Articles

Read the latest articles relevant to your clinical practice, including exclusive insights from Healthed surveys and polls.

By reading selected clinical articles, you earn CPD in the Educational Activities (EA) category whenever you click the “Claim CPD” button and follow the prompts. 

Filter results

Jane Heller

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.The Conversation 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.
Dr Linda Calabresi

Got a patient with multiple sun spots on their head that need treatment? Well it looks like the old, tried and true 5FU cream is still the way to go, according to a randomised trial just published in the New England Journal of Medicine. Among more than 600 randomly assigned patients, Dutch researchers compared the effectiveness of four topical treatments commonly used to treat multiple actinic keratoses as part of a ‘field treatment’. In addition to the 5% fluorouracil cream (Efudix), the study looked at the effectiveness of 5% imiquimod cream (Aldara), methyl aminolevulinate photodynamic therapy (MAL PDT or Metvix PDT) and 0.015% ingenol mebutate gel (Picato gel). After 12 months, the study showed that the Efudix was the most effective in terms of maintaining a reduction of at least 75% of actinic keratoses from the baseline. In other words, this cream was the best of the four therapies, at getting rid of these sun spots completely. “And the differences between fluorouracil cream and imiquimod, PDT and ingenol mebutate were significant,” the study authors said. They found the likelihood of success for those patients using fluorouracil was almost 75%, compared with only 54% for imiquimod, 38% for PDT and 29% for those using ingenol mebutate. And this independent study didn’t do anything tricky with the dosing regimen either. “In our trial, we used the most commonly prescribed dosing regimens of the therapies studied,” they said. In terms of sticking to the dosing regimen, patients were much better adhering to the schedule when they were taking ingenol mubutate (99% adherence) or PDT (97%) rather than the fluorouracil (89%) or the imiquimod (88%), but this appeared to directly correlate with how often they had to take the therapy and for how long. Overall, however this adherence rate did not reflect treatment satisfaction rate. “Satisfaction with treatment and improvement in health-related quality of life at 12 months after the end of treatment were highest in the fluorouracil,” the study authors reported. Nothing like a treatment actually working to make a patient feel happy about having had it. A bonus of this study, according to the researchers was the inclusion of patients with the more severe actinic keratosis lesions (Grade III lesions), patients who have been commonly excluded from previous similar trials of topical treatments. “[Including these patients] is more representative of patients seen in daily practice,” they said. In addition to effectiveness, cost is another appealing factor for fluorouracil over the other treatments. This study has the capacity to change practice. The study authors quote the prevalence actinic keratoses among whites aged 50 and over as being at 37.5%. While cryotherapy remains the treatment of choice for single lesions, where there are multiple lesions present field treatment should be considered. Currently the guidelines for this field treatment don’t advocate one treatment over any other, more or less suggesting all four of the treatments in this study as being efficacious. However, as these Dutch researchers say “our results could affect treatment choices in both dermatology and primary care.”

Reference

Jansen MHE, Kessels JPHM, Nelemans PJ, Kouloubis N, Arits AHMM, van Pelt HPA, et al. Randomized Trial of Four Treatment Approaches for Actinic Keratosis. N Engl J Med. 2019 Mar 7; 380(10): 935-46.  DOI: 10.1056/NEJMoa1811850
Healthed

Cutaneous disorders are among the most common conditions presented to primary care doctors. Many are easily identifiable and may be dealt with effectively without the need for cutaneous biopsy. Nevertheless, in many instances the diagnosis is not obvious on clinical grounds. The rash may display atypical features or may not respond to therapy as predicted. In these cases, and when dealing with cutaneous tumours or worrying pigmented lesions, cutaneous biopsy with histological assessment becomes necessary. The art of cutaneous biopsy is to derive the maximum amount of information from the minimum amount of tissue, causing least discomfort to the patient. This will be achieved if due regard is given to the advantages and shortcomings of the various techniques available for biopsying cutaneous tissue, and if the pathologist is supplied with a good clinical history.

Clinical History

For several reasons, clinical history assists greatly in the interpretation of skin biopsies. Clinicopathological correlation is particularly important in many inflammatory cutaneous disorders. As the histological features can be very similar, clinical notes may help us to arrange a list of provisional diagnoses in order of likelihood. The key features to discuss with regard to cutaneous rashes include:
  • duration
  • distribution
  • description (macular, papular, vasculitic or vesicular)
  • drugs or other possible aetiological agents
  • provisional clinical diagnosis.
As there is wide variation in the normal microscopic picture from different sites, the area biopsied should also be stated. For biopsies performed to distinguish between squamous cell carcinoma and keratoacanthoma, the rate of growth of the lesion is important. When sending specimens of pigmented lesions, the degree of clinical suspicion should be stated, together with any history of melanoma within the individual or within the individual’s family. Any condition associated with cutaneous disorders, such as systemic lupus erythematosus, pregnancy or bone marrow transplant, should be mentioned in the clinical notes. The clinical history should also include the type of biopsy procedure used (see below) as this determines the way we handle the specimen in the laboratory. For example, the whole of an incisional biopsy will be blocked in order to gain the maximum amount of information, whereas an excisional biopsy will be transversely sectioned in order to fully assess the lateral excision margins in the case of a tumour biopsy.

Excision Biopsy

This is the best technique to use for pigmented lesions and cutaneous tumours. It allows for histological assessment and diagnosis of the lesion, and assessment of surgical excision margins. If appropriate, an orientation suture can be placed at one end of the excision, e.g. the superior end of the specimen, so that if the excision is inadequate, the margin involved can be indicated on an accompanying diagram. Occasionally, excision biopsy is appropriate for inflammatory cutaneous disorders where the condition is characterised by the formation of vesicles. The best chance of removing an intact vesicle (which greatly aids diagnosis) may be through excision.

Incision Biopsy

With incision biopsy, a thin elliptical biopsy is taken radially through the edge of the tumour or through the edge of a macular or annular rash. Incision biopsy is superior to punch biopsy for diagnosing rashes, more tissue is displayed on histological section and scarring is often reduced. A typical incision biopsy is 5-6 mm in length and about 2 mm in width. It should be deep enough to extend into the subcutaneous adipose tissue. The biopsy should run radially from the centre or central areas of the lesion to include approximately 1 mm of normal cutaneous tissue surrounding the lesion.

Punch Biopsy

Punch biopsies are easier to perform and, in general, are more convenient. Nevertheless, they nearly always yield less information than an incision biopsy. For tumours, the biopsy should be taken centrally. For cutaneous eruptions, the biopsy should be taken from an area typical of the rash. In some cases, multiple biopsies may increase the amount of information. In this procedure, it is best not to include normal skin. Punch biopsies come in various sizes. As 2 mm punches often yield inadequate information for diagnosis, a 3 mm punch biopsy is the smallest that should be used.

Shave Biopsy/Curettage

This technique is suitable for superficially-located lesions with plaque-like clinical features, e.g. seborrhoeic keratoses. It is not an appropriate technique for nodular lesions, cutaneous rashes or melanocytic lesions.

General comments concerning cutaneous biopsies

Preparation of the skin surface: Be gentle when cleaning the skin surface prior to biopsy; try not to disturb any overlying scale as the keratin layers sometimes contain diagnostic information (e.g. this is where dermatophytic fungi may be seen). Let any alcohol preparation dry before collecting specimens for immunofluorescence. Local anaesthesia: Only a small amount of local anaesthetic is required for punch biopsy procedures (0.5 mL maximum). Too much local anaesthetic within the tissues can distort the histological appearances and simulate dermal oedema. Marking the lesion: It is often prudent to mark the target area for biopsy with an ink marker, as some lesions can blanch following introduction of local anaesthetic. The erythema in many lesions is due to vascular dilatation occurring as part of the inflammatory disorder. Local anaesthetic can cause vasoconstriction and diminish the erythema clinically. This may result in a poorly targeted biopsy yielding subdiagnostic histology. Depth of biopsy: It is best to continue into the subcutaneous adipose tissue so that the entire dermis is represented on histological section. This helps greatly with the categorisation of many inflammatory skin disorders and also demonstrates the deep border of any cutaneous tumour. When performing a punch biopsy, the biopsy instrument appears to ‘give’ when it penetrates the dermal connective tissue into subcutaneous adipose tissue. A similar sensation will be noticed when dissecting free an incision biopsy. Care with biopsy tissue: All too often, after biopsy tissue has been retrieved from the patient, crush artefact occurs during its transfer into formalin. Crush artefact greatly distorts the histological appearance and repeat biopsy may become necessary. Rather than grasping the biopsy tissue with non-tooth forceps, it should be transferred to the specimen container using needle tips, a skin hook or fine forceps, delicately grasping one edge of the biopsy. Fixative: Ordinary blue, 10% buffered formalin supplied with the specimen jars is suitable for nearly all cutaneous biopsies, except those submitted for microbiological culture or immunofluorescent examination. Labelling: Please label all specimen containers with the patient’s name and details, which should match those stated on the request slip. Unlabelled specimens can still be processed and interpreted if they arrive with labelled paperwork; however, the medico-legal status of any generated report is doubtful. The report will usually be generated with a ‘specimen received unlabelled’ comment attached.

Conclusion

Diagnosing cutaneous conditions can be challenging. The chances of success are improved when the clinician, is armed with a variety of biopsy techniques for use in the correct clinical setting, and when the pathologist is supplied with an adequate clinical history.   - 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.
Myriam Gharbi, Joseph H Drysdale, Hannah Lishman, Rosalind Goudie, Mariam Molokhia, Alan P Johnson, Alison H Holmes, Paul Aylin & Alastair D Hay

So here’s the exception that proves the rule. Urinary tract infections need immediate treatment with antibiotics to avoid an increased risk of sepsis and death. That’s the quite definitive conclusion from a large retrospective study involving GP data from the UK recently published in the BMJ. After analysing the records of over 150,000 patients, aged 65 and over presenting to their GP with a suspected or confirmed UTI, the researchers found those whose antibiotic treatment was delayed or deferred were up to eight times more likely to develop sepsis in the following 60 days compared to the group who were given antibiotics from the beginning. And those patients who were not given antibiotics at all, they were twice as likely to die as their medicated counterparts. Most of the infections were caused by Escherichia Coli, and trimethoprim or nitrofurantoin were the most common antibiotics prescribed. As the study showed, sepsis is not a common sequela of UTI, occurring in just .5% of cases. But the fact remains if antibiotics were delayed or withheld altogether the incidence jumped to 2.2% and 2.9% respectively which is significant and totally unnecessary. Understandably outcomes were worse the older the patient, and men had more adverse outcomes than women, but even accounting for multiple variable factors the basic conclusion remained the same. “Our study suggests the early initiation of antibiotics for UTI in older high-risk adult populations (especially men aged >85 years) should be recommended to prevent serious complications”, the study authors said. Of concern to the researchers was the relatively large number of older patients (about 7%) who were diagnosed with a UTI but not treated. They suggest antimicrobial stewardship programmes encouraging more judicious use of antibiotics may be at least, in part, to blame. That, and the risk of elderly patients developing Clostridium difficile infection following antibiotic use. But while ‘delayed or deferred’ antibiotic treatment was not generally associated with serious adverse outcomes for some self-limiting illnesses such as upper respiratory tract infections, this study suggests it is not a good idea for UTIs. “In our study, deferred antibiotics were associated with less severe adverse outcomes than no antibiotics for older adults but still showed a significantly higher risk of mortality compared with immediate antibiotics,” the researchers said. An accompanying editorial by a UK GP academic says the study highlights one of the many dilemmas that occur in general practice. “[GPs face] the daily challenge of ensuring that patients who are unlikely to benefit are not treated, whereas those who require antibiotics receive the right class, at the right time, at the right dose, and for the right duration,” he wrote. And while agreeing with the study authors concluding advice, that all older patients with suspected UTI should be treated from day one he does suggest further research is needed. Research could help determine the most appropriate antibiotic in this situation, and if there are any particular groups in this 65 and over cohort who it would be safe to leave off antibiotic treatment until the result of the culture and sensitivities are known. - Myriam Gharbi, NIHR Health Protection Research Unit, Imperial College London; Joseph H Drysdale, Department of Primary Care and Public Health, Imperial College London; Hannah Lishman, Medical School, St George's University of London UK; Rosalind Goudie, Nuffield Department of Population Health, University of Oxford, UK; Mariam Molokhia, Department of Primary Care and Public Health Sciences, King's College, London, UK; Alan P Johnson, Healthcare-Associated Infections and Antimicrobial Resistance Division, London, UK; Alison H Holmes, NIHR Health Protection Research Unit, Imperial College London; Paul Aylin, NIHR Health Protection Research Unit, Imperial College London This article is referenced from THEBMJ. Read the original article. - Alastair D Hay, Centre for Academic Primary Care, Bristol Medical School: Population Health Sciences, University of Bristol, Canynge Hall, Bristol, UK This article is referenced from THEBMJ. Read the original article.

Dr Cameron Webb

Western Australian health authorities recently issued warnings about Murray Valley encephalitis, a serious disease that can spread by the bite of an infected mosquito and cause inflammation of the brain. Thankfully, no human cases have been reported this wet season. The virus that causes the disease was detected in chickens in the Kimberley region. These “sentinel chickens” act as an early warning system for potential disease outbreaks.

What is Murray Valley encephalitis virus?

Murray Valley encephalitis virus is named after the Murray Valley in southeastern Australia. The virus was first isolated from patients who died from encephalitis during an outbreak there in 1951. The virus is a member of the Flavivirus family and is closely related to Japanese encephalitis virus, a major cause of encephalitis in Asia. Murray Valley encephalitis virus is found in northern Australia circulating between mosquitoes, especially Culex annulirostris, and water birds. Occasionally the virus spreads to southern regions, as mosquitoes come into contact with infected birds that have migrated from northern regions.

How serious is the illness?

After being transmitted by an infected mosquito, the virus incubates for around two weeks. Most people infected don’t develop symptoms. But, if you’re unlucky, you could develop symptoms ranging from fever and headache to paralysis, encephalitis and coma. Around 40% of people who develop symptoms won’t fully recover and about 25% die. Generally, one or two human cases are reported in Australia per year. Since the 1950s, there have been sporadic outbreaks of Murray Valley encephalitis, most notably in 1974 and 2011. The 1974 outbreak was Australia-wide, resulting in 58 cases and 12 deaths. It’s likely the virus has been causing disease since at least the early 1900s when epidemics of encephalitis were attributed to a mysterious illness called Australian X disease.

Early warning system

Given the severity of Murray Valley encephalitis, health authorities rely on early warning systems to guide their responses. One of the most valuable surveillance tools to date have been chooks because the virus circulates between birds and mosquitoes. Flocks of chickens are placed in areas with past evidence of virus circulation and where mosquitoes are buzzing about. Chickens are highly susceptible to infection so blood samples are routinely taken and analysed to determine evidence of virus infection. If a chicken tests positive, the virus has been active in an area. The good news is that even if the chickens have been bitten, they don’t get sick. Mosquitoes can also be collected in the field using a variety of traps. Captured mosquitoes are counted, grouped by species and tested to see if they’re carrying the virus. This method is very sensitive: it can identify as little as one infected mosquito in a group of 1,000. But processing is labour-intensive.

How can technology help track the virus?

Novel approaches are allowing scientists to more effectively detect viruses in mosquito populations. Mosquitoes feed on more than just blood. They also need a sugar fix from time to time, usually plant nectar. When they feed on sugary substances, they eject small amounts of virus in their saliva. This led researchers to develop traps that contain special cards coated in honey. When the mosquitoes feed on the cards, they spit out virus, which specific tests can then detect. We are also investigating whether mosquito poo could be used to enhance the sugar-based surveillance system. Mosquitoes spit only tiny amounts of virus, whereas they poo a lot (300 times more than they spit). This mosquito poo can contain a treasure trove of genetic material, including viruses. But we’re still working out the best way to collect the poo.

Staying safe from Murray Valley encephalitis

There is no vaccine or specific treatment for the virus. Avoiding mosquito bites is the only way to protect yourself from the virus. You can do this by:
  • wearing protective clothing when outdoors
  • avoiding being outdoors when the mosquitoes that transmit the virus are most active (dawn and dusk)
  • using repellents, mosquito coils, insect screens and mosquito nets
  • following public health advisories for your area.
The virus is very rare and your chances of contracting the disease are extremely low, but not being bitten is the best defence.The Conversation

- Ana Ramírez, PhD candidate, James Cook University; Andrew Francis van den Hurk, Medical Entomologist, The University of Queensland; Cameron Webb, Clinical Lecturer and Principal Hospital Scientist, University of Sydney, and Scott Ritchie, Professorial Research Fellow, James Cook University

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

Australian GPs are confident and competent at managing kids with bedwetting issues, new research confirms. But they are less sure what to do with children with daytime wetting or when childhood enuresis persists into adulthood, according to the study findings recently published in the Australian Journal of General Practice. As you may remember, back in late 2016, health professionals on the Healthed database were invited to participate in a survey designed by leading paediatric urologist, Dr Patrina Caldwell to investigate their knowledge and experience with managing urinary incontinence in childhood. Almost 1500 Australian health professionals responded, mostly GPs. Researchers found that 88% of survey participants reported being slightly or very knowledgeable about managing childhood urinary incontinence. Their confidence seems well-founded at least for nocturnal enuresis. Having been given multiple answer options about first-line management, 93% of participants correctly selected urotherapy and enuresis alarm training as the ideal first-line management for childhood enuresis. This is despite less than half (48%) being able to correctly identify the commonest cause of the condition as being abnormal physiology of sleep and bladder function. Over a third of people incorrectly thought childhood enuresis was simply a delay in developing toileting skills. However, it is a different kettle of fish when it comes to managing daytime urinary incontinence which only 81% of participants felt at least somewhat confident managing. Of concern was the finding that 18% of health professionals would treat this condition with inappropriate and potentially harmful treatments. More specifically, a small percentage of participants chose tricyclic antidepressants which used to be a popular treatment option but is now no longer recommended as first-line therapy for daytime urinary incontinence due to its potential side-effects. The situation was even worse for adult patients who had problems with enuresis that had persisted since childhood. Only 61% of participants felt they were even slightly knowledgeable managing these patients, although most chose the most appropriate first-line therapy of urotherapy and desmopressin. According to the study authors, the knowledge of the health professionals with regard to the various categories of urinary incontinence was largely reflective of the prevalence of each of the different conditions in their clinical experience. Most GPs were currently managing at least a few cases of nocturnal enuresis but the other two conditions were much rarer.

Reference

Caldwell PHY. Manocha R, Hamilton S, Scott KM, Barnes EH. Australian community health practitioners’ knowledge and experience with managing urinary incontinence that begins in childhood. Aust J Gen Pract. 2019 Jan; 48(1-2); 60-5. Available from: https://www1.racgp.org.au/ajgp/2019/january–february/managing-urinary-incontinence-that-begins-in-child
A/Prof Sanjaya Senanayake

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.
Dr Linda Calabresi

Despite the incidence of cerebral palsy decreasing, it is still Australia’s most common cause of physical disability in childhood, experts say. And with the condition affecting over two in every 1000 live births, it is more than likely a GP will be caring for these patients in their clinical practice. The authors of a review in the latest Medical Journal of Australia highlight areas where the treating health professional, including the GP can play a role in improving these children’s health outcomes as well as their quality of life. “While there is currently a limited range of evidence-based treatments that change the underlying pathology of cerebral palsy, there are many areas in which health care professionals can change the natural history of cerebral palsy and improve participation and quality of life for children with this condition,” they said. They refer to a framework for management of patients with cerebral palsy, known as the six Fs. These Fs help both clinicians and families of the affected child set realistic goals and develop appropriate pathways to meet them. The six Fs are: Function – encourage the child to try activities and celebrate not only what they can achieve but the attempt. Family –  the family environment is vitally important to the child’s health outcomes both physically and psychologically. Significant attention, support and resources need to be directed to this. Fitness – Overall physical fitness is at least as important as exercises directed at helping overcome the particular physical disability of a child with cerebral palsy. Fun – Caregivers need to ensure the child with cerebral palsy does not miss out on this key component of childhood. Friends – Social interaction and the development of quality relationships need to be incorporated as a management goal. Future – This is all about setting realistic goals and expectations and the mapping out plans of how to achieve them, keeping in mind the other five Fs. In addition to this very grounding framework of management, the review authors went on to describe the current state of play of treatment for the various physical manifestations of cerebral palsy. Spasticity and dystonia are the most common signs of the disease and along with physical therapies such as physiotherapy, occupational therapy, splints and orthotics there are a number of medications and even some surgical options for treatment. Baclofen, diazepam and Botulinum toxin A are well-known options to treat the spasticity and dystonia. But apparently there is emerging evidence for the use of other medications such as gabapentin and clonidine. There are also some highly specialised surgeries being performed for subsets of cerebral palsy children such as deep brain stimulation for children with dystonic and dyskinetic movement, selective dorsal rhizotomy for severe spasticity in the lower limbs and even intrathecal baclofen to avoid the side effects of oral baclofen. The review also highlights three potential problem areas for children with cerebral palsy that are of particular relevance for GPs caring for children with this condition. Hip displacement is more of a risk in children with cerebral palsy, and if it is missed it can result in hip dislocation. Regular clinical and radiographic assessment is recommended. “The pelvic x-ray is taken in a standardised supine position and is usually repeated between six and 12 months, depending on the severity of cerebral palsy and the rate of progression of migration of the femoral head out of the acetabulum,” they said. Referral is recommended once migration approaches 30% Another major issue to check for in children with cerebral palsy is pain, with evidence suggesting up to 75% of young patients are regularly experiencing this. The review authors recommend carers ask about this directly, as children may not volunteer this information despite chronic pain’s well-known effect on quality of life. Pain treatment is generally fairly standard, however specific treatments are available for pain arising from unique symptoms such as dystonia or spasticity. Finally, the review authors advise treating clinicians to watch out for feeding and swallowing problems, and as a consequence of these, deficiencies in nutrition. There is a wide range of potential issues concerning eating and drinking that can affect children with cerebral palsy, including swallowing difficulty, managing utensils, posture, risk of aspiration, sensory difficulties and even excessive drooling. All of these can be managed, but the key first step is identifying there is an issue before nutritional deficiencies manifest in comorbidities such as osteoporosis. Unfortunately, as yet, we still cannot cure cerebral palsy. However, with early interventions, close monitoring and targeted therapies the natural history of cerebral palsy is being altered for the better.

Reference

Graham D, Paget SP, Wimalasundera N. Current thinking in the health care management of children with cerebral palsy. Med J Aust. 2019 Feb; 210(3): 129-35. DOI: 10.5694/mja2.12106
Jayne Lucke

Abortion is a common experience for Australian women. Around one in six have had an abortion by their mid-30s, according our new research published today in the Australia New Zealand Journal of Public Health. Narratives about abortion often stigmatise women who have had one or seek access to one. But our research shows women from all walks of life may have an abortion: married, single, child-free, and mothers. In fact, women who have already had children are more likely to have a termination than those who haven’t. Women make decisions about whether or not to have an abortion in the context of their complex lives. And it’s by no means an easy decision. Our research investigated the factors associated with abortion as women move from their late teens into their mid-30s. We found women with lower levels of control over their reproductive health, whether through family violence, drug use or ineffective contraception, are more likely than their peers to terminate a pregnancy. If we want to reduce the rate of unintended pregnancies and abortion in Australia, we need to empower women to have control over their fertility and support them with appropriate health services.

Women’s experiences

We used data from five surveys of the Australian Longitudinal Study on Women’s Health to examine factors associated with “induced” abortions which were not undertaken because of a foetal abnormality. We looked at a cohort of more than 9,000 women born between 1973-78 who were first surveyed at ages 18-23 years. At the fifth survey they were aged 31-36 years. Overall, by their mid-30s, 16% of the women in this study had reported at least one abortion. We also looked at the proportion of women who reported a new abortion at each survey. At the first survey, when women were aged 18-23, 7% reported having had an abortion. In subsequent surveys, 2-3% of women reported having an abortion since the last survey. While most women reported only one new abortion, around one in ten reported two abortions, and around 2% reported three abortions. Abortion is understandably more common for women when they are in their 20s than it is when women reach their 30s. This may be because many women in their 30s are actively trying to be pregnant, or may be using contraception more effectively if they’re trying to avoid becoming pregnant. Compared with married women, those who were in a de facto relationship, were single, or divorced were more likely to have had an abortion. Women with children were more likely to have an abortion than women who did not have children. In the fourth survey, the majority of women (72%) said they hoped to have one or two children, 20% wanted three or more, while 8% didn’t want to have children. Perhaps unsurprisingly, women who had an abortion in the later surveys were more likely to have previously reported using ineffective contraception, or to have had a past abortion, than women who didn’t terminate a pregnancy in their 30s. Women whose alcohol use had recently become riskier and women who reported using any illicit drugs in the past 12 months were also more likely to have an abortion. Violence was also a big factor. Women who recently experienced partner violence were more likely to terminate a pregnancy than women who reported no violence. Even women who reported childhood sexual abuse had a significantly increased likelihood of abortion in their twenties (but not in their 30s). In fact, women reporting violence of any kind, and at any time, had a significantly increased likelihood of having an abortion.

What can we do about it?

Australia is going through a much-needed process of law reform to ensure women across the country have access to abortions as part their women’s health service. Queensland is the most recent state to remove abortion from the criminal code. Alongside this, we need to improve training and resources to for health providers to identify and help women who may be at risk of unintended pregnancy, particularly those who are using illicit drugs or are experiencing partner violence. We need better ways of reaching all vulnerable women, but especially young women experiencing reproductive coercion. We also need to ensure that all women are provided with good access to information about effective contraceptive choices. While the oral contraceptive pill and condoms are the most common methods Australian women use, long-acting reversible methods (such as intra-uterine devices and implants) can be good options for many women wanting effective contraception.The Conversation

- Jayne Lucke, Chair, Australian Research Centre in Sex, Health & Society, La Trobe University and Angela Taft, Professor and Director, La Trobe University

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

Chronic rhinosinusitis is a misery-generating condition – literally. According to a large study just published in The Journal of the American Medical Association, having chronic rhinosinusitis significantly increases your risk of depression and anxiety. And if you also have nasal polyps the risk is higher still. The Korean study was admittedly observational but it did include almost 50,000 individuals from the general population and followed them up for 11 years. Researchers found, over the duration of the study, those people with chronic rhinosinusitis were 54% more likely to develop depression and 57% more likely to develop anxiety than those people who did not suffer this condition. And if nasal polyps accompanied the rhinosinusitis the increase in likelihood for both mental illnesses jumped to the early 60s (61% and 63% respectively). So what are the implications of this study? Well – they are fairly straightforward really. “Physicians should be aware of the potential comorbidities observed in patients with [chronic rhinosinusitis] and provide therapy to reduce the risk of depression and anxiety in these patients,” the study authors helpfully concluded. What we don’t know of course, being simply an observational study without any intervention to test, is whether effectively treating the rhinosinusitis helps the depression or anxiety, and importantly, whether surgically removing the polyps can make a difference to this psychological side-effect. The researchers actually even distance themselves from the conclusion that chronic rhinosinusitis causes depression and anxiety, citing the chicken and egg phenomena. “Whether depression and anxiety amplify the symptoms of [chronic rhinosinusitis] or whether these conditions are the consequence of [chronic rhinosinusitis]is unknown,” they said. But they do say their findings support previous research that has suggested an association between the conditions. They also say their study allowed analysis of the specific phenotype responsible for the chronic rhinosinusitis – whether it be predominantly T1 or T2 response derived. What they found was the association held true regardless of the phenotype – suggesting this was more to do with personality and symptoms than physiology. All in all, what the study authors suggest is that given how common chronic rhinosinusitis is in the population, it is worthwhile keeping a high indexation of suspicion for the development of depression and anxiety not only for the patients’ current quality of life but also because these conditions can affect health outcomes down the line. “[T]hese psychiatric comorbidities may influence not only the diagnosis of [chronic rhinosinusitis] but also its therapeutic and surgical outcomes,” the study authors said.  

Reference:

Kim JY, Ko I, Kim MS, Yu MS, Cho BJ, Kim DK. Association of Chronic Rhinosinusitis With Depression and Anxiety in a Nationwide Insurance Population. JAMA Otolaryngol Head Neck Surg. 2019 Feb 7.  DOI: 10.1001/jamaoto.2018.4103 [Epub ahead of print].
Sullivan Nicolaides Pathology

Allergic disorders result from an inappropriate, usually IgE-mediated, immune response upon exposure to either environmental or food allergens. Common manifestations of allergy include rhinoconjunctivitis, asthma, eczema, acute urticaria and anaphylaxis. Disorders, such as chronic urticaria, hereditary angioedema and T-cell contact dermatitis (metal allergy), while clinically similar in some ways, are not IgE-mediated. Allergic disease manifests in different ways through life and the likely causative agents can also change with age (see Table 1).

Tests used in the diagnosis of IgE-mediated allergy

Total IgE Higher levels of total IgE are often found in patients with allergic conditions. However, normal total IgE does not exclude allergy. Total IgE is also elevated in other conditions including parasitic infections and allergic bronchopulmonary aspergillosis. It is used increasingly in determining anti-IgE therapy in moderate to severe asthmatics. Allergen-specific IgE Allergen-specific IgE can be detected for a large variety of allergens. The presence of a specific IgE to allergen can suggest allergic disease and is detected via a blood test (RAST or radioallergosorbent test) or skin prick test. RAST tests detect many of the different proteins within an individual allergen. Recombinant allergen testing Of the many proteins within a substance, only a few may cause allergic symptoms. Recombinant allergen testing looks for specific characterised protein within an allergen. Interpretation of RAST tests The presence of detectable specific IgE to an allergen does not confirm the patient is allergic to that substance. All results must be interpreted in conjunction with the clinical history of the patient. Low levels of detectable specific IgE can confirm the presence of allergy in the right clinical context. RAST testing aids in the assessment of, and identification of allergic sensitisation, but is not to be used alone as the deciding factor for inclusion or exclusion of allergy. As the level of specific IgE increases, the likelihood of clinical relevance also increases. As shown in Table 2, different allergens have different specific IgE level cutoffs at which serious allergy is >95% likely (positive predictive value or PPV). The range of values is vastly different between allergens and is affected by age and also by geographic region. Table 2 defines levels at which exposure, or a challenge, would be highly hazardous for a patient. Importantly, many patients could have serious reactions at much lower levels.   [table id=1 /]   [table id=2 /]

RAST tests

RAST tests are available for a range of allergens, however Medicare criteria limits rebates based on the number, type and frequency of tests. Medicare Australia limits rebates for RAST tests to a maximum of four specific allergens and/or mixes per pathology request and a maximum of four RAST test episodes per year. When ordering RAST tests, it is advisable to include allergens the patient feels are relevant and those likely for the clinical scenario. For common clinical scenarios we recommend the following: Childhood eczema Age <2 years: Milk, Egg, Wheat, Peanut Age >2 years: Milk, Egg, Peanut, Dust mite Additional allergens or an extended RAST combined allergy panel may be ordered. Asthma and allergic rhinoconjunctivitis Dust mite, Grass mix, Animal dander Additional allergens may be ordered or substituted if relevant (e.g. cat dander instead of animal dander). An extended RAST inhalant panel is also available. Default panel if no allergens are specified and no clinical notes are provided Age <5 years: Dust mite, Grass mix, Food Mix Age >5 years: Dust mite, Grass mix, Animal Mix Anaphylaxis Anaphylaxis is a severe life-threatening allergic reaction. It is recommended these patients require specialist assessment by a clinical immunologist or allergist. Initial testing should look for the causative allergen if possible. It is important to note that a negative RAST test does not exclude the allergen tested. RAST testing recommendations ­
  • Test individual likely causative allergen i.e. food, stinging insect. ­
  • Tryptase, if done within 2-6 hours of reaction, can support the occurrence of an allergic reaction. ­
  • Useful as an assessment of mastocytosis (condition with increased numbers of mast cells)

Extended RAST panels

Extended RAST panels have been developed to represent the common allergens encountered clinically in practice. They are particularly relevant in our geographic region and replace the skin prick test panel which is no longer available. Additional allergens may also be requested. All results must be interpreted in conjunction with the patient’s clinical history. Extended RAST Food Panel ­
  • Covers common food-related allergens
  • Almond; Hazelnut; Sesame seed; Banana; Mango; Shrimp (prawn); Cashew; Milk (cow); Soybean; Codfish; Peanut; Walnut; Egg white; Rice; Wheat
Extended RAST Nut Allergy Panel ­
  • Broad collection of commonly consumed nuts, including peanuts ­
  • Individual nut testing with appropriate clinical history is preferred ­
  • Recommend to discuss results with a clinical immunologist or allergist
  • Almond; Macadamia; Pine nut; Brazil; Peanut; Sesame seed; Cashew; Peanut (Ara-h2); Walnut; Hazelnut; Pecan
Extended RAST Combined Allergy Panel ­
  • Combination of common food and environmental allergens ­
  • Replaces the skin prick test panel (no longer available)
  • Almond; Dust mite; Mould mix; Cashew nut; Egg white; Peanut; Cat dander; Grass mix; Shrimp (prawn); Codfish; Hazelnut; Soy; Dog dander; Milk (cow); Wheat
  • * Preferable for children (<12 years) due to low serum volume
Extended RAST Inhalant Panel ­
  • Covers common environmental allergens ­
  • Useful for asthma and allergic rhinitis
  • Acacia (wattle); Blomia tropicalis; Dust mite; Alternaria alternate; Cat dander; Eucalyptus; Aspergillus fumigatus; Cladosporium; Horse dander; Bahia grass; Common ragweed; Johnson grass; Bermuda grass; Dog dander; Perennial rye grass

Recombinant allergens

Omega-5 gliadin ­
  • A component of wheat ­
  • Associated with anaphylaxis ­
  • Often in the context of eating wheat and physical activity within 1-2 hours
Alpha-gal (mammalian meat allergy) ­
  • Associated with anaphylaxis; often delayed following consumption of meat (beef, lamb, pork) ­
  • Related to tick bites
Peanut Allergy Risk Assessment ­
  • Peanuts like all food is made up of many different proteins ­
  • Ara-h2 is associated with anaphylaxis to peanut ­
  • Can assist with risk assessment and should be done in conjunction with a clinical immunologist or allergist ­
  • A negative Ara-h2 in peanut positive patient does not imply there is no risk to anaphylaxis
  • Results of RAST tests can also be of use in monitoring ongoing allergy in patients in conjunction with their treating clinician

How to order allergy tests

RAST tests - standard panels Medicare Australia limits rebates for RAST tests to a maximum of four specific allergens and/or mixes per pathology request and a maximum of four RAST test episodes per year. Extended RAST tests (Medicare rebate + $120* per panel)
  • Extended RAST Food
  • Extended RAST Nut
  • Extended RAST Combined
  • Extended RAST Inhalant
Please note, extended RAST panels are not bulk billed. Recombinant allergen tests (Medicare rebate + $60* each)
  • Alpha-gal
  • Omega-5 gliadin
  • Peanut (Ara-h2)
  • Peanut Allergy Risk Assessment
  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.
Dr Linda Calabresi

It’s a controversial topic here in Australia. But a new UK study, just published in the New England Journal of Medicine, gives strong support the role of e-cigarettes as a smoking cessation therapy. The randomised controlled trial of almost 900 adult smokers wanting to quit found the one-year abstinence rate was 18% among the e-cigarette users compared to 9.9% among those who were randomised to receive nicotine replacement therapy. Much of the difference could be attributed to adherence to the assigned product. After 12 months, 80% of the e-cigarette group were still using the device whereas only 9% of the alternative group were still taking their nicotine replacement therapy despite being able to choose between the patch, gum, lozenge, nasal spray, inhalator, mouth spray, mouth strip, and microtabs (or any combination of these). Participants in both groups underwent the same multi-session behavioural support as per best practice guidelines. This study provides some of the strongest evidence to date that e-cigarettes are significantly better than nicotine replacement therapy in helping people quit smoking, the study authors suggest. “This is particularly noteworthy given that nicotine replacement was used under expert guidance, with access to the full range of nicotine-replacement products and with 88.1% of participants using combination treatments,” they said. The researchers suggested e-cigarettes had better adherence rate because they were more effective at reducing the symptoms of withdrawal when quitting smoking, because the refillable devices are better at delivering nicotine compared with options such as gum or patches. They also suggest the nicotine dose provided by e-cigarettes was easier to tailor to individual needs than other replacement options. And even though people using the e-cigarettes were more likely to get mouth or throat irritation, this side effect was generally mild and tolerable especially compared to withdrawal symptoms such as constipation, mouth ulcers and weight gain. In general, the researchers claim replacing cigarettes with e-cigarettes is a definite positive in terms of health outcomes and much better than other nicotine replacement options, but they suggest the high rate of adherence in the e-cigarette group may have some negative connotations. “This can be seen as problematic if e-cigarette use for a year signals ongoing long-term use, which may pose as-yet-unknown health risks,” they said. As an accompanying editorial points out, fundamentally nicotine is highly addictive. While electronic cigarettes have been proven to be a great tool in helping people get off normal cigarettes, there may be an issue if non-smokers, especially teenagers take up vaping, making them vulnerable to becoming smokers further down the track. “The cigarette company may well see e-cigarettes as addictive bait that will lead young people toward smoking,” the US editorial authors suggest. They suggest this potential problem could be relatively easily averted by ensuring e-cigarettes aren’t manipulated to enhance their appeal, specifically the authorities should not allow the manufacture of flavoured nicotine products. However, they too acknowledge e-cigarettes have a significant role to play in solving this public health problem – ‘by helping people who are users of combustible tobacco products stop smoking by switching to vaping.’

References:

Hajek P, Phillips-Waller A, Przulj D, Pesola F, Smith KM, Bisal N, et al. A Randomized Trial of E-Cigarettes versus Nicotine-Replacement Therapy.  N Engl J Med. 2019 Jan 30;  DOI: 10.1056/NEJMoa1808779 [Epub ahead of print] Drazen JM, Morrissey S, Campion EW. The Dangerous Flavors of E-Cigarettes. N Engl J Med. 2019 Jan 30. DOI: 10.1056/NEJMe1900484 [Epub ahead of print]

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.The Conversation 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.
Clinical Articles iconClinical Articles

Got a patient with multiple sun spots on their head that need treatment? Well it looks like the old, tried and true 5FU cream is still the way to go, according to a randomised trial just published in the New England Journal of Medicine. Among more than 600 randomly assigned patients, Dutch researchers compared the effectiveness of four topical treatments commonly used to treat multiple actinic keratoses as part of a ‘field treatment’. In addition to the 5% fluorouracil cream (Efudix), the study looked at the effectiveness of 5% imiquimod cream (Aldara), methyl aminolevulinate photodynamic therapy (MAL PDT or Metvix PDT) and 0.015% ingenol mebutate gel (Picato gel). After 12 months, the study showed that the Efudix was the most effective in terms of maintaining a reduction of at least 75% of actinic keratoses from the baseline. In other words, this cream was the best of the four therapies, at getting rid of these sun spots completely. “And the differences between fluorouracil cream and imiquimod, PDT and ingenol mebutate were significant,” the study authors said. They found the likelihood of success for those patients using fluorouracil was almost 75%, compared with only 54% for imiquimod, 38% for PDT and 29% for those using ingenol mebutate. And this independent study didn’t do anything tricky with the dosing regimen either. “In our trial, we used the most commonly prescribed dosing regimens of the therapies studied,” they said. In terms of sticking to the dosing regimen, patients were much better adhering to the schedule when they were taking ingenol mubutate (99% adherence) or PDT (97%) rather than the fluorouracil (89%) or the imiquimod (88%), but this appeared to directly correlate with how often they had to take the therapy and for how long. Overall, however this adherence rate did not reflect treatment satisfaction rate. “Satisfaction with treatment and improvement in health-related quality of life at 12 months after the end of treatment were highest in the fluorouracil,” the study authors reported. Nothing like a treatment actually working to make a patient feel happy about having had it. A bonus of this study, according to the researchers was the inclusion of patients with the more severe actinic keratosis lesions (Grade III lesions), patients who have been commonly excluded from previous similar trials of topical treatments. “[Including these patients] is more representative of patients seen in daily practice,” they said. In addition to effectiveness, cost is another appealing factor for fluorouracil over the other treatments. This study has the capacity to change practice. The study authors quote the prevalence actinic keratoses among whites aged 50 and over as being at 37.5%. While cryotherapy remains the treatment of choice for single lesions, where there are multiple lesions present field treatment should be considered. Currently the guidelines for this field treatment don’t advocate one treatment over any other, more or less suggesting all four of the treatments in this study as being efficacious. However, as these Dutch researchers say “our results could affect treatment choices in both dermatology and primary care.”

Reference

Jansen MHE, Kessels JPHM, Nelemans PJ, Kouloubis N, Arits AHMM, van Pelt HPA, et al. Randomized Trial of Four Treatment Approaches for Actinic Keratosis. N Engl J Med. 2019 Mar 7; 380(10): 935-46.  DOI: 10.1056/NEJMoa1811850
Clinical Articles iconClinical Articles

Cutaneous disorders are among the most common conditions presented to primary care doctors. Many are easily identifiable and may be dealt with effectively without the need for cutaneous biopsy. Nevertheless, in many instances the diagnosis is not obvious on clinical grounds. The rash may display atypical features or may not respond to therapy as predicted. In these cases, and when dealing with cutaneous tumours or worrying pigmented lesions, cutaneous biopsy with histological assessment becomes necessary. The art of cutaneous biopsy is to derive the maximum amount of information from the minimum amount of tissue, causing least discomfort to the patient. This will be achieved if due regard is given to the advantages and shortcomings of the various techniques available for biopsying cutaneous tissue, and if the pathologist is supplied with a good clinical history.

Clinical History

For several reasons, clinical history assists greatly in the interpretation of skin biopsies. Clinicopathological correlation is particularly important in many inflammatory cutaneous disorders. As the histological features can be very similar, clinical notes may help us to arrange a list of provisional diagnoses in order of likelihood. The key features to discuss with regard to cutaneous rashes include:
  • duration
  • distribution
  • description (macular, papular, vasculitic or vesicular)
  • drugs or other possible aetiological agents
  • provisional clinical diagnosis.
As there is wide variation in the normal microscopic picture from different sites, the area biopsied should also be stated. For biopsies performed to distinguish between squamous cell carcinoma and keratoacanthoma, the rate of growth of the lesion is important. When sending specimens of pigmented lesions, the degree of clinical suspicion should be stated, together with any history of melanoma within the individual or within the individual’s family. Any condition associated with cutaneous disorders, such as systemic lupus erythematosus, pregnancy or bone marrow transplant, should be mentioned in the clinical notes. The clinical history should also include the type of biopsy procedure used (see below) as this determines the way we handle the specimen in the laboratory. For example, the whole of an incisional biopsy will be blocked in order to gain the maximum amount of information, whereas an excisional biopsy will be transversely sectioned in order to fully assess the lateral excision margins in the case of a tumour biopsy.

Excision Biopsy

This is the best technique to use for pigmented lesions and cutaneous tumours. It allows for histological assessment and diagnosis of the lesion, and assessment of surgical excision margins. If appropriate, an orientation suture can be placed at one end of the excision, e.g. the superior end of the specimen, so that if the excision is inadequate, the margin involved can be indicated on an accompanying diagram. Occasionally, excision biopsy is appropriate for inflammatory cutaneous disorders where the condition is characterised by the formation of vesicles. The best chance of removing an intact vesicle (which greatly aids diagnosis) may be through excision.

Incision Biopsy

With incision biopsy, a thin elliptical biopsy is taken radially through the edge of the tumour or through the edge of a macular or annular rash. Incision biopsy is superior to punch biopsy for diagnosing rashes, more tissue is displayed on histological section and scarring is often reduced. A typical incision biopsy is 5-6 mm in length and about 2 mm in width. It should be deep enough to extend into the subcutaneous adipose tissue. The biopsy should run radially from the centre or central areas of the lesion to include approximately 1 mm of normal cutaneous tissue surrounding the lesion.

Punch Biopsy

Punch biopsies are easier to perform and, in general, are more convenient. Nevertheless, they nearly always yield less information than an incision biopsy. For tumours, the biopsy should be taken centrally. For cutaneous eruptions, the biopsy should be taken from an area typical of the rash. In some cases, multiple biopsies may increase the amount of information. In this procedure, it is best not to include normal skin. Punch biopsies come in various sizes. As 2 mm punches often yield inadequate information for diagnosis, a 3 mm punch biopsy is the smallest that should be used.

Shave Biopsy/Curettage

This technique is suitable for superficially-located lesions with plaque-like clinical features, e.g. seborrhoeic keratoses. It is not an appropriate technique for nodular lesions, cutaneous rashes or melanocytic lesions.

General comments concerning cutaneous biopsies

Preparation of the skin surface: Be gentle when cleaning the skin surface prior to biopsy; try not to disturb any overlying scale as the keratin layers sometimes contain diagnostic information (e.g. this is where dermatophytic fungi may be seen). Let any alcohol preparation dry before collecting specimens for immunofluorescence. Local anaesthesia: Only a small amount of local anaesthetic is required for punch biopsy procedures (0.5 mL maximum). Too much local anaesthetic within the tissues can distort the histological appearances and simulate dermal oedema. Marking the lesion: It is often prudent to mark the target area for biopsy with an ink marker, as some lesions can blanch following introduction of local anaesthetic. The erythema in many lesions is due to vascular dilatation occurring as part of the inflammatory disorder. Local anaesthetic can cause vasoconstriction and diminish the erythema clinically. This may result in a poorly targeted biopsy yielding subdiagnostic histology. Depth of biopsy: It is best to continue into the subcutaneous adipose tissue so that the entire dermis is represented on histological section. This helps greatly with the categorisation of many inflammatory skin disorders and also demonstrates the deep border of any cutaneous tumour. When performing a punch biopsy, the biopsy instrument appears to ‘give’ when it penetrates the dermal connective tissue into subcutaneous adipose tissue. A similar sensation will be noticed when dissecting free an incision biopsy. Care with biopsy tissue: All too often, after biopsy tissue has been retrieved from the patient, crush artefact occurs during its transfer into formalin. Crush artefact greatly distorts the histological appearance and repeat biopsy may become necessary. Rather than grasping the biopsy tissue with non-tooth forceps, it should be transferred to the specimen container using needle tips, a skin hook or fine forceps, delicately grasping one edge of the biopsy. Fixative: Ordinary blue, 10% buffered formalin supplied with the specimen jars is suitable for nearly all cutaneous biopsies, except those submitted for microbiological culture or immunofluorescent examination. Labelling: Please label all specimen containers with the patient’s name and details, which should match those stated on the request slip. Unlabelled specimens can still be processed and interpreted if they arrive with labelled paperwork; however, the medico-legal status of any generated report is doubtful. The report will usually be generated with a ‘specimen received unlabelled’ comment attached.

Conclusion

Diagnosing cutaneous conditions can be challenging. The chances of success are improved when the clinician, is armed with a variety of biopsy techniques for use in the correct clinical setting, and when the pathologist is supplied with an adequate clinical history.   - 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.
Clinical Articles iconClinical Articles

So here’s the exception that proves the rule. Urinary tract infections need immediate treatment with antibiotics to avoid an increased risk of sepsis and death. That’s the quite definitive conclusion from a large retrospective study involving GP data from the UK recently published in the BMJ. After analysing the records of over 150,000 patients, aged 65 and over presenting to their GP with a suspected or confirmed UTI, the researchers found those whose antibiotic treatment was delayed or deferred were up to eight times more likely to develop sepsis in the following 60 days compared to the group who were given antibiotics from the beginning. And those patients who were not given antibiotics at all, they were twice as likely to die as their medicated counterparts. Most of the infections were caused by Escherichia Coli, and trimethoprim or nitrofurantoin were the most common antibiotics prescribed. As the study showed, sepsis is not a common sequela of UTI, occurring in just .5% of cases. But the fact remains if antibiotics were delayed or withheld altogether the incidence jumped to 2.2% and 2.9% respectively which is significant and totally unnecessary. Understandably outcomes were worse the older the patient, and men had more adverse outcomes than women, but even accounting for multiple variable factors the basic conclusion remained the same. “Our study suggests the early initiation of antibiotics for UTI in older high-risk adult populations (especially men aged >85 years) should be recommended to prevent serious complications”, the study authors said. Of concern to the researchers was the relatively large number of older patients (about 7%) who were diagnosed with a UTI but not treated. They suggest antimicrobial stewardship programmes encouraging more judicious use of antibiotics may be at least, in part, to blame. That, and the risk of elderly patients developing Clostridium difficile infection following antibiotic use. But while ‘delayed or deferred’ antibiotic treatment was not generally associated with serious adverse outcomes for some self-limiting illnesses such as upper respiratory tract infections, this study suggests it is not a good idea for UTIs. “In our study, deferred antibiotics were associated with less severe adverse outcomes than no antibiotics for older adults but still showed a significantly higher risk of mortality compared with immediate antibiotics,” the researchers said. An accompanying editorial by a UK GP academic says the study highlights one of the many dilemmas that occur in general practice. “[GPs face] the daily challenge of ensuring that patients who are unlikely to benefit are not treated, whereas those who require antibiotics receive the right class, at the right time, at the right dose, and for the right duration,” he wrote. And while agreeing with the study authors concluding advice, that all older patients with suspected UTI should be treated from day one he does suggest further research is needed. Research could help determine the most appropriate antibiotic in this situation, and if there are any particular groups in this 65 and over cohort who it would be safe to leave off antibiotic treatment until the result of the culture and sensitivities are known. - Myriam Gharbi, NIHR Health Protection Research Unit, Imperial College London; Joseph H Drysdale, Department of Primary Care and Public Health, Imperial College London; Hannah Lishman, Medical School, St George's University of London UK; Rosalind Goudie, Nuffield Department of Population Health, University of Oxford, UK; Mariam Molokhia, Department of Primary Care and Public Health Sciences, King's College, London, UK; Alan P Johnson, Healthcare-Associated Infections and Antimicrobial Resistance Division, London, UK; Alison H Holmes, NIHR Health Protection Research Unit, Imperial College London; Paul Aylin, NIHR Health Protection Research Unit, Imperial College London This article is referenced from THEBMJ. Read the original article. - Alastair D Hay, Centre for Academic Primary Care, Bristol Medical School: Population Health Sciences, University of Bristol, Canynge Hall, Bristol, UK This article is referenced from THEBMJ. Read the original article.

Clinical Articles iconClinical Articles

Western Australian health authorities recently issued warnings about Murray Valley encephalitis, a serious disease that can spread by the bite of an infected mosquito and cause inflammation of the brain. Thankfully, no human cases have been reported this wet season. The virus that causes the disease was detected in chickens in the Kimberley region. These “sentinel chickens” act as an early warning system for potential disease outbreaks.

What is Murray Valley encephalitis virus?

Murray Valley encephalitis virus is named after the Murray Valley in southeastern Australia. The virus was first isolated from patients who died from encephalitis during an outbreak there in 1951. The virus is a member of the Flavivirus family and is closely related to Japanese encephalitis virus, a major cause of encephalitis in Asia. Murray Valley encephalitis virus is found in northern Australia circulating between mosquitoes, especially Culex annulirostris, and water birds. Occasionally the virus spreads to southern regions, as mosquitoes come into contact with infected birds that have migrated from northern regions.

How serious is the illness?

After being transmitted by an infected mosquito, the virus incubates for around two weeks. Most people infected don’t develop symptoms. But, if you’re unlucky, you could develop symptoms ranging from fever and headache to paralysis, encephalitis and coma. Around 40% of people who develop symptoms won’t fully recover and about 25% die. Generally, one or two human cases are reported in Australia per year. Since the 1950s, there have been sporadic outbreaks of Murray Valley encephalitis, most notably in 1974 and 2011. The 1974 outbreak was Australia-wide, resulting in 58 cases and 12 deaths. It’s likely the virus has been causing disease since at least the early 1900s when epidemics of encephalitis were attributed to a mysterious illness called Australian X disease.

Early warning system

Given the severity of Murray Valley encephalitis, health authorities rely on early warning systems to guide their responses. One of the most valuable surveillance tools to date have been chooks because the virus circulates between birds and mosquitoes. Flocks of chickens are placed in areas with past evidence of virus circulation and where mosquitoes are buzzing about. Chickens are highly susceptible to infection so blood samples are routinely taken and analysed to determine evidence of virus infection. If a chicken tests positive, the virus has been active in an area. The good news is that even if the chickens have been bitten, they don’t get sick. Mosquitoes can also be collected in the field using a variety of traps. Captured mosquitoes are counted, grouped by species and tested to see if they’re carrying the virus. This method is very sensitive: it can identify as little as one infected mosquito in a group of 1,000. But processing is labour-intensive.

How can technology help track the virus?

Novel approaches are allowing scientists to more effectively detect viruses in mosquito populations. Mosquitoes feed on more than just blood. They also need a sugar fix from time to time, usually plant nectar. When they feed on sugary substances, they eject small amounts of virus in their saliva. This led researchers to develop traps that contain special cards coated in honey. When the mosquitoes feed on the cards, they spit out virus, which specific tests can then detect. We are also investigating whether mosquito poo could be used to enhance the sugar-based surveillance system. Mosquitoes spit only tiny amounts of virus, whereas they poo a lot (300 times more than they spit). This mosquito poo can contain a treasure trove of genetic material, including viruses. But we’re still working out the best way to collect the poo.

Staying safe from Murray Valley encephalitis

There is no vaccine or specific treatment for the virus. Avoiding mosquito bites is the only way to protect yourself from the virus. You can do this by:
  • wearing protective clothing when outdoors
  • avoiding being outdoors when the mosquitoes that transmit the virus are most active (dawn and dusk)
  • using repellents, mosquito coils, insect screens and mosquito nets
  • following public health advisories for your area.
The virus is very rare and your chances of contracting the disease are extremely low, but not being bitten is the best defence.The Conversation

- Ana Ramírez, PhD candidate, James Cook University; Andrew Francis van den Hurk, Medical Entomologist, The University of Queensland; Cameron Webb, Clinical Lecturer and Principal Hospital Scientist, University of Sydney, and Scott Ritchie, Professorial Research Fellow, James Cook University

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

Australian GPs are confident and competent at managing kids with bedwetting issues, new research confirms. But they are less sure what to do with children with daytime wetting or when childhood enuresis persists into adulthood, according to the study findings recently published in the Australian Journal of General Practice. As you may remember, back in late 2016, health professionals on the Healthed database were invited to participate in a survey designed by leading paediatric urologist, Dr Patrina Caldwell to investigate their knowledge and experience with managing urinary incontinence in childhood. Almost 1500 Australian health professionals responded, mostly GPs. Researchers found that 88% of survey participants reported being slightly or very knowledgeable about managing childhood urinary incontinence. Their confidence seems well-founded at least for nocturnal enuresis. Having been given multiple answer options about first-line management, 93% of participants correctly selected urotherapy and enuresis alarm training as the ideal first-line management for childhood enuresis. This is despite less than half (48%) being able to correctly identify the commonest cause of the condition as being abnormal physiology of sleep and bladder function. Over a third of people incorrectly thought childhood enuresis was simply a delay in developing toileting skills. However, it is a different kettle of fish when it comes to managing daytime urinary incontinence which only 81% of participants felt at least somewhat confident managing. Of concern was the finding that 18% of health professionals would treat this condition with inappropriate and potentially harmful treatments. More specifically, a small percentage of participants chose tricyclic antidepressants which used to be a popular treatment option but is now no longer recommended as first-line therapy for daytime urinary incontinence due to its potential side-effects. The situation was even worse for adult patients who had problems with enuresis that had persisted since childhood. Only 61% of participants felt they were even slightly knowledgeable managing these patients, although most chose the most appropriate first-line therapy of urotherapy and desmopressin. According to the study authors, the knowledge of the health professionals with regard to the various categories of urinary incontinence was largely reflective of the prevalence of each of the different conditions in their clinical experience. Most GPs were currently managing at least a few cases of nocturnal enuresis but the other two conditions were much rarer.

Reference

Caldwell PHY. Manocha R, Hamilton S, Scott KM, Barnes EH. Australian community health practitioners’ knowledge and experience with managing urinary incontinence that begins in childhood. Aust J Gen Pract. 2019 Jan; 48(1-2); 60-5. Available from: https://www1.racgp.org.au/ajgp/2019/january–february/managing-urinary-incontinence-that-begins-in-child
Clinical Articles iconClinical Articles

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.
Clinical Articles iconClinical Articles

Despite the incidence of cerebral palsy decreasing, it is still Australia’s most common cause of physical disability in childhood, experts say. And with the condition affecting over two in every 1000 live births, it is more than likely a GP will be caring for these patients in their clinical practice. The authors of a review in the latest Medical Journal of Australia highlight areas where the treating health professional, including the GP can play a role in improving these children’s health outcomes as well as their quality of life. “While there is currently a limited range of evidence-based treatments that change the underlying pathology of cerebral palsy, there are many areas in which health care professionals can change the natural history of cerebral palsy and improve participation and quality of life for children with this condition,” they said. They refer to a framework for management of patients with cerebral palsy, known as the six Fs. These Fs help both clinicians and families of the affected child set realistic goals and develop appropriate pathways to meet them. The six Fs are: Function – encourage the child to try activities and celebrate not only what they can achieve but the attempt. Family –  the family environment is vitally important to the child’s health outcomes both physically and psychologically. Significant attention, support and resources need to be directed to this. Fitness – Overall physical fitness is at least as important as exercises directed at helping overcome the particular physical disability of a child with cerebral palsy. Fun – Caregivers need to ensure the child with cerebral palsy does not miss out on this key component of childhood. Friends – Social interaction and the development of quality relationships need to be incorporated as a management goal. Future – This is all about setting realistic goals and expectations and the mapping out plans of how to achieve them, keeping in mind the other five Fs. In addition to this very grounding framework of management, the review authors went on to describe the current state of play of treatment for the various physical manifestations of cerebral palsy. Spasticity and dystonia are the most common signs of the disease and along with physical therapies such as physiotherapy, occupational therapy, splints and orthotics there are a number of medications and even some surgical options for treatment. Baclofen, diazepam and Botulinum toxin A are well-known options to treat the spasticity and dystonia. But apparently there is emerging evidence for the use of other medications such as gabapentin and clonidine. There are also some highly specialised surgeries being performed for subsets of cerebral palsy children such as deep brain stimulation for children with dystonic and dyskinetic movement, selective dorsal rhizotomy for severe spasticity in the lower limbs and even intrathecal baclofen to avoid the side effects of oral baclofen. The review also highlights three potential problem areas for children with cerebral palsy that are of particular relevance for GPs caring for children with this condition. Hip displacement is more of a risk in children with cerebral palsy, and if it is missed it can result in hip dislocation. Regular clinical and radiographic assessment is recommended. “The pelvic x-ray is taken in a standardised supine position and is usually repeated between six and 12 months, depending on the severity of cerebral palsy and the rate of progression of migration of the femoral head out of the acetabulum,” they said. Referral is recommended once migration approaches 30% Another major issue to check for in children with cerebral palsy is pain, with evidence suggesting up to 75% of young patients are regularly experiencing this. The review authors recommend carers ask about this directly, as children may not volunteer this information despite chronic pain’s well-known effect on quality of life. Pain treatment is generally fairly standard, however specific treatments are available for pain arising from unique symptoms such as dystonia or spasticity. Finally, the review authors advise treating clinicians to watch out for feeding and swallowing problems, and as a consequence of these, deficiencies in nutrition. There is a wide range of potential issues concerning eating and drinking that can affect children with cerebral palsy, including swallowing difficulty, managing utensils, posture, risk of aspiration, sensory difficulties and even excessive drooling. All of these can be managed, but the key first step is identifying there is an issue before nutritional deficiencies manifest in comorbidities such as osteoporosis. Unfortunately, as yet, we still cannot cure cerebral palsy. However, with early interventions, close monitoring and targeted therapies the natural history of cerebral palsy is being altered for the better.

Reference

Graham D, Paget SP, Wimalasundera N. Current thinking in the health care management of children with cerebral palsy. Med J Aust. 2019 Feb; 210(3): 129-35. DOI: 10.5694/mja2.12106
Clinical Articles iconClinical Articles

Abortion is a common experience for Australian women. Around one in six have had an abortion by their mid-30s, according our new research published today in the Australia New Zealand Journal of Public Health. Narratives about abortion often stigmatise women who have had one or seek access to one. But our research shows women from all walks of life may have an abortion: married, single, child-free, and mothers. In fact, women who have already had children are more likely to have a termination than those who haven’t. Women make decisions about whether or not to have an abortion in the context of their complex lives. And it’s by no means an easy decision. Our research investigated the factors associated with abortion as women move from their late teens into their mid-30s. We found women with lower levels of control over their reproductive health, whether through family violence, drug use or ineffective contraception, are more likely than their peers to terminate a pregnancy. If we want to reduce the rate of unintended pregnancies and abortion in Australia, we need to empower women to have control over their fertility and support them with appropriate health services.

Women’s experiences

We used data from five surveys of the Australian Longitudinal Study on Women’s Health to examine factors associated with “induced” abortions which were not undertaken because of a foetal abnormality. We looked at a cohort of more than 9,000 women born between 1973-78 who were first surveyed at ages 18-23 years. At the fifth survey they were aged 31-36 years. Overall, by their mid-30s, 16% of the women in this study had reported at least one abortion. We also looked at the proportion of women who reported a new abortion at each survey. At the first survey, when women were aged 18-23, 7% reported having had an abortion. In subsequent surveys, 2-3% of women reported having an abortion since the last survey. While most women reported only one new abortion, around one in ten reported two abortions, and around 2% reported three abortions. Abortion is understandably more common for women when they are in their 20s than it is when women reach their 30s. This may be because many women in their 30s are actively trying to be pregnant, or may be using contraception more effectively if they’re trying to avoid becoming pregnant. Compared with married women, those who were in a de facto relationship, were single, or divorced were more likely to have had an abortion. Women with children were more likely to have an abortion than women who did not have children. In the fourth survey, the majority of women (72%) said they hoped to have one or two children, 20% wanted three or more, while 8% didn’t want to have children. Perhaps unsurprisingly, women who had an abortion in the later surveys were more likely to have previously reported using ineffective contraception, or to have had a past abortion, than women who didn’t terminate a pregnancy in their 30s. Women whose alcohol use had recently become riskier and women who reported using any illicit drugs in the past 12 months were also more likely to have an abortion. Violence was also a big factor. Women who recently experienced partner violence were more likely to terminate a pregnancy than women who reported no violence. Even women who reported childhood sexual abuse had a significantly increased likelihood of abortion in their twenties (but not in their 30s). In fact, women reporting violence of any kind, and at any time, had a significantly increased likelihood of having an abortion.

What can we do about it?

Australia is going through a much-needed process of law reform to ensure women across the country have access to abortions as part their women’s health service. Queensland is the most recent state to remove abortion from the criminal code. Alongside this, we need to improve training and resources to for health providers to identify and help women who may be at risk of unintended pregnancy, particularly those who are using illicit drugs or are experiencing partner violence. We need better ways of reaching all vulnerable women, but especially young women experiencing reproductive coercion. We also need to ensure that all women are provided with good access to information about effective contraceptive choices. While the oral contraceptive pill and condoms are the most common methods Australian women use, long-acting reversible methods (such as intra-uterine devices and implants) can be good options for many women wanting effective contraception.The Conversation

- Jayne Lucke, Chair, Australian Research Centre in Sex, Health & Society, La Trobe University and Angela Taft, Professor and Director, La Trobe University

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

Chronic rhinosinusitis is a misery-generating condition – literally. According to a large study just published in The Journal of the American Medical Association, having chronic rhinosinusitis significantly increases your risk of depression and anxiety. And if you also have nasal polyps the risk is higher still. The Korean study was admittedly observational but it did include almost 50,000 individuals from the general population and followed them up for 11 years. Researchers found, over the duration of the study, those people with chronic rhinosinusitis were 54% more likely to develop depression and 57% more likely to develop anxiety than those people who did not suffer this condition. And if nasal polyps accompanied the rhinosinusitis the increase in likelihood for both mental illnesses jumped to the early 60s (61% and 63% respectively). So what are the implications of this study? Well – they are fairly straightforward really. “Physicians should be aware of the potential comorbidities observed in patients with [chronic rhinosinusitis] and provide therapy to reduce the risk of depression and anxiety in these patients,” the study authors helpfully concluded. What we don’t know of course, being simply an observational study without any intervention to test, is whether effectively treating the rhinosinusitis helps the depression or anxiety, and importantly, whether surgically removing the polyps can make a difference to this psychological side-effect. The researchers actually even distance themselves from the conclusion that chronic rhinosinusitis causes depression and anxiety, citing the chicken and egg phenomena. “Whether depression and anxiety amplify the symptoms of [chronic rhinosinusitis] or whether these conditions are the consequence of [chronic rhinosinusitis]is unknown,” they said. But they do say their findings support previous research that has suggested an association between the conditions. They also say their study allowed analysis of the specific phenotype responsible for the chronic rhinosinusitis – whether it be predominantly T1 or T2 response derived. What they found was the association held true regardless of the phenotype – suggesting this was more to do with personality and symptoms than physiology. All in all, what the study authors suggest is that given how common chronic rhinosinusitis is in the population, it is worthwhile keeping a high indexation of suspicion for the development of depression and anxiety not only for the patients’ current quality of life but also because these conditions can affect health outcomes down the line. “[T]hese psychiatric comorbidities may influence not only the diagnosis of [chronic rhinosinusitis] but also its therapeutic and surgical outcomes,” the study authors said.  

Reference:

Kim JY, Ko I, Kim MS, Yu MS, Cho BJ, Kim DK. Association of Chronic Rhinosinusitis With Depression and Anxiety in a Nationwide Insurance Population. JAMA Otolaryngol Head Neck Surg. 2019 Feb 7.  DOI: 10.1001/jamaoto.2018.4103 [Epub ahead of print].
Clinical Articles iconClinical Articles

Allergic disorders result from an inappropriate, usually IgE-mediated, immune response upon exposure to either environmental or food allergens. Common manifestations of allergy include rhinoconjunctivitis, asthma, eczema, acute urticaria and anaphylaxis. Disorders, such as chronic urticaria, hereditary angioedema and T-cell contact dermatitis (metal allergy), while clinically similar in some ways, are not IgE-mediated. Allergic disease manifests in different ways through life and the likely causative agents can also change with age (see Table 1).

Tests used in the diagnosis of IgE-mediated allergy

Total IgE Higher levels of total IgE are often found in patients with allergic conditions. However, normal total IgE does not exclude allergy. Total IgE is also elevated in other conditions including parasitic infections and allergic bronchopulmonary aspergillosis. It is used increasingly in determining anti-IgE therapy in moderate to severe asthmatics. Allergen-specific IgE Allergen-specific IgE can be detected for a large variety of allergens. The presence of a specific IgE to allergen can suggest allergic disease and is detected via a blood test (RAST or radioallergosorbent test) or skin prick test. RAST tests detect many of the different proteins within an individual allergen. Recombinant allergen testing Of the many proteins within a substance, only a few may cause allergic symptoms. Recombinant allergen testing looks for specific characterised protein within an allergen. Interpretation of RAST tests The presence of detectable specific IgE to an allergen does not confirm the patient is allergic to that substance. All results must be interpreted in conjunction with the clinical history of the patient. Low levels of detectable specific IgE can confirm the presence of allergy in the right clinical context. RAST testing aids in the assessment of, and identification of allergic sensitisation, but is not to be used alone as the deciding factor for inclusion or exclusion of allergy. As the level of specific IgE increases, the likelihood of clinical relevance also increases. As shown in Table 2, different allergens have different specific IgE level cutoffs at which serious allergy is >95% likely (positive predictive value or PPV). The range of values is vastly different between allergens and is affected by age and also by geographic region. Table 2 defines levels at which exposure, or a challenge, would be highly hazardous for a patient. Importantly, many patients could have serious reactions at much lower levels.   [table id=1 /]   [table id=2 /]

RAST tests

RAST tests are available for a range of allergens, however Medicare criteria limits rebates based on the number, type and frequency of tests. Medicare Australia limits rebates for RAST tests to a maximum of four specific allergens and/or mixes per pathology request and a maximum of four RAST test episodes per year. When ordering RAST tests, it is advisable to include allergens the patient feels are relevant and those likely for the clinical scenario. For common clinical scenarios we recommend the following: Childhood eczema Age <2 years: Milk, Egg, Wheat, Peanut Age >2 years: Milk, Egg, Peanut, Dust mite Additional allergens or an extended RAST combined allergy panel may be ordered. Asthma and allergic rhinoconjunctivitis Dust mite, Grass mix, Animal dander Additional allergens may be ordered or substituted if relevant (e.g. cat dander instead of animal dander). An extended RAST inhalant panel is also available. Default panel if no allergens are specified and no clinical notes are provided Age <5 years: Dust mite, Grass mix, Food Mix Age >5 years: Dust mite, Grass mix, Animal Mix Anaphylaxis Anaphylaxis is a severe life-threatening allergic reaction. It is recommended these patients require specialist assessment by a clinical immunologist or allergist. Initial testing should look for the causative allergen if possible. It is important to note that a negative RAST test does not exclude the allergen tested. RAST testing recommendations ­
  • Test individual likely causative allergen i.e. food, stinging insect. ­
  • Tryptase, if done within 2-6 hours of reaction, can support the occurrence of an allergic reaction. ­
  • Useful as an assessment of mastocytosis (condition with increased numbers of mast cells)

Extended RAST panels

Extended RAST panels have been developed to represent the common allergens encountered clinically in practice. They are particularly relevant in our geographic region and replace the skin prick test panel which is no longer available. Additional allergens may also be requested. All results must be interpreted in conjunction with the patient’s clinical history. Extended RAST Food Panel ­
  • Covers common food-related allergens
  • Almond; Hazelnut; Sesame seed; Banana; Mango; Shrimp (prawn); Cashew; Milk (cow); Soybean; Codfish; Peanut; Walnut; Egg white; Rice; Wheat
Extended RAST Nut Allergy Panel ­
  • Broad collection of commonly consumed nuts, including peanuts ­
  • Individual nut testing with appropriate clinical history is preferred ­
  • Recommend to discuss results with a clinical immunologist or allergist
  • Almond; Macadamia; Pine nut; Brazil; Peanut; Sesame seed; Cashew; Peanut (Ara-h2); Walnut; Hazelnut; Pecan
Extended RAST Combined Allergy Panel ­
  • Combination of common food and environmental allergens ­
  • Replaces the skin prick test panel (no longer available)
  • Almond; Dust mite; Mould mix; Cashew nut; Egg white; Peanut; Cat dander; Grass mix; Shrimp (prawn); Codfish; Hazelnut; Soy; Dog dander; Milk (cow); Wheat
  • * Preferable for children (<12 years) due to low serum volume
Extended RAST Inhalant Panel ­
  • Covers common environmental allergens ­
  • Useful for asthma and allergic rhinitis
  • Acacia (wattle); Blomia tropicalis; Dust mite; Alternaria alternate; Cat dander; Eucalyptus; Aspergillus fumigatus; Cladosporium; Horse dander; Bahia grass; Common ragweed; Johnson grass; Bermuda grass; Dog dander; Perennial rye grass

Recombinant allergens

Omega-5 gliadin ­
  • A component of wheat ­
  • Associated with anaphylaxis ­
  • Often in the context of eating wheat and physical activity within 1-2 hours
Alpha-gal (mammalian meat allergy) ­
  • Associated with anaphylaxis; often delayed following consumption of meat (beef, lamb, pork) ­
  • Related to tick bites
Peanut Allergy Risk Assessment ­
  • Peanuts like all food is made up of many different proteins ­
  • Ara-h2 is associated with anaphylaxis to peanut ­
  • Can assist with risk assessment and should be done in conjunction with a clinical immunologist or allergist ­
  • A negative Ara-h2 in peanut positive patient does not imply there is no risk to anaphylaxis
  • Results of RAST tests can also be of use in monitoring ongoing allergy in patients in conjunction with their treating clinician

How to order allergy tests

RAST tests - standard panels Medicare Australia limits rebates for RAST tests to a maximum of four specific allergens and/or mixes per pathology request and a maximum of four RAST test episodes per year. Extended RAST tests (Medicare rebate + $120* per panel)
  • Extended RAST Food
  • Extended RAST Nut
  • Extended RAST Combined
  • Extended RAST Inhalant
Please note, extended RAST panels are not bulk billed. Recombinant allergen tests (Medicare rebate + $60* each)
  • Alpha-gal
  • Omega-5 gliadin
  • Peanut (Ara-h2)
  • Peanut Allergy Risk Assessment
  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.
Clinical Articles iconClinical Articles

It’s a controversial topic here in Australia. But a new UK study, just published in the New England Journal of Medicine, gives strong support the role of e-cigarettes as a smoking cessation therapy. The randomised controlled trial of almost 900 adult smokers wanting to quit found the one-year abstinence rate was 18% among the e-cigarette users compared to 9.9% among those who were randomised to receive nicotine replacement therapy. Much of the difference could be attributed to adherence to the assigned product. After 12 months, 80% of the e-cigarette group were still using the device whereas only 9% of the alternative group were still taking their nicotine replacement therapy despite being able to choose between the patch, gum, lozenge, nasal spray, inhalator, mouth spray, mouth strip, and microtabs (or any combination of these). Participants in both groups underwent the same multi-session behavioural support as per best practice guidelines. This study provides some of the strongest evidence to date that e-cigarettes are significantly better than nicotine replacement therapy in helping people quit smoking, the study authors suggest. “This is particularly noteworthy given that nicotine replacement was used under expert guidance, with access to the full range of nicotine-replacement products and with 88.1% of participants using combination treatments,” they said. The researchers suggested e-cigarettes had better adherence rate because they were more effective at reducing the symptoms of withdrawal when quitting smoking, because the refillable devices are better at delivering nicotine compared with options such as gum or patches. They also suggest the nicotine dose provided by e-cigarettes was easier to tailor to individual needs than other replacement options. And even though people using the e-cigarettes were more likely to get mouth or throat irritation, this side effect was generally mild and tolerable especially compared to withdrawal symptoms such as constipation, mouth ulcers and weight gain. In general, the researchers claim replacing cigarettes with e-cigarettes is a definite positive in terms of health outcomes and much better than other nicotine replacement options, but they suggest the high rate of adherence in the e-cigarette group may have some negative connotations. “This can be seen as problematic if e-cigarette use for a year signals ongoing long-term use, which may pose as-yet-unknown health risks,” they said. As an accompanying editorial points out, fundamentally nicotine is highly addictive. While electronic cigarettes have been proven to be a great tool in helping people get off normal cigarettes, there may be an issue if non-smokers, especially teenagers take up vaping, making them vulnerable to becoming smokers further down the track. “The cigarette company may well see e-cigarettes as addictive bait that will lead young people toward smoking,” the US editorial authors suggest. They suggest this potential problem could be relatively easily averted by ensuring e-cigarettes aren’t manipulated to enhance their appeal, specifically the authorities should not allow the manufacture of flavoured nicotine products. However, they too acknowledge e-cigarettes have a significant role to play in solving this public health problem – ‘by helping people who are users of combustible tobacco products stop smoking by switching to vaping.’

References:

Hajek P, Phillips-Waller A, Przulj D, Pesola F, Smith KM, Bisal N, et al. A Randomized Trial of E-Cigarettes versus Nicotine-Replacement Therapy.  N Engl J Med. 2019 Jan 30;  DOI: 10.1056/NEJMoa1808779 [Epub ahead of print] Drazen JM, Morrissey S, Campion EW. The Dangerous Flavors of E-Cigarettes. N Engl J Med. 2019 Jan 30. DOI: 10.1056/NEJMe1900484 [Epub ahead of print]
Clinical Articles iconClinical Articles