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Abstract & Commentary
Synopsis: The pneumococcus may cause necrotizing fasciitis.
Source: Ballon-Landa GR, et al. Necrotizing fasciitis due to penicillin-resistant Streptococcus pneumoniae: Case report and review of the literature. J Infect. 2001;42:272-290.
Physicians dread the confrontation with necrotizing fasciitis (NF). It can be tricky to diagnose, present in various forms, and have a catastrophic clinical outcome. Group A streptocococci are by far the most common cause of NF, but other bacteria including the clostridia can produce the syndrome. Another streptococcus is a featured cause of NF in this report, the pneumococcus, Streptocococcus pneumoniae (SP).
The report is that of a 32-year-old Hispanic man from San Diego, Calif, who presented with trauma-induced left flank pain and overlying erythema. The pain initially waned but he represented 2 days after the trauma complaining he could not sleep. He was afebrile but tachycardic, at 110 beats/minute. The only other physical finding was erythema of the flank region. There was marked leukocytosis of 41,000 WBC/mm3. A chest CT did show a broken left 10th rib and some underlying atelectasis without infiltrate.
The next hospital day, his clinical condition worsened, and the white blood cell count increased to 51,000/mm3. The ecchymosis extended from the flank across the abdomen, surgical exploration revealed extensive necrosis of the subcutaneous tissue of the flank and abdominal wall. Following persistent hypotension and acidosis, the patient was taken back to surgery the following day for further debridement, this time including the left chest wall. Surgical specimens grew pure cultures of a serotype 9V SP, and tissue Brown and Brehm stains showed lancet-shaped diplococci. Blood cultures remained negative. The MIC of the isolate was 2.0 µg/mL for penicillin and 0.5 µg/mL for ceftriaxone. The initial therapeutic regimen of meropenam, levofloxacin, and metronidazole was changed to vancomycin and clindamycin.
Interestingly, Ballon-Landa and colleagues next compared their isolate to a clone called France 9V-3, a penicillin-resistant SP that has spread worldwide. Indeed, the comparison to France 9V-3 to the patient’s isolate of penicillin-binding protein genes pbp1a, pbp2b, and pbp2x polymorphisms revealed apparent identity, as did the pulse field gel electrophoresis patterns.
In their review of the literature yielding 11 cases, several aspects stood out. Six patients were younger than 45 years of age, 9 had SP bacteremia, 4 were on immunosuppressive drugs, 5 underwent surgery, and only 2 died.
Comment by Joseph F. John, MD
One of the major findings of this report is the ability of penicillin-resistant SP to cause severe NF and septic shock. We have seen cases like these in New Jersey indistinguishable from NF caused by group A streptococcus. Of course, all group A streptococci remain susceptible to low concentrations of penicillin, but other bacteria like Staphylococcus aureus, Enterococcus faecalis, and now some SP, such as this penicillin-resistant strain, will not respond to a pure penicillin G regimen, although high-dose parenteral penicillin might have been effective. NF should probably be treated with broad antibiotic regimens initially pending identification of the causative pathogen. Ballon-Landa et al favor a regimen including clindamycin, shown in some animal studies to have improved efficacy over penicillin.
Ballon-Landa et al emphasize the importance of the increasing rate of penicillin resistance in invasive strains of SP in the United States—up to 25% of strains by 1998. It will be interesting to see if this rate increases as we approach 2002.
One striking aspect of the review of the 11 SP-associated NF cases is that not one had a respiratory syndrome. The lack of an obvious sino-pulmonary entry point for the SP that cause NF suggests a possible changing ecology for SP or specific virulence factors in the NF strains that allow them to metastasize silently from asymptomatic foci in the respiratory tract. More studies will be needed to test such hypotheses. Ballon-Landa et al emphasize that the pneumolysis of SP induced nitric oxide, a mediator of septic shock. Cell wall components are able to stimulate cytokine production including IL-1, IL-6, and IL-8, all of which can adversely affect host tissue and contribute to tissue damage.
The 55 references in this case report and literature review highlight the wealth of information now available about the pneomococcus. Clinicians, including infectious diseases consultants, should remain alert to the ability of SP to produce skin (cellulites), invasive soft tissue, and myofacial infections in both compromised and normal hosts.
Joseph John, Professor of Medicine and Microbiology, University of Medicine and Dentistry-New Jersey, Robert Wood Johnson Medical School, is Co-Editor of Infectious Disease Alert.