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A Theory of P. Jirovecii co-infection in severe COVID-19 Cases

  1. The Problems of a Simple-Virus Explanation of COVID-19 (and Clues).

    1. Unpredictable Outcomes: There is a disparity in severity of symptoms and case fatality rate (both among similar individuals and between geographic areas) that is not adequately explained. This disparity is causing mass confusion on the the nature of and best treatment for COVID-19. There are too many other cases of young, healthy persons being swiftly killed by COVID-19, and old people getting through it with little trouble. These outlier cases need better explanation.

    2. Lungs packed with sticky granular mucus is not typical of a viral infection. (but is more typical of bacterial/fungal infections)

    3. COVID-19 appears to respond to anti-parasitical treatments such as Hydroxychloroquine (HCQ) and Ivermectin, which are not known to be directly effective against viruses.

    4. Unpredictable case progression timelines.

    5. Negative/severe COVID-19 outcomes appear to correlate with high population density and/or congregate housing. Mild cases appear to correlate with lower population density areas.

    6. Large and growing number of asymptomatic cases, falling case fatality rate.

  2. A Theory: COVID-19 associated ARDS is a result of fungal co-infection of Pneumocystis Jirovecii (aka P. Carinii), the organism that causes Pneumocystis Pneumonia (PCP).

    1. While with either organism often causes only asymptomatic infections on it’s own, the presence of both can induce ARDS. COVID-19 caused lymphopenia allows for the rapid progression into severe PCP.

    2. Secondary fungal infection would somewhat explain the difficulty in turning critical cases around. Standard treatments of steroids, antibiotics, ventilator would not help at all, perhaps make it worse. However this particular organism does respond to anti-parasitic medications (more below).

    3. This theory is easily tested by PCR testing of sputum from ARDS-state COVID-19 patients.

  3. Asymptomatic Cases: This theory would better explain an abundance of asymptomatic COVID-19 cases. For most symptoms to manifest it is required that:

    1. T-Lymphocyte count is depleted by SARS CoV-2 to a critical level (around 400/μL), and;

    2. Either;

      1. Latent P. Jirovecii infection already in patient, or;

      2. Exposure to P. Jirovecii during period of severe lymphopenia.

  4. Unpredictable case progression timeline – Two possible paths to ARDS:

    1. Fast Track: Pre-existing, latent P. Jirovecii colonization being brought to a florid state by SARS-CoV-2 induced lymphopenia.

    2. Slow Track: Newly acquired infection of P. Jirovecii to COVID-19 patients already in immunosuppressed state if/when exposed to colonized healthcare workers or other P. Jirovecii asymptomatic carriers.

  5. Progression to ARDS: COVID-19 and PCP have identical symptom progressions into an ARDS state. COVID-19 progression to ARDS is predicted by T-lymphocyte count in the range of around 400/μL, same as severe PCP onset (median 375/μL). (Normal T-lymphocyte count for healthy adults is 2000-4000/μL). Additionally both PCP and COVID-19 also have the unusual symptom of the lungs being filled with sticky, granular mucus that cannot be coughed up, leading to death by hypoxemia.

  6. Response to anti-parasitic medications: Both COVID-19 and PCP appear to respond to anti-parasitical treatments (HCQ, Ivermectin, Artemisinin, et al.), despite the fact that neither organism is technically a parasite. The P. Jirovecii organism was originally classified at a protozoan disease for this reason and is often referred to as the protozoan P. Carinii. If critical-COVID ARDS is the result of P. Jirovecii, this would explain the apparent efficacy of HCQ as both an ARDS treatment and prophylaxis, and would suggest new avenues of treatment (such as Artemisinin-types). For example, the nation of Madagascar is using A. Annua (a common malaria treatment) as a COVID-19 prophylaxis with apparent success (CFR 0.0095%).

  7. Latent, asymptomatic P. Jirovecii colonies are extremely common in healthy adults. Some regions have an overall latent infection rate of greater than 50% of adults. Latent, colonizing infections can persist for long periods of time, unnoticed but still transmissible. Symptoms (PCP) only develop if a colonized individual becomes severely immunosuppressed, such as with AIDS, organ transplant, or taking a course of steroids like Prednisone. P. Jirovecii fungus can only replicate in respiratory tissue, and therefore is more commonly found circulating asymptomatically among high-density populations and congregate housing environments. Furthermore, latent P. Jirovecii infections have been shown to be transmissible while totally asymptomatic. If considered as a complicating co-infection with COVID-19, it would explain the apparent increase in negative outcomes of COVID-19 patients from these high-density populations.

  8. VIII. Healthcare workers with latent respiratory P. Jirovecii colonization are a known cause of nosocomial transmission to immunosuppressed patients, resulting in PCP. This phenomenon has seen in repeated outbreaks in kidney transplant clinics. HIV/AIDS patients also frequently suffer from PCP, so the COVID/AIDS comparisons may be more accurate than first suspected.

  9. Large and growing number of asymptomatic cases, falling case fatality rate: If severe COVID is the result of two concurrent infections, public-health emergencies will only manifest in areas where P. Jirovecii is endemic among the population. Such a place would have a high population density, crowded community spaces (public transit), poor indoor ventilation, and high levels industrial pollution (suppressed immune systems). NYC, N. Italy, and Wuhan are all good candidates. Since the virus spreads more easily than the fungus, it would stand to reason that the virus would spread beyond areas where it’s public health impacts were first noticed (high numbers of severe cases and deaths), and into areas where you would have high percentages of positive tests, but also high levels of asymptomatic cases and low death rates due to the absence of P. Jirovecii. And indeed, outside of cities like those described above, public health emergencies are not materializing except in medical and congregate living facilities likely to be P. Jirovecii reservoirs (nursing homes).

  10. Possible Conclusions:

    1. All patients seen for COVID-19 should have Lymphocyte count done, as well as PCR testing of sputum for P. Jirovecii in cases with shortness of breath.

    2. Treatments should include measures for stabilizing/raising T-Lymphocyte count (perhaps donor plasma), and PCP prophylaxis. Sulfamethoxazole, HCQ, Ivermectin, and Artemisinin should be considered for trials in this application.

    3. Measures should be taken in hospital settings to prevent transmission of P. Jirovecii. Procedures have been already established for organ transplant clinics.

    4. Steroids should not be given when contraindicated by lymphopenia.

    5. Public health measures should be focused on areas already shown to have problems with endemic fungal and bacterial respiratory pathogens (legionella may be a good indicator), and congregate living facilities.