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NAME: Haemophilus influenzae (type b)

SYNONYM OR CROSS REFERENCE: Hib, meningitis, Haemophilus meningitis , childhood pneumonia, bacteremia, epiglottitis, septic arthritis, cellulitis, osteomyelitis, pericarditis, bacterial meningitis, Pfeiffer's bacillus(Footnote 1,Footnote 2,Footnote 3,Footnote 4).

CHARACTERISTICS: Haemophilus influenzae type b (Hib) is a gram negative coccobaccilus(Footnote 5). This respiratory tract membrane obligate parasite requires hemin (X-factor) and NAD (V- factor) for in vitro growth. Hib is non motile and non acid-fast. Hib is aerobic(Footnote 6), but also able to grow in facultative anaerobic conditions(Footnote 5). H.influenzea are classified into six antigenically distinct serotypes (a to f) based on capsular polysaccharide antigen. One such antigen is polyribosyl-ribitol phosphate (PRP) and this antigen characterizes serotype b(Footnote 3). Three biochemical tests (indole, urease, and ornithine decarboxylase) subdivide H.influenzea into 8 biotypes(Footnote 5). Although most Hib strains belong to biotype I and II, standard Hib strains, which belong to biotype VI, also exist.


PATHOGENICITY/TOXICITY: Infection with Haemophilus influenzae (type b) can cause meningitis (50% of all cases - adults and children), epiglottitis (17%), pneumonia (15%), septic arthritis (8%), cellulitis (6%), osteomyelitis (2%), or generalized bacteremia (2%)(Footnote 6). A small proportion of children (0.5-3%) children will have asymptomatic infections.

Meningitis may begin as minor upper respiratory infection(Footnote 3). Symptoms include behavioural or mental status change, fever, vomiting, headaches, and signs of meningeal irritation such as bulging fontanelle in infants, or stiff neck in older children or adults. In adults, complete recovery is common with treatment(Footnote 7), but for children there is a 2-5% mortality rate, even with treatment. Sequelae such as hearing loss, mental retardation, seizures, vision loss, and motor and speech delay may develop in 15-30% of cases(Footnote 3).

Epiglotitis is an acute infection of the upper airway that causes oedema and inflammation of the epiglottis and adjacent tissues and may lead to complete airway obstruction in hours(Footnote 3). Symptoms include severe sore throat and fever. Speaking, swallowing or breathing may be impaired and respiration may be noisy. To assist with breathing, patients may adopt a tripod or sniffing posture. Airways obstruction results in a 5-10% mortality rate.

Cellulitis often affects the face, head or neck(Footnote 3). Cellulitis causes localized tissue inflammation and may lead to proptosis, loss of visual acuity, limitation of extraoccular movement and death. 12-25% of affected children may have concomitant meningitis.

Other illnesses associated with infection include pneumonia (pulmonary infection with purulent excretion), osteomyelitis (bone infection), septic arthritis (joint infection) and pericaditis (infection of the pericardial membrane surrounding the heart)(Footnote 3).

EPIDEMIOLOGY: In the prevaccine era, 1 in 200 children under 5 years developed Hib related illnesses, especially between 6 and 12 months(Footnote 3). Following vaccine introduction in 1986(Footnote 8), the incidence declined by 97%(Footnote 3). Currently, Hib is more prevalent in developing countries, and aboriginal peoples are more at risk(Footnote 2). Adult cases are rare and sickness is usually concomitant with another immunosuppressive state(Footnote 9). A bimodal seasonal pattern of infection, peaking in September/December and March/May has been observed for meningitis(Footnote 10).

HOST RANGE: Hib is a human obligate parasite(Footnote 5).


MODE OF TRANSMISSION: Respiratory droplet transmission as well as via contact with discharge from nose and throat during infectious periods. The portal of entry is most commonly the nasopharynx(Footnote 11).

INCUBATION PERIOD: 2 - 4 days(Footnote 12)

COMMUNICABILITY: Hib is not highly contagious(Footnote 6). Secondary infection may occur in the case of particularly close contact with patients. Not communicable 48 h after initiation of efficient antibiotic treatment(Footnote 13).


RESERVOIR: Humans are the only known reservoir(Footnote 3).

ZOONOSIS: None(Footnote 2)

VECTORS: None(Footnote 2)


DRUG SUSCEPTIBILITY: Hib is susceptible to chloramphenicol and third generation cephalosporins (e.g. cefotaxime, ceftriaxone, and cefuroxime)(Footnote 3).

DRUG RESISTANCE: Resistance has been shown for ampicillin, co-trimoxazole, clarithromycin, tetracycline, chloramphenicol, and rifampicin(Footnote 14).

SUSCEPTIBILITY TO DISINFECTANTS: Phenolic disinfectants, 1% sodium hypochlorite, 70% ethanol, formaldehyde, glutaraldehyde, iodophore and peracedic acid are effective against Hib(Footnote 15).

PHYSICAL INACTIVATION: Hib is inactivated by UV(Footnote 16), microwave(Footnote 17), and gamma(Footnote 18) radiation, moist heat (121°C for at least 20 min(Footnote 19)), and dry heat (165-170°C for 2 h).

SURVIVAL OUTSIDE HOST: Hib does not survive long term in the environment(Footnote 6), but can survive more than 18 hrs in mucous and 12 hrs on plastic (Footnote 20).


SURVEILLANCE: Monitor for symptoms. Diagnosis is most often confirmed by bacterial culture(Footnote 3). Newer techniques include detection of the PRP polysaccharide by latex agglutination or countercurrent immunoelectrophoresis and PCR.

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: The primary treatment for Hib is appropriate antibiotics(Footnote 3). Intravenous antibiotics are often required but depending on illness, oral administration may follow for 7-10 days. If airways are blocked, more invasive procedures may be indicated.

IMMUNIZATION: Currently, vaccination targets the PRP antigen and is effective for Hib but not other Haemophilus influenzae serotpyes(Footnote 21). Vaccine is usually given between 2 months and five years of age.

PROPHYLAXIS: Rifampin prophylaxis is indicated for direct contacts, as directed by a doctor(Footnote 3). Pregnant women should not receive prophylactic treatment.


LABORATORY-ACQUIRED INFECTIONS: There are 5 cases of laboratory acquired infections(Footnote 22).

SOURCES/SPECIMENS: Bacteria may be in the cerebrospinal fluid, serum, urine(Footnote 3), blood, pleural fluid, joint fluid and middle ear aspirates(Footnote 6).

PRIMARY HAZARDS: LAIs are caused by inhalation(Footnote 22), autoinoculation(Footnote 23) or ingestion.



RISK GROUP CLASSIFICATION: Risk Group 2(Footnote 24)

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, and cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes(Footnote 25).

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, or other sharp objects should be strictly limited(Footnote 25). Additional precautions should be considered with work involving animals or large scale activities(Footnote 25).


SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (30 min)(Footnote 25).

DISPOSAL: All material should be decontaminated before disposal with steam sterilization, incineration or chemical disinfection(Footnote 25).

STORAGE: Samples and biological material should be store in appropriately labelled sealed containers(Footnote 25).


REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: July 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©
Public Health Agency of Canada, 2010


Footnote 1
Tristram, S., Jacobs, M. R., & Appelbaum, P. C. (2007). Antimicrobial resistance in Haemophilus influenzae. Clinical Microbiology Reviews, 20 (2), 368-389. doi:10.1128/CMR.00040-06
Footnote 2
Ulanova, M., & Tsang, R. S. (2009). Invasive Haemophilus influenzae disease: changing epidemiology and host-parasite interactions in the 21st century. Infection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases, 9 (4), 594-605. doi:10.1016/j.meegid.2009.03.001
Footnote 3
Burns, I. T., & Zimmerman, R. K. (2000). Haemophilus influenzae type B disease, vaccines, and care of exposed individuals. The Journal of Family Practice, 49 (9 Suppl), S7-13; quiz S14.
Footnote 4
PACE, G. (1952). Two cases of meningitis due to Pfeiffer bacillus treated with chloramphenicol. [Su due casi di meningite da bacillo di Pfeiffer trattati con cloroanfenicolo] Sicilia Sanitaria, 5 (11), 625-630.
Footnote 5
Kilian, M. (2007). haemophilus. In P. R. Murray, Baron E.J., J. H. Jorgensen, M. L. Landry & M. A. Pfaller (Eds.), Manual of clinical microbiology (9th ed., pp. 636). Washington, DC: ASM Press.
Footnote 6
Center for Disease Control and Prevention. (2009). Haemophilus influenzae . In W. Atkinson, S. Wolfe, J. Hamborsky & L. McIntyre (Eds.), Epidemiology and prevention of vaccine- preventable diseases (11th ed., pp. 71-83). Washington D.C.: Public Health Fondation.
Footnote 7
Tang, L., Chen, S., & Wu, Y. (1998). Haemophilus influenzae meningitis in adults. Diagnostic Microbiology and Infectious Disease, 32 (1), 27-32. doi:DOI: 10.1016/S0732- 8893(98)00061-3
Footnote 8
Greenberg, D. P., Doemland, M., Bettinger, J. A., Scheifele, D. W., Halperin, S. A., IMPACT Investigators, Waters, V., & Kandola, K. (2009). Epidemiology of pertussis and Haemophilus influenzae type b disease in Canada with exclusive use of a diphtheria-tetanus- acellular pertussis-inactivated poliovirus-Haemophilus influenzae type b pediatric combination vaccine and an adolescent-adult tetanus-diphtheria-acellular pertussis vaccine: implications for disease prevention in the United States. The Pediatric Infectious Disease Journal, 28 (6), 521-528. doi:10.1097/INF.0b013e318199d2fc
Footnote 9
Farley, M. M., Stephens, D. S., Harvey, R. C., Sikes, R. K., & Wenger, J. D. (1992). Incidence and clinical characteristics of invasive Haemophilus influenzae disease in adults. CDC Meningitis Surveillance Group. The Journal of Infectious Diseases, 165 Suppl 1 , S42-3.
Footnote 10
Theodoridou, M. N., Vasilopoulou, V. A., Atsali, E. E., Pangalis, A. M., Mostrou, G. J., Syriopoulou, V. P., & Hadjichristodoulou, C. S. (2007). Meningitis registry of hospitalized cases in children: epidemiological patterns of acute bacterial meningitis throughout a 32- year period. BMC Infectious Diseases, 7 , 101. doi:10.1186/1471-2334-7-101
Footnote 11
Heymann, D. L. (2008). Control of Communicable Diseases Manual (19th Edition ed.). Washington, D.C.: American Public Health Association.
Footnote 12
Weber, R. (2005). Communicable disease epidemiology and control: a global perspective (2nd ed.) CABI publishing.
Footnote 13
Hawker, J., Begg, N., Blair, L., Reintjes, R., & Weinberg, J. (2005). In Khan M., Bonnett C. and Pattinson F. (Eds.), Communicable Disease Control Handbook (2nd ed.). New Delhi: Blackwell Publishing Ltd.
Footnote 14
Campos, J., Roman, F., Perez-Vazquez, M., Aracil, B., Oteo, J., Cercenado, E., & Spanish Study Group for H. influenzae type f. (2003). Antibiotic resistance and clinical significance of Haemophilus influenzae type f. The Journal of Antimicrobial Chemotherapy, 52 (6), 961- 966. doi:10.1093/jac/dkh004
Footnote 15
Collins, C. H., & Kennedy, D. A. (1999). Decontamination. Laboratory-Acquired Infections: History, Incidence, Causes and Prevention. (4th ed., pp. 160-186). London, UK: Buttersworth.
Footnote 16
Katara, G., Hemvani, N., Chitnis, S., Chitnis, V., & Chitnis, D. S. (2008). Surface disinfection by exposure to germicidal UV light. Indian Journal of Medical Microbiology, 26 (3), 241-242.
Footnote 17
Wu, Y., & Yao, M.Inactivation of bacteria and fungus aerosols using microwave irradiation. Journal of Aerosol Science, In Press, Corrected Proof doi:DOI: 10.1016/j.jaerosci.2010.04.004
Footnote 18
Farkas, J. (1998). Irradiation as a method for decontaminating food. A review. International Journal of Food Microbiology, 44 (3), 189-204.
Footnote 19
Csucos, M., & Csucos, C. (1999). Microbiological obseration of water and wastewater . United States: CRC Press.
Footnote 20
Smith-Vaughan, H., Crichton, F., Beissbarth, J., Morris, P. S., & Leach, A. J. (2008). Survival of pneumococcus on hands and fomites. BMC Research Notes, 1 , 112. doi:10.1186/1756-0500-1-112
Footnote 21
Public Health Agency of Canada. (2006). Active immunizing agent. Canadian immunization guide (7th ed., pp. 248-349) Minister of Public Works and Government Services Canada.
Footnote 22
Collins, C. H., & Kennedy, D. A. (1999). Laboratory acquired infections. Laboratory acquired infections: History, incidence, causes and prevention (4th ed., pp. 1-37). Woburn, MA: BH.
Footnote 23
Jacobson, J. T., Orlob, R. B., & Clayton, J. L. (1985). Infections acquired in clinical laboratories in Utah. Journal of Clinical Microbiology, 21 (4), 486-489.
Footnote 24
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).
Footnote 25
Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.