Staphylococcus Aureus
Topic: Staphylococcus Aureus
Name
Instructor
Course
Institution
Date
Abstract
Microorganisms or microbes are regarded as microscopic, living, and single celled or multicellular organisms that form an important component of medical microbiology. Although some microorganisms are beneficial, majority of them are harmful and causes infectious diseases to both humans and animals. In many cases, majority of microorganisms are ubiquitous in nature, and consists of prokaryotes that includes bacteria and archaea and various forms of eukaryotes that consists of fungi, protozoa, and viruses. Of all the microorganisms important to medical microbiology, Staphylococcus aureus is recognized as one of the most common bacterium species of the Firmicutes family that colonizes the human respiratory tract and the skin. Although this microorganism is not always pathogenic, it causes a variety of mild to severe diseases that may lead to coma and even death. Some of these infections include skin and wound infection, impetigo, furuncles, cellulitis, endocarditis, Meningitis, osteomyelitis, septic phlebitis, Pneumonia, food poisoning, and bacteraemia (blood stream infection).
Key words: Microorganisms, Bacteria, Staphylococcus aureus
Total words 161
STAPHYLOCOCCUS AUREUS
Introduction
Staphylococcus aureus is recognized as one of the most widespread bacterium species of the Firmicutes family that colonizes the human respiratory tract or system, alimentary canal, and the skin (dermis) (Lee and Bishop, 2010). Although this microorganism is not always pathogenic, it causes mild to severe infections that can even lead to coma and death. These include skin and wound infections such as impetigo, furuncles, and cellulitis, endocarditis (infections of the heart valve), Meningitis (infection of the brain membranes), Pneumonia, food poisoning, and bacteraemia (bloodstream infection) (Boost et al., 2008). This occurs specifically because of the S. aureus inoculation into the body either through a broken skin or through invasive surgical procedures. Unlike other bacterial species, S. aureus has a very unusual repertoire of virulence factors that makes it to endure the effects of the host immune system, and as well as maintain a fine regulation of the virulence expression (Bogaert et al., 2004).
Majority of Staphylococcus aureus strains are sensitive to a wide range of antibiotics, and all its infections and related signs and symptoms are successfully treated and managed (Huether and McCance, 2004). Nevertheless, some strains of Staphylococcus aureus (for example meticillin-resistant Staphylococcus aureus) that result from the use and misuse of antibiotics compounds are resistant to antibiotics and tend to require different and much stronger types of antibiotics to treat them (Cosgrove et al., 2009).
Staphylococcus aureus
Staphylococcus aureus was first discovered as the cause of infection in the year 1880 in Aberdeen, United Kingdom, by a medical surgeon and researcher by the name Sir Alexander Ogston from pus obtained from a surgical abscess in a knee joint (Madigan et al., 2009). Anton Rosenbach later in 1884 isolated two strains of Staphylococcus forming S. aureus (that formed golden colonies on bacterial media) and S. albus (that formed white colonies on bacterial media) (Lee and Bishop, 2010). In early 1930s, a “coagulase test” that enabled scientists to identify the plasma-coagulating enzyme secreted by S. aureus was established making it easier to diagnose and treat infections caused by the microbe (Menichetti, 2005). In 1941, penicillin was discovered as the first line treatment for S. aureus infections, while in 1959 methicillin was introduced after penicillin proved to be ineffective in the treatment and management staph infections. Later in 1961, Methicillin-Resistant S. Aureus (MRSA) was detected in a British hospital, from where it migrated to other geographical areas in United States, Europe, Asia, and Australia (Zhu et al., 2008). Since then, various scientific advancement and discoveries have been done to strengthen the S. aureus infections treatment and prevention, and to minimize the risks of antibiotics resistance. Currently, it is now easier to treat and manage this microbe’s infections than it was some few decades ago (Clauditz et al., 2006).
Staphylococcus aureus is a member of the family Staphylococcaceae, and it derives its name from a Greek word “staphyle” that means a bunch of grapes, and “cocci” that means cluster, thus the name a cluster of grapes (Lee and Bishop, 2010). Staphylococcus aureus is a facultative anaerobic Gram-positive bacterium, and when viewed under the microscope it appears like grape-like (staphylo) clusters with golden-yellow colonies, thus the name Staphylococcus (Cosgrove et al., 2009). This microbe is also catalase positive, meaning that it produces the enzyme catalase that reduces or catalyzes hydrogen peroxide into oxygen and water. This microbial mechanism together with the coagulase test is used in diagnostic tests to distinguish staphylococci species from other bacteria strains such as streptococci and enterococci (Bogaert et al., 2004).
Figure 1: Gram stain of S. aureus cells
In terms of clinical manifestation, Staphylococcus aureus is considered as a classic opportunist microbe responsible for a variety of mild to life threatening infections but it also occur as a commensal (Staley et al., 2007). Approximately 3 out of 10 healthy and immunocompentent individuals carry this microbe in their skins, intestinal tract, and respiratory systems (nose and pharynx), and its existence in the body is not indicative of an infection. Apart from the skins and the respiratory system, this microbe also colonizes the areas around the groin, armpits (axilla), groin, and under skin folds most specifically among overweight and obese people (Quinn and Cole, 2007). Although in most occasions colonization predisposes an individual to more infections, in case of any S. aureus infection an individual with more colonies tends to exhibit less severe infections compared to individuals who are less colonized or noncolonized (Chambers, 2001).
S. aureus occur in the environment and they are transmitted through air droplets, physical contact with contaminated body fluids from infected body surfaces and wounds, skin-to-skin contact with an infected individual via production of hyaluronidase that digest tissues (Menichetti, 2005) , and contact with infected individual personal items such as towels, beddings, and clothing. Infections also results from poor personal hygiene and failure to cover open wounds. Of the variety of clinical manifestations (Rooijakkers et al., 2005), S. aureus causes a variety of diseases and infections that range from skin infections such as pimples, impetigo, boils (furuncles), cellulitis folliculitis, carbuncles, and abscesses, respiratory diseases such as pneumonia (lung infections) , meningitis (inflammation of membrane lining the brain), and osteomyelitis (bone and bone marrow infections) (Arias and Murray, 2009). Other infections caused by S. aureus include septic phlebitis (infection of the blood vessels), endocarditis (infection of the heart valves), and blood infection disorders such as toxic shock syndrome, septicemia, and bacteremia, and food poisoning. Individuals affected with S. aureus infections and diseases exhibit a number of signs and symptoms that are dependent on the type of infection it present (Matthews et al., 1997). Common signs and symptoms for skin infections include localized collection pus; the affected region may be swollen, red, and painful, chills, low blood pressure, and high fever for bacteremia or sepsis, and severe pain for meningitis, osteomyelitis, and septic phlebitis. Other common signs and symptoms include nausea, vomiting, diarrhea, and stomach pains for food poisoning and irritability malaise, fever or chills, and breathing difficulties for pneumonia (Bryant et al., 2003).
Several pathophysiological processes are involved in the development of S. aureus diseases and infections. These range from production and release of potent protein toxins and expression of cell surface proteins that bind and inactivate diseases fighting antibodies (Huether and McCance, 2004). The microbe expresses its virulence once it gains entry into the body via a broken skin or through invasive surgical procedures. Once inside the body, Staphylococcus aureus produces a number of enzymes, surface proteins, clumping factors, and various types of complement inhibitors that inactivate the host immune system from attacking the bacterium (Rooijakkers et al., 2005). These enzymes include coagulase that clots plasma and as well as coat the bacterial cell wall to protect it from destruction by the host immune system and Hyaluronidase that breaks down hyaluronic acid thus allowing the microbe to spread and invade other neighboring body tissues and cells (Miller and Diep, 2008). Other core enzymes produced that aid the activity and spread of the microbe include deoxyribonuclease that breaks down the host nucleic acids (DNA) (Lee and Bishop, 2010), lipase that digest lipids into free fatty acids increasing their surface area, and staphylokinase that digests connective tissues such as fibrin. S. aureus also instill its virulence by secreting exotoxins such as superantigens, exfoliative toxins, and cell membrane toxins such as alpha, beta, and delta toxins that lyse and destroy neutrophils (Arias and Murray, 2009). It also instill its virulence by evading the host immune system via production of Protein A that binds or anchors the microbe to the “peptidoglycan pentaglycine bridges through the transpeptidase sortase A” (Cimolai, 2008), which bind and inactivate diseases fighting antibodies. This protein also protects the bacterial species from being recognized by the host macrophages. It also evade the host immune system by producing staphylococcal pigments such as staphyloxanthin that act as a virulence factor (Clauditz et al., 2006), most specifically by functioning as an antioxidant that assists the bacterial species in evading the “superoxides or oxygen radicals” the host cells uses to destroy any invading pathogens (Agata et al., 2008).
Figure 2: Pathophysiological mechanisms of S. aureus infections
All S. aureus diseases and infections are characterized with inflammation of mucous membrane, pain, fever or chills, and malaise, and they are diagnosed by evaluating the catalase and coagulase enzyme function (catalase test is normally positive for all Staphylococcus species while coagulase test is specific S. aureus) (Rooijakkers et al., 2005). According to Francoisand Schrenzel (54), the medical microbiology laboratory plays a very significant role in the diagnosis, treatment and monitoring of diseases caused by this microbe (Ryan and Ray, 2004). The lab provides references for identifying various strains of S. aureus, and provides rapid test incorporating genetic materials that allows real time isolation and characterization of clinical samples (Iwase et al., 2010). In regard to treatment and management, penicillin is the first line choice for S. aureus infections treatment but in areas where penicillin resistance is common, a variety of penicillinase-resistant β-lactam antibiotic such as cloxacillin and flucloxacillin are used (Cosgrove et al., 2009). In severe cases of pneumonia, meningitis and osteomyelitis and to avert possible risks of resistance, a combination therapy involving β-lactam antibiotic such as cloxacillin and flucloxacillin, Aminoglycoside antibiotics such as streptomycin and gentamicin, and Augmentin (Coamoxiclav) can be incorporated in the treatment protocols (Boost et al., 2008).
Irrespective of the antibiotics success in the treatment and management of S. aureus diseases and infections, continued use, overuse, and misuse or inappropriate use have triggered resistance that has in the recent past increased the implications for mortality and morbidity and increased cost of treatment and management (Bryant et al., 2003). To promote safety and quality of treatment, it is important to maintain sensible use of antibiotics in managing bacterial infections and for the establishment of novel antibiotics that circumvent resistance. It is also very important for the members of the public to maintain good personal hygiene and to cover any open wound with clean occlusive dressing to prevent transmission (Agata et al., 2008).
Conclusion
Staphylococcus aureus is regarded as one of the most common bacterium that colonizes the human respiratory tract or system, alimentary canal, and the skin. It is categorized as one of the five most common causes of infections following injury and surgery (Lee and Bishop, 2010). Currently, S. aureus diseases and infections affects more than 5 million people worldwide, with around 500,000 of the total patients population being in U.S. alone thus posing a very huge public health challenges in terms of its prevention and management and risks of resistance (Chambers, 2001). Nevertheless, its prevalence and incidence rate is projected to increase in the near future due to the consequences of the use, overuse, and misuse of antibiotics compounds and emergence of new strains that are resistance to the available antibiotics (Staley et al., 2007).
Total words 1965
Bibliography
Agata, E.C.,e t al 2008. The Impact of Different Antibiotic Regimens on the Emergence of Antimicrobial-Resistant Bacteria. PLoS ONE 3(12): e4036.
Arias, C.A. and Murray, B.E. 2009. Antibiotic-resistant bugs in the 21st century -a clinical super-challenge. N. Engl. J. Med. 360(5), 439-443
Bogaert, D., et al. 2004. Colonisation by Streptococcus pneumoniae and Staphylococcus aureus in healthy children. Lancet 363:1871–1872
Boost, M.V., et al. 2008. “Prevalence of Staphylococcus aureus carriage among dogs and their owners”. Epidemiol. Infect. 136 (7): 953–964.
Bryant, B., et al 2003. Pharmacology for health professionals. Sydney: Mosby Elsevier
Chambers, H.F.2001. “The changing epidemiology of Staphylococcus aureus?”. Emerg Infect Dis 7 (2): 178–82.
Cimolai, N.2008. “MRSA and the environment: implications for comprehensive control measures”. Eur. J. Clin. Microbiol. Infect. Dis. 27 (7): 481–93.
Clauditz, A., et al. 2006. “Staphyloxanthin plays a role in the fitness of Staphylococcus aureus and its ability to cope with oxidative stress.” Infection and immunity 74 (8): 4950–3.
Cosgrove, S.E., et al. 2009. “Initial low‐dose gentamicin for Staphylococcus aureus bacteremia and endocarditis is nephrotoxic.” Clin Infect Dis 48 (6): 713–721.
Francois, P. and Schrenzel, J. 2008. “Rapid Diagnosis and Typing of Staphylococcus aureus”. StaphylococcuWEINERs: Molecular Genetics. London: Caister Academic Press.
Huether, S. and McCance, L. 2004. Understanding Pathophysiology. St. Louis: Mosby
Iwase, T., et al. 2010. “Staphylococcus epidermidis Esp inhibits Staphylococcus aureus biofilm formation and nasal colonization.” Nature 465 (7296): 346–9.
Lee, G. and Bishop, P. 2010. Microbiology and Infection control for health professionals (4th Ed.). Frenchs Forest, N.S.W: Prentice Hall
Madigan. M.T., et al. 2009. Brock Biology of Microorganisms (12th edition). London: Pearson – Benjamin Cummings.
Matthews, K.R., et al.1997. “Identification and Differentiation of Coagulase-Negative Staphylococcus aureus by Polymerase Chain Reaction”. Journal of Food Protection 60 (6): 686–8.
Menichetti, F. 2005. “Current and emerging serious Gram-positive infections”. Clin Microbiol Infect 11 (Suppl 3): 22–8.
Miller, L.G. and Diep, B.A. 2008. Clinical practice: colonization, fomites, and virulence: rethinking the pathogenesis of community-associated methicillin-resistant Staphylococcus aureus infection. Clin Infect Dis 46:752–760
Rooijakkers, S.H., et al. 2005.Staphylococcal innate immune evasion. Trends Microbiol 13:596–601
Ryan, K.J. and Ray, C.2004. Sherris Medical Microbiology (4th ed.). London: McGraw Hill.
Staley J.T., et al. 2007. Microbial Life (2nd edition). New York: Sinauer.
Quinn, G., and Cole, A. 2007. “Suppression of innate immunity by a nasal carriage strain of Staphylococcus aureus increases its colonization on nasal epithelium”. Immunology 122 (1): 80–9
Zhu, J., et al. 2008. “Single mutation on the surface of Staphylococcus aureus Sortase A can disrupt its dimerization.” Biochemistry 47 (6): 1667–74.
