Relationship between pathogen and host

Host Bacterial Pathogen Relationship | Pathogens and Disease | Oxford Academic

relationship between pathogen and host

() The Relationship between Host Lifespan and Pathogen Reservoir Potential: An Analysis in the System Arabidopsis thaliana-Cucumber. What is the significance of host-pathogen interactions? This interaction between the host and the The relationship between a host and pathogen is dy-. When a pathogenic microorganism (bacterium, virus or protozoal parasite) infects the human body, a battle ensues between the host's innate & adaptive.

Pathogenic variability in hosts[ edit ] Although pathogens do have the capability to cause disease, they do not always do so.

Host − Pathogen interactions and immune evasion

This is described as context-dependent pathogenicity. Scientists believe that this variability comes from both genetic and environmental factors within the host.

One example of this in humans is E. Normally, this bacteria flourishes as a part of the normal, healthy microbiota in the intestines. However, if it relocates to a different region of the digestive tract or the body, it can cause intense diarrhea.

relationship between pathogen and host

Current pathogenic treatment methods[ edit ] Currently, antimicrobials are the primary treatment method for pathogens. These drugs are specifically designed to kill microbes or inhibit further growth within the host environment.

Multiple terms can be used to describe antimicrobial drugs. Antibiotics are chemicals made by microbes that can be used against other pathogens, such as penicillin and erythromycin. Semi-synthetics are antimicrobials that are derived from bacteria, but they are enhanced to have a greater effect.

In contrast to both of these, synthetic are strictly made in the lab to combat pathogenicity. Each of these three types of antimicrobials can be classified into two subsequent groups: Bactericidal substances kill microorganisms while bacteriostatic substances inhibit microbial growth. Consequently, antifungal and antiparasitic drugs are often less effective and more toxic than antibiotics. A second characteristic of fungal and parasitic infections that makes them difficult to treat is the tendency of the infecting organisms to switch among several different forms during their life cycles.

A drug that is effective at killing one form is often ineffective at killing another form, which therefore survives the treatment. The fungal branch of the eucaryotic kingdom includes both unicellular yeasts such as Saccharomyces cerevisiae and Schizosaccharomyces pombe and filamentous, multicellular molds like those found on moldy fruit or bread.

Host–pathogen interaction - Wikipedia

Most of the important pathogenic fungi exhibit dimorphism—the ability to grow in either yeast or mold form. The yeast-to-mold or mold-to-yeast transition is frequently associated with infection. Histoplasma capsulatum, for example, grows as a mold at low temperature in the soil, but it switches to a yeast form when inhaled into the lung, where it can cause the disease histoplasmosis Figure Figure Dimorphism in the pathogenic fungus Histoplasma capsulatum.

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  • The dynamic host bacterial pathogen relationship: resistance, tolerance, and disease

A At low temperature in the soil, Histoplasma grows as a filamentous fungus. B After being inhaled into the lung of a mammal, Histoplasma undergoes a morphological switch triggered by the more Protozoan parasites have more elaborate life cycles than do fungi.

relationship between pathogen and host

These cycles frequently require the services of more than one host. Malaria is the most common protozoal disease, infecting — million people every year and killing 1—3 million of them. It is caused by four species of Plasmodium, which are transmitted to humans by the bite of the female of any of 60 species of Anopheles mosquito.

Plasmodium falciparum—the most intensively studied of the malaria -causing parasites—exists in no fewer than eight distinct forms, and it requires both the human and mosquito hosts to complete its sexual cycle Figure Gametes are formed in the bloodstream of infected humans, but they can only fuse to form a zygote in the gut of the mosquito.

Three of the Plasmodium forms are highly specialized to invade and replicate in specific tissues—the insect gut lining, the human liver, and the human red blood cell.

Figure The complex life cycle of malaria. A The sexual cycle of Plasmodium falciparum requires passage between a human host and an insect host. B - D Blood smears from people infected with malaria, showing three different forms of the parasite that appear more Because malaria is so widespread and devastating, it has acted as a strong selective pressure on human populations in areas of the world that harbor the Anopheles mosquito.

The malarial parasites grow poorly in red blood cells from either homozygous sickle cell patients or healthy heterozygous carriers, and, as a result, malaria is seldom found among carriers of this mutation. For this reason, malaria has maintained the sickle cell mutation at high frequency in these regions of Africa. Even when they are obligate parasites, they use their own machinery for DNA replication, transcription, and translation, and they provide their own sources of metabolic energy.

relationship between pathogen and host

Viruses, by contrast, are the ultimate hitchhikers, carrying little more than information in the form of nucleic acid.

The information is largely replicated, packaged, and preserved by the host cells Figure Viruses have a small genomemade up of a single nucleic acid type—either DNA or RNA —which, in either case, may be single-stranded or double-stranded.

Whilst many bacterial pathogens are intracellular in nature, others do not need to invade the host cell, but instead use various secretion processes which effect the delivery of toxins and other virulence factors into the host cell. Examples of bacteria which have developed the ablity to make a hollow projection a so-called translocon which on contact with the host cell can deliver anti-host factors into it, often resulting in host cell apoptosis so-called Type III secretioninclude Escherichia coli, Shigella flexnerii, Yersinia pestis and Chlamydia trachomatis which cause diverse syndromes of food poisoning, dysentery, bubonic plague and genito-urinary tract infection, respectively see Figure 1.

However, some bacteria such as Francisella tularensis causative of tularemia and Burkholderia spp. Type III Secretion System and Translocon graphic design by University of Massachusetts Biochemistry department Another serious human pathogen, Bacillus anthracis, causative of anthrax, has well-developed virulence mechanisms involving the secretion of three proteins, one of which, protective antigen PAbinds host cell receptors to effect entry of either lethal factor LF or edema factor EF.

Under these conditions, LF is released into the cytoplasm, whereas EF remains bound to the late endosomal perinuclear membrane. In the cytoplasm, LF cleaves and inactivates mitogen-activated protein kinase kinases MAPKKs to disrupt phosphorylation and transcription in the nucleus, ultimately preventing protein synthesis and causing cell death; whilst EF, a calcium and calmodulin-dependent adenylate cyclase, causes a rapid increase in perinuclear cAMP resulting in cellular, tissue and ultimately organ edema.

Viral pathogens, on the other hand, do need to invade a host cell to complete their replication cycles. The immune evasion tactics used by HIV are so far-reaching that they have so far stymied progress towards the advanced development of an effective vaccine.

HIV cases are controlled by anti-retroviral drugs, whilst vaccine candidates are being identified and evaluated. Variola major causative of smallpox has also evolved host immune evasion tactics, by secreting a protein which inhibits the activation of complement enzymes and another, chemokine-binding protein, type II, which blocks signals calling for immune cells and inflammation at the infection site.