Late Spring 2008
Eight or nine months into treatment, as my heart made slow progress on Rifampin, I hunted around the Internet reading abstracts about bartonella and its related cardiac problems. It was hard to find anecdotal accounts of some of the rarer strains in humans. I began mining veterinary articles, which -- perhaps because the subjects were nonverbal -- included more elaborate description of the physical details of the subjects. These were the first articles I found that truly characterized cardiac bartonella. It was around that time that I found a near-description of my own cardiac symptoms in a veterinary article about twelve dogs with heart problems related to bartonella vinsonii subsp. berkhoffii, a strain of bartonella that had known transmission from animal to human. It had been recognized for some time in coyotes, with documented coyote-to-human transmission. On a parallel track, one world-class researcher in Raleigh, NC, Edward B. Breitschwerdt, was on his own obsessive quest to understand rarer strains of bartonella and their impact on human populations. Among other fascinating cases, he has written about a set of twins who seemingly contracted bartonella in utero: one died of a cardiac defect just nine days after birth. His papers on B. vinsonii subsp. berkhoffii in humans were published over a year and a half after I read the article on B. vinsonii subsp. berkhoffii in dogs, and saw my own symptoms in those purebreds and former strays.
B. vinsonii subsp. berkhoffii is a particularly virulent strain when it comes to the heart, at least in dogs. Alarmingly, eleven out of twelve of the dogs in the first article I read, even with treatment, died -- the dog who survived had been on continuous treatment with veterinary Cipro for three years. Clearly, this strain was a different beast from bartonella henselae. The symptomatic notes on the twelve dogs showed an alarming and dramatic infection that seized the dogs quickly, often before they had a chance to get help. A cocker spaniel, a Newfoundland, a coonhound, and two German shepherd were described as having "collapse," whereas a five-year old bull mastiff and a four-year old boxer succumbed to "sudden death." B. vinsonii subs. berkhoffii has also been found in human hearts, and sudden death -- which occurred in the elite orienteers with bartonella elizabethae, another strain that occurs in dogs -- is often an indicator of myocarditis.
Dogs are actually, it turns out, a better model for understanding human diseases than cats. In fact, it is no accident that I found the most descriptive detail of my heart symptoms in veterinary papers and extremely old medical texts, as those patients often had a more comprehensive, intimate relationship with their doctors that involved longer observation periods. In a recent article by Breitschwerdt's team entitled, "Bartonellosis: an emerging infectious disease of zoonotic importance to animals and human beings," the authors state, "it is increasingly obvious that the dog is a natural model for human bartonellosis and vice versa." This same article, published in 2010 -- a year after I was dying in my bedroom in acute respiratory distress breathing with a ventilator as my condition became more deadly, noted that two dogs were diagnosed with b. vinsonii subsp. berkhoffii leading to acute respiratory distress requiring ventilatory support. Other dogs developed "rapid cardiopulmonary decompensation" from this strain. The authors note, importantly, that a limited understanding of bartonella as "cat scratch fever" (bartonella henselae) does not give a clear picture of more damaging, non-self-limiting strains of bartonella in humans. In other words, when it comes to bartonella species, a cat is not a dog.
I was living a parallel reality to those dogs. My infection, after all, had affected my heart with torturous, crushing, utterly debilitating cardiac symptoms just a few days after I was bit. But B. vinsonii subsp. berkhoffii had begun to sound like a ringer for my heart symptoms, even before I remembered and verified the dog bite. For one thing, the technician at the lab that did my blood smear told me he thought I might have a rare strain of bartonella. On my blood slide, the bartonella organisms are bunched in the middle of the cell, whereas in most slides I have seen of bartonella they are clinging to the side. The technician explained this is a visual quirk, that actually the bartonella must be clustered in the concave part of the red blood cells.
I could not find any images of bartonella vinsonii slides, but I did find a slide of b. elizabethae that looked a lot like mine. So both of these became contenders as strains that might have infected me. Because of its lethality and the descriptions of the dogs just collapsing, I felt most strongly that b. vinsonii subsp. berkhoffii was my strain. It is known to cause endocarditis, myocarditis, arrhythmia, uveitis, choriditis, limping, splenomegaly, polyarthritis, and epistaxis in dogs, and endocarditis as well as neurological problems in humans. B. elizabethae, on the other hand, causes lethargy, anemia, and weight loss in dogs, and endocarditis in humans. I called my friend that day and left her a voicemail that said, "I think I've got doggie bartonella!" and I started barking on her voicemail. She reminded me of this message later, when I had my memories about the dog bite.
Around the time of my veterinary readings, unbeknownst to me, Dr. Martin Lerner announced some startling new data from the previous seven years of cardiac observations on ME/CFS patients. At the ME/CFS Conference in Westminster, London, he said that he had identified two distinct groups of ME/CFS patients: one with a herpesvirus illness (EBV, HHV6, HCMV) with no coinfections, and the other with a combination of herpesvirus infections and a co-infection such as Lyme, babesiosis, adult rheumatic fever, or mycoplasma pneumoniae myocarditis. For the first time that I know of, Lerner was publicly acknowledging a subgroup of ME/CFS cardiomyopathy patients whose hearts were likely coinfected with zoonotic, often tick-borne, infections (Lyme, babesiosis). Remember, Dr. Lerner found T-wave inversions and T-wave flattening on Holter monitoring in 90 percent of ME/CFS patients he studied, declaring this heart damage a biomarker. He also found ME/CFS patients to have abnormal tissue biopsies of the heart, and abnormal contraction of the heart indication weakening of the left ventricle. Meanwhile, Dr. John Chia, an infectious disease specialist from California with an interest in enteroviruses, announced his research that showed 135 out of 165 (82 percent) of the ME/CFS patients he tested by stomach biopsy had enterovirus antigens in their stomach tissue, compared with 7 out of 34 (20 percent) of controls, data that validated Richardson's earlier work on enteroviruses with a cardiac-affinity. While Chia's focus was not specifically on the heart (as Lerner's ongoing research has been), both of these raised an interesting possibility: was my heart first infected by a virus, back in 1992, only to be ravaged later by a dramatic attack of virulent bartonella?
In a particularly prescient moment of emailing my home visit doc in 2007 to convince him of my heart infection, I had sent him an article on the latest cardiac understanding of AIDS along with a letter: "Also notable is the attached article AIDS cardiac issues. The fact that pericarditis, pericardial effusion, and all sorts of heart infections are common amongst AIDS patients – and often caused by unusual factors such as staph – leads me to think that this could be a vast untapped area in CFIDS research where the immune parameters and co-infections are so similar to AIDS. Pericarditis leading to cardiac tamponade is one of the only conditions I could find in which chambers of the heart collapsed, which is interesting as Dr. Paul Cheney has found similar heart collapse in upright echocardiograms of CFIDS patients."
Two years after sending that letter to my doctor who thought that having blood like a dead person was not a cause for alarm, after I had been on an antimicrobial regimen for two years, the Whittemore Peterson Institute heralded the discovery of the retrovirus XMRV in ME/CFS patients, and this threw another curve ball. As it turned out, my letter to my hear-no-evil doctor was right on the money: most ME/CFS patients are infected with a retrovirus that seems to pave the way for secondary infections, just like HIV.
In a Q & A in the IACFS Newsletter (Vol. 3, Issue 1, April 2010), lead XMRV scientist Judy Mikovitz answered several questions about Lyme and other coinfections and their relation to XMRV, stating "The hypothesis that chronic XMRV infection creates an underlying immune deficiency is consistent with many co-pathogens including Lyme." She elaborated:
Q; With the known % of CFS patients positive for Mycoplasma species (~60% in multiple studies), Chlamydia pneumoniae (~10% in multiple studies), HHV-6 (~30% in some studies) and other infections, is there any concordance with XMRV positivity?
A: We have only done those analyses on the 101 in the original study, HHV6A was 10%, EBV ~14% and nothing else more than 10%. We are working with several groups at Lyme and those numbers may approach 30%-40 of those tested.
Q: Do you feel that XMRV could act to cause dysfunction of the immune system, allowing opportunistic infections (such as in 4, above), similar to HIV-1 in AIDS?
A: Absolutely that is our working hypothesis
I was correct in asserting to my doctor that ME/CFS patients, initially infected with XMRV, might later present with secondary infections similar to those of AIDS patients, who often get the spirochetal illness syphilis (similar to Lyme) as well as bartonella. I'm not sure why this reality has been obscured for so long in ME/CFS research, but I'm reminded of the sobering article I read about cardiac implications of HIV/AIDS -- about how they were not well tracked in the early years of the epidemic, as patients simply did not live long enough for their heart problems to become full blown. Having a new chronicity brought on a greater understanding of the illness running a progressive course. Funding and ACT-UP tactics, of course, also helped.
My life was still circumscribed beyond imagination, and by July of 2008, my cardiac symptoms were still quite severe after almost a year of treatment, even though I had had significant improvements from the previous cardiac torture. "The best I can imagine in life is a slow, progressive anorexia of everything," I wrote on July 22. My heart had still not returned to its pre-Cipro state for any extended period of time, and that was a relief, but it still slipped back to that state with some regularity without homing there, and on November 20, 2008 I wrote in my journal "Tonight the effort of breathing felt like it would end me. Death still feels very close, and still I think of little else but playing the game of survivor." It was a few weeks before my 40th birthday, and I had spent almost all of my adult years too sick to have a life.
On December 1, 2008, after my revelation about the dog bite and its connection to my cardiac symptoms, it occurred to me the local animal control officer might know something about where the white dog was taken, what shelter. I did some research and found the officer's name online -- her name, Candy LaFlam, seemed like a drag queen name more befitting of a flamboyant afghan handler than a small-town rabies monitor. My friend called her for me, since I was too weak to speak on the phone. The officer, a friendly woman who ran a dog-sitting business, had an immediate recognition when my friend described the dog that bit me. She said she was pretty sure she knew the dog personally. The man on Ireland street was actually the owner of the dog, she said, and he was pulling the wool over my eyes about not being the owner and about his intention to contact animal control. The man in fact had found the dog and brought it in to the animal control officer and told her he wanted to keep it, so she was mandated to quarantine it for ten days to make sure it was healthy. The dog had some blindness due to old age, with glazed and glossy eyes. It was about 30 pounds, part "miniature Eskimo dog," with dirty white fur, and partially deaf -- a male. After her ten-day quarantine, she returned the dog to the man. At some point later, she found the same dog dead by the Gorge. She brought the dog's body back to the man, not knowing how it died. My friend got the impression that Candy was somewhat unsure of the man's story then, but if the dog had a lethal strain of bartonella, sudden collapse at the Chesterfield Gorge would have been quite plausible.
Finally, I had my answer. The dog that bit me had been sick enough to die at the same beautiful Gorge where I had escaped to in my early weeks in Massachusetts, before it bit me.
At that point, however, I could not get tested for this strain, and had to be content with my general blood smear showing I had some strain of bartonella. Bartonella vinsonii subsp. berkhoffii is thought to be more likely in dogs from rural populations, where there is more tick exposure, and it is one of only a short list of dog strains of bartonella that also infect humans: B. vinsonii subsp. berkhoffii, B. henselae, B. clarridgeiae (Candidatus B. washoensis), B. quintana, B. rochalimae, and B. elizabethae. Human labs were not doing specific testing for most of these strains, so I tried veterinary labs. One veterinary lab I contacted about testing my blood, Zoologix, offers a panel test for the most common strains of bartonella found in both humans and dogs, but Zoologix refused to process my blood. Just this year, Dr. Breitschwerdt's lab,Galaxy Diagnostics, began testing humans for b. vinsonii subsp. berkhoffii, but since I have been on bartonella meds for almost three years, and since dangerous hypersensitivity reactions can be induced by stopping and restarting my bartonella drugs, Dr. Breitschwerdt agreed in a private correspondence that I would have a hard time getting an accurate test for B. vinsonii subsp. berkhoffii or other dog strains now. He wrote me: "the optimal testing time point is prior to administration of antibiotics. We do get positive Bartonella PCR/DNA sequencing for some patients while taking antibiotics, but this is not optimal as these bacteria are extremely hard to detect and antibiotics suppress the numbers and the growth in the enrichment culture step." I may never know exactly which strain I have.
I do know this: white animals have often been seen in mythological traditions as harbingers. The white dove, for example, is seen as a good omen, and the birth of a white bison is meaningful in many Native American traditions, especially amongst the Plains Indians such as the Lakota, who view it as a symbol of rebirth when the people of the world have fallen upon troubled times. I suspect some species of bartonella will be recognized as some of the most virulent, life-threatening infections of our troubled times. Tragically, Dr. Breitschwerdt experienced this first hand, when his own work quite surprisingly jumped species after his father -- a tough-as-nails former ironworker and WWII vet -- got sick with a bizarre neurological disease. His story demonstrates why it was so hard for me to connect the dog bite with my symptoms for years, and why it's so hard for many people to recognize dangers in their own back yards. Dr. Breitschwerdt, a veteran of zoonotic illness research, did not immediately suspect bartonella, despite the fact that his father had previous tick exposures but a negative test for Borrelia burgdorferi, the spirochete that causes Lyme. Dr. Breitschwerdt describes his father's symptoms as "retrospectively obvious" but, perhaps because of the nearness of the situation, he did not see them clearly right away.
Dr. Breitschwerdt ultimately found evidence of not one, but three strains of bartonella in his own Dad -- B. henselae, B. alsatica, and B. vinsonii subsp. berkhoffii -- and his father was treated and released from the hospital repeatedly, but his condition worsened until he ultimately died in a severely encephalopathic state. Despite appropriate and aggressive antimicrobial treatment for bartonella, and the fact that his son was a leading researcher on bartonella, Dr. Breitschwerdt's father could not fight the infection that had invaded his brain. Many of his symptoms, leading to his death, were identical to mine -- he had a lesion on his eyebrow like the one I had on my finger, he went into a stupor-like state that was described as nearly comatose, he had seizures and jerking movements similar to my myoclonic activity. By his final blood draw, just days before his death, his blood was only showing evidence of one strain of bartonella, thus indicating his antimicrobial therapies had worked against the other two strains. The remaining strain in his blood was B. vinsonii subsp. berkhoffii!
Dr. Breitschwerdt's article about his father, and the veterinary article on the dogs who died of bartonella vinsonii subsp. berkhoffi, are frightening to read. I know, from stopping my meds a few times, that my bartonella infection is not even close to being eradicated. My bartonella drugs are liver-toxic. If my liver conks out, I'll have to stop my only working meds. Many of my symptoms in recent years, as well, hint at an encephalopathic state, and Dr. Breitschwerdt's father demonstrated how bad this can be: he had hallucinations, dementia, symptoms initially thought to be a stroke, tremors, nonverbal states, severe agitation, inability to recognize his own family members, and near-constant confusion. Similar neurological symptoms from bartonella have been observed, it should be noted, in much younger patients, so these symptoms were not related to age. I have had many similar symptoms since contracting bartonella, though I have not detailed them here. As I write this today, however, I can barely read through my own words. I have a constant, maddening thumping on the right side of my head that has been almost continuous for the past year. My hyperacusis is still so severe I cannot listen to music and can handle very little sensory input in general. It is hard to open and close my right hand. I read things on the Internet and have to read the simplest paragraphs over and over again to understand them, as they initially appear nonsensical. These are just my neurological symptoms of the moment.
Had I finished this article on bartonella a year and a half ago when I wrote most of it (including the speculation about B. vinsonii subsp. berkhoffii), had the ice storm not come and thrown me into the hospital, then into increasingly severe neurological, immunological, and other symptoms until I almost died of respiratory distress, I would not have known about Dr. Breitschwerdt, his recent articles, and the death of his father. Most of these articles were only published in the recent months. In a moving departure from the overly-technical tone of most scientific articles, Dr. Breitschwerdt makes poignant observations about death and dying and the human medical system -- from his perspective as a trained veterinarian watching his father die. "In human medicine, unlike veterinary medicine, no physician claimed or accepted the responsibility to be my father's doctor," writes Dr. Breitschwerdt. He adds, "I found the human healthcare system to be frayed, if not broken."
These realities were not lost on me, and I am grateful to Dr. Breitschwerdt for validating my reality -- especially the deep emotional pain I felt when no one would take on the responsibility of my care -- both in terms of practical caregiving responsibilities and medical care -- and the tragic, broken reality when doctors finally did help me. My home visit doc unceremoniously dumped me after I sent him a letter requesting that he stop speaking to my family about my case. He wrote back that I had clearly shown I did not trust him, and that he could not operate in a medical relationship without "trust" (he was not willing to take actions to regain my trust, like admit he had been wrong about my Lyme disease). My LLMD later foisted off my case on a primary care doctor, implying that my condition was so serious and complicated it had become a liability. My own life, post-bartonella, has become more and more broken.
"Some years ago in a conversation with my mother," writes Dr. Breitschwerdt in the article about his father. "I suggested that the term natural death may well represent an oversimplification of the processes that end a person's life." Indeed, while hundred-year-old cardiology texts can describe the intimate, painful reality of a "natural death," the term natural death is used in modern society as a way of avoiding and anesthetizing the process of dying. This is exactly why a person dealing with a persistent, chronic, potentially lethal infection that invades the heart and brain but evades detection will face denial, derision, and perhaps a grueling and untimely death without a steadfast advocate fighting by her side. I believe there is another reason why veterinarians might be better at this job than human doctors: they are less hierarchical. They don't see a lowly groundhog as unworthy of human interest. They notice, in other words, what is underfoot. By working closely with animals and witnessing the close bond between humans and animals, they don't harbor as strong of an illusion that humans are above animal, and hence immune to insidious little forces of nature crawling up their pant legs. It is the same type of character that makes me admire the often-unlikable Dr. House: when he exhumes a dead cat to save a patient from a zoonotic pathogen, I want him to drive to Ireland Street for me, invade that man's back yard, and dig.
Natural causes are not inevitable. Adolf Hitler once said, "Nature is cruel, therefore we are also entitled to be cruel." It is true that nature is cruel, and that human nature is cruel, but it is Hitler's use of the word "entitled" that gets to me. I think this is what Dr. Breitschwerdt is getting at about natural death. To use that term to diminish the experience of actual death, of death death, is cruel. To walk away from a limping dog, a complicated illness, a person who needs care, is cruel. To not exhume the cat, in its own way, is cruel. It was not, after all, curiosity that killed it -- but rather a lack thereof. Nothing, in other words, entitles us to speed nature along by denying someone's symptoms and then call it a "natural death." Nothing entitles us to deny the complicated, often protracted process of a person dying.
I find it interesting that some drugs, developed for rare medical conditions, are called orphan drugs, and the conditions they treat are called orphan conditions. I wonder when some of us, trapped in the cogwheel of obscure physical realities, will stop being medically abandoned, orphaned, cast astray? Almost as if by vampirism, I have become that dog with the quivering back legs, the dog that tried to wander from its own fate and thought it was being rescued, then found itself dragged back to near where it would die -- yet in one, life-affirming moment, said no with its teeth. I am thankful for the impulse behind that no, the fight that still lives on in me.