This is Julia Hugo Rachel. Like millions around the world I was accused of having a mental illness, had my child taken away from me and spent years in mental and physical agony. Then I found I was not mentally ill but instead had a virus and was cured. There are many people like me and this book, Viral Assault, will show victims, families and friends that there is hope. This is my story.

To the millions of victims and their families who have suffered from Chronic Fatigue Syndrome, it is the most baffling of diseases. All of us know only too well the exhaustion that becomes part of daily life, the depression that seems to accompany the inability to get anything done, the lack of will, the loss of weight. But beyond the common symptoms, the underlying causes seem to be incoherent and elusive, defying both logic and discovery.

To the victims, the results of CFS could not be clearer as is the remarkable collapse of daily existence where often high functioning individuals fall to the bottom of the human heap. Doctors and even friends and family can often dismiss the symptoms as psychological, a mental disturbance that can be easily fixed with some rest and a bit of therapy. To the few doctors who really understand CFS, the reality is much more complex. 

Although there is no definitive answer available yet to medical science, it seems clear that there is a basket of illnesses that in some way can trigger CFS as a consequence of a patient becoming infected. Exactly what happens in the body is not known but the effects are clearly devastating. What is known is that these illnesses clearly attack an already weakened immune system in some victims while others feel no additional effects. 

What is also known is a treatment that can be successful for one patient may have little impact on another. This creates a huge and very complex puzzle for medical science: why is one treatment successful and not another? Why do one group of patients respond to one set of protocols while another seemingly identical group of patients remain ill?

I have been fortunate to receive treatment from Dr. Jose Montoya, perhaps the world’s most experienced and successful specialist in treating CFS. But even he is baffled by the disease’s complexity and calls for a huge international effort to focus the research across multiple disease specialties in the hope of refining and then treating newly identified common elements that link all the illnesses together.

It’s an enormous and complex task that requires harnessing resources in government and the private sector to look with fresh eyes at CFS, an illness which is believed to impact between 1-4m people each year in America alone and perhaps 25m people worldwide with further devastation on the 100m or so family members who have to cope with the fallout of a loved one descending into despair and possible suicide.

My own experience of CFS was largely confined to myself and my son, Blake, but since beginning the journey towards a cure I have met with hundreds of people and corresponded with thousands of others who have all confirmed that the heartbreak and despair I felt for me and my son is something that truly binds all CFS sufferers together.

I have clarity around something else: there are a range of illnesses that may include PTSD, Epstein-Barr, HHV-6A, Dengue Fever, Q Fever, the swine Flu and others such as a head injury that seem to trigger CFS in some people. This is what I hear anecdotally from victims and what I have also learned from doctors in the field. The problem with such a conclusion is that the research is stove piped (the expert on one disease tends to know little about any other disease). And then the experts on CFS are constrained by what information they can gather on the precursor illnesses because there is so little sharing of information across the different specialties. 

Because there are so many possible links to CFS and ME, for this section, we will divide and conquer, looking at each illness piece by piece and examine the link to chronic fatigue. This was how I eventually saved my son’s life: by first looking at the causes and following the effects until I eventually I found the right doctor with the right answers and the right treatment.

Though this list is condensed, it will help to give an understanding of the possible connections and show that more than one possibility still exists for determining chronic fatigue’s true cause.  

Epstein- Barr:

The CDC defines Epstein-Barr, which is also known by the name human herpesvirus 4, as a virus which is actually very common among humans and falls into the herpesvirus family. Called EBV for short, the virus is spread through bodily fluids, primarily saliva and is known to cause infectious mononucleosis as well as other illnesses.

The symptoms of this virus fall closely in line with CFS and include symptoms such as fatigue, fever, inflamed throat, swollen lymph nodes in the neck, enlarged spleen, swollen liver and rash. EBV is also very common among teenage children which is where it separates itself from CFS which is generally seen in adults. The symptoms can last for weeks or even months depending on the severity of the case, but those symptoms vary patient to patient depending on their immune system and its strength.  

Like Chronic Fatigue Syndrome, there is currently no cure for EBV, and sufferers are left to turn to the basics in hopes of getting better. Drinking water, no extreme exercise for 6 months, avoiding those who have been infected and using over the counter treatments for the more manageable symptoms of EBV are all in the CDC’s recommendations for improving conditions of the virus. Though it seems such treatments would do little to help, some sufferers attest a little help goes a long way. 

Though it is not listed by the CDC, many sufferers of EBV also report problems with their eyesight along with their other symptoms. 

A  study published back in the late 1980s  by JAMA Ophthalmology titled Ocular Involvement Associated With Chronic Epstein-Barr Virus suggested eye problems are usually limited to an issue known as transient follicular conjunctivitis, but it suggested that other injuries had also been reported.  For this specific test, the doctors focused on three sufferers of EBV who had chronic versions of the virus as well as eye problems associated with the virus. 

For each of the three patients, different variations of treatment seemed to relieve their cases of ocular difficulties associated with EBV. For one, a topical acyclovir ointment was used to help the inflamed and swelling areas. An antiviral drug used to treat herpes and AIDS can also be effective. For another patient, topical steroid therapy was what helped to soothe and treat inflammation in the corneas of the eyes. The final form of treatment which researchers found to be beneficial was cataract and vitreous surgery.

While the symptoms can be treated, the EBV virus never actually goes away and can affect those who have been infected later in life after becoming “reactivated.” This reactivation can occur at any time with varying severity. 

Though EBV can be very challenging, it can also morph into mononucleosis or Mono which affects as many as 2 per 1,000 teens and those in their early 20s every year. Some of those affected can die from the virus because of their suppressed immune system. This suppression can lead to the contraction of other illnesses as well. 

One such sufferer who contracted mono caused by EBV described the process of contracting the virus and the difficulty of being a host. Lecia Bushak described her story in an article on


“The week I turned 23, I came down with the infamous “kissing disease,” known medically as infectious mononucleosis — or more commonly as mono. I was a late bloomer; most people get mono when they’re in high school or college — and it was, quite frankly, a shock to me. I racked my mind to figure out the last time I had made out with someone randomly in a club, and it seemed to have been years. Regardless, I was stuck with an illness that knocked me off my feet for a solid three months… It’s the fatigue that truly defines the experience of mono: that and the accompanying lack of motivation to keep going that can affect you for months afterwards. The first day the exhaustion hit me, I had biked across the Queensboro Bridge into Manhattan, gone for a swim at the gym, and then biked back — all before my shift at work. Though the workout was admittedly intense, I came home and felt more tired than normal; a heavy fatigue weighed my limbs down. Little did I know, the Epstein-Barr virus had made its way into my system possibly weeks or even months before and had been incubating for quite some time, waiting to strike. The EBV has an incubation period of 30-50 days from actually contracting it. The fatigue was just the beginning.

A few days later, the exhaustion worsened and I also became moody and depressed: I was plagued with a sudden desire to go home to my parents’ house and give up on everything. Within a day, the fever struck. I denied the illness for a while, continuing to go to work until the fever got so bad that my entire body felt like it was burning up. The fever lasted about a week, and by now I had called in sick to work and also gone to an urgent care center in Queens, where doctors did blood tests on me to figure out what was wrong.

At a certain point, while waiting for my test results, I decided I could no longer be alone in NYC without anyone to take care of me. I could barely get out of bed, let alone walk down the street to get groceries, so I went home, where my parents gently tried to get me to eat plain rice, toast, soup, and drink water, though I had no appetite. That week, I got a call from the urgent care doctor notifying me that I had mono, and there was nothing I could do but rest and drink fluids to flush the virus out of my system.

Mono is typically diagnosed by looking at your throat, skin, or pressing on your abdomen. It is also diagnosed through blood tests, such as the mononucleosis test or the complete blood count (CBC). Doctors can also test your liver enzymes, which are heightened by the virus, and can show whether your liver is inflamed. Symptoms may include a heinously sore, white-covered throat (which I was lucky enough to not develop — as the illness affects everyone differently), severe fatigue, headache, nausea, loss of appetite, an inflamed liver and a swollen spleen. So yes, I could feel the swollen organs in my abdomen during the worst of the illness, and this is why people with mono can’t return to their active lifestyles or playing sports for months (Getting hit by a basketball could burst your spleen when it’s in its vulnerable post-mono state).

Needless to say I was shocked at the diagnosis, and wondered how I possibly could have been infected with the illness stereotyped as the “making out” disease rampant at frat parties. Could it be that my daily commute on a crammed train, being sneezed on by sickly strangers, had finally gotten to me? Or that my schedule of two jobs, working seven days a week, had worn me down too much? It could have been a floating sprinkle of saliva from a coughing commuter or a passerby. The fact is, there’s no real way to trace where you got mono, but it typically happens by exchanging saliva or other bodily fluids with an infected person (hence the “kissing disease” label). And mono hit me hard — probably because I was stressed, working myself to the bone, and wasn’t taking care of myself.

The second week of the illness was the worst: I couldn’t eat, I slept most of the day, and I couldn’t walk down the stairs without someone supporting me. My stomach felt swollen and nauseated from my inflamed liver. I was so mentally and physically drained that I couldn’t even gather the energy to check my phone or my e-mail; the thought of communicating with people seemed overwhelmingly tiring. The highlight of those two weeks was watching The Hobbit.

With mono in particular, it’s extremely important to give yourself proper rest, even though you may be frustrated at your significant decline in productivity. Students in high school or college often have to take weeks or months off from school, depending on how hard the illness hits them. I lay in bed for three weeks, slowly being nursed back to moderate health by my parents' healthy nourishment. I drank plenty of water and tea, ate chicken soup, and gradually moved to more solid foods like eggs, toast, and kasha with strawberries and bananas. But most importantly, disconnecting and forcing myself to relax actually helped me learn how to manage my energy, stress, and health — and learn how to be patient — in the long run.

As stated before, mono and depression often go hand in hand. When you’re dragged down by a heavy, seemingly endless fatigue every day, it’s hard not to feel unproductive and down. Once I was already back at work, a month after mono’s initial onset, I was advised to refrain from going to the gym or resuming my ordinary physical activity. For three months, I was banned from alcohol (to allow my liver to recover), exercise, and pushing myself too hard at anything. Every day during those months, my heavy fatigue would roll around at 3PM and sometimes earlier, so I would go home straight to bed to relax and sleep. Mono forced me to lose my competitive edge for a short time, but it also forced me to slow down and enjoy the journey. And once my recovery became complete — when I got the liver test results back that showed my enzyme levels had returned to normal — I felt more capable in moving forward in a constructive, healthy, and balanced way.

Overall, I suggest heeding Candea Core-Starke’s quote: "When an illness knocks you on your ass, you should stay down and relax for a while before trying to get back up."



The HHV-6 foundation describe the virus like this: “little is known about the prevalence of HHV-6A or how it is acquired, but one small study found very low levels of HHV-6A in the saliva of half of healthy adults.” Low levels can be easily tolerated by most adults but greater levels like those Blake had can cause serious problems. 

However, a variant on this virus HHV-6B, is known more for its affect on children and toddlers and it has been argued that the virus can be passed to children in utero.

“With chromosomal integration, all cells have the virus from the beginning," said senior study author Caroline Hall, a pediatrician at the University of Rochester in an interview with  But, "it is unclear whether the presence of the virus during development affects a child's health." 

HHV-6A has recently been discovered in the uterus of women who are infertile as well as in the thyroid tissue of patients with Hashimoto’s thyroiditis. Other findings suggest the virus may be an indicator of multiple sclerosis.  

Symptoms of HHV-6B can include fever, diarrhea and sometimes a rash known as roseola. Other versions of the virus HHV-6B can cause febrile seizures, encephalitis or intractable seizures.

Like EBV, the virus is also one that can recur at any point in a sufferer's life and the HHV-6 Foundation describes the process of reactivation. 

“Reactivation can occur in the brain, lungs, heart, kidney and gastrointestinal tract, especially in patients with immune deficiencies and transplant patients. In some cases, HHV-6 reactivation in the brain tissue can cause cognitive dysfunction, permanent disability and death. Except in acute or initial infections, the viral DNA can typically be found only by biopsy, as it does not circulate in peripheral blood.” 

While the fact that reactivation is so simple for such a virus, further recent studies have linked the virus to a much more serious factor: infertility. 

Jayson Maclean from Cantech Letter reports that HHV-6A has recently been linked to unexplained infertility, specifically in women. 

The study from University of Ferrara in Italy and the University of Geneva in Switzerland consisted of 66 women, 30 of whom were defined as infertile for unexplainable reasons while 36 were determined to be fertile women who had one or more successful pregnancies in their lives. 

Upon examination of each of the subject, the researchers found evidence of the HHV-6A virus in the uterine lining of 43 percent of women who fell into the infertile groups. It should be noted that each of the women in the group were in the “unexplained infertility” category. 

As for the women who were fertile, there was no evidence of the virus in their uterine lining at all. 

“Our study indicates, for the first time, that HHV-6A infection might be an important factor in female unexplained infertility development,” said the study’s authors in an interview with Cantech Letter. 

The article points out that  “Currently, 25 per cent of infertility cases in women go unexplained, thus the new findings offer a ray of hope for many of those wishing to have children but are faced with unknown factors contributing to infertility.”

Other than the issues the virus is known to cause pregnant women, it has also been linked with other diseases, some known to cause death. Medscape reviewed the virus and the history of studies involving it to bring to light the following:

“In patients infected with HIV, HHV-6 infection may up-regulate HIV replication and hasten the progression toward AIDS. HHV-6 also has been implicated in the pathogenesis of white-matter demyelination in persons with AIDS dementia complex; however, causality has not been proven.” 

It’s connection to HIV/AIDS has not been explored in broader contexts yet, though it is known that this virus is connected to numerous other health issues and diseases. The problem is that,  often, the virus appears to be no more than a mild illness before its more extreme effects begin to hit. This leaves sufferers assuming they have contracted a much less serious flu and keeps them from checking with doctors to explore if it may be something more serious. 

And though no vaccine exists, antivirals like ganciclovir (Valcyte) and foscarnet  (IV infusion) are among the recommendations for easing of symptoms. Further, more simplistic remedies like natural remedies have also been known to help sufferers. 

HHV-6 and EBV Connections to CFS:

The struggle of living life without a cure is one that is known across the board for sufferers of  CFS, Epstein-Barr and HHV-6. However further connections have recently emerged between these viruses which prove that they may be more closely connected than originally thought. 

According to the HHV-6 Foundation, the virus HHV-6 “has long been suspected as one trigger for CFS. HHV-6 reactivation in transplant patients can cause symptoms similar to CFS, including fatigue, cognitive dysfunction and autonomic dysfunction” 

A 2012 study that specific evidence of infection of the central nervous system is difficult to obtain because HHV-6 can last for years in the central nervous system even after it is no longer in the blood stream.  This makes it very hard to study in part because it can be almost impossible to find. 

HHV-6B reactivates in 97 percent of transplant patients and “will multiply in the saliva in response to ordinary stress or high workload, HHV-6A is the virus most often associated with CFS.”

A 2012 European study found that “82 percent of fine needle biopsy tissue samples from patients with Hashimoto’s thyroiditis were positive for both HHV-6A DNA and messenger RNA, proving that these were active infections.” 

On the other end of the spectrum, just 10 percent of the tissues from control subjects who had thyroid cysts were found to be positive with HHV-6, but none of these control subjects were found to have a current or active infection of HHV-6. This means remnants from previous infections were still wreaking havoc in other portions of the body. 

Another study conducted in 2001 in Sweden claimed to have established that 40 percent of the 291 sufferers of CFS also had chronic lymphocytic thyroiditis. This was established by the use of fine needle thyroid biopsies, and just half of the subjects in the study had abnormal thyroid levels. Using the facts of the study for a fictional scenario, “if 40% of CFS patients suffer from subacute thyroid disease, and 82% of it is caused by HHV-6A, then as many as one third of all CFS patients could be suffering from active HHV-6A infection of the thyroid tissue.” While this specific scenario has not been reported, there is documentation by CFS doctors and specialists that suggests most CFS patients have a history of thyroid disease. 

But the thyroid and central nervous systems are not the only locations in the body these viruses have been known to impact. In fact, according to a 2007 study “HHV-6 is well known for invading the hippocampus and other parts of the limbic system, and also establishes residence in the human sensory ganglia (particularly HHV-6A) along with other neurotropic herpes viruses”.

Michael VanElzakker , a Tufts University researcher for PTSD neuroimaging laboratory and the Massachusetts General Hospital Psychiatric Neuroscience division published a theory in 2013 which discussed a  possible cause of Chronic Fatigue Syndrome. 

“For years, CFS researchers have been looking in plasma and blood cells for a pathogenic agent that causes the myriad of symptoms experienced by patients with the condition. However, according to VanElzakker, they may have been looking in the wrong place (plasma) and need to search instead in the tissues of the peripheral and central nervous system. During infection, the sensory vagus nerve sends a signal to the brain to initiate ‘sickness behavior,’ an involuntary response characterized by fatigue, fever, myalgia, depression, and other symptoms that are often observed in patients with CFS.,” the article on his work describes. 

“However, VanElzakker proposes that when sensory vagal ganglia and paraganglia are themselves infected with any virus or bacteria, these symptoms would be exaggerated. He notes that many of the symptoms of sickness behavior (such as fatigue, sleep changes, myalgia, cognitive impairment, depression and zinc depletion) are also mediated by pro-inflammatory cytokines and observed in CFS. Although VanElzakker proposes that any neurotropic virus or bacteria could trigger CFS, HHV-6 is at the top of his list.”  

And as though living with these viruses weren’t enough already, Blake endured another virus during his bout with CFS, a virus which also happens to be part of the genus of herpesvirus: Cytomegalovirus.


Though less is known about this virus, it is one that is only known to affect humans and monkeys. The virus is also much more closely related to HHV-6 than we might have originally expected as the type of Cytomegalovirus which most often affects humans is known as human CMV (HCMV) or human herpesvirus-5 (HHV-5). Like the other illnesses, this virus is also spread through contact, urine, and saliva.

One definition further refines the characteristics beyond just HHV-6 and Cytomegalovirus. 

“All herpes viruses share a characteristic ability to remain latent within the body over long periods. Although they may be found throughout the body, CMV infections are frequently associated with the salivary glands in humans and other mammals. Other CMV viruses are found in several mammal species, but species isolated from animals differ from HCMV in terms of genomic structure, and have not been reported to cause human disease.” 

This virus actually affects more people than one would expect, and can infect almost anyone, according to the Mayo Clinic. Luckily for most people, the virus will not produce obvious symptoms and is more likely to remain dormant so long at the host is relatively healthy. However, when it comes to women who are pregnant or those with compromised immune systems, the virus is a whole other story. 

Depending on the person who has been infected, symptoms will vary. For example, in babies with the virus, possible symptoms include: yellow skin and eyes (jaundice), purple skin splotches or a rash or both, small size at birth (or low birth weight), enlarged spleen, enlarged and poorly functioning liver, pneumonia and seizures. 

In adults with compromised immune systems, other symptoms may occur and often resemble  infectious mononucleosis and fever, pneumonia, diarrhea, ulcers in the digestive tract, possible causing bleeding, hepatitis, inflammation of the brain (encephalitis, behavioral changes, seizures, coma, visual impairment and blindness). 

But according to the Mayo Clinic, “most people infected with CMV who are otherwise healthy experience few if any symptoms. When first infected, some adults may have symptoms similar to mononucleosis, including fatigue, fever and muscle aches.”

The difference with Cytomegalovirus is that the contact types differ from the other viruses listed above. This virus is also related to those viruses which cause chicken pox and herpes simplex. 

The spread can come through numerous forms, including through touching your eyes or the inside of your nose or mouth after coming into contact with the body fluids of an infected person. This is the most common way CMV is spread because it's absorbed through the mucous membranes, through sexual contact with an infected person, through the breast milk of an infected mother, through organ transplantation or blood transfusions or through the placenta, from an infected mother to her unborn child, or during birth.

Q Fever: 

Caused by infection with Coxiella burnetii, Q fever  “is a bacterium that affects humans and other animals. This organism is uncommon, but may be found in cattle, sheep, goats, and other domestic mammals, including cats and dogs. The infection results from inhalation of a spore-like small-cell variant, and from contact with the milk, urine, feces, vaginal mucus, or semen of infected animals. The incubation period is 9–40 days. Humans are vulnerable to Q Fever, and infection can result from even a few organisms. The bacterium is an obligate intracellular pathogenic parasite.” 

The virus is found everywhere on earth other than New Zealand and is considered very sustainable as just one organism is able to cause an infection. Commonly contracted through the inhalation of contaminated dust, contact with contaminated milk, meat, or wool, and particularly birthing products, ticks can also transfer the fever to other animals.  

Though it can be passed between humans, it is considered rare, but studies have shown that men are often more affected than women, which may be attributed to different employment rates in typical professions.

Symptoms range from the more common flu-like symptoms with abrupt onset of fever, malaise, profuse perspiration, severe headache, muscle pain, joint pain, loss of appetite, upper respiratory problems, dry cough to pleuritic pain, chills, confusion, and gastrointestinal symptoms, such as nausea, vomiting, and diarrhea. But the difficulty with Q Fever is that half of those afflicted exhibit no symptoms at all, making the host unaware that they have even been infected. 

The disease can mutate to pneumonia within a few days in some cases, which “can result in a life-threatening acute respiratory distress syndrome.” 

Though not as common, the fever is known to cause one type of hepatitis, granulomatous, which involves malaise, fever, liver enlargement, and pain in the right upper quadrant of the abdomen. 

Finally, Q Fever may also appear in a chronic form which “is virtually identical to inflammation of the inner lining of the heart (endocarditis), which can occur months or decades following the infection. It is usually fatal if untreated. However, with appropriate treatment, the mortality falls to around 10 percent.” 

Treatment with antibiotics is known to work well for Q Fever, but preventative vaccinations are also available. 

Interestingly enough, the virus which causes Q Fever was developed as a biological weapon and investigated by the U.S. as a weapon in the 1950s. Human trials were even conducted on volunteers to determine test dosages as well as infection rates. 

The weapon was “dispensed biological (under the name) Agent OU with ships and aircraft, during Project 112 and Project SHAD, and manufactured in large quantities at Pine Bluff Arsenal, with 5,098 gallons in the arsenal in bulk at the time of demilitarization in 1970.”  

The causal virus is currently ranked as a "Category B" bioterrorism agent by the CDC and can be contagious. It is also extremely “stable in aerosols in a wide range of temperatures.”

The microorganisms associated with Q fever can survive on surfaces up to 60 days and the number of bacilli needed to infect half of people is the lowest known among diseases. 

More current studies on Q Fever were conducted in April 2007, by Jensen T.K. and colleagues, regarding the presence of Coxiella burnetii in 90 aborted placentas of mammals over a two year period.

Results of the study were published at describe the necessity of proper food production in keeping this bacteria from the public. 

“Not only are methods of isolation and detection of bacteria popular in current microbiology research, the significance of regulation of food safety has not gone unstudied. Because Coxiella burnetii has been known to possibly be found in milk, milk pasteurization has never been so crucial in the promotion of sanitary food production. Milk pasteurization aims to kill all harmful bacteria through extensive heat treatment. Due to the fact that this bacterium is perceived to be one of the toughest heat resistant organisms existing, questions were raised from O. Cerf and R. Condron involving the effectiveness of upholding the requirement for milk to be pasteurized under rigorous temperature and time-sensitive conditions because of previous notions that Q fever could possibly be transmitted through food. The conclusion was that infection arising from the consumption of unpasteurized milk does not inevitably lead to the clinical disease of Q fever, brought on by either inhalation or arthropod bites.” 

Q Fever and CFS:

But the importance of Q fever for our story is its connection to CFS. Some patients who suffered from Q fever, subsequently contracted CFS as highlighted in the notes from this study Dr. Dragan Ledina from the Department of Infectious Diseases, Split University Hospital Center, Split; Croatia
“Some authors observed symptoms of chronic fatigue in a small number of patients after the acute phase of Q fever; in many cases serological assay confirmed the activity of Coxiella burnetii infection. The effect of antibiotic therapy on post-Q-fever fatigue syndrome has not been studied in south-east Europe thus far.”

The study goes on to examine case reports as well, studying the illness in three different patients.  

“Three patients are presented with post-Q-fever fatigue syndrome. All fulfilled the CDC criteria for chronic fatigue syndrome. IgA antibodies to phase I of the growth cycle of Coxiella burnetii were positive in two patients and negative in one. Two patients were treated with doxycycline for two weeks in the acute phase of illness and one with a combination of erythromycin and gentamycin. After 4–12 months they developed post-Q-fever fatigue syndrome and were treated with intracellular active antibiotics for 3–12 months. Efficacy of the treatment was observed in two patients, but in one patient the results were not encouraging.” 

The study concluded that the results suggested the involvement of the preemptive virus to Q fever in the beginnings of CFS. It was the first study and report on such a connection between the two in Mediterranean countries. Proof of those IgA antibodies to phase I of the growth cycle of Coxiella burnetii is not considered to be representative for diagnosing CFS however, and the study concludes by recommending antibiotics as well as further studies.

Mycoplasma Pneumoniae:

Mycoplasma Pneumoniae has also been linked to CFS/ME. M. Pnumoniae Is a form of atypical bacterial pneumonia related to cold agglutinin disease. 

The small bacterium is in the class Mollicutes and is caused by a human pathogen. It’s notable not only because of the lack of a peptidoglycan cell wall but also because of its resistance to antibacterial treatment. Infections are often extremely difficult to stop with this bacterium and even after treatment, it is known for its ability to mimic host cell surface composition, morphing and changing to fit the host in each new case. 

But that isn’t where the idiosyncrasies of this bacterium end. 

“In addition to evasion of host immune system by intracellular localization, M. pneumoniae can change the composition of its cell membrane to mimic the host cell membrane and avoid detection by immune system cells. M. pneumoniae cells possess a number of protein and glycolipid antigens that elicit immune responses, but variation of these surface antigens would allow the infection to persist long enough for M. pneumoniae cells to fuse with host cells and escape detection. The similarity between the compositions of M. pneumoniae and human cell membranes can also result in autoimmune responses in several organs and tissues.” 

“It’s characterized by symptoms like atypical pneumonia, tracheobronchitis, and upper respiratory tract disease and primary atypical pneumonia is one of the most severe types of manifestation, with tracheobronchitis being the most common symptom and another 15 percent of cases, usually adults, remain asymptomatic. These infections usually appear over a time of several days and “can be confused with a number of other bacterial pathogens and conditions that cause pneumonia.”  

The reason this bacterial infection becomes important in understanding CFS is it’s possible connection or causation with chronic fatigue. 

A study by Nasralla M, Haier J and Nicolson GL. claimed to have found a connection in that they described multiple mycoplasma infections were detected in blood of patients with chronic fatigue syndrome and/or fibromyalgia. 

The study was done with the goal to search for the presence of mycoplasma species in blood samples from patients with CFS and/or fibromyalgia. Prior to this study, over 60 percent of patients with CFS/fibromyalgia syndrome were found to have mycoplasma blood infections.

For the study, sufferers of Chronic fatigue syndrome/fibromyalgia syndrome were tested for signs of multiple mycoplasma infections in their blood. Over 90 sufferers of CFS/ fibromyalgia were tested, and should they test positive for any mycoplasma infection, were then investigated for the presence of Mycoplasma fermentans, Mycoplasma pneumoniae, Mycoplasma hominis and Mycoplasma penetrans in blood. 

The study revealed numerous accounts of the bacterial infection in the blood with the numbers as follows: Mycoplasma pneumoniae (54/91), Mycoplasma fermentans (44/91), Mycoplasma hominis (28/91) and Mycoplasma penetrans (18/91). 

The study found multiple mycoplasma infections in 48 of 91 patients, with double infections being detected in 30.8% and triple infections in 22%, but only when one of the species was Mycoplasma pneumoniae or Mycoplasma fermentans. Patients infected with more than one mycoplasma species generally had a longer history of illness, suggesting that they may have contracted additional mycoplasma infections with time. 

In a European based study titled High prevalence of Mycoplasma infections among European chronic fatigue syndrome patients. Examination of four Mycoplasma species in blood of chronic fatigue syndrome patients results were found to be similar to those conducted in the U.S., showing geographic location likely plays no role in the connection, but it does help to show just how widely spread this connection truly is. 

Compared to the American versions, in this study, nearly 69 percent of the 261 European patients with CFS patients and 36 healthy volunteers proved to be infected by at least one species of Mycoplasma. 

Because of these various findings and studies, it is considered by some that that one or multiple types of Mycoplasma could be a precursor to chronic fatigue syndrome and possibly other similar viruses as well. 

Dengue fever:

Dengue is a mosquito-borne tropical disease caused by a virus with related symptoms taking anywhere between a few days to two weeks to emerge. Unlike other infections, Dengue may appear in five different forms. 

“Infection with one type usually gives lifelong immunity to that type, but only short-term immunity to the others. Subsequent infection with a different type increases the risk of severe complications. A number of tests are available to confirm the diagnosis including detecting antibodies to the virus or its RNA,” according to Wikipedia. 

In any variant, possible symptoms range from high fever, headache, vomiting, muscle and joint pains, and a characteristic skin rash. But in some instances, the disease develops into the life-threatening dengue hemorrhagic fever, resulting in bleeding, low levels of blood platelets and blood plasma leakage, or into dengue shock syndrome, which is characterized by dangerously low blood pressure. 25,000 people die every year from the disease which is spread by mosquitos. 

Matthew Karsten of “The Expert Vagabond” blog described his symptoms of Dengue, which he contracted while in Mexico.

“This felt like I’d drunk a whole bottle of tequila and was hit by a truck on the way home. My symptoms included pounding headaches that lasted all day, cold chills in 90 degree weather, and severe muscle pain all over my body. I was a mess. 

“I spent a full day hiding in my bedroom under blankets with a fever-induced haze...The next day my horrible fever was gone. The headaches were gone. I felt better. In fact I felt so good I decided to go surfing.”

“The waves were the best I’d seen them! But walking down to the beach barefoot with my surfboard is when I first noticed some new pain. My feet were really sore…My fingertips hurt too. Trying to attach the GoPro to my surfboard was difficult, it felt like I was grabbing thumbtacks. After an hour of riding the waves I gave up. My hands and feet were in a lot of pain.”

Upon returning from the beach trip, Karsten took to the internet to figure out just what was going on with him. Because he had contracted the virus after a night out, he thought it could be some mix of hangover symptoms or the result of being drugged by the bartender, but when his further symptoms didn’t fit that profile, he searched for other explanations. 

“I knew something was wrong when I couldn’t tie my shoes because the pain was so bad. Red dots started appearing all over my hands and feet. I described my symptoms on Facebook asking for advice. A few people mentioned the possibility of Dengue. So I borrowed a friend’s car and drove myself to the closest hospital the next town over. The staff sent me to the emergency room where I proceeded to wait for 4 hours in freezing cold AC while people puked up their lunch around me. Compared to everyone else waiting for treatment, my ailment wasn’t an emergency. Locals streamed in with broken arms, legs, kids puking up yellow goo, and women in labor. Other than painful hands and feet due to capillaries bursting under my skin, I felt fine. So I gave up and left.” 

With another day wasted, Karsten endured another night of pain before making it to a doctor who actually was able to help, even if his initial response did not fit what Karsten was expecting.  

“The following day I drove 25 minutes to the town of Bucerias on the recommendation of fellow blogger Christine, whose husband had been infected with the disease and described my symptoms to Dr. Mauro. He was a very pleasant man who spoke excellent English. He seemed doubtful it was Dengue, because most people suffer a lot more than I had. But he sent me across the street to have blood work done just in case.” 

When the results came back, Karsten was found to have Dengue just as he had expected, and he was told that he “must have a very strong immune system to only suffer one day of fever — normally people are out for a week, or require hospitalization.’’ 

But his case isn’t a unique one. An article from the ME Association discusses the prevalence of such a story in travellers as well as its connection to and onset of extreme fatigue, saying “Overseas travellers and backpackers returning from more exotic locations form a subgroup of patients with post infectious fatigue syndromes that may then progress into an ME/CFS-like illness.  Although dengue fever is already well recognized to be a cause of prolonged debility this is the first research paper to look at the development of a more specific post-infectious fatigue syndrome.  A number of other tropical infections are also known to cause post-infectious fatigue syndromes and this highlights the importance of including questions about overseas travel when a diagnosis of ME/CFS is being considered.”

It goes on to explain the importance of identifying and studying such a connection between Dengue and CFS. 

“The fact that a high percentage of people with dengue fever experience significant post-infectious fatigue indicates that this infection could be used as a model to study and compare some of the endocrine and immunological abnormalities that have been found in ME/CFS with dengue patients who do or do not develop post-infection fatigue.”

Because Karsten’s case of Dengue occurred before the vaccine TV003 was available, he was not able to have access to medication which has proved 100 percent effective in trials. 

Studies were only released in March of 2016 about this vaccine but since then, it has been able to help numerous sufferers from contracting worse versions of the fever. 

This vaccine could actually be considered a possible medication to sufferers of CFS. Doctors in Singapore used a sample of 71 males and 56 females with an average age 36 years for a study
Which showed that a “significant post-infectious fatigue was observed in approximately 25% of the hospitalized patients.  Risk factors for the development of fatigue included older age, female sex, and the presence of chills.” 

 “The study adds further confirmation to the fact that a wide range of infections, predominantly viral, can trigger an ME/CFS-like illness. It also adds some support to the disease model involving immune dysfunction (including excessive immune chemical/cytokine production), hypothalamic-pituitary-adrenal axis dysfunction, and autonomic nervous system dysfunction.  The results also help to confirm that debilitating and prolonged post-infectious fatigue is not simply a ‘Western disease’.”

What is clear from all the available current research is that many illnesses can lead to CFS but just why this happens or how it occurs in some patients and not in others is a mystery. We also know that CFS can occur after treatment for other, completely unrelated illnesses.

According to a study form the National Center for Biotechnology Information, 33 percent of women who undergo Breast Cancer treatment end up with CFS. Though it is not known if this is from the initial assault of the chemicals associated with chemotherapy or the radiation treatment that causes a MCS (multiple chemical sensitivity) like-assault. It should also be noted that MCS is a predominant factor in Gulf War Illness. 

Given the complex nature of the illness and the millions of people who suffer from it (even these numbers are unclear with opinions ranging from one to four million in America alone), it might be logical to assume that CFS would be a high priority for the medical establishment. Nothing could be further from the truth. The NIH currently allocates just $7 million a year for research, a fraction of the sum available to other illnesses which have a fraction of the impact. Despite efforts by lobbyists for those suffering from CFS, there is still no coordinated effort to attack and understand the challenge and to find a cure.

There are isolated approaches based around the precursor illness that can lead to CFS. For example, the HHV-6 Foundation outlines what patients of both CFS and HHV-6 should take as next steps, suggesting “CFS patients who test positive for HHV-6 on a plasma PCR DNA test should have a follow-up quantitative whole blood test to rule out chromosomally integrated HHV-6 or CIHHV-6.” 

The patients with CIHHV-6 will always test positive with the plasma test because HHV-6 is integrated into the chromosome of every cell, thus keeping the strain going. But, the inherited condition effects very small percentage of the population – perhaps less than one percent. It also seemed to appear more in those who suffer from central nervous system dysfunction. 

A study from Montoya in 2012 and Pantry in 2013 go on to say “some have theorized that CIHHV-6 patients may be unable to mount a proper immune defense against community acquired strains of HHV-6, and thus develop CNS symptoms that resemble CFS.”

Until more studies have been done, patients of CFS, HHV-6, EBV and others will not know definitively if the relationship between the viruses is a cause and CFS the effect. 

What does seem clear to me is that a very broad range of people from all over the world have been impacted by CFS. As far as we can tell, all of them also had one or more other illnesses that seems to have weakened the immune system or impacted the gene structure in some way to help create the environment where CFS can flourish. How this happens or why some people become victims and others do not remains a mystery. 

We know so much more today about all the individual illnesses that led to the near death of my son. Now we need to start building on that knowledge so that the next generation of CFS sufferers can have a realistic hope of an early diagnosis and a complete cure.

This is Julia Hugo Rachel. Next week, I’ll be sharing how we finally got my son on the road to recovery and the miracle of his transformation today. 


Julia Hugo Rachel

CFS: Many Causes, One Result

One woman’s journey into medical hell and the lessons that will help cure millions.