Floridians need to be aware that jellyfish can not only be a source of an unpleasant sting, but also of allergic reactions. In fact, life threatening allergy (anaphylaxis) was first described in 1901 by two scientists; Charles Richet and Paul Portier who were studying jellyfish. They began their studies at the behest of Prince Albert of Monaco who was an avid oceanographer. He asked them to study the sting of the Portuguese man-of-war. They used the venom from both the man-of-war and the sea anemone in dog studies.
Because the concept of vaccination was new to science, they wondered if they could “vaccinate” dogs with the venom to build up protection. Unexpectedly (because they used too large of doses) and to their dismay, the second injection caused some of the dogs to die suddenly, because they failed to provide “phylaxis” (now called prophylaxis). They called the events aphylaxis (eventually termed anaphylaxis) meaning “against” “protection”. As a dog lover I’m sorry for the dogs, but I guess it would have been worse if they had experimented on the prince.
Jellyfish belong to the phylum Cnidaria which refers to the cnida, a specialized explosive organelle that causes stings. The cnida produce a variety of proteins which can lead to allergic sensitization: congestin, hyaluronidase, collagenase, proteinase, hypnotoxin, thalassin, nuclease, and phosphatase.
There are 10,000 species of jellyfish and their numbers are increasing due to global warming. The most common jellyfish allergy is skin allergy either immediate or delayed. The immediate reaction is hives that occur in addition to the “stings”. The hives respond to antihistamine therapy but the stings do not. The delayed reaction is akin to poison ivy allergy in that an itchy blistering develops several days after the immediate stings. This type of allergy responds best to steroids, either topical or oral.
The next most common reaction is food allergy reaction with itchy rash and GI symptoms after ingesting jellyfish. In some cultures, the umbrella (outer portion) of the jellyfish is a common food.
Anaphylaxis is the rarest form of allergy but can be life threatening. Most cases occur in people with frequent and repeated contact with jellyfish especially surfers and open water swimmers.
The short answer is yes, the long answer requires explanation. First of all, asthma and hypertension are both very common conditions with 9% of American adults having asthma and up to 25% having hypertension. Certain factors can contribute to both conditions: stress, obesity, sedentary life style, excess salt intake, and sleep-disturbed sleep. Correcting these factors can help both conditions.
In terms of medications, many of the medicines used to treat asthma and hypertension can act on opposing sides of the autonomic nervous system. The autonomic nervous system controls the smooth muscles found in both our bronchial tubes and our blood vessels and heart. Unfortunately, medicines that can relax heart and blood vessel smooth muscle (thereby lowering BP) can sometimes constrict bronchial smooth muscle (narrowing airways and causing asthma).
Coreg contains a beta-blocker meaning it blocks the beta input into blood vessels and the heart and thereby relaxes them and lowers BP. Unfortunately, it also blocks beta input into bronchial tubes which causes them to tighten, thereby causing asthma. Many of the medications used to treat asthma work through the beta system as stimulants (agonists). Many inhalers contain short acting or long acting beta agonists: albuterol, Advair, Symbicort, Breo, Dulera. Blocking the beta system reduces their benefit.
Luckily scientists have come to understand this dichotomy. This has led to the development of “cardio-selective” beta blockers. These drugs are much less likely to have negative effect on asthma as they are formatted to work mostly on the heart and blood vessels. Perhaps your doctor could switch you from Coreg (a non-cardio selective) to a cardio-selective beta blocker.
Over the past thirty years there has been a dramatic increase in both obesity and food allergy. In fact, the rate of increase for both conditions has followed the same identical track. For this reason, and others, scientists at Washington University School of Medicine have done exhaustive research to see if there might be a common cause. As it turns out a high fat diet is the answer. The rise in obesity is directly linked to the high fat content of “The Western Diet”. As it turns out, a high fat diet also can lead to food allergy for three main reasons: mast cells, gut permeability, and change in microbiota.
Mast cells are the “worker bees” for allergic conditions. They are the cells that contain and release histamine and other allergic mediators. A high fat diet leads to an accumulation of excess Mast cells inside the intestine walls. A high fat diet also makes the walls of the intestine more porous (or “leaky”) thus allowing greater penetration of food allergens.
Finally, a high fat diet alters the normal healthy microbiome towards one that is pro-inflammatory. This increase in total body inflammation promotes both allergic and auto-immune conditions.
PFAS stands for pollen food allergy syndrome. It used to be called OAS (oral allergy syndrome) but the new name better characterizes the pathogenesis. Using highly technical immunologic terms, it is called Class II food allergy. Class I food allergy refers to the common/classic form of food allergy where sensitivity occurs due to ingesting the food. In Class II food allergy, the sensitivity occurs from exposure to pollen and leads to cross reactivity with a food.
The symptoms involve immediate itching and sometimes mild swelling of the lips, tongue, mouth and throat. Sometimes the itching can even extend from the oral cavity to the back of the nose or ears. Occasionally these oral symptoms are accompanied by difficulty swallowing and/or nausea. Almost always the symptoms are both self-limiting and mild. But the immediate nature of the onset makes people fearful of possible anaphylaxis. That is why its important to distinguish PAS from traditional food allergy issues.
The most common pollen-food cross reactivities are: mugwort pollen and peach and chestnut; ragweed pollen and banana, melons, kiwi and peaches; grass pollen and tomato, peach, and apple; and birch pollen and apple, apricot, carrot, celery, cherry, chestnut, hazelnut, kiwi, peanut, pear, raspberry, soybean, strawberry, tomato and walnut.
Of interest, cooking a food can sometimes degrade the cross-reactivity protein so that PAS doesn’t occur. Otherwise, avoidance is the best therapy.
The two main tests being used during this pandemic are nasal swabs to detect active infection, and antibody tests to detect prior infection.
The nasal swab uses a polymerase chain reaction (PCR) which is a chemical tool that amplifies tiny amounts of nucleic acid to allow detection of viral RNA.
Antibody tests fall into two main categories: detection and protective value. The two main detection assays are for either spike glycoprotein (allows the virus to enter human cells) or nucleocapsid phosphoprotein (the most abundant protein). Both can confirm a prior corona virus infection.
Neutralizing antibody assay is used to determine if the presence of antibodies can “kill” (neutralize) the corona virus in a test tube. This type of testing will be used to determine how effective corona virus vaccines will be.
We have launched our new Mobile Check In app. You may download it by clicking the download on the right side of this page, or by scanning the QR Code in the office. You can check in from the parking lot. If you are going to be waiting for your shot in the car just click the box that says “yes, in car” and in the comment section please add the color and make of your car.
Of course, you can still check in from the IPad in the lobby.
The Journal of Allergy and Clinical Immunology recently published research on an experimental H4-antihistamine investigated at the University of Hanover. The research is part of a global effort to find more effective therapies for atopic dermatitis (eczema). The prevalence of atopic dermatitis has doubled in the past 30 years with occurrence in between 15% to 30% of children and 2% to 10% of adults. It is characterized by chronic relapsing itching of the skin which develops bumps and scaling, and can weep fluid in its severe form. The itch is very problematic often disrupting life activities and sleep.
Current therapies include improving skin barrier function through moisturizers and wet wraps, dilute bleach baths to reduce skin bacteria overgrowth, topical and systemic steroids, topical calcineurin inhibitors, topical phosphodiesterase inhibitor, phototherapy, and for very severe cases injectable monoclonal antibodies. To date, the available antihistamines have proven to be of very modest value. The traditional antihistamines block either H1: Benadryl, Claritin, Allegra, Zyrtec, Xyzal or H2: Zantac, Pepcid, Tagamet, and Axid. These are of modest benefit because the skin cells have only a small number of H1 and H2 receptors. But as it turns out, there are many H4 receptors on skin cells, hence research to find an effective and safe H4 antihistamine.
The drug ZPL-3893787 just might fit the bill. Recently developed by German scientists it proved to be extremely effective in a large-scale clinical trial. It led to a very remarkable lessening of itch but also to healing of the skin. The H4 receptors in the skin mediate both pruritis and inflammation. By blocking the H4 receptor “ZPL” seems to both stop the itch and heal the skin. If further studies give similar results it will prove to be a “God-send” for atopic dermatitis patients.
All three of my children have food allergies. My two daughters have minor symptoms but my son has eosinophilic esophagitis and has had to have his esophagus dilated twice. Why the difference?
The short and sweet answer is gender. First off, all food allergy is quite common, affecting up to 15% of Americans at some time during their lives. The resultant symptoms can vary from trivial to life threatening anaphylaxis (such as severe peanut allergy). Also, the “target organ” of the food allergy can vary from the skin, to the sinuses, to the lungs, to the GI tract. Eosinophil esophagitis (EOE) tends to be one of the more troublesome manifestations. The allergy leads to inflammation in the esophagus causing heart burn, reflux, and sometimes strictures, with resultant sticking of food. If mild the lodged food can be vomited out, but sometimes it has to be removed via endoscopy.
As it turns out, EOE is four times more common in males than in females. It also tends to be more severe in males than in females with more frequent development of strictures. The gender difference turns out to be due to a protective effect of estrogen, specifically 17-Beta-Estradiol. Estrogen can affect physiologic processes beyond reproductive function by its effect on the immune system. Estrogen receptors have been found on T and B lymphocytes, other white blood cells and on natural killer cells, all of which can mediate allergic inflammation. By downregulating the inflammatory response, estrogen protects the esophagus from the severe inflammation that can occur in males.
Researchers at the University of Michigan and the University of Cincinnati have recently found estrogen receptors in esophageal tissue of both sexes. Based on these findings they plan to investigate the plausibility of using a dilute estrogen solution to swallow as part of a healing therapy. They hope
that very dilute concentrations would work in males, but not adversely affect their hormonal balance.
A recent article in the Journal of Allergy and Clinical Immunology discussed current research into why asthma patients cough.
The answer, as it seems to be to many complex questions, is multifactorial. The human brain is the source of a myriad of protective reflexes from blinking to coughing. Protecting the airway compels a complex and delicate neural network. Think about the high degree of neurologic coordination required for swallowing without aspirating, even though the esophagus and trachea lie against one another. There is no question that asthmatics have a more delicate (“hair trigger”) cough reflex. What makes their cough-nerves more sensitive?
It seems to be a function of both structural issues and functional issues. The main structural issue is airway narrowing, which is why asthmatics wheeze and have shortness of breath. The narrowing of the airway “tugs” on the cough-nerves and by stretching them makes them more sensitive. One example of this heightened sensitivity is coughing due to laughing. When we laugh, we move a greater volume of air in and out of our lungs and this in turn leads to very slight cooling of the airway. This slight cooling is perceived as an airway threat and hence the coughing.
The functional issue is inflammation. You can think of this as “burning” the cough-nerve fibers. Because protecting our airway is so important the cough-nerve fibers are unmyelinated; that is, they don’t have the protective myelin coating that most nerves in the human body have. This makes them very vulnerable just as a bare copper wire would more easily spark.
Treating the cough of asthma boils down to expanding the narrowed airways and reducing inflammation.
By: Sasha Klemawesch, MD
Do you get misty-eyed every time you’re standing in RayJay, waiting for kickoff, listening to the National Anthem? Or do other drivers give you the side-eye when they catch you singing R-e-S-p-E-c-T into your air mic while sitting at a red light? No matter what genre you prefer, everyone has been moved by music at some point.
Cultures throughout history have recognized and made use of this, specifically, sound’s healing power. For example, aboriginal healers used the low frequency tones of the Yidaki instrument during their treatment of sick tribal members. Ancient Egyptians believed vowels to have held sacred power, so priests chanted them for healing prayers. Priestesses meanwhile played Ras (rattles) and harps during therapeutic rituals, both of them typically doing so in reverberant chambers which augmented the ultrasonic vibrations they were creating.
This latter phenomenon is the basis for modern science’s foray into sound therapy. Vibroacoustic treatment as we know it today started in Scandinavia in the 70’s; where early reports cited reduction in muscle tension, pain and anxiety after exposure. Since then, there have been a variety of research studies done in the area of sound and music therapy, including (more recently):
- Just 2 weeks of vibroacoustic treatment using classical music, done 30 min a day for 5 days a week, led to statistically significant reduction in depression among nursing home residents.
- NIH observed a group of patients with issues ranging from cancer to cardiovascular and infectious diseases to mood disorders, who underwent vibroacoustic sound treatment, and found a 53% “cumulative reduction in pain and symptoms” including tension, nausea, and fatigue.
- Yet another study found that vibroacoustic therapy helped decrease maladaptive behaviors and acting-out among children on the Autism spectrum.
One of the theories behind its effectiveness is the idea that our bodies are constantly using energy (at the cellular level seen as persistent micro-vibrations), and injury, stress or other sicknesses sap the speed and intensity of these micro-vibrations, further compounding fatigue, immunologic dysfunction, and overall chronic illness. It may seem a little new-agey to those with more western allopathic mindsets, but the goal of vibroacoustic therapy is to replenish this cellular energy and “get us vibrating at the optimal frequency”. And when you add music to the equation you are accessing a whole additional set of benefits with how much music affects the brain. Now the eastern vs western, alternative vs allopathic medicine debate is for another time, but it’s hard to argue with the results to date in the vibroacoustic therapy arena. In fact, you could say, it’s a pretty sound option for treatment!