Why staphylococcus aureus is gram positive




















FDA came as respite for clinicians. However, new antibiotic discovery efforts and non- antibiotic approaches to tackle MRSA should not be diminished considering the ability of the pathogen to acquire resistance to newer drugs quickly after their introduction in clinics. In this chapter, we present a comprehensive outlook of S. They are often in clusters resembling bunch of grapes when observed under light microscope after Gram staining.

The scanning electron microscopic observation reveals roughly spherical shaped cells with smooth surface [ 2 ]. The diameter of the cells ranges from 0. The transmission electron microscopy of cells shows thick cells wall, distinctive cytoplasmic membrane and amorphous cytoplasm [ 4 ]. The yellow colour of the colonies is imparted by carotenoids produced by the organism.

The organism is often haemolytic in blood agar due to production of four types of haemolysins alpha, beta, gamma and delta [ 6 , 7 ]. Nearly all isolates of S. The organism is salt tolerant, which is able to grow in mannitol-salt agar medium containing 7. The organism is catalase positive and oxidase negative. The primary objective in laboratory diagnosis is to identify whether the diagnosed S.

Since MRSA emerged as problematic pathogen, a systematic diagnostic approach is necessary for early diagnosis so that treatment with appropriate antibiotics can be initiated as early as possible.

For the species identification, slide and tube coagulase tests, latex agglutination tests and PCR-based tests are used. For detection of MRSA, determination of minimum inhibitory concentration MIC of methicillin or oxacillin or cefoxitin using broth micro-dilution method, cefoxitin disk screen, oxacillin agar screen and latex agglutination test for PBP2a and molecular methods for detection of mecA are employed [ 8 ].

The process of S. The organism is in carrier state in the anterior nares and can remain so without causing infections for weeks or months. The colonization proceeds to infection under certain predisposing factors such as prolonged hospitalization, immune suppression, surgeries, use of invasive medical devices and chronic metabolic diseases.

Localized skin abscess develop when the organism is inoculated into the skin from a site of carriage. This can further spread and results in various clinical manifestations of localized infections such as carbuncle, cellulitis, impetigo bullosa or wound infection. The organism can enter into blood and spread systemically to different organs causing sepsis. This haematogenous spread may result in endocarditis, osteomyelitis, renal carbuncle, septic arthritis and epidural abscess.

Without a blood stream infection, specific syndromes can occur due to extra cellular toxins of S. These are toxic shock syndrome, scalded skin syndrome and foot borne gastroenteritis [ 9 ].

The clinical infections of S. These two types are distinct in clinical manifestations of the infections, antibiotic susceptibility and the genetic background of the infecting S. For decades, S. However, the community S. The important clinical S. Other clinical infections are epidural abscess, meningitis, toxic shock syndrome and urinary tract infections [ 9 , 10 ].

These factors enable the organism to be successful as pathogen that causes wide range of human and animal infections. Virulence factors help in attachment to host cells, breaking down the host immune shield, tissue invasion, causing sepsis and elicit toxin-mediated syndromes.

This is the basis for persistent staphylococcal infections without strong host immune response [ 11 ]. Based on their mechanism of action and role in pathogenesis, staphylococcal virulence factors are classified as represented in Table 1 [ 9 , 12 ]. Virulence factors of S. The anterior nares are the principal ecological niche, where the organism colonizes in humans.

The nasal carriage of S. The average nasal carriage of S. Since, the nasal carriage increases the risk of development of surgical site, lower respiratory and blood stream infections in hospitals, efforts are made to eliminate the carriage using various strategies. Methods such as local application of antibiotics eg. The beta-lactam antibiotics exert their antibacterial activity by inactivation of penicillin-binding proteins PBPs , which are essential enzymes for bacterial cell wall synthesis.

However, these antibiotics have only a low affinity towards PBP2a, thus this enzyme evades from inactivation and carry out the role of essential PBPs resulting in cell wall synthesis and survival of bacteria even in presence of beta-lactam antibiotics. Penicillin is the first beta-lactam antibiotic discovered in and found to be effective weapon against S.

In s, sooner after its introduction into clinics, there were reports of S. These strains produced plasmid-encoded beta-lactamase enzyme penicillinase which enzymatically cleaved the beta-lactam ring of penicillin rendering the antibiotic inactive [ 31 , 32 ].

In s, the penicillin resistance was restricted to hospital isolates of S. Meanwhile, scientists who were challenged with penicillinase-mediated resistance in S. Methicillin was introduced into clinics in ; however, in less than a year, resistance of S. Over the next 10 years, increasing number of MRSA outbreaks was reported in different parts of the world especially from the European countries [ 36 , 37 ].

The notable feature of these reports is that, the incidences were from hospitals and thus MRSA emerged as a hospital-borne pathogen.

The mechanism of resistance to beta-lactam antibiotics in these MRSA isolates was uncovered in [ 38 ]. The gene is part of a 21—60 kb mobile genetic element referred to as staphylococcal cassette chromosome mecA SCC mecA.

There are two hypotheses that explain the evolutionary origin of MRSA. The single clone hypothesis suggests that the mobile genetic element entered the S.

The second and the most agreed hypothesis is that MRSA strains evolved number of times by means of the horizontal transfer of the mobile genetic element into phylogenetically distinct methicillin-susceptible S.

SCC mec elements are highly diverse in their structural organization and genetic content Figure 1 and have been classified into types based on the combination of mec and ccr , which share variations five classes in mec and eight in ccr. To date, at least 11 types of SCCmec elements have been identified [ 41 — 43 ].

Basic structure of SCC mec. SCC mec constituted by mec gene and ccr gene complexes. The ccr gene complex encodes the integration and excision of entire SCC element. The gene complexes are flanked by characteristic nucleotide sequences, inverted repeats IR and direct repeats DR , at both ends. J joining regions are J1 between right chromosomal junction and ccr complex, J2 between ccr and mec complexes and J3 between mec complex and left chromosomal junctions.

Adopted from Ref. Scattered case reports of MRSA infections in healthy population whom had no exposure to health care facilities were published in the s and mids. Beginning in , case series of MRSA infection and colonization of patients lacking health care-associated risk factors were reported from six continents, in diverse states, nations and regions [ 51 , 53 ].

HA-MRSA strains were resistant to many classes of non-beta-lactam antibiotics, thus display multi-drug resistant phenotypes. The concern about this clone is high virulence and increase in resistance to non-beta-lactam antibiotics [ 50 , 53 ]. Since then, hospital outbreaks of S.

The first beta-lactam antibiotic penicillin G was discovered in by Alexander Fleming and the drug was used in human as chemotherapeutic agent in [ 59 ]. The antibiotic was potent against Gram positive pathogens [ 60 ] and a power weapon against Staphylococcal infections. However, first reports of S. Such penicillin-resistant isolates carried a plasmid gene, blaZ which encoded a beta-lactamase enzyme, referred to as penicillinase [ 33 , 34 ]. The enzyme is capable of cleaving the beta-lactam ring of penicillin resulting inactivation of the antibiotic [ 31 , 32 ].

The emergence and spread of penicillinase-mediated resistance in S. This has spread in alarm proportions and became pandemic in the s. As discussed earlier, the penicillinase resistance in S. Risk and outcome of nosocomial Staphylococcus aureus bacteraemia in nasal carriers versus non-carriers.

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Many strains have developed resistance Antibiotic resistance Bacteria are microscopic, single-celled organisms. If carriers take antibiotics, the antibiotics kill the strains that are not resistant, leaving mainly the resistant strains.

These bacteria may then multiply, and if they cause infection, the infection is more difficult to treat. Whether the bacteria are resistant and which antibiotics they resist often depend on where people got the infection: in a hospital or other health care facility or outside of such a facility in the community.

Because antibiotics are widely used in hospitals, hospital staff members commonly carry resistant strains. When people are infected in a health care facility, the bacteria are usually resistant to several types of antibiotics, including almost all antibiotics that are related to penicillin called beta-lactam antibiotics Penicillins Penicillins are a subclass of antibiotics called beta-lactam antibiotics antibiotics that have a chemical structure called a beta-lactam ring.

Carbapenems, cephalosporins, and monobactams Strains of bacteria that are resistant to almost all beta-lactam antibiotics are called methicillin-resistant Staphylococcus aureus MRSA. Methicillin is a type of penicillin.

MRSA strains are common when infection is acquired in a health care facility called hospital-acquired infection. Some strains of MRSA cause infections that are acquired outside of a health care facility called community-acquired infection , including mild abscesses and skin infections. The number of these community-acquired infections is increasing.

Staphylococcal infections may be difficult to treat because many of the bacteria have developed resistance to antibiotics. Folliculitis Folliculitis Folliculitis and skin abscesses are pus-filled pockets in the skin resulting from bacterial infection.

A hair root follicle is infected, causing a slightly painful, tiny pimple at the base of a hair. Impetigo Impetigo and Ecthyma Impetigo is a superficial skin infection, caused by Staphylococcus aureus, Streptococcus pyogenes, or both, that leads to the formation of scabby, yellow-crusted sores and, sometimes, small Impetigo may itch or hurt.

Abscesses Skin abscesses Folliculitis and skin abscesses are pus-filled pockets in the skin resulting from bacterial infection. Cellulitis Cellulitis Cellulitis is a spreading bacterial infection of the skin and the tissues immediately beneath the skin. This infection is most often caused by streptococci or staphylococci. Redness, pain, and Cellulitis spreads, causing pain and redness. Toxic epidermal necrolysis Stevens-Johnson Syndrome SJS and Toxic Epidermal Necrolysis TEN Stevens-Johnson syndrome and toxic epidermal necrolysis are two forms of the same life-threatening skin disease that cause rash, skin peeling, and sores on the mucous membranes.

See also Introduction Both lead to large-scale peeling of skin. Breast infections mastitis Breast Infection A breast infection mastitis can occur after delivery postpartum infection , usually during the first 6 weeks and almost always in women who are breastfeeding. If the baby is not positioned The area around the nipple is red and painful. The bacteria may then infect the nursing infant.

Pneumonia often causes a high fever, shortness of breath, and a cough with sputum that may be tinged with blood. Lung abscesses Abscess in the Lungs A lung abscess is a pus-filled cavity in the lung surrounded by inflamed tissue and caused by an infection. A lung abscess is usually caused by bacteria that normally live in the mouth and are They sometimes enlarge and involve the membranes around the lungs and sometimes cause pus to collect called an empyema Types of fluid Pleural effusion is the abnormal accumulation of fluid in the pleural space the area between the two layers of the thin membrane that covers the lungs.

Fluid can accumulate in the pleural These problems make breathing even more difficult. Bloodstream infection is a common cause of death in people with severe burns. Symptoms typically include a persistent high fever and sometimes shock. Osteomyelitis causes chills, fever, and bone pain. The skin and soft tissues over the infected bone become red and swollen, and fluid may accumulate in nearby joints. Other infections require samples of blood or infected fluids, which are sent to a laboratory to grow culture , identify, and test the bacteria.

Laboratory results confirm the diagnosis and determine which antibiotics can kill the staphylococci called susceptibility testing Testing of a Microorganism's Susceptibility and Sensitivity to Antimicrobial Drugs Infectious diseases are caused by microorganisms, such as bacteria, viruses, fungi, and parasites.

Doctors suspect an infection based on the person's symptoms, physical examination results, If a doctor suspects osteomyelitis, x-rays, computed tomography CT , magnetic resonance imaging MRI , radionuclide bone scanning Radionuclide Scanning In radionuclide scanning, radionuclides are used to produce images. A radionuclide is a radioactive form of an element, which means it is an unstable atom that becomes more stable by releasing These tests can show where the damage is and help determine how severe it is.

Bone biopsy is done to obtain a sample for testing. The sample may be removed with a needle or during surgery. People can help prevent the spread of these bacteria by always thoroughly washing their hands with soap and water or applying an alcohol-based hand sanitizer.

Some doctors recommend applying the antibiotic mupirocin inside the nostrils to eliminate staphylococci from the nose. However, because overusing mupirocin can lead to mupirocin resistance, this antibiotic is used only when people are likely to get an infection.



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