- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
International Common Names
- English: acute anthrax, bacillus anthracis; pharyngeal anthrax, bacillus anthracis, in pigs; splenic fever
Local Common Names
- France: charbon
- Germany: Milzbrand
- Italy: carbonchio
- Netherlands: miltvuur
- Spain: pustula maligna
OverviewTop of page
Anthrax is a per-acute, acute or sub-acute disease, primarily affecting herbivores as a soil-borne infection, but also capable of affecting other mammals, including man, and occasionally birds.
The name 'anthrax' is derived from the Greek anthrakos, meaning coal, referring to the characteristic eschar in the human cutaneous form of the disease. The French and Italian names for the disease, charbon and carbonchio, similarly reflect this manifestation. In other languages, the names refer to others of its manifestations or to its sources of infection, for example, Milzbrand (German) and miltvuur (Dutch), meaning 'spleen fire', or pustula maligna (Spanish) referring to the appearance it occasionally takes, referred to in English as ‘malignant pustule’. Its names in other national languages and local dialects reflect historical familiarity with the different syndromes before it was realized that they were manifestations of a single aetiological agent, Bacillus anthracis. These names, however, come from the manifestations of the disease in humans and these manifestations are not seen in animals.
Anthrax appears to have been well recognized from the dawn of recorded history. The ‘grievous murrain’ upon asses, horses, oxen and sheep constituting the fifth plague of Egypt (Exodus 9, ca. 1250 BC) may be one of the earliest documented outbreaks of anthrax in livestock. The Greeks and Romans were seemingly well acquainted with the disease and in post-Roman Europe it featured in the eleventh century text ‘The Medicine of Quadrupeds’. In America, the description of ‘bloody murrain’ in 1847 (Cole, 1847) suggests that anthrax was well recognized under that name, and this record even includes references to an allegedly successful vaccination of cows with ‘the vaccine virus (pus)’.
The first scientific (as opposed to historical) report of the disease in animals was that of Chabert in 1780 (cited in Wilson and Miles, 1946). Anthrax is also commonly associated with Pasteur's well-known pioneering work on livestock vaccines a century later.
As a result of the combination of widespread application of the vaccine developed by Sterne in the 1930s (Sterne, 1937) together with improvements in veterinary public health, industrial hygiene, export-import controls and other surveillance and control measures, anthrax is no longer the global scourge it once was. Nevertheless, it continues to be seen, at least sporadically, in livestock and wildlife in a large number of countries. The nature of its persistent spores is such that every country must remain on alert against importation of the disease on materials of animal origin and/or resurgence of indigenous disease from burial and other sites with long-standing contamination.
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's Handistatus and WAHID databases on disease occurrence. For further information on this disease from OIE, see the website: www.oie.int.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Aepyceros melampus||Wild host||Other: All Stages|
|Axis axis (Indian spotted deer)||Wild host||Other: All Stages|
|Bos indicus (zebu)|
|Bos taurus (cattle)||Domesticated host, Experimental settings||Cattle & Buffaloes: All Stages|
|Camelus bactrianus (Bactrian camel)||Domesticated host, Wild host||Other: All Stages|
|Camelus dromedarius (dromedary camel)||Domesticated host|
|Canis aureus||Wild host||Other: All Stages|
|Canis familiaris (dogs)||Domesticated host, Experimental settings||Other: All Stages|
|Canis mesomelas (black-backed jackal)||Wild host||Other: All Stages|
|Capra hircus (goats)||Domesticated host||Sheep & Goats: All Stages|
|Cavia porcellus (domesticated guinea pig)||Experimental settings||Other: All Stages|
|Cervus porcinus||Wild host||Other: All Stages|
|Cervus unicolor||Wild host||Other: All Stages|
|Elephantidae||Wild host||Other: All Stages|
|Equus asinus (donkeys)||Domesticated host||Other: All Stages|
|Equus burchellii||Wild host||Other: All Stages|
|Equus caballus (horses)||Domesticated host||Other: All Stages|
|Hippopotamus amphibius||Wild host||Other: All Stages|
|Hyaena||Wild host||Other: All Stages|
|Kobus kob||Wild host||Other: All Stages|
|Lama glama (llamas)||Domesticated host, Wild host||Other: All Stages|
|Oryx gazella||Wild host||Other: All Stages|
|Ovis aries (sheep)||Domesticated host, Experimental settings||Sheep & Goats: All Stages|
|Panthera leo (lion)||Wild host||Other: All Stages|
|Rhinoceros unicornis||Wild host||Other: All Stages|
|Struthio||Wild host||Other: All Stages|
|Sus scrofa (pigs)||Domesticated host, Wild host||Pigs: All Stages|
|Syncerus caffer||Wild host||Other: All Stages|
|Tragelaphus strepsiceros||Wild host||Other: All Stages|
Hosts/Species AffectedTop of page
As indicated in the epidemiology section, anthrax is primarily a disease of herbivorous mammals but it is believed that very few hot-blooded animals are wholly resistant to it. Among domestic livestock, by far the largest numbers of reports are in cattle, but this may be, at least in part, because attempts are rarely made to diagnose unexpected deaths in sheep, goats and donkeys, and deaths are rarely reported in these animals. Certainly sheep, goats, horses, donkeys and camels are readily susceptible to anthrax.
In the wild, anthrax does not affect all herbivorous species equally and there is an apparent preference by the disease for particular species in any one region. Zebras, for example, are the most commonly affected in the Etosha National Park in northern Namibia with Kudu only occasionally affected; the most recent published percentages of all recorded anthrax deaths (uncorrected for total populations) were zebra 45% versus Kudu 0.8% (Lindeque and Turnbull, 1994). In the Kruger National Park, South Africa, the Kudu is the principal host accounting for greater than 50% of all recorded anthrax cases with zebra falling into a relatively small group of ‘other affected species’ (de Vos and Bryden, 1996). The hosts table gives example species which are affected by anthrax.
Carnivores are significantly more resistant than herbivores and, in enzootic areas, resistance in wild carnivores is enhanced by the naturally acquired immunity which is acquired as a result of frequent exposure from scavenging carcasses of anthrax victims (Turnbull et al., 1992). Numerous reports exist of infection in carnivorous birds inadvertently fed infected meat in zoos. Among herbivorous birds, reports exist of anthrax occurring in ostriches. Representing omnivores, pigs show a high resistance to infection under experimental conditions (Redmond et al., 1997), but outbreaks in pigs are a periodic livestock problem.
Systems AffectedTop of page blood and circulatory system diseases of large ruminants
blood and circulatory system diseases of pigs
blood and circulatory system diseases of small ruminants
digestive diseases of large ruminants
digestive diseases of pigs
digestive diseases of small ruminants
respiratory diseases of large ruminants
respiratory diseases of pigs
respiratory diseases of small ruminants
skin and ocular diseases of large ruminants
skin and ocular diseases of pigs
skin and ocular diseases of small ruminants
urinary tract and renal diseases of large ruminants
urinary tract and renal diseases of pigs
urinary tract and renal diseases of small ruminants
DistributionTop of page
Anthrax is a notifiable disease in most countries and annual notifications are forwarded by many countries to the Office International des Epizooties (OIE) in Paris where they are recorded as a multiple species listed disease. The first occurrence of an OIE listed disease should be reported within 24 hours with follow up weekly, six monthly and annual reports. Information given in the Geographical Distribution table largely derives from the OIE data published on the internet. [For current information on disease incidence, see OIE's WAHID database]. As is clear from the table, the disease is widely distributed and many countries report at least occasional cases occurring each year.
Disease reports are also submitted by Member States (MS) monthly to the African Union - Interafrican Bureau for Animal Resources (AU-IBAR). In 2011, 21 MS reported anthrax outbreaks to AU-IBAR recording a total of 629 outbreaks, 5655 cases and 1735 deaths. The highest number of outbreaks were reported by Ethiopia (452), followed by Somalia (44) and South Africa (25). The highest number of deaths was also recorded by Ethiopia (1102), followed by Zimbabwe (119), Guinea Bissau (109) and Cote d’Ivoire (103). (AU-IBAR, 2011).
Useful as the information collated by OIE and AU-IBAR is, it suffers from severe limitations, beyond the control of the institutions, resulting either from the failure of some countries to send in returns or from the poor quality of the data submitted by many others. This frequently reflects poor surveillance and reporting within the countries concerned. The indications from this are that the true incidence in animals is well above that actually being reported.
The Geographical Distribution table also fails to distinguish countries with few and sporadic cases of anthrax from those in which the disease is strongly endemic. It would be wrong, needless to say, to regard the presence of anthrax in the UK or France in the same light as the presence of anthrax in Zambia or Zimbabwe. Several countries in temperate or cool parts of the globe, for example Scandinavian countries in the northern hemisphere and New Zealand in the southern hemisphere, which have harboured anthrax in the past through importation of contaminated animal materials, have now become free of the disease through appropriate import controls. Other such countries are striving to do the same and several smaller countries have succeeded, such as Belize, Cuba, Cyprus, Czech Republic, Iceland, Ireland, Jamaica, Malta and Taiwan. Malaysia has also succeeded in becoming anthrax-free (Rahim, 1997).
Interestingly, probably not one of the countries where anthrax is shown as ‘present’ in the distribution table regard the disease as economically important. The Director of Veterinary Services in one endemic African country described anthrax to this author as "not economically important but potentially a political nuisance – occasionally people contract it from their animals and die". This is probably a commonly held view in many endemic regions. Consequently there was no way to assess economic impact directly in the table. Several countries have large (>10,000 doses administered annually) vaccination programmes. These programmes represent at least considerable economic input into control of the disease. These vaccination programmes are in operation in: Armenia, Azerbaijan, Iran, Kuwait, Uruguay, Kyrgystan, Tajikstan, Turkey, Turkmenistan, Uzbekistan, Vietnam, Botswana, Eritrea, Ghana, Lesotho, Libya, Madagascar, Mali, Morocco, Mozambique, Namibia, Niger, Nigeria, South Africa and the Sudan (OIE, 2001). In some reports, the numbers of doses administered annually appear to be vast, for instance in 1999, Romania administered almost 150 million doses, Uruguay 25 million doses, Ukraine 16 million doses and Uzbekistan greater than 10 million doses.
In summary, the OIE data for the most part tells us that most countries where anthrax occurs do recognize that it exists in their midst and, that the geographical regions where it is found have not changed significantly over more than a decade of reporting to OIE. However there is probably a lot of under-reporting and mis-reporting worldwide.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Armenia||Disease not reported||200707||, 1971; OIE, 1997; OIE, 2009|
|Azerbaijan||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Bahrain||Disease not reported||OIE, 2009|
|Bangladesh||Present||NULL||Halilov, 1997; OIE, 2009|
|Bhutan||Disease not reported||OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||Restricted distribution||NULL||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998; OIE, 2009|
|-Gansu||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|-Guangxi||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|-Guizhou||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|-Hong Kong||No information available||OIE, 2009|
|-Hunan||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|-Nei Menggu||Present||Shuang et al., 1997|
|-Qinghai||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|-Sichuan||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|-Tibet||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|-Xinjiang||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|-Yunnan||Present||Xudong et al., 1996; Liang and Xiao, 1997; Liang, 1998|
|Georgia (Republic of)||Reported present or known to be present||, 1971; OIE, 1997; OIE Handistatus, 2005; OIE, 2009|
|India||Restricted distribution||NULL||, 1971; Nair, 1997; OIE, 1997; OIE, 2009|
|-Andaman and Nicobar Islands||Present||, 1971; OIE, 1997|
|-Andhra Pradesh||Present||Rao et al., 1998|
|-Arunachal Pradesh||Present||, 1971; OIE, 1997|
|-Assam||Present||, 1971; OIE, 1997|
|-Bihar||Present||, 1971; OIE, 1997|
|-Gujarat||Present||, 1971; OIE, 1997|
|-Himachal Pradesh||Present||, 1971; OIE, 1997|
|-Karnataka||Present||, 1971; OIE, 1997|
|-Madhya Pradesh||Present||, 1971; OIE, 1997|
|-Maharashtra||Present||, 1971; OIE, 1997|
|-Meghalaya||Present||, 1971; OIE, 1997|
|-Odisha||Present||, 1971; OIE, 1997|
|-Tamil Nadu||Present||, 1971; OIE, 1997|
|-Tripura||Present||, 1971; OIE, 1997|
|-Uttar Pradesh||Present||, 1971; OIE, 1997|
|-West Bengal||Present||, 1971; OIE, 1997|
|Indonesia||Present||NULL||, 1971; Hardjoutomo, 1990; Hardjoutomo, 1996; OIE, 1997; OIE, 2009|
|-Nusa Tenggara||Localised||Martindah and Wahyuwardani, 1998|
|Iran||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Iraq||Restricted distribution||OIE, 2009|
|Israel||Disease not reported||200711||, 1971; OIE, 1997; OIE, 2009|
|Japan||Disease not reported||200008||, 1971; OIE, 2009|
|Jordan||Restricted distribution||NULL||, 1971; OIE, 1997; OIE, 2009|
|Kazakhstan||Present||NULL||Amireev et al., 1997; OIE, 2009|
|Korea, DPR||Disease not reported||OIE Handistatus, 2005|
|Korea, Republic of||Disease not reported||20080326||, 1971; OIE, 2009|
|Kuwait||Disease not reported||1993||, 1971; OIE, 2009|
|Kyrgyzstan||Restricted distribution||NULL||, 1971; Abikarimov et al., 1997; OIE, 1997; OIE, 2009|
|Laos||Present||NULL||Kittiphone, 1997; OIE, 2009|
|Lebanon||Disease not reported||1999||, 1971; OIE, 1997; OIE, 2009|
|Malaysia||Disease not reported||OIE, 2009|
|-Peninsular Malaysia||Disease not reported||OIE Handistatus, 2005|
|-Sabah||Disease never reported||OIE Handistatus, 2005|
|-Sarawak||Disease never reported||OIE Handistatus, 2005|
|Mongolia||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Myanmar||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Nepal||Disease not reported||2004||OIE, 1997; Pradhan and Bohara, 1997; OIE, 2009|
|Oman||Disease never reported||OIE, 2009|
|Pakistan||Restricted distribution||NULL||, 1971; OIE, 1997; OIE, 2009|
|Philippines||Restricted distribution||NULL||, 1971; Alcasid, 1997; OIE, 1997; OIE, 2009|
|Qatar||No information available||OIE, 2009|
|-Russia (Asia)||Present||, 1971; Monisov et al., 1997; OIE, 1997|
|Saudi Arabia||Disease not reported||OIE, 2009|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease not reported||NULL||, 1971; OIE, 2009|
|Taiwan||Last reported||1999||OIE Handistatus, 2005|
|Tajikistan||Present||NULL||, 1971; Nazarov, 1997; OIE, 1997; OIE, 2009|
|Thailand||Disease not reported||2000||, 1971; OIE, 1997; Pollarp, 1997; OIE, 2009|
|Turkey||Present||NULL||, 1971; özkam et al., 1993; OIE, 1997; OIE, 2009|
|Turkmenistan||Last reported||2003||OIE Handistatus, 2005|
|United Arab Emirates||Disease never reported||OIE, 2009|
|Uzbekistan||, 1971; Abdourashitov, 1997; OIE, 1997; OIE Handistatus, 2005|
|Vietnam||Restricted distribution||NULL||, 1971; OIE, 1997; OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease not reported||1999||, 1971; OIE, 1997; OIE, 2012|
|Angola||No information available||NULL||, 1971; OIE, 1997; OIE, 2009|
|Benin||Last reported||2012||, 1971; OIE, 1997; OIE, 2012|
|Botswana||Last reported||2008||, 1971; OIE, 2012|
|Burkina Faso||Present||, 1971; OIE, 2012|
|Burundi||Reported present or known to be present||OIE Handistatus, 2005|
|Cameroon||Present||, 1971; OIE, 1997; OIE Handistatus, 2005; OIE, 2012|
|Cape Verde||Present||2009||OIE, 2012|
|Central African Republic||Present||2011||, 1971; OIE Handistatus, 2005; OIE, 2012|
|Chad||Present||2010||, 1971; OIE, 1997; OIE, 2012|
|Congo||No information available||OIE, 2009|
|Congo Democratic Republic||Restricted distribution||2011||OIE, 2012|
|Côte d'Ivoire||Present||2011||, 1971; OIE, 1997; OIE Handistatus, 2005; AU-IBAR, 2011|
|Djibouti||Disease not reported||OIE, 2009|
|Egypt||Disease not reported||1974||, 1971; OIE, 2012|
|Eritrea||Present||2010||, 1971; OIE, 1997; OIE, 2012|
|Ethiopia||Present||2011||, 1971; OIE, 1997; OIE, 2012|
|Gabon||No information available||OIE, 2009|
|Gambia||No information available||NULL||, 1971; OIE, 1997; OIE, 2009|
|Ghana||Present||2011||, 1971; OIE, 1997; OIE, 2012|
|Guinea||Present||2012||, 1971; OIE, 1997; OIE, 2012|
|Kenya||Present||2012||, 1971; OIE, 1997; OIE, 2012|
|Lesotho||Present||2012||, 1971; OIE, 1997; OIE, 2012|
|Libya||Last reported||2009||, 1971; OIE Handistatus, 2005; OIE, 2012|
|Madagascar||Absent, reported but not confirmed||NULL||, 1971; OIE, 1997; OIE, 2009|
|Malawi||Disease not reported||OIE, 2009|
|Mali||Disease not reported||2008||, 1971; OIE, 1997; OIE, 2009|
|Mauritania||Reported present or known to be present||, 1971; OIE, 1997|
|Mauritius||Disease never reported||OIE, 2009|
|Morocco||Present||2010||, 1971; OIE, 1997; OIE, 2012|
|Mozambique||Present||2005||, 1971; OIE, 1997; OIE, 2012|
|Namibia||Present||2011||, 1971; OIE, 1997; OIE, 2012|
|Niger||Restricted distribution||, 1971; OIE, 1997; OIE Handistatus, 2005; OIE, 2012|
|Nigeria||Disease not reported||OIE, 2009|
|Réunion||Last reported||1957||OIE Handistatus, 2005|
|Rwanda||Restricted distribution||OIE, 2012|
|Sao Tome and Principe||Disease not reported||OIE Handistatus, 2005|
|Seychelles||Disease not reported||OIE Handistatus, 2005|
|Sierra Leone||Present||OIE, 2012|
|South Africa||Present||, 1971; OIE, 1997; OIE, 2012|
|Sudan||Disease not reported||2005||, 1971; Musa et al., 1993; OIE, 1997; OIE, 2009|
|Swaziland||Disease not reported||OIE, 2012|
|Tanzania||Present||2011||, 1971; OIE, 1997; OIE, 2012|
|Togo||Present||, 1971; OIE, 1997; OIE, 2012|
|Tunisia||Disease not reported||2007||, 1971; OIE, 1997; OIE, 2012|
|Uganda||Restricted distribution||, 1971; OIE, 1997; OIE, 2012|
|Zambia||Restricted distribution||, 1971; Tuchili et al., 1993; OIE, 1997; OIE, 2012|
|Zimbabwe||Present||, 1971; OIE, 1997; OIE, 2012|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Restricted distribution||NULL||, 1971; OIE, 1997; OIE, 2009|
|-Alberta||Present||Coupland and Henderson, 1996|
|-Manitoba||Present||, 1971; OIE, 1997|
|-Ontario||Present||Lusis and Smart, 1996|
|-Saskatchewan||Present||, 1971; OIE, 1997|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease not reported||2006||, 1971; OIE, 1997; OIE, 2009|
|USA||Restricted distribution||NULL||, 1971; OIE, 1997; OIE, 2009|
|-Minnesota||Present||, 1971; OIE, 1997|
|-Nevada||Present||, 1971; OIE, 1997|
|-North Dakota||Present||, 1971; OIE, 1997|
|-South Dakota||Present||, 1971; OIE, 1997|
|-Texas||Present||, 1971; OIE, 1997|
Central America and Caribbean
|Barbados||Disease never reported||OIE Handistatus, 2005|
|Belize||Disease never reported||OIE, 2009|
|British Virgin Islands||Disease never reported||OIE Handistatus, 2005|
|Cayman Islands||Disease never reported||OIE Handistatus, 2005|
|Costa Rica||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Cuba||Disease never reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||Disease not reported||OIE Handistatus, 2005|
|Dominican Republic||Disease never reported||OIE, 2009|
|El Salvador||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Guadeloupe||Disease never reported||OIE, 2009|
|Guatemala||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Honduras||Disease never reported||OIE, 2009|
|Jamaica||Disease not reported||OIE, 2009|
|Martinique||Disease never reported||OIE, 2009|
|Nicaragua||Disease not reported||200709||, 1971; OIE, 2009|
|Panama||Disease never reported||OIE, 2009|
|Saint Kitts and Nevis||Disease never reported||OIE Handistatus, 2005|
|Saint Vincent and the Grenadines||Disease never reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Last reported||1938||OIE Handistatus, 2005|
|Argentina||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Bolivia||Absent, reported but not confirmed||NULL||, 1971; OIE, 1997; OIE, 2009|
|Brazil||Present||NULL||, 1971; Langenegger, 1994; OIE, 1997; OIE, 2009|
|Chile||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Colombia||Disease not reported||200701||, 1971; OIE, 1997; OIE, 2009|
|Ecuador||Disease not reported||19900630||, 1971; OIE, 1997; OIE, 2009|
|Falkland Islands||Disease never reported||OIE Handistatus, 2005|
|French Guiana||Disease never reported||OIE, 2009|
|Guyana||Disease not reported||OIE Handistatus, 2005|
|Paraguay||Last reported||2002||, 1971; OIE, 1997; OIE Handistatus, 2005|
|Peru||Disease not reported||200801||, 1971; OIE, 1997; OIE, 2009|
|Uruguay||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Venezuela||No information available||NULL||, 1971; OIE, 1997; OIE, 2009|
|Andorra||Disease not reported||OIE Handistatus, 2005|
|Austria||Disease not reported||1988||, 1971; OIE, 1997; OIE, 2009|
|Belarus||Disease not reported||1999||, 1971; OIE, 1997; OIE, 2009|
|Belgium||Disease not reported||NULL||, 1971; OIE, 1997; OIE, 2009|
|Bosnia-Hercegovina||Last reported||2003||OIE Handistatus, 2005|
|Bulgaria||Disease not reported||200609||, 1971; OIE, 1997; OIE, 2009|
|Croatia||Disease not reported||200710||, 1971; OIE, 1997; OIE, 2009|
|Cyprus||Disease not reported||OIE, 2009|
|Czech Republic||Disease not reported||OIE, 2009|
|Denmark||Disease not reported||1988||, 1971; OIE, 2009|
|Estonia||Disease not reported||1996||, 1971; OIE, 2009|
|Finland||Present||NULL||, 1971; OIE, 2009|
|France||Restricted distribution||NULL||, 1971; Vaissaire et al., 1996; OIE, 1997; OIE, 2009|
|Germany||Disease not reported||200008||, 1971; OIE, 2009|
|Greece||Restricted distribution||NULL||, 1971; OIE, 1997; OIE, 2009|
|Hungary||Disease not reported||2007||, 1971; OIE, 2009|
|Iceland||Disease not reported||OIE, 2009|
|Ireland||Disease not reported||OIE, 2009|
|Isle of Man (UK)||Last reported||1948||OIE Handistatus, 2005|
|Italy||Disease not reported||NULL||, 1971; Battisti et al., 1994; OIE, 1997; OIE, 2009|
|Jersey||Disease not reported||OIE Handistatus, 2005|
|Latvia||Disease not reported||198901||, 1971; OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease not reported||1998||, 1971; OIE, 1997; OIE, 2009|
|Luxembourg||Disease not reported||OIE, 2009|
|Macedonia||Disease not reported||OIE, 2009|
|Malta||Disease not reported||OIE, 2009|
|Moldova||Reported present or known to be present||, 1971; OIE, 1997; OIE Handistatus, 2005|
|Montenegro||Disease not reported||OIE, 2009|
|Netherlands||Disease not reported||1994||, 1971; OIE, 2009|
|Norway||Disease not reported||1993||, 1971; OIE, 2009|
|Poland||Disease not reported||2001||, 1971; OIE, 2009|
|Portugal||Disease not reported||OIE, 2009|
|Romania||Present||NULL||, 1971; OIE, 1997; OIE, 2009|
|Russian Federation||Present||OIE, 2009|
|-Russia (Europe)||Present||, 1971; Monisov et al., 1997; OIE, 1997|
|-Southern Russia||Present||, 1971; OIE, 1997|
|Serbia||Disease not reported||OIE, 2009|
|Slovakia||Disease not reported||1995||, 1971; OIE, 2009|
|Slovenia||Present||NULL||, 1971; OIE, 2009|
|Spain||Disease not reported||2004||, 1971; Serrano, 1994; OIE, 1997; OIE, 2009|
|Sweden||Present||NULL||, 1971; OIE, 2009|
|Switzerland||Disease not reported||199708||, 1971; OIE, 1997; OIE, 2009|
|UK||Disease not reported||200606||, 1971; OIE, 1997; OIE, 2009|
|-Northern Ireland||Last reported||1990||OIE Handistatus, 2005|
|Ukraine||Disease not reported||20071013||, 1971; OIE, 1997; OIE, 2009|
|Yugoslavia (former)||Reported present or known to be present||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Reported present or known to be present||OIE Handistatus, 2005|
|Australia||Restricted distribution||NULL||, 1971; OIE, 1997; OIE, 2009|
|-New South Wales||Present||, 1971; OIE, 1997|
|-Victoria||Present||, 1971; OIE, 1997|
|-Western Australia||Present||, 1971; OIE, 1997|
|French Polynesia||Disease never reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease not reported||OIE, 2009|
|Papua New Guinea||Present||Hugh-Jones, 1999|
|Samoa||Disease never reported||OIE Handistatus, 2005|
|Vanuatu||Disease never reported||OIE Handistatus, 2005|
|Wallis and Futuna Islands||No information available||OIE Handistatus, 2005|
PathologyTop of page
Most of the available information on the pathology of anthrax derives from studies carried out from the 1940s to the 1960s (Barnes, 1947; Young et al., 1946; Ross, 1955; 1957; Widdicombe et al., 1956; Gleiser, 1967; Gleiser et al., 1968; Dalldorf et al., 1971). It was then observed that the lymph nodes act as centres for the proliferation and dissemination of the bacilli which leads to septicaemia and death. Mucosal or cutaneous infection results in oedema, cellular infiltration and multiplication of the bacilli with the regional lymph nodes becoming enlarged, haemorrhagic and containing the bacilli. Inhalation anthrax involves less activity at the site of invasion and changes in lung parenchyma, such as hyperaemia, oedema and cellular infiltration are mild or absent (Young et al., 1946). The bacilli do not multiply in the lung itself but lead to infection of the mediastinal lymph nodes; the alveolar lining acts merely as a point of entry by the bacilli with multiplication and subsequent bacteraemia only occurring after infection of the lymph nodes draining the lungs (Barnes, 1947). There was no evidence that inhaled anthrax spores reached the blood stream directly from the lungs (Ross, 1957).
The earliest histological changes in the lymph nodes and spleen are necrosis of germinal centres. As infection proceeds, the nodes become oedematous and then haemorrhagic. Veins and capillaries within the nodes become filled with thrombi composed of leukocytes, platelets, fibrin and bacteria (Dalldorf et al., 1971). On the basis of pulmonary lesions, resistance in resistant species was explained in terms of an ability by these species to ‘wall off’ the pathogen at an early stage with an intense fibrinous and cellular response not mounted by susceptible species (Gleiser, 1967).
DiagnosisTop of page
The disease case history is of major importance in the diagnosis of anthrax (Turnbull et al., 1998). Clinical manifestations to look for are:
- Ruminants: Sudden death, bleeding from orifices, subcutaneous haemorrhage, without prior symptoms or following a brief period of fever and disorientation should lead to suspicion of anthrax.
- Equines and some wild herbivores: Some transient symptoms (fever, listlessness, dyspnoea and agitation) may be apparent.
- Pigs, carnivores, and primates: Local oedemas and swelling of the face and neck or of lymph nodes, particularly mandibular, pharyngeal and/or mesenteric.
At death in most susceptible species (the pig being a notable exception), the blood contains 107 to 108 bacilli per ml provided the animal has not been treated (numbers may also be lower in immunized animals which succumb to the disease). For reasons unknown, numbers of B. anthracis at death are very low in pigs (hundreds per millilitre or less).
A blood smear should be obtained with a swab from a small incision in the ear or from an ear clipping; the ear is usually recommended as being accessible and supplied with an extensive capillary network. Blood smears can also be obtained by means of a syringe from an appropriately accessible vein. The blood characteristically clots poorly or not at all upon death in anthrax victims and is dark and haemolyzed. The smear is dried, fixed and stained with polychrome methylene blue (M'Fadyean stain) (Turnbull et al., 1998). Large numbers of the capsulated bacilli will be seen in smears from relatively fresh carcasses of most species. The capsule should be clearly demarcated and pink in colour around the blue-black, often square-ended bacilli. Colourless haloes around rod-shaped bacteria cannot be judged positive. A Gram-stain will not reveal the capsule and may result in mistaken diagnosis, particularly if the carcass is not very fresh. B. anthracis does not compete well with putrefactive bacteria and, with increasing age of the carcass, the capsulated bacilli become harder to visualize (Turnbull et al., 1998).
The bacterium can be cultured from blood, from a swab of an ear clipping or from another appropriate specimen on blood agar or another nutrient agar. The haemorrhagic nasal, buccal or anal exudate will also carry large numbers of B. anthracis, which can be cultured from swabs or from samples contaminated with the exudate, but there may also be numerous other contaminating bacteria present.
If anthrax is suspected the carcass should not be opened in order to avoid contamination of the environment by spilled body fluids and subsequent spore formation (Turnbull et al., 1998). If, mistakenly, the carcass has been opened, the dark unclotted blood and markedly enlarged haemorrhagic spleen are usually immediately apparent. The mesentery may be thickened and oedematous and peritoneal fluid may be excessive. Petechial haemorrhages may be visible on many of the organs and the intestinal mucosa may be dark-red and oedematous with areas of necrosis. Where anthrax has been diagnosed after a carcass has been opened, special attention should be paid to de-contamination of the site at which the post-mortem was carried out and of the tools and materials that were used (Turnbull et al., 1998). Appropriate personal protective clothing should also be used if handling or disposing of suspect carcasses or contaminated materials.
In pigs, as indicated above, blood smears may not reveal the capsulated bacilli and, if cervical oedema is present, smears and cultures should be made with fluid from the enlarged mandibular and suprapharyngeal lymph nodes. If intestinal anthrax is responsible for death in pigs, this may only become apparent at necropsy. Smears and cultures should be made from the mesenteric fluid and lymph nodes. In other animals, in addition to any haemorrhagic exudates that may be observed, severe inflammation and oedematous swelling of the lips, tongue, gums, jowls and throat may be diagnostic indicators (Turnbull et al., 1998).
In the unopened carcass, the bacilli, unable to sporulate in the absence of oxygen, are destroyed by the putrefactive processes (Turnbull et al., 1998). Smears, as a diagnostic procedure, become unreliable about 24 hours after death although ‘shadons’ (capsular material) may still be observed some time after the bacilli themselves can no longer be seen. B. anthracis can often be cultured from carcass skin residues for some days after death but, with increasing length of time between death and examination, this becomes progressively less easy (Turnbull et al., 1998). Diagnosis then becomes increasingly dependent on isolation of spores from soil or other environmental samples contaminated by the oral, buccal or anal exudates (Turnbull et al., 1998).
It may not be possible to find the bacilli in smears or to isolate B. anthracis from animals that were treated before death; treatment can rapidly sterilize the blood and tissues but, if sufficient toxin has been formed, the animal may still go on to die (Turnbull et al., 1998).
For differential diagnosis, other causes of sudden death that should be considered are botulism, blackleg (Clostridium chauvoei), per-acute babesiosis, chemical poisoning (heavy metals, other poisons), ingestion of toxic plants, snake bite, lightning strike or metabolic disorders such as lactic acidosis, magnesium deficiency and bloat (Turnbull et al., 1998).
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Jugular pulse||Sign|
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Sign|
|Digestive Signs / Abdominal distention||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Ascites, fluid abdomen||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Bloat in ruminants, tympany||Sign|
|Digestive Signs / Bloody stools, faeces, haematochezia||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Decreased amount of stools, absent faeces, constipation||Sign|
|Digestive Signs / Diarrhoea||Sign|
|Digestive Signs / Dysphagia, difficulty swallowing||Sign|
|Digestive Signs / Rumen hypomotility or atony, decreased rate, motility, strength||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Cyanosis, blue skin or membranes||Sign|
|General Signs / Decreased, absent thirst, hypodipsia, adipsia||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Diagnosis|
|General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass||Sign|
|General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass||Sign|
|General Signs / Icterus, jaundice||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Laryngeal, tracheal, pharyngeal swelling, mass larynx, trachea, pharynx||Other:All Stages,Pigs:All Stages||Sign|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Other:All Stages,Pigs:All Stages||Sign|
|General Signs / Neck swelling, mass cervical region||Other:All Stages,Pigs:All Stages||Sign|
|General Signs / Pale mucous membranes or skin, anemia||Sign|
|General Signs / Pelvic or perineal swelling, mass||Sign|
|General Signs / Petechiae or ecchymoses, bruises, ecchymosis||Sign|
|General Signs / Sudden death, found dead||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Diagnosis|
|General Signs / Swelling skin or subcutaneous, mass, lump, nodule||Sign|
|General Signs / Swelling, mass external abdomen||Sign|
|General Signs / Thoracic swelling, mass, thorax, chest, ribs, sternum||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Other:All Stages||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Abnormal behavior, aggression, changing habits||Sign|
|Nervous Signs / Coma, stupor||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Nervous Signs / Disoriented, memory loss||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Other:All Stages||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Sign|
|Nervous Signs / Tremor||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Cattle & Buffaloes:Cow,Other:Adult Female,Pigs:Sow,Sheep & Goats:Mature female||Sign|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Diagnosis|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Skin / Integumentary Signs / Alopecia, thinning, shedding, easily epilated, loss of, hair||Sign|
|Skin / Integumentary Signs / Moist skin, hair or feathers||Sign|
|Skin / Integumentary Signs / Skin edema||Cattle & Buffaloes:All Stages,Other:All Stages,Sheep & Goats:All Stages||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Sign|
|Skin / Integumentary Signs / Skin fistula, sinus||Sign|
|Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene||Sign|
|Urinary Signs / Haematuria, blood in urine||Sign|
|Urinary Signs / Haemoglobinuria or myoglobinuria||Sign|
|Urinary Signs / Red or brown urine, pink||Sign|
Disease CourseTop of page
Little is known about how animals acquire anthrax. It is generally believed that ingestion of the spores while grazing or browsing is the usual route of infection. B. anthracis is not an invasive organism and needs a lesion in the skin or mucosa in which to lodge and initiate infection. For animals taking up the spores while grazing or browsing, the generally accepted theory is the necessary lesions are produced in the alimentary canal mucosa by grit or spiky leaves, grass or thorns. Fly-bites, as an alternative route of mechanically transmitted infection, have been discussed. Inhalation of spores while grazing over contaminated sites, which are dry and dusty, is another possible means of infection.
Once lodged in a lesion in the skin or mucosa, local germination and multiplication can occur giving a localized anthrax lesion. Apparently, however, spores reaching the lungs by inhalation do not germinate there (Barnes, 1947; Henderson et al., 1956; Ross, 1957; Friedlander et al., 1993). In either case, systemic infection begins with the spores being phagocytosed by macrophages and carried to regional lymph nodes. They germinate inside the macrophages and the capsulated vegetative bacilli are released from the macrophage to multiply in the lymphatic system. The spores then, in terms used by workers in the 1950s, continuously feed the blood stream with the vegetative bacilli in a manner analogous to continuous culture. Initially, during the incubation period, the spleen and other parts of the reticuloendothelial system filter out the bacteria. Eventually the system breaks down due to toxin action. During the last few hours of life (fulminant-systemic-phase), the bacteria build up rapidly in the blood (doubling time approximately 0.75 to 2 hours depending on host species) to levels of 108/ml or more together with massive toxaemia at the time of death. The action of the toxin on the endothelial cell lining of the blood vessels results in their breakdown, causing internal bleeding and the characteristic terminal haemorrhage to the exterior which is an essential part of the organism's cycle of infection.
The incubation period in the susceptible herbivore ranges from about 36 to 72 hours, during which time the host shows no readily discernible symptoms. With the onset of the hyper-acute systemic phase, the animal becomes distressed, appears to have difficulty breathing and ceases eating and drinking. Swellings in the sub-mandibular fossa may be apparent. Temperatures usually become slightly elevated. Finally the animal lapses into coma followed by death from shock. In highly susceptible species, the period between onset of visible symptoms and death may be just a few hours; the course of these events is more protracted in more resistant species.
The two known virulence factors of anthrax are its poly-D-glutamic acid capsule and the tri-partite protein toxin. The role of the capsule in pathogenesis is not fully understood beyond its function as an anti-phagocytic barrier. Although an essential virulence factor, it is a poor immunogen.
The basic disease mechanism is vascular injury with oedema, haemorrhage and thrombosis recognized as being the result of action of the toxin on the endothelial cell membranes rendering them permeable to plasma and causing adhesion of leukocytes and platelets with widespread intravascular thrombosis (Dalldorf et al., 1971). The molecular action of the toxin, and its detailed role in the pathogenesis of anthrax, has been progressively elucidated over the past two decades.
What for a long time was regarded as a single three-component toxin, has now come to be regarded as two related toxins. The lethal toxin, comprised of a protective antigen (PA) in combination with the lethal factor (LF), and the oedema toxin, composed of PA in combination with the oedema factor (EF). All three proteins are produced simultaneously during the exponential phase of growth of the organism.
Anthrax toxin is thus considered to fit the binary toxin (A-B) model in line with several other bacterial protein toxins. The crystal structure of PA was elucidated and refined to 2.1Å by Petosa et al. (1997) and it bears no resemblance to other bacterial toxins of known three-dimensional structure (Liddington et al., 1999).
EF is an 89 kDa protein and an adenylate cyclase. Being calmodulin dependent (calmodulin is the major intracellular calcium receptor in eukaryotic cells), it only functions in eukaryotic cells. By catalysing the abnormal production of cyclic-AMP, EF induces the altered water and ion movements that lead to the characteristic oedema of anthrax. The role of oedema toxin in the anthrax disease process may be to prevent mobilization and activation of poly-morpho-nuclear leukocytes and thereby prevent the phagocytosis of the bacteria (Leppla, 1991).
The genes for both the virulence factors of B. anthracis are carried on plasmids. Those for the toxin components and their transcriptional activator atxA, are located on a single high molecular weight 182 kb plasmid designated pXO1. The genes for capsule expression, assembly and degradation (CapA, CapB CapC and dep) and their transcriptional activator, acpA, are located on the smaller 95 kb pXO2 plasmid. A wild type strain may be differentially or fully cured of these plasmids. Strains cured of one or both plasmids have reduced virulence. Toxigenic, non-capsulated strains form the basis of live spore vaccines.
Both pXO1 and pXO2 have been fully sequenced (Okinaka et al., 1999) and the sequence for the whole B. anthracis chromosome was completed in 2003 (Read et al., 2003).
EpidemiologyTop of page
Anthrax is primarily a disease of herbivores and the eco-epidemiological cycle of the causative agent, Bacillus anthracis, is maintained through shedding the bacilli at death in large numbers within blood leaking out through the nose, mouth or anus or within spilled body fluids when the carcass is opened by scavengers. In the cycle’s simplest form, the spores formed on exposure to the air then become the infecting source for future hosts grazing over the site.
In general, carnivores and omnivores are more resistant to anthrax but occasionally do contract it from feeding on the carcasses of herbivorous animals that have died of the disease.
There are various elaborations of this cycle, for example, when herbivorous animals acquire the disease from osteophagia (chewing on bones to obtain necessary minerals). As reviewed by Quinn and Turnbull (1998) biting flies have been proposed as the cause of explosive epidemics and have been shown experimentally to be able to spread the disease. Non-biting flies have been incriminated as the principal vector of anthrax in browsing herbivores (de Vos and Bryden, 1996).
Anthrax is a seasonal disease, although, because conditions and circumstances that predispose to outbreaks vary from location to location, seasonality shows correspondingly different patterns in different locations. The primary conditions affecting the incidence of anthrax in any one place are temperature and rainfall (or drought). Climate probably acts in two ways. Directly, by influencing the way in which an animal makes contact with the spores, through, for example, grazing closer to the soil in dry periods when the grass is sparse, or enforced grazing at restricted sites when water becomes scarce. Alternatively, climate can act indirectly through its effect on the general health of the animal and its level of resistance to infection.
Anthrax enzootic areas are generally found in warmer climates. This is probably attributable to the relationship between temperature and water activity and rates of sporulation of bacilli that have been shed from victims of the disease. The vegetative form appears to survive poorly outside the animal host and the outcome of the race to sporulate or die is temperature dependent. Sporulation may not be achieved below certain temperatures and the disease can be expected to die out with time. As with every rule, however, there are apparent exceptions and some modification of this theory may be needed to explain the persistence of anthrax in the bison community of the Great Lakes region of northern Canada.
The relationship between temperature, water activity and germination may also play a role in the eco-epidemiology of anthrax, though to a lesser extent than with sporulation. Below a certain temperature and/or water activity, germination will not take place even in the presence of germinants. Above that temperature and/or water activity, germinants present may induce germination, but, if adequate nutrient is not present (as in the average environmental circumstance), the emerging vegetative cells will die out. Cooler climates therefore again become unfavourable to perpetuation of the disease.
Seasonality in industrialized countries is also influenced by human activities, primarily those involving importation of animal products. Spread of infection from these to the livestock of the importing countries via animal feedstuffs or more indirectly through industrial effluent, results in an incidence reflecting the seasonality of the country or countries from which the imports originated.
Despite being a disease that has been so well known for so long, many seemingly simple epidemiological questions remain unanswered. How an animal contracts the disease remains the realm of theory; experimental oral LD50s or MIDs (minimum infectious doses) are far higher than animals would ever be expected to encounter in natural circumstances (Druett et al., 1953; Schlingman et al., 1956; de Vos, 1990; Redmond et al., 1997; Carter and Pearson, 1999). Outbreaks are generally considered to be of the point source type with direct herbivore-to-herbivore transmission thought not to occur and certainly has been found to not occur under laboratory conditions. However, it is hard to explain periodic explosive epidemics in terms of point source infection. The proposed role of biting flies in such events is unproven and possibly would not explain a second anomaly which occurs in respect to large explosive outbreaks. This is that explosive epidemics usually affect only one species while the incidence in other, equally susceptible species in the vicinity remains sporadic. Strain differences are an obvious explanation, but these have never been detected and shown to account for this anomaly.
Impact: EconomicTop of page
As indicated in the overview section, anthrax, although so widely encountered across the globe, is seemingly regarded more as a nuisance than as having significant economic consequences. The true economic impact of anthrax is impossible to assess with the data available. However, reported, often mandatory vaccination programmes are so extensive in some countries that they, if not the disease itself, must represent a significant national economic burden.
Zoonoses and Food SafetyTop of page
It has been well documented that many cases of cutaneous anthrax result from butchering carcasses and preparing the meat destined for human consumption. Although poorly documented, there is little doubt that, in endemic areas of Africa and other parts of the globe, human pharyngeo-gastrointestinal anthrax occurs amongst those who eat the meat of these types of carcasses (Ndyabahinduka et al., 1984; Dietvorst, 1996a; Dietvorst, 1996b; van den Bosch, 1996). As the course of the disease is rapid, there is no loss of condition in the affected animal and the meat appears good. The hazards of eating the swollen spleen are traditionally recognized and this is generally buried. Also recognized is that a small proportion of those who consume the meat may become ill with gastrointestinal symptoms and some may even die. However, the value of the meat is frequently seen as outweighing the risks of ill-effect and farmers/owners will often ignore veterinary instructions to bury or burn sudden death carcasses.
Continued public education together with improvement of meat inspection and of follow-up decontamination and disinfection procedures is the prescription in countries where these practices persist (Balogh et al., 1994).
The issue of action to be taken on milk derived from a dairy herd/flock in which anthrax has occurred has occasionally arisen in the past. This was revisited by the UK Department of Health in 1995 (unrestricted document PL/CO3). The summary states "the milk from animals known or suspected at the time of milking of being infected with anthrax will be treated as the Anthrax Order 1991 requires and excluded from the supply. Where milk has already entered the public supply or where there is a suspicion that bulk milk may contain milk from an animal that could be suffering from anthrax or has died from the disease, pasteurization should suffice to protect the consumer against the risk of anthrax after consuming the milk." Heat treatment of milk involves boiling for 10 to 40 minutes and is regarded as adequate because it was judged that contamination would be at a very low level. This, in turn, was based on the judgement that, in the infected animal, anthrax bacilli does not pass to the milk until the disease has become bacillaemic. By this time, milk secretion will have ceased or the animal will be so obviously ill that no attempt would be made to milk it.
An inadequately resolved issue is the appropriate holding period for livestock between vaccination and slaughter. The figures found in official and semi-official documents range from 10 days to 6 weeks and appear to have been chosen on an arbitrary basis.
There is also a potential for Bacillus anthracis to be used as a biological weapon, as seen recently in the USA. Such use can result in three types of disease in humans: inhalation anthrax, cutaneous anthrax and gastrointestinal anthrax. Details of these diseases can be found in the weblinks.
Disease TreatmentTop of page
The first sign of anthrax in a herd is unexpected death of one or more animals. Following this first incident of anthrax in a herd, the remaining animals should be moved immediately from the site where the index case(s) died. Animals should be checked at least three times daily for 2-weeks for signs of illness (rapid breathing, elevated body temperature) or of submandibular or other oedema. Any animal showing these signs should be separated from the herd and treated with antibiotics immediately. Intravenous sodium benzylpenicillin according to manufacturer's instructions, usually in the range 12,000-22,000 units per kg of body weight. This should be followed 6-8 hours later by intramuscular injection of long acting benethamine penicillin for which manufacturers' instructions usually recommend dose within range 6000-12,000 units per kg of body weight. Alternatively another appropriate long-acting preparation such as ClamoxylR (15 mg/kg), a long-acting preparation of amoxycillin can be administered and are normally successful. If long-acting preparations are unavailable, procaine penicillin (dose recommended by manufacturers is usually 6000-12,000 units/kg) can be used for intramuscular injection but should be administered again after 24 and 48 hours. Streptomycin acts synergistically with penicillin and penicillin/streptomycin mixtures are available commercially but involve an extra cost factor. Recommended doses of streptomycin to be administered together with penicillin intramuscularly are 5-10 mg per kg body weight in large animals and 25-100 mg per kg body weight in small animals.
Attention should be paid to manufacturers' recommendations regarding precautions and limitations of use and aspects relating to withdrawal periods after use in food animals.
If there is concern that the antibiotic treatment will not control the outbreak, the herd should be vaccinated. Live spores constitute the active ingredient of the vaccine and therefore treatment should not be done simultaneously with vaccination. Deaths usually cease within 8 to 14 days of vaccination. Herd quarantine can be lifted 21 days after the last death. Decontamination of the site(s) where the index case or other case(s) died should be carried out.
In certain countries, treatment is not permitted and slaughter is mandatory.
Prevention and ControlTop of page
Control measures for anthrax are aimed at breaking the cycle of infection and involve four main components:
- site quarantine
- correct disposal of carcasses of animals that have died of anthrax
- decontamination by appropriate methods of the sites where the animals died and of any materials subsequently contaminated
- vaccination where there is risk of the outbreak spreading
A contingency plan for the prevention and control for anthrax was included as Appendix VI in the WHO anthrax guidelines (WHO, 2008). This proposed that affected premises should be quarantined for at least 20 days after the last case. Any susceptible livestock, or risk items (carcasses, hides, skins, etc.) moved from the premise should be traced and the appropriate action taken. Milk is covered separately (see zoonoses and food safety section).
The preferred method of carcass disposal is in situ incineration by a method that ensures thorough scorching of the contaminated ground in the vicinity of the carcass. Practical details are given in Appendix III of the WHO anthrax guidelines (WHO, 2008). Where lack of fuel prevents this, burial 1.5 to 2 m below ground may be the only option. Numerous reports exist, however, of fresh outbreaks occurring after disturbance of known or suspected anthrax burial sites, and burial should always be discouraged in favour of incineration where possible. Where local regulations permit it, transfer of a carcass to a body bag and transport to a permanent incinerator may be considered. In some European countries, rendering is an option. In either case, care must be taken to avoid spreading contamination while manipulating the carcass and subsequent decontamination measures must be effective.
Appropriate decontamination methods include dry heat, autoclaving, incineration, fumigation with sporicidal fumigants (formaldehyde, ethylene oxide), disinfection with sporicidal disinfectants (hypochlorite, formalin, glutaraldehyde, hydrogen peroxide, peracetic acid) or irradiation. It has been suggested that dry heat at 160°C for one hour (Mitscherlich and Marth, 1984) or irradiation at ±20 kGy (Bowen et al., 1996) is sufficient depending on the degree of contamination and the bulk of the material. Different procedures and, where relevant, chemicals will be appropriate for different materials and circumstances. Sensitive and valuable equipment will need to be fumigated or irradiated, not autoclaved or incinerated. Hypochlorites are not suitable for metal objects or materials with a high organic content. Formalin is often the best and easiest sporicidal disinfectant to apply but is hazardous to operators and animals. Soil can be incinerated, but whether this is practical depends on the quantity of contaminated soil present. Where contaminated sites are too large to practically decontaminate, the only approach may be to isolate them, for example by concreting them over. The topic is further discussed by Turnbull (1996) and Turnbull et al. (1998).
Livestock vaccines in almost all countries are suspensions of spores of an attenuated strain of B. anthracis usually with saponin as an adjuvant (Turnbull et al., 1998). In most countries, this is the Sterne strain 34F2 although countries of the former USSR use a different strain attenuated in an analogous manner. The attenuation has resulted in the inability of these strains to form the capsule while still elaborating the toxin. The basis of protection is the development of antibodies to the protective antigen.
ReferencesTop of page
Abdourashitov TA, 1997. Epizootic status for anthrax in the Uzbekistan Republic. In: Cherkasskiy BL, ed. Inter-regional WHO/FAO Workshop on Anthrax, 5-6 October, 1997, Almaty, Kazakhstan. Abstract papers, pp. 72-73.
Abikarimov ST, Baatyrbekov ES, Shevchenko VP, 1997. On anthrax incidence and preventive interventions in the Kyrgyz Republic. In: Cherkasskiy BL, ed. Inter-regional WHO/FAO Workshop on Anthrax, 5-6 October, 1997, Almaty, Kazakhstan. Abstract papers, pp. 68-69.
African Union-Interafrican Bureau for Animal Resources, 2011. Panafrican Animal Health Yearbook 2011. Pan African Animal Health Yearbook, 2011:xiii + 90 pp. http://www.au-ibar.org/index.php?option=com_flexicontent&view=items&cid=71&id=109&Itemid=56&lang=en
Ahmed N, 1997. The current status of surveillance and control of anthrax in Bangladesh. In: Joshi DD, ed. Proceedings of the International Workshop on Anthrax, 9-11 March, 1997, Kathmandu, Nepal. Kathmandu: The National Zoonoses and Food Hygiene Research Centre, Tahachal, 129-133.
Alcasid RN, 1997. Anthrax in the Philippine. In: Joshi DD, ed. Proceedings of the International Workshop on Anthrax, 9-11 March, 1997, Kathmandu, Nepal. Kathmandu: The National Zoonoses and Food Hygiene Research Centre, Tahachal, 124-125.
Amaneldyev K, 1997. Urgent issues of anthrax incidence in Turkmenistan. In: Cherkasskiy BL, ed. Inter-regional WHO/FAO Workshop on Anthrax, 5-6 October, 1997, Almaty, Kazakhstan. Abstract papers, pp. 70-72.
Amireev SA, Bismildin FB, Spataev MB et al. , 1997. Ways to improve epidemiological surveillance of anthrax in the Kazakhstan Republic. In: Cherkasskiy BL, ed. Inter-regional WHO/FAO Workshop on Anthrax, 5-6 October, 1997, Almaty, Kazakhstan. Abstract papers, pp. 66-67.
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