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Infectious diseases

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An uncommon fungal infection from farm animals

Trichophyton verrucosum is a cosmopolitan zoophilic dermatophyte. The normal host for this organism is cattle and occasionally horses. Human infection is acquired through direct contact with these animals or contaminated fomites, usually following minor trauma to the skin. Figure 1. Case 4 developed lesion after contact with beef cattle

Aim

To review cases of T. verrucosum infection diagnosed over a five year period.

Method

The Sullivan Nicolaides Pathology data base from 2009 – 2014 was searched for isolates of T. verrucosum. The laboratory services Queensland and extends into New South Wales as far south as Coffs Harbour.

Results

Seven cases of T. verrucosum over a five year period time frame that identified more than 12,500 dermatophyte infections in total. The most recent case (7) was a 54-year-old retired meat worker who owns a small property with one beef and three dairy calves all of which suffered from fungal infection. After clearing lantana and sustaining multiple scratches he developed a non-healing inflammatory lesion on his forearm which healed after three weeks of oral griseofulvin with some residual scarring. Biopsy, bacterial and fungal cultures all demonstrated fungal infection and cultures grew T. verrucosum. Scrapings collected from his infected cattle also demonstrated large spore ectothrix infection and grew this dermatophyte. Cases included six males and one female (Table 1). The age ranged from 27–71, mean 45 years. All except one (Case 5) had association with cattle with one also with horses. The site of infection was the forearm (5) (figure 1), leg (1) and face (1). Case 6 developed her leg lesion after birdwatching and camping on a cattle property although did not have direct contact with cattle. Three patients underwent skin biopsy and histology and in only one was hyphae seen on tissue sections. Four of five bacterial cultures also grew T. verrucosum on bacterial agar. Unlike other dermatophytes growth is enhanced at 37^OC. The cases were concentrated in SE Queensland and Northern NSW. Four of the cases required systemic antifungal therapy to clear and a number were treated with several courses of antibiotics prior to the diagnosis being established.

Case No.	Location	Sex/Age	Site	Fungal Microscopy	Contact	Treatment
1	Kyogle, NSW	M/32	Forearm	No hyphae	Cattle	Bifonazole T
2	Avondale, NSW	M/64	Forearm	Hyphae 1+	Cattle/horses	Terbinafine
3	Clarenza, NSW	M/27	Forearm	No hyphae	Cattle	No treatment
4	Charleville, Qld	M/35	Forearm	No hyphae	Cattle	Ketaconazole T
5	Boonah, Qld	F/71	Lower leg	Hyphae 1+	Cattle property	Ketoconazole O
6	Kingstown, NSW	M/29	Face	Hyphae 1+	Cattle	Griseofulvin O
7	Buccan, Qld	M/54	Forearm	Hyphae 1+	Cattle	Griseofulvin O

Table 1: Culture positive cases T. verrucosum infection SNP 2009-2014

Conclusion

verrucosum is an unusual zoonotic infection of the skin causing a highly inflammatory response involving the scalp, beard or exposed areas of the body in contact with cattle and horses.

Fluorescence under Wood’s ultra-violet light has been noted in cattle but not in humans. Unlike other dermatophytes, growth is enhanced at 37^OC. Systemic therapy is usually required to clear the infection which is frequently mistaken for an inflammatory bacterial infection, initially being treated with antibiotics. Advice on clearing the infection from animals was seen as important. To read more or view the original summary click here - General Practice Pathology is a regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Expert/s: Dr Linda Calabresi

Infectious diseases

Clinical Articles

Offer Q fever vaccine to all rural Australians

Anyone living in country Australia should consider being vaccinated against Q fever, according to researchers. The recommendation was made on the basis of their study, published in the Medical Journal of Australia which showed that living in a rural area for more than three months was associated with an increased risk of contracting Q fever even if there was little contact with farm animals, the traditional reservoir of the infection. In fact, the risk among country dwellers was 2.5 times higher than among people who had never lived rurally, according to the study which looked for evidence of past infection among 2740 blood donors in Queensland and NSW. “The prevalence of Q fever, caused by Coxiella burnetii, is substantial in Australia despite the availability of a safe and effective vaccine,” the study authors wrote. They point to stats that show that between 2013 and 2017 there were more 2500 notifications of Q fever in this country. They say this is very likely to be an underestimate, as most infections (up to 80%) are asymptomatic and sometimes they may have non-specific symptoms. But what we do know is that when Q fever does cause significant symptoms the morbidity can be substantial - pneumonia, hepatitis, endocarditis, and osteomyelitis. In addition, 10-15% of symptomatic patients will develop a protracted post-Q fever fatigue syndrome. To check just how many people have or have had the condition, researchers assessed blood donors from metropolitan Sydney and Brisbane, as well as blood donors in rural areas, namely the Hunter New England region of NSW and Toowoomba in Queensland. As well as collecting data on exposure, occupation and vaccination, the sera of the subjects was tested for both the C. burnetii antibody (as a measure of past exposure) and C. burnetii DNA (measuring current infection). No patient in the study was found to be currently infected with Q fever. Overall, 3.6% of the participants had evidence of past infection. And even though seroprevalence was higher in the rural areas compared to metropolitan areas, a significant proportion of those people from the city who tested positive for past Q fever had a history of living in the country at some time in the past. As you would expect, people working with sheep, cattle or goats, abattoir workers and people who had assisted at an animal birth were at highest risk. Vaccination of these people is already recommended. Non-farming people who just lived in rural areas were found to be at risk. “Having lived in a rural area, but with no or rare contact with sheep, cattle or goats, was itself an independent predictor of antibody seropositivity after accounting for the effects of other exposures”, the study authors said. Hence the recommendation we vaccinate everyone living in the country. But, as an accompanying editorial points out, expanding the current vaccination program is not without its challenges. Screening for humoral antibody and cell-mediated skin testing is required prior to vaccination so the need for at least two GP visits, access to intradermal skin testing and the cost are all potential barriers, the editorial authors said. There is also an issue with a lack of evidence about the safety and effectiveness of the Q fever vaccine in children. Nonetheless, all the experts agree: if we want to reduce the burden of Q fever in Australia, we will need to look beyond the select populations we are currently targeting for vaccination because there are obviously risk factors other than sheep, cattle and goats, at play.

References

Gidding HF, Faddy HM, Durrheim DN, Graves SR, Nguyen C, Hutchinson P, Massey P, Wood N. Seroprevalence of Q fever among metropolitan and non‐metropolitan blood donors in New South Wales and Queensland, 2014–2015. Med J Aust. 2019 Apr; 210(7): 309-15. DOI: 10.5694/mja2.13004 Francis JR, Robson JM. Q fever: more common than we think, and what this means for prevention. Med J Aust. 2019 Apr; 210(7): 305-6. DOI: 10.5694/mja2.50024

Expert/s: Dr Linda Calabresi

Infectious diseases

Clinical Articles

Diagnosing Measles

The Department of Health requires suspected cases of measles to be notified immediately without waiting for laboratory confirmation. Measles is an urgent, highly contagious, notifiable disease. Secondary infections occur in 75-90% of susceptible household contacts Transmission of the measles virus is by respiratory droplets and direct contact with respiratory secretions
Serological testing and PCR are the mainstays of laboratory diagnosis

Background

Measles is a highly contagious disease with secondary infections occurring in 75 – 90% of susceptible household contacts.¹ With suboptimal vaccination coverage in some areas, measles outbreaks remain an unfortunate reality in Australia.² A single case therefore has significant public health implications.

Clinical features

Transmission of measles virus is by respiratory droplets and direct contact with respiratory secretions. The virus can also survive on inanimate objects in the patient’s environment for at least 30 minutes. After an incubation period of 10 days (range 7 – 18 days) patients develop a prodrome consisting of fever, malaise, cough, coryza and non-purulent conjunctivitis. Koplik’s spots may develop during this time. These are whitish spots on an erythematous background on the buccal mucosa classically arising opposite the molar teeth. After about four days, a morbilliform rash appears, initially on the face and head, then extending to the trunk and limbs (Figure 1). The rash lasts 3 – 7 days. Patients usually make a full recovery, but complications including otitis media, pneumonia, seizures, and rarely encephalitis (subacute sclerosing panencephalitis) can occur. The case fatality rate in stable populations is estimated at around 2%, but rates up to 32% have been seen in refugee and displaced populations.⁴

Laboratory testing

Serological testing and PCR are the mainstays of laboratory diagnosis. In the early stages of infection, a single serology result demonstrating negative measles IgG and positive IgM in the context of the clinical picture outlined above provides strong evidence for a case of measles. It is important to note that serology can be negative in the early stages of infection. In a minority of patients, IgM may not be detected up to four days after the rash onset.⁵ Definitive serological diagnosis can be established with acute and convalescent sera, usually taken 10 – 14 days apart. A diagnostic rise in measles-specific IgG is a reliable indicator of recent infection. In early infection, PCR is performed on nose and throat swabs. Nose and throat swabs are usually pooled and analysed together in the testing laboratory. Swabs sent in viral or universal transport media are acceptable for testing, as are ‘dry’ swabs (no transport media). Swabs using bacterial transport media should be avoided as rates of viral detection may be lower. Other specimens that can be used for PCR are first pass urine and anticoagulated blood. When positive, PCR provides rapid confirmation of the clinical picture.

Case definition for measles

Initial investigation of suspected Measles

▪ Generalised maculopapular rash usually lasting three or more days and ▪ Fever (at least 38° if measured) present at the time of rash onset and ▪ Cough, coryza, conjunctivitis and Koplik’s spots

Notify immediately.

Laboratory Testing – Serology (IgG & IgM) and PCR.

Treatment and prevention

Treatment of measles remains supportive only. Infection control measures are important in order to avoid secondary cases. In the clinic;

The receptionist receiving patients should be alert to possible measles cases.
Those presenting with fever and rash should be given a single use mask and isolated from other patients
Consultation rooms used for assessment of suspected measles cases should be left vacant for at least 30 minutes after the consultation.³

Measles vaccination as part of the routine immunisation schedule for clinic patients is of the utmost importance. It is also important is ensuring that clinic staff vaccinations are kept up-to-date.

Notification

Due to its public health importance, the Department of Health requires all suspected cases of measles to be notified immediately without waiting for laboratory confirmation. This will help facilitate timely follow-up of the contacts, vaccination where required and will help prevent further transmission of the virus.

References

Perry RT, Halsey NA. The Clinical Significance of Measles: A Review. J Infect Dis. 2004 May 1; 189(S1): S4-16. DOI: 10.1086/377712
Victorian Department of Health, Blue Book, Infectious Diseases Epidemiology and Surveillance, Measles. [Accessed 8.9.2014] Available at: https://www2.health.vic.gov.au/public-health/infectious-diseases/disease-information-advice/measles
Kouadio IK, Kamigaki T, Oshitani H. Measles outbreaks in displaced populations: a review of transmission, morbidity and mortality associated factors. BMC Int Health Hum Rights. 2010 Mar 19; 10: 5 [Accessed 8.9.2014]. DOI: 10.1186/1472-698X-10-5

- General Practice Pathology is a regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Expert/s: Dr Linda Calabresi

Infectious diseases

Clinical Articles

Update on Q fever in Australia

With several hundred cases diagnosed each year, Australia has one of the highest rates of Q fever worldwide. Q fever is a bacterial infection which spreads from animals; mainly cattle, sheep and goats. It can present in different ways, but often causes severe flu-like symptoms. Importantly, the bacteria that cause Q fever favour dry, dusty conditions, and inhalation of contaminated dust is a common route of infection. There are now fears the ongoing droughts in Queensland and New South Wales may be increasing risk of the disease spreading. But there are measures those at risk can take to protect themselves, including vaccination.

What is Q fever and who is at risk?

Q fever is an infectious illness caused by the bacterium Coxiella burnetii, one of the most infectious organisms around. Q fever is zoonotic, meaning it can transmit to people from infected animals. It’s usually acquired through either direct animal contact or contact with contaminated areas where animals have been. Goats, sheep and cattle are the most commonly reported Q fever hosts, although a range of other animals may be carriers. Because of this association with livestock, farmers, abattoir workers, shearers, and veterinarians are thought to be at the highest risk of Q fever. People who also may be at risk include family members of livestock workers, people living or working near livestock transport routes, tannery workers, animal hunters, and even processors in cosmetics factories that use animal products. Q fever can be difficult to diagnose (it has sometimes been called “the quiet curse”). Infected people usually develop flu-like fevers, severe headaches and muscle or joint pain. These symptoms typically appear around two to three weeks after infection, and can last up to six weeks. A small proportion of people will develop persistent infections that begin showing up later (up to six years post-infection). These can include local infections in the heart or blood vessels, which may require lifelong treatment.

Are Q fever rates on the rise?

In Australia, 500 to 800 cases of Q fever (2.5 – 5 cases per 100,000 people) were reported each year in the 1990s according to the National Notifiable Diseases Surveillance System. A national Q fever management program was designed in 2001 to combat this burden. This program provided subsidised vaccination to at-risk people including abattoir workers, beef cattle farmers and families of those working on farms. Results were positive. Q fever cases decreased during the program and following its conclusion in 2006, leading to a historic low of 314 cases (1.5 cases per 100,000 people) in 2009. But since 2010, Q fever cases have gradually increased (558 cases or 2.3 per 100,000 were reported in 2016), suggesting further action may be necessary. Every year, the highest numbers of people diagnosed are from Queensland and NSW. And the true number of affected people is likely to be under-reported. Many infected people do not experience severe symptoms, and those who do may not seek health care or may be misdiagnosed.

Q fever and drought

The reason people are more susceptible to Q fever in droughts lies in the bacteria’s capacity to survive in the environment. Coxiella burnetii spores are very resilient and able to survive in soil or dust for many years. This also helps the bacteria spread: it can attach to dust and travel 10km or more on winds. The Q fever bacteria is resistant to dehydration and UV radiation, making Australia’s mostly dry climate a hospitable breeding ground. Hot and dry conditions may also lead to higher bacterial shedding rates for infected livestock. The ongoing drought could allow Q fever to spread and reach people who were previously not exposed. One study suggested drought conditions were probably the main reason for the increase in Q fever notifications in 2002 (there were 792 cases that year). This was the fourth driest year on record in Australia since 1900. We still need more evidence to conclusively link the two, but we think it’s likely that drought in Queensland and NSW has contributed to the increased prevalence of Q fever in recent years.

How can people protect themselves?

National guidelines for managing Q fever primarily recommend vaccination. The Q-VAX® vaccine has been in use since 1989. It’s safe and has an estimated success rate of 83–100%. However, people who have already been exposed to the bacteria are discouraged from having the vaccination, as they can develop a hypersensitive reaction to the vaccine. People aged under 15 years are also advised against the vaccine. Because the vaccine cannot be administered to everyone, people can take other steps to reduce risk. NSW Health recommends a series of precautions.

Author provided/The Conversation, CC BY-ND

What else can be done?

Vaccination for people in high-risk industries is effective to prevent Q fever infection, but must be administered well before people are actually at risk. Pre-testing requires both a skin test and blood test to ensure people who have already been exposed to the bacteria are not given the vaccine. This process takes one to two weeks before the vaccine can be administered, and it takes a further two weeks after vaccination to develop protection. This delay, along with the cost of vaccination, is sometimes seen as a barrier to its widespread use. Awareness of the vaccine may also be an issue. A recent study of Australians in metropolitan and regional centres found only 40% of people in groups for whom vaccination is recommended knew about the vaccine, and only 10% were vaccinated. We also need to better understand how transmission occurs in people who do not work with livestock (“non-traditional” exposure pathways) if we want to reduce Q fever rates. Nicholas J Clark, Postdoctoral Fellow in Disease Ecology, The University of Queensland; Charles Caraguel, Senior lecturer, School of Animal and Veterinary Science, University of Adelaide; Jane Heller, Associate Professor in Veterinary Epidemiology and Public Health, Charles Sturt University; Ricardo J. Soares Magalhaes, Senior Lecturer Population Health & Biosecurity, The University of Queensland, and Simon Firestone, Academic, Veterinary Biosciences, University of Melbourne This article is republished from The Conversation under a Creative Commons license. Read the original article.

Expert/s: Jane Heller, Charles Caraguel, Simon Firestone, Ricardo J. Soares Magalhaes, Dr Nicholas J Clark

Infectious diseases

Clinical Articles

Here’s what You Need to Know About Melioidosis, the Deadly Infection that Can Spread After Floods

The devastating Townsville floods have receded but the clean up is being complicated by the appearance of a serious bacterial infection known as melioidosis. One person has died from melioidosis and nine others have been diagnosed with the disease over the past week. The bacteria that causes the disease, Burkholderia pseudomallei, is a hardy bug that lives around 30cm deep in clay soil. Events that disturb the soil, such as heavy rains and floods, bring B. pseudomallei to the surface, where it can enter the body through through a small break in the skin (that a person may not even be aware of), or by other means. Melioidosis may cause an ulcer at that site, and from there, spread to multiple sites in the body via the bloodstream. Alternatively, the bacterium can be inhaled, after which it travels to the lungs, and again may spread via the bloodstream. Less commonly, it’s ingested. Melioidosis was first identified in the early 20th century among drug users in Myanmar. These days, cases tend to concentrate in Southeast Asia and the top end of northern Australia.

What are the symptoms?

Melioidosis can cause a variety of symptoms, but often presents as a non-specific flu-like illness with fever, headache, cough, shortness of breath, disorientation, and pain in the stomach, muscles or joints. People with underlying conditions that impair their immune system – such as diabetes, chronic kidney or lung disease, and alcohol use disorder – are more likely to become sick from the infection. The majority of healthy people infected by melioidosis won’t have any symptoms, but just because you’re healthy, doesn’t mean you’re immune: around 20% of people who become acutely ill with melioidosis have no identifiable risk factors. People typically become sick between one and 21 days after being infected. But in a minority of cases, this incubation period can be much longer, with one case occurring after 62 years.

How does it make you sick?

While most people who are sick with melioidosis will have an acute illness, lasting a short time, a small number can have a grumbling infection persisting for months. One of the most common manifestations of melioidosis is infection of the lungs (pneumonia), which can occur either via infection through the skin, or inhalation of B. pseudomallei. The challenges in treating this organism, though, arise from its ability to form large pockets of pus (abscesses) in virtually any part of the body. Abscesses can be harder to treat with antibiotics alone and may also require drainage by a surgeon or radiologist.

How is it treated?

Thankfully, a number of antibiotics can kill B. pseudomallei. Those recovering from the infection will need to take antibiotics for at least three months to cure it completely. If you think you might have melioidosis, seek medical attention immediately. A prompt clinical assessment will determine the level of care you need, and allow antibiotic therapy to be started in a timely manner. Your blood and any obviously infected body fluids (sputum, pus, and so on) will also be tested for B. pseudomallei or other pathogens that may be causing the illness. While cleaning up after these floods, make sure you wear gloves and boots to minimise the risk of infection through breaks in the skin. This especially applies to people at highest risk of developing melioidosis, namely those with diabetes, alcohol use disorder, chronic kidney disease, and lung disease.

Sanjaya Senanayake, Associate Professor of Medicine, Infectious Diseases Physician, Australian National University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Expert/s: A/Prof Sanjaya Senanayake

Infectious diseases

Clinical Articles

Why People Born Between 1966 and 1994 Are at Greater Risk of Measles – and what to Do About It

Australia was declared free of measles in 2014. Yet this summer we’ve seen nine cases of measles in New South Wales, and others in Victoria, Western Australia, South Australia and Queensland. High vaccination rates in Australia means the measles virus doesn’t continuously spread, but we still have “wildfire” outbreaks when travellers bring measles into the country, often unknowingly. If you haven’t received two doses of measles vaccine, you are at risk of contracting measles.

How can you catch it?

Measles is a highly contagious virus that spreads by touching or breathing in the same air as an infected person. The virus stays alive in the air or on infected surfaces for up to two hours. An infected person is contagious from the first day of symptoms (fever, cough and runny nose). These general symptoms start about four days before the rash develops, meaning contagious people can spread the virus even before they realise they have measles. If you’re not immune to the virus, through vaccination or past infection, the chance of becoming ill after being near someone with measles is 90%. Being in the same café, waiting in line at the checkout or flying on the same aeroplane as an infected person could be enough to pick up the disease.

Why is it so dangerous?

Measles causes a fever, cough, and a rash that starts around the hairline and then spreads to the whole body. It can also cause middle ear infections (otitis media), chest infections (pneumonia), and diarrhoea. Swelling and inflammation to the brain (encephalitis) occurs in 1 in every 1,000 cases and can lead to permanent brain damage or death. In 2017, 110,000 people died from measles worldwide. Even after surviving the initial illness, measles can cause a devastating and fatal complication known as subacute sclerosing panencephalitis (inflammation of the brain) many years later.

Why are people in their 20s to 50s more at risk?

To protect yourself against measles, you need two doses of measles-mumps-rubella (MMR) vaccine. Children in Australia routinely get this vaccine at 12 and 18 months of age. The second dose is given in combination with the chickenpox vaccine. It’s important to have two doses of MMR vaccine, especially if you haven’t reached your mid-50s. Most people older than this would have been infected with measles before vaccination was routine. People aged in their 20s to early 50s (those born from 1966 and 1994) are most likely to have only had one dose of MMR vaccine. While we’ve had the measles vaccine in Australia since 1968, a two-dose program was only introduced in 1992. A brief school-based catch-up program from 1993 to 1994 offered school children a second dose. Another school-based program provided children with catch-up vaccinations in 1998*. For those who missed out on the school program, catch-up vaccinations were given on an ad-hoc basis via GP clinics. So not everyone in this age group would have received two doses of the measles vaccine. If you are this age, you may not be not fully protected against measles. Checking with a GP or immunisation nurse is the best way to be sure. They will check your records, and may do a blood test if you have no proof of immunisation. Even if you can’t be sure of past vaccinations, it’s still safe to have an extra vaccine. And it’s free for those who need a catch-up dose. If you have a child under 12 months of age and you’re heading to a country with measles, an early additional vaccine dose can be given to protect your baby from measles. This ideally should be done at least a month before you travel, to ensure an immune response has time to develop. The routine scheduled doses at 12 months and 18 months will still need to be given later.

What if you’re not protected?

Unfortunately, there is no treatment for measles. Getting adequately vaccinated is the best form of defence against this serious disease. If you think you’ve been exposed or may be ill from measles, see your GP or call Health Direct or your public health department as soon as possible. If exposed, but not yet ill, it may not be too late to get a protective vaccine and ensure you don’t spread the disease to others. If you are unwell, and suspect measles, call ahead to let the clinic know so they can make provisions to keep you away from other patients in the waiting room. Other, more common, diseases can look like measles, so an urgent specific test (throat swab) must be done to confirm the infection. If measles is proven, public health workers will trace your contacts and your treating doctor will monitor you for complications.

Are we at risk of measles returning in Australia?

Australia currently has all-time high vaccine coverage, with 94.5% of five-year-old children fully immunised at the end of 2017. By keeping vaccine coverage near or above 95%, herd immunity where there are enough people vaccinated helps prevent measles from spreading to others, including those who cannot be vaccinated. But in our interconnected world, we must work together to reduce the threat of measles worldwide by boosting immunisation programs in regions with low coverage, including in the Asia Pacific. Measles have resurfaced in some countries due to falls in vaccine coverage from unfounded safety concerns as well as weak health systems. In the first six months of last year, for instance, Europe had 41,000 cases of measles, nearly double the total number of the previous year. This, among other factors, has prompted the World Health Organisation to list vaccine hesitancy as a top ten threat to global health in 2019. A continued global coordinated effort will be required to maintain elimination and prevent resurgence of this deadly disease in Australia. * Correction: this article has been updated to note a school-based catch-up program also operated in 1998.

- Kristine Macartney, Professor, Discipline of Paediatrics and Child Health, University of Sydney and Lucy Deng, Staff Specialist Paediatrician, National Centre for Immunisation Research and Surveillance; Clinical Associate Lecturer, Children's Hospital Westmead Clinical School, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Expert/s: Prof Kristine Macartney

Infectious diseases

Clinical Articles

Ross River Virus Spread and Suppression

Ross River virus is Australia’s most common mosquito-borne disease. It infects around 4,000 people a year and, despite being named after a river in North Queensland, is found in all states and territories, including Tasmania. While the disease isn’t fatal, it can cause debilitating joint pain, swelling and fatigue lasting weeks or even months. It can leave sufferers unable to work or look after children, and is estimated to cost the economy A$2.7 to A$5.6 million each year. There is no treatment or vaccine for Ross River virus; the only way to prevent is to avoid mosquito bites. Mosquitoes pick up the disease-causing pathogen by feeding on an infected animal. The typical transmission cycle involves mosquitoes moving the virus between native animals but occasionally, an infected mosquito will bite a person. If this occurs, the mosquito can spread Ross River virus to the person.

Animal hosts

Ross River virus has been found in a range of animals, including rats, dogs, horses, possums, flying foxes, bats and birds. But marsupials – kangaroos and wallabies in particular – are generally better than other animals at amplifying the virus under experimental infection and are therefore thought to be “reservoir hosts”. The virus circulates in the blood of kangaroos and wallabies for longer than other animals, and at higher concentrations. It’s then much more likely to be picked up by a blood-feeding mosquito.

Dead-end hosts

When we think of animals and disease we often try to identify which species are good at transmitting the virus to mosquitoes (the reservoir hosts). But more recently, researchers have started to focus on species that get bitten by mosquitoes but don’t transmit the virus. These species, known as dead-end hosts, may be important for reducing transmission of the virus. With Ross River virus, research suggests birds that get Ross River virus from a mosquito cannot transmit the virus to another mosquito. If this is true, having an abundance of birds in and around our urban environments may reduce the transmission of Ross River virus to animals, mosquitoes and humans in cities.

Other reservoir hosts?

Even in areas with a high rates of Ross River virus in humans, we don’t always find an abundance of kangaroos and wallabies. So there must be other factors – or animals yet to be identified as reservoirs or dead-end hosts – playing an important role in transmission. Ross River virus is prevalent in the Pacific Islands, for instance, where there aren’t any kangaroos and wallabies. One study of blood donors in French Polynesia found that 42.4% of people tested had previously been exposed to the virus. The rates are even higher in American Samoa, where 63% of people had been exposed. It’s unclear if the virus has recently started circulating in these islands, or if it’s been circulating there longer, and what animals have been acting as hosts.

What about people?

Mosquitoes can transmit some viruses, such as dengue and Zika between people quite easily. But the chances of a mosquito picking up Ross River virus when biting an infected human is low, though not impossible. The virus circulates in our blood at lower concentrations and for shorter periods of time compared with marsupials. If humans are infected with Ross River virus, around 30% will develop symptoms of joint pain and fatigue (and sometimes a rash) three to 11 days after exposure, while some may not experience any symptoms until three weeks after exposure. To reduce your risk of contracting Ross River virus, take care to cover up when you’re outdoors at sunset and wear repellent when you’re in outdoor environments where mosquitoes and wildlife may be frequently mixing. This article is republished from The Conversation under a Creative Commons license. Read the original article.

Expert/s: Eloise Stephenson, Dr Cameron Webb, Emily Johnston Flies

Infectious diseases

Clinical Articles

Parvovirus Infection: Trivial Except when It’s Not

Each year, around late winter to spring, we see an increase in the number of serologically-confirmed infections with parvovirus B19. These infections are usually trivial in nature and benign in outcome, but there are important exceptions to this rule. This article will review the typical presentation and course of infection with parvovirus B19, discuss its potential adverse outcomes and in whom that potential is greatest. Parvovirus B19 was discovered and named in 1975 by virologists working at the University of Sydney. It is the predominant genotype (of three) which are pathogenic for humans. Infection is common, occurring sporadically and in clusters, it has a clear seasonality (late winter through to spring) and also has an epidemic cycle with a 4–5 year periodicity. While 50–80% of adults have parvovirus IgG and are regarded as immune, there remains a significant proportion of the adult population who are susceptible to infection.

Infection and its complications

Humans are the only known host for parvovirus B19. The anaemia and thrombocytopenia which are usually subclinical in a normal individual may, in those with increased red blood cell turnover (for example, sickle-cell disease, haemoglobinopathies), lead to significant falls in haemoglobin and, potentially, aplastic crisis. Because B19 is cytotoxic to fetal red blood cell precursors, fetal infection may cause severe anaemia, high cardiac output failure and non-immune hydrops. Unlike rubella, which has a similar presentation and with which it can cross-react in serological assays, B19 has no association with congenital malformations.

Clinical presentation

The clinical presentation of infection is highly variable; Fifth disease, slapped cheek disease and erythema infectiosum all refer to the same febrile exanthem, without significant sequelae, occurring in young children, while an adult frequently presents with fever and arthralgia/arthritis but with no rash at all. However, the same adult with sickle-cell disease may present in aplastic crisis and, in pregnancy, there is a risk of hydrops fetalis, myocarditis and fetal death. In general, the typical presentation of B19 infection in children and its benign outcome require laboratory confirmation relatively infrequent. By contrast, the more variable and dramatic clinical presentation in adults, the absence of any rash rather than the presence of a typical one and, in women, the threat of adverse pregnancy outcomes lead to a much greater reliance on laboratory diagnosis.

Laboratory diagnosis

Generally, diagnosis of parvovirus B19 infection is serological. IgM is usually detectable from just before the onset of symptoms and present in >90% of people by the time of onset of the rash. Detectable IgM is suggestive of infection but not conclusive, unless an IgG seroconversion is also demonstrated or (if IgG was also present at the time IgM was detected) there has been a significant rise when testing is repeated after two weeks. When infection has been diagnosed in a pregnant woman, there is little reason to attempt definitive diagnosis in the fetus. Parvovirus PCR can provide that confirmation however it requires amniocentesis to obtain the required specimen.

Erythema infectiosum (Fifth disease, slapped cheek disease)

These terms all refer to the same presentation of parvovirus B19 infection in childhood. After an incubation period of 4–14 days, and a non-specific prodrome of fever, malaise and rhinorrhoea, a red, macular rash appears on the cheeks, fading to become more lacy and erythematous after a few days. There is no such typical presentation in an adult (see above), with rash being variable or absent. Joint pain and swelling, however, are almost as typical of adult infection as a slapped-cheek rash is in childhood.

Parvovirus B19 infection in pregnancy

Around 40% of women of child-bearing age are susceptible to parvovirus infection. The highest infection rates are seen in school teachers, day-care workers and women with school-aged children in the home. The obvious common factor is their greater likelihood of being exposed to children with erythema infectiosum and that exposure being sustained for longer. Transmission is thought to be through respiratory droplets, with infectivity lasting from one week prior to the rash until the time of onset of the rash. Between 25 and 50% of susceptible household contacts of a case will acquire infection, of whom up to 50% will do so asymptomatically. Therefore, unless women are aware of their potential exposure there is a significant risk of acquisition going undetected. The incidence of parvovirus infection in pregnancy is approximately 1–2% and vertical transmission occurs in about 50%. The risk of hydrops is low (estimated incidence, 3–6%) but there is an overall excess fetal loss of 10% for infection acquired in the first 20 weeks of pregnancy. The fetus is particularly susceptible to hydrops in the second trimester when haematopoiesis is occurring in the liver. During this time, there is a 34-fold increase in red cell mass and a reduction in the life span of the red blood cells. In pregnant women with proven recent infection, the overall fetal death rate of hydrops or its treatment is 0.6% according to ASID guideline.

Management of proven parvovirus B19 infection in pregnancy

When maternal infection is proven or is highly likely, it is not necessary to prove that vertical transmission has occurred, but the fetus should be monitored by frequent ultrasonography. This allows the early detection and assessment of both myocardial dysfunction and fetal hydrops, but more importantly, it makes possible the early detection of fetal anaemia, prior to the development of hydrops. The peak systolic velocity (PSV) of the waveform in the middle cerebral artery can detect moderate to severe fetal anaemia with a sensitivity of 100%, followed by intra-uterine transfusion. General Practice Pathology is a regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Expert/s: Dr Ian Chambers

Infectious diseases

Clinical Articles

Health Check: How Long are You Contagious with Gastro?

There’s no way you’d want to go to work when you’ve got the telltale signs of gastro: nausea, abdominal cramps, vomiting and diarrhoea. But what about when you’re feeling a bit better? When is it safe to be around colleagues, or send your kids to school or daycare? The health department recommends staying home from work or school for a minimum of 24 hours after you last vomited or had diarrhoea. But the question of how long someone is contagious after recovering from gastro is a very different question. What causes gastro? To better understand how long you can be contagious with gastro, we need to look at the various causes. Viruses are the most common causes of gastro. Rotavirus is the leading cause in infants and young children, whereas norovirus is the leading cause of gastro in adults. There are around 1.8 million cases of norovirus infection in Australia each year. This accounts for almost 40% of the total cases of gastro. Bacterial gastroenteritis is also common and accounts for around 1.6 million cases a year. Of those cases, 1.1 million come from E. coli infections. Other bacteria that commonly cause gastro include salmonella, shigella and campylobacter. These bacteria are often found in raw or undercooked meat, seafood, and unpasteurised milk. Parasites such as giardia lamblia, entamoeba histolytica and cryptosporidium account for around 700,000 cases of gastro per year. Most of the time people recover from parasitic gastroenteritis without incident, but it can cause problems for people with weaker immune systems. Read more: Health Check: I feel a bit sick, should I stay home or go to work? Identifying the bug Most cases of diarrhoea are mild, and resolve themselves with no need for medical attention. But some warrant further investigation, particularly among returned travellers, people who have had diarrhoea for four or five days (or more than one day with a fever), patients with bloody stools, those who have recently used antibiotics, and patients whose immune systems are compromised. The most common test is the stool culture which is used to identify microbes grown from loose or unformed stools. The bacterial yield of stool cultures is generally low. But if it does come back with a positive result, it can be potentially important for the patient. Some organisms that are isolated in stool cultures are notifiable to public health authorities. This is because of their potential to cause serious harm in vulnerable groups such as the elderly, young children, pregnant women and those with weakened immune systems. The health department must be notified of gastro cases caused by campylobacter, cryptosporidium, listeria, salmonella, shigella and certain types of E.coli infection. This can help pinpoint outbreaks when they arise and allow for appropriate control measures. You might feel better but your poo isn’t Gastro bugs are spread via the the faecal-oral route, which means faeces needs to come into contact with the mouth for transmission to occur. Sometimes this can happen if contaminated faecal material gets into drinking water, or during food preparation. But more commonly, tiny particles of poo might remain on the hands after going to the toilet. Using toilet paper to wipe when you go to the toilet doesn’t completely prevent the contamination of hands, and even more so when the person has diarrhoea. The particles then make their way to another person’s mouth during food preparation or touching a variety of contaminated surfaces and then putting your fingers in your mouth. After completely recovering from the symptoms of gastro, infectious organisms can still be shed into stools. Faecal shedding of campylobacter, the E. coli O157 strain, salmonella, shigella, cryptosporidium, entamoeba, and giardia can last for many days to weeks. In fact, some people who have recovered from salmonella have shed the bacteria into their stools 102 days later. Parasites can remain alive in the bowel for a long period of time after diarrhoea finishes. Infectious cryptosporidium oocysts can be shed into stools for up to 50 days. Giardia oocysts can take even longer to be excreted. So, how long should you stay away? Much of the current advice on when people can return to work, school or child care after gastro is based on the most common viral gastroenteritis, norovirus, even though few patients will discover the cause of their bug. For norovirus, the highest rate of viral shedding into stools occurs 24 to 48 hours after all symptoms have stopped. The viral shedding rate then starts to quickly decrease. So people can return to work 48 hours after symptoms have stopped. Yes, viral shedding into stools can occur for longer than 48 hours. But because norovirus infection is so common and recovery is rapid, it’s not considered practical to demand patients’ stools be clear of the virus before returning to work. While 24 hours may be appropriate for many people, a specific 48-hour exclusion rule is considered necessary for those in a higher-risk category for spreading gastro to others. These include food handlers, health care workers and children under the age of five at child care or play group. If you have a positive stool culture for a notifiable organism, that may change the situation. Food handlers, childcare workers and health-care workers affected by verotoxin E.coli, for example, are not permitted to work until symptoms have stopped and two consecutive faecal specimens taken at least 24 hours apart have tested negative for verotoxin E. coli. This may lead to a lengthy exclusion period from work, possibly several days. How to stop the spread Diligently washing your hands often with soap and water is the most effective way to stop the spread of these gastro bugs to others. Consider this: when 10,000 giardia cysts were placed in the palm of a hand, handwashing with soap eliminated 99% of them. To prevent others from becoming sick, disinfect contaminated surfaces thoroughly immediately after someone vomits or has diarrhoea. While wearing disposable gloves, wash surfaces with hot water and a neutral detergent, then use household bleach containing 0.1% hypochlorite solution as a disinfectant.

Expert/s: Healthed

Infectious diseases

Clinical Articles

Typhoid in the modern era

The microbiology laboratory has made great strides in introducing clinically useful diagnostics over the past couple of decades, particularly in recent years with the development of molecular assays that ‘narrow the gap’ and provide early diagnoses. While introducing new tests, it has also been important to evaluate and discard old tests that may not contribute greatly to patient outcomes. One such test that has come under the spotlight is the classic Widal agglutination test in the diagnosis of typhoid. The Widal test, developed by George Fernand Widal in 1896, uses a suspension of killed Salmonella typhi as antigen to detect agglutinating antibodies to somatic O antigens and flagellar H antigens present in serum of typhoid patients. There are many reasons for its lack of clinical utility. Antibodies are not present in the acute illness and take time to develop. Significant cross reactivity can occur with other infectious agents that mimic typhoid including malaria, dengue, endocarditis, tuberculosis and chronic liver disease. Other limitations are of a technical nature and include non-standardisation of the antigen preparation used in the assay, interference with serological responses following typhoid vaccination commonly provided to travellers, and prior exposure and antibodies in patients most susceptible to typhoid, especially those from endemic areas visiting friends and relatives (VFRs). Unless multiple antigens are included, it generally does not detect the other causes of enteric fever, S. Paratyphi A, B and C. It is now time to discontinue this simple agglutination test for typhoid in modern medicine and consider more appropriate diagnostic tests. Typhoid fever Typhoid fever is a life-threatening illness caused by the bacterium Salmonella Typhi. Whereas Salmonellae which cause gastroenteritis are zoonoses, humans are the only reservoir for S.Typhi and S. Paratyphi which cause enteric fever. Typhoid fever is still common in the developing world where it affects about 21.5 million people each year but is much less common in the Lucky Country such as ours where good sanitation prevails. About 100 cases are notified each year in Australia. In 2014, 92% of cases were acquired overseas. India continues to be the most common country of acquisition and in 2014 accounted for more than half of cases. Most transmission occurs through contaminated drinking water or food. Large epidemics are most often related to faecal contamination of water supplies or street-vended foods. A chronic carrier state – excretion of the organism for more than one year – occurs in about 5% of infected persons. Where no travel history is present, the likely source of infection is contaminated food or water from a human carrier akin to ‘Typhoid Mary’. Such an outbreak was reported in Auckland, New Zealand, this year where 20 local cases and one death occurred when a carrier from Samoa helped prepare food at a church community gathering. The incubation period is typically eight to 14 days but may be much longer. Without therapy, the illness may last for three to four weeks and death rates range between 12% and 30%. Increasing resistance to available antimicrobial agents, including fluoroquinolones, has occurred in recent years. Resistance to antimicrobials including amoxycillin, and trimethoprim+sulfamethoxazole has limited the options for treatment; reduced susceptibility to quinolones is common in infections acquired on the Indian subcontinent and in Southeast Asia. While awaiting the results of susceptibility testing, azithromycin or ceftriaxone should be used for initial therapy for infections acquired in these regions. Diagnosis of enteric fevers Two sets of blood cultures are the single most useful diagnostic procedure for diagnosis of enteric fever. Other bodily fluids and tissues may yield positive cultures including faeces, urine, and if seeded, bones and joints, liver and gall bladder. Food handlers, healthcare workers, carers of children, and carers of the elderly, and others who are not able to maintain their own personal hygiene, should further be excluded from working with food or caring for people until two consecutive stool specimens – collected at least 48 hours apart and the first specimen collected not sooner than 48 hours post-cessation of antibiotics – are culture negative. Prevention Both an oral live attenuated multi-dose vaccine and a killed vaccine are available. Booster doses after 3-5 years are generally required if continued exposure occurs. Vaccine efficacy is of the order of only 80%. What to order Blood culture x 2 (Salmonella Typhi and Salmonella Paratyphi) Faeces for Bacterial PCR and MCS; Urine MCS Collection Centres: Faeces and urine samples are accepted at all collection centres. Blood cultures are collected only at designated collection centres. Sample Blood (use blood culture bottles), faeces, urine Transportation Ambient Costs Medicare rebate applies Typhoid Mary Mary Mallon, better known as Typhoid Mary, was an Irish immigrant to New York and the first person in the United States identified as an asymptomatic carrier of the pathogen associated with typhoid fever. Over the course of her career as a cook, she was presumed to have infected 51 people, three of whom died. She was twice forcibly isolated by public health authorities and died after a total of nearly three decades in isolation. General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Expert/s: Dr Jenny Robson

Infectious diseases

Clinical Articles

New Virus Putting Babies in Hospital

In the last few months of 2017, over 200 Australian infants were hospitalised due to infection with the little known human parechovirus, say Australian public health experts in the latest issue of the MJA. The infected infants were admitted with conditions such as severe sepsis and meningoencephalitis. Less common presentations included acute abdomen from intussusception, pseudo-appendicitis and even bowel perforation. According to the MJA review, parechovirus was originally included under the echovirus umbrella back in the 1960’s, but became an entity in its own right, in the 90’s. There are close to 20 genotypes of the virus, but to date only three (genotypes 1,3 and 6) are thought to cause human disease. For the most part parechovirus causes mild gastro or respiratory tract infections. However, one of the genotypes – genotype 3 - has been found to be considerably more dangerous, especially in babies. “It is now recognised as a leading cause of sepsis-like illness and central nervous system infection, particularly in young infants,” the review authors wrote. The first ‘epidemic’ in Australia of this parechovirus genotype occurred in spring-summer of 2013-2014. Another outbreak occurred two years later – the spring-summer of 2015-2016. This most recent ‘epidemic’ appeared to start in Victoria last August and has now spread nationwide with over 200 infants hospitalised to December. For GPs, the key presenting features to be on the lookout for are fever, irritability and sepsis-like illness – which aren’t very specific. More helpfully - while not all infected children will have a rash, if the presenting infant is ‘red, hot and angry’ -think parechovirus, the authors recommend. Infants younger than three months are most likely to be hospitalised and, of course, really young infants (less than a month old) are at greatest risk of complications so should be sent to hospital earlier rather than later. To diagnose this infection, specific PCR testing needs to be requested of either stool or CSF. Just testing for enteroviruses will not be sufficient. Unfortunately, as yet there is no specific treatment for parechovirus. Given the presentation is the same as that of bacterial sepsis, the review authors suggest antibiotics be commenced until cultures come back negative and bacterial infection is excluded. But other than that, the treatment is mainly supportive and close monitoring and perhaps hospitalisation is required. Of particular concern are a number of studies that suggest infection that is severe enough to require the child be hospitalised is associated with high risk of neurological sequelae. As a consequence, the authors recommend that all children hospitalised with parechovirus be followed up with a paediatrician – at least until they start school- ‘to monitor development and learning, and manage complications including seizures.’ In terms of a vaccine, there is not one yet developed against parechovirus. They suggest research efforts should focus on developing vaccines that target the most pathogenic genotypes of a virus rather than trying to eradicate the entire genus such as has occurred in China with the vaccine against EV71 – a specific enterovirus that causes a complicated hand, foot and mouth disease. Regardless the need to find a vaccine is a priority. “The high morbidity in young children provides a strong case for prevention,” they concluded. Ref: MJA doi: 10.5694/mja18.00149

Expert/s: Dr Linda Calabresi

Infectious diseases

Clinical Articles

Here’s what you need to know about the new flu vaccines for over-65s

In an attempt to avoid a repeat of last year’s horror flu season, Health Minister Greg Hunt yesterday announced the government would fund two new flu vaccines in 2018 to try to better protect the elderly. While influenza affects people of all ages, infections among the elderly are more likely to require hospitalisation or cause serious complications such as pneumonia and heart attacks. Of the 1,100 Australians who died last year from flu-related causes, 90% were aged 65 and over. The two free vaccines for over-65s work in different ways: FluZone High Dose is a high-dose version; Fluad adds an additional ingredient to boost its effectiveness. Both are recommended for use only in people aged 65 and over. But neither is perfect. And it’s important to remember flu vaccines are, at best, only partially protective.

Why do we need new vaccines for flu?

Australia’s National Immunisation Program provides free influenza vaccine for the elderly, as well as other high-risk groups including pregnant women, those with chronic diseases and Indigenous Australians.

Read more: Flu vaccine won't definitely stop you from getting the flu, but it's more important than you think

Older people’s immune systems don’t respond to flu vaccines as well as younger people’s. Recent studies have also shown that flu vaccines don’t appear to be as effective in the elderly at protecting against flu and its complications. Compounding this problem is that the flu subtype that tends to affect older people (A/H3N2) is different to that which affects younger people (A/H1N1). Although the seasonal flu vaccine now contains four strains to cover all the relevant subtypes present, the protection against H3N2 infection appears to be poorer than against other strains. Two strategies are attempting to improve the effectiveness of flu vaccines. One is to increase the dose of the flu strains in the vaccine. This is the basis for Sanofi’s High Dose FluZone vaccine, which contains four times the amount of flu antigen than the standard dose. Another way is to add a substance that improves the immune response, known as an adjuvant, in combination with the flu strains. This is the basis for Seqirus’ (CSL) Fluad vaccine, which contains the adjuvant MF59. This vaccine has been used overseas for many years, but has only been become available in Australia this year.

How much better are these vaccines than the current vaccine?

Compared to the standard flu vaccine, the high-dose version has been shown to better stimulate the immune system of older users to make protective antibodies. It has been shown to better reduce rates of flu infection in over-65s than the standard vaccine. And, interestingly, it also seems to protect against pneumonia. One common criticism of clinical trials is that they don’t include the types of people who are found in the “real world”. But population based observational studies suggest that the high-dose vaccine is more protective than the standard-dose vaccine where H3N2 is the predominant circulating strain – as it was last year.

Read more: Here's why the 2017 flu season was so bad

What about the Fluad (adjuvanated) vaccine? Compared to the standard vaccine, adjuvanted flu vaccine has been shown to better stimulate the immune system of older users to make protective antibodies. Unlike the high-dose vaccine, there have not been clinical trials that show a difference in infection rates compared with the standard vaccine. But observational data suggests the adjuvanted vaccine is more protective against hospitalisation with influenza or pneumonia – to a similar degree as the high-dose vaccine. One problem with both these vaccines is that they only contain three strains, rather than the four strains in the current vaccine. The strain missing from the new vaccines is an influenza B type. But the benefits of better protection against the most common three strains in the new vaccine appear to outweigh the potential loss of protection against the missing B strain.

Are the new vaccines safe?

Both vaccines are safe, but commonly cause mild side effects, and very rarely can cause serious side effects. However, these risks from the vaccine are less than from getting influenza infection. The main side effect of vaccines relates to their effect in stimulating the immune system. In many people they cause a sore arm and, less commonly, a fever. The side effects of these new flu vaccines are slightly more common than with standard vaccines. Generally, these side effects are mild and don’t last long. None of the flu vaccines used in Australia contains live virus and therefore can’t cause flu infection. However, the vaccination season (April to June) usually occurs around the same time as when another respiratory virus (RSV) circulates, so this respiratory infection is commonly misattributed to vaccination.

Read more: Health Check: when is 'the flu' really a cold?

Rare but serious side effects, such as Guillain Barre Syndrome (where the immune system attacks nerves), have been described after flu vaccination. Studies suggest that the risk of these side effects are less common after the flu vaccine than after flu infection. People with allergies should discuss flu vaccines with their doctor. In the past, there has been concern that the flu vaccines, which are manufactured in eggs, may elicit allergic reactions in people with egg allergy. However, it is now thought that people with egg allergies can receive flu vaccines safely under appropriate supervision. In 2009, an adjuvanted vaccine (Pandemrix) was thought to be implicated in cases of narcolepsy (a disease associated with excessive sleepiness) in Europe. However, this primarily occurred in children (rather than the elderly), and with a different adjuvant (ASO3) than is being used in Fluad (MF59)

Which vaccine should I get?

The two vaccines have not been compared head to head, so it isn’t known which one is better. The available data suggest they are similar to each other. In practice, what vaccine you’ll receive will depend on what’s available at your GP or pharmacy. It is important to note that these vaccines are only recommended for use in people 65 years of age or older, and are not recommended for use in people under this age. The standard vaccine will still be available for younger people. There are no data to support the use of multiple doses of vaccines of the same or different types.

Read more: Flu is a tragic illness. How can we get more people to vaccinate?

Neither of the new vaccines is perfect – they simply reduce your risk of getting flu to a slightly greater effect than the standard vaccine. Like other flu vaccines, there is still the chance that the vaccine strains don’t match what’s circulating. Despite the common perception that the flu is mild illness, it causes a significant number of deaths worldwide. To make an impact on this, we need better vaccines, better access to vaccines worldwide and new strategies, such as increasing the rate of vaccination in childhood. Allen Cheng, Professor in Infectious Diseases Epidemiology, Monash University This article was originally published on The Conversation. Read the original article.

Expert/s: Prof Allen Cheng