Todar's Online Textbook of Bacteriology Bacillus cereus chapter presents information on Bacillus anthracis, the bacterium that causes anthrax.
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Currently, the recommended duration of PEP is 60 days, using one of the following antimicrobial agents: For these reasons, beta lactams are not recommended as first line agents for the prophylaxis or treatment of B. Components of both the innate and adaptive arms of the immune system participate in protection against infection with B. The most important of these mechanisms appears to be production of anthrax toxin, leading to effective paralysis of both innate and adaptive immune responses.
In fact, administration or inherent production of antibodies directed against protective antigen PA , a component of anthrax toxin, both provide a significant measure of protection against anthrax. People with increased exposure to B. Little is known about human-specific factors that may predispose a person to infection with B.
The histopathology of inhalational anthrax has been extensively described from humans infected during an accidental release of B. These patients had hemorrhagic lymphadenitis and hemorrhagic mediastinitis, and cases in which dissemination occurred often had hemorrhagic meningitis and hemorrhagic lesions in the submucosa of the gastrointestinal tract. More recent cases of inhalational anthrax from the outbreak in the United States confirmed observations from Sverdlovsk of extravascular fluid accumulation, especially in the form of pleural effusions.
Cutaneous anthrax demonstrates ulceration, edema, coagulative necrosis, vasculitis, perivascular inflammation, and tissue hemorrhage. Gastrointestinal GI anthrax pathology has not been systematically described in the published literature, but surgical findings from patients with GI anthrax often show ulceration of mucosal layers along the GI tract, mesenteric lymphadenitis, bowel edema, and hemorrhage.
The pathogenesis of inhalational anthrax is the most thoroughly studied aspect of this disease. Inhalational anthrax begins with the phagocytosis of spores by alveolar macrophages and dendritic cells in the lung. These spores are transported by these cells to regional mediastinal lymph nodes and undergo germination into the bacillary form. Shortly after germination, bacilli encapsulate and begin producing anthrax toxin. Early toxin production is critical for promoting survival of bacilli within professional phagocytes. Bacilli also express several virulence factors that promote escape from phagosomes and, ultimately, the phagocyte.
These factors include a cholesterol-dependent cytolysin, anthrolysin O, and several phospholipases. Once the bacilli have escaped from phagocytes, they begin replicating and gain entry into the systemic circulation, where they disseminate to other organ systems. The toxin components [protective antigen PA , edema factor EF , and lethal factor LF ] work together in many different target cell types to disable the host immune response, damage host tissues, and promote survival and dissemination of B.
Some examples of mechanisms utilized by B. Both ET and LT inhibit neutrophil actin-based motility, leading to impaired chemotaxis and phagocytosis of bacilli. Both ET and LT cause cardiovascular dysfunction, hypotension, and shock, with associated mortality, in animal models. The main forms of anthrax are cutaneous, gastrointestinal GI , inhalational IA , injection-related, and meningeal sometimes referred to as "primary" when it occurs in isolation. Cutaneous anthrax is the most common form and is associated with the lowest mortality, whereas anthrax meningitis, either isolated or occurring with another form of the disease, is almost always fatal.
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Cutaneous anthrax typically manifests on exposed skin surfaces i. The lesion may begin as a papule, but evolves with central ulceration, eschar formation, and peri-lesional edema. There may be vesicles that precede the ulcer or are present as satellite lesions. The eschar is usually very dark and "coal-like," and this appearance is responsible for the species name "anthracis," derived from the Greek word for coal Figure 1. Systemic signs and symptoms, such as fever, leukocytosis, and hypotension, may be present, especially in severe forms of this disease.
Malignant edema is one severe form of facial cutaneous anthrax that may present with airway compromise. Untreated cutaneous anthrax may lead to dissemination, septic shock, and death, but appropriate antimicrobial therapy leads to clinical cure in the vast majority of cases. GI anthrax is usually acquired by eating the meat from an animal that died from anthrax. There are two main forms of GI anthrax: Oropharyngeal anthrax may present as a severe ulcerative pharyngitis, with airway compromise as a major concern.
This disease mimics diphtheria in many respects, with pseudomembrane formation and systemic toxicity. The clinical presentation of intestinal anthrax is that of gastroenteritis, with nausea, vomiting, diarrhea, abdominal pain, fevers, chills, and malaise. There may also be evidence for GI hemorrhage, with hematemesis, melena, or hematochezia. A notable feature of GI anthrax is the development of ascites, sometimes in massive quantities.
Disease onset after ingestion of the implicated source is fairly rapid, occurring between 15 and 72 hours in one series. Inhalational anthrax IA is often described as a biphasic illness, with the initial phase presenting as an influenza-like illness ILI characterized by malaise, cough, fever, and chills, followed by rapid progression to the next phase of acute respiratory failure, hypotension, altered mentation, multisystem organ failure, and death.
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Conversely, most patients with ILI do not experience dyspnea, whereas this is a common feature of IA. Injection-related anthrax is newly described, with the most extensive clinical experience coming from injection drug use IDU among patients in Glasgow, Scotland. The main source of B. Inoculation of spores into the subcutaneous tissues or muscle during IDU resulted in the development of severe soft tissue infections i.
Clinical features include soft tissue edema, local excessive bruising or hemorrhage at the injection site, local pain at the injection site Figure 3. Most patients present with rapid onset of clinical sepsis, with hypotension, coagulopathy, and multi-organ failure. Injection-related anthrax may mimic necrotizing fasciitis NF , but surgical exploration does not reveal NF. The Scottish series revealed fat necrosis, massive tissue edema, and excessive hemorrhage in the operative bed. Delayed or secondary lesions may appear despite initial debridement and stabilization of the patient.
Clinical presentation includes acute bacterial meningitis with fever, headache, confusion, neck stiffness, seizures, and focal motor deficits. Signs of meningismus may be absent. A petechial rash may be seen and mistaken for meningococcemia. The cerebrospinal fluid analysis typically reveals a neutrophil-predominant pleocytosis, elevated protein, and hypoglycorrhachia, and the Gram stain may show large "boxcar"-shaped gram-positive rods growing in chains Figure 4.
Little is known about the long-term complications associated with anthrax. Short-term complications relate to the species. Bacillus anthracis is readily cultivated from clinical specimens. With the exception of cutaneous anthrax, blood cultures are useful for the diagnosis of anthrax because of the propensity of this organism to disseminate from primary site of infection. All form oval spores located centrally in an unswollen sporangium.
The endospore is a dehydrated cell with thick walls and additional layers that form inside the cell membrane.
Anthrax and Microbiology of B. anthracis
It can remain inactive for many years, but if it comes into a favorable environment, it begins to grow again. It initially develops inside the rod-shaped form. Features such as the location within the rod, the size and shape of the endospore, and whether or not it causes the wall of the rod to bulge out are characteristic of particular species of Bacillus.
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Depending upon the species, the endospores are round, oval, or occasionally cylindrical. They are highly refractile and contain dipicolinic acid. Electron micrograph sections show they have a thin outer endospore coat, a thick spore cortex , and an inner spore membrane surrounding the endospore contents. Such weaponization has been accomplished in the past by at least five state bioweapons programs—those of the United Kingdom , Japan , the United States , Russia , and Iraq —and has been attempted by several others. French physician Casimir Davaine demonstrated the symptoms of anthrax were invariably accompanied by the microbe B.
Throughout the 19th century, Anthrax was an infection that involved several very important medical developments. The first vaccine containing live organisms was Louis Pasteur's veterinary anthrax vaccine. Both the pXO1 and pXO2 plasmids are required for full virulence and represent two distinct plasmid families. The pXO1 plasmid kb contains the genes that encode for the anthrax toxin components: These factors are contained within a The PAI also contains genes which encode a transcriptional activator AtxA and the repressor PagR, both of which regulate the expression of the anthrax toxin genes.
This capsule allows B. Expression of the capsule operon is activated by the transcriptional regulators AcpA and AcpB, located in the pXO2 pathogenicity island 35 kb. Whole genome sequencing has made reconstruction of the B. A contributing factor to the reconstruction is B. The lack of diversity is due to a short evolutionary history that has precluded mutational saturation in single nucleotide polymorphisms. A short evolutionary time does not necessarily mean a short chronological time.
When DNA is replicated, mistakes occur which become genetic mutations. The buildup of these mutations over time leads to the evolution of a species. These prolonged periods of dormancy have greatly reduced the evolutionary rate of the organism. The first three strains are pathogenic or opportunistic to insects or mammals, while the last three are not considered pathogenic. The strains of this group are genetically and phenotypically heterogeneous overall, but some of the strains are more closely related and phylogenetically intermixed at the chromosome level.
PlcR is a global transcriptional regulator which controls most of the secreted virulence factors in B. It is chromosomally encoded and is ubiquitous throughout the cell. The plcR gene is part of a two-gene operon with papR. The organism also produces three plasmid-coded exotoxins: The symptoms in anthrax depend on the type of infection and can take anywhere from 1 day to more than 2 months to appear.
All types of anthrax have the potential, if untreated, to spread throughout the body and cause severe illness and even death. Chest imaging reveals widening of the mediastinum, enlargement of and bleeding into lymph nodes, and bloody fluid collections around the lungs.
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Range of 1 to 12 days following exposure; incubation period is typically closer to 1 day. The first symptom is a small sore at the point of infection that develops into a blister and later into a painless ulcer covered by a black scab. Often there is marked swelling around the ulcer. Symptoms are fever, ulcers in the back of the mouth and throat, severe sore throat, difficulty swallowing, and lymph node and neck swelling. Initial symptoms are nausea and vomiting.
The disease may progress rapidly to bloody diarrhea, abdominal pain, and shock. Inflammation or abscess at the injection site sometimes progressing to cellulitis or necrotizing fasciitis. Some patients progress to sepsis without extensive local infection. X-ray of a patient with inhalational anthrax showing bilateral effusion and widening of the mediastinum. A patient with a cutaneous anthrax lesion on the arm. Post-exposure prophylaxis should begin immediately in persons suspected of exposure to B. If susceptibility of the B.
Raxibacumab can also be used for prophylaxis in special circumstances. Once started, antibiotic therapy should be continued for 60 days post-exposure.
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A 3-dose post-exposure anthrax vaccine regimen at 0 weeks, 2 weeks, and 4 weeks is recommended by the CDC, in conjunction with antibiotics. The greatest risk of anthrax infection occurs during the period when spores are first aerosolized primary aerosolization. After this primary period, B. However, the extent to which re-aerosolized spores are infectious is not known.
Re-aerosolization depends on a number of variables:. Surfaces should be decontaminated to help eliminate the risk of secondary aerosolization, and this should be done in coordination with local health, public health, and environmental authorities. AVA is a cell-free filtrate made from cultures of a strain of anthrax not capable of causing disease.
Bacillus anthracis (Anthrax)
A 5-dose series is required for immunization, with annual boosters. Anthrax Immune Globulin AIG antitoxin is a therapy derived from the plasma of individuals previously immunized with the anthrax vaccine. This investigational product consists of antibody directed against the anthrax protective antigen. Patients already presenting with symptoms of anthrax infection may be treated with AIG in addition to antibiotic therapy.
Raxibacumab ABthrax , a human monoclonal protective antigen-targeted antibody developed by Human Genome Sciences HGS , targets anthrax toxins after they have been released by anthrax bacteria, when antibiotics might not be effective. Enter Search Phrase Search. Publications Find an article or report by keywords: Find an article or report or see all by area, author, or year:.