Summer is here, and just as we are shedding layers and welcoming the sunshine, insects are lining up to feast on our flesh.
While ticks and the scary diseases they carry are among the most fearsome of warm-weather insects, another tiny pest is making a meal out of mankind in a truly horrifying fashion.
Chiggers, miniature mites that live in grassy, wooded areas or near water, come alive in the summer season when warmer temperatures create ideal conditions for feeding and breeding.
Related to spiders and ticks, chiggers are petite parasites that are nearly invisible to the naked eye. Though they be but small, their effects are mighty and their approach to growth truly disturbing.
The creepy life cycle of a chigger begins when it hatches from an egg. These juvenile larval mites (band name) then feed on the skin of an animal or human host before falling off and transitioning into their adult form.
These six-legged larvae rely on the flesh of their hosts to supply the nutrients they need to grow into their eight-legged, non-parasitic best selves.
Typically, chigger larvae attach to clothing, favoring areas such as waistbands, bra lines and sock lines where skin and clothing are in close contact.
To satisfy their appalling appetites, chigger larvae move from clothing to skin, releasing a powerful digestive enzyme to make our cells slurpable.
As the enzyme liquifies skin cells, it hardens the surrounding tissue, creating a straw-like tube — known as a stylostome — that allows the chiggers to drink from our dermis like a morbid milkshake.
Because mites have mouths that can pierce but not tear or consume, this skin straw enables them to suck up liquified skin cells and, in some cases, blood for their gnarly nourishment.
Bottoms up.
The enzyme that kills skin cells also causes the intense itching that we associate with a chigger attack. The irritation peaks during the first 24-48 hours after contact, then subsides over the following two weeks.
The most common areas for chiggers to attach and attack are the ankles, lower legs, backs of the knees, waist and groin.
Chigger bites are not immediately apparent, as symptoms can take up to 3 hours after contact to appear.
Symptoms include red spots or pimples on the skin and severe itching.
Because chiggers feed on the skin rather than burrow into it, a rash usually appears only after the mites have detached, and treatment focuses on alleviating itching rather than parasite removal.
Treatment options include cleaning the affected area with soap and water, applying calamine lotion, cold compresses, and permethrin, and/or taking antihistamines.
You can prevent becoming chigger lunch by wearing protective clothing, using insect repellent, treating clothing with insect repellent, and avoiding outdoor activity in grassy, wet, or wooded areas during the summer months.

The H5N1 strain of bird flu has for the first time been found in Australia, the country’s agriculture ministry confirmed. It means the highly contagious variant has now reached every continent.
The disease was found in a migratory seabird, a brown skua, in remote Western Australia, Agriculture Minister Julie Collins said on Saturday.
The bird was found on a beach at the Cape Le Grand National Park near the town of Esperance, about 700km (434 mi) south-east of Perth, according to local media.
Australia was previously the only continent where the H5N1 bird flu strain had not been found.
Collins added that there was a second suspected case of bird flu – a southern petrel that was found exhausted on an Esperance beach, though she added that there was no “evidence of mass mortalities at this time”.
Threatened Species Commissioner Fiona Fraser said authorities would know “within a few days” if the virus was present in any other animal populations in Australia, according to a report by the national broadcaster, the ABC.
The report also quoted the country’s Chief Veterinary Officer Beth Cookson who said authorities had been “preparing for this event for a long time” and that the committee for emergency animal disease had convened on Saturday.
The H5N1 strain of bird flu was detected on the remote Australian territories of Heard and McDonald Islands in October last year – located in the southern Indian Ocean.
A study released this week estimated that around 13,000 baby seals from a group of 17,000 on Heard Island were killed by the H5N1 strain of bird flu since last August, more than 75% of the entire group. They also found higher than expected deaths in penguin populations.
Scientists believe bird flu was likely introduced to the islands last August from migrating birds from the French-owned Crozet Islands, about 1,800 km away.
Bird flu is a disease caused by a virus that infects birds and sometimes other animals, such as foxes, seals and otters.
The major strain – circulating among wild birds worldwide – is a type of the virus known as H5N1. It emerged in China in the late 1990s.

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A traveler infected with measles may have exposed passengers at Los Angeles International Airport and guests at a nearby hotel after arriving in Los Angeles County earlier this month, health officials said Wednesday.
The Los Angeles County Department of Public Health said it is investigating a confirmed measles case involving a traveler who arrived aboard Cathay Pacific Flight CX 884 on June 11. The traveler was infectious while passing through Los Angeles County, potentially exposing others at LAX and the Hilton Los Angeles Airport Hotel.
The case marks the sixth measles infection reported in Los Angeles County this year. Health officials said the risk of exposure could increase as summer travel ramps up and Los Angeles welcomes international visitors for FIFA World Cup events being held in the region.
MEASLES CASES CONFIRMED AT FOUR MAJOR US AIRPORTS ACROSS COUNTRY AMID PEAK HOLIDAY TRAVEL
According to health officials, anyone who was at the Tom Bradley International Terminal between 10 a.m. and noon on June 11 may have been exposed. Officials also identified a potential exposure at the Hilton Los Angeles Airport Hotel, located at 5711 W. Century Blvd., between 11:15 a.m. and 12:15 p.m. that same day.
The Centers for Disease Control and Prevention is working with local health departments to notify passengers who were seated near the infected traveler on the international flight.
People who were at either location during the listed times could develop symptoms between seven and 21 days after exposure, officials said. The last day to monitor for symptoms is July 2.
AT LEAST 46 CHILDREN DEAD AMID MEASLES OUTBREAK AS VIRUS SPREADS GLOBALLY
“As measles cases increase, it is important that residents take steps to make sure they are fully protected,” Los Angeles County Health Officer Dr. Muntu Davis said. “The MMR vaccine is the safest and most reliable way to prevent measles and protect yourself, your family, and your community.”
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Symptoms include fever, cough, runny nose, red and watery eyes, followed by a rash that typically begins on the face before spreading to the rest of the body.
Fox News Digital reached out to the Los Angeles County Department of Public Health for additional comment but did not receive a response.

Amna Nawaz:
A growing body of research suggests popular weight loss drugs like Ozempic and Wegovy may also help treat or prevent certain cancers. It’s the latest unexpected benefit to be associated with GLP-1s, which are now taken by one in eight American adults.
William Brangham has more.
William Brangham:
The results in these cases come from what are known as observational studies, not more rigorous clinical trials, and researchers say there are still many open questions.
That said, this was the hot topic at a recent conference of America’s top cancer doctors, where a number of observations all pointed in the same direction, that GLP-1s appeared to help fight cancer above and beyond the benefits that you would expect from weight loss alone.
So, to understand these implications and the limitations of these studies, we turn to Dr. Neil Iyengar. He’s director of breast oncology and cancer survivorship at the Winship Cancer Institute at Emory University.
Dr. Iyengar, thank you for being here.
There is this growing body of observational evidence that GLP-1s do seem to help with regards to cancer. Big picture, what have those studies found?
Dr. Neil Iyengar, Emory University School of Medicine: Well, thanks for having me.
I think this is really exciting and important data. We have known for a very long time that obesity is associated with an increased risk of at least 13 different cancers, possibly 20 different cancers. And so reversing obesity has been a key area of research.
Up until now, we haven’t had powerful methods for weight loss as we do with the GLP-1 receptor agonists. These studies that you have pointed out really identify an exciting hypothesis or theory. And I say that because, as you mentioned, these are observational studies.
But the data really support the idea that weight loss through a GLP-1 receptor agonist cannot only help to prevent many of the obesity-related cancers, but may actually help to prevent a recurrence of some of these cancers even after a cancer diagnosis.
William Brangham:
I mean, it’s quite striking.
I just want to read some of the details from some of these studies. One analysis from the University of Pennsylvania found women between the ages of 45 and 80 who were taking these drugs were about 30 percent less likely to develop breast cancer than those who were not.
Another surveyed patients identified with seven types of early-stage cancer and found GLP-1s significantly reduced the risk of spread in four of them, lung, breast, colon, and liver cancers. Again, do you believe that this is principally a function of weight loss being the real actor here?
Dr. Neil Iyengar:
I do.
It’s been clear from prior studies where we have used methods like diet or exercise, which induce lower amounts of weight loss. But even at those lower-levels of weight loss, we see some reduction, not as profound as what you have just read, but we see some reduction in the risk of obesity-related cancers.
What we do know from studies that have looked at larger weight loss procedures, like bariatric surgery, for example, is that the more weight loss we can induce in people who are struggling with obesity, the lower the risk of developing cancer or cancer recurrence.
So it’s not surprising that, when we look at these large observational data sets, a GLP-1 receptor agonist, which can typically induce 15 to 20 percent or even greater weight loss, similar to what bariatric surgeries do, that these drugs can also reduce the risk of cancer.
And it does seem that it’s primarily through the weight loss function. We also know that GLP-1s have some anti-inflammatory effects as well. And we’re learning about some possible immune-related effects as well. But I think it’s really driven through the large amounts of weight loss that these drugs can induce, as opposed to prior or other diabetes drugs.
And that’s where we’re probably likely to see success with the GLP-1s and cancer risk reduction.
William Brangham:
So let’s say those studies go forward and they do show this real effect.
How much of a shift would this be in your field of cancer, in oncology?
Dr. Neil Iyengar:
I think that we are standing really at the precipice of a massive possible shift in the global health burden, not only of obesity, but obesity-related cancers.
We know that one in seven male cancer-related deaths and one in six female cancer-related deaths are related to obesity. If we can reduce the obesity problem, which we know we can do with the GLP-1s, this really stands to remarkably shift the global burden of obesity-related cancers.
But we have to do this cautiously, because there are mixed data for the effects on various types of cancers, interactions with different types of cancer therapies. This is why it is so essential that we continue studying these drugs in a prospective, rigorous way, so we can optimally and safely use them to reduce cancer burden.
William Brangham:
I mean, given what we know now — you’re a specialist in treating breast cancer.
Again, with the data that we have currently, would you suggest to your patients that they take a GLP-1 either for current cancer patients or as a preventative?
Dr. Neil Iyengar:
I think this is a tricky question right now, because this is where we have to rely on the available data, which is observational, as we’ve been discussing.
And so where I worry is, we don’t have data on how the GLP-1s may or may not interact with cancer therapies. So, for a patient who has completed their cancer therapy and is cancer-free, I think, if they are dealing with obesity, then this could be a successful approach for, A, reducing obesity, and, B, reducing the risk of cancer recurrence due to obesity.
But for patients who are currently on treatment, especially chemotherapy or immune therapy, we don’t know yet precisely how these drugs may interact. They may possibly make side effects worse. They may possibly make some treatments like immunotherapy less effective for cancer treatment.
That’s really where we don’t know enough to recommend the use of a GLP-1 in that setting. So, ultimately, I would say, for a cancer survivor who has completed their therapy and is struggling with obesity, it is worth having that discussion with your oncologist and with your doctors about whether it is safe to use a GLP.
But if you’re on active therapy, certainly, have that conversation with your oncologist. I would caution against it until we generate more data.
William Brangham:
All right, that is Dr. Neil Iyengar of Emory University.
Thank you so much for being here.
Dr. Neil Iyengar:
Thank you for having me.

A new study is raising questions about one of the most widely held ideas in Alzheimer’s research—suggesting the disease may not start with plaques in the brain after all.
Researchers at the University of California, Riverside (UCR) say the earliest changes could instead happen inside nerve cells, where two key proteins appear to interfere with each other.
For years, much of the focus has been on amyloid beta, or a-beta, because it forms clumps in the brains of people with Alzheimer’s. That link appeared well supported, especially since genetic mutations that increase a-beta levels are known to cause early-onset forms of the disease.
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But attempts to treat Alzheimer’s by removing these clumps have been largely unsuccessful, with thousands of trials failing to stop or reverse its progression.
Michael Kane, chief medical officer at Indiana Center for Recovery, told Newsweek that the findings of this study should not be seen as dismissing the amyloid theory entirely, but rather as refining it.
“I see these findings less as a rejection of the amyloid theory and more as a possible link between amyloid beta and tau,” he said.
Connection Between Amyloid Beta and Tau
Scientists have long known that another protein, tau, is also involved. Both a-beta and tau build up in the brains of people diagnosed with Alzheimer’s, yet how they are connected has remained unclear.
“In addition to having dementia, Alzheimer’s diagnosis requires both a-beta and tau buildup in the brain,” said study lead author Ryan Julian, a chemistry professor at UCR. “But many labs focus on the role of one and ignore the other.”
The new study, published in Proceedings of the National Academy of Sciences, Nexus, looks at what happens when the two proteins are present inside the same cell.
Kane said this connection is one of the most significant aspects of the research.
“Amyloid beta and tau have both been central to Alzheimer’s research for decades, but the field has struggled to explain exactly how they interact. This study gives scientists a more specific place to look,” he said.
What Happens Inside Nerve Cell
Tau normally supports structures called microtubules, which act as internal pathways, helping nerve cells move essential materials to where they are needed.
The researchers found that the part of tau that attaches to these structures is very similar to amyloid beta. That similarity led them to examine whether a-beta could attach to microtubules in the same way.
Using a fluorescent marker to track the protein, the team observed that a-beta can bind to microtubules with similar strength to tau.
“Our work shows amyloid beta and tau compete for the same binding sites on microtubules, and that a-beta can prevent tau from functioning correctly,” Julian said.
Kane said this mechanism could represent an earlier stage of disease development than previously recognised.
“The damage may start earlier, with the cell’s machinery becoming less stable,” he said.
Disruption That May Come First
The researchers suggest that this competition could be an important early step.
If a-beta builds up inside a neuron, it may push tau away from the microtubules. Without tau in place, the cell’s transport system may begin to break down.
At the same time, tau may start to change behavior—clumping together and moving into areas of the cell where it is not normally found.
This points to a different way of thinking about the disease. Instead of protein buildup being the starting cause on its own, the two processes may be part of a wider problem inside cells.
Kane cautioned that while the explanation is biologically plausible, it remains a working model. “A plausible mechanism is not the same as proof that this is what drives Alzheimer’s in patients,” he said.
Ageing May Play Role
The study also highlights a process called autophagy, which normally clears unwanted proteins from cells, including a-beta.
As this process becomes less efficient with age, amyloid beta may begin to accumulate inside neurons. This could increase the chances of it competing with tau and interfering with normal cell function.
What It Could Mean Going Forward
The findings may help explain why some earlier approaches to treatment have struggled to make a difference.
They also suggest that future research may look more closely at how these proteins interact inside cells, rather than focusing only on removing them once they have formed clumps.
Julian said the idea helps bring together different strands of research.
“This idea helps make sense of many results that previously seemed unrelated,” he said. “It gives us a clearer picture of what may be going wrong inside neurons and where new treatments might start.”
Kane said the study could point scientists toward new types of therapeutic strategies, but warned against overstating its immediacy.
“It could point researchers toward targets inside the neuron, such as protecting microtubules or preventing amyloid beta from interfering with tau—but I would not describe it as an immediate treatment breakthrough,” he said.
He added that the most important next step is confirming whether the process occurs in people.
“Researchers need to know when it happens, who it happens in, and whether it tracks with memory loss or functional decline over time,” he said.
Kane also urged caution in interpreting the findings.