Poly-Microbial Condition or Disease - Term Paper Example

Running Head: Poly-microbial Condition or Disease Poly-microbial Condition or Disease Name Institution Poly-microbial Condition or Disease Introduction Poly-microbial diseases are those conditions that are caused by a number of pathogenic players. The pathogens can come from different kingdoms, from dissimilar genera that exist within a specific kingdom, from different species that exist in a genus and lastly from different sub-strains that exist within a strain (American Academy of periodontology, 1996). In poly-microbial conditions, there are complicated interactions that exist between two or a number of etiologic agents, which lead to synergistic clinical pathologies and symptoms that trigger an array of responses from the host. Examples of such diseases are outlined below: Chickenpox – in which 15% of children who had an invasive group A Streptococcal infection also previously had a viral varicella-zoster disease. Gastroenteritis – which do bacteria and viruses cause. Genital infections – it is noted that 22.7% of 494 ladies suffered from mixed bacterial, chlamydial, fungal and viral infections. Hepatitis – infections come about as a result of hepatitis D, C and B viruses. Intra-abdominal infections- contains gram negative, gram positive, anaerobic and aerobic bacteria. Lyme disease – also manifests with babesiosis. Multiple sclerosis- manifests as a result of retrovirus and Epstein Barr virus. Necrotizing fasciitis – anaerobic, aerobic, gram negative, gram-positive bacteria are thought to cause it. Otisis media- bacteria and viruses are detected in approximately 65% of the cases. Periodontal diseases – are as a result of a combination of fungi, viruses and bacteria. Pertussis- bacteria other than Bordetella pertussis colonize 58% of patients. Epidemiology It especially attacks the Latino adults with not more than a high school education in the United States. Periodontal disease was noted to be highest in Mexican American males. It impacts an individual’s physical, mental and emotional well-being (Scott & Simile, 2005). The oral pain associated with it negatively affects the nutritional sleep and intake, contributes to missed days at work and can lead to more health complications. Oral health has been associated with heart disease, diabetes and pregnancy outcomes that are adverse. The pregnancy complications include low birth weight, pre-term birth and general infections that may manifest during it (Scott & Simile, 2005). Causal agents Periodontal diseases are a varied group of clinical entities in which the induction of inflammatory processes lead to the destruction of attachment apparatus, the loss of the supporting alveolar bones and if untreated the eventual tooth loss. It is the main cause of teeth loss in adult (Vega et al, 2009). Periodontal disease’s etiology has been centralized on microbial by-products, bacterial plaque and the immune response of the host. Bacteria are the primary causal agents of periodontal disease. The three bacteria involved are B. forsythus, P. gingivalis and A. actinomycetemcomitans. However, other listed pathogens that cause the disease are herpes viruses, indigenous organisms (T. denticola, E. nodatum, P. micros, Campylobacter rectus and P. nigrescens/intermedia) and yeast (Vega et al, 2009). The two chief periodontal disease categories that result in the loss of the teeth’s supporting structures is: aggressive and chronic periodontitis. Periodontal disease can further be characterized by the nature of bone loss (generalized or localized) and as such the disease’s severity (advanced, moderate, slight). Chronic periodontitis is the most common and tooth destruction is consistent with mineralized and bacterial plaque. It is as such a poly-microbial disease that has variable microbial patterns. On the other hand aggressive periodontitis shows rapid bone destruction and attachment loss. The destruction observed is not equivalent to the quantity of microbial deposits. Pathogenesis The pathogenic bacteria should be able to: Colonize the host Damage host tissues Evade the host’s defense mechanisms The mechanisms for each of the steps required for pathogenesis have been recognized for a number of the various periodontal pathogens. Colonization Adhesion is the chief element in subgingival bacteria colonization either directly to periodontal tissues or via the association with various organisms through coadhesion and coaggretion. During the biofilm development, there are spots of low and high bacterial biomass, which are interlaced with aqueous channels that provide for essential nutrient movement. The nutrients are mainly derived from gingival crevicular fluid and it is also used for metabolic waste product removal. While there is an attempt in the subgingival microbial complex expansion due to limited space; the apical migration of epithelium and the destruction of attachment apparatus near the tooth provides for subgingival biomass expansion. As a consequence of polymicrobial infection, bacteria act in concert and as such support aggregation and nutrition factors that are necessary for biofilm development. For instance, bacterial derived proteinases obliterate tissue and as such provide polypeptides that are used for organism growth. Host defenses Periodontal pathogens use numerous means to hamper host defense mechanisms that serve to prolong their periodontal pocket presence. An example is leukptoxin which is manufactured by A. actinomycetemcomitans. The aforementioned cytotoxic protein kills leukocyte subsets in vitro that are inclusive of peripheral blood monocytes and polymorphonuclear leukocytes. Leukotoxin is a gene sequenced and cloned on the basis of its sequence homology and was found to be in the family of toxic bacteria which is inclusive of toxins such as Actibobacillus and Pasteurella haemolytica that produce devastating infections in swine and cattle respectively. Another means by which pathogens evade host defenses is through the production of factors that are immunosuppressive, polymorphonuclear chemotaxis inhibition, Fc binding protein production and proteases secretion that result into the cleaving of immunoglobulin G (IgG). The pathogens may also induce lymphocyte cell cycle arrest. CDT’s (cytolethal distending toxin) biological effects extend above immunosuppression and as such could also play a role in cell invasion. P. gingivalis leads to the production of proteinases that cleave IgG, IgA1 and IgA2 which is inclusive of the hydrolysis of immunoglobulin that is already bound to bacterial surface. Lipopolysaccharide (LPS) manufactured by P. gingivalis is not able to stimulate the expression of E-selectin on endothelial cells as such it hinders leukocyte extravasation. Damage tissue Although the main cause of connective tissue destruction is from proteolytic host cell activity, bacteria produce a great number of enzymes that lead to the damage of extracellular matrix proteins that are inclusive of collagenase. Human gingival fibrolasts that are incubated with T. denticola show a variety of pathologic responses that include cell detachment, cell death and reduced cell proliferation. The pathogen is able to lyse and agglutinate red blood cells and also induce membrane blebbing of the epithelial cells. It is also noted that T. denticola components such as membrane lipids, surface proteases and lipoproteins may contribute to periodontal tissues inflammatory reaction that contributes to the damage of tissues. Alkaline phosphatases and A. actinomycetemcomitans lead to the induction of bone resorption. A. actinomycetemcomitans leads to the production of a factor which stops fibroblast proliferation that is seen in cell cultures which modulates tissue turnover. Diagnosis The diagnosis of the disease is made mainly through traditional clinical assessments and supplemental tests. In traditional clinical assessments a dentist relies on factors such as; Absence or presence of the clinical inflammation signs (for instance bleeding upon probing) The probing depths Pattern and extent of the loss of bone and clinical attachment Patient’s dental and medical histories Presence or absence of miscellaneous symptoms that are inclusive of ulceration, pain and the amount of observable calculus and plaque. The measurements of the loss of clinical attachment and probing depths obtained by periodontal probes are valid methods used for the assessment of periodontal status. There are computer linked periodontal probes are available (Armitage, 2003). In supplemental tests the qualitative and quantitative assessment of sub gingival micro flora and gingival crevicular fluid is tested. The results from the aforementioned tests can provide useful information with regard to a patient’s periodontal disease. The aforementioned risk assessment tests may also be made use of with regard to the establishment of a therapy’s endpoint before a patient is put on a given periodontal maintenance program. However, their clinical utility is yet to be developed, as more research needs to be conducted (Armitage, 2003). Prognosis Prognosis is the prediction of the course, duration and the outcome of an infection based on the general knowledge of its pathogenesis and the presence of the disease’s risk factors. It is determined after a diagnosis is made but just before the development of a treatment plan. Clinical attachment (CAL) is used to determine prognosis. The following are the features assessed during the prognosis of an individual tooth: Mobility Probing depth Bone loss percentage The crown to root ratio The presence and severity of furcation The distribution and type of bone loss Root morphology Bleeding upon probing Caries/ pulpal involvement Occlusal relationship and tooth position Patient risk factor The following factors affect prognosis; rate of progression, age, medical status, patient cooperation, economic considerations, the knowledge and dentist’s ability, oral habits for instance stress, alcohol abuse and smoking. Treatment The treatment has relied mainly on mechanical therapy; root debridement that is done through surgical access or without it. It is a therapy geared towards the reduction of overall plaque mass. Mechanical debridement advantages are as follows; Removal of endotoxin and calculus The disruption of plaque biofilm complex Induction of a protective antibody response to various pathogens An increase in beneficial bacteria for instance streptococci Removal of specific subgingival pathogenic organisms that results in better clinical health or stabilization. Chronic periodontitis is treated with root planning (debridement) and scaling that does not entail the use of local or systemic antimicrobials. When this treatment method is done during routine periodontal maintenance then the periodontal pathogens are inhibited to a level, which maintains host and pathogen equilibrium. This ensures that progressive attachment loss is avoided. The maintenance of good oral hygiene is also another mode of treatment. Good oral hygiene ensures that there is good plaque control. It has been noted it changes subgingival flora to a state that is compatible to periodontal health. The use of surgery and/or antibiotics is also seen as a way of treatment. It is especially used in the treatment of pathogens for instance P. gingivalis and A. actinomycetemcomitans, which invade epithelium. The aforementioned pathogens are not responsive to standard mechanical debridement. Systemic antibiotics are recommended for the aggressive treatment aggressive periodontal disease. These antibiotics are also used in conjunction with root planning and scaling that exists in deep periodontal pockets that are nonresponsive. The use of systemic antibiotics has a number of advantages, which include the treatment of potential microbial reservoirs (buccal mucosa, tonsils, tongue) and multiple sites; the treatment of organisms that exist at pocket bases and also in the tissues. This is due to the systemic absorption and the delivery into oral tissue, saliva and gingival crevicular fluid. However, it also has a number of disadvantages, which are; bacterial resistance, compliance, kills beneficial bacteria, side effects (which are inclusive of gastrointestinal irritation and super-infections) and also the point that periodontal destruction is mainly localized to few teeth. Systemic antibiotic local delivery alleviates numerous concerns since it is able to reach base pocket bacteria. It also retains activity for a sufficient amount of time that allows bacteriostatic or bactericidal effects on the offending pathogens. Gingival crevicular fluid can be replaced 40 times in 60 minutes and as such it should be retained on the root surfaces or be administered in a very slow controlled release. Local delivery gives a higher drug concentration in base pockets than an equal systemic agent. Antimicrobials have also been used in its treatment. Locally delivered and systemic antimicrobial agents that are directly administered into periodontal pockets have been used. Its upside is the availability of various drugs and specific combinations to choose from and the lower cost compared to locally delivered antimicrobials. The local delivery of antimicrobials is not a systemic antibiotics substitute when indicated in particular periodontal diseases. Antibiotic selection during the use of local delivery is noted to be empirical. Therefore in instances where a person needs to be aware of specific antimicrobial and bacteria susceptibility (i.e nonresponsive or aggressive disease), antibiotic susceptibility and microbiologic testing are recommended. Lastly, antimicrobials should not be utilized as replacement for mechanical therapy but should be used together with mechanical therapy so as to optimize therapeutic effectiveness. Antimicrobials are not as effective because of biofilm matrix and architecture, which impairs the penetration of antimicrobials. The biofilm may also contain inactivating substances and also change the phenotype of biofilm bacteria for instance slower growth, which may lead to resistance of antimicrobial agents. Therapeutic strategies are being utilized and are aimed at the modulation of a host’s immune-inflammatory response. The therapeutic practices utilized in clinical practice are inclusive of the administration of a very low-dose doxycycline, which stops matrix metalloproteinases. Other agents that impair specific cytokines or stop PGE have also manifested therapeutic potential. Current preventive measures Currently there only exist preventive measures to keep periodontal diseases in check. This is because it is caused by complex microbial pathogens, which makes it difficult to develop a vaccine. Also contrary to other infections in which treatment correlates with the removal of offending pathogen; the successful treatment of periodontal disease is not dependent on the removal of pathogens but in an alteration where homeostasis or symbioses is able to take place between the defensive host and offending bacteria. The preventive measures will be outlined below. Periodontal disease can be prevented through good oral hygiene and a healthy lifestyle. Good oral hygiene includes flossing and brushing which is important in keeping advanced periodontal lesions in check. A healthy lifestyle entails having appropriate diet and making good choices such as tobacco and alcohol cessation. Water fluoridation in the community is effective in the prevention of dental caries that occur in both adults and children. The fluoridation of water benefits a multitude of residents served by it regardless of their economic and social status. Milk and salt fluoridation schemes are depicted to have the same effects when utilized in the community preventive programmes. Measures taken by individuals and professionals which are inclusive of the use of gels, fluoride mouth rinses, toothpastes and dental sealant applications aid in the prevention of dental caries. The introduction of fluoridated toothpaste is seen as a valuable strategy that ensures that people are appropriately exposed to fluorides. The availability and accessibility of good oral health care goes along way in preventing periodontal diseases (WHO, 2012). Bibliography 1. American Academy of Periodontology (1996). Position paper. Epidemiology of periodontal diseases. Journal Periodont, 67: 935-945 2. Armitage, G.C., (2003). Diagnosis of Periodontal Diseases. Journal Periodontal, 74: 1237-1247. 3. Gibbons, R.J. & Van Route, J., (1980). Bacterial Adherence and the Formation of Dental Plaques. P. 63-104. In E.H. Beachey (ed.), Bacterial Adherence. London: Chapman & Hall. 4. Ranney, R.R., Debski, B.F., & Tew, J.G (1981). Pathogenesis of gingivitis and periodontal disease in children and young adults. Journal of Pediatrician Dentist. 3:89-100. 5. Scott, G & Simile C., (2005). Access to dental care among Hispanic or Latino Subgroups: United States, 2000-2003. Centers for Disease Control Division of Health Interview Statistics. Advance Data from Vital and Health Statistics, 354. 6. Socransky S.J, & Haffajee A.D., (1991). Microbial mechanisms in the pathogenesis of destructive periodontal diseases: A critical assessment. Journal of Periodontology, 26: 195-212. 7. Vega, W.A., et al. (2009) Health disparities in the Latino population. Journal of Epidemiologic Reviews, 31, 99-112 8. World Health Organization (2002). Oral Health. Strategies and approaches in oral disease prevention and health promotion. Retrieved September 6th 2012 from http://www.who.int/oral_health/strategies/cont/en/index.html Read More