Respiratory tract infections, neoplasms and childhood disorders

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Thechild’s presentations are common for both flu and cold. Thefatigue, ache, fever, chills, sore throat, running nose and hackingcough are all presentations of cold and flu. However, the persistenceand severity of the symptoms are what defines the difference betweenthe two. According to the US Centers for Disease Control andPrevention (CDC), the cough, sore throat and fatigue are some of themajor symptoms of flu (, 2015). The reason cold and flu havethe same presentations is that they both affect the respiratorysystem, despite the fact that they are caused by different viruses.Patricia thought that the child had flu because according to, flu is characterized by rapid onset of symptoms, while coldis less aggressive.

Accordingto the CDC, there are about 2000 influenza viruses that are increnulation every year. Doctors use antigenic characterization togive an indication of the virus’ ability to react against theimmune response of the body. The HI test (Hemagglutinin InhibitionAssay) is used to evaluate the similarity between the flu viruses.When Marshall was exposed to the flu strain, his antibodies latchedonto the virus, attaching healthy cells alongside them, consequentlyinfecting them. In the body, the flu virus undergoes changes thatlead to the variability in HA and NA antigens. There is influenzaType A, B and C. Influenza type A and B are common in humans. Thetype A is broken down into two main strains, which are H1N1 and H3N2viruses. According to Nakajima et al., (2012), histopathological,type A is variable. Its viral replication peaks after two days, andlittle of the virus is shed after the first one week. It is mainlyreplicated in the upper and lower respiratory tracts. Marshall’scase is that of flu vs. cold because of the rate of progression ofthe symptoms.

Pathophysiology– Influenza A damaged Marshall’s epithelial cells of therespiratory tract. Once infected, the cells break and leave spacesbetween the basal cells, which happens in a process known asnecrosis. This leads to the release of extracellular fluid, resultingin a flooded respiratory passage (Krug, 2012). Given that theciliated cells cannot move around the airways, mucus accumulates.This leads to a congestive infection. The antigens move the virusinto the epithelia cells, and release them from the host cells. It iscrucial that flu is medically diagnosed because it can be confusedwith a common cold, and the presentations may be an indication of theonset of pneumonia, which is a more serious respiratory infection.Moreover, through a proper investigation and medical diagnosis,unwarranted use of antibiotics is prevented. Also importantly,medically diagnosing influenza contributes to prevention of thedisease as a contagious illness within the community.


Forvirulence, Hemagglutinin and neuraminidase are essential (Xu et al.,2012). This is because they are the major target of the virus.Hemagglutinin attaches to the epithelial cells and facilitatecellular infection. On the other hand, neuraminidase slices the bond,and allows for further infection. Identification of the H and Nproteins is necessary for the typing of type A. in the body, theantigenic drift is less frequent than the antigenic drift.Transmission occurs as a result of direct contact with the virus orthrough the air during sneezes. The viral shading may take up to 24hours, during which the host puts others in risk of picking up thevirus from them.

Onceinside the victim, the flu virus multiplies into millions withinseconds (Krug, 2012). Most of the cells get attached to the mucus andother fluids inside the host, and destroys them. This leads to theaccumulation of mucus within the respiratory tract, which is why thepatients often cough and have a runny nose. To counter the virus, theimmuno-cells attack them actively, and they use a lot of energy to dothis, and this is the reason the victim feels exhausted. However, thegeneral impact of the virus depends on some viral and host factors,which determine the severity (Treanor, 2014). Young children and theold people are the worst affected.

Asearlier identified, there are three main antigens of influenza, whichare influenza A, influenza B and influenza C. Of these, influenza Ais the worst. The type A virus is divided into groups according totheir glycoproteins with HA and NA activity. The reason antigen A isquite deadly is that it has high mutation rates, and frequent geneticre-assortment (X). This makes it hard to manage within thecommunity. Moreover, there are many minor changes in its proteinstructure, making it a possible global pandemic. According to Treanor(2014), the type A, besides causing injury to the respiratory system,it has the capability of shutting down the entire immune system.

Whilethe clinical aspects of the virus have remained constant over time,Influenza A has been always dynamic. It can evolve rapidly, becauseof two mechanisms. First, there is an antigenic shift between humansand non-human hosts, and the second is an antigenic drift causingmutations that lead to fast evasion of the host. For this reason,influenza A keeps altering genetically, in response to environmentand drugs. Over the past one century, there have been four majorshifts. The latest was the H1N1 strain, which began circulation in1977 (Krug, 2012). That is why the WHO continues to recommenddifferent immunizations, which are developed based on evidence fromclinical investigation of emerging variants of the influenza A virus.


Bacterialpneumonia is an infection of the lungs. It can affect one or both ofthe lungs. One of the major similarities between influenza andpneumonia is that they both affect the functioning of the respiratorysystem. One of the explanations why Marshall may be at risk ofcontracting bacterial pneumonia is because the bacteria that causesflu leads to the inflammation of the epithelial cells, filling thepassage with mucus. The virus in this mucus may spread to the lungs’air sacs, hence filling them with fluid that may facilitate thedevelopment of bacterial pneumonia. One way of contracting bacterialpneumonia is Community-Acquired Pneumonia (CAP). This is getting aninfection outside a healthcare setting, just as Marshall did.Haemophilus influenzae is one of the leading bacteria thatcause CAP. It lives in the upper respiratory tract, and it is thesecond most common cause of bacterial pneumonia. To add to this,Marshall falls within the description of high risk population, whichis children of his age. At the same time, flu weakens the immunesystem, making it vulnerable to bacterial pneumonia. The combinationof these two facts explains why he might be at risk of contractingbacterial pneumonia.

Thecauses of the development of pneumonia are both extrinsic andintrinsic. Extrinsic causes are not external, while intrinsic causesare related to the host. Given that Marshall already has influenza,there may be loss of protective upper airway reflexes, which may leadto intoxication and other neurologic simulators of pneumonia (Krug,2012). Once the bacteria from the infected upper airways gets intothe lungs parenchyma, a series of events, such as loss of localdefense, may lead to the development of pneumonia.

One of the major symptoms of bacterial pneumonia is cyanosis.Cyanosis is blue coloration of the skin found around the mouth. Thecause of cyanosis is the lack of sufficient oxygen in the blood,hence this color. According to research by Yadlapati et al. (2013),oxygen of the arterial and venous blood in pneumonia are closelyassociated to cyanosis. The research also indicated that cyanosis ofpneumonia patients is a result of insufficient venous bloodsaturation. The mean venous saturation was found to be 31.5%, and inmost cases, patients with cyanosis record a low of 24.7% (Stadie,1919). When pneumonia attacks the system, the body fails to absorbsufficient oxygen through the lungs. In response, the body suppliesthe oxygen to the vital organs first, such as the brain and kidneys.This measure leaves other parts of the body with little supply ofoxygen, hence the blue coloring of the parts around the mouth. Inpneumonia patients, incomplete saturation is the main cause ofdiscoloration. When hemoglobin and oxyhemoglobin in the small bloodvessels occurs, the discoloration results.

References: (2015). Symptoms &amp treatment. Retrieved 5December 2015 from

Krug, R. M. (Ed.). (2012).&nbspTheinfluenza viruses.Springer Science &amp Business Media.

Nakajima, N., Sato, Y., Katano, H.,Hasegawa, H., Kumasaka, T., Hata, S., … &amp Sata, T. (2012).Histopathological and immunohistochemical findings of 20 autopsycases with 2009 H1N1 virus infection.&nbspModernPathology,&nbsp25(1),1-13.

Stadie, W, C. (1919). The oxygen of the arterial and venous blood inpneumonia and its realtion to cyanosis. Rockefeller UniversityPress, No 30 (3):215.

Treanor, J. J. (2014). Influenzaviruses. In&nbspViralInfections of Humans&nbsp(pp.455-478). Springer US.

Xu, R., Zhu, X., McBride, R.,Nycholat, C. M., Yu, W., Paulson, J. C., &amp Wilson, I. A. (2012).Functional balance of the hemagglutinin and neuraminidase activitiesaccompanies the emergence of the 2009 H1N1 influenzapandemic.&nbspJournalof virology,&nbsp86(17),9221-9232.

Yadlapati, A., Grogan, T.,Elashoff, D., &amp Kelly, R. B. (2013). Correlation of a novelnoninvasive tissue oxygen saturation monitor to serum central venousoxygen saturation in pediatric patients with postoperative congenitalcyanotic heart disease.&nbspTheJournal of extra-corporeal technology,&nbsp45(1),40-45.

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