Olmsted Can't Find SSPE Either

This past weekend, Age of Autism had their "Weekly Wrap" by Dan "The Amish don't have autism" Olmstead entitled, "Do MMR + Hg + SSPE = ASD?"  Dan Olmsted opines via Kathy Blanco that:

"I wonder whether autistic enterocolitis isn’t a kind of SSPE with a weakened (vaccine) virus," Kathy Blanco wrote in an e-mail this week, with a link to a blog post HERE  that reports: "Hidden government documents have revealed that leading professionals have had serious concerns about the safety of the single measles vaccines for many years. Secret government documents that have been under lock and key for thirty years have revealed that the UK government has known for many years that the single measles vaccine can cause the debilitating neurological disorder SSPE or Subacute Sclerosing Panencephalitis."

Whether "autism" is in effect a variant form of SSPE is well worth wondering.

Not worth wondering at all.  There is no variant of SSPE.  SSPE is subacute sclerosis panencephalitis and is a distinct diagnosis even though there are atypical cases.  SSPE is almost always fatal within about 3-7 years after a measles infection although cases that have occurred in adolescents and adults with aggressive treatment administered can remain alive for several more years although severely debilitated.

Olmsted and Blanco are relying upon the frantic hand-waving of Dr. Rebecca Carly, a bat-guano insane physician who lost her medical license for well, being bat-guano insane.  The symptoms and clinical course of SSPE are:

Subacute sclerosis panencephalitis (SSPE) is a persistent and chronic encephalitis secondary to measles virus infection that causes widespread demyelination of the central nervous system (CNS). (1) SSPE was described first by Dawson (2) in 1934, in an individual with rapidly progressive encephalitis. Later, in 1945, van Bogaert (3) described another individual with the same clinical presentation but in whom the disease exhibited a more
gradual course. The disease is so called because it typically develops over a period of less than 9 months (subacute), (4) because of the nature of the pathological lesions (sclerosis), and from the fact that the whole brain is affected (i.e. panencephalitis). (5–7)

The age at presentation is usually 8 to 11 years, (19,37,38) with onset usually occurring 6 years after measles infection. (6,19) Affected individuals present with poor school performance and progressive intellectual deterioration, personality changes, and behaviour abnormalities; this is followed by steady motor decline, myoclonus, focal paralysis, seizures, autonomic failure, and rigidity, finally leading to death with akinetic mutism. (5,16,19,38,39) These changes are characterized in four stages (see Table I). Motor regression is eventually seen in 100% of individuals with SSPE, cognitive decline in 86%, myoclonus in 74%, generalized seizures in 16%, and focal seizures in 10%. (16)

Does this sound like an ASD in any way?  Well of course not providing you are a rational and sane person.  In fact the differential diagnoses are: multiple sclerosis, acute demyelinating encephalomyelitis, Hashimoto’s encephalopathy, paraneoplastic limbic encephalitis, lafora disease, mitochondrial diseases and other rare neurodegenerative disorders. Olmsted and Blanco account for this disparity in symptoms between SSPE and ASDs with their usual torture of anything resembling a logical train of thought:

“At the level of the immune response, the newborn tends towards a TH2 response to pathogens and gradually shifts towards a TH1 response with age. If this transition does not take place appropriately, the infant is likely to be at greater risk of mounting aberrant immune responses in later life, as seen in patients with allergies. Given that, under normal circumstances the age of this transition will be different for different children, it seems inevitable that a ubiquitous viral exposure of all 15-month-old children could induce an immune response that is consistent with the individual dynamics of this TH2-TH1 transition.” (Wakefield AJ, and Montgomery SM. Autism, viral infection, measles-mumps-rubella vaccination. Israeli Med Ass J 1999;1:183-187 ).

Using their tortured "logic", wouldn't this create a clinical course worse than what is observed with SSPE?  But then again, these are people who believe that autism is a fate worse than death.  Furthermore, the epidemiology of SSPE is:

Overall, 4 to 11 cases of SSPE are expected for every 100 000 cases of measles, but the incidence is higher among children aged less than 5 years (18 ⁄ 100 000, compared with 1.1 ⁄ 100 000 after 5 years of age). (9) The highest incidence of SSPE relative to the rate of measles is reported in the Middle East, where the rate is 360 ⁄ 100 000 in individuals infected before 1 year of age. (11) The incidence varies dramatically depending on the age at which the measles infection is acquired and vaccination status. (8,11–13)

How does this explain their "autism epidemic"?  I can't help but wonder (for only a second though) why they chose to co-opt SSPE  when there are so many other disease presentations that they could more easily contrive to fit with their mental convolutions.  For instance, West Nile Virus or Herpes Simplex Virus-1 and 2 have more in common with features of some ASDs and have clinical courses they could more easily manipulate to fit with their paradigm but alas, there are no vaccines to blame so that wouldn't work.  Their basis for their "hypothesis" is hilariously inept:

The official concerns about the measles vaccine and SSPE Blanco cites go back to the early 1970s. But from the very earliest autism reports, there's been evidence that some kids were neurologically vulnerable to live virus vaccines -- perhaps because, as Blanco notes, they've been immunologically "set up" by early or simultaneous exposures to such toxins as mercury.

Actually the "official" concerns pre-date the 1970s but it isn't as though the AoA braintrusts are ever interested in facts.  Going back to Dr. Carly's "expose" she writes:

‘There has been some concern recently about the suggestion that measles vaccines might occasionally give rise to Subacute Sclerosing Panencephalitis. Professor Sir Charles Stuart-Harris, as chairman of the Joint Committee on Vaccination and Immunisation, has asked whether members of the Association would be prepared to notify cases we see.’

Note the words ‘might occasionally' which in my opinion, were specifically chosen to cover the fact that this was a growing problem.

This document, along with many others uncovered, means that the measles vaccination was proving problematic to the neurological well being of young children as far back as 1972. If this were the end of the matter, then it would be easy to assume that the problems had been overcome. However, the problem of vaccine-induced SSPE continued to persist even when the measles vaccination was combined with the mumps and the rubella vaccination to form the MMR triple vaccine.

No Dr. Carly, that's not what your not-so-secret document means.  There are several publications in the literature such as Schneck et al. 1968 and Payne et al. 1969 that implicated measles vaccine as the causative agent because there were no measles infection reported but measles vaccination was in temporal relationship to SSPE.  Public health officials, at that time, made a rational assumption that SSPE could be caused by measles vaccine virus since it is a live viral vaccine and cases of SSPE were being reported in the absence of a measles infection but in measles-vaccinated children.

Olmsted adds:

But is there anything that might suggest SSPE, like polio, could be a product of a co-factor interacting with the measles virus (or vaccine)? Well, here's something Mark and I came across: "Further Epidemiological Studies of Subacute Sclerosing Panencephalitis," by Detels et al., from The Lancet of July 7, 1973 (right around the same time the Brits were noticing SSPE could be an outcome of measles vaccination, as it happens).

This case-control study in various areas of the United States found that among 43 SSPE patients who had clinical measles, the median age at original infection was 15 months, whereas among controls who didn't have SSPE, the median age was 43 months. That matches exactly what Wakefield et al. were saying in that study Blanco sites -- "it seems inevitable that a ubiquitous viral exposure of all 15-month-old children could induce" an aberrant immune response. He was talking about the MMR, of course, which was originally given at 15 months but has since been moved forward to 12 months. But clearly, the risk of neurological problems from measles increases when the infection occurs earlier.

Here is the 1973 Lancet study he neglects to link to and what they really state:

Our data indicate that events accompanying measles infection differ between S.S.P.E. patients and controls. Measles occurred at a much younger age among patients, although their controls were selected as having been lifelong friends. Clinical measles did not occur in 11 patients, 6 of whom also did not receive measles vaccine. High measles-antibody titre was present in these patients and several had known intra-family exposure to measles at an early age. Presumably these patients had inapparent measles infection. It is probable that some of the cases with no clinical history of measles and in some with measles under age one, the infection occurred while there was partial immunity to this virus as a result of passively acquired maternal antibody. When the infection occurred the host response may have been incomplete, permitting the virus to persist in tissues.

Even then, investigators were beginning to understand that subclinical measles infections were occurring prior to onset of SSPE and that is why wild-type measles was suspected because some subjects weren't vaccinated and did have exposure to measles.   That doesn't stop Olmsted from abusing more information from this 40 year old study to suit his agenda.  Again from Detels et al:

Our data and those of others, however, indicate that unusual measles, while perhaps a necessary component, is not a sufficient explanation for the pathogenesis of S.S.P.E. S.S.P.E. is more common among males than females (though this was not striking in our series) and at a higher rate in non-urban settings. In urban inner-city areas where crowding is intense, the proportion of patients who are infected with measles below age one or concomitantly with chickenpox, might be expected to exceed the proportion in rural areas, so the rarity of S.S.P.E. patients in cities suggests that additional determinants play a key role.

This is what Olmsted somehow extracted from this excerpt:

They automatically turn toward other viral co-factors as a possibility, because these guys are virus hunters. But their observation -- SSPE as a largely rural phenomenon, strikingly absent in central urban areas -- also could point to toxic co-factors, such as pesticides. That's what we believe the rural character of the early poliomyelitis epidemics is pointing to. (The father of another of Kanner's early cases was a plant pathologist who spent most of his career in Puerto Rico, which shows the degree to which commercial agriculture, including chemically intensive coffee growing, occurs on that island.)

There is one viral co-factor in SSPE that seems quite clear: "Additional evidence that unusual circumstances accompany the measles infection was the significant excess of chickenpox associated with measles in SSPE patients. While this occurred in only 6 instances it is of note because of the relatively early age of clinical measles in patients versus controls, decreasing the likelihood of this sequence."

So atypically catching measles and chickenpox about the same time at 15 months is a big fat risk factor for setting up a persistent measles infection that results in a neurological catastrophe. If I were in charge of the U.S. vaccination schedule, I would have a bit of a breakdown over that fact.

However, they are all using information from over 40 years ago prior to the advent of molecular techniques that could distinguish viruses and better epidemiological surveillance to rule out confounding information.  And who in their right mind would be using decades old information that has been monumentally revised to dictate vaccine policy?  Right, an anti-vaxx wingnut. Why would they rely upon such dated information when there are so many more contemporary studies that employ molecular testing?  Simple.  They intentionally ignore these studies because they find the information inconvenient to their preposterous conjecture.

Let's take a look at some work that has been done in the last 40 years heck within the last seven years that completely refutes what Olmstead, Blanco and Carly prattle on about.  First, there appears to be an increased risk of SSPE among certain ethnicities although it hasn't been determined if there is a genetic pre-disposition associated with certain ethnic groups or whether the increased incidence of SSPE is due to socio-economic disparities. 

Ethnicity and genetic factors

There is evidence of ethnic differences, including increased risk associated with Hispanic and Asian ethnicity in the USA⁵⁹ and UK,²² respectively. A relatively low SSPE incidence was observed in black Americans.⁵⁵ One South African study reported distribution of cases by race roughly proportionate to the racial distribution in the population, but a measles incidence in black babies markedly higher than that for white infants.¹² Other South African studies calculated higher risks of SSPE in the ‘coloured’ (mixed race or of Indian/Sri Lankan origin) compared with the white population with lowest incidence in the black population.⁴⁷,^,66 In Israel, SSPE was reported almost exclusively in Sephardi Jews (of Afro-Asian origin) and Arabs, and not Ashkenazi Jews (of Euro-American origin).³¹ A later Israeli study found differences between Arabic and Jewish populations, but Sephardi and Ashkenazi Jews were not distinguished.¹⁰ Real ethnic differences may exist but this could reflect socio-economic circumstances that affect the likelihood of early measles exposure.

There is no strong evidence of a genetic factor associated with SSPE risk. Where cases have been reported in a twin, the condition has been discordant even in identical twins.⁶⁷ Familial aggregation has rarely been reported.⁶⁸,^,69 Two cases in two families have been observed in England and Wales. The probability of two families having more than one case by chance was calculated as under 1 in 10 000, suggesting some genetic tendency.⁸

There is also inconsistency among studies with regards to a male preponderance and in studies that do observe a male bias, may be due to differing latency between measles infection and onset of SSPE.  Olmsted tries to use this male preponderance as "proof" because of the male preponderance observed with ASD prevalence.  Of course he fails.

Age at onset and sex ratios

Worldwide average onset ages for SSPE ranged between 6 and 13 years, except Papua New Guinea at 4.9 years¹¹ (Table 1) and individual ages at onset ranged from 0 to 56 years in the papers reviewed. The average period from initial measles infection to SSPE symptom onset (latency) ranged between 4 and 10 years. A higher incidence has mainly been reported in boys (Table 1); the reason for this is not clear. However, data from South Africa (1984–90),¹² Japan (1999)¹³ and Papua New Guinea (1997–2000)¹⁴ indicated more equal distribution between the sexes.

An increase in age at onset once measles transmission has been greatly reduced or interrupted has been observed²²,^,49,58 together with an apparent lowering of male predominance in some countries.¹⁴,^,53,59 SSPE cases in Romania exceptionally moved to a slight female predominance.⁴² This suggestion of later onset in females is upheld by data from the SSPE Registry in England and Wales, based on 345 cases with onset between 1962 and 2005. The latency using only cases in whom age or date of measles infection was known n = 274, (and age at onset), in male cases had a different distribution to female cases (Figure 1), which was apparent before puberty. Females had a later age at SSPE onset (10.14 vs 12.21, P = 0.005 Kruskal–Wallis test) and a longer latency (8.32 vs 9.73, P = 0.03 Kruskal–Wallis test). Brazilian, US and South African data also supported the suggestion of later female onset.¹⁷,^,55,60 In two of three published adult onset case series, there were similar numbers of men and women (gender m/f 4/4⁶¹ and 7/6⁶²), in the third case series there was a male predominance (25/14).⁶³

And this section addresses Olmstead's wankery about co-infections and rural dwelling predominance:

Other factors

Rural dwelling has been reported as having a higher associated risk than urban dwelling,¹⁶,^{,36,49,53,64,52,65,70} but some studies have found no difference²³,^{,24,32,34,37,38,40,43,55,57} or, unusually, an urban excess.⁸ Animal or sick animal contact (more common in rural settings) has been a suggested risk,¹⁶,^{,18,20,54,64,70} but was not substantiated by other studies.⁴⁰,^,70 Close temporal association with another infection, either near the time of SSPE onset or initial measles infection, has also been reported¹⁶,^,31,64 as has an increased incidence of serious head injury in cases; though this may be due to early undiagnosed disease.⁸,^,42,39,54

Other suggested risk factors have included larger number of siblings and a later birth order (consistent with increased risk of early disease), lower socio-economic status and more crowded homes.⁸,^{,26,31,50,52,54} Uneven geographical distribution has been reported within countries, with a small number of very local clusters,⁴⁶,^,49,70 but no overall geographical pattern has emerged.

I saved the best for last though and could have actually just trotted this out in the beginning to completely demolish Olmstead's and Blanco's twaddle to save myself a lot of trouble but where's the fun in that?

Every SSPE biopsy sample submitted for molecular sequencing has always been wild-type virus and never vaccine strain measles virus.

6.4. Only wild-type virus sequences have been found in SSPE

The description of specific clades and genotypes of MV has allowed the evaluation of mutations found in the MV RNA sequences from SSPE brain material against wild-type (clades B–G) viruses. All the vaccine viruses are derived from the Edmonston strain (clade A) but no clade A virus has been found in SSPE brain material. The sequences found in SSPE brain are related to the wild-type viruses circulating at the time of initial infection of the child and not to those circulating at the time of onset of symptoms. Hence, the virus which initially infected the child, appears to persist and SSPE is not due to a super-infection by viruses circulating during the onset of symptoms (Jin et al., 2002) (Rima et al., 1995); Rota, personal communication). To the best of the authors’ knowledge no vaccine virus, genotype A, sequences have been obtained from SSPE cases. SSPE has been vastly reduced in incidence after successful control of measles by vaccination (Dyken et al., 1989). In contrast, vaccine strains have been identified in MV infections in immuno-compromised patients who died from MIBE (Bitnun et al., 1999) and giant cell pneumonia (Mawhinney et al., 1971).

Even in SSPE cases who did not have any reported measles disease but had measles vaccination, only wild-type measles strains were identified:

Although measles is a monotypic virus, 22 genotypes of wild-type virus are recognized; many genotypes have been associated with endemic circulation of measles virus in certain geographic regions or have been documented in connection with an outbreak or epidemic in an area [4, 5]. The measles vaccine virus strains belong to genotype A and can be distinguished from wild-type virus of the same genotype by means of sequence analysis [6 –8]. Analyses of measles virus sequences in brain tissue samples obtained from patients with SSPE have identified only wild-type measles virus, and the virus genotypes identified have been consistent with the genotype of measles virus that circulated in the area where the patients lived and to which the patients had been exposed ⩾10 years before the onset of symptoms of SSPE [6, 9 –13]. Genetic studies have supported epidemiologic evidence that measles vaccine virus does not cause SSPE [6, 14, 15]. In cases of SSPE that developed in children or adults who had no history of measles but who did have a history of vaccination against measles virus, analysis of measles virus sequences derived from the patients confirmed the presence of the wild-type genome, indicating that the individuals had an undiagnosed measles virus infection [6, 7, 9] 

To sum it up, the barmy trifecta of Olmsted, Blanco and Carly state that the measles vaccines are causing some kind of abhorrent SSPE masquerading as autism because some forty year old studies and super, (not so) secret meeting notes by public health officials who postulated that measles vaccines could cause SSPE.  That, in spite of hundreds of studies since that cannot find any association between measles vaccines and SSPE these dunderheads are doubling down on their deception to frighten people even more about vaccination in order to perpetuate their own delusion and to pay homage to their Saint Andy Wakefield.

Not only has MMR and measles vaccination reduced the incidence of SSPE and other measles encephalopathy, MMR vaccination also contains protection for congenital rubella syndrome which is well-documented to cause autism spectrum disorders.  We have a vaccine that prevents autism and other neuropathy and these dunderheads continue to try and find a way to discourage uptake.  Only in anti-vaxx land could this possibly make sense.