Dermatological emergencies are uncommon, but can cause devastating complications and death if not recognised and treated early. Some skin conditions require treatment in an intensive care unit. Here are some of the most serious skin conditions and what you should know about recognising them.
1. Necrotising fasciitis
Necrotising fasciitis is a severe infection of the skin, the tissue below the skin, and the fascia (fibrous tissue that separates muscles and organs), resulting in tissue death, or necrosis. The infection is rapid, fast-spreading and fatal if not detected and treated early. If not treated with antibiotics and surgery early, toxic shock and organ failure are common.
Necrotising fasciitis may occur in anyone. Previously healthy young people are often affected.
The cause may be one or more bacteria entering the body via an external injury or punctured internal organ. Group A streptococci bacteria, which are the organisms implicated in “strep throat”, are among the most common causes.
Early necrotising fasciitis is easily missed, as similar symptoms are commonly seen in less severe infection. The initial area is painful, red and swollen. This progresses to a dark, blistered, malodorous and blackened area, which is a sign of tissue death. Other symptoms include fever, intense pain, low blood pressure and shock.
The most important risk factors for necrotising fasciitis include diabetes, peripheral vascular disease, trauma, alcohol and intravenous drug use, and use of non-steroidal anti-inflammatory drugs.
Treatment of necrotising fasciitis is immediate hospitalisation, surgical removal of all dead tissue, and intravenous antibiotics. Patients often require intensive care. Management of shock and other complications reduces the risk of death. Use of a hyperbaric chamber (to increase oxygen delivery to the tissue) and immune therapy may also be required.
Around a quarter of people diagnosed with necrotising fasciitis will die, and sepsis occurs in up to 70% of cases.
2. Scalded skin syndrome
Staphylococcal scalded skin syndrome is an uncommon major skin infection. It typically affects newborn babies, young children and adults with reduced immune systems or kidney failure. This syndrome is caused by toxins produced by the bacterium Staphylococcus aureus, which is common in throat, ear and eye infections.
Around 15-40% of adults carry Staphylococcus aureus on the skin surface and have no problems. But these adults may inadvertently introduce the bacteria into nurseries or daycare centres. Because young children have weak immunity to specific toxins, they’re at increased risk of scalded skin syndrome.
Scalded skin syndrome is characterised by a red, blistering rash resembling burns. Early symptoms include fever, skin redness and skin tenderness. Other symptoms may include sore throat or conjunctivitis.
Within 24-48 hours, fluid-filled blisters form on the entire body. The blisters may rupture, leaving areas resembling burns. Large areas of the skin peel off and fall away with only minor touch.
Common skin rashes and what to do about them
Scalded skin syndrome requires hospitalisation for intravenous antibiotics and treatment of the wounds. Ruptured blisters require wound dressings, and the skin surface requires intense care to avoid further damage.
Other treatment includes intravenous fluid and electrolyte maintenance to prevent shock and other complications, paracetamol for pain and fever, and avoidance of severe sepsis. Sepsis is when chemicals released into the bloodstream to fight an infection trigger inflammatory responses throughout the body, which can be life-threatening.
Complications of scalded skin syndrome include severe infection, pneumonia, cellulitis (a bacterial skin infection) and dehydration. Most children treated appropriately recover well and healing is complete within a week.
3. DRESS syndrome
Standing for “drug reaction with eosinophilia and systemic symptoms,” DRESS syndrome is a severe reaction that affects the skin and internal organs. The patient may have an extensive rash, fever, enlarged lymph nodes and damage to the liver, kidneys, lungs, heart, blood components or pancreas. Symptoms usually start two to eight weeks after the responsible drug has been taken.
The death rate is estimated between 10 and 20%, most often due to liver failure.
The most common drugs responsible include anticonvulsants, antidepressants, non-steroidal anti-inflammatory drugs, antibiotics and sulfa drugs (a type of synthetic antibiotic). The severe reaction is thought to occur due to a pre-existing genetic change in the immune system, a triggering illness (most often a viral infection) and defective breakdown of the drug by the body.
Early diagnosis is essential. The responsible drug must be stopped immediately and patients may require intensive care or burn unit management. More intensive treatment is needed if organs are involved.
4. Life-threatening drug reactions
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are variants of a life-threatening reaction that affects the skin and mucous membranes (mouth, eyes, genitals, respiratory or gastrointestinal tracts).
These are unpredictable reactions that leave sufferers critically unwell, with widespread death of the outer skin layer (epidermis), which peels off. The rash generally begins on the trunk and extends to the limbs and face, and there is intense skin pain. Before the rash appears, symptoms include fever, sore throat, runny nose, conjunctivitis and general aches.
It’s almost always caused by medications. The most common medications causing this reaction are anticonvulsants, antibiotics, allopurinol (gout medication), non-steroidal anti-inflammatory drugs and an HIV drug. The reaction usually occurs in the first eight weeks after taking the drug. It’s more likely to happen if the patient has cancer, HIV or specific genes that may play a role.
This reaction can be fatal by causing dehydration and malnutrition, severe infection, respiratory failure, gastrointestinal complications and multi-organ failure.
The responsible drug has to be stopped, and treatment (in a burns unit and intensive care unit) includes wound care, fluid management, pain management and prevention of infection. Long-term complications, including scarring, eye, oral, genital, lung disease and mental health disorders, are common. Around a quarter of people with this reaction will die.
Everyone has had the unpleasant experience of a rash on the skin – pink, red or purple, flat or bumpy, itchy, scaly, pus-filled, or just plain unsightly. This variety isn’t surprising, because the skin is a complicated organ.
Infections, allergic reactions, immune system problems and even bad reactions to medication can all manifest as a rash.
Here are a few of the most common types.
Almost every prescription medication available can cause a rash as a side effect, and more than 80% of those are “exanthematous drug eruptions”, meaning a widespread rash accompanied by other symptoms such as headache, fever and feeling generally unwell.
This rash usually appears within two weeks of starting a new medication, as a widespread, symmetrical rash with pink-to-red spots that are flat or elevated and firm, and that might join together in patches.
This type of rash is a hypersensitivity reaction, in which the attacking soldiers of the immune system (called “T-cells”) detect the drug and try to clear it from the body by releasing inflammatory proteins.
Very rarely, a drug can cause a severe and life-threatening rash called “toxic epidermal necrolysis” where the skin begins to peel off in sheets. It’s more common in Han Chinese people with a specific genetic variant, and requires intensive care or burn unit treatment.
Most drug eruptions go away within a week once the patient stops taking the problem medication, or within several weeks in protracted cases. In the meantime, or if the drug is essential, steroid creams (which reduce inflammation) and emollient (softening) moisturisers can bring some relief.
Allergic contact dermatitis
Allergic contact dermatitis is caused by direct skin contact with a substance to which the person is allergic. The immune system’s T-cells overreact to the allergen and release proteins that call more immune cells to the area, making it red and swollen.
It’s often itchy and can be blistered or dry but bumpy. The reaction is often delayed by 48-72 hours, so it can be difficult to determine exactly what caused the reaction. It should also die down by itself over a few days, as long as the allergen is no longer on the skin.
Contact allergies can develop suddenly after years of exposure to an allergen. Jewellery containing nickel, fragrances in lotions, household cleaners, preservatives in hair products, and latex in gloves or condoms are common sources. A dermatologist can carry out a patch test to determine whether a substance is the allergen, by applying it to a small patch of skin.
Active dermatitis is treated with emollient moisturisers and steroid creams, or with oral steroids or drugs to suppress the immune system if very severe. Further episodes can be prevented by becoming aware of the sources of the allergen, reading labels carefully, and using gloves to handle allergen-containing products.
Atopic dermatitis or atopic eczema (often just called eczema) is very common in children from three months old onwards, but appears in adults too, often with hay fever and asthma.
Atopic dermatitis features patches of intensely itchy red skin, sometimes with blisters and weeping patches. Children often have open sores and scabs, because it’s so itchy that it’s hard to refrain from scratching.
Over time the skin becomes thickened and rough from frequent scratching and rubbing. Childhood atopic dermatitis tends to improve as the child grows up, but may continue. Far less commonly, atopic dermatitis can also appear first in adulthood.
Atopic dermatitis is a disease of the immune system, in which
structural defects in the skin barrier make it easier for irritants to penetrate into the skin. This throws the delicate balance of the microbial community on our skin out of whack, causing the immune system to go into overdrive. Triggers include stress, sweating, coarse fibres in clothing, inhalation of allergens such as pollen, irritants such as soap or perfumes, and eating food we’re allergic to.
Steroid creams can help treat a bad flare of atopic dermatitis, but shouldn’t be used constantly. In very severe cases, immunosuppressant drugs are prescribed. Ongoing control of atopic dermatitis often includes using emollient moisturisers to combat dry skin, keeping cool, avoiding hot water or irritants, and reducing allergens such as dust mites in the home.
For severe cases that don’t respond to these methods, the drug dupilumab has just been approved for use in Australia. This drug blocks a specific cell receptor to prevent immune cells from detecting two overactive inflammatory proteins.
Atopic dermatitis can have a big impact on quality of life, due to insomnia from the constant itchiness, and restrictions on clothing, body products, pets or activities. Its presence on prominent parts of the body like the face and hands can also reduce self-esteem. Evening sedatives to improve sleep and psychotherapy can help reduce the impact on everyday life.
Psoriasis is another chronic immune disorder. It can start at any age and can be lifelong, and is usually present as red plaques (raised or thickened skin) with well-defined edges and silvery-white scales, ranging from a few millimetres to several centimetres across. The overactive inflammation can also damage the joints and lead to psoriatic arthritis.
Psoriasis is caused by too many new skin cells being produced and moving up to the surface of the skin too quickly. It’s not known exactly why, but there’s usually an overabundance of inflammatory messenger proteins in the skin.
It can be triggered or aggravated by a streptococcal infection such as tonsillitis, smoking, hormonal changes such as menopause, and some medications. Genetics play an important role in susceptibility to psoriasis and also in what treatments are effective.
Chronic plaque psoriasis, the most common form, can be very resistant to treatment. Small areas can be treated with creams containing steroids, coal tar, or vitamin D. If a lot of the body is covered by plaques, oral immunosuppressant drugs are used, or phototherapy, which uses targeted UV light to destroy over-active immune cells. Moderate sun exposure sometimes improves psoriasis, but sunburn can worsen it – a tricky balance in Australia’s high-UV environment.
These treatments can usually improve the plaques, but it can be very difficult to clear it completely. There are several new drugs coming onto the market for severe psoriasis that hasn’t responded to other treatment.
Tinea, or ringworm, is not caused by worms at all but a fungal infection. Tinea is usually named according to the body site it’s on, but the same few kinds of fungus can cause tinea in many parts of the body and it can be spread from one part of the body to another, such as by scratching or using a contaminated towel.
Tinea pedis, on the foot, is an important type because spores can live for weeks in communal showers and changing rooms, making it a common source of infection that can then spread to the trunk, arms and legs (tinea corporis) or groin (tinea cruris, or jock itch). Cats, dogs and other animals are a common source of ringworm fungus, but many types can be spread between people too.
Typically, tinea spreads in a circular or oval patch, often healing in the middle so that it appears to be a red scaly ring of infection. Sometimes it can also become a fungal abscess that looks like a boil, feels boggy, and has pustules.
On the feet it can look like ringworm circles, patchy fine dry scales on the sole, blisters on the instep or a moist, red peeling area between the toes (athlete’s foot).
In the groin, it can have a scaly, red raised border and be extremely itchy.
Tinea is diagnosed by microscopic examination and laboratory culture of skin scrapings. It’s usually treated with antifungal creams, or oral antifungal drugs if it persists. It can become chronic in the warm, moist folds of the body.
Shingles is a famously painful, blistering rash caused by the reactivation of chicken pox virus, varicella-zoster virus, usually years or decades after the original infection.
The virus lies dormant in nerves near the spine and migrates down the sensory nerve to the skin when it is reactivated, but it’s not known why the virus is reactivated. Some possible triggers are radiotherapy, spinal surgery, other infections, or cancers.
Shingles starts with pain in the skin that is often described as burning or stabbing, followed in one to three days by a rash of raised red bumps that become blisters and then crust over. The rash is usually confined to a narrow arc of skin, along the sensory nerve that was harbouring the virus.
Patients often have a fever, headache and swollen lymph nodes. Recovery takes two to four weeks but the pain can persist after the rash has healed, called post-herpetic neuralgia.
If it’s caught within three days of onset, antiviral medication can reduce the severity of symptoms and length of the infection. Otherwise, treatment consists of powders or solutions to dry out the rash, as well as pain relief and rest.
Australians aged over 70 are eligible for a free zoster vaccine, which reduces the risk of shingles by half.
This article is part of our series about skin: why we have it, what it does, and what can go wrong. Read other articles in the series here.
Skin cancer is one of Australia’s most common cancers, with data showing almost a million cases of skin cancer in 2015.
Skin cancer is primarily caused by excessive exposure to ultraviolet (UV) radiation from the sun, causing DNA damage to skin cells. If this damage is not repaired by the body’s internal DNA repair machinery, then faulty cell replication can occur – triggering the abnormal growth of cells – which eventually become cancers.
People with pale skin types are more vulnerable to skin cancer and, broadly, the more sun they are exposed to – and the greater the intensity of the UV radiation – the higher their risk.
Cutaneous malignant melanoma is the most aggressive skin cancer claiming more than 1,700 lives in 2016. Squamous cells carcinoma and basal cell carcinoma are far more common but far less life threatening. Despite being very amenable to treatment if identified at an early stage, squamous cells carcinomas still caused 560 deaths in 2016.
International comparisons highlight the extent to which we and our Kiwi friends are undisputed world champions in skin cancer. Unfortunately, we’ve long occupied gold and silver on the skin cancer Olympic podium.
A conservative estimate of the cost of treating melanoma in Australia exceeds A$270 million annually. If we add non-melanoma skin cancers (now called “keratinocyte cancers” after their cell of origin) and the bill is likely more than A$1billion a year.
Most Australians (and Kiwis) have the wrong type of skin for their environment. Basically, through migration, our two countries have been populated by many people with fair skin whose ancestors come from much less sunny climates. Lack of protective pigmentation leaves skin cells especially vulnerable to the DNA-damaging rays from the sun.
Common skin rashes and what to do about them
During human evolution, our early hominid ancestors in Africa lost their covering of body hair and developed pigmented skins, presumably as protection against the harsh tropical sun. With subsequent migration out of Africa into Europe, the protective benefits of dark skin became less important for survival and were likely a hindrance to effective vitamin D production. There was selective pressure for less pigmented skin with more distance from the equator.
In contrast, those who migrated out of Africa to Asia, Australia and the islands of Melanesia were constantly exposed to sunlight. So they retained their protective pigmentation. This explains why the recent European migrants to the Americas and Oceania arrived in the “new worlds” with skin types poorly suited to their new environments. This was in stark contrast to the well-adapted skin of the indigenous inhabitants.
While melanin provides protection against the damage caused by exposure to UV radiation, it’s not a “suit of armour”. Melanoma rates are far lower in people with pigmented skin such as Aboriginal people, but not non-existent.
A major factor is geography – that is proximity to the equator (the line on the globe that gets the greatest amount of sun). Generally speaking, the closer to the equator someone lives, the greater the amount and intensity of sun exposure they receive. That gradient is seen in a comparison of skin cancer rates across Australian states with Queensland reporting much higher rates than New South Wales, which is in turn higher than Victoria.
Another is the earth’s elliptical orbit around the sun. The planet is about 1.7% closer to the sun in January, during the southern summer, and 1.7% further away in July – northern summer. So that means when the sun is strongest the southern hemisphere is 3.4% closer to the sun than the north is during their summer. This increases UV by about 7%.
Add to that the lower pollution levels and clearer air in the southern hemisphere – due largely to much lower population densities – resulting in UV levels about 7% higher than in the northern hemisphere.
Taking all these factors together, southern hemisphere locations receive about 15% more UV radiation than the equivalent northern latitude location in any given year.
What about the ozone hole?
Many believe the ozone hole – a naturally-occurring pool of ozone-depleted air arising over the poles – explains much of our excess skin cancer rates. Stratospheric ozone does reduce the amount of UV reaching the Earth’s surface. When the ozone layer was damaged by the release of CFCs and halon from refrigerants from the 1960s onwards, more UV reached ground level.
So the depletion of the ozone layer caused legitimate concern and prompted the establishment of the “Montreal protocol” designed to eliminate ozone-damaging pollutants and repair the ozone hole.
As the ozone hole over the south pole breaks up in spring, pockets of ozone depleted air drift across Tasmania, southern Victoria and the southern part of New Zealand’s south island. The effects are minor and transient, and are being closely monitored by NASA and other agencies.
In reality, ozone depletion has made no appreciable difference to skin cancer rates in Australia and New Zealand. The quantum of additional UV exposure was modest – and at a time of year when most skin was covered so as to stay warm. Happily, the Montreal Protocol has proven successful in facilitating ozone repair.
Are we making any headway?
Melanoma rates in the under 40s age group (those who grew up with “Slip Slop Slap”) are coming down. This makes sense given the timing of the programs and the decades-long lag between protecting our skin and the benefits of “avoided” skin cancers. But rates in the 60+ age group are still going up and as a result so are the overall rates. We anticipate and hope those will fall over the next decade.
Comparisons with NZ suggest they have a lot to learn from our skin cancer messaging campaigns. But we both still have a long way to go to decrease the burden of skin cancer.
Terry Slevin, Adjunct Professor, School of Psychology, Curtin University; Education and Research Director, Cancer Council WA; Chair, Occupational and Environmental Cancer Committee, Cancer Council Australia and David Whiteman, Professor and Group Leader at the Cancer Control Group, QIMR Berghofer Medical Research Institute
This article is part of our series about skin: why we have it, what it does, and what can go wrong.
Our skin is a big deal – literally. It’s the largest organ in the body and one of the most complicated. It has many roles in the maintenance of life and health, but also has many potential problems, with more than 3,000 possible skin disorders.
Not only does the skin hold everything in, it also plays a crucial role in providing an airtight, watertight and flexible barrier between the outside world and the highly regulated systems within the body. It also helps with temperature regulation, immune defence, vitamin production, and sensation.
The skin is unique in many ways, but no other organ demands so much attention and concern in both states of disease and health. There is a huge focus on skin health, with fierce competition to have glowing, clearer, healthier, younger and fresher skin. And this focus can cause secondary problems with self-esteem and mental health.
So, what exactly is our skin meant to do and how does it impact our life?
The structure of the skin
The skin is divided into three layers known as the epidermis, dermis and subcutis. These layers are well defined but together they allow the skin to function effectively.
The epidermis is the outermost, cellular layer of the skin which varies in thickness depending on the body site. On average it’s less than half a millimetre thick. The epidermis resembles a “brick wall” of cells known as keratinocytes, which are bound tightly together and act to prevent free movement of moisture, pathogens and chemicals into or out of the body.
Keratinocytes replicate from the basal layer and work their way up to the outer surface (known as the stratum corneum) over a period of about 28 days. Once they reach the surface the tight bonds between them break apart and they are shed.
Other than keratinocytes, pigment-producing cells known as melanocytes and immune cells known as Langerhans cells also exist within the epidermis. Melanocytes inhabit the basement membrane, at the base of the epidermis and produce a pigment known as melanin both innately (giving the skin its natural colour), and in response to ultraviolet light (UV) exposure (giving the skin a sun tan).
The melanin is a brown pigment that is taken up into the overlying keratinocytes. This pigment will then absorb UV light (from the sun) when it hits the skin, thereby protecting the basal calls underneath from UV damage.
The epidermal cells also develop hair follicles, sweat glands and sebaceous (oil) glands which extend down into the layer below known as the dermis. The small ducts from each of these glands open onto the skin surface. Sweat and sebum (oil) provide an antibacterial and protective barrier on the skin.
The dermis lies beneath the epidermis and is 20-30 times thicker. It’s made up of a dense layer of fibrous (collagen) and elastic (elastin) tissue. The dermis gives the skin its integrity, strength and elasticity; and houses blood vessels, glands and hair follicles, as well as nerves and their receptors.
Beneath the dermis lies the subcutis (also known as the hypodermis), a specialised layer of adipose (fat) and fibrous tissue. The thickness of this layer varies dramatically depending on the site and a person’s body shape and weight. It cushions the body from external trauma, insulates from the cold and stores energy (fat).
The function of the skin
The extraordinary array of functions performed by healthy skin is still coming to light. The basic day-to-day functions include:
Working as a barrier – protecting against water loss as well as physical and chemical injury, and bugs
Helping us fight off bugs, allergens, toxins and carcinogens via the parts of our immune system that exist in our skin
Regulating our temperature by dilating and constricting our blood vessels near the skin surface, controlling the transfer of heat out of the body. Temperature is also regulated by evaporative cooling due to sweat production and by the insulating effect of erect hairs on the skin surface. Heat loss is also affected by the insulating layer of subcutaneous fat
Protecting us from UV radiation by producing melanin
Giving us the sense of touch _ providing interaction with physical surroundings, allowing all fine and gross motor activities and allowing pleasurable and sexual stimulation
Beauty and physical attraction – the quality and condition of the skin greatly contributes to the perception of health, wellness, youth and beauty.
What is normal skin and how can you optimise it?
Normal healthy skin has many important roles and thus should be treated with care and respect. Many people only start focusing on the skin once there is an abnormality or at least a perceived problem.
Common concerns include dryness, sensitivity, oiliness, congestion, wrinkles, sun damage and signs of ageing. Although these states are all within the spectrum of normal functional skin, they may be considered problematic if severe or undesirable.
Normal, healthy skin that is not exposed to excessive physical or environmental insults may not require any specific care or protection, but for those who want to optimise or improve their skin, some basic steps can make a big difference.
The key to skin care is consistency and routine, and it can take time to appreciate the changes. A basic regime of daily protection from excessive UV radiation, protection from excessive irritation and drying (by avoiding drying soaps, excess water or irritating chemicals) and aiding of the skin’s barrier properties (using a moisturising protective layer) will result in noticeable improvement in almost all skin.
Switching and changing products and routines is usually counterproductive and will prevent you from seeing expected improvement in time. It’s worth looking after your skin, as you’ll wear it every day for the rest of your life.
Australians over the age of 40 can now calculate their risk of developing melanoma with a new online test. The risk predictor tool estimates a person’s melanoma risk over the next 3.5 years based on seven risk factors.
Melanoma is the third most common cancer in Australia and the most dangerous form of skin cancer.
The seven risk factors the tool uses are age, sex, ability to tan, number of moles at age 21, number of skin lesions treated, hair colour and sunscreen use.
The tool was developed by researchers at the QIMR Berghofer Medical Research Institute. Lead researcher Professor David Whiteman explained he and his team determined the seven risk factors by following more than 40,000 Queenslanders since 2010, and analysing their data.
The seven risk factors are each weighted differently. The tool’s algorithm uses these to assign a person into one of five risk categories: very much below average, below average, average, above average, and very much above average.
“This online risk predictor will help identify those with the highest likelihood of developing melanoma so that they and their doctors can decide on how to best manage their risk,” Professor Whiteman said.
After completing the short test, users will be offered advice, such as whether they should see their doctor. A reading of “above average” or “very much above average” will recommend a visit to the doctor to explore possible options for managing their melanoma risk.
But Professor Whiteman cautions that people with a below average risk shouldn’t become complacent.
“Even if you are at below average risk, it doesn’t mean you are at low risk – just lower than the average Australian,” he said.
An estimated one in 17 Australians will be diagnosed with melanoma by their 85th birthday.
The test is targeted for people aged 40 and above as this was the age range of the cohort studied.
However, melanoma remains the most common cancer in Australians under 40.
Professor Whiteman said that the test may be useful for those under 40, but it may not be as accurate, as that wasn’t the demographic it was based on.
But he added complete accuracy couldn’t be guaranteed even for the target demographic.
“I don’t think it’s possible that we’ll ever get to 100%. I think that’s a holy grail that we aspire to, but in reality, cancers are very complex diseases and their causality includes many, many, factors, including unfortunately some random factors.”
The prognosis for melanoma patients is significantly better when it is detected earlier. The University of Queensland’s Professor of Dermatology H. Peter Soyer explained that the five-year survival rate for melanoma is 90%. But this figure jumps to 98% for patients diagnosed at the very early stages.
“At the end of the day, everything that raises awareness for melanomas and for skin cancer is beneficial,” Professor Soyer said.
Dr Hassan Vally, a senior lecturer in epidemiology at La Trobe University, said the way risk is often communicated is hard for people to grasp. But he said this model would provide people with a tangible measure of their risk of disease, and point them towards what they may be able to do to reduce it.
“Everything comes back to how people perceive their risk, and how can they make sense of it.
“If it makes people more aware of their risks of disease that’s a good thing, and if that awareness leads to people taking action and improving their health then that’s great.”
An outbreak of plague has been occurring in Madagascar, with more than 2,000 cases and 170 deaths reported since August 2017.
This island nation is one of the few remaining hotspots for plague in the world, with cases usually reported between September and April each year.
But this outbreak has been unusual, as it has affected many different areas in Madagascar, including heavily populated cities.
What is plague, and how is it treated?
Plague is a serious disease caused by the bacteria Yersina pestis. It has a high death rate if untreated. There are several different clinical forms, including bubonic plague (affecting the lymph nodes), pneumonic plague (affecting the lungs) and septicaemic plague (involving the bloodstream).
Outside of outbreak situations, deaths from plague are usually due to delays in recognition and diagnosis, rather than a lack of treatment options. Although antibiotic resistant strains have been described, plague can generally be treated with a number of commonly available antibiotics.
Why does plague still exist?
Plague was responsible for hundreds of millions of deaths in three devastating pandemics, including the Plague of Justinian in the 6th century, the Black Death in the 14th century, and the Third Pandemic that originated in China in the 19th century.
In these pandemics, it’s generally thought plague was introduced by rats (often transported on ships) then transmitted to local rats in domestic settings. Fleas then transmit the bacterium between infected rats and humans. But there’s still some debate on the transmission pathways of plague in these pandemics. The classical cycle between an animal reservoir (rats) to humans through an insect vector (fleas) is common to many animal-associated infectious diseases, known as zoonoses.
The pattern of plague cases seems to have changed to a more complex ecology over the past 50 years. There has been a shift in cases from Asia to Africa and the re-emergence of disease in other areas such as the United States.
It’s now recognised there are many potential pathways of transmission from animals to humans in different settings. In the US, plague is thought to be transmitted from wild rodents in rural areas, such as prairie dogs and rock squirrels.
In some African countries, it’s thought cases arise where there is human encroachment into forest areas. Outbreaks have also been linked to the consumption of infected camel and goat meat in Libya, and from exposure to infected guinea pigs during preparation for cooking.
In recent years, there’s been interest in the impact of climate change on the potential for outbreaks. The prevalence of plague in animals in Kazakhstan is associated with higher temperatures in spring and rainfall in summer, as are outbreaks in the US. Tree ring studies also suggest similar climatic conditions may have triggered the Black Death and the Third Pandemic.
How can it be controlled?
Modern plague control includes finding cases and treating them, and where cases are detected, clearing homes of fleas using insecticides. Plague cases in hospitals need to be cared for safely to prevent spread to health care workers and other patients.
In affected communities, people should act to keep rats out of homes. This includes making sure food is stored and disposed of safely. Avoiding bites from fleas is also important, using insect repellents and ridding animals of fleas. Although rat control using poisons can also be used, this should only be done after fleas have been controlled, as fleas can leave dying rats and make things worse.
At a national and international level, systems to respond to outbreaks are required to make sure the public receives reliable information, to deploy logistics and resources to where they are required, and co-ordinate the various national and international organisations involved in the response.
How easily can it spread between countries?
Although the concept of quarantine arose from efforts to control plague spread, travel and trade restrictions are not often warranted given their potential economic impact. The wider fallout from outbreaks can be severe. For example, a relatively small outbreak, mostly localised to the city of Surat in India in 1994, provoked widespread panic. This resulted in a national collapse in tourism and trade that was estimated to cost up to US$2 billion.
In this current outbreak, only the Seychelles has implemented travel bans, and it’s thought the risk of transmission is low. Few confirmed cases have been reported in travellers from Madagascar during the current outbreak.
The World Health Organisation has been working with neighbouring countries to improve preparedness efforts. This includes improving surveillance at airports and sea ports, developing contingency plans and pre-positioning of antibiotics and protective equipment.
What is the future for plague?
It’s not possible to eradicate plague, as it is widespread in wildlife rodents outside the sphere of human influence. Outbreaks generally are managed reactively by “firefighting teams” deployed to clear houses of fleas, identify and treat cases and give pre-emptive treatment to contacts at risk.
A more preventative approach, such as the identification of areas at risk using climate models and animal surveys to focus flea and rat control efforts would be better. But this requires a better understanding of transmission pathways in each region where disease persists.