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Fatal case of post-influenza, community-associated MRSA pneumonia in an Ontario teenager with subsequent familial transmission

Canada Communicable Disease Report

15 February 2007 Volume 33  Number 04

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H Adam, PhD (1), A McGeer, MD (2), A Simor, MD (3)

  1. Clinical Microbiology Fellowship Program, University of Toronto, Toronto, Ontario

  2. Mount Sinai Hospital and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario

  3. Sunnybrook Health Sciences Centre and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario

Introduction

Infections due to community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) are increasing worldwide(1). Persons at particular risk of CA-MRSA include children, First Nations populations, athletes, military trainees, men who have sex with men, intravenous drug users, prison populations and the homeless(1-3).While CA-MRSA is less common in Canada than in the United States, several studies have documented its emergence in Canada(4-6). In a recent review of MRSA in Ontario, it was estimated that 13% of infections were community-associated, as determined by the location of MRSA acquisition reported by laboratories(7).

While most CA-MRSA infections are of skin or soft tissue, necrotizing pneumonia due to CA-MRSA is well described and often fatal, even when it occurs in young, immunocompetent people(8). In one comparison of community and hospital-associated MRSA pneumonia, patients with CA-MRSA pneumonia were younger (14.8 years versus 70.1 years), more commonly had influenza-like illness before admission for pneumonia, high temperatures (> 39o C), heart rate > 140 beats per minute and lower survival rates at 48 hours after admission (63% versus 94%)(8). Other recent studies highlight the association between severe community-acquired pneumonia due to S. aureus and preceding viral infection. It has been proposed that a viral infection preceding S. aureus pneumonia may lead to severe necrotizing pneumonia, resulting in admission to the intensive care unit (ICU), intubation and often death(9,10).

The spread of CA-MRSA occurs through direct contact with a colonized or infected patient, or with their contaminated personal belongings(1). The spread of CA-MRSA within households (11,12) and potentially between families has led to the suggestion that family members may act as an important reservoir for CA-MRSA(13).

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Case report

Patient A.
In February 2006, a 17-year-old, previously healthy, high school student presented to an emergency department in Scarborough, Ontario, with complaints of fever, shortness of breath and a dry cough that had started 2 days earlier. His father also had symptoms of an upper respiratory tract infection. At the time of presentation, the patient had temperatures up to 39.5o C and an oxygen saturation of 83%. Chest radiography revealed extensive bilateral lung infiltrates. The patient quickly developed respiratory distress and became hypotensive. His condition was diagnosed as severe community-acquired pneumonia with septic shock, and he was moved to the ICU, where he was intubated and ventilated. Within 12 hours of ICU admission, the patient required high-frequency oscillatory ventilation. He needed significant inotropic support and was given activated protein C for presumed septic shock. A bronchoscopy was performed, which revealed patchy necrosis of the epithelial surface of the airways suggestive of a necrotizing pneumonia. Bronchoalveolar lavage (BAL) fluid was collected. The patient was treated with numerous antimicrobials during the first 24 hours, including azithromycin, ceftazidime, ciprofloxacin, clindamycin, cloxacillin and vancomycin. Despite aggressive supportive care, the patient's status continued to deteriorate, and he died on the fifth day after admission. A postmortem examination was not conducted.

Cultures of BAL fluid yielded both MRSA and influenza A virus. Microbiologic investigations of the MRSA isolate demonstrated that it was CMRSA-10 (similar to genotype USA300(4)) by pulsed-field gel electrophoresis pattern and positive for the Panton-Valentine leukocidin gene (pvl).

Neither the patient nor his household contacts had any history of exposure to health care in Canada or any recognized risk factors for CA-MRSA exposure in Canada (e.g., sports teams, incarceration). A travel history revealed that the young man and his family had travelled to Houston, Texas, a few weeks before his illness. They stayed with family members there, one of whom had had a recent MRSA infection.

Patient B.
Two months after the death of Patient A, his previously healthy 19-year-old sister had recurrent furunculosis and soft-tissue abscesses involving her perineum and buttocks, caused by MRSA. She had four recurrences over a period of 3 months.

Patients C.
The father of patients A and B has also had one episode of skin and soft-tissue infection due to MRSA.

Patient A is assumed to have acquired his MRSA in Texas, where he had close contact with a person known to have been infected with MRSA and where CA-MRSA is much more common that in Canada(14). Patients B and C may have become colonized with MRSA during their visit to Texas or during patient A's illness. Decolonization with mupirocin ointment, chlorhexidine gluconate soap, rifampin and doxycycline has been recommended for patients B and C because of the recurrent nature of the infections and for the other family contact (the mother of patients A and B).

Discussion

Cases of both severe community-acquired pneumonia caused by CA-MRSA following influenza infection and familial spread of CA-MRSA are appearing worldwide. This report describes a Canadian family in which both of these evolving phenomena occurred.

Patients are at risk of potentially lethal, necrotizing pneumonia associated with CA-MRSA after an influenza infection. The occurrence of these cases is likely to increase as the CA-MRSA incidence rises. Continued emphasis on influenza vaccination is the most effective means to minimize the risk of severe post-influenza CA-MRSA pneumonia. Empiric therapy of severe, community-acquired pneumonia in immunocompetent patients should include treatment for CA-MRSA in communities where this has become an emerging pathogen. Empiric use of vancomycin (or possibly linezolid) may be indicated in cases of post-influenza bacterial pneumonia, and pandemic planners developing algorithms for the care of severely ill patients during the pandemic should be aware of the emergence of CA-MRSA and its potential contribution to pneumonia during the pandemic.

Guidelines for the prevention and management of CA-MRSA have recently been developed for Canadian practitioners(1) and are available on-line from the Canadian Committee on Antibiotic Resistance (www.ccar-ccra.com/english/ca-mrsa.shtmlnew window). The guidelines summarize the currently available information on CA-MRSA in Canada, including the epidemiology, microbiology and management. Recommendations to limit familial spread of CA-MRSA are included in the guidelines. In order to limit the spread of CA-MRSA, patients must be advised to cover infected lesions, practise regular hand washing and avoid sharing personal items(1).

This case highlights the need for awareness of and preparation for the inevitable increase in CA-MRSA rates in Canadian centres and the small but significant risk of fatality from communityacquired pneumonia following influenza infection in young healthy adults.

Several methods of testing were used for the diagnosis of influenza in respiratory specimens, virus isolation accounting for the greatest proportion of positive influenza detections (49.1% or 3,236/6,590). Other reported methods of laboratory confirmation included virus antigen detection (38.3% or 2,522/6,590), nucleic acid amplification (12.5% or 824/6,590) and to a minor extent, serologic testing (0.1% or 8/6,590).

Acknowledgments

The authors thank B. Willey and O. Imas for their assistance.

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References

  1. Barton M, Hawkes M, Moore D et al. Guidelines for the prevention and management of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA): A perspective for Canadian health care practitioners. Can J Infect Dis Med Microbiol 2006;17:4C-24C.

  2. Moran G, Krishnadasan A, Gorwitz R et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med 2006;355:666-74.

  3. Fridkin S, Hageman J, Morrison M et al. Methicillin-resistant Staphylococcus aureus disease in three communities. N Engl J Med 2005;352:1436-44.

  4. Gilbert M, MacDonald J, Gregson D et al. Outbreak in Alberta of community-acquired (USA300) methicillin-resistant Staphylococcus aureus in people with a history of drug use, homelessness or incarceration. Can Med Assoc J 2006;175:149-54.

  5. Mulvey M, MacDougall L, Cholin B et al. Community-associated methicillin-resistant , Staphylococcus aureus Canada. Emerg Infect Dis 2005;11:844-50.

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  7. McGeer A, Fleming C, Green K et al. Antimicrobial resistance in common hospital pathogens in Ontario. QMPLS News 2006;104:1-10.

  8. Gillet Y, Issartel B, Vanhems P et al. Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotizing pneumonia in young immunocompetent patients. Lancet 2002;359:753-59.

  9. Gonzalez B, Hulten K, Dishop M et al. Pulmonary manifestations in children with invasive community-acquired Staphylococcus aureus infection. Clin Infect Dis 2005;41:583-90.

  10. Hageman J, Uyeki T, Francis J et al. Severe community-acquired pneumonia due to Staphylococcus aureus, 2003-04 influenza season. Emerg Infect Dis 2006;12:894-9.

  11. Faden H, Ferguson S. Community-acquired methicillin-resistant Staphylococcus aureus and intrafamily spread of pustular disease. Pediatr Infect Dis J 2001;20:554-5.

  12. Osterlund A, Kahlmeter G, Bieber L et al. Intrafamilial spread of highly virulent Staphylococcus aureus strains carrying the gene for Panton-Valentine leukocidin. Scand J Infect Dis 2002;34:763-87.

  13. Huijsdens X, van Santen-Verheuvel M, Spalburg E et al. Multiple cases of familial transmission of community-acquired methicillin-resistant Staphylococcus aureus. J Clin Microbiol 2006;44:2994-6.

  14. Purcell K, Fergie J. Epidemic of community-acquired methicillin-resistant Staphylococcus aureus infections. Arch Pediatr Adolesc Med 2005;159:980-5.


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