Control guideline for public health units

Public health priority: Urgent.

PHU response time: Respond to any report of meningococcal disease on day of notification. Enter probable and confirmed cases on NCIMS within 1 working day and enter serogrouping results within 1 working day.

NSW Public Health Units should follow the National CDNA Guidelines for public health units, in the investigation, management and follow up of cases and contacts of meningococcal disease.​

Version​ ​Date Revised by ​​ Changes​ Approval​​
1.0​ July 2014​​ Developed by the IMD SoNG Working Group​ ​CDNA
​1.1 ​April 2015 Updated reference to Therapeutic Guidelines: Antibiotic 2014 ​CDNA
1.2​ ​Feb 2017 Communicable Diseases Branch​​ ​Alteration to Section 3 Vaccination​ refer to Immunisation Handbook ​​
​1.3 ​Feb 2018 CDNA Document updated for currency. A new section added with a description of available and funded vaccines and new reference to the fact that schedules change. Specific advice on vaccination for confirmed IMD cases, and for higher-risk contacts eligible for vaccination added. CDNA​
1.4​​ ​Aug 2020 ​Communicable Diseases Branch Alteration to section 3 Vaccination to provide detail of changes to funding from July 2020 ​A/Director CDB
Last updated: 06 August 2020
  1. Summary
  2. The disease
  3. Routine prevention activities
  4. Surveillance objectives
  5. Data management
  6. Communications
  7. Case definition
  8. Laboratory testing
  9. Case management
  10. Control of environment
  11. Contact management
  12. Special situations
  13. References
  14. Appendices

1. Summary

Public health priority


Case management

Isolate case and practise standard and droplet precautions for 24 hours after initiation of appropriate antibiotic treatment. Exclude from child-care, school, other educational institution or work until 24 hours of antibiotics completed.

Contact management

Provide information to identified contacts and urgently arrange for clearance antibiotics to be given to eligible higher-risk contacts. Vaccination is advised for eligible higher-risk contacts if case confirmed to be caused by some vaccine preventable serogroups (A, C, W or Y).

2. The disease

Infectious agents

Neisseria meningitidis is a Gram-negative diplococcus. There are 13 serogroups of N.meningitidis, with six serogroups (A, B, C, W, X and Y) accounting for the majority of cases of invasive meningococcal disease (IMD) worldwide.[1] From 2002 to 2015 the predominant meningococcal serogroup in Australia was serogroup B.[2] Notifications of serogroup W (MenW) increased nearly five-fold between 2014 and 2016, and in 2016, MenW was the predominant meningococcal serogroup notified in Australia.[3]


N. meningitidis is a commensal of humans, the only natural host. The bacteria normally colonise the mucosa of the upper respiratory tract without causing disease. The mean duration of carriage, in settings where prevalence is stable, has been estimated as about 21 months.[4] The carriage rate varies from around 3–25 percent of the population, depending primarily on age.[5] In European and North American studies carriage rates have been shown to be very low in the first years of life and then to sharply increase in teenagers, reaching a maximum in those aged between 20 and 24 years.[6] Meningococcal carriage is also associated with male gender, coincident viral or bacterial respiratory tract infections, low socio-economic status, smoking, frequency of intimate kissing and the number and closeness of social contacts.[6,7]

Mode of transmission

Transmission is primarily by respiratory droplets from the upper respiratory tract. Saliva has been shown to inhibit the growth of meningococci and salivary contact (e.g. by sharing drink bottles) is not considered to be a significant means of transmission.[8]

Incubation period

Usually from 1 to 7 days (rarely up to 10 days). Individuals who become asymptomatic carriers of meningococci are very unlikely to develop IMD.[1]

Infectious period

Until the organisms are no longer present in discharges from the nose and throat. With effective antibiotic therapy meningococci usually disappear from the nasopharynx within 24 hours.[9]

Clinical presentation and outcome

Invasive infections due to N. meningitidis can present as a spectrum of clinical illness, with meningitis and septicaemia, or a combination of the two, being the most common. Disease expression can also include pneumonia, septic arthritis, epiglottitis, pericarditis, gastrointestinal symptoms, conjunctivitis and urethritis.[10] Meningococcal meningitis typically presents with fever, meningeal signs (e.g. headache, neck stiffness, photophobia) and altered mental status.[10]

Septicaemia, with or without meningitis, can have a fulminant and rapidly fatal course (sometimes less than 24 hours) with initial symptoms that are nonspecific (e.g. fever, muscle aches, vomiting), especially in children.[11] The septicaemic form can be difficult to diagnose before the onset of the characteristic haemorrhagic (i.e. petechial or purpuric) rash that does not blanch under pressure. Appearance of a rash can be relatively late (median onset 13-22 hours) [12] or there may be no rash at all. Additionally, in the early stages of illness there is sometimes a maculopapular rash that blanches under pressure. This rash may progress to become haemorrhagic and non-blanching or may fade away.[13]

Leg pain, cold extremities, and abnormal skin colour – described as pallor or mottling – are frequently reported in the first 12 hours of meningococcal disease (median onset 7-12 hours), particularly in children and adolescents.[12]

Infrequently, chronic meningococcal septicaemia can also occur.

Overall mortality for IMD is approximately 5-10 percent of infected individuals.[14] An increase in case fatality rate (CFR) has been associated with a range of factors, including age,[15,16] the N. meningitidis serogroup,[17,18] concurrent HIV infection[19] and whether cases are associated with an outbreak.[20] Most deaths occur in the first 24 hours[21] and early diagnosis and treatment is associated with reduced CFR.[22,23]

Long term sequelae affect 10-20 percent of recovered IMD cases, including deafness, other neurological deficits, skin loss requiring grafts and partial or full amputation of limbs.[1]

People at increased risk of disease

Transmission from a symptomatic case is uncommon – the vast majority of cases are sporadic with transmission assumed to have occurred from prolonged close contact with an asymptomatic carrier in the network of close contacts.

Household contacts

The contacts most at risk of meningococcal disease are other members of the household of a case of IMD, during the first week after the case is detected.[24] Studies carried out in Europe and America before the routine use of clearance antibiotics showed that household contacts of a case of IMD had a 500 to 800-fold greater risk of meningococcal disease than the general population.[24,25] The risk was highest in the first week after onset of illness in the case and fell rapidly thereafter.[24]

Intimate contacts

The frequency of intimate kissing, involving close contact with respiratory droplets from the nasopharynx, increases the risk of both carriage [7,26] and disease.[27,28] However, contact with saliva per se, such as through sharing drinks or superficial mouth kissing, is not thought to significantly increase risk of carriage or disease. [8]

Child-care contacts

There is limited evidence in favour of providing clearance antibiotics to child-care contacts of sporadic cases of IMD. A Belgian study found that the relative risk of secondary IMD among day-care (aged under three years) and pre-school contacts (aged two to five years) was much less than that for similarly aged household contacts of an index case.[24] A British study of pre-school settings (including day care, play-groups and other pre-school groups) (most were aged less than four years) found that the relative risk of a cluster of cases in pre-school in the four weeks after an index case was 27.6 and the absolute risk was 49/100,000 contact children.[29]

School and university contacts

United States (US) and United Kingdom (UK) studies have demonstrated a modestly increased risk of further cases in schools attended by index cases.[30,31] However, subsequent cases do not necessarily occur in the same classroom as the index case, with others occurring, for example, in contacts who share extracurricular activities with index cases.[30] In the US the relative risk of further cases among school students (5-18 years of age) was 2.3.[30]

Healthcare workers and others with close contact with a case after onset of symptoms

Even though transmission from a symptomatic case is uncommon there is, however, a small increased risk of disease in people who have very close contact with a symptomatic case prior to completion of 24 hours of antibiotic therapy. Those healthcare workers who have unprotected close airway exposure to large particle respiratory droplets (e.g. during airway management) from a case of IMD around the time of admission, are at increased risk of disease in the 10–day period after exposure.[32] However, the risk is very low; in one study absolute risk was estimated to be 0.8/100,000,[33] far below the risk in household contacts.

Other groups/individuals at higher risk

Laboratory personnel who work with N. meningitidis are at increased risk of IMD.[34,35] Other risk factors for IMD include congenital or acquired immunoglobulin deficiencies and complement deficiencies, anatomic or functional asplenia, travel to or residence in countries where meningococcal disease is hyperendemic or epidemic,[36] exposure to cigarette smoke,[37,38] concurrent respiratory tract infections[39,40] and crowded living conditions or recreation spaces.[41,42,43] Indigenous Australians are at significantly increased risk compared to the non-indigenous population.[23,44]

Disease occurrence and public health significance

IMD is endemic in Australia but the incidence has varied dramatically over time, with major epidemics following both world wars. More recently, incidence increased through the 1990s, but declined to historically low levels following a peak around the early 2000s.[45,46] Cases occur throughout the year, but there is a marked seasonality, with the highest number of notifications and hospitalisations occurring between June and September each year.[47] All age groups can be affected, but there is a bimodal age distribution, with the highest rates of disease in children aged under 5 years and a second peak in adolescents and young adults aged 15-19 years.[2]

While the overall incidence and mortality associated with IMD is low, the clinical and public health management of the disease can be demanding. This is related to the often dramatic course of the disease, the potential for deaths and serious complications, the fact that incidence is highest in young children, teenagers and young adults, and that clusters of cases may occur, albeit infrequently. Hence, it is essential that the public health follow-up of IMD is undertaken as a priority, that guidelines are followed closely, and that information provided to families of those affected, contacts and the media is consistent and evidence-based.

Universal childhood vaccination using the conjugate serogroup C vaccine, introduced in 2003, along with catch-up vaccination of children and adolescents through school based programs, has been associated with a marked reduction in serogroup C IMD cases in Australia.[2,16]

3. Routine prevention activities


Vaccines are available in Australia for serogroups A, B, C, W and Y meningococcal disease.

The Australian Immunisation Handbook 10th Edition, updated online version provides current guidance on meningococcal immunisation.

Meningococcal C conjugate vaccine (MenCCV) - Available through the National Immunisation Program. Recommended for all children at 12 months of age. From July 2018 this will be replaced with 4vMenCV.

Meningococcal B vaccine (MenBV) - [Available under the National Immunisation Program for certain groups from July 2020], or by private script. Recommended for infants and young children, adolescents, young adults living in close quarters, some laboratory personnel and individuals with certain medical conditions.

Quadrivalent meningococcal vaccines (4vMenCV and 4vMenPV) which protect against serogroups A, C, W and Y. [Available under the National Immunisation Program for certain groups] or on private script. Recommended for [infants and young children, adolescents], occupational exposures, some travel and certain medical conditions. This can be also offered to those who wish to protect themselves or their family from these serogroups of meningococcal disease.

Check the National Immunisation Schedule and the relevant jurisdictional schedule for up-to-date information on currently funded vaccines, as schedules change from time to time. For example, in early 2017, some states implemented a time-limited adolescent ACWY vaccination program to address the changing epidemiology of serogroup W disease.

Risk mitigation

The main aims of public health measures for meningococcal disease are:

  • to provide information to contacts to allay anxiety and provide advice on the action to take should they develop symptoms consistent with IMD and
  • to identify and provide clearance antibiotics and vaccination where indicated to ”higher risk” contacts of cases in order to reduce the risk of further cases resulting from transmission of a virulent strain of the organism.

4. Surveillance objectives

  • To promptly identify cases and their close contacts in order that appropriate public health action can be taken.
  • To identify clusters of cases and outbreaks in order that appropriate public health action can be taken.
  • To monitor the epidemiology of the disease, including the impact of immunisation, to inform prevention strategies.
  • To monitor the effectiveness of current control measures and to provide an evidence base for further review of national guidelines.

5. Data management

Probable and confirmed cases of meningococcal disease should be entered onto the notifiable diseases database within one working day of notification. Ensure that data on Aboriginal or Torres Strait Islander status and vaccination history are collected and entered into the jurisdictional database. Serogroup, sub-serogroup and case outcome should be added to the database when available.

6. Communications

Where applicable in a jurisdiction the laboratory or clinician notifies the state/territory communicable diseases branch or public health unit (PHU) of the case’s age, sex, date of onset, clinical status, laboratory findings and vaccination history (if relevant).

7. Case definition

Probable and confirmed cases of invasive meningococcal disease are notifiable.

Confirmed case

A confirmed case requires either:

  1. laboratory definitive evidence or
  2. laboratory suggestive evidence and clinical evidence.

Laboratory definitive evidence

  1. Isolation of Neisseria meningitidis from a normally sterile site or
  2. detection of specific meningococcal DNA sequences in a specimen from a normally sterile site by nucleic acid amplification testing.

Laboratory suggestive evidence

  1. Detection of Gram-negative diplococci in Gram stain of specimen from a normally sterile site or from a suspicious skin lesion or
  2. high titre IgM or significant rise in IgM or IgG titres to outer membrane protein antigens of N. meningitidis

Clinical evidence (for a confirmed case)

Disease which in the opinion of the treating clinician is compatible with invasive meningococcal disease.

Probable case

A probable case requires clinical evidence only.

Clinical evidence (for a probable case)

A probable case requires the absence of evidence for other causes of clinical symptoms and either:

  1. clinically compatible disease including haemorrhagic rash or
  2. clinically compatible disease and close contact with a confirmed case within the previous 60 days.

The current surveillance case definition can be located at the Australian national notifiable diseases and case definitions.

Although meningococcal conjunctivitis is not included in the IMD surveillance case definition, cases should still be notified in order to enable a public health response as, on occasion, it may precede invasive disease[48] or IMD in a contact[49] (refer to Section 12).

8. Laboratory testing

Testing guidelines

All patients with suspected meningococcal infection should have blood collected as soon as possible for culture, polymerase chain reaction (PCR) testing, c-reactive protein and full blood count. Where appropriate, a sample of cerebrospinal fluid (CSF) should be collected for PCR, microscopy and culture. For meningococcal conjunctivitis (refer to Section 12 Special Situations).

For further details of specimen collection, handling requirements and availability of testing, which may vary between locations, contact the relevant laboratory (refer to Appendices: National Neisseria Network (NNN) Laboratories).

Molecular testing by Polymerase Chain Reaction (PCR)

PCR-based diagnosis provides confirmation of IMD from blood, CSF or other normally sterile sites with validity comparable to that of culture-based diagnosis. Additionally, PCR methods can provide diagnostic information pertinent to patient care and public health management. For these reasons it is recommended that CSF and/or EDTA blood samples from which DNA was extracted for PCR-based diagnosis as well as the remaining DNA extract, both be sent to the appropriate NNN laboratory (refer to Appendices: National Neisseria Network (NNN) Laboratories).

Early antibiotic therapy has contributed to PCR, particularly in blood specimens, now being the most common means of laboratory diagnosis of IMD. PCR-based assays are generally directed at the ctrA gene. Test sensitivity is >95 percent for CSF using ctrA gene PCR [50] and approximately 87 percent when testing blood samples.[51] Data are not available for skin lesions.

PCR tests for serogroup determination should be performed both from a confirmatory and epidemiological point of view. Serogroup identification can guide the public health response, particularly vaccination recommendations. PCR-assays for detecting regions in the siaD gene specific for serogroups B, C, W and Y are widely performed in Australia.

Although meningococcal DNA can be detected up to 72 hours after initiation of systemic antibiotics, caution should still be taken when interpreting negative PCR results. In probable cases results should be assessed in conjunction with clinical presentation, duration and severity of disease and the timing of the initiation of systemic antibiotics in relation to collection of the specimen. [51]


Detection of Gram-negative diplococci by Gram stain of CSF or specimens from other normally sterile sites constitutes laboratory suggestive evidence in the CDNA case definition. In conjunction with a clinically compatible illness, this fulfils criteria for a confirmed case of IMD. The reported sensitivity of Gram stain on CSF is about 62 percent[52,53] and of skin lesion aspirates or biopsies about 50 percent.[53,54] Prior use of antibiotics reduces the likelihood of a positive Gram stain and culture.


Culture of N. meningitidis from blood, CSF or other normally sterile sites confirms a diagnosis of IMD. Additionally, cultures provide isolates for strain differentiation and antibiotic susceptibility testing. When meningitis is present CSF offers the best chance of yielding an organism for culture, but sensitivity is reported to decline from 72 percent to 42 percent after antibiotic treatment.[52] The sensitivity of blood culture is reported to vary from 24-47 percent [52,55] but falls to 5 percent or less if antibiotics have been given before collection. [52]

Nasopharyngeal (throat) swabs

The collection of throat swabs is not recommended for either cases of IMD or their contacts.


Serum antibody tests for the diagnosis of IMD are not routinely available, but are performed in some laboratories. Serological diagnosis is based on the demonstration of a single elevated level of IgM antibody or seroconversion to outer membrane protein (OMP) antigens. As the OMP antigens amongst the Neisseria genus cross-react, the test may be positive in disseminated gonococcal infection.

An assay to detect IgM antibody to serogroup C capsule is also available and will detect an antibody response to recent C capsule vaccination or invasive infection with serogroup C N. meningitidis.

Serological diagnosis is retrospective but may be useful in circumstances where IMD was suspected clinically and when other tests were negative or not performed; it is not recommended for clinical diagnosis of acute cases.

Strain differentiation

Strain differentiation or typing can assist in establishing linkages between cases or cases and carriers that are identified epidemiologically. Laboratory typing results can exclude true relatedness of apparently linked cases if they emerge as being distinct. Also, if the method used is highly discriminating and the prevalence of particular types is taken into account, detection of indistinguishable case isolates can provide quite strong evidence of relatedness.

Isolates and samples for typing are referred to NNN Laboratories (refer to Appendices). Historically, phenotyping (serotyping) has been used to separate isolates into serogroups (using capsular polysaccharides), serotypes and sub-serotypes (using OMP).

Genotyping (molecular) techniques are now used by most state laboratories to type strains in addition to serotyping. Techniques available include pulsed-field gel electrophoresis (PFGE), porA/ porB, or fetA sequencing and multi-locus sequence typing (MLST).[56] Whole genome sequencing, where available, can also be used to establish strain relatedness of cases and guide public health interventions.

Further information is available from the Public Health Laboratory Network (PHLN) case definition website.

9. Case management

Response times

Public health action should commence immediately where the clinical picture is consistent with IMD – in the opinion of the treating clinician – or definitive or suggestive laboratory evidence is received. Begin investigation and response on the same day of notification of a probable or confirmed case of IMD or of confirmed meningococcal conjunctivitis.

Although meningococcal conjunctivitis is not included in the surveillance case definition for IMD, cases should still be notified in order to enable a public health response as, on occasion, it may precede invasive disease [48] or IMD in a contact [49] (refer to section 12 special situations).

Response procedure

Case investigation

The response to a notification will usually be carried out in collaboration with the case’s medical team. Ensure that action has been taken to:

  • discuss with the treating doctor the need to interview the case or the relevant care-giver in order to provide information and seek a contact history
  • establish what the case or the relevant care-giver has already been told about the diagnosis before beginning the interview
  • confirm the onset date and symptoms/signs of illness and assess whether the clinical evidence is consistent with a diagnosis of IMD
  • confirm results of existing relevant laboratory tests, or recommend that the tests be done
  • review case and contact management undertaken to date. For instance, establish if the treating team has provided clearance antibiotics to household contacts
  • facilitate the support of the case and/or family with a social worker, Aboriginal or Torres Strait Islander Liaison Officer or interpreter as required.

Case treatment

Treatment is the responsibility of the treating doctor. For antibiotic treatment recommendations refer to the current edition of Therapeutic Guidelines: Antibiotic. Some antibiotics, including penicillin, do not reliably clear nasopharyngeal carriage of meningococci, [1] so appropriate clearance antibiotics must also be used (refer to Table 2).


Vaccination of cases is not recommended unless the case has underlying risk factors as outlined in the Australian Immunisation Handbook.

Isolation and restriction

Droplets and nasopharyngeal secretions are considered to be infectious from the onset of the acute illness until completion of 24 hours treatment with effective systemic antibiotics.[9] Hence, during this period both standard and droplet precautions should be practised for suspected, probable or confirmed cases, especially while undertaking airway management during resuscitation.

Active case finding

Contacts (refer to below) who develop symptoms consistent with IMD should be advised to seek medical advice urgently and to inform the PHU.

A single case of serogroup A meningococcal disease in an Aboriginal or Torres Strait Islander person may be the sentinel event of a community outbreak and requires appropriate action.

10. Control of environment

None routinely required (refer to Section 12. Special situations).

11. Contact management

Identification of contacts

The aim of identifying contacts is to:

  • clarify their degree of contact with the case
  • provide them with information about meningococcal infection and their level of risk aimed at both allaying unnecessary anxiety and advising them of what action to take if they develop symptoms
  • recommend clearance antibiotics and vaccination if indicated (Table 1).

Contact definition

Public health follow-up focuses on identifying the subset of ‘higher-risk’ contacts who require information and clearance antibiotics and vaccination in some instances. Other lower-risk contacts groups may be given information only.

In establishing the timing and degree of contact with a case, the time period of interest is from 7 days prior to the onset of symptoms in the case to the time the case has completed 24 hours of appropriate antibiotic treatment.

Higher-risk contacts fall into the following groups:

  1. Household or household-like contacts: of a case are those who lived in the same house (or dormitory-type room) or were having an equivalent degree of contact with the case in the 7 days prior to the onset of the case’s symptoms until completion of 24 hours of appropriate antibiotic treatment.
  2. Intimate kissing and sexual contacts: in the 7 days prior to the onset of the case’s symptoms until completion of 24 hours of appropriate antibiotic treatment.
  3. Child-care: to be considered a higher-risk contact, children and staff in childcare should have an equivalent degree of contact with the case as a household contact. An exposure assessment should be conducted to assess the degree of contact at the childcare centre. As a guide, two full days (where one full day is approximately 6-8 hours) of attendance in the same care group as the case or a cumulative of around 20 hours in the same care group as the case in the 7 days prior to onset of case symptoms should be considered a higher-risk contact. Other childcare contact is considered lower-risk. Child-care includes any situation where children under 5 years of age are cared for with other children away from home. This setting includes kindergartens and pre-schools (pre-primary).
  4. Passengers: seated immediately adjacent to the case during long distance travel (>8 hours duration) by aeroplane, train, bus or other vehicle.[57]
  5. Healthcare workers who have had unprotected close exposure of their airway to large particle respiratory droplets of a case during airway management (e.g. suctioning, intubation), or mouth to mouth resuscitation up until the case has had 24 hours of appropriate antibiotic treatment.[33,48]

Table 1: Public health responses in defined settings in which a single case of invasive meningococcal disease (or meningococcal conjunctivitis) has occurred 1

Settings​ Clearance antibiotics 2 Vaccination 3 Information 4
Household and other higher risk contacts of a case (refer to Contact definition in Section 11) Yes Yes Yes
School and universities

Only students who are household-like contacts of a caserefer to Contact definition Section 11

Only students who are household-like contacts of a case refer to Contact definition Section 11​​


Yes - all other students in the same classroom (schools) or tutorial groups (universities)
​Passengers in seats directly beside a case during long duration travel (>8 hours) ​Yes ​No ​Yes
​Childcare facilities ​Only children and staff who are household-like contacts of a case – refer to section 11 Contact management Only children and staff who are household-like contacts of a case – refer to Vaccination Section 11 ​Yes
Those exposed to a case after the onset of symptoms No, unless meet other criteria for higher risk contacts No Yes
Healthcare workers Only healthcare workers who have performed airway management (e.g. suctioning, intubation) of a case without wearing a mask No Yes
Sporting team and work contacts (including both shared office or open air settings) No No Yes
  1. Response for probable and confirmed cases of invasive meningococcal disease plus confirmed meningococcal conjunctivitis.
  2. Only those in close and prolonged contact with a case in the 7 days prior to the onset of symptoms, and only very close contacts after the onset of the case’s symptoms, and prior to completion of 24 hours of appropriate treatment, require clearance antibiotics.
  3. Vaccination recommendations only apply when IMD is caused by serogroups A, C, W and Y, but not to B. Refer to Vaccination below.
  4. For lower-risk contacts, information should be provided as soon as possible and by no later than the end of the next business day.

Clearance antibiotics

The main rationale for provision of clearance antibiotics is to eliminate meningococci from any carrier within the network of contacts close to each case, thereby reducing the risk of further transmission of what may be a more virulent strain of the organism within the social network and preventing further cases of invasive disease. Clearance antibiotics given to household contacts was estimated to be 89 percent effective in preventing secondary cases.[58]

Clearance antibiotics should also be provided for contacts of meningococcal conjunctivitis because secondary cases of IMD have occurred.[49]

Wider provision of clearance antibiotics outside the recommended groups should be avoided due to the risk of doing more harm than good, including elimination of protective flora, risk of side effects and development of antibiotic resistance. Following even a single case of IMD there may be considerable demands and pressure from parents or others for clearance antibiotics to be administered more widely than is recommended. It is important that public health personnel do not acquiesce to these demands, but rather provide reassurance on the low risk of IMD in contacts and carefully explain the purpose for clearance antibiotics.

All identified contacts, regardless of whether or not they are eligible to receive clearance antibiotics, should be advised to remain alert for symptoms and to seek medical review if appropriate.

The current (April 2019) Therapeutic Guidelines: Antibiotic lists ciprofloxacin, ceftriaxone and rifampicin as suitable agents. Characteristics of these agents are shown below in Table 2. Clearance antibiotics should be given to contacts of confirmed cases of IMD as soon as possible after the contact is identified. However, there is no purpose in administering antibiotics if more than four weeks have elapsed since the most recent contact with the case.

Table 2: Characteristics of agents used for nasopharyngeal clearance of meningococci

Agent Ciprofloxacin Ceftriaxone Rifampicin


agent for

  • Adults and children of all ages
  • Women taking the oral contraceptive pill (OCP)
  • Pregnant women
  • Situations where access to and/or compliance with rifampicin may be poor, such as in remote Indigenous communities
  • Young children
  • Adult or child ≥12 years: 500 mg orally, as 1 dose
  • Children aged 5–12 years: 250 mg stat
  • Children under 5 years: 30mg/kg up to maximum of 125 mg stat

    *Ciprofloxacin suspension contains 250mg/5ml

  • Child under 12 years: 125 mg IM as 1 dose
  • Adult: 250 mg IM, as 1 dose
  • Child: Neonate <1 month: 5 mg/kg orally, 12-hourly for 2 days
  • Child ≥ 1 month: 10 mg/kg up to 600 mg orally, 12- hourly for 2 days.
  • Adult: 600 mg orally, 12-hourly for 2 days
  • 91-100% effective in elimination of nasopharyngeal carriage [57]
  • Single dose
  • Oral
  • 97-98% effective in elimination of nasopharyngeal carriage [59]
  • Well tolerated
  • Single dose
  • No adverse reactions or drug interactions of importance
  • 81-98% effective in elimination of nasopharyngeal carriage [59]
  • Oral, available in syrup
  • Previous allergy
  • Pregnancy
  • Drug interaction
Not for use in infants less than 4 weeks old.
  • Severe liver impairment
  • Alcohol abuse
  • Pregnancy
  • Allergic reactions, including anaphylaxis.
  • Compatible with breastfeeding but can cause diarrhoea in the infant.

IM administration:

  • painful and may require concomitant local anaesthetic
  • compatible with breastfeeding but can cause diarrhoea in the infant.

2-day course could reduce compliance:

  • Compatible with breastfeeding but may cause diarrhoea in infants. Monitoring of infants for jaundice is recommended
  • Side effects: orange discolouration of soft contact lenses, tears and urine; gastrointestinal disturbance; dizziness; drowsiness; headache.
  • Drug interactions including hormonal contraceptives, anticoagulants and anticonvulsants.


Meningococcal vaccination may be offered to higher-risk contacts to further reduce the small risk of secondary cases. The rationale for vaccination in this context is to protect individuals from infection with an invasive strain of meningococcus that may still be circulating in their social network, including among persons who did not receive clearance antibiotics.

In addition to clearance antibiotics, vaccination with an appropriate vaccine is indicated for unimmunised household-like contacts of cases of IMD and meningococcal conjunctivitis confirmed to be caused by serogroup C, A, W or Y.

Public health units should facilitate access to appropriate vaccine either directly or through existing jurisdictional arrangements with primary care or immunisation providers.

Contacts should be informed that, depending on their age, further doses may be required if they wish to have long term protection against meningococcal A, C, W and Y disease [Australian Immunisation Handbook]. Completion of the vaccination course, if necessary, is at the discretion of the contact and can be arranged via their primary care provider.

Vaccination with 4CMenB vaccine, however, is not recommended after a single case of IMD caused by serogroup B, primarily because it is a multi-dose course, and a single (first) dose is unlikely to confer protection to the contact during the period of higher risk of disease.

Vaccination of household contacts with 4CMenB vaccine should, however, be considered if a second serogroup B case occurs in the same household (even if >30 days later), as this may indicate increased susceptibility of family members to IMD and/or ongoing transmission within the household.


Following confirmation of IMD, provide information to the network of contacts (or to the responsible guardians of children in the network) about the disease and how it is spread. For lower-risk contacts, information should be provided as soon as possible and by no later than the end of the next business day. A fact sheet, appropriate to the cultural and literacy needs of recipients, should be provided (refer to example at Appendix 2: Meningococcal disease: Information for the public). This information should include the message that contacts, or anyone close to them, who develop symptoms consistent with meningococcal disease, should seek urgent medical attention.

Isolation and restriction

None required

12. Special situations


Outbreaks of meningococcal disease can be particularly challenging for public health authorities due to the intense public concern and media interest they generate, [23] the potential for significant morbidity and mortality and the limited published evidence to guide best practice. [60]

The term ‘outbreak’ is taken to mean the occurrence of more cases than expected for the population or group under consideration. The objective of public health management of outbreaks of IMD is to interrupt transmission and prevent further cases. Once an outbreak is either suspected or recognised there is an immediate need to initiate a coordinated response. Elements of this response include:

  • a situation review to determine if there is an outbreak and its extent
  • the establishment of a response team(s) and, if appropriate, a site visit
  • establishment of heightened surveillance
  • determination of the population at risk and calculation of age-specific and region-specific attack rates where indicated
  • decisions on what action is to be taken, tailored to the setting
  • provision of adequate information to all contacts and other people as indicated, including healthcare providers, affected communities or groups, the media and the wider public
  • ensuring the provision of clearance antibiotics (and immunisation where indicated) as required for the setting and
  • review of all actions taken and the preparation and dissemination of final documentation and a report.


Sporadic case - a single case in the absence of previous known close contact with another case (refer to Contact definition above).

Primary (index) case - a case that occurs in the absence of previous known close contact with another case and is subsequently associated with a co-primary or secondary case.

Co-primary case - a close contact who develops disease within 24 hours of onset of illness in a primary case.

Secondary case - a close contact who develops disease more than 24 hours after onset of illness in a primary case where the available microbiological characterisation of the organisms is the same.

Organisation-based outbreak - two or more probable or confirmed (where the available microbiological characterisation of the organisms is the same) cases with onset in a four week interval, among people who have a common organization-based affiliation (such as attending the same high school, extended families and/or social groups) but no close contact with each other, in a grouping which makes epidemiological sense.

Community outbreak - three or more confirmed or probable cases of IMD where there is no direct epidemiologic link between the cases, with onset in a 3 month interval among persons residing in the same area and the primary attack rate is at least 10 per 100,000.[57] Rate calculations should not be annualised. This is not an absolute threshold and should be considered in the context of other factors, e.g. completeness of case reporting, whether there is continuing occurrence of cases after recognition of a suspected outbreak and population vaccination coverage where relevant.

Identification of outbreaks

The following changes in epidemiology of meningococcal disease are suggestive of an outbreak [61]:

  • an increased rate of disease. In small populations it may be more useful to focus on the number of cases rather than the rate
  • clustering of cases in an age group or a shift in the age distribution of cases and
  • phenotypic and/or genetic similarity among strains causing disease in the population.

Suspected outbreaks should be reviewed in order to identify the microbiological features of the cases and any epidemiologic links between cases. Microbiological investigation should focus on confirmation of the diagnosis and rapid characterisation of organisms in as much detail as locally possible. Cases that occur closely in time and place, but are infected with different serogroups (or serotypes, sub-serotypes or genotypes if known), should be managed as sporadic cases.[62] The identification of possible epidemiological links should include a search for contacts in common, particularly in childcare, educational institutions or other groupings or organisations.[30,63,64,65,66] Examples include attendance at nightclubs or parties.[67]

Organisation-based outbreaks

In settings such as childcare centres and aged care facilities, the population at risk is a natural grouping that makes epidemiological sense. Identification of populations at risk may be more difficult in other organisational settings, such as schools, universities and workplaces; or in extended families or social groups.

Clearance antibiotics should be considered for a wider group than household-like contacts, even though the evidence for preventing further cases is not strong.[29,68] Co-primary or secondary cases should not be counted when determining whether criteria for provision of organisation-based clearance antibiotics have been met. This is because they are the household-like contacts.

If cases have occurred in a household-like setting, then this may not meet criteria for an organisational outbreak. For example, two cases in university students in the same class who share accommodation do not define a university-based outbreak, since the risk is assumed to arise from the household-like setting of the shared accommodation.

The use of meningococcal vaccine in addition to clearance antibiotics should be considered if the outbreak is due to a vaccine-preventable serogroup. [62,67,69,70,71]

Community outbreaks

These outbreaks are difficult to define and manage. At-risk populations are usually defined geographically by using natural or administrative boundaries that most closely fit the residence data for the majority of the outbreak cases. However, physical or administrative boundaries do not limit factors that contribute to the increasing risk of meningococcal disease and accurate identification of the at-risk population should not be inappropriately constrained by them.

Assess carefully all available epidemiological information, including both confirmed and probable cases, serotyping and/or genotyping data, dates of onset, direct and indirect links between cases, the size of the population or identifiable sub-population containing the cases and meningococcal vaccine uptake rates (where relevant).[54]

From an epidemiologic perspective, when determining if the criteria for an outbreak are met, secondary and co-primary cases should be counted as one case[57] for the purpose of calculating community attack rates.

Vaccination of the population at risk should be considered if an outbreak of a vaccine preventable serogroup is identified, as defined above. Other factors should be taken into account, including logistic and financial considerations. The decision to vaccinate a large population is a difficult one for several reasons:

  • when the issue is first raised, there is usually a small number of cases with a relatively low attack rate in the total population;
  • cases may be widely dispersed in time and space, making it difficult to determine whether this is an outbreak or a fluctuation within expected limits for sporadic disease and
  • the costs of the vaccine and other resources required to vaccinate the group are considerable.

Community-wide clearance antibiotics should not be used. The widespread use of clearance antibiotics in community outbreaks has not been shown to be of value. It may result in:

  • the eradication of benign strains of N. meningitidis and bacteria of other species that induce protective antibodies
  • the generation of drug resistant strains and
  • an increase in the prevalence of drug-related adverse events.

Aboriginal and Torres Strait Islander communities

Based on outbreaks reported in the 1980s and early 1990s, the risk of sustained transmission of IMD in Aboriginal and Torres Strait Islander communities, is probably higher than in the general community.[72] For this reason a low threshold should be used to initiate disease control measures. Action targeted to all community members should be considered if there are 2 or more cases in a remote Aboriginal or Torres Strait Islander community within a 4 week period and where available characterisation indicates they are the same strain. The nature of any action will depend on factors including the size of the community and the serogroup of the organism.

Clusters of serogroup W disease occurred in Aboriginal communities in some states in 2016/17, and population-based vaccination interventions were undertaken in response.

Meningococcal conjunctivitis

Primary meningococcal conjunctivitis may also precede invasive disease in a case or in a close contact.[48,49] Hence, it is recommended that contacts of individuals with meningococcal conjunctivitis receive information and clearance antibiotics as for contacts of IMD cases.

Conjunctival swabs should be collected from suspect cases of meningococcal conjunctivitis as soon as possible for microscopy and culture. Gram staining of conjunctival exudate or scrapings from suspect cases of meningococcal conjunctivitis consistently reveals Gram-negative diplococci and abundant polymorphonuclear leukocytes. This provides a preliminary diagnosis of meningococcal conjunctivitis (with N. gonorrhoeae and M. catarrhalis considered in differential diagnosis), but culture is essential for diagnostic confirmation, strain characterization and antibiotic susceptibility testing.[49]

13. References

  1. Heymann DL. Control of Communicable Diseases Manual 19 ed. Washington: American Public Health Association, USA; 2008.
  2. Lahra MM, Enriquez RP. Annual report of the Australian Meningococcal Surveillance Programme, 2011. Commun Dis Intell. 2012;36(3):E251-62.
  3. Australian Government Department of Health. Meningococcal W Disease. 2017. Accessed on 26/04/2017. Available from: (
  4. Trotter CL, Gay NJ, Edmunds WJ. The natural history of meningococcal carriage and disease. Epidemiol Infect. 2006;134(3):556-66.
  5. Christensen H, May M, Bowen L, Hickman M, Trotter CL. Meningococcal carriage by age: a systematic review and meta-analysis. Lancet Infect Dis. 2010;10(12):853-61.
  6. Caugant DA, Maiden MC. Meningococcal carriage and disease--population biology and evolution. Vaccine. 2009;27 Suppl. 2:B64-70.
  7. MacLennan J, Kafatos G, Neal K, Andrews N, Cameron JC, Roberts R, et al. Social behaviour and meningococcal carriage in British teenagers. Emerg Infect Dis. 2006;12(6):950-7.
  8. Orr HJ, Gray SJ, Macdonald M, Stuart JM. Saliva and meningococcal transmission. Emerg Infect Dis. 2003;9(10):1314-5.
  9. Abramson JS, Spika JS. Persistence of Neisseria meningitidis in the upper respiratory tract after intravenous antibiotic therapy for systemic meningococcal disease. J Infect Dis. 1985;151(2):370-1.
  10. Rosenstein NE, Perkins BA, Stephens DS, Popovic T, Hughes JM. Meningococcal disease. N Engl J Med. 2001;344(18):1378-88.
  11. Isaacs D. Commentary: Controversies in SIGN guidance on management of invasive meningococcal disease in children and young people. BMJ. 2008;336(7657):1370-1.
  12. Thompson MJ, Ninis N, Perera R, Mayon-White R, Phillips C, Bailey L, et al. Clinical recognition of meningococcal disease in children and adolescents. Lancet. 2006;367(9508):397-403.
  13. Steven N, Wood M. The clinical spectrum of meningococcal disease. K C, editor. Chichester: John Wiley & Sons; 1995.
  14. Goldacre MJ, Roberts SE, Yeates D. Case fatality rates for meningococcal disease in an English population, 1963-98: database study. BMJ. 2003;327(7415):596-7.
  15. Dang V, Jamieson FB, Wilson S, Rawte P, Crowcroft NS, Johnson K, et al. Epidemiology of serogroup B invasive meningococcal disease in Ontario, Canada, 2000 to 2010. BMC Infect Dis. 2012;12:202.
  16. Gunaratnam P, Massey P, Durrheim D, Torvaldsen S. Invasive meningococcal disease in elderly people, New South Wales, Australia, 1993 to 2012. Western Pac Surveill Response J. 2013;4(4):4-10.
  17. Jensen ES, Schonheyder HC, Lind I, Berthelsen L, Norgard B, Sorensen HT. Neisseria meningitidis phenotypic markers and septicaemia, disease progress and case-fatality rate of meningococcal disease: a 20-year population-based historical follow-up study in a Danish county. J Med Microbiol. 2003;52(Pt 2):173-9.
  18. Trotter CL, Chandra M, Cano R, Larrauri A, Ramsay ME, Brehony C, et al. A surveillance network for meningococcal disease in Europe. FEMS Microbiol Rev. 2007;31(1):27-36.
  19. Cohen C, Singh E, Wu HM, Martin S, de Gouveia L, Klugman KP, et al. Increased incidence of meningococcal disease in HIV-infected individuals associated with higher case-fatality ratios in South Africa. AIDS. 2010;24(9):1351-60.
  20. Brooks R, Woods CW, Benjamin DK, Jr., Rosenstein NE. Increased case-fatality rate associated with outbreaks of Neisseria meningitidis infection, compared with sporadic meningococcal disease, in the United States, 1994-2002. Clin Infect Dis. 2006;43(1):49-54.
  21. van Deuren M, Brandtzaeg P, van der Meer JW. Update on meningococcal disease with emphasis on pathogenesis and clinical management. Clin Microbiol Rev. 2000;13(1):144-66.
  22. Smith I, Bjornevik AT, Augland IM, Berstad A, Wentzel-Larsen T, Halstensen A. Variations in case fatality and fatality risk factors of meningococcal disease in Western Norway, 1985-2002. Epidemiol Infect. 2006;134(1):103-10.
  23. Guimont C, Hullick C, Durrheim D, Ryan N, Ferguson J, Massey P. Invasive meningococcal disease--improving management through structured review of cases in the Hunter New England area, Australia. J Public Health (Oxf). 2010;32(1):38-43.
  24. De Wals P, Hertoghe L, Borlee-Grimee I, De Maeyer-Cleempoel S, Reginster-Haneuse G, Dachy A, et al. Meningococcal disease in Belgium. Secondary attack rate among household, day-care nursery and pre-elementary school contacts. J Infect. 1981;3(1 Suppl.):53-61.
  25. CDC. Meningococcal disease. In: Atkinson W HJ, Wolfe S, editor. Epidemiology and Prevention of Vaccine-Preventable Diseases The Pink Book: Course Textbook. 12 ed. Washington DC: Public Health Foundation; 2012.
  26. Kristiansen BE, Tveten Y, Jenkins A. Which contacts of patients with meningococcal disease carry the pathogenic strain of Neisseria meningitidis? A population based study. BMJ. 1998;317(7159):621-5.
  27. Tully J, Viner RM, Coen PG, Stuart JM, Zambon M, Peckham C, et al. Risk and protective factors for meningococcal disease in adolescents: matched cohort study. BMJ. 2006;332(7539):445-50.
  28. Stanwell-Smith RE, Stuart JM, Hughes AO, Robinson P, Griffin MB, Cartwright K. Smoking, the environment and meningococcal disease: a case control study. Epidemiol Infect. 1994;112(2):315-28.
  29. Davison KL, Andrews N, White JM, Ramsay ME, Crowcroft NS, Rushdy AA, et al. Clusters of meningococcal disease in school and preschool settings in England and Wales: what is the risk? Arch Dis Child. 2004;89(3):256-60.
  30. Zangwill KM, Schuchat A, Riedo FX, Pinner RW, Koo DT, Reeves MW, et al. School-based clusters of meningococcal disease in the United States. Descriptive epidemiology and a case-control analysis. JAMA. 1997;277(5):389-95.
  31. Hastings L, Stuart J, Andrews N, Begg N. A retrospective survey of clusters of meningococcal disease in England and Wales, 1993 to 1995: estimated risks of further cases in household and educational settings. Commun Dis Rep CDR Rev. 1997;7(13):R195-200.
  32. Materna B HK, Harriman K, Rosenberg J, Shusterman D, Windham G, Atwell J, et al. Occupational transmission of Neisseria meningitidis - California, 2009. MMWR. 2010;59(45):1480-3.
  33. Gilmore A, Stuart J, Andrews N. Risk of secondary meningococcal disease in health-care workers. Lancet. 2000;356(9242):1654-5.
  34. Sejvar JJ, Johnson D, Popovic T, Miller JM, Downes F, Somsel P, et al. Assessing the risk of laboratory-acquired meningococcal disease. J Clin Microbiol. 2005;43(9):4811-4.
  35. Kessler AT, Stephens DS, Somani J. Laboratory-acquired serogroup A meningococcal meningitis. J Occup Health. 2007;49(5):399-401.
  36. Anon. Updated recommendation from the Advisory Committee on Immunization Practices (ACIP) for revaccination of persons at prolonged increased risk for meningococcal disease. MMWR. 2009;58(37):1042-3.
  37. Lee CC, Middaugh NA, Howie SR, Ezzati M. Association of second hand smoke exposure with paediatric invasive bacterial disease and bacterial carriage: a systematic review and meta-analysis. PLoS Med. 2010;7(12).
  38. McCall BJ, Neill AS, Young MM. Risk factors for invasive meningococcal disease in southern Queensland, 2000-2001. Intern Med J. 2004;34(8):464-8.
  39. Tuite AR, Kinlin LM, Kuster SP, Jamieson F, Kwong JC, McGeer A, et al. Respiratory virus infection and risk of invasive meningococcal disease in central Ontario, Canada. PLoS One. 2010;5(11):e15493.
  40. Jansen AG, Sanders EA, A VDE, AM VANL, Hoes AW, Hak E. Invasive pneumococcal and meningococcal disease: association with influenza virus and respiratory syncytial virus activity? Epidemiol Infect. 2008;136(11):1448-54.
  41. Baker M, McNicholas A, Garrett N, Jones N, Stewart J, Koberstein V, et al. Household crowding a major risk factor for epidemic meningococcal disease in Auckland children. Pediatr Infect Dis J. 2000;19(10):983-90.
  42. Deutch S, Labouriau R, Schonheyeder HC, Ostergaard L, Norgard B, Sorensen HT. Crowding as a risk factor of meningococcal disease in Danish preschool children: a nationwide population-based case-control study. Scand J Infect Dis. 2004;36(1):20-3.
  43. Honish L, Soskolne CL, Senthilselvan A, Houston S. Modifiable risk factors for invasive meningococcal disease during an Edmonton, Alberta outbreak, 1999-2002. Can J Public Health. 2008;99(1):46-51.
  44. Menzies R, Turnour C, Chiu C, McIntyre P. Vaccine preventable diseases and vaccination coverage in Aboriginal and Torres Strait Islander people, Australia 2003 to 2006. Commun Dis Intell. 2008;32 Suppl.:S2-67.
  45. Patel MS. Australia's century of meningococcal disease: development and the changing ecology of an accidental pathogen. Med J Aust. 2007;186(3):136-41.
  46. Australia's notifiable disease status, 2010: Annual report of the National Notifiable Diseases Surveillance System. Commun Dis Intell. 2012;36(1):1-69.
  47. Chiu C, Dey A, Wang H, Menzies R, Deeks S, Mahajan D, et al. Vaccine preventable diseases in Australia, 2005 to 2007. Commun Dis Intell. 2010;34 Supp:S1-167.
  48. Stansfield RE, Masterton RG, Dale BA, Fallon RJ. Primary meningococcal conjunctivitis and the need for prophylaxis in close contacts. J Infect 1994;29(2):211-214.
  49. Bigham JM, Hutcheon ME, Patrick DM, Pollart AJ. Death from invasive meningococcal disease following close contact with a case of primary meningococcal conjunctivitis - Langley, British Columbia, 1999. Can Commun Dis Rep 2001; 27(2):13-18.
  50. Porritt RJ, Mercer JL, Munro R. Detection and serogroup determination of Neisseria meningitidis in CSF by polymerase chain reaction (PCR). Pathology. 2000;32(1):42-5.
  51. Bryant PA, Li HY, Zaia A, Griffith J, Hogg G, Curtis N, et al. Prospective study of a real-time PCR that is highly sensitive, specific, and clinically useful for diagnosis of meningococcal disease in children. J Clin Microbiol. 2004;42(7):2919-25.
  52. Cartwright K, Reilly S, White D, Stuart J. Early treatment with parenteral penicillin in meningococcal disease. BMJ. 1992;305(6846):143-7.
  53. van Deuren M, van Dijke BJ, Koopman RJ, Horrevorts AM, Meis JF, Santman FW, et al. Rapid diagnosis of acute meningococcal infections by needle aspiration or biopsy of skin lesions. BMJ. 1993;306(6887):1229-32.
  54. Health Protection Agency. Guidance for public health management of meningococcal disease in the UK. 2012.
  55. Carrol ED, Thomson AP, Shears P, Gray SJ, Kaczmarski EB, Hart CA. Performance characteristics of the polymerase chain reaction assay to confirm clinical meningococcal disease. Arch Dis Child. 2000;83(3):271-3.
  56. Australian Meningococcal Surveillance Programme annual report, 2010. Commun Dis Intell. 2011;35(3):217-228.
  57. CDC. Prevention and Control of Meningococcal Disease - Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR 2005;54:1-21.
  58. Purcell B, Samuelsson S, Hahne SJ, Ehrhard I, Heuberger S, Camaroni I, et al. Effectiveness of antibiotics in preventing meningococcal disease after a case: systematic review. BMJ. 2004;328(7452):1339.
  59. ECDPC. Public Health management of sporadic cases of invasive meningococcal disease and their contacts. Stockholm: ECDC, 2010.
  60. Stuart JM. Managing outbreaks : the public health response. In: Meningococcal Disease; Methods and Protocols. Totawa, NJ: Humana Press Inc.; 2001. p. 257-272.
  61. Guidelines for the prevention and control of meningococcal disease; Supplement. Canada Communicable Disease Report 2005;31S1:1-21.
  62. Stuart JM, Monk PN, Lewis DA, Constantine C, Kaczmarski EB, Cartwright KA. Management of clusters of meningococcal disease. PHIS Meningococcus Working Group and Public Health Medicine Environmental Group. Commun Dis Rep CDR Rev 1997;7(1):R3-5.
  63. Davison RP, Lovegrove DR, Selvey LA, Smith HV. Using the national guidelines to manage a meningococcal group C outbreak in a Brisbane boarding school - some discretionary judgements are needed. Commun Dis Intell 2003; 27(4):520-523.
  64. M F, L Y, G H. Unusual cluster of mild invasive serogroup C meningococcal infection in a university college. Communicable Diseases Intelligence 1999;23;261-264
  65. Miles TA, Lewis PR, Cook L, Bruderlin KI. An outbreak of meningococcal disease in a secondary school - implications for public health practice. Commun Dis Intell 2004; 28(3):345-347
  66. Robinson P, Taylor K, Tallis G, Carnie J, Rouch G, Griffith J, et al. An outbreak of serogroup C meningococcal disease associated with a secondary school. Commun Dis Intell 2001;25(3):121-125
  67. Jeffs J, Jalaludin B, Munro R, Patel M, Kerr M, Daley D, et al. A cluster of meningococcal disease in western Sydney, Australia initially associated with a nightclub. Epidemiol Infect 1998; 120(3):263-270.
  68. Begg N. Policies for public health management of meningococcal disease. J Epidemiol Community Health 1999;53(9):516
  69. O'Hallahan J, Lennon D, Oster P, Lane R, Reid S, Mulholland K, et al. From secondary prevention to primary prevention: a unique strategy that gives hope to a country ravaged by meningococcal disease. Vaccine 2005;23(17-18):2197-2201.
  70. Samuelsson S, Hansen ET, Osler M, Jeune B. Prevention of secondary cases of meningococcal disease in Denmark. Epidemiol Infect 2000; 124(3):433-440.
  71. Kristiansen BE, Knapskog AB. Secondary prevention of meningococcal disease. BMJ 1996;312(7031):591-592.
  72. Simpkins D, Wood N, Jelfs J, McIntyre PB, Menzies R, Lawrence G, et al. Modern trends in mortality from meningococcal disease in Australia. Pediatr Infect Dis J 2009;28(12):1119-1120.

14. Appendices

Appendix 1 - PHU checklist [PDF]
Appendix 2 - Meningococcal disease fact sheet
Appendix 3 - Core data form [PDF]
Appendix 4 - Follow up of contacts of a case form [PDF]
Appendix 5 - Timeline form
Appendix 6 - Case audit form [PDF]
Appendix 7 - Information for close contacts regarding clearance antibiotics and vaccination [DOC]
Appendix 8 - Ciprofloxacin: an antibiotic for contacts of persons with a meningococcal infection [DOC]
Appendix 9 - Rifampicin: an antibiotic for contacts of persons with a meningococcal infection [DOC]
Appendix 10 - Ceftriaxone: an antibiotic for contacts of persons with a meningococcal infection [DOC]
Appendix 11 - Information for people who have close contact with a person with meningococcal disease [DOC]
Appendix 12 - Information for low level contacts [DOC]
Appendix 13 - National Neisseria Network (NNN) Laboratories [PDF]

Contact page owner: Communicable Diseases