The abnormally small heads seen among children infected with Zika virus have haunted all those living in regions where mosquitoes carry the pathogen, including the United States. It turns out that just one genetic change in a viral protein could cause the defect—yet another piece of evidence of just how easy it could be for a virus to transform from mild to a serious global concern.

A group of Chinese researchers identified one particular mutation in the virus most associated with microcephaly, the birth defect associated with last year’s outbreak.

The breakthrough could be crucial for future outbreaks. Although concerns over Zika have diminished since last year, the problem has not disappeared. With so many areas of the U.S. now covered in stagnant floodwaters, questions linger about what impact recent storms could have on the transmission of the virus.

“[Zika] will come back at some point,” Dr. Michael Diamond, an infectious diseases specialist at the Washington University School of Medicine in St. Louis (but who was not involved in the research), tells Newsweek. “I can’t tell you when, but it will come back at some point. And if it comes back, are we going to be in the same place that we were last time—with nothing—or are we going to continue to study it, understanding it might come back worse than it is now?”

The new finding is a first step toward knowing how and why the Zika virus causes birth defects—and which forms of the virus might be particularly dangerous.

The research was published in Science on Thursday.

The genetic abnormality alters the course of the disease. “This specific mutation can indeed make the virus more aggressive,” Alysson Muotri, a researcher at the University of California, San Diego who has also studied the Zika virus in animal models but was not involved in the new paper.

Microcephaly was not always a common birth defect seen in children affected by Zika. The problem may simply have gone unnoticed during earlier outbreaks because fewer infected women were pregnant. But as the epidemic changed—expanding in Brazil, most notably—the problem became more noticeable, says Diamond.

Researchers, including Cheng-Feng Qin, a virologist at the Beijing Institute of Microbiology and Epidemiology and an author of the paper, also wondered if the virus had mutated, becoming more virulent and damaging to the developing human brain.

To test this theory, Qin took nearly 100 newborn mice, separated them into four groups, and injected one of four different strains of the virus into their brain. One of the strains was associated with an outbreak that happened in 2010; three strains were isolated during the outbreak from 2015 to 2016. He also tested the virus on human brain stem cells.

For developing mice infected with one particular strain, called VEN/2016, their brain became far smaller than the brain of mice infected with other strains. The brain of mice infected was still smaller if it was infected with a virus created to carry just the one mutation found in that version of the virus—a substitution of one amino acid, serine, for another, asparagine—in a protein called prM.

Mexico Zika Virus South AmericaAn Edes aegypti mosquito inside a test tube as part of research on preventing the spread of the Zika virus and other mosquito-borne diseases at a control and prevention center in Guadalupe, Mexico, on March 8, 2016.REUTERS/DANIEL BECERRIL/FILES

But though the results were strong, the method used left many researchers with questions.

Injecting the virus straight into mice’s brain meant that the virus didn’t go through the usual path it would take to affect a developing fetus. In most cases, a mosquito bites a pregnant woman, then the virus spreads through her body and crosses the placenta to reach the fetus.

“Inside the brain, it works. The question is, Does it work outside the brain?” said Jean Pierre Schatzmann Peron, an immunologist at the University of Sao Paolo in Brazil. Since the mutated protein identified in this study is found on the surface of the virus, it could have an impact on the likelihood of the virus making it through that path. Perhaps the human immune system would detect the modified protein on the surface of the virus and kill it, for example.

And why would this mutation make the virus work better or differently, he asked. “What does it change? There are a lot of other questions that have to be answered after this.”

Qin and the Chinese team are working on some answers. They’re currently studying factors that interact with the mutated protein.

But ideally, Diamond noted, scientists would use similar experiments with monkeys or chimpanzees, allowing the virus with this mutation to infect the animals from mosquitos and watching how it affected fetal development. “That experiment needs to be done,” he said.

A more aggressive Zika virus could also be exacerbated by other issues that make an infant more susceptible to microcephaly. “This [mutation] can change the biology of the virus, but it doesn’t fully explain what’s going on,” says Muotri. Environmental factors, genetic background of the person, previous exposure to other viruses or vaccines could all play a role. “It’s not only about the viral genetics,” says Muotri. “There are probably other factors that play a role.”

In the U.S., 100 children infected with Zika have been born with microcephaly. Children with this birth defect may have seizures, hearing loss, difficulty seeing or moving, and may not learn to sit, stand or walk at the same rate as other children. They may also have intellectual disabilities.

Though the mosquito that spreads Zika can be found throughout the southern United States—and even as far north as New Jersey and Northern California—it hasn’t been widespread in the United States. About 5,500 cases of Zika were reported in the U.S. outside of territories like Puerto Rico and the U.S. Virgin Islands since the beginning of 2015. Only 225 of those cases were due to mosquito bites that happened in those states; most were residents who were likely traveling when they were infected.

But as Diamond points out, the virus could re-emerge anytime, and we need to be prepared.



Aedes aegypti mosquitoes spread Zika all over the Americas, leaving a trail of microcephaly cases in their wake.


SIXTY YEARS AGO, a team of scientists went looking for yellow fever in the jungles that line the northwestern edge of Lake Victoria. What they found instead, in the blood of a rhesus monkey, was a new virus, one they named for the area’s dense vegetation: Uganda’s Zika Forest. Within a few years, Zika virus was showing up in humans, causing a pink rash and mild flu-like symptoms. And for the next six decades, as it spread eastward on the wings of the Aedes aegypti mosquito, its symptoms stayed the same.

That all changed when the virus jumped the Pacific Ocean and landed on the shores of Brazil sometime around 2014. As Zika sickened thousands, reports of microcephaly—a birth defect characterized by abnormally small heads and underdeveloped brains—began pouring in from doctor’s offices and hospitals around the country. In April of last year, scientists at the US Center for Disease Control and Prevention formally declared that Zika was to blame for the microcephaly cases. Since then, researchers have been rushing to tease apart how the Zika virus went from tepid to toxic, in hopes of finding vaccine or drug targets to prevent the most devastating manifestations of the infection.

New evidence suggests it might all come down to one measly mutation.

In a paper published Thursday in Science, researchers from some of China’s largest academic institutions report that a single genetic change, which likely happened around May of 2013, swapped one amino acid on one of the virus’s three structural proteins—a tiny tweak with catastrophic effects. The research highlights the importance of a global genetic surveillance system for emerging pathogens, and opens the door to developing better predictive tests for expectant mothers.

The Chinese researchers started out by comparing three contemporary strains of the virus—isolated from patients in the Caribbean, Samoa, and Venezuela in 2015 and 2016—with a more ancestral Cambodian strain from 2010. When they injected the viruses into baby mice, they saw something shocking. The Cambodian strain killed fewer than a quarter of the mice, leaving the rest with some brain damage. The three modern strains? Killed every mouse. And compared to the older virus, the newer version from Venezuela killed significantly more neural progenitor cells—the cells that give rise to new neurons in the developing brain—leading to mice with much smaller brains.

Using the old Cambodian strain as a reference, the scientists then compared the genomes of the newer ones, trying to tease apart any differences that could account for their enhanced lethality. They discovered that Zika had developed multiple mutations before the virus broke out in Brazil, all of which persisted in the American strains.

In particular, they identified one mutation that switched a single amino acid—from serine to asparagine—appearing around May 2013. And they believe it’s that change that strikes a disastrous blow to the brains of unborn children. Of all the mutations they engineered into a reference strain, only the serine to asparagine swap led to more neuronal death and smaller brains in baby mice than the older Cambodian strain. While it may still take a constellation of mutations to create the worst forms of microcephaly, this one shines brightest.

This answers a big question scientists have been wrestling with since microcephaly cases started ballooning: Do they have a genetic cause? There are other possible explanations to the birth defect’s surprising appearance in Brazil; perhaps microcephaly wasn’t showing up in places like India and Africa because a lot of women were exposed to Zika as children, so they already had immunity to the diseases. Especially in rural areas, there might just not have been enough microcephaly to be detected. But now there’s convincing evidence that the birth defect is in fact the product of viral evolution. The paper’s authors write that their findings “offer an explanation for the unexpected causal link of Zika to microcephaly, and will help people to understand how Zika evolved from an innocuous mosquito-borne virus into a congenital pathogen with global impact.”

“The results of the paper are very intriguing and beautifully laid out,” says Pardis Sabeti, a Harvard computational biologist and accomplished virus hunter. She and her colleagues published a series of papers earlier this year tracking the genetic spread of Zika around the Americas. Her team stressed the importance of sequencing the genomes of emerging threats like Zika in as close to real-time as possible, both to inform public health responses on the ground and make studies like this one possible. “Viruses continually mutate, and the more opportunities we give them to take hold in a population the more opportunities they have to change in ways with great consequences,” Pardis says.

What the Science study authors still don’t know is whether the microcephaly-associated mutation helps Zika survive and spread. Cheng-Feng Qin, a virologist at the Beijing Institute of Microbiology and Epidemiology and co-author of the paper, says that’s what they’re trying to figure out next. “One possibility is that the mutation affects the interaction between some unidentified host proteins and the virus,” he says. “The other hypothesis is the mutation could have impacts on viral assembly and maturity in neural progenitor cells.” Viruses are about just one thing: making more of themselves, whatever it takes. So it’s possible the mutation somehow helps Zika transmit more effectively, and the toxicity to fetal nerve cells is either part of transmission or an unrelated byproduct. Or it could just be a random tweak that doesn’t happen to harm the virus.

That’s the million dollar question right now, says Aaron Brault, a microbiologist with the CDC’s Division of Vector-Borne Diseases who has been studying Zika since 2015 at the agency’s Fort Collins laboratory. If the mutation helps Zika spread, that means the microcephaly-causing mutation somehow provides an evolutionary advantage, and could be selected for in nature. “This paper opens the door to understanding whether or not this mutation might arise again,” says Brault. Like, say, in Africa, where the disease has circulated for a long time but hasn’t yet caused birth defects like those seen in the Americas. It also makes it clear that the mutation, at the very least, is a persistent one. “This mutation is present in every sequence of the virus generated in the western hemisphere since 2013,” he says. “It’s not going anywhere.”

Over the past two years, the CDC has been working to fast-track a number of diagnostic tests so that doctors and patients can be better informed early on of potential birth defects related to Zika. But those tests have had issues, missing some Zika cases while picking up related infections like dengue and chikungunya. A blood test designed to only pick up this particular mutated protein would likely be a much better indicator of microcephaly than any test out there now. And while Zika cases in the Americas are no longer raging—they’ve dropped to fewer than a thousand cases this summer, compared to 35,000 during the outbreak’s peak in January 2016—public health officials say it’s no time to slack off. If Zika’s taught them anything, it’s that a crisis is always just one mutation away.

Bed bug found at Henninger High School for second time in a week


by CNYCentral

An official from the Syracuse City School District says another bug found at Henninger High School has been determined to be a bed bug.

The discovery comes after three bed bugs were found at the same school last week. Administrator for Communications Michael Henesey said the latest bug was found Tuesday.

Extra staff have been brought in to vacuum, clean and disinfect all surfaces in the room where the bug was found and the rooms adjacent to it.

The school’s principal is also relaying information to parents, Henesey said.

Bed bugs may travel to new homes in your dirty laundry

bed-bugs (1)

Katherine Ellen Foley

Bed bugs are incredible world travelers.

In the past couple of decades, bed bug populations have exploded all over the world, particularly in the US, parts of Europe, and Australia. According to a 2015 survey by National Pest Management Association and the University of Kentucky, these critters show up in nursing homes, hospitals, schools, and even office buildings.

These horrific nuisances shouldn’t be nearly as prevalent as they are. They hate to travel on their own and they have particular tastes, feasting exclusively on blood and living only in the hardest-to-reach nooks and crannies. One of the explanations researchers have come up with for why bed bugs can be found all over the world is that we humans may be enabling their spread through the laundry we lug around when we travel.

In a study published on Sept. 28 in Scientific Reports, scientists from the University of Sheffield found that indeed, dirty, smelly clothes are the preferred to be hiding spot of these pests when compared to clean laundry. This suggests that if you’re traveling, you should be extra wary of keeping your dirty clothes stored away tightly, so no parasitic hitchhikers can catch a ride back to your home.

The researchers selected four people to wear cotton clothing for three hours while they went about their days. After the three-hour period, volunteers took their clothing and sealed them into bags. Researchers stocked an air-tight room with two bags of dirty clothes and two bags of clean clothing alternating in a circle. They then placed a container carrying a family of bed bugs in the middle of the circle, and opened it up, allowing the insects to venture around where they wanted. After four days (about the amount of time it typically takes for bugs to find a new home), more bed bugs had moved from their original container to settle in the dirty laundry than the clean clothing.

The scientists also wanted to see whether or not the presence of a living human being influenced the bugs’ travel decisions. When we humans breathe, we exhale carbon dioxide. Although we can’t smell this gas, mosquitoes and some stinging insects, like wasps, can. They use it as a cue to tell them that there’s a meal (in the case of a mosquito) or a threat (in the case of a wasp) in the vicinity. The researchers thought that maybe the same would be true for bed bugs, who love to slurp up our blood. So they pumped these same rooms with carbon dioxide to mimic people. Only a few more bed bugs migrated to dirty or clean laundry in the presence of carbon dioxide, which suggests that the real draw for them is the smelly laundry.

“Soiled clothing left in an open suitcase, or left on the floor, of an infested room is more likely to attract bed bugs,” the authors write. “When packed into a suitcase, they will accompany their host back home.”

To be sure, this was a relatively small study with just a handful of bugs and a small amount of clothing. Everyone produces different body odor, and different types of clothing smell differently when worn. Polyester gives off a completely different stench than the cotton that was tested, for example. But even so, if you’re traveling, it’s probably best to keep dirty clothes in a separate compartment in your suitcase, and wash them immediately when you get home. That way, if you unintentionally bring any insect souvenirs back with you, you’ll kill them before they have a chance to infest your home.

The Same Movie Theater Keeps Getting Accused Of Spreading Bed Bugs

Giant ant, honey I Shrunk the kids

The movie theater experience is supposed to be a fun time that everybody in the family can enjoy. However, one theater is not enjoying the experience themselves, as they are being repeatedly accused of infecting moviegoers with bed bugs. This is obviously causing the theater money as well as being a PR nightmare, though it appears that the accusations might be unfounded.

The general manager of the Mounds 10 Theater in Anderson, Indiana admits that the theater did have a bed bug problem earlier this year, but an exterminator was called in and the issue was dealt with. However, according to Fox 59, there have been at least five additional inspections for bed bugs over the past four months, and each of them has turned up nothing. This hasn’t stopped the problem as a family believes they were infected with bed bugs, and brought the annoying insects home with them, after seeing a screening of IT at the theater as recently as two weeks ago. However, once again an inspection was done and no bed bugs were found.

Bed bugs are brutal and can be a serious blow to any establishment that ends up with them. A hotel that gets a reputation for the irritating little things has some significant work to do to get their reputation back. The same can certainly be said for movie theaters. It would be bad enough if the theater actually had bed bugs, but it seems that in this case, the theater is dealing with all the negative press that comes with the accusation, without actually having the problem.

Apparently, you can be infected with bed bugs for some time before suffering any of the effects, so it is possible that the people accusing the theater of bed bugs did actually pick them up someplace else, though it would certainly be a remarkable confluence of events that would see multiple people picking up the bugs elsewhere, and then also visiting the movie theater. Of course, something like that must have happened at least once, as that was likely how the theater became infected the one time it was apparently a legitimate issue. Apparently, Indiana as a state has some issues with bed bugs overall, so perhaps so many people getting infected elsewhere isn’t such a crazy idea.

At this point, this theater in Indiana has been so thoroughly inspected for bed bugs that may be the least likely place to find them in the state. Hopefully, if the theater is totally in the clear, they can find some way to end these incessant accusations so they don’t need to spend all their money on repeated pest inspections, though it is certainly nice to see the company step up and do the work to make sure everything is ok, even though they certainly believe the theater is clean.

This “Kissing Bug” Can Kill Your Dogs And Your Children Too


As scary as they may seem most bugs are harmless. But it’s reasonable to be afraid of the bug called “kissing bugs.” That sounds quite friendly, doesn’t it? But they’re also known as: “The Assassin Bug.” They live under porches, in cracks between walls, under rocks, under cement, in forested areas, or in outdoor dog houses or chicken coups.

They can cause the spread of a highly dangerous disease called American Trypanosomiasis, or “Chagas Disease.”


Unfortunately, Hundreds of dogs have died from a rare parasitic disease known as Chagas. This disease is mostly spread in Texas, where almost 400 dogs have died from it.

A parasite known as Trypanosoma Cruzi causes “Chagas Disease.” “Kissing Bug” carries this parasite. It feeds with blood around the eyes and mouth of a pet while they are sleeping.

Transmission occurs when the fecal material gets rubbed into the bite wound or into a mucous membrane. Dogs also can get diseased by eating the bugs.

Chagas disease is known as the “silent killer” because it can be diagnosed only in later stages, only after it attacks the heart muscles and eventually causes heart failure.

Symptoms include massive swelling of the eyelids and even anaphylactic shock, which can cause asphyxiation and eventually death. At first, the symptoms can be same as they are for flu.

But eventually, they will become more painful.

They are in every southern state in America, and most Midwestern states. These bugs often bite unsuspecting children who play by wooded areas.

Love Bug Season Is Upon Us

By: Guarantee Floridian

Spring time is here! Which means sunshine, blooming flowers, and the infamous love bug plague. As Floridians, we’ve all experienced these too-friendly pests and their flocks in numbers. This is especially true for any of us with vehicles, as our cars, trucks, and motorcycles become plastered with them every time we have to run an errand. While love bugs are harmless, they are quite a nuisance and an annoyance.

Love Bug Myth

There’s been a long-standing myth that the love bug was an experiment-gone-wrong on the campus of the University of Florida in Gainesville. However, this myth isn’t actually true. Love bugs are a natural insect, though they don’t originate from the United States. They come from South America and eventually migrated their way up to North America. Some say that certain shipments from South America to North America in the 1940s helped to bring love bugs to Texas.

Love Bug Issues

Fortunately, love bugs don’t cause any harm to us in the form of bites, stings, or possible transmitted diseases. However, they can “leave their mark,” so to speak. Many find that failing to remove love bug remains from their cars will result in damage to the car’s paint. Furthermore, the longer they remain on the vehicle, the more difficult it becomes to get them off completely. To prevent this from becoming as big of an issue, try treating your car with a protective wax to help make it easier to get rid of the love bug aftermath of driving around.

Prevention and Control Tips

For those who simply hate the thought of these buzzing lovers floating into their home, a pest control professional can help by treating the area. There are also some tips that you can take yourself to help minimize the flocks of love bugs that swarm and enter your home during the spring and late summer seasonal bursts.

Try the following tips to help control your love bug population this spring:

  • Applying insect spray to doors and other exterior areas to help keep them from lounging on access points into your home
  • Turn on ceiling fans and other smaller fans to blow them outward and away from the home
  • Light mosquito repellent candles, which can also work to keep love bugs at bay
  • Keep your lawn mowed, as love bug larva grow in the thatch, or area between the soil and the green matter of your lawn

UCR study: Tayras, sloths and porcupines can be hosts for deadly parasite

A UCR study is the first to show that tayras, long, slender animals that look similar to weasels, are hosts for parasite-spreading kissing bugs. (UCR image)


UC Riverside scientists have identified new hosts for a parasite that causes Chagas disease, a chronic, debilitating condition that is spread by insects called “kissing bugs.”

The research, which was published this month in the journal PeerJ, broadens the list of animals that can transmit the disease, which should help control the deadly scourge that afflicts more than 8 million people worldwide.

The new hosts include tayras, solitary weasel-like animals; new world monkeys; sloths; porcupines; and coatis — which are the South American cousins of racoons.

“There are 152 species of kissing bug, but we don’t know much about most of them, including the animals they feed on that can act as reservoirs for the parasite,” Christiane Weirauch, a professor of entomology in UCR’s College of Natural and Agricultural Sciences, said in a UCR news release. “Overall, the existing data is piecemeal, scattered, and biased toward a handful of heavily studied and well-documented species, while little data exists for insects that are found in very secluded habitats.”

The research, led by Anna Georgieva, an undergraduate majoring in biology, and Eric Gordon, a graduate student researcher in Weirauch’s lab, will support efforts to control the disease, particularly in poor, rural populations in South America, according to a UCR release.

Chagas disease is caused by the parasite Trypanosoma cruzi, which is transmitted to animals and humans by members of the assassin bug subfamily called kissing bugs that feed on blood and are named for their tendency to bite people around the mouth.

According to the Centers for Disease Control and Prevention, kissing bugs become infected with T. cruzi by biting an infected animal or person and, once infected, they pass T. cruzi parasites in their feces. When they bite a person and ingest blood, they defecate on them.

A person can become infected if bug feces enters their body through mucous membranes or skin lesions caused by the bite wound or scratching. Research also suggests that animals can become infected by eating other animals that harbor the parasite.

Although Chagas disease is common in rural areas, identifying new hosts among tree-dwelling, and sometimes nocturnal animals is a challenge, the release states. To sidestep this problem, the researchers identified new hosts by studying their blood—which they isolated straight from the guts of kissing bugs. The sample included 64 kissing bug samples collected from Central and South America between 2005 and 2015 that were preserved in ethanol.

“Our modern approach using DNA allowed us to determine this wide variety of animal hosts without a bias towards ones that are already known, unlike some older detection methods” Georgieva said in the UCR news release.

DNA analyses of the ingested blood revealed host associations for 24 of the samples. Among the newly identified hosts was the tayra, which has never before been named as a host for kissing bugs.

“Education and pesticide application around homes has helped reduce the impact of kissing bugs associated with homes and domestic animals, but now more and more cases of Chagas disease are driven by species most often associated with more rural hosts,” Gordon said in the statement. “One important consideration in controlling Chagas disease in wild animals is the possibility of bioaccumulation of the parasite in certain carnivores near the top of the food chain.

“If kissing bugs also feed on these carnivores, as has occurred for the tayra in our study, they are likely to be one of the important links in the transmission chain of the disease in the wild. If a vaccine becomes available one day in the future, they are good candidates to target for immunization to halt the natural spread of the parasite and potentially help to eradicate the pathogen.”


Do you know how long the researchers were in South America? Or are they working with researchers down there who sent them the specimens?

Gordon: “Weirauch lab members have spent months in total collecting these samples in South America (two and a half weeks in French Guiana, three weeks in Costa Rica, one month in Ecuador) but we have also received many additional specimens from other researchers, for example, those working in Mexico, Peru and Nicaragua.

Weirauch: “During these trips we also study and collect thousands of other specimens. Many are plant pests, some are beneficial insects, all belong to the true bugs.”

Why was this study done at UCR? Are other colleges in South America or researchers working on similar studies? 

Gordon: “This study was conducted at UCR because the Weirauch Lab at UCR or “the True Bug Lab” is the leading group of researchers in the study of the evolutionary relationships of the Reduviidae, or assassin bugs, which are the insect family that kissing bugs belong to. In the process of gathering samples for the study of that larger group, we have amassed many samples of kissing bugs which we used to conduct this study.”

Are other colleges in South America or researchers working on similar studies?

Gordon: “Other researchers in North America and South America have been working on similar studies (see for example Gorchakov et al. 2016  and Gottdenker et al. 2012, but many others exist). In comparison to most other studies, ours is somewhat different in having worked on specimens sometimes stored for years in ethanol as well as having many specimens collected from a wild environment as opposed to in association with domestic or man-made habitats.”

Judges courtroom closed after court deputy finds bed bugs

By Alexis Means

TOLEDO, Ohio (WTVG) – Courtroom eight at the Lucas County Common Pleas Courthouse remains closed after a bed bug was found on a chair. The owner of Del Roy Products and Pest Control inspected the courtroom with a magnifying glass and flashlight.

“You basically would just go along and follow the cracks and seams. That’s exactly what we did. When we got to the second row of chairs and there it was a dead bed bug. Then we found some larvae which is small white little worm,” said the owner of Del Roy Products and Pest Control Cornelius Pryba.

They treated the room.

” We us the insecticide treatment at Del Roy that consists of three applications at 14 days a part,” said Pryba.

He used a product called Bedlam Plus to kill the bed bugs. They spayed the chairs, baseboards and the switch plate covers.

“Basically it’s a bed bud monitor trap,” said Pryba.

He called the trap an extra set of eyes.

“So when we go back and do our inspection. I proceed to set some around the bottom of the seats of the chairs which would tell me if they are coming down the stem. If they are in here they’re coming from the baseboards,” said Pryba.

Heat can also be used to kill the insects. No word on if the courtroom will reopen on Monday.

“There’s no reason to get rid of those chairs at the courthouse at this point based on our inspection and first treatment. In the event I would have found a contaminated chair with the evidence I show you here with that picture then I would have strongly encouraged them to skedaddle those chairs out of here,” said Pryba.

The county will have Del Roy Products and Pest Control treat the courtroom two more times.

Deposit Elementary School warns families about bed bugs

By Chloe Vincente

DEPOSIT (WBNG) — The Deposit Elementary School is taking caution after the district said bed begs were discovered on personal items of some students.

Bed bugs are parasitic insects that can be difficult to see due to their small size.

Marianne Yourdon, a Communicable Disease Nurse at the Broome County Health Department, said “Bed bugs are flat. They’re reddish brown in color they’re about one to seven millimeters in size which is about the size of the head on Lincoln on a penny.”

On Wednesday, Deposit Schools Superintendent Denise Cook sent this message to families regarding bed bugs:

Recently it was brought to our attention that bed bugs had been brought into our elementary building. Bed bugs have been a popular topic for years and have been found in schools, hospitals, churches, theaters, and even fine hotels. Many of the schools in our area deal with this situation on a daily basis. I wanted to provide you with some information about the situation.
In no way is this an infestation. The source of the bugs has been identified and we are taking every step necessary to isolate the problem. Each day, we are inspecting student’s backpacks and clothing, washing student’s clothing (as necessary), bagging and isolating school and student belongings, and cleaning hard surfaces in the area. Additionally, we have employed organic pesticides and are working with families who are affected by the situation.
You may be wondering why we haven’t used chemical pesticides. Schools follow very strict regulations about the use of harmful chemicals around children. If the situation intensifies enough that we feel it would be necessary to use chemical pesticides, we would notify you because we would have to close school for a period of time. Because the school is not the source of the bugs, treating the problem with chemical pesticides would not prevent the bugs from re-entering the building. It would, however, expose our staff and students to potential health risks. Therefore, this is a lasts resort in this situation.
Today, I met with the Medical Director of the Broome County Health Department who assured me that we are following the expected protocol and regulations set forth by New York State. Because bed bugs (and lice) are not known to cause any health conditions or spread disease, they do not present a valid reason to keep students from attending school. On the contrary, the District has a legal obligation to continue providing all students with an education.
Please don’t hesitate to send your children to school tomorrow. As you know, bed bugs can be found in any establishment in any town. We will continue to be diligent, isolate the problem and treat it on a daily basis. You can help at home by checking your child’s backpack and clothing before and after school. I’ve attached the fact sheet that was sent home with the elementary students today. Please don’t hesitate to email me, Kelli Parsons, or the school nurse with any questions. 

Denise Cook

Cook said that no bed bugs have been found in classrooms, just on personal property of a couple students.

The Broome County Health Department said it’s not all that uncommon for schools to encounter bed bugs.

“I get calls occasionally where a child has come in with a bed bug either on their clothing or on their backpack,” said Yourdon.

Heather Steffan has two children at Deposit Elementary School. She said the school system is doing its best. She just hopes it doesn’t affect her household. She said, “They’re trying to fix it and I get that I just don’t want it at my house and I hope they don’t get it and bring it back.”

Steffan said overall, she isn’t too concerned but she is monitoring her children for signs of bites. “I just make sure when I get them home they don’t have any thing, not bugs no irritation,” she said.

Typically bed bugs don’t cause any major health problems. Health experts said they can be pesky, and cause discomfort

“They don’t carry human disease the main problem would be if someone was allergic to them. and it is kind of a nuisance and it can lead to difficulty sleeping if you’re getting bit. Yes, this is not anything you want in your home.”

Superintendent Cook said the school is checking student’s belongings and clothing to ensure no bugs are being brought into the school

She said it is safe for parents to send their kids to school.

The district will continue to provide families with updates.


Information and Perspectives on Bed Bug Prevention, Protection and Safety

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Information and Perspectives on Bed Bug Prevention, Protection and Safety

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Information and Perspectives on Bed Bug Prevention, Protection and Safety

Information and Perspectives on Bed Bug Prevention, Protection and Safety