The answer is “yes” and “no.”
A few basics first. Up until a decade ago, the belief was held that the lungs were sterile. If virulent pathogens managed to get into this sterile environment and colonize, infection would develop. This is no longer held true. The lungs are not sterile. In fact, studies reporting uncontaminated cultures taken from the trachea and bronchi show “communities” of bacteria reside permanently at the carina and intermediate bronchi. These cultures show the same microbes found in the oropharynx are also found in these areas, thus further establishing the mouth-lung relationship. At the level of the lung alveolus where oxygen/carbon dioxide transfer occurs, bacteria have a difficult time surviving. There is little nutrition (protein & iron) available and the immune response is pretty intense (Dickson et al., 2014).
Second, we (normals) all aspirate throughout the day and night. Microaspiration of secretions, with or without food particles, is ongoing and is the vehicle that feeds the microbes from the oropharynx into the lower airway system. Microaspiration is part of a system that helps regulate the microbe “communities” in the lower airway (Dickson et al., 2016)
Third, the billions of microbes found throughout the airway live in symbiosis with each other until a serious illness or injury occurs. This health status change results in changes to the overall body immune resistance allowing more virulent pathogens to rapidly multiple and overcome other weaker microbes. Thus, changes in the immune status affect the whole airway protection system, particularly the mucociliary elevator in the trachea and bronchi. The virulent pathogens make their way to the lung alveolae resulting in inflammatory responses. The alveolae swell shut allowing protein fluid to fill the air sacs, and the pathogens feed off it (Dickson et al., 2017.)
Fourth, the virulent pathogens in the oropharynx are aspirated into the lower airway continuing to supply an ever-increasing virulent bacteria load at the carina and lower air passages. So does the amount of aspiration matter? Yes, particularly in patients who have a compromised immune system (high white blood cell count & high neutrophil count). Macroaspiration adds large loads of bacteria from the oropharynx to the bacteria load already in the lower airway increasing the bad microbe community in the airway. Thus, aspiration of pathogens from the oropharynx into the lower airway does not initiate pneumonia, but feeds it (Dickson, 2016; Werno et al., 2012).
That being said, it may not be the amount (or load) of bacteria aspirated that is important, but which virulent pathogens are being aspirated. The term, “aspiration pneumonia” is being viewed in some medical circles as a “junk” term. It simply states the mechanism by which the pneumonia occurred, but not the pathological cause. The cause is bacteria, and different species are more prevalent in some environments than others. For example, Hospital-Acquired Pneumonia is cultured as Pseudomonas aeruginosa, Staphylococcus aureus, MRSA, MSSA, & Kiebsiella pneumoniae. Nursing Home-Acquired Pneumonia is cultured as Streptococcus pneumoniae, MRSA, and Staphylococcus aureus. There is a call to alter the term to, “Pneumonia from Aspiration.” So, the answer may be “no” to the question if the amount matters. (Ferguson et al., 2018).
Regardless, oral hygiene, or “oral infection control” (my term), helps to reduce (not eliminate) the primary source of microbes in the oropharynx feeding the lower respiratory system. While microaspiration may continue to occur, improving airway protection at the larynx will reduce the incidences of macroaspiration and large volumes of pathogens entering the lower airway. Hydration is another all-important factor. Water is needed a) to turn over the oropharyngeal environment to help move bacteria, b) to assist with body hydration levels that feed the mucous productions systems, and 3) to assist with supporting the salivation system and its immune properties.
Dickson, R.P., Erb-Downward, J.R., & Huffnagle, G.B. (2014). Towards an ecology of the lung: New conceptual models of pulmonary microbiology and pneumonia pathogenesis.Lancet Respiratory Medicine, 2, 238-246.
Dickson, R.P., Erb-Downward, J.R., Martinex, F.J., & Huffnagle, G.B. (2016). The microbiome and the respiratory tract. Annual Review of Physiology, 10, 481-504.
Dickson, R. P. (2016). The microbiome and critical illness. Lancet Respiratory Medicine, 4, 59- 72.
Dickson, R.P., Erb-Downward, J.R., Freeman, C.M. . . . Curtis, J.L (2017). Bacterial topography of the healthy human lower respiratory tract. mBio 8:e02287-16. https;//doi.org/10.1128/nBio.02287-16.
Ferguson, J. Ravert, B., & Gailey, M. (2018). Aspiration: /æspəˈreɪʃən/: Noun: An ambiguous term used for a diagnosis of uncertainty. Clinical Pulmonary Medicine, 25, 177-183
Werno, A.M., Anderson, T.P., & Murdoch, D.R. (2012). Association between pneumococcal load and disease severity in adults with pneumonia. Journal of Medical Microbiology, 61, 1129-1135.
Manuscript by John R. Ashford, Ph.D.
SA Swallowing Services, PLLC
April 2, 2019