A parasite is an organism which lives on or in another organism called the host. The parasite needs the host to live, but the host gains no benefit from having the parasite. The 3 main classes of parasite are protozoa (unicellular organisms), worms, and arthropods (insects and arachnids).
In comparison to acute bacterial or viral infections, a parasitic infection lasts much longer due to their well-evolved and effective methods of avoiding the immune system, a parasite is successful if it can successfully avoid or subvert immune responses directed against it. Many parasites are able to survive years in a host causing little or minimal harm, however for some parasites it is beneficial to cause disease in the host.
Parasites can cause harm to the host by:
- Competing for nutrients in the host
- Disrupting host tissue
- Destroying host cells
- Mechanical blockage
Endoparasties – Live inside the host
Ectoparasites – Live outside of the host
Protozoan Parasite Immunity
Protozoa are defined as single celled, eukaryotic microorganisms that lack cell walls. Not all protozoa are parasitic however.
Innate Immunity against Protozoa
Similar mechanisms to the removal of bacteria and viruses are in place to remove protozoa threats; this includes the complement system, NK cells and phagocytosis. However, many protozoa are breed and species specific, different species can be more susceptible to different pathogens.
Acquired Immunity against Protozoa
The acquired immune response to protozoa includes both humoral (antibodies, Helper T-cells and B cells) and cell mediated responses (Cytotoxic T-cells, macrophages, NK cells and cytokines).
Antibodies specific to protozoa surface antigens are released to control parasite numbers in the blood and tissues; this is aided by TH2 (T-helper 2 cells).
The cellular mediated immunity targets the intracellular infections and is mainly TH1 (T-helper 1 cell) driven. For the effective removal of most protozoa, the combination of TH1 and TH2 aided responses are required to target the protozoa at different stages of their life cycle.
Protozoa Evasion of Immunity
The mechanisms that protozoa have evolved to avoid the immune system are:
- The avoidance of attachment and phagocytosis
- Immunosuppression of the host immune system (e.g. destruction of T cells)
- The blockage of antigen presentation (Expression in association with MHC Class II)
- Alter surface antigens (Antigenic variation)
- Block surface antigen expression to avoid detection (Parasite coats itself with host proteins)
Vaccinations to prevent possible protozoa infections have provided limited success, frequent boosters are needed and the vaccine must contain a mix of species and strains of protozoa to maximise its success.
Immunity to Helminths (Worms)
The definition of a helminth is a parasitic worm which typically inhabits the intestines of vertebrates e.g. tapeworms, roundworms and flukes. Helminths have become adept to the parasitic lifestyle making them hard to control as they can employ many evasive manoeuvres against the immune system. However, unlike protozoa they do not replicate within the host and any disease that may arise as a result of their infection is usually only mild.
Innate Immunity against Helminths
The efficiency of the innate immune response depends a lot on the host, whether or not the host becomes infected in the first place also depends on the host genetics and factors. For example the age, gender and genetics of the host will play an important role in whether the host is infected at all. These factors mean different levels of hormones in the body; it is this that is thought to affect the parasite. It is also possible for the parasite to synchronise their reproductive cycle (altered levels of hormones) with the host to maximise their evasion abilities.
Acquired Immunity against Helminths
Helminths are relatively large and have a thick extracellular cuticle making them almost immune to phagocytosis and other conventional immune responses. Even complement is unable to perforate the cuticle to lyse the parasite. The host immune system has developed a method to combat this, by targeting the weaker points of the parasite, for example the digestive tract of the parasite
The main mechanism of the acquired immune response to combat the parasite is to elicit a very strong TH2 response. This results in high levels of IgE, IL-4 and antibodies as well as an accumulation of eosinophils and mast cells. This causes raised blood levels of IgE and eosinophils (eosinophilia).
IgE is able to bind to the parasite and eosinophils have an IgE Fc receptor (FcR). Macrophages and platelets also possess this receptor. The IgE coating the parasite bind the eosinophils (and macrophages and platelets) activating them and resulting in the death of the parasite. IL-5 secretion is also stimulated, (produced by TH2 cells) which mobilises the bone marrow pool and results in the release of the large number of eosinophils.
Eosinophils are equipped to destroy the parasite because they are able to release their granule contents directly onto the thick cuticle of the worm, which causes damage to them (as well as possible damage to the host). The granules contain oxidants, nitric oxide and major basic protein all of which damage the helminth cuticle. This process is more effective against the parasite during its larval stage, as opposed to its adult stage. Although IgE has a main role in the protection against helminths, the other immunoglobulin components also play a part, having a variety of mechanisms such as the inhibition of egg production or interfering with development.
The cell mediated immune branch of acquired immunity is less effective against helminth infection. Sometimes, cytotoxic T-cells are effective against worms embedded in the mucosal surfaces of the host. Or the induction of a delayed hypersensitivity can attract mononuclear cells to the worm, which are able to prevent their growth or migration.
Helminth Evasion of Immunity
Helminths are able to survive and function even in the presence of a fully functional immune system, using such mechanisms as:
- Their size alone prevents normal immune responses such as phagocytosis
- Their thick extracellular coat is hard to penetrate
- They are able to adsorb host proteins, masking them from the immune system
- Molecular mimicry
- Anatomical seclusion
- Shedding of surface antigens
- Interference with the presentation of antigens
- They can be immunosuppressant
- They can employ anti-immune mechanisms
- They are able to migrate
- Production of enzymes to prevent antibody adherence e.g. anti Ig/anti C5a
Vaccinations against helminths are not readily available; due to the poor host immunity against them an effective vaccine is hard to create. The two targetable antigens of helminths are their surface proteins and the products they excrete. Due to the ineffectiveness of vaccines, drug treatments are used much more commonly.
Immunity to Arthropods
Arthropods are vector for many diseases such as those carried by fleas, ticks or mosquitoes; they can spread parasites by injecting their saliva. Saliva consists of proteins that are able to induce an immune response in the host, or block immune/inflammatory responses – reducing antigen presentation or cytokine production can do this. The result is a reduced immunity to the arthropods and the parasites it transmits.
The host is however able to produce an immune response against antigens in the saliva which stimulate a TH1 response inducing basophil infiltration or stimulate a TH2 response leading to the production of IgE.