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Semi-protected edit request on 21 November 2020

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I would like to enhance this page's coverage of the robustly established relationship between SARS-CoV-2 and pneumonia.

Change "Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can also result in pneumonia."

to

"Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can also result in pneumonia. The virus infects and destroys the cells of the alveoli, both those that are ciliated and those that produce mucus and surfactant . Because the cilia cannot function properly, fluid and cellular debris accumulate in the alveoli, which can cause pneumonia . Teddymhill (talk) 02:06, 21 November 2020 (UTC)

This can only be supported with very high quality references. A newspaper article would not be sufficient, nor an animal study. The pathogenesis is probably more complicated than you have indicated: there is diffuse alveolar damage and immunothrombosis. Hence not supporting this addition at this time. JFW | T@lk 21:27, 21 November 2020 (UTC)

References

  1. https://www.seattletimes.com/seattle-news/health/facts-about-novel-coronavirus-and-how-to-prevent-covid-19/
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373339/
  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431901/

Please harmonize the internal contradiction about the cause of pneumonia

In the Cause section you cite #28 Jain 2015, a paper which puts viruses well ahead of bacteria in causing pneumonia. Later, in the Bacteria section you state that "Bacteria are the most common cause" with a different reference (#35 Sharma 2007), putting a direct contradiction into this article, just a few lines

PS: Just as in the telephone game the numbers have been misquoted. It says "20% haemophilus" but it was 20 cases or 7% in the original paper!

Good catch here @JS. I can help make this edit. As for the review article, this is one of differences between medical writing on Misplaced Pages and writing for a peer-reviewed medical journal- the use of the WP:MEDRS guideline preferring high-quality secondary sources to primary research sources. It is not always perfect- i.e.- susceptibilty to the 'telephone game' errors, however, some feel that there are strengths as well to this approach given that anyone can edit these articles. I will not have time to review the citations for a few days, but will try to circle back soon. Citations to consider: Primary source, presently ref # 28 Jain et al 2015. . Outdated secondary source (does not meet WP:MEDDATE): JenOttawa (talk) 16:39, 22 November 2021 (UTC)
P.S- if anyone wants to beat me to this improvement please do go ahead!!! There are a lot of outdated references in the aforementioned sections. JenOttawa (talk) 16:46, 22 November 2021 (UTC)

References

  1. Jain, Seema; Self, Wesley H.; Wunderink, Richard G.; Fakhran, Sherene; Balk, Robert; Bramley, Anna M.; Reed, Carrie; Grijalva, Carlos G.; Anderson, Evan J.; Courtney, D. Mark; Chappell, James D. (2015-07-30). "Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults". The New England Journal of Medicine. 373 (5): 415–427. doi:10.1056/NEJMoa1500245. ISSN 1533-4406. PMC 4728150. PMID 26172429.
  2. Sharma, Sat; Maycher, Bruce; Eschun, Gregg (May, 2007). "Radiological imaging in pneumonia: recent innovations". Current Opinion in Pulmonary Medicine. 13 (3): 159–169. doi:10.1097/MCP.0b013e3280f3bff4. ISSN 1070-5287. PMID 17414122. {{cite journal}}: Check date values in: |date= (help)

Keiko died from this! This is for real!!!

Here is the whale Keiko of the free willy movie, it DOES exist as a disease in wild animals! "Killer whale Keiko dies of pneumonia.." The Free Library. 2003 The Register Guard 19 Mar. 2022 https://www.thefreelibrary.com/Killer+whale+Keiko+dies+of+pneumonia.-a0112803638 --82.207.238.166 (talk) 11:50, 19 March 2022 (UTC)

Semi-protected edit request on 10 May 2022 - Genetics of Pneumonia

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It has been found that vulnerability to Pneumonia and its severity may be linked to underlying genetic mechanisms. These mechanisms, such as the CYP1A1 gene (CYP1A1) regulating inflammatory responses and sepsis, can influence the efficacy of the immune system which can either be detrimental or beneficial in combating Pneumonia.

Individuals with certain genetic variants can be at risk for a higher susceptibility to Pneumonia. For example, individuals with mutations in Bruton’s tyrosine kinase (BTK). These mutations lead to the development of a disease called X-linked agammaglobulinemia which inhibits the formation of white blood cells and mature B cells. Without functional BTK, the development cycle of B lymphocytes is stopped at the pre-B cell stage which results in the loss of mature lymphocytes in the bone marrow and lymphatic system. In BTK, the mutation of arg525 to gln was particularly responsible for the lowered functionality of BTK. Due to decreased white blood cell count, this immune deficiency increases one’s susceptibility to Pneumonia greatly.

A broad mapping study aimed at identifying loci associated with pulmonary function and Pneumonia in humans mapped 137 loci of interest. 116 of the 137 loci were found to be responsible for both pulmonary function and susceptibility to Pneumonia. Furthermore, 336/340 SNPs were shared between Pneumonia and pulmonary function . Genes that are responsible for pulmonary function play an integral role in overall lung development and inflammation pathways that are key to an immune response. Individuals with an impaired pulmonary function due to certain predisposed developmental, inflammatory, or cardiovascular traits were found to be at a higher risk for Pneumonia. This high degree of overlap of genes and the correlation between pulmonary function traits and susceptibility to Pneumonia could mean that there is a major genetic factor.

There are nine disease genes currently known to increase susceptibility to idiopathic interstitial Pneumonia. Three of the disease genes are responsible for the production of surfactant by alveoli in the lungs: Surfactant protein C (SFTPC), Surfactant protein A2 (SFTPA2), and Adenosine triphosphate-binding cassette subfamily A member 3 (ABCA3). Surfactant is a mixture of proteins and fats that helps keep the alveoli from collapsing when a person exhales and also protects lung cells from infection. Mutations at these loci have age-dependent effects, however, it is not yet possible to predict which family members will develop Pneumonia at what age. The other six disease genes are associated with telomeres: Telomerase reverse transcriptase , Telomerase RNA component , Dyskerin , Telomere repeat binding factor 1-interacting nuclear factor 2 , Regulator of telomere elongation helicase , Poly(A)-specific ribonuclease . Mutations in these genes impede the ability of the body to repair damage in the telomeres of chromosomes and thus they become shorter, which can also increase the risk of developing Pneumonia, amongst many other diseases. Currently, doctors do offer genetic testing for these 9 disease genes in cases where two or more individuals in the same family have Pneumonia.

During the COVID-19 pandemic, patients infected with COVID-19 were found to have twice the risk of developing pneumonia. Doctors have developed a DNA test that uses multiple polymerase chain reactions to detect DNA and antibiotic resistance of streptococcus pneumoniae in a patient’s blood sample. This can be done in the span of four hours which is much quicker than the conventional method of growing bacterial cultures which is prone to false negatives due to patients receiving antibiotics before the sample is collected. The test expedites the treatment procedure with doctors being able to prescribe antibiotics at an earlier stage and making it more effective in the treatment of Pneumonia.

References

Chen, Shaw, Petty, North. (2020, December 11). Host genetic effects in Pneumonia. Cell. https://www.cell.com/ajhg/fulltext/S0002-9297(20)30446-8

Genetics in community-acquired Pneumonia : Current Opinion in Pulmonary Medicine. (2019). LWW. https://journals.lww.com/co-pulmonarymedicine/Abstract/2019/05000/Genetics_in_community_acquired_Pneumonia.17.aspx

ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia

Khadzhieva, Kuzovlev, Salnikova. (2019, December). Pneumonia: host susceptibility and shared genetics with pulmonary function and other traits. PubMed. https://pubmed.ncbi.nlm.nih.gov/31487037/

Kropski, YOung, Cogan, Mitchell, Lancaster, Worrell, Markin, Liu. (2017, June 1). Genetic Evaluation and Testing of Patients and Families with Idiopathic Pulmonary Fibrosis. National Library of Medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5470751/

Waterer, Wunderink. (2010). Genetic susceptibility to Pneumonia. PubMed. https://pubmed.ncbi.nlm.nih.gov/15802163/

Guin, Debleena, et al. “Human Genetic Factors Associated with Pneumonia Susceptibility, a Cue for Covid-19 Mortality.” MedRxiv, Cold Spring Harbor Laboratory Press, 1 Jan. 2021, https://www.medrxiv.org/content/10.1101/2021.06.03.21258106v1.full.

“DNA Test Can Quickly Identify Pneumonia in Patients with Severe COVID-19, Aiding Faster Treatment.” ScienceDaily, ScienceDaily, 15 Jan. 2021, https://www.sciencedaily.com/releases/2021/01/210115091340.htm.

  1. Guin, Debleena, et al. “Human Genetic Factors Associated with Pneumonia Susceptibility, a Cue for Covid-19 Mortality.” MedRxiv, Cold Spring Harbor Laboratory Press, 1 Jan. 2021, https://www.medrxiv.org/content/10.1101/2021.06.03.21258106v1.full.
  2. Genetics in community-acquired Pneumonia : Current Opinion in Pulmonary Medicine. (2019). LWW. https://journals.lww.com/co-pulmonarymedicine/Abstract/2019/05000/Genetics_in_community_acquired_Pneumonia.17.aspx
  3. Chen, Shaw, Petty, North. (2020, December 11). Host genetic effects in Pneumonia. Cell. https://www.cell.com/ajhg/fulltext/S0002-9297(20)30446-8
  4. Khadzhieva, Kuzovlev, Salnikova. (2019, December). Pneumonia: host susceptibility and shared genetics with pulmonary function and other traits. PubMed. https://pubmed.ncbi.nlm.nih.gov/31487037/
  5. Khadzhieva, Kuzovlev, Salnikova. (2019, December). Pneumonia: host susceptibility and shared genetics with pulmonary function and other traits. PubMed. https://pubmed.ncbi.nlm.nih.gov/31487037/
  6. ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia
  7. ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia
  8. Kropski, YOung, Cogan, Mitchell, Lancaster, Worrell, Markin, Liu. (2017, June 1). Genetic Evaluation and Testing of Patients and Families with Idiopathic Pulmonary Fibrosis. National Library of Medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5470751/
  9. “DNA Test Can Quickly Identify Pneumonia in Patients with Severe COVID-19, Aiding Faster Treatment.” ScienceDaily, ScienceDaily, 15 Jan. 2021, https://www.sciencedaily.com/releases/2021/01/210115091340.htm.

Editor3456123123 (talk) 00:26, 11 May 2022 (UTC)

 Not done: it's not clear what changes you want to be made. Please mention the specific changes in a "change X to Y" format and provide a reliable source if appropriate. —Sirdog (talk) 05:46, 14 May 2022 (UTC)
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