Polio outbreaks in Syria

Recently on the news there has been many reports on the recent outbreak of Polio within Syria, which thought to have originated in Pakistan.  So far there has been twenty-two children recorded paralysed, ten of these have be confirmed to infected with the polio virus and the further twelve victims are being investigated. The origin of Pakistan indicated a high risk for the virus to have spread over a broad area, not just the Deir al-Zol region where those infected live. Although vaccinations have decreased the rates of polio, the spread of polio has never stopped in Afghanistan, Nigeria and Pakistan.

Polio is a highly infectious disease, where transmission is via the mouth by infected food or water.  It is usually in areas with poor sanitation due to infection of the food or water by feces of a polio victim. Furthermore the virus can be transmitted by direct contact with the infected person. Certain categories of people are most vulnerable to infection, such as pregnant women, very young children (often younger than five) and those with a weak immune system. The virus causes many symptoms,the worst being paralysis invading the nervous system and infecting the brain and spinal cord, and can be fatal due to immobilizing breathing muscles. Other symptoms include flu-like symptoms that last for a few days or weeks, such as fever, sore throat, headache, vomiting, fatigue, back and neck pain, arm and leg stiffness, muscle tenderness, muscle spasms, and meningitis. These symptoms tend to be those of nonparalytic polio or the beginning symptoms of the paralytic polio. Paralytic polio however advances onto harsher symptoms such as severe muscle pain, loose or floppy limbs or in the worst case as previously described paralysis of different parts of the body.

The Polio outbreak within Syria refers to symptomatic polio, which accounts for 4-8% of all cases. Polio can be defined as either symptomatic or asymptomatic. Symptomatic polio can be broken down further into a mild form called nonparalytic (where many patients can make a full recovery) or abortive polio and a severe form called paralytic polio (occurring in 0.1% to 2% of cases). Paralytic polio (as mentioned above) also may be classified as:

Spinal polio - attacks motor neurons in the spinal cord and causes paralysis in arms and legs and breathing problems

Bulbar polio - affects neurons responsible for sight, vision, taste, swallowing, and breathing

Bulbospinal polio - both spinal and bulbar polio

There is no cure for Polio, so in more economically developed countries polio is cut out my vaccinations given at birth. Therefore the best form of treatment is prevention in the form of immunisation, however medication can be given to ease the symptoms of those infected. These treatments can include antibiotics to treat consequent infections, pain killers, and ventilators for those with lung paralysis.

References:

http://www.reuters.com/article/2013/10/29/us-syria-crisis-polio-idUSBRE99S0FI20131029

http://www.medicalnewstoday.com/articles/155580.php

http://www.who.int/mediacentre/factsheets/fs114/en/

http://www.cdc.gov/polio/about/

Ebola Virus

Ebola virus was first found within the Ebola River in the Congo, of which it named after. Ebola first appeared in 1976 in two simultaneous outbreaks, in Nzara, Sudan, and in Yambuku, Democratic Republic of Congo (DRC). Outbreaks often occur in remote villages near rainforests, so the disease typically does not spread far, and so far has only affected Africa, mainly the western and central regions.

The Ebola virus causes severe VHF (viral haemorrhagic fever), which affects many organs throughout the body, so is known as a multisystem syndrome. VHF particularly affects the vascular system, and therefore the body’s ability to regulate itself is impaired. Research shows that it also causes low counts of platelets and white blood cell. The symptoms can be very severe and life threatening, including internal bleeding or bleeding underneath the skin.  However initial symptoms include fever, intense weakness, muscle pain, headache and sore throat. Then the secondary symptoms are caused by kidney and liver impairment which cause the internal bleeding but more commonly, vomiting, diarrhoea and rashes begin to appear.  

The transmission of the virus is first from animals to humans by direct contact with blood, secretions, organs or bodily fluids of the infected animal. It is secondly past from human to human by similar contact of blood, secretions and bodily fluid of the infected human.  People can cause transmission as long as their blood or secretions are infected with the Ebola Virus. Within Africa it is believed transmission from animals to humans is due to close contact with monkeys, antelopes, chimpanzees, fruit bats or porcupines.  Furthermore the direct contact transmission from person to person can be due to infected semen, close contact with infected deceased during burial. Another example is in the healthcare industry because within less economically developed countries, such as those in Africa there are not sufficient sterile precautions and an inadequate protection barrier.  Examples of these include lack of gloves or goggles which can lead to direct exposure with the infected patient’s blood.

Many patients infected with the Ebola virus can be diagnosed with malaria, typhoid fever, shigellosis, cholera, leptospirosis, plague, rickettsiosis, relapsing fever, meningitis, hepatitis and other VHFs. Although the Ebola virus can be distinguished with further blood tests, due to it causing elevated liver enzymes, henceforth an enzyme-linked immunosorbent assay (ELISA) can be carried out.   However There is currently no treatment or vaccine available to treat humans or animal, therefore unfortunately it cannot be cured or prevented. The Lack of cure drives fatality rates up to 90% of those infected with the virus. The healthcare provided is often intensive rehydration with fluids containing electrolytes.

References:

http://www.bmj.com/content/310/6991/1344

http://www.who.int/mediacentre/factsheets/fs103/en/

http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/vhf.htm

http://www.patient.co.uk/doctor/viral-haemorrhagic-fevers#

Tourette's Syndrome

Tourette’s syndrome is a life long neurological condition (affecting the brain and nervous system) that is characterised by a combination of involuntary noises and movements called tics. The full name is Gilles de la Tourette’s syndrome, which originates from the 19^th Century when firsts signs of tics were identified by a French doctor named Georges de Gilles de la Tourette. Tics can be vocal-phonic or motor, and are repetitive, fast involuntary contractions of muscles. Examples of vocal movements can be simple such as saying a word or grunting, or more complex such as phrasing a whole sentence. Involuntary swearing is a socially disabling tic symptom which is present in 10-30% of people diagnosed with Tourette’s. Physical movements can also be simple or complex, such as jerking or making a series of movements. Names of complex tics include echolalia, which is a vocal tic where the patient repeats other people’s words, or coprolalia (swearing.) Furthermore a motor tic known as copropraxia, is where involuntary production of rude gestures occurs.  

The presence of comorbid behavioural symptoms often makes diagnosis a lot harder, but a key feature of diagnosis can be at least two motor tics and one vocal tic present since childhood. Tics relating to Tourette’s syndrome usually develop at a young age, the average being six years old, and rarely develop in adulthood. Although tics do develop in men and women, men are four times more likely to develop them than women. Tics can also be caused by other medical conditions such as Huntington’s disease and physiological effects of substances such as stimulants. Quite often Tourette’s syndrome occurs with other disorders for example Obsessive-compulsive disorders, attention-deficit disorders and hyperactivity disorders, in which 60% of diagnosed patients also have these disorders.

Why do tics occur?   The main explanation for the involuntary reactions is due to genetically inherited genes; however tics tend to be intensified by anxiety and stress. This therefore explains the peak in severity during teenage years and on the other hand tics are eased by mental and physical concentration.  This therefore supports the need for schools and workplaces to take into account the implications of tics, but still provide education and jobs so that the severities of tics for the patients are reduced. Nevertheless there is a disabling of social capabilities with the disorder, finding it hard to face daily activities. This is hugely unfortunate because research shows that the syndrome is compatible with success at school and in the workplaces and it has no effect on intellectual disability. Moreover patients can voluntarily supress their tics for a short period of time, although this is researched to cause inner tension and subsequent rebound in tic severity.

Finally the treatment available involves behavioural treatments and prescription of drugs. Behavioural training involves practices such as habit reversal training which influences tic expressions to be delayed or abolished because patients can recognise the prior urge associated with the involuntary movement. This method has proved to be very successful in about half of patients treated; unfortunately access to this type of treatment is currently limited in many countries.  Drug prescription is not given to every patient with Tourette’s syndrome, its usually provided to patients who do not respond to behavioural training or alternatively if the tics provide injury or pain or furthermore social discomfort such as bullying. Haloperidol and pimozide are examples of neuroleptics which are prescribed to patients with Tourette’s as the most effective medication, despite the metabolic side effects. More recent antipsychotics have been researched to provide the same benefits but without side effects. For young patients with other conditions such as ADHD, clonidine and guanfacine examples of a2 adrenergic agonists can be used as treatment due to the fewer adverse effects than other drugs. On the other hand Benzodiazepines should be avoided as long term treatment for tics due to tolerance and addiction. The final types of treatment are Botulinum toxic injections or surgery such as functional neurological procedure.

References:

http://www.nhs.uk/conditions/Tics/Pages/Introduction.aspx

http://www.nhs.uk/Conditions/Tourette-syndrome/Pages/Introduction.aspx

http://www.nhs.uk/conditions/Tics/Pages/Introduction.aspx

http://childstudycenter.yale.edu/ocd/ocd/patients.aspx

Political drive to screen for Pre-Dementia

Dementia is a progressive and largely irreversible clinical syndrome that is characterised by a widespread impairment of mental function. This includes problems with memory loss, thinking speed, mental agility, language, understanding and judgement.  Dementia is a common condition that affects about 800,000 people in the UK. The risk of developing dementia increases as you get older, and the condition usually occurs in people over the age of 65.

Throughout the world there has been a ‘political drive’ to assess elderly patients for Dementia, due to the large amount diagnosed and past neglect of services and research in dementia has fuelled international calls for action and earlier treatment. The Alzheimer’s Society estimated that in 2005 there were 574,717 people in England with dementia. In addition the Society estimated that the total cost of dementia in the wider UK population totalled £17.03 billion, or an average of£25,472 per person with late-onset dementia. The NHS bears 8% £1.36 billion or £2.69 million per 100,000 population) of this total cost, as shown below.

The cost of £25,475 per person with late-onset dementia is the primary reason for the demand for screening or case finding of mild cognitive impairment and dementia, in aim to reduce NHS costs. In England, the government has announced that it will reward GP’s around £3600 annually, per practice for assessing patients aged over 75.This also includes those in a ‘at-risk group’ which is those patients with established diabetes or vascular disease. People with diabetes have an increased risk of developing dementia, due to high blood glucose concentrations which damage blood vessels, and the risk of vascular dementia increases with blood vessel damage. This is also being enforced in other places around the world such as in the United States, under the new Affordable Care Act which is a recent new health reform, the Medicare insurance programme will cover an annual wellness visit with a physician. This wellness visit will include detection of cognitive impairment or any measurable change in thinking abilities.

This screening process aiming to diagnose patients early will beneficial so healthcare assistants can give counselling and provides an opportunity for patients to organise financial affairs and future guardianship whilst they are still competent.

However the ‘political drive’ is controversial, because screening is not recommended by the UK National Screening Committee, Royal Australian College of General Practitioners guidelines or the US Preventative Services Task Force.  This is because there is no evidence for the usefulness or curative pharmacological intervention. A further reason is that only 5-10% of people with mild cognitive impairment progress to Dementia, therefore costs of screening may not outweigh the costs of early diagnosis. Furthermore many people who develop dementia do not meet the definitions of mild cognitive impairment before diagnosis. Also very interestingly, research has shown that the development of people with dementia is higher in people who don’t have symptoms of mild cognitive impairment than in those who do. A major issue created by screening, is adding increase risks to the patients: this is because there is no drugs to prevent the progression, many patients turn to therapies such as Vitamin E, cholinesterase inhibitors or memantine. These can increase damage to a patient’s health rather than improve it, for example cholinesterase inhibitors increase of hip fractures, syncope and pacemaker insertion.

It is difficult to assess whether the beneficial advantages of screening patients for cognitive impairment outweighs the negative risks and effects of the treatment. Nevertheless, within the UK and the US and many other places around the world they think it’s extremely worthwhile.

Reference:

http://www.bmj.com/content/347/bmj.f5125

http://www.nhs.uk/Conditions/dementia-guide/Pages/about-dementia.aspx

http://www.nice.org.uk/media/7EF/1A/DementiaCostingCommissioningAssessment.pdf

http://www.mayoclinic.com/health/vascular-dementia/DS00934/DSECTION=risk-factors

The Return of the Black Death

Last month within Kyrgyzstani, a fifteen-year-old boy died of bubonic plague after being bitten by an infected flea. This is of huge interest because naively I thought the bubonic plague had died out, but today 1000-3000 cases occur globally each year. Although 90% of infections occur in Africa, by contrast in the US annually on average seven people catch the plague. In July this year, camping sites around Los Angeles were closed because a squirrel tested positive for plague.

The bubonic plague is caused by a bacterium, Yersinia pestis and transmission of the infection occurs by rats, squirrels and other rodents. The biggest problem for epidemics is when rodents begin to die, as the infected fleas need a new host. Buboes within the lymph glands (in the groin) begin to swell and cause immense pain; this is where the name ‘Bubonic’ plague comes from.

An example of an epidemic of the Bubonic plague was during the 1300’s when it was known as the ‘Black Death.’ At the time it wasn’t known what caused the blisters and swellings, but recent work from archaeologists identified the bacterium Yersinia pestis within skeleton DNA. It was known as the Black Death due to high death rates down to the lack of medical advancement and antibiotics. It became fatal because it caused haemorrhaging of blood vessels in the fingers and nose leading to gangrene. This became infected and spread to the lungs causing pneumonic plague. This increased the risk because pneumonic plague could be spread by droplet infection such as coughs or sneezes.

Bubonic is only one type of plague the infected bacterium can also cause pneumonic plague as I previously mentioned and then the third one is septicemic plague. The transmission is the same, however its symptoms such as weakness, abdominal pain and bleeding beneath skin or other organs is caused by the multiplication of the bacterium within the bloodstream. Skin and other tissues may turn black and die, especially on fingers, toes, and the nose. Septicemic plague can occur as the first symptom of plague, or may develop from untreated bubonic plague.

 

Reference:

http://www.bbc.co.uk/news/world-asia-23843656

http://www.mayoclinic.com/health/plague/DS00493/DSECTION=symptoms

http://www.cdc.gov/plague/symptoms/

THE WEEK/ISSUE 936/7^th September 2013