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Invasive Pneumococcal Disease

Queensland Health Guidelines for Public Health Units

Revision History

1.0 February 2010  Full revision of guideline. 
2.0 June 2018 Full revision of guideline.

Infectious Agent

The bacterium Streptococcus pneumoniae (also referred to as pneumococcus). More than 90 different serotypes of S. pneumoniae, based upon differences in the capsular polysaccharides, have been identified [1].

Notification Criteria

Laboratory Definitive Evidence

  1. Isolation of S. pneumoniae from a normally sterile site

  2. Detection of S. pneumoniae from a normally sterile site by nucleic acid testing.

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Notification Procedure

Pathology Laboratories

To notify on confirmation of diagnosis by usual means.

Reporting to NOCS

Report only confirmed cases.

Confirmed case:

A confirmed case requires laboratory definitive evidence only.

Objectives of surveillance

To define the epidemiology of invasive pneumococcal disease (IPD) in Queensland (in particular, to monitor the impact of vaccines upon the burden of IPD).

Community outbreak criteria

An increase in the expected number of cases of the same serotype of S. pneumoniae in a defined population.

Public Health Significance and Occurrence

S. pneumoniae is a leading cause of bacterial pneumonia, meningitis, and sepsis worldwide. The highest incidence of IPD occurs in young children and in the elderly [2].

Since the introduction of the first conjugate pneumococcal vaccine in 2000 (PCV7), global reductions in disease burden in children younger than 5 years of age have been observed. The number of deaths attributable to pneumococcal disease has halved since 2000 among HIV negative children younger than 5 years of age, from approximately 600,000 to 294,000 deaths in 2015. Despite these reductions, pneumococcal disease burden remains high, particularly in low income countries. Pneumonia, from all causes, accounts for approximately 16% of childhood deaths in low and middle-income countries, compared to 5% in high income countries; S. pneumoniae is a leading cause of these pneumonia deaths [3].

Groups at increased risk for serious IPD include individuals at the extremes of age (particularly aged younger than 2 years and 65 years and older), those with underlying organ dysfunction (asplenia, splenic dysfunction, chronic heart, lung, liver, and kidney disease) and immunocompromising conditions (HIV infection, antibody defects, complement deficiencies, neutropenia, and malignancies) [2]. Other conditions that increase risk of IPD are smoking cigarettes or exposure to second-hand smoke, cerebrospinal fluid leak, and having a cochlear implant [4]. In Australia, the incidence of IPD in Aboriginal and Torres Strait Islander people remains several-fold greater than that in non-Indigenous people [5].

IPD outbreaks, caused by the same serotype of S. pneumoniae are very uncommon but are well-recognised. IPD outbreaks have occurred among adults in crowded living conditions (e.g. military camps, prisons, shelters for the homeless and residential aged care facilities) [2], childcare centres [6], and in marginalised groups within the broader population (eg. in remote Aboriginal communities) [5].

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Clinical Features

S. pneumoniae frequently colonises the nasopharynx and from there pneumococci can spread directly via the airway to the lower respiratory tract, causing pneumonia, or to the sinuses or middle ears [7]. Common manifestations of non-invasive pneumococcal disease include middle ear infections, sinusitis and bronchitis [8]. Following nasopharyngeal carriage and contiguous spread of disease to other sites in the respiratory tract, progression to pneumonia requires additional factors (e.g viral infection, lung injury, impaired host defences, etc) [9].

Invasive pneumococcal disease (IPD) is defined by the isolation of S. pneumoniae from a usually sterile site; most often from blood, but also from CSF, joint aspirate etc. The commonest manifestations of IPD are pneumonia with bacteraemia, empyema and/or bacteraemia, and meningitis [8]. Although S. pneumoniae is a frequent cause of non-bacteraemic pneumonia, pneumonia without bacteraemia or empyema is not invasive disease [8,10]. In developing countries, non-bacteraemic pneumonia causes the majority of pneumococcal deaths in children [8]. Bacteraemia without a known site of infection is the most common manifestation of IPD in children younger than 2 years of age [10].

Signs and symptoms of pneumococcal pneumonia include fever and chills or rigors. Other signs and symptoms include pleuritic chest pain, cough productive of mucopurulent sputum, dyspnoea, tachypnoea, hypoxia, tachycardia, malaise, and weakness. Nausea, vomiting, and headache occur less frequently.

Complications of pneumococcal pneumonia include empyema, pericarditis, and endobronchial obstruction, with atelectasis and lung abscess formation. Pneumococcal pneumonia has been demonstrated to complicate influenza infection [4].

Pneumococcal meningitis has similar clinical symptoms, cerebrospinal fluid profile, and neurologic complications to other forms of purulent bacterial meningitis. Signs and symptoms may include headache, lethargy, vomiting, irritability, fever, neck stiffness, cranial nerve signs, seizure, and coma. Neurologic sequelae are common among survivors [4].

Fulminant pneumococcal infection presents with a rapidly progressive clinical course and is more common in patients with asplenia or immunocompromise, although it can occur in non-immunocompromised individuals [11]. Features of fulminant IPD include sepsis, purpura fulminans, and Waterhouse-Friderichsen syndrome [12].


Humans. Pneumococci are commonly carried asymptomatically in the upper respiratory tract of healthy people worldwide.

Mode of Transmission

Transmissibility of pneumococcal bacteria is not fully understood, however, pneumococcal disease is not generally regarded as highly contagious [2]. Transmission occurs through respiratory droplets from people with pneumococcal disease or more commonly, healthy individuals who carry the organism in their nasopharynx [13]. Modes of transmission include droplet spread, direct oral contact, or indirectly though articles freshly soiled with respiratory discharges (including fingers and hands).

There are many healthy, asymptomatic carriers of S. pnemoniae [8]. Person to person transmission of the organisms is common, but illness among casual contacts and attendants is infrequent.

Incubation Period

Unknown; probably short, 1 – 4 days.

Period of Communicability

The period of communicability for pneumococcal disease is unknown, but presumably transmission can occur as long as the organism appears in respiratory secretions [14]. Discharges from the nose and mouth usually no longer contain infectious numbers of pneumococci within 24 hours of initiation of effective antibiotic therapy [15].

Susceptibility and Resistance

Susceptibility is general and disease may occur in persons susceptible to the serotype involved. In otherwise immunocompetent adults, the incidence of IPD is increased with alcohol abuse, congestive heart failure, chronic lung disease, cigarette smoking, asthma, recent influenza infection, diabetes mellitis, institutionalisation, neurological disorders, and men [9]. Among immunocompetent, non-elderly adults, cigarette smoking is the strongest independent risk factor for IPD. Cigarette smoke impairs mucociliary clearance, enhances bacterial adherence, and disrupts the respiratory epithelium [16].

Colonisation with specific serotypes may elicit serotype-specific antibodies. While protection is serotype-specific, cross protection is found in some cases. In addition to anticapsular antibodies (whether acquired naturally or by vaccination), other factors are also involved in eradicating pneumococci, including anatomical barriers, cilia, and other immune processes [9].

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All cases of IPD in children younger than 5 years of age should have any predisposing risk factors (including Indigenous status and passive smoking) and vaccination history recorded on the case report form.

If there is adequate capacity (within a PHU), the above details should be obtained for other IPD cases, giving priority to those age groups eligible for funded pneumococcal vaccination.


Exclusion from work, school or childcare is not necessary. The person can return when he or she feels well.

Standard and droplet transmission-based precautions are recommended:

Pneumococcal infection is spread via respiratory droplets as noted above. In hospital and residential care settings, the infected person should be cared for in a single room using droplet transmission-based precautions in the first 24 hours after commencing appropriate antibiotic treatment. Where single rooms are unavailable, cohorting of cases should be implemented.

The importance of infection control should be reinforced to protect at-risk individuals, for example, in residential aged care. Hand hygiene (washing hands with soap and water or using alcohol-based hand rub) should always be performed after coughing, sneezing, or using tissues. Education should be provided about respiratory etiquette, including use of a tissue or the arm when coughing or sneezing. Used tissues should be disposed immediately into the bin and hand hygiene should immediately follow.


Contact Tracing

Because secondary cases of IPD are uncommon, chemoprophylaxis is not indicated for contacts of patients with such infection [17].

Other Control Measures

IPD may occur as a result of multiple factors, including genetic factors, comorbidities, overcrowding, hygiene conditions, nutrition, poverty, and vaccine uptake. Most of these factors are very difficult to change. Vaccines are the most cost-effective way to prevent IPD and to reduce disparities in IPD rates between populations worldwide [18]. See prevention measures below.

Outbreak Control Measures

The epidemiology of an outbreak of IPD within a facility or community should be defined, including the implicated serotype. Vaccination is not likely to be useful in acute control but may be considered if the implicated serotype is contained in the available vaccine. Chemoprophylaxis is generally not indicated. Enhanced infection control should form the mainstay of the response to the outbreak.

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Preventive Measures

The pneumococcal vaccine is the main form of prevention. Yearly influenza vaccination is also important because the flu increases pneumococcal disease risk [17].

For recommendations on the use of pneumococcal vaccines, see the current Australian Immunisation Handbook.

It is particularly important that anyone with hyposplenia or asplenia – either functional or anatomical – is adequately vaccinated against pneumococcal and other invasive bacterial diseases.

For further details on the Spleen Australia Registry, see .

Literature and registry data indicate that being on a spleen registry reduces the risk of invasive pneumococcal disease and meningococcal disease by 69% compared to patients not registered [19]. To reduce the risk for people living without a functioning spleen, Queensland Health engages Spleen Australia to maintain a state-wide registry and provide a range of clinical support services, free of charge, to eligible Queenslanders and their doctors.


Report to notifying agency.


Prepare a summary report of the investigation for the Communicable Diseases Branch, Queensland Health, on request.


  1. Geno KA, Gilbert GL, Song JY, Skovsted IC, Klugman KP, Jones C, et al. Pneumococcal capsules and their types: past, present and future. Clinical Microbiology Reviews 2015; 28(3): 871–899
  2. Janoff EN, Musher DM. Streptococcus pneumoniae. In: Bennett J, Dolin R, Blaser MJ. Mandell, Douglas and Bennett’s Principals and Practice of Infectious Diseases, 8th edition. Philadelphia: Elsevier Saunders 2015; p 2309–2327
  3. World Health Organization. Executive summary: SAGE October 2017, pneumococcal conjugate vaccine session [online]. Geneva: World Health Organization. Available from URL: [cited November 2017]
  4. Centers for Disease Control and Prevention. Pneumococcal Disease [online]. In: CDC. Epidemiology and prevention of vaccine-preventable diseases: the pink book: course textbook, 13th edition. CDC: Atlanta 2015; p 279–296. Available from URL: [cited November 2017]
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  10. Centers for Disease Control and Prevention. Pneumococcal disease: clinical features [online]. CDC 2017 [cited November 2017]. Available from URL:
  11. Natio R, Miyazaki T, Kajino K, Daida H. Fulminant pneumococcal infection. BMJ Case Reports 2014, doi: 10.1136/bcr-2014-205907
  12. Hale AJ, LaSalvia M, Kirby JE, Kimball A, Baden R. Fatal purpura fulminans and Waterhouse-Friderichsen syndrome from fulminant Streptococcus pneumoniae sepsis in a young asplenic adult. ID cases 2016; 6: 1–4, doi: 10.1016/j.idcr.2016.08.004
  13. Donkor ES. Understanding the pneumococcus: transmission and evolution. Frontiers in Cellular and Infection Microbiology 2013; 3:7, doi:  10.3389/fcimb.2013.00007
  14. Centers for Disease Control and Prevention. Pneumococcal disease: transmission [online]. CDC 2017 [cited November 2017]. Available from URL:
  15. Heymann DL (ed). Control of communicable diseases manual, 20th ed. Washington: American Public Health Association 2015, p 465–469
  16. Nuorti JP, Butler JC, Farley MM, Harriosn LH, McGeer A, Kolczak MS, et cal. Cigarette smoking and invasive pneumococcal disease. New England Journal of Medicine 2000; 342: 681–689
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  19. Arnott A, Jones P, Franklin L, Bunn C, Mcnamara J, Pratt N, et al. A registry for patients with asplenia/hyposplenism reduces the risk of infections with encapsulated organisms: time for a national registry? [internet]. Alfred Health Week Research Poster Display 23–27 October 2017 [cited November 2017]. Available from URL:

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Last updated: 20 June 2018