules and donkeys) are of intermediate susceptibility and carnivores, pigs and humans are relatively resistant. In many species of animals anthrax is characterised terminally by the development of a rapidly fatal septicaemia that results in sudden death, and by the presence of the organism in blood and body fluids at death. The principal lesions are those of widespread oedema, haemorrhage and necrosis.

aetiology

Bacillus anthracis is a large (1 -1,5 x 3 -10 μm), gram-positive, capsulated, endospore-forming, non-motile rod that produces a potent tripartite exotoxin. Germination of B. anthracis spores occurs at temperatures between 20 to 40°C at a relative humidity of greater than 80%. This means that it will stay in its endospore form in the environment during arid and cold conditions. Due to low activity in the environment and the fact that it causes fatal disease, this bacterium is genetically stable with only minor regional genetic differences.

It is a BSL3 bacterium. Bacillus anthracis is easily cultured on blood agar where it produces non-haemolytic ground glass surface like colonies. Bacillus cereus produces similar colonies, but are strongly beta-haemolytic.

Special methods have been developed for selective enrichment of B. anthracis from contaminated samples. A diagnostic multiplex PCR identifies it by the detection of genes that code for the protective antigen and the capsule. Note that vaccine strains will test positive for the protective antigen, but not the capsule.

A variant of Bacillus cereus that has acquired the B. anthracis virulence plasmid is known as Bacillus cereus biovar anthracis. It is also the cause of anthrax but has a different ecological niche to B. anthracis, being found in the humid, forested areas of West Africa.

epidemiology

Anthrax still occurs virtually worldwide. It is relatively common in southern and Eastern Europe, the countries of the former USSR, southern and central America, Asia and Africa. In North America, Western Europe and Australia, it occurs sporadically. To find out about the current reported cases or outbreaks of anthrax visit the WAHID interface of the WOAH.

The map below shows a compilation of outbreaks and cases reported to the WOAH (2016 – 2023). Note that some countries may have cases of anthrax, but don’t report them. These are those countries that have no colour overlay.

Environmental survival of Bacillus

The endospore allows Bacillus to survive in the environment in a dormant state (cryptobiotic). Endospores are highly resistant to temperature extremes, UV light, desiccation and disinfectants. Spores germinate when conditions are suitable for growth. (We can use this fact when selectively growing endospore producing bacteria in the laboratory – samples containing endospores can be heated to 80°C which will destroy vegetative contaminating bacteria allowing the spores to germinate in suitable media). Thus Bacillus anthracis can be selectively cultured from soil and carcase samples that have been exposed to air.

Bacillus anthracis can only survive in the soil for prolonged periods as an endospore. Under nutrient-rich and high moisture conditions that allow it to germinate, it will easily be killed by competing soil bacteria and fungi. This is why there are a high number of viable B. anthracis spores in arid low lying areas i.e. areas where water accumulates during seasonal rainfall, but dries up rapidly.

Bacillus cereus, a related and common environmental saprophyte, is able to proliferate rapidly in soils and produce bacteriocins which allow B. cereus to out-compete other soil microorganisms. Unlike B. anthracis, Bacillus cereus is also resistant to many antibacterials produced by other bacteria and fungi. This is why this bacterium is a common sample contaminant.

“The Anthrax Belt” of Australia

In Australia, most cases are limited to the “Anthrax Belt” which extends from the northern area of Victoria, through the central pastoral grazing areas of New South Wales to southern Queensland. Each year, from January to March a number of cases are reported to the state veterinarians. The anthrax belt and the most recent cases are shown in the map below. The anthrax belt is in the historical region of stock movement. Thus the endospores of B. anthracis are still found in the soils of this region.

Socio-economic importance – why should anthrax be notifiable?

1. Anthrax is a global, potentially fatal disease of animals and humans that is monitored by the WOAH. Australia is a signatory to the WOAH.
2. Anthrax in livestock and humans is more common in developing countries where there may be insufficient funds and infrastructure to implement adequate surveillance and control programmes for animal diseases. In addition, humans, due to poverty and other socio-economical factors, are often prepared to eat meat and/or utilise hides or wool/hair from sick or dead animals.
3. As spores can remain dormant in soil for many years, and only affect animals when the soil is disturbed, stockowners tend to become complacent and do not vaccinate their animals. This may result in a build up of susceptible populations resulting in outbreaks of anthrax.
4. In some American, African and Asian countries, anthrax regularly causes severe losses in wildlife that may significantly reduce the numbers of valuable or endangered species.
5. As B. anthracis is pathogenic for most mammals including humans, is easily obtainable, grows prolifically on artificial nutrient media and can be delivered to large populations by aerolisation or in water or food supplies, it is an ideal candidate for use in bioterrorism and biological warfare. It is also a large bacterium, making it a good candidate for genetic manipulation. In fact, it is this, that has led to a renewed interest in the bacterium spurred on by 66 human deaths in Sverdlovsk, Russia in April 1979, repeated attempts of the Japanese terrorist group Aum Shinrikyo in the 1990s to disperse anthrax and botulism and in persons who handled contaminated letters in the USA in 2001 as well as an increase in “internationalized” warfare that has occurred since the Gulf War in 1990. The CDC estimated in 1997 that it would cost $26.2 billion per 100,000 persons exposed to the bacterium.

Host susceptibility and transmission of Bacillus anthracis

1. Animals vary in their susceptibility to disease, but generally those animals that develop a high terminal bacteraemia are the most susceptible to infection; these include domestic ruminants, most wild ruminants, mice and guinea pigs. Their opened carcasses provide a source of numerous environmentally resistant bacterial endospores. Those with a variable number of bacteria in their bloodstream at death are usually intermediate in their susceptibility and include equids and rabbits. Relatively resistant species include humans, pigs, carnivores, ratites (emus, cassowaries and ostriches) and rats.  Animals that are resistant to infection when they die, have a low terminal bacteraemia, making them less important in environmental contamination.
2. Generally, adults (especially middle-aged) are more susceptible than juveniles. (This is opposite to most infectious diseases, where it is the juvenile that is the most susceptible)
3. Certain animal species ingest many endospores because of their social behaviour and feeding habits. Cattle more commonly die from anthrax as they tend to exhibit osteophagia (bones harbour bacterial endospores), due to phosphate deficiencies, and eat close to the ground.
4. Stress and overcrowding of animals, especially wildlife, are often associated with outbreaks of this disease.
5. Viable spores or bacteria have been demonstrated under natural conditions in the lymph nodes and spleen of healthy cattle and pigs. Inhaled spores have also been found dormant in the lungs of animals. It is thought some animals in endemic areas with low-grade exposure to B. anthracis may carry the bacterium and only exhibit the peracute disease when subjected to severe physiological stress.

Transmission of Bacillus anthracis

• The transmission of B. anthracis in animals is usually by the ingestion of endospores in contaminated feed or water. Although rare, animals may also become infected percutaneously via skin lesions or by inhalation.
• Biting flies, especially those with long mouth parts, may transmit B. anthracis mechanically percutaneously. Animals, like horses, with thin skins are especially susceptible.
• Most (95%) of human cases originate as a result of percutaneous infections. Infection may also occur following the ingestion of insufficiently cooked infected meat and by the inhalation of spores found on wool and animal hides (Wool sorters’ disease).

Animal, bacterial and environmental factors that are associated with the transmission of Bacillus anthracis

1. A high terminal bacteraemia as well as impaired blood clotting in affected animals result in the spread of bacteria throughout the body and their occurrence in excretions e.g. faeces and nasal discharges. These contaminate the environment.
2. Carcasses of animals dying with a high terminal septicaemia when opened will allow numerous bacteria to escape and sporulate in the presence of air. Vegetative bacteria in the carcass of an animal that died from anthrax are rapidly killed by putrefaction (3 days at 30-35°C). They can persist for 1 week in bone marrow and 2 weeks in the skin, under the same conditions. These bacteria will survive for up to 4 weeks in carcasses at 5 – 10°C due to slower putrefaction at these temperatures.
3. Predators, scavengers, and carrion-eating birds promote the development and dispersion of spores by opening up infected carcasses, allowing the poorly clotted blood to spill and dragging or carrying their organs and tissues to other areas, and eating parts of them to distribute the spores in their faeces. They may also disperse the bacteria and spores by means of their contaminated coats or feathers. Note that vegetative bacteria and some spores are destroyed in the intestinal tract of scavengers.  For example, vultures will destroy large numbers of spores in their intestinal tract = 10-fold reduction.
4. Humans may also open infected carcasses and transport them or their organs and tissues over long distances.
5. The endospores can survive in the environment for prolonged periods (years). Soils rich in calcium (pH 9) are thought to promote the survival of the endospores of B. anthracis. B. anthracis spores survive better in the subsurface (15cm depth) of these soils where there are low numbers of competing microorganisms. High nutrients and biological activity in the soil, as well as the presence of products in the soil produced by certain plants and B. anthracis bacteriophages limits endospore survival. Sporulation is restricted in cold environments.
6. Endospores in run-off water accumulate in low-lying, poorly drained areas such as pans or flood plains whereas those entering fast-flowing rivers are diluted and washed away. Note that endospores, once released from a river bed, will float to the surface of water as they are hydrophobic. This is a primary reason why anthrax is often seasonal in endemic areas.
7. Biting flies, such as stable flies (tabanids), can act as mechanical vectors of the vegetative organisms by feeding on infected animals and within a short space of time transfer the infection to susceptible animals in the immediate vicinity of the moribund animal.
8. (Blowflies feed on body fluids of carcasses and, when replete, rest in trees on which they deposit faecal and vomit material blood containing numerous bacteria and spores. In Africa, browsing animals, such as kudu (Tragelaphus strepsiceros), can become infected by eating contaminated leaves. In addition, many trees in Africa are thorny which inflict mouth wounds that act as portals of entry for B. anthracis.)

pathogenesis

The outcome of infection related to the form of the disease that will develop is dependent on host susceptibility and infective dose. Once the endospores have been ingested, inhaled or have gained entrance through skin wounds, they are taken up by phagocytic cells. There they germinate, multiply and locally invade the animal’s tissues and are carried via the lymphatics to the regional lymph nodes.

At the site of infection, susceptible hosts show a mild inflammatory response.

The very thick poly-gamma-D-glutamic acid capsule of Bacillus anthracis assists the bacteria early in infection from being destroyed by the immune system mainly because they inhibit Complement opsonisation and Complement-mediated lysis. Bacteria that are uncapsulated are rapidly destroyed. In fact, the live attenuated Sterne vaccine is a strain of Bacillus anthracis that is still toxigenic, but has no capsule.

Once the bacteria have overcome the immune response, they enter the bloodstream causing a bacteraemia and localise in many organs and tissues with subsequent necrosis and haemorrhage. The bacterium in resistant hosts often remains localised resulting in a severe localised reaction consisting of oedema and necrosis.

The intracytoplasmic toxins of B. anthracis, namely protective antigen (PA), lethal factor (LF) and oedema factor (EF) form a complex (tripartite toxin). Protective antigen targets the plasma membrane of cells and inserts and reorganizes to form a seven-sided ring (pore) allowing the entry of either LF or EF into the cytosol. All cells in the body are potential targets. It is thought, however, that cells of the immune system such as macrophages are the primary targets. This is a typical AB toxin with LF and EF being the A subunit and PA the B subunit.

Lethal factor (LF) is a zinc dependent metalloprotease that cleaves mitogen activated phosphoproteases (MAPP) decreasing the transcriptionof certain genes within cells and hence protein production. This effect is varied but it can result in the death of macrophages and endothelial cells, decrease the production of pro-inflammatory kinins and inhibit antigen presentation by dendritic cells. This allows the bacteria to escape from the lymph nodes and spread further.

Oedema factor (EF) is a calcium and calmodulin-dependent adenylate cyclase that binds to calmodulin causing cleavage of ATP to cAMP resulting in water Na:K pump reversing with the resultant loss of water and chloride ions from the cell.

Below is a diagrammatic representation of the tripartite toxin interaction and its effects within a cell.

The summative effects of the toxins are to severely impair the immune system, increase capillary endothelial permeability and delay blood clotting. Together, it results in severe oedema, haemorrhages and haemoconcentration. In addition, there is unchecked growth of the bacteria that utilize available oxygen. As a consequence affected animals in extremis are markedly hypoxic. The neuromuscular irritability and convulsions exhibited in some animals in the terminal stages of anthrax are probably as a consequence of decreased serum calcium and increased serum potassium.

The pictures below show the effects of impaired blood clotting in peracute anthrax

Clinical signs in animals

The incubation period of anthrax under natural conditions ranges in susceptible herbivores from 36 – 72 hours (very short). The course of the disease may be peracute, acute, or subacute to chronic.

Peracute anthrax

Wild ruminants and goats usually develop this form of the disease. The course of the disease is usually less than 2 hours and most animals are found dead without signs of illness being noted. Terminal clinical signs include difficulty in breathing, congestion and cyanosis of mucous membranes, and collapse showing convulsions and paddling of the legs. Blood‑stained fluid may be noted in some exudes from the nostrils, mouth and anus before death.

Acute anthrax

This is mostly encountered in domestic ruminants and equids. The disease course is usually less than 72 hours. Affected animals may show a high fever, depression and weakness, and petechiation (pin-point haemorrhages) of visible mucous membranes, difficulty in breathing and loss of appetite with digestive disturbances, such as depressed rumination in ruminants and colic in horses. In some diarrhoea that may be bloody and milk that is blood-stained or yellow may be present. Some animals may abort. Swellings under the skin in the region of the throat and ventral parts of the chest, abdomen and perineum may be present, particularly in equids.

Subacute to chronic anthrax

This form of the disease usually develops in omnivores, carnivores and partially immune herbivores.

The course of the disease usually extends for more than 3 days before recovery or death. The most frequent sign is a subcutaneous edematous swelling of the throat and neck as a result of primary infection of the pharynx and its regional lymph nodes. The swelling may become so extensive that it interferes with respiration and may result in suffocation and with the ingestion or swallowing of food and water. The infection usually remains localised but it may progress to a septicaemia, which is often fatal. Primary invasion may occur in the intestines with the development of localized lesions which result in digestive disturbances, such as loss of appetite, vomiting and bloody diarrhoea.

Infection in humans (for information only)

A brief outline of anthrax in people is provided below. If you want to know more consult your public health notes and online documents. A link to the CDC information brochure on anthrax in people is provided. 

In humans the disease is mostly occupational with livestock workers and meat preparers (housewives) having the highest case incidence. The incubation period in people is generally 1 to 8 days.

Cutaneous form

This is the most common form. Infection generally occurs after direct contact with tissues or products e.g. blood, meat, wool, hair or skins of diseased animals. Bacteria usually enter the body through pre-existing wounds in the skin or by the bites of infected flies. The incubation period varies from 1 – 12 days. A papule develops at the site of infection that is surrounded by a zone of hyperemia and edema of adjoining tissues. Central necrosis of the lesions occurs with the formation of an eschar that later becomes ulcerated. The lesion usually resolves but a fatal septicaemia (± 1% of cases) may supervene.

Oropharyngeal and gastro-intestinal forms

Eating uncooked or underdone B. anthracis‑infected meat causes oropharyngeal or gastro-intestinal anthrax, especially if there is pre-existing trauma in these areas. This practice is common in countries where the people cannot afford to buy high quality food. Lesions similar to the cutaneous carbuncle develop most commonly in the wall of the terminal ileum or caecum and colon, but the oropharynx, stomach and other parts of the small intestines are occasionally affected. The clinical signs depend on the location of the lesions and include fever, nausea, vomiting, anorexia, abdominal pain and bloody diarrhoea. Involvement of the oropharynx results in fever, ulcers in the oropharynx and swelling of the face and neck.

Inhalation form

Pulmonary anthrax, also referred to as woolsorter’s disease or mediastinal anthrax, occurs when dust particles laden with anthrax spores are inhaled and deposited in the alveoli where they are phagocytosed and multiply. They are also transported to the mediastinal lymph nodes in which they multiply. From here bacteria may enter the blood and initiate a rapidly fatal septicemia, which includes meningitis. This form usually manifests as an acute atypical pneumonia and lymphadenitis followed by signs of cardiac failure. The incubation period varies considerably, but in the Sverdlovsk epidemic, it was found to be 2 – 43 days. Virtually all untreated cases are fatal. Humans are usually highly resistant to this form, requiring a high infectious dose within air-born droplets, which does not usually occur when performing post-mortem examinations.

Welder’s anthrax is a rare fatal lung disease in metal workers in the USA caused by anthrax toxin produced by Bacillus cereus. It is thought that the soil near metal works is rich in iron promoting the growth of environmental bacteria and that the high dust loads experienced by the workers increase the lung’s susceptibility to infection. The only successful treatment has been with raxibacumab, a monoclonal anthrax antitoxin.

Diagnosis and management of anthrax  in Australia

If anthrax is suspected, the following steps are followed and all information gained should be recorded in a notebook. Wear full PPE:

1. Obtain the history of the outbreak.
2. Examine the sick animals, if any.
3. Do not perform a post-mortem examination as this would result in sporulation of the bacteria with contamination of the environment by the spores and possibly infection of the prosector.
4. Take and examine blood or oedema fluid smears from the carcasses. A rapid protective antigen detection immunochromatography test is available. Have the diagnosis confirmed by laboratory examination (Dial the Disease hotline and if required send the sample to your nearest State Government Veterinary Laboratory).
5. Make and examine by light microscopy smears of blood or fluid from oedematous swellings. Note that unless the animal is close to death, bacteria are very few in number in the blood of living animals. Blood smears made from blood obtained by the direct collection from an available blood vessel (jugular vein) in recently dead animals or by making a small incision into the ear, tail tip or hoof coronet, or smears made from the fluid of oedematous swellings (e.g. resistant species) should be examined microscopically after fixing them and staining them with Giemsa, CAMS-DiffQuick, polychrome methylene blue (M’Faydean), 0.03% azure blue in 0.01% KOH or toludine blue staining methods. In smears made from fresh carcasses, large rectangular bacilli are found either singularly or in short chains that stain magenta-red and possess a thick light pink staining capsule. In decomposed carcasses putrefactive processes usually alter the appearance of B. anthracis, but capsule remnants often called “ghost cells” or “shadons” may still be seen in smears.

Laboratory confirmation

1. Bacterial isolation and identification. This should be done if anthrax is suspected but unconfirmed by blood smear examination or lateral flow assay. Preferably, samples should be collected from fresh carcasses. Samples should include blood taken from an accessible blood vessel such as the jugular vein, tip of the tongue, a superficial lymph node or blood-contaminated soil. If the carcass has been opened, specimens of the spleen or several lymph nodes should be collected. If all that is left of a carcass are bones (metacarpal bones), bone chips should be taken from the edge of eye sockets, mandible or ischium.
2. PCR typing on isolates to detect the pag and cap virulence genes. A PCR test distinguishes between the Sterne vaccine stain (lacking pX02) and wild isolates of B. anthracis. It can also be used to detect species in the environment.
3. The enzyme immunoassay (EIA) that detects serum antibodies to the toxin antigens, primarily the protective antigen component, can be used in chronic cases.  Note that vaccinated animals will also have antibodies. (No need to learn).

Control

Control measures should be aimed at breaking the cycle of infection and consist of:

1. Active surveillance
2. Prophylactic measures, and
3. Disease regulatory actions – Ausvetplan manual file:/https://www.animalhealthaustralia.com.au/our-publications/ausvetplan-manuals-and-documents/. It is listed as a Category 3 emergency animal disease

Active surveillance

Identification of high-risk areas and early detection of outbreaks can result in the institution of timely control measures, which will limit the impact anthrax has on animals and humans in a country. It is also the responsibility of countries that are part of the international disease surveillance network of the WOAH to report any outbreaks within their boundaries.

Prophylactic measures

1.  Vaccination

A live, avirulent, spore vaccine (Sterne vaccine) given subcutaneously provides effective immunity for approximately 9 – 12 months. It is safe to use in most domestic and wild animal species, but is not recommended in humans. (There is a vaccine for people). The vaccine can in some domestic goats and llamas cause disease or severe localized swelling and thus it is recommended for these species that a quarter of the dose be administered initially with the full dose one month later.  Horses should be vaccinated twice, 1 month apart. Animals should not be treated immediately before and after vaccination with antimicrobials as such treatment will destroy the organisms in the vaccine. In Australia animals are vaccinated annually for 3 years after an outbreak has occurred on that property. This is done at no additional cost to the farmers.  Farmers in a high risk area (anthrax belt) can apply to the local State veterinary services to vaccinate their livestock. The price of the vaccine is capped at $1 per dose. Note that there is no vaccine subsidisation for animals vaccinated for export.

2.  Carcass management

When handling infected carcasses and contaminated material and surfaces, protective clothing, gloves and masks, should be worn.

Unopened carcasses should be destroyed on site by incineration with minimal updrafts (down-directed blowtorches or portable incinerators). If one of these is not possible, the carcass should be left unmoved and the carcass and the area liberally doused with 5% formaldehyde. It should be adequately closed off from other animals, particularly scavengers, and humans, by fencing and covering using any available material. Warning signs should be posted around the site. After the carcass has decomposed, the site can then be scorched with fire to minimize the number of viable spores in the soil and vegetation.

3.  Decontamination procedures

Where possible, all excreta, blood, wool, hides, or other contaminated material such as bedding, water and instruments must be placed in a bag and either incinerated or autoclaved at 120°C for 30 minutes before safe disposal. Irradiation facilities should be used, if available.

Where incineration or heat sterilization procedures cannot be applied, disinfectants are used. Although many disinfectants can be used, the most effective are 5% formaldehyde and 2% glutaldehyde. Chlorine compounds at a concentration of 10 000 ppm of active chlorine can also be used, but they are inactive in the presence of organic material. Contaminated surfaces should be first disinfected using a recommended disinfectant for a contact time of 2 hours, then cleaned thoroughly and again disinfected. Materials, such as boots, can be soaked overnight in disinfectant. Five per cent formaldehyde is suitable for soil and sewage sludge decontamination.

Where it is not possible to use a liquid disinfectant such as in laboratories and safety cabinets, the area is properly sealed off and fumigation is applied using 37% formalin, the fumes of which are allowed to steam from a kettle. Exposure to the formalin fumes should be for at least 4 hours but a longer period is preferable (e.g. overnight). Where the facilities are available, ethylene oxide can be used.

The efficacy of all decontamination procedures should be tested using for example Bacillus subtilis var. globigii spore disks in or on the materials/areas to be decontaminated. These disks are recovered after the heat sterilization, disinfection or fumigation process and cultured to determine the viability of the spores.

Treatment of animals (not usually done in Australia, at the discretion of state veterinarians)

1. Antimicrobial therapy

Antimicrobial and supportive therapy is indicated in clinical cases and those that are suspected to have been in contact with B. anthracis spores. Treatment is recommended even in terminal cases as it will reduce, if not eliminate the number of bacteria in the body thereby reducing the subsequent contamination of the environment.  Bacteriocidal antimicrobials, such as penicillin are recommended. Penicillins should be administered at a dosage rate recommended by their manufacturers. A treatment regimen consisting of the administration of short-acting penicillin followed, 6 – 8 hours later by long-acting penicillin is most practical. However, if they are not available, procaine penicillin can be used at 12-hour intervals for three successive treatments, and thereafter once a day for a further 5 days. It must be noted that treatment will interfere with the development of immunity. Therefore these animals should be kept isolated and vaccinated no earlier than 10 days after treatment has terminated.

2. Hyperimmune serum therapy

This is rarely used in animals as it has little advantage over antibiotic therapy. If available, it can be life-saving in cases that don’t respond to antibiotic therapy. Two registered monoclonal antibodies directed towards Bacillus anthracis, namely  obiltoxaximab and raxibacumab can be used in severe cases.

 In an outbreak situation the following should be done:

1. Notify the relevant state authorities immediately.
2. Determine the extent of the outbreak.
3. Quarantine the farm or the area concerned for at least 20 days after the last case or two weeks after vaccination. The longer of the two quarantine periods should be applied.
4. Dispose of carcasses in an appropriate fashion.
5. The site where the animal has died should be disinfected with 5% formaldehyde after disposal of the carcass.
6. Vaccinate all uninfected domestic ruminants and equids in the quarantine areas, as well as those in a buffer zone around the quarantine area. The state governments maintain emergency vaccine supplies that are provided free of charge during an outbreak.
7. Uninfected animals should be removed from the focus of infection and kept in isolation in the quarantine area under observation for at least 2 weeks after vaccination.
8. Disinfect infected premises, vehicles, clothing, animal products, instrumentation and soil.
9. Trace any susceptible livestock or animal products that have left the quarantine area in the 20-day period before the first anthrax case occurred and take appropriate measures where necessary.
10. Non-infected bordering properties: vaccinate, then quarantine for 2 weeks.

Human treatment (no need to learn)

Antibiotic therapy is given directly post-exposure. Vaccines have been developed for use in humans. In China and the former USSR live spore vaccines and in the UK and USA inactivated bacterin (BioThrax) are prophylactically and post-exposure with antibiotics of military and other persons at risk. Its use reduces the treatment duration to 1 to 2 weeks (used to be 6) thus reducing the risk that treated people will develop Clostridioides difficile infection.

END OF CHAPTER