Wednesday, 4 March 2020

The Plague a snapshot, 3,000 BC till today

Plague, a very brief History
Imagine if you will an illness that could easily spread from person to person and result in death within a couple of days. An illness that could spread through a city like wildfire and (during the Black Death) kill 60% of population. In some areas it was 80 percent and whole areas were depopulated as the few survivors fled. A few areas were relatively spared and while some of this was understandable, some of it was completely inexplicable, as if the disease was striking at random.
Mass Grave 1720-21 Epidemic, France
Nowhere was safe. It could cross city walls. Contact with a victim was not needed.It was an enemy that became simply known as 'The Pestilence' or 'The Plague'.
“They died by the hundreds, both day and night, and all were thrown in ... ditches and covered with earth. And as soon as those ditches were filled, more were dug. ...I ... buried my five children with my own hands ... So many died that all believed it was the end of the world.” Agnolo di Tura (14th century, Sienna)
Plague in humans has been detected both in Europe and Central Asia as far back as 5,000 years ago, suggesting it was already widespread by that time. While the Bronze Age had already started in Mesopotamia, it would take another 500 years to reach these regions technically this was still in late Neolithic times.
There were three massive pandemics of 'plague' in recorded history and the likelihood of a Pandemic in prehistory. Added to that, there were countless localised epidemics. 
A prehistoric Pandemic. In the first blog, I talked of the evidence emerging that a primitive form of plague caused the near extinction of the first Neolithic farmers in Europe, not long before the arrival of Indo-Europeans (see here).
The Justinian Plague was the next pandemic (541–542 AD) coming from Egypt. It is said to have killed 13–26% of the population of the middle east, Europe and Northern Africa. Some historians think it might have killed more than that.
The Black Death. (1347 to 1351 in Europe) is the most famous pandemic of all and the worst pandemic ever encountered. It is described as  “the Greatest Catastrophe to ever visit mankind” (Ole J. Benedictow)
Spread of the Black Death (Flappiefh, Wiki)
Siege of Kaffa. Most accounts start with Gabriele de’ Mussi’s classic account of the siege of Kaffa (Caffa). Kaffa (modern day Feodosia) on the Crimean coast was bought by the Genoese off the Golden Horde in 1266 and it (along with other settlements and enclaves) allowed them to dominate the trade throughout the Black Sea region.
Associated with river traffic (e.g. Danube, Dnieper, Dniester, Don and Kuban Rivers) it allowed them deep access into the hinterland, which included lucrative trade with the heart of Mongolian (Mongolian/Turkic) occupied Russia. It became one of the worlds most celebrated ports and one of Europe’s largest slave markets.
In 1307 Toqtai Kahn expelled the Europeans (after a year’s siege) for trading in Turkic slaves, but they were invited back by his successor and they built bigger and stronger than ever. In 1343 there was a religious brawl in Kana near Constantinople where a Moslem was killed. The ‘perpetrators’ (and a great many others) fled to Kaffa. The people of Kaffa refused to hand them over to the Moslem authorities but now they faced Jani beg, a proud and militarily aggressive  Kahn with a large army. He besieged Kaffa  in 1343, but was defeated by an Italian expeditionary force in February 1344. He returned in 1345 for another year and Gabriele de’ Mussi takes up the story:
“Oh God! See how the heathen Tartar races, pouring together from all sides, suddenly invested the city of Kaffa and besieged the trapped Christians there for almost three years. There, hemmed in by an immense army, they could hardly draw breath, although food could be shipped in, which offered them some hope.
“But behold, the whole army was affected by a disease which overran the Tartars and killed thousands upon thousands every day. It was as though arrows were raining down from heaven to strike and crush the Tartars’ arrogance. All medical advice and attention was useless; the Tartars died as soon as the signs of disease appeared on their bodies: swellings in the armpit or groin caused by coagulating humours, followed by a putrid fever.
“The dying Tartars... lost interest in the siege. But they ordered corpses to be placed in catapults and lobbed into the city in the hope that the intolerable stench would kill everyone inside. What seemed like mountains of dead were thrown into the city, and the Christians could not hide or flee or escape from them, although they dumped as many of the bodies as they could in the sea. And soon the rotting corpses tainted the air and poisoned the water supply ... one infected man could carry the poison to others, and infect people and places with the disease by look alone.”
He goes on to describe that the fleeing sailors took the plague to the European ports.
" Alas! our ships enter the port, but of a thousand sailors hardly ten are spared. We reach our homes; our kindred and our neighbours come from all parts to visit us. Woe to us for we cast at them the darts of death! Whilst we spoke to them, whilst they embraced us and kissed us, we scattered the poison from our lips. Going back to their homes, they in turn soon infected their whole families, who in three days succumbed, and were buried in one common grave.”

His compelling account, some of which is written in the first person has become part of established dogma even through to today. Historical documents show him to be in Sienna,  not in Kaffa, at the time of the siege and there are just too many contradictions for his account be accepted.
While the besieging Mongols may not have known that throwing corpses over the wall  would not be very effective, they didn't need to do it, rats would have breached the city fortifications and the plague would already be raging throughout the city. Muslims would not disrespect their own dead in this way.
It is true that the Crusaders had catapulted the heads of Moslem (civilian) captives over fortress walls in the past, but whole bodies that had died of the plague? The highly paid contractors that built and maintained the ‘counterweight trebuchets’ would hardly agree to such grisly work.
The Plague spread from Crimea in a slower, step-wise fashion and took a year to reach Europe, which is not in keeping with de’ Mussi’s account.

However it gained entry, the Black Death is estimated to have killed 30% to 60% of the population of Europe and devastated the Middle East and Northern Africa,. It took 200 years and more for Europe’s population to recover.
Asia and the Black Death
The 'Black Death' pandemic originated in the North West China (1331). By 1393 census the population of China had dropped an incredible 50%. Of course, China was in considerable chaos at the time between plague, famine and rebellions that saw an end to the Mongol rule in China.
There was also massive depopulation all over the great Steppe as far as the Korean Peninsula. How India escaped this time is another puzzle.

The ‘Third Plague Pandemic’, starting in China in 1855, was the weakest of the three and faced the most effective response and yet ten million died in  the first onslaught in British India alone and a further 12.5 million over the next thirty years.
Recurrence is the rule.
In the three historical pandemics, Plague didn’t rage through a community and then disappear. Characteristically there would be frequent highly lethal recurrences, becoming less frequent over time. The third Pandemic wasn't declared 'over' by the WHO till 1960 when world wide cases dropped to 200/ year.
In Britain the Black Death two years at first 1348- 1349 where it killed over 40% of the population. It returned in 1361–62, this time with 20% mortality. There were milder recurrences throughout the 14th and 15th centuries, the last outbreak being the Great Plague of London in 1665–66 which killed about a quarter of London’s population over an eighteen month period. 
The Justinian Plague 541–542 AD kept flaring up especially in the first 50 years, the last time being 750 AD. Evagrius Scholasticus from Antioch in Syria describes four recurrences in his life time. The first gave him bubonic plague while he was a school boy. Other recurrences caused the death of ‘several of my children, my wife, and many of my kin, as well as of my domestic and country servants’ . The fourth one was when he was fifty six and he lost “a daughter and her son”.
These recurrences didn't seem to be the emergence of a new strain, but from a re-infection of the local rodent populations. The Plague of those times remained dormant for periods in a way we don't understand even today.
Our forbears may have thought disease to be initiated by miasma (tainted air given off by rubbish and dead bodies), along with various supernatural explanations, but we shouldn't dismiss their intelligence or their powers of shrewd observation.
In an effort to deal with the frequent recurrences , a sophisticated and effective system of containment was devised. Isolation (to deal with leprosy) was well known since biblical times and in 1377 ‘quarantine’ was first introduced in Dubrovnik, where visitors had to wait in isolation for thirty days to make sure they didn’t have the plague before they entered the city.
Venice became foremost in developing systems to controlling spread, building the first plague hospital or 'lazaretto' 1423 on a small island and going on to perfect a system of maritime cordons. Merchandise from ships was unloaded to designated buildings. Procedures for so-called “purgation” of the various products were prescribed in minute bureaucratic detail; wool, yarn, cloth, leather, wigs, and blankets were considered the products most likely to transmit disease. Treatment of the goods consisted of continuous ventilation. Wax and sponge were immersed in running water for 48 hours.
The ship's captain needed to obtain a certificate of the sanitary status of a port of origin. He also needed to certify the health of his crew. Once there was an outbreak, a ship arriving from such a port needed to fly a yellow flag and lookouts were stationed on the church tower of San Marco to identify them.
The captain was taken in a lifeboat to the health magistrate’s office and was kept in an enclosure where he spoke through a closed window. If ordered to the quarantine station, passengers and crew were isolated and the vessel was thoroughly fumigated and retained for 40 days to see if cases would emerge.
The word "quarantine" originates from Italian quaranta giorni, meaning "forty days".
Why were the ancient ancient pandemics, so much worse?
Plague can be treated with antibiotics but even today, untreated Septicaemic and Pneumonic forms of plague are usually rapidly fatal, and even (untreated) the Bubonic form still has a terrifying mortality 30-40%. Transmission via infected material is not totally impossible but can be avoided by simple precautions, so most contemporary forms of plague do  
World wide distribution of Plague 1998
not carry much of a risk of person to person spread. “Uncomplicated bubonic plague is not contagious and patients do not place their family, other social contacts or care givers at risk”. New Mexico Dept of health 2013.
The Bubonic form almost always comes from a flea bite and the Septicaemic form (10-15% of cases) is most commonly a complication of the Bubonic form. Neither is particularly infectious (unless they spread to the lungs). It is only the uncommon Pneumonic form (usually 5% of cases) (and the very rare pharyngeal form) that are highly infectious.
The Pneumonic form is usually contacted directly or may be a rare complication of the Septicaemic form. Sometimes contemporary epidemics may involve a very high proportion of the especially dangerous Pneumonic cases, most likely when the infection is spread by close contact from other Pneumonic cases.
The role of rats (or another rodent) and their fleas was discovered in 1898 (Paul-Louis Simond) and remains the cornerstone of our understanding of transmission of contemporary plague but it is so persuasive and fits so well with our current (limited) contemporary experience that it is still unquestioned by many as the only significant means of spread of the common bubonic form.

Our contemporary experience does not explain previous Pandemics
 Contemporary experience does not explain the speed of spread, the (even greater) lethality, some clinical aspects and the much higher person to person spread seen in the first two 'historical' pandemics.
 In the past, this has caused some historians to question whether it was Y. Pestis or something else. Researchers have been able to show Plague DNA in the dental root canal of victims and while some descriptions of symptoms are ambiguous, many are not. So yes, it was Plague.
Were the reports exaggerated?
“Oh happy people of the future, who have not known these miseries and perchance will class our testimony with the fables”. Francesco Petrarca, Italian renaissance poet and scholar.
Poorer hygiene, poorer rat control and diet may have made our forbears more vulnerable. Recent research on  the so called ‘human flea’ suggests a new vector that could facilitate human to human spread, even of the Bubonic form.
Has 'Herd' Immunity Grown Greater?
While an individual who survived the plague only had partial immunity, Mihai Netea (at Radboud University) was able to show people from countries exposed to the Black Death had (over many centuries) evolved changes in their immune system that made them more resistant to the Plague.

Are we dealing with different strains that behaved differently? 
This is a rather a rhetorical question, because we know that different strains of Y.Pestis can have subtle and not so subtle clinical differences, they can differ biochemically and have differences in their plasmids, the significance of which we don't fully understand. 
 The most primitive form of plague in Neolithic times did not block the digestion of the rat flea and yet it seems to have been catastrophically devastating . One idea is that it had to be the far more dangerous Pneumonic form. In the first blog I discussed fleas that could transmit plague without being 'blocked'. Recent suspicion is directed at the (so called) 'human flea' which could result in human-to-human transmission without the need for rodents. We just don’t know.
The Italian writer Giovanni Boccaccio wrote 'the Decameron'. The background story is a small group that hides out from 1348 epidemic in Florence, and pass the time by telling amusing tales but he also describes his own observations of the disease:  “certain swellings in the groin or under the armpit ... soon after ...  black or purple spots appeared ... a certain sign of death.” 
This suggests that during the Black Death a large number of cases of the normal Bubonic form rampantly proceeded to the fatal septicaemic form.Reports of people coughing up blood might suggest some or even many of the septicaemic forms involved the lungs, making direct human to human transmission more likely and, of course, Pneumonic forms are very dangerous, spreading and killing quickly.
Not only were people of Europe and Asia more vulnerable to the plague, in the Justinian Plague, the Black Death and maybe in the Neolithic Plague they encountered particularly deadly strains that behaved somewhat differently.
Apart from the massive loss of life from these pandemics,  lethal recurrences and food shortages (e.g. England’s population declined from 7 million to 2 million in 1400) there were widespread social consequences. It is said that the Black Death contributed to the end of Serfdom in Western Europe.  The Justinian Plague was said to have prevented the Byzantines being able to hold their conquests in Italy and Northern Africa when they had tried to take back the western part of the Roman Empire. It may have aided the Anglo-Saxon conquest of England.

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Wednesday, 5 February 2020

Plague, a Brief Scientific Background

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Without any doubt Yersinia pestis is the greatest catastrophe to ever visit mankind. ‘Yersinia’ is a family of bacteria and ‘pestis’ is short for ‘pestilence'. It became known as 'The Plague' or simply 'plague'
"Yersinia pestis is the nastiest thing alive. It's the most virulent bacterial organism known to mankind.” Olaf Schneewind.
How Bacteria Evolve
Bacteria can evolve by two methods:
(a) mutation. This often results in a defective gene but sometimes it can be successful.  
(b) the major method of bacterial evolution is receiving genetic material  from another bacteria.
The donating bacteria sends a bundle of genes that ‘teaches’ the receiver how to survive in different environments, resist antibiotics or fight a host’s resistance, something the donating bacterium can already do. It is more common with related species but can occur across species and then it results in a major change in the recipient.
There are three ways this transfer of genetic material can happen. 
1. Certain viruses (phages) attack bacteria. They replicate viruses inside their host by placing their own genetic material inside the bacterial DNA.  Eventually they will release a protein that dissolves the cell membrane and kills their host, spreading the infection. Some, ‘temperate’ phages don’t immediately kill their bacterial host, being content to survive inside it for a time. They even protect their host in several ways, one of which might be introducing genetic material that is helpful to the host, often taken from elsewhere.  Bacteria have their own immune system so they may survive the viral attack and keep the genetic ‘gift’.
The more important way bacteria can give and receive new genes (and abilities) in a process called conjugation, where two bacteria construct a bridge-like connection joining their protoplasm.
Transfer of a plasmid (wiki)
2. In one form, the ‘host’ detects that the recipient is missing useful genetic material and makes a copy of a section of its own DNA which it sends across the bridge between the two cells.
3. Presumably this process is the origin of the third and maybe the most important form of transfer,  the copying and transfer of a bundle of useful genetic material called ‘plasmids’. Plasmids are small circular independent DNA fragments separate to the main genes of the cell and having the power to replicate independently of the rest of the DNA.
Of course, evolution of a particular (strain or) species of bacteria using Plasmids isn’t as simple as that. Once transferred the plasmid has to find a way to live and replicate in the (new cell or) new species, and the receiving bacterium has to evolve (through natural selection and more genetic changes) to make use of what the plasmid is offering it, if that is possible.
Evolution of Y. Pestis
Sometime in the late Neolithic period,  Y. Pestis evolved from Yersinia pseudotuberculosis, a soil-living bacterial infection that can cause colitis in rodents (and other animals). It can rarely be transmitted to humans through ingestion (e.g. water contaminated by faeces). It is very different type of infection to plague and while it can be nasty enough, it is usually not fatal or spread from human to human.
Y. Pestis is like nothing seen before or since.
Like all infections, there are different strains, there is something like 36 known strains of Y. Pestis (some living, some extinct) and several have significantly differences between them.
What makes Plague so virulent is only just starting to be understood with recent major advances in DNA analysis but contradictory opinions still abound.
With the change from Y. Pseudotuberculosis to Y. Pestis there was the addition of at least 6 genes and inactivation of as much as 13% of its genome. (It doesn’t want to waste its resources producing proteins it no longer needs). This gives an idea of the tremendous change in life style it underwent.
New plasmids were added. Many of these aren’t held in common across all species of Y. Pestis and are referred to as ‘cryptic’ (role unknown). Even for those we think we understand, there are variations in size of the same plasmid, so plasmids in different strains that we have given the same name to may have different amounts of genetic material.
Three plasmids are involved in the virulence of Y. pestis.
 (a) ‘pYV’ was already present in Y. Pseudotuberculosis and is especially nasty. It gives rise to something called the ‘type III secretion’ system. The surface of the bacteria produce needle-like probes which can detect environmental conditions and attach to host cells and inject toxins directly into them, killing the cell, avoiding the extracellular fluid and avoiding much of the immune response. 
Worse, it preferentially attacks the body’s first responders (macrophages, neutrophils, or dendritic cells) crippling the immune response and allowing the infection to establish itself inside lymph tissue.

Perhaps this is why surviving an episode of plague only gives partial immunity. It may be part of why frequent recurrences of the same strain of Y. Pestis in the same area is the rule rather than the exception. Sometimes the same patient can be re-infected by the same strain.
The plague may form a reservoir in wild rodents, waiting to re-infect, and while it doesn’t like fresh air and sunshine it can remain in soil and water in endemic areas. It can live inside the single celled organism amoeba proteus that likes to swallow and digest bacteria.Whether soil and water reservoirs can contribute to recurrences (through ingestion, mainly by rodents but possibly other animals and even humans) is unknown. 
Two additional plasmids are unique to most strains of Y. Pestis.
b) The first one  pPCP1 is critical importance and allowed Y.Pestis to attack the respiratory system (Pneumonic Plague) and blood (Septicaemic Plague), both clinical variants are almost always fatal if untreated.
The primitive form of Y. Pestis was able to totally devastate neolithic communities throughout the West but we are unsure of how it manifested and how it spread, more on this in next month's blog.
The next step and the rat flea.
Around 2,000 BC (during the Bronze Age) the pestilence evolved again by the incorporation of another major plasmid. It was a quantum change what was already a very dangerous infection.
This third important plasmid (called the pFra or pMT1) gave Y. Pestis a number of  adaptations that allowed it to colonise and block the rodent flea’s midgut.
Infected rat flea (wiki)
Fleas bite to drink blood from their hosts and use two mouth parts. One part sucks blood from the host. The other part squirts saliva in to prevent blood clotting and because of this second part, fleas (like mosquitos) can readily transfer a range of diseases from one host to another.
The new plasmid contained genes that allowed the Y.Pestis to survive and replicate in the toxic environment of the foregut of the flea, resist being ingested and form a biological film which blocks the flea’s digestion.
Being unable to swallow the flea now regurgitates blood into the bite site to clear its blocked digestive track and this is teaming with bacteria. The bacteria no longer has to rely on saliva to transfer infection, it has a far superior method.
Successful infection relies on a combination of the virulence of the organism, the resistance of the host and the dose of infection. A higher the dose of infection in the initial assault is more likely to overwhelm a new host’s initial resistance and establish a solid beach head of infection.
Most (but not all) fleas have adapted to live, reproduce, and preferentially feed on a narrow range of hosts. They don’t spend all their time on the host, they (and their lava) live part of their life in nests and surrounds. The tiny rat flea is one of the more selective ones, but, having their digestive track blocked, they start to starve and they become voracious feeders, not only biting nearby rodents repeatedly, but much more readily biting dogs, cats, and humans.
Y. Pestis was already very lethal but now it truly became the worst pestilence to ever be visited on mankind.
What are the main rodents?
The main reservoir of the plague is wild rodents (e.g. gerbils, marmots, prairie dogs, chipmunks, wood rats, ground squirrels, deer mice and voles). It may be fatal in these animals but they usually have high resistance. Cats, rabbits, some wild carnivores, goats, camels, and sheep can also get the Plague.
It usually gains entry to humans via ‘domestic’ rats which also roam in the wild and encounter the infection from the ‘reservoir’ in the wild. A major player was the black rat (roof rat) and still is in some parts of the world. This rat prefers to build their nests high and dry. Wood structures and thatched roofs especially suited it. It likes temperate, not cold climates but the larger, burrowing,  brown rat (sewer rat, Norwegian rat) was important in transmitting plague in colder climates.
The Main Clinical Forms of the Plague
Plague can loosely take three (main) clinical forms.
They are all caused by the same organism  attacking at different sites of the body.
(Image from Centres for Disease Control)
Bubonic form, is the major presentation, accounting for 85 % and more of cases in most epidemics. It is most usually caused by the bite of an infected flea though rarely it can be caught handling contaminated material when there is an open wound on the skin. It attacks the lymph glands (groin, armpit or neck ) which become very painful and swollen by inflammation and necrotic tissue. It is accompanied with sudden onset of fever and chills, headache, fatigue or malaise and has a staggering mortality of 50%. 
Septicaemic form may also come from a flea bite which avoids the lymphatic system, maybe causing a local abscess and reaching the blood directly (no buboes). More commonly it is a complication of bubonic or pneumonic plague. It occurs in 10% to 15% of cases with a mortality of a 100% in untreated cases.
Death usually occurs at a terrifying speed (2-3 days after onset). The plague toxins cause shock, multi organ failure and something called disseminated intravascular coagulation (showing up as bruising, bleeding and gangrene at the extremities).
Pneumonic form is the rarest clinical type of infection (less than 5 %) but can be far higher in some strains. It also has 100% mortality in untreated cases and death occurs in 2 to 6 days.
It can be a complication of septicaemic plague but mostly it is passed directly from human to human. It is the only clinical form of plague that can readily pass from human to human directly.
It takes close proximity with the victim (less than six feet). While the bacteria can live in the soil for up to a year, it is readily killed by sunlight and fresh air and can only last for less than an hour in droplet form in the air. Patients are most infectious when they develop a moist cough in the final stages.
Bubonic and Septicaemic plague are almost never transferred directly from human to human.
(Caution: While I say the bubonic form is not highly infectious beyond flea bites, all care needs to be taken in handling infected patients and their body fluids. There are exceptions to every rule.)
Climate and the Plague
Plague is a complex story of humans, rats,  rat fleas and probably human fleas (see below). Climate can impact incidence in contradictory ways. For instance, in medieval temperate Europe, black rats and their fleas are less active in winter and sometimes plague followed this pattern (not always).
On the other hand, famine almost always preceded a serious human pandemics (weakening human resistance)  and famine could be triggered by a sudden burst of cold weather and poor harvests. Climate changes may impact on the behaviour of wild rodent populations and so on.
Is there something missing in all this?
Only about 30 of the approximately 3000 known species of fleas are proven plague vectors and Xenopsylla cheopis (the Oriental rat flea) is thought to be the most effective.
The rodent flea story is a compelling one and there is a lot of evidence for it.
How did Primitive Plague decimate the neolithic farmers of Europe
There is no doubt that the primitive forms of Y.Pestis was highly virulent, but this occurred before  Y.Pestis ‘learned’ to colonise and block the foregut of the rat flea.
We have to postulate another way of entry into human settlements and its ongoing propagation.
Hunters and gathers are at higher risk of being bitten by hungry fleas of recently deceased rodents lying in wait in nests. This would cause a bubonic infection.
If a form of primitive Y.Pestis was more lethal to rats living in close proximity to humans in some wholesale way, this would result in a lot of hungry rat fleas close to humans. Obvious rat deaths (so called ‘rat falls’ of sick and dying rats from ceilings) is not usually a feature of later plague outbreaks, but they have occurred. Such an event could cause an outbreak of bubonic plague even with the more primitive strain but it would only spread via rats, not from human to human. 

Another idea suggested was that maybe this early (primitive) plague may have been mainly a pneumonic form. Ingestion of poorly cooked infected meat gives rise to a ‘pharyngeal’ plague variant. It can mimic tonsillitis and be transmitted to humans in droplet form, resulting in a pneumonic outbreak in contacts of the initial case. Cats develop a similar form of plague and can introduce a pneumonic form into a human settlement.
While Pneumonic plague is uncommon in most epidemics, it is not true of all.  The 1994 plague in Surat, India had a large percentage of pneumonic cases and it was initially misidentified as a more common respiratory illness. The 2017 outbreak in Madagascar was mainly pneumonic and the Black Death in Bergen, Norway, in 1349, was initially pneumonic and only later changed to a mainly Bubonic type infection (presumably when Norwegian brown rats and their fleas became involved).
What about later episodes?
Could there be alternate forms of transmission of the bubonic form that we haven't previously suspected?
Rat fleas stick closer to their hosts than other fleas, and a healthy rat flea is unlikely to bite an infected human. In any case, it has been long taught that a healthy flea of any species biting an infected human would be unlikely to get infected. This is because it is thought that there isn’t enough concentration of bacteria in the blood of humans to overwhelm its initial protective mechanisms.
Rita Greer, The Great Plague
Rodents can carry 500-1,000 times more plague bacteria per unit of blood than humans who would be overwhelmed before reaching anything like this.
Humans with the septicaemic form of the plague have (by definition) a far higher amount of bacteria in the blood than the bubonic form but is it enough? Many experts would doubt it.
This seems to mean that (apart from Pneumonic plague) humans do not spread plague and this would be astounding. It would mean that, in the worst epidemics in history humans are passengers, not active participants, they are mostly along for the ride in what is essentially a plague in rats.
Questioning the exclusive role of rats
Some researchers have pointed to outbreaks of the garden variety of Plague in situations where it is thought that the rat population was low.
For rat centred spread of bubonic plague, Plague would have to be transferred to the local rat population and then spread amongst it. After that, it takes the bacteria 12–16 days to block the digestive tract of the flea and then the flea doesn’t live too long after that. 
According to recent mathematical modelling, the spread during the Black Death period was too fast for this method of transmission in several localities. The researchers suggested there must be another plague vector and suspicion has fallen on Pulex irritans often called the ‘human flea’ or ‘house flea’ which gets its name because of its irritating bite.
Pulex Irritans (the Human Flea) has a wide distribution, can live on a very wide range of hosts: birds, humans, dogs and cats, to name a few.
Whether 'human' fleas can even be a vector for plague has been hotly debated. These fleas are not susceptible to having their foregut blocked. The ones in favour of the human flea being a vector suggest that if a blocked foregut is not necessary, transfer of infection can go faster. The few cases of North American plague is transmitted from certain wild squirrels by a flea that doesn’t have its digestion blocked, and transmission is indeed quicker.
During a 2013 outbreak of plague in rural in Madagascar, researchers caught rats in traps and also fleas in 'candle' traps in village houses. 73% of the fleas were Pulex Irritans ‘human fleas’ and about 4 % of them were carrying Y.Pestis. 2/3 of these had not recently fed suggesting the fleas were infected and not just carrying infected blood in their latest meal.
None of the rats were carrying human fleas, suggesting the human fleas had most likely contracted the plague from humans. None of the other flea species including the usual ‘vectors’ had plague DNA, but their numbers were lowish. 
Can Pulex Irritans transmit Plague from humans to humans? This research needs to be confirmed, but our new suspect has been caught, not only leaving finger prints at the crime scene but also holding the murder weapon.
Don’t think to throw away the rat theories. It is still a major pathway for transmission and for entry into the human population but maybe there is a second pillar holding up the plague banner and waving it.
For pet lovers
The ‘cat’ and dog fleas are thought to be poor vectors. Cats and dogs might bring infected rat fleas indoors on their bodies where they might bite humans.
Your favourite pet can get the plague by biting an infected rodent (and eating it or being bitten by it) or they can be bitten by a rat flea. Cats are much more susceptible to the plague and usually develop enlarged submandibular nodes and sneezing, passing on the plague to their owners in the pneumonic form. Direct transmission from dogs is rare but has occurred. Dogs are often asymptomatic.
Another reason why the plague is so lethal (in case we needed another reason).
A predator species doesn’t want to be too efficient in eliminating its prey.
Similarly, an infective agent wants to infect and replicate (a lot) in its host but it wants to balance this need to replicate against the risk of an overwhelming infection killing the host. 
Ideally it should form a reservoir in the host population and maybe even have asymptomatic ‘carriers’. 
This would require a less lethal strain, forming a reserve, though from time to time more lethal strains would emerge.
At the same time as the possible evolutionary pressure for the infection not to be super-virulent, hosts develop resistance over time by the Darwinian selection.
The same thing happened with the Plague but unfortunately this process mainly benefited rodents, especially wild rodents, and not humans. Rodents are the main hosts.
It is speculative, but plague that is more virulent in humans might be more readily transmitted by human fleas. So selection may favour strains that are more deadly to humans.
Human resistance has been slow to develop and no reliable vaccine has yet been developed.
It remains endemic in Africa but in modern times it has become somewhat less of a problem with better rat, flea control, better public health and antibiotics. 

Next month's Blog: The Great Plague, major epidemics

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