• Rosalie Greenberg, MD

How Hidden is Borrelia burgdorferi (Lyme disease) and Other Tick-borne Infections?


I recently logged onto the virtual Inflammatory Brain Disorders Conference presented by The Foundation for Children with Neuroimmune Disorders and wanted to share some of my thoughts with you. Lecturers from the United States and abroad spoke on diagnostic and therapeutic approaches to these disorders. Overall, I found the conference to be quite informative. I am writing because a few remarks interested me.


#1. A hot topic in psychiatry and neurology these days is autoimmune encephalopathy. The National Institutes of Health defines autoimmune encephalitis as “a group of conditions that occur when the body's immune system mistakenly attacks healthy brain cells, leading to inflammation of the brain.”

One of the early conference presenters said that the increase in the number of autoimmune encephalitis cases is secondary to better diagnostic testing rather than a true increase in rate. I disagree with this assessment. This reminds me of what people used to say 20 years ago about autism. It was not uncommon to hear medical professionals’ comment that the numbers didn’t really increase, we just got better at diagnosing it. Below are statistics corroborated by both the Centers for Disease Control and Prevention and by the American Academy of Pediatrics, showing the rise in the rate of autism in the United States: 1980: 1 to 2 per 10,000 children

1990: 1 in 500

2000: 1 in 250 2004: 1 in 166 2009: 1 in 110

2020: 1 in 68

Given the dramatic escalation of cases in the past two decades, there can be little disagreement regarding the validity in the escalation of the actual rate and not merely the diagnostic techniques.

I’ve been a child psychiatrist for over 40 years and the kids I see today are sicker than those I saw during my training. Many appear multi-dimensionally impaired. Few can be diagnosed solely as having ADHD. More often they have problems socially and/or difficulty with emotional regulation, struggle with impulse control and/or are dealing with learning issues.

For the last few decades, I have specialized in pediatric mood disorders, especially depression and bipolar disorder (previously called manic depressive illness.) Since the late 1990s, there has been a surge in the number of children who have received the diagnosis of pediatric bipolar disorder. Similar to what has occurred with autism, I believe the increase in number of individuals affected by this type of mood disorder is real and not just due to improved identification.

I have observed that a number of the youth given the diagnosis of pediatric bipolar disorder are often found to be suffering from either Pediatric Autoimmune Neuropsychiatric Disorders After Streptococcal Infection (PANDAS) or Pediatric Acute-onset Neuropsychiatric Syndrome (PANS). PANDAS occurs in susceptible individuals following a group A Streptococcal infection. PANS refers to disorders resulting from infections or other insults, creating an underlying autoimmune encephalopathy and manifested as multiple, mainly psychiatric symptoms. There is actually a newer diagnostic category created in part, to decrease the number of children who perhaps were incorrectly diagnosed with pediatric bipolarity. The new term is Disruptive Mood Dysregulation Disorder (DDMD) and refers to a condition manifested by extreme irritability, anger and frequent, intense temper outbursts causing significant impairment. I strongly suspect many of these youngsters are also manifesting a PANDAS or PANS.

In a study I published looking at 27 bipolar youth with a mean age of a little over seven-years-old, I found that 89% showed evidence of exposure to an infection; 74% had positive blood tests and clinician confirmed tick-borne disorders and 25% were positive for PANDAS. Many of the children could also be classified as suffering from a form of PANS. Treatment of the infection(s), as well as strengthening the immune system, were very helpful in lessening psychiatric symptoms in some cases. Mental symptoms in those with tick-borne illness are in part believed to be secondary to an autoimmune encephalitic process.

In my view, given the examples above, I believe the rates of escalation of pediatric psychiatric illness, at least in part due to autoimmune encephalitis, is climbing significantly more than is realized.


#2. A member of the Stanford Immune Behavioral Health Clinic and Research Team said in her presentation that Lyme disease is responsible for only 1% of their PANS cases. I find this surprising and question this figure. In my child and adolescent psychiatry practice in New Jersey, a Lyme endemic state, I have found that over 60% of the kids I have seen in the last five years have testing evidence of infectious tick-borne exposure. The additional appropriate clinical diagnosis in many of these children is PANS plus the additional diagnosis of PANDAS in some. Recognition and treatment of Lyme disease and accompanying other infections (called co-infections) such as Babesia, Bartonella, Anaplasma and Ehrlichia can result in significant clinical improvement.

Recent statistics indicate that there are at least 476,000 new cases of Lyme disease per year. Children and adolescents make up one quarter of this group (i.e. 114,000 youth.) When people think of Lyme they think of Lyme arthritis and think that the disorder mainly affects joints. Too often the neuropsychiatric manifestations of Lyme are overlooked. Given my personal practice experience, I think that the inadequacy of present tick-borne infection (TBI) testing by major labs accounts for a significant underdiagnosis and under-recognition of these disorders, especially in children. Ways in which the present recommended standardized testing is biased against the identification of Lyme disease in kids will be discussed in another blog.

Given that Lyme disease has been found in all 50 states, and in my experience the frequency of neuropsychiatric effects in youth do not appear rare, it is hard to believe that Lyme disease accounts for only 1% of the cases seen in the Stanford Immune Behavioral Health Clinic.


#3. Presenters made clear that there has been no evidence of Streptococcal bacteria in the brains of individuals with PANDAS. This is important because the symptoms present in the individual with the illness can’t be attributed to direct actions of the bacteria, meaning it is the action of the immune system that is causal. This would also explain the limited efficacy of antibiotics in treatment. They might kill the bacteria but they don’t usually call off the immune system’s self-attack.

What occurs is PANDAS with Streptococcal bacteria is in stark contrast to the perniciousness of the Lyme bacteria Borrelia burgdorferi. The Borrelia spirochete, the causal agent of Lyme disease, can enter the brain as has been documented in autopsies performed on infected fetus’ as well as older individuals. The potential ramifications of this are disturbing. Unless the bacteria are fully eradicated from the body, including the brain, they can serve as an ongoing source of immune system stimulation, perpetuating the autoimmune response. In addition, the antibiotic or antibacterial agent used in treatment has to be able to go through the blood-brain barrier to get rid of the intracranial infectious agents. The presence of the bacteria in the brain also increases the likelihood of the illness being more complex and harder to cure.


#4. A few of the speakers mentioned the Mycoplasma pneumoniae bacteria as a possible cause of autoimmune encephalitis. The most common Mycoplasma infection is Mycoplasma pneumoniae which causes “walking” or “atypical” pneumonia and is a leading cause of respiratory illness. It can also result in other problems including gastrointestinal, cardiovascular, musculoskeletal, renal and neurologic symptoms (manifestations of encephalitis). There are actually more than 200 known species of mycoplasma, and 23 of them can cause disease in humans including: Mycoplasma pneumoniae, Mycoplasma fermentans, Mycoplasma hominis, and Mycoplasma genitalium.

A lesser-known fact is that Ixodes ticks, the carriers of Borrelia burgdorferi, the Lyme bacteria, also can carry different Mycoplasma species. It is possible that other Mycoplasma species can interfere with testing for M. pneumoniae causing false positive results. In my practice, I have found that a majority of my patients who test positive for Mycoplasma pneumoniae, are very likely to also show evidence of tick-borne infections. The medical literature shows that as many as 75% of Lyme disease patients have Mycoplasma co-infections.

Physicians have to keep in mind that if they have a Mycoplasma pneumoniae precipitated PANS patient who is very difficult to treat or refractory to treatment, it may be because there are other infections present, especially tick-borne infections.


Please remember that the views expressed in this blog are no substitute for direct individual physician assessment.



RG



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