Dear Editor, In 2002 Hawkes realized that epidemiologically multiple sclerosis (MS) behaves like an STD [1]. Although the epidemiological similarity between the two diseases is true, this thesis was not discussed extensively, perhaps because it implied that some children might have been victims of abuse, which sounds false and potentially unfair. We believe that transverse myelitis and MS are the result of an infectious disease, eventually sexually transmitted by chlamydia/gonococcus, which is caused by a subclinical bacterial urethritis/inflamatory pelvic disease (IPD) among adults. In children it is the same disease but caused by common uropathogens/enterobacteria. Both UTI and MS are much more common in girls than in boys [2, 3]. These UTIs would favor herpetic proliferation via toll-like receptors (TLRs), since the virus is endemic and always present, and it is not possible to eradicate it completely [4, 5, 6]. Herpes viral load is counteracted by interferon alpha 1 (IFN alpha-1), present in different cell types, from macrophages to lymphocytes passing through endothelia and fibroblasts. Interferon alpha 1, when interacting with its specific receptors, produces in the intracellular the action of antiviral RNAse and the inhibition of viral protein synthesis [7, 8]. TLR2/4 when stimulated by lipopolysaccharides (LPS) from bacteria reduce the production of IFN alpha increasing the viral load [9, 10, 11]. Viral proliferation can be stimulated via LPS, ie, pathogen-associated molecular protein (PAMP), which by stimulating inflammation, by interacting with TLR2/4, would reduce IFN-alpha1 and, consequently, increase viral load. On the other hand, the stimulation of these same receptors by fibronectin or hyaluronic acid, tissue “chunks”, damage associated protein (DAMP), would increase the biosynthesis of IFNalpha1 reducing the viral load [12, 13]. Herpes proliferation would favor the exteriorization of MHC type 2 complexes [14, 15, 16], which characterizes transverse myelitis and MS, favoring the chemotaxis of Th17 and Th1 CD4s. Intestinal parasites and dysbiosis - transmissible by water - produce chronic elevations of Th17 CD4 [17], which by itself reduce the blood-brain barrier [18]. Urine infections in childhood are caused by enterobacteria, [19] which are epidemiologically important agents, as they cause diarrhea [20] that occur anywhere in the world, although more frequent in the third world [21]. Transmissible through water, enterobacter are the main responsible for infant mortality in poor regions and among the elderly they determine longevity [22, 23, 24], are more prevalent than imagined and both positively affect rheumatoid factors (25, 26) and produce reactive arthritis [27, 28]; when asked if there would be a cause/effect relationship between dysbiosis and rheumatic diseases, it is heard: “cross reaction” [29]. The choice of assigning an obscure origin to autoimmune diseases is to opt for the uncertain, since the positivity of the test is attributed to an obscure origin, to the detriment of what the test actually measured and in what clinical conditions the test is positive. I ask: It would not be possible for enterobacteria, according to the magnitude of the intestinal dysbiosis that they produce, to increase the levels of Th17 and that - in the same individual - there is a subclinical urethritis/itu/IPD, whose magnitude would favor the inhibition of IFNalpha1 and consequently would favor the proliferation of herpes in the tissues previously affected? Could this unfortunate encounter be the cause of MS and transverse myelitis? Bacterial urethritis is often asymptomatic, elevating the same interleukins that MS, IL-8 and IL-18 [30, 31, 32, 33], in addition to Th17 and Th1 [34, 35]. Outpatient treatment of a possible post coital cystitis, for example, would not eradicate bacterial vaginosis or chlamydia, making them potentially resistant, perpetuating the IPD/UTI insidiously [36, 37]. The pathophysiology of transverse myelitis in MS could be explained as a result of neurodegeneration dependent on lymphocyte infiltration of Th17 and Th1, which when interacting with local type II MHC [38, 39, 40] would release IL-17A causing IL-6 and TNF alpha release with subsequent neurodegeneration, of course inflammatory and demyelinating [40]. The thesis proposed by Haewek explains absolutely all aspects of the disease, covering epidemiological, biochemical and clinical aspects such as the topography of the lesions, specifically lymphocytic infiltration, in MS. If this text is correct, the neurodegeneration of MS could be stopped through dewormers, antibiotics, beta glucan, probiotics and by far the most difficult: to avoid reinfection, since the health factors linked to intestinal dysbiosis persist, after all, they are linked to socio-economic aspects, which are difficult to change. After resolution of urethritis/cystitis/pyelonephritis/DIPA garlic capsules, perhaps via organo sulfur molecules, would favor the release of IFN-alpha1 and IFN-gamma [41, 42, 43]. The patients with increased levels of antinuclear autoantibodies would be infected with vaginosis bacterial, and receive diagnosis of lupus [44].