Copyright 2009 S.H. Shakman,  Institute Of Science; all rights reserved.


– by Stuart-Hale Shakman PhD (History)


(first drafted circa 1995 as per appendix; revisited 2004, Sept 29 2009, published Dec 4 2009)





        (1) BLACK



        (4) WHITE








Overview of  related works by E.C. Rosenow MD (author of 300+ articles 1902-1958 as per Index Medicus; head of experimental bacteriology at the Mayo Foundation from 1915-1944).


  Dr. Rosenow's studies included multiple sclerosis (MS) as early as 1916, but he paid particular attention to it in his later years, presenting evidence of having established an etiologic relationship with an organism consistently isolated from nasopharynx and infected oral “foci”, i.e., infections in tonsils and in and around teeth, and concluding that MS was due to a non-hemolytic neurotropic streptococcic infection or intoxication emanating from such oral foci.

  In his last 2 published articles, both of which referred to MS and the last also to ALS (amyotrophic lateral sclerosis), Rosenow emphasized the use of intradermal injections of both autogenous streptococcic vaccine and thermal antibody.  These were to be continued over an indefinite period presumably due to the continued presence of foci implicated in his earlier studies, although these last articles did not contain specific reference to these oral foci or the concept of "focal infection".

  Thus, notably absent from Rosenow's last two works (1957-8) was reference to the need to remove these infected (oral) foci.  On the one hand we may speculate that this absence was due not to abandonment of the importance of this principle, but rather so as to not cast a possibly injurious shadow on the independently-favorable results obtained with vaccine alone (particularly in its form as thermal antibody.  However, insofar as Rosenow's definitive animal experiments and a range of additional supporting, reproducible and irrefutable experiments, the combination of removal of foci in conjunction with vaccine and antibody appear to be indicated as the most prudent course of action.

  It would appear that Rosenow may have grown somewhat "battle weary" on the subject of oral focal infection, and perhaps partly in reaction had developed therapeutic methods which were effective even if the offending foci were not removed.  In other words, to use a boxing analogy, even with one hand tied behind his back - his best and early sure-knockout punch (removal of causative oral foci), Rosenow managed to develop a strategy which reportedly could keep the pathogen in check.  Of course, the effectiveness of these therapeutic methods further validate his work identifying the source of the offending organisms as those oral foci from which they have been obtained and made into effective therapeutic substances.

  Of Rosenow's regimen for MS, it is noted that his administration of vaccine twice weekly is in agreement with Florence Sabin's assessment that antibody is produced for about 3 days following injection.  In discussing long-term vaccine-therapy for MS, Dr. Rosenow described a schedule of subcutaneous injections of up to 1 ml of vaccine weekly and up to 2 ml of "thermal streptococcic antibody" twice weekly or daily:    One-half milliliter of the stock or autogenous [multiple sclerosis] thermal streptococcic antibody from 10 billion streptococci per milliliter was injected separately subcutaneously, but at the same time or more often (as vaccine), if favorable results ensued.  This dose was increased to 2 ml. and was given twice weekly or daily, provided local reactions at the point of injection were minimal or negative and provided clinical results were favorable. … Since such injections were harmless and had to be repeated over long periods, some member of the family or a nurse was instructed to give the injections." 




  Wholly independent of Rosenow and the general "cause of MS" literature, the indirect link between oral infections and MS seems firmly established, via optic neuritis; i.e., oral foci, or dental infections, are known to cause optic neuritis; and optic neuritis is a precursor to MS.




        (1) BLACK


  Black, 1913, summarized and listed some 41 articles from the early dental literature, from 1839 to 1912, which had discussed the apparent causal relation between diseases of the teeth and diseases of the eye.  Black refers to various eye and ear ailments, including optic neuritis and even loss of sight, which were cured by dental treatment.  (See 13T1-13T41)  Two of these were cited by Black as relating to the subject of optic neuritis, McConachie 1903 and Allport 1904.  [see FOCAL INFECTION CHRON FILE, McConachie 1903, Allport 1904, Black 1913.




  A number of recent articles accessed through MEDLINE clearly support this correlation between dental infection and optic neuritis.  For example:   Bocca etal (1989) discussed possible interactions between ophthalmic and dental pathologies.  Ilewicz etal. (1990) demonstrated relations between oral foci and diseases of the eye (intraocular and retrobulbar optic neuritis, iritis, retinitis and keratitis) with positive electrocutaneous pulp viability test results in 31 of 43 patients.  Chaabouni etal. (1991) reported improvement in 3 of 4 optic neuritis patients with treatment of acute dental infection first and, secondly, association of corticosteroids.  Philippe, etal., (1993) discussed the case of 23-year-old woman with unilateral acute edematous optic neuritis which recovered on removal of a nasolabial cyst of probable dental origin.




The prominent editor (N. R. Miller) of the authoritative contemporary ophthalmology text (Walsh and Hoyt, 1982, p. 238-241), on the one hand recognizes the established connection between optic neuritis and multiple sclerosis: "... optic neuritis may occur at any time during the course of well-documented multiple sclerosis .... in many instances the conclusion that a syndrome of progressive optic neuropathy does exist in patients with multiple sclerosis seems inescapable."  Miller refers to a number of "disorders that have been associated with an anterior optic neuritis", including herpes zoster, ulcerative colitis, peptic ulcer disease, post-infectious encephalomyelitis, measles, rubella, chicken pox, influenza, lymphatic meningitis, poliomyelitis, coxsackie virus infection, psittacosis and infectious mononucleosis; and disorders which have been associated with retrobulbar optic neuropathy, including syphilis, diphtheria, scarlet fever, encephalomyelitis, petrussis, mumps, measles, and infectious mononucleosis.  Miller also notes that "Both anterior and retrobulbar forms of optic neuritis have been reported after various vaccinations", including anti-rabies, smallpox, combined smallpox, tetanus and diphtheria, combined measles, mumps and rubella, bivalent influenza and swine influenza.

  However, Miller dismisses the concept of a relation between oral focal infection and optic neuritis, referring erroneously to Leon E. White's 1928 article as having disproved it:  "Early approaches to the treatment of optic neuritis concentrated on a search for a focus of infection, particularly with respect to the paranasal sinuses, tonsils and teeth.  White (1928) examined a group of patients with optic neuritis who had had a variety of operative procedures directed at these organisms and found that their prognosis was identical with that of patients with untreated optic neuritis." [Miller, 1982, p. 243]  Mr. Miller has obviously not read White (1928), nor Black (1913), nor other relevant materials.


        (4) WHITE


  Whereas, the White article ("Location of Focus in Optic Nerve Disturbances", 1928) was actually an enthusiastic endorsement of Rosenow's work as concerns the relation between eye diseases and non‑vital teeth and infected tonsils, and was critical only of an irresponsible fad of needless sinus operations, which fad seems to have preceded and been independent of the "oral sepsis/focal infection/elective localization progression.  Talk about sloppy research, here's the authoritative book in the field of ophthalmology, and it's just plain giving out 100% 180-degree WRONG information.  Lord help us all.




  As mentioned above, while Miller somehow denies the oral/optic connection (perhaps not wanting to be rendered obsolete by a dentist), he does acknowledge optic neuritis as a precursor of MS.  Unquestionable acceptance of this relationship continues to the present time.  For example, Beck, RW etal, in the New England Journal of Medicine, Dec. 9, 1993, reported that optic neuritis patients treated with steroids were found to have lowered rates for developing M.S. within two years; however it was noted that the effects of steroid shots eventually wears off. [as reported in Science News 144, Dec. 11, 1993, wherein is stated "optic neuritis, a symptom associated with M.S.]

  Mapelli, etal, 1991, p. 117-121, in an article entitled "Progression of Optic Neuritis to Multiple Sclerosis: A prospective study in an Italian population", reported development of MS in 10 of 40 optic neuritis patients followed for 12 years.  Seven of these ten developed MS within 2 years.  The authors summarize reported the risk of ON leading to MS as found in other studies to vary greatly, from 11.5 to 85% in U.S. and European studies, and from 8.3 to 27% in Japanese studies.

  Slamowits and Macklin, 1991, p. 47, refer to "increasing evidence that optic neuritis and multiple sclerosis have a higher degree of association (perhaps 80%) than previously thought (as low as 11%)."

  Frenkel etal, 1991, p. 49, refer to Risso and Lessell's 1988 [Neurology 38:185-190] retrospective covering 15 years following diagnosis of optic neuritis, wherein 74% of females (average 7.2 years) and 34% males (average 10.4 years) developed multiple sclerosis.

  Adams 1989, p. 105, "The optic pathway is involved in most MS patients, estimated by Lumsden (1970) at 93 percent of cases and by Ulrich and Groebke-Lorenz (1983) at 100 percent of cases.  Surprisingly only 44 percent of patients in the latter study had had clinical optic neuritis."

  Mims 1983 [Mims, Cedric, New Scientist, 30 June 1983, 938-40, "Multiple Sclerosis, the case against viruses."]   p. 938, on Multiple Sclerosis: "It often begins with misty vision or other eye trouble (optic neuritis) to be followed later by weakness in the limbs, numbness or tingling ..."

  A 1994 Johnson & Johnson Vision Products advertisement features a mock eye-chart illustration, with "MS" on the top line in large letters, "DIABETES" on the next line in slightly smaller letters, then "GLAUCOMA" on next line in next size, then "CATARACTS", and finally on the bottom line in the smallest letters "HIGH BLOOD PRESSURE".  The text states "By examining your eyes, your eye doctor may detect the early onset of diseases like diabetes, high blood pressure, and multiple sclerosis."  The connection between optic neuritis and multiple sclerosis would appear to be generally accepted.

  Hence the question must be asked and emphasized:





  Let's try it again:  If A causes B, and B causes C, then it would appear that A causes C.  Call it math (the "old" math) or call it logic, the fact is that oral focal infection must be recognized as an etiological factor in multiple sclerosis.


  So what's new?  Rosenow told us that in 1916.




For your reading enjoyment, following are excerpts, etc. from various discussions of MS in the medical literature through 1995, with emphasis on the suspected role of infection, and with occasional side-comments.



  Sept. 1995: Waksman, BH, Nature 377, Sept 1995, 105-6, More genes versus environment"


  Waksman notes that Ebers, GC, etal, Nature 377, Sept. 14, 1995, 1550-151, seek to counter Kurtzke [JF, Clin. Microbiol. Rev. 6, 382-427 (1993)] "and those sharing his view that existing epidemiological data point to a specific infectious (presumably viral) agent as a direct cause of MS.  No such agent has ever been successfully linked to MS ..., either by direct isolation or by indirect (for example, serological) means, despite claims for some twenty different viruses. ...

  "The situation in MS is reminiscent of that in poliomyelitis ... The incidence of neurological disease increases in individuals of higher socioeconomic status within a population (because this tends to be associated with viral transmission delayed to late childhood or early adolescence) and in populations living at temperate latitudes ... .  A similar requirement in MS for late viral transmission has been demonstrated in a well controlled, population-based study that showed an almost tenfold increase in the risk of contracting Ms as the age (up to puberty) of infection with common childhood viruses (such as measles) increased."

[Byron Waksman, Dept. of Pathology, NYU, 300 East           54th St., New York, Ny 10022, USA.



  Steinman, L., Nature 375, 29 June 1995, 739-40, "Multiple Sclerosis - Presenting an odd autoantigen": p. 739 "The identification of key antigens in human autoimmune diseases is a crucial step towards the development of specific intervention."  p. 801: "MS lesions may develop if pro-inflammatory factors - including the autoantigen itself - accumulate locally beyond a threshold of control as a result of stress-producing events such as local immune responses to viral antigens."  [van Noort JM, etal, Nature 375, 29 June 1995, 739; 798-801, "The small heat-shock protein aB-crystallin as candidate autoantigen in multiple sclerosis"]



  1995:  Burt RK, W Burns, A Hess, Bone Marrow Transplantation 16 (1995), 1-5, "Bone marrow transplantation for multiple sclerosis", note that "Total lymphoid irradiation (TLI) has been used to treat several presumed autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus, chronic inflammatory demylinating polyneuropathy and MS.  In each of these cases, TLI is palliative, not curative, presumably due to incomplete ablation of the immune system."

  [We note that these same conditions were addressed by Rosenow and by autohemotherapy]

  For MS patients with a poor prognosis, the authors propose an aggressive course of action "such as complete immune ablation and hemapoietic stem cell rescue."  This "is designed to ablate an aberrant immune system and then .. reconstitute a new immune system." (p. 2)

  The authors note that

  --  in animal models "it is of interest that unmanipulated autologous marrow is as effective in maintaining remission as allogeneic or syngenic hematopoietic stem cell support." (p. 2)

  --  "Although infrequently reported, patients with a coincidental autoimmune disease who undergo BMT for other reasons have durable remissions of their autoimmune disorder.  For instance, patients with psoriasis or ulcerative colitis have maintained long-term clinical remissions arfter allogeneic BMT for leukemia." (p.3)

  --  "... the mechanism by which marrow transplantation could induce a durable remission in patients with a regenerating immune system is unclear."  Some possible explanations are offered, including considerations which would give a preferential advantage to autologous BMT.

  --  the mortality of autologous BMT for breast cancer or solid tumors of 3-5% or less, and for T-cell-depleted allogeneic BMT of less than 20%.

  --  "Animal studies from three separate institutions suggest that BMT may be beneficial."



  October 1994:  Some 8 decades after Dr. Rosenow's initial studies of this condition, it was estimated that more than a quarter million Americans have MS.  About half of these cases were of a "relapsing, remitting" type, progression of which had reportedly been halted in 80% of patients given interferon, vs 65% of patients given a placebo. [Los Angeles Times 11 Oct 94, p. A22.]

  Unfortunately this leaves the remainder, 20% of group A and 35% of group B, still falling deeper into the devastating grasp of this insidious, chronic disease.  And 100% of both groups which might be able to abort the cause of the syndrome altogether through the elimination of the causative foci, in most cases probably diseased or non-vital teeth (as seemingly conclusively demonstrated by Rosenow); or at a minimum to control its progression through subcutaneous injections of autologous "antigen" and "antibody, ideally in combination with removal of oral foci of infection.



  Waksman 1989 [Byron H. Waksman, Nature 337 (16 Feb. 1989), "Multiple Sclerosis, Relation to a Retrovirus?"] discusses the "pathogenesis of the characteristic inflammatory destructive lesions of MS, rheumatoid arthritis, insulin-dependent diabetes, chronic thyroiditis, and other similar diseases [which] is explained by many as an immunological reaction to tissue antigen triggered by viral infection (measles, rubella, Epstein-Barr virus) in early life in genetically predisposed individuals."

  p. 104, "The evidence that MS in susceptible individuals is initiated by viral infection, at least in some cases, is increasingly persuasive.  For the epidemic in the Faeroe Islands that followed the arrival of British troops in 1940, it seems that approximately two years of exposure to the putative infectious agent was necessary and that the period from infection to onset of clinical disease was about 6 years (J. Kurtzke).  Susceptibility was low before puberty. ... [MS elsewhere may be] associated with infections (measles, mumps, rubella, Epstein-Barr virus) caught   significantly later in age than in HLA-matched controls (A Compston, O. Anderson)", from 2-5 weeks after infection the exacerbation rate was increased more than three-fold.

  p. 105, Waksman, "Hypothetical sequence of pathogenic events in MS" lists as first in the "acute phase", systemic virus infection (measles, variacella, influenza), and in the middle of the "chronic phase", "systemic virus infection - reactivation of process."

  Waksman relates that "more than 20 viruses have been incriminated as the possible cause of multiple sclerosis since 1946. ... Yet none of these candidates has stood the test of time." [see also AIDS/MS, KILLING COUSINS]



  Confavreux C etal, "Association of amyotrophic lateral sclerosis and multiple sclerosis", Revue Neurologique, 1993, 149(5):351-3, discussed a case first diagnosed as multiple sclerosis, which after a 10 year asymptomatic period, exhibited symptoms of amyotrophic lateral sclerosis.  "Muscle weakness and atrophy increased in the limbs and the bulbar territority and the patient died nine months later.  The autopsy showed characteristic 'old' plaques of multiple sclerosis in the cerebrum with anterior horn cell and pyramidal tracts degeneration, typical of amyotrophic lateral sclerosis, in the spinal cord.  Although exceptional, this association of amyotrophic lateral sclerosis and multiple sclerosis leads to the discussion of an etiological immunological dysregulation common to these two diseases." [MEDLINE]

  To the extent that Dr. Rosenow referred to ALS, he had grouped it with MS due to similar results with strains from these diseases.



  Scolding (1989), 620-2, "... complement has ... been implicated in the pathogenesis both of multiple sclerosis and experimental allergic encephalomyelitis."  Of course this would also suggest that such blood fluids might be commandeered into an autogenous vaccine in the form of autohemotherapy.



  Scott 1985, p. 199, "Good evidence suggests that MS is at least triggered by some sort of infection, and the viruses are the favoured candidates.

[Scott, Andrew, Pirates of the Cell, The Story of Viruses from Molecule to Microbe, Basil Blackwell Ltd., Oxford 1985]


  Johnson 1985 [Johnson RT in Koetsier; Vinken, PJ, etal., Handbook of Clinical Neurology, North Holland, 1985]


  "(1) epidemiological data have indicated that MS is related primarily to environmental exposure in childhood followed by a long latency period."

  (2) Studies in "other demyelinating diseases have documented multiple mechanisms by which viruses can have long incubation periods...

  (3) "studies in patients with MS have consistently shown abnormal immune responses, particularly to viral antigens."

  p. 320, discusses the role of experimental encephalitis as "the prototype autoimmune disease" and "since the 1950s it has been studied as an experimental model of MS" [apparently due to the general (except Rosenow) failure to infect animals with MS] and discuss demyelinating acute encephalitis which occasionally follows measles and vaccina virus infections.

  "Between 1967 and 1971, four chronic neurological diseases proved to have viral etiologies.  The transmission of Kuru and Creutzfeldt-Jakob disease and the recovery of viruses from subacute sclerosing parencephalitis and progressive multi-focal leukoencephalopathy led to widespread speculation that MS would soon be transmitted or prove to have consistent viral recovery (Johnson 1975)

  p. 320-1, Johnson discusses "uneven geographical distribution of MS, with a decided north-south difference in prevalence.  p. 321,  For example, per 100,000, there is an incidence of 30-80 cases in Northern Europe and Northern U.S., vs. 6-20 in Southern Europe and Southern U.S., vs. 1.0 in equatorial areas.  These differences are not quite so well-defined in the southern hemisphere.  There is a higher prevalence for women than for men, and for whites over blacks.

  Studies in South Africa and Israel indicate that persons migrating after age 15 carry the risk of birth place, whereas before that age they adopt the risk of their new home.

  "Virtually all studies support the relation to an early childhood exposure occurring betwen the ages of 10 and 15, or the necessity of repeated exposures during childhood up to the age of puberty.  This is followed by a latency period of a number of years before the onset of clinical disease." [sounds just like the description of AIDS prior to learning the latent period is not latent; all signs point to Rosenow and oral foci].

  p. 322, Johnson discusses apparent epidemics of MS in the Faeroes between 1943 and 1960, following the British occupation of 1940; and in Iceland a sudden rise in 1923 and again after 1944, following World War I occupation by Canadian Americans and British.

  "These findings of apparent epidemics suggest that MS is not only related to a childhood exposure but is transmissible. ... The age of acquisition of an infection may influence the clinical manifestations.... Parallels between the epidemiology of MS and poliomyelitis have been made". [Pozkanzer etal, 1963]   [We are often reminded that Dr. Rosenow's work involved a phases of related microorganisms in the causation of both of these neurological diseases.]

  "In 3 case-controlled series the patients with MS were found to have a history of measles at a later age (Sullivan etal 1984).  This is a particularly intriguing finding, since the established late complication of measles virus infection - subacute sclerosing panencephalitis - is associated with infection under 2 years of age."

  p. 326, "One of the circumstantial arguments for the viral etiology of MS is based on guilt by association, since several other human demyelinating diseases have established viral etiologies", including postinfectious encephalomyelitis, subacute sclerosing panencephalitis, and progressive multifocal leukoencephalopathy.

  p. 329, Immunological studies - more than 30 studies since 1962 have shown MS patients in contrast to controls to have higher levels of serum antibodies against measles, as well as parainfluenza 3, influenza C, variacella, herpes simplex, rubella and Epstein-Barr viruses.  Johnson cites other studies, including one in which "intrathecal antibody synthesis occurred to as many as eleven different agents in the same patients (Salmi etal 1983).  These findings might suggest that multiple viruses can cause MS ...."

  329,  Johnson also points out, in seeming accordance with Rosenow, that "It is important to note that the finding of higher serum antibody titers to measles is not specific to MS.  Similar findings have been reported in lupus erythematosus, Reithe's syndrome, and chronic liver disease."

  p. 330, "there are many claims of the transmission of MS to primates and smaller animals, but none either recovered a characterizable virus or could be confirmed by other laboratories (Innes and Kurland 1952).

  "The isolation of parainfluenza type I virus from tissue culture derived from two patients dying of MSS has been pursued extensively and unsuccessfully."


  Newmark, Peter, 1985,

  "Even if a virus can be proved to be implicated in MS, it is likely to be merely the initiator of a chain of immunological events leading to demyelination of nerve fibres rather than a direct cause.  It seems probable that the initial viral infection somehow triggers an autoimmune reaction against components of the myelin sheath of nerves."

  However, Newmark indicates that it is not yet "clear how the disease progresses from the triggering event."



  Thoden van Velzen, 1984, notes that Sznieielski 1979 [Sznieielski, S. etal, Toxicon 17, 363-371, 1979] showed that bacterial toxins might preferentially injure the myelin sheath thus interfering with nerve function.



  Störtbecker 1967, p. 301, specifically referred to the potential significance of bacterial products emanating from dental foci of infection in the pathogenesis of multiple sclerosis.

  Johnson in Koetsier, Vol. 3, p. 329, "In 1962, Adams and Imagawa reported that complement-fixing and neutralizing antibody titers against measles virus were higher in patients with MS than in a control group [75% in MS patients vs. 00% in controls] ...findings have been confirmed in over 30 subsequent studies.  Other studies also have found higher levels of serum antibodies against parainfluenza, influenza C, varicella, herpes simplex, rubella, and EBV. ... These findings might suggest that multiple viruses can cause MS ..."



  Mims 1983 [Mims, Cedric, New Scientist, 30 June 1983, 938-40, "Multiple Sclerosis, the case against viruses."] p. 940:  "It looks mery much as if MS is a virus-induced auto-immune disease of the nervous system."  Mims discusses four possible ways "in which such cross-reacting immune responses could be so generated".  [Certainly three, and probably all four, are wrong, worthless, useless, fictional, imaginary.]

  The discovery of two other 'slow' virus diseases in the 1960s, subacute sclerosing panencephalitis and progressive multifocal leucoencephalopathy were found to be caused by the measles virus and a polymavirus respectively, plus evidence that MS is caused by childhood infection, "were an immense stimulus to M.S. research."

  p. 939, "Between the mid-1960s and 1980 scientists recovered no fewer than 9 different viruses or virus-like agents, including herpes simplex, parainfluenza virus I, measles, and coronavirus from MS brains.  Unfortunately none of this work has proved to be repeatable. ... A guilty virus would offer the prospect of a vaccine to prevent the disease."

  Subsequently, Almo Salmi and colleagues in Finland "charted antibody responses to 16 common viruses in the serum and CSF of MS patients, and concluded that a given patient might synthesize antibodies to as many as eleven different viruses in his brain.  In addition some patients synthesized antibodies to other common microbial antigens such as mycoplasma pneumoniae or diptheria and tetanus toxoids. ...

  "The most likely explanation of these antibody observations is that early in the disease ... antibody producing cells circulating in the blood very occasionally enter areas of the brain" through a presumably temporary breakdown in the blood-brain barrier.  Free from the immune control presumably normally exerted on them in the blood, this according to Mims, "the antibody forming cells synthesize whatever antibody they are programmed to synthesize", e.g. those associated with childhood disease.... antibody producing cells are also present in the inflamed brains of patients suffering from mumps or measles encephalitis, but nearly all of them, which arrived from the blood, are producing antibody in response to the presence of the infecting virus.  In contrast, the antibodies in MS patients appear to be formed as an accidental result of the disease process, and not because the viruses are actually present in the brain."

  [Thank the good lord that antibodies are " formed as an accidental result of the disease process" or we'd all be long gone.]

  p. 938, DISEASE WAITING FOR INFECTION, OR WHAT?  Mims speculates, "The cause of MS may not be a mystery much longer.  Although there is probably no specific MS virus, MS may well result when antibodies to other viruses enter the brain."


  Innes 1952,

 p. 574, cites  "several diseases of established micro-organismal origin" which also fail to show symptoms generally typical of bacterial or viral diseases through much of their course, e.g. lues, leprosy and certain phases of tuberculosis and brucellosis.

  p. 575, Incidence:  "3 to 4 times as many cases were found in selected cities of Canada and northern U.S. as in comparable cities of the southern U.S."

  p. 575 That MS may occur more frequently among members of the same family than expected by chance "might indicate some genetic predisposition rather than interfamilial infection..."

 p. 577, discussing negative results of attempts to experimentally transmit MS, cites efforts by Rothfield, Freund and Hornowski (1920) who injected blood and CSF from four cases of MS in rabbits and guinea pigs:  "Many died, but the cause of death was diagnosed to be either coccoidiosis or tuberculosis..."; Teage (1921) as reported by Cornwall (1936), likewise observed coccoidiosis in rabbits and pneumonia in guinea pigs after injections of blood and CSF from MS patients.

  p. 579, In discussing positive results, Behr 1924 reported successful transmission in rabbits with washings from the ethmoids, on the assumption that retrobulbar neuritis, a frequent finding in MS, might be due to an infectious pathway through the nasal passages and ethmoids.

  p. 588, concludes that "... the virus hypothesis is still neither proved nor disproved ...; even if a virus were found, it might not evoke in animals a disease exactly like MS."


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