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Anthrax and Its Potential for Bioterrorism - Research Paper Example

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The paper "Anthrax and Its Potential for Bioterrorism" focuses on the critical analysis of the major peculiarities of Anthrax and its potential for bioterrorism. Bacillus anthracis pose a threat not only to animals but to man as well. It has the potential to be used as a weapon for bioterrorism…
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Anthrax and Its Potential for Bioterrorism
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Anthrax and Its Potential for Bioterrorism Bacillus anthracis pose a threat not only to animals but to man as well. It has a potential to be used as a weapon for bioterrorism because a kilo of anthrax spores is highly portable, relative cheap to produce, and has the capacity to kill at least 30,000 people. There are clinical signs associated with anthrax in both animals and humans. One good news is that it is not impossible to manage and cure a person from infection by anthrax. Vaccines are available and, provided exposure to anthrax has been detected early enough, it is possible to conduct vaccination among those who have been exposed to the bacteria. Recovery from the disease is also highly possible. Anthrax and Its Potential for Bioterrorism The United States National Institute of Allergy and Infectious Diseases (NIAID) categorized anthrax as a “Category A” high priority disease because of its potentials as a biological weapon or for bioterrorism (Dyer, 2010, p. 1). The bacterial pathogens that can cause anthrax are Bacillus anthracis, Francislla tularensis, and Yersinia pestis (Dyer et al., 2010). However, the study of Fasanella et al. (2010, p. 1) identified only “the encapsulated, large rod, and spore-forming Bacillus anthracis” as the cause of the disease for both animals and man. According to Fontanella et al. (2010, p. 1), “human anthrax usually results from a cutaneous infection caused from the handling of infected animal products or, in rare cases, by ingesting or inhaling spores from contaminated animal products.” Epidemiology From more than 250,000 screens performed in 2010, Dyer et al. (2010) identified 3,073 human-B anthracis, 1,383 human-F. tularensis, and 4,059 human-Y. pestis proteins, all of which are uncharacterized. According to Fasanella et al. (2010, p. 1), animal anthrax “primarily affects herbivore ruminants, such as cattle, sheep, and goats, which are the most susceptible animal hosts.” Animals usually get the disease after ingestion of soil-borne anthrax sore (Fasanella et al., 2010, p. 1). The study of Fasanella et al. (2010) confirmed that house flies or insects could be mechanical vectors for the spread of anthrax. Unweaponized, anthrax infections in humans are rare and “it occurs primarily as a professional disease in farmers and veterinarians through direct exposure to spores from infected animals or animal products such as hides or wool” (Cao et al., 2009). Risk Factors for Anthrax Without bioterrorism, the risk factors for Anthrax outbreaks include “gleysolic or organic soils, old anthrax grave sites, soil disruptions or flooding, hot, dry temperatures, and heavy precipitation events” (Epp et al., 2010, p. 747). An unusually warm and dry spring conditions followed by heavy rainfall can be a key factor for an outbreak (Epp et al., 2010). Clustering was observed in an anthrax outbreak among cattle in Saskatchewan, Canada, in 2006 (Epp et al., 2010). Clustering is an “unusual occurrence of events in space, time, or both” (Epp et al., 2010, p. 743). In Saskatchewan, Canada, most of the anthrax outbreaks occurred during the months of June, July, August, and September (Epp et al., 2010). Pathogenesis According to Cao et al. (2009, p. 4679), the lethal toxin of Bacillus anthracis plays a key role in the pathogenesis of anthrax. At the same time, the protective antigen is the most important part of the anthrax toxin and builds the lethal toxin by combining with the lethal factor Phenylalanine-427 (Cao et al., 2009). The anthrax bacteria start infection by the entry of anthrax spores through abrasions in the skin, ingestion, or inhalation (Cao et al., 2009). Most anthrax infections are “highly lethal” (Cao et al., 2009, p. 4679). Kalamas (2004) confirmed that anthrax is often a fatal through the three possible routes that the bacteria enter the human body: inhalation, abrasion or cutaneous, and gastrointestinal or ingestion. Within hours from its introduction in the human body, most anthrax spores germinate into vegetative bacteria that “produce various virulence factors” (Kalamas, 2004, p. 534). According to Kalamas (2004), the vegetative bacteria can enter the bloodstream and the three toxins of anthrax form two binary toxins, “edema toxin and lethal toxin” that are responsible for overt symptoms and death. Potential for Bioterrorism Bacillus anthracis is a “rod-shaped, gram-positive, spore-forming bacterium” (Cao et al., 2009, p. 4679). The spores are “highly resistant to adverse environments, can survive for long periods, and are easy to produce” (Cao et al., 2009). Even before 2001, there were 18 cases of inhalation of anthrax (Kalamas, 2009). From 3 October to 2001 to 16 November 2001, there were 22 cases of inhalation and cutaneous anthrax in the US that resulted to five deaths (Kalamas, 2009, p. 533). Despite the signing of Biological Weapons Agreement in the 1970s banning bioweapons, at least 17 countries have been developing bioweapons (Kalamas, 2004). The United Nations Special Commission, for example, has discovered that “Iraq had weaponized anthrax pores into Scud warheads in 1995” (Kalamas, 2004, p. 234). Anthrax aerosolized spores were accidentally released to the atmosphere in 1979 and resulted to 79 cases in which 68 died (Kalamas, 2004). The risk of mass deaths from anthrax is real. A 1993 US Congressional Office of Technology report estimated that at least 3 million casualties would result from an aerosol release of 100 kilograms of weaponized anthrax spores using the upwind of the Washington, DC area (Kalamas, 2004). This means that as little as one kilo of the highly portable anthrax can cause 30,000 deaths. It should be easier and a lot cheaper to produce anthrax compared to a nuclear bomb. In addition, anthrax endosphores “are resistant to drying, heat, ultraviolet light, gamma radiation, and many disinfectants” (Kalamas, 2004). Anthrax spores “can germinate in the blood, tissues of animals, or human hosts rich in amino acids, nucleosides, and glucose” (Kalamas, 2004). The vegetative bacilli have a poor survivor rate outside of an animal or human host and “will form spores when local nutrients are exhausted” (Kalamas, 2004). Anthrax can remain dormant in the soil for decades (Kalamas, 2004). The attacks of 2001 have raised public awareness on the feasibility of large-scale attacks using anthrax in aerosols (Kalamas, 2004). However, it must be pointed out that even before 2001, Kortepeter and Parker (1999) has already identified anthrax as a threat and as a potential biological weapon that can be used by terrorists. Associated Signs and Symptoms/Clinical Evaluation Anthrax “causes black, coal-like lesions” and once germination takes place, the replicating bacteria releases large amounts of toxin (Kalamanas, 2004). This can lead to “edema, hemorrhage, necrosis, and septic shock” (Kalamas, 2004, p. 535). The initial symptoms can “begin with the insidious onset of flu-like symptoms with fevers, chills, sweats, malaise, fatigue, myalgias, headache, and nonproductive cough” (Kalamas, 2004, p. 535). Patients can have significant gastrointestinal complaints like nausea and vomiting (Kalamas, 2004). In the case of gastrointestinal anthrax, the symptoms can progress rapidly to “bloody diarrhea, coffee ground emesis, an acute abdomen, and sepsis” (Kalamas, 2004, p. 537). The second stage of anthrax infection can be characterized by “chest discomfort, dyspnea, and stridor resulting from a hemorrhagic, necrotizing mediastinitis” (Kalamas, 2004, p. 535). Subarachnoid hemorrhage can happen in 50% of patients (Kalamas, 2004). Rapid diagnostic tests for anthrax can only be executed at national research laboratories (Kalamas, 2004). According to Kalamas (2004), the rapid diagnostic tests can use such as ELISA for circulating toxins and capsular antigen or PCR. However, rapid diagnosis is used primarily for confirmation of the diagnosis and determining susceptibility to antibiotics (Kalamas, 2004). Nevertheless, preliminary diagnosis can be done in hospital laboratories where a standard blood culture is used that can show evidence of growth within 6 to 24 hours (Kalamas, 2004). Sputum culture and grain stain cannot be employed because of a lack of pneumonic process (Kalamas, 2004). Meanwhile, David et al. (2010) reported that diagnosis of cutaneous anthrax can be made by polymerase chain reaction test of serious fluid. Vaccines Anthrax vaccines available in the US is a cell-free infiltrate of B anthracis given at 0, 2, and 4 weeks, and again at 6, 12, and 18 months boosted annually to maintain immunity (Kalamas, 2004). The research of Praunitz et al. (2009) indicated the possibility of anthrax micro-needle vaccines. However, Praunitz et al. (2009) used micro-needle vaccines for rabbits and not humans in which the vaccine provided complete protection from anthrax on rabbits. Vaccines that can provide long term immunity are not yet available for the public but especially in the light of the research of Wattiau (2009) on unvaccinated workers who have developed immunity to anthrax, long-term vaccines can be available to the public in the future. The research of Loving et al. (2009) also shows that there can be adaptive immunity anthrax after aerosol exposure. Decontamination and Infection Control Measures After 2001, the Advisory Committee on Immunization Practices (ACIP) recommended that the use of anthrax vaccine should be reserved for those who have risk of exposure especially those with risks of repeated exposure (Kalamas, 2004). However, the ACIP did not recommend pre-exposure vaccination to those who are not at risk for repeated exposures to aerosolized B anthracis spores through their occupation (Kalamas, 2004). Vaccination and pre-emptive handling of anthrax cases are now highly feasible especially with the methodology developed by Legrand et al. (2008) for estimating the location and spatial extent of covert anthrax release. Indications for Laboratory and Radiographic Testing In anthrax infection, sore throat and rhinnorhea are typically absent and signs of illness and laboratory findings are often nonspecific (Kalamas, 2004). Further, “a chest radiograph may appear only mildly abnormal during the early stages of infection” (Kalamas, 2004, p. 535). A “chest CT scan may be diagnostically important, because it will often reveal characteristic abnormalities such as pleural effusions, perihilar infiltrates, and mediastinal edema” (Kalamas, 2004, p. 536). Differential Diagnosis Although the lung is the initiate site of contact, inhalational anthrax is not considered pneumonia (Kalamas, 2004). The World Health Organization (2008) elaborated a list of differential diagnosis for a wide range of infectious diseases but the diseases lack the characteristic oedema of anthrax. Other details on differential diagnosis are on pages 3-4 of the World Health Organization (2008) material. Management and Treatment Anthrax patients would require “some degree of critical care in the form of ventilator or hemodynamic support” (Kalamanas, 2004, p. 534). Without antibiotics, the mortality rate from anthrax can be at least 20% (Kalamanas, 2004). The onset of symptoms from anthrax can be from two to forty-three days from exposure, “suggesting that the use of antibiotics among high-risk exposed persons may be effective in preventing later infections due to delayed germination” especially as “early diagnosis of inhalation anthrax is difficult and requires a high index of suspicion” (Kalamas, 2004, p. 535). According to Kalamas (2004, p. 536), although not well-documented in humans, “physiologic sequelae of severe anthrax infection in animal models reveal hypocalcemia, hypoglycemia, hyperkalemia, depression of the respiratory center, and terminal acidosis and suggest that in addition to antibiotics, correction of electrolyte disturbances and acid-base imbalance, glucose infusion, and early mechanical ventilation may improve survival.” Treatment cannot be delayed because a delay of antibiotic administration can substantially decrease the chances for survival (Kalamas, 2004). Thus, patients suspected for anthrax must be treated for anthrax until the disease can be excluded (Kalamas, 2004). Penicillin can be used but the Centers for Disease Control and Prevention (CDC) recommends ciprofloxacin 400 mg intravenously every 12 hours or doxycycline 100 mg intravenously every 12 hours for inhalational anthrax (Kalamas, 2004). The duration of the therapy can be from 60 to 100 days supplemented with anthrax vaccines in three doses at 2-week intervals (Kalamas, 2004). The World Health Organization (2008, p. 5) confirmed that “anthrax is responsive to antibiotic therapy provided this is administered early in the course of treatment.” Further, the World Health Organization (2008, p.5) has pointed out that “ciprofloxacin and doxycycline are generally not suitable for children.” The World Health Organization (2008, p. 5) also pointed out that, “in severe life-threatening cases, intravenous penicillin or another primary antibiotic” can be combined for treatment. Recent Studies on Anthrax Cao et al. (2009) has found that F427D and F427N mutants can inhibit the anthrax lethal toxin and has expressed the possibility of developing vaccines for anthrax based on the results of their study. Abrami et al. (2010) provides details on the sequence of events leading to the endocytosis of the anthrax toxin, highlighting the role of clathrin, actin and unconventional adaptors. The finding of Abrami et al. (2002) can be used to help improve the treatment regimen for anthrax. This is because “bacterial toxins endowed with enzymatic activity generally have targets, or require co-factors, that reside in the cytoplasm of the target cell” (Abrami et al., 2010, p. 1). The study of Chen et al. (2010) on the rapid identification of genetic modification in the anthrax bacteria will also be useful in the development of a vaccine for anthrax. At the same time, the medications should be administered with another one or two antibiotics (Kalamas, 2004). However, cephalosorins and trimethoprim-sulfamethoxazole should not be used for therapy (Kalamas, 2004). The research of Joyner et al. (2010) indicated that climate change changes will affect how anthrax can spread in the future. Concluding Statement In conclusion, while the use of anthrax for bioterrorism is a real threat, nations are not defenseless against the threats. Vaccines can be developed and treatments are available. References Abrami, L., Bischofberger, M., Kunz, M., Groux, R., & van der Goot, F. (2010). Endocytosis of the anthrax toxin is mediated by Clathrin, Actin and unconventional adaptors. Plos Pathogens, 6 (3), 1-4. Cao, S., Guo, A., Liu, Z., Tan, Y., Wu, G., Chengcai, Z., Zhao, Y., & Chen, H. (2009). Investigation of new dominant-negative inhibitors of anthrax protective antigen mutants for use in therapy and vaccination. Infection and Immunity, 77 (10), 4679-4687. Chen, P., Willner, K., Butani, A., Dorsey, S., Matroner, G., Stewart, A., Lentz, S., Cook, C., Akmal, A., Price, L., Keim, P., Mateczun, Brahmbhatt, T., Bishop-Lilly, K., Zwick, M., Read, T., & Sozhamnnan, S. Rapid identification of genetic modification in Bacillus anthracis using whole genome daft sequences generated by 454 pyrosequencing. Plos One, 5 (8), 1-9. David, S., Peter, J., Raju, R., Padmaja, P., & Mohanraj, P. (2010). Oculocutaneous anthrax: detection and treatment. Clinical Opthalmology, 4, 713-716. Dyer, M., Neff, C., Dufford, M., Rivera, C., Shattuck, D., Josep, B., Murali, T., & Sobral, B. (2010). The human-bacterial pathogen protein interaction networks of Bacillus anthracis, Francisella tularensis, and Yersinia pestis. Epp, T., Argue, C., Waldner, C., & Berke, O. (2010). Spatial analysis of an anthrax outbreak in Saskatchewan, 2006. CVJ, 51, 743-748. Fasanella, A., Scasciamacchia, S., Garofolo, G., Giangaspero, A., Tarsitano, E., & Adone, R. (2010). Plos One, 5 (8), 1-5. Kalamas, A. (2004). Anthrax. Anesthesiology clinics of North America, 22, 533-540. Kortepeter, M. & Parker, G. (1999). Potential biological weapons threats. Emerging Infectious Diseases, 5 (4), 523-527. Joyner, A., Lukhnova, L., Pazilov, Y., Temiralyea, G., Hugh-Jones, M., Aikimbayev, A., & Blackburn, J. (2010). Modeling the potential distribution of bacillus anthrax under multiple climate change scenarios for Kazakhstan. Legrand, J., Egan, J., Hall, I., Cauchemez, S., Leach, S., & Ferguson, N. (2008). Estimating the location and spatial extent of a covert anthrax release. Plos Computatoin Biology, 5 (1), 1-10. Loving, C., Osorio, M., Kim, Y., Nunez, G., Hughes, M., & Merkel, T. (2009). Infection and immunity, 4529-4537. Praunitz, M., Mikszta, J., Cormier, M., & Andrianov, A. (2009). Microneedle-based vaccines. Curr Top Microbiol Immunol, 369-393. Wattiau, P., Govaerts, M., Frangoulidies, D., Fretin, D., Kissling, E., Hessche, M., China, B., Pincin, M., Pirenne, Y., & Hanquet, G. Immunologic response of unvaccinated workers exposed to anthrax, Belgium. Emerging Infectious Diseases, 15 (10), 1637-1640. World Health Organization (2008). Anthrax in humans and animals. 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