Anthrax paper (assignment)

CHAPTER I

INTRODUCTION

1.1  Background

            Historically, in the mid-1800s, inhalational anthrax related to the textile industry became known as woolsorters’ disease (in England) and ragpickers’ disease (in Germany and Austria), because of the frequency of infection in mill workers exposed to imported animal fibers contaminated with anthrax disease. In 1962, nine anthrax epizootics have been recorded in the bison herds of northern Canada resulting in the deaths of at least 1309 bison. Large anthrax outbreaks in humans have occurred throughout the modern era more than 6,000 (mostly cutaneous) cases occurred in Zimbabwe between October 1979 and March 1980, and 25 cutaneous cases occurred in Paraguay in 1987 after the slaughter of a single infected cow. On September 11, 2001, the United States experienced 22 cases of anthrax, including 5 deaths, and forever changing the realm of public healths. Until now the dissemination of this disease still persists in many countries, because the animal such as cattle and pig as one of host also widely cultivated.

            The dissemination of microorganism spores running quickly years by years, so that the disease case is increase. Anthrax is caused by infection with Bacillus anthracis, a gram-positive spore-forming rod. The spore form of this organism can survive in the environment for many decades. Certain environmental conditions appear to produce anthrax zones, areas where in the soil is heavily contaminated with anthrax spores. Such conditions include soil rich in organic matter (pH < 6.0) and dramatic changes in climate, such as abundant rainfall following a prolonged drought. Partly because of its persistence in soil, anthrax is a rather important veterinary disease, especially of domestic herbivores. In addition to encountering anthrax while grazing in areas of high soil contamination, these herbivores may also acquire the disease from the bite of certain flies. Vultures may mechanically spread the organism in the environment. So, the disease spread up wherever by various kind of host and environment condition. That’s why the dissemination of this disease moved quickly.

            Therefore, several treatments by result of research activities for infected animal must be conducted by scientist, farmer, and the agencies working in animal health or veterinary. This aimed to minimize the dissemination of this disease include maintaining health in worldwide. Hence, this paper would explain about the disease especially in animal involve bacteriology, pathogenesis, prevalence, clinical features, and the treatment.

 

1.2  Problem

The problem is:

a.    How about the bacteriology of anthrax disease?

b.    How about the pathogenesis of anthrax disease?

c.    How about the prevalence of anthrax disease?

d.   How about the diagnosis of anthrax disease?

e.    How about the clinical features of anthrax disease?

f.     How about the treatment of anthrax disease?

1.3  Purpose

The purpose involved:

a.    To know about the bacteriology of anthrax disease.

b.    To know about the pathogenesis of anthrax disease.

c.    To know about the prevalence of anthrax disease.

d.   To know about the diagnosis of anthrax disease.

e.    To know about the clinical features of anthrax disease.

f.     To know about the treatment of anthrax disease.

CHAPTER II

DISCUSSION

2.1  Bacteriology

            Bacillus anthracis as the causative agent of anthrax, it’s a large, gram-positive, aerobic, spore-forming bacillus that measures 1.0 to 1.5 μm by 3.0 to 10.0 μm. Unlike other saprobic bacillus species (B. subtilis and B. cereus ), it is nonmotile, is nonhemolytic on sheep’s-blood agar, grows readily at a temperature of 37°C, and forms large colonies with irregularly tapered outgrowths (a “Medusa’s head” appearance). In vitro it grows as long chains, but in the host it appears as single organisms or chains of two or three bacilli. It forms mucoid colonies and exhibits a prominent capsule when grown on nutrient agar containing 0.7 percent sodium bicarbonate in the presence of 5 to 20 percent carbon dioxide.           When nutrients are exhausted, resistant spores are formed that can survive in the soil for decades. Spores do not form in host tissues unless the infected body fluids are exposed to ambient air. B. anthracis spores germinate when exposed to a nutrient-rich environment, such as the tissues or blood of an animal or human host. Although B. anthracis is one of the most molecularly monomorphic bacteria, it has been possible to separate all known strains into five categories (providing some clues to their geographic sites of origin) on the basis of variable numbers of tandem repeats in the variable region of the vrrA gene.

2.2  Pathogenesis

            B. anthracis has a nearly worldwide distribution, existing in the soil in the form of extremely resistant spores and causing infection in humans and in farm and wild animals that have grazed on contaminated land or ingested contaminated feed like meat or visceral organs.

          When in the animal transmission, anthrax tend to occur in association with particular climatic and weather events, such as heavy rainfall, flooding, and drought. In anthrax-prone areas, the close grazing of animals on fresh shoots of grass after rainfall often leads to outbreaks of the disease due to the ingestion of organisms picked from contaminated soils (inhalation and ingestion). During severe outbreaks, biting flies may transmit the disease from one animal to another but this is a very minor mode of transmission (cutaneous). The principal mode of transmission is ingestion of infective micro-organisms. Non-biting blowflies may contaminate vegetation by depositing vomit droplets after feeding on a carcass infected with B. anthracis. Animals feeding on such vegetation then become infected. Wild carnivores become infected through the consumption of infected animals that have died from anthrax. Outbreaks of anthrax have been reported in some animals after ingestion of feeds containing meat and bone meal based concentrates originating from carcasses contaminated with anthrax bacterial spores.

            When in the human transmission, infection is initiated with the introduction of the spore through a break in the skin by directly contact with anthrax spores or biting fly (cutaneous anthrax) or entry through the mucosa (gastrointestinal anthrax). After ingestion (poor undercooked meat) by macrophages at the site of entry, germination to the vegetative form occurs, followed by extracellular multiplication and capsule and toxin production that induce releasing large number of B. anthracis. But another way also happen here, the inhalational anthrax begins after exposure to the necessary inoculum, with the uptake of spores by pulmonary macrophages. These macrophages carry the spores to tracheobronchial or mediastinal lymph nodes. Here, B. anthracis finds a favorable milieu for growth and is induced to vegetate. The organism begins to produce an antiphagocytic capsule and at least three proteins, which appear to play a major role in virulence.

            The principal virulence factors of B. anthracis are encoded on two plasmids, one involved in the synthesis of a polyglutamyl capsule that inhibits phagocytosis of vegetative forms and the other bearing the genes for the synthesis of the exotoxins it secretes. The exotoxins are binary, composed of a B (binding) protein that is necessary for entry into the host cell and an A (enzymatically active) protein. The B component is known as the protective antigen and is common to both toxins. The A component of the edema toxin is the edema factor, a calmodulin-dependent adenylate cyclase that is responsible for the prominent edema at sites of infection, the inhibition of neutrophil function, and the hindrance of the production by monocytes of tumor necrosis factor and interleukin-6.                       The A component of the second toxin, lethal toxin, is a zinc metalloprotease that inactivates mitogen-activated protein kinase, leading to the inhibition of intracellular signaling. Lethal toxin stimulates the release by macrophages of tumor necrosis factor α and interleukin-1β, a mechanism that appears to contribute to the sudden death from toxic effects that occurs in animals with high degrees of bacteremia (reaching  to  bacilli per milliliter of blood, visible on Gram’s staining) and terminally high levels of lethal toxin.

2.3  Prevalence

            Between 1979 and 1980, in association with war and the interruption of veterinary public health practices, Zimbabwe was the site of the largest outbreak of anthrax, with about 10,000 cases, almost all of which were cutaneous infections. Between 20,000 and 100,000 cases of anthrax have been estimated to occur worldwide annually, but in the United States, the annual incidence was only 127 in the early part of the 20th century, and it subsequently declined to less than 1 case per year, a rate maintained for the past 20 years. Until now, there had not been a case of inhalational anthrax in the United States in more than 20 years. Thus, the recent occurrence of 12 cases of anthrax, 6 involving inhalation and none with the conventional exposure to infected animals or animal products, has spotlighted the current consideration of anthrax as a weapon of bioterrorism.

            We were forced to recognize the possibility that anthrax may be used as a biologic weapon in 1979, when at least 66 people in Sverdlovsk died in the largest known epidemic of inhalational anthrax. This epidemic followed the accidental release of anthrax spores into the atmosphere by a research facility involved in “weaponizing” anthrax by preparing finely milled, nonclumping (electrostatically neutral) spores that are optimal for dissemination and inhalation and that produce toxins when they germinate. After the Gulf War, Iraq admitted producing and deploying such weaponized anthrax in missiles, so a clear threat remains.

            The different disease infection of human has made a different case-fatality rate, on 24 July to 4 August 1989 in Haiti, cutaneous anthrax infection with penicillin treatment have 5% to 20% of case-fatality rate (Raymond A. Smego et al., 1998), while the case-fatality rate on 2001 in eastern United States of inhalational anthrax infection with intensive care was 45% and untreated Gastrointestinal anthrax infection about 25%-75% (John D. Grabenstein, 2008).

            Then, (Michael E. Bales et al., 2002) stated that on 2001 in southwest Texas 1,638 animal of at least 11 animal species were infected with Bacillus anthracis, on 1993 in southeast North Dakota there are 8 cases of anthrax in livestock by soil contamination or ingestion infection, on 1976 in Foard and Cottle Counties Texas there are more than 160 cases where significantly higher attack in bulls and horses that infected by biting flies or cutaneous infection, on 1961 in Philadelphia there is fatal cases of inhalation anthrax where aerosolized B. anthrachis spread up and attach at a goat hair and healed each other.

2.4  Diagnosis

         

          Several diagnosis method can be carried out as follows:

2.4.1 Blood Smear Rationale

          In most species, at death from anthrax (the pig being a notable exception) the blood is usually teeming with the capsulated anthrax bacilli, provided the animal has not been treated. Published figures for terminal B. anthracis blood counts are (approximate cfu/ ml) mice, rats -, sheep and goats , rhesus monkeys –, chimpanzees , zebras –, elephants –, springbok , blue wildebeest , cheetah .

2.4.2 Diagnosis Based on Tests for Antigents

            A simple, rapid and highly sensitive and specific chromatographic device, a more reliable and more sensitive alternative to the Ascoli test and utilizing a monoclonal capture antibody detecting the anthrax–specific protective antigen, has now been designed and shown to be useful for rapid on-site diagnosis in the field.

2.4.3 Molecular Diagnosis

            Genetically-based confirmation by PCR is becoming increasingly accepted on a stand-alone basis for many types of specimen and is increasingly available worldwide through commercial kits. It is still advisable to attempt to confirm bacteriologically (i) a positive to avoid the chance of a false positive, and (ii) a negative in case the PCR test was insufficiently sensitive.

2.5  Clinical Features

            Horses may show acute symptoms and die in 2–3 days. Intestinal lesions may result in colic and diarrhoea. N. M. Swartz (2001) associated large oedemas on the breast, abdomen, neck, and shoulders with cases transmitted by biting flies and the recovery sometimes occurs. Pigs are regarded as more resistant to anthrax than cattle, sheep, goats and horses, but herd outbreaks with significant mortality can occur. Their greater resistance is reflected in the greater evidence of local signs, such as swellings of the throat and pharyngeal and cervical lymph glands.

            Among cattle and sheep, the period of illness is often so short that the affected animals may be found dead without signs of illness having been noticed. Nevertheless, sometimes anthrax is not always rapidly fatal to cattle and sheep, and an affected animal may be ill for several days before death occurs. Any of the following symptoms may be observed: high temperature, shivering and twitching, harsh dry coat, fits, bright staring eyes, colicky pains, dejection, refusal of food, and marked decrease or complete loss of milk. Occasionally a small trickle of blood from the nostrils is visible and there may also be blood in the dung.

            In the post-mortem appearances, the unopened carcasses may be swollen and blood may ooze from the nostrils or other natural openings of the body. These conditions are not always present and their absence does not indicate that the case is not anthrax.

2.6  Treatment (Post-exposure Prophylaxis)

            As the animal treatment, the treatment is seldom possible and done for animals infected with anthrax because of the rapid and fatal course of the disease once symptoms become apparent. However, if time permits, antibiotic drugs (Penicillin, oxytetracycline, doxycycline, dihydrostreptomycin, chloramphenicol, and rifampin) may be used with good effect. If animals are likely to be continually exposed to infection, for example by grazing over infected pastures, vaccination with anthrax spore vaccine is recommended.

            This vaccine is safe to use and protects the animals for six months or more. Animals remain in a susceptible state, however, for about ten days after vaccination, and should be isolated as far as possible from contact with possible sources of infection during this period. When the circumstances appear to warrant treatment with antibiotics or vaccine, a veterinary surgeon should be consulted. As a note: Antibiotics and vaccines should not be used at the same time because antibiotics interfere with the development of immunity. If animals require antibiotics shortly after vaccination they should be revaccinated 10 days after the antibiotic treatment has stopped.

CHAPTER III

CONCLUSION AND SUGGESTION

3.1  Conclusion

Based on the discussion, we conclude that:

1.    Bacillus anthracis as the causative agent of anthrax, it’s a large, gram-positive, aerobic, spore-forming, grows readily at a temperature of 37°C, and forms large colonies with irregularly tapered outgrowths.

2.    The anthrax cycle begins from anthrax spores that survive in the soil of pasture area and then infect human also animal by cutaneous, inhalational, and ingestion infection where cutaneous is highest infection.

3.    The increment of prevalence of the disease can be seen in animal and human cases where untreated condition increasing case fatality rate while treated condition decreasing case-fatality rate.

4.    Several diagnosis methods that can be carried out such as Blood smear rationale, Diagnosis based on the antigents (Ascoli test), and molecular diagnosis where Ascoli test more simple, rapid, and sensitive.

5.    The clinical signs of infected animals sometimes unvisible (suddenly death), but sometimes such as shivering and twitching also diarrhea as onset of infection.

6.    The treatment can be done by therapy of antibiotic drugs and vaccination, but it must be used in different time.

3.2  Suggestion

Based on this paper, the author give the suggestion that anthrax disease is a hazardous infection as well for human and animals. Therefore, know the sources and cycle of the disease and then cut and close the cycle are important.

REFERENCES

Bales, E. B., et al. 2002. Epidemiologic Response to Anthrax Outbreaks: Field Investigations, 1950-2001. Emerging Infectious Disease. Vol.8(2): 1163-1174.

Borio, L., et al. 2001. Death Due to Bioterrorism-Related Inhalational Anthrax. JAMA. Vol.286(20): 2554-2559.

Bush, M. L., et al. 2001. Index Case of Fatal Inhalational Anthrax Due to Bioterrorism in the United States. N Eng J Med. Vol.345(22): 1607-1610.

Grabenstein, D. J. 2008. Countering Anthrax: Vaccines and Immunoglobulins. Clinical Infectious Disease. Vol.46(1): 129-136.

Hughes, M. J. and Gerberding, L. J. 2002. Anthrax Bioterrorism: Lessons Learned and Future Directions. Emerging Infectious Disease. Vol.8(10): 1013-1015.

Jerningan, A. J., et al. 2001. Bioterrorism-Related Inhalational Anthrax: The First 10 Cases Reported in the United States. Emerging Infectious Disease. Vol.7(6): 933-944.

Smego, A. R., et al. 1998. Cutaneous Manifestations of Anthrax in Rural Haiti. Clinical Infectious Disease. Vol.26(1): 97-102.

Swartz, N. M. 2001. Recognation and Management of Anthrax. N Eng J Med. Vol.345(22): 1621-1626.