Question

When microbe and human first interact there are variables that come into play that dictate which outcome is to occur (colonization on host, no effect, disease/infection). Please write out a synopsis and explanation of 3 factors involved that will lead to one of these three outcomes.

Answer 1

To understand interaction between microbial-host interaction, we need to understand the following terminology

Relationships between two organisms can be very complex. A larger organism that supports the survival and growth of a smaller organism is called the host. The interaction of the two is symbiotic. Symbiosis refers to the living together of organisms and includes commensalism, mutualism and parasitism. Parasites are those organisms that live within a host organism and are metabolically dependant on the host. Any organism that causes a disease is a parasite. If an organism lives on the surface of its host, it is an ectoparasite; if it lives internally, it is an endoparasite. The host in which the parasite either attains sexual maturity or reproduces is the final host. A host that serves as a temporary but essential environment for some stages of development is an intermediate host. A host infected with a parasitic organism that also can infect humans is called a reservoir host. An infectious disease is any change from a state of health in which part or all of the host body is not capable of carrying on its normal functions due to the presence of a parasite or its products.

The first step in the infectious process is the attachment and entrance of the microbe into a susceptible host and its cells. Entrance may be accomplished through body surfaces, sexual contact, blood transfusions, organ transplantation, or by insect or some animal vectors. Adsorption or attachment to the cell surface refers to the penetration into the host system. Viral Pathogenesis - In case of virus, viral proteins on envelopes (spikes or capsid proteins) maximize contact with the host cell. Binding of a virus to its receptor typically results in penetration of the cell or the delivery of virus nucleic acid to the cytoplasm of the cell. The interaction between a virus and its host cells can result in a variety of effects. Cytopathic viruses are those that ultimately kill the host cell; by triggering apoptosis or local necrosis of the cells. Noncytopathic viruses do not immediately produce cell death and result in latent or persistent infections. As a result, noncytopathic viruses can be subdivided into productive and non-productive. Noncytopathic viruses that produce persistent infection with the release of only a few new viral particles at a time are said to be productive. Viruses that do not actively make virus at detectable levels for a period of time (latent infection) are considered non- productive. The last step in the infectious process is shedding of the virus back into the environment. This is necessary to maintain a source of viruses in a population of hosts. During this period, an infected host is contagious and can spread the virus.

Bacterial Pathogenesis - An essential feature in the development of an infectious disease is the initial transport of the bacterial pathogen to the host. The most obvious means is direct contact- from host to host (coughing, sneezing, body contact). Infected hosts shed bacteria into their surroundings which can settle on various surfaces, resuspended in air or water, followed by indirectly transmitted to a host. Soil, water and food are indirect vehicles that harbour and transmit bacteria to hosts. In this context, colonization means the establishment of a site of microbial reproduction on or within a host. It does not necessarily result in tissue invasion or damage. Adherence structures (pili and fimbriae) are specialised adhesion molecules that bind to complimentary receptor sites on the host. Bacterial attack may be accomplished through production of lytic substances that alter the host tissue by (i) attacking the extracellular matrix, basement membranes of integuments and intestinal linings (ii) degrading carbohydrate-protein complexes between cells or on the cell surface (iii) disrupting the cell surface. The presence of viable bacteria in the blood stream is called bacteremia. The presence of bacteria or their toxins in the blood often is termed septicaemia. Virulence gene expression is often regulated by environmental factors. The gene for diphtheria toxin from Corynebacterium diptheriae is carried on the temperate bacteriophage B, and its expression is regulated by iron. The gens that encode major virulence factors in many bacteria Yersinia spp., Pseudomonas aeruginosa) are found on large segments of DNA, called pathogenicity islands.

Host Defense Primary defences - Mucous membranes with cilia, pH regulation, flushing mechanisms and antimicrobial products are efficient transition sites where the host tissues interface with their environment. Secondary defences - The host blood and interstitial fluids contain evolutionary conserved, antimicrobial proteins that are very efficacious. The whole lot of immune cells (lymphocytes, monocytes, dendritic cells, B cells etc.) helps in antigen presentation and effective antibody response against microbial invasion. Lytic cytokines secreted by the immune cells help in microbial lysis.

Evasion of Host Defenses by Microbes Viruses have evolved a variety of ways to suppress or evade the host's immune response. These mechanisms are now becoming recognized through genomics and the functional analysis of specific gene products. Some viruses may muate and change antigenic sites on the virion proteins, or down-regulate the expression level of viral cell surface proteins. Some viruses (HIV) infect T cells and diminish the functionality of the host immune system. Measles virus and cytomegalovirus cause the fusion of host cells. This allows these viruses to move from an infected cell to an uninfected cell without exposure to the antibody-containing fluids of the host. Herpesvirus infect neurons that express little or no MHC molecules. Some bacterial cells possess capsules that prevent complement activation. Other gram-negative bacteria lengthen the O chains in their lipopolysaccharide to prevent complement activation. Strains like Neisseria gonorrhoeae generate serum resistance. Streptococcus pneumonia can produce a slippery mucoid capsule that prevents the phagocyte from effectively contacting the bacterium. S. Pyogenes release a protease that cleaves the C5a complement factor and thus inhibits complement's ability to attract phagocytes to the infected area.