Discuss about the Immunology for Infection Control in Healthcare.
Fever refers to a temporal rise in one’s body temperature above the normal 37 degrees Celsius, usually as a sign of an illness and/or infection. Peters fever developed after the immune system detected the presence of harmful foreign microbes that needed to be destroyed. In response, the liver generated sufficient heat in the body according to Lehne, Moore, Crosby, & Hamilton (2013), that could destroy the microbes and at the same time activate the body’s protective cells such as the CD8+ T Cells and the neutrophils to fight the microbes.
a. First, the increase in body temperature usually beyond 37.9 degrees Celsius leads to the death of bacterial microbes within the body (Lehne et al, 2013). On the other hand, an increase of this temperature to 38.8 degrees from the normal 37.0 degrees Celsisus will render the viruses in the body to be unable to undergo replication and are immobilized thus preventing them from spreading to other parts of the body.
b. Secondly, fever activate lymphocytes to fight viruses, bacteria among other pathogens that have entered the body through various routes of entry such as inhalation, ingestion, among others. For instance, the high body temperature resulting from a fever triggers CD8+ cytotoxic T-cells of the immune system which helps in the destruction of cancer-causing cells and the virus-infected cells (Craft et al 2015). Research shows that CD8+ cytotoxic T-cell numbers increase with an increase in temperature of an individual. Body temperature increase as a result of fever also enables the activation of neutrophils whose role is to target and destroy bacterial cells that are infectious. Thus, according to Lehne et al, 2013), hyperthermia triggers the activities of lymphocytes and more so the CD8+ cytotoxic T Cells which destroy both tumour and virus-infected cells. The enzymatic activities and the high temperatures makes the pathogens unable to survive and therefore die off.
Once the Influenza virus reaches the respiratory tract it leads to inflammation tracheal superficial epithelium necrosis and even on the bronchial mucosa (Boland & Santall, 2011). Usually it predisposes the body to secondary bacterial invasion. Among the most dreaded bacterial infection include pneumonia. The body can be able to develop immunity to the Influenza virus but there is need to prevent the bacterial infection. Therefore, Peter was given phenoxymethylpenicillin for 10 days as prophylaxis with an intention of preventing the development of any bacterial load, suspected to have been part of the infection (Bullock & Maria, 2014). Through this prophylaxis, Peter will not be infected and/or suffer from bacterial infections including pneumonia.
Phenoxymethylpenicillin is useful in the treatment of mild and moderate gram positive bacterial infections. Administered orally, Phenoxymethylpenicillin can be useful for prophylaxis to protect a patient from other susceptible organisms (Lee & Bishop, 2016). The drug destroys the inter-peptide links of the peptidoglycan molecule within the cell wall of the gram positive bacteria. Cell walls that have the cross-links of the peptidoglycan weak and vulnerable to collapsing disintegrate particularly when the infectious bacteria try to divide. Human cells are eukaryotic and thus have no cell wall making Phenoxymethylpenicillctive very safe for humans as the cells cannot be damaged. Some of the gram positive bacteria treated by this drug include Streptococcus pneumonia and viridans among others.
Antibiotics cannot be effective in treating a viral infection because they have no target on any viruses. Viruses replicate very fast and can only be targeted by anti-viral medication and/or vaccinations (Lee & Bishop, 2016). Unlike in bacterial infections where antibiotics target to destroy the cell wall of the pathogens and/or interfere with cellular DNA repair for instance, viruses have no cell wall and their replication mechanism make it impossible for antibiotics to destroy them.
The first mode of transmission that must have led to Peter’s flu infection is through inhaling influenza contaminated air from an infected person (Craft, 2016). This must have been through talking with an infected individual within 6 feet, who spread the viral droplets to him.
Secondly, Peter might have acquired the virus from by touching deposited cough/sneeze nuclei and/or droplet from an infected person and then without his knowledge rubbed his nose, mouth and eyes with the virus cough nuclei. Usually, cough and sneeze nuclei are left deposited on surfaces. People who have habit of rubbing their nose, eyes and mouth are likely to transmit the virus to themselves (Porth, 2014). These droplets can be deposited on surfaces within a 6-feet distance from a coughing and/or sneezing infected individual.
To break the modes of transmission of influenza virus, there is need for those suffering from the flu to use handkerchiefs while coughing and sneezing by partially blocking their mouths and noses (Lee & Bishop, 2016). This prevents the splashing and spreading of droplets and nuclei to others.
Secondly, people should avoid congested and crowded places as they may most likely inhale the flu nuclei from others.
The physiological basis for the first symptoms including fever, running nose, sneezing and lymphadenopathy indicate the body’s initial immune response to pathogenic infections. The fever for instance indicates that the immune system wants to destroy harmful microbes by raising the body temperature (Porth, 2014). The running nose is as a result of the body’s immune response of producing excess mucus that contains protective macrophages that not only deter the movement of microbes but also destroy them. Lymphadenopathy is a result of the lymphatic system’s response to infections by providing a platform for macrophage and pathogen interaction in the lymph nodes (Bullock & Maria, 2014). Sneezing is an immune response that is partly voluntary and partly involuntary aimed at ejecting pathogens within the upper respiratory tract.
The second symptoms include aching joints, tiresome feeling and headaches. Physiologically, aching of joints and feeling tired is as a result on insufficient energy within the body. This means that the body’s energy production has gone down as a result of infection and the energy used up in generating heat to destroy the microbes. As the immune system responds to the infection, the body has to generate sufficient heat to destroy the viruses and probably the bacterial load within it. Thus, much energy is by priority allocated to heat generation, leaving other essential organs with lesser energy (Boland & Santall, 2011). Headaches are a result of reduced oxygen supply to the blood as the throat is infected, making Peter the patient, to breath in air in short breaths. The short breaths taken in have insufficient levels of oxygen necessary for the body that now requires more energy. This is the same reason as to why the patient feels tired.
The third signs of influenza include swollen and red throat, and a yellow-white exudate on the tonsils. Physiologically, the redness is as a result of increased temperature and pain on the throat resulting from destruction of infectious microbes by the neutrophils and CD8+ cytotoxic T-cells (Engelhardt, 2012). Another reason is that once the Influenza virus reaches the respiratory tract it leads to inflammation tracheal superficial epithelium necrosis and even on the bronchial mucosa. This inflammation is the cause of the swelling, heat and pain leading to redness (Marieb & Hoehn, 2016). The yellow exudate on the tonsils results also as a by-product of this inflammation in the upper respiratory tract. Therefore, as the body fights the pathogens, the parts of the immune system within the patient are put to full functionality so as to return the body to its normal state.
One of the major differences between viruses and bacteria is that bacteria have all the cell organelles necessary for growth and for multiplication and they that they reproduce by binary fusion. Viruses on the other hand majorly carry information in form of DNA and RNA as a protein/membranous package (Engelhardt, 2012). They therefore have no organelles for reproduction and instead rely on those of the host cell for reproduction. Secondly unlike bacteria which rely on themselves for reproduction, viruses integrate into the DNA and RNA of the host cell to be translated into multiple forms of the same virus. The host cell will then burst, releasing the multiple forms of the virus. Therefore, a virus must have a host cell to reproduce.
References
Boland, M. (Director), Santall, J. (Presenter), & Video Education Australasia, (2011). Infection Control in healthcare (Videorecording). Bendigo Australia: VEA.
Bullock, S., Maria, E. (2014), Fundamentals of Pharmacology (7th ed.), Frenchs Forest, Australia: Pearson Australia
Craft, J., Gordon, C., Heuther, S., McCance, K., Brashers, V., & Rose, N. (2015) Understanding pathophysiology 2. Chatswood, Australia Elsevier.
Lee, G., & Bishop, P. (2016). Microbiology and Infection Control for health Professionals (6th Ed.). Melbourne, Victoria: Pearson Australia.
Lehne, R. A., Moore, L., Crosby, L., & Hamilton, D. (2013), Pharmacology for Nursing Care (8th ed.), St Louis, Mo: Saunders/Elsevier.
Marieb, E.N., & Hoehn, K. (2016), Human Anatomy and Physiology (10th global Edition), Harlow, UK: Pearson Education.
Porth, C. M., & G. (2014), Pathophysiology Concepts of altered health states (9th ed.), Philadelphia, PA: Lippincott Williams & Wilkins.
Engelhardt, O. (2012). Many ways to make an influenza virus – review of influenza virus reverse genetics methods. Influenza and Other Respiratory Viruses, 7(3), 249-256. https://dx.doi.org/10.1111/j.1750-2659.2012.00392.x
Influenza A virus hemagglutinin (HA); Influenza A virus neuraminidase (NA); Influenza A virus matrix protein M2 (M2); Influenza A virus PB1-F2 protein (PB1-F2). (2009). Science-Business Exchange, 2(18), 6-6. https://dx.doi.org/10.1038/scibx.2009.753
Influenza A virus vaccine H1N1/influenza virus vaccine. (2012). Reactions Weekly, &NA;(1421), 31. https://dx.doi.org/10.2165/00128415-201214210-00102
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