RespiratoryTract Infection, Neoplasm, and the Childhood Disorders
RespiratoryTract Infection
Influenzais a viral infection that affects the respiratory tract. The casestudy considered in this paper involves Marshall, who work-up feelingtired and achy. Marshall’s cheeks became warm and red while at thedaycare. He avoided playing with other children and started crying bythe time his mother arrived from the place of work. By the afternoonof the same day, Marshall had developed a new set of symptoms thatinclude fever, a sore throat, chills, runny nose, and a dry cough.This case study analysis will explain why the presentation byMarshall made Patricia think that suffered from influenza,Pathophysiology of influenza virus, and probability of Marshallgetting a secondary bacterial pneumonia.
Question1: Why presentation by Marshall made Patricia think that sufferedfrom influenza
Althoughinfluenza and cold are both viral diseases that have most commonsymptoms, the presentation of these symptoms is slightly different.The presentation of symptoms can be differentiated in two ways.First, the symptom of influenza occurs faster compared to coldsymptoms. In most cases cold symptoms begin with a sore throat thatlasts for a day or two before the rest of the symptoms can appearclearly (Kalra, Khatak & Khatak, 2011). All influenza symptoms,on the other hand, appear quickly and can be diagnosed within half aday or within the same day that the patients start feeling sick. Inthe case of Marshal, most of the symptoms became visible between thetime the boy woke up and the afternoon of the same day. By theafternoon, Marshall had developed fever, sore throat, chill, dry andhacking cough, and runny nose.
Secondly,influenza symptoms are more severe than the cold symptoms. Forexample, Marshall was unable to play with other kids, started cryingby the time Patricia arrived, and his condition had worsened by theafternoon. This severity rules out the possibility of Marshall’scondition being a cold. Therefore, the speed and the severity ofsymptoms made Patricia think that Marshall suffered from influenzaand not cold.
Amedical diagnosis of influenza is critically important because ithelps the health care professionals distinguish it from other healthconditions that have similar symptoms. Although it has beenestablished that influenza symptoms are quite severe and tend todevelop quickly compared to cold symptoms a medical diagnosis(including a lab test) is the only sure way to confirm influenzainfection (Sakurai & Shibasaki, 2012). In addition, an accuratediagnosis of influenza reduces chances of prescribing the wrongmedication. For example, there is a limited probability ofunwarranted use of antibiotics when scientific and medical proceduresare used to diagnose influenza. Therefore, medical diagnosis is partof a solution to the challenge of antibiotic resistance.Additionally, the findings of a medical diagnosis can be used by thestakeholders (including the Department of Health) to developstrategies for preventing this contagious viral illness. Therefore, amedical diagnosis of influenza leads to an accurate treatment, thuspreventing trial and error therapy.
Question2: Pathophysiology of influenza virus
Influenzais caused by a negative sense, encapsulated, and a single strandedRNA virus. The virus belongs to the family known as Orthomyxoviridae.Influenza A is the most common type of virus and it causes themajority of the human influenza and all avian influenza. The core ofthe RNA has about 8 segments of genes that coat influenza proteins,such as neuraminidase and hemagglutinin (Wohlbold & Krammer,2014). The two types of proteins (neuraminidase and hemagglutinin)determine the virulence of the virus, since they play the criticalrole of neutralizing anti-bodies that are produced by the immunesystem to fight influenza. The protein hemagglutinin helps the virusbind to the epithelial cells of the respiratory system, whichculminates in cellular infection. The other protein, neuraminidase,plays the role of cleaving the bind between the human cells and thenewly formed virions. This allows the cellular infection to spread toother neighboring cells.
Proteinsneuraminidase and hemagglutinin are the major factors that are usedto classify different sub-types of influenza A. The RNA polymerasedoes not have the error-checking mechanisms, which implies that theantigenic drift that occurs from one year to another subject at leastone host to the risk of infection (Wohlbold & Krammer, 2014). Thesegmented genome may also cause the re-assortment of differentsegments of genome from various strains of influenza in theco-infected host.
Differentstrains of influenza are species-specific. The specificity ofdifferent strains is determined by the ability of hemagglutininproteins to bind to different receptor of the sialic acid found onthe surface of the epithelial cells of the respiratory tract. Forexample, the avian influenza is differentiated from human influenzabecause it binds to alpha-2, 3-sialic acid receptor, while the humanvirus that binds to alpha-2, 6-sialic acid receptor (Wohlbold &Krammer, 2014). Strains of influenza virus may survive the treatmentand infect other species by acquiring genes from different otherstrains.
Theconcepts of antigenic shift and drift also explain the high virulenceand the capacity of influenza A virus to overcome medication andantibodies. It is estimated that the virus mutates more than othertypes of microbes by 300 times (Wohlbold & Krammer, 2014). Theprocess of antigenic drift involves the production of point mutationsby RNA polymerase at regains that are prone to errors along thegenome. This mutation increases the ability of the virus to evadeindividuals with acquired immunity. The process of antigenic shift,on the other hand, involves the re-assortment of genes in between twostrains, which occurs during the co-infection of one host.
Therefore,the capacity of antigen A to exert effects on the target host can beexplained by two major features. The first characteristic is thepossession of two types of proteins (including neuraminidase andhemagglutinin) that facilitate the binding of the virus and thespread of a viral infection. The second feature is the ability of thevirus to mutate frequently and acquire new genomes.
Question3: Probability of Marshall getting a secondary bacterial pneumonia
Theprobability of Marshall suffering from secondary bacterial infectioncan be explained by the damage that occurs in the mucous membrane.First, an infection caused by the influenza virus results in thecorrosion of the mucus membrane that is found in the nasopharynx(Liderot, Ahl & Ozenci, 2013). This infection encourages theprocess of secretion of mucus. The excess mucus enhances the adhesionof bacteria to the surface of the epithelium while inhibiting theactivity of macrophage on pneumococci. This increase would increasethe risk of Marshall suffering from a bacterial infection that couldbe attributed to influenza as the primary infection. Pneumonia is ahealth condition that subjects the alveoli to the risk ofinflammation (Liderot, Ahl & Ozenci, 2013). Cyanosis results froma decline in the exchange of gases across the membrane of the alveoliand the subsequent decrease on the saturation of hemoglobin.
Conclusion
Patriciathought that Marshall suffered from influenza because the symptomswere severe and developed faster that the symptoms of a common cold.Influenza A infection is mainly facilitated by two major proteinsthat include neuraminidase and hemagglutinin. A secondary infectionin a patient with influenza is attributed to damage on mucousmembrane and a decline in the immune system.
References
Kalra,M., Khatak, S. & Khatak, M. (2011). Cold and flu: Conventionalvs. botanical and nutritional therapy. InternationalJournal of Drug Development and Research,3 (1), 314-327. Retrieved May 12, 2016, fromhttp://www.ijddr.in/drug-development/cold-and-flu-conventional-vs-botanical–nutritional-therapy.pdf
Liderot,K., Ahl, M. & Ozenci, V. (2013). Secondary bacterial infectionsin patients with seasonal influenza A and pandemic H1N1. BioMedResearch International,13, 1-6. Retrieved May 12, 2016, fromhttp://www.hindawi.com/journals/bmri/2013/376219/
Sakurai,A. & Shibasaki, F. (2012). Updated values for molecular diagnosisfor highly pathogenic avian influenza virus. Viruses,4, 1235-1257. Retrieved May 12, 2016, fromhttp://www.mdpi.com/1999-4915/4/8/1235/pdf
Wohlbold,T. & Krammer, F. (2014). In the shadow of Hemagglutinin: Agrowing interest in influenza viral neuraminidase and its role as avaccine antigen. Viruses,4, 2465-2494. Retrieved May 12, 2016, fromhttp://www.mdpi.com/1999-4915/6/6/2465/pdf