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Influenza and bacterial pneumonia
International Journal of Antimicrobial Agents 34 (2009) 293–294
Contents lists available at ScienceDirect
International Journal of Antimicrobial Agents journal homepage: http://www.elsevier.com/locate/ijantimicag
Editorial
Influenza and bacterial pneumonia
Influenza virus A type H1NI is currently causing a smouldering world-wide outbreak which originated in Mexico. There are predictions of a major outbreak occurring in the Autumn when the ‘influenza season’ returns to the Northern hemisphere. A possible scenario similar to that of the 1918/1919 “Spanish flu” pandemic, which had a very high mortality, frequently affecting previously healthy young individuals, is causing great concern. There has been considerable interest in the cause of this high death rate in 1918–1919. Causes of death in influenza include an overwhelming viral infection (the influenza virus does enter the blood-stream) – sometimes associated with disseminated intravascular coagulation (DIC) – myocarditis, encephalitis, and secondary bacterial infection, usually pneumonia, which can lead to respiratory failure. A recent paper [1] sheds light on the cause of death in the 1918–1919 influenza pandemic. Morens and colleagues at the United States National Institutes of Health examined stored postmortem samples obtained from 58 people who had died of influenza during the 1918–1919 pandemic. They re-cut tissue sections and examined them histologically. They also carried out a literature search for publications reporting the results of pathology and microbiology investigations on individuals who died of influenza during the pandemic. Morens and colleagues conclude that “The examination of re-cut lung tissue sections from 1918-1919 influenza case material revealed, in virtually all cases, compelling histologic evidence of severe bacterial pneumonia”. From their own study, and also their literature search, they found that Streptococcus pneumoniae was the single most common infecting bacterium. Streptococcus haemolyticus (presumably pyogenes) was also common as was mixed bacterial infection. Staphylococcus aureus was a relatively rare isolate. This latter finding is in contrast to the 1957–1958 ‘Asian’ influenza pandemic when S. aureus was the commonest bacterial respiratory pathogen [2]. S. aureus, more than 50% of which were meticillin-resistant, was also found to be the commonest cause of childhood influenza-related deaths in the United States in the 2003–2004 ‘influenza season’ [3]. There is no available cure for influenza although antiviral dugs such as the neuraminidase inhibitors oseltamivir and zanamivir can reduce the duration of symptoms of influenza by a day or so, and may also reduce the severity of complications. The mainstay of the treatment of influenza complicated by pneumonia must therefore be antibacterial agents with a spectrum that includes pneumococci and staphylococci. The possibility of infection caused by meticillinresistant staphylococci (MRSA) – both hospital and community acquired – will be a serious risk.
The time to start antibacterial therapy during the course of influenza will undoubtedly pose problems. Theoretically, this should be when there is clinical and X-ray confirmation of pneumonia but this will not be possible in most cases during a pandemic. Indeed, an abnormal chest X-ray may not signify bacterial pneumonia. In a report of 30 patients admitted to hospital in California with H1N1 influenza up to 17 May 2009, radiographic abnormalities were present in 15 of 25 patients X-rayed although evidence of bacterial super-infection was not found in any of the 30 patients (investigations in some cases included endotracheal or bronchoalveolar lavage) [4]. It has to be assumed that the Xray abnormalities were due primarily to the virus infection in this group of mainly young patients (mean age 27.5 years). Clinicians cannot therefore necessarily rely on an abnormal chest X-ray, or the presence of physical signs of pneumonia, to diagnose bacterial pneumonia and commence antibiotics. C-reactive protein (CRP) may help to differentiate between viral and bacterial pneumonia [5]. The decision to commence antibacterial agents will have to be made on clinical judgement in most cases. Stockpiling of antibiotics, as with antiviral agents and vaccines, is required but this will cause problems in terms of availability, cost, storage and turnover. The antibiotics to be stockpiled for community use will depend on national and local guidelines and also the predominant local pathogens and their sensitivity to antibiotics. The drugs could include inter alia amoxicillin/clavulanate, doxycycline, second and third generation cephalosporins, respiratory fluoroquinolones, macrolides and co-trimoxazole [6]. Assisted ventilation facilities will also be required. This will prove difficult as it is likely that a city with a population of around one million with three or four major hospitals will probably have, in the absence of an influenza epidemic, a maximum of 10 available ventilators, and frequently less, on any one day (personal observation). Four of the 30 Californian H1N1 patients required assisted ventilation [4]. During a pandemic intensive care facilities will be overwhelmed. Funding: None. Competing interests: None declared. Ethical approval: Not required. References [1] Morens DM, Taubenberger JK, Fauci AS. Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness. J Infect Dis 2008;198:962–70. [2] Robertson L, Caley JP, Moore J. Importance of Staphylococcus aureus in pneumonia in the 1957 epidemic of influenza A. Lancet 1958;2:233–6.
0924-8579/$ – see front matter © 2009 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved. doi:10.1016/j.ijantimicag.2009.06.004
294
Editorial / International Journal of Antimicrobial Agents 34 (2009) 293–294
[3] Bhat N, Wright JG, Broder KR, Murray EL, Greenberg ME, Glover MJ, et al. Influenza-associated deaths among children in the United States, 2003–2004. N Engl J Med 2005;353:2559–67. [4] CDC. Hospitalized patients with novel influenza A (H1N1) virus infection—California, April–May 2009. MMWR 2009;58:1–5. [5] Cals JWL, Butler CC, Hopstaken RM, Hood K, Dinant G-J. Effect of point of care testing for C reactive protein and training in communication skills on antibiotic use in lower respiratory tract infections. Br Med J 2009;338:b1374.
[6] Gupta RK, George R, Nguyen-Van-Tam JS. Bacterial pneumonia and pandemic influenza planning. Emerg Infect Dis 2008;14:1187–92.
A.M. Geddes Medical School, University of Birmingham, Birmingham, B15 2TT, UK E-mail address: [email protected]
Contents lists available at ScienceDirect
International Journal of Antimicrobial Agents journal homepage: http://www.elsevier.com/locate/ijantimicag
Editorial
Influenza and bacterial pneumonia
Influenza virus A type H1NI is currently causing a smouldering world-wide outbreak which originated in Mexico. There are predictions of a major outbreak occurring in the Autumn when the ‘influenza season’ returns to the Northern hemisphere. A possible scenario similar to that of the 1918/1919 “Spanish flu” pandemic, which had a very high mortality, frequently affecting previously healthy young individuals, is causing great concern. There has been considerable interest in the cause of this high death rate in 1918–1919. Causes of death in influenza include an overwhelming viral infection (the influenza virus does enter the blood-stream) – sometimes associated with disseminated intravascular coagulation (DIC) – myocarditis, encephalitis, and secondary bacterial infection, usually pneumonia, which can lead to respiratory failure. A recent paper [1] sheds light on the cause of death in the 1918–1919 influenza pandemic. Morens and colleagues at the United States National Institutes of Health examined stored postmortem samples obtained from 58 people who had died of influenza during the 1918–1919 pandemic. They re-cut tissue sections and examined them histologically. They also carried out a literature search for publications reporting the results of pathology and microbiology investigations on individuals who died of influenza during the pandemic. Morens and colleagues conclude that “The examination of re-cut lung tissue sections from 1918-1919 influenza case material revealed, in virtually all cases, compelling histologic evidence of severe bacterial pneumonia”. From their own study, and also their literature search, they found that Streptococcus pneumoniae was the single most common infecting bacterium. Streptococcus haemolyticus (presumably pyogenes) was also common as was mixed bacterial infection. Staphylococcus aureus was a relatively rare isolate. This latter finding is in contrast to the 1957–1958 ‘Asian’ influenza pandemic when S. aureus was the commonest bacterial respiratory pathogen [2]. S. aureus, more than 50% of which were meticillin-resistant, was also found to be the commonest cause of childhood influenza-related deaths in the United States in the 2003–2004 ‘influenza season’ [3]. There is no available cure for influenza although antiviral dugs such as the neuraminidase inhibitors oseltamivir and zanamivir can reduce the duration of symptoms of influenza by a day or so, and may also reduce the severity of complications. The mainstay of the treatment of influenza complicated by pneumonia must therefore be antibacterial agents with a spectrum that includes pneumococci and staphylococci. The possibility of infection caused by meticillinresistant staphylococci (MRSA) – both hospital and community acquired – will be a serious risk.
The time to start antibacterial therapy during the course of influenza will undoubtedly pose problems. Theoretically, this should be when there is clinical and X-ray confirmation of pneumonia but this will not be possible in most cases during a pandemic. Indeed, an abnormal chest X-ray may not signify bacterial pneumonia. In a report of 30 patients admitted to hospital in California with H1N1 influenza up to 17 May 2009, radiographic abnormalities were present in 15 of 25 patients X-rayed although evidence of bacterial super-infection was not found in any of the 30 patients (investigations in some cases included endotracheal or bronchoalveolar lavage) [4]. It has to be assumed that the Xray abnormalities were due primarily to the virus infection in this group of mainly young patients (mean age 27.5 years). Clinicians cannot therefore necessarily rely on an abnormal chest X-ray, or the presence of physical signs of pneumonia, to diagnose bacterial pneumonia and commence antibiotics. C-reactive protein (CRP) may help to differentiate between viral and bacterial pneumonia [5]. The decision to commence antibacterial agents will have to be made on clinical judgement in most cases. Stockpiling of antibiotics, as with antiviral agents and vaccines, is required but this will cause problems in terms of availability, cost, storage and turnover. The antibiotics to be stockpiled for community use will depend on national and local guidelines and also the predominant local pathogens and their sensitivity to antibiotics. The drugs could include inter alia amoxicillin/clavulanate, doxycycline, second and third generation cephalosporins, respiratory fluoroquinolones, macrolides and co-trimoxazole [6]. Assisted ventilation facilities will also be required. This will prove difficult as it is likely that a city with a population of around one million with three or four major hospitals will probably have, in the absence of an influenza epidemic, a maximum of 10 available ventilators, and frequently less, on any one day (personal observation). Four of the 30 Californian H1N1 patients required assisted ventilation [4]. During a pandemic intensive care facilities will be overwhelmed. Funding: None. Competing interests: None declared. Ethical approval: Not required. References [1] Morens DM, Taubenberger JK, Fauci AS. Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness. J Infect Dis 2008;198:962–70. [2] Robertson L, Caley JP, Moore J. Importance of Staphylococcus aureus in pneumonia in the 1957 epidemic of influenza A. Lancet 1958;2:233–6.
0924-8579/$ – see front matter © 2009 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved. doi:10.1016/j.ijantimicag.2009.06.004
294
Editorial / International Journal of Antimicrobial Agents 34 (2009) 293–294
[3] Bhat N, Wright JG, Broder KR, Murray EL, Greenberg ME, Glover MJ, et al. Influenza-associated deaths among children in the United States, 2003–2004. N Engl J Med 2005;353:2559–67. [4] CDC. Hospitalized patients with novel influenza A (H1N1) virus infection—California, April–May 2009. MMWR 2009;58:1–5. [5] Cals JWL, Butler CC, Hopstaken RM, Hood K, Dinant G-J. Effect of point of care testing for C reactive protein and training in communication skills on antibiotic use in lower respiratory tract infections. Br Med J 2009;338:b1374.
[6] Gupta RK, George R, Nguyen-Van-Tam JS. Bacterial pneumonia and pandemic influenza planning. Emerg Infect Dis 2008;14:1187–92.
A.M. Geddes Medical School, University of Birmingham, Birmingham, B15 2TT, UK E-mail address: [email protected]