Journal
of Hospital
Infection
(1991) 19, l-3
EDITORIAL
Nosocomial
spread
of Haemophilus
influenzae
The potentially contagious nature of infections caused by Haemophilus injluenzae type b in children is well recognized.’ Carriage rates are often high in families where a case has arisen2 and guidelines have been issued for the use of rifampicin prophylaxis to prevent secondary household cases.3,4 Spread within communities of children such as orphanages’ and nurseries6 has also been described and there have been reports of cross infection in both acute7 and long-stay’-” paediatric hospitals. In this issue Howard et al. (p. 70) draw attention to the rare occurrence of spread of H. injluenzae type b amongst adult in-patients, and Hekker et al. (p. 25) to the poorly understood situation regarding hospital outbreaks of non-typable strains of H. in&enzae. In comparison with children, adult infections due to H. influenzae type b are uncommon. Over a period of three years, only 15/207 (7.2%) cases of invasive disease due to H. injkenzae type b presenting in Welsh hospitals occurred in patients over 15 years of age.12 The decline in incidence of cases with increasing age is associated with a corresponding rise in the prevalence of protective antibodies in the population. I3 However, protection can wane with advancing age and only 8% of subjects over 79 years of age were shown to have bactericidal antibodies in one study. l4 When cross-infection due to H. injluenzae type b has arisen, it has generally affected older age group patients.l’-i7 It is possible that with an increasing elderIy population, H. influenzae type b disease may become more common and the potential for hospital cross infection may rise. Most of the instances of nosocomial spread of non-typable H. influenxae have also involved adult patients, and outbreaks have been described involving respiratory,‘s2’ general medica121m22 and geriatric23 units. These infections have generally been seen in older individuals with underlying respiratory pathology predisposing to haemophilus infection. One report implicates a spirometer as a possible source of infection” and another the method of drug nebulization.*i Others have suggested person-to-person spread.‘*a2’ The extent of cross infection due to H. influenzae is impossible to judge in the absence of readily available markers of strain identity. The outbreaks referred to above have all been initially recognized by the presence of unusual antibiotic resistance patterns. Simon et aZ.24 concluded that 29% of patients with H. injluenzae pneumoniae and bronchitis and 43% of patients with respiratory tract colonization acquire the organism following admission. As most of the descriptions of cross-infection due to 0195-6701/91/090001+03
$03.00/O
0 1991 The Hospital 1
Infection
Society
2
Editorial
this organism record a worsening of clinical condition on acquisition of the organism, it is possible that the spread of H. &$uenxae in hospitals could represent a much larger clinical problem than is currently recognized. Barrier isolation and respiratory precautions have been recommended for children with invasive H. influenzae type b infections until 24 hours after initiation of effective therapy. 25 It would seem prudent to extend this advice to adults; however, the infrequency of infection in this group and the lack of will often render such counsel impractical, distinguishing features particularly in the initial period following admission when infectivity is likely to be greatest. Rifampicin prophylaxis is recommended for children with H. injluenzae type b disease to prevent secondary spread within households and repeated episodes of disease in the same individual.3,4 It may also have a place in the control of hospital epidemics, particularly when they involve long-stay paediatric units where the degree of contact between patients may be equivalent to the household setting. The potential role of rifampicin prophylaxis when spread occurs on adult wards is less clear, especially as carriage rates in contacts have been low in all the cases so far described. Another control measure to be considered in paediatric long-stay units is the administration of a conjugate H. injluenzae type b vaccine. In such institutions, secondary cases can arise over prolonged periods of time; for over a 6-month example, Glode et ~1.~ reported five cases of meningitis period. Significant protection is achieved in most infants 2 months after the first dose of a course of Haemophilus b/meningococcal protein conjugate.26 Infection control measures to limit the spread of non-typable H. influenzae have included isolation or cohort nursing, exclusion of staff shown to be carriers of the epidemic strain, removal of a point source, chemotherapy of infected patients and isolation of readmissions until screening swabs have been shown to be negative for the epidemic strain. More information is needed to clarify whether nosocomial spread of non-typable H. influenzae is more common than the few outbreaks of easily recognizable strains might imply. If it is, the problem needs to be further defined in terms of the morbidity and mortality it causes, and the likely mechanisms of spread, before appropriate preventive measures can be confidently recommended. A. J. Howard
Ysbyty Gwynedd
Gwynedd Bangor LL57 2PW
References 1. Glode MP, Daum RS, Goldmann DA, Leclair J, Smith A. Haemophilus influenzae type b meningitis: a contagious disease of children. Br &fed J 1990; 280: 899-901, 2. Gilbert GL, MacInnes SJ, Guise IA. Rifampicin prophylaxis for throat carriage of’
Editorial
3. 4. 5. 6. 7.
8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26.
3
Haemophilus infruenzae type b in patients with invasive disease and their contacts. Br MedJ 1991; 302: 1432-1435. American Academy of Pediatrics Committee on Infectious Diseases: revision of recommendations for use of rifampicin prophylaxis for contacts of patients with Hemophilus influenzae infection. Pediatrics 1984; 74: 301-302. Cartwright KAV, Begg NT, Hull D. Chemoprophylaxis for secondary Haemophilus injkenzae type b disease. Communicable Disease Report 1991; 1: R2-R6. Simasathien S, Duangmani C, Echeverria P. Haemophilus injluenzae type b resistant to ampicillin and chloramphenicol in an orphanage in Thailand. Lancet 1980; 2: 1214-1217. Ginsburg CM, McCracken GH, Rae S, Parke JC. Haemophilus influenzae type b disease. Incidence in a day-care center. JAMA 1977; 238: 604-607. Barton LL, Granoff DM, Barenkamp SJ. Nosocomial spread of Haemophilus izjluenzae type b infection documented by outer membrane protein subtype analysis. Pediatrics 1983; 102: 82&824. Glode MP, Schiffer MS, Robbins JB, Khan W, Battle CV, Armenta E. An outbreak of Haemophilus influenzae type b meningitis in an enclosed hospital population. Pediatrics 1976; 88: 3640. Yogev R, Lander HB, Davis AT. Effect of TMP-SMX on nasopharygeal carriage of ampicillin-sensitive and ampicillin-resistant Haemophilus influenzae type b. Pediatrics 1978; 93: 394397. Shapiro ED, Wald ER. Efficacy of rifampicin in eliminating pharyngeal carriage of Hemophilus infEuenzae type b. Pediatrics 1980; 66: 5-S. Bachrach S. An outbreak of Haemophilus injluenzae type b bacteraemia in an intermediate care hospital for children. J Hosp Infect 1988; 11: 121-126. Howard AJ, Dunkin KT, Musser JM, Palmer SR. Epidemiology of invasive disease due to Haemophilus influenzae type b in Wales. Br Med J 1991; in press. Fothergill LD, Wright J. Influenza1 meningitis. The relation of age incidence to the bactericidal power of blood against the causal organism. J Immunol 1933; 24: 2733284. Norden CW. Prevalence of bactericidal antibodies to Haemophilus influenzae type b. J Infect Dis 1974; 130: 489-494. Patterson JE, Madden GM, Krisiunas EP et al. A nosocomial outbreak of ampicillin-resistant Haemophilus injluenzae type b in a geriatric unit. J Infect Dis 1988; 157: 1002-1007. Smith PE, Stricof RL. Shayegani M, Morse DL. Cluster of Haemophilus injluenzae type b infections in adults. JAMA 1988; 260: 1446-1449. Howard AJ, Owens D, Musser JM. Cross-infection due to Haemophilus injkenzae type b in adults. J Hosp Infect 1991; 19: 7G-71. Sturm AW, Mostart, Rouing PJE, van Klingeren B, van Alphen L. Outbreak of multi-resistant non-encapsulated Haemophilus injuenzae infections in a pulmonary rehabilitation centre. Lancet 1990; 335: 214-216. Gough J, Kraak WAG, Anderson EC, Nichols WW, Slack MPE, McGhie D. Cross-infection bv non-encansulated Haemofihilus influenzae. Lancet 1990: 336: 159-160. Hekker TAM, van der Schee AC, Kempers J, Namavar F, van Alphen L. A nosocomial outbreak of amoxycillin-resistant non typable Haemophilus influenzae in a pulmonary ward. j’ Hosp Infect 1991; 19: 25-31. Barclay K, Keaney MGL, Clew E, Gray J. Multiresistant Haemophilus in3uenzae. Lancet 199Q; 335: 549. Scott GM, Thomason R, Rebec MP, Kibbler CC, Smith MD, Holton J. Outbreak of multiresistant Haemophilus influenzae infection. Lancet 1990: 335: 925. Mehtar S, Law CA.- An outbreak of P-lactamase producing Haemophilus injhenzae (biotype III) on a geriatric ward. J Hasp Infect 1980; 1: 357-358. Simon HB, Southwick FS, Moellering RC, Sherman E. Haemophilus injluenzae in hospitalized adults: current perspectives. Am J Med 1980; 69: 219-226. Peter G, Ed. In Report of the Committee on Infectious Diseases, 20th Edition. American Academy of Pediatrics, Evanston, Illinois 1986; 169-174. Ahonkhai VI, Lukacs L, Jonas LC et al. Haemophilus influenzae type b conjugate vaccine (meningococcal protein conjugate) (Pedvax HIB): Cl’ mica1 evaluation. Pediatrics 1990; 85: 6766681.
of Hospital
Infection
(1991) 19, l-3
EDITORIAL
Nosocomial
spread
of Haemophilus
influenzae
The potentially contagious nature of infections caused by Haemophilus injluenzae type b in children is well recognized.’ Carriage rates are often high in families where a case has arisen2 and guidelines have been issued for the use of rifampicin prophylaxis to prevent secondary household cases.3,4 Spread within communities of children such as orphanages’ and nurseries6 has also been described and there have been reports of cross infection in both acute7 and long-stay’-” paediatric hospitals. In this issue Howard et al. (p. 70) draw attention to the rare occurrence of spread of H. injluenzae type b amongst adult in-patients, and Hekker et al. (p. 25) to the poorly understood situation regarding hospital outbreaks of non-typable strains of H. in&enzae. In comparison with children, adult infections due to H. influenzae type b are uncommon. Over a period of three years, only 15/207 (7.2%) cases of invasive disease due to H. injkenzae type b presenting in Welsh hospitals occurred in patients over 15 years of age.12 The decline in incidence of cases with increasing age is associated with a corresponding rise in the prevalence of protective antibodies in the population. I3 However, protection can wane with advancing age and only 8% of subjects over 79 years of age were shown to have bactericidal antibodies in one study. l4 When cross-infection due to H. injluenzae type b has arisen, it has generally affected older age group patients.l’-i7 It is possible that with an increasing elderIy population, H. influenzae type b disease may become more common and the potential for hospital cross infection may rise. Most of the instances of nosocomial spread of non-typable H. influenxae have also involved adult patients, and outbreaks have been described involving respiratory,‘s2’ general medica121m22 and geriatric23 units. These infections have generally been seen in older individuals with underlying respiratory pathology predisposing to haemophilus infection. One report implicates a spirometer as a possible source of infection” and another the method of drug nebulization.*i Others have suggested person-to-person spread.‘*a2’ The extent of cross infection due to H. influenzae is impossible to judge in the absence of readily available markers of strain identity. The outbreaks referred to above have all been initially recognized by the presence of unusual antibiotic resistance patterns. Simon et aZ.24 concluded that 29% of patients with H. injluenzae pneumoniae and bronchitis and 43% of patients with respiratory tract colonization acquire the organism following admission. As most of the descriptions of cross-infection due to 0195-6701/91/090001+03
$03.00/O
0 1991 The Hospital 1
Infection
Society
2
Editorial
this organism record a worsening of clinical condition on acquisition of the organism, it is possible that the spread of H. &$uenxae in hospitals could represent a much larger clinical problem than is currently recognized. Barrier isolation and respiratory precautions have been recommended for children with invasive H. influenzae type b infections until 24 hours after initiation of effective therapy. 25 It would seem prudent to extend this advice to adults; however, the infrequency of infection in this group and the lack of will often render such counsel impractical, distinguishing features particularly in the initial period following admission when infectivity is likely to be greatest. Rifampicin prophylaxis is recommended for children with H. injluenzae type b disease to prevent secondary spread within households and repeated episodes of disease in the same individual.3,4 It may also have a place in the control of hospital epidemics, particularly when they involve long-stay paediatric units where the degree of contact between patients may be equivalent to the household setting. The potential role of rifampicin prophylaxis when spread occurs on adult wards is less clear, especially as carriage rates in contacts have been low in all the cases so far described. Another control measure to be considered in paediatric long-stay units is the administration of a conjugate H. injluenzae type b vaccine. In such institutions, secondary cases can arise over prolonged periods of time; for over a 6-month example, Glode et ~1.~ reported five cases of meningitis period. Significant protection is achieved in most infants 2 months after the first dose of a course of Haemophilus b/meningococcal protein conjugate.26 Infection control measures to limit the spread of non-typable H. influenzae have included isolation or cohort nursing, exclusion of staff shown to be carriers of the epidemic strain, removal of a point source, chemotherapy of infected patients and isolation of readmissions until screening swabs have been shown to be negative for the epidemic strain. More information is needed to clarify whether nosocomial spread of non-typable H. influenzae is more common than the few outbreaks of easily recognizable strains might imply. If it is, the problem needs to be further defined in terms of the morbidity and mortality it causes, and the likely mechanisms of spread, before appropriate preventive measures can be confidently recommended. A. J. Howard
Ysbyty Gwynedd
Gwynedd Bangor LL57 2PW
References 1. Glode MP, Daum RS, Goldmann DA, Leclair J, Smith A. Haemophilus influenzae type b meningitis: a contagious disease of children. Br &fed J 1990; 280: 899-901, 2. Gilbert GL, MacInnes SJ, Guise IA. Rifampicin prophylaxis for throat carriage of’
Editorial
3. 4. 5. 6. 7.
8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26.
3
Haemophilus infruenzae type b in patients with invasive disease and their contacts. Br MedJ 1991; 302: 1432-1435. American Academy of Pediatrics Committee on Infectious Diseases: revision of recommendations for use of rifampicin prophylaxis for contacts of patients with Hemophilus influenzae infection. Pediatrics 1984; 74: 301-302. Cartwright KAV, Begg NT, Hull D. Chemoprophylaxis for secondary Haemophilus injkenzae type b disease. Communicable Disease Report 1991; 1: R2-R6. Simasathien S, Duangmani C, Echeverria P. Haemophilus injluenzae type b resistant to ampicillin and chloramphenicol in an orphanage in Thailand. Lancet 1980; 2: 1214-1217. Ginsburg CM, McCracken GH, Rae S, Parke JC. Haemophilus influenzae type b disease. Incidence in a day-care center. JAMA 1977; 238: 604-607. Barton LL, Granoff DM, Barenkamp SJ. Nosocomial spread of Haemophilus izjluenzae type b infection documented by outer membrane protein subtype analysis. Pediatrics 1983; 102: 82&824. Glode MP, Schiffer MS, Robbins JB, Khan W, Battle CV, Armenta E. An outbreak of Haemophilus influenzae type b meningitis in an enclosed hospital population. Pediatrics 1976; 88: 3640. Yogev R, Lander HB, Davis AT. Effect of TMP-SMX on nasopharygeal carriage of ampicillin-sensitive and ampicillin-resistant Haemophilus influenzae type b. Pediatrics 1978; 93: 394397. Shapiro ED, Wald ER. Efficacy of rifampicin in eliminating pharyngeal carriage of Hemophilus infEuenzae type b. Pediatrics 1980; 66: 5-S. Bachrach S. An outbreak of Haemophilus injluenzae type b bacteraemia in an intermediate care hospital for children. J Hosp Infect 1988; 11: 121-126. Howard AJ, Dunkin KT, Musser JM, Palmer SR. Epidemiology of invasive disease due to Haemophilus influenzae type b in Wales. Br Med J 1991; in press. Fothergill LD, Wright J. Influenza1 meningitis. The relation of age incidence to the bactericidal power of blood against the causal organism. J Immunol 1933; 24: 2733284. Norden CW. Prevalence of bactericidal antibodies to Haemophilus influenzae type b. J Infect Dis 1974; 130: 489-494. Patterson JE, Madden GM, Krisiunas EP et al. A nosocomial outbreak of ampicillin-resistant Haemophilus injluenzae type b in a geriatric unit. J Infect Dis 1988; 157: 1002-1007. Smith PE, Stricof RL. Shayegani M, Morse DL. Cluster of Haemophilus injluenzae type b infections in adults. JAMA 1988; 260: 1446-1449. Howard AJ, Owens D, Musser JM. Cross-infection due to Haemophilus injkenzae type b in adults. J Hosp Infect 1991; 19: 7G-71. Sturm AW, Mostart, Rouing PJE, van Klingeren B, van Alphen L. Outbreak of multi-resistant non-encapsulated Haemophilus injuenzae infections in a pulmonary rehabilitation centre. Lancet 1990; 335: 214-216. Gough J, Kraak WAG, Anderson EC, Nichols WW, Slack MPE, McGhie D. Cross-infection bv non-encansulated Haemofihilus influenzae. Lancet 1990: 336: 159-160. Hekker TAM, van der Schee AC, Kempers J, Namavar F, van Alphen L. A nosocomial outbreak of amoxycillin-resistant non typable Haemophilus influenzae in a pulmonary ward. j’ Hosp Infect 1991; 19: 25-31. Barclay K, Keaney MGL, Clew E, Gray J. Multiresistant Haemophilus in3uenzae. Lancet 199Q; 335: 549. Scott GM, Thomason R, Rebec MP, Kibbler CC, Smith MD, Holton J. Outbreak of multiresistant Haemophilus influenzae infection. Lancet 1990: 335: 925. Mehtar S, Law CA.- An outbreak of P-lactamase producing Haemophilus injhenzae (biotype III) on a geriatric ward. J Hasp Infect 1980; 1: 357-358. Simon HB, Southwick FS, Moellering RC, Sherman E. Haemophilus injluenzae in hospitalized adults: current perspectives. Am J Med 1980; 69: 219-226. Peter G, Ed. In Report of the Committee on Infectious Diseases, 20th Edition. American Academy of Pediatrics, Evanston, Illinois 1986; 169-174. Ahonkhai VI, Lukacs L, Jonas LC et al. Haemophilus influenzae type b conjugate vaccine (meningococcal protein conjugate) (Pedvax HIB): Cl’ mica1 evaluation. Pediatrics 1990; 85: 6766681.
