Staphylococcus Aureus Infection in Humans

Classification and Morphology

The genus Staphylococcus has various species, which are mainly divided depending on their ability to cause clotting of the blood plasma. This process is referred to as the coagulase reaction. Staphylococcus aureus is coagulase-positive, implying they cause clotting. The organisms are mainly found in the axillae and nasal cavities of humans existing as commensals. A quarter of humans and animals are estimated to host the pathogen in these parts of the bodies (Tong, Davis, Eichenberger, Holland, & Fowler, 2015). The aureus species is the most pathogenic in the particular genus.

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Staphylococcus aureus is a gram-positive bacterium. Its shape is a coccus which usually is clustered together in a grape-like form. Each bacterium has a diameter of approximately one micrometer. At times, the cocci can also be found in chains or pairs. Their ability to grow in clumps is an identification test following culture in the laboratory. This formed the basis of their index identification by Sir Alexander Ogston, a surgeon. After culturing a pus sample from an abscess of the knee joint, he described that they looked like bunches of grapes.

Due to the potential of the bacteria to cause infections in both the community and the hospital, typing the samples is necessary during investigations of related disease outbreaks. The typing processes employed should be easily replicable and also show ease of use and interpretation.

The previous method of typing was phage-typing. The marker that the test is founded on is not easily reproducible and requires maintenance of large amounts of phages, limiting the typing to few specialized laboratories. This heralded the use of molecular typing methods that mainly analyze restriction fragment length polymorphisms. The best method currently employed is the field gel electrophoresis (Tong et al., 2015). The bacterial DNA is spliced into large fragments by restriction enzymes.

Pathogenesis

In humans, the skin acts as the initial barrier against bacterial infections. Keratin, produced by keratinocytes, is at the foundation of this protective function. The occurrence of trauma renders the individual susceptible as pathogens gain entry to the underlying tissues (Kobayashi, Malachowa, & DeLeo, 2015). Another protection mechanism is the involvement of polymorphonuclear neutrophils (PMNs). They form the primary cellular defense against bacterial infection. This role is carried out through phagocytosis. It can be followed by the destruction of the pathogen using reactive oxygen species and other degradative enzymes.

The pathogenesis of Staphylococcus aureus is dependent on its ability to subvert these protective mechanisms. The bacteria produce immune evasion molecules, cause lysis of PMNs, coagulase enzymes, and cytotoxins. The pathogen releases N-formyl peptides. These peptides are chemotactic and attract PMNs. However, the staphylococcal pathogen has developed chemotactic inhibitory proteins that prevent the accumulation of neutrophils within affected regions. Some of the leukocytes reach the site of infection. They encounter cytolytic toxins that destroy them, effectively limiting the response of the immune system.

The bacteria also produce protein A. This molecule binds to the Fc region of the immunoglobulin G, hence preventing opsonization of the pathogens. This implies that they cannot be targeted for destruction, ensuring their survival. Another anti-phagocytic molecule is clumping factor A which binds to fibrinogen in the blood and deposits it on the bacterial surface (Kobayashi, Malachowa, & DeLeo, 2015).

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The pathogens have evolved to formulate mechanisms that prevent destruction by reactive oxygen species produced by leukocytes. The enzymes reductase, catalase, alkyl hydroperoxide, and superoxide dismutase protect them from this risk. Staphyloxanthin, the staphylococcal pigment, has antioxidant properties, further augmenting the role of these enzymes. Due to the ability of the bacteria to cause cytolysis of the PMNs, the cytotoxic molecules are released from these inflammatory cells into the tissues.

This results in the destruction of the surrounding tissues, hence the characteristic feature of the staphylococcal organisms to cause the formation of abscesses. These leukocytic factors include alpha-hemolysin, leucocidin, and gamma-hemolysin. Alpha-hemolysin is closely linked with the development of Staphylococcal skin infections.

The bacteria have superantigens, toxic shock syndrome toxin (TSST), and enterotoxins. Superantigens cause widespread stimulation of the immune system without the involvement of formal recognition of antigens. Large amounts of cytokines are released, causing the symptoms and signs of toxic shock syndrome. The final pathogenic factor is an exfoliative toxin. It shows proteolytic activity, causing blistering and loss of the epidermis.

Symptoms of Infection

The main entry of the organism is broken skin. It leads to the formation of abscesses that are pus-filled lesions.

The abscesses can be classified into pustules, furuncles, and carbuncles in order of increasing size.

The organism causes impetigo, which is found mainly in young children. It is a superficial, blister condition that primarily affects the face and limbs.

Cellulitis. The pathogen is responsible for the widespread inflammation of the dermis and underlying connective tissue.

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Accidental and post-operative wound infections.

The organism may be disseminated through the body via the blood, causing the following conditions septic arthritis, endocarditis (mainly in intravenous drug users), osteomyelitis, meningitis, and septicemia. The conditions instigated by its toxins include toxic shock syndrome, scalded skin syndrome, and staphylococcal food poisoning (Center for Disease Control and Prevention, 2018).

Laboratory Identification and Diagnosis

Clinical specimens are grown on blood agar. The examples include pus swabs, sputum, blood, feces, and nasal swabs. Following culture, the bacteria produce opaque, raised, round colonies that are at least a millimeter in diameter (“Lab 15,” 2019). They are beta-hemolytic and have creamy gold colonies. They are sensitive to novobiocin. On Gram staining, they are positive and found in clusters. They are able to grow on mannitol salt agar and are coagulase positive. They are also favorable for clumping factor and protein A. In the laboratory, they are also assessed for sensitivities to the various antibiotics used in the treatment of staphylococcal infections.

Treatment and Antibiotic Resistance

Initially, the pathogens were susceptible to penicillin, especially methicillin. Penicillins act by inhibiting cell wall synthesis. They work on peptidoglycans; hence, gram-positive bacteria are sensitive to their action causing lysis of the bacterial organism.

For staphylococcal skin infections, management involves incision and drainage for superficial infections. Antibiotics are employed in severe disease, which fails to respond to the previous intervention.

Over time, the organism has gained adaptations to subvert the actions of penicillin. This resistance can be easily transmitted to other bacteria through plasmids, thus limiting the effectiveness of these drugs. Alternative drugs for treatment include trimethoprim-sulfamethoxazole, doxycycline, vancomycin, and clindamycin (Tong et al., 2015). Methicillin-resistant Staphylococcus aureus is treated mainly using vancomycin or linezolid. Vancomycin-resistant strains are treated using a combination of quinupristin-dalfopristin or linezolid.

Due to the ability of the pathogen to rapidly develop resistance against antibiotics, other therapies such as vaccination have been broached to manage the infections. However, human trials have been unsuccessful so far.

Infection can be prevented through handwashing and proper cleansing of both surgical and other traumatic wounds. The use of indwelling catheters should also be done in an aseptic manner. Antimicrobials should be used sparingly and appropriately to prevent the development of resistance.

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References

Center for Disease Control and Prevention. (2018). Staphylococcal (Staph) Food Poisoning. Web.

Kobayashi, S., Malachowa, N., & DeLeo, F. (2015). Pathogenesis of Staphylococcus aureus abscesses. The American Journal of Pathology, 185(6), 1518-1527. Web.

Lab 15: Isolation and Identification of Staphylococci. (2019). Web.

Tong, S., Davis, J., Eichenberger, E., Holland, T., & Fowler, V. (2015). Staphylococcus aureus Infections: Epidemiology, pathophysiology, clinical manifestations, and management. Clinical Microbiology Reviews, 28(3), 603-661. Web.

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