Drosophila has been used to model infection by the Gram-positive bacterium Staphylococcus aureus. S. aureus asymptomatically colonizes about 20-30% of the human population, and most humans are exposed to it at some point in life. However, it can also be an opportunistic pathogen that seriously threatens human health, especially in immunocompromised people, due to its ability to infect a variety of tissues, form a biofilm, and gain antibiotic resistance. Methicillin-resistant staphylococcus aureus (MRSA) is one of the best-known antibiotic resistant strains, but S. aureus samples resistant to other "last-resort" antibiotics have also been isolated.
The interaction between S. aureus and Drosophila has been studied through many different approaches. S. aureus is commonly used to investigate the phagocytosis of Gram-positive bacteria, particularly the molecular recognition between phagocyte and target. Injecting S. aureus into fly hemolymph provides a model for bacteremia and sepsis. Drosophila are also used to screen for new antibiotic drugs and delivery systems, especially against MRSA strains, and to screen S. aureus mutants to dissect their response to host defenses.
The Disease Ontology includes multiple clinical manifestations of S. aureus infection: toxic shock syndrome (DOID:14115), impetigo (DOID:8504), Ritter's disease (DOID:9063), lymphangitis (DOID:9317), tracheitis (DOID:9392), staphyloenterotoxemia (DOID:96), and hordeolum (DOID:9909).
[updated Aug. 2022 by FlyBase; FBrf0222196]
S. aureus infections range in severity from mild skin infections to severe necrotizing pneumonia. It is simultaneously the leading cause of bacteremia, infective endocarditis, and can also cause osteoarticular, skin and soft tissue, pleuropulmonary, and device-related infections. (Oliveira et al. 2018 and references therein, pubmed:29921792).
The S. aureus population in humans is dominated by about ten S. aureus lineages. Individual isolates within each lineage have unique combination of mobile genetic elements (MGEs) often encoding virulence and resistance genes. S. aureus evolves due to point mutation and selection, but also dramatically due to the horizontal transfer of these MGE between strains or from other species or genera. Because of the mobility of MGE, there are prospects for increasingly virulent and resistant strains to emerge that could severely affect healthcare and agriculture more effectively than the current pathogens. (Lindsay 2010, pubmed:19811948.)
Apoptosis is pivotal in certain diseases caused by S. aureus, such as atopic dermatitis and sepsis. Many S. aureus toxins, such as staphylococcal enterotoxins (SEs) and alpha-toxin (α-toxin), show proapoptotic activities. Cell apoptosis of the host immune system may conceivably facilitate S. aureus infection, and apoptosis of tissue cells can also trim the immune response by influencing cytokine production and T cell differentiation. (Zhang et al. 2017, pubmed:28942840.)
New S. aureus isolates were identified in the 1960s that were resistant to methicillin, a β-lactam antimicrobial active at that time against nearly all S. aureus strains. Although methicillin is not used any more (other members of the family that are used are oxacillin and nafcillin), the name "methicillin-resistant S. aureus (MRSA)" persists. Such MRSA isolates were initially largely confined to the health care environment, and they became major causes of nosocomial infections, particularly among patients after procedures or with devices that necessitate piercing the skin. These MRSA strains were believed to be acquired in health care environments and have been termed health care-associated or HA-MRSA. They are often resistant to multiple classes of non β-lactam antibiotics. (David and Daum 2017, pubmed:28900682.)
