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You may have seen mention in the media of the introduction of separate meningococcal vaccination programs in South Australia  and Western Australia  – they’re being implemented in response to a number of outbreaks of meningococcal disease in those states. The South Australian Health Department, together with the University of Adelaide and vaccine manufacturer GSK, have announced that they are offering the meningococcal B vaccine to 60,000 adolescents in grades 10, 11 or 12 from 2017. Testing has proved the B strain to be responsible for 19 of the 24 meningococcal meningitis cases this year in SA. While WA is providing a one-off administration of the vaccine that protects against the W strain in a program directed at children and young adults (aged four years and under and 15 – 19 years of age) living in Kalgoorlie, Boulder, Coolgardie and Kambalda - 5 cases caused by the W strain have occurred in Kalgoorlie in the past 2 months.

What do we know about this life-threatening illness?

Neisseria meningitidis (a meningococcus), is a leading cause of bacterial meningitis, producing sepsis (blood poisoning), pneumonia and other localised infections3. We know it causes death in around 1 in 20 of individuals infected1,2 in high-income countries, and several times higher in developing countries. Further, approximately half of all survivors have neurological complications, including hearing, visual or cognitive impairment1, loss of fine motor skills, seizures, hydrocephalus and limb amputations due to tissue cell death3.

There are 13 serogroups of Neisseria meningitidis but most human disease is caused by only 5 of them - A, B, C, W & Y4. Meningococcal bacteria can live harmlessly in our throat and nose; around 10% of people will be colonised by these bacteria at any one time without ever becoming ill – they are ‘healthy carriers’. It isn’t completely understood why in some people these common bacterial colonisers are able to evade the body’s natural defences and cross the blood-brain barrier to cause meningitis1. There are, however, several risk factors which increase susceptibility, including: specific age groups, medical conditions causing lowered immune defences and genetic factors1. When it comes to someone transmitting the bacteria to another person, this is more likely to occur in smokers (higher incidence of being a carrier), in those people with close contact (i.e. with saliva, such as during coughing, kissing or sharing eating utensils) or living in the same household. You can’t catch the bacteria through casual contact or, unlike measles, from merely being in the same room as someone with the infection1.

Australia and Meningococcal Meningitis

From the 1950s, serotypes B & C were responsible for most disease recorded in Australia, but, with the introduction of the C strain vaccine into the National Immunisation Program in 2003, the incidence of meningococcal infections due to this serotype dropped from 3.5 cases per 100,000 in 2001 to 1.1 per 100,000 in 2011. Subsequently the majority of IMD cases in Australia have been due to the B strain5.

Statistics available for 2016 show that Victoria has had 57 meningococcal meningitis cases this year to date - up from 50 cases in 2015 and 26 cases in 2014. In New South Wales there have been 63 cases so far in this year, with 43 in 2015 and 35 in 2014 (of which 39 cases were not strains B or C). In WA numbers have been static from 2014 to 2015 with 17 cases annually and usually only 1 to 2 W strain cases, but there have been 20 cases this year with the W strain accounting for 12.

In Australia, the disease has a peak incidence during the cooler months of winter and early spring, but smaller outbreaks also occur at other times. Age groups with the highest incidence of disease are under 4 years and again, to a lesser extent, between 15 and 24 years of age5.

Number of invasive meningococcal disease cases reported to the National Notifiable Diseases Surveillance System compared with laboratory confirmed data from the Australian Meningococcal Surveillance Programme, Australia, 1991 to 20145.

Global incidence

It is estimated that there are approximately 1.2 million cases of invasive meningococcal disease (IMD) causing approximately 135,000 deaths across the globe each year. The world-wide burden of IMD varies by region: countries are grouped into ‘high, moderate and low-incidence’ and Africa falls into the first category by virtue of the frequent epidemics that occur in 25 countries of sub-Saharan Africa - the so-called ‘meningitis belt’. These epidemics strike during the dry season (Dec-June)6, alternating with an endemic incidence during the rainy season (June-Oct)7.

Distribution of common and predominant meningococcal serogroups by region. Predominant strains are highlighted in bold text3

  Population Health Metrics 2013, 11:17 

Available vaccines

Vaccines used to protect against meningococcal meningitis disease in Australia come in 2 forms – one cannot be used under 2 years of age, is shorter-acting and will not eliminate the bacteria from the individual’s respiratory tract (polysaccharide vaccine), whereas the other covers a wider range of ages, has a longer duration and reduces nasopharyngeal carriage of the bacterium (conjugate vaccine).

The Australian National Immunisation Program provides one dose of serogroup C vaccine (in combination with Haemophilus influenzae type b (Hib)) to infants at the age of 12 months8. Another, a meningococcal B vaccine, is available on the private market so is without government subsidy at this time.

So the 4 formulations of meningococcal vaccines currently available for use in Australia8:

  • Meningococcal C conjugate vaccines, also in combination with Hib
  • Recombinant multicomponent meningococcal B vaccines
  • Meningococcal A, C, W135 and Y conjugate vaccines
  • Meningococcal A, C, W135 and Y polysaccharide vaccines

Travel and meningococcal meningitis

Specific itineraries that are more likely to warrant the recommendation of the meningococcal vaccine are:
- Travel to the meningitis belt in sub-Saharan Africa
- Annual Hajj pilgrimage and Umrah (the ACWY vaccine is a requirement for entry into Saudi Arabia)
- Travel to a region with a current outbreak of IMD
- Young people travelling in groups or living in dormitories i.e. at college
- Extensive close contact with the local community in regions of high IMD incidence
- Some medical conditions, including functional or anatomical asplenia, HIV infection and haematopoietic stem cell transplant.

As always, the final decision on what is best for any traveller will be decided during a pre-travel consultation with a medical practitioner.

For more information please call Travelvax’s travel health advice line on 1300 360 164.


1. Adriani, K.S, Brouwer, M.C., & van de Beck, D. (2015) Risk factors for community-acquired bacterial meningitis in adults. The Netherlands Journal of Medicine (73:2) p.53 – 60. Accessed 20.12.16 Available at:
2. Van de Beek, D., Brouwer, M.C., Thwaites, G.E. & Tunkel, A.R. (2012) Bacterial meningitis 2 – Advances in treatment of bacterial meningitis. Accessed 20.12.16 Available at:
3. Jafri, R.Z, Messonnier, N.E., Tevi-Benissan, C., Durrheim, D., & Eskola, J. et al. (2013) Global epidemiology of invasive meningococcal disease. Population Health Metrics (11:17) Accessed 20.12.16
4. Halperin, S.A, Bettinger, J.A, Greenwood, B., Harrision, L.H., & Jels, J. et al (2012) The changing and dynamic epidemiology of meningococcal disease. Vaccine (30S) p.B26-B36. Accessed 20.12.16 Available at:
5. National Centre for Immunisation Research and Surveillance Meningococcal Disease Factsheet July 2015. Accessed 20/12/16 Available from:
6. Department of health Meningococcal (2014) Australian Meningococcal Surveillance Programme annual report (40: 2). Communicable Disease Information. Accessed 20.12.16 Available from:
7. Koutangani, T., Mainasara, H.B., Mueller, J.E (2015) Incidence, Carriage and Case-Carrier Ratios for Meningococcal Meningitis in the African Meningitis Belt: A systematic review and meta-analysis. PLOS One (6) Accessed 20.12.16 Available at:
8. Australian Government Department of Health and Ageing. Australian Immunisation Handbook, 10th edition, 2013. Canberra: DoHA; 2013. Meningococcal meningitis. Available at:
9. US CDC Health Information for International Travel 2016 (Chapter 3. Infectious diseases related to travel – Meningococcal Meningitis) Accessed 20.12.16 Available from:


Wounded dog in Durbar Square, Kathmandu, Nepal

September 28th is World Rabies Day and we thought it worthwhile to acknowledge the event with some reminders on how to manage a potential rabies exposure – what to do in the way of first aid and what medical treatment should involve – as a well as sharing a link to a recent article in the guardian online.

The story we wanted to share was written by a young woman who survived rabies infection – an extremely rare occurrence unfortunately. The young woman’s name is Jeanna Giese and the piece: Experience: I was bitten by a rabid bat
I had become the first known person ever to survive rabies without a vaccination, and the treatment became known as the Milwaukee protocol. 

It is important, however, to point out that the Milwaukee Protocol has been attempted many times since it was published, with little or no success. It is thought that Jeanna’s case was caused by a less virulent strain of bat rabies virus that allowed her immune system to mount a vigorous, early immune response. There have been similar other rare cases of survivors, with or without treatment, usually infected with bat variant rabies virus.

Things to know about rabies

Rabies is present in almost every country on earth, but most human cases occur in South Asia – particularly India. While dogs are responsible for most of the estimated 55,000 deaths each year, virtually any mammal can carry the virus, typically passing it on by biting another animal – or a person.
When you’re overseas, patting, feeding or even approaching animals – domestic or wild, healthy, sick or injured – is problematic: The virus is always fatal once its symptoms manifest themselves so you can’t ignore a potential exposure.
You know all this, right? Well, here are a few things you might not know about rabies…
You don‘t have to be bitten to get infected – Though rare, transmission can occur through infected saliva contacting the mucous membranes of your nose or eyes, or via a lick on a scratch or other break in the skin.
Infection isn’t immediate – After multiplying in the wound, the virus inevitably reaches nerve tissue. It then travels via the nervous system to the brain, where it continues to multiply with progressively more gruesome and painful clinical symptoms. If rabies post-exposure prophylaxis (PEP) is administered before the virus enters the nervous system, death can be prevented.
Animals may not appear rabid – The Hollywood image of a dog foaming at the mouth is a far less common sign of rabies than sudden, unexplained paralysis or a change in behaviour. A friendly cat may suddenly be very aggressive, while a normally playful puppy becomes shy and withdrawn. Not eating, eating strange (non-food) objects, pawing the mouth, appearing to choke, difficulty swallowing, chewing the bite wound, seizures, hypersensitivity to touch or sound are among the other sign an animal is infected.
Rabies incubation periods can vary – It usually takes 3-8 weeks for the rabies virus to incubate, but human cases have ranged from just days to years. That’s why it is important to receive post-exposure prophylaxis (PEP) as soon as possible and start within 48 hours. If medical care was not sought at the time of the bite it is still possible to get PEP well after the potential exposure, because if the incubation period is at the protracted end, the PEP may still be effective. 

Rabies is 100% preventable

While it’s 100% deadly, rabies is also 100% preventable. But, a series of steps needs to be taken in the right order to prevent infection.
1 – The wound needs to be cleansed thoroughly with lots of soap and water.
2 – If available, alcohol or iodine (such as betadine) should be applied. The wound should be covered with gauze to prevent infection (but not bound), or left uncovered.
3 – It is critical to seek expert medical attention as soon as possible. (Don’t wait for confirmation that the animal was infected. That could take days – even weeks.) It’s important to find a medical facility experienced in rabies treatment that stocks (or can obtain quickly) both Human Rabies Immune Globulin (HRIG) and the first dose of rabies cell culture vaccine. Injected at the site of the wound, HRIG contains rabies antibodies that immediately inactivate and control the rabies virus until the vaccine begins to work.
4 - Have a tetanus booster, if one is required.
5 - Observe the wound for redness and discharge. Bacterial infection may occur after animal bites and antibiotics may be required.

Vaccination provides lifelong protection

Discuss pre-travel rabies vaccination with your travel doctor or GP if you are:
– Travelling to a rabies-endemic country, irrespective of length of stay. Children in particular are at greater risk.
– Planning to live and work overseas in a rabies-endemic country.
– Wanting the protection that immunisation offers.
The course of rabies vaccine is relatively expensive. On the plus side, no booster is required unless you will be at risk of regular exposure through your occupation, or if indeed you have an exposure.
The advantages of pre-exposure vaccination are:
- If bitten or potentially exposed to the virus you will need only 2 injections over 3 days, not the 4-5 over 14-28 days required if you haven’t been vaccinated.
- The HRIG is not necessary, greatly simplifying treatment after a potential exposure. (HRIG is notoriously difficult to obtain overseas and always very expensive when you can.)
For regular travellers, rabies vaccination is a life-long investment in peace-of-mind travel.

© Pavla |

In tropical regions, chickenpox (or varicella) is a disease affecting older children or adults that’s more likely to strike during the ‘tourist’ season when it’s dry and the temperatures are cooler. For temperate climates, which most Australians live in, spikes of infection occur mostly in winter or spring1.

Proof indeed!
Before the chickenpox (varicella) vaccine was introduced into our national immunisation program in 2005 (a single dose was given to children under 14 years of age), each year over 200,000 cases of chickenpox were reported and around 1,500 of those needed hospitalisation. Even worse, an average of 7 deaths annually resulted2. Now, some 11 years later, that annual number of cases is now around 2,4003, and the greatest benefit has been seen in children aged 1-4 years and indigenous Australians4.

The USA added the vaccine to its routine vaccination program in 1996 in response to an estimated 4 million chickenpox cases each year, including 11,000 to 13,500 hospitalisations and 100 to 150 chickenpox-related deaths. The result was an astounding 85% reduction in the incidence of chickenpox. However because of continued outbreaks in schools and high rates of ‘breakthrough’ infections among immunised children3, a second dose was included in the routine childhood immunisation schedule in 2006. The National Notifiable Diseases Surveillance System has since documented an overall 97% reduction in the incidence of chickenpox since the varicella vaccination program was implemented5.

What do we do next?
Leading Australian immunisation resources, the Australian Technical Advisory Group on Immunisation (ATAGI) and the National Health and Medical Research Council (NHMRC), through the Australian Immunisation Handbook, have recommended a second vaccine dose as it provides protection similar to that of natural infection, adds to herd immunity and minimises the chance of breakthrough infection in children under 14 years of age, but acknowledge that the lack of funding means that it must be paid for by parents and carers privately.

The disease
Varicella-Zoster Virus (VZV), better known as chickenpox, is one of eight herpes viruses that can cause infection in humans and it’s highly contagious - up to 90% of household contacts will develop the disease. The virus is transmitted via the upper respiratory tract by aerosol spread of infected respiratory secretions or contact with the vesicular fluid from those infected. There is a 10 to 21 day incubation period and infected individuals are contagious from 2 days before the onset of the typical vesicular rash until all the rash vesicles are crusted. Typically the illness commences with a prodromal phase with symptoms such as fever, malaise. 1-2 days later the typical itchy, blister-like rash begins to appear. Initially the blisters (vesicles) affect the trunk and face and then spread to the rest of the body. Each vesicle has a red base which develops into a pustule that eventually forms a crust. New vesicles continue to appear for 3 to 7 days, with an average of 300 lesions (but can number from 10 up to 1,500).

Some 5% of children exposed actually get subclinical infections with subsequent immunity without knowing that they had contracted the infection.

Serious complications of acute varicella infection are rare, occurring in approximately 1% of cases. These may present as secondary bacterial infections of the skin lesions, pneumonia, encephalitis and hepatitis. Infection is usually more severe in adolescents and adults2. Following infection, antibodies are produced which will keep the virus at bay; however as we age, we become more susceptible and the virus can emerge and cause the painful herpes zoster infection, also known as shingles.

Vaccines: What we have and who do we give it to?
In Australia there are 2 vaccines containing live, attenuated varicella zoster virus, plus 2 others used only in children that are in combination with measles, mumps and rubella.
While not publicly funded, varicella vaccination is also recommended for non-immune adults at high risk of developing the disease: healthcare professionals, child-care workers, non-immune women prior to falling pregnant and parents. Also, household contacts with no immunity should be vaccinated to prevent the virus’ spread to immunosuppressed individuals. The vaccine schedule for the 14 years and older age group is 2 doses administered at least 4 weeks apart. An important note is that varicella-containing vaccines are contraindicated for pregnant women and pregnancy should be avoided for at least 28 days after vaccination.

If you’re travelling overseas
The risk of chickenpox is as high in developed countries as in developing ones. Very few countries include the vaccine in their routine childhood schedules - Canada, Costa Rica, Germany, Greece, Korea, Latvia, Luxembourg, Qatar, Saudi Arabia, UAE, Uruguay, USA and some parts of Spain & Italy1 - but coverage is increasing. Non-immune adults and children should consider vaccination, especially if planning longer stays or extensive travel.


Talk to anyone born prior to the 1960s and they will tell you about how polio used to be a terrifying reality. Hundreds of thousands of children across the globe were left paralysed in its wake and confronting images of wards full of iron lung machines circulated. With the introduction of the Salk vaccine in the mid-1950s, polio outbreaks became less frequent – the last epidemic to hit Australia was in the early 1960s. By 1966, the oral Sabin vaccine came into use and this was replaced with a more effective inactivated vaccine in 2005.  

About polio

Polio is a potentially serious viral illness spread through contact with infected faeces or saliva. It is made up of 3 types of wild polio virus WPV 1, 2 & 3 – all of which can cause disease. Polio has a variable incubation period of 3-21 days. Infected individuals are most infectious from 10 days before to 10 days after the onset of symptoms. In 90% of cases, polio infection passes without symptoms but, if they are present, they include headache, fever, vomiting, tiredness, neck and back stiffness, limb pain with or without paralysis. Severe paralytic polio occurs as a complication of WPV in 1 in 200 cases. It affects the spinal cord in 79% of cases, which leads to acute flaccid paralysis (AFP) affecting the limbs (mainly the legs and is asymmetrical). Paralytic polio can lead to death in 2 - 5% of children and 15 – 30% of adults. There is no cure and treatment is supportive; immunisation is the only way to prevent infection.

The largely asymptomatic nature of polio is a major hurdle in the eradication efforts as authorities try to identify cases in often remote regions of the world.


Figure from Global Polio eradication initiative 2011 report

 Eradication efforts

In 1988, the World Health Assembly (WHA) resolved to target polio with a view to achieving eradication by the year 2000 and formally founded the Global Polio Eradication Initiative (GPEI). At the time the GPEI was established, more than 1000 children a day worldwide were diagnosed with polio. Since then, in excess of 2.5 billion children have been immunised against polio and there has been some success in eradicating certain strains of WPV: the last case of WPV type 2 was reported in 1999 and the last WPV type 3 in 2012.

By 2006 the number of WPV cases had reduced by more than 99% and only four countries showed no interruption in WPV transmission, namely Afghanistan, India, Nigeria and Pakistan. India was removed from the list of endemic countries in March 2014 and in October 2015 Nigeria was also taken off the list.

In 2016 year-to-date, there have been 22 cases of polio reported across the globe compared to 350, 000 in 1988 and until last week (11th of August) the only 2 countries reporting wild polio were in fact Afghanistan and Pakistan. But in a major setback to the global eradication campaign, Nigeria has notified the WHO that after more than 2 years without wild polio 2 children have been diagnosed with paralytic polio in the northern state of Borno.

Polio Global Eradication Initiative – Data and monitoring

It was in 2012 that the World Health Organisation (WHO) instigated the Polio Eradication and Endgame Strategic Plan 2013 -2018 which outlined an all-inclusive strategy addressing how to deliver a polio-free world by 2018.


The Regional Commission for the Certification of Polio Eradication declared the WHO’s 11 country South-East Asia Region free of circulating wild poliovirus in March 2014 when India’s polio status changed. The region was the 4th of the 6 WHO regions to be certified as having interrupted all indigenous WPV circulation (the Americas in 1994, the Western Pacific in 2000 & the European Region in 2002).

Current situation

While the eradication programme has had successes, many factors stand in the way of reaching the eradication goal:

- The growing conflict and insecurity in the Horn of Africa and Middle East has played a major role in precipitating outbreaks in this area
- Increased instability in Pakistan, allowing continued transmission
- Disruption to immunisation activities in these areas has led to low population immunity and ongoing insecurity hampers the efforts to respond to outbreak reports
- Rapid detection of cases can be hindered in some areas by suboptimal surveillance
- Supplementary immunisation activities have had insufficient impact on stopping transmission in Pakistan and Afghanistan – this is mainly due to poor planning which results in the same groups of children missing vaccine doses.

Recommendations for travellers

In May 2014, the WHO declared the international spread of wild poliovirus from endemic areas into polio-free areas a ‘public health emergency of international concern’ and instituted some temporary recommendations: currently these only apply to Afghanistan & Pakistan and require that residents are to be vaccinated against polio and supplied with an International Certificate of Vaccination or Prophylaxis.

According to the US Centers for Disease Control and Prevention (CDC): Long-term travelers (staying >4 weeks) to the polio-infected countries may be required to show proof of polio vaccination when departing the polio-infected country. To meet these WHO requirements, long-term travelers should receive polio vaccine between 4 weeks and 12 months before the date of departure from the polio-infected country.

Australian children receive a primary course of polio vaccinations as part of the National Immunisation Program. For those adults who have completed a primary course and will be travelling to countries where wild poliovirus transmission still occurs, a single booster dose is recommended. However travel requirements do occasionally change in response to outbreaks, so up to date advice should be sought from your travel health provider or through the Australian Government Department of Health website.

© Artofphoto |

Both food poisoning and stomach flu can give rise to nausea, vomiting, cramps and diarrhoea - but the two conditions are in fact of different aetiology. Consuming food that has been contaminated with viruses, bacteria or parasites at some point during production causes food poisoning, whereas stomach flu is a viral infection of the digestive system. Stomach flu is most commonly brought on by norovirus or rotavirus, and is different from the conventional flu, which attacks the respiratory system. Both food poisoning and stomach flu cause a condition known as gastroenteritis –inflammation of the gut, which may involve the stomach, the small and/or large intestine.

According to the World Health Organization (WHO) report on the estimates of the global burden of foodborne diseases in 2010, there were approximately 600 million foodborne illnesses causing 420,000 deaths. 

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© Paulus Rusyanto |

With final packing and preparations well underway for those lucky travellers heading to the Olympic Games, there are just 16 days until the official opening ceremony. Travelvax has compiled a medical checklist outlining a few specific concerns for travel to Brazil, as well as the predictable stomach upsets, sunburn and security.

Events of the 2016 Olympic and Paralympic Games, while primarily set in Rio de Janeiro during August and September, will also take place in Belo Horizonte, Brasilia, Manaus, Salvador and São Paulo. To these areas, more than 200 member nations will arrive bringing over 10,000 athletes; in excess of 1 million visitors are expected to view the spectacle. As could be expected, the risk of spreading communicable diseases is increased with such large numbers - crowding, shared accommodation, travellers from all continents, as well as the diverse and varying ecology of Brazil, will put travellers and host-country residents at risk.

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