This case showed an unusually severe clinical presentation. This is similar to previous reports on PVL-producing S. aureus  causing conditions such as necrotizing pyogenic skin infections, cellulitis, tissue necrosis, septic arthritis, bacteremia, purpura fulminans (typically characterized by disseminated intravascular coagulation and purpuric skin lesions) and community-acquired necrotizing pneumonia.
PVL disease often can be observed in young and healthy people without previous medical history, who might be in close contact to others due to accommodation in barracks or dormitories, or who might be engaged in close contact sport. These risk factors are conceivable in a school child. PVL-positive S. aureus have also been transmitted by contaminated articles like sharing towels, razors, poor hand hygiene or illicit drug use. In our case, a transmission by intramuscular injection appears possible, but cannot be proven retrospectively.
The causative strain belonged to CC8. It lacked some of the most prevalent enterotoxins (egc-cluster) as well as exfoliative toxins (etA, etB or etD) and epidermal cell differentiation inhibitors (edinA, edinB or edinC). On the other hand, it carried, beside PVL, several different enterotoxin genes (sed, sej, ser, seb, seq). The clinical role of these toxins, a possible impact on the virulence, and possible synergistic effects are not yet understood. Thus it cannot be determined how much they contributed to the fatal course of the disease in addition to the PVL. PVL alone is a potent virulence factor, especially with regard to skin and/or soft tissue infections and pneumonia. While enterotoxin genes sed, sej and ser are common in that clonal complex , PVL appears to be rare among CC8-MSSA. The majority of PVL-MSSA infections from geographic areas other than Trinidad and Tobago can be attributed to other clonal complexes, such as CC1, CC5, CC22, CC30, CC80, CC121 and CC152 [3, 10]. This could suggest geographic differences in the molecular epidemiology of the PVL-producing MSSA. While PVL genes are uncommon in CC8-MSSA, there is a common and widespread MRSA strain from the same lineage, which is known as USA300. Interestingly, this strain has also been described in Colombia , geographically close to Trinidad and Tobago. Thus it is tempting to speculate on a possible phylogenetic relationship between USA300 and the strain described in this study. Further investigations on PVL-positive S. aureus in the southern Caribbean and South America are warranted.
Unfortunately, some symptoms, including the hypotension, tachycardia, leukocytopenia, and abnormal liver function tests suggestive of shock, were not adequately addressed until our patient was admitted into the ICU. Some laboratory reports arrived at the ICU only after the death of our patient. Information on the presence of PVL was also obtained only after our patient died. Such problems commonly plague health care providers in the developing world where the facilities and technologies are often not readily available.
The autopsy findings and histological reports proved the involvement of the lungs and consequently their failure. Except for the vague history of flu-like symptoms and the persistent productive cough of whitish sputum noted during the last few hours of his life, there were no major clinical features that suggested pneumonia. An involvement of the kidneys was also noted in this patient in the autopsy findings. These findings emphasize the need for aggressive management of cases of infections by PVL producing S. aureus organisms since it appears that no organ or tissues can be spared.
By both phenotypical and molecular methods, it was shown that this strain was susceptible to several relevant antibiotics. A combination of a bactericidal drug, such as a beta-lactam, plus a compound that reduces toxin synthesis, such as clindamycin or rifampicin, is strongly advocated since beta-lactams alone have in vitro been shown to increase PVL in synthesis studies . However, susceptibility tests need to be performed urgently in order to assess the efficiency of the therapy and to rule out PVL-MRSA. Thus, the initial choice of antibiotics in the presented case appeared to be correct, but nevertheless the case resulted in a fatal outcome. This emphasizes the severity of PVL-associated disease.