in nervous system 2, Please discuss the mechanisms that Clostridium tetani and b

Question

in nervous system

2, Please discuss the mechanisms that Clostridium tetani and botulinum treptococcus pneumoniae and yrypanosoma cruzi and brucei. utilize to cause disease in the nervous system. You must state what disease these microorganisms cause. In addition, please discuss the host immune defenses that the microbes would have to overcome to be successful at causing disease. (Hint: A. Include the three routes of entry to gain access to the nervous system and the role of the blood brain barrier. B.) Explain what physical trauma has to do with microbial diseases of the nervous system. C. Include a discussion on quorum sensing, and its relationship to diseases in the nervous system.) Include a discussion what roles personal hygiene and sequential timing play in microbial nervous system diseases. Please include methods to prevent Clostridium tetani and botulinum from causing disease. Also, include a section on whether or not we can eradicate Trypanosoma spp.and why we probably cannot develop a vaccine for Trypanosoma infections.Lastly, please include a section on the relationship between toxoids and Clostridiuim tetani and botulinum.

Explanation / Answer

Tetanus, also called lockjaw, is a serious infection caused by Clostridium tetani. C. tetani usually enters a host through a wound to the skin, then it replicates. Once an infection is established, C. tetani produces two exotoxins, tetanolysin and tetanospasmin. Tetanospasmin released in the wound is absorbed into the circulation and reaches the ends of motor neurons all over the body. The toxin acts at several sites within the central nervous system, including nerve terminals, the spinal cord, and brain, and within the sympathetic nervous system. By binding to peripheral motor neuron terminals, the toxin enters the nerve axons, and is transported across synaptic junctions to the nerve-cell body in the brain stem and spinal cord by retrograde intraneuronal transport, until it reaches the central nervous system, where it rapidly binds to gangliosides at the presynaptic membrane of inhibitory motor nerve endings.

Clostridia spp. secrete potent collagenases that aid infection by disrupting tissue barriers while providing amino acids as a carbon source. toxins produced are zinc metalloproteases that cleave proteins involved in neurotransmitter release. BoNT prevents the release of neurotransmitters, resulting in flaccid paralysis, and TeNT prevents the release of inhibitory neurotransmitters, resulting in spastic paralysis.

Botulism is a serious illness that causes flaccid paralysis of muscles. It is caused by a neurotoxin, generically called botulinum toxin, produced by the Clostridium botulinum. Since botulism poisoning most commonly comes from foods improperly canned at home, the most important step in preventing botulism is to follow proper canning procedure. C. botulinum is only able to produce the neurotoxin during sporulation, which can only happen in an anaerobic environment. They are resistant to degradation by enzymes found in the gastrointestinal tract. This allows for ingested toxin to be absorbed from the intestines into the bloodstream. Host defenses are essentially absent. There is little, if any, innate immunity. No host defenses are known.

Trypanosomes infect a variety of hosts and cause various diseases, including the fatal human diseases sleeping sickness, caused by Trypanosoma brucei, and Chagas disease, caused by Trypanosoma cruzi. their modes of transmission include oral infection through contaminated food, congenital transmission, blood transfusions, organ transplants, and by accidental laboratory inoculation. The mitochondrial genome of the Trypanosoma, as well as of other kinetoplastids, known as the kinetoplast, is made up of a highly complex series of catenated circles and minicircles and requires a cohort of proteins for organisation during cell division. Both diseases are characterized by an increase in the number of macrophages and the presence of macrophage activation markers. The trypomastigotes enter the human host through the bite wound or by crossing mucous membranes. The host cells contain macromolecules such as laminin, thrombospondin, heparin sulphate, and fibronectin that cover their surface. These macromolecules are essential for adhesion between parasite and host and for the process of host invasion by the parasite. The trypomastigotes must cross a network of proteins that line the exterior of the host cells in order to make contact and invade the host cells. The molecules and proteins on the cytoskeleton of the cell also bind to the surface of the parasite and initiate host invasion. Trypanosomiasis in humans progresses with the development of the trypanosome into a trypomastigote in the blood and into an amastigote in tissues.Infective T. cruzi trypomastigotes invade host cells using at least two different strategies, either by an active process recruiting host-cell lysosomes to the area of parasite cell contact or by an alternative pathway, in which the parasite infects phagocytic cells through conventional phagocytosis/endocytosis mechanism.

Good personal hygiene is one of the most effective ways to protect ourselves and others from many illnesses.

coontrol.

Wound infections are controlled by administration of antimicrobial agents (e.g., penicillin, chloramphenicol) coupled with tissue debridement (for more severe forms of clostridial wound infections). The administration of tetanus toxoid is a preventive measure. C tetani infection is treated with antimicrobial agents (metronidazole or penicillin) and by local wound debridement. Other measures include tetanus immunoglobulin and supportive therapy.The best means of control is to eliminate the toxin source via proper food handling. Once the food poisoning is diagnosed, treatment measures should include an attempt to neutralize unbound toxin. Supportive care is of primary importance.

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