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PDF | Medical Parasitology is the branch of medical sciences dealing with complexity of parasites and host-parasite relationships, the entrenchment of .. pediatric Mediterranean visceral leishmaniasis, Journal of Clinical Microbiology, vol. .. Moghimi S.M., Hunter A.C., and Murray J.C. (): Nanomedicine: current. Host-Parasite Relation. Every mammalian ing, the relationship between host and parasite determines Clinical Microbiology and Infection, vol. 17, no. [ ] H. W. Murray, J. D. Berman, C. R. Davies, and N. G. Saravia. A parasitic relationship is one in which one organism, the parasite, Host pathogen interaction - Medical Microbiology (Austria).
For this reason, several adaptations have evolved to promote prolonged survival in the outside world and so maximize the chances of successful host contact e.
- Lecture One BIOL 5331 Host-Parasite Relationships Medical Microbiology.
The prolific replication of parasites is another device to achieve the same end. Nevertheless, where parasites fail to make contact with a host, their powers of survival are ultimately limited.
Host Parasite Relationship
Adaptation to host signals can therefore have a reproductive cost i. The evolution of parasitism As so many organisms are parasitic and every group of animals is subject to invasion by parasites, the development of parasitism as a way of life must have occurred at an early stage in evolution and at frequent intervals thereafter. How this occurred is not fully understood, and it may well have been different in different groups of organisms. In many, parasitism most probably arose as a consequence of accidental contacts between organism and host.Host Parasite Relationships 2
Of many such contacts, some would have resulted in prolonged survival and, under favourable nutritional circumstances, prolonged survival would have been associated with enhanced replication, giving the organism a selective advantage within the environment. Many parasites of humans and other mammals may have originated via the route of accidental contact, but it is clear that others have become adapted to these hosts after initially becoming parasitic in other species.
For example, parasites of blood-feeding arthropods have ready access to the tissues of the animals on which the arthropods feed. Where the parasite becomes specialized for the non-arthropod host it may lose the ability to be transmitted by blood feeding. Where the arthropod host is retained in the life cycle the parasite is faced by competing demands for survival in each host, which probably explains why, for example, arboviruses are restricted to only a few families of RNA viruses and a single DNA virus, African swine fever virus.
Bacterial parasites evolved through accidental contact In the case of bacteria, it is easy to see how accidental contact in environments rich in free-living bacteria could lead to successful invasion of external openings such as the mouth and eventual colonization of the gastrointestinal tract.
Initially, the organisms concerned would have had to be facultative parasites, capable of life both within or outside host organisms many pathogenic bacteria still have this property, e. Many bacterial parasites have evolved to live inside host cells Bacteria that became parasitic by accidental contact would have lived outside host cells at first and would not have had the advantages of being intracellular.
The evolution of the intracellular habit required further modifications to allow survival within host cells, but could easily have been initiated by passive phagocytic uptake. Subsequent survival of the microbe would depend upon the possession of surface or metabolic properties that prevented digestion and destruction by the host cell. The success of intracellular life can be measured not only by the large number of bacteria that have adopted this habit, but also by the extent to which some organisms have integrated their biology with that of the host cell.
The endpoint of such integration is perhaps to be seen in the evolution of the eukaryote mitochondrion, which may have evolved from symbiotically associated heterotrophic purple bacteria Fig. Many lines of evidence suggest that mitochondria of modern eukaryote cells evolved from bacteria that established symbiotic mutualistic relationships with ancestral cells. The pathway of virus evolution is uncertain Clearly, parasitism by bacteria, which are undoubtedly ancient organisms they can be traced back 3—5 billion years in the fossil recorddepended upon the evolution of higher organisms to act as hosts.
Whether the same is true of viruses is open to question, and depends upon whether viruses are considered primarily or secondarily simple. If viruses evolved from cellular ancestors by a process of secondary simplification, then parasitism must have evolved long after the evolution of prokaryotes and eukaryotes. If viruses are primitively non-cellular then it is possible that they became parasitic at a very early stage in the evolution of cellular life, at some point when, because of environmental change, independent existence became impossible.
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A third alternative is that viruses were never anything other than fragments of the nuclear material of other organisms and have in effect always been parasitic. Modern viruses may, in fact, have arisen by all three pathways.
Eukaryote parasites have evolved through accidental contact The evolution of parasitism by eukaryotes is likely to have arisen much as it may have done in prokaryotes i. Examples can be found among protozoan and worm parasites to support this view: Parasite adaptations to overcome host inflammatory and immune responses We can view the evolution of parasitism and the adaptations necessary for life within another animal as being exactly analogous to the adaptations necessary for life within any other specialized habitat: However, it is always necessary to remember that in one major respect parasitism is quite different from any other specialist mode of life.
This difference is that the environment in which a parasite lives, the body of the host, is not passive; on the contrary, it is capable of an active response to the presence of the parasite. The attractiveness of animal bodies as environments for parasites means that hosts are under continual pressures from infection, and these pressures are increased when hosts live: Pressure of infection has been a major influence in host evolution Pressure of infection has been a major selective influence in evolution, and there is little doubt that it has been largely responsible for the development of the sophisticated inflammatory and immune responses we see in humans and other mammals.
In evolutionary terms, all infection has its costs to the host because it diverts valuable resources from the activities of survival and reproduction; there has therefore been pressure to develop means of overcoming infection whether or not it causes disease. Of course, this is not the focus of clinical microbiology, which legitimately places emphasis on the costs of infection in terms of frank disease, but it should be remembered because it explains more fully the nature of the continuing battle between host and parasite — the former attempting to contain or destroy, the latter attempting to evade or suppress — and why the emergence of new, and the return of old, infectious diseases are a constant threat.
Parasites are faced not only with the problems of surviving within the environment they experience initially, but also of surviving in that environment as it changes in ways that are likely to be harmful to them. The inflammatory and immune responses that follow the establishment of infection are the most important means by which the host can control infections by those organisms able to penetrate its natural barriers and survive within its body. These responses represent formidable obstacles to the continued survival of parasites, forcing them to evolve strategies to cope with harmful changes in their environment.
Indeed, they are often the very reason why such organisms are major pathogens. Nevertheless, transmission and survival of many parasites depends upon the existence of particularly susceptible host individuals e.
Quite subtle changes in either can completely change the balance of the relationship, towards greater or lesser pathogenicity, for example. Perhaps the most important recent illustration of this situation is the dramatic and explosive appearance of HIV infections. This group of viruses was originally restricted to non-human primates, but changes in the virus have permitted extensive infections in humans. Similarly, changes in an avian influenza virus allowing human infection resulted in the major pandemic early in the twentieth century and the recent emergence of the new H1N1 flu in is another example; there is also current concern about the potential spread of avian virus such as H5N1.
Of a different nature, but relevant to the general theme, is the acquisition of drug resistance in bacteria and protozoa Fig. Although the underlying genetic and metabolic changes do not by themselves influence pathogenicity, the expression of such changes in the face of intense and selective chemotherapy certainly does, so allowing overwhelming infection to occur.
The problem of hospital-acquired MRSA infection is a perfect example.
The activity of many antibiotics can be blocked by bacterial enzymes coded for by genes located on cytoplasmic DNA in plasmids. The ability of bacteria to transfer plasmids between individual organisms means that strains or species previously susceptible to an antibiotic can acquire the ability to produce such enzymes and so gain antibiotic resistance directly from resistant organisms.
These newly resistant forms are then differentially selected under antibiotic treatment, the susceptible individuals being deleted from the population. Primary antibiotic resistance also occurs through genetic mutations. Host adaptations to overcome changes in parasites Changes in the host can also alter the balance of a host—parasite relationship. There are no exactly equivalent examples in humans, but in evolutionary time there have been major selective influences on populations prompting changes to permit survival in the face of life-threatening infections.
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The ability of the host to prevent establishment of infection by using its defense mechanisms. Lack of resistance to organism and establishment of disease. Can be divided according to the degree of Pathogenecity into: Cause disease in non- immune host to that organism. Having low pathogenecity and infect people with low immunity. Pseudomonas 9 Infection is simply invasion of cells and multiplication by microorganisms without tissue destruction.
Virulence is an ability to invade and destroy tissue to produce disease. Virulence is measured by the Lethal dose 50 LD50 which is the number of organisms or mg. When the LD 50 is small, the microorganism is considered highly virulent and when it is high the organism is said to be of low virulence.