Prevention comes at a price..

“Treatment without prevention is simply unsustainable”- Bill Gates

So as not to bore you too much, I thought I’d use this short entry to focus on two of my passions in life: infectious diseases and horses. Unless a seasoned equestrian, you’ll probably have never heard of strangles; an upper respiratory infection affecting horses, donkeys and ponies. Strangles is highly contagious and caused by the Streptococcus equi bacteria. Whilst progress has been made to contain the infection in recent years, there has been an unexpected knock-on effect from preventative measures.


General symptoms are unpleasant, however strangles gets its name from large abscesses that develop at the lymph nodes of a victim’s throat. These threaten to rupture and release pus, thereby preventing the horse eating and extending it’s neck. Infected animals must be quarantined with appropriate hygiene precautions in place, until the infection has run it’s course. Most patients require no treatment, however strangles can severely impact animals of extreme age; in which case antibiotics may be prescribed. Up to 10% of animals exposed to strangles will carry the disease furthermore.

Although asymptomatic, carriers pose a problem as S. equi remains in bean-sized amounts in the neck pouch. These areas of dried pus are known as chondriods and permit convenient transmission. Carriers were not known of until recently; leading to the introduction of compulsory horse testing before moving location. Great right? Well yes, unless your beloved companion is discovered to be a carrier.


Diagnostic techniques include antibody testing and nasal scopes. Whilst diagnosis seems beneficial all around, compulsory testing has caused controversy. The wider population has been largely protected from infection. However implications have, in some cases, resulted in the euthanasia or abandonment of animals, due to the carrier “status”. Increased education has ensured the equine community is now more open about strangles infections; leading to victims being treated like a bad smell. The advances in strangles containment seem to be positive for vets, owners, farmers and animals alike.


The RSPCA Appeal

This prevention however, comes at a price (quite literally)… As with everything equestrian, strangles tests are unsurprisingly costly; a compulsory addition to the growing list of expenses for owners. At £50 for a blood antibody test and a further £300 for a scope, would you put your hand in your pocket just to transport an animal? Whilst preventative methods have been positive for reducing the number of cases, expense has acted as a potential deterrent for many prospective owners. The result is a growing number of unwanted animals, many of which are infected with strangles. As abandoned animals are usually left to roam free, despite efforts, treasured pets and livestock will come into contact once more with the infection. It seems like we can’t win; animal testing should be economically feasible for all owners. Is it really surprising that the RSPCA is appealing for help with the horse abandonment crisis?

In this case Bill I feel you should stand corrected; prevention can also be unsustainable.



Reviewing a review..

Infections may account for up to 15% of early miscarriages and up to 66% of late miscarriages

*Gasps of terror*

According to the latest Giakoumelou review, the role of infection in miscarriage, a whopping 78% of 101 tissue samples from miscarriages were found to be infected with bacteria. I doubt I’m alone in the fact, when I initially read these numbers I thought wow, that’s a huge problem. Why has this remained unnoticed and how can this be prevented?

Blood vessel picture

First and foremost, I’ll introduce the theory around this subject. It is often overlooked that pregnancy is an abnormal situation for woman. Immune systems are honed throughout our lives to attack anything that contains different genetic coding. So when an embryo, which also contains paternal DNA, takes up residence in the womb, factors must be in place to prevent the immune system seeing this as a threat. This is particularly important when you remember that the placenta is the site of gas, nutrient and waste material exchange; therefore blood vessels must exist in close proximity, to permit diffusion into the mother’s bloodstream.

So what prevents rejection of the foetus? Immunity is regulated by a group of proteins known as cytokines. Some cytokines are inflammatory and activate the immune system; triggering defences against pathogens, injuries and potential allergens. On the other hand, regulatory cytokines inhibit the immune system; preventing hypersensitivity and reactions to basically everything (including developing pregnancies and food). Current opinion is that when pregnancy begins, regulatory cytokines are up-regulated; preventing an immune attack and allowing the pregnancy to continue. If inflammatory cytokines are activated, there is an increased likelihood of the immune system attacking the embryo.


The Delicate Pregnancy Cytokine See-Saw

Where do infections come into this? Miscarriage sadly is not uncommon; occurring in around 1 in 5 pregnancies. Experts currently believe, the inflammatory cytokines activated upon infection are enough to harm and potentially abort a foetus; disrupting the normal tolerance-rejection harmony of pregnancy. This is fairly logical in my opinion.

The review however, made some pretty bold claims and upon further inspection, some claims weren’t entirely supported by the data presented.

Review pros:

  • Evidence from multiple sources showed pathogens such as malaria, HIV, influenza and bacterial vaginosis are associated with an increased risk of miscarriage. Evidence supported that the studied infections were detrimental to pregnancy outcome.
  • Review highlighted a crucial area for future research; finding how infections actually result in miscarriage. Such research has the potential to uncover fertility issues and enhance the chances of successful conception or IVF attempts.
  • Proposed a viable screening programme, implemented could protect women hoping to fall pregnant.

The cons:

  • The data acquired for this review was predominantly from less developed countries, with a higher prevalence of stated diseases. Countries with a higher prevalence, will automatically have an increased incidence of infected mothers.
  • A study based on high-prevalence groups will not accurately reflect the worldwide population.
  • Each given study only tested for a single disease; many infections are associated with other infections. This combination may influence miscarriages and therefore data lacks comprehensiveness.
  • A causal relationship between infections and miscarriage was described but not supported. Researchers continue to investigate the exact mechanisms that may terminate pregnancies. This relationship therefore, needs solid supporting evidence.
  • Although study states that further education is needed regarding the risks of infections in pregnancy, this seems premature.

Under the current UK NHS regime, infection testing for pregnant women is only offered on an optional basis. This suggests the trends described in the paper may not be consisted within the population of the UK.

The study argues further education is needed regarding the risk of infections in pregnancy. How could you educate the population when experts themselves do not clearly understand the exact mechanisms? With the UK’s drug-me-up mentality, it is likely that an education campaign will cause a stampede of women demanding tests and treatments; even though the incidence of many infections in the UK is relatively low. Aside from the previously discussed problems (see antibiotic post), some infection therapies are also associated with birth defects, among other foetal problems; therefore an education campaign should not be pursued unnecessarily.

The review certainly raises some concerning figures as previously highlighted. Although there is a clear link between infections and miscarriage, the conclusions drawn from this review would have been more convincing with mechanistic evidence. This would improve the scope of securing government funding for a compulsory screening programme. Whilst I agree these preventative measures should take place worldwide, the screening programmes should be tailored to developing countries who are exposed to higher risks of infections. Relative to the UK, a revised trial may be effective for understanding miscarriages; this would help determine the current position of miscarriages in the UK and potentially save government funding for worthwhile causes.

Although the paper raises many questions, this is what scientists live for right? The authors are perhaps causing premature alarm by publishing the article, without supportive evidence. Further research is certainly needed to uncover the full picture. In the meantime, always question what you read folks!


Plague; a thing of the past right?

When the plague is mentioned, I get flashbacks of history classes at school; mainly men in scary beak suits, “The Great Plague” and stray chamber pots contributing to disease spread. The reality in fact, is that the plague is still alive and kicking today. In 2015, the USA had 16 new cases of the plague confirmed by the CDC; the highest number of cases this century. Surprisingly, new cases are not unusual.

Black Death

The Beak Suit

There are three types of plague, caused by the Yersinia pestis bacteria; bubonic, pneumonic and septicemic. The bubonic plague is spread mainly by ticks infected by the bacteria. With the bubonic type, patients may experience distinctive lumps, also called buboes, at lymphatic sites such as the groin. Bubonic plague is the least severe of the three types; patients can usually be successfully treated by antibiotics. Alternatively, the pneumonic type attacks the lungs of victims; making it the most severe of the three. This type of plague is airborne, transmitted by coughing and therefore spreads rapidly. With the highest fatality rates, patients can die within 24 hours if untreated. Scary right? When Y. pestis has the opportunity to enter a patient’s bloodstream, the infection can become septicemic, which is often lethal.

Bubonic plague pneumonic plague Sept plague

Bubonic, Pneumonic and Septicemic plague respectively.

Unfortunately, experts believe that the people of London in the Middle Ages (1346-53) were hit by a combination of both bubonic and pneumonic plague. This pandemic was famously known as The Black Death. The extreme poverty and living conditions at the time meant that spread of the disease was inevitable. The Black Death wiped out around a third of the population in London during the course of the infection. Eventually, low temperatures of winter were thought to kill off fleas and slow disease spread. Interestingly however, since the great outbreaks, the plague has never been completely eradicated.

If you’re still up for reading this article, the bad news continues. Whilst infection is not quite on the same scale as the middle ages, Yersinia pestis is still responsible for between 1000 and 3000 cases of plague every year. The disease persists as before in areas with poor hygiene and overcrowding: Asia, Africa and South America in particular. Worryingly, more developed countries such as North America continue to experience plague outbreaks.

Priarie dog

The Devilish culprit- A Prairie dog

Why has the USA struggled to eradicate the plague? Modern antibiotics have dramatically reduced plague fatality rates. Over 80% of new plague cases are of the bubonic type, which is easier to treat and recover from. Nearly all of the cases in the USA are restricted to the western side of the country and are more commonly seen in summer, when people spend more time outside. One of the main carriers of plague in North America is the Prairie dog. Prairie dogs are social animals, helping infected ticks spread rapidly; both to other prairie dogs and nearby humans.

An animal reservoir makes a disease much harder to eradicate. In the UK there is a similar problem with persistent tuberculosis cases; leading to the ongoing debate over badger culling or vaccination for disease eradication. Whilst the UK remains undecided on the best course of action, scientists at the National Wildlife Health centre in the USA, are in the process of developing vaccines for prairie dogs; in the hope this will greatly reduce the amount of infections.

It’s only a different set of circumstances that’s keeping [plague] in its place“.

Throughout the USA the plague caused 4 fatalities in 2015; the highest number this century. In comparison to monsters like cardiovascular disease and cancers, this number is minuscule. As previously discussed however, a rise in bacterial infections is worrying; particularly when antibiotics are one of the “circumstances” that are repressing the plague. The 2015 plague mortality figure suggests these circumstances are not fool-proof. A rise in fatalities demonstrates treatments are becoming less effective and indicates preventative measures should be introduced. Other studies have also confirmed that certain plague patients have acquired strains with resistance to the normal antibiotics.

Controversially, the lax attitude of the CDC has resulted in persistence of plague cases. Instead of eradicating the disease at the source, the easy option of treating plague patients was taken. It is undeniably time we stopped putting faith in antibiotics. Prevention therefore is arguably better than cure; removing the need to rely upon antibiotics that will one day be ineffective. Vaccines could prevent the carrier stage; decreasing transmission to humans. However, implementation takes time; especially when working with animal carriers who dislike being jabbed with needles.

Vaccines will be hugely beneficial. Once established in the USA it is possible that preventative efforts could be distributed worldwide. Studying the plague highlights the importance of not ignoring the neglected infections; a disease that wiped out 50 million people in the 14th century has not yet lost the ability to do it again. Realistically, the plague is unlikely to make a return whilst we keep eradication firmly in our sights; so don’t worry too much.

Antibiotic advances?

“People will die” “We just have to take action now” 

As an individual who refuses to go to the doctor, unless I am feeling on the verge of death, I was initially surprised when I heard about the issues with antibiotic resistance due to over-prescription. Apparently, it’s normal to rush to the doctors and demand medication at the first sign of a cold appearing. Although comforting, such actions have resulted in a strain of bacteria that now shows resistance to all current antibiotics; including the “last resort”- Colistin. These bacteria carry a resistance gene known as mcr-1. Resistance to all available treatments gives the bacteria the ability to spread rapidly, which leaves us with the threat of a worldwide epidemic.

As of today, numerous antibiotics are available. There are two main groups; bacteriocidal and bacteriostatic. Although well-known, it is often ignored that antibiotics only work on bacterial infections; for example tuberculosis. Antibiotics will not work on viruses, fungi or parasites and in these instances, prescription can do more harm than good. Antibiotics can damage the natural “good” bacteria (or microbiota), which keep our body conditions constant and healthy. Consequently, antibiotics should only be prescribed for serious infections or when the immune system is failing. For the average adult, the immune system will not fail when a bout of flu hits.


During the antibiotic discovery boom of the 1980s, bacterial diseases were considered a thing of the past. For every minor infection and illness, antibiotics were prescribed, which pressurised unnatural and rapid evolution of bacterial strains. Scientists failed to anticipate bacteria would take up arms and fight back against the latest threat to their survival. Because human medicine had pushed resistant bacteria to survive, evolution favoured strains that were unaffected by common antibiotics. “Superbugs” such as MRSA began to spread; these terrors are currently wreaking havoc in hospitals.

1900s Discovery Timeline

Modern society arguably overlooks the research that goes into producing antibiotics. There is a clear lack of understanding for the correct applications for these drugs. Alexander Fleming accidentally discovered the first antibiotic in 1928, during his work with the fungus Penicillium notatum.  Fleming’s remarkable observation led to the production of Penicillin. Unfortunately, typical antibiotic discovery is not usually as convenient. The last 30 years has seen a dramatic lag in antibiotic production. The inability to culture many natural antibiotic compounds in a laboratory has inhibited drug development. Meanwhile, the current antibiotics that were revolutionary in the 80’s have lost effectiveness. Worryingly, in 2014 10% of Toronto’s gonorrhoea cases were resistant to treatments. Whilst the general healthy population remain oblivious to the lost efficiency, individuals with weakened immune systems have silently suffered.

January 2015 saw a huge breakthrough; the first novel antibiotic in over 30 years was discovered. Teixobactin was produced by extracts from natural soil microbes; researchers had to overcome many barriers to mimic natural growth conditions and culture this elusive strain in a lab. Teixobactin is now showing promise in human trails. Although a temporary resolve for many resistant bacteria, Teixobactin is ineffective against the mcr-1 strains; posing a large risk for epidemics.

The problem remains very real; antibiotic resistance will re-emerge, leaving us in the same position in another 30 years. Are these “advances” really advances at all, or will we always be in a constant battle with nature for survival? It’s clear that Mother Nature will always be one step ahead. One thing is for sure, antibiotic prescription should not be taken lightly. The more we expose bacteria to, the faster they’ll evolve to evade us again. Doctors and patients both have a responsibility to rely on antibiotics only when desperately needed; this may slow the tide of emerging super-bugs.

Ebola returns

Everyone’s talking about Ebola these-days, as if it’s the height of fashion. Notably in the media at the moment is the Paula Cafferkey case. One particular headline that drew my attention was along the lines of “[Paula Cafferkey] contracts Ebola again”; a statement that seems to have shocked the nation. I thought I’d take this opportunity therefore to explain a little about Ebola and what a virus actually does; I hope to highlight this headline is slightly misleading to an unknowing reader.

Viruses enter cells through many methods. Every virus adopts a different method of entry; hence exposure to one virus will not protect you from alternative infections. Ebola is a filovirus, meaning it is able to form filamentous particles that contain its RNA (a single stranded variation of the well-known DNA double helix). These particles can then spread around a host to infect alternative sites. Ebola virus enters through specific receptors on host cells; upon attachment, this stimulates the host cell to suck the virus inside.

Viruses are typically lazy; they are not capable of self-replication so must rely on their host in order to replicate. Every virus encodes proteins that allow it to hijack a host cell. Luckily for Ebola, its RNA is single stranded and this form acts as a perfect template for viral protein formation (confused? see video). For us, the problem arises here. Once a virus has been replicated, traditionally it can only be completely removed upon death of the infected host cell.

As Ebola RNA acts as the perfect template for replication, viral proteins can form quickly. These proteins quickly overwhelm the immune system, before it can generate a response to fight off the infection. Some individuals (the lucky ones), are naturally equipped with antibodies which can slow down viral spread.  Most of us however, need to make do with the current recommended treatments for Ebola; aka the wait-it-out drug, alongside other experimental treatments to alleviate symptoms. These do a grand job, or not in the case of Paula Cafferkey.

The current Ebola strain circulating is a new Zaire strain (ZEBOV). ZEBOV is a sneaky opponent, with its ability to hide in special areas of the body known as “immuno-privileged sites” (a phrase for areas that are concealed from the immune system). Ebola has recently been shown to be capable of surviving for up to 9 months in recovered patients sperm. ZEBOV can remain hidden in areas such as these, until an opportunity arises for it to replicate again. The host then experiences a second potentially fatal wave of infection, whilst ZEBOV demonstrates it has not yet learnt to be subtle in its ways.

The Symptoms of Ebola

ZEBOV can be considered a diva. Instead of remaining inconspicuous, Ebola causes a storm inside its host; mass inflammation, bleeding, nausea, diarrhoea and shock symptoms. Although our body makes a feeble attempt at fighting off the infection, symptoms arguably facilitate viral spread; enabling viral particles to infect those in close proximity.

Viruses essentially want to replicate to the point where everyone is infected. The human genome now contains around 100,000 pieces of permanent retroviral DNA; making up an estimated 5-8% of the total size. Consequently ZEBOV is potentially in the early stages of its evolution. Unless it quickly loses its fatality however, it is unlikely to reach the permanent infection stage. (Which is good news for us, but not for those who are already infected!).


To return to my initial point; Cafferkey did not “contract” the virus again. A more accurate headline would perhaps describe the virus as recurrent or capable of reactivation, after undefined periods of latency in immuno-privileged sites. Until ZEBOV evolves to become less aggressive, our immune systems will continue to react dangerously; threatening virus and host survival. We can only hope that preventative treatments and therapies begin to emerge, or that Mother Nature kindly favours a less virulent strain. Despite this, the ZEBOV outbreak in West Africa is currently under control, again supporting that fatal pathogens are usually short-lived. Conclusively, the presence of persistent ZEBOV DNA in humans remains a frightening prospect. The importance of continual patient monitoring should not be overlooked.

A micro-overview..

Infectious disease is a term used to encompass a range of infections caused by pathogenic microorganisms. Viruses, fungi, bacteria and parasites can all be responsible for a variety of diseases; including HIV, aspergillosis, tuberculosis and malaria respectively. Whilst many individuals believe that only certain species of microorganisms are pathogenic, there are in fact naturally-occurring, “friendly” organisms that can also cause harm. These traitors can alter themselves to become pathogenic in response to sensing a change in their host. So just to make everyone feel that bit more vulnerable; you’re never entirely safe from the ambition of the tiny terrors that live inside you. However rest easy- if you’re healthy and your immune system is competent, they’re unlikely to cause any major problems.Emoji

So how do we acquire these infections? Transmission may occur through air, consumption of contaminated food, water, physical contact, by exchange of bodily fluids or by animal bites. The possibilities are sadly, almost endless. The Ebola virus requires direct contact to spread. In West Africa, hands on burial techniques and a motile population resulted in rapid spread of the virus; largely contributing to the 2014 epidemic. Evidence suggests human habits are largely influential to pathogen transmission. Despite education, we usually make the same mistakes twice (or more) and microorganisms take full advantage of this.

Why do these microorganisms make us sick? Pathogens aim to survive long enough to reproduce. Pathogens are therefore capable of generating a range of symptoms to enhance replication and transmission. The influenza virus upon infection damages the respiratory tract; causing symptoms such as coughing and sneezing. Sneezing expels viral particles from the host into the surrounding area; increasing the likelihood of transmission to a new host. In this case, simple hygiene practices may halt flu attacks.

A pathogenic army ready to take over the world.

Contrary to science-fiction beliefs, fatal pathogens are at a disadvantage and accordingly uncommon. Host mortality prevents pathogenic spread; consequently fatal strains are usually short-lived. Some scientists believe that overpopulation encourages transmission of potentially fatal pathogens. However, the most successful pathogens are typically less severe. Influenza remains infectious by annually altering its genetic material. Whilst changes are not largely dissimilar, they are enough to cause symptoms, allowing spread. Pathogenic success therefore depends not only on virulence, but also on transmission ability. Community intervention efforts may further inhibit pathogenic armies (humans, fight back!).

In summary, the pathogen-host relationship is a love-hate one. Although counter-productive for pathogens to kill their hosts, this does happen in some cases. The 2014 Ebola outbreak killed over 11,000 people; epidemics such as this highlight a need for increased research and education to advance the understanding of infectious diseases. Unfortunately, humans are ignorant of the fact that such diseases do not spread on their own. We play a crucial role within a pathogens life-cycle, therefore outbreaks are OUR responsibility to control. Current attitudes suggest a need for improved education; helping communities to minimize pathogenic transmission. Consequently, like it or not, infectious diseases should be everyone’s concern.

Picture sources (left to right- 1, 2, 3, 4)

Ebola Mosquito MRSAWaterfall Fungi