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		⚫	== Semi-protected edit request on 10 May 2022 - Genetics of Pneumonia ==
	== Proportions don't add up. ==
		⚫	{{edit semi-protected\|Pneumonia\|answered=yes}}

			It has been found that vulnerability to Pneumonia and its severity may be linked to underlying genetic mechanisms. These mechanisms, such as the ] (CYP1A1) regulating ] and ], <ref>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. </ref> can influence the efficacy of the immune system which can either be detrimental or beneficial in combating Pneumonia.
	The proportion of cases in the Bacteria and Virus sections are inconsistent and/or dont't add up. Together, they amount to more than 100%. It appears that the proportions recited in the Bacteria section are the proportions of bacterial-pneumonia cases, whereas the proportions in the Virus section are the proportions of total pneumonia cases. The breakdown by adult and children in the Virus section, without a percent value for total virus cases, adds to the confusion. Could someone clarify? <!-- Template:Unsigned IP --><small class="autosigned">— Preceding ] comment added by ] (]) 23:45, 11 March 2020 (UTC)</small> <!--Autosigned by SineBot-->

			Individuals with certain genetic variants can be at risk for a higher susceptibility to Pneumonia. For example, individuals with mutations in ] (BTK).<ref>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</ref> These mutations lead to the development of a disease called ] which inhibits the formation of white blood cells and mature ]. 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 ]. In BTK, the mutation of arg525 to gln was particularly responsible for the lowered functionality of BTK.<ref>Chen, Shaw, Petty, North. (2020, December 11). Host genetic effects in Pneumonia. Cell. https://www.cell.com/ajhg/fulltext/S0002-9297(20)30446-8</ref> Due to decreased white blood cell count, this immune deficiency increases one’s susceptibility to Pneumonia greatly.
	== Links about Coronavirus as cause ==

			A broad ] study aimed at identifying ] 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. <ref>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/</ref> Furthermore, 336/340 ] were shared between Pneumonia and pulmonary function <ref>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/</ref>. 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.
	at link 11
	https://pubmed.ncbi.nlm.nih.gov/21435708/

			There are nine disease genes currently known to increase susceptibility to ]. Three of the disease genes are responsible for the production of ] by alveoli in the lungs: Surfactant protein C (SFTPC), Surfactant protein A2 (SFTPA2), and Adenosine triphosphate-binding cassette subfamily A member 3 (ABCA3).<ref>ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia</ref> Surfactant is a mixture of proteins and fats that helps keep the ] 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 ]: 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 ] and thus they become shorter, which can also increase the risk of developing Pneumonia, amongst many other diseases.<ref>ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia</ref>
	It says that infections comes together bacterial and viral. But on virus infection, it gives feel like, viruses can cause pneumonia.
			Currently, doctors do offer genetic testing for these 9 disease genes in cases where two or more individuals in the same family have Pneumonia.<ref>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/</ref>

			During the COVID-19 pandemic, patients infected with COVID-19 were found to have twice the risk of developing pneumonia.<ref>“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.</ref> Doctors have developed a DNA test that uses multiple polymerase chain reactions to detect DNA and antibiotic resistance of 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.
	"Dual viral infections are common, and a third of children have evidence of viral-bacterial co-infection. In adults, viruses are the putative causative agents in a third of cases of community-acquired pneumonia, in particular influenza viruses, rhinoviruses, and coronaviruses. Bacteria continue to have a predominant role in adults with pneumonia."

			=== References ===
	On page, there are no clear understanding of a thing. The last sentence says, the bacterial infections are dominant.
			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
	Nowdays, because of "corona pandemic" maybe not. I tend not to believe for governments, because of lack pictures of the virus in public domain. Today EM microscopes can easily make resolution of 0.1 nm, what about some virus that 100 nm?

			ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia
	It should be checked twice links. <!-- Template:Unsigned IP --><small class="autosigned">— Preceding ] comment added by ] (]) 02:14, 13 April 2020 (UTC)</small> <!--Autosigned by SineBot-->

			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/
	::I'm not entirely sure what you are asking, but bacteria are the most common cause of Pneumonia in general. In infants and toddlers, RSV is generally the most common cause. The link you provided isn't contradicting itself. Dual infections often happen with viral infections leading to a bacterial infection as well. I'm not sure if that is what you are confused about? ] (]) 23:00, 5 May 2020 (UTC)

			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/
	== "Necrotizing pneumonia" listed at ] ==
	]
	An editor has asked for a discussion to address the redirect ]. Please participate in ] if you wish to do so. <!-- from Template:RFDNote --> ''' —''' ] (]) (])  01:42, 29 April 2020 (UTC)

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

			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.
	{{u\|Mikalra}} added the Jain 2015 NEJM study which showed the limitations of advanced diagnostics in determining the aetiology of CAP (]). This study, while groundbreaking, does not comply with ]. Currently the observation on this problem is cited in the body of the article to a source called EBMED05, which is now 15 years old and should be updated in line with MEDRS.

			“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.
	Oddly the updated ATS guideline does not discuss the poor yield of investigations, but the Jain study is cited in ]. I'm sure this would be a good alternative to EBMED05 for this information as well as some other bits. ] \| ] 14:47, 1 September 2020 (UTC)
			{{Reflist}} ] (]) 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 ] if appropriate.<!-- Template:ESp --> —](]) 05:46, 14 May 2022 (UTC)

			== ] ==
	:This study didn't use 'advanced diagnostics,' but routine laboratory diagnostics such as PCR and urinary antigen testing. You're right that "the observation on this problem is cited in the body of the article to a source called EBMED05;" the Jain study is an example of that problem and is a large and relatively recent report in institutions equipped to address the question.] (]) 15:54, 1 September 2020 (UTC)

			On Misplaced Pages there are 5 links to "]" which then redirects here, yet "hypostatic" does not appear anywhere within this article. The disambiguation for ] only gives one medically relevant definition: "Hypostasis ''(])'', corpse's discoloration". That might be helpful, but it's for a different organ. I can only take an educated guess at what hypostatic pneumonia means, and I wouldn't be sure the right place to describe it if I knew. ] (]) 20:12, 26 September 2022 (UTC)
	For many healthcare settings, the diagnostics used in Jain2015 were definitely "advanced". In the UK the viral PCR panel in pneumonia only includes influenza and RSV unless the host is immunocompromised. ] \| ] 15:01, 2 September 2020 (UTC)

			== ''Cause'' section should probably be updated to take into account the prevalence of SARS-CoV-2 amongst pneumoniae causes ==
	:{{ping\|Mikalra}} The Jain 2015 reference is not an appropriate source, so it has been removed again. Please review ] for explanation. ] \| ] 11:13, 3 September 2020 (UTC)

			This is important because such beliefs may lead the public to not consiser SARS-CoV-2 as a potential cause of pneumonia and lead to unjustified intakes of antibiotics. ] (]) 06:09, 29 September 2023 (UTC)
⚫	== Semi-protected edit request on 21 ~~November~~ ~~2020~~ ==

			== Is pneumonia the same as asthma? ==
⚫	{{edit semi-protected\|Pneumonia\|answered=yes}}
	I would like to enhance this page's coverage of the robustly established relationship between SARS-CoV-2 and pneumonia.

			No, they're different as ] is a ] and can cause ] , but ] is a disease of the ]; filling the ] with a fluid and can result a cause of death, for more information, watch the ] video or search the article ]. Also the article ]
	Change "Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can also result in pneumonia."
			] (]) 11:20, 8 April 2024 (UTC)

			== Add A Fact: "Child dies of pneumonia every 43 seconds" ==
	to
			{{atop

			\| result = {{nd}}—I will go out on a limb to say this is the type of statistic that generally tugs the heartstrings more than it meaningfully educates. It would be an unencyclopedic addition. <span style="border-radius:2px;padding:3px;background:#1E816F">]<span style="color:#fff"> ‥ </span>]</span> 03:10, 7 November 2024 (UTC)
	"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 <ref>https://www.seattletimes.com/seattle-news/health/facts-about-novel-coronavirus-and-how-to-prevent-covid-19/</ref>. Because the cilia cannot function properly, fluid and cellular debris accumulate in the alveoli, which can cause pneumonia <ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373339/</ref><ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431901/</ref>. ] (]) 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. ] \| ] 21:27, 21 November 2020 (UTC)

⚫	{{~~Reflist-~~talk}}

			I found a fact that might belong in this article. See the quote below
	== Please harmonize the internal contradiction about the cause of pneumonia ==
			<blockquote>
			A child dies of pneumonia every 43 seconds
			</blockquote>
			The fact comes from the following source:
			: https://data.unicef.org/topic/child-health/pneumonia/

	In the '''Cause''' section you cite , 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 apart. It's also problematic that the latter is just a review pointing somewhere else - like in the children's telephone game. The former reference is better and an actual research publication. It would be great if somebody rewrote both section to remove or qualify this contradiction and make the article better. JS

			Additional comments from user: It is alarming how these illnesses affect children, highlighting the urgent need to prevent and reverse the current situation.
	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!

			This post was generated using the ] browser extension.
	== Semi-protected edit request on 22 February 2021 ==

			] (]) 16:37, 5 November 2024 (UTC)
	{{edit semi-protected\|Pneumonia\|answered=no}}
			{{abot}}
	] (]) 20:10, 22 February 2021 (UTC)kkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkkmmkmkmkmkmk

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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.

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.
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
Chen, Shaw, Petty, North. (2020, December 11). Host genetic effects in Pneumonia. Cell. https://www.cell.com/ajhg/fulltext/S0002-9297(20)30446-8
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/
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/
ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia
ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia
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/
“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)

Hypostatic pneumonia

On Misplaced Pages there are 5 links to "hypostatic pneumonia" which then redirects here, yet "hypostatic" does not appear anywhere within this article. The disambiguation for hypostasis only gives one medically relevant definition: "Hypostasis (livor mortis), corpse's discoloration". That might be helpful, but it's for a different organ. I can only take an educated guess at what hypostatic pneumonia means, and I wouldn't be sure the right place to describe it if I knew. DAVilla (talk) 20:12, 26 September 2022 (UTC)

Cause section should probably be updated to take into account the prevalence of SARS-CoV-2 amongst pneumoniae causes

This is important because such beliefs may lead the public to not consiser SARS-CoV-2 as a potential cause of pneumonia and lead to unjustified intakes of antibiotics. MathieuSchopfer (talk) 06:09, 29 September 2023 (UTC)

Is pneumonia the same as asthma?

No, they're different as asthma is a difficulty for breathing and can cause tiredness , but pneumonia is a disease of the lungs; filling the alveolus with a fluid and can result a cause of death, for more information, watch the Videowiki/Pneumonia video or search the article Pneumonia. Also the article Asthma 112.198.178.96 (talk) 11:20, 8 April 2024 (UTC)

Add A Fact: "Child dies of pneumonia every 43 seconds"

Not done—I will go out on a limb to say this is the type of statistic that generally tugs the heartstrings more than it meaningfully educates. It would be an unencyclopedic addition. Remsense ‥ 论 03:10, 7 November 2024 (UTC)

The following discussion is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.

I found a fact that might belong in this article. See the quote below

A child dies of pneumonia every 43 seconds

The fact comes from the following source:

https://data.unicef.org/topic/child-health/pneumonia/

Additional comments from user: It is alarming how these illnesses affect children, highlighting the urgent need to prevent and reverse the current situation.

This post was generated using the Add A Fact browser extension.

Laiasolagonzalez (talk) 16:37, 5 November 2024 (UTC)

The discussion above is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion. Categories: