Autism: A Stealth Disease

                   -Lawrence Broxmeyer M.D.

Lawrence Broxmeyer, MD © 2011 All Rights Reserved. Registered: US Library of Congress

FORWARD:Were he alive today, John Langdon Down, a subset of whose children were autistic, would certainly have felt almost vindicated.The U.S. National Institutes of Health reports that Indiana University, in (http://clinicaltrials.gov/ct2/show/NCT01086475) collaboration with the Department of Defense is currently and actively recruiting participants to determine the effectiveness of an anti-tubercular antibiotic to determine if it can improve social impairment in children with autism, Asperger’s Disorder, and the Pervasive Developmental Disorders. This particular anti-tuberculosis drug, first tested in the laboratory at the Eastern Virginia Medical School, previously worked to improve the sociability of mice with limited social behavior. Study investigators there said that the study held potential towards similarly changing  the social skills in kids with autism. It also worked against schizophrenia. Why is a drug heretofore used only for tuberculosis now being tested to treat autistic children? The answer lies partially in the history of medicine itself.

Tuberculosis, caused by Mycobacterium tuberculosis, infects an estimated one third of the world’s population. Globally, at least one person is infected with TB per second, and someone dies of TB every ten seconds. Tuberculosis kills two to three million people each year, more than any other infectious disease in the world today.

The consensus that autism is from intrauterine infection has been growing.In a 2007 issue of Science, Patterson [1] hypothesized that by far the most important environmental risks for autism and also schizophrenia, consists of intrauterine infection before birth. Fatemi [2], in 2009, mentions the same: that based on major agreement and several decades of studies, again that maternal infection is responsible, leading towards autism and schizophrenia.

 ________________

Child psychiatrist Leo Kanner first shaped our present notion of autism. Yet there is nothing really new about what Kanner called “autism”, and psychiatrist D.A. Treffert of the University of Wisconsin presents convincing evidence to this effect.

Treffert points out that autistic disorders, like mental retardation, have been with man from the earliest times. In fact, until 1943, autistic disorders were simply incorporated into the larger category of “mental retardation”, and both, to this day, cause mistaken diagnosis.

What Down thought of as “mental retardation” included what Kanner then labeled infantile “autism”. But clear and unmistakable evidence of the autistic disorder can be found in J. Langdon Down’s 1887 “developmental” form of mental retardation.[3]

Desperate to put some space between himself and Down,  Kanner, in 1964 calls Down  ‘one of the outstanding lights in the history of ‘mental retardation’.[4] Yet the American Psychiatric Association’s DSM (Diagnostic and Statistical Manual of Mental Disorders) of 1968 not only mentions mental retardation while defining autism, but insists that its true classification is “Schizophrenia, Childhood Type”. Today it is realized that well over half of all autistic individuals are mentally retarded.

By  refusing to acknowledge that his autism could include mental retardation, Kanner attempts to skirt the delicate issue that his cases were indeed a subset of Down’s “mentally retarded” children. But really Down got there first and fully a century after Down, autistic disorders are still classified as “developmental”, just the way Down named them.

However, even beyond such omission of proper credit, Kanner’s more serious exclusion was his inability to come to grips with what  Down considered the most prominent root cause for his children’s mental disabilities. Down’s children, Down said “for the most part”, originated from tuberculosis in their parents.[5]  Thus, by using the term “developmentally disabled”, Down was really creating a euphemism which the public found more palatable than “the developmentally disabled from tuberculosis”.[Ibid][6]

One of the STEALTH forms of “cell-wall deficient” atypical tuberculosis colonies that grew from the brain of a child who expired from the disease. Such forms of tuberculosis are extremely difficult to detect and require special stains and culture media not used routinely in today’s laboratories. [From Korsak T., Acta Tuberc. Pneumol. Belg., 66:445-469 1975].

Today, Langdon Down is considered wrong for saying that Down Syndrome was from parental tuberculosis and rather that it is a “genetic” abnormality, an extra chromosome on Chromosome 21, called “trisomy”. But to this day no one has come up with the actual cause for this genetic abnormality. This was probably why the discoverer of the extra chromosome, Frenchman Jérome Lejeune, hesitated to publish results that were  otherwise clear cut . When Lejeune faced McGill geneticists at a 1958 Montreal International Congress of Genetics, announcing that he had located an extra chromosome in the karyotype of Down’s patients, he was received with interest but skepticism. Considerable skepticism.

Dr. Jérome Lejeume found an extra chromosome on Chromosome 21 in Down Syndrome. However, to this day nobody has come up with the actual cause for this genetic abnormality and studies such as Shy-Ching Lo’s 2004 study at the Armed Forces Institute of Pathology have since shown that such karyotypic changes can result from infection itself.

Since then, Warthin [7], Rao [8], Lakimenko [9] and Golubchick [10] have all shown how tuberculosis itself can cause chromosomal change reminiscent of those found in Lejeune’s trisomy. Warthin showed tuberculosis’s early penitration right into the corpus luteum itself, in which 90% of Down’s abnormal meiotic chromosomal splitting occurs. Rao also found that the tubercle bacillus is capable of inducing such chromosomal changes as result in Down’s nondisjunction of the human egg. And Lakimenkoand Golubchick both proved just how devastating TB could be to the chromosomal apparatus of cell cultures of the human amnion,  in not one, but two separate studies. These investigators showed an increase in  pathological mitoses, arrest of cell division in metaphase, and the actual appearance of chromosomal adhesions absent in control cultures. Indeed Lakimenko and Golubchick demonstrated  that early tubercular involvement was not only destructive against chromosomes, but the very spindles that separated them. Total ovarian destruction occurs in 3% of woman with pelvic tuberculosis[11], again the site where Down and autism’s chromosomal abnormalities usually occurs.

Until about 1980, autism and schizophrenia (splitting of the mind) are considered basically one and the same, separated only after a “genetic” link for autism and schizophrenia isn’t found in the same family. But as late as 2010 Ploeger[12] still sees schizophrenia and autism as probably sharing a common origin, both with physical abnormalities which form during the first month of pregnancy. Ploeger sees this as happening, to be more precise, from 20 to 40 days after fertilization, when the embryo is highly susceptible to disruption.

Three years before this, Rzhetsky[13], using a proof-of-concept biostatistical analysis of 1.5 million patient records, finds significant genetic overlap in humans with autism, schizophrenia……..and tuberculosis.

REFERENCES:

1.   Patterson, PH Maternal effects on schizophrenia risk. Science 2007; 318:576-577

2.   Fatemi, SH Multiple Pathways in Prevention of Immune-mediated Brain Disorder: implications For the Prevention of Autism. J Neuroimmunol 2009 December 10;217(1-2):8-9

3.  Treffert DA Dr. Down and “developmental disorders”, J. Autism Dev Disorder. 36(7):965-6 2006, Oct

4.  Kanner L.  A history of the care and study of the mentally retarded. Springfield, Illinois, Charles. C. Thomas 1964. 150 pages.

5.  Down JLH: Observations on an ethnic classification of idiots. Lond Hosp Clin Lect Rep 3: 259-262, 1866)

6.  Down JL: On Some of the Mental Affections of Childhood and Youth, J & A Churchill, 1887.

7.  Warthin AS Cowie DM A contribution in the casuistry of placental and congenital tuberculosis. Journ. Inf. Dis. 1:140 1904

8.  Rao VV, Gupta EV, Thomas IM     Chromosome damage in untreated tuberculosis patients. Tubercle. 1990 Sep;71(3):169-72

9.  Lakimenko LN  .Changes in the mitotic regime of a cell culture under the influence of sensitins  Biull Eksp Biol Med. 1976 Feb;81(2):237-9

10. Golubchik IS, Iakimenko LN, Lazovskaia AL   Effect of tuberculin on the mitotic regime in cell cultures Biull Eksp Biol Med. 1972 May;73(5):105-7

11. Nogales-Ortiz F Tarancon I  The Pathology of Female Genital Tuberculosis. Obstet. Gynecol. 53:422, 1979

12. Ploeger A Raijmakers ME  The association between autism and errors in early embryogenesis: what is the causal mechanism?    Biol Psychiatry 2010 Apr 1;67(7):602-7. Epub 2009 Nov 22

13. Rzhetsky A  Wajngurt D  Park N and Zheng T  Probing genetic overlap among complex human phenotypes.  Proceedings of the National Academy of Sciences, Chicago, Vol. 104  No. 28 pp. 11694-699 July 10, 2007

Office of the Medical Superintendent, The Earlswood Asylum for Idiots in Surrey England, 1887

So it was in the teachings of John Langdon Down, a subset of whose  “mentally retarded” children were autistic, that Leo Kanner really found his “autism”.

Dr. John Langdon Down [18 November 1828 – 7 October 1896]. According to George T. Capsone, M.D., Down’s original report attributed Down syndrome to maternal tuberculosis.

Down, one of the outstanding medical scholars of his day, was certain to gain entrance into the prominent London Hospital when he decided instead to go into an avenue few would even entertain, as Superintendent of the Earlswood Asylum for Idiots in Surrey.  But for Down it was pre-ordained. At the age of 18, he had what might be described as a transformative experience. A heavy summer storm drove his family to take shelter in a cottage. Down: “I was brought into contact with a feeble minded girl, who waited on our party and for whom the question haunted me – could nothing for her be done? I had then not entered on a medical student’s career but ever and anon… the remembrance of that hapless girl presented itself to me and I longed to do something for her kind.”[1]Down therefore becomes a doctor for reasons that were the purist of them all, and soon excels to the head of his class.  His pursuits are brought to a temporary halt when he acquires tuberculosis, sending him back to his family’s home in Torpoint. Gradually he recovers. Down then goes through an obstetrics residency before obtaining his MD to assume the position of head of the Earlswood Asylum. He is now quite knowledgeable about pregnancy, the complications and diseases of pregnancy, and the neonates that come as a result of pregnancy. In addition to that his surgical skills allow him to do autopsies during which he contributes much to expand knowledge of conditions of the brain such as cerebral palsy.In his Lettsonian Lectures[2], Down follows the psychiatric nomenclature of his time, classifying his most severe cases of mental retardation in the young under the category of ‘idiocy’.  Like Kanner, he specifies that some of his  mentally retarded children had exceptional intellect in specific areas, such as memorization, music or mathematics. In fact, a noticeable subset of Down’s patients did not appear physically to even have mental retardation.In a more recent survey of the literature, Gillberg and Coleman[3]  relate that quite a number of reports of individuals with Down Syndrome also meet the criteria for autism.By 1867, Down had appeared, in the Lancet, linking childhood mental illness with tuberculosis.[4] To Down, in fact, children who inherited Down Syndrome “for the most part, arose from tuberculosis in the parents,” and not genetics.[5] Capone mentions  Down’s original report attributed the condition to maternal tuberculosis.[6]  As a result of such tuberculosis from conception or soon thereafter, and nothing else, such children’s life expectancy would be shortened, as the same tuberculous infection would lead to their early demise.The only thing really wrong about John Langdon Down’s theory was that it was way ahead of its time.He knew that tuberculosis was, as it still is, the most common cause of death from a single infectious agent in children[7], killing upwards of 250,000  children each year[8], yet exceedingly difficult to diagnose[9]. He also knew that TB was the  single leading cause of death among women of reproductive age between 15-44, one million of whom presently die, according to WHO, each year.[10]Moreover, brain and central nervous system tuberculous account for 20-45% of all types of tuberculosis among children, much higher than its 2.9-5.9% for all adult tuberculosis.[11]In fact tuberculosis of the nervous system has consistently been the second most common form of TB in the very young outside of the lung.

And of those infants and children that did survive, nearly 20-25% manifest mental retardation, and mental disorders[12]- serious and long term behavioral disturbances[13], seizures[14]and motor (movement) handicaps  in addition to the various other anomalies associated with autistic and Down’s “neurodevelopment”  behavior problems.

For his Lancet study, Down submits one-hundred post-mortem records of children who had passed away at his institution. He had found no fewer than 62% of these children to have tubercular deposits in their bodies. For some unknown reason, boys had more than twice the incidence of tubercles in their organs as did girls, a finding which concurred with the male predominance he later notes in  childhood mental disease in general. Such male preponderance is today not only documented in Down Syndrome but autism as well. Tuberculosis might be more frequently transmitted by the mother than the father but it was the male offspring that were more tubercular.Caldecott[15] in a 1909 British Medical Journal, noted that Down showed his children rarely lived beyond 20 years as a consequence of brain and nervous system disease, and that they died of…………. tuberculosis.

REFERENCES:

1.  Down, J. Langdon. Address Christian Union, June 27, 1879.

2.  Down JL On Some Of The Mental Affectations of Childhood and Youth. The Lettsonian Lectures. London J&A Churchill, 1887.

3.  Gillberg C Coleman M The Biology of the Autistic Syndromes in Clinics in Developmental Medicine No. 153/4  3rd Edition Mac Keith Press pp.340, 2000, p. 140

4.  Down JL On Idiocy and its Relation To Tuberculosis The Lancet vol ii 1867.

5.  Down JLH: Observations on an ethnic classification of idiots. Lond Hosp Clin Lect Rep 3: 259-262, 1866.

6.  Capone, GT Down Syndrome: Advances in Molecular Biology and the Neurosciences, Developmental and Behavioral Pediatrics, Lippincott Williams & Wilkins, Inc. Vol. 22, No. 1, February 2001

7.  Walia R Hoskyns W Tuberculous meningitis in children: problem to be addressed effectively with thorough contact tracing Eur J Pediatr. 159(7):535-8 2000  Jul

8.  Titone L Romano A Epidemiology of paediatric tuberculosis today Infez Med 2003 Sep;11(3):127-32

9.  Mahadevan B Mahadevan S Tuberculin reactivity in tuberculosis meningitis Indian J. Pediatr. 2005 Mar:72(3):213-5

10. WHO TB Is Single Biggest Killer Of Young Women Press Release Geneva, Switzerland WHO/40 26 May 1998

11. Molavi A, Lefrock JL: Tuberculous meningitis. Med Clin North Am, 1985; 69:315-331

12. Garg PK tuberculosis of the central nervous system. Post grad Med J 75:133-40 1999

13. Schoeman JF Springer P Adjunctive thalidomide therapy for childhood tuberculous meningitis: results of a randomized study. J. Child Neurol 2004 Apr;19(4):250-7

14. Takamatsu I The current situation and treatment of childhood tuberculosis Kekkaku 1999 Apr;74(4):365-75

15. Caldecott H: Discussion of paper by Shuttleworth GE: Mongolian imbecility. Br Med J 2:661-665, 1909.

 

Department of Psychiatry, Burgholzli Hospital, Zurich Switzerland, 1930

The word “autism” originates from Swiss psychiatrist Eugene Bleuler, first appearing in English in an April, 1913 issue of the American Journal of Insanity [1], heralded at an address he delivered for the opening of Johns Hopkins very own Henry Phipps Psychiatric Clinic.

Paul Eugen Bleuler Born April 30, 1857 – Died July 15,1939 (aged 82) Zollikon, Switzerland He coined the word schizophrenia in 1908, and autism later on.  Bleuler described the main symptoms of schizophrenia as 4 A’s: flattened Affect, Autism, impaired Association of ideas and Ambivalence.

Bleuler uses “autism”,  Greek for “self”, to describe schizophrenics’ (literally people with a splitting of the mind) seeming difficulty in connecting with other people, and, in certain cases, withdrawing into their own world, and showing  self-centered thought.  But, to Bleuler, schizophrenia, and thereby autism, still came from an organic cause such as infection, and, as such, were sometimes curable. Until about 1980, autism and schizophrenia are considered basically one and the same. To that point Bleuler’s definition holds.

Bleuler also uses “autism” to describe doctors that are not attached to scientific reality, wont to build, on what Bleuler calls “autistic ways”,  that is, through methods in no way supported by scientific evidence, an event more and more in evidence as psychiatrists moved away from tissue based outcomes into the realm of subjective behavior labeling.

REFERENCES:

1.   Bleuler E, Autistic Thinking ,American Journal of Insanity Vol 69 No. 5 April 1913 p. 873

Child Psychiatry Service, John’s Hopkins University Hospital, Pediatric Division Baltimore, 1933

Internal medicine trained Leo Kanner teaches himself the basics of child psychiatry and at the instigation of Adolph Meyer, joins the Henry Phipps Psychiatric Clinic at John Hopkins Hospital in Baltimore.

By 1903, Henry Phipps, wealthy partner of Andrew Carnegie, sought charitable outlets for his wealth. He then joined Lawrence F. Flick, a doctor with a vision, to open a center solely dedicated to the study, treatment, and prevention of tuberculosis, hands down the number one infectious killer in the United States.

Not until May, 1908 did Philadelphia steel magnate Phipps get around to visiting Johns Hopkins’ tuberculosis division, which he had funded. At that point Phipps turned to ask Hopkin’s Dean and legendary pathologist William Henry Welch if he needed help sponsoring other projects at the Hospital. Welch answers Phipps by handing him a copy of “A Mind That Found Itself”[1], an agonizing assessment of mental asylums written by Clifford W. Beers, and published with the help of Swiss born pathologist Adolph Meyer. Phipps turns around and  within a month agrees to donate $1.5 million to fund a psychiatric clinic for Johns Hopkins Department of Psychiatry. By 1912 the Henry Phipps Psychiatric Service at Johns Hopkins Hospital provides the first inpatient psychiatric facility in the United States for the mentally ill.

Welch likes Meyer. Meyer, although unable to secure an appointment from his alma mater, the University of Zurich, is,  like Welch, a pathologist………. a neuropathologist to be exact. Also Welch takes to him because Meyer initially seems to reject Freud as the be all and end all for psychiatry. And there is another level of understanding: Meyer and Welch share the rapport of two superb medical networkers and politicians. Welch sees to it that Meyer becomes the head of Hopkins Psychiatry.

Dr. Adolph Meyer. Born September 13, 1866 Niederwenigen – Died March 17, 1950 (age 83) Baltimore. Head of Johns Hopkin’s psychiatry. One of the most influential figures in American psychiatry in the first half of the Twentieth Century. The first academic department of child psychiatry in the world was founded by Leo Kanner in 1930 under Meyer’s auspices and direction.

But it is the very same second-rate, vague, “psychobiological” views that characterize Meyer’s psychiatric approach that will prove in the end, to be  disappointing. Designed to be all things to all people, Meyer’s “psychobiology”  assesses mental patients physical and psychosocial problems concomitantly, but turns out to be all things to no one. Meyer is much more orientated towards taking extensive histories of his patients…….getting all the “facts”, then in rooting out the pathology behind mental illness on the autopsy table. Besides, the positions of Meyer and Freud closely resemble one another in that each insists heavily on the study of psychogenic factors in neurotic disorders. Welch, on the other hand, was committed to bringing the German model, which relied heavily on the lab,  to US medicine. So with Meyer, Welch didn’t precisely get what he thought he was getting.

Nevertheless, thanks to neurologist/pathologist Adolph Meyer, Leo Kanner becomes the first “child psychiatrist” at Johns Hopkins,……… and,  by default,  the United States. Meyer is bent on changing American psychiatry, and will dominate psychiatry from his Johns Hopkins chair during the first half of the twentieth century.

Meyer has long been interested in the psychiatric treatment of children. So he arranges with Hopkins pediatrician Edwards Park for Kanner to become a liaison between pediatrics and psychiatry at the institution. This gives Kanner enhanced influence in reaching an audience of pediatricians who otherwise would have found little value in the psychiatric evaluation of children.  Meyer has already decided that the psychosocial aspects of mental disease are more important than tissue diagnosis of brain pathology. He closes his laboratory, and instead prefers to talk to his patients, taking extensive histories in the manner of Kraepelin and Sigmund Freud.

REFERENCES:

1.   Beers CW A Mind That Found Itself 232 pages University of Pittsburgh Press; 1st edition June 30, 1981.

 

Vienna, Austria, Office of Sigmund Freud, Neurologist, 1883

“Loudest of all is the cry: tuberculosis! Is it contagious? Is it acquired? Where does it come from? Is Master Koch of Berlin right in saying that he has discovered the bacillus responsible for it?”[1]        -Sigmund Freud  October 9, 1883

Long before Leo Kanner, Freud speculated that autism was an impairment in social functioning in which the satisfaction of instincts was, to one degree or another, withdrawn from the influence of other people.

Sigmund Freud, 1921 [Born 6 May 1856 – Died 23 September 1939 (aged 83)] Sigmund Freud saw patients of whom he described the “satisfaction of the instincts is partially or totally withdrawn from the influence of other people.”, a description that could fit present day concepts of autism. The influence of Freud’s psychogenic hypothesis was not lost on Dr. Leo Kanner. In a 1960 interview, Kanner bluntly described parents of autistic children as “just happening to defrost enough to produce a child.”

Freud’s prior neurophysiological interests leads him to the psychiatry clinic of famous brain anatomist and psychiatrist Theodore Meynert. Under Meynert’s direction, Freud proved unusually adept at diagnosing organic brain disorders, particularly the effects of localized injuries. But what he did not seem to pick up was Meynert’s absolute belief that the roots and cause of mental illness lie in the diseases and pathology in a human beings brain and central nervous system. Freud is unhappy with a career that might pursue such orthodoxy, as he expresses in a letter to his fiancée in 1884. Instead he is looking for “a lucky hit”.That “lucky hit” would, of course, eventually turn out to be psychoanalysis and his talking cure.But even after he abandons Meynerts’s brain approaches, Freud continues to admit that his wide-ranging psychoanalytic theories would eventually need to be rooted in the tissue neuroscience of Meynert. Otherwise, it would only take “a few dozen years” to “blow away” the “artificial structure of hypotheses” involved in psychoanalysis.[2]There are obvious holes In Freud’s theories. But, for decades, nobody is picking them up. No one could deny the tremendous impact his thoughts had on those working with children with emotional problems. Nevertheless Freud’s theories at times seem to distort the treatment of the serious mental illnesses, among them, the notion that bad mothering could cause conditions such as schizophrenia. Not only did this leave irrevocable guilt, in certain cases, on the families involved, but often on the patients themselves. Yet such thoughts influenced a generation of thinkers.  Kanner refers to remnants of it in his cold hearted moms, who he finds often among his “autistic” children. In his book Child Psychiatry Kanner acknowledges Freud’s merit more often than not, although he later lashes out that Freud’s influence had gone too far in his followers insistence that Freud’s theories were just about infallible.Leaving Maynert, Freud joins neurologist Charcot in Paris, who was working on the medical disorder “hysteria”. “Hysteria” was a wastebasket category that included, among other things depression, and “conversion” disorders which produced pain with no obvious organic cause. It was in conversion hysteria, that Charcot could sometimes, briefly, eliminate symptoms through hypnosis.  Freud felt that such hysteria had nothing to do with disease or brain pathology, which immediately put him at odds with most of the medical establishment.The first to mention tuberculosis induced neuroses such as hysteria was Cardanus[3] , who described a case cured in 20 days because it “merely involved the intellect”. Thus the first “talking cure” might have been well over 200 years before Freud.Once in private practice, Freud persists in using  post-hypnotic suggestion to cure hysterical symptoms, to little avail.  Finally his great breakthrough comes not with one of his own patients but when he utilizes the records of a patient who his friend and colleague Josef Breuer saw, called “Anna O.”, the first patient upon whom a “talking cure” was affected. “Anna O” was Bertha Pappenheim, a 21 year old who developed a host of physical and mental problems while attending to her father, dying of tuberculosis. Some of her symptoms included an intractable cough, severe headache, malaise, partial paralysis, and vision problems……….all thought by Freud to be “hysterical”. Suffering from epilepsy, one of her arms was paralyzed as a result of complex seizures.Based on all of these symptoms, Breuer, in his chart notes, seriously considers that Anna O. has tuberculosis meningitis. Then, discovering that her paralyzed arm was the arm that cradled her dying father, he makes the leap that she was unconsciously immobilizing her arm as self-inflicted punishment because she inwardly blamed herself for her father’s death. Breuer then tries to get her to “talk out” her repressed memories to affect a cathartic cure. Breuer’s  case proves pivotal, by Freud’s own admission. It would be the beginning of a “psychoanalysis” which Freud would embellish from that point on.

Freud presses Breuer for joint publication of Studies on Hysteria,accomplished in 1895. But even in this book, the gulf between Breuer and Freud became obvious. Breuer was an internist, trained in internal medicine. So he looked for neurologic disease processes behind Anna’s hysteria, while Freud used a psychological point of reference. What unfolded In the case of Anna O, would prove to be medical misjudgments with lasting consequences.

As the years went on it became obvious to others that Anna O.’s more noteworthy symptoms pointed towards specific, infectious brain pathology, typical of complex partial seizures, originating in the temporal lobe. German born research psychologist H.J. Eysenck[4] and others speculate that Anna O wasn’t suffering from hysteria or neurosis at all, but brain involvement from tuberculosis, a disease that not only did two of her siblings die from at the ages of 2 and 18, but that her mother had and that she was again exposed to from nursing her tubercular ridden, dying father.

According to Thornton’s more in depth account, Anna’s father had a tubercular abscess  just under the lining (or “pleura”) of one lung, a frequent complication of the tuberculosis which was then highly prevalent in Vienna. Nursing him exposed her to constant contact. Moreover, in the midst of Breuer’s talking therapy[5], her father’s lung abscess was surgically incised and drained at home, subjecting the girl, who changed his dressings, to direct exposure to his tubercular bacilli. The virulence of the strain that exuded out of the purulent drainage from her father’s chest tube was best attested to by the fact that it would soon kill him. Thornton makes it crystal clear that Freud’s account of Anna O. was totally deceptive and that there had been no “talking cure” or catharsis, something he believed Freud knew very well.

Eysenck, famed for his Eysenck Personality Scale,  says that it was not Breuer or Freud who really cured “Anna O.” but repeated hospitalizations for tubercular symptoms which occurred subsequent to their psychoanalytic “treatment”.

Eysenck had a good case and H.F. Ellenberger[6] agreed. Tracking down actual chart records, Ellenberger notes that Anna O.’s condition actually got much worse during Breuer’s treatment, to the point where she had to be treated in a TB sanitarium. Again, Freud was aware of all of this but his account still proclaimed Anna O.’s pristine talking cure. Breuer, not nearly so enamored with the treatment he himself had originated, broke with Freud. And Jung was the first to point out publically that the alleged success of the treatment of Anna O. was anything but. Jung insists that there was no cure at all in the sense with which it was originally presented. Again, he mentions, Anna O was not suffering from a neurosis at all, but from the mental and physical changes of tuberculous meningitis.

Even Freud’s case study of “Dora”, which established Freud’s theories about lesbians and female hysterics, was not untainted by physical disease.  “Dora” was Ida Bauer, born in Vienna in 1882, of Bohemian Jewish ancestry. Ida’s father, Philip, died of tuberculosis in 1913; one year after her mother died of the same disease.

During the course of their sessions, young Ida mentions to Freud that her father had a lover who Freud labels Frau K and whose husband made sexual advances towards her which she found outright repugnant, coming from the much older man. Her father seemed to ignore this in an attempt to preserve his own illicit relationship with Frau K, who together with her husband, were friends of the family.

Because of this, Ida’s father told her that the husband’s advances were all a figment of her imagination. But later, Frau K’s husband, Herr K, would tell a much different tale. Indeed he had tried to seduce young Ida. Although Freud accepted Ida’s account, his take on it was a series of specious leaps at best. Instead of accepting Ida’s valid repugnance for a much older man, Freud insists that she was repressing both her own love for Herr K, as well as an incestuous love of her father, and at the same time a homosexual attraction for Frau K.

From a more medically based perspective, Ida’s father had in fact developed tuberculosis when she was six years old, a disease he was never able to entirely shake and had constant relapses from, punctuated by fever and coughing until his death in 1913. Furthermore, tuberculosis characteristically doesn’t do its greatest damage, for unknown reasons, between age 5 and 15. Dora comes to Freud at 14. Ida’s mother also dies from tuberculosis. Freud doesn’t chart this, feeling it insignificant. Ida begins to suffer her own lung involvement at age 8 with constant episodes of shortness of breath that seem to assuage with enforced rest for a six month period. Her family doctor, full well knowing the stigma of even mentioning the possibility of tuberculosis, puts down that the shortness of breath was from “nervous causes”.[7]

At age 12, Ida’s shortness of breath is joined by spasmodic episodes of “nervous” coughing, generally lasting 3 to 5 weeks and associated with loss of voice. Rather than attribute Ida’s coughing spells to TB, or her voice loss to a tubercular attack on the 6th recurrent laryngeal nerve, Freud immediately seizes upon a series of hypothesis that few besides himself could even fathom, much less have thought up.

Ida’s coughing, claims Freud, expressed her sexual longing for her father, and her rivalry with Frau K regarding this. And her throat irritation and consequent coughing was, Freud maintained, a combined symbolization of her desire to take Frau K’s place in performing fellatio on her father.

As if this wasn’t enough, supposedly, the ceaseless coughing could also express Ida’s desire to replace her father in his affair with Frau K. Freud thereby assumes that Ida K has lesbian tendencies as well. Later she would marry in what proved to be an entirely heterosexual relationship without a mention of any homoerotic tendencies whatsoever.

At the time of its release, Studies on Hysteria was not well received by  European medicine. And It was not until years later that psychoanalysis was recognized as a legitimate psychiatric tool.

In 1918, Sigmund Freud, during  a speech at the Fifth International Congress of Psychoanalysis in Budapest insisted that: ‘The neuroses threaten public health no less than tuberculosis”. [8]

But he never saw the possible interconnection between the two. Or if he did, he kept it to himself.

REFERENCES:

1. Freud S Freud  EL Letters of Sigmund Freud Courier Dover Publications, 1992, 470pps. P68

2. Freud, Sigmund. Jenseits des Lustprinzeps. Leipzig-Vienna-Zurich (1920). GW, 13, 1-69; Beyond the pleasure principle. SE, 18: 7-64. p. 60

3. Cardanus, J Dignot, admirared num. 3. Ii, de phthisis, obs 14 . J.G. Schenck, Ed. Francofurti, Beyeri, 1665, p.265

4.  Eysenck HJ  Mead M Eysenck SBG  Decline and Fall of the Freudian Empire Transaction Publishers, 2004 224 pages.

5. Thornton, E.M. Freud and Cocaine: The Freudian Fallacy. Blond & Briggs, 1983.

6.  Ellenberger HF The Discovery of the Unconscious: The History and Evolution of Dynamic Psychiatry Basic Books, 1970 932 pages

7.  Wenegrat B Theater of Disorder: Patients, Doctors, and the Construction of Illness Oxford University Press US, 2001 292 pages p100

8.  Danto, EA Freud’s Free Clinics: Psychoanalysis and Social Justice 1918-38  New York  Columbia University Press 348 p. 2005 p.17

 

Child Psychiatry Service, John’s Hopkins University Hospital, Pediatric Division Baltimore, 1934

Kanner , with little use for medical diagnostics himself, seems made-to-order for Meyer. Kanner will laud Meyer for shifting the emphasis of psychiatry “from organs and their diseases to patients as improperly functioning persons.”[1]

But diseased organs can themselves lead to “improperly functioning persons”.

Dr. Leo Kanner (1955). Born June 13, 1894; Died April 3, 1981 (aged 86). By 1943 Kanner published a study of 11 children identified with early infantile autism which became known as Kanner Syndrome. This seminal paper, entitled “Autistic Disturbances of Affective Contact”, together with the work of Hans Asperger, formed the basis of the modern study of autism. However neither Kanner nor Asperger came down strongly in favor of an organic or infectious cause.

Kanner  never  really seemed that interested in “organs and their diseases”. While still in Berlin, finishing medicine, his lowest grade on his finals is as a result of being unable to diagnosis a then premier infectious brain disorder leading to mental symptoms.[2]Neurologist Karl Bonhoeffer documents that Kanner misinterpreted the symptoms of tabes dorsalis, a neurologic end-stage syphilis of the brain and nervous system. (Ibid)

Not really attracted to being a  general internist, and still in Berlin, Kanner gravitates into the then new, and relatively limited field of electrocardiography, or EKG tracings of the heart‘s rhythms. Once at Hopkins, Kanner writes his first edition of Child Psychiatry in 1935, borrowing the name from the German term Kinderpsychiatrie. And by 1943, bent upon making his mark, discovers a “new“ syndrome.  Without mention of Bleuler, who originated the word “autism”, Kanner uses it  to describe, what he feels to be a novel psychiatric illness in children, emphasizing an “autistic aloneness” and “insistence on sameness”. Ironically, Kanner, known to rant and rage over mere psychiatric labels without treatment, creates another one……………. “autism”.

REFERENCES:

1.   Kanner L The Pediatric-Psychiatric Alliance Can Med Assoc J 1938 Jan;38(1):71-74

2.   Neumarker K Leo Kanner: his years in Berlin, 1906-24. The roots of autistic disorder in History of psychiatry 14 (54 Pt 2): 205-18 2003.Jun)

Office of The Director, Department of Medical Genetics, New York State Psychiatric Institute July, 1936

Leo Kanner and Franz J. Kallmann, have a couple of things in common.  Both have connections with the University of Berlin.  Kallmann worked for 4 years at Berlin’s psychiatric institute, under the same Karl Friedrich Bonhoeffer who graded a portion of Kanner’s final exams. Although Kanner is only 3 years older than Kallmann, and Kanner is trained in Internal Medicine, both would move quickly, upon their arrival to America, to make their impact on psychiatry.

Dr. Franz J. Kallmann Born July 24, 1897 Neumarkt, Silesia – Died May 12, 1965 (aged 67), New York. Kallmann was one of the first to study the genetic basis of psychiatric disorder. He spent most of his career in New York, where he pioneered the use of twin studies in the assessment of the relative roles of heredity and the environment in the pathogenesis of psychiatric disease.

Landing in New York, Kallmann establishes the Medical Genetics Department of the New York State Psychiatric Institute. From then on, one thing is certain. With Franz J. Kallman, American psychiatry got much more of the hereditary patterns in mental disease than it was willing to accept or pursue. Prominent British geneticist Penrose judged Kallmann’s work unconvincing.

A year after Kanner writes “Child Psychiatry”, Kallmann becomes interested in twins and their genetic disposition. But there arises an inconvenient truth: identical twins, who have virtually the same DNA, do not always develop the same mental disorders.

Kallmann focuses on what he calls the “genetics of schizophrenia.” In a lecture,  he finds  it desirable to prevent the reproduction of relatives of schizophrenic patients. He defines them as  undesirable from a eugenic point of view, especially at the beginning of their reproductive years.

By 1938, Kallmann, who escaped Nazi Germany because he was half Jewish, has doubled down, calling for the “legal power” to sterilize “tainted children and siblings of schizophrenics” and to prevent marriages involving “schizoid eccentrics and borderline cases.”  In his mind, Kallmann feels the need to stamp out every recessive gene behind schizophrenia.[1] It was a thought that began  incubating in him while still in Germany. Leo Kanner is appalled by Kallmann’s  thoughts and words. He sees dangerous implications. This time he is correct.

Kallmann is a zealot in every sense of the word. He finds a genetic basis for just about everything. He proclaims that human tuberculosis is genetically based.  His agenda in doing so is quite transparent.

Proponents like Kallmann for a “genetic” or “hereditary” view of mental illness have always relied on identical twin studies. In these, if there is a heavy degree of “concordance”, meaning that both identical twins come down with the illness, it is supposed that “genetic” influences are involved. This is so especially if at the same time fraternal twins showed a lower rate in being “concordant for” or contracting the same disease.

But it was also known that an infectious disease like tuberculosis brought in the same numbers in identical twin studies as did schizophrenia or autism, putting the accuracy of such twin studies deeply in question. Kallmann[2][3]himself, found that approximately 85% of identical (homozygous) twins had the same disease (were concordant) if their co-twin had either tuberculosis or schizophrenia.

Kallmann’s study for the hereditary basis of schizophrenia is published in 1938. It acknowledges  long time boss and Nazi mentor, Ernst Rudin.[4]  While still in Germany, Kallmann saw Rudin catapulted to director of the Kaiser Wilhelm Institute for Psychiatry and its eugenics division through Rockefeller Foundation money, creating the medical specialty known as Psychiatric Genetics. Rudin was not only assisted by Kallmann but another protégée named Otmar Verschuer. Back in Germany, Rudin, a year later, sees to it that the German version of Kallmann’s book is used by the Nazi T4 Unit as a blueprint for the murder of mental patients and “defectives”, many of them children. 250,000 are killed under this program by gas and lethal injection. The Rockefeller-Rudin operation had become a section of the Nazi state. Rudin was now head of their Racial Hygiene Society.

Meanwhile, in America, geneticist Franz Kallmann becomes an early leader of the American Society of Human Genetics (ASHG), a true pioneer in the study of the genetic basis of psychiatric disorders. Kallmann’s American Society of Human Genetics, organizes the “Human Genome Project”. It is the most ambitious project ever dealing with basic genetics. In 1988, Congress provides funds for the National Institutes of Health (NIH) and other groups to begin mapping out human DNA. The project began officially on October 1, 1990, with a projected budget of $3 billion over the next 15 years.

As B. W. Richards points out,  advances regarding the discovery of genetic markers for diseases such as autism, Down Syndrome, and schizophrenia, although good for diagnostics, have done little to get at the actual cause of such chromosomal aberrations. Richards: “Despite dramatic advances in the fields of biochemistry and cytogenetics, revealing many new causes of mental retardation, a large proportion of mentally retarded patients are still undiagnosable in respect of etiology (cause).”[5]

What did result, thanks to such take no prisoners actions like Kallmann’s, was that bacteriology was purposely confined to a specialty of medicine outside the schools of biology, botany and zoology, in no small part responsible for bacteriology’s slow acceptance.

Bacteriologists, in retaliation, steered clear and gave no credence to any of the proclamations of geneticists. Unbelievably, the situation had gotten so out of hand that  as late as 1945, bacteriologist Rene Dubos, discoverer of the first antibiotic ever, had to muster all the courage in him to name his milestone paper “The Bacterial Cell”.  Such are and always were the politics of medicine.

REFERENCES:

1. Muller-Hill B. Murderous Science: Elimination by Scientific Selection of Jews, Gypsies, and Others in Germany, 1933–1945.Woodbury, NY: Cold Spring Harbor Laboratory Press; 1988: 11, 31, 42–43, 70

2. Kallman FJ Resiner D Twin studies on the significance of genetic factors in tuberculosis. Am. Rev. Tuberc. 47:549, 1943

3. Kallman FJ The genetic theory of schizophrenia. Analysis of 691 twin index families. Am. J. Psychiat. 103:309 1946

4. Torrey EF, Yolken RH Psychiatric Genocide: Nazi Attempts to Eradicate Schizophrenia. Schizophr Bull. September 2009

5.  B. W. Richards Recent Advances in Medical Knowledge of Causes of Mental Retardation Can Med Assoc J. 1963 December 14; 89(24): 1230–1233.

 

Office of the Director, Child Psychiatry, John’s Hopkins Hospital, Baltimore, 1943

To make certain that his theory sticks, Kanner cherry-picks eleven children, leaving out those presently with seizures or mental retardation even though these are very much in today’s autistic spectrum. Some studies have mental retardation occurring  in approximately two-thirds of individuals with autism and seizures in approximately one-third.

Dr. Leo Kanner. His first autistic case was Donald T. first seen in October, 1938, at the age of 5 years. In August, 1937, Donald was placed in a tuberculosis preventorium in order to provide for him “a change of environment.”

Kanner produces a 33-page[1] medically sketchy paper.He outlines 11 case histories, all the while convincing himself that despite findings such as a history of seizures, which could point to a brush with serious disease, that his subjects problems were purely psychiatric or behavioral. At the same time he says that unlike childhood schizophrenia, autism is the result of “inborn autistic disturbances of affective contact“   …….a sort of congenital lack of interest in other people. Yet most of his children are thought deaf, neither talking, nor responding if questioned, and could have severe cranial nerve disruption from a serious central nervous system infection.

“Physically”, Kanner insists, despite findings which suggest otherwise, “the children were essentially normal”.  But five out of his 11 subjects, through measurement “had relatively large heads” , which could indicate possible degrees of hydrocephalous. Hydrocephalous also known as “water on the brain,” is a medical condition in which there is an abnormal accumulation of   cerebrospinal fluid (CSF) in the ventricles, or deep cavities in the brain. This may cause increased intracranial pressure inside the skull and progressive enlargement of the head, convulsions , and mental disability. One of its causes in infants is perinatal infection. At one time, the diagnosis of acute hydrocephalus was so commonly associated with tuberculous meningitis that the terms were used interchangeably.

But apparently  of more concern to Kanner is the children’s parent’s: “In the whole group, there are very few really warmhearted fathers or mothers.”When, in his first case, Kanner finds out through Donald T’s mother that the child had been placed in a “tuberculosis preventorium” for “a change of environment”, Kanner never questions her as to why.

The Sea Breeze Tuberculosis Preventorium at Coney Island, Brooklyn, New York: where poor children who had been determined to have contracted tuberculosis in tenement city neighborhoods could go. Some of these children were fitted with casts there. Picture appeared in “The Seashore and Fresh Air Treatment at Sea Breeze Hospital”, presented by John W. Brannan, M.D. at the Sixth International Congress on Tuberculosis, Vol. 2; W. F. Fell Company, 1908. American Preventoriums were designed to protect children from the ravages of TB and existed from 1909 to approximately 1970.

All but forgotten, tuberculosis preventoriums were  America’s answer to preventing  tuberculosis epidemics among the  urban poor. This was accomplished by ripping “pre-tubercular” children from their homes and placing them into residential institutions.[2]  From the very beginning of the 20th century and well into it, such primitive “preventoriums” where looked towards as the only solution to break the chain in a disease which by 1900 killed at least 15% of urban populations, with no treatment in sight. By 1907 von Pirquet came up with a children’s tuberculin skin test with all the flaws of our present adult tuberculin skin test. Not only were there false negative tests done on seriously infected children whose immune system could not muster a positive skin reaction, but even when the test proved positive it was often impossible to distinguish mere previous exposure from active disease. Nevertheless, the imprecise designation “pre-tubercular” was used to designate children with positive skin tests who didn’t seem to have active disease. These were the children targeted for preventoriums.

Kanner knows from the onset that his “autism” will  be challenged,  on many levels. Other psychiatrists, presented with these same children would call them mentally retarded or schizophrenic.

The fact was that psychiatrically, all would be considered by many as a form of childhood schizophrenia. To make the differentiation stick, Kanner emphasizes ‘extreme solitude from the very beginning of life’ and a preserved intelligence. But many of Down’s developmentally disabled children had normal intelligence also, and certainly did not appear to have mental retardation.[3] Kanner argues that his children, unlike schizophrenics, did not seem to have delusions or hallucinations. In addition, he says, schizophrenia doesn’t emerge in as early as the 30 months after birth that autism seemed to.

But more tellingly, in 1949, Kanner vacillates, admitting that he sees no need for his ‘infantile autism’ to be separated from ‘schizophrenia’.[Ibid] The American Psychiatric Association (APA) balks in accommodation, and decades later still won’t acknowledged autism as anything other than just that:  ‘schizophrenia, childhood type.’[4]By then, Kanner deplores the APA’s decision.[5]  Yet despite this, until 1980 his “autism” is not[6] “autism”, it is childhood schizophrenia.

One year after the APA’s 1968 decision, prominent Bellevue child psychiatrist Lauretta Bender argues that children with autism generally grow up to have schizophrenia anyway. And on top of that, despite the ever increasing rallying cry by American psychiatric gurus as to childhood schizophrenia’s extreme rarity, Bender documents thousands of cases of it while at Bellevue.[7] German psychiatry, which long maintained its influence over Europe, the Soviet and Eastern Bloc countries, also insisted that childhood autism is the initial form of schizophrenia, with development into schizophrenia more or less inevitable.

Moreover, some in the field understood that clear and unmistakable evidence of the Autistic disorder could be found in J. Langdon Down’s 1887 “developmental” form of mental retardation,[8]which Down attributed mostly to tuberculosis in the child’s parents.[9][10]  The stage was set for a battle royale.

REFERENCES:

1.  Kanner L Problems of Nosology and Psychodynamics of Early Infantile Autism American Journal of Orthopsychiatry 19:416-26 1949

2.  Connolly CA Saving Sickly Children: The Tuberculosis Preventorium In American Life, 1909-1970 New Brunswick Rutgers University Press 182pp. 2008

3.  Treffert DA Dr. Down and “developmental disorders”, J. Autism Dev Disorder. 36(7):965-6 2006, Oct

4.  APA (1968) Diagnostic and Statistical Manuel of Mental Disorders, Second Edition Washington, DC American Psychiatric Association

5.  Neumarker K Leo Kanner: his years in Berlin, 1906-24. The roots of autistic disorder in History of psychiatry 14 (54 Pt 2): 205-18 2003.Jun

6.  American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders 3rd Ed Washington DC 1980)

7.  Bender L A Longitudinal Study of Schizophrenic Children with Autism Hospital  and Community Psychiatry 20(8):230-37 1969.

8.  Treffert DA Dr. Down and “developmental disorders”, J. Autism Dev Disorder. 36(7):965-6 2006, Oct

9.  Down JLH  Observations on an ethnic classification of idiots. London Hosp Clin Lects Reps 3:259-262, 1806

10. Down JL: On Some of the Mental Affections of Childhood and Youth, J & A Churchill, 1887.

Johns Hopkins Department of Pathology, Baltimore, 1946

Though his office was but a short distance away from Leo Kanner’s, Johns Hopkins TB pathologist Arnold Rich lived in a completely different world. In Rich’s world there were no psychiatric hypothetical’s, no diagnoses not verifiable by laboratory reagents and microscopic findings.

Although it appeared that Rich and Kanner worked in completely different arenas, at times they unknowingly touched directly on one another’s work, but never more closely than when Rich began to focus on perinatal infectious disease.

Arnold Rice Rich [1893-1968]. Became Pathologist-in-Chief of the Johns Hopkins Hospital after William Henry Welch. His continued research clarified the pathogenesis of the spread of the tubercle bacilli in the body and revolutionized the concept of the disease “tuberculosis” and its myriad manifestations, culminating in his The Pathogenesis of Tuberculosis, in 1944, revised in 1951 and subsequently translated into Spanish and Japanese.

Rich was a teaching dynamo at Hopkins, completing his authoritative Pathogenesis of Tuberculosisin 1944, with a second edition in 1951. It took him nine years to compile, and still remains a model of what a scientific monograph should be.By  virtue of his astute powers of observation, Rich had always stood out from the rest, even at Hopkins. His name still remains on the lung condition called “The Hamman-Rich Syndrome”, as well as  the small tuberculous masses (tuberculomas) that metastasized, not infrequently, to among other areas, the human brain, and became known as “Rich’s foci”. He was also the first to describe the high prevalence of occult prostate cancer in elderly males, as well as first to describe widespread pulmonary vascular obstruction in children with the hereditary heart condition called Tetralogy of Fallot.During Rich’s tenure, much as in the past, the prevailing emphasis at Hopkins laboratory research was either with the living or recently deceased but the way in which Phipps psychiatry under Meyer neglected its bench work research gave it a somewhat remote character to the rest of Hopkins, preventing closer association.In addition it seemed that Meyer’s protégée, Dr. Leo Kanner was looking only at the very tip of the very same extensive iceberg that John Langdon Down had come to grips with so long ago. When Kanner spoke of an “inborn” condition affecting mentation, Rich, as well as Down previously, had a fairly good idea of what he was speaking about and to Rich it was no more a condition caused by heredity than the nonsensical documents that crossed his desk weekly claiming human TB to be hereditary or caused by the wrong genes.Rich, like Down, knew that TB was the most common cause of death from a single infectious agent in young children and neonates[1] , commonly attacking their central nervous system.[2] The German’s had their own name for childhood tuberculosis, “kindertuberkulose”, and in the many that survived, besides leaving their tiny bodies gnarled, nearly 20-25% manifested mental retardation and psychiatric disorders.[3] And for various reasons many did survive.So until this significant pool of neonates infants and toddlers was fully evaluated for such protean mental complications, Arnold Rich truly couldn’t understand the psychiatrist’s  fussing over “inborn” features of a “psychiatric” disease whether labeled “autism” or anything else that very possibly was caused by organic infection.  It just didn’t make sense.

A neurologist friend had confided in him that Kanner’s autism seemed more like a disease caused by post-encephalitic phenomena than anything else. Rich knew that tuberculosis was fully capable of causing such an encephalitis, described by one pediatric infectious disease specialist[4] as indolent or slow to developand heal, often as painlessly as any other central nervous infection around.

Rich looked up at the picture of William Henry Welch (1850-1934). Welch had been both Rich’s predecessor at Hopkins Pathology, as well as Dean of Medicine  and founder of the Johns Hopkins University Medical School. Welch was unique. Welch was different. He was a mover and a shaker, an organizational genius who would single-handedly  force American medicine up to and eventually beyond what they had in Europe.  A bacteriologist and a pathologist, he would one day be called the Dean of American Medicine. During his watch American life expectancy would jump by at least twenty years. And Welch would be a major factor in that leap.

William Henry Welch, MD [1850-1934] The first dean of the Johns Hopkins University School of Medicine. Often referred to as “the Dean of American Medicine”. He was convinced that the maternal to fetal transmission of tuberculosis was common.

Rich was proud both of the association and to have personally known the physician considered both the father of American medicine and one of its most influential members. Welch had studied in Germany under the great masters, including stints with Koch, Cohnheim, and psychiatrist/neurologist Meynert. Welch therefore full well realized the importance of seeking out diseased tissue in the mentally ill.  Meynert decried those like Kraepelin and Meyer, who seemed preoccupied with labeling symptoms instead of going after the real tissue cause of brain or central nervous system illness.[5] And having also worked with Koch, Welch held a keen appreciation for the destruction, both inside and outside of the mind, that tuberculosis could cause.With regards to the immediate problem in front of him, Rich had read Knoph’s review[6]   in which he mentioned of Welch that: “He too was of the opinion that a direct bacillary transmission, that is to say, prenatal infection (of tuberculosis), takes place much more frequently then believed.”Like Rich, Knoph also knew that few fetal autopsies and exhaustive studies where done to prove fatal tuberculosis on dead fetuses. And those studies preformed had to contend with the fact that tuberculosis, a microbe which grew only with sufficient oxygen, was most often impossible to isolate in the low-oxygen content of fetal blood or tissue. It’s not that TB had any trouble surviving under low-oxygen conditions. It just did so in undetectable forms, causing a diagnostic nightmare.Rich questioned the wisdom of Welch in choosing someone like Adolph Meyer to run Hopkin’s psychiatry. Meyer seemed such a far cry from Hopkins neurologist D.J. McCarthy, previously on staff at Phipps Tuberculosis[7], and an authority on tuberculous of the nervous system in infants and children. McCarthy not only knew that cerebral tuberculosis occurred with much greater frequency in infancy and childhood than realized, but reported a distinct and causative relationship between tuberculosis and adolescent schizophrenia itself. In fact McCarthy’s investigation at Johns Hopkins Phipps tuberculous pavilion  for the mentally ill revealed that practically all of the patients isolated there where schizophrenic.  This seemed particularly relevant when taken in the light of Lauretta Bender’s argument that children with autism generally grow up to have schizophrenia anyway. [Ibid]Although eventually the term “childhood schizophrenia” was displaced altogether, there were nevertheless some children who displayed both the early-appearing social and communicative deficits characteristic of autism and the emotional instability and disordered thought processes that resembled schizophrenia.Rich wondered if either Kanner or Meyer had as extensive a knowledge of the infectious orientation of German psychiatry as did pathologist William Henry Welch, who once walked with its giants.

REFERENCES:

1.  Walia R Hoskyns W Tuberculous meningitis in children: problem to be addressed effectively with thorough contact tracing Eur J Pediatr. 159(7):535-8 2000 Jul

2.  Weaker NJ Jr Connor JD Central nervous system tuberculosis in children: a review of 30 cases. Pediatr Infect Dis J 9:539-543 1990

3.  Garg PK tuberculosis of the central nervous system. Post grad Med J 75:133-40 1999

4.  Gutierrez KM, Prober CG Encephalitis Postgraduate Medicine 103(3): 123-5, 129-30, 140-3 March 1998

5.  Meynert T Uber die Nothwendigkeit und Tragweitge einer anatomischen Richtung in der Psychiatrie Wiener Medizinische Wochenschrift, 18:573-76, May 1868

6.  Adolphus Knoff,   The Period of Life At Which Infection From Tuberculosis Occurs Most Frequently, The American Journal of Public Health, pp. 934-952, Sept, 1915).

7.  McCarthy D.J.    Tuberculous Affectations of The Nervous System In Infancy and Childhood in Tuberculosis in Infancy And Childhood Ed. By T.N. Kelynack, MD. William Wood and Company pp. 376,  p.43-54, 1908.

 

 

Psychiatric Asylums on the European and American continent, late Nineteenth Century

When Johns Hopkins pathologist William Henry Welch studied under psychiatrist Maynert, it was in the late nineteenth century, a time during which there was fear that tuberculosis would destroy the entire civilization of Europe. It was also the time that the first massive increase in psychiatric illness and confinement to mental asylums occurred.[1]

And although there was a sociological shift of patients going from family care and poorhouses to 19th century asylums, this in itself could not account for the inexorable increase in asylum census. To distinguished psychiatrist/writer E. Fuller Torrey, severe psychiatric illnesses, such as schizophrenia are comparatively new diseases, less than 250-years-old, the confinement for which, even as a college student, reminded Torrey of the tuberculosis sanitariums of a slightly earlier era.[2]

The upward spiral had became obvious. By 1884, in Germany, Karl Kahlbaum, perhaps the most underrated psychiatrist in history, and the true  originator of American outcome based psychiatric classification, first described schizophrenia as a separate entity. Kahlbaum: “It must be the experience of all psychiatric institutions that the number of youthful patients has recently undergone a considerable increase”.[3][4]  It was between  1700 to 1900 that tuberculosis was responsible for the deaths of approximately one billion (one thousand million) human beings. The annual death rate from TB when Koch discovered its cause was an incredible seven million people per year.

During this time frame there was no autism as understood by Leo Kanner, just the autism Bleuler used to describe schizophrenia.

There  were others who also saw this 19th century ground-swell of mental illness as representing something new, including auditory hallucinations, as never witnessed before. Historians like Hare and Wilkins, among others, point out that it was only then that schizophrenia, with its a hallucinations and delusions, was really even mentioned, representing no small part of the late Nineteenth century psychiatric flare-up.[5][6]

Almost unheard of in the medical literature before this, chronic delusions and hallucinations – such as hearing voices, became common in asylum admissions at the same time Clouston, by 1892, was documenting them in mental illness as a result of a killer pandemic of tuberculosis.[7]

Max Jacobi, the originator of the school that infectious illness led to mental illness, was the first to ascribe characteristic symptoms for this associated with tuberculosis[8].  Just as autism was thought to be a disease of “affect” by Kanner, Jacobi in particular considered an unpredictable, emotional (affective) changeability as characteristic and at times even diagnostic for latent, undiagnosed TB.

Incredibly Greding[9],  found pulmonary tuberculosis during autopsy in 70% of mental defectives and in 50% of the mentally affected with seizure disorders. Seizures, not uncommon in autism, occur in 20-30% of its patients based on the majority of studies.[10]

Barr would talk about the relationship between tuberculosis and mental defectiveness at the 6th International Tuberculosis Congress held in Washington in 1908[11][12].  There Jacques Moreau expressed his belief that epilepsy and the convulsive disorders were derived from tuberculosis. A year previously, Anglade spoke not only on how tuberculosis caused epilepsy in infants and the young, but how such epileptics eventually became mentally defective through sclerotic brain changes caused by the disease.[13]

Subsequently Baruk discovered that when either proteins extracted from tuberculosis, or the spinal fluid taken from schizophrenics were introduced into healthy animals, a condition occurred where the body and its functions seemed frozen in time, called catalepsy. Catalepsy is not only associated with one form of  schizophrenia but  with epilepsy itself.[14]Patients with catatonia, an extreme form of withdrawal in which the individual retreats into a completely immobile state, can also exhibit catalepsy. Wing[15] related in 2000 that the incidence of catatonia could be as high as 17% in adolescent autistics.

Historically prominent Viennese pathologist Ernst Löwenstein decided to take things a step beyond. Having developed a potato flour and egg based tuberculosis growth media, still very much with us, he set about to prove that TB could be cultured from the blood of patients with “schizophrenia”.[16]  Yet despite 9 independent confirmative studies finding either the  tuberculosis bacillus itself or it’s much harder to stain yet commoner viral forms, other studies appeared which couldn’t confirm these results . Whether this was from defective laboratory procedure, especially when dealing with difficult to stain and culture viral (or cell-wall-deficient forms) of tuberculosis, to this day remains a possibility.

Undeterred and In answer to these negative studies, Weeber[17], Melgar[18], and Lowenstein himself[19]  again found tuberculosis in the blood of schizophrenic patients in studies, which to this day, remain unaddressed.

 

___________________________

 

As far back as 1769, Scotsman Robert Whytt [20], reporting on approximately 20 cases, described the localization of tuberculosis in the meninges,  membranes which cover the brain and spinal cord. Realizing that the localization of tuberculosis there was often associated with mental disturbances, Whytt thus gave us the first description of tuberculous meningitis, at that time called morbus cerebralis Whyttii.  In describing the disease, Whytt noticed not only small masses called “tubercles” in the brain tissue, but hydrocephalus, an excess of ‘water in the brain’.

There is a circulating duct system of fluid in the brain and spinal cord. Just as the brain has a covering called the meninges, these membranes manufacturer and contain a cerebrospinal fluid which later circulates through channels of deep cisterns in the brain and then down the spinal cord. A block in this circulation, whether from a congenital condition or disease, can lead to an increase of cerebrospinal fluid around the brain. In the case of infants and young children, because the bones of their skulls are still unfused, this can result in an enlargement of the head. No matter the age, mental disturbances and even retardation can result as complications of such ‘hydrocephalus’. So intertwined was hydrocephalus with tuberculosis, that medical experts, by the end of the 19th Century, considered acute hydrocephalus as just another name for tuberculous meningitis.[21]

Since 1854, Wunderlich had recognized psychotic episodes, including schizophrenia, could be caused by small masses of tuberculosis (“tubercles”) in the brain.[22] But as time passed, it became more obvious, just how commonly. The tubercles of tuberculosis, which often themselves formed masses called tuberculomas, were  launched through the bloodstream to the brain, and often found in infants and humans with no neurologic symptoms. But Marie documented symptomatic cases of tubercles as a cause of psychosis such as schizophrenia.[23]

TB meningitis was just the tip of the iceberg, and other investigators, as early as in 1908, uncovered  a more generalized inflammation of the brain matter, tuberculous encephalitis “as also being behind specific psychosis[24]So the term tuberculous  “meningoencephalitis” was considered more accurate than just tuberculous meningitis.

 

REFERENCES:

1. Torrey EF Severe Psychiatric Disorders May be Increasing. Psychiatric Times 19:4  2002, April

2. E. Fuller Torrey, M.D., and Judy Miller. The Invisible Plague: The Rise of Mental Illness from 1750 to the Present. Piscataway, New Jersey, Rutgers University Press, 2—2. xiii, 416 pp.

3. Kessler, Ronald C, Archives Of General Psychiatry 1994

4.  Kessler RC McGonagle KA  Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry. 1994 Jan;51(1):8-19, p.12

5.  Hare, E. (1983) Was insanity on the increase? BMJ, 142, 439 –445.

6.  Wilkins R Hallucinations in Children and Teenagers Admitted to Bethlem Royal Hospital in the Nineteenth Century and Their Possible Relevance to the Incidence of Schizophrenia Journal of Child Psychology and Psychiatry 28:569-80 1987

7.  Clouston TS Phthisical insanity, in History of Psychiatry 2005Dec 64(4): 479-95

8.   Jacobi M Annalen der Irrenheilanstalt zu Siegburg. Köln, Dumont & Schauberg, 1837 pp.26, 63

9.  Greding J Sämmtliche medicinische Schriften C.W. Greding, Ed. Greiz, Henning, 1790  vI:277-350; II:145-162, 327-33

10.  Kagan-Kushnir T Roberts W Snead C Screening Electroencephalograms in Autism Spectrum Disorders: Evidence-Based Guideline J Child Neurol March 2005 vol. 20 no. 3 197-206

11.  Barr MW The relationship between tuberculosis and mental defect 6th Internat. Congr. Tuberc. Washington 1908. Philadelphia, Fell, 1908 (III, p. 88).

12.  Barr MW The relation between tuberculosis and mental defect. 6th Internat. Congr. Tuberc. Washington 1908. Philadelphia, Fell, 1908 (III, p. 88

13.  Anglade and Jacquin, Hérédo-tuberculose et idioties congénitales. Encéphale, 1907, 1, 136-57

14.  Baruk H Psychiatric , Paris, Masson, 1938 (pgs. 202, 292, 865

15.  Wing L, Shah A. Catatonia in autistic spectrum disorders. Br. J. Psychiatry. 2000;176:357-362

16.  Löwenstein E Das Vorkommen der Tuberkelbazillämie bei verschiedenen Krankheiten. Münch. Med. Wschr., 1931,78, 261-263

17.  Weeber R Ueber Blut- und Liquorbazillose. Wien. Med Wschr., 1937, 87, 285-6,

18.  Melger R Tuberculosis y psicosis Rev. Asoc. Méd. Argent.,1943, 57, 1061-4

19.  Lowenstein E Tubercle bacilli in spinal fluid. J.  Nerv. Ment. Dis., 1945, 101, 576-82

20.  Whytt R Observation on the dropsy of the brain. Edinburgh, Balfour, 1768 pp.1-48

21.  Chisholm H Encyclopedia Britannica Cambridge University Press 1911

22.  Wunderlich C.A. Handbuch der Pathologie und Therapie Stuttgart, Ebner & Seubert, 1854 II, 2 p. 1638

23.  Marie A Tuberculose et psychose. Bull. Soc. Méd. Paris, 1930, 2, 457-461

24.  Lépine J. Tuberculose-encephalite. Psychoses. 6th Internat. Cong. Tuberc. Washington, 1908. Philadelphia, Fell, 1908, vol.1, pt.2 p.1076

 

Department of Pathology John’s Hopkin’s 1948

Arnold Rich was working on a problem which might have major implications towards Kanner’s child psychiatry but he was having a problem with regards to the frequency of maternal to fetal transfer of tuberculosis.[1]It was an issue with seminal significance in addressing Down’s “developmental disorders”, of which autism was a subset. It was also a matter which had been addressed by some of the greatest minds in medicine.

On the one hand Rich knew that: “It is now well established that tuberculous infection can be transmitted from mother to fetus through the placenta.”  He references Warthin[2] in The Journal of Infectious Diseases, who said it was commonand then Siegel‘s study[3] in the American Review of Tuberculosis.  Siegel documented infants that had died from the disease one or two days after birth. Husted’s study[4] even included tuberculous stillbirths.

Dr Aldred Scott WARTHIN, MD (1866-1931) Head of Pathology at the University of Michigan, Ann Arbor. Warthin saw that fetal tissues were relatively immune to the action of the tubercle bacillus. Yet such infection was transmitted through the placenta, even in mothers without signs of infection to her fetus. This created a situation where a truly latent tuberculosis was both possible and probable, with tissue changes developing some time after birth, and at a rate “much more frequently than is generally supposed.”

But to further establish the importance of a link between maternal and perinatal tuberculosis, Arnold Rich would go into the numbers involved in the general population. Of all the infectious diseases TB was and always has been a disease of alarmingly large numbers.

Even since Norris’s original review, it had been known that for some reason pregnancy, especially late pregnancy, and child bearing itself dangerously reanimated any form of tuberculosis in a woman’s body, no matter how silent. Thus in the first half of the twentieth century, the method of choice was early termination of pregnancy in the tuberculous mother.[5]   Menstruation itself had a similar deleterious effect, causing its own flare-up of tuberculosis in the body.

One of Warthin’s tissue mounts. The transmission of the tubercle bacilli to the fetus from a mother with unrecognized, latent STEALTH tuberculosis with no maternal symptoms. Two miliary tubercles (see the two pale discreet almost circular areas) have formed in the placenta, brought there through the maternal bloodstream [A.S. Warthin, MD, Ph.D. “Miliary Tuberculosis of The Placenta JAMA Vol LXI, No. 22 1951-52].

The numbers in front of Rich were incredible.In a disease that according to the World Health Organization consistently kills more women of childbearing age than any other[Ibid], the age at which female tuberculosis mortality began to rise above male mortality coincided with the average age of  the onset of female menstruation. But the age at which it really surpassed that of males coincided with the period during which over two-thirds of all pregnancies occurred.Rich conservatively estimated that a little over 2 million woman between 18-30 were pregnant in 1940. And since the total US population for woman of this age was approximately 17,700,000, it followed that 1 out of every 8 women in the United States was pregnant in this age range and 1 in 10 bore living children. This produced a pool of 200,000  opportunities to not only reanimate dormant and often undiagnosed maternal tuberculosis, with its drastically increased female mortality rate, but, with such reactivation, the possibility for the transmission of that disease to the fetus and new born.In such a reanimation of latent tuberculosis, it was also striking that TB meningitis, infrequent  in adults, frequent in infants and toddlers, seemed to noticeably increase in child-bearing women from the reactivation of old deposits of cerebral tuberculosis.[6]Rich already realized that regarding TB’s fatality in the neonate, infant and early childhood  there was a definite pattern. Tuberculosis was definitely most fatal during the first year or two of life. After the second year, the death rate for infected toddlers fell markedly, probably through a decidedly greater ability to form protective antibodies between 2 and 5 then in infancy.[7]  Though the disease was still deadly for the remainder of the first 5 years, by far the safest period was that between 5 years and puberty where the death rate from TB drastically plummeted.  Often termed the ‘Golden Age of Resistance’, for some reason children between 5 and 15 are more resistant to TB than adults, and, above all infants.  It was an interesting fact, creating a possible theoretical underpinning for Bender’s assertion as to how autistic involvement in the very young, hardest hit in the first 30 months, could come back as a related schizophrenia with adolescence, towards the end of the ‘Golden age of Resistance”.There was a time when it was felt that newborns were completely devoid of resistance[8]to tuberculosis. But there  had since been sufficient studies to completely contradict this. In Braily’s study[9] at Rich’s own Johns Hopkins Hospital, of 65 infants who became tuberculin positive during the first year of life, two-thirds were alive and well at the end of five years. So the acquisition of tuberculosis by infants was not necessarily a death sentence. However its complications, including those involving the brain and nervous system,  could soon impact the individual for the rest of his or her life.

As to whether a tuberculous focus in the brain killed, Rich would soon find,  would be something that he could only refer accurately to as what card players call “the luck of the draw.”

It is not generally appreciated that the development of small rounded nodules caused by tuberculosis, sometimes cheesy or “caseous” in the brain is a relatively common occurrence in children and childhood tuberculosis. It is usually symptomless. Such small nodules often then become arrested and encapsulated by the body’s immune system. They are, to this day, called “Rich’s Foci”.  Many of us unknowingly have them.

But, stressed Rich, it was when small tubercle nodules happened to land in that part of the surface cerebral cortex near the meninges, or covering of the brain, no matter how small in size, that serious troubles began. Such infectious nodules often extended into this protective covering  through which fluid (cerebrospinal fluid) percolates on its journey through the brain and into the spine. Such a discharge of tuberculosis into the spinal fluid of the meninges (in its subarachnoid space), can lead and often does, to potentially fatal meningitis. The disease festers and is spread throughout the central nervous system. There need not be extensive infection, just one tiny nodule in the wrong place, near the meninges.

On the other hand, the development of small tubercles deeper in the brain substance, though relatively common, often gave rise to no symptoms whatsoever. Rich himself had seen one inch tuberculous masses, lodged in a silent area of the brain, yet entirely harmless.

A severe hypersensitivity reaction to tuberculoprotein could also occur in any tissue in the body, including the brain, in infants already hypersensitized to tuberculous protein while in their mother’s womb. Burn and Finley[10] showed damage and death of cells as well as acute inflammation in the meninges in such instances. The inflammation that resulted required no TB bacilli, just the sustained diffusion of the protein of the tuberculosis bacilli  or its active split products through the placenta into a previously sensitized infant.

Through it all, one thing was certain. Tuberculosis did not always kill. That infants could survive even a massive dose of tuberculosis was amply demonstrated in the tragedy called the Lubeck episode[11]. At Lubeck, of 251 infants mistakenly injected with large numbers of virulent human tubercular bacilli, incorrectly thought to be the TB vaccination called BCG, 71.3% survived.

The number of possible complications in those infants and children that survived TB’s onslaught, including those to the brain and nervous system, Rich knew, would be enough to keep symptom-based psychiatry perturbed and under siege for some time to come.

REFERENCES:

1.  Rich AR The Pathogenesis of Tuberculosis Chas C Thomas Publsh. Springfield Illinois, 1946

2.  Warthin AS Cowie DM A contribution in the casuistry of placental and congenital tuberculosis. Journ. Inf. Dis. 1:140 1904

3.  Siegel M Pathological findings and pathogenesis of congenital tuberculosis Am Rev Tuberc 29:297 1934

4.  Husted E Un cas de tuberculose millaire congenitale Acta Path et Microbiol Scand Supp 16:163. 1933)

5.  Kobrinsky S Preganancy and Tuberculosis Canad. M.A.J. Nov. 1948 vol. 59; 462-4

6.  Whitney JS Facts and Figures About Tuberculosis Natl. Tuberc. Assn 1931

7.  Halber W Hirszfeld H Untersuchungen uber die Antikorperentstehung bei Kindern im Zuzammenhang mit dem Alter Zeitschrift. F. Immunitatsf., 1927, 53, 391

8.  Cummins SL Tuberculosis in primitive tribes. Internat. Jour. Pub. Health 1920, 1, 137

9.  Brailey M Mortality in tuberculin positive infants. Bull. Johns Hopkins Hosp., 1936, 59,1

10.   Burn CG Finley KH The role of hypersensitivity in the production of experimental meningitis Journ. Exp. Med. 1932, 56, 203

11.   Die Sauglingstuberkulose in Lubeck. Arbeit. A. d. Reichsgesndhtsamte. 1935, 69

 

Penn State Department of Psychology, 1949

But Psychiatry was already under siege. In 1949, psychologist Philip Ash, in a University of Pennsylvania postdoctoral dissertation, proved that three psychiatrists faced with a single patient, and given identical information at the same moment in time, were able to reach the same diagnostic conclusion approximately twenty per cent of the time.[1] Subsequently, Aaron T. Beck, one of the founders of cognitive behavioral therapy, published a similar study in 1962 [2],which although it found psychiatric agreement a bit higher, at between 32% and 42%, still left its doubts regarding the reliability of a psychiatric diagnosis.

Added to this came the The Rosenhan experiment[3], a well known probe into the validity of psychiatric diagnosis conducted by Stanford psychologist David Rosenhan in 1972.

Dr. David L. Rosenhan (1929 – February 6, 2012) was an American psychologist best known for the Rosenhan experiment, a study challenging the validity of psychiatric diagnosis.

Published in  Science and entitled “On being sane in insane places“, Rosenhan’s study consisted of two parts. The first involved the use of mentally healthy associates or fake patients, who briefly pretended auditory hallucinations in an attempt to gain admission to 12 different psychiatric hospitals in 5 different US states. All of these mentally healthy persons were admitted and diagnosed with psychiatric disorders. All were also forced to admit they had mental illness and to take antipsychotic drugs as a condition for their release.

The second part of Rosenhan’s experiment involved asking staff at a psychiatric hospital to actually detect  “fake” patients in a group that was all mentally ill. No fake patients were sent in this Phase II of the Rosenhan experiment, yet staffs at various institutions falsely identified large numbers of actual mental patients as pretenders.

The study was considered an important and influential criticism of psychiatric diagnosis. Rosenhan concluded “It is clear that we cannot distinguish the sane from the insane in psychiatric hospitals”. It also illustrated the dangers of depersonalization and the mere slapping on of a label that goes on in these institutions. [Ibid]

As a result of such intrusions, the American Psychiatric Association (APA), in 1973, asked psychiatrist Robert Spitzer to chair a classification task force to try to thrash out more precise medically oriented parameters. The problem was that such a classification would still be symptom or syndrome focused. The end result was a  classification manual, along the lines of Emil Kraepelin’s rejuvenated ideas, entitled the Diagnostic and Statistical Manual of Mental Disorders (3rd ed.) or DSM-III.[4] Though DSM-III was indeed more reliable [5] than its predecessors, it still offered no clear definition of the cause of the many different “mental illnesses” it defined.

Without causes, the mere categorizing of psychiatric diseases did not mean that they were valid to begin with, and not the result of direct physical illness. The APA admitted it had no idea of what caused its manual’s supposed “mental” illnesses, while at the same time it felt completely confident in its ability to diagnose and “treat” them.

“The Diagnostic and Statistical Manual” (DSM), Paul McHugh, then Chair of Psychiatry at Johns Hopkins said, has “permitted groups of ‘experts’ with a bias to propose the existence of conditions without anything more than a definition and a checklist of symptoms. This is just how witches used to be identified.” [6]

REFERENCES:

1. Spiegel A The Dictionary of Disorder New Yorker 56-63 2005 Jan

2.  Beck, A. T. (1962). Reliability of psychiatric diagnoses: A critique of systematic studies. American Journal of Psychiatry, 119, 210-216

3.  David L. Rosenhan, “On Being Sane in Insane Places,” Science, Vol. 179 (Jan. 1973), 250-258.

4.  American Psychiatric Association (APA) Diagnostic and statistical manual of mental disorders (3rd ed.). Washington, DC: American Psychiatric Association 1980

5.  Hyler, S. E., Williams, J. B., & Spitzer, R. L. (1982). Reliability in the DSM-III field trials. Archives of General Psychiatry, 39, 1275–1278

6.  McHugh Psychiatry Research Reports The American Psychiatric Association. Division of Research. Summer 2001)

 

Johns Hopkins Department of Pathology 1949

Rich knew of numerous cases where the human placenta was infected in tuberculous mothers and readily admitted that infection could easily pass from mother to fetus. But it was in the frequency that he could find the disease reaching  fetal tissue, limited by the diagnostic capabilities of his time, that Rich would have to speak of TB’s transfer from the placenta to the fetus as “rare”. William Henry Welch, who besides being a pathologist like Rich was also a bacteriologist, never would have agreed.

Welch was already on record[1] that the mere inability to pick up TB in the fetus or newborn wasn’t an argument against frequent transmission to them. There were just too many factors involved, such as the hostile low oxygen of fetal blood which could tame even the most virulent TB bacilli for some time, making diagnosis difficult to impossible.

It wasn’t only Welch that Rich put himself at odds with. German investigator Baumgarten who saw infection of the fetus by the spores of TB coming from the maternal placenta as a common occurrence.[2] In fact, to Baumgarten , all tuberculosis, including neurotuberculosis, was most commonly acquired in the womb, in utero, in most cases, though there remained a  lesser possibility, that it could occur through infected sperm.

Ophuls mentioned that it was a well established fact that the semen of tuberculous individuals contains tubercle bacilli, even in the absence of genital TB.[3]  It was obvious then that the ovum from which the fetus will develop could also become infected. Kobrinsky cites Sitzenfrey as having “demonstrated the presence of bacilli in the interior of the ovum while still within the Graafian follicle”.[4] Friedmann, carefully studying the possibility in rabbits, concluded: “It should be regarded as proved that tubercle bacilli can enter the fertilized egg cell, that the latter does not perish as a result of the invasion, but may develop into a well-formed animal. In addition, the bacilli transmitted in this way may still be present in certain organs of the newborn.”[5] And among these organs were the brain and the central nervous system.

That tuberculosis is a sexually transmitted disease is a certainty. By 1972, Rolland[6]   wrote Genital Tuberculosis, a Forgotten Disease? And  in 1979, Gondzik[7] and Jasiewicz showed that even in the laboratory, genitally infected tubercular male guinea pigs could infect healthy females through their semen by a ratio of 1 in 6 or 17%. This prompted him to warn his patients that not only was tuberculosis a sexually transmitted disease, but also the necessity of the application of suitable contraceptives, such as condoms, to avoid it. Gondzik’s statistics are chilling; his findings significant. Even in syphilis at its most infectious stage, successful transmission in humans was possible only in 30% of contacts.

Schmorl’s work supported Baumgarten and Welch’s contention of routine tubercular transmission to the fetus through the placenta. Schmorl’s work again showed that indeed, tuberculous infection of the placenta in tuberculous mothers was much more common than formerly believed.[8]

But perhaps all of this work was upstaged by Leon Charles Albert Calmette at Pasteur.

REFERENCES:

1.  Welch WH  Papers and Addresses Vol. 2 Bacteriology, The Johns Hopkins Press, Baltimore, 1920 p.47

2.  Baumgarten P Ueber die Wege der tuberkulosen Infection. Zeitschrift. F. klin. Med., 6:61 1883

3.  Ophuls W Routes of Infection in Tuberculosis California State Journal of Medicine Vol XIV, No. 7 pp. 272-276 July, 1916

4.  Kobrinsky S Preganancy and Tuberculosis Canad. M.A.J. Nov. 1948 vol. 59; 462-4

5.  Friedmann: Experimentelle Beitrage zur Frage kongenitaler Tukerkelbazillenubertragung und kongenitaler Tuberkulose. Virch. Arch., 1905, clxxxi,150

6.  Rolland R., Schellekens L. Genital tuberculosis, a forgotten disease. Ned Tijdschr Geneeskd 1972; 116(52): 2377–2378.

7.  Gondzik M., Jasiewicz J. Experimental study on the possibility of tuberculosis transmission by coitus. Z Urol Nphrol 1979; 72(12): 911–914.

8.  Schmorl: Zur Frage der Genese de Lungentuberkulose. Munch. Med. Woch., 1902, il, 1379.1419

Institute Pasteur, Paris France, February, 1933

Calmette was on to something.

He had confirmed that TB’s attack form going through the virtual filters of the placenta into fetal blood was viral, filter passing forms of tuberculosis. These were not being picked up by Rich’s traditional TB stains or cultures. Nevertheless, they were responsible for wasting and death,[1] even while traversing a perfectly normal placenta.[2]

Léon Charles Albert Calmette Born July 12, 1863 Nice, France – Died October 29, 1933 (aged 70) Paris. Served as Director of the Pasteur Institute. Together with Valtis and Lacomme, concluded the frequent transmission of tuberculosis, in its stealth filterable forms. from mother to fetus. Calmette also was of the belief that even just an acute febrile episodes from reactivated TB in an expectant mother was capable of breaking down the barrier effect of an otherwise normal placenta. In JAMA, Myers supports Calmette, saying “it is possible that a greater number of children are infected before birth than we had ever suspected”, and furthermore that “in fact, a considerable number [of such infants] make good recoveries”.

In going against the grain of a scientific research such as that done by Pasteur’s Leon Charles Albert Calmette, Johns Hopkins Rich, for all his authority regarding the pathogenesis of tuberculosis, was skating on thin ice.Since its founding on June 4, 1887, the Pasteur Institute, for over a century, was a beacon for research.  HIV, tuberculosis, polio and the plague had all been probed. In addition, since 1908, eight Pasteur scientists had received the Nobel Prize for medicine. It was while working in Pasteur, that Calmette developed the world’s first and to this day, only, recognized vaccine for tuberculosis, the BCG.Calmette was fully aware of the void that Robert Koch, the discoverer of tuberculosis, had left for future scientists. Koch had done it on purpose. A confirmed monomorphist, Koch insisted that the TB bacilli had only one form which caused disease. Extremely influential, Koch moved to make certain that his operatives kept this view as the one most scientists, to this day, have adapted.

During the original presentation of his discovery, Koch isolated TB from a total of 33 cases, including patients with bloodbourn tuberculosis, as well as tuberculosis of the brain. In Berlin, towards the end of the 19th century, tuberculosis was the number one killer. Of all deaths, the death of every third newborn and of almost every second adult aged 25–40 – were caused by tuberculosis. In collaboration with Dr. Max Birnbaum, nine years after discovering the tubercle bacilli, Koch writes a little known treatise describing, among other things, forms of social withdrawal in tuberculous children with central nervous system involvement.

Koch knew better. Bacteria and mycobacteria certainly could have more than one form. With Almquist, he had observed different forms of typhoid in the blood of its victims. Nevertheless Koch would now began an intensive campaign to seize and rule the scientific and lay mind that “legitimate” tuberculosis only assumed, one form. Thus Brock[3] points out that despite the fact that Koch was a first-rate researcher, a keen observer and an ingenious technical innovator, he went from an “eager amateur” country doctor to “an imperious and authoritarian father figure whose influence on bacteriology and medicine was so strong as to be downright dangerous”. And nowhere, according to Brock, was Koch a more dangerous and “opinionated tyrant” than in his rigid insistence on monomorphism, the idea that microbes could assume one truely infectious form and one form only. Yet Klebs[4], who actually examined Koch’s own tubercular cultures, wrote otherwise. In addition to the traditional rods in Koch’s culture plates, spherical forms were regularly found, as well as branching, slender filamentous, and granular forms. Many of these could actually pass a filter and therefore be interpreted as being “filterable viruses”.

Koch’s one-form rigidity wasn’t making friends. There was widespread opposition from others who sensed his lack of evidence. They gravitated towards the more realistic, better documented theories of Nageli and Max von Pettenkoffer,  which showed that bacteria change forms as they evolve. Nageli and von Petterkoffer’s view retained wide support almost to the turn of that century. Koch reflexively opposed Nageli’s ideas as soon as he heard them. Much of Koch’s clash with Pasteur was also based on Pasteur’s discovery of variability among microbes. In that scuffle, mentions Brock, Koch could at times be so personally vicious as to be shocking.

Vicious or not, by 1939, bacteriologists Vera and Rettger[5] of Yale were contradicting him. Vera: “The single point on which all investigators have agreed is that the Koch bacillus does not always manifest itself in the classical rod shape. While at times and most commonly the organism appears as a granular rod, coccoid bodies, filaments and clubs are not rare.”

To marginalize such thought, Koch and his followers, to this day, have banished all forms except one to the wastebasket hinterland of “involutional”, or “degenerative” forms of the mycobacteria. They didn’t count. No matter how many studies showed that all of these forms could regenerate to the classical TB rod.  Koch and his minions thus somehow prevailed. To Brock, Koch and his cohorts represent a prime instance of the excessive influence of a “cult of personality”.  The problem was that someone somewhere down the line would have to pay for such cult generated ignorance.

Let it be said to their credit that, from the onset, the French saw right through Koch. Tuberculosis had many forms, including a filterable viral-like stage in its growth cycle. Although Fontes[6] was the first to document these, Macjunkin[7] and Calmette soon followed. Again and again, either cultures or extracts of organs from tuberculous victims, after thorough filtration through Chamberlain L2 Filters, produced tuberculosis when injected into experimental animals. And importantly, such forms passed right through the placenta from mother to fetus.

Some animals injected with viral, filter passing TB might appear normal during the time of observation, but when tested with tuberculin showed positive tuberculin skin tests beginning approximately 25 days after being injected with tubercular tissue or microbes. Other animals lost weight rapidly. And some died of a rapid progressive infection. It all depended upon the virulence of the filterable TB being used.[8]

In a series of 21 dead infants, born to tuberculous women, Calmette, along with Valtis and Lacomme concluded that their observations proved the frequent transmission of tuberculosis from the mother to the fetus by means of filterable forms of tuberculosis. At the same time Calmette established that such viral forms of tuberculosis were in the spinal fluid of perinatal meningitis.[9]

It would take time until mainstream microbiology would  be forced to even acknowledge such viral forms. It would take a Nobel nominee by the name of Lida Holmes Mattman.

REFERENCES:

1. Calmette A Valtis J Les éléments virulents filtrables du bacille tuberculeux.
Annales de médecine, 1926, 19: 553-560.

2. Calmette A Valtis J Lacomme M Transmission Intra-Utérine Du Virus Tuberculeux de la Mère à L’enfant. Comptes rendus hebdomadaire des séances de l’Académie des Sciences, Paris, 1926 , 183: 835-837. Presse Médicale, 1926,90:1409

3. Brock Thomas D Robert Koch – A Life in Medicine and Bacteriology ASM Press pp. 392,  January,1999 p.4

4.  Klebs E Weitere Beitrage sur Geechichte der Tuberkulose. In: Arch F. Exper. Pathol u. Pharmacie, v 17, No. ½, pp.1-52 m. 3 Taf. 1883

5. Vera HD Rettger LF Morphological Variation of the Tubercle Bacillus and Certain Recently Isolated Soil Acid Fasts, With Emphasis on Filterability J. Bacteriology 1940 June; 39 (6) 659-687

6.  Fontes ann. De l’inst. Oswaldo Cruz, 1910

7.  MacJunkin, F. J. Exper. Med., 33:751, 1921

8.  Arloing F  Dufourt  Presse med. January 5, 1927, p. 17

9.  Calmette A Tubercle Bacillus Infection and tubercujlosis in Man and Animals, Williams & Wilkins Baltimore 1923) (Calmette A Valtis J. Virulent filterable elements of the tubercle bacillus Ann. Med. 19:553 1926

Pathology Lab of Arnold Rich, Johns Hopkins 1950

There was a struggle going inside the mind of Arnold Rich, and its implications would affect Western medicine for decades to come. Under variations in the forms TB can assume, Rich’s words don’t always  match his conclusions. He concedes that depending upon the type of culture plate that tuberculosis is incubated on the shape of the organism changes, partly because of culture medium, partly because of the age of the culture itself. Even the conditions under which this growth occurs, such as temperature and amount of oxygen figured in. He emphasizes that non-acid fast stainingrods may be present, especially in young cultures, whereas in older cultures and  infected tissues, “beaded forms” were common.

Koch had noticed these beaded forms.  Somewhat granular and protruding from stalks, Koch felt them to be potential “spores” through which infection could be propagated.  But Koch was unable to observe the granules break off into separate segments.

Much[1], on the other hand, for decades, not only watched the granules break off (“Much’s granules”), but regenerate into classical TB bacilli. Much was also able to document that they weren’t always acid-fast, and that this could be why they had not been recognized as the spores of what would, with time, again become the acid-fast staining TB bacilli microbiologists looked for.

Then there was  M.C. Kahn’s work. Kahn, using ideal technique[2], described, in the most precise manner, his direct observations of the actual growth of minute filter-passing granular forms of TB into fully developed and virulent bacilli, capable of independent proliferation and producing progressive tuberculosis.

Whether granular or otherwise, such viral-like or cell-wall-deficient (CWD) forms of tuberculosis, often mistaken for mycoplasma,  are today widely known as “L-forms“, named after the Lister Institute by  one of its scientists, Emmy Klieneberger[3],   L-forms are cell-wall-deficient by virtue of a breech in their cell wall which allows them the plasticity to assume other forms including granular forms.

Little recognized in Rich’s time, L-forms of tuberculosis have since even been found in mother’s milk.[4]

Rich, working in the 1940’s wanted to believe very much in these viral forms of tuberculosis. They explained the many times that he knew he was dealing with tuberculosis but could not, even as a pathologist see the germ. Nevertheless, this knowledge, relatively new at the time, was not substantiated enough. After all, Kahn had observed the transformation of granular forms to mature bacilli in vitro, in a culture plate. This did not mean to Rich that every TB bacilli once in humans had to go through this same cycle in its reproduction.  So, despite Kahn directly assuring him by personal communiqué that he had solidified his findings in vivo, in laboratory animals, Rich was not ready to acknowledge granular “viral” cell-deficient forms of tuberculosis, which were key to the mystery of how certain forms of TB sieved through the placenta’s chorionic villi into the fetus, escaping detection.

Rich’s statement that in certain cases, even when the maternal placenta was laced with TB bacilli  “acid-fast stains of a large number of sections of the fetal tissues failed to disclose  a single bacillus” was correct. Welch had predicted it. The viral cell-wall-deficient forms could only be picked up by special stains, cultures and techniques which Rich had no access to.

In the meantime Rich’s hypothetical statement of “rare” transmission was having difficulty. Many infants were reacting to the TB skin test weeks to months after birth, even without known exposure after birth.

REFERENCES:

1. Much H Uber die granulare, nach Zieh nicht farbbare. Form des Tuberkulosevirus.    Beit. Z. Klin. D. Tuberk., 1907, 8, 85, 357

2. Kahn, MC The developmental cycle of the tubercle bacillus as revealed by single cell cultures. Am. Rev. Tuberc., 1929, 20, 150

3. Klieneberger- Nobel E.   Origin, development and signifincance of L-forms in bacterial cultures. J Gen Microbiol 1949; 3: 434–442

4. Garvin DF L forms isolated from infection in Microbial Protoplass, Spheroplasts and L Forms Guze LB, Ed Williams & Wilkins Baltimore pp.472-483 1968

 

The Department of Biological Sciences at Wayne State University in Detroit, Michigan, 1982

The answer to the discovery of how to unravel the mechanism behind autism and a host of other diseases of unknown cause lay in a doctor named  Lida Holmes Mattman.

Lida Holmes Mattman [1912–2008] Once the director of laboratories for the United Nations, Mattman joined the faculty at Wayne State University in 1949. She also taught at Harvard, Howard Hughes Institute and Oakland University. Mattman taught and used a new method to diagnose tuberculosis in 72 hours. Conventional methods took three to four weeks. Her book, Cell Wall Deficient Forms: Stealth Pathogens, Third Edition describes these techniques, recruiting methods widely used abroad. By 2001 Mattman concluded that “there is little doubt that the minute filterable forms of bacteria move from the mother’s capillaries to those of the fetus.” But what really troubled her, in the case of tuberculosis were those cases, established in the 1970’s which reaffirmed that even healthy mothers, with no symptoms were able to pass to their infants cell-wall-deficient forms of TB which nevertheless could kill or injure them. So “stealth” were these particular forms of TB that it once took Mattman eight animal passages before isolating the tubercular pathogen from the menstrual blood of a mother who’s infant had became ill a few days after birth.

Microbiologist and virologist Mattman , a Ph.D., an immunologist, and a 1997 nominee for the Nobel Prize in Medicine, knew something that few scientists on the planet still truly understand. Bacteria had a life cycle and could assume many forms. She also knew which special stains, cultures and techniques would have to be used to detect them.Mattman, of course, had access to modern techniques that her predecessors didn’t, including electron microscopy, immunofluorescence, PCR and other molecular assessment techniques.Her book, “Cell Wall Deficient Forms,” first written[1] in 1974, was regarded as an invaluable education tool among researchers, students and physicians in the field of microbiology. The problem was that at that point not all of them were accepting it.By 2001Mattman concluded , regarding the human placenta, that: “There is little doubt that the minute filterable form of bacteria move from the mother’s capillaries to those of the fetus.”She was referring, of course, to those tiny filterable bacteria either without a cell wall or having a breach in that cell wall. Mattman  was an expert on such forms, and her bookabout them which went into its Third Edition[2] in 2001.  When Mattman’s “Cell wall deficient Forms” of bacteria, which she also referred to as “stealth pathogens”, lose or have their cell wall disrupted, they become plastic, having the ability to assume many forms. Some are so tiny that they pass a 22μm filter, the so-called viral stage of a bacteria.  Cell wall disruption also changed the way these microbes stained. Cell Wall Deficient tuberculosis did not stain with the same “acid-fast” stain that classical TB bacillus did.

Tuberculosis was one of the first placental infections to be accurately described. Since Lehmann’s first description, the subject had came under intense scrutiny. Mattman spent considerable time talking about the transplacental passage of cell wall deficient forms (CWD forms) of TB and the mycobacteria to the fetus.

She knew that of all the pathogens, tuberculosis and its fellow mycobacteria relied on their stealth, cell-wall-deficient forms for their singular survival record inside humans. Thus she was drawn, early on, to the subject.  Her 1970 paper remains a classic on such forms.[3]

Calmette, said Mattman, knew that TB must traverse the placenta in its viral stage since the placenta, in most cases, remained intact with no obvious damage.  Calmette noted that after such infection with cell wall deficient tuberculosis quick fetal death might occur. But if the child is born alive it could result in death through emaciation by one month. And there were those cases in which the infant suffered no ill effects.[4]These were the infants that were infected but nevertheless vigorous.

The emergence of what in this micropictograph looks like fingers of the human hand (which will become the typical, familiar tubercular rods) emerging from STEALTH pleomorphic (multi-shaped) cell-wall-deficient tubercular growth [Xalabarder, C., Publ. Instit. Antituberc. Sup., 7:1-83, 1970]

But what really troubled Mattman where those cases, only established in the early 1970’s in which seemingly healthymothers, with no symptoms, where also able to pass to their infants cell wall deficient forms of TB which nevertheless killed their offspring.[5] So “stealth” were the cell wall deficient tuberculosis in the menstrual blood from one mother who’s offspring became ill a few days after birth, that it took eight animal passages to finally yield the pathogen.Mattman warned that tuberculosis mainly grew as pleomorphic (many formed) stealth pathogens[Ibid p. 189]  In one long series, American labs were only picking up 50% of tubercular sputum samples by not looking for its cell wall deficient (CWD) forms.[6]Brieger[7] at Cambridge demonstrated such mainly pleomorphic stealth growth when he inoculated tuberculosis directly into the amniotic sac, the outer layer of which is part of the placenta. Rapidly, cell-wall-deficient granules formed that did not stain with traditional acid-fast stain. Within 3 days, other cell-wall-deficient forms, the long branching fungal filaments of TB, appeared. TB is a mycobacteria with both bacterial and fungal  (“myco” means fungal) forms.  Brieger then did the same with fowl tuberculosis in chicken embryos with similar results.[8] Cell-wall deficient forms again formed, again not identifiable by traditional stains.

Histopathology of placenta with inflammatory cells and the tiny threadlike violet acid-fast bacilli of Mycobacterium tuberculosis (see arrows). Ziehl-Neelsen stain. Courtesy of Centers for Disease Control and Prevention.

While American traditionalists remained skeptical of the clinical significance of Mattman’s  stealth, cell-wall-deficient forms, the Russians never doubted them.[9][10][11]  Instead they churned out study after study, proving the destructiveness of cell wall deficient tuberculosis to the central nervous system . By 1996 Insanov[11] warned that an infection with cell wall deficient forms in children not only made standard treatment less effective, but created a disease with a gradual, insidious onset, and a slow accumulation of cerebral damage in children. This made the disease more difficult to diagnose, because its slow burn into young nervous systems allowed months to year before its full spectrum of damage was obvious.  Insanov showed that cell wall deficient forms in tuberculosis meningitis accounted for an incredible 87.6% of the tuberculosis found in children with TB meningitis and 87.3% of those in adults. How could such statistics be ignored?

It’s not that Americans hesitated to acknowledge the importance of “latent” tuberculosis[12] and how it could persist within a child or adult for years without causing disease. They just couldn’t seem to correlate the phenomena with Mattman’s stealth pathogens.

To Lida Holmes Mattman, it was bad enough that most 21st century bacteriologists still ignored those cell wall deficient bacterial forms responsible for much adult illness of ‘unknown’ cause. But with such stubbornness, perhaps, there was a just retribution involved in that, the same researchers that ignored her findings were suffering along with the general population.  But when it came to innocent children and newborns not being able to be diagnosed or treated properly for diseases because of such recalcitrance, that is where she drew the line.

REFERENCES:

1.  Mattman LH Cell Wall Deficient Forms CRC Press, Cleveland  pp. 411 1974

2.  Mattman, LH Cell Wall Deficient Forms – Stealth Pathogens 3rd Edition. CRC Press Boca Raton 2001

3.  Mattman, L. H. (1970), Cell Wall Deficient Forms of Mycobacteria. Annals of the New York Academy of Sciences, 174: 852–861

4.  Calmette A Valtis J  Lacomme A Nouvelles recherches expérimentales sur l’ultravirus tuberculeux, C.R. Acad. Sci., 186, 1778-1781, 1928

5.  Dorozhkova IR Deshkekina MF Ereneeva AS Zemskova ZS Ilyiash NI and Zhukova EK  On the question of inborn tuberculosis, Tuberk Probl. 10, 80-83, 1972

6.   Pollock HM  Wieman EF  Smear Results in the Diagnosis of Mycobacterioses Using Blue Light Fluorescence Microscopy, J. Clin. Microbiol., 5:329-331, 1977.

7.  Brieger EM The Host Parasite Relationship in Tuberculous Infection, Tubercle, 30:242-253, 1949

8.   Brieger EM Glauert AM  A Phase-Contrast Study of Reproduction In Mycelial Strains of Avian Tubercle Bacilli, J. Gen. Microbiol., 7:287-294, 1952

9.   Gadzhiev GS Characteristics of the mycobacteria in children with tuberculous meningitis Probl Tuberk. (11):8-10 1990

10.  Golanov VS Andreev LP Characteristics of bacterial discharge in patients with different forms of pulmonary tuberculosis Probl Tuberk 5:43-5 1994

11.   Insanov AB Gadzhiev FS Comparative analysis of the results of spinal fluid microbiological study in children and adults who suffered from tuberculous meningitis. Probl tuberk. 1996; (5):25-8

13.   Parrish NM Dick JD Mechanisms of latency in Mycobacterium tuberculosis. Trends Microbial 6(3):107-12 1998)

 

CONCLUSION:

Most of us agree with Ploeger that “developmental diseases” like autism and Down Syndrome occur in the fetus before birth. We also know that the changes that occur and the symptoms that result are likely from an intrauterine infectious process. Actually the evidence for mental illness, including autism and schizophrenia, as being the result of an infectious disease is quite extensive.

Medical residents are often told “Don’t look for zebras”. Don’t look for the exotic or the esoteric cause of a disease. And the best diagnosticians among them never forget this. For the purposes of this paper, part of not looking for zebras would have to include asking what infectious process statistically most affects not only women of childbearing age, but their children….and at the same time is nerve-seeking (neurotropic) by its very nature. According to statistics such as can be obtained from WHO (World Health Organization) and a host of other sources, that disease, hands down, is tuberculosis and the mycobacteria.

Just as appropriate, were this the case, might be the admonishment of a resident who brings up the issue of vaccines or their ingredients as a direct as opposed to an indirect influence on autism. One must distinguish primary cause from aggravating circumstance. First of all, most of the vaccines in today’s infant/maternal schedules have a direct contraindication to such potential chronic, even dormant tubercular infection.  And physician/researcher Hartz, after extensive human trials, appeared in a older issue of The Journal of the American Medical Association (JAMA), insisting that mercury compounds were “positively injurious and detrimental to one afflicted with tuberculosis”.[1] In addition some of the oil adjuvants used to increase a vaccines potency are lipids or oils that are cholesterol precursors, becoming cholesterol in the body[2] This cholesterol surge is a big boost for any dormant systemic tuberculosis already in the body, who’s very ability to maintain infection is linked to its ability to acquire cholesterol. So crucial is this unique ability of TB to use cholesterol in the body for both carbon and energy sources, that if it were not for its ability to grow off of cholesterol, tuberculosis, like other pathogens, would be unable to resist eradication through cytokine attack and the attempts of certain activated white blood cells called macrophages to starve it of essential nutrients. It is a true survival mechanism acquired after eons and eons which has made TB, from a historic sense, probably the most successful pathogen on the planet.[3]

So in comparative and simpler terms, one might look at an injection of certain vaccine adjuvants, squalene among them, whether inside or outside of a vaccination, as lighting up chronic foci of tuberculosis like a Christmas tree.

J. Langdon Down, who really was the first to deal with autism in a subset of his children thought that Down’s children, “for the most part”, originated from TB in their parents. He was also the first to use “developmentally disabled” for such cases, a euphemism which the public liked and could much more readily absorb than the developmentally disabled from tuberculosis. Was John Landon Down just pulling from an imaginary shortlist when he focused on the fact that, in most cases, his developmentally disabled children, a subset of who were autistic, resulted from parental tuberculosis? Not at all.  Down was a high-end product of English science, and what the British lacked in the well-organized and well-financed state run laboratories of the Germans, they more than made up for in their astute powers of observation. Down also could, even then, draw on an extensive library of research on the subject which pointed towards the same direction as his thoughts. It was only then, and after compiling compelling statistical evidence, that he came to the conclusion he came to and published his thoughts.

Time went by, and evidence accrued. Antidepressants, hailed as “new breakthrough drugs” in mental illness, were really discovered as a by-product of the tuberculosis research in the 1950’s. Having proven  anti-tuberculous activity, they weren’t used clinically as antidepressants until the 1960’s. The first being  imipramine, now called a tricyclic antidepressant (TCA). Almost concomitantly came antidepressants known as monoamine oxidase inhibitors (MAO’s), also with anti-tubercular activity.  This was only after It was noted that TB patients given MAO inhibitors experienced a state of elation and euphoria where only depression had existed before.

Yet from their onset, results and studies, no matter how much they confirmed TB’s role in mental illness, were tainted by a public that would hear none of them. After all, to be diagnosed insane or tubercular were two of the greatest stigmas that could be thrust not only upon a patient but his or her immediate family. So insanity or mental illness was either given medical labels that few understood, or reduced to a “nervous disorder” and TB was always that “not me” illness, often referred to as a “chest ailment”, during which “nervous disorders” often occurred.

In 1997Adhikari and Pillay[4] were quite straightforward on a subject traditionalists never have admitted to as other than “a rarity”. Pillay wrote in Tuberculosis in the Newborn: An Emerging Problem: “Congenital TB can result from hematogenous (blood) dissemination of M. tuberculosis after maternal mycobacteremia, rupture of a placental tubercle into the fetal circulation, or ingestion of infected amniotic fluid or maternal blood at delivery. The mother might not have symptoms of TB disease, and subclinical maternal genital TB also can result in an infected neonate”. This seems straightforward enough. The fetus can be infected by the mother with TB while still in her womb. The mother might not have symptoms of TB. And that it was an “emerging problem”. But there was another emerging problem happening at about the same time. Autism had already begun to skyrocket.

By 1999, Pillet, in the Archives of Pediatrics, went over the difficulties in early diagnosis of neonatal tuberculosis. His conclusion as so many others before him was that its frequency was being underestimated and its diagnosis often difficult because its initial manifestations were often delayed. [5] By stating this, Pillet was saying what Insanov and Welch had already brought up in the distinct delay of disease process as a result of the cell-wall-deficient (CWD) forms of tuberculosis in the newborn which would take time to revert to classical disease.  This is also what Calmette and Mattman brought attention to. Calmette was warning pathologists CWD forms caused few tissue changes to the placenta and Mattman was warning even healthy, otherwise asymptomatic pregnant woman that a focus of tuberculosis somewhere in their body could generate stealth, cell-wall-deficient forms of tuberculosis into the blood to infect their fetuses. Rich had already  pointed out the extreme activation of even silent TB that occurs during pregnancy, a fact that he had acquired from Norris before him.

In October of 2003 Gourion[6] and others appeared in the Journal of Autism and Developmental Disorders reporting on how neonatal cerebral tuberculosis had evolved into a member of the autistic spectrum of disorders, namely Asperger’s syndrome (AS).

More importantly, a cross comparison between neuropathology and imaging studies done on TB meningoencephalitis (Hosoglu, 1998) (Ozates 2000) and those from the autistic spectrum, including Asperger’s (McAlonan 2002) (Gilberg 1993) (Happe & Frith 1996), seemed to match, including a study of the decreased metabolism in the brain’s cingulate gyri.     (McAlonan 2002) (Gilberg 1993) (Happe & Frith 1996) (Haznedar 2000) This was important.

In linking Asperger’s syndrome (AS), a known disease in the autistic spectrum to neonatal TB meningitis Gourion, Pelissolo, and Lepine joined Schoeman’sprevious implication[7] that tuberculosis and its neonatal brain lesions were behind the neurodevelopmental disorders, including the autistic spectrum of infancy, childhood and beyond.

_______________________

No one who has ever witnessed the pathetic “head banging” of an autistic child can truly come away unswayed. Many explanations have been offered  by workers in the field, some of them unconvincing. That pain relief is a possibility has occurred to a few.  They mention a child is more likely, for example to bang his head when he has an ear infection or is suffering from some other physical discomfort in the head. This makes sense, but some of the other explanations do not. Five out of 11 of Kanner’s initial subjects, through measurement, “had relatively large heads”, which could indicate possible degrees of hydrocephalus. Delacato, evaluating 474 children diagnosed as autistic found 81percent of these to have enlarged ventricles on computerized tomography[8], a premier radiologic feature of hydrocephalus. Edwards and many others have documented the chronic headaches that can result from hydrocephalus[9], one of whose more frequent causes in infants is perinatal infection. In fact hydrocephalus itself is often listed as a possible cause for autism. As previously mentioned, at one time, the diagnosis of acute hydrocephalus was so commonly associated with cerebral tuberculosis that the terms were used interchangeably.

For the sake of the “developmentally disabled” children in our midst today alone, no less those that grow to adolescence and adulthood , it is both our obligation and responsibility to carefully review the historic debate of tuberculosis’s stealth role in the psychiatrically impaired and developmentally disabled.

Perhaps the current Government sponsored trials using anti-tuberculous medicine for autism will bring us more in that direction.

REFERENCES:

1.  Hartz HJ  Ultimate Results in the Treatment of Pulmonary Tuberculosis With Mercury Succinimid  Journal of the American Medical Association 55(11):915-918 p. 917)

2.  Carlson BC Jansson AM, Anders Larsson The Endogenous Adjuvant Squalene Can Induce a Chronic T-Cell-Mediated Arthritis in Rats. American Journal of Pathology, Vol. 156, No. 6, June 2000 pp 2057-2065.

3.  Pandey AK Sassetti Mycobacterial persistence requires the utilization of host cholesterol. PNAS March 18, 2008 vol. 105 no. 11 pp. 4376-4380

4.  Adhikari M, Pillay T, Pillay DG. Tuberculosis in the newborn: an emerging problem. Pediatr Infect Dis 1997;16:1108-12

5.  Pillet P, Grill J  Congenital Tuberculosis: Difficulties in Early Diagnosis Arch Pediatr 6(6):635-9 1999 Jun

6.  Gourion D Pelissolo A Neonatal Tuberculous Meningitis in a Patient with Asperger‘s Syndrome Journal of Autism and Developmental Disorders, Vol 33(5):559-60 October, 2003

7.  Schoeman CJ Herbst I The effect of tuberculous meningitis on the me and motor development of children South African Medical Journal 87(1):70-72 1997

8.  Delacato, D.F., Szegda, D.T. and Parisi, A. Neurophysiological View of Autism: Review of Recent Research As It Applies to the Delacato Theory of Autism. Developmental Brain Dysfunction. 7, nos. 2-3 (March-June 1994):129-131.

9. Edwards, J.E., Britz, G.W. and Marsh H.  Chronic Headaches Due to Occult Hydrocephalus. 96, no. 2 (February 2003): 77-8.

Lawrence Broxmeyer, MD © 2011 All Rights Reserved. Registered: US Library of Congress

This entry is filed under autism, Autism: A Stealth Disease, medical history of autism.

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