William Rawls - Unlocking Lyme: Myths, Truths, and Practical Solutions for Chronic Lyme Disease

Microbe is a general term that includes bacteria, viruses, protozoa, and certain species of fungi.

Even before Lyme disease, Dr. Burgdorfer, a prominent researcher of tick-borne diseases, was familiar with other species of Borrelia and Rickettsia. Rickettsia rickettsii, the cause of Rocky Mountain spotted fever was already known, as were several other species of Borrelia that had been associated with human disease in other parts of the world (Burgdorfer 1993).

It was once thought that the white-tailed mouse was the single primary reservoir for Borrelia and that most all other hosts, including humans, were dead-end hosts. A dead-end host is one in which the microbe cannot complete its reproductive cycle and cannot be transmitted to other hosts. It is now apparent that Borrelia can adapt and spread through a wide range of hosts and is not solely dependent on the white-footed mouse (Levy 2013, Radolf 2012).

The iceman was carrying more than just Borrelia. Intestinal worms were identified, and his total burden of microbial parasites was likely much greater than a person living today in the developed world. Even with a greater microbial burden, however, he could accomplish physical tasks that someone suffering from chronic Lyme disease today would find nearly impossible. His body was, to a certain extent, tolerating the burden of microbes.

It was once thought that humans were dead-end hosts for Borrelia, that ticks that have bitten humans are not infective, but current information may suggest otherwise. Borrelia is very well adapted to a variety of hosts, including humans. When ticks engage in partial feeding (they feed on one creature, drop off, and later bite and feed on another creature), ticks that have bitten humans carrying Borrelia are likely infectious to other humans. In addition, after a nymph tick completes feeding on a human carrying Borrelia, it molts into an adult and is infectious to other creatures, including humans (Levy 2013, Cook 2015).

The ability of Borrelia (and other microbes) to live inside cells may contribute to autoimmunity. To live inside cells, the microbes must turn off the ability of the immune system to recognize the cell as abnormal. Eventually, however, the cell is recognized, and the immune system makes antibodies to that cell type.

Cyst forms occur in a wide range of atypical forms in a variety of shapes. Also, granules composed of budded-off cell wall containing cellular components, surface proteins, and linear/circular DNA that can form into active spirochetes (Buhner, Brorson 2009, Merilinen 2016).

Biofilms in the large colon protect the lining of the gut and are important for normal health.

The microbial mix of the body, called the microbiome, is a complex mix of several thousand-possible species. Though most are friendly flora, there are always opportunists in the mix that can cause disease if unrestrained (potential pathogens). When totaled, a healthy host can support 100 trillion microbes, about three pounds of body weight, without having noticeable symptoms.

Borrelia adds to the total burden of potential pathogens in the microbiome. There are many species of microbes with similar characteristics to Borrelia. Having an infection with multiple microbes at once can tip the balance toward symptomatic illness (more on this in upcoming chapters).

It was once thought that B. burgdorferi s.s. was the primary species causing Lyme disease in the United States, and B. afzelii and B. garinii were the primary species in Europe, with only B. burgdorferi s.s. causing Lyme disease both in the United States and in Europe, but that assumption is no longer valid. Many species of Borrelia have been associated with Lyme-disease-like syndromes.

Separating life-forms into groups, species, and strains is the job of taxonomists (people who name life- forms). These people have a very challenging job, especially when it comes to separating and naming different species of bacteria.

Soft ticks (as opposed to more common hard ticks) typically are found in rodent-infested cabins and feed at night. The bites are painless. About a half dozen species of Borrelia cause tick-borne relapsing fever worldwide, three of which are present in the United States (B. hermsii, B. recurrentis, and B. miyamotoi).

Louse-borne relapsing fever is mostly limited to poverty stricken areas of Africa (Ethiopia, Sudan) where lice infestations are endemic. B. recurrentis is the offending microbe. This louse-borne form of relapsing fever is associated with severe acute disease, but poor health status of those infected is likely a factor. With treatment, mortality is 1%, but antibiotics are often not available, and without treatment, mortality is 70%.

Host-microbe familiarity is usually the most important factor that defines virulence, but other factors unique to the microbe can also affect virulence; there are exceptions to every rule.

Epidemics occur when a microbe skips from its established reservoir host to a naive host. (Virulence is increased when microbes skip to new hosts.) Strains of influenza virus that are well adapted to humans only cause mild-to-moderate illness. Every now and then, however, a strain of influenza jumps from another animal to humans (typically from birds), and the results are devastating. This is what happened with the 1918 flu epidemic that killed millions (Hoag, Study revives bird origin for 1918 flu pandemic, Nature, Feb 2014). Generally, epidemics of poorly adapted microbes are not sustainable; they run their course and eventually burn out.

Sometimes the spider bites a bat, and the bat spreads the virus to other bats. Humans can become infected with the virus if they come in contact with the bat or the bats excrement. When that happens, the results are devastating (Quammen 2015).

All microbes are greedy and aggressive; they will take as much as they can get. If immune function is disturbed, even normal flora can cause harm. This is best illustrated by the fact that when someone dies, it is normal flora, no longer constrained by the immune system, which rapidly break down tissues and cause a dead body to decompose.

For a long time, science held to the assumption, defined by Robert Koch in 1884 (Kochs postulates) that microbial illnesses were caused by single specific microbes. While this still holds true for infections with high virulence microbes, it is much less true with low virulence microbes, in which multiple microbes together can cause illness (Peterson 2014).

This observation holds true for both developed and undeveloped countries. In developed countries, the total burden of potentially harmful microbes tends to be lower than developed countries, but risk of exposure is still proportional to the pyramid. In countries where living standards are poor, the microbial burden of all types of microbes is high, but it is proportioned with a greater preponderance of low-virulence microbes over high virulence.

This, of course, is a generalization; there are many other potential species of microbes beyond these four that may be associated with chronic Lyme disease (both known and unknown). The list includes less virulent species of Rickettsia, Ehrlichia, and Anaplasma.

For the white-footed mouse, Borrelia would be a 1 on the virulence scale, the relationship is ancient. For a dog, Borrelia would be a 2; dogs can get mild arthritis from chronic infection with Borrelia, but generally are not severely affected. It implies that dogs have a longer and closer relationship with Borrelia than humans.

Why some people get very sick and others do not get sick at all may be a function of the strain of the microbe, the variability of the hosts virulence to that microbe, or possibly environmental or seasonal factors that are not yet evident. Less virulent species of Rickettsia, Ehrlichia, and Anaplasma may be more commonly associated with chronic Lyme disease than once thought.