Covid male sterility papers + HPV, herpes

as previously discussed:

https://onlinelibrary.wiley.com/doi/10.1111/andr.12859

A recent report published in JAMA Network Open revealed that in an analysis 38 semen samples from COVID-19 patients, 6 (four at the acute stage of infection and, alarmingly, two who were recovering) tested positive for the virus by RT-PCR.1 Importantly, at this point, we have no idea whether the actual virus was viable and infectious. Nevertheless, the possibility that this coronavirus could have a pathophysiological impact on the testes was suggested by additional data indicating that active COVID-19 infection dramatically reduced the testosterone-to-LH ratio, suggesting a significant impact on the responsiveness of Leydig cells to LH stimulation.2 In many ways, we should not be surprised by these observations because the blood-testes barrier is known to offer little defense against viral invasion, given the wide range of pathogenic viruses (HIV, hepatitis, mumps, papilloma) that are known to be capable of damaging the testes and rendering the host infertile.

Furthermore, the spike protein that gives the COVID-19 virus its corona is known to target ACE2 (angiotensin-converting enzyme 2), which is highly expressed by several cell types in the testes including Leydig cells, Sertoli cells, and the germ line. As a result of these factors, several opinion pieces have been published already, raising the possibility of testicular damage and infertility consequent to COVID-19 infection.24 

However, it is also possible that the virus could gain access to male germ cells once they leave the testes, either in the epididymis or following ejaculation. In this Opinion Article, I shall be focusing on this post-testicular route of infection pointing out, for the first time, that the mature spermatozoon has all of the machinery needed to bind this virus, fuse with it, and even achieve reverse transcription of the viral RNA into proviral DNA. Such considerations raise the possibility that spermatozoa could act as potential vectors of this highly infectious disease. This happens in insects5—why not us?

IN ADDITION TO-

https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.26667

The other side of COVID-19 pandemic: Effects on male fertility

RECONCILE ABOVE WITH

The outbreak of novel coronavirus disease 2019 (COVID-19) has become a major pandemic threat worldwide. According to the existing clinical data, this virus not only causes respiratory diseases and affects the lungs but also induces histopathological or functional changes in various organs like the testis and also the male genital tract. The renin-angiotensin system (RAS), also ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2.

Because the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases. As the COVID-19 pandemic has affected the male genital system in direct or indirect ways and showed a negative impact on male reproduction, this paper focuses on the possible mechanisms underlying the damage caused by COVID-19 to the testis and also other components of the male genital tract.

SO THE SPIKE PROTEIN ALONE TARGETS ACE2, FOUND IN THE BALLS, LIKE URINE* (*THAT PART WAS A JOKE)

and they wanna force all young men to get it

college age men too

and all young women

when other papers cite it might act like an STD?

Huh.

Highlight:

  • The male genital system presents high ACE 2 expression therefore, it will be highly important to investigate and clarify the relationship between COVID-19 and the male genital tract.

I’m not even a man but I can feel my lady balls shrink reading that.

If we look at the mechanisms of these changes caused by SARS-CoV-2 in the testis, as mentioned above, this virus uses ACE 2 for entry into the cells through its surface spike (S) proteins. S proteins have two subunits, S1 and S2, which are responsible for receptor recognition and membrane fusion. Studies have shown that SARS-CoV-2 enters into the host cell through the binding of its C-terminal domain of the S1 subunit to ACE 2. Additionally, some studies have reported that the level of autophagy receptor SQSTM1/p62 in SARS-CoV-2 infected cells has increased, suggesting a decrease in autophagy flux.

So, SARS-CoV-2 itself or via ACE 2 can directly induce or inhibit the autophagy pathway to achieve virus survival.

As a result, SARS-CoV-2 may cause male reproductive disorders by regulating the level of autophagy in male germ cells.4 On the contrary, another hypothesis is that testis degeneration in the COVID-19 cases is attributed to an increase in testicular temperature as an indirect effect of the inflammation.5

or :-

Do the jabs cause inflammation?

Can spike proteins microwave your balls? Do they nuke your little swimmers?

BUT WAIT. THERE’S MORE.

Another molecule effective at entering the cell of the SARS-CoV-2 is host proteases like transmembrane serine protease 2 (TMPRSS2), which cleaves the viral S protein to induce a conformational change that allows to a fusion of the virus and host cell membranes.34 TMPRSS2 is the key molecule for the successful infection process.35 

This protease is more expressed in human tissues than ACE 2; co-expression of ACE 2 and TMPRSS2 has been shown in the testis, endometrium, and placenta. Researchers investigated the coexpression of these two molecules in the testis and accordingly, they found that ACE 2 is predominantly expressed in myoid cells, spermatogonia, Leydig, and Sertoli cells, while TMPRSS2 is expressed in spermatogonia and (elongated) spermatids of the testicular tissue34 (Figure 3).

I warned you about endometriosis-like function. Maybe naturally having endo is protection?

It’s lifelong inflammation. Kinda like cancer. You literally have to cut the tissues out.

Like Fight Club, they’d have to take your balls.

Shocked men aren’t more protective of their bollocks and demanding ONE safety study.

ModRNA has owners. Repossession is plausible, legally.

STD angle:

“Recent studies have reported that SARS-CoV-2 is easily found in human bodily fluids.35 The presence of a virus in a semen sample is still a topic of discussion and research due to the small number of studies. For example, two different studies have analyzed SARS-CoV-2 presence in semen samples and according to these studies, SARS-CoV-2 (+) semen samples were found in two patients from 23 cured patients and four patients from 15 patients in the acute phase. Another study reported that SARS-CoV-2 was not detected in the semen samples of 34 COVID-19 patients.31

“It is also known that the prostate gland secretes prostate fluid, one of the main seminal components, and muscles of the gland help in pushing the seminal fluid through the urethra during ejaculation.31 The critical point is that, as we mentioned above, a small percentage of the prostate hillock and club cells express ACE 220 and also TMPRSS2 is highly expressed by the epithelium of the human prostate;37 so it is more likely to get SARS-CoV-2 infection, which may affect its secretions.31 

These mechanisms could explain  the SARS-CoV-2 (+) semen samples of the studies.23

“If the presence of the virus in semen is definitively proved by studies, assisted reproduction techniques will also be affected. For instance, testing all male patients like HIV or Hepatitis B/C cases, and using appropriate sperm washing techniques, or paying extra attention to sperm freezing for COVID-19 positive patients.35

“Like SARS-CoV-2, most viruses enter the human body through nasal and oral routes, and viral particles may break the blood-brain barrier.” but don’t worry about shedding?

“It has been reported that the brain cells (glial cells and neurons) also express ACE 2 receptors, making them a possible target to induce neuronal death for SARS-CoV-2. Importantly, the central nervous system plays a critical role in endocrine control and spermatogenesis.31 

The Hypothalamic-Pituitary-Gonadal Axis (HPGa) exerts a vital role in reproduction; in other words, HPGa can inhibit the body’s reproductive functions via hormones.3138

We have our mechanism for sterility, people.

Gonadotropin-releasing hormone (GnRH) expressing neurons from the hypothalamus secretes GnRH and it activates the release of the follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland. A low level of GnRH causes a decrease in FSH and LH, resulting in impaired function of the Sertoli and Leydig cells.31 Ma et al.39 showed that COVID-19 patients had significantly higher serum LH levels but decreased testosterone/LH and FSH levels than healthy men, suggesting potential hypogonadism. Taken together, patients with COVID-19 have been found to present a reduced testosterone/LH ratio, indicating possible subclinical damage to male gonadal function.5 Additionally, activation of the HPGa and subsequent alterations in hormone concentrations play a critical role in poor sperm quality.38

Therefore, besides its direct effects on testis, SARS-CoV-2 may affect fertility indirectly via the central nervous system.31

Like a remote control, for your balls.

In conclusion, all preliminary findings mentioned above suggest that the COVID-19 pandemic affects the male genital system in direct or indirect ways and shows a negative impact on male reproductive health, inducing spermatogenic failure. Additional studies are necessary to answer all the questions and further investigations are warranted, but ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2. As the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases.

SPERMATOGENIC FAILURE

and onward

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13654

Could COVID-19 have an impact on male fertility?

duh

The pandemic caused by Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to several hypotheses of functional alteration of different organs. The direct influence of this virus on the male urogenital organs is still to be evaluated. However some hypotheses can already be made, especially in the andrological field, for the biological similarity of the SARS-CoV and SARS-CoV2. As well as SARS-CoV, SARS CoV-2 uses the ‘Angiotensin Converting Enzyme-2’ (ACE2) as a receptor to enter human cells. It was found that ACE2, Angiotensin (1-7) and its MAS receptors are present, over in the lung, also in the testicles, in particular in Leydig and Sertoli cells. A first hypothesis is that the virus could enter the testicle and lead to alterations in testicular functionality. A second hypothesis is that the binding of the virus to the ACE2 receptor, could cause an excess of ACE2 and give rise to a typical inflammatory response. The inflammatory cells could interfere with the function of Leydig and Sertoli cells. Both hypotheses should be evaluated and confirmed, in order to possibly monitor fertility in patients COVID-19+.

Specific genes relating to male fertility have already been found e.g.

https://onlinelibrary.wiley.com/doi/full/10.1002/mrd.23314

oddly recommended with covid papers?

Male infertility is a rising problem around the world. Often the cause of male infertility is unclear, and this hampers diagnosis and treatment. Spermatogenesis is a complex process under sophisticated regulation by many testis-specific genes. Here, we report the testis-specific gene 1700102P08Rik is conserved in both the human and mouse and highly expressed in spermatocytes. To investigate the role of 1700102P08Rik in male fertility, knockout mice were generated by CRISPR-Cas9. 1700102P08Rik knockout male mice were infertile with smaller testis and epididymis, but female knockout mice retained normal fertility. Spermatogenesis in the 1700102P08Rik knockout male mouse was arrested at the spermatocyte stage, and no sperm were found in the epididymis. The deletion of 1700102P08Rik causes apoptosis in the testis but did not affect the serum concentration of testosterone, luteinizing hormone, and follicle-stimulating hormone or the synapsis and recombination of homologous chromosomes. We also found that 1700102P08Rik is downregulated in spermatocyte arrest in men.

Together, these results indicate that the 1700102P08Rik gene is essential for spermatogenesis and its dysfunction leads to male infertility.

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13712

As the incidence and severity of SARS-CoV-2 are reported to be higher in males than females, Shastri et al. performed a study to determine the time to viral clearance after infection in a total of 68 individuals (48 males and 20 females) with median age of 37 years (Shastri et al., 2020).

They observed that females were able to achieve viral clearance significantly earlier than males.

Furthermore, a serial follow-up evaluation of three families with both male and female patients demonstrated that female members of the same household cleared the SARS-CoV-2 infection earlier in each family (Shastri et al., 2020). In order to determine the reason for delayed clearance in males, they also checked the expression of ACE2 in tissue-specific repositories.

It was found that testicular tissues were one of the tissues showing ACE2 expression in 3 independent RNA expression databases (Human Protein Atlas, FAMTOM5 and GETx). Interestingly, the ovarian tissue showed very low expression of ACE2 (Shastri et al., 2020).

so women may be the red herring here

ACE2 and fat study, so expect fatty side effects

https://onlinelibrary.wiley.com/doi/full/10.1111/dth.13989

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13791

Impact of COVID-19 and other viruses on reproductive health

They admit the male HPV link I posted about previously.

Male infertility is linked to some viral infections including human papillomavirus (HPV), herpes simplex viruses (HSV) and human immunodeficiency viruses (HIVs). Almost nothing is known about severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) effect on fertility. The possible risk factors of coronavirus disease 2019 (COVID-19) infection on fertility comes from the abundance of angiotensin-Converting Enzyme-2 (ACE2), receptor entry of the virus, on testes, a reduction in important sex hormone ratios and COVID-19-associated fever. Recent studies have shown a gender difference for COVID-19 rates and comorbidity. In this review, we will discuss the potential effect of COVID-19 on male fertility and talk about what needs to be done by the scientific community to tackle our limited understanding of the disease. On the other side, we will focus on what is known so far about the risk of COVID-19 on pregnancy, neonatal health and the vertical transfer of the virus between mothers and their neonates. Finally, because reproduction is a human right and infertility is considered a health disease, we will discuss how assisted reproductive clinics can cope with the pandemic and what guidelines they should follow to minimise the risk of viral transmission.

Remember, viral entry via SPs cause inflammation that might cause sterility? WELL-

Virus entry begins when the virus surface enzyme called Spike (S) glycoprotein binds to the angiotensin-converting enzyme 2 (ACE2) located on the host cell membrane (Hoffmann et al., 2020; Wang et al., 2020). S protein contains two different domain regions: S1 and S2, each one has its own role in virus entry. S1 domain is the part that binds directly to the host ACE2 receptor while the S2 domain helps the virus to fuse with the target cell membrane using its functional elements (Glowacka et al., 2011; Hoffmann et al., 2020). This process is also mediated by a Transmembrane Serine Protease 2 (TMPRSS2) located on the surface of the target cell membrane used for the priming of the S protein causing the virus entry (Hoffmann et al., 2020; Shen, Mao, Wu, Tanaka, & Zhang, 2017; Wang et al., 2020).

When the fusion of the virus with the target cell membrane occurs, the virus releases its genome and using the host cell organelles to replicates its RNA and releases new mature virion to target other cells (Boopathi, Poma, & Kolandaivel, 2020; Jiang, Hillyer, & Du, 2020) Figure 1.

wait wait wait the wild virus replicates its RNA too?

minor flex –

3.1 Human papillomavirus (HPV) and its impact on male fertility

Human papillomavirus (HPV) is a non-enveloped DNA virus and sexually transmitted worldwide. In some cases, it causes either warts or precancerous lesions (Ljubojevic & Skerlev, 2014). More than 170 HPV types have been identified and completely sequenced (Chouhy, Bolatti, Pérez, & Giri, 2013). Recent studies suggest that HPV infection affects male fertility. In cases of idiopathic asthenozoospermia, HPV DNA was observed in the sperm cells of infertile patients (Foresta et al., 2010; Lee, Huang, King, & Chan, 2002) confirming its role of infertility. Strong association between HPV infection and impairment of sperm parameters, especially a reduction in sperm motility and concentration, was observed in HPV-infected men (Garolla et al., 2012; Jeršovienė, Gudlevičienė, Rimienė, & Butkauskas, 2019). Garolla and coworkers (Garolla et al., 2012) reported that HPV can bind to the head of a spermatozoon and impair sperm motility in men. Certain sperm DNA exons undergo apoptotic fragmentation on HPV-infected men suggesting that HPV types degrade different exons of important genes (Lee et al., 2002). Collectively, these evidences suggest that HPV plays a role in male factor infertility.

3.2 Herpes simplex viruses (HSVs) and their impact on male fertility

Herpes simplex viruses (HSVs) are enveloped DNA viruses of the family Herpesviridae. HSVs include two distinct viruses HSV-1 and HSV-2 (Whitley & Roizman, 2017). HSVs are sexually transmitted and targets reproductive system. HSV-1 causes oral and, occasionally, genital sores while HSV-2 is common cause of genital herpes which may lead to infertility problems in both males and females. HSV DNA was detected in semen from about 50% asymptomatic infertile males (Amirjannati et al., 2014; Bezold et al., 2007; Monavari et al., 2013; Neofytou, Sourvinos, Asmarianaki, Spandidos, & Makrigiannakis, 2009). A strong association of HSV infection and low sperm count, poor motility, and increased apoptotic cells were reported (Monavari et al., 2013). Haematospermia and a lower seminal volume and abnormal viscosity were found in HSV-2-infected males which indicate prostate dysfunction (Kurscheidt et al., 2018). Bezold et al. (2007) reported significantly reduced sperm concentration and motility as well as reduced citrate concentrations and neutral α-glucosidase in HSV-infected males, suggested impaired epididymal and prostate function.

The manwhore diseases are listed alongside HIV, lol.
The wages of sin is death, in men as well as women.
How will PUAs recover? They won’t. God Willing.

The concern show that SARS-CoV-2 may affect male reproductive organ and thus results in male infertility stems from several observations. Early studies both in China and Italy showed that males are more susceptible to COVID-19 compared to females (Guan et al., 2020; Livingston & Bucher, 2020).

A recent large cohort observational study from United Kingdom featuring around 20 thousands COVID-19 patients reported that males represented 60% of cases and considered the male sex as one of the risk factors for COVID-19 (Docherty et al., 2020).

DS: MRAs: crickets

More alarming is the result of a new systematic review—included 48 recently published articles and 16 databases—where it found that men are more likely to suffer or to die from the complications of COVID-19 compared to women (Serge, Vandromme, & Charlotte, 2020).

DS: suffer or die? Binary?

Large proportion of these vulnerable males is in their childbearing age, and thus their reproductive ability can be affected.

Finally, like influenza, COVID-19 patients suffer from fever, which may affect sperm production. It was reported that febrile illnesses had an impact on semen parameters (Sergerie, Mieusset, Croute, Daudin, & Bujan, 2007). Total sperm count and motility percentage were reduced significantly at days 15, 37 after fever episode before going back to normal after several weeks (Sergerie et al., 2007). Increase of sperm DNA fragmentation index and alteration in the nuclear protein composition of ejaculated spermatozoon were reported after fever episode (Evenson, Jost, Corzett, & Balhorn, 2000).

Different viruses use different routes to enter into the host cells. SARS-CoV-2 uses the same ACE2 receptor used by its cousin, the SARS-CoV virus, with the help of TMPRSS2 (see Figure 1). Single cell expression analysis has detected the expression of ACE2 RNA not only in the lung epithelial cells, but also in several other organs, among them are the kidneys and the bladder (Fan et al., 2020; Lin et al., 2020; Tipnis et al., 2000). Protein expression analysis also confirmed the presence of ACE2 protein in multiple tissues (Hamming et al., 2004).

Interestingly, the highest expression of ACE2 was found in the testes (Fan et al., 2020). The high expression of the ACE2 receptor in the testes raises a concern that the SARS-CoV-2 has the route to enter some if not all testicular cells and thus could cause damage.

To further analyse the types of testicular cells vulnerable for SARS-CoV viruses, Wang et al. studied single-celled ACE2 expression in the human testes (Wang & Xu, 2020). They found that ACE2 is mainly expressed in spermatogonia, leyding and Sertoli cell, while spermatocytes and spermatids had very low expression (Wang & Xu, 2020). Interestingly, TMPRSS2 expression is similar to ACE2, where TMPRSS2 was also enriched in spermatogonia and spermatids. It has been also shown that ACE2 positive spermatogonia cells express genes that are important for virus reproduction and transmission, while ACE2 positive leyding and Sertoli cells express genes that are required for cell–cell junctions and immunity.

Collectively, these results highlight the risk of COVID-19 on testicular cells and on the spermatogenesis process.

The only direct evidence for the effect of COVID-19 on male reproductive function comes from a study where sex hormones namely testosterone (T), luteinising hormone (LH) and follicle-stimulating hormone (FSH) among others were compared between COVID-19 patients and healthy controls. While the T level was not different between the two groups, the ratio of T to LH and the ratio of FSH to LH were significantly decreased in COVID-19 patients (Ma et al., 2020).

This might be the first direct evidence for the influence of COVID-19 on testicles’ ability to produce sex hormones; however, the results of this study should be followed by a more direct analysis of the seminal fluid of COVID-19 patients to evaluate the effect—if any—on sperm count, volume, morphology or motility. It has been reported that SARS-CoV causes orchitis in addition to other complications (Xu et al., 2006), so it is also possible that SARS-CoV-2 may cause the same complication in males.

Y NO DO THIS ON JABBEES?

And it may kill pregnant women only:

Pregnant women have been shown to be at high risk of comorbidity and mortality related to influenza infections (Rasmussen, Jamieson, & Bresee, 2008; Rasmussen, Jamieson, & Uyeki, 2012). The previous SARS infection showed that pregnant women had higher fatality rate (25%) compared to the general population (10%; Wong et al., 2004). With the rise of numbers of pregnant women and children affected by COVID-19, it is worth to know if pregnant women are a high-risk group for COVID-19 death or increased hospitalisation and also to evaluate the risk of vertical transfer either from the mother to the foetus or from the neonates to the mother.

Neonatal health is another important concern in the COVID-19-infected mothers. In a study from Wuhan, 33 neonates were born to mothers with COVID-19, and no health complications were reported except for shortness in breath in four cases (Zeng et al., 2020). Other studies, including less number of cases, did not report any neonatal health issues except for low birthweight (<2,500 g) and premature delivery (Cao et al., 2020; Chen & Lou, 2020). Two other studies from China and Iran reported two neonatal deaths out of 19 cases studied (Hantoushzadeh et al., 2020; Zhu, Wang, et al., 2020). No cases of miscarriages have been reported in the first trimester of COVID-19 pregnancies. Overall, it seems that neonates delivered by COVID-19 pregnant mothers have no increased risk of clinical complications compared to normal pregnancies and some of the reported neonatal complications could be related to mothers’ overall health status rather than a consequence of COVID-19 infection.

Then why jab them?

The risk of vertical transfer of SARS-CoV-2 between the mother and the foetus is possible knowing that the ACE2 receptor is expressed in the placenta and uterus (Levy et al., 2008); however, most published data do not support this predication as most neonates born for mothers affected by COVID-19 tested negative (Chen et al., 2020; Liu et al., 2020; Yu et al., 2020). A few studies have reported a vertical transfer of SARS-CoV-2 from the mother to the neonates (Hantoushzadeh et al., 2020; Yu et al., 2020), but these studies should be carefully interpreted as they occur less frequently and possibly resulted because of the neonatal exposure to SARS-CoV-2 after delivery.

One way to get you on the hook financially is reproductive tech.

Risk of ovarian hyperstimulation syndrome should be taken very seriously during COVID-19 pandemic crisis and all guidelines clearly stated that reproductive endocrinologists should adopt gonadotropin-releasing hormone (GnRH) antagonist as a default protocol for ovarian stimulation with GnRH-agonist trigger to minimise the risk of ovarian hyperstimulation syndrome (OHSS), hospital admissions and intensive care unit (ICU) occupancy (ASRM; Carugno et al., 2020ESHREJSF).

Isn’t that an endometriosis fertility treatment? Odd. So you’re saying it works?

Many health issues related to COVID-19 have been addressed in this review. Pregnancy and maternal health have been discussed. Many reports have evidences against a direct link between COVID-19 and maternal death. Neonates born to a COVID-19 mothers are not at increased risk of adverse health consequence compared to the ones born for COVID-19-unaffected mothers, and the possibility of viral vertical transfer has not been confirmed. Large cohort studies should be followed to confirm these results; additionally, first-trimester COVID-19 cases should be included and be evaluated for the risk of miscarriages.

The gender difference in COVID-19 incidence, comorbidity and death rates—males are at higher risk—requires prompt actions to understand the source of difference biologically and behaviourally. Viral infection by HPV, HSV, HIVs, HBV, HCV and MuV challenges reproductive health and can be considered as a risk factor for male infertility. These viruses have been detected in semen and can impair testicular function. Some viruses such as HIV, MuV and SARS-CoV are associated with orchitis resulting in male infertility, so it would be interesting to study if SARS-CoV-2 can cause the same problem. Because many males at childbearing age are affected by COVID-19, the high expression of ACE2 receptor in the testes and the association of COVID-19 with fever; a multidimensional andrological translational research project was suggested (Salonia et al., 2020). This project aims to develop international collaboration for data registry, hormonal studies and genomic studies to better understand the sex difference for COVID-19 health-related consequences.

re the endo treatment


GnRH agonists are a group of drugs that have been used to treat women with endometriosis for over 20 years [1]. They are modified versions of a naturally occurring hormone known as gonadotropin releasing hormone, which helps to control the menstrual cycle.

At present, the usual length of treatment with a GnRH agonist is 3–6 months. However, in Germany, 12 months treatment with add-back therapy (5 mg of norethisterone per day) has been approved, and other countries may do the same in the future.

Paper: Pneumonic plague as bioweapon, signs

https://www.nejm.org/doi/full/10.1056/NEJMra1409755

In this article, we review the clinical management of deliberate infection with several pathogens of greatest bioweapons concern. On the basis of historical incidents coupled with information on ease of dissemination, contagiousness, mortality rates, public health impact, ability to engender panic, and the need for special preparedness,1-3 the Centers for Disease Control and Prevention (CDC) stratifies pathogens and toxins into three risk categories — A, B, and C — with category A meriting the highest level of concern and preparedness.4,5 In this review, we consider diseases that are caused by category A agents for which there are high-quality clinical data in the unclassified literature (see the Supplementary Appendix, available with the full text of this article at NEJM.org). The category A viral hemorrhagic fever viruses are beyond the scope of this review.

Pneumonic Plague

Pneumonic plague is caused by infection with the fleaborne bacterium Yersinia pestis. This organism, found worldwide and responsible for the “Black Death,” can cause several forms of illness: bubonic (the most common) (Figure 1D), septicemic, and pneumonic plague.41 Because of the focus of this review, only pneumonic plague is discussed.

How fucking fascinating.

CARDINAL FEATURES OF PNEUMONIC PLAGUE

In a deliberate attack, primary pneumonic plague — rather than secondary spread from bubonic or septicemic forms — would occur 1 to 3 days after inhalation of the released bacterium or after droplet transmission from another infected person. The initial presentation of pneumonic plague is nonspecific and is difficult to differentiate from an ordinary pneumonia in its early stages. Hemoptysis, a unique feature, might be present, and rapid progression to respiratory failure and death would occur with greater frequency than in ordinary pneumonias.41

I imagine this would make the death count impossible to distinguish from regular pneumonia.

Remember: “Hemoptysis, a unique feature, might be present…”

About that….

https://tribune.com.pk/story/2146154/1-coronavirus-scare-looms-karachi/

“Maintaining that the 2019-nCoV may cause mild to severe respiratory disease, initially clinically presented as fever, dry cough, myalgia (muscle pain), fatigue and gradually progressing to a more severe productive cough that produces phlegm, episodic headaches, hemoptysis (coughing up blood) and occasional diarrhoea.”

http://www.china.org.cn/china/Off_the_Wire/2020-01/26/content_75650590.htm

“About 55 percent of the patients developed dyspnoea. Less common symptoms were sputum production, headache, hemoptysis and diarrhea.”

https://www.msn.com/en-us/health/medical/is-it-a-cold-the-flu-or-coronavirus-how-to-tell-the-difference/ar-BBZzIsH

“Common coronavirus symptoms can include: — Fever — Dry cough — Shortness of breath — Aching muscles — Fatigue

Less typical coronavirus symptoms: — Phlegm buildup — Headache — Hemoptysis — Diarrhea ”

What PP is versus what we’re told CV is by the MSM.

“Hemoptysis, a unique feature…”

Why has nobody else done it this way? aka the empirical one

look at signs, look at symptoms

unique feature…

u n i q u e   f e a t u r e

I can’t be the only smartass.

But if I must.

DIAGNOSIS OF PNEUMONIC PLAGUE

Because the clinical features of pneumonic plague are nonspecific, diagnosis is largely based on the results of culture. Sputum, blood, or lymph-node aspirates could yield positive culture results. Chest radiography would reveal a severe pneumonic process. Serologic testing can also be useful but would not play much of a role during acute illness.41 Rapid antigen tests are available in regions in which plague is endemic, but none are FDA-approved.

Oh no!

So we’d see tests be useless early on…

and… a shortage of testing kits…

especially for America… who I imagine would call some state of emergency.

TREATMENT AND PREVENTION OF PNEUMONIC PLAGUE

The treatment of pneumonic plague involves a 10-day course of an aminoglycoside antibiotic agent, such as streptomycin or gentamicin. Doxycycline is considered a second-line treatment.41 However, a randomized, controlled trial of potential treatments for bubonic plague revealed equivalency between gentamicin and oral doxycycline; it is unclear whether these results can be extrapolated to pneumonic plague.42 There has been increased interest in the use of fluoroquinolones as primary treatment in mass-casualty settings.42 A 7-day course of doxycycline or ciprofloxacin would be used as postexposure prophylaxis.41 No vaccine against plague is available. Because pneumonic plague can be transmitted from person to person through respiratory droplets, droplet precautions must be implemented for all patients.41

Why do the Chicoms want disease-ridden people in hospitals that can supposedly do nothing for them?

https://www.medscape.com/viewarticle/500621_2

..supplemented with 10% fetal calf serum and penicillin/streptomycin. To make the quail QT6/ACE2 cell line, the gene encoding the receptor for SARS-CoV, human angiotensin-converting enzyme 2…

Rest behind a paywall. Great. It’s a 2005 paper about treating coronavirus.

https://www.nejm.org/doi/full/10.1056/NEJM199709043371004

Yersinia pestis is the causative agent of plague, a zoonotic disease transmitted to humans through flea bites and typically characterized by the appearance of a tender and swollen lymph node, the bubo. Human-to-human transmission can occur, through either the bite of fleas (bubonic plague) or respiratory droplets, causing an overwhelming infection called pneumonic plague.

Our history books missed out that part.

Suddenly those masks don’t look so stupid.

The last plague pandemic began in Hong Kong in 1894 and spread throughout the world, establishing many endemic foci. Antibiotics and enforcement of public health measures significantly decreased the morbidity and mortality associated with the disease but did not allow its eradication. In fact, plague is now considered a reemerging disease1 ….

We report high-level resistance to multiple antibiotics, including all the drugs recommended for plague prophylaxis and therapy, in a clinical isolate of Y. pestis. The resistance genes were carried by a plasmid that could conjugate to other Y. pestis isolates. This report should serve as a warning of the risk of the spread of resistance in Y. pestis, a species previously considered universally susceptible to antibiotics.

…Strain 17/95 was resistant not only to all the antibiotics recommended for therapy (chloramphenicol, streptomycin, and tetracycline) and prophylaxis (sulfonamides and tetracycline) of plague4 but also to drugs that may represent alternatives to classic therapy, such as ampicillin, kanamycin, spectinomycin, and minocycline. The isolate remained susceptible to cephalosporins, other aminoglycosides, quinolones, and trimethoprim, and treatment with trimethoprim, despite its lack of synergism with sulfonamides, most likely led to the patient’s recovery….

https://www.nejm.org/doi/full/10.1056/NEJMoa2001316

The initial cases of novel coronavirus (2019-nCoV)–infected pneumonia (NCIP) occurred in Wuhan, Hubei Province, China, in December 2019 and January 2020. We analyzed data on the first 425 confirmed cases in Wuhan to determine the epidemiologic characteristics of NCIP.

LOL: https://www.theguardian.com/world/2019/nov/13/two-people-diagnosed-with-pneumonic-plague-in-china

identified by local hospitals using a surveillance mechanism for “pneumonia of unknown etiology” that was established in the wake of the 2003 severe acute respiratory syndrome (SARS) outbreak with the aim of allowing timely identification of novel pathogens such as 2019-nCoV.4 In recent days, infections have been identified in other Chinese cities and in more than a dozen countries around the world.5 Here, we provide an analysis of data on the first 425 laboratory-confirmed cases in Wuhan to describe the epidemiologic characteristics and transmission dynamics of NCIP.

Suspicious.

Furthermore, children might be less likely to become infected or, if infected, may show milder symptoms, and either of these situations would account for underrepresentation in the confirmed case count. Serosurveys after the first wave of the epidemic would clarify this question.

re Pneumonic plague above: “Serologic testing can also be useful but would not play much of a role during acute illness.”

If it looks like a duck, walks like a duck and quacks like a duck – sure, it could be a chicken in a duck suit for kinky reasons but I’m inclined on probability to call it a fucking duck.

delays to hospitalization were much longer, with 89% of patients not being hospitalized until at least day 5 of illness (Figure 2). This indicates the difficulty in identifying and isolating cases at an earlier stage of disease. 

re pneumonic plague, above: “The initial presentation of pneumonic plague is nonspecific and is difficult to differentiate from an ordinary pneumonia in its early stages.”

It’s the same hymn sheet. I can’t be the only one seeing this.

Our preliminary estimate of the incubation period distribution provides important evidence to support a 14-day medical observation period or quarantine for exposed persons.

re pneumonic plague, above: “In a deliberate attack, primary pneumonic plague — rather than secondary spread from bubonic or septicemic forms — would occur 1 to 3 days after inhalation of the released bacterium or after droplet transmission from another infected person.”
“The treatment of pneumonic plague involves a 10-day course of an aminoglycoside antibiotic agent, such as streptomycin or gentamicin. ”
“Because pneumonic plague can be transmitted from person to person through respiratory droplets, droplet precautions must be implemented for all patients.41

That takes about…. 14 days.

Our study suffers from the usual limitations of initial investigations of infections with an emerging novel pathogen, particularly during the earliest phase, when little is known about any aspect of the outbreak and there is a lack of diagnostic reagents.

re pneumonic plague: “The initial presentation of pneumonic plague is nonspecific and is difficult to differentiate from an ordinary pneumonia in its early stages.”

re pneumonic plague: “diagnosis is largely based on the results of culture”

Furthermore, the initial focus of case detection was on patients with pneumonia, but we now understand that some patients can present with gastrointestinal symptoms, and an asymptomatic infection in a child has also been reported.17

https://www.cdc.gov/plague/symptoms/index.html

“Pneumonic plague: Patients develop fever, headache, weakness, and a rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery mucous. Pneumonic plague may develop from inhaling infectious droplets or may develop from untreated bubonic or septicemic plague after the bacteria spread to the lungs. The pneumonia may cause respiratory failure and shock. Pneumonic plague is the most serious form of the disease and is the only form of plague that can be spread from person to person (by infectious droplets).”

That’s why hide it.

https://www.mayoclinic.org/diseases-conditions/plague/symptoms-causes/syc-20351291

“Pneumonic plague affects the lungs. It’s the least common variety of plague but the most dangerous, because it can be spread from person to person via cough droplets. Signs and symptoms can begin within a few hours after infection, and may include:

  • Cough, with bloody mucus (sputum)
  • Difficulty breathing
  • Nausea and vomiting
  • High fever
  • Headache
  • Weakness
  • Chest pain

Pneumonic plague progresses rapidly and may cause respiratory failure and shock within two days of infection. Pneumonic plague needs to be treated with antibiotics within a day after signs and symptoms first appear, or the infection is likely to be fatal.”

repeating coronavirus paper:

Although delays between the onset of illness and seeking medical attention were generally short, with 27% of patients seeking attention within 2 days after onset.

Complete coincidence.

Back to CV paper generally

Early infections with atypical presentations may have been missed, and it is likely that infections of mild clinical severity have been under-ascertained among the confirmed cases.18 We did not have detailed information on disease severity for inclusion in this analysis.

In conclusion, we found that cases of NCIP have been doubling in size approximately every 7.4 days in Wuhan at this stage. Human-to-human transmission among close contacts has occurred since the middle of December and spread out gradually within a month after that. Urgent next steps include identifying the most effective control measures to reduce transmission in the community. The working case definitions may need to be refined as more is learned about the epidemiologic characteristics and outbreak dynamics. The characteristics of cases should continue to be monitored to identify any changes in epidemiology — for example, increases in infections among persons in younger age groups or health care workers. Future studies could include forecasts of the epidemic dynamics and special studies of person-to-person transmission in households or other locations, and serosurveys to determine the incidence of the subclinical infections would be valuable.14

re Pneumonic plague above: “Serologic testing can also be useful but would not play much of a role during acute illness.”

These initial inferences have been made on a “line list” that includes detailed individual information on each confirmed case, but there may soon be too many cases to sustain this approach to surveillance, and other approaches may be required.19

Study allowed by Chinese Government, who arrested 8 doctors for trying to release some piece of information, can’t imagine what.

If they’d been told to give people antibiotics for a virus though, I imagine they had some pointed questions.

Especially if the Chicoms wanted to buy time to buy up global supply and produce more.

https://en.wikipedia.org/wiki/Pneumonic_plague

“Pneumonic plague is a severe lung infection caused by the bacterium Yersinia pestis. Symptoms include fever, headache, shortness of breath, chest pain, and cough. They typically start about three to seven days after exposure.”

Long lag time.

PP can cause meningitis, which might explain the headache.

from CV article above: “”Common coronavirus symptoms can include: — Fever — Dry cough — Shortness of breath — Aching muscles — Fatigue”

https://www.cdc.gov/coronavirus/about/symptoms.html

“For confirmed 2019-nCoV infections, reported illnesses have ranged from people with little to no symptoms to people being severely ill and dying. Symptoms can include:

  • Fever
  • Cough
  • Shortness of breath”

All three just so happen to be also the symptoms of pneumonic plague.

“CDC believes at this time that symptoms of 2019-nCoV may appear in as few as 2 days or as long as 14 after exposure”

So three, three days on the low end. How familiar.

About dat headache symptom…

Click to access 23064.pdf

Coronaviruses as Encephalitis

-Inducing Infectious Agents

so why is headache not described as a symptom?

also

“In acute encephalitis, viral replication occurs in the brain tissue itself, possibly causing destructive lesions of the
gray matter, as was described after herpes simplex virus (HSV), rabies, or some arbovirus infections. ”

Yes, herpes can reach the brain. Again, I must remind you. Yes, it can.

This concludes why I’m banned from appearing on tv (pretty much).

I couldn’t make it up

The wages of sin are death.

https://www.theguardian.com/society/2018/jun/21/alzheimers-link-to-herpes-virus-in-brain-say-scientists

“Free love”

How’s that sexual revolution?

Still doubling down huh?

Yeah, your parents couldn’t have a point, they were just squares.

I don’t think it is the herpes, although that damage is real.

I think it’s the aluminium still.

STDs and child disease

I was reading this

https://www.theguardian.com/science/blog/2017/oct/16/itvs-victoria-illustrates-how-19th-century-sexism-helped-syphilis-to-spread

because I wrote that piece on syphilis.

As well as causing infertility, syphilis can induce miscarriages and stillbirths. Some children born to syphilitic mothers will never show any signs of infection. Others die in infancy or develop serious health complications.

And antibiotics are failing.

And it struck me, wait, that continues on. It never disappeared.

Except women are still the ones blamed despite men counting more partners in studies (most sluts are men, mathematically and willingness plays into this) and there are links to psychiatric conditions.

No pill for ruining your legacy.

http://www.sciencemag.org/news/2017/02/herpes-virus-may-be-trigger-autism

Top of my mind.

“It’s a very important paper,” says Karen Jones, a behavioral neuroimmunologist at the University of California, Davis, who was not involved with study. “It’s also really important to remember that not every mom who has HSV-2 is going to have a kid with autism.”

The idea virgin brides will prevent any STDs or medical grievances is absurd.
Chastity applies to men as well for good reason. Purity is physical?

This idea either sex can both have their cake and eat it is childish. Have it All is a lie sold to weaklings. Adults make difficult decisions, you don’t pop into the Perfect Husband/Wife mold overnight, it takes years and plenty of omissions!
To put your future wife and children at risk like that when sex toys exist should count as abuse, since abused children have similar problems, including catching the diseases of the parents.

http://bigthink.com/videos/kathleen-mcauliffe-and-impact-of-disease-on-sexual-attraction-and-fecal-transplants

The microbiome sexuality link remains strong.
Any sex, but especially anal.
Wow, I wonder which sex was brainwashed into being obsessed with that?

The focus on women is based on the fact we carry, we aren’t the source of the problem.
That’s medically impossible to be both cause and effect.
Fresh infections cause the most damage. Whose fault is that?

Feminist trying to remove stigma of STIs

http://www.independent.co.uk/life-style/love-sex/i-have-herpes-woman-tells-the-world-about-life-and-love-with-the-sti-to-battle-stigma-10185284.html

There is a stigma for a reason. (Birth defects and miscarriage).

It’s terrible you weren’t told by the presumably random man who gave it to you, it’s awful wearing protection didn’t stop it, but if you choose to have casual sex – it happens. I’d feel sorry for you if you got it from your husband, though. Because again, it’s female fertility that suffers.

How clean is your pap smear? That metal speculum?

http://medidex.com/medical-devices/99-issues-relating-to-disposable-and-reusable-vaginal-specula.html

I was tipped off about this and I’m mortified as a woman.

“SMTL carried out a survey of mainly GP practices with regard to their use of disposable and reusable vaginal specula. Disturbing reprocessing practices were revealed in some surgeries, including some practices completely ignoring MDA advice. Most users performing in-house reprocessing were not complying with best practice as recommended by the Department of Health through their various device bulletins and HTM documents.

Many GP practices could reduce the level of risk by investing in better reprocessing systems, contracting out their reprocessing completely, or through the use of disposable specula. Practices may also be able to reduce their costs by using disposable specula or by contracting out their reprocessing.”

Imagine the lawsuits. The NHS has been pushing ALL women above a fixed age to have this exam.

“There is little in the literature relating to the issues surrounding reusable vaginal specula.”

Perhaps this is partially behind the soaring HPV rates?

“They concluded that HPV infected cells can be found on instruments inserted into the vagina of women with HPV infection, and that if these instruments are not cleaned and sterilized properly, they will be a potential source of infection for subsequent patients.”

HPV can cause cancer, btw.

“correct pasteurisation (immersion in water at 80 C for 5 minutes) would inactivate papillomaviruses, herpes viruses, and HIV.

That isn’t the same as clean. Are women told this? I’ve never heard of it. Uninformed consent. Bleeding is a “common” side effect of these exams, hence the HIV bolded.

“Although there is little in the literature regarding cross-infection from inadequately sterilized specula, we live in an increasingly litigious society. One strand in the defence against patient claims of cross infection from poorly decontaminated and sterilized instruments would be complete documentation of the process, including logbooks, written operating procedures, training records, test results and maintenance data. The other possibility is to use pre-sterilized disposable CE marked equipment from a reputable manufacturer. Either would make it more difficult for a patient to mount a successful legal claim.”

Oh, they don’t really care about patients at all, they want the NHS to avoid the mass of lawsuits.

Here’s Feminist Midwife explaining the infectious problems with these supposedly ‘safe’ exams, I wish feminism would complain about important problems like this (guys, you’re sticking your dick in this too, it matters, and you might think a woman’s cheating when she isn’t).

http://www.feministmidwife.com/2013/03/12/very-clean-pap-smears/

Apparently, even the disposable ones can be contaminated by the awkward, common habit of touching lots of things with gloved hands and then the speculum, when it’s clean out of the container. (We must assume it’s clean out of the container or I’m out. Yet checking manufacturing/personnel would be vital).

Can someone look into probes for me? I can only find information like this: “High-Level Disinfection destroys all microorganisms except some endospores” ~ forum source

And forceps are a problem too. Contamination news story in Canada Don’t these devices have hinges? Springs? Things that gather dirt and grime and cannot, in most cases, be taken apart for cleaning?

IV fluid too?? FFS!

Study on HPV infection from non-sexual means at the clinic e.g. gloved hands!
And HPV is in semen.
“The incidence of anal cancer among homosexual men exceeds that of cervical cancer in unscreened women.”
I’m going to stop looking now, it’s too disgusting.

UPDATE

Further information

http://jid.oxfordjournals.org/content/176/4/1076.full.pdf “The data suggest that further study of nonsexual spread of high-risk genital HPV via fomites is warranted.”

http://www.cancer.org/acs/groups/cid/documents/webcontent/003167-pdf.pdf “A woman with multiple sexual partners should use condoms to lower her risk of sexually transmitted infections no matter what other form of contraception she uses.” Rather defeats the purpose of the Pill, doesn’t it? “Certain types of sexual behavior increase a woman’s risk of getting HPV infection, such as having sex at an early age and having many sex partners.” Why don’t men get the vaccine when they’re passing it on?

Update: it gets worse, the lubes used by doctors are probably bad for us too.

Should you be worried about your vagina absorbing the ingredients in your lube?