Povidone-iodine: The “new-old” ally against COVID-19

Abstract

The SARS-CoV-2 pandemic has infected over 95 million people worldwide and over 2 million in Colombia. The healthcare personnel (HCP) in our country account for more than 3,800 cases and 197 deaths until January 2021 (1). Being a highly contagious virus, it has changed medical practice and exposed HCP who are at risk of becoming victims with every patient they see. The primary routes of transmission of SARS-CoV-2 are through respiratory droplets and contact with infected patients or any nearby surfaces or objects which the patient has used. Airborne transmission of the virus is possible when conducting aerosol generating procedures (2). Among HCP, those who are more exposed to aerosols are more vulnerable to get the disease: anesthesiologists, emergency physicians, internists and intensivists, as well as ENT doctors, ophthalmologists, maxillofacial surgeons, head and neck surgeons, dentists, gastroenterologists, pulmonologists, respiratory therapists, scrub nurses, nursing staff, inter alia. SARS-CoV-2 had a strong affinity for angiotensin II converting enzyme (ACE2) which is mainly present in the nasal and oral mucosae, where it initially replicates before invading the lung (3). The nasalpulmonary axis has been suggested as the route for the development of pneumonia in patients. The saliva is the primary reservoir, with a high viral load of COVID-19 (1.2x108 infectious copies /mL). The virus may be detected in the saliva in 91.7 % of the patients. A key factor to fight the disease is to reduce the viral load in the saliva and nasal secretions, in order to reduce the transmission of the disease; hence, the potential use of povidoneiodine has been suggested (3-5). Since 1800 iodine has been recognized as an effective bactericidal agent. Then povidone-iodine was discovered in 1955, as an ideal and less toxic alternative for surgical asepsis, with a gram-positive, gramnegative, spores, fungal, viral and protozoa germicidal effect. Among the oral antiseptic agents, it has the broadest spectrum to reduce any bacterial, viral or fungal load, and more effective virucidal action than chlorhexidine or benzalkonium chloride (6). Povidone-iodine disrupts the metabolic pathways in the cell wall of microorganisms causing irreversible damage. It is a potent virucidal agent, which inhibits neuraminidase and hemagglutinin, blocking the attachment of the virus to the cell receptors and preventing the release and spread of the virus from the infected cells. Its efficacy has been assessed in similar coronaviruses such as SARS and MERS (7). In vitro studies have shown that it also destroys SARS-CoV-2 when used for gargling or as mouth rinse at 0,23 %, for 15 seconds, reducing the viral activity by 99.99 %. Experimental models have shown that povidone-iodine at a concentration of 1,25 % does not alter the ciliary motility and is well tolerated by the nasal epithelium (8). Povidone-iodine has been well tolerated in the upper airway at a dose range between 1 % to 10 %, with no evidence of thyroid dysfunction, olfactory disorders or changes in mucociliary clearance, even with extended use (9). The lack of solid evidence has prevented WHO and FDA approval of povidone-iodine, specifically for use in SARS CoV-2. A recent Cochrane systematic review failed to find any evidence for the systematic adoption of this intervention; however, it highlights the relatively few publications on the topic (10). Considering the efficacy of povidone-iodine with similar viruses and its routine use for nasal and oral decontamination in surgery, several countries have developed protocols for its use. It may be considered a useful public health intervention and part of the personal protection strategy (11). For HCP, these protocols (Table 1) suggest the routine use of povidone-iodine as nasal drops