Treating COVID with antibiotics could be a much easier way to make people better off
A recent study conducted in an Egyptian hospital showed that treating moderate to severe COVID patients with one of two antibiotics (ceftazidime or cefepime, in combination with a steroid) resulted in similar recovery times compared to patients receiving treatment standard.
If you have a cold, don’t ask your doctor for antibiotics, that’s the rule of thumb. They are for bacterial infections, not viral ones. We are not only told that they will not work, but that by using antibiotics when they are not needed, we are helping bacteria to become resistant to them.
Yet, in a recent study conducted in an Egyptian hospital, we showed that treating moderate to severe COVID patients with one of two antibiotics (ceftazidime or cefepime, in combination with a steroid) resulted in similar recovery times compared to to patients receiving standard treatment.
This standard treatment, authorized by the Egyptian government and endorsed by the World Health Organization, consisted of at least seven different drugs, suggesting that treating COVID with antibiotics could be a much easier way to make things better.
Yet in doing so, we went against established medical convention that antibiotics are not for viruses. So why did we break this rule?
Traditionally, creating new drugs to treat disease takes a long time. Trying to develop a new treatment can take years, is very expensive and has a very low success rate. Nevertheless, this process is generally acceptable when it comes to targeting common diseases.
However, this time-consuming process is not sustainable when there is a high threat posed by an emerging infectious disease, such as Zika, Ebola, Mers and now COVID. Without quick action or ready-to-use effective treatments, emerging diseases can turn into pandemics that claim many lives. There have been hundreds of millions of confirmed cases of COVID, for example, and more than 5.4 million deaths worldwide.
For this reason, faced with a new threat, drug developers and big pharma are looking for faster alternatives to the typical drug development process. A practical strategy is drug reassignment. This is where drugs already created and approved for one-time use are tested to see if they can also help treat the new disease.
Since the drugs have already been shown to be safe and so much is known about how they work, this is potentially a much less risky and time-consuming way to find a cure for the new disease. This is a strategy that has been used often in the past – and my colleagues and I wanted to try using it during COVID due to the pressing need.
Find a new purpose
Drug repurposing starts with using computational techniques to model how existing drugs and the new pathogen — in this case, the coronavirus — might interact. Promising drugs are then tested in real laboratory studies to validate the computer results and confirm that they might be useful in the clinic.
In the case of a viral disease such as COVID, a drug whose reuse is envisaged must have one of these three qualities: it must either be able to inhibit one or more stages of the replication cycle of the coronavirus; relieve the bad effects of the virus; or manipulate the immune system so the body can deal with the virus.
And surprisingly, antibiotics are often the substances that show potential. Although viruses are different from bacteria, they are sometimes also susceptible to antibiotics. The statement that antibiotics don’t work against viruses doesn’t apply 100% of the time.
For example, in response to the Zika crisis about five years ago, a US study evaluated over 2,000 drugs already approved by the US Food and Drug Administration to see if they could potentially be used safely during the pregnancy against the virus. The study found that the antibiotic azithromycin could reduce the proliferation of the virus in the brains of unborn children, potentially protecting against microcephaly, a condition caused by the virus in newborns.
In addition, tests have also shown that the antibiotic novobiocin has a strong antiviral effect against the Zika virus. And a 2016 drug redirection study in Thailand identified minocycline as a promising antiviral drug against dengue virus, with the antibiotic inhibiting the growth of the virus at different stages of its life cycle.
All of these studies gave us confidence that repurposing antibiotics as COVID treatments was a plausible idea.
But why ceftazidime or cefepime?
Research had previously shown a number of antibiotics to be effective in preventing the coronavirus from reproducing in laboratory tests – including ceftazidime and others in the same class, known as ‘beta-lactams’ . So we knew that this class of drugs had potential.
And when we ran computer simulations of how ceftazidime and cefepime (another beta-lactam) interact with the virus, they were both effective in disrupting its protease, a key enzyme the virus uses to reproduce. .
Ceftazidime and cefepime are also widely used broad-spectrum antibiotics to treat critically ill patients who develop infections in hospital. As COVID patients often end up with other infections at the same time, we also thought these drugs could help seriously ill patients by eliminating other infections they might have, helping to prevent conditions such as pneumonia. .
However, it is not clear to what extent the effect of the antibiotics in our study on Egyptian hospitals was due to the elimination of co-infections compared to what was due to them by attacking the coronavirus directly. Indeed, the idea that beta-lactams have antiviral properties is based on computer simulations and laboratory experiments – it has not been definitively proven.
Nevertheless, our work has demonstrated that these drugs can fight the coronavirus. Although we should always use antibiotics with caution, they may therefore have a role to play against COVID in the future.
Eid, RA, et al. (2021) Efficacy of ceftazidime and cefepime in the management of patients with COVID-19: single center report from Egypt. Antibiotics. doi.org/10.3390/antibiotics10111278.
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