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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

Infectious diseases

Clinical Articles

Unprecedented Rise In Scarlet Fever In England And Asia

Scarlet fever is on the rise. According to the latest issue of The Lancet Infectious Diseases, cases of scarlet fever in the UK reached a 50 year high last year with a seven fold increase in new cases in the last five years. In addition, similar increases having been reported in a number of Asian countries including Vietnam, China, South Korea and Hong Kong. But public health authorities remain perplexed as to why the disease appears to be making a comeback. Detailed analysis of the causative organism shows different strains of the strep bacteria have been responsible for the UK and Asian outbreaks, so they are unsure if they are linked at all or whether the resurgence has to do with external factors such as the immune status of the population or environmental factors. So far it would seem that Australia is yet to be affected by this increased incidence however experts are warning we should not be complacent. Unlike in England, scarlet fever is not a notifiable disease in this country except in WA. And even in the UK, data suggests marked under-reporting. Scarlet fever is highly contagious and usually affects children under the age of 10, although it can occur in adults as well. While the bacterial infection, caused by Streptococcus pyogenes or group A Streptococcus (GAS) was a common cause of death in the 1800s, these days it is readily treated with antibiotics usually penicillin. However, failure to recognise the condition and treat it appropriately can lead to complications such as pneumonia, and liver and kidney damage. Children with the infection typically experience sore throat, headache and fever along with the characteristic popular pink-red rash that feels like sandpaper and the so-called strawberry tongue. Diagnosis is usually made via a throat swab. In an accompanying comment, Australian infectious diseases researchers Professor Mark Walker and Stephan Brouwer from the University of Queensland said, “Scarlet fever epidemics have yet to abate in the UK and northeast Asia. Thus, heightened global surveillance for the dissemination of scarlet fever is warranted.” In other words, be alert, people! Ref: Lancet Infect Dis 2017 Published Online November 27, 2017 http://dx.doi.org/10.1016/ S1473-3099(17)30693-X Online/Comment http://dx.doi.org/10.1016/ S1473-3099(17)30694-1

Expert/s: Dr Linda Calabresi

Infectious diseases

Clinical Articles

Schistosomiasis

Schistosomiasis, also known as bilharzia, is the second most prevalent tropical disease after malaria and is a leading cause of morbidity in many parts of the world. It is not uncommon in Australia because of the many travellers who visit endemic areas and swim or bathe in freshwater lakes and streams. Places commonly implicated include Lake Kariba and Lake Malawi in Africa. Immigrants and refugees from bilharzia endemic countries are also likely to present with untreated infection. With increasing travel to and migration from Africa and the Americas knowledge of the dangers and means of avoiding schistosomiasis is essential. Schistosomiasis is caused by trematodes of the genus Schistosoma. The principal schistosomes of medical importance, S japonicum, S mansoni, S mekongi (intestinal schistosomiasis) and S haematobium (urinary schistosomiasis), infect people who enter water in which infected snails (intermediate hosts) are living. The larval cercariae shed by the snail actively penetrate unbroken skin and develop into schistosomulae that migrate through the lungs to the liver where they mature into adults. Female worms lay eggs that pass through the vessels and tissues to the lumen of the gut or bladder (depending on localisation of worms). A proportion of eggs escape from the host and may be found in faeces or urine. The host's immune response to eggs that become lodged in the tissues is largely responsible for disease, Figure 1.

Geographic distribution

This is governed by the distribution of the intermediate host snail. S haematobium Africa, Middle East, India (only Maharashtra) S japonicum Philippines, Indonesia (only Sulawesi), parts of China S mansoni Africa, Middle East, some Caribbean Islands, parts of South America (Brazil, Surinam, Venezuela) S mekongi Laos and Cambodia S intercalatum 10 countries within the rainforest belt of West Africa.

At-risk groups

Owing to the absence of suitable snail hosts, transmission cannot occur in Australia. A history of overseas travel or residence is essential for this diagnosis. Chronic schistosomiasis is more likely to be seen in migrants and refugees from endemic areas. In Australia, where the definitive host is freshwater and marine birds, non-human trematodes may cause schistosomal dermatitis (cercarial dermatitis, swimmer's itch). Onset is usually within 15 minutes of skin contact with cercariae.

Clinical presentation

Disease due to schistosomiasis depends on the infecting species and the intensity of infection. Acute schistosomiasis occurs two to 12 weeks post infection and symptoms last for periods varying from one day to a month or more; recurrence of symptoms 2-3 weeks later is common. Between 40-95% of individuals, not previously exposed to infection, develop symptoms which include fever, malaise, headache, abdominal pain, diarrhoea and urticaria. Many have eosinophilia. After the initial acute onset, most become asymptomatic, although those with S haematobium infections may develop microscopic or macroscopic haematuria. Rare complications result from ectopic deposition of eggs in the spinal cord and brain. Most travellers are only mildly infected and are therefore often asymptomatic and unlikely to develop the severe manifestations of chronic schistosomiasis. Severe disease occurs in patients with heavy and prolonged infection. Hepatosplenomegaly, portal hypertension, ascites and oesophageal varices may result from intestinal schistosomiasis. And frank haematuria with varying degrees of impairment of the urinary bladder and ureters may occur with S haematobium infections.

Diagnosis

The prepatent period of S japonicum, S mansoni and S mekongi is 6-8 weeks, and for S. haematobium 10-12 weeks. Examination of faeces or urine before this time often yields false negative results. Similarly, with serology, testing too early may result in false negative results. Antibody development occurs slightly before eggs are detected. Eosinophilia (greater than 0.60 x10³/mL) is present in up to 80% of patients with infections; however, its absence does not exclude infection.

Parasitologic examination

Diagnosis is by demonstration of eggs of S japonicum, S mansoni and S mekongi in faeces, or eggs of S haematobium in urine. At least two stool or urine specimens should be submitted for examination over a period of 10 days. Whilst eggs may be found in all specimens of urine, there is some evidence of a diurnal periodicity with a peak of excretion around midday. Collection of the terminal portion of urine collected between noon and 2 pm is therefore recommended. Schistosome eggs can also be demonstrated in rectal snips or bladder biopsies. Viability of eggs can be assessed if the biopsies are received fresh.

Serologic examination

At our laboratory, antibodies are detected by enzyme immunoassay (EIA) using purified egg S mansoni antigen. Antibodies to this antigen may be undetectable in the pre-patent period lasting 8-10 weeks. The test detects genus specific antibodies. In the absence of a diagnosis based on egg identification, travel history provides the best assessment of likely species.

Interpretation

Parasitologic Faeces is concentrated (modified formalin-ethyl acetate) and urine either centrifuged or filtered; all of the concentrate or sediment is examined. Because of the low sensitivity of these techniques, a negative faecal or urine examination does not exclude schistosomiasis. Microscopic examination of eggs enables the species of parasite to be determined. At least two examinations on different days are recommended. Serologic Schistosome serology cannot distinguish between past or current infection nor differentiate the species of infection. Clinical history and further investigations should be considered when establishing the diagnosis. Recent infections may be serologically negative.

Preventative measures

Cercariae can burrow through the mucosa of the mouth as well as through unbroken skin. All fresh water in endemic areas should be considered suspect, although snails tend to live in slow-flowing and stagnant waters, rather than in rapids and fast-flowing waters. If freshwater contact is unavoidable, bathing water should be heated to 50°C for five minutes or treated with iodine or chlorine as for the treatment of drinking water. Water can also be strained through paper filters, or allowed to stand for 2-3 days before use. This exceeds the usual life span of the cercariae. Of course, the container must be kept free of snails. High waterproof boots or hip waders are recommended if wading through streams or swamps. It is wise to carry a pair of rubber gloves to protect hands when contact with fresh water is anticipated. Vigorous towel drying, and rubbing alcohol on exposed skin immediately after contact with untreated water, may also help reduce cercarial penetration. Vegetables should be well cooked and salads avoided as these may have been washed in infected water, allowing cercariae to attach themselves to the leaves.

Treatment

Praziquantel (Biltricide) 20 mg/kg bodyweight every four hours for 2-3 doses depending upon the species is recommended. In travellers, this is likely to achieve cure rates in the order of 90%. Tablets are scored and available as a 600mg dose dispensed six per pack. In patients at risk of chronic disease, such as refugees and migrants, it is important to be aware of complications that may arise from chronic infection: liver fibrosis, portal hypertension and its sequelae, and colorectal malignancy in the intestinal forms; obstructive uropathy, superimposed bacterial infection, infertility and possibly bladder cancer.

Follow-up

Follow-up schistosomiasis serology is recommended in 12 to 36 months after treatment. Follow-up serology may differ between immigrants and returned travellers. Travellers may show a more rapid serological decline post-treatment due to a shorter duration of infection and lower parasite burden. Immigrants may even show a rise in titre within the first 6-12 months post-treatment. Persisting titres should not automatically justify retreatment, this should be based on symptoms, parasite identification or eosinophilia. Viable eggs may continue to be excreted for up to one month after successful treatment. Non-viable and degenerate eggs can be found in tissue biopsies for years after infection has occurred.

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

Zika Now In Fiji

In what could represent a major blow to tourism in the region, the US Centers for Disease Control have, this week, issued a level 2 warning that mosquitoes in Fiji have been found to be infected with Zika virus and have transmitted the infection to humans. Because of the strong link between Zika virus infection and severe birth defects, the CDC is strongly advising against women who are pregnant or who are even planning on becoming pregnant travelling to the area. And as the virus can also be transmitted through the sex, the advice for pregnant women whose partner has travelled to Fiji is to use condoms or refrain from sex for the duration of the pregnancy. The warning also signals an alert for Australian doctors to consider Zika virus in patients who present with symptoms such as fever, rash and headache following travel to Fiji. However, one of the major problems in curtailing the spread of this virus has been the fact that infected adults may display very few if any symptoms and maybe unaware that have contracted the disease. What’s more an infected male can harbour the Zika virus in his semen for much longer than in other bodily fluids, so the CDC recommends that men travelling to a Zika-prone country, that now includes Fiji, avoid conceiving a child for six months after leaving the area or from the time they develop symptoms if they indeed do develop symptoms. Women clear the virus more quickly and therefore the recommendation from the CDC is that they avoid falling pregnant two months after potential exposure or from when symptoms appear, assuming their partner did not travel. For those people, including pregnant women who can’t avoid travel Fiji or other Zika-prone area, the CDC advises they take precautions to avoid mosquito bites and continue these precautions for three weeks after returning home. These include the use of specific insect repellents and the wearing of long-sleeved clothing. Ref: https://wwwnc.cdc.gov/travel/notices/alert/zika-virus-fiji

Expert/s: Dr Linda Calabresi

Infectious diseases

Clinical Articles

Flu Season Pretty Bad

This year, the number of laboratory-confirmed influenza (flu) virus infections began rising earlier than usual and hit historic highs in some Australian states. If you have been part of any gathering this winter, this is probably not news. States in the south-east (central and southern Queensland, New South Wales, Victoria, Tasmania and South Australia) are more inflamed by flu than those in the north and west. For example, Queensland has seen more hospital admissions than in the last five years, mostly among an older population, while younger demographics more often test positive without needing hospitalisation. Meanwhile, flu numbers in New Zealand and elsewhere in the Pacific have not matched the same elevated levels. But is Australia really experiencing the biggest flu season on record in 2017, or are we just testing more and using better tools? This is hard to answer for certain because the information we need is not usually reported until later and public databases only show the past five years. We can say for sure that 2017 is on track to be a historically big flu year.
Read more: Have you noticed Australia’s flu seasons seem to be getting worse? Here’s why

Really, a big flu season

Flu can be a nasty illness. Sometimes it’s deadly. Other times it can be mild. But even for cases that fall in the middle you may not be able to work for days, or you’ll have to look after ill children home from school, or visit the very sick who have been hospitalised. Years ago, detection of influenza viruses mostly relied on slow, finicky methods such as testing for virus in artificial cell cultures. But, in Australia today, most laboratories use either sensitive tools to detect viral gene sequences in samples from the patient’s airway, or less sensitive but rapid dipstick methods, where a special strip is placed in a sample to detect viral proteins. These tools have been in use since 2007 in the larger Australian laboratories, so it’s unlikely we are just seeing more positives in 2017. While newer versions of these tests are being rolled out this year, they are unlikely to detect more cases. Equally, it’s unlikely more people with suspected flu decided to change their behaviour in 2017 and get tested, compared to 2016, or the year before. As in all years, there are many people in the community with flu who don’t get tested. The proportion of people with flu who are tested likely remains roughly the same year to year. State-wide flu reports provide reliable, laboratory-confirmed results. By looking at them, we can also be confident that “man flu” and severe common colds aren’t contributing to this specific and large increase in flu. We’re very likely seeing a truly huge flu season.

Why so bad this year?

Flu, caused by infection with an influenza virus, is mostly a disease with an epidemic peak during July and August in non-tropical countries. Flu viruses are broadly grouped into two types: Influenza-A and Influenza-B. Influenza-B viruses have two main sub-types while the Influenza-A viruses are more variable. The Influenza-As you get each year are usually A/H3N2 (the main player so far this season) or A/H1N1, which lingers on from its 2009 “swine flu” pandemic. Multiple flu viruses circulate each year and serial infections with different strains in the same person in a single season are possible. H3N2 has played a big role in the past five flu seasons. When it clearly dominates we tend to have bigger flu seasons and see cases affecting the elderly more than the young. H3N2 is a more changeable beast than the other flu viruses. New variants can even emerge within a season, possibly replacing older variants as the season progresses. This may be happening this winter, driving the bigger-than-normal season, but we won’t know for certain until many more viruses are analysed. Outside winter, flu viruses still spread among us. This year, in particular, we’re being encouraged to get vaccinated even during the peak of flu season. Vaccines are a safe way to decrease the risk that we or loved ones will get a full-blown case of the flu. Yet Australian flu vaccination rates are low. Data are scant but vaccination rates have increased in adults and some at-risk groups, but remain lower than for childhood vaccines.

Read more: Disease risk increasing with unvaccinated Australian adults

The flu vaccine

Each season new flu vaccines are designed based on detailed characterisation of the flu viruses circulating in the previous season. But the viruses that end up dominating the next season may change in the meantime. It is not clear whether that was a factor for this year’s high numbers in Australia this year or precisely what the vaccine uptake has been in 2017. Much of this detail will not be reported until after the epidemic ends. Some testing suggests this year’s vaccine is well matched to the circulating viruses. The flu vaccine is not the most effective of vaccines, but it is safe and the only preventive option we have for now. Of those vaccinated, 10-60% become immune to flu virus.

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

Future flu vaccines promise to account for the ever-changing nature of flu virus, reducing the current need for yearly vaccination. Until they are available, though, it remains really important to book an appointment with your vaccine provider and get a quick, safe vaccination, because we are unarguably in the midst of the biggest flu season Australia has seen in years. We have both vaccines and drugs to help us prevent and minimise disease and the extra load on hospitals caused by flu. The young, elderly, those with underlying disease and Indigenous Australian people are most at risk of the worst outcomes and this is reflected by government-funded vaccination for these groups. Ian M. Mackay, Adjunct assistant professor, The University of Queensland and Katherine Arden, Virologist, The University of Queensland This article was originally published on The Conversation. Read the original article.

Expert/s: A/Prof Ian M. Mackay, Dr Katherine Arden

Infectious diseases

Clinical Articles

Man flu is real, but women get more autoimmune diseases and allergies

Men and women respond differently to diseases and treatments for biological, social and psychological reasons. In this series on Gender Medicine, experts explore these differences and the importance of approaching treatment and diagnosis through a gender lens.
We know that sex hormones drive characteristic male and female traits such as breast enlargement and hip widening in women, or increased muscle mass and growth of facial hair in men. But now we also recognise they have a major impact on the immune system - our body’s inbuilt mechanism that helps fight and protect us against disease. Research suggests this has an evolutionary basis: survival of the species may mean men are harder hit by viruses, but a woman’s reactive immune system leaves her more susceptible to autoimmune diseases and allergies.

Viruses see men as weaker

Men die significantly more often from infectious diseases than women. For instance, men are 1.5 times more likely to die from tuberculosis, and twice as likely to develop Hodgkin’s lymphoma following Epstein–Barr virus (EBV) infection. Men are also five times more likely to develop cancer after infection with human papillomavirus (HPV), than women. This is because women’s immune systems mount a stronger response against foreign invaders, particularly viruses. While the male hormone testosterone tends to dampen immune responses, the female hormone oestrogen increases the number of immune cells and the intensity of their response. So women are able to recover more quickly from an infection. All this may reflect a sneaky evolutionary trick used by viruses to enable their survival. Women have developed multiple mechanisms to transmit infections; mainly through passing bugs from mother to child during gestation or birth, or through breastfeeding. So women are better vessels for viruses. Meanwhile, viruses have singled men out as the weaker sex. While popular culture has come up with the term “man flu”, suggesting men are over-dramatising flu symptoms, evidence suggests they may in reality be suffering more due to this dampening down of their immune responses.

Read more - Health Check: is man flu real?

However, this increased susceptibility of men to infection may not be an advantage for the long-term (over tens of thousands of years) survival of a disease-causing organism (pathogen), if it induces such severe disease that it results in the death of the host. Pathogens modify themselves so they can be transmitted by women during pregnancy, birth or breast feeding. Because of this, many have adapted to be less aggressive in women allowing wider infection, generally across a population. However, this feature alone is not likely to be sufficient to ensure the ongoing survival of a virus. The fitness of both sexes is necessary to reproduce long-term and thus provide new hosts for invading pathogens. Thus, the hit to the male sex must somehow be balanced by other advantages to their immune system.

Autoimmune diseases

Autoimmune diseases occur when the immune system turns on and attacks the body’s own cells or tissues, initiating a chronic cycle that results in damage or destruction of specific organs. These diseases include type 1 diabetes, lupus, rheumatoid arthritis, multiple sclerosis, and up to 80 different diseases that affect systems such as the intestine, bones, joints and nervous systems.The most striking sex differences in the immune system are seen in autoimmune diseases. Autoimmune disease affects about 8% of the population, but 78% of those affected are women. Women are three times more likely than men to develop these types of disease.

Read more - Explainer: what are autoimmune diseases?

In the case of lupus, the immune system mistakenly attacks the person’s own DNA (the structure that carries a person’s genetic code) causing damage to multiple organs that will lead to weight loss, anemia and eventually heart and kidney failure. Nine out of ten patients with lupus are women and clinical observations suggest that, again, hormones are the culprits. These differences of susceptibility between males and females tend to appear after puberty, and flare-ups increase during pregnancy. On the contrary, menopause is associated with a lower disease severity. Studies have linked oestrogen levels with the exacerbation of lupus. Oestrogens directly act on a particular immune cell (called the plasmacytoid dendritic cell) to promote their capacity to secrete inflammatory signals, which exacerbate lupus symptoms. Although these dendritic cells are generally important for fighting viral infections, in the context of lupus and multiple sclerosis, they cause significant harm.

Hormones and allergies

One in nine Australians (more than 2.5 million in total) suffer from asthma – a disease that causes swelling and narrowing of the airways. This makes it difficult to breathe when we encounter environmental allergens such as pollen. Twice as many women develop asthma compared to men. Interestingly, males are more susceptible to asthma before to the onset of puberty but, after puberty, females are more affected and develop more severe asthma than men. Until now, the reasons for this were not obvious, but hormones were speculated to play a role. In a recent study, we showed that high levels of testosterone in males protect them against the development of allergic asthma. During puberty, the level of testosterone increases. Testosterone acts as a potent inhibitor of a recently discovered immune cell called an innate lymphoid cell (ILC2), which accumulates in the lungs and initiates asthma. ILC2 cells release inflammatory signals that drive the swelling and airway narrowing characteristic of asthma when people are exposed to pollen, dust mites, grass or other common allergens. Testosterone reduces the numbers of ILC2 in the lungs of males, while female hormones provide no protective effect.

Read more: Do kids grow out of childhood asthma?

Immunity and sex are far more intricately linked than we had previously appreciated. More research needs to be done to better understand the triggers involved in the different responses of males and females. But the recent discoveries open the door for tactics to potentially target hormonal pathways or receptors that are preferentially expressed on male or female immune cells.

Read the first article in our Gender Medicine series - Medicine’s gender revolution: how women stopped being treated as ‘small men’ Gabrielle Belz, Professor, Molecular Immunology, Walter and Eliza Hall Institute and Cyril Seillet, Senior research scientist, Walter and Eliza Hall Institute This article was originally published on The Conversation. Read the original article.

Expert/s: Prof Gabrielle Belz, Dr Cyril Seillet

Drugs and devices, Infectious diseases, Vaccination

Videos

New pneumococcal 15-valent conjugate vaccine that includes coverage against serotype 3

In this Product Explainer, Public Health Physician and Infectious Diseases Epidemiologist Prof Paul Van Buynder explains the burden of pneumococcal disease in both children and adult population. He explains why PCV 15 has increased serotype coverage and why improved immunogenicity against serotype 3 is important both from a clinical and public health perspective (5 mins).

Expert/s: Prof Paul Van Buynder