In: Biology
Could you please answer each point in details.
a. Discuss the mechanisms that Pseudomonas aeruginosa, Staphylococcus aureus, Propionibacterium acnes, and Streptococcus pyogenes utilized to cause disease on skin and in the eyes.
b.State what disease these microorganisms cause..
c.list and explain the host immune defenses that the microbe would have to overcome to be successful at causing disease (Include a discussion of what role personal hygiene plays in microbial skin and eye infections)..
d. List and explain what the microbes could contain that would allow them to overcome these host immune responses.
e.Explain how these infections could lead to more serious conditions such as endocarditis (discuss the relationship between local and systemic infections and septicemia). Include a discussion about what roles quorum sensing and sequential timing play in microbial skin and eye diseases.
Answer:
Pseudomonas aeruginosa is a common gram negative bacterium and can cause serious illnesses – especially nosocomial infections like pneumonia and septicemia. It uses a wide range of organic material for food; in animals, its versatility enables the organism to infect damaged tissues or those with reduced immunity. The symptoms of such infections are generalized inflammation and sepsis which can be fatal. Since these bacteria like moist environments, such as hot tubs and swimming pools, they can cause skin rash or swimmer's ear (dermatitis). Pseudomonas is also a common cause of postoperative infection in radial keratotomy surgery patients, skin lesion ecthyma gangrenosum, puncture wounds of the foot (osteomyelitis).
Staphylococcus aureus can cause skin boils, food poisoning, cellulitis and toxic shock syndrome. The infection is due to direct infection or due to the production of toxins by the bacteria.
Propionibacterium species are nonpathogenic, gram-positive anaerobic bacilli. They are common contaminants of blood and body fluid cultures. They cause most common skin disease – acne.
Streptococcus pyogenes are most common bacteria and cause sore throat.
Microorganisms produce various toxins that help them to parasitize the host. Virulence factor in P. aeruginosa is pyocyanin required for initial colonization and exotoxin A to inactivate eukaryotic elongation factor 2. Because of this inactivation protein synthesis is stopped and cell undergo necrosis and die. The pathogen also uses exoenzyme, ExoU, that helps in degrading plasma membrane of eukaryotic cells, leading to lysis. Virulence factors in S. aureus and other bacteria are various enzymes such as coagulate that coats the bacterial cell to prevent phagocytosis. Virulence factors that help in spreading of infection include exotoxins, hyaluronidase, deoxyribonuclease, lipase, staphylokinase/streptokinase, M proteins and beta-lactamase. These toxins cause fever and rashes on skin and supresses sntibody synthesis in the body.
Host have also evolved to fight or overcome these virulent factors by using their defense responses. When the bacterial growth/infection is restricted to only one site or a particular tissue where the pathogen has attacked initially, then it is called as localized infection. When the infection or bacterial cells are spread to other tissues (other than initial attack site) then it is called systemic infection. During a localized bacterial infection the barriers that bacteria faces is mucus that contains antimicrobial peptides on epithelial cell layers, tissue-resident immune cells such as macrophages, and the neutrophils are later recruited to the site of bacterial infection. In most cases, this leads to a rapid resolution of the infection, thereby preventing the spread of bacteria. As a consequence, bone marrow granulopoiesis is unaffected and does not differ from steady-state conditions. Sometimes bacteria is powerful enough to overcome these host defence mechanisms and is successful in spreading to other tissues. In such cases, i.e. during systemic infection more neutrophils are recruited and to counterbalance neutrophil depletion and to provide a supply of urgently needed neutrophils to combat systemic bacterial spread, a haematopoietic response programme termed 'emergency granulopoiesis' is initiated, which is characterized by the large-scale de novo generation of neutrophils from myeloid progenitors in the bone marrow. The expansion of bone marrow granulopoiesis is paralleled by a decrease in bone marrow lymphopoiesis. This overwhelming immune response to infection is called as septicemia. Inflammation may result in organ damage and it can be life threatening disorder.
Quorum sensing refers to cell to cell communication which helps in regulating gene expression by the production of small molecules called autoinducers. These molecules act as signaling molecules and their accumulation leads to altered gene expression and coordinate behavior. Quorum sensing is known to control the gene expression of many bacterial virulence factors like pyocyanin, thus playing role in pathogenesis.
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