Many chronic diseases are linked or associated with infectious pathogens. A disease is said to be linked or associated with an infectious pathogen when that pathogen is found more frequently in patients with the disease than in healthy controls. Often, infectious pathogens associated with a disease may be suspected of playing a causal role in that disease — and some scientists believe a substantial portion of chronic diseases may in part be caused by infectious agents — though association alone does not automatically prove causality (because correlation does not imply causation).
Indeed, the terms linked and associated are used here in a strict technical sense: they mean there is a frequent co-occurrence of certain pathogens in certain diseases; but it should not be read that linked and associated imply there is a proven causal relationship between pathogen and disease. An observed association only flags up the possibility that there might be a causal relation.
For an infectious pathogenic microbe that has been noted to frequently accompany a disease, there are several logical possibilities that can explain this observed association:
The pathogen is an "innocent bystander" that plays no causal role in the etiology of the disease, but for some reason is more prevalent in patients with the disease (perhaps because the disease compromises the immune response, for example).
The pathogen predisposes to disease development (increases the risk of getting the disease), but the pathogen does not cause the disease (for example, genital herpes increases the risk of acquiring HIV).
The pathogen is a necessary, but not sufficient, cause of the disease: in other words, the pathogen can cause the disease, but does so only in combination with one or more other causal factors (such as host genetic factors, or toxin exposure).
The pathogen is a direct and singular cause of the disease, but this causality has yet to be proven.
Determining whether a pathogen plays a causal role in a chronic disease is often difficult for the following reasons:
The time between contracting an infectious pathogen and the appearance of the first disease symptoms can be lengthy, sometimes decades.
An infectious pathogen may not cause disease in every person.
An infection may be asymptomatic in its acute phase (when first contracted), and so go unnoticed; symptoms may only appear much later — in the form of a chronic disease.
Sometimes, only specific strains of a pathogen are linked to a disease; other strains of the same microbe may be harmless.
A pathogen may precipitate the disease only in combination with one or more other causal factors.
There may be more than one pathogen that can precipitate a given disease.
A given pathogen may not always cause the same disease — infection with it may lead to one of several different diseases.
There may be pathogens that are not readily detectable that play a causal role in a disease.
For obvious ethical reasons, you cannot inoculate infectious pathogens into humans to see if these do cause the disease or not.
A pathogenic microbe may cause disease by relatively easy to track direct means, such as by infecting and destroying cells; or may cause disease via more complex and convoluted indirect means, such as through the damage created by inflammatory cytokines or autoimmune processes that are induced by the microbial infection (for example, tuberculosis infection induces an inflammatory cytokine that then itself causes severe tissue damage).
A pathogenic microbe may not necessarily be present in the diseased tissues or organs (bacterial toxins for example can travel and damage tissues at sites distant from the infection site; and inflammatory or autoimmune processes precipitated by infectious pathogens can also act at tissue sites far removed from the infection).
In spite of the difficulties in obtaining proof of causality, evolutionary biologistPaul W. Ewald and physicistGregory M. Cochran are noted for their assertion that many common chronic diseases of currently unknown etiology are likely caused by chronic low-level microbial infection, countering the prevailing view that genes are predominantly responsible for the development of chronic disease. Ewald and Cochran support their thesis with the logic of evolutionary biology, with Ewald explaining that: "chronic diseases, if they are common and damaging, must be powerful eliminators of any genetic instruction that may cause them."
In other words, any disease-causing gene that reduces survival and reproduction will eliminate itself over a number of generations, just by evolutionary pressures; therefore such genetic diseases are self-extinguishing. Ewald says the only genetic diseases that will persist are those that provide a compensating benefit. For example, genes that encode for sickle cell anemia disease are maintained and persist down generations, as these genes also protect against malaria, which kills millions worldwide each year.
Infectious pathogens are one of several potential causes of disease; other causal factors include: environmental toxins, certain types of radiation exposure, diet and lifestyle factors, stress, genetics, and epigenetics. All these factors are generally explored as potential causes of a disease.
Diseases may also be multifactorial, such that the disease only manifests when multiple causal factors occur in combination. For example: in a murine model, Crohn's disease can be precipitated by a norovirus, but only when both a specific gene variant is present and a certain toxin has damaged the gut. Thus a pathogen's causal role in a disease may well be contingent upon several other causal factors.
Infectious pathogen-associated diseases include many of the most common and costly chronic illnesses. About 70% of all deaths in the United States result from chronic diseases, with the treatment of chronic diseases accounting for 75% of all US healthcare costs (amounting to $1.7 trillion in 2009).
List of diseases associated with infectious Bacteria
In the list of diseases associated with infectious pathogens given below, bear in mind that there is no definitive proof that the associated pathogens do play a causal role in the disease, just a possibility that they might. Further research is required to determine whether or not these pathogens participate causally in their associated diseases. Note that this list covers some of the most common human diseases associated with infectious pathogens, but it is not intended to be a comprehensive list.
Amyotrophic lateral sclerosis, the most common of five forms of motor neuron disease, is associated with echovirus (an enterovirus) infection of the central nervous system, and with retrovirus activity (it is not known whether this retrovirus activity arises from a human endogenous retrovirus, or from an exogenous retrovirus).
Infection with Borrelia species bacteria is associated with anorexia nervosa. In rare cases, anorexia nervosa may arise after infection with Streptococcus species bacteria. Anorexia (which is distinct from anorexia nervosa) is associated with the protozoan parasite Dientamoeba fragilis.
Some estimates currently attribute 15% to 20% of all cancers to infectious pathogen causes. In future, this percentage may be revised upwards if the pathogens currently associated with cancers (such as those listed below) are proven to actually cause those cancers. (Note: for the sake of completeness, some infectious pathogens known to cause cancers are included in the list, in addition to the infectious pathogens associated with cancers.)
One study found ileocecal Crohn's disease is associated with viral species from the enterovirus genus (but note that all the study cohort with ileocecal Crohn's disease had disease-associated mutations in either their NOD2 or ATG16L1 genes). Crohn's disease is associated with Mycobacterium avium subspecies paratuberculosis. In a murine model, Crohn's disease is precipitated by the norovirus CR6 strain, but only in combination with a variant of the Crohn’s susceptibility gene ATG16L1, and chemical toxic damage to the gut. In other words, in this mouse model, Crohn’s is precipitated only when these three causal factors (virus, gene, and toxin) act in combination.
Diabetes mellitus type 1 is associated with viral species from the enterovirus genus, specifically echovirus 4 and Coxsackie B virus (the latter it is thought may infect and destroy the insulin producing beta-cells in the pancreas and also damage these cells via indirect autoimmune mechanisms). One study found Coxsackie B1 virus associated with a higher risk of the beta cell autoimmunity that portends type 1 diabetes; though Coxsackie B3 and B6 viruses were found to be associated with a reduced risk of such autoimmunity (possibly due to immune cross-protection against Coxsackie B1 virus). In boys, human parechovirus infection has been linked to a subsequent appearance of diabetes-associated autoantibodies.
Obesity is associated with adenovirus 36, which is found in 30% of obese people, but only in 11% of non-obese people. It has further been demonstrated that animals experimentally infected with adenovirus 36 (or adenovirus 5, or adenovirus 37) will develop increased obesity. Adenovirus 36 induces obesity by infecting fat cells (adipocytes), wherein the expression of the adenovirus E4orf1 gene turns on both the cell's fat producing enzymes and also instigates the generation of new fat cells. Evidence suggests that obesity can be a viral disease, and that the worldwide obesity epidemic that began in the 1980s may be in part due to viral infection.
Cross reference: Pathogens and their associated diseases
For some selected pathogens, the set of their disease associations is shown in the bar graphs below. For each bar below, the pathogen in question has been found more frequently in patients with the listed diseases than it has in healthy controls — but it has not been proven that the pathogen plays any causal role in the listed diseases; though usually investigations to examine whether it might participate causally are ongoing. By contrast, the diseases below enclosed in brackets ( ) indicate that the pathogen is a proven cause of that disease.
^Freeman EE, Weiss HA, Glynn JR, Cross PL, Whitworth JA, Hayes RJ (2006). "Herpes simplex virus 2 infection increases HIV acquisition in men and women: systematic review and meta-analysis of longitudinal studies.". AIDS20 (1): 73–83. doi:10.1097/01.aids.0000198081.09337.a7. PMID16327322.
^Ewald, Paul W. (2002). Plague Time: The New Germ Theory of Disease. Anchor. p. 3. ISBN0-385-72184-6. Bad genes and bad environments have often been falsely accused, or, at least they have taken more than their share of the blame. Viruses and bacteria are the primary offenders.
^Cochran, Gregory M.; Ewald, Paul W.; Cochran, Kyle D. (2000). "Infectious Causation of Disease: An Evolutionary Perspective". Perspectives in Biology and Medicine43 (3): 406–48. doi:10.1353/pbm.2000.0016. PMID10893730.
^ abEwald, Paul W. (2002). Plague Time: The New Germ Theory of Disease. Anchor. p. 56. ISBN0-385-72184-6. Chronic diseases, if they are common and damaging, must be powerful eliminators of any genetic instruction that may cause them. Only if a genetic instruction provides some compensating benefit can the disease it causes persist as a common ailment.
^Kockaya, Guvenc; Wertheimer, Albert (2010). "What are the top most costly diseases for USA? The alignment of burden of illness with prevention and screening expenditures". Health02 (10): 1174–8. doi:10.4236/health.2010.210172.
^"The Role of Chronic Disease in Higher Health Costs and Lower U.S. Economic Growth". Almanac of Chronic Disease. Partnership to Fight Chronic Disease. 2009. p. 23.
^Shima, Kensuke; Kuhlenbäumer, Gregor; Rupp, Jan (2010). "Chlamydia pneumoniae infection and Alzheimer’s disease: a connection to remember?". Medical Microbiology and Immunology199 (4): 283–9. doi:10.1007/s00430-010-0162-1. PMID20445987.
^Kountouras, Jannis; Boziki, Marina; Gavalas, Emmanuel; Zavos, Christos; Grigoriadis, Nikolaos; Deretzi, Georgia; Tzilves, Dimitrios; Katsinelos, Panagiotis et al. (2009). "Eradication of Helicobacter pylori may be beneficial in the management of Alzheimer's disease". Journal of Neurology256 (5): 758–67. doi:10.1007/s00415-009-5011-z. PMID19240960.
^Kusbeci, Ozge Yilmaz; Miman, Ozlem; Yaman, Mehmet; Aktepe, Orhan Cem; Yazar, Suleyman (2011). "Could Toxoplasma gondii Have any Role in Alzheimer Disease?". Alzheimer Disease & Associated Disorders25: 1–3. doi:10.1097/WAD.0b013e3181f73bc2. PMID20921875.
^Itzhaki, RF; Wozniak, MA (2008). "Herpes simplex virus type 1 in Alzheimer's disease: the enemy within". Journal of Alzheimer's disease13 (4): 393–405. PMID18487848.
^Corcia, P; Giraud, P; Guennoc, AM; De Toffol, B; Autret, A (2003). "Acute motor axonal neuropathy, enterovirus and Amyotrophic lateral sclerosis: can there be a link?". Revue neurologique159 (1): 80–2. PMID12618659.
^McCormick, A. L.; Brown, R. H.; Cudkowicz, M. E.; Al-Chalabi, A.; Garson, J. A. (2008). "Quantification of reverse transcriptase in ALS and elimination of a novel retroviral candidate". Neurology70 (4): 278–83. doi:10.1212/01.wnl.0000297552.13219.b4. PMID18209202.
^ abcdefgFallon, BA; Nields, JA (1994). "Lyme disease: a neuropsychiatric illness". The American Journal of Psychiatry151 (11): 1571–83. PMID7943444.
^Sokol, MS (2000). "Infection-triggered anorexia nervosa in children: clinical description of four cases". Journal of child and adolescent psychopharmacology10 (2): 133–45. doi:10.1089/cap.2000.10.133. PMID10933123.
^ abPhillips, Anna C.; Carroll, Douglas; Khan, Naeem; Moss, Paul (2008). "Cytomegalovirus is associated with depression and anxiety in older adults". Brain, Behavior, and Immunity22 (1): 52–5. doi:10.1016/j.bbi.2007.06.012. PMID17703915.
^Addolorato, G.; Mirijello, A.; d’Angelo, C.; Leggio, L.; Ferrulli, A.; Abenavoli, L.; Vonghia, L.; Cardone, S. et al. (2008). "State and trait anxiety and depression in patients affected by gastrointestinal diseases: Psychometric evaluation of 1641 patients referred to an internal medicine outpatient setting". International Journal of Clinical Practice62 (7): 1063–9. doi:10.1111/j.1742-1241.2008.01763.x. PMID18422970.
^Prager, M; Türel, Z; Speidl, WS; Zorn, G; Kaun, C; Niessner, A; Heinze, G; Huk, I et al. (2002). "Chlamydia pneumoniae in carotid artery atherosclerosis: a comparison of its presence in atherosclerotic plaque, healthy vessels, and circulating leukocytes from the same individuals". Stroke; a journal of cerebral circulation33 (12): 2756–61. doi:10.1161/01.STR.0000039322.66575.77. PMID12468766.
^Yamashita, Y; Fujimoto, C; Nakajima, E; Isagai, T; Matsuishi, T (2003). "Possible association between congenital cytomegalovirus infection and autistic disorder". Journal of autism and developmental disorders33 (4): 455–9. doi:10.1023/A:1025023131029. PMID12959425.
^Finegold, Sydney M.; Molitoris, Denise; Song, Yuli; Liu, Chengxu; Vaisanen, Marja‐Liisa; Bolte, Ellen; McTeague, Maureen; Sandler, Richard et al. (2002). "Gastrointestinal Microflora Studies in Late‐Onset Autism". Clinical Infectious Diseases35 (Suppl 1): S6–S16. doi:10.1086/341914. PMID12173102.
^Barzilai, O; Sherer, Y; Ram, M; Izhaky, D; Anaya, JM; Shoenfeld, Y (2007). "Epstein-Barr virus and cytomegalovirus in autoimmune diseases: are they truly notorious? A preliminary report". Annals of the New York Academy of Sciences1108: 567–77. doi:10.1196/annals.1422.059. PMID17894021.
^Larizza, D.; Calcaterra, Valeria; Martinetti, Miryam; Negrini, Riccardo; De Silvestri, Annalisa; Cisternino, Mariangela; Iannone, A. M.; Solcia, Enrico (2006). "Helicobacter pylori Infection and Autoimmune Thyroid Disease in Young Patients: The Disadvantage of Carrying the Human Leukocyte Antigen-DRB1*0301 Allele". Journal of Clinical Endocrinology & Metabolism91: 176–9. doi:10.1210/jc.2005-1272.
^Dickerson, Faith B; Boronow, John J; Stallings, Cassie; Origoni, Andrea E; Cole, Sara; Krivogorsky, Bogdana; Yolken, Robert H (2004). "Infection with herpes simplex virus type 1 is associated with cognitive deficits in bipolar disorder". Biological Psychiatry55 (6): 588–593. doi:10.1016/j.biopsych.2003.10.008. PMID15013827.
^Pisani, P; Parkin, DM; Muñoz, N; Ferlay, J (1997). "Cancer and infection: estimates of the attributable fraction in 1990". Cancer epidemiology, biomarkers & prevention6 (6): 387–400. PMID9184771.
^Barzon, L; Trevisan, M; Masi, G; Pacenti, M; Sinigaglia, A; MacChi, V; Porzionato, A; De Caro, R et al. (2007). "Detection of polyomaviruses and herpesviruses in human adrenal tumors". Oncogene27 (6): 857–64. doi:10.1038/sj.onc.1210699. PMID17684484.
^Abramowitz, Laurent; Jacquard, Anne-Carole; Jaroud, Fatiha; Haesebaert, Julie; Siproudhis, Laurent; Pradat, Pierre; Aynaud, Olivier; Leocmach, Yann et al. (2011). "Human papillomavirus genotype distribution in anal cancer in France: The EDiTH V study". International Journal of Cancer129 (2): 433–439. doi:10.1002/ijc.25671.
^Botelho, Monica Catarina; MacHado, Jose Carlos; Correia Da Costa, Jose Manuel (2010). "Schistosoma haematobiumand bladder cancer: What lies beneath?". Virulence1 (2): 84–7. doi:10.4161/viru.1.2.10487. PMID21178421.
^Barbanti-Brodano, Giuseppe; Sabbioni, Silvia; Martini, Fernanda; Negrini, Massimo; Corallini, Alfredo; Tognon, Mauro (2006). "Polyomaviruses and Human Diseases". Advances in Experimental Medicine and Biology 577. pp. 319–41. doi:10.1007/0-387-32957-9_23. ISBN978-0-387-29233-5.|chapter= ignored (help)
^Samaras, V; Rafailidis, PI; Mourtzoukou, EG; Peppas, G; Falagas, ME (2010). "Chronic bacterial and parasitic infections and cancer: a review". Journal of infection in developing countries4 (5): 267–81. doi:10.3855/jidc.819. PMID20539059.
^Ishii, A; Matsuoka, H; Aji, T; Ohta, N; Arimoto, S; Wataya, Y; Hayatsu, H (1994). "Parasite infection and cancer: with special emphasis on Schistosoma japonicum infections (Trematoda). A review". Mutation research305 (2): 273–81. doi:10.1016/0027-5107(94)90247-X. PMID7510038.
^Chaturvedi, A. K.; Gaydos, C. A.; Agreda, P.; Holden, J. P.; Chatterjee, N.; Goedert, J. J.; Caporaso, N. E.; Engels, E. A. (2010). "Chlamydia pneumoniae Infection and Risk for Lung Cancer". Cancer Epidemiology Biomarkers & Prevention19 (6): 1498–505. doi:10.1158/1055-9965.EPI-09-1261.
^Joh, Joongho; Jenson, A. Bennett; Moore, Grace D.; Rezazedeh, Arash; Slone, Stephen P.; Ghim, Shin-je; Kloecker, Goetz H. (2010). "Human papillomavirus (HPV) and Merkel cell polyomavirus (MCPyV) in non small cell lung cancer". Experimental and Molecular Pathology89 (3): 222–6. doi:10.1016/j.yexmp.2010.08.001. PMID20699096.
^Rivera, Zeyana; Strianese, Oriana; Bertino, Pietro; Yang, Haining; Pass, Harvey; Carbone, Michele (2008). "The relationship between simian virus 40 and mesothelioma". Current Opinion in Pulmonary Medicine14 (4): 316–21. doi:10.1097/MCP.0b013e3283018220. PMID18520265.
^Chia, J K S; Chia, A Y (2007). "Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach". Journal of Clinical Pathology61 (1): 1–2. doi:10.1136/jcp.2007.050054. PMID17873115.
^Chia, J.; Chia, A.; Voeller, M.; Lee, T.; Chang, R. (2009). "Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence". Journal of Clinical Pathology63 (2): 165–8. doi:10.1136/jcp.2009.070466. PMID19828908.
^Chapenko, S; Krumina, A; Kozireva, S; Nora, Z; Sultanova, A; Viksna, L; Murovska, M (2006). "Activation of human herpesviruses 6 and 7 in patients with chronic fatigue syndrome". Journal of Clinical Virology37: S47–51. doi:10.1016/S1386-6532(06)70011-7. PMID17276369.
^Seishima, Mariko; Mizutani, Yoko; Shibuya, Yoshinao; Arakawa, Chikako (2008). "Chronic Fatigue Syndrome after Human Parvovirus B19 Infection without Persistent Viremia". Dermatology216 (4): 341–6. doi:10.1159/000116723. PMID18277075.
^Kerr, JR; Bracewell, J; Laing, I; Mattey, DL; Bernstein, RM; Bruce, IN; Tyrrell, DA (2002). "Chronic fatigue syndrome and arthralgia following parvovirus B19 infection". The Journal of rheumatology29 (3): 595–602. PMID11911112.
^Wildman, MJ; Smith, EG; Groves, J; Beattie, JM; Caul, EO; Ayres, JG (2002). "Chronic fatigue following infection by Coxiella burnetii (Q fever): ten-year follow-up of the 1989 UK outbreak cohort". QJM95 (8): 527–38. doi:10.1093/qjmed/95.8.527. PMID12145392.
^Chia, John K. S.; Chia, Laura Y. (1999). "Chronic Chlamydia pneumoniae Infection: A Treatable Cause of Chronic Fatigue Syndrome". Clinical Infectious Diseases29 (2): 452–3. doi:10.1086/520239. PMID10476765.
^McManus, T. E.; Marley, A-M.; Baxter, N.; Christie, S. N.; Elborn, J. S.; O'Neill, H. J.; Coyle, P. V.; Kidney, J. C. (2008). "High levels of Epstein-Barr virus in COPD". European Respiratory Journal31 (6): 1221–6. doi:10.1183/09031936.00107507. PMID18287127.
^Natelson, BH; Ye, N; Moul, DE; Jenkins, FJ; Oren, DA; Tapp, WN; Cheng, YC (1994). "High titers of anti-Epstein-Barr virus DNA polymerase are found in patients with severe fatiguing illness". Journal of medical virology42 (1): 42–6. doi:10.1002/jmv.1890420109. PMID8308519.
^ abRichardson, S. J.; Willcox, A.; Bone, A. J.; Foulis, A. K.; Morgan, N. G. (2009). "The prevalence of enteroviral capsid protein vp1 immunostaining in pancreatic islets in human type 1 diabetes". Diabetologia52 (6): 1143–51. doi:10.1007/s00125-009-1276-0. PMID19266182.
^Díaz-Horta, O; Bello, M; Cabrera-Rode, E; Suárez, J; Más, P; García, I; Abalos, I; Jofra, R et al. (2001). "Echovirus 4 and type 1 diabetes mellitus". Autoimmunity34 (4): 275–81. doi:10.3109/08916930109014696. PMID11905853.
^Kawashima, H; Ihara, T; Ioi, H; Oana, S; Sato, S; Kato, N; Takami, T; Kashiwagi, Y et al. (2004). "Enterovirus-related type 1 diabetes mellitus and antibodies to glutamic acid decarboxylase in Japan". Journal of Infection49 (2): 147–51. doi:10.1016/j.jinf.2004.01.012. PMID15236922.
^Laitinen OH, Honkanen H, Pakkanen O, et al. (February 2014). "Coxsackievirus B1 is associated with induction of β-cell autoimmunity that portends type 1 diabetes". Diabetes63 (2): 446–55. doi:10.2337/db13-0619. PMID23974921.
^Kolehmainen P, Koskiniemi M, Oikarinen S, et al. (September 2013). "Human parechovirus and the risk of type 1 diabetes". J. Med. Virol.85 (9): 1619–23. doi:10.1002/jmv.23659. PMID23852688.
^Visser, LH; Van Der Meché, FG; Meulstee, J; Rothbarth, PP; Jacobs, BC; Schmitz, PI; Van Doorn, PA (1996). "Cytomegalovirus infection and Guillain-Barré syndrome: the clinical, electrophysiologic, and prognostic features. Dutch Guillain-Barré Study Group". Neurology47 (3): 668–73. doi:10.1212/WNL.47.3.668. PMID8797462.
^Morken, Mette Helvik; Valeur, JøRgen; Norin, Elisabeth; Midtvedt, Tore; Nysæter, Gunnar; Berstad, Arnold (2009). "Antibiotic or bacterial therapy in post-giardiasis irritable bowel syndrome". Scandinavian Journal of Gastroenterology44 (11): 1296–303. doi:10.3109/00365520903274401. PMID19821794.
^Stensvold, C. R.; Lewis, H. C.; Hammerum, A. M.; Porsbo, L. J.; Nielsen, S. S.; Olsen, K. E. P.; Arendrup, M. C.; Nielsen, H. V.; Mølbak, K. (2009). "Blastocystis: unravelling potential risk factors and clinical significance of a common but neglected parasite". Epidemiology and Infection137 (11): 1655–63. doi:10.1017/S0950268809002672. PMID19393117.
^Lin, Ching-Yih; Su, Shih-Bin; Chang, Chih-Ching; Lee, Tsung-Ming; Shieh, Jiunn-Min; Guo, How-Ran (2009). "The Association Between Chlamydia pneumoniae and Metabolic Syndrome in Taiwanese Adults". Southern Medical Journal102 (12): 1203–8. doi:10.1097/SMJ.0b013e3181c043d9. PMID20016424.
^Sotelo, Julio; Martínez-Palomo, Adolfo; Ordoñez, Graciela; Pineda, Benjamin (2008). "Varicella-zoster virus in cerebrospinal fluid at relapses of multiple sclerosis". Annals of Neurology63 (3): 303–11. doi:10.1002/ana.21316 (inactive 2014-03-25). PMID18306233.
^Munger, Kassandra L.; Peeling, Rosanna W.; Hernán, Miguel A.; Chasan-Taber, Lisa; Olek, Michael J.; Hankinson, Susan E.; Hunter, David; Ascherio, Alberto (2003). "Infection with Chlamydia pneumoniae and Risk of Multiple Sclerosis". Epidemiology14 (2): 141–7. doi:10.1097/01.EDE.0000050699.23957.8E. PMID12606878.
^Arcari, Christine M.; Gaydos, Charlotte A.; Nieto, F. Javier; Krauss, Margot; Nelson, Kenrad E. (2005). "Association between Chlamydia pneumoniae and Acute Myocardial Infarction in Young Men in the United States Military: The Importance of Timing of Exposure Measurement". Clinical Infectious Diseases40 (8): 1123–30. doi:10.1086/428730. PMID15791511.
^Gabrylewicz, Bogna; Mazurek, Urszula; Ochała, Andrzej; Sliupkas-Dyrda, Elektra; Garbocz, Piotr; Pyrlik, Andrzej; Mróz, Iwona; Wilczok, Tadeusz; Tendera, Michał (2003). "Zakażenie wirusem cytomegalii w świeżym zawale serca. Powiązania przyczynowo-skutkowe?" [Cytomegalovirus infection in acute myocardial infarction. Is there a causative relationship?]. Kardiologia Polska (in Polish) 59 (10): 283–92. PMID14618212.
^Andréoletti, Laurent; Ventéo, Lydie; Douche-Aourik, Fatima; Canas, Frédéric; De La Grandmaison, Geoffroy Lorin; Jacques, Jérôme; Moret, Hélène; Jovenin, Nicolas et al. (2007). "Active Coxsackieviral B Infection Is Associated With Disruption of Dystrophin in Endomyocardial Tissue of Patients Who Died Suddenly of Acute Myocardial Infarction". Journal of the American College of Cardiology50 (23): 2207–14. doi:10.1016/j.jacc.2007.07.080. PMID18061067.
^Atkinson, R L; Dhurandhar, N V; Allison, D B; Bowen, R L; Israel, B A; Albu, J B; Augustus, A S (2004). "Human adenovirus-36 is associated with increased body weight and paradoxical reduction of serum lipids". International Journal of Obesity29 (3): 281–6. doi:10.1038/sj.ijo.0802830. PMID15611785.
^Ley, Ruth E.; Turnbaugh, Peter J.; Klein, Samuel; Gordon, Jeffrey I. (2006). "Microbial ecology: Human gut microbes associated with obesity". Nature444 (7122): 1022–3. doi:10.1038/4441022a. PMID17183309.
^ abMell, L. K.; Davis, RL; Owens, D (2005). "Association Between Streptococcal Infection and Obsessive-Compulsive Disorder, Tourette's Syndrome, and Tic Disorder". Pediatrics116 (1): 56–60. doi:10.1542/peds.2004-2058. PMID15995031.
^Takahashi, M; Yamada, T (1999). "Viral etiology for Parkinson's disease--a possible role of influenza A virus infection". Japanese journal of infectious diseases52 (3): 89–98. PMID10507986.
^Miman, Ozlem; Kusbeci, Ozge Yilmaz; Aktepe, Orhan Cem; Cetinkaya, Zafer (2010). "The probable relation between Toxoplasma gondii and Parkinson's disease". Neuroscience Letters475 (3): 129–31. doi:10.1016/j.neulet.2010.03.057. PMID20350582.
^Qayoom, S; Ahmad, QM (2003). "Psoriasis and Helicobacter pylori". Indian journal of dermatology, venereology and leprology69 (2): 133–4. PMID17642857.
^Herndon, BL; Vlach, V; Dew, M; Willsie, SK (2004). "Helicobacter pylori-related immunoglobulins in sarcoidosis". Journal of investigative medicine52 (2): 137–43. doi:10.2310/6650.2004.17876. PMID15068230.
^Lian, W; Luo, W (1995). "Borrelia burgdorferi DNA in biological samples from patients with sarcoidosis using the polymerase chain reaction technique". Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih / Chinese Academy of Medical Sciences10 (2): 93–5. PMID7647327.
^Krause, Daniela; Matz, Judith; Weidinger, Elif; Wagner, Jenny; Wildenauer, Agnes; Obermeier, Michael; Riedel, Michael; Müller, Norbert (2010). "The association of infectious agents and schizophrenia". World Journal of Biological Psychiatry11 (5): 739–43. doi:10.3109/15622971003653246. PMID20602604.
^Rantakallio, P; Jones, P; Moring, J; Von Wendt, L (1997). "Association between central nervous system infections during childhood and adult onset schizophrenia and other psychoses: a 28-year follow-up". International Journal of Epidemiology26 (4): 837–43. doi:10.1093/ije/26.4.837. PMID9279617.
^Brown, Alan S.; Begg, Melissa D.; Gravenstein, Stefan; Schaefer, Catherine A.; Wyatt, Richard J.; Bresnahan, Michaeline; Babulas, Vicki P.; Susser, Ezra S. (2004). "Serologic Evidence of Prenatal Influenza in the Etiology of Schizophrenia". Archives of General Psychiatry61 (8): 774–80. doi:10.1001/archpsyc.61.8.774. PMID15289276.
^Cook, PJ; Honeybourne, D; Lip, GY; Beevers, DG; Wise, R; Davies, P (1998). "Chlamydia pneumoniae antibody titers are significantly associated with acute stroke and transient cerebral ischemia: the West Birmingham Stroke Project". Stroke; a journal of cerebral circulation29 (2): 404–10. doi:10.1161/01.STR.29.2.404. PMID9472881.
^Ponzetto, A; Marchet, A; Pellicano, R; Lovera, N; Chianale, G; Nobili, M; Rizzetto, M; Cerrato, P (2002). "Association of Helicobacter pylori infection with ischemic stroke of non-cardiac origin: the BAT.MA.N. project study". Hepato-gastroenterology49 (45): 631–4. PMID12063957.
^Leonardi, S; Pavone, P; Rotolo, N; La Rosa, M (2005). "Stroke in two children with Mycoplasma pneumoniae infection. A causal or casual relationship?". The Pediatric Infectious Disease Journal24 (9): 843–5. doi:10.1097/01.inf.0000177284.88356.56. PMID16148858.
^Kang, J.-H.; Ho, J.-D.; Chen, Y.-H.; Lin, H.-C. (2009). "Increased Risk of Stroke After a Herpes Zoster Attack: A Population-Based Follow-Up Study". Stroke40 (11): 3443–8. doi:10.1161/STROKEAHA.109.562017. PMID19815828.