What is Long COVID?
USDHHS Guidance on “Long COVID” as a Disability Under the ADA, Section 504, and Section 1557
"This guidance explains that long COVID can be a disability under Titles II (state and local government) and III (public accommodations) of the Americans with Disabilities Act (ADA),3 Section 504 of the Rehabilitation Act of 1973 (Section 504),4 and Section 1557 of the Patient Protection and Affordable Care Act (Section 1557).5 Each of these federal laws protects people with disabilities from discrimination.6 This guidance also provides resources for additional information and best practices. This document focuses solely on long COVID, and does not address when COVID-19 may meet the
legal definition of disability. The civil rights protections and responsibilities of these federal laws apply even during emergencies.7 They cannot be waived."
Is ‘Long Covid’ similar to ‘Long SARS’?
COVID Long-Haulers Are Fighting for Their Future
Life After COVID-19 | Institute of Human Anatomy Update
This is a thorough explanation of why a negative COVID test is not
required to return to work or school for people who have tested positive
for COVID 19 in the past and who had symptoms. This is the official
stance of the CDC as well (the exception to this is if a person needs to
travel, a negative test may be required in that case). This seems
counterintuitive to many people because people are assuming that a
negative test will indicate when a person's infection is over and they
are no longer contagious. The reason is basically because the testing
is done as PCR testing, which detects viral RNA particles regardless of
whether the infection is current or past, meaning it does not
differentiate who is contagious and who is not. Anyone who has had
COVID 19 could test positive regardless of whether they are still sick
or over the infection. Instead of a testing-based strategy to determine
who is safe to return to school, work, or daily life, a symptom-based
strategy is what is being used. The guidelines for this are that a
person is required to quarantine for at least 10 days after onset of
symptoms, have no fever (without fever-reducing meds such as Tylenol or
ibuprofen), and have improvement in symptoms. For patients with severe
cases or who are immune-compromised 20 days of quarantine is required
instead of 10. A symptom-based strategy also uses fewer tests so that
those tests will be there if needed for a spike in cases, etc.
What we now know about long COVID and our brains
Long COVID is also called Post-COVID-19 Neurological Syndrome (PCNS) in research.
What is Post-COVID-19 Neurological Syndrome?
"The
physical stress of infection might end, but COVID-19 patients can carry
emotional and neurological scars from the experience for months and
years, often in the form of post-traumatic stress disorder (PTSD). For
example a large Chinese study earlier this year revealed that an
alarming 96.2 per cent of recovering COVID-19 patients have clinical
evidence of severe post-traumatic stress disorder (PTSD).... COVID-19
and acute stroke share common pathobiology at a cellular level."
The COVID-19 Pandemic and Caregiver Discrimination Under Federal Employment Discrimination Laws
The symptoms of an infection are caused by the person's own body fighting the pathogen, not the pathogen itself. Understanding why the body is fighting the way that it is is a good place to start in figuring out how to resolve the disease. The most common symptoms of long COVID are fatigue, shortness of breath, coughing, joint pain, and chest pain. Some people have additional symptoms including headache, fever, depression, pounding heart (palpitations) and a loss of taste.
Posttraumatic stress disorder in convalescent severe acute respiratory syndrome patients: a 4-year follow-up study
Mast cell activation symptoms are prevalent in Long-COVID
"In the present study, there was a high prevalence of MCA symptoms
in LC patients prior to MCAS treatment. The symptom data and spider web
plots illustrated that LC patients’ symptoms are virtually identical to
those experienced by MCAS patients. These results support, but do not
provide definitive proof of, our earlier hypothesis that LC might often
arise out of a SARS-CoV-2-driven provocation of primary or secondary
MCAS. Theories to explain promotion of MCA in LC include: 1) complex interactions of stressor-induced cytokine storms with epigenetic-variant-induced states of genomic fragility to induce additional somatic mutations in stem cells or other mast cell progenitors; 2) cytokine or SARS-CoV-2 coronavirus activation of mast cells and microglia; 3) dysregulation of genes by SARS-CoV-2 coronavirus leading to loss of genetic regulation of mast cells; 4) development of autoantibodies which react with immunoglobulin receptors on mast cells, and 5) increase in Toll-like receptor activity by the coronavirus.
In this study, MCA symptoms were significantly increased in LC. Uncontrolled, aberrant mast cells may in part underlie the pathophysiology of LC. Inflammation caused by COVID-19 is complicated, and other immune disturbances that have been seen in the acute infection such as excess dysfunction of the macrophage and serotonin release from platelets might or might not play roles in LC"
Some long Covid patients may have hidden damage to their lungs - BBC NewsA special type of MRI, which measures how well oxygen can get into a person's bloodstream from the lungs, is showing some sort of widespread inflammation in the lungs that can seriously reduce oxygen exchange.
Long-term neurological manifestations are being seen in people who have recovered from COVID 19,
including in children. These can include acute encephalitis but may
also appear as more general symptoms such as headache, fatigue,
confusion, and more serious problems such as memory problems, problems
with speech, psychotic symptoms, even seizures. In some cases this
seems to be part of the Multisystem Inflammatory Syndrome in Children
that can be one presentation of COVID 19. References and relevant
studies:
Invasive Aspergillosis as an Under-recognized Superinfection in COVID-19
"Taken together, these early findings suggest that invasive aspergillosis
may be an important, yet under-recognized, complication of SARS-CoV-2
infection. The frequency of post-COVID-19 aspergillosis is likely to
differ significantly between hospitals and geographic sites, as has been
observed with postinfluenza aspergillosis"
"We are living in an unprecedented era of fungal infections,
characterized by the emergence of previously unrecognized human
pathogens and well-recognized pathogens causing new manifestations of
disease. The spectrum of “at-risk” populations for invasive Aspergillus
infections is expanding, with increased appreciation of diseases such
as chronic pulmonary infection and postinfluenza aspergillosis. Fungal
superinfections are difficult to distinguish from severe COVID-19 based
on clinical or imaging findings, and a high index of suspicion is
necessary to diagnose aspergillosis. If aspergillosis is a complication
of COVID-19 in a significant minority of critically ill hospitalized
patients, failure to recognize or diagnose the disease will likely lead
to excess mortality. For this reason, it is imperative to establish the
incidence, clinical characteristics, and outcomes of COVID-19-associated
aspergillosis as quickly as possible."
In Long COVID, GI and Mental Health Symptoms 'Go Hand in Hand'
"In an analysis of nearly 750 individuals who had COVID-19, those with mental health symptoms either before or after their infection were more than 16 times more likely to have post-COVID GI symptoms (adjusted odds ratio [aOR] 16.5, 95% CI 6.97-38.9), reported John Blackett, MD, MS, of the Mayo Clinic in Rochester, Minnesota, and colleagues."
EWAS of post-COVID-19 patients shows methylation differences in the immune-response associated gene, IFI44L, three months after COVID-19 infection.
"We explored the epigenetic signatures of COVID-19 in peripheral blood
using data from an ongoing prospective observational study of COVID-19
called the Norwegian Corona Cohort Study. A series of EWASs were
performed to compare the DNA methylation profiles between COVID-19 cases
and controls three months post-infection. We also investigated
differences associated with severity and long-COVID. Three
CpGs-cg22399236, cg03607951, and cg09829636-were significantly
hypomethylated (FDR < 0.05) in COVID-19 positive individuals.
cg03607951 is located in IFI44L which is involved in innate response to
viral infection and several systemic autoimmune diseases. cg09829636 is
located in ANKRD9, a gene implicated in a wide variety of cellular
processes, including the degradation of IMPDH2. The link between ANKRD9
and IMPDH2 is striking given that IMPDHs are considered therapeutic
targets for COVID-19. Furthermore, gene ontology analyses revealed
pathways involved in response to viruses. The lack of significant
differences associated with severity and long-COVID may be real or
reflect limitations in sample size. Our findings support the involvement
of interferon responsive genes in the pathophysiology of COVID-19 and
indicate a possible link to systemic autoimmune diseases."
Long COVID and employment
COVID-19 Workplace Safety Plan | PDF version
Job Accommodation Network, definition of a disability
EEOC What You Should Know About COVID-19 and the ADA, the Rehabilitation Act, and Other EEO Laws
EEOC Coronavirus 19
How to treat Long COVID?
Safety and efficacy of low dose naltrexone in a long covid cohort; an interventional pre-post study
