from http://home.no.net/harah/oprys/articles/bruno/prelude.htm
SABIN and Bodian - and how polio can develop - with weak
to strong manifestations - leading to a vast number now potentially falling
ill with 'Post Polio Syndrome
------------------------------------------------------------------------
"Non-paralytic" Polio as Prelude to Post-Polio Sequelae.
------------------------------------------------------------------------
Dr. Richard L. Bruno
Chairperson
International Post-Polio Task Force
and
Director
The Post-Polio Institute
Englewood Hospital and Medical Center
Englewood, New Jersey 07631
Phone: (201) 894-3724 Toll Free: 1-877-POST-POLIO
PPSENG@AOL.COM
emphasis added by Janine Roberts, site editor. (who now needs to read more of Bodian)
Cincinnati, 1947. The Summer arrives bringing heat, humidity . . . and fear.
Polio is coming again and the terror has never been greater. 1946 had brought
America's worst epidemic ever, the death rate rising to an all-time high. But
as July became August and then September, there was an eerie calm. While there
had been 167 cases of polio during a previous Cincinnati summer, only 40 cases
were reported by the end of August. Why were there so few cases of polio? Had
the "The Summer Plague" miraculously come to an end? No, the poliovirus
had not disappeared. It was attacking Cincinnati wearing a disguise.
For at least four weeks during August and early September, pediatricians saw
a new illness they called the "Summer Grippe." It's symptoms -- headache,
fever, stomach pain, nausea, sore throat, and generalized aching -- came on
suddenly in children between one and ten years old. The kids were not sick enough
to go to the hospital and saw their doctor once if at all. Albert Sabin, a doctor
at The Children's Hospital of Cincinnati in 1947 and developer of the oral polio
vaccine a decade later, reported that there were at least 10,000 cases of "Summer
Grippe" in Cincinnati and that "in some parts of the city hardly a
child escaped." 1
Why was Sabin, a preeminent polio researcher, interested in the "Summer
Grippe?" Because many of the children had a stiff neck, the "red
flag" symptom that would require immediate hospitalization and the
terrifying diagnosis "rule out poliomyelitis." However, since "Summer
Grippe" symptoms did not lead to paralysis and disappeared within a week,
pediatricians were not interested in hospitalizing children. But Sabin was.
He remembered that there had been an unusually mild polio outbreak in Denmark
in 1934 when, although only 27 patients were paralyzed, 600 more reported
a "slight fever." Sabin also recalled the unusual increase in influenza
in Copenhagen during August and September, 1934, and the 100 cases of polio
that came with it. He wondered if a mild form of the poliovirus could have caused
the "slight fever" and flu in Denmark in 1934 and the "Summer
Grippe" in Cincinnati in 1947. 2 Sabin decided to find out.
A Medical Detective Story
From August 22 to September 9, Sabin admitted 13 children to The Children's
Hospital with "Summer Grippe" symptoms. The children had fevers of
around 103, almost all were listless and had headaches, many had sore throats
and most had stomach pain. These fluish, feverish, and sometimes fussy children
had spinal taps and bodily fluid specimens taken. Eight were diagnosed with
"Summer Grippe." Two had a stiff neck and were diagnosed with "non-paralytic
polio;" one had "dysentery," another had a sinus infection and
a third had pneumonia. None of the children was seriously ill and they all left
the hospital in about nine days.
With the children gone, Sabin returned to his laboratory to see if a poliovirus
caused the "Summer Grippe." Remarkably, Sabin found antibodies (cells
produced by the immune system that render a virus harmless) to the Lansing (or
Type II) poliovirus in the blood of five of the eight children with "Summer
Grippe," in the child with the sinus infection and in one of the two children
who had non-paralytic polio. But Sabin knew that antibodies could have been
present because the children had been exposed to poliovirus during the epidemic
of 1946. So he followed the accepted procedure to prove that the Type II poliovirus
had indeed been present in the children: Sabin exposed monkeys to specimens
collected from his patients and watched the monkeys for about a month to see
if weakness or paralysis developed.
I believe this exposure of monkeys was by means of making a hole in their skull and injecting in human cells taken from sick children - this assault would have included toxins, nanoparticles, human cell debris etc..
Then, Sabin performed autopsies on the animals to look for damage to the spinal
cord and brain that was the unique "calling card" of the poliovirus.
Specimens from "Summer Grippe" patients did indeed damage monkeys:
specimens from one patient paralyzed a monkey, specimens from three damaged
motor neurons in the spinal cord, and specimens from four damaged the brain
stem neurons responsible for keeping the brain awake. Specimens from only one
of the children who had non-paralytic polio paralyzed a monkey in spite of her
lack of Type II antibodies. However, when Sabin exposed monkeys to specimens
from seven different patients diagnosed during August with non-paralytic polio,
only one monkey became paralyzed while the other animals had no evidence of
nerve damage.
A Kinder, Gentler Poliovirus?
Sabin concluded that a mild or "low virulence" Type II poliovirus
caused the flu-like symptoms of the "Summer Grippe." Although Sabin's
"mild" poliovirus did not cause even muscle weakness in humans, it
did more than twice the damage to monkeys' nervous systems than did the virus
causing non-paralytic polio in Cincinnati that Summer. What's more, Sabin's
low virulence poliovirus did something even the most virulent paralytic poliovirus
did not do: sicken at least 10,000 kids. At it's worst the paralytic poliovirus
in Cincinnati felled only 167. Some mild virus!
Yet not everyone agreed that a kinder, gentler poliovirus caused the "Summer
Grippe," not even the editor of the journal that published Sabin's findings.
David Bodian, editor of The American Journal of Hygiene, told Sabin in a letter
that the evidence supporting Sabin's conclusion was "very far from being
satisfactory" and that the paper would be "subject to serious criticisms."
3 Bodian, a Johns Hopkins pathologist, is the unsung hero of the polio vaccine.
It was Bodian who discovered that damage to neurons in the brain stem and spinal
cord was the calling card of the poliovirus and that as many as 60% of spinal
cord motor neurons had to be killed by the poliovirus for any muscle weakness,
let alone paralysis, to occur. Bodian should have been the one scientist
to readily accept Sabin's claim that a low virulence poliovirus not only caused
"Summer Grippe" symptoms but also killed neurons, although not
enough neurons to cause weakness or even a stiff neck. Bodian didnot.
JR comment - Bodian it seems showed how much damage to the motor neuron cells the body had to have before paralysis symptoms became evident - this is very differernt from proving that this damage 'was the calling card of the poliovirus'. This requres further checking.
Bodian wrote to Sabin that a "causal relationship" between the poliovirus
and the "Summer Grippe" had not been proved saying, "it is
equally plausible to assume that the (polio) virus was found in accidental relationship
with the illness." Sabin wrote back that bodily fluid collected "during
the same period" from 24 additional patients with non-paralytic poliomyelitis
did not cause nerve damage in monkeys, supporting his claim that he had "caught"
a poliovirus unique in that it caused "Summer Grippe" symptoms and
damaged neurons in monkeys at a much higher rate than did the non-paralytic
poliovirus floating around Cincinnati that Summer. But Sabin could not actually
prove a causal relationship between a his "stealth" poliovirus and
the "Summer Grippe," admitting to Bodian, "It is, in fact (a)
matter of probable guilt by association." Sabin was missing two important
cards if his claim that two different polioviruses were circulating simultaneously
were to trump Bodian's criticisms: one card Sabin wouldn't hold until 1952;
the final card wouldn't be dealt until 1955.
In 1949, David Bodian himself discovered that it was not just the Type II poliovirus
that damaged human neurons, but that there were three types of poliovirus that
caused illness in humans, each requiring a unique antibody to render it harmless.
4 So in 1952, Sabin tested bodily fluid saved from his 1947 paralytic and non-paralytic
polio patients (but, unfortunately, not from the "Summer Grippe" kids)
for the other types of poliovirus. He discovered Type I antibodies and concluded
that the Type I poliovirus -- not Type II -- was responsible for paralytic and
non-paralytic polio in 1947. 5 So Sabin was right: there were two different
types of poliovirus circulating simultaneously in Cincinnati that Summer. But
did the "high virulence" Type I poliovirus cause "typical polio"
while a "low virulence" Type II virus caused the "Summer Grippe?"
That answer would come years later and from thousands of miles away.
To Iceland From The Heartland
In September, 1948, three cases of paralytic polio were diagnosed in Akureyri,
Iceland. 6 And although not another case of polio was reported, over the next
few months more than 1100 Icelanders reported typical polio symptoms (fever,
neck pain, muscle weakness and even some paralysis) as well as symptoms not
associated with polio (tingling, numbness and "general tiredness").
Although fluid samples from four patients were sent to Bodian's laboratory for
testing, neither poliovirus nor antibodies were found. Yet, doctors in Iceland
concluded that there were only two possible causes for what has come to be called
Iceland Disease: "Either a strain of polio (virus) of low virulence was
responsible for this epidemic" or "some unknown (neuron-damaging)
virus has been present."
Hard evidence for a low virulence poliovirus did not come for six more years.
1955 brought an extensive polio epidemic to Iceland caused by the Type I poliovirus,
along with two new outbreaks of Iceland Disease. 7 Incredibly, not one case
of polio was reported in towns with Iceland Disease in spite of the fact that
only 7% of the children had antibodies to Type I poliovirus. Incredibly, 100%
of children in the Iceland Disease towns had antibodies to Type II poliovirus.
Just as Sabin thought happened in Cincinnati, children in Iceland had been exposed
to a low virulence Type II poliovirus that damaged their nervous systems, caused
symptoms of Iceland Disease, but prevented infection by a high virulence Type
I poliovirus.
How could an infection by one type of poliovirus prevent infection by another
without protective antibodies? That answer came during the 1959 Singapore study
of Sabin's own oral polio vaccine. 8 Children were given all three live attenuated
(totally non-virulent) polioviruses developed for the vaccine. Unexpectedly,
the Type II poliovirus was found to be "dominant." Just as a flock
of dominant blue jays blocks less aggressive robins from roosting in your back
yard, the dominant Type II poliovirus blocks all other polioviruses -- even
the naturally-occurring Type I poliovirus that was
causing Singapore's 1959 polio epidemic -- from entering your blood stream.
So children in Iceland and Singapore were protected from paralytic polio by
a Type II poliovirus that blocked a high-virulence Type I poliovirus from entering
their blood. And a Type II poliovirus protected the children of Cincinnati from
paralysis by blocking a Type I poliovirus from entering their blood but at the
price of the "Summer Grippe," a very much milder version of Iceland
Disease. When the "Summer Grippe" epidemic was "at its peak by
the end of August, there were not more than 40 reported cases of poliomyelitis."
Only after the "Summer Grippe" had left town by mid-September did
polio cases start to increase, reaching a total of 170, the highest number in
Cincinnati history. (cf 9,10)
Polio By Any Other Name
Knowing that there are relatively "mild" polioviruses, that damage
the spinal cord and brain without causing paralysis or even weakness, is important
as we try to explain the cause of Post-Polio Sequelae (PPS) today. As early
as 1941, Bodian cautioned that "the clinical diagnosis of a non-paralytic
case (of polio) may rest on the failure to detect minimal degrees of muscle
weakness," predicting the 1953 finding that at least 39% of those diagnosed
with NPP in fact had demonstrable muscle weakness. 11-13 Bodian showed that
paralytic and non-paralytic polio are not separate entities but a single process
whose pathophysiology and clinical manifestations lie on a continuum. 15
He reported that the appearance of paralysis and its severity increased as the
percentage of motor neurons killed increased; rhesus monkeys could have apparently
normal muscle function with only 40% of their anterior horn cells remaining.
17, 18
In 1997 Canadian researcher Alan McComas supported this conclusion, finding
the "limbs not considered to have been involved" in paralytic polio
survivors had lost on average 40% of their motor units. 19 These findings
contradict the common wisdom that the absence of paralysis is synonymous with
the absence of CNS damage, and the notion that NPP survivors' motor neurons
could not be experiencing metabolic failure and death to which late-onset muscle
weakness has been attributed. 19
New fatigue and non-paralytic polio. The focus of PPS research during
the past 15 years on new muscle weakness has ignored the most frequently reported
and most disabling late-onset symptom, fatigue. 10 Certainly "brain fatigue,"
with its associated trouble with attention and staying awake, cannot be attributed
to spinal motor neuron damage. 20
Bodian made scores of comparisons at autopsy between poliovirus-induced spinal
cord and brain lesions. In animals without paralysis, he found that "lesions
in the brain are more extensive and numerous than in some monkeys which did
develop paralysis" and that some "animals with non-paralytic poliomyelitis
do not have any lesions in the spinal cord but have a characteristic distribution
of lesions in the brain ." 21, 22 (Notably, the brain lesions Bodian
found were in the same areas damaged in monkeys injected with specimens from
Sabin's "Summer Grippe" patients.) Bodian stated that "although
non-paralytic infection may be associated with severe neuronal damage in the
spinal cord," the poliovirus "is capable of producing an encephalitis,
with or without associated clinical symptoms, in the absence of any pathological
change in the spinal cord" (italics Bodian's). 17 Bodian also found that
the "degree of involvement of brain centers" in humans having paralytic
polio is comparable to the brain lesions in animals with non-paralytic polio
18. Bodian concluded that "all available evidence shows conclusively that
every case of poliomyelitis, human or experimental, exhibits lesions of the
brain," and that, "As far as the pathologist is concerned all cases
of poliomyelitis are 'encephalitic'." 22
The finding that lesions in the brain activating system can be the only damage
resulting from poliovirus infection may explain 1) why fatigue is reported more
frequently than muscle weakness in both paralytic and non-paralytic polio survivors,
2) the lack of correlation between the severity of late-onset fatigue and the
number of limbs paralyzed, hospital admission or length of hospital stay, impaired
breathing or use or respirator during the acute polio episode, and 3) the neuropsychologic,
neuroendocrine, neuroanatomic, and EEG abnormalities associated with post-polio
fatigue and the occurrence of central sleep apnea and abnormalities of sleep
architecture in polio survivors. 16,20,23-28 With the occurrence of late-onset
fatigue, we are seeing today what Bodian predicted in 1949: that symptoms resulting
from "lesions in the central gray of the mid-brain and hind-brain and in
the mid-brain tegmentum and reticular formation" would be more often observed
if they were not overshadowed by "paralysis of skeletal muscles."
10
Prevalence of poliovirus-induced illness. Unfortunately, it is impossible to
know how many Americans had their CNS damaged by the poliovirus, damage that
set the stage for PPS. Although infectious disease texts state there is a 1:10:50
ratio of paralytic polio, non-paralytic polio, and a "minor illness"
with symptoms identical to the "Summer Grippe," the data do not support
this claim. 12,29 In Cincinnati during 1947, the ratio of paralytic to non-paralytic
cases was 1:1.2 while the ratio of paralytic polio patients to "Summer
Grippe" cases was at least 1:106 1, 2 Across the U.S., the incidence of
reported NPP cases varied widely depending on location and year, ranging from
0% to 80% of cases during the 1940's (mean ratio of paralytic to non-paralytic
cases: 7:3) to 25% - 65% during the 1950's (mean ratio of paralytic to non-paralytic
cases: 1:1). 2,11 (R. Bruce, C.D.C., personal communication.)
There are a several of factors that caused the marked variability in reported
cases of paralytic and non-paralytic polio:
Patients did not present for diagnosis. Failure to present for diagnosis may
have resulted from symptoms being very mild or not seen as indicative of poliovirus
infection (especially in infants) and patients, especially those who were poor,
not having access to or having to travel for medical care. A study of polio
diagnoses in a San Francisco city hospital from 1950 to 1953, and the reported
cases of polio in Cincinnati during 1947, show that 15% more paralytic and 121%
more non-paralytic polio cases were diagnosed among patients living in the city
versus those living in outlying areas. 2,11 * Urban patients were thought to
be more likely to present for diagnosis, being nearer to hospitals, versus those
living in areas where they had to travel for medical care. Those with mild symptoms
-- as in the "Summer Grippe," non-paralytic polio or even mild paralytic
polio, especially in infants and young children -- may never have been diagnosed.
Although diagnosis may have been more accurate and reporting to public health
authorities more likely at city hospitals, and especially at university medical
centers such as Sabin's in Cincinnati, the number of cases of both paralytic
and non-paralytic polio reported by rural hospitals would have been underestimates
of the true incidence;
Paralytic polio was under diagnosed. Studies document the underdiagnosis
of paralytic polio. 11,12 Shaw and Levin reported that "mild degrees of
muscle weakness may be easily overlooked" if manual muscle testing were
employed without a functional assessment of strength: "Many patients who
are eager for activity, who can readily walk out of the hospital, and who are
persuasively non-paralytic will thus be found to have very definite muscle weakness
which cannot be detected while they are recumbent in bed." 11 The failure
to detect muscle weakness was also attributed to "too short a period of
observation without opportunity for follow-up;" eighteen months to 6 years
after having been diagnosed with non-paralytic polio, 39% of patients were found
to have weakness in at least one muscle group; 11,12
Polio cases were not reported. The number and severity of polio cases during
the epidemics may also have prevented overwhelmed physicians from reporting
the occurrence of polio, especially NPP, to local public heath authorities.
This occurred even at Sabin's Children's Hospital in Cincinnati. (Dr. J. Englert,
personal communication.) Even if polio cases were reported locally, between
1915 to 1934 a varying number of states failed to report cases to the federal
government, thereby preventing documentation of the true incidence of polio
and even the extent of large polio outbreaks, such as the 1916 epidemic. 2 What
is more, the C.D.C. did not separately tabulate non-paralytic and paralytic
polio cases until 1951, and did not itself require the reporting of polio cases
until the late 1950's. (R. Bruce, C.D.C., personal communication.)
These factors have not only caused inaccuracies in archival polio incidence
and prevalence data, but also they have impaired the ability of recent surveys
to accurately estimate the actual number of living polio survivors. For example,
the 1987 National Health Interview Survey (N.H.I.S.) relied on respondents to
report whether they had had polio and if they had paralytic or NPP. 30 The N.H.I.S.
estimated that there are 641,416 living American paralytic polio survivors,
832,852 NPP survivors and 159,919 who reported they had had polio but did not
know whether that had been paralyzed. This survey documented 1 paralytic case
for 1.3 non-paralytic cases, a ratio similar to that reported during the 1950's
but much lower than the 7:3 ratio of paralytic to non-paralytic cases reported
during the 1940's. The fact that 10% of the N.H.I.S. respondents did not know
whether they had been paralyzed makes clear that retrospective surveys, which
rely on patient reports of early-life symptoms and diagnoses, may not be able
to accurately determine the prevalence of paralytic polio, let alone the prevalence
of NPP or a "minor illness" such as the "Summer Grippe."
"Polio suspects" and PPS. It may be possible to control for the sources
of diagnostic and reporting error described above and approximately estimate
the number of living Americans who did have a "minor illness" and
thereby estimate the total number of polio survivors who had CNS damage and
therefore are at risk for PPS today.
As early as 1935, the Mayo Clinic's centralized records-linkage system recorded
not only cases of paralytic and non-paralytic polio, but also what were called
polio "suspects . . ."
". . . a term used by the physicians in polio epidemic years to describe
persons with an acute fibrile illness suspiciously similar to polio but without
paresis or evidence of central nervous system involvement from clinical history
and/or cerebrospinal fluid examination. Many of these persons were family members
and contacts of cases. Some may have had abortive polio and may constitute the
'tip of the iceberg,' since so many cases of polio never came to the attention
of the physician." 31
Although the population-based Mayo data are not representative of polio incidence
in other regions of the country, especially in urban centers, they do significantly
reduce, if not eliminate, errors resulting from improper diagnosis and underreporting.
Between 1935 and 1955, for each paralytic polio patient, 0.65 polio "suspects"
were recorded in the Mayo system. Applying this ratio to the N.H.I.S. estimate
of 641,416 paralytic polio survivors, there would be at least 416,920 living
polio "suspects" having had symptoms similar to those of the "Summer
Grippe." Since 38% of Sabin's "Summer Grippe" patients had pleocytosis,
indicating CNS involvement, 158,430 Americans would be at risk for PPS in addition
to the estimated 1.63 million paralytic and non-paralytic polio survivors.
Clinical Implications
"Non-paralytic" polio and "Post-Polio Syndrome." The diagnostic
criteria for "Post-Polio Syndrome" reflect the principal clinical
concerns of the 1950's and the 1980's: acute paralysis and new muscle weakness,
respectively.Post-Polio Syndrome criteria require the "onset of new weakness"
in an individual with a "prior episode of paralytic polio confirmed by
history, physical exam," as well as EMG changes "consistent with prior
anterior horn cell disease." 32 Unfortunately, these criteria do not take
into account the studies described above which make clear that non-paralytic
polio -- and even a "minor illness" such as the "Summer Grippe"
-- can be associated with the death of neurons in the spinal cord and brain
that sets the stage for late-onset symptoms.
Recent studies make clear that NPP survivors do have late-onset symptoms. A
population-based study of 828 polio survivors found that new muscle weakness
and fatigue were reported, respectively, in 38% and 34% of those who had been
paralyzed, and in 14% and 21% of those who had had NPP. 23 A study of 34 sets
of twins found PPS symptoms in 71% of the twins who had had paralytic polio
and "PPS-like symptoms" in 42% who had had no symptoms of paralysis.
33 The presence of PPS-like symptoms, as well as muscle biopsies "showing
long-standing signs of denervation" in some of the non-paralyzed twins,
caused the authors to conclude that the acutely non-paralyzed twin "had
also suffered subclinical nonparalytic polio (and that) symptoms of PPS m
ight also be sequelae of nonparalytic polio." Indeed, 13% of the non-paralyzed
twins had been acutely diagnosed as having "non-paralytic polio."
34
Further, the 1987 N.H.I.S. found that 28% of NPP survivors reported new health
problems related to polio. 30 45% more paralytic polio survivors reported limitations
as compared to those who had had NPP, while NPP polio survivors reported 46%
more limitation in life activities than did the general population.
EMG changes indicative of denervation may not be present in those who had "Summer
Grippe," NPP or even in those who had acute transient paralysis. Sabin
stated that "transitory" and reversible paralysis may be seen because
"not all nerve cells attacked by the poliomyelitis virus are irreversibly
damaged." 35 Bodian documented that motor neurons did recover function
after poliovirus infection even if all of the intracellular organelles, except
for the nucleus, had been destroyed. 17 Thus, an individual could have been
acutely paralyzed without neuronal death or axonal degeneration, the poliovirus-infected
neurons recovering and restoring muscle function without EMG evidence of chronic
denervation. Such a scenario would be more likely in those who had been weakened
or mildly paralyzed acutely and especially in those who had NPP or "Summer
Grippe."
However, it is important to note that neurons which recovered from poliovirus
infection were internally damaged, their cellular machinery for metabolism,
protein manufacturing, neurochemical packaging transportation likely having
been significantly impaired. 36,37 Bodian suggested that such poliovirus-damaged
neurons "may be vulnerable for life to metabolic factors such as changes
of senescence;" this vulnerability and eventual metabolic failure are thought
to be the likely causes of late-onset muscle weakness and fatigue in polio survivors
with or without acute evidence of paralysis or EMG evidence of denervation.
19,26,38-40.
Therefore, "Post-Polio Syndrome" should not be used as the generic
descriptor for late-onset problems in polio survivors, since its diagnostic
criteria exclude those without a history of paralysis, EMG evidence of denervation
and new muscle weakness. The Post-Polio Syndrome definition should either be
modified to include other frequently reported and disabling symptoms, especially
fatigue, or its name should be changed to "Post-Polio Muscle Weakness Syndrome."
In either case, the requirement of a history of paralytic polio and EMG evidence
of denervation should be removed.
So the story of the poliovirus and its effects on the body may be like the fable
of the elephant and the blind men: everyone infected by the poliovirus may be
left holding a slightly different piece of the "animal." Doctors must
remember that polio survivors' symptoms today depend, not on a diagnosis given
40 years ago, but on how many neurons were killed by the poliovirus in any given
area of the spinal cord and brain. The one to six million North Americans who
had "non-paralytic" polio must be assertive and advocate for themselves,
showing doctors the research describing the varied effects of poliovirus on
the nervous system and making clear that non-paralytic polio survivors do develop
PPS. And "non-paralytic" polio survivors must follow the same prescription
as survivors of paralytic polio to manage their PPS: listen to your body, stop
activities before symptoms start and discard the "use it or lose it"
philosophy and begin to "conserve to preserve" your remaining, poliovirus-damaged
neurons. 41-45
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