Pathogen penetration

The mycorrhizal symbiosis involves several mechanisms in control of plant diseases, (i) Creating a mechanical barrier for the pathogen penetration and subsequent spread... 

Dando SJ, Mackay-Sim A, Norton R, et al. Pathogens penetrating the central nervous system infection pathways and the cellular and molecular mechanisms of invasion. Clin Micmbiol Rev. 2014 27(4) 691-726. 

It is of interest that the activation of POs often takes place in stomata guard cells, since P. infestans mainly penetrates into plant tissues through stomata slits. The localisation of phenolic compounds - some of them seemingly being used by POs as a substrate - and PO activity was visible in guard cells. (Maksimov et al., 2011). As such, the immune reaction occurred in close proximity to pathogen structures. 

In some infections the pathogenic organisms are located intracellularly within phagocytic cells and, therefore, remain relatively protected from drugs which penetrate cells poorly, such as the penicillins and cephalosporins. In contrast, erythromycin, rifampicin and chloramphenicol readily penetrate phagocytic cells. Legionnaires disease is an example of an intracellular infection and is treated with rifampicin and/or erythromycin. 

Although viral infections are important causes of both otitis media and sinusitis, they are generally self-limiting. Bacterial infections m complicate viral illnesses, and are also primary causes of ear and sinus infections. Streptococcus pneumoniae and Haemophilus influenzae are the commonest bacterial pathogens. Amoxycillin is widely prescribed for these infections since it is microbiologically active, penetrates the middle ear, and sinuses, is well tolerated and has proved effective. 

Plants are continually exposed to a vast array of potential phytopathogenic fungi nevertheless, plants resist to most of them by blocking fungal development soon after penetration. Resistance against pathogens can be distinguished in resistance at the species level (non-host resistance) and resistance at the cultivar level (race-cultivar resistance). Plants lack a circulatory system and antibodies and have evolved a defense mechanism that is distinct from the vertebrate immune... 

Figure 1. Transverse section of barley leaf epidermal cells taken perpendicular to the long axis of the cells and anticlinal to the leaf surface. The section has been labeled by the EMSIL technique (see Methods) utilizing purified C. sativus endopolygalacturonase and monoclonal antibody EPG-4, which is specific for this enzyme, in order to localize the substrate of the enzyme at the typical site penetrated by the fungal pathogen. Bar = 1 pm. Inset Comparable cell wall region as in Fig. 1 but labeled with monoclonal antibody JIM 5 to localize non-esterified pectin. Bar = 1 pm. Note the identical labeling patterns obtained with either method.

Figure 2. Advanced stage of barley leaf penetration by C. sativus. The pathogen has penetrated the anticlinal cell wall junction between two host epidermal cells (e). The fungal appressorium (a) is visible above the cell comer. The host cell comer matrix has been displaced by an enlarged hyphal element (h) situated between the thin cell walls of the host epidermal cells. The host epidermal cell walls have been densely labeled with the cellulase-gold probe. An intercellullar hyphal element (ih) is present within the penetrated host cell. Bar = 1 pM.

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