Staph bacteria, including S. aureus and S epidermis. The bacterial infection can happen in the mouth, nose, feet, anal regions, or genitalia.
Warmth, swelling, redness, and discomfort are some of the warning signs and symptoms. Additionally, the disease caused a fever, chills, sweats, and edema. Additionally, an abscess, furuncle, or puss may be present.
S. aureus is the main culprit behind Staphylococcus infections. On the skin and delicate tissues, the bacteria produce sores. The S. aureus has a number of ways to get around the host immune system. When leukocytes attack, the bacteria creates antiphagocytic microcapsules to protect itself. It generates molecules causes lysis of the host cell as well as lead to the formation of fibrin capsule that surrounds the abscess.
Epidemiology
Group A Streptococcus infections are present in many parts of the world and particularly in the United States. An estimate of 9,000 to11, 500 people are affected by the infections annually in the US. The disease results in approximately 1,000 to 1,800 deaths per annum. In the vagina, the case of invasive Group A Step is about 150 to 175 per annum (Tong et al., 2015).
Prevention and Treatment
Group A Streptococcus can be prevented through proper hygiene routine especially washing of hand after sneezing or coughing. Proper washing is also necessary after and before caring for patients, preparing foods as we as before eating. The wound should also be kept clean, and the patient should watch for signs of infections such as redness, pain or swelling. Treatment of Group A Streptococcus infections involves the use of antibiotics such as penicillin, vancomycin, and methicillin.
Group A Streptococcal or flesh eating disease
Causative Agent
It is a bacterial infection caused by Streptococcus pyrogens. Besides, the disease can be caused by other bacteria such as Staphylococcus aureus, Clostridium and E. coli.
Symptoms
The symptoms include nausea, vomiting and fever symptoms that also occur in flu patients, gangrene or death of the area affected with discoloration, peeling, and scaling of the skin.
Pathogenesis
After entry, the bacteria secretes pyrogenic exotoxin A, which causes a series of events resulting in the destruction of tissues. Exotoxin A increases the production of cytokines that lead to the destruction of endothelial lining. The damage of endothelial lining leads to leaking of fluid into the extravascular space which causes the blood flow to reduce, increased tissue hypoxemia and eventually tissue death. Thrombosis and vasculitis occur in the tissues adjacent to the affected areas that further enhances the formation of the necrosis that involves the subcutaneous nerves (Davies, 2001).
Epidemiology
Necrotizing enterocolitis (NEC) is a global issue that has emerges as the most common gastrointestinal emergency in the past 25 years. It has 1 to 7.7% admission of instances of neonatal intensive care units (NICU). The disease has high occurrence on premature infants with 90% of infection reported. The death case stood at 2% in the United States, and the condition worsens in patients with diabetes, HIV/ AIDS, abortion and injected drugs. The most pathogenic factor reported among children include the bacterial colonization, mucosal injury and formula feeding.
Prevention and treatment
Prevention involves proper hygiene through quick treatment of the infected wounds, keeping wounds clean and dry as well as washing hands and maintaining them clean can help prevent the occurrence of the infection. Furthermore, the disease can be treated by use of antibiotics, surgical operation and supportive treatment.
Tetanus/Lock Jaw
Causative agents
Tetanus is severe of bacterial infection Clostridium tetani. The bacteria can originate from dirt, dust, and animal dropping.
Symptoms
Symptoms include difficulty in swallowing, spasms and stiffness of muscles of the neck, jaw, abdomen, back and chest, high blood pressure, sweating, and fever.
Pathogenesis
The bacterial toxins enter the lower motor neurons and move axonally to the brainstem or spinal cord. On reaching the spinal cord, the poison is transported across-synaptic to the inhibitory nerve terminals. The toxins block the vesicular release of inhibitory neurotransmitters resulting lower motor neurons disinhibition. The toxins cause muscle rigidity or spasms usually occurring as lockjaw, the rigidity of abdominal muscles and laryngeal, dysphagia and opisthotonus (Hassel, 2013).
Epidemiology
Tetanus is present in worldwide but commonly occur in the densely populated areas in hot and damp climates with organic matter- rich soils. The Clostridium tetani are found mainly in soils and intestinal tracts of humans and humans. It is transmitted primarily through contaminated wounds which may be minor or major. The infection may occur after burns, surgery, crush wounds, dental infections as well as animal bites (Hassel, 2013).
Prevention and Treatments
The Prevention include cleaning of wounds to eliminate the bacteria, vaccination. Besides, treatment includes surgical operation, antibiotics and use of tetanus immune globulin (TIG) can also be employed to neutralize the toxins in the systems.
Clostridial myonecrosis/ Gas Gangrene
Causative Agents
Clostridial myonecrosis is a bacterial infection caused Clostridium perfringens. It can also occur due to other bacteria such Clostridium septicum and Clostridium novyi.
Symptoms
The symptoms include fever, swelling of the area adjacent to the wound, excessive sweating, increase heart rate, blister having foul smelling discharge, as well as pale skin that turns gray, purple, dark red or black.
Pathogenesis
The C. perfringens proliferate in poorly oxygenated or dead tissues. It releases the theta toxins, alpha toxins as well as Kappa toxins. The theta toxins cause injury to the vesicles, leukocyte degeneration, hemolysis, cytolysis, as well as destruction white blood cells. The Kappa toxin, stimulate the spread of necrosis via the tissue planes by damaging the connective tissue. The alpha toxin, on the other hand, phospholipase C activity that results in the lysis of platelets, myocytes, leukocytes, fibroblasts, and red blood cells (Stevens, 2000).
Epidemiology
The bacteria can be present in the mouth, intestine as well as the vagina. The disease has a higher occurrence in the United States with 100 cases reported annually. The overall mortality rate is approximately 20%-30% if property treatment is undertaken. In the event of no cure, the process causes death at the rate of 100% (Stevens, 2000). Besides, cases that are spontaneous have a mortality rate of 67-100%. The risk level of attack increase with age with the older people having higher death rate than young patients.
Prevention and treatment
Prevention of involves practicing proper hygiene through cleaning the wound and covering. Treatment, on the other hand, includes use of antibiotics, reconstructive surgery (skin graft), amputation of the affected area as well as hyperbaric oxygen therapy to treat
References
Davies, H. (2001). Flesh-eating disease: a note on necrotizing fasciitis. Canadian Journal of Infectious Diseases and Medical Microbiology, 12(3), 136-140.
Hassel, B. (2013). Tetanus: pathophysiology, treatment, and the possibility of using botulinum toxin against tetanus-induced rigidity and spasms. Toxins, 5(1), 73-83.
Stevens, D. L. (2000). The pathogenesis of clostridial myonecrosis. International Journal of medical microbiology, 290(4-5), 497-502.
Tong, S. Y., Davis, J. S., Eichenberger, E., Holland, T. L., & Fowler, V. G. (2015). Staphylococcus aureus infections: epidemiology, pathophysiology, clinical manifestations, and management. Clinical microbiology reviews, 28(3), 603-661.
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