Stem Rust Fungus

Puccina graminis is the scientific name for stem rust fungus, which affects wheat and barley crops. Wheat makes up much of the staple diet in 97% of countries. Between barley and wheat, they make up 25% of the world’s food supply, and help keep billions of people from being malnourished.

Over the years, the fungus has caused devastation numerous times; the fungus can effect fields that are nearing harvest, and can reduce crop yields by up to 80%, Different strains effect different crops, but the strain that effects wheat is the most damaging to human food stocks.


Stem rust is a parasitic fungus- it feeds on living tissues of its host. It can infect either cereal plants or Berberis (Barberry), a genus of shrubs which grow freely in temperate and sub-tropical regions. It forms five different types of spores.

The disease is transmitted when spores from infected plants are carried to other crops by the wind. It can also be transmitted if it’s grown in soil where an infected plant previously was. It can pass thousands of miles in certain conditions through soil. The pattern of the infection is used to determine the source (a fan of infection implies it’s local, overall coverage for a distant field).

Mode of Infection

Spores need water in order to germinate. They use hypha (thread-like structures) to penetrate the stomata of the leaves or stem of the plant to gain access to water, and in turn, to other internal tissues. Hypha secrete enzymes such as cellulases which digest plant cells and then they absorb nutrients into the fungus. The hyphae branch to form a mycelium that feeds and grows, hidden in the stem or leaves of healthy-looking plants.

The fungus grows best in hot days (25-30°C), mild nights (15-20°C), and wet leaves (from rain, dew or irrigation). The spore relies on this water to germinate.

Pathogenic Effects

Symptoms start 7-15 days after the plant has become infected. Rust-red pustules break through the epidermis of the stem of leaf, which can contain up to 100,000 similarly coloured spores; any of these can be blown by the wind to infect more plants.  This can happen many times over a crop’s growth cycle, until black spores (which can last over a winter) are finally formed. It’s at that stage that the crop itself becomes blackened and worthless.


  • Absorbs nutrients, reducing crop yield
  • Pustules break the epidermis, making transpiration more difficult for the plant to control; their metabolism becomes less efficient; the plant is more likely to dry out; secondary infections become more likely
  • Mycelium grows into vascular tissue, absorbing water and nutrients; interference of supply to crop
  • Weakens stems so plants are more likely to be damaged or topply due to the weather, reducing harvest efficiency

Controlling Stem Rust in Wheat

Stem rust is fast-acting upon its host. Some farming practices encourage its spread;

  • High nitrate soils favour the fungus; fertilisers encourage the fungus.
  • Many farmers in HICs deliberately avoid disturbing the soil; if there are any spores in the soil, they are likely to be near the top where they can more easily infect the next crop
  • Regular irrigation provides both water for the plants to grow, and the virus.

To avoid the virus, start by avoiding such practices, where possible. Then;

  • Use bigger spaces between plants to reduce moisture and increase distances for spores to have to travel
  • Reduce fertiliser application
  • Use earlier-maturing crops which avoid the time of maximum spread
  • Remove wild Berberis so part of the life cycle is interrupted, reducing further spread

Fungicides can be used to control the growth of stem rust, but the cost of this can make it uneconomic to grow the crop at all.

Genetic Resistance

The main method of fighting the fungus historically has been to just develop more hardy breeds of crop. In the mid 1900’s, scientists discovered genes that hep gives resistance to rust attacks, especially Sr31. Wheat strains were breed to have this variant that were very resistant to the fungus, and by the ’70s, the virus seemed to be under control.

In 1999, an unknown strain of wheat stem rust fungus appeared in Uganda, known as Ug99. This strain can overcome almost all of the known resistance genes in wheat; Sr31 has no protective effect. The spores have been covered to other East African countries, and even as far as Yemen and Iran, and are continuing to spread. Scientists have calculated that 80-90% of wheat could be susceptible to this strain.

Scientists are working to develop new strains of resistant wheat to prevent Ug99 from spreading into some of the most important wheat-growing areas of the world. A package of genes have been found that can be engineered into various varieties, giving resistance to all stem rust strains and infections. However, the cost, environmental and ethical concerns in some countries about GM crops (many of which can be counter-acted by sterilising plants carrying the modification, though this creates a dependancy on the original supplier and can hinder development in LICs) mean that this solution is not yet widely adopted.




MRSA stands for methicillin-resistant Staphylococcus aureus. MRSA has developed in hospitals in response to the use of drugs there. When anti biotics are used, certain bacteria may survive- those which have the necessary genes or alleles (depending on the antibiotic) to resist it. The resistant pathogens then have less competition, and can multiply their population rapidly up to the original levels, and most of the new bacteria will also be resistant to the drugs. Some will even become more resistant.

Penicillin, the first discovered antibiotic, was first introduced clinically during WWII- then 90% of the strains were sensitive to the drug, so this was usually successful. Resistent strains soon started to emerge; within about 5 years halfof all strains had become resistant, and today this proportion has reached 90%.

The issues with penicillin resistance were initially overcome by finding how penicillin worked and then making varient forms which performed a similar task, and would not be broken down by the same enzymes in the bacteria; the drugs created included methicillin, flucloxacillin, ampicillin and amoxillin, which are still used today. However, some strains have become resistant to these today, and now form MRSA.

The normal varient, Staphylococcus aureus can be found in the nose and on the skin of roughly 30% of people, and is fairly harmless, as long as it does not manage to get into abrasions, cuts, or other wounds. Even if they do infect, symptoms tend to be relatively mild, such as forming pimples or possibly conjunctivitis in the eye. More extreme reactions can occur, especially when the normal varient can enter into skin, bone, muscle, blood or the urinary tract.


For non-methicillin-resisant Staphylococcus aureus, if a cut or abrasion is infected, it may cause:

  • Pimples
  • Boils

An eye infection can lead to conjunctivitis.

More severe versions can cause pneumonia and heart disease, and can be fatal.

MRSA can also cause skin ulcers.


MRSA is rare among the general public, and is typically only found in hospitals. It is very capable of surviving away from the human body on dry surfaces, meaning it can easily be picked up by touching a contaminated surface, and visitors should regularly be washing their hands.

Up to 9% of patients in hospital may have MRSA. This is largely due to being in a confined environment, which leads to the disease spreading easily between those present. Patients may be on treatments that reduce the sensitivity of their immune systems, or have other illnesses which pose this symptom.


Probably 30% of hospital infections could be avoided by closer adherence to hygiene rules. However, many factors which cause infection are just due to being in a hospital environment, not cleanliness.

Sufferers of MRSA often have to have a long stay in the hospital, while the bacteria are removed using vancomycin and other antibiotics.

1918 Flu

The death toll from the Spanish flu was somewhere between 20 million and 100 million worldwide, after the end of WWI. It was partly so high because  so many of the countries infected had been decimated by war, but it is hard to determine how many people really died due to a lack of documentation. If such  a disease emerged again today, it would kill more people in a year than heart disease, cancer, stroke, lung disease, AIDs and Alzheimer’s disease combined.

Spanish flu has largely been forgetting due to occurring so soon after the upheaval of the deaths of 9 million soldiers and a further 9 million civilians during WWI.

The name itself is deceptive- it did not origin in Spain, nor was it most devastating to Spain. However, Spain immediately started reporting about the disease. It is unknown where the virus originated from, but it may well be from the Far East, and it was spread by the active troops across Europe.

In 2005, scientists from the USofA processed the genetic code of the 1918 flu virus; the sample was taken by extraction from a female patient buried in Alaskan permafrost. The pandemic was found to have been caused by gradual genetic changes from a flu virus that had originated in birds.

Flu most frequently effects humans, birds and pigs. Interspecies infections can quite easily lead to deaths, even in otherwise mild strains.


Typical Spanish flu symptoms included:

  • Spots over cheek bones within hours of admission to wards
  • Cyanosis (skin turning blue) extending across he face from the ears
  • Starting to struggle for breath within hours
  • Sudden collapse
  • Infection of the lungs by other diseases in addition

The collapses were especially common. In South America, a mine operator collapsed at control of a lift and sent at least 20 miners plummeting back down the mine shaft to their deaths.

Spanish Flu death-causing symptoms included:

  • Bleeding from the nose and ears
  • Swollen hearts
  • Solidified lungs weighing up to 6x their normal weight
  • Accumulation of fluid in delicate tissues such as the lungs

Clogged up lungs from the disease would have offered little ability for gas exchange across the lung surface by the volume of water. Thus the patient would have drowned; it was called  “Drowning death”.

It was common for those who survived the initial infection to then be infected by another disease, such as pneumonia, which would then kill them.

Causes of symptoms: 

The influenza virus weakens respiratory epithelia and cilia (a type of cell that wafts dirt out of the lungs), and immune cell dysfunction, leaving them weakened to other infections.

Distinguishing features

Most influenza break outs focus upon the young and old, and have the greatest death toll upon these age groups, due to having a weaker immune system. The Spanish flu also specifically targeted young healthy adults.

One theory for this was “cytokine storming”. Cytokines are small chemicals used to signal between various white blood cell types to co-ordinate fighting infections. Cytokines work a lot like hormones, and travel through the blood. They encourage inflammation, swelling, increasing vasopermeability (ability for chemicals to move through blood vessels) and attract other white blood cells. This fights infection, but sometimes damages organ tissue. It can lead, eventually, to internal scarring and organ failure.

Cytokine storms are thus when the cytokines overreact to a pathogen and this can lead to deaths.


All strains of flu are viruses, and belong to the family orthomyxovirus. Influenza A is the worst sort of the virus group. Its genome includes genes for the coding of only 10 proteins. 2 of these- haemoggluttin and neuraminidase are the most important, and flu strains tend to be named after these. The Spanish flu and 2009’s swine flu were both H1N1. H2N3, H5N1 (Bird flu) and H7N7 are all common strains.

Haemoggluttin binds receptors on the outside of the virus with the membrane of the target cell. Neuraminidase lets new viruses formed within the cell leave and move out to attack further cells.

Viruses have to integrate their genetic material into a host cell. They themselves have RNA, rather than DNA, so have to have specialised enzymes to convert their RNA into DNA. The host cell then incorporates this DNA into its own nucleus- much the same way that a computer will absorb the coding to produce certain types of virus itself. When the host produces its own proteins, it also produces copies of the virus proteins, which eventually combine to form more viruses- this continues until the host cell has used up all its contents in the worst case scenario. Typically, viruses will be released gradually from the host cell over time.


The viruses of Haemoggluttin and Neurominidase can be extracted. Each year this is done to produce a new flu vaccination. The body can then produce antibodies specific to those proteins, and learn how to tackle the virus more effectively if it should enter the body. However, the viruses always mutate over the year, so new jabs have to be developed frequently.

They are also individually targeted by other jabs. TamiFlu is an example of this. The UK government spent £500 million on TamiFlu during the swine flu outbreak of 2009- but in practice, for many, this does little more than just paracetamol to relieve symptoms.

Finding one set treatment is hard, as mutations in the virus genome mean an antibody that works one year may well not by the start of the next. The body has to constantly adapt to every new strain.


Salmonella is part of a large family of bacteria (Enterobacteriaceae) which live inside the human gut, as well as the guts of various other species. More than 2,500 types of salmonella have  been identified. All could cause disease in humans, although in practice only a small proportion are responsible for most outbreaks of the disease.

Salmonella is generally divided into two groups- those which specifically target humans, and tend to have the most severe symptoms, and those which target species less specifically, are associated with food poisoning and tend to be milder.

Salmonella typhi alone is responsible for 27 million cases of typhoid a year, and 217,000 annual deaths.


Typhoidal Salmonella will enter the blood stream and into circulation, where it can reach the lymph nodes, gall bladder, liver, spleen and many other parts of the body, where it can enter into human cells. Symptoms start within a few weeks of ingestion, and get progressively worse throughout infection as the greater numbers of bacteria over stimulate the victim’s immune system. The actions of the immune system can result in tissue damage and even death.

Non typhoidal Salmonella will enter into the gut’s epithelial cells (The gut lining) and the immune system is quickly alerted, leading to gut inflammation. This typically results in:

  • Shedding of gut cells
  • Substantial fluid loss
  • Diarrhoea
  • Abdominal pains/ cramps

Symptoms of non-typhoidal varients typically start 6-24 hours after infection and last for 4-7 days, before quickly clearing.


Salmonella is typically contracted by ingesting something contaminated by faeces from another infected individual, or carrier. The most common source is polluted water, so Salmonella is most common in areas with poor, or no, water sanitation.

Contact with cattle and chickens are also typical methods of contraction. Bacteria often can be found in raw meat or other products from these animals, as well as their faeces. Pets can also pass the infection, especially amphibians and reptiles.

Some people remain carriers long after their own infection is over.


Occasionally, non typhoidal Salmonella will enter the victim’s blood stream and can cause bacteraemia (when bacteria multiply in the bloodstream), which can be fatal, and in those with weaker immune systems form typhoid-like symptoms. It is estimated that there are 1.3 x10^9 cases and 3 million deaths of non-typhoidal Salmonella each year.

Salmonella move to the gut shortly after being ingested; they are then able to out-compete the bacteria which naturally occur in the gut for nutrients and will start to attack the gut cells.

Salmonella produces tiny syringe-like structures called Type 3 Secretion Systems (T3SSs), which inject proteins from the bacteria into victim’s cells. In the intestines, these T3SS1 proteins will cause the cell membrane to form lumps and eventually absorb the bacterium responsible, and it becomes trapped in a membrane within the cell. T3SS2 is used by bacteria already inside human cells, and produces virulence factors- a type of chemical which allows infection to be ignored- to avoid being killed by the human immune system. Essentially, our cells absorb the bacteria in the hopes of being able to kill them before infection occurs, but the bacteria stop this from occuring once inside; instead of killing them, the pathogens enter into a protected environment.


Proper cooking of any meats and eggs should kill off bacteria housed within our food. Similarly, boiling water before drinking it should prevent any bacteria surviving to be ingested.

The best method to avoid Salmonella food poisoning is just to regularly wach your hands, especially when handling food.

If a mild form of the disease is encountered, generally not much interference is needed. The human immune system is generally pretty effective, and naturally will come up with methods to fight it over time.

In more severe forms, antibiotics are typically used to halt the increase in bacterial presence, and reduce the severity of symptoms. Patients may need rehydration therapy and antibiotics if there are signs that the disease has entered the blood.

Salmonella typhi supposedly has a sugar coating around itself, which stops it being recognised by the immune system, leading to food poisoning. By not getting an immune response, S. typhi can spread through our bodies fairly freely.

There are no vaccines to protect against non-typhoidal Salmonella. Two vaccines are available in the UK against typhoid, and use of them is rrecommended before travelling to anywhere with high typhoid levels. These vaccines only offer limited protection, however. Improved vaccines will be needed in the future.

It may be possible to prevent infection by Salmonella by developing drugs which target the virulence factors that stop the immune system detecting them.


Malaria kills 1-3 million people a year, mainly among children under 5. This is about 500 every hour, and it tends to come back in recurrent bouts throughout life.

It has been known since the 1890s that mosquitoes transmit malaria by protozoa such as Plasmodium falciparumP. falciparum is the main transmitter in humans, causing 90% of modern cases.

There are eventually 3 outcomes of malaria:

  • Infected blood cells are recognised by the immune system and killed
  • Drug treatments kill the infected cells
  • The patient dies


Symptoms become less serious as a person becomes older, as their immune system becomes stronger. This is why the majority of deaths are from young children. Malaria does have a tendency, however, of returning and reinfecting a person multiple times; each time the protozoa uses a different set of genes and the person has to be reinfected several times before they gain immunity to all of the responsible genes.

Common symptoms:

  • Fever
  • Chills

These symptoms are seen as being caused due to the release of toxins by the protozoa. Symptoms increase as the new merozites- the sort of cell produced by the protozoa- are released.

The invasion of a red blood cell can be seen by some obvious changes. The normal disc shape turns highly uneven and lumpy. As the P. falciparum is released from host cells, the lumps move further to the outside of the cell, creating the bumps on the outside of the cell. The knobs also produce a sort of protein which takes the red blood cell out of commission and away from the other red blood cells. Normally mis-shapen cells are taken to the spleen and destroyed, but the cells are no longer reach the spleen, so are not destroyed, allowing the merozites to be freely produced.

More serious physical symptoms:

  • Infected blood cells bind with uninfected cells, that can block blood capillaries
  • Infected blood cells bind to blood vessel linings in the brain, which can cause cerebral malaria, which is the biggest cause of death.


Mosquito saliva contains anticoagulants, which allow them to suck up blood through their probosces, but the anticoagulants are irritant and thus cause itching. The saliva also contains the Plasmodium parasites, which enter directly into the blood.

Within a few minutes, a certain type of cell, known as sporozites, have reached the host’s liver.


Once inside the host’s liver cells, the Plasmodium falciparum cell nucleus divides rapidly, creating a cell with many nucleus. Then each new nucleus buds off from the original parent cell, with a little cytoplasm, forming a new type of cell called a merozite. The liver cell bursts, releasing the merozites.

Merozites  then infect red blood cells and digest the haemoglobin in them as a food source. The merozites each undergo nuclear division several times, and produce up to 32 new offspring each. The blood cell bursts and within just a few minutes, merozites are released and each one then enters a new red blood cell.

The cycle of release of the merozites occcur every 3-4 days.


Injection is normally a quite effective method of prevention . If the insect involved can be removed, the transmission is far less effective than even with the injection, however.

Vaccines must be suitable for use among small children, as they have the highest fatality rates. The variety of malarial forms and antigens makes finding a single vaccine very challenging. Researchers are working on finding a vaccine that recognises antigens present in the most severe forms of malaria first. The idea behind this is to reduce acute symptoms and keep the infant alive long enough for them to fight an infection naturally.

When in the past marshland has been drained for farming, this has reduced the number of mosquitoes, and thus the rate of incidence of malaria. However, this does have a large environmental cost, due to species which have then lost their habitats. A method of separation without environmental damage is even easier- installing glass into windows. Mosquito nets are another very easy, very effective method.

Insecticides are a popular method of eradication of malaria. However, this is not a sensible method in most areas, because the effected areas are massive, and thus the insecticide needed would be massively expensive and infeasible to deliver. Delivery to small, localised waters is feasible, and could be done easily.

Drugs to prevent malaria can be taken before and throughout visiting a country where malaria is endemic. The best known sorts are based of quinine. Quinine has been used by native American peoples in Bolivaria and Peru using natural bark from a Cinchona tree to treat malaria before scientists researched its use properly. The bark of the tree was then transferred back to imperialist powers which found the native peoples from the sixteenth century on-wards.

Quinine derivatives have since had to be added, thanks to the increasing incidence of strains resistant to quinine. Some are even more effective than quinine was originally. Chloroquinine is one of these. In a red blood cell, the merozite digests the haemoglobin, and uses amino acids from it in order to grow. The haem group left is normally toxic, but Plasmodium neutralise it by converting it into another chemical, haemozoin. Chloroquinine interferes with this conversion.The haem then builds up and kills of the merozites itself.

Other drugs target enzymes involved in Plasmodium DNA replication and growth. Artemisinins are a new class of drugs discovered from research based on Chinese traditional medicine for malaria. It is unknown how artmesinins work, but they have been used for over 2,000 years to cure malaria.

These methods could help save many lives from the disease in the tropics. The main limiting factors seem to be extreme poverty, a lack of infrastructure for distribution, poor governance, and disturbances, as well as any other number of human failures to develop nations evenly worldwide.