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Taiwan opens borders to tourists as restrictions eased after 2.5 years
Rabbit virus has evolved to become more deadly, new research finds
A common misconception is that viruses become milder over time as they become endemic within a population. Yet new research, led by Penn State and the University of Sydney, reveals that a virus — called myxoma — that affects rabbits has become more deadly over time. The findings highlight the need for rigorous monitoring of human viruses, including SARS-CoV-2, monkeypox and polio, for increased virulence.
“During the COVID-19 pandemic, many people have incorrectly assumed that as the SARS-CoV-2 virus becomes endemic, it will also become milder,” said Read. “However, we know that the Delta variant was more contagious and caused more severe illness than the original strain of the virus, and Omicron is even more transmissible than Delta. Our new research shows that a rabbit virus has evolved to become more deadly, and there is no reason why this couldn’t happen with SARS-CoV-2 or other viruses that affect humans.”
According to Read, myxoma was introduced to Australia in the early 1950s to quell an out-of-control non-native rabbit population. Known as ‘myxomytosis,’ the disease it caused resulted in puffy, fluid-filled skin lesions, swollen heads and eyelids, drooping ears and blocked airways, among other symptoms. The virus was so deadly that it killed an estimated 99.8 percent of the rabbits it infected within two weeks.
Over time, however, the virus became milder, killing only 60% of the rabbits it infected and taking longer to do so.
“Scientists at the time believed this outcome was inevitable,” said Read. “What they called the ‘law of declining virulence’ suggested that viruses naturally become milder over time to ensure that they do not kill their hosts before they’ve had a chance to be transmitted to other individuals.”
Yet, when Read and his team began to study the myxoma virus in rabbits in 2014, they found that the virus had regained the upper hand and was once again killing rabbits at a higher rate. In their most recent study, which published on Oct. 5 in the Journal of Virology, they examined several myxoma virus variants collected between 2012-2015 in the laboratory to determine their virulence. The team determined that the viruses fell into three lineages: a, b and c.
Interestingly, Read said, the rabbits in their study exhibited different symptoms than those induced by viruses collected in the first decades after the release.
“Instead of developing puffy, fluid-filled lesions, these rabbits developed flat lesions, suggesting a lack a reduced immune response,” said Read. “In addition, these rabbits had significantly more bacteria distributed throughout multiple tissues, which is also consistent with immunosuppression. We interpreted this ‘amyxomatous’ phenotype as an adaptation by the virus to overcome evolving resistance in the wild rabbit population.”
Lineage c, however, produced a slightly different response in rabbits. Rabbits infected with lineage c had significantly more swelling at the base of the ears and around the eyelids, where mosquitoes typically bite. These areas also contained extremely high amounts of virus.
“Insect transmissibility is dependent on high amounts of virus being present in sites accessible to the vector,” said Read. “We hypothesise that lineage c viruses are capable of enhanced dissemination to sites around the head where mosquitoes are more likely to feed and that they are able to suppress inflammatory responses at these sites, allowing persistent virus replication to high amounts.”
Read said that the team’s findings demonstrate that viruses do not always evolve to become milder.
“By definition an evolutionary arms race occurs when organisms develop adaptations and counter-adaptations against each other,” said Read. “With myxoma, the virus has developed new tricks, which are resulting in greater rabbit mortality. However, over time the rabbits will likely evolve resistance to these tricks. An analogous arms race may be occurring with SARS-CoV-2 and other human viruses as humans become more immune. This is why it’s so important for vaccine manufacturers to keep up with the latest variants and for the public to stay up to date on their vaccines. Better still would be to develop a universal vaccine that would work against all variants and be effective for a longer period of time.”
Other authors of the paper include Peter Kerr, formerly of CSIRO Health and Biosecurity, now deceased; Isabella Cattadori, professor of biology, Penn State; Derek Sim, associate research professor of biology, Penn State; June Liu, postdoctoral researcher, CSIRO Health and Biosecurity; and Edward Holmes, professor of medicine and health, University of Sydney.
The National Institute of Allergy and Infectious Diseases supported this research, which was initially stimulated by a seed grant from Penn State’s Huck Institutes of the Life Sciences.
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Materials provided by Penn State. Original written by Sara LaJeunesse. Note: Content may be edited for style and length.
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Clinical trial to evaluate antiviral drug for monkeypox begins in the Democratic Republic of the Congo
A clinical trial to evaluate the antiviral drug tecovirimat, also known as TPOXX, in adults and children with monkeypox has begun in the Democratic Republic of the Congo (DRC). The trial will evaluate the drug’s safety and its ability to mitigate monkeypox symptoms and prevent serious outcomes, including death. The National Institute of Allergy and Infectious Diseases (NIAID), part of the U.S. National Institutes of Health, and the DRC’s National Institute for Biomedical Research (INRB) are co-leading the trial as part of the government-to-government PALM partnership. Collaborating institutions include the U.S. Centers for Disease Control and Prevention (CDC), the Institute of Tropical Medicine Antwerp, the aid organization Alliance for International Medical Action (ALIMA) and the World Health Organization (WHO).
TPOXX, made by the pharmaceutical company SIGA Technologies, Inc. (New York), is approved by the U.S. Food and Drug Administration for the treatment of smallpox. The drug impedes the spread of virus in the body by preventing virus particles from exiting human cells. The drug targets a protein that is found on both the virus that causes smallpox and the monkeypox virus.
“Monkeypox has caused a high burden of disease and death in children and adults in the Democratic Republic of the Congo, and improved treatment options are urgently needed,” said NIAID Director Anthony S. Fauci, M.D. “This clinical trial will yield critical information about the safety and efficacy of tecovirimat for monkeypox. I want to thank our DRC scientific partners as well as the Congolese people for their continued collaboration in advancing this important clinical research.”
Since the 1970s, monkeypox virus has caused sporadic cases and outbreaks, primarily in the rainforest areas of central Africa, and in west Africa. A multi-continent outbreak of monkeypox in areas where the disease is not endemic, including Europe and the United States, has been ongoing since May 2022 with the majority of cases occurring in men who have sex with men. The outbreak has prompted recent public health emergency declarations from the WHO and the U.S. Department of Health and Human Services. From Jan.1, 2022 to Oct. 5, 2022, the WHO has reported 68,900 confirmed cases and 25 deaths from 106 countries, areas and territories.
According to the WHO, cases identified as part of the ongoing global outbreak are largely caused by monkeypox virus Clade IIb. Clade I, which is estimated to cause more severe disease and higher mortality than Clade IIa and Clade IIb, especially in children, is responsible for infections in the DRC. The Africa Centres for Disease Control and Prevention (Africa CDC) has reported 3,326 cases of monkeypox (165 confirmed; 3,161 suspected) and 120 deaths in the DRC from Jan. 1, 2022 to Sept. 21, 2022.
People can become infected with monkeypox through contact with infected animals, such as rodents, or nonhuman primates or humans. The virus can transmit among humans by direct contact with skin lesions, body fluids, and respiratory droplets, including through intimate and sexual contact; and by indirect contact with contaminated clothing or bedding. Monkeypox can cause flu-like symptoms and painful skin lesions. Complications can include dehydration, bacterial infections, pneumonia, brain inflammation, sepsis, eye infections and death.
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The trial will enroll up to 450 adults and children with laboratory-confirmed monkeypox infection who weigh at least 3 kilograms (kg). Pregnant women are also eligible to enroll. The volunteer participants will be assigned at random to receive either oral tecovirimat or placebo capsules twice daily for 14 days, with the dose administered dependent on the participant’s weight. The trial is double-blinded, so participants and investigators do not know who will receive tecovirimat or placebo.
All participants will stay at a hospital for at least 14 days where they will receive supportive care. Study clinicians will regularly monitor participants’ clinical status throughout the study, and participants will be asked to provide blood, throat swab, and skin lesion swab samples for laboratory evaluations. The study is primarily designed to compare the average time to healed skin lesions among those receiving tecovirimat versus those receiving placebo. Investigators will also gather data on multiple secondary objectives, including comparisons of how quickly participants test negative for monkeypox virus in the blood, overall severity and duration of disease, and mortality between groups.
Participants will be discharged from the hospital once all lesions have scabbed over or flaked off, and after they test negative for monkeypox virus in the blood for two days in a row. They will be followed for at least 28 days and will be asked to return for an optional study visit after 58 days for additional clinical and laboratory tests. An independent Data and Safety Monitoring Board will monitor participant safety throughout the duration of the study.
The trial is led by co-principal investigators Jean-Jacques Muyembe-Tamfum, M.D., Ph.D., director-general of INRB and professor of microbiology at Kinshasa University Medical School in Gombe, Kinshasa; and Placide Mbala, M.D., Ph.D., operations manager of the PALM project and head of the Epidemiology Department and the Pathogen Genomic Laboratory at INRB.
“I am happy that monkeypox is no longer a neglected disease and that soon, thanks to this study, we will be able to prove that there is an effective treatment for this disease,” said Dr. Muyembe-Tamfum.
For more information, please visit clinicaltrials.gov and search identifier NCT05559099. The trial timeline will depend on the pace of enrollment. A separate NIAID-supported trial of TPOXX is ongoing in the United States. For information about the U.S. trial, visit the AIDS Clinical Trials Group (ACTG) website and search TPOXX or study A5418.
PALM is short for “Pamoja Tulinde Maisha” a Kiswahili phrase that translates to “together save lives.” NIAID and the DRC Ministry of Health established the PALM clinical research partnership in response to the 2018 Ebola outbreak in Eastern DRC. The collaboration has continued as a multilateral clinical research program composed of NIAID, the DRC Ministry of Health, INRB and INRB’s partners. PALM’s first study was the randomized controlled trial of multiple therapeutics for Ebola virus disease, which supported the regulatory approvals of the NIAID-developed mAb114 (Ebanga) and REGN-EB3 (Inmazeb, developed by Regeneron) treatments.
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It takes guts: Fungus living inside cave crickets reveals fungal evolution steps
Sometimes, the answers to questions about evolution can be found in the strangest of places. For example, researchers from Japan have now discovered that a fungus found in cave cricket feces can help to shine a light on fungal evolution.
In a study published last month in Mycologia, a research group led by the University of Tsukuba has revealed that a previously undescribed fungus could provide the key to understanding how fungi in the group Kickxellomycotina evolved.
Fungi are a highly diverse group of organisms that inhabit many different habitats and ecological niches. The subphylum Kickxellomycotina is no exception: these fungi can range from living as saprobes (fungi that feed on decaying wood, leaves, and other organic matter) on soil or dung, to inhabiting the guts of arthropods. However, the evolutionary transition between these life cycles is unclear.
“During a survey of fungi that underwent early evolutionary divergence, we found a new fungus that grows on cave cricket feces,” says senior author of the study, Professor Yousuke Degawa. “On the basis of its morphology and ecology, we concluded that this fungus is a member of the Kickxellales.”
The Kickxellales is a group within the Kickxellomycotina, and up until now these fungi were considered to be mostly saprobes. The researchers found that the new fungus, named Unguispora rhaphidophoridarum, represented a new genus. However, it did not grow under the same conditions as other fungi in the Kickxellales, and instead demonstrated a new life cycle for this group — one where the fungus inhabits the gut of its host, and is also dependent on its host for survival.
The researchers use the term ‘amphibious fungi’ (not to be confused with aquatic hyphomycetes — a group of fungi that colonize decaying deciduous leaves in streams and rivers — which are also called amphibious fungi) to describe fungi like U. rhaphidophoridarum. This new genus has two life stages: one inside the host gut and the other outside, such as on feces and exuvia (the molted exoskeletons of arthropods). Most of the species in the gut-inhabiting group within the Kickxellomycotina are found in aquatic insects.
“Our findings suggest that the Kickxellomycotina evolved in association with the guts of animals, including arthropods,” says Professor Degawa.
Although it is difficult to determine how ancestral fungi in the Kickxellomycotina lived, the results of this study offer a new way of looking at how some of them evolved to inhabit the guts of animals. Future investigations of fungi in this group that have life cycles associated with the animal gut will uncover the evolutionary stages between saprobes and gut-inhabiting fungi, as shown by Unguispora.
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Materials provided by University of Tsukuba. Note: Content may be edited for style and length.
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Scientists have found that bacteria and fungi in the human mouth can join forces to form a so-called …
Scientists have found that bacteria and fungi in the human mouth can join forces to form a so-called superorganism that is stronger and more tenacious than regular microbes. These superorganisms have been isolated from saliva samples collected from toddlers with severe childhood tooth decay. These pathogens are able to colonize teeth, resist standard antimicrobial drugs, and are tougher to remove than either the bacteria or fungi on their own. They can also form appendages that act like limbs, which they use to move and even ‘leap’ on the surface on teeth, spreading quickly even though the microbes are non-motile on their own. The findings have been reported in the Proceedings of the National Academy of Sciences.
This study began with a simple discovery that was almost accidental, made while toddlers’ saliva samples were being analyzed. The researchers watched as bacteria and fungi assembled together, then developed abilities the scientists “never thought [the microbes] would possess.” The microbes seemed to be walking and leaping, which the investigators called “emergent functions” that benefit the assembled bacterial and fungal superorganism in novel ways, explained co-corresponding study author Hyun (Michel) Koo, a professor at Penn Dental Medicine. “It’s almost like a new organism – a superorganism with new functions.”
Biofilms, including those studied by Koo’s lab, are known to take on abilities that regular microbial communities don’t posses. They have found that dental biofilms formed by Streptococcus mutans bacteria and Candida albicans fungi can lead to severe tooth decay.
Cavities form in teeth when sugar from the diet feeds mouth microbes, which generate plaques, releasing acid that destroys the enamel on teeth.
When the researchers identified the superorganism clusters, they used microscopy to learn more about how it behaved on teeth. The model included the microbes, a tooth-like substance, and human saliva. The superorganisms were found forming highly organized structures. The bacteria were clustered within a network of yeast filaments known as hyphae, which project from yeast cells. It was all held within a glue-like polymer.
The researchers found that after the superorganism formed, it started moving. The researchers were surprised to find that together, these microbial pathogens were stickier and more resistant to removal or destruction, whether it was physical force or chemical.
Some bacteria are known to use filaments or appendages to move around. But these microbes cannot do so on their own. The superorganism also moves in an intriguing way; the fungal hyphae anchor onto a surface, and transports the bacteria across surfaces. Koo said it is “like bacteria hitchhiking on the fungi.” They can also move quickly, and over ‘long’ distances, at over 100 microns per hour.
“That is more than 200 times their own body length,” said first study author Zhi Ren, a postdoctoral fellow in the Koo lab, “making them even better than most vertebrates, relative to body size. For example, tree frogs and grasshoppers can leap forward about 50 times and 20 times their own body length, respectively.”
It may be easier to stop tooth decay in children now that researchers have identified these superorganisms. The research has also provided insight into unique microbial behaviors. There may be other microbes that join forces in this way, waiting to be discovered.
Sources: University of Pennsylvania, Proceedings of the National Academy of Sciences
How poliovirus takes over cells from within
For the first time, researchers at Umeå University, Sweden, can now show how the dreaded poliovirus behaves when it takes over an infected cell and tricks the cell into producing new virus particles. Polio was thought to be almost eradicated, but infection has now been rediscovered in London and New York.
“We now have a completely different understanding of how the virus acts and thus better opportunities for research to perhaps find new ways to curb the virus’ progress in the future,” says Lars-Anders Carlson at the Department of Medical Chemistry and Biophysics at Umeå University.
The dreaded poliovirus belongs to the same large family, enteroviruses, as several common colds. It has been known for some time that enteroviruses drastically rearrange the inside of infected, but it has not been known exactly how, simply because technology has not allowed us to see so deeply into the cells. Thanks to the advanced cryo-electron microscope in Umeå, researchers have for the first time been able to take three-dimensional images of how the poliovirus forms and takes over human cells.
“We were surprised to see how the virus transforms processes in the cell that are otherwise used to destroy viruses to produce new viruses instead,” says Lars-Anders Carlson.
The researchers were able to identify the site in the cell where the poliovirus forms new virus particles, by seeing sites with half-assembled viruses. Surprisingly, this “virus factory” in the cell turned out to be surfaces in the cell that resembled an otherwise normal process in the cell, autophagy. Autophagy is a relatively recently discovered process in cells that was subject of the 2016 Nobel Prize. Normally, autophagy serves to break down particles that the cell wants to get rid of, such as virus particles. But the poliovirus manages to reprogram this defence mechanism against viruses to produce more virus instead.
The researchers found that certain proteins are particularly important. The VSP34 protein is used by the virus to build new virus particles. When the researchers inhibited VSP34, they could see that the virus could barely assemble whole viruses, but mostly only half virus particles. Another important protein is called ULK1, which slows down the production of viruses. The researchers could see that the amount of virus exploded when this protein was inhibited. This confirms the theory that the poliovirus breaks down this “brake.”
Once the virus has multiplied in the cell, the particles must be released to infect new cells. This is done by releasing the particles in small packets, called vesicles. Here, the researchers also made a surprising discovery; a careful sorting of what is packed into the vesicles takes place. Only viruses that are correctly formed and carry the genetic material of the virus are placed in the vesicles, while empty virus particles are not allowed in. In this way, the virus may spread more efficiently.
“The new knowledge we are contributing about the role of autophagy in virus formation may provide new insights for the development of future antivirals that could complement vaccines. We have good reason to believe that our findings are valid for the large group of viruses to which poliovirus belongs, enteroviruses. There is no vaccine against most enteroviruses, but an antiviral that acts on the autophagy system could be effective against many of them. However, there is still a long way to go,’ says Lars-Anders Carlson.
Polio is rightly a dreaded disease that can cause paralysis and death. The poliovirus starts in the intestines but can then attack the spinal cord. There is still no cure for the disease, but the only way to prevent it is to be vaccinated. In much of the world, vaccination campaigns have been so successful that the disease is considered virtually eliminated. However, polio has persisted in some countries in Asia, Africa and the Middle East. The poliovirus is mainly transmitted through feces. In 2022, the virus was again detected in sewage in New York and London. In addition, New York has had the first new case in ten years of a person getting paralysed due to polio infection.
The reappearance of polio in developed countries may be partly due to a decline in vaccination rates, as the disease was considered almost eradicated, and also due to increasing resistance to vaccination.
The study was a collaboration with researchers at the National Institutes of Health, USA, and Monash University, Australia. It is published in the scientific journal Nature Communications.
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Materials provided by Umea University. Note: Content may be edited for style and length.
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90% Are Completely Cured – A New Far Superior Treatment for Life-Threatening Intestinal Infections
While normal therapy is often insufficient to treat stubborn bowel disease, recent research found that a novel, ground-breaking method could completely cure 90% of patients.
Feces transplantation in the intestine is a very effective cure – far superior to today’s conventional treatment – for a potentially fatal infection that affects between 2,500 and 3,000 individuals in Denmark each year.
That is the finding of a recent study that was carried out by scientists from Aarhus University and Aarhus University Hospital. Their findings were recently published in the journal The Lancet Gastroenterology & Hepatology.
In the study, the researchers explored the ground-breaking fecal transplantation treatment for patients infected with Clostridioides difficile (C. difficile), an infection that often strikes old or weak people.
According to Simon Mark Dahl Baunwall, a Ph.D. candidate at the Department of Clinical Medicine and a doctor at the Aarhus University Hospital, the study’s findings are very encouraging.
“Our new study shows that we can effectively cure the infection through the early use of fecal microbiota transplantation (FMT) after completing the standard treatment, to prevent relapses,” he says.
Antibiotics are presently the standard treatment for C. difficile, but the infection is tenacious and may reoccur in many individuals.
Because the typical treatment methods are insufficient, the infection can be lethal in some cases.
Currently, only the most difficult cases with three or more infections have been identified are eligible for FMT treatment.
However, the study, which involved 42 patients, indicated that the new treatment could completely cure the large majority of patients.
“We found that treatment with FMT after completing the standard treatment cured 19 out of 21 patients, whereas only seven out of 21 treated with a placebo or another antibiotic were cured. In other words, the probability of curing the infection is three times greater after treatment with FMT than with our current standard treatment alone,” explains Simon Mark Dahl Baunwall.
FMT treatment is performed by transferring healthy donor feces, which contain a complete microbial intestinal ecosystem, to patients with disorders in their intestinal microbiota.
In the study, the effect of the treatment was so significant that the project had to be stopped for ethical reasons.
“In rare cases, it can happen that you discover that the treatment you are investigating is so effective that it is ethically indefensible to continue,” says Simon Mark Dahl Baunwall.
“Our study is one example, in that the new FMT treatment is so much better than the standard treatment with antibiotics that it would be unethical to continue because the patients in the control group would risk not receiving the FMT treatment.”
Denmark is the country in Europe that is furthest advanced with the roll-out of the treatment to the patient group in question. However, a survey last year revealed that only 25 percent of the patients who could benefit from FMT treatment were offered it. In Europe as a whole, the figure is just one in ten.
There are also many indications that FMT is not just an effective treatment for patients with C. difficile: the treatment is also being tested on a wide range of other diseases where disturbances in the intestinal microbiota may be a triggering factor.
“At the moment, many studies of FMT treatment for various diseases are being carried out worldwide, with the most promising of these indicating beneficial effects in patients with inflammatory bowel disease and multi-resistant bacteria,” says Simon Mark Dahl Baunwall.
Reference: “Faecal microbiota transplantation for first or second Clostridioides difficile infection (EarlyFMT): a randomised, double-blind, placebo-controlled trial” by Simon Mark Dahl Baunwall, MD, Sara Ellegaard Andreasen, MD, Mette Mejlby Hansen, MSc, Jens Kelsen, Ph.D., Katrine Lundby Høyer, MD, Nina Rågård, BSc, Lotte Lindgreen Eriksen, MD, Sidsel Støy, Ph.D., Tone Rubak, MD, Prof Else Marie Skjøde Damsgaard, DMSc, Susan Mikkelsen, Ph.D., Prof Christian Erikstrup, Ph.D., Jens Frederik Dahlerup, DMSc and Christian Lodberg Hvas, Ph.D., 21 September 2022, The Lancet Gastroenterology and Hepatology.
DOI: 10.1016/S2468-1253(22)00276-X
The study was funded by the Innovation Fund Denmark.
COVID-19 vaccine may be lifesaving for pregnant woman and their unborn children
Stillbirth is a recognized complication of COVID-19 in pregnant women caused by harmful changes to the placenta induced by the virus. Termed SARS-CoV-2 placentitis, it can render the placenta incapable of providing oxygen to the fetus, leading to stillbirth and neonatal death. Researchers now suggest that pregnant women who get the COVID-19 vaccine may be protected from SARS-CoV-2 placentitis and stillbirth. In a new article published in the American Journal of Obstetrics & Gynecology, researchers conclude that the vaccine not only protects pregnant women but may also be lifesaving for their unborn children.
The extensive examination of published literature involved reviewing nearly 100 papers looking at COVID-19’s impacts on pregnant women and the effects on the placenta and pregnancy outcome. Sarah Mulkey, M.D., Ph.D., a prenatal-neonatal neurologist in the Division of Prenatal Pediatrics at Children’s National Hospital and co-author of the article, says the findings make a strong case for vaccination.
“The COVID-19 virus fortunately does not cause birth defects like other viruses such Zika, but it can cause severe injury to the placenta that can result in stillbirth and other pregnancy complications,” says Dr. Mulkey. “I hope patients who are pregnant or planning to become pregnant can learn how the COVID vaccine may help keep them and their baby healthy throughout pregnancy from some of the worst effects of this virus.”
While stillbirths can have many causes, the data analyzed supports that the COVID-19 vaccine is beneficial for pregnancies and for reducing the risk of stillbirth by reducing the risk of the virus impacting the placenta.
“In the multiple reports of SARS-CoV-2 placentitis that have been associated with stillbirths and neonatal deaths, none of the mothers had received COVID-19 vaccinations,” says David Schwartz, M.D., lead author, epidemiologist and perinatal pathologist. “And although not constituting proof, we’re not aware, either personally, via collegial networks, or in the published literature, of any cases of SARS-CoV-2 placentitis causing stillbirths among pregnant women having received the COVID-19 vaccine.”
Earlier in 2022, Dr. Schwartz led a team from 12 countries that found SARS-CoV-2 placentitis destroyed an average of 77.7% of placental tissue, resulting in placental insufficiency and fetal death, all occurring in unvaccinated mothers.
Fortunately, the large majority of pregnancies affected by a COVID-19 infection do not result in stillbirth. The development of SARS-CoV-2 placentitis is complex and likely involves both viral and immunological factors. The characteristics of a SARS-CoV-2 variant may also affect risk.
“Placental pathology is an important component in understanding the pathophysiology of SARS-CoV-2 infection during pregnancy,” says Dr. Mulkey
As part of the Congenital Infection Program at Children’s National, Dr. Mulkey has been following infants born to mothers who had SARS-CoV-2 infection during pregnancy since the beginning of the pandemic. She will present the results of the early neurodevelopment of these infants at ID Week in Washington, D.C., on Oct. 22, 2022. Dr. Mulkey will also lead the neurodevelopmental follow-up of a large cohort of infants born to mothers with SARS-CoV-2 infection during pregnancy to better understand any long-term neurological effects to offspring.
The study builds upon Dr. Mulkey’s longitudinal studies on Zika virus infection in pregnancy and long-term impacts on the child.
More information:
David A. Schwartz et al, SARS-CoV-2 Placentitis, Stillbirth and Maternal COVID-19 Vaccination: Clinical-Pathological Correlations, American Journal of Obstetrics and Gynecology (2022). DOI: 10.1016/j.ajog.2022.10.001
David A. Schwartz et al, SARS-CoV-2 Placentitis, Stillbirth and Maternal COVID-19 Vaccination: Clinical-Pathological Correlations, American Journal of Obstetrics and Gynecology (2022). DOI: 10.1016/j.ajog.2022.10.001
Journal information:
American Journal of Obstetrics & Gynecology
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American Journal of Obstetrics and Gynecology
American Journal of Obstetrics & Gynecology
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American Journal of Obstetrics and Gynecology