Cause Anthrax

1 cause

1.1 bacteria
1.2 exposure
1.3 mode of infection

cause
bacteria

photomicrograph of gram stain of bacterium bacillus anthracis, cause of anthrax disease

bacillus anthracis rod-shaped, gram-positive, aerobic bacterium 1 9 μm in size. shown cause disease robert koch in 1876 when took blood sample infected cow, isolated bacteria, , put them mouse. bacterium rests in endospore form in soil, , can survive decades in state. herbivores infected whilst grazing, when eating rough, irritant, or spiky vegetation; vegetation has been hypothesized cause wounds within gastrointestinal tract permitting entry of bacterial endospores tissues, though has not been proven. once ingested or placed in open wound, bacteria begin multiplying inside animal or human , typically kill host within few days or weeks. endospores germinate @ site of entry tissues , spread circulation lymphatics, bacteria multiply.

the production of 2 powerful exotoxins , lethal toxin bacteria causes death. veterinarians can tell possible anthrax-induced death sudden occurrence, , dark, nonclotting blood oozes body orifices. anthrax bacteria inside body after death outcompeted , destroyed anaerobic bacteria within minutes hours post mortem. however, anthrax vegetative bacteria escape body via oozing blood or through opening of carcass may form hardy spores. these vegetative bacteria not contagious. 1 spore forms per 1 vegetative bacterium. triggers spore formation not yet known, though oxygen tension , lack of nutrients may play roles. once formed, these spores hard eradicate.

the infection of herbivores (and humans) inhalational route proceeds follows: once spores inhaled, transported through air passages tiny air sacs (alveoli) in lungs. spores picked scavenger cells (macrophages) in lungs , transported through small vessels (lymphatics) lymph nodes in central chest cavity (mediastinum). damage caused anthrax spores , bacilli central chest cavity can cause chest pain , difficulty in breathing. once in lymph nodes, spores germinate active bacilli multiply , burst macrophages, releasing many more bacilli bloodstream transferred entire body. once in blood stream, these bacilli release 3 proteins named lethal factor, edema factor, , protective antigen. 3 not toxic themselves, combination incredibly lethal humans. protective antigen combines these other 2 factors form lethal toxin , edema toxin, respectively. these toxins primary agents of tissue destruction, bleeding, , death of host. if antibiotics administered late, if antibiotics eradicate bacteria, hosts still die of toxemia because toxins produced bacilli remain in system @ lethal dose levels.

the lethality of anthrax disease due bacterium s 2 principal virulence factors: poly-d-glutamic acid capsule, protects bacterium phagocytosis host neutrophils, , tripartite protein toxin, called anthrax toxin. anthrax toxin mixture of 3 protein components: protective antigen (pa), edema factor (ef), , lethal factor (lf). pa plus lf produces lethal toxin, , pa plus ef produces edema toxin. these toxins cause death , tissue swelling (edema), respectively.

to enter cells, edema , lethal factors use protein produced b. anthracis called protective antigen, binds 2 surface receptors on host cell. cell protease cleaves pa 2 fragments: pa20 , pa63. pa20 dissociates extracellular medium, playing no further role in toxic cycle. pa63 oligomerizes 6 other pa63 fragments forming heptameric ring-shaped structure named prepore. once in shape, complex can competitively bind 3 efs or lfs, forming resistant complex. receptor-mediated endocytosis occurs next, providing newly formed toxic complex access interior of host cell. acidified environment within endosome triggers heptamer release lf and/or ef cytosol. unknown how complex results in death of cell.

edema factor calmodulin-dependent adenylate cyclase. adenylate cyclase catalyzes conversion of atp cyclic amp (camp) , pyrophosphate. complexation of adenylate cyclase calmodulin removes calmodulin stimulating calcium-triggered signaling, inhibiting immune response. specific, lf inactivates neutrophils (a type of phagocytic cell) process described cannot phagocytose bacteria. throughout history, lethal factor presumed cause macrophages make tnf-alpha , interleukin 1, beta (il1b). tnf-alpha cytokine primary role regulate immune cells, induce inflammation , apoptosis or programmed cell death. interleukin 1, beta cytokine regulates inflammation , apoptosis. overproduction of tnf-alpha , il1b leads septic shock , death. however, recent evidence indicates anthrax targets endothelial cells line serous cavities such pericardial cavity, pleural cavity, , peritoneal cavity, lymph vessels, , blood vessels, causing vascular leakage of fluid , cells, , hypovolemic shock , septic shock.

exposure

the spores able survive in harsh conditions decades or centuries. such spores can found on continents, including antarctica. disturbed grave sites of infected animals have been known cause infection after 70 years.

occupational exposure infected animals or products (such skin, wool, , meat) usual pathway of exposure humans. workers exposed dead animals , animal products @ highest risk, in countries anthrax more common. anthrax in livestock grazing on open range mix wild animals still occurs in united states , elsewhere. many workers deal wool , animal hides routinely exposed low levels of anthrax spores, exposure levels not sufficient develop anthrax infections. lethal infection reported result inhalation of 10,000–20,000 spores, though dose varies among host species. little documented evidence available verify exact or average number of spores needed infection.

historically, inhalational anthrax called woolsorters disease because occupational hazard people sorted wool. today, form of infection extremely rare in advanced nations, no infected animals remain. last fatal case of natural inhalational anthrax in united states occurred in california in 1976, when home weaver died after working infected wool imported pakistan. minimize chance of spreading disease, deceased transported ucla in sealed plastic body bag within sealed metal container autopsy.

in november 2008, drum maker in united kingdom worked untreated animal skins died anthrax. gastrointestinal anthrax exceedingly rare in united states, 2 cases on record, first reported in 1942, according centers disease control , prevention. in december 2009, outbreak of anthrax occurred amongst heroin addicts in glasgow , stirling areas of scotland, resulting in 14 deaths. source of anthrax believed dilution of heroin bone meal in afghanistan.

also during december 2009, new hampshire department of health , human services confirmed case of gastrointestinal anthrax in adult female. cdc investigated source , possibility contracted african drum used woman taking part in drum circle. woman apparently inhaled anthrax [in spore form] hide of drum. became critically ill, gastrointestinal anthrax rather inhaled anthrax, made unique in american medical history. building infection took place cleaned , reopened public , woman recovered. jodie dionne-odom, new hampshire state epidemiologist, stated, mystery. don t know why happened.

mode of infection

inhalational anthrax, mediastinal widening

anthrax can enter human body through intestines (ingestion), lungs (inhalation), or skin (cutaneous) , causes distinct clinical symptoms based on site of entry. in general, infected human quarantined. however, anthrax not spread infected human noninfected human. but, if disease fatal person s body, mass of anthrax bacilli becomes potential source of infection others , special precautions should used prevent further contamination. inhalational anthrax, if left untreated until obvious symptoms occur, fatal.

anthrax can contracted in laboratory accidents or handling infected animals or wool or hides. has been used in biological warfare agents , terrorists intentionally infect exemplified 2001 anthrax attacks.