Koch's postulates have been modified by some epidemiologists, based on the sequence-based detection of distinctive pathogenic nucleic acid sequences in tissue samples. When using this method, absolute statements regarding causation are not always possible. Higher amounts of distinctive pathogenic nucleic acid sequences should be in those exhibiting disease, compared to controls. In addition, the DNA load should become lower with the resolution of the disease. The distinctive pathogenic nucleic acid sequences load should also increase upon recurrence.
Other conditions are met to establish cause or association including studies in disease transmission. This means that there should be a high disease occurrence in those carrying a pathogen, evidence of a serological response to the pathogen, and the success of vaccination prevention. Direct visualization of the pathogen, the identification of different strains, immunological responses in the host, how the infection is spread and, the combination of these should all be taken into account to determine the probability that an infectious agent is the cause of the disease. A conclusive determination of a causal role of an infectious agent for in a particular disease using Koch's postulates is desired yet this might not be possible.[1]
The leading cause of death worldwide is cardiovascular disease, but infectious diseases are the second leading cause of death worldwide and the leading cause of death in infants and children.[2]
Other causes
Other causes or associations of disease are: a compromised immune system, environmental toxins, radiation exposure, diet and other lifestyle choices, stress, and genetics. Diseases may also be multifactorial, requiring multiple factors to induce disease. 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.[3]
List of diseases associated with infectious bacteria and viruses
A list of the more common and well-known diseases associated with infectious pathogens is provided and is not intended to be a complete listing.
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).[40] Crohn's disease is associated with Mycobacterium avium subspecies paratuberculosis.[41] In a murine model, Crohn's disease is precipitated by the norovirus CR6 strain,[3][42] 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.
Depression is associated with cytomegalovirus[45] and West Nile virus,[46] and the protozoan parasite Toxoplasma gondii.[47] It is thought that depression may be precipitated by the effect of immune signals (such as pro-inflammatory cytokines) reaching the brain from infections located in the peripheries of the body.[48][49]
Diabetes mellitus type 1 is associated with viral species from the enterovirus genus,[53][54] specifically echovirus 4[55] 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).[56][57] 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).[58] In boys, human parechovirus infection has been linked to a subsequent appearance of diabetes-associated autoantibodies.[59]
Obesity is associated with adenovirus 36, which is found in 30% of obese people, but only in 11% of non-obese people.[89][90] It has further been demonstrated that animals experimentally infected with adenovirus 36 (or adenovirus 5, or adenovirus 37) will develop increased obesity.[91] 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.[92] 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.[93][94]
Obesity is also associated with higher gut levels of certain Bacillota bacteria in relation to Bacteroidota bacteria. Overweight individuals tend have more Bacillota bacteria (such as Clostridium, Staphylococcus, Streptococcus, and Helicobacter pylori) in their gut, whereas normal weight individuals tend have more Bacteroidota bacteria.[95]
Schizophrenia is associated with bornavirus,[50] the bacterium Chlamydia trachomatis,[102] as well as Borrelia species bacteria.[44] Schizophrenia is also linked to neonatal infection with Coxsackie B virus (an enterovirus), which one study found carries an increased risk of adult onset schizophrenia.[103] Prenatal exposure to influenza virus in the first trimester of pregnancy increases the risk of schizophrenia by 7-fold.[104]
Infectious pathogen-associated diseases include many of the most common and costly chronic illnesses. The treatment of chronic diseases accounts for 75% of all US healthcare costs (amounting to $1.7 trillion in 2009).[115]
History
One of first examples of systematic study of disease causation was Avicenna, in the tenth century. The history of infection and disease were observed in the 1800s and related to the one of the tick-borne diseases, Rocky Mountain spotted fever. The cause of viral encephalitis was discovered in Russia based upon epidemiological clustering of cases. The virus causing this illness was isolated in 1937. The rash typical of Lyme borreliosis was identified the early 1900s.[1] Historically, some chronic diseases were linked or associated with infectious pathogens.[116][117][118]
^Barbanti-Brodano, Giuseppe; Sabbioni, Silvia; Martini, Fernanda; Negrini, Massimo; Corallini, Alfredo; Tognon, Mauro (2006). "BK Virus, JC Virus and Simian Virus 40 Infection in Humans, and Association with Human Tumors". Polyomaviruses and Human Diseases. Advances in Experimental Medicine and Biology. Vol. 577. pp. 319–41. doi:10.1007/0-387-32957-9_23. ISBN978-0-387-29233-5. PMID16626046.
^Lawson, James S; Günzburg, Walter H; Whitaker, Noel J (2006). "Viruses and human breast cancer". Future Microbiology. 1 (1): 33–51. doi:10.2217/17460913.1.1.33. PMID17661684.
^Chia, J K S; Chia, A Y (2007). "Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach". Journal of Clinical Pathology. 61 (1): 1–2. doi:10.1136/jcp.2007.050054. PMID17873115. S2CID15705222.
^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 Pathology. 63 (2): 165–8. doi:10.1136/jcp.2009.070466. PMID19828908. S2CID30686099.
^Chia, John K. S.; Chia, Laura Y. (1999). "Chronic Chlamydia pneumoniae Infection: A Treatable Cause of Chronic Fatigue Syndrome". Clinical Infectious Diseases. 29 (2): 452–3. doi:10.1086/520239. PMID10476765. S2CID31939562.
^ abcdeFallon, BA; Nields, JA (1994). "Lyme disease: a neuropsychiatric illness". The American Journal of Psychiatry. 151 (11): 1571–83. doi:10.1176/ajp.151.11.1571. PMID7943444.
^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 Virology. 42 (1): 42–6. doi:10.1002/jmv.1890420109. PMID8308519. S2CID29428623.
^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. S2CID25206855.
^Caini, Saverio; Gandini, Sara; Dudas, Maria; Bremer, Viviane; Severi, Ettore; Gherasim, Alin (2014). "Sexually transmitted infections and prostate cancer risk: A systematic review and meta-analysis". Cancer Epidemiology. 38 (4): 329–338. doi:10.1016/j.canep.2014.06.002. ISSN1877-7821. PMID24986642.
^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". Neurology. 47 (3): 668–73. doi:10.1212/WNL.47.3.668. PMID8797462. S2CID71592645.
^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 Journal. 102 (12): 1203–8. doi:10.1097/SMJ.0b013e3181c043d9. PMID20016424. S2CID6078949.
^Haahr, Sven; Höllsberg, Per (2006). "Multiple sclerosis is linked to Epstein-Barr virus infection". Reviews in Medical Virology. 16 (5): 297–310. doi:10.1002/rmv.503. PMID16927411. S2CID30832378.
^Sotelo, Julio; Martínez-Palomo, Adolfo; Ordoñez, Graciela; Pineda, Benjamin (2008). "Varicella-zoster virus in cerebrospinal fluid at relapses of multiple sclerosis". Annals of Neurology. 63 (3): 303–11. doi:10.1002/ana.21316. PMID18306233. S2CID36489072.
^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". Epidemiology. 14 (2): 141–7. doi:10.1097/01.EDE.0000050699.23957.8E. PMID12606878. S2CID29730230.
^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 Diseases. 40 (8): 1123–30. doi:10.1086/428730. PMID15791511. S2CID11713973.
^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 Cardiology. 50 (23): 2207–14. doi:10.1016/j.jacc.2007.07.080. PMID18061067.
^Miman, Ozlem; Kusbeci, Ozge Yilmaz; Aktepe, Orhan Cem; Cetinkaya, Zafer (2010). "The probable relation between Toxoplasma gondii and Parkinson's disease". Neuroscience Letters. 475 (3): 129–31. doi:10.1016/j.neulet.2010.03.057. PMID20350582. S2CID5141917.
^Qayoom, S; Ahmad, QM (2003). "Psoriasis and Helicobacter pylori". Indian Journal of Dermatology, Venereology and Leprology. 69 (2): 133–4. PMID17642857.
^Herndon, BL; Vlach, V; Dew, M; Willsie, SK (2004). "Helicobacter pylori-related immunoglobulins in sarcoidosis". Journal of Investigative Medicine. 52 (2): 137–43. doi:10.1136/jim-52-02-23. PMID15068230. S2CID206994992.
^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 Psychiatry. 11 (5): 739–43. doi:10.3109/15622971003653246. PMID20602604. S2CID37312321.
^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 Epidemiology. 26 (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 Psychiatry. 61 (8): 774–80. doi:10.1001/archpsyc.61.8.774. PMID15289276.
^Cleary, J; Pearson, M; Oliver, J; Chapman, S (2008). "Association Between Histoplasma Exposure and Stroke". Journal of Stroke and Cerebrovascular Diseases. 17 (5): 312–9. doi:10.1016/j.jstrokecerebrovasdis.2008.01.015. PMID18755412.
^Institute of Medicine (US) Forum on Microbial Threats (1 July 2004). "PREFACE". In Knobler, Stacey L; O'Connor, Siobhán; Lemon, Stanley M; Najafi, Marjan (eds.). The Infectious Etiology of Chronic Diseases: Defining the Relationship, Enhancing the Research, and Mitigating the Effects: Workshop Summary. National Academies Press. pp. xi–xii. ISBN978-0-309-08994-4.
^Institute of Medicine (US) Forum on Microbial Threats (1 July 2004). "SUMMARY AND ASSESSMENT". In Knobler, Stacey L; O'Connor, Siobhán; Lemon, Stanley M; Najafi, Marjan (eds.). The Infectious Etiology of Chronic Diseases: Defining the Relationship, Enhancing the Research, and Mitigating the Effects: Workshop Summary. National Academies Press. p. 2. ISBN978-0-309-08994-4.
^Institute of Medicine (US) Forum on Microbial Threats (1 July 2004). "OVERVIEW". In Knobler, Stacey L; O'Connor, Siobhán; Lemon, Stanley M; Najafi, Marjan (eds.). The Infectious Etiology of Chronic Diseases: Defining the Relationship, Enhancing the Research, and Mitigating the Effects: Workshop Summary. National Academies Press. pp. 13–14. ISBN978-0-309-08994-4.