Pillar One: Serious Illness or Frailty (Immunosuppression)

            The first “Pillar,” or factor, for pneumonia to develop, is the presence of a serious illness (Bartlett and Gorbach, 1975).  Disease development over time is a consequence of genetic inheritance and/or environmental factors. But in every case, illness alters the body’s internal stability placing it at a higher risk for exacerbating consequences. Illnesses produce both physical and psychological stresses and the immune system is the first responder with a pro-inflammatory response, or increased inflammation (Morey, Boggero, Scott, & Segerstrom, 2015). Stress has been shown to have adverse effects on cardiovascular, gastrointestinal, and endocrine functions, particularly if the stress is severe and prolonged (Yaribeygi et al., 2017).  The effects of stress may also further alter the immune system responses related to these diseases and allow secondary, opportunistic diseases to develop. The immune system is comprised of two systems: The Innate and the Adaptive Immune Systems.  The Innate Immune System is constantly vigilant and primarily provides an immediate but short-lived, imprecise pro-inflammatory response to pathogen invasion; it has no memory of previous pathogens or attacks, and, if left unchecked, can cause inflammatory damage to healthy cells (Yatim and Lakkis, 2015, Meyer, 2001; Dettmer, 2021).  The Adaptive Immune System is initiated when the innate system defenses are eluded and pathogen molecules are detected (Janeway et al., 2001; Dettmer, 2021). This system is slower to respond taking 4 to 7 days to reach effective strength (InformedHealth.org, 2020; Janeway et al., 2001).

            Aging results in the gradual loss of mechanisms in the major organ systems that maintain the equilibrium of structure and function of adult tissue. Aging also leads to a decline in the ability to reproduce cells, increased susceptibility to disease and tissue dysfunction, and increased risk of mortality (Barzilai et al., 2012; Rando & Chang, 2012).  This increased susceptibility to disease with aging is due to the reduced ability to mount immune responses against stressors, or immunosenescence. (Meyer, 2001; Meyer, 2004; Banu, 2020; Xu, Wong, Hwang, & Larbi, 2020; Dettmer, 2021).

            Identifying and monitoring disease onset and progression are routinely documented by body fluid assay results.  Blood tests, such as the Complete Blood Count (CBC), monitor the levels of activation of leukocytes in the blood and give insight into the body’s immunity status and disease severity (Farkus, 2020). These tests are essential when assessing patients with the potential for developing pneumonia. They provide measures from a large spectrum of cells circulating in the blood system: white blood cells, red blood cells, and platelets. White blood cell types are differentiated into innate immune fighters: neutrophils (bacteria), monocytes/macrophages (viruses, bacteria, fungi, and protozoa), basophils (allergies), and eosinophils (allergies), and adaptive immune fighters: lymphocytes-T-cells (bacteria and viruses).  A white blood cell count with a high neutrophil count indicates the innate immune system is responding to tissue damage with inflammation somewhere in the body (Blumenreich, 1990).  Red blood cell count (RBC), hemoglobin, and hematocrit monitor the level of oxygen-carrying cells in the bloodstream. A reduction of circulating red blood cells and/or hemoglobin (iron protein) concentrations is a marker for anemia (Chaparro & Suchdev, 2019), which can quickly reduce muscle strength and initiate functional inefficiency leading to dysphagia, aspiration, hemorrhages, kidney failure, malnutrition, dehydration, heart disease, lung disease, and some cancers (George-Gay & Parker, 2003). 

Pillar Two: Impaired Laryngotracheal Protection

            Moving food and liquid materials from the oral cavity into the esophagus requires one of the most complex biomechanical systems in the body. Muscle weakness of the laryngeal/pharyngeal musculature is one of the primary associated causes of oropharyngeal dysphagia.  Aspiration is the direct consequence of impaired oropharyngeal/esophageal muscle strength, coordination and/or mucosal sensation (Bock et al., 2017). It is the consequence of reduced or altered biomechanical closure of the laryngeal valves necessary to prevent entry of material (saliva, mucous, liquids, thicker foods, regurgitated stomach chum) into the lower respiratory system (Bartlett & Gorbach, 1975; Huxley et al., 1978).  However, aspiration is not the cause of BAP. In healthy individuals, larynx protection of the lower airway begins with arytenoid adduction approximating the aryepiglottic folds to midline and tilting anteriorly to the base of the epiglottis, nearly totally obliterating the laryngeal vestibule. Next epiglottis inversion covers the closed larynx aditus and adduction of the ventricular and true vocal folds further seal off the airway resulting in apnea (Vose & Humbert, 2019).   Aspiration of material is not a simple event. Aspiration is the consequence of impaired physiological factors, such as timing, force, pressure, amplitude, and velocity, that impair the movement of the bolus through the pharynx into the esophagus.

            Aspiration events are relatively common among healthy individuals.  Bartlett and Gorbach (1975) reference the early work of Amberson in 1937 who reported finding contrast material in the lungs of patients the following day after placing contrast material in their mouths while asleep.  Huxley and colleagues (1978) reported that 45 percent of normal subjects aspirated during deep sleep, and 70% of patient with depressed consciousness aspirated. Similar findings were reported by Gleeson, Eggli, and Maxwell (1997). In healthy people, there are no ill-effects even though the aspirate contains bacterial organisms. Evidence continues to support the premise that microaspiration of trace amounts of liquids, including secretions, is a normal occurrence (Bartlett & Gorbachev, 1975, Dickson et al., 2016; Bock et al., 2017; Todd et al., 2013; Dickson et al., 2014).  Microaspiration is defined as subclinical aspiration of small droplets (Lee et al., 2010 Am J Med), and is highly associated with BAP development. It is, however, difficult to observe and document.  It is more commonly reported with intubated ventilator patients. Seepage around the inflated endotracheal cuff is microaspirated into the lower respiratory system.  Macroaspiration, or aspirating larger amounts of foods or liquids, is suspected during meals but also is not directly observed.  The common belief is that macroaspiration during meals, or prandial aspiration, may be responsible for pneumonia.  Clinical research is lacking in support of this factor.  Feinberg et al. (1996) did not find a simple and obvious relationship between prandial aspiration and pneumonia.  Wet vocal quality and coughing may or may not indicate aspiration and instrumental swallowing studies should be administered if there is concern. Miller and associates (2005) state that macroaspiration is not associated with an increased rate of pulmonary infection. 

Pillar Three: Poor Oral Environment Conditions

            Aspiration does not cause pneumonia; a poorly cared for and infected oral cavity does!!  The oral cavity is a complex and generally diverse ecosystem and the second largest reservoir of microbes in the human body. It is composed of soft tissue mucosa and hard surfaces, such as the teeth.  Saliva provides the primary watery mechanical and chemical protective covering over all oral surfaces and plays a critical role in oral homeostasis and tissue repair (Fenoll-Palomares et al. 2004;Pedersen et al, 2018; Brizuela & Winters 2023). Teeth are composed primarily of the hard substance, carbonated phosphate or enamel, and are the only body structures that do not regenerate through metabolism (Farci and Soni 2023; Talal et al. 2020; Loesche, 1996). These surfaces serve as collection areas for microbes. There are over 700 species of oral microbes thriving in this cavity (Chen et al. 2010), and approximately 100 billion microbes are swallowed in saliva per day. These microbes form communities (commensal) in biofilms in the oral cavity and provide protection from pathogens, nutrition for themselves, and help maintain oral surfaces. These biofilms develop from saliva and flora interactions and grow to form on the surfaces of the teeth and oral mucosa.  Among these commensal microbes are pathobionts or microbes that are opportunistic and will turn pathogenic under certain conditions, including periodontal disease. When the oral environments become less communal and the diversity of the microbe communities lessens with the rise of these pathobionts, this is called dysbiosis. Poor oral cleanliness is the primary cause of buildup of biofilms, or plaque, on the teeth. Continued lack of proper oral cleaning results in inflammatory disease developing around the base of the teeth and the gingiva (gums) and beds for further colonization of destructive pathogens.  This is called gingivitis, and severe forms of gingivitis is known as periodontitis.  The pathogens thriving on the oral surfaces have been linked to systemic diseases, such as cardiovascular disease, endocarditis, stroke, low birth weight, respiratory infections and diseases, pancreatic cancer, diabetes, inflammatory bowel disease, and nutritional problems (Haumschild et al. 2009; Li et al 2000). Oral inflammatory disease is a result of the body’s immune system attacking the oral pathogen, and more specifically neutrophils. Evidence that periodontal disease is a primary causative factor in BAP development is strong (Scannapieco & Mylotte, 1996; Scannapieco, 1999; Scannapieco, Bush, & Paju, 2003; Awano et al., 2008; Holmstrup et al. 2017; Gomes-Filho et al., 2020; Jerônimo et al., 2020; Kouanda et al., 2021; Wu et al., 2022).  Aspiration is not the primary cause of BAP but oral bacterial pathogens are. To prevent BAP, oral cleaning programs have been proven to be very effective in both nursing home and hospitals, particularly intensive care units.

References (In Progress)

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 November 1, 2023