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IS THE DEFINITION OF PATHOGENICITY TOO BROAD?
Pathogenicity is defined and used by most researchers to include any organism able of causing disease. This broad definition would include an organism able to cause a disease to another organism that it is not necessarily associated with. Should the term be expounded to include any organism able of causing disease or limited to only organisms that interact and associate with a host for self-benefit (i.e. completion of their life cycle)? Hunt (1994) mentioned the need to consider toxin producing saprophytes capable of causing disease as pathogens. In the field of medical sciences, several authors highlighted the importance of commensal bacteria becoming pathogenic in immune impaired hosts (Brown et al., 2012; Pallen and Wren, 2007; Pirofski and Casadevall, 2012). Some recently termed a symbiont (commensal or mutualist) with the potential of causing dysregulated inflammation resulting in disease under specific conditions a pathobiont. It was applied to the gut (Mazmanian et al., 2008; Round and Mazmanian, 2009) and skin microbiota (Chen et al., 2018). Pathobiont seems restricted to inflammatory responses. If not, it is unclear if it will be applied in other disciplines as terms with similar meaning far outdates it.
In plant pathology, McNew (1960) mentioned that causal agents can range from facultative saprophytes where parasitism is incidental to facultative or obligate parasites with commensal tendencies. To add to the complexity, some diseases can be perceived as mutualistic or pathogenic depending on environmental conditions. For example, noduleforming bacteria (Rhizobium leguminosarum) causing galls in legumes divert and live of host nutrients. In return, the bacteria provide nitrogen to the host via nitrogen fixation. This interaction can be regarded as mutualistic or commensal in a nitrogen deprived environment but pathogenic in a nitrogen-rich environment (McNew, 1960). Surely commensal or mutualistic symbionts that might have pathogenic abilities cannot be disregarded from the concept of pathogenicity since these organisms are directly associated with their host and receive mutual benefit from the interaction. Whether to include saprophytes might require some clarification.
WHAT IS A DISEASE?
It is difficult to specifically define disease (Godlee, 2011; Scully, 2004; Sharma, 2004). It is often confused with condition (symptom), injury or pathogen (cause) (Sharma, 2004). To be noted from the various definitions of disease (Appendix A: Table 2.1); it is a malfunctioning of host cells or tissue (abnormality) as a result of continuous irritation, is not direct physical injury, express symptoms and can be caused by the environment, infectious agents, inherent defects (genetic) or a combination of these. Complexity is added as the lines between pathology, disability, ageing and psychiatric conditions are vague (Scully, 2004).
Disease and nutrition are synergetic. Undernutrition, stunting and the mere failure to achieve one’s full genetic potential can lead to, or be as a result of, disease. Nutrition impacts on the health of the host thus affecting susceptibility. Nutrient uptake is influenced by many environmental factors whether physical, biological or social (Perkins et al., 2016). With beings of advanced intelligence and conscience (i.e. humans), the state of healthy or diseased can even be influenced by one’s psyche. Disease can be caused by abiotic and/or biotic factors (Sharma, 2004). Basically, only three factors are required for a disease to occur; organism, environment and time. This, of course, would exclude all infectious diseases, but disease none the less. Environment (space) and time are the only abiotic factors and can never be removed from a scenario. Physically, the host, pathogen and other biotics can be removed from an environment, but never time and space. These latter two factors can only change, they cannot be avoided. They should form the basis when starting to consider disease occurrence and development. The host forms the response organism. When considering infectious diseases, the pathogen becomes the causal agent and other biotics influential agent/s. Surely all five factors (two abiotic and three biotic) are needed to consider all diseases (Sharma, 2004) and the measure by which they interact change the disease effect (Casadevall et al., 2011).
CHAPTER 1: GENERAL INTRODUCTION
References
CHAPTER 2: REVIEW OF LITERATURE: THE CONCEPT AND SPECIFICITY OF PATHOGENICITY
Abstract
1. Introduction
2. Is the definition of pathogenicity too broad?
3. What is a disease?
4. What is a pathogen?
5. The construct of pathogenicity
5.1 Ability vs capability vs capacity
5.2 Organism vs microorganism vs parasite vs pathogen vs infectious agent
5.3 Cause vs produce vs incite vs induce
6. What is the cause?
7. Conclusion
8. References
CHAPTER 3: POSTHARVEST DECAY OF NECTARINE AND PLUM CAUSED BY PENICILLIUM SPP
Abstract
1. Introduction
2. Materials and methods
3. Results
4. Discussion
5. Conclusion
6. Acknowledgements
7. References
CHAPTER 4: IMPACT OF RIPENESS ON THE INFECTION AND COLONISATION OF PENICILLIUM DIGITATUM AND P. EXPANSUM ON PLUM
Abstract
1. Introduction
2. Materials and methods
3. Results
4. Discussion
5. Conclusion
6. Acknowledgements
7. References
CHAPTER 5: IMPACT OF RIPENESS ON THE INFECTION AND COLONISATION OF PENICILLIUM DIGITATUM AND P. EXPANSUM ON NECTARINE
Abstract
1. Introduction
2. Materials and methods
3. Results
4. Discussion
5. Conclusion
6. Acknowledgements
7. References
CHAPTER 6: GENERAL DISCUSSION
References
