Staphylococcus aureus

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Staphylococcus aureus
File:Staphylococcus-aureus.jpg
Scientific classification
Domain: Bacteria Phylum: Firmicutes Class: Bacilli Order: Bacillales Family: Staphylococcaceae Genus: Staphylococcus
Species
Staphylococcus aureus

Description and significance

Staphylococcus aureus is a gram-positive spherical cocci that grows in a loose, irregular cluster resembling clusters of grapes. The cluster formation is due to the cell division occuring in three planes, with the daughter cell remaining in nearby. Staphylococcus aureus may also be found singly, in pairs and in short chains of three or four cells. The bacterium can never be found in long chains. They are non motile and non spore forming. On an ordinary medium, Staphylococcus aureus can grow within a temperature range of 10-42°C. The optimum pH ranges in between pH 7.4-7.6. The bacterium thrives best in an oxygen rich environment. S. aureus can grow on all common laboratory media such as milk, nutrient gelatin or agar. When grown on a nutrient agar and incubated for 24 hours the colonies appear to be 2-4mm in diameter. The colonies appear circular, smooth, convex, shiny, and opaque.

Staphylococcus aureus was first observed in 1871 by von Recklinghausen but not isolated. Then in 1881 a surgeon by the name of Alexander Ogston documented two kinds of micrococci. The already known streptococci, arranged in chains and the other cocci arranged in clusters. Ogston named the cocci cluster Staphylococci because “Staphyle” in Greek means "bunches of grapes" and “kokakos” meaning a "berry". Unfortunately, Ogston did not provide a description of the genus and therefore it was not recognized. In 1884 Rosenbach successfully isolated and grew Staphylococcus aureus from pus. Rosenbach is credited with proposing the genus Staphylococcus and the species Staphylococcus aureus. He kept the genus name Staphlococcus because the bacteria was similar to that studied by Ogston. Rosenbach proposed the nomenclature for Staphylococcus aureus based on the yellow pigmentation of the colony.

In recent years the Staphylococcus aureus species has become a serious health issue. The bacteria has built up a strong resistance to treatment. By unlocking the genome sequence, researchers could understand the nature of its resistance, virulence, genetic flexibility, epidiology and physiology. Comparing the genome sequence of S. aureus with the genomes of a less virulent form and nonpathogenic species could help researchers have a better understanding of the nature of Staphylococcal aureus infections.

Genome structure

The Staphylococcus aureus genome contains about 2.800 to 2.903 million base pairs of DNA. The bacteria has about 2,600 genes in its chromosome. The first whole genome sequence of S. aureus strains were completed by shot-gun random sequencing in 2001. S. aureus plasmids contains genes that encode resistance to antibiotics, heavy metals, or antiseptics. Some virulence genes have been reported to be carried on plasmid, such as exfoliative toxin B and some superantigens. Approximatly 75% of S. aureus genome comprises a core component of genes present in all of the strains.

Describe the size and content of the genome. How many chromosomes? Circular or linear? Other interesting features? What is known about its sequence? Does it have any plasmids? Are they important to the organism's lifestyle?

Cell structure and metabolism

Staphylococcus aureus cell wall contains a thick peptidoglycan layer and teichoic acid. The polysaccharide peptidoglycan in the cell wall gives the bacterium structure and rigidity and induces the release of cytokines. Teichoic acid is an antigenic component that aids adhesion of the cocci to the host cell surface. The bacterium contains no flagella. Some young cultures posses microscopically visible capsules. Many noncapsulated strains of S.aureus have small amounts of capsular material on the surface.

Staphylococci are facultative anaerobes that grow by aerobic respiration or by fermentation that yields lactic acid. S. aureus ferments sugars by producing acid but no gas.

Phagocytosis is a mechanism used by the host organism to combat a staphylococcal infections. S. aureus produces leukocidin, which cause the destruction of leukocytes allowing the bacteria to escape phagocytosis. Leukocidin is produced in skin lesions such as boils which results in cell destruction of white blood cells and is one of the factors responsible for pus formation.

Describe any interesting features and/or cell structures; how it gains energy; what important molecules it produces.

Ecology

Staphylococcus aureus is commonly found on the skin and in various mucous membranes of man and other animals. About 20-30% of healthy people in the United States are carriers of the bacteria. These individuals are usually unaware that they are carriers of the bacteria and usually never get sick from it. In hospitals the percentage is higher because of more possible contact with infected cases.

Describe any interactions with other organisms (included eukaryotes), contributions to the environment, effect on environment, etc.

Pathology

Staphylococcus aureus is one of the most common pathogenic bacteria. The organism may cause disease through tissue invasion and toxin production. The bacteria could cause a wide range of infections both internally and externally. It may cause skin infections, bone infections, pneumonia, food poisoning, Toxic shock syndrome, life threatening bloodstream infections and other serious illnesses.

Staphyolococcus aureus may cause boils usually by entering the skin through a hair folicle or a cut. They may be red, swollen and painful, and sometimes have pus. They can turn into impetigo, which turns into a crust on the skin and usually common among newborns. The organism could also cause internal abscesses. In recent years Staphylococcus aureus has become one of the leading causes of hospital acquired infections. People prone to staphylococcal infections include newborns, drug users, breastfeeding women, and people with skin disorders, surgical incisions, a weakened immune system, or chronic diseases.

Extracellular and cell associated factors may influence virulence. Cell surface proteins, extracellular enzymes and toxins are present on most strains of S. aureus and increases the species ability to act as a successful pathogen.

Protein A and clumping factors are both cell surface proteins. Protien A induces platelet damage and hypersensitivity. The cocci clumps when introduced to human plasma because of this researchers use a coagulase test to help identify the bacterium. Some strains may not always test positive because they may be capsulated.

Coagulase, nucleases, lipases, hyaluronidase and protein receptors are all extracellular enzymes that play an important role in pathogenesis. The bacteria can convert fibrinogen to fibrin, has a heat stable nuclease, produces lipid hydralases which aids in infecting the skin, breaks down connective tissue, and possess receptors that facillitate adhesion to the host cell and tissue.

Toxins such as alpha hemolysin, enterotoxin, toxic shock syndrome toxin(TSST), and exfoliative (epidermolytic)toxin produced by S. aureus may cause the bacerium to be more virulent. Alpha hemolysin is a protein that is inactivated at 70^oC but activated at 100^oC. It is toxic to macrophages, lysosomes, muscle tissues, renal cortex, and the circulatory system. Enterotoxin is also a superantigen responsible for causing food poisoning which may lead to nausea, vomiting, and diarrhea. Toxic shock syndrome toxin is a superantigen as well and causes toxic shock syndrome in the infected host. It may prove to be a potentially fatal multisystem disease. The infected host can experiance a fever, hypotension, myalgia, vomiting, diarrhea and mucosal hyperemia. The exfoliative (epidermolytic)toxin is responsible for staphycoccal scalded skin syndrome(SSSS). It is an exfoliative skin disease which causes the outer layer of the epidermis to be separated from the underlying tissues. Symptoms associated with the disease are a fever, malaise and irritability following an upper respiratory infection.

Staphylococcus aureus has a high incidence of drug resistance with methicillin-resistant strains resistant to ß-lactams and most other antibiotics. Infections are enhanced in the presence of foreign materials inside the body such as tampons, surgical packing or intravenous catheters.

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

Application to Biotechnology

In an anaerobic environment Staphylococcus aureus can reduce mannitol to lactic acid, which differentiates it from other species of staphylococci. The bacterium is the only coagulase positive and ß-hemolytic staphylococcus. When grown on a nutrient agar containing phenolphtalein diphosphate the bacterium produces phosphatase. When ammonia vapor is introduced to the culture, the colonies assume a bright pink color due to the presence of free phenophalein. Researchers use this test to distinguish between Staphylococcus aureus from S. epidermidis.

Does this organism produce any useful compounds or enzymes? What are they and how are they used?

Current Research

Enter summaries of the most recent research here--at least three required

Methicillin-resistant staphylococcus aureus

Methicillin-resistant staphylococcus aureus (MRSA) is a strain of Staphylococcus aureus that is resistant to commonly used antibiotics such as methicillin. MRSA emerged in the early 1960's. MRSA is predominantly a nosocomial pathogen causing hospital aquired infections as well as community aquired infections. Currently available statistics from the Kaiser foundation in 2007 indicate that about 1.2 million hospitalized patients have MRSA, and the mortality rate is estimated to be between 4%-10%.

Screening for MRSA

In order to prevent the spread of the bacterium in hospitals, patients who are infected need to be identified as soon as possible. Many antibiotics are ineffective for treating sever infections and early identification of patients is an essential precautions to take to prevent the spread. As of 2008 Illinois, New Jersey, and Pennsylvania have passed laws requiring hospitals to screen certain patients upon admission for MRSA. All three states require hospitals to screen patients admitted to intensive care units and high risk patients in other parts of the hospital to identify those colonized with MRSA.

Eradication of MRSA

It is possible to reduce the risk of MRSA infections and transmission. Washing hands regularly, use an alcohol based hand rub, have good housekeeping skills by using disinfectants such as quaternary ammonium compounds, skin wounds should be covered with dressings to avoid exposure or isolating the infected.

Normally skin infection may not need treatment. While others may require incision and drainage of the infected area and the use of antibiotics.

Methicillin-resistant staphylococcus aureus is resistant to many types of antibiotics. Vancomycin (eg Vancocin) is the most popular antibiotic used to treat infections. MRSA can also be treated with teicoplanin such as Targocid or linezolid such as Zyvox. Treatment for sever MRSA infections may be given by vaccines or through and intravenous drip.

Sometimes a patient has recurrent infections caused by MRSA. Combination therapy is required if decolonization is going be attempted. Decolonization does not always work. The patient is being subjected to more antibiotics which could cause other factors such as elimination of indigenous flora (giving rise to Clostridium difficile pseudomembraneous colitis) or development of more resistant organisms.

References

http://www.nih.org/NIHnewWebsite/nihPublicHealth/pdfs/MRSAParentsGuide.pdf

http://www.emedicine.com/ped/topic2704.htm

http://www.merck.com/mmhe/sec17/ch190/ch190r.html