Parasites are symbiotic species that rely on their host for nutrients, like predators rely on prey. This is at the expense of the host, which often suffers illness as a result, or a damaged reproductive function. Unlike predators that have a lower reproductive capacity compared to their prey, parasites have a higher reproductive potential than their host.
An ecological niche is the set of tolerances and requirements a species has in its immediate living space. For example, birds make use of a tree’s branches to house nests, while fungi make use of a tree’s trunk to grow. The same habitat can have many different niches that can be populated by different species.
Parasites have very narrow niches because they are specific to their host. Human head lice cannot survive anywhere except the human scalp. This also means that the molecular processes that parasites rely on in their host are very similar and overlap with those of the host – one reason developing effective treatments against them is challenging. This interdependence means that some processes carried out by the host on behalf of its parasite renders the parasite degenerate i.e. unable to fulfil them by itself, and lacking in structures and organs other species might have.
The aforementioned head lice are an example of an ectoparasite, parasites that reside on the surface of their host. Internal parasite such as tapeworm are called endoparasites.
Tapeworms reside in the small intestine where they can conveniently tap into the host’s nutrients, and so interfere with the normal absorption of the host’s nutrients into its bloodstream, thereby depriving the host to potentially dangerous levels of malnutrition and other side effects such as anaemia and fatigue.
Lice live on the body, such as pubic lice or on eyelashes, or the scalp in the case of head lice, and feed on the host’s blood. Sensitivity to lice saliva causes itchiness, and some lice can be vectors (carriers) of dangerous infectious agents such as Epidemic typhus and Trench fever.
A vector species may act as a bridge between the parasite and its host by transmitting it to the host where the parasite reaches sexual maturity – its definitive host. The vector or another species may also act as an intermediate host for a required precursor stage of the parasite’s life cycle.
In the absence of competing species (interspecific competition), a parasite occupies its fundamental niche. Upon competing with others, a different niche may emerge for them, termed the realised niche. It is possible that multiple species rely on the same resources, and following competitive exclusion, one species goes extinct locally. If both endure, it is because they are able to accommodate sufficiently different realised niches by partitioning their resources.
Transmission and virulence
Transmission is the path of the parasite to its host.
Virulence is the severity of the parasite effects on its host.
Many factors present in host populations can exacerbate parasite transmission. High densities of hosts (overcrowding) increase parasite transmission, alongside transmission routes that do not require hosts to be active. Examples of these include waterborne parasites and vectorborne parasites. For example, getting bitten by the anopheles mosquito carrying malaria does not require the human host (definitive host) to come into contact with another infected human.
Parasites can change their host’s behaviour to extreme lengths to benefit their interests. This includes changing host behaviour, reproduction, movement or behaviour towards predators or their habitat. This effect influences parasite fitness, thereby constituting the parasite’s extended phenotype. An extended phenotype is the far-reaching effect of an organism’s expression. While feather colour is a bird’s phenotype, its nest is its extended phenotype.
An extreme example of parasites shifting host behaviour comes from the “zombie-making”, “mind-controlling” lancet liver fluke (flatworm) and Sacculina (barnacle).
The lancet liver fluke has a complex life spanning no less than three hosts. It lives in cow livers and expels its eggs through their faeces. These are picked up by snails which cough them up inside slime balls which are eaten by ants. Once inside an ant, the lancet liver fluke hijacks its brain and leads it to stand exposed at the top of a blade of grass, in order to maximise the probability of a cow eating it to start everything anew.
Sacculina invades crabs and takes advantage of their reproductive system to make it produce its own offspring as if they were the crab’s. If the crab is male, the parasite will shift it into female to accomplish its goal.
Among these changes, parasites can also suppress the immune system of the host to maximise their own growth, reproduction and transmission. Not all hosts have the same amount of parasites, and the different sexual and asexual stages of parasite development help maintain a high evolution rate and population growth.
The immune response
Different cells have different molecules presented on their surface to the immune system. These are often protein-based and enable the identification of:
-cells from other organisms of the same species
-abnormal body cells
The specific immune response is split into humoral immunity and cell-mediated immunity. Humoral is to do with the blood and antibodies. Distinguishing between an antigen and an antibody is very important.
Antigen = protein or carbohydrate foreign (not normally present) to a host’s organism
Antibody = protein made as a response to detecting an antigen which binds to the antigen and prevents the pathogen from harming the host.
Parasites mimic host antigens in order to avoid being detected, and to minimise the host’s immune reaction to them. Due to their rapid evolution, the host’s developed detection of the parasite over time cannot keep up with the parasite’s changing antigen profile.
Immunity against invading pathogens is a crucial part of maintaining health. The body has adaptations which prevent invasion by pathogens, as well as processes in place to deal with those that manage to penetrate the body’s primary defenses. The skin and mucous membranes (e.g. mouth) are examples of such defenses. Sweat contains lysozyme which is an enzyme that breaks down bacterial walls. The skin flora is made up of all the microorganisms that live on the skin without causing disease. They populate the surface of the body, so invading pathogens can be stopped in their tracks by the resident flora.
Connective tissue, tears, mucus and ciliated epithelium also help protect against infection. Connective tissue forms during scarring and alongside blood clotting, it maintains the barrier against infection. Tears and mucus contain digestive enzymes that maintain eye and respiratory system health by disintegrating microorganisms and keeping a hostile environment to prevent infection. Ciliated epithelium has hair-like protrusions that wave to move out particles that are inhaled for example. They also act in response to these particles by triggering sneezing.
Localised inflammation is also a first response to infection or other types of assaults. Its purpose is to remove the infectious agent and encourage tissue repair. It achieves this by swelling the area with blood containing phagocytes and molecules involved in the immune response such as cytokines.
If pathogens do invade the body, the subsequent immune response is split between:
The non-specific immune response is inflammation and phagocytosis. The specific immune response involves the formation of memory following an infection, in order to better fight and prevent recurrent infections by the same agent that is highly specifically identified.
Neutrophils are the most abundant white blood cell that identifies foreign agents in the body and digests them by phagocytosis. Macrophages are present in tissue and have a similar phagocytic function, but additionally present fragments of the invading agent as antigens to the type of lymphocyte (T cell) that requires this information to identify the invader and mount a specific response against it.
All these cells are able to produce small proteins called cytokines that act in cell signalling to bridge the cell-mediated and humoral responses and regulate the action of all the different cells available.
Antibodies are made by B cells or T cells which come from stem cells from bone marrow. B cells release antibodies, while T cells secrete antibodies which stay on the surface of the cell. Helper T cells stimulate cytotoxic T cells, B cells and phagocytes.
B cell –> O – – – – – –
T cell –> O-
where “–” is an antibody. Apologies for the horrendous visual representation.
So when a bacterium invades, B cells would release antibodies with a shape complementary to that of the bacterium’s antigen. This antibody would then bind to the antigen. T cells on the other hand would secrete the antibodies on their surface, then personally greet the bacterium and bind to it via the antibody. You could say the B cell is shooting the bacterium, while the T cell is strangling it. But for goodness’ sake, don’t write that in the exam.
When a pathogen invades the body and a B cell releases the appropriate antibody to manage the infection, it’s not just the one B cell. They come in their thousands, they are clones of a B cell with a specific antibody, and they are called plasma cells. Plasma cells release a high amount of antibodies, but they are short-lived. Other cells called memory cells may survive for much longer, up to several years. Memory cells are involved in the secondary immune response which happens if a high enough amount of antigens are present. The memory cells replicate into a large number of plasma cells which then release enough antibodies.
The response not dependent on antibodies involves all the aforementioned phagocytosis-inducing cells like macrophages and neutrophils, as well as cytotoxic T-lymphocytes and the cytokine response to invaders.
White cells (the most common ones are neutrophils) engulf any foreign particles such as dust or bacteria, then digest them and dispose off of the remains. It’s badass, trust me. I’ve got proof:
The enzymes used to break invaders down are lysosomes which fuse with the vesicle which contains the bacteria. All this action happens within the white cell. At the end, the undigested leftovers are disposed off of by exocytosis (kind of like a burp).
T killer cells (a.k.a. cytotoxic) recognise their target and release toxic chemicals to kill them.
The blue cell in the centre is a tumour cell, while the surrounding cells are killer T cells about to release their toxic cargo found in the vesicles stained red. Bye-bye, tumour cell.
Vaccinations prevent symptoms of an illness (such as flu) from developing, by creating a primary immune response to an unharmful substance that the body identifies as a pathogen. This could be an antigen, or the pathogen itself – dead or otherwise modified to prevent disease. Some vaccines are really successful and have prevented many diseases so far, yet the flu vaccine remains a challenge due to the above points. The virus changes its antigens, and there is great variation to start off with.
There are ethical considerations surrounding vaccination. On the one hand, large scale vaccination can prevent escalation of epidemics via herd immunity. When more people are immune to a certain infectious agent, transmission from person to person becomes more difficult even when a small number of cases do occur.
Therefore, anyone getting vaccinated would want to ensure others follow suit. On the other hand, the personal decision to get vaccinated can interfere with the goal of achieving a good immunity status for a given population against an illness. Some people would be cautious to get themselves or their children vaccinated due to suspected long term side effects.
The balance of personal autonomy versus achieving greater societal goals that require everyone to synchronise in their decision making has to be accomplished.
Active immunity refers to immunity acquired as a result of an illness. This is also the type of immunity induced via vaccination, as the body is responding in the same way when it encounters the pathogenic antigen and responds appropriately.
Passive immunity is the type of immunity acquired directly via the relevant antibodies rather than by developing them afresh following disease or other ways of contacting antigens. An example is the immunity passed to a foetus via the placenta during gestation.
Epidemiology is the study of breakouts and spread of infectious diseases.
Where disease is present constantly over time, it is said to be endemic, for example as tuberculosis is endemic to parts of India. When an otherwise absent or infrequent disease surges in cases in a population, it creates an epidemic. If an epidemic spreads internationally, then it becomes a pandemic.
Parasite life cycles
As seen previously, parasites can require multiple hosts to complete their life cycle. Parasites can include protozoa, bacteria and viruses.
Malaria is transmitted via a vector which carries it without being affected, before passing it onto the final host of the parasite. In this case it is carried by the mosquito which transfers it via its bite in saliva.
Symptoms upon infection include fever, headache, vomiting and fatigue.
The reproductive cells of the parasite (gametocytes) fuse inside the mosquito which then delivers the sporozoites into the host via the bite. The Plasmodium falciparum sporozoites get taken up by the lymphatic system in a human, and later they pass through the liver where they asexually reproduce, and then travel to red blood cells before releasing their gametocytes again.
Their reproduction in the liver doesn’t bring any symptoms, but once they invade red blood cells and destroy them to invade more red blood cells, fever occurs in waves as new parasites move from the liver cells into red blood cells.
Red blood cells can become sticky due to so-called adhesion knobs on their surface. The parasite can easily hide inside the red blood cells to evade the host’s immune system, as well as in the liver.
Tuberculosis (TB) is an infectious disease of the lungs which causes constant coughing with blood, shortness of breath, fever and weight loss over the years. Every year 2 million people die from TB out of 8/10 million who get the disease. Far more people, around 2 billion, carry the TB bacteria on them without having the disease.
TB is passed on between people by inhaling droplets from the air infected with the bacteria Mycobacterium tuberculosis. When the infection is confirmed, patients are isolated for up to 4 weeks and put on a course of antibiotics for up to 6 months.
When bacteria reach the alveoli, the immune system reacts by surrounding them with white blood cells, which results in the formation of scar tissue. The shortness of breath symptom is caused by less oxygen reaching the circulatory system due to a decreased surface area for diffusion in the lungs, as many alveoli are damaged.
Treatment involves a course of antibiotics which can be lengthy, resulting in many patients stopping at the first signs of amelioration of their symptoms. This causes resistance in the bacteria, which come back to cause disease. Moreover, antibiotic-resistant strains have emerged. There are multi-drug resistant strains which are not affected by the main antibiotics (isoniazid and rifampicin), and even totally drug resistant TB. Managing antibiotic use is crucial to preventing resistance. This includes keeping some antibiotic types as a backup by not using them at all (last resort drugs).
There is a vaccine that protects partially against TB and is administered to children, slightly reducing their probability of contracting the infection, as well as substantially reducing the probability that if they get infected it will cause the disease symptoms. Other prevention strategies include isolating symptomatic patients, and solving crowding problems in households, as prolonged contact between carriers can contribute to the spread of the infection to susceptible people.
Influenza, what a joy! I think by this point we know that flu is caused by a virus that has an infinite mutation potential that makes vaccines very fleetingly efficient (taken on a yearly basis). But! Who is influenza and what does it do?
Influenza is a virus part of the mind-blowingly named Orthomixovirus family, and is transmitted between hosts via droplets carried by sneezing or coughing. It presents symptoms between 2 and 10 days post-infection, such as fever, cough and nasal congestion. Unlike the rhinoviruses that cause the common cold, influenza actually damages tissue. However, the symptoms are mostly the result of the body’s own immune response caused by a release of proinflammatory cytokines from infected cells.
The mechanism of infection of influenza consists of its outer hemagglutinin protein being cleaved by proteases present in human cells. These are found in the throat and lungs, so other tissues don’t get infected as a result. More virulent strains like the bird flu strain H5N1 on the other hand, can have their hemagglutinin cleaved by other types of proteases, hence enable their spread to other parts of the body.
HIV and AIDS
The human immunodeficiency virus causes acquired immune deficiency syndrome. Upon infection, it replicates in helper T cells. HIV is a lentivirus with the expected viral components such as its genetic material (RNA in this case) and capsid.
Upon infection via transmission of infected bodily fluids such as blood or semen, the virus seeks its host cell, the helper T cell which is a key component of the immune response. As HIV hijacks the cell’s machinery to replicate, it destroys it and thus impedes the immune response, leaving the victim with a compromised immunity and therefore susceptible to opportunistic infections.
Part of the HIV replication strategy is the embedding of its genetic material into the host cell’s DNA. The virus contains RNA which has to first be converted into DNA. This is what the reverse transcriptase enzyme does (transcription is DNA to RNA, so reverse transcription is RNA to DNA).
Some drugs for AIDS take advantage of this DNA embedding step by preventing it, and therefore slowing down the replication process of the virus. The reason antibiotics don’t work on any viruses is quite simple. We’ve seen that prokaryotes like bacteria are a cell of their own with many different structures and organelles such as a cell wall, while viruses are neither a cell nor alive. You can imagine you can’t really target something as vague as a piece of genetic information in a protein capsid.
Bacteria have complex cell walls with many components and various enzymes building them up or performing other metabolic functions within the cell. Any of these parts or processes can be targeted, as long as it is distinct from its host (that is ourselves with our eukaryotic cells that do not, for example, have cell walls and thus won’t be harmed by the antibiotic if that’s the part it targets). Viruses have no cell walls, no ribosomes, nothing really taking place.
Viruses are a special little topic indeed. Here we are talking about life in one of its most bizarre, misunderstood and disturbing expressions. Viruses are the stuff of horror movies.
They are tiny microscopic entities that have absolutely no activity whatsoever. In the presence of a larger organism of their specific fit (and there are viruses to target anything), they come alive by hijacking its life tools: nutrients, energy, ribosomes, you name it.
They only carry the genetic information they need to invade and replicate. Invade and replicate. A bit of a glitch of life, or the perfect expression of it?
Both DNA and RNA viruses make use of their host’s transcription and translation machinery such as ribosomes and enzymes to enable protein synthesis. Retroviruses on the other hand bring their own reverse transcriptase enzyme to enable the production of DNA using their RNA template once inside the host cell. Once the RNA is reverse transcribed into DNA (DNA->RNA is transcription, hence RNA->DNA is reverse transcription), the normal protein synthesis pathway can take place.
Lytic cycle and latency
As if the horror movie wasn’t bad enough as it is, it now has a truly creepy plot twist. Not only does the viruses invade, replicate and kill the host cell, making it burst (lyse) hence the lytic cycle, but it can invade and just lie quietly inside the host cell’s genetic material until a later time. This is latency also known as the lysogenic cycle.
Instead of expressing the virus genes to create more viruses, the genetic material of the virus simply incorporates itself into the host DNA. With it, it replicates with each cell division and spreads until a later time when a genetic separation event (such as a recombination event resulting in excision of the viral DNA) allows the viral DNA, termed prophage because it precedes the virus (phages are viruses that target bacteria) to split from the main host genetic material and activate its lytic cycle all over again.
This results in the synthesis of viral components including viral proteins and viral genetic material, and their assembly (which can be spontaneous) into new viruses. The host cell is compromised and the viruses are free to spread again.
Challenges in treatment and control
Researching treatments for parasitic infections can be challenging, not least because some parasites are difficult to culture in the lab. Mycobacterium tuberculosis is a great example of this, taking weeks to grow in lab conditions. In terms of the flu and flu vaccination, rapid evolution means that an updated vaccine must be administered seasonally.
Human elements such as sanitation, crowding and politics can all contribute to the challenge of tackling infections, both regarding transmission rates and virulence. Availability of advanced care and treatment in different countries illustrates this, as someone coming with malaria to the UK would be expected to make a recovery with little risk, compared to someone where malaria is endemic and there is no access to those resources. These multiple factors are explored in depth using malaria as an example.
Malaria is endemic to a wide stretch around the equator that covers South and Central America, Africa, the Middle East and South-East Asia. A disease is endemic when it occurs routinely in an area. An epidemic, on the other hand, is a temporary explosion of cases of a disease in an area.
Numbers of people surpassing 100,000,000 are newly infected yearly, with hundreds of thousands dying as a result. There are three conditions conductive to malaria being endemic, and that determine which efforts to curb the disease are most likely to bear fruit in a particular region:
1. High human density
2. High anopheles mosquito density
3. High rates of transmission from mosquitoes to humans and from humans to mosquitoes (as you remember, the gametophytes of the Plasmodium parasite fuse inside the mosquito to create sporozoites; these are transmitted to humans and undergo further development to produce gametophytes again, which get transmitted back to mosquitoes)
Economically speaking, it may be more worthwhile to prevent the disease than to treat it. This is feasible in areas like China where the money needed by the affected Chinese provinces to execute this is a small percentage of the healthcare budget, but not necessarily in other parts of the world affected by malaria, such as Tanzania, where these measures would by comparison be equivalent to a large portion of the budget (a fifth).
Social and enconomic infrastructures determine the outcome of infection, as treatment with antimalarials depends on the progression of the disease and the state of the patient. A vaccine is not in use yet, but trials are undergoing for a vaccine that could confer tolerance to the parasite (as opposed to immunity).
Under complete medical supervision and early treatment of an infected individual in the UK (acquired from an endemic region, as Plasmodium is not present in Europe; it can’t reproduce in the anopheles mosquito below 20 degrees Celsius), recovery is virtually guaranteed. Travellers can start treatment prior to travel or infection as a means of prevention, and use mosquito repelling substances. Both these approaches might not be available or practical to someone living in an endemic area, and within an area there might be people of different socio-economic status with different options or none at all regarding treatment and prevention.
Mass efforts to address this include low cost measures such as nets repelling to mosquitoes, and awareness of the symptoms of the disease and its transmission. Female mosquitoes bite at dusk and at night, and covering skin can minimise the risk of getting bitten.
Ethical issues exist surrounding the different control methods, as well as the process of the scientific community‘s validation of their efficacy. Enough evidence must support the use of a certain practice, especially if it is a drug or something that could make matters worse. Administering untested drugs to patients that are unable to consent, such as children, who are often more susceptible to malaria and can suffer from anaemia worse as a result of the infection, is an ethical issue.
Political ethical issues exist in the process of researching new treatments and prevention methods, and deciding whether enough evidence supports their deployment in various parts of the world. For example, this happened between the WHO (World Health Organisation) and the IPTi Consortium (funded by the Bill & Melinda Gates Foundation). IPT stands for intermittent preventative therapy, and involves administering various drugs to infants alongside their other vaccinations, every several months soon after birth.
It has shown great promise, with several studies confirming its efficacy at preventing malaria even after the drugs have left the body, and at better outcomes of anaemia. However, there are some contradictory or inconclusive studies, and the WHO decided that there was not enough evidence to start IPT in children in sub-Saharan Africa. There are multiple drugs available for IPT, with different and potentially unknown effects, as well as the risk of increasing drug resistance of the Plasmodium parasite through excessive use of certain drugs.
Eventually the WHO malaria chief, Dr. Akira Kochi, was replaced by a member of the IPTi Consortium. This resulted in the go-ahead given to administer IPT to children in high-transmission areas where resistance to the drugs used was low.