Chronic Illness Treatment

According to cyrex laboratories: “The detection of antibodies to P. gingivalis indicates the patient has increased risk of rheumatoid arthritis and cardiovascular autoimmunity. Periodontitis is a dysbiotic inflammatory disease induced by an oral pathogen and is associated with an adverse impact on systemic health.  P. gingivalis plays a role in upper gastrointestinal tract, respiratory tract, and in colon disorders and is commonly associated with periodontitis.1,2 P. gingivalis may also contribute to extra-intestinal tissue disorders such as rheumatoid arthritis (RA), cardiovascular disease, respiratory disease, and chronic obstructive pulmonary disease.”2

According to cyrex laboratories: “The detection of antibodies to S. mutans indicates the patient may have increased risk of autoimmune cardiovascular disorders.

Inflammatory cytokines lead to
autoimmunity as seen in the pathogenesis of psoriasis and autoimmune cardiovascular disorders.”

According to cyrex laboratories: “The detection of antibodies to H. pylori indicates the patient has increased risk of gastrointestinal disorders, neurological disorders, rheumatic diseases, thyroid autoimmunity and lupus. Two major groups of H. pylori have been classified.3  Systemic inflammation caused by H. pylori can
lead to extra-intestinal autoimmunity effecting heart, pancreas and thyroid tissues.” 3-5

According to cyrex laboratories: “The detection of antibodies to C. jejuni indicates the patient may have increased risk of bowel disorders, neurological disorders and
arthritis. Extraintestinal manifestations of C. jejuni infection are rare and may include meningitis, endocarditis, septic arthritis, osteomyelitis, neonatal sepsis1 and even Guillain-Barré syndrome (GBS)6,7 or Miller Fisher syndrome.3 Molecular mimicry between microbial antigens and human tissue and in this particular case, between C. jejuni and
ganglioside, serve as the causative mechanism for GBS.” 8

According to cyrex laboratories: “The detection of antibodies to Y. enterocolitica indicates the patient has increased risk of gastrointestinal disorders, eye inflammation, thyroid autoimmunity, reactive arthritis. Due to cross-reactivity or molecular mimicry with human tissues, Y. enterocolitica may play a role in some arthritic and thyroid disorders. Indeed IgG antibodies to Y. enterocolitica were significantly higher in patients with Graves’ disease and patient with Hashimoto’s thyroiditis.”9

According to cyrex laboratories: “The detection of antibodies to C. difficile indicates the patient has increased risk of gastrointestinal disorders including irritable bowels, ulcerative colitis and Crohn’s disease. Studies have shown an increase in the prevalence and severity of C. difficile infection among inflammatory bowel disease (IBD) patients and patients with IBD are more likely to have serum antibodies to C. difficile toxin B.10

According to cyrex laboratories: “The detection of antibodies to C. albicans indicates the patient has increased risk of gastrointestinal disorders and multiple extraintestinal autoimmunities. C. albicans is present in the oral cavity of up to 75% of the population.13,14  The potential for systemic Candida to ignite autoimmunity is high due to the homology between the fungus and multiple human tissues.11 When a comparison of anti-Candida IgG antibodies in healthy controls versus patients with autoimmune reactivitty was conducted, only 10% of healthy controls showed elevation in C. albicans antibody, while C. albicans antibodies were present in 60% of tissue antibody positive individuals.12 Candida infection is also considered a trigger of Celiac disease.”

According to cyrex laboratories: “The detection of antibodies to Rotavirus indicates the patient has increased risk of gastrointestinal disorders, type 1 diabetes, eye autoimmunity.” 15

According to cyrex laboratories: “The detection of antibodies to E. histolytica indicates the patient has increased risk of skeletal and neurological disorders.”

According to cyrex laboratories: “The detection of antibodies to G. lamblia indicates the patient has increased risk of gastrointestinal disorders including intestinal permeability and autoimmunity against gastrointestinal tract tissues. Clinical features may range from diarrhea to constipation, nausea, headache, and flatulence. Published case reports and epidemiologic studies have associated giardiasis with the development of allergies,16 reactive arthritis,17 chronic enteric disorders,18,19 and chronic fatigue.18 Furthermore, recurrent Giardiasis may mimic the symptoms of Celiac disease and may simulate clinical and histological picture of active Celiac disease, therefore, patients with persistent giardiasis and failure to thrive should be tested for possible Celiac disease.”20

According to cyrex laboratories: “The detection of antibodies to Cryptosporidium indicates the patient has increased risk of colon autoimmunity, Celiac disease and nonceliac gluten sensitivity.  Autoantigen remodeling by the parasite is an additional mechanism by which Cryptosporidium can induce autoimmunity.22 Human tropomyosin-5, which is over-expressed at the site of C. parvum infection was shown to be an autoantigen capable of inducing a significant B- and T-cell immune response in ulcerative colitis.”21

According to cyrex laboratories: “The detection of antibodies to B. hominis indicates the patient has increased risk of irritable bowel disorders and subsequent fibromyalgia.” 23

According to cyrex laboratories: “The detection of antibodies to HSP60 + C.Hsp60 indicates the patient has increased risk of multiple autoimmunities including arthritis, lupus, gastrointestinal disorders, lung disorders, heart autoimmunity, and neuroautoimmunity.” 24-26

According to cyrex laboratories: “The detection of antibodies to Chlamydias indicates the patient has increased risk of neuroautoimmunities, systemic inflammation, autoimmune cardiovascular disorders, pelvic inflammatory disease, infertility, or Fitz-Hugh-Curtis syndrome.” 27,28

According to cyrex laboratories: “The detection of antibodies to Streptozymes indicates the patient has increased risk of neurological disorders including obsessive compulsive disorder (OCD), pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS), rheumatic heart disorders and reactive arthritis.” 29,30

According to cyrex laboratories: “The detection of antibodies to Streptococcal M Protein indicates the patient has increased risk of neurological disorders including, obsessive compulsive disorder (OCD), pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS), rheumatic heart disorders and reactive arthritis. Antigenic similarity between strep M proteins with heart α-myosin and the resulting antibody and T-cell-mediated immune responses is responsible for injury to the heart valves. The stimulation of inflammation cascades and molecular mimicry between streptococcal M protein and human tissue antigens are not the only mechanisms for the induction of autoimmunity.” 31-33

According to cyrex laboratories: “The detection of antibodies to Mycoplasmas indicates the patient has increased risk of lupus, arthritis and anti-phospholipid syndrome.” 34-37

According to cyrex laboratories: “The detection of antibodies to Acinetobacter indicates the patient may have increased risk of multiple sclerosis (MS).  Evidence of sinusitis in MS patients indicate that Acinetobacter is one of the major causative agents of MS and measurement of Acinetobacter IgG antibodies could be used as a marker of disease activity.38 The measurement of IgG antibody against Acinetobacter as well as neural antigens such, as myelin basic protein and neurofilaments, was recommended, by study authors, for the identification of possible MS.39 It starts with a sinus infection, which leads to the formation of antibodies against the enzymes released by the bacteria. Then autoreactive antigens breach the blood-brain barrier, where Acinetobacter IgG can bind to myelin and other neurological tissues. At this time, antigen-antibody complexes are formed and inflammatory molecules are released, which leads to MS.”

According to cyrex laboratories: “The detection of antibodies to Klebsiella indicates the patient has increased risk of joint, skeletal and eye autoimmunities. Klebsiella spp. are among the most common causes of a variety of community-acquired and hospital-acquired infections. K. oxytoca has been found in patients with septicemia, bacteremia, septic arthritis, soft tissue infections, cholecystitis, urinary tract infections, colic and Celiac disease.” 40

According to cyrex laboratories: “The detection of antibodies to M. avium indicates the patient has increased risk of gastrointestinal disorders, thyroid autoimmunity, type 1 diabetes, arthritis and multiple sclerosis. Whether inhaled or ingested, M. avium is taken up primarily into macrophages, where they can reside, undetected by the immune system, for many years in a latent stage.41 A physical stressor can release the M. avium and clinical manifestations can emerge.41 M. avium can grow on tap water pipes, and plastic water bottles.32 M. avium has been found in the drinking water of the United States,14 as high as 700,000 or 7 x 105 organisms per liter of water. By drinking two liters of water per day, after a little over two months, an individual could have ingested pathogenic levels of microorganisms. Pierce2 concluded that M. avium antigens are the cause of Crohn’s disease and ulcerative colitis in addition to other autoimmune diseases such as type-1 diabetes, thyroiditis, rheumatoid arthritis and sarcoidosis.”

According to cyrex laboratories: “The detection of antibodies to Aspergillus indicates the patient has increased risk of chronic fatigue syndrome, fibromyalgia, a variety of autoimmunities including neuroautoimmunity. The genus Aspergillus, which includes nearly identified 200 species, including fumigatus, niger and flavus, has a tremendous impact on public health both beneficially, in numerous industrial applications, and negatively, as a pathogen. The most common mode of invasion is via inhalation. Molds, through the production of enzymes such as serine chymotrypsin-like proteinase, cleaves lungs and gut barrier proteins and then finds their way into the blood. In the blood, immune system reaction against them results in the release of proinflammatory cytokines and the production of antibody against mold antigens. The molds and their mycotoxins, enzymes and proinflammatory cytokines alter the blood brain barrier function and allow for the entry of autoreactive T-helper 1 (Th1), Th17 and antibodies into the nervous system causing damage to microglia, astrocytes and neurons, which leads to the neuroautoimmunity commonly seen in patients exposed to molds.” 43-44

According to cyrex laboratories: “The detection of antibodies to Penicillium indicates the patient has increased risk of chronic fatigue syndrome, fibromyalgia, a variety of autoimmunities including neuroautoimmunity. The most common mode of invasion is via inhalation. Due to their small size, Penicillium spores rest in the lower lung. These spores and their products can induce significant immunomodulatory responses in lung cells and inflammation in animal models of lung disease.” 45

According to cyrex laboratories: “The detection of antibodies to Stachybotrys indicates the patient has increased risk of chronic fatigue syndrome, fibromyalgia, a variety of autoimmunities including neuroautoimmunity. Although exposure to S. chartarum is often associated with indoor air, however, it is important to note that rural air can harbor S. chartarum. 46

According to cyrex laboratories: “The detection of antibodies to Citrullinated EBV indicates the patient has increased risk of a variety of autoimmunities including joint, lupus, neurological, thyroid, and liver, and type 1 diabetes and multiple food immune reactivity. Rheumatoid arthritis patients appear to have elevated antibody levels to EBV, yet the mechanism linking EBV pathogenesis in RA has not been elucidated. Patients with CIDP show impaired B cell expression of the inhibitory Fc-γ receptor (FcγRIIB), which alters the state of EBV persistence, leading to increased viral replication and antiviral immune responses. Epidemiological studies suggest that childhood EBV exposure is an important determinant of MS risk.” 47-56

According to cyrex laboratories: “The detection of antibodies to Hepatitis C-specific peptide, which cross-reacts with liver tissues, indicates the patient has increased riskof liver autoimmunity. Chronic HCV infection is known to induce autoimmune reactions and can be associated with Sjögren’s Syndrome and autoimmune thyroid disorders.” 57

According to cyrex laboratories: “The detection of antibodies to Cytomegalovirus indicates the patient has increased risk of type 1 diabetes, arthritis, lupus and neurological disorders. CMV establishes a lifelong latent infection following primary infection and, in some hosts, can periodically reactivate with shedding of infectious virus. Due to its potential for cross-reactivity with heart myosin and nervous system myelin, patients at risk for coronary disorders and/or demyelinating disorders, should be screened and treated for CMV antibodies. 58-63

According to cyrex laboratories: “The detection of antibodies to Human Herpesvirus-6 indicates the patient has increased risk of chronic fatigue syndrome, fibromyalgia, lupus, and autoimmunities of the nervous system, joints and thyroid. Most humans acquire HHV-6 during early childhood and after initial infection, the virus latently remains in the host. Depending on a person’s genetic susceptibility, a persistent HHV-6 infection may lead to neurological autoimmunity via a cascade of events that starts with elevated HHV-6 IgG and release of proinflammatory cytokines, which opens the blood-brain barrier allowing HHV-6 IgG to react to neurons and cause the release of myelin. 64

According to cyrex laboratories: “The detection of antibodies to B. burgdorferi indicates the patient has increased risk of Lyme disease, Lyme arthritis, Lyme neuroborreliosis, blood-brain barrier damage and neurological disorders.  In some untreated cases, symptoms of pathogenic invasion have involved neurologic, cardiac, or articular complications. Early spirochete dissemination mainly affects the nervous system and can present as meningitis and cranial neuritis predominantly in children, while some patients experience heart disorders such as atrioventricular blockade, myopericarditis and cardiomyopathy, and more common in the US than Europe, the musculoskeletal system can be involved resulting in arthritidis. Borrelia pathogenesis can break the blood brain barrier, which allows invasion of the central nervous system, resulting in neuroborreliosis.” 65-70

According to cyrex laboratories: “The detection of antibodies to B. burgdorferi indicates the patient has increased risk of Lyme disease, Lyme arthritis, Lyme neuroborreliosis, blood-brain barrier damage and neurological disorders.  In some untreated cases, symptoms of pathogenic invasion have involved neurologic, cardiac, or articular complications. Early spirochete dissemination mainly affects the nervous system and can present as meningitis and cranial neuritis predominantly in children, while some patients experience heart disorders such as atrioventricular blockade, myopericarditis and cardiomyopathy, and more common in the US than Europe, the musculoskeletal system can be involved resulting in arthritidis. Borrelia pathogenesis can break the blood brain barrier, which allows invasion of the central nervous system, resulting in neuroborreliosis.” 65-70

According to cyrex laboratories: “The detection of antibodies to B. burgdorferi indicates the patient has increased risk of Lyme disease, Lyme arthritis, Lyme neuroborreliosis, blood-brain barrier damage and neurological disorders.  In some untreated cases, symptoms of pathogenic invasion have involved neurologic, cardiac, or articular complications. Early spirochete dissemination mainly affects the nervous system and can present as meningitis and cranial neuritis predominantly in children, while some patients experience heart disorders such as atrioventricular blockade, myopericarditis and cardiomyopathy, and more common in the US than Europe, the musculoskeletal system can be involved resulting in arthritidis. Borrelia pathogenesis can break the blood brain barrier, which allows invasion of the central nervous system, resulting in neuroborreliosis.” 65-70

According to cyrex laboratories: “The detection of antibodies to B. burgdorferi indicates the patient has increased risk of Lyme disease, Lyme arthritis, Lyme neuroborreliosis, blood-brain barrier damage and neurological disorders.  In some untreated cases, symptoms of pathogenic invasion have involved neurologic, cardiac, or articular complications. Early spirochete dissemination mainly affects the nervous system and can present as meningitis and cranial neuritis predominantly in children, while some patients experience heart disorders such as atrioventricular blockade, myopericarditis and cardiomyopathy, and more common in the US than Europe, the musculoskeletal system can be involved resulting in arthritidis. Borrelia pathogenesis can break the blood brain barrier, which allows invasion of the central nervous system, resulting in neuroborreliosis.” 65-70

According to cyrex laboratories: “The detection of antibodies to B. burgdorferi indicates the patient has increased risk of Lyme disease, Lyme arthritis, Lyme neuroborreliosis, blood-brain barrier damage and neurological disorders.  In some untreated cases, symptoms of pathogenic invasion have involved neurologic, cardiac, or articular complications. Early spirochete dissemination mainly affects the nervous system and can present as meningitis and cranial neuritis predominantly in children, while some patients experience heart disorders such as atrioventricular blockade, myopericarditis and cardiomyopathy, and more common in the US than Europe, the musculoskeletal system can be involved resulting in arthritidis. Borrelia pathogenesis can break the blood brain barrier, which allows invasion of the central nervous system, resulting in neuroborreliosis.” 65-70

According to cyrex laboratories: “The detection of antibodies to Babesia may indicate the patient has increased risk of blood-brain barrier damage, neurological disorders and arthritis. Tick-borne pathogens can have serious, long-lasting effects on the host. Infection with Babesia usually results in a subclinical or mild illness, but the infection can occasionally cause severe illness in immunocompromised patients and persons lacking a spleen.” 70-72

According to cyrex laboratories: “The detection of antibodies to Ehrlichia  may indicate the patient has increased risk of blood-brain barrier damage, neurological disorders and arthritis. Tick-borne pathogens can have serious, long-lasting effects on the host. Infections with Ehrlichia targets neutrophils adherent to endothelium in tissues, resulting in subsequent tissue damage and systemic proinflammatory responses.”

According to cyrex laboratories: “The detection of antibodies to Bartonella may indicate the patient has increased risk of blood-brain barrier damage, neurological disorders and arthritis. Tick-borne pathogens can have serious, long-lasting effects on the host. Bartonella infection can present with nonspecific clinical features indicating upper respiratory tract infection or viral
pneumonia. 75-78

• Rocky Mountain Spotted Fever (RMSF)
• Citrobacter freundii
• Treponema pallidum
• Toxoplasma
• Human T-Lymphotropic virus -I (HTLV-I)
• Herpes simplex virus 1
• Herpes simplex virus 2
• Mycoplasma fermentans
• Parvovirus
• Varicella-zoster virus
• Dengue viruses 1-4
• Coxsackie virus A & B
• Colorado tick fever virus
• Borrelia Lonstari
• Bartonella quintana
• Bartonella elizabethae
• Bartonella bacilliformis
• Babesia WA-1
• Adenovirus

1. Hajishengallis. Peridodontitis: from microbial immune subversion to systemic inflammation. Nature Rev Immunol, 2015; 15:30-44.
2. Whitney, et al. Serum immunoglobulin G antibody to Porphyromonas gingivalis in rapidly progressive periodontitis: titer, avidity, and subclass
   distribution. Infect Immune, 1992; 60(6): 2194-2200.
3. Danesh, et al. Helicobacter pylori infection and early onset myocardial infarction: case-control and sibling pairs study. BMJ, 1999; 319:1157-1162.
4. Larizza, et al. Helicobacter pylori infection and autoimmune thyroid disease in young patients: the disadvantage of carrying the human leukocyte
   antigen-DRB1*0301 Allele. J Clin Endocrinol Metabol, 2006; 91(1):176-179.
5. Frulloni, et al. Identification of a novel antibody associated with autoimmune pancreatitis. N Engl J Med, 2009; 361(22):2135-2142.
6. Yuki, et al. A bacterium lipopolysaccharide that elicits Guillain-Barré syndrome has a GM1 ganglioside-like structure.
   J Exp Med, 1993; 178:1771-1775.
7. Yuki and Koga. Bacterial infections in Guillain-Barré and Fisher syndromes. Curr Opin Neurol, 2006; 19:451-457.
8.  Ang, et al. The Guillain-Barré syndrome: a true case of molecular mimicry. Trends Immunol, 2004; 25(2):61-66.
9. Wenzel, et al. Antibodies to plasmid-encoded proteins of enteropathogenic Yersinia in patients with autoimmune thyroid disease. Lancet, 1988;
   1(8575-6):56.
10. Shakir, et al., Determination of serum antibodies to Clostridium difficile toxin B in patients with inflammatory bowel disease. Gastroenterol Hepatol (N
    Y), 2012; 8(5):313-317.
11.  Vojdani, et al. Immunological cross reactivity between Candida albicans and human tissue. J Clin Lab Immunol, 1996; 48:1-15.
12. Nieuwenhuizen, et al. Is Candida albicans a trigger in the onset of coeliac disease? Lancet, 2003; 361:2152-2154.
13.  Ruhnke. Skin and mucous membrane infections. In: Calderone RA, ed. Candida and Candidiasis: ASM Press, Washington, DC, pp. 307-325., 2002.
14. Kumamoto. Inflammation and gastrointestinal Candida colonization. Curr Opin Microbiol, 2011; 14(4):386-391.
15. Honeyman, et al. Evidence for molecular mimicry between human T cell epitopes in rotavirus and pancreatic islet autoantigens. J Immunol,
    2010; 184(4):2204-2210.
16.  Di Prisco, et al. Possible relationship between allergic disease and infection by Giardia lamblia. Ann Allergy, 1993; 70:210-213.
17. Tupchong, et al. Beaver fever-a rare cause of reactive arthritis. J Rheumatol, 1999; 26:2701-2702.
18. Wensaas, et al. Post-infectious gastrointestinal symptoms after acute Giardiasis. A 1-year follow-up in general practice. Fam Pract, 2010; 27:255-259.
19. Wensaas, et al. Irritable bowel syndrome and chronic fatigue 3 years after acute giardiasis: historic cohort study. Gut, 2012; 61:214-219.
20. Tchidjou, et al. Celiac disease in an adoptive child with recurrent Giardia infection. Int J Health Sci (Qassim), 2015; 9(2):193-197.
21. Onuma, et al. Autoimmunity in ulcerative colitis (UC): a predominant colonic mucosal B cell response against human tropomyosin isoform 5. Clin Exp
    Immunol, 2000; 121(3):466-471.
22. Bouzid, et al. Cryptosporidium pathogenicity and virulence. Clin Microbiol Rev, 2013; 26(1):115-134.
23. Cole, et al. Migraine, fibromyalgia, and depression among people with IBS: a prevalence study. BMC Gastroenterol, 2006; 6:26.
24. Yokota, et al. Autoantibodies against chaperonin CCT in human sera with rheumatic autoimmune diseases: comparison with antibodies against other
    Hsp60 family proteins. Cell Stress Chaperones, 2000; 5(4):337-346.
25. Gammazza, et al. Elevated blood Hsp60, its structural similarities and cross-reactivity with thyroid molecules, and its presence on the plasma
    membrane of oncocytes point to the chaperonin as an immunopathogenic factor in Hashimoto’s thyroiditis. Cell Stress Chaperones,
    2014; 19(3):343-353.
26. Patil, et al. Possible significance of anti-heat shock protein (HSP-65) antibodies in autoimmune myasthenia gravis. J Neuroimmunol,
    2013; 257(1-2):107-109.
27. Lindholt, et al. Serum antibodies against Chlamydia pneumoniae outer membrane protein cross-react with the heavy chain of immunoglobulin in the
    wall of abdominal aortic aneurysms. Circulation, 2004; 109:2097-2102.
28. Wucherpfennig and Strominger. Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin
    basic protein. Cell, 1995; 80(5):695-705.
29. Vojdani. Obsessive compulsive disorder and differentiation between non-autoimmune OCD and the autoimmune version of the disease
    called PANDAS. Latitudes, 2003; 6(2):106.
30. Dileepan, et al. Group A Streptococcus intranasal infection promotes CNS infiltration by streptococcal-specific Th17cells. J Clin Invest, 2016;
    126(1):303-317.
31. Bronze and Dale. Epitopes of streptococcal M proteins that evoke antibodies that cross-react with human brain. J Immunol, 1993; 151(5):2820-2828.
32. Arnold and Richter. Is obsessive-compulsive disorder an autoimmune disease? CMAJ, 2001; 165(10):1353-1358.
33. Müller, et al. Increased titers of antibodies against streptococcal M12 and M19 proteins in patients with Tourette’s syndrome. Psychiatry Res, 2001;
    101(2):187-193.
34. Cole, et al. Arthritis of mice induced by Mycoplasma arthritidis. Ann Rheum Dis, 1976; 35:14-22.
35. Kirchhoff, et al. Pathogenetic mechanisms in the Mycoplasma arthritidis polyarthritis of rats. Rheumatol Int, 1989; 9(3-5):193-196.
36. Steele, et al. Mycoplasma pneumoniae as a determinant of the Guillain-Barré syndrome. Lancet, 1969; 2:710.
37. Biberfeld. Antibodies to brain and other tissues in cases of Mycoplasma pneumoniae infection. Clin Exp Immunol, 1971; 8:319-333.
38. Hughes, et al. Cross-reactivity between related sequences found in Acinetobacter spp. Pseudomonas aeruginosa,
    myelin basic protein and myelin oligodendrocyte glycoprotein in multiple sclerosis. J Neuroimmunol, 2003; 144:105-115.
39. Ebringer, et al. The role of Acinetobacter in the pathogenesis of multiple sclerosis examined by using Popper sequences. Medical Hypotheses, 2012;
    78:763-769
40. Darby, et al. Cytotoxic and pathogenic properties of Klebsiella oxytoca isolated from laboratory animals. PLoS ONE, 2014; 9(7):e100542.
41. Hermon-Taylor, et al. Causation of Crohn’s disease by Mycobacterium avium subspecies paratuberculosis. Can J Gastroenterol, 2000; 14(6):521-539.
42. Tatchou-Nyamsi-König, et al. Survival of Mycobacterium avium attached to polyethylene terephtalate (PET) water bottles. J Appl Microbiol, 2009;
    106(3):825-832.
43. Gugnani. Ecology and taxonomy of pathogenic aspergilli. Front Biosc, 2003; 8:s346-s357.
44.  Dagenais, et al. Pathogenesis of Aspergillus fumigatus in invasive aspergillosis. Clin Microbiol Rev, 2009; 447-465.
45. Pathak, et al. Innate immune recognition of molds and homology to the inner ear protein, cochlin, in patients with autoimmune inner ear disease.
    J Clin Immunol, 2013; 33(7): 10.1007/s10875-013-9926-x.
46. Miller, et al. Stachybotrys chartarum: cause of human disease or media darling? Med Mycol, 2003; 41:271-291.
47. Panza, et al. Immunoglobulin G subclass profile of anticitrullinated peptide antibodies specific for Epstein Barr virus-derived and histone-derived
    citrullinated peptides. J Rheumatol, 2014; 41:407-408.
48. Pratesi, et al. Deiminated Epstein-Barr virus nuclear antigen 1 is a target of anti-citrullinated protein antibodies in rheumatoid arthritis. Arthritis
    Rheumatism, 2006; 54(3):733-741.
49. Lünemann, et al. Dysregulated Epstein-Barr virus infection in patients with CIDP. J Neuroimmunol, 2010; 218:107-111.
50. Nociti, et al. Epstein-Barr virus antibodies in serum and cerebrospinal fluid from multiple sclerosis, chronic inflammatory demyelinating
    polyradiculoneuropathy and amyotrophic lateral sclerosis. J Neuroimmunol, 2010; 225:149-152.
51. Gross, et al. EBV and systemic lupus erythematosus: a new perspective. J Immunol, 2005; 174:6599-6607.
52. Janegova, et al. The role of Epstein-Barr virus infection in the development of autoimmune thyroid diseases. Endokrynol Pol, 2015; 66(2):132-136.
53. Esposito, et al. Human transaldolase and cross-reactive viral epitopes identified by autoantibodies of multiple sclerosis Patients. J Immunology, 1999;
    163:4027-4032.
54. Pool, et al. Epstein-Barr virus and molecular mimicry in systemic lupus erythematosus. Autoimmunity, 2006; 39(1):63-70.
55. van Sechel, et al. EBV-induced expression and HLA-DR-restricted presentation by human B cells of alpha B-crystallin, a candidate autoantigen in
    multiple sclerosis. J Immunol, 1999; 162(1):129-135.
56. Bogdanos, et al. Virus/self double reactivity characterises the humoral immune response in autoimmune hepatitis-2. J Hepatol, 2000; 32(Suppl 2):45.
57. Manns and Obermayer-Straub. Cytochromes P450 and uridine triphosphate-glucuronosyltransferases: model autoantigens to study drug-induced,
    virus-induced, and autoimmune liver disease. Hepatology, 1997; 26(4):1054-1066.
58.  Rider, et al. Human cytomegalovirus infection and systemic lupus erythematosus. Clin Exp Rheumatol, 1997; 15(4):405-409.
59. Lunardi, et al. Antibodies against human cytomegalovirus in the pathogenesis of systemic sclerosis: a gene array approach. PLoS Med, 2006; 3(1):e2.
60. Pak, et al. Association of cytomegalovirus infection with autoimmune type 1 diabetes. Lancet, 1988; 2(8601):1-4.
61. Lawson, et al. Mouse cytomegalovirus infection induces antibodies which cross-react with virus and cardiac myosin: a
    model for the study of molecular mimicry in the pathogenesis of viral myocarditis. Immunology, 1992; 75:513-519.
62.  Zheng and Zhang. Cross-reactivity between human cytomegalovirus peptide 981-1003 and myelin oligodendroglia glycoprotein peptide 35-55 in
    experimental autoimmune encephalomyelitis in Lewis rats. Biochem Biophys Res Communications, 2014; 443(3):1118-1123.
63. Hiemstra, et al. Cytomegalovirus in autoimmunity: T cell crossreactivity to viral antigen and autoantigen glutamic acid decarboxylase. Proc Natl Acad
    Sci U S A, 2001; 98(7):3988-3991
64. Goodman, et al. Human herpesvirus 6 genome and antigen in acute multiple sclerosis lesions. J Infect Dis, 2003; 187:1365-1376
65. Steere. Lyme disease. N Engl J Med, 1989; 321:586-596.
66. Vojdani, et al. Novel diagnosis of Lyme disease: potential for CAM intervention. eCAM, 2007.
67. Girschick, et al. Treatment of Lyme borreliosis. Arthritis Res Therapy, 2009; 11:258. doi:10.1186/ar2853
68. Magnarelli, et al. Cross-reactivity in serological tests for Lyme disease and other spirochetal infections. J Infect Dis, 1987; 156(1):183-188.
69. Bruckbauer, et al. Crossreactive proteins of Borrelia burgdorferi. Eur. J. Clin Microbiol Infect Dis, 1992; 11:224-232.
70. Benvenga, et al. Homologies between proteins of Borrelia burgdorferi and thyroid autoantigens. Thyroid, 2004; 14(11):964-966.
71. Homer, et al. Babesiosis. Clin Microbiol Rev, 2000; 13(3):451-469.
72. Krause, et al. Increasing health burden of human babesiosis in endemic sites. Am J Trop Med Hyg, 2003; 68(4):431-436.
73. Ruebush, et al. Human babesiosis on Nantucket Island: clinical features. Ann Intern Med, 1977; 86:6-9.
74. Lepidi, et al. Comparative pathology and immunosistology associated with clinical illness after Ehrlichia phagocytophila-group infections. Am J Trop Med
    Hyg, 2000; 62(1):29-37.
75. Klotz, et al. Cat-scratch disease. Am Fam Physician, 2011; 83(2):152-155.
76. Adal, et al Cat scratch disease, bacillary angiomatosis, and other infections due to Rochalimaea. N Engl J Med, 1994:330:1509-1515.
77. Zbinden, et al. IgM to Bartonella henselae in cat scratch disease during acute Epstein Barr virus infection. Med Microbiol Immunol, 1998; 186:167-170.
78. Massei, et al. High prevalence of antibodies to Bartonella henselae among Italian children without evidence of cat scratch disease. Clin Infect Dis, 2003;
    38:145-148.