1. Suruchi Chandra, MD Autism Research Institute ACIM June, 2013
The Neuropsychiatric Manifestations of Lyme Disease and Other Tick Borne Infections
Suruchi Chandra, MD
Autism Research Institute
ACIM June, 2013

2. Is it a neuropsychiatric illness or infection?

3. Mounting Evidence of the Autism Environment Connection
CDC:1 in 50 US children now has autism.
Rising rates of autism
California
Genetic heritability and shared environmental factors among twin pairs with autism.
Association of ASD rates with environmental toxins in multiple studies.

4. Causes of ASD
Causes are likely unique, individualized and multifactorial.
Emerging research is pointing to changes in our environment along with genetic vulnerabilities.
Environment includes:
Chemical toxins
Electromagnetic fields
Changes in diet and nutrition
Microbiome
Infections

5. Prenatal inflammation linked to autism risk
The risk of autism among children in the study was increased by 43 percent among mothers with CRP (C- reactive protein) levels in the top 20th percentile, and by 80 percent for maternal CRP in the top 10th percentile.
Elevated CRP is a signal that the body is undergoing a response to inflammation from, for example, a viral or bacterial infection.

6. Maternal Infection Requiring Hospitalization During Pregnancy and Autism Spectrum Disorders
Journal of Autism and Developmental Disorders, Volume 40, Number 12.
Maternal immune activation causes age- and region-specific changes in brain cytokines in offspring throughout development Paula A. Garay et al Brain, Behavior, and Immunity.

7. Possible role of viruses in ASD
Association of autism with polyomavirus infection in postmortem brains.
Polyviral infections tend to occur more frequently in the brains of autistic patients compared to controls (40% versus 7.7%, respectively; P = .08).
J Neurovirol Mar;16(2):141-9.
Case studies: An 11 year old and 31 year old man developed all the symptoms considered diagnostic of autism after herpes encephalitis.

8. Possible Infectious Contributors to Autism Spectrum Disorders
An infectious contributor ideally would be:
Chronic
Widespread and increasing in prevalence
Challenging to diagnose
Potentially transmitted during pregnancy or early in life
Multisystemic with prominent neurological, immune and gastrointestinal features
Potentially a chronic and active infection
Resistant to short term antibiotic treatment, although symptoms might temporarily and partially improve with a few weeks of antibiotics

9. Misconceptions about Lyme Disease
All patients recall a tick bite or bulls eye rash.
Lyme disease is only a concern in Northeastern states.
ELISA is a sensitive screening test
Only one infectious pathogen is transmitted by the tick bite.
A short course of antibiotics resolves all cases of Lyme disease.
Lyme disease may present as chronic and complex ‘medically unexplained symptoms.’

12. Of the 522 adults, 8% tested positive.
Babesiosis: An Underdiagnosed Disease of Children
Of the 52 children on Block Island RI tested, 12% were positive for Babesia.
Of the 522 adults, 8% tested positive.
25% of the seropositive children and 20% of the seropositive adults reported symptoms compatible with this infection during the previous month.
Pediatrics Vol. 89 No. 6 June 1, 1992 pp

13. Is Lyme disease always polymicrobial? The Jigsaw hypothesis.
Lyme disease may be due to a tick borne complex.
This hypothesis suggests that multiple co-infections are present in the clinical syndrome.
In one study of 240 patients diagnosed with Lyme disease, 11% were found to have evidence of concurrent Babesia infection.
Owen, DC. Med Hypotheses. 2006;67(4): Epub 2006 Jun 30.

15. Development of immune response to Lyme borreliosis from tick bite
ISRN Immunology Volume 2012 (2012)
Development of immune response to Lyme borreliosis from tick bite
Both the IgM and IgG immune response showed an undulatory distribution with antibodies coming and going in untreated patients over weeks

16. Late stage neuropsychiatric symptoms of Lyme disease
Cognitive Problems
Depression
Mood Swings
Psychosis
Violent behaviors/irritability
OCD
Anxiety/Panic Attacks
Sleep disorders
Seizures
ADHD-like symptoms
Autism-like behavior
Chronic Fatigue Syndrome/Fibromyalgia
Lyme disease can
attack the CNS in the form of neuroborreliosis without
involving other systems.
Joksovic , P et al. Current Psychiatry, December 2011.

17. ‘Medically Unexplained Symptoms’
Chronic Lyme Disease may present as:
Chronic Fatigue
Fibromyalgia
Somatoform Disorders
These terms are descriptors of symptoms and do not explain the underlying etiology of the illnesses.

18. Maternal-Fetal Transmission of the Lyme Disease Spirochete, Borrelia burgdorferi
“The Lyme disease spirochete may also spread transplancentally to organs of the fetus. The mother in this case developed Lyme disease during the first trimester of pregnancy; spirochetes were seen in the spleen, kidney, and bone marrow of the infant at term. In addition, the infant had several cardiovascular abnormalities. However, no spirochetes were found in his heart and no organ inflammation was seen.”
Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT.
Ann Intern Med Jul;103(1):67-8.

19. Support for this hypothesis includes:
Positive reactivity in several studies with autistic spectrum disorder patients for B. burgdorferi (22%, 26% and 20–30%)
Multiple cases of mothers with Lyme disease and children with ASD

20. Support for this hypothesis includes:
Fetal neurological abnormalities associated with tick-borne diseases
Improvement in autistic symptoms from antibiotic treatment
Similarities between tick-borne diseases and ASD regarding symptoms, immune reactivity, temporal lobe pathology, and brain imaging data.

21. Serologic Markers of Lyme Disease in Children With Autism
Serologic testing for Lyme disease was conducted on two populations: 37 children aged 2-18 years who had autism and 27 unaffected siblings
None of the children with autism and none of the unaffected controls showed serologic evidence of Lyme disease by the CDC two-tier testing.
JAMA May 1;309(17):1771-3
Dr. Cowden: This study you sent used the CDC-recommended 2-tier testing with EIA & Western Blot.  To my knowledge, there are no studies showing the sensitivity of CDC 2-tier Lyme testing approaching 99%, as this article incorrectly states.  The first attached article found a 29%-32% sensitivity of that methodology, which means they would have missed a bunch of kids who actually had Lyme but tested negative for Lyme.  The second attached article found a 74% sensitivity of the 2-tier testing (still a bunch of false negatives).  The third attached article says the 2-tier testing has 90% sensitivity in late-stage Lyme disease but <40% in early-stage Lyme disease (& I would say somewhere between 40-90% for intermediate stages of Lyme).
______________________________________________________________________________________________________________________________________
On ELISA testing, one child with autism tested positive for anti–Borrelia burgdorferi IgG, and four had borderline positive results for IgM. However, all were found to be negative on confirmatory Western blot testing.
Similarly, four of the control subjects tested positive for anti–B. burgdorferi IgG, one had borderline positive results for IgG, and one was positive for IgM. However, all were found to be negative on confirmatory Western blot testing.
Ms. Ajamian and her colleagues said one possible limitation of the study is the absence of information about the lifestyles of the patients and controls, including the amount of time they spent outdoors. The researchers also pointed out that their analysis did not address the question of whether Lyme disease might cause autism-like behavioral deficits.

22. The CDC clinical criteria for Lyme Disease which exist for the purpose of monitoring the rate of Lyme disease nationally are quite narrowly defined in order to ensure a high degree of specificity in the diagnosis.
These criteria are mainly useful for the early stages and rheumatological presentations of Lyme Disease.
The CDC criteria are not very helpful for helping the clinician to detect late stage neurologic Lyme Disease.
The CDC clinical criteria for Lyme Disease which exist for the purpose of monitoring the rate of Lyme disease nationally are quite narrowly defined in order to ensure a high degree of specificity in the diagnosis. These criteria are mainly useful for the early stages and rheumatological presentations of Lyme Disease, such as when a patient appears with an erythema migrans rash, arthritis, a Bell's palsy, or early central neurologic Lyme disease (meningitis or encephalitis). The CDC criteria are not very helpful for helping the clinician to detect late stage neurologic Lyme Disease. For example, the most common manifestation of late neurologic Lyme Disease is cognitive dysfunction (often referred to as "encephalopathy"). A patient who presents with new onset encephalopathy and a positive blood test for Lyme Disease would not be considered by the CDC to be a case of Lyme disease. Although the CDC recognizes that Lyme encephalopathy exists, encephalopathy is not part of the "surveillance case definition". Hence, physicians who rely on the narrow surveillance case criteria of the CDC for clinical diagnosis will fail to diagnose some patients who in fact do have Lyme disease; in these cases, the patient's treatment will either not occur or be delayed. Such delay in treatment may result in an acute treatable illness becoming a chronic less responsive one.
Other physicians who use a broader more inclusive set of clinical criteria for the diagnosis of Lyme disease will make the diagnosis of Lyme Disease and initiate treatment. The latter group of doctors, by treating some patients for "probable Lyme Disease", will make use of antibiotic responsiveness to confirm their diagnostic impression. These physicians, by erring on the side of not letting a patient with probable Lyme Disease go untreated, will help many patients who otherwise would not get treatment; undoubtedly, however, because of the inclusiveness of their diagnostic approach, these physicians will also treat some patients with antibiotics who do not have Lyme Disease. These physicians would argue that the serious consequences for physical, cognitive, and functional disability associated with chronic Lyme Disease outweigh the risks of antibiotic therapy.

23. Emerging Infectious Determinants of Chronic Disease
Infectious agents likely determine more neurodevelopmental disorders and other chronic conditions than currently appreciated.
The inability to detect an agent does not rule out infectious etiology.
Existing tools and methods may not be sensitive enough to link known agents with chronic disease.
They may be unable to detect as yet uncharacterized novel or emerging microbes.
Diagnostic assays may not access intracellular, sequestered, or nonreplicating agents.
O'Connor SM, Taylor CE, Hughes JM.
Emerg Infect Dis Jul;12(7):

24. All five children in the study showed improvement in their autistic symptomology after beginning long term antibiotic treatment for Lyme disease.

25. Common Underlying Pathophysiology
Oxidative stress
Mitochondrial dysfunction
IDO upregulation
Increased kynurenic acid
Excitation/ inhibition ratio
Microglial activation
Gastrointestinal disturbances
Immune dysfunction
Molecular mimicry
Zinc imbalances
Lyme
Autism

26. Tick Borne Illnesses, Hypotonia, and Mitochondrial Dysfunction
Dr. Charles Ray Jones, who has treated more than 10,000 children for Lyme disease, finds that hypotonia is present in over 90% of cases of gestational Lyme disease.
In Ehrlichia chaffeensis-infected DH82 cells, mitochondria do not incorporate BrdU and transcriptional level of the mitochondrial gene NADPH2 is significantly reduced indicating the inhibition of mitochondrial metabolism.
Liu et al. Microbes Infect Mar;13(3):232-8.

27. Hijacking mitochondria: bacterial toxins that modulate mitochondrial function
It is now clear that bacterial pathogens produce a plethora of proteins known as "toxins" and "effectors" that target a variety of physiological host processes during the course of infection. One of the targets of host targeted bacterial toxins and effectors are the mitochondria.
IUBMB Life May;64(5):

28. These studies identify microglia as a previously unappreciated source of inflammatory mediator production following challenge with B. burgdorferi.
Chronic neuroinflammation in the frontal cortex of a patient with Lyme neuroborreliosis. First column (A, D and G) immunoreactive microglia forming clumps in the frontal cortex of a patient with Lyme neuroborreliosis.
Second column (B, E, H) On frontal sections of the control patient, activated microglia or astrocytes are not visible.
JMiklossy et al. Journal of Neuroinflammation :40
J Neuroimmunol 2002 Sep;130(1-2):22-31.

29. The Prevalence of Gastrointestinal Problems in Children Across the United States With Autism Spectrum Disorders From Families With Multiple Affected Members
Parents reported significantly more GI problems in children with ASD compared with their unaffected siblings. The 2 most common Gl problems in children with ASD were constipation (20%) and chronic diarrhea (19%).
Journal of Developmental & Behavioral Pediatrics:
June Volume 32 - Issue 5 - pp
Copyright Suruchi Chandra, 2012

30. Lyme Disease and the Gastrointestinal System
Gastrointestinal signs and symptoms are common in the early stages of Lyme disease. Ali Zaidi, 2002)
Chronic gastritis, chronic duodenitits, and chronic colitis were found in children and adolescents with Lyme disease and associated with the detection of B burgdorferi DNA in the GI tract despite prior antibiotic treatments. (Fried,2002)

31. Simultaneous Gastrointestinal Infections in Children and Adolescents
81 pediatric patients were assessed for infections associated with abdominal pain, reflux, heartburn, and/or blood in stool.
PCR testing of gastrointestinal biopsies from the stomach, duodenum, and/or colon was conducted.
35 had Bartonella spp.
24 had Mycoplasma fermentans
14 had Helicobacter pylori
13 had Borrelia burgdorferi
Practical Gastroenterology, November 2004.

32. Tick Borne Illnesses Result in Increased Oxidative Stress Markers and Decreased Reduced Glutathione
Lipid peroxidation products, malondialdehyde (MDA), 4- hydroxynoneal (4-HNE) were increased about 2-4 fold in the plasma of patients with Lyme. (Luczaj, 2011) Patients with tick borne encephalitis (TBE) had increased generation of oxygen derived free radicals and decreased activity of superoxide dismutase (SOD), glutathione reductase (GSSG-R), glutathione peroxidase (GSH-Px) in CSF. (Pancewicz, 2002)

33. Zinc/Copper Imbalances and Chronic Infections
Zinc levels are lower and copper levels are increased in pulmonary tuberculosis and other chronic infections.
Zinc and copper levels normalize after anti- tubercular therapy.
Zinc and copper given together was found to be more effective in treating Trypanosoma infection than either zinc or copper alone.

34. The immune response to B
The immune response to B. burgdorferi may elicit the production of antibodies capable of damaging or modifying normal host tissues.
B. burgdorferi antigens may mimic the thyroid gland and be an environmental trigger of autoimmune thyroid diseases.
Antibodies against the OspA epitopes of B. burgdorferi have been shown to cross react with neural tissue.
National Institute of Allergy and Infectious Disease. Lyme disease: the role of
autoimmune reactivity, retrieved from
lymedisease/research/pages/autoimmune.aspx; 2007.
Benvenga S, Guarneri F, Vaccaro M, Santarpia L, Trimarchi F. Homologies between proteins of Borrelia burgdorferi and thyroid autoantigens. Thyroid Nov;14(11):964-6

35. Antibiotic Treatment in Mice
Persistence of Borrelia burgdorferi Following
Antibiotic Treatment in Mice
Antimicrobial Agents and Chemotherapy, May 2008, p , Vol. 52, No. 5
After antibiotic treatment, mice remained infected with nondividing but infectious spirochetes, especially if treatment was started during the chronic stage of infection.
FIG. 1. Immunohistochemical labeling of multiple B. burgdorferi spirochetes (arrows) in ligament tissue of the tibiotarsal joint of a saline solution-treated (control) mouse (A) and of a single spirochete (arrow) in ligament tissue of the tibiotarsal joint of a ceftriaxone-treated mouse (B). Both images are from mice at 4 months after inoculation with B. burgdorferi

36. A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy
Patients with well documented Lyme disease, 3 weeks of prior IV antibiotics, and objective memory impairment.
Patients received either 10 weeks of treatment with IV ceftriaxone or IV placebo.
IV ceftriaxone therapy resulted in short term cognitive improvement but relapse in cognition occurred after the antibiotic was discontinued.
Fallon BA et al.
Neurology Mar 25;70(13):

37. Several granules along Borrelia after 24 h of incubation with ceftriaxone at the middle and end regions.
Kersten et al. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, May 1995, p. 1127–1133

38. Possible Contributors to Autism Spectrum Disorders
Effects are complex and
bi-directional
ASD
Genetics
Nutrition GI
Dysfunction
Toxins
Microbes
Immune Dysfunction
Hormones

39. History of Borrelia
First description of a case of probable Lyme disease appeared in the writings of Reverend Dr. John Walker in 1764
Borrelia DNA has been found in an infected Ixodes ricinus tick from Germany dating back to 1884
Recent autopsy of a 5,300 year old mummy found DNA sequence of Borrelia

40. Autism: modern day illness
It is unlikely that autism is simply related to an infection Modern day changes have likely contributed to the development of these disorders: Exposome Changes in microbiotica Dietary and nutrition changes
Environmental exposures to chemicals arise from both external and internal sources. The exposome represents the combined exposures from all sources that reach the internal chemical environment

41. Body’s Terrain Water/Hydration status Nutritional Status
Environmental Toxins including metals
Electromagnetic pollution
Stress
Negative emotions
Overuse of medications
Lack of movement and exercise
Lack of sunlight
Poor tissue oxygenation
Tissue acid-base imbalance
Are we weaker than ever before and more prone to chronic infections?

42. Biomedical and Integrative Approach to ASD
Dietary changes
Nutritional supplementation
Methylation support
Reduce exposure to toxins
Detoxification
Mitochondrial support
HPA axis support
Address GI symptoms and dysbosis

43. Mitochondrial Dysfunction in Autism
JAMA. 2010;304(21):
50-80% of children with autism had one or more biomarkers for mitochondrial dysfunction.
The cells of children with autism were exposed to higher levels of oxidative stress.
Half the children had mtDNA over replication, indicating an effort to overcome some form of damage or dysfunction.
©2010 True Health Medical Center

44. Holistic Model for Treatment of Mitochondrial Dysfunction
Avoid toxins that may interfere with function
Avoid medicines that interfere with mitochondrial function
Use herbs that protect and support mitochondria
Individualized mitochondrial cocktail
High ORAC/antioxidant foods
Reduce excess consumption of omega 6 oils
Treat any chronic bacterial issues and infections
Copyright Suruchi Chandra, 2012

45. Children with ASD have altered gut microbiota
Desulfovibrio species and Bacteroides vulgatus were present in significantly higher numbers in stools of severely autistic children. (Finegold SM, 2010) Lower relative abundances of Bifidobacteria species and the mucolytic bacterium Akkermansia muciniphila were found in children with autism. (Wang L, 2011) Sutterella species were found in ileal mucosal biopsy specimens from patients diagnosed with ASD but not in control children with GI symptoms. (Williams BL, 2012)
Copyright Suruchi Chandra, 2012

46. Refined foods, rarely fermented, and often grown with antibiotics
Modern practices that have established a potential influence on microbial diversity:
Caesarian delivery
Formula feeding
Refined foods, rarely fermented, and often grown with antibiotics
Refrigeration
Chlorinated water
Widespread antimicrobial use

47. Gut microbiota
At least 500 different species of bacteria Probiotics have only a few species Functions: Nutrient extraction immune system development defense against pathogens

48. Normal gut microbiota modulates brain development and behavior
Results suggest that the microbial colonization process initiates signaling mechanism that affect neuronal circuits involved in motor control and anxiety behavior.
Proc Natl Acad Sci 2011, February 15.

49. Microbiota and Short-Course Antibiotic Challenge
Six healthy study volunteers received oral amoxicillin (1.5 g/day) for 5 days.
The fecal microbiota showed a major shift in dominant species after just 24 hours of antibiotic treatment.
After 4 days of treatment, the average similarity to pre-treatment microbiota was 74%.
After 60 days, the average similarity to the pre-treatment microbiota was 89%.
In one subject, there were significant changes even at 2 months after treatment.
J Clin Microbiol Nov;43(11):
Resilience of the dominant human fecal microbiota upon short-course antibiotic challenge.

50. Send to:
Display Settings:
Abstract
Pathways involved in bidirectional communication between the gut microbiota and the brain.
John F. Cryan & Timothy G. Dinan
Nature Reviews Neuroscience 13,   (October 2012)

51. Disruption of the gut microbiome as a risk factor for microbial infections.
We suggest that modern lifestyle advances may be depleting specific microbes that enhance immunity against pathogens. Validation of the notion that absence of beneficial microbes is a risk factor for infectious disease may have broad implications for future medical practices.
Curr Opin Microbiol Apr 15.

52. Microbiome and environmental toxins
Tissue content of mercury in rats given methylmercuric chloride orally: influence of intestinal flora.
Antibiotics-treated rats given labeled metyhlmercuric chloride orally had significantly more mercury in their tissues, especially in kidney, brain, lung, blood, and skeletal muscle, and also excreted less mercury in the feces than conventional rats.
Biodegradation of chlorpyrifos by lactic acid bacteria during kimchi fermentation.
Arch Environ Health May-Jun;35(3):
J Agric Food Chem. 2009 Mar 11;57(5):1882-9

53. Impairment of innate immune killing mechanisms by bacteriostatic antibiotics
In essence, certain drugs may be functioning at odds with our immune system rather than in synergy to achieve bacterial killing.
Certain pharmaceutical therapies could allow bacteria to persist longer in host tissue environments where innate immune responses are normally summoned.
The FASEB Journal. Online January 10, 2007,

54. Treatment of Dysbosis Preserve and restore natural diversity
We are still in the infancy stages of treatment,
Over 1000 human associated microorganisms have been identified in the human microbiota. Probiotics usually contain only a few different species.
Preserve and restore natural diversity
Avoid unnecessary antibiotics and antibiotic treated meat
Probiotics
Prebiotics/fibers
Fermented foods
Reduce Stress
Dietary Changes
Target possible pathogenic biofilm formation
Copyright Suruchi Chandra, 2012

55. Treatment of Dysbosis Possible future treatments:
Herbs to balance and restore gut microbiota – need studies to better understand and support use.
Human probiotics
Fecal transplant
Identification and targeted treatments for Desulfovibrio species
Copyright Suruchi Chandra, 2012

56. Treatment in the setting of an uncertain diagnosis
Many cases of chronic neurologic Lyme will not have confirmatory testing
Patient may have an infection that has not yet been identified
Herbal antimicrobials are a better option in the setting of an uncertain diagnosis

57. Long Term Antibiotic Use in Tick Borne Illnesses May:
Promotes dysbosis and fungal overgrowth in the GI system
Affect behavior and brain development
Decrease natural immunity in GI system
Contribute to the development of antibiotic resistant bacteria
Promote cyst or round body formation
Become another toxic burden on an already taxed liver
Not be effective against microbes that exist in biofilm formation.

58. Herbal Protocol Treatments for Tick Borne Illnesses
Stephen Buhner
Core Protocol:
Andrographis, Cat’ Claw, Japanese Knotweed, Astragalus, and Similax
Byron White
Dr. William Lee Cowden
Nutramedix herbs:
Cumanda, Banderol, Samento, Lakato, Houttuynia, Enula, Mora, and Quina

59. In Vitro Effectiveness of Samento and Banderol Herbal Extracts on the Different Morphological Forms of Borrelia Burgdorferi
Control
Banderol (1:300 dilution)
The cells inside the colonies are
>90% dead.
Samento (1:300 dilution)

60. In Vitro Effectiveness of Samento and Banderol Herbal Extracts on the Different Morphological Forms of Borrelia Burgdorferi
Samento + Banderol (1:300 dilution)
Doxycyline

61. Hottuyniae Herba protects rat primary cortical cells from amyloid beta induced neurotoxicity via regulation of calcium influx and mitochondria –
Mediated apoptosis.
Houttuyniae Herba water extract inhibited the amyloid beta induced elevation of intracellular calcium level, reactive oxygen species overproduction, mitochondrial membrane potential disruption, and caspase 3 activation.
Hum Ex Tocicol Jul; 31 (7)

62. Anti-inflammatory activity of Mirtraphylline isolated from Uncaria tomentosa bark.
Mitraphlline inhibited around 50% of the release of interleukins 1 alpha, 1 beta, 17, and TNF-alpha. This activity was similar to dexamethasone. It also reduced almost 40% of the production of interleukin 4 (IL-4) while the corticoid did not.
J Ethnpharmacol Oct 11;143 (3):

63. oxidative stress induced by 2,4-dichlorophenol (2,4-DCP) and catechol
Protective activity of the Uncaria tomentosa extract on human erythrocytes in
oxidative stress induced by 2,4-dichlorophenol (2,4-DCP) and catechol
Food Chem Toxicol Sep; 49 (9):
Neuroprotective effects of aqueous extracts of Uncaria tomentosa: Insights from
6-OHDA induced cell damaged transgenic Caenorhabditis elegegans model.
Neurochem Int Mar14;62 (7):

64. Case Studies

65. Case 1 9 year old boy with history of PDD Presents with Poor focus
Impulsivity
Fatigue
Anxiety
Low tone
Delays in fine motor skills

66. Treatment History IVIG IV EDTA/DMPS HBOT 40 Leucovorin 50 mg
Fluoxetine
Memantine
Neuro feedback therapy

67. Mother’s History
Mother had history of: Multiple tick bites as an adolescent Chronic fatigue Fibromyalgia ‘Foggy thinking’ Chronic depression After her son’s visit she took 4 drops of Banderol and had a herxheimer reaction

68. Treatment Stopped Leucovorin, Namenda, and IVIG
Started a vitamin, mineral, and herbal based protocol
After two months, mother reported that he was ‘doing better than ever.’
Started Lakato herbal and 10 days later experienced poor focus, hyperactivity, and school difficulties.
Stopped the Lakato and within one week was back to his baseline.

69. Mother’s Test Results Advanced Laboratory Polyclonal Borrelia Culture
Result: Growth
Positive Growth of spirochetes in the blood which stained positive via immunohistochemical method using polyclonal antibody for Borrelia species.

70. Lyme IgG WB IGENEX Positive Ehrlichia chaffeensis IgM 20 Positive
Borrelia and co-infection testing was done when patient was experiencing a herxheimer reaction while on Lakato IGENEX Panel:
Lyme IgM WB IGENEX Negative
CDC/NYS Negative
Lyme IgG WB IGENEX Positive
Ehrlichia chaffeensis
IgM 20 Positive
IgG <40 Negative
Babesia duncani
IgM 80 Positive

71. Case 2
8 year old boy with history of Asperger's and possible bipolar disorder
Treated with risperidone and fluoxetine
Genova ONE test results all within normal range
With minerals, vitamins, and adaptogenic support came off medications.

72. Case 2 Started Cumanda Developed auditory hallucinations
Became aggressive
Started hitting his own head

73. Lyme IgG WB IGENEX positive Babesia duncani IgM <20 Negative
Borrelia and co-infection testing was done after patient had been on Cumanda. IGENEX Panel:
Lyme IgM WB IGENEX Negative
CDC/NYS Negative
Lyme IgG WB IGENEX positive
Babesia duncani
IgM <20 Negative
IgG 80 Positive
Bartonella henselae
IgM 20 Positive
IgG <40 Negative

74. Treatment N acetyl cysteine cream
Treatment with less broad spectrum antimicrobials including herbs for possible parasitic infection
After 9 months of antimicrobial treatment, teachers and mother felt he was indistinguishable from other children
Still struggles under stressful situations

75. Conclusion
All of these infections are emerging diseases. We still have much to learn about them.
Consider Lyme disease and the associated co-infections in the differential of any severe or atypical psychiatric disease.
Lyme disease is a clinical diagnosis. Serologies can be used to support a diagnosis.
For late stage Lyme disease, consider a treatment approach that is multi-faceted and addresses all forms of Borrelia, co-infections, and secondary complications of the infection.