This week I am participating in a debate on how to manage patients with MS on DMTs during the COVID-19 pandemic. Rather than a didactic lecture, I am going to debate several issues with Dr Kerstin Hellwig in relation to two case scenarios (see below), which will highlight the evolving complexities of how to manage MS during these troubling times. If you haven’t registered yet please do so ASAP as places are limited.
Case 1: A 36-year old male has been on ocrelizumab for 2 years; this is his second DMT after having previously received interferon β-1a. He was due his 6th dose of ocrelizumab in March 2020 but this has been postponed indefinitely by his MS centre.
Do you agree with this decision?
What are his chances of getting severe COVID-19 with B-cell depletion?
What about secondary bacterial infections in the event he does get COVID-19?
When will it be safe to resume ocrelizumab treatment?
He is worried that on ocrelizumab therapy he will be unable to show response to an anti-SARS CoV-2 vaccine? Is this a factor to consider when reviewing his treatment?
Would you consider switching his treatment to allow him to be ‘vaccine-ready’ and if yes to what therapy would you switch?
Case 2: A 28-year old woman with highly active RRMS. Previously suffered relapses on dimethyl fumarate in the past. She was treated with oral cladribine in June and July 2019. She is due her second course in late June and July 2020. She had been told be her treating neurologist that she should delay her next course of treatment until after the COVID-19 pandemic is over.
Do you agree with this decision?
How effective is one course of oral cladribine and will it be sufficient to protect her during the current pandemic?
If she received her 2nd year of oral cladribine should she be shielded and for how long?
Could measuring her lymphocyte counts assist in management of this patients?
What is a safe lymphocyte count?
Would delaying her second course of oral cladribine affect her ability to be vaccinated with an anti-SARS-CoV-2 vaccine in the next 12-24 months?
CoI: multiple
#MSCOVID19: new normal
Will we ever get back to managing MS proactively or is this the new normal?
I saw a new patient with probable MS via video consultation this week. He was from a BAME background and I could sense that he has very active MS despite only having had two relatively mild attacks in the last 14 months; an episode of transient diplopia lasting a few days and a mild sensory relapse lasting just shy of two weeks. An MRI done two and a half years ago when he presented with optic neuritis was abnormal. At the moment he is fully functional without any physical disability apart from some persistent fatigue.
Without being able to do a physical examination of this patient (I need to know if there are subtle motor and cerebellar signs), arrange an MRI and do a semi-urgent lumbar puncture to confirm the diagnosis and check neurofilament levels, I can’t do an accurate prognostic profile. If he has definite MS (diagnosis to be confirmed) he would only be eligible for platform therapies and ocrelizumab. But as ocrelizumab is an irreversible treatment I want to be confident of the diagnosis. In addition, I want to be able to offer this patient other options and not only one highly-effective therapy.
What should I do? Well, I have had to tell a sort-of-a-porky and book a Gd-enhanced MRI claiming it is urgent when in reality a diagnostic/prognostic MRI for multiple sclerosis is not a neurological emergency. If this patient has to wait prerequisite 3-4 months, or possibly longer, for us to complete the diagnostic workup because of the COVID-19-induced changes to our MS service there is high likelihood of him having a catastrophic relapse and ending up disabled. ‘Time is Brain’ is how I justified asking for an urgent MRI to myself.
Managing MS during the COVID-19 pandemic is clearly suboptimal and people with MS or possible MS are getting a raw deal. I suspect the same is happening across other specialities. I know it is happening in oncology, I saw it with my own eyes on the medical wards.
Have you seen what is install for the NHS post-COVID-19? The following graph is from a recently launched online ‘NHS Waiting List Estimation Tool’, which shows you the backlog in terms of outpatient appointments that are waiting for the NHS post-COVID-19. People are talking about COVID-19 burnout amongst NHS staff, it is going to be much worse post-COVID-19 when we have to try and clear the backlog created by the reconfiguration of the NHS to deal with COVID-19.
If any of you have had bad experiences, delays in diagnosis, monitoring or treatment please let us know. I shudder to think about how much brain will be lost due to the change in the way we manage MS induced by COVID-19. I sincerely hope this does not become the new normal.
CoI: multiple
#MSCOVID19: antibody positive
Would knowing that you were anti-SARS-CoV-2 antibody-positive change your behaviour?
The WHO and other public health agencies are trying to play down the importance of having antibodies to SARS-CoV-2 saying they don’t yet have the data to say these antibodies protect you from reinfection. Yes and no. No in that we don’t have data yet in relation to SARS-CoV-2, but YES in relation to other viral infections.
If you have been infected with SARS-CoV-2, either asymptomatically or symptomatically (COVID-19), and have developed an antibody response (IgM and/or IgG) to the viral proteins then you are likely to be protected from reinfection in the short (months) and intermediated (years) term. We know from other coronavirus infections that these antibody levels wane with time and the protection is lost, which is why we can get repeated infections with other common coronaviruses. I suspect the same may happen with SARS-CoV-2 as well; in other words, immunity may not be life long.
It is also clear that people who have asymptomatic and mild infections have lower antibody levels than people with severe infections and hence their immunity may be less effective and less longlasting. It also seems that having antibodies to other coronaviruses, i.e. previous coronavirus infections, may protect from getting severe COVID-19. The latter implies that some of these antibodies may be cross-protective.
A lot of effort is going into the testing of convalescent plasma from COVID-19 patients, which contains anti-SARS-CoV-2 antibodies, as a treatment in severe COVID-19. The preliminary results are looking promising. In addition, many academic laboratories and pharma companies are trying to develop commercial neutralizing monoclonal anti-SARS-CoV-2 antibodies as a treatment to prevent and treat COVID-19.
All of this evidence, and basic immunology, suggests that having anti-SARS-CoV-2 antibodies is likely to indicate that you will be immune to reinfection in the short to intermediate-term and even if you were reinfected you would get an asymptomatic or mild infection. The whole premise of herd immunity is built on these assumptions, which is why the WHO and public health officials should get off the fence.
But why are they sitting on the fence? I suspect it has to do with behavioural psychology. They don’t want to see antibody-positive people relaxing their guard and acting normally, i.e. no social distancing, no handwashing, no masks, etc. They would set a bad example for people who are antibody negative.
But knowing what I know about virology and immunology if I was antibody-positive it would be a great relief to me and my family. I would be at low risk of getting COVID-19, I could see patients face-2-face without putting them at risk and I could reassure my family that I am not going to infect them. I could even potentially visit and help vulnerable people living near me without fear of infecting them. It is for these reasons that I had my blood taken yesterday to find out if I have had SARS-CoV-2 infection or COVID-19. If antibody-positive then that severe flu-like illness I had over Christmas could have been the sentinel event. There is increasing evidence that SARS-CoV-2 was already circulating in London in December and I was unwell for 3 weeks with many symptoms compatible with COVID-19. If it was that event I could have been infected by patients or staff whilst working on the general medical wards. If on the other hand, if I was antibody negative then I will remain super vigilant and may not cancel my life insurance policy just yet.
Long et al. Antibody responses to SARS-CoV-2 in patients with COVID-19. Nature Medicine (2020), Published: 29 April 2020.
We report acute antibody responses to SARS-CoV-2 in 285 patients with COVID-19. Within 19 days after symptom onset, 100% of patients tested positive for antiviral immunoglobulin-G (IgG). Seroconversion for IgG and IgM occurred simultaneously or sequentially. Both IgG and IgM titers plateaued within 6 days after seroconversion. Serological testing may be helpful for the diagnosis of suspected patients with negative RT–PCR results and for the identification of asymptomatic infections.
CoI: none
#MSCOVID19: loss of smell
As you are aware that about 30% of people with COVID-19 present with loss of smell (anosmia) and/or loss of taste (ageusia). The loss of smell happens because the coronavirus damages the nerve endings in the olfactory epithelium in the nose. The good news is that it looks like most people recover their sense of smell and taste, but the recovery can take many months. At present we don’t know how many affected people don’t recover smell.
As MS affects smell and taste pathways within the brain it is likely that pwMS are a greater risk of developing abnormal smell and taste function with COVID-19 and may also take longer to recover function. This will need to be studied in the MS population to see if these assumptions or hypotheses are correct.
We do know that losing smell and taste affects your quality of life and is often associated with depression. Is there anything you can do to address this problem? Smell specialists recommend smell training, which can be self-administered. Two very good web resources are run by the UK charities Fifth Sense and Abscent. To start smell training you will need to create your own smell kit; this web resource from Abscent is self-explanatory.
I am interested to know if any of you who have COVID-19 are suffering from a persistent loss of smell and taste and how has it affected your life? Please let us know if smell training makes a difference.
Lapostolle et al. Clinical Features of 1487 COVID-19 Patients With Outpatient Management in the Greater Paris: The COVID-call Study. Intern Emerg Med 2020 May 30. doi: 10.1007/s11739-020-02379-z.
Clinical features of COVID-19 have been mostly described in hospitalized patients with and without ICU admission. Yet, up to 80% of patients are managed in an outpatient setting. This population is poorly documented. In France, health authorities recommend outpatient management of patients presenting mild-to-moderate COVID-19 symptoms. The aim of this study was to describe their clinical characteristics. The study took place in an emergency medical dispatching center located in the Greater Paris region. Patients included in this survey met confirmed COVID-19 infection criteria according to the WHO definition. We investigated clinical features and classified symptoms as general, digestive, ear-nose-throat, thoracic symptoms, and eye disease. Patients were included between March 24 and April 6 2020. 1487 patients included: 700 (47%) males and 752 (51%) females, with a median age of 44 (32-57) years. In addition to dry cough and fever reported in more than 90% of cases, the most common symptoms were general symptoms: body aches/myalgia (N = 845; 57%), headache (N = 824; 55%), and asthenia (N = 886; 60%); shortness of breath (N = 479; 32%) and ear-nose-throat symptoms such as anosmia (N = 415; 28%) and ageusia (N = 422; 28%). Chest pain was reported in 320 (21%) cases and hemoptysis in 41 (3%) cases. The main difference between male and female patients was an increased prevalence of ear-nose-throat symptoms as well as diarrhea, chest pains, and headaches in female patients. General symptoms and ear-nose-throat symptoms were predominant in COVID-19 patients presenting mild-to-moderate symptoms. Shortness of breath and chest pain were remarkably frequent.
CoI: none in relation to this post
#MSCOVID19: New UK Government guidelines
Dare you disagree with Government guidelines? The following are excerpts of the new guidelines posted last night on the Government’s website. Unfortunately, people on ‘immunosuppression therapies sufficient to significantly increase the risk of infection’ are still on the list with no justification of what this risk should be. Based on the experience emerging from pwMS getting COVID-19 on MS disease-modifying therapies (DMTs) this statement is incorrect. On balance pwMS on DMTs don’t appear to be at increased risk of getting COVID-19, severe COVID-19 or dying from COVID-19. In terms of dying from COVID-19, the same risk factors playing out in the general population appear to be playing out in pwMS, i.e. older age, comorbidities and disability. Advanced disability is linked to age; pwMS who are disabled tend to be older.
The good news is that shielding is now less intense and people who are shielding can at least go out and meet with people albeit at a distance. This will be good news for many people. Please be aware that this virus does not appear to be spread outdoors unless you are in close contact with people.
Guidance on shielding and protecting people who are clinically extremely vulnerable from COVID-19 (Updated 31 May 2020)
Clinically extremely vulnerable groups
Expert doctors in England have identified specific medical conditions that, based on what we know about the virus so far, place some people at greatest risk of severe illness from coronavirus. Disease severity, history or treatment levels will also affect who is in this group.
Clinically extremely vulnerable people may include:
- Solid organ transplant recipients.
- People with specific cancers:
- people with cancer who are undergoing active chemotherapy
- people with lung cancer who are undergoing radical radiotherapy
- people with cancers of the blood or bone marrow such as leukaemia, lymphoma or myeloma who are at any stage of treatment
- people having immunotherapy or other continuing antibody treatments for cancer
- people having other targeted cancer treatments which can affect the immune system, such as protein kinase inhibitors or PARP inhibitors
- people who have had bone marrow or stem cell transplants in the last 6 months, or who are still taking immunosuppression drugs
- People with severe respiratory conditions including all cystic fibrosis, severe asthma and severe chronic obstructive pulmonary disease (COPD).
- People with rare diseases that significantly increase the risk of infections (such as severe combined immunodeficiency (SCID), homozygous sickle cell).
- People on immunosuppression therapies sufficient to significantly increase risk of infection.
- Women who are pregnant with significant heart disease, congenital or acquired.
- Other people have also been classed as clinically extremely vulnerable, based on clinical judgement and an assessment of their needs. GPs and hospital clinicians have been provided with guidance to support these decisions.
More information about who has been classed as clinically extremely vulnerable is available on the NHS Digital website.
If you’re still concerned, you should discuss your concerns with your GP or hospital clinician.
Staying at home and shielding
People classed as clinically extremely vulnerable are advised to take additional action to prevent themselves from coming into contact with the virus. If you’re clinically extremely vulnerable, you’re strongly advised to stay at home as much as possible and keep visits outside to a minimum (for instance once per day).
This is called ‘shielding’ and the advice is now updated:
- If you wish to spend time outdoors (though not in other buildings, households, or enclosed spaces) you should take extra care to minimise contact with others by keeping 2 metres apart.
- If you choose to spend time outdoors, this can be with members of your own household. If you live alone, you can spend time outdoors with one person from another household (ideally the same person each time).
- You should stay alert when leaving home: washing your hands regularly, maintaining social distance and avoiding gatherings of any size.
- You should not attend any gatherings, including gatherings of friends and families in private spaces, for example, parties, weddings and religious services.
- You should strictly avoid contact with anyone who is displaying symptoms of COVID-19 (a new continuous cough, a high temperature, or a loss of, or change in, your sense of taste or smell).
The Government is currently advising people to shield until 30 June 2020 and is regularly monitoring this position.
For full details please refer to the Government’s website.
CoI: multiple
#MSCOVID19 musings on Friday #11 post-lockdown
I am trying something new instead of blogging, i.e. a podcast and a vlog. This week I cover some initial thoughts on how COVID-19 has affected MS Services and potentially MS research.
CoI: multiple
#MSCOVID19: Why is cladribine so misunderstood?
Because cladribine and alemtuzumab are classified as immune reconstitution therapies (IRTs), and probably work in a similar way, they are tarnished with the same brush. However, cladribine’s immune depletion and reconstitution, and adverse event profile are very different to alemtuzumab’s and therefore cladribine should be considered on its own when weighing up the risks and benefits of treating highly-active MS during the COVID-19 pandemic. For example, the advice that pwMS need to shield after cladribine treatment is a very harsh call and in my opinion unnecessary. Why?
The following are the points concerning cladribine in the latest version (19-May-2020) of the ABN GUIDANCE ON THE USE OF DISEASE-MODIFYING THERAPIES IN MULTIPLE SCLEROSIS IN RESPONSE TO THE COVID 19 PANDEMIC
EXECUTIVE SUMMARY
5. The effect of DMTS on the risk of SARS-CoV2 infection and COVID 19 disease remains uncertain and we commend pwMS and MS teams to continue to submit data to the UK MS Register study of COVID 19. We recommend that patients are counselled on the effect of a DMT on their individualised risk of COVID 19 disease, taking into account its duration of action; any comorbidities; and also the DMT’s impact on the efficacy of any future SARS-CoV2 vaccine. Patients should be informed if their treatment choice requires shielding [especially cladribine and alemtuzumab].
11. Cladribine should be started cautiously on a case-by-case basis when the risk of SARS-CoV2 is very high. Re-treatment should be delayed until the risk of infection is level 3 or below.
14. pwMS with mild symptoms of COVID-19 should not stop first-line DMTs, but infusions [and cladribine administration] should be delayed until symptoms resolve.
C. THE RISK OF COVID-19 IN PEOPLE WITH MS [PWMS] ON DISEASE MODIFYING THERAPIES [DMTS]
11. There is very limited experience4 of pwMS on cladribine becoming infected with SARS-CoV2 and the SmPC warns of herpetic viral infections being “common”. However, it may be considered on a case-by-case basis. When and where the rate of SARS-CoV2 infection is very high, the risks of increased infection for three months after cladribine administration, and the advice to shield, may outweigh its benefits.
D. DMTS IN PwMS WITH ACTIVE COVID 19 INFECTION
14. pwMS with mild symptoms of COVID-19 should not stop a first line DMT, but infusions [and cladribine administration] should be delayed until symptoms resolve.
We know that anti-SARS-CoV-2 immunity requires innate immune responses (neutrophils and macrophages) and T-cell responses (predominantly CD8+ responses) to clear the virus. Cladribine does not deplete monocytes and neutrophils and has a modest impact on CD8+ve T-cells. Therefore t is unlikely to have a major impact on anti-SARS-CoV-2 immunity.
On cladribine, T lymphocytes are in general depleted by about 40% and the vast majority of patients don’t drop their counts below 500/mm3. In the T-cell compartment, the CD8+ T-cells are much less affected than CD4+ T-cells. This is important because CD8+ T-cells are the cells responsible for fighting viral infections and explains, apart from a small risk of herpes zoster reactivation, why we didn’t see an increase in viral infections compared to placebo in cladribine treated subjects in the phase 3 trial programme.
In the phase 3 programme about a quarter of patients had a transient grade 3 or 4 lymphopaenia, but this tended to occur after the second course in year 2 in subjects who were redosed when their lymphocyte counts in year 1 had not yet recovered to above 800/mm3 (per-protocol dosing). We have used the trial data to model grade 3 and 4 lymphopaenia (<500/mm3), and estimate that less 7% of cladribine treated subjects will develop lymphocyte counts less than 500/mm3 if we stick to the cladribine redosing guidelines. This is important because most of the cases of zoster were in subjects who developed grade 3 or 4 lymphopaenia, which implies the risk of getting herpes zoster in real-life (post-marketing) is likely to be much lower than what we saw in the clinical trials.
Should we be so hung up about the lymphocyte count? When we explore the safety data of oral cladribine, from both the trial programme and post-marketing surveillance, we really don’t see a significant viral infection signal in cladribine-treated subjects. The viral infections that did occur tended to be non-specific upper respiratory tract infections and were mild to moderate. The following presentation is data that we recently presented at the AAN and EAN meetings and illustrates how uncommon viral infections are in pwMS treated with cladribine.
Based on these data I really don’t think it is necessary to for pwMS to shield during the current pandemic. All they need to do is maintain social distancing, practice good personal hygiene and avoid contact with potentially infectious people. This means that pwMS working in high-risk professions (healthcare and care sector workers with direct patient contact) who are treated with cladribine should not have direct patient-facing activities until they have recovered their lymphocyte counts to a safe level (>500/mm3 in people less than 60 years of age and >800/mm3 in those older than 60 years).
Although, cladribine is a remarkably good depleter of B-cells the B-cell numbers return quite quickly. The reconstituted B-cells are initially naive B-cells, which come from the bone marrow and are not memory B-cells. This is important for vaccine-readiness if a SARS-CoV-2 vaccine does emerge.
In comparison to cladribine, ocrelizumab and rituximab are given as maintenance or continuous therapy there is a small increase in the incidence of serious infections over with time and the development of hypogammaglobulinaemia, which is not seen with cladribine. Once the immune system reconstitutes post-cladribine it can fight infections, immune survey the body for cancers and mount immune responses to new viral infections, such as SARS-CoV-2, and vaccines. In relation to vaccines both live and inactivated component vaccines can be given after cladribine.
The other important thing about cladribine is the monitoring requirements are low. Once you have had a course you only need a full blood count to be done 3 and 7 months after starting treatment. The rationale for this is that the 3-month time-point is where the nadir occurs and the 7-month time point is to check for recovery of lymphocyte counts.
Another advantage of cladribine is that as a small molecule it penetrates the CNS; cerebrospinal fluid (CSF) levels are about 25% of what is found the peripheral blood and at a level that would target B- and T-cells within the brain and spinal cord. I think this property of cladribine is very important and is one of the reasons why we are exploring cladribine as a treatment for progressive MS in the CHARIOT-MS trial.
I think cladribine is a very misunderstood DMT and has been hard done by in the COVID-19 treatment guidelines which in general are not evidence-based nor are they necessarily based on basic immunological principles.
As the COVID-19 pandemic is likely to have a long tail with a vaccine 18 to 24 months away I think we the MS community should reconsider our position on oral cladribine as cladribine addresses many of the issues of treating highly active MS in these troubling times and it has the added advantage of leaving people with MS with a reconstituted vaccine-ready immune system if and when a SARS-CoV-2 vaccine arrives.
Please note that I am not saying cladribine is safe; no DMT is safe. However, cladribine has a very well-defined risk-benefit profile that is less risky than what is been suggested in the ABN guidelines. The risk-benefit profile of cladribine simply allows you to counsel patients with highly-active MS about their treatment options during the COVID-19 pandemic and cladribine deserves to be part of that discussion.
CoI: multiple, but in particular I was the principal investigator on the oral cladribine phase 3 trial and have been involved with the development of oral cladribine as a treatment for MS since 2002.
#MSCOVID19 Anti-CD20 therapies and vaccines
Have we optimised the dose of anti-CD20 therapies to target the real MS or smouldering MS, i.e. disease progression independent of relapse activity (PIRA)?
I did an iWiMS webinar on Wednesday covering anti-CD20 therapies and the risk of COVID-19 and severe COVID-19. I covered vaccine responses and how to be vaccine-ready or vaccine responsive to a future SARS-CoV-2 vaccine if you are on an anti-CD20 therapy.
I also discussed optimising the dose of anti-CD20 therapies making the point we may need much higher doses than what we currently use to treat MS. The latter is because we have been blinkered by the impact of anti-CD20 therapy on focal inflammatory events, i.e. relapses and MRI lesions, when the real MS (disability/smouldering MS) appears to more responsive to higher doses of anti-CD20 therapies.
I re-recorded my lecture to spend more time on why these issues are important for people with MS. I have also shared my slides below.
CoI: multiple
#MSCOVID19 info wars
It is one thing calling for scientists to turbocharge the development of a coronavirus vaccine but quite another to get the population to have the vaccine. The anti-vaxxers are organising rapidly and have started circulating content with false information to achieve their aims. The movie plandemic is one example and is covered in a very good article in the New York Times today.
The primary reason I started this blog was to counteract anti-science movements and to provide people with MS and their families a rational interpretation of MS-related research. It is interesting to note that there is now good data science to show how anti-science movements, despite having very few initial supporters, get their message across and sow enough confusion to get undecided people to support their movement.
What I find fascinating, albeit scary, is how dynamic and multifaceted the anti-vaccination campaigns are, which explains their explosive growth in recent times (see figure and paper below). It also shows how gullible people are in general. The study below highlights why we scientists need to fight back using the same tactics. Simply sitting in our ivory towers using traditional media and unidirectional channels will not be good enough to fight the anti-vaccination and other anti-science movements.
I have a vested interest in this. One of our lines of research is to use an anti-EBV vaccine to prevent MS. If people don’t want vaccines how are we going to get this prevention strategy adopted by funders, ethics committees and more importantly the general population?
Can you help? Yes, please help fight fake news, by reporting it and calling it out for what it is. And don’t believe the fabricated conspiracy theories that are peddled to support these anti-science movements. The vast majority of conspiracy theories are wrong.
Johnson et al. The online competition between pro- and anti-vaccination views. Nature published: 13 May 2020
Distrust in scientific expertise is dangerous. Opposition to vaccination with a future vaccine against SARS-CoV-2, the causal agent of COVID-19, for example, could amplify outbreaks, as happened for measles in 2019. Homemade remedies and falsehoods are being shared widely on the Internet, as well as dismissals of expert advice. There is a lack of understanding about how this distrust evolves at the system level. Here we provide a map of the contention surrounding vaccines that has emerged from the global pool of around three billion Facebook users. Its core reveals a multi-sided landscape of unprecedented intricacy that involves nearly 100 million individuals partitioned into highly dynamic, interconnected clusters across cities, countries, continents and languages. Although smaller in overall size, anti-vaccination clusters manage to become highly entangled with undecided clusters in the main online network, whereas pro-vaccination clusters are more peripheral. Our theoretical framework reproduces the recent explosive growth in anti-vaccination views, and predicts that these views will dominate in a decade. Insights provided by this framework can inform new policies and approaches to interrupt this shift to negative views. Our results challenge the conventional thinking about undecided individuals in issues of contention surrounding health, shed light on other issues of contention such as climate change, and highlight the key role of network cluster dynamics in multi-species ecologies.
CoI: we are planning to do an anti-EBV vaccine study to prevent MS
#MSCOVID-19: how to prevent yourself from getting COVID-19 in your own home
What can do I to prevent myself from being infected with coronavirus if someone in my household gets COVID-19?
This is a topic that I have not covered directly, but it is obviously very important and an oversight on my part. Apologies.
The following advice is pretty intuitive and has been hacked from an amazing website, by the Univesity of Southampton, called Germ Defence. If you have the time can I suggest you ignore this post and go through Germ Defence’s short online programme? Although not COVID-19 specific it gives out generic and very sensible advice and only takes 10 minutes to complete.
Ideally, the person who has COVID-19 should spending as much in their own space so that you are less likely to come in contact with them. This could be in their own room or a room in the house that other people should not enter. I am aware that this may not be feasible depending on your circumstances.
It is important not to share a bed with the person who has COVID-19 or you think may have coronavirus.
Please open your windows and limit the amount of time you are in a room with the person who has COVID-19. Also, try to spend time outdoors if you can.
If possible socially distance at home; i.e. try and keep 2 meters away from the person with COVID-19.
Try and organise your home so that you have more space between seats. If it is possible arrange to use shared areas of your home, for example, the bathroom, at different times, so that only one person is in there at any time.
Try and kill any viruses by frequent cleaning. It may be impossible to avoid shared areas of the home, such as kitchens and bathrooms, so keeping them clean, very clean, is important. Try and use a disinfectant to clean surfaces that the affected person may touch, e.g. taps, fridge, door handles, toilet seat, toilet handle, remote controls, computer keyboards, gaming consoles, etc. Wipe down surfaces such as tables, kitchen tops, fridge and freezer doors, seats, remote controls, keyboards, etc.
Place bottles of disinfectant in key areas of the house so that they are quick and handy to use.
Try to avoid sharing or touching things that other people have used, e.g. bottles, kettle, towels, fridge, taps, toothpaste, remote controls, telephone, etc., unless you know that they have been cleaned recently with disinfectant.
It can take up to 3 days (72 hours) for the coronavirus to completely die on hard surfaces. So if there are things that you can’t clean, can you put them somewhere out of the way for 3 days before you use them. If 3 days isn’t possible, then aim for as long as possible.
The person with COVID-19 should wear a mask. Similarly, if you need to spend time with the person who has COVID-19 then wearing a mask can stop you breathing any infectious particles that are spread through coughing and sneezing.
Try and not touch your face, in particular your nose and mouth. This is very hard so you need to concentrate and train yourself to be aware of what your hands and fingers are doing.
Try to limit the time you spend close to other people in the house as well. They may be incubating and shedding the virus asymptomatically.
CoI: none