Human Heartworm Disease
Dirofilariasis is a long ignored disease indigenous to most areas of the United States. When a person has this disease there are no obvious signs that are visible to the physician and there are no approved serological test for the disease. A physician essentially has no tools to help them diagnose this disease. The patients may present very diverse and nondescript medical issues but nothing will likely point that physician at making a correct diagnosis except for the patients own self reported symptoms of Formication. Even if the doctor could diagnose this disease there is still no approved treatment plan for the disease in humans. Prescribing highly toxic medications to a patient where the doctor can not even prove that the patient has this disease is very unlikely. So, we desperately need to develop a test for this disease as it is nearly impossible to study any disease where you can not even tell who has it. Unfortunately only the patient knows if they have the disease, but without testing they will just be ignored.
One insect bite is all it takes to acquire this very stealthy disease. The odds of you developing this disease is approximately equal to the probability of your dog acquiring Heartworm. Fortunately your dog will be successfully tested and treated, while you will not be. Because there is no test in humans nobody ever gets diagnosed with the occult form of this disease, which is the actual default condition in humans. Without even a single diagnosis there can be no statistics to collect, and without statistics there is no money set aside for research that might otherwise develop a viable test for the disease. It is an endless cycle of waiting because without a medical test it is not even possible to find the subjects with whom to study the pathology and progression of the disease. Even the best of scientists can not possibly study a disease if they can not determine who has the disease.
HDRI is committed to raising the awareness of this disease and promote the necessity for actual research on this disease, as there are clearly dire consequences to the health for those who are unfortunate enough to acquire this stealthy disease. Please keep reading to understand why this is.
Life cycle and Immunology in Humans
From the moment the insect bites a human the filaria crawls into the open wound made by the arthropod vector in taking their blood meal. The L3 stage filaria then begins a transformation needed to evade the hosts immune system. Once in the skin it transforms by molting and then begins covering itself with a thin protective layer of carbohydrates that serve to shield it it from any granulating immune cells or their toxic compounds of the host immune cells that might try to harm it. It also begins wrapping up some very targeted mRNA into exosome like particles and starts dumping these as secretomes into the host circulatory system. These rogue mRNA capsules are designed to be pulled into the hosts own cells to begin the rogue production of many different protein molecules that help circumvent the hosts own immune system, and thereby make it nearly impossible for the host to form a suitable defense against the new parasitic invader. So the the hosts own endothelial cells are tricked into producing byproducts that are designed expressly to suppress its own immune system and thus help the parasite to stay hidden from any kind of effective immune response. The carbohydrate protective layer makes them all but impervious to the destructive cytokines and other defenses normally used against parasites. Furthermore antibodies are know to not adhere well at all to carbohydrates so they have little effect on the adult filaria.
Once this stage is set the filaria migrates into the circulatory system proper where it then spends the rest of its life migrating around within the veins where the heart and lungs are directly downstream. Should an adult filaria actually die, for any reason, the filaria cadaver will pass through the right ventricle and then finally get lodged into the lungs to cause a potential a blood flow blockage, ischemia, and possibly produce a coin lesion. If it happens to gets calcified it might then be discovered by accident on an x-ray taken for a completely different medical reason. The lung tissue whose blood supply had been cut off at that particular site may die in the process. Needless to say when an adult filaria dies it can lead to a myriad of medical complications yet the source of that damage can not be known without exploratory surgery.
Since the host immune response is being altered by the parasite, the host is no longer immunoincompetent to handle several other types of infections. There is disagreement in the journal archives about Th1 vs Th2 suppression and clearly the competency of the human immune system needs to be better studied in this circumstance. In one specific case study the flow cytometry shows that the CD8+ is suppressed to near zero while the total IgG antibody count is near the upper limit. Specific Antibody tests show both the EBV and HSV specific antibodies are completely off the chart of their respective tests but without the CD8+ the host may be unable to kill off the viral infected host cells. This specific case study is clearly without a competent immune response and is unable to eliminate at least two latent viral infections for more than 35+ years.
Then there is Wolbachia. With Dirofilariasis you actually get two diseases at the same time. Dirofilariasis requires Wolbachia in order to complete its life-cycle so it brings this disease along with its immune evasion bag of tricks. Wolbachia lives within the human cell and is therefore extremely hard to get rid of. It may take a course of 6-9 months of doxycycline to effectively kill this bacterium. The good news is that killing the Wolbachia makes the Dirofilaria that much weaker and this will probably be at least a portion of the treatment protocol needed to cure a human of Dirofilaria.
As the host immune system attempts to fight back all the cytokines are essentially dumped directly into the flowing bloodstream, having little effect on the carbohydrate protection layer on the adult filaria before it is swept downstream where this will have damaging effects on the endothelial lining of the entire vascular system. Any microfilaria produced remain unprotected and can be quickly tagged and labeled by antibodies for destruction and removal by the macrophages. It would not be until the remnants of the microfilaria have passed completely through the heart, lungs, and any internal organs or muscles that these fragments would even be available as a blood draw for any microscopic inspection. Much of this garbage is quite likely to just to be caught and filtered by the lungs capillaries while this needed cleanup is dealt with and this condition could then exasperate other conditions such as asthma or other breathing disorders. Clearly the lungs are subjected to the degrading effects of the cytokines and other immune cell degranulation causing even more damage damage. Systemic pain will be constant but will vary in severity in accordance to both the health of the host and the health of the filaria. There will also be a constant flow of histamines as a chemical messenger that is needed to activate immune system responses that are no longer working due to this immunosuppression.
The mRNA also have the effect of making the endothelial layer of the vascular system more permeable to aid the microfilaria in their journey to the skin surface where they could be picked up by another arthropod during a blood meal. This vascular damage is documented in laboratory animals but can not be studied in humans. Regardless of the unsuccessful journey of the microfilaria in humans these mRNA, immunologic fragments, and cytokines are all still at work causing problems for the host. Between the mRNA and the 24×7 flow of cytokines and histamines into the bloodstream the result will be a much more permeable membrane throughout the entire vascular system and all internal organs.
This is where Leaky Gut Syndrome (LGS) comes into play, and a whole cascade of new immunological problems will follow. Because the boundary layer of the small intestines is only about one or two cell layer thick, and its a literal war zone for the gut immune system and microbiota, any degradation of this barrier coming from the vascular system side will have major consequences for the host. The microscopic damage to the intestines from the inside will then allow macro sized molecules of food to pass directly into the host circulation which will then trigger an enormous number of IgG antibodies in the bloodstream. Food intolerance will follow as well as possible malnutrition due to poor absorption of the required nutrients. Gas, cramps, and diarrhea are all subject to the dietary intake while they become most sensitive to the proteins, fats, and oils that are consumed and Food Intolerance will be the result as the immune system begins reacting to many peptide sequences now seen in the blood that should never have been there and Irritable Bowel Syndrome (IBS) or Inflammatory Bowel Disease (IBD) may be the result. Since this is not an “allergy” (Ig-E mediated reaction) the normal food allergy tests given by doctors are of no help to isolate the problem, but the ALCAT(*) food sensitivity test may help these individuals to sort out which specific foods they need to stay away from, but the sensitivity list does change over time as the LGS disease progresses.
This all puts the host immune system into overdrive and requires the expenditure of massive amounts of energy to sustain it just as the level of nutrients needed to support this battle drop. This gives the host a net negative energy balance and may result in symptoms of Chronic Fatigue Syndrome (CFS) that will very in severity based on the level of the infection and the particular diet of the host. From here it is a forever downward spiral towards depression and anxiety with a possible statistical increase of alcoholism, drug use, and potentially even suicide. Without support from the clinical medical institutions this final outcome is almost ensured in any extreme case of the disease. These people are in pain, are forced to withdraw from any social life due to the their worsening medical conditions, and are without hope of life ever improving.
Its accumulative in nature
This disease is also accumulative in nature. Once even a single filaria is able to take hold the mRNA released into the bloodstream set the stage for the next arrival. Subsequent exposure via any infected vector will essentially get a free ride past all the hosts natural defenses. The mRNA actually decrease the number of effector cells available to fight the incoming filaria. These new arrivals will have little opposition while they molt and transform themselves and go off to join the rest in the vascular system. Since there is no evidence that the adult filaria actually die of natural causes, except for the presence of coin lesions, their numbers will only grow over time.
The danger from the lack of sound medical advise
Reducing the exposure to the disease is the only real method to prevent acquiring even more disease unless it becomes possible to get prophylactic prescription for Moxidectin from their personal physician as a preventative treatment, but even that will not do anything for the adult filaria themselves. This prescription will clearly not happen without first getting a diagnosis and there is still no test for the disease. Exposure reduction is therefor the only available preventative to a worsening disease. But one must realize these people are desperate for a cure, to end the 24×7 torture session they live with. Psychologically, since they get no moral support from the medical institutions at all, they are ready to try anything to kill off this disease without any medical supervision what so ever. There are a multitude of products out there that claim to kill parasites and these people will literally try anything they can get their hands on. Many products are just predatory in nature and provide absolutely no benefit for adult Dirofilaria yet they can have some severe consequences. For example, some products have naturally occurring cyanide and arsenic (e.g. apricot pits or apple seeds) and other lethal compounds, while others are sold specifically for animals off the shelf without a prescription. These people are despite and will try every one of them in hope to find the one that works because they are offered absolutely no guidance at all. They will easily fall prey to these bogus products that simply will not work. We need to be giving them at least some level of medical guidance so that they don’t kill themselves trying every substance they find on the market. The medical establishment has clearly fallen short of their duty.
Diethyl Carbamazine (DEC) is the one drug without arsenic that can be prescribed for Dirofilaria. It however has four major problems. First, it is only 40% effective at clearing out adult Dirofilaria. Second, it is not available for prescription in the US. It was taken off the market due to its toxicity and so it is only available to your physician through the CDC under the compassionate care program and only then under specific circumstances. Last of all, since no diagnosis is yet possible there will be no prescription made available from the CDC for Dirofilaria even if your doctor asks for it. Fourth, there is also no way to determine if the drug even worked other than simply asking the patient what they feel. Everything depends on finding a valid test for this disease.
Relationships of disease presentation
In the medical journal literature there are several forms of Dirofilariasis infection mentioned in various clinical case studies. These includes ocular, pulmonary coin lesions, and subcutaneous. The subcutaneous infection is limited to a single adult and can easily be removed surgically in most cases.
A nodule is caused by a single adult filaria not being able to penetrate deep into the vascular system and is instead caught up and quarantined by the immune system. Other filaria from that same bite may also be present but were successful in reaching the bloodstream. When they enter the bloodstream the infection is in the occult phase of the disease which is the default condition in humans. The ocular form of the disease occurs when the filaria is still in its pre-adult form and then crawls into the veins at the back of the eye and thereby becomes visible to a physician. Sometimes they even penetrate all the way into the eye itself but this is far less common. The pulmonary coin lesion form of the disease happens when the filaria dies, passes through the heart, and gets caught in the lungs, where the arteries branch and narrow.
Note that all these visible manifestations except for the subcutaneous nodule is predicated on their first being the occult form of the disease present. These other types simply can not happen without the occult form existing first, and the probability of either ocular or pulmonary occurring in general is rather slim. What is significant here is that when the infection is not one of these other visible forms of the disease it will continue on as the undiagnosed occult infection and will very likely last for the lifetime of the host. If the filarias death were a common occurrence we would see a lot more of pulmonary Dirofilariasis coin lesions in x-rays when the same person was previously diagnosed with a subcutaneous skin nodule infection. Logically the people with subcutaneous infections should have a much higher rate of pulmonary issues, yet there is no mention of any such association in the journal literature. They have not even bothered to look for this association. At the time of this writing there have been no scientific studies located that even try to follow up on these clinically diagnosed infections. There has never been a cohort study needed to make such an association but logically this association should be true.
The threat of disease vectors
The filaria count in the initial bite is likely very important because a group effort will provide much more mRNA into the bloodstream than a single filaria possibly can. The more the host immune system is turned off prior to their entering the vasculature the better their chances of overall survival.
The largest mosquito can carry as many as 21 microfilaria while a horsefly (Tabanidae) bite can carry well over 200 L3 stage filaria. Yet in the literature coming from textbooks or journal articles, or from either the CDC or NIH you won’t even see horseflies mentioned yet they pose a much greater threat than a smaller mosquito. It also seems that what information is currently being published is just being ignored by the scientific community and no cross correlation of this data is being made with respect to humans. The medical advise for doctors hasn’t changed to reflect what is currently published deep in the journal archives.
For instance, there are many more arthropods (Ceratopogonidae , Culicidae, Simuliidae, Stomoxys calcitrans, Tabanidae ) capable of carrying this disease. But you won’t be reading about this anywhere, because researchers, doctors, and scientists are not yet concerned enough with this disease despite its ubiquitous prevalence throughout the US, and the entire world, excluding only Antarctica. Midges and sand fleas were both indigenous to the Gulf region and many service dogs have come back from the Gulf region Heartworm positive while some service members have been diagnosed with Formication. Logically there may be a connection here but clinically we may never know the answer because there is no test. Gastro-Intestinal doctors also note a fair amount of patients experiencing Formication symptoms, while people with LGS/IDS/IDB are extremely likely to need their assistance. Is there a correlation here too? There are no studies looking for any correlations.
Probability of successful infection
Obviously not all infections are equal, but it you get bitten by a arthropod vector with only one or two filaria then you may have a better chance for your immune system to kill them off before they start suppressing the the immune system and reducing your ability to fight back. If you get bitten by one horsefly with a lot of filaria (200+) then chances are at least one will succeed in evading the immune system. On the other hand repeated exposure by many smaller infected arthropods such as black flies, sand fleas, or Midges will also likely succeed. Its the total exposure over a given period that would matter. What is clearly important here is the lifecycle of the vector in terms of the number of times it may bite, because they need to bite more than once in order to acquire the disease and a second time to transfer that disease to a human. Mosquitos live about three weeks and rarely bite twice, but there are many of them so it is statistically a problem. Horseflies on the other hand can live up to 60 days and have ample opportunity to bite more than once thus making them a significant problem for not just how many filaria they can transfer at one time but also for how many hosts they can infect in their given lifetime. The risk of exposure by various vectors clearly needs to be studied in more detail.
(*) Disclosure: HDRI has no financial interest in any laboratories associated with ALCAT testing. The information is provided here in hope that it might be useful to someone.
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