Encephalitis and Ether Anesthesia
Central Middlesex Hospital, 1943


Air Toxics Found Causative For
Encephalitis and Positive Virus Test Results
Via Ether Anesthesia

This is Jim West's review of: J.H. Humphrey, M.B., b.Ch., et al.
"Cranial Nerve Palsies with Herpes Following General Anaesthesia"
British Medical Journal
, 3/4/44

In 1944, a study of 13 encephalitis victims (2 deaths and 11 various paralyzed) at the Central Middlesex County General Hospital, focused upon air toxics as the cause, in the form of anesthesia formulations. The formulations and dosage levels varied considerably, yet, bear fundamental similarities to the record-high air toxics experienced by the WNV encephalitis victims in Queens/Bronx in 1999.

The anesthesia consisted of various mixtures of oxygen, ether, nitrous oxide, trichloroethylene, cyclopropane, and pentothal, suspected of forming synergistic compounds of higher toxicity, due to a soda-lime absorber which acted as a catalyst.

The Queens/Bronx atmosphere consisted of similar chemicals, a greater variety of chemicals, at record-high levels, recognized by the EPA as fatally dangerous: ether, ozone, aromatic nitros, sulfides, petroleum aromatics (and organochlorines, organophosphates, furans, and formaldehydes), combined in sunlight which served as a catalyst to form a more poisonous set of neurotoxic compounds known as photochemical smog.

The Middlesex report provides two tables:

Table I. Clinical Summary of Cases
No. Sex Age Operation
Date
Nature of
Operation
Anesthetic Duration of Operation Post-Op
Vomiting
Herpes Cranial Nerves Involved Comment
1 M 53 6/28/43 Bone graft Pent., cyclo., O2 induction -- trilene maintenance 1 1/2 hours - - Subjective V Not discovered until 4 1/2 months later
2 F 21 6/28/43 Appendicectomy Pent., cyclo., O2 + a little ether 1/2 hour + + V (all fivs.) and motor XII  
3 F 19 6/28/43 Appendicectomy Pent., cyclo., O2 + a little ether 1/2 hour + + V (all fivs.) and motor Followed case 2 on table
4 F 25 7/30/43 Appendicectomy Pent., cyclo., O2 + a little ether 1/2 hour - + III, V (all fivs.), XII, X  
5 F 62 7/30/43 Cholecystectomy Pent., cyclo., O2 + a little gas-O2-ether 1 3/4 hours - + + III, V (all fivs.), mainly subjective, XII, X Followed case 4 on table
6 M 41 8/22/43 Appendicectomy Gas, O2, ether, "to-and-fro" (on circle machine) 3/4 hour + + Subjective, right V (all divs.)  
7 F 45 8//343 Laparotomy Pent., cyclo., O2 1/2 hour + - Subjective, bilateral V (1 and 2 divs.), R VII  
8 F 56 8/4/43 Cholecystectomy Pent., cyclo., O2, ether 1 hour - - III, V, VII, X, XII Died in coma on 2nd post-operative day
9 F 46 8/17/43 Removal of cyst-adenoma of breast

Pent., trilene + O2 induction -- +cyclo. maintenance

1/2 hour + + V (all divs.), R. VII  
10 F 39 10/21/43 Hysterectomy Cyclo., O2 + a little ether 1 1/2 hours - + + III, V, VI, VII, VIII Very severe headache. R. extensor plantar response
11 M 74 10/27/43 Cystoscopy and suprapubic cystomy Cyclo., O2 3/4 hour - + - V (+motor), L. VI, VII Died on 16th post-operative day
12 F 18 10/27/43 Appendicectomy Cyclo., O2 35 minutes - + V., R. VII Under treatment for myasthemia gravis
13 F 36 10/27/43 Evacuation of uterus, severe blood loss Cyclo., O2 5 minutes - + L. V, transient L. VII Followed case 12 on table
Pent. = pentothal. Cyclo. = cyclopropane. Gas = nitrous oxide. O2 = oxygen. Trilene = trichloroethylene.

 

Regardless of the specifics, the Middlesex study, in conjunction with other studies, confirms that low dosages of neurotoxins can cause rapid virus proliferation.

Table II. Results Of Tests for
Antibodies Against Herpes
No. [Clinical]
Herpes
Herpetic
History
Time of Taking Serum
After Operation
Strain 10 MRC Strain
1 - - 13 weeks + +
2 + - 19 weeks

+

+
3 + -

6 weeks

+

+

4

+

-

4 days

+ +
5 + - 3 days + +
6 + + Not done na na
7 - - 7 days + +
8 - - 2 days + +
9 + + 11 days + +
10 + + 6 weeks + +
11 - - 4 days + +
12 + + 1 day + +
13 + + 1 day + +

 

Poisoning has long been considered causative for herpes. In 1888, the "leading authority" of skin diseases in Britain, Dr. Hutchinson stated,

"That it [an arsenic pharmaceutical] causes the outbreak of herpes is now, I think, generally admitted...." -- "Disease of the Skin", Transactions Of The Pathological Society, p362

A Harvard Medical website section by Keith A. Johnson and J. Alex Becker graphically describes herpes encephalitis, where it mentions:

"HSV is ubiquitous, but fortunately, only 1 or 2 cases per million infected individuals develop the encephalitis of HSV each year in the US. It is the most frequently fatal of all encephalitides."

The causative agent, the supposed "herpesvirus", is not quite ubiquitous in humans as stated above. Also, we should assume that herpes tests include the more inclusive serum antibody tests, rather than clinical observation, as the chart above shows. Such studies in the 1930s and more recently have shown herpes to be present in 65-70% of hospital patient populations. The clinical symptoms and physiology similar to the WNV encephalitis in New York City where it can be fairly assumed that herpesvirus was not tested for because HV is not an avian/mosquito virus. The herpesvirus is interesting because if tested for in encephalitis victims during August and September of 1999, it very likely could be found in far greater frequency and quantity than WNV. To date, WNV testing has a quantitative difficulty, whereas herpesvirus is quite tangible. WNV is a flavivirus (like the SLE and the Kunjin) and there are 73 flaviviruses. There are 251 known herpesviruses and they are present in virtually every species of animal, fish, reptile, mammal, and avian. They also represent well-known neurological diseases. A listing of herpesviruses is reminiscent of the NYCDEC's dead animal list for the summer of 1999. Here are a few: Equine herpesvirus 5, Epstein-Barr virus, Black stork herpesvirus, Bald eagle herpesvirus, Banded krait herpesvirus, Black footed penguin herpesvirus, Bobwhite quail herpesvirus, Bovine herpesvirus 5, Falcon inclusion body disease, Goat herpesvirus, Green lizard herpesvirus, Herpesvirus salmonis, Human herpesvirus 7, Lake Victoria cormorant herpesvirus, Map turtle herpesvirus, Medical Lake macaque herpesvirus, Owl hepatosplenitis herpesvirus, Papio Epstein-Barr herpesvirus, Parrot herpesvirus, Siamese cobra herpesvirus, Squirrel monkey herpesvirus, Turkey herpesvirus 1, Woodchuck herpesvirus marmota 1.

The Middlesex report:

"The most significant samples are the early ones from [anaesthesia-caused encephalitis] patients without herpetic histories, since in these cases the formation of antibodies would have been too rapid to be due to the herpes occurring at that time, quite apart from the fact that some never developed the condition." [...] If herpes or any other virus infection is involved it must have been 'lit up' by the anaesthetic. There is some experimental evidence for this possibility in the observation of Fiala (1943) that subdural or intravenous injection of vaccinia virus in rabbits is not normally followed by encephalitis, but is so if the rabbits are under urethane anaesthesia..."

The Middlesex anaesthesia victims acquired encephalitis and concurrently, herpes virus lesions rapidly, faster than normal virus incubation periods.

"All the cases showed a definite incubation period between operation and the first appearance of symptoms, ranging from 24 hours to three days. This is very short, by accepted standards, for a virus infection. [...] If herpes or any other virus infection is involved it must have been 'lit up' by the anaesthetic. [...] There is some experimental evidence for this possibility in the observation of Fiala (1943) that subdural or intravenous injection of vaccinia virus in rabbits is not normally followed by encephalitis, but is so if the rabbits are under urethane anaesthesia..."

Herpes supposed virus strains were identified by serum tests and animal experiments in all cases. Clinical appearance of herpes vesicles on the "lips, the chin, and occasionally the buccal mucous membrane and soft palate" occurred on the third day of 9 of 12 patients who survived the first 3 days, immediately following anaesthesia occurred. All herpes vesicles occurred near the sites of air toxics entry, i.e., there is no mention of genital herpes. Only 3 of the cases had a prior history of herpes.

"The clinical evidence [regarding cause for paralytic encephalitis] favours two possible theories, or a combination of both, but the experimental results are strongly in favour of a toxic theory. If the latter is adopted there must have been great susceptibility, since one anaesthesia (Case 13) was of five minutes' duration and the patient developed well-marked palsy."

"The only drug that could be incriminated is trichloroethylene plus soda-lime, and this only on the assumption that it could have persisted in the machine or in the soda-lime between the anaesthesias in which it was used. On two occasions as long as three days elapsed between the use of trichloroethylene and the anaesthetic which was followed by palsies, and during the intervals there had been given nine and twelve closed-circuit cyclopropane or ether anaesthesias respectively on the same machine without any ill effects. [...] The fact that only a small proportion showed symptoms would mean that there must be great variation in susceptibility. such variations are well known in toxicology."

Thus, trichloroethane was suspected.

Only 2 of the cases used trichloroethylene, but the final summary describes the soda-lime absorber as suspect in conjunction with trichloroethylene, by assuming that the absorber catalyzes an unknown toxin from trichloroethylene and the absorber allows transfer of the unknown toxin from surgical session to surgical session.

"The first case of the series was missed until 4 1/2 months later, when a chance remark of the patient's drew attention to his [herpes] lesion. It seems to us possible that mild case may have occurred elsewhere, and the facts recorded above have been published in the hope that the observations of others may help to shed light upon the problem"

"It is now over three months since we ceased using trichloroethylene in association with soda-lime, and although many trichloroethylene anaesthesias, some lasting up to three hours have been given, no further palsies have occurred."

It seems evident that soda-lime catalyzes the production of an unknown toxin, and/or phosgene via reaction products from trichloroethylene so that very low dosages can trigger an inflammatory reaction in the nervous system called encephalitis, accompanied by the rapid activation and proliferation of herpes virus. There are at least as many synergistic unknowns in MTBE and photochemical smog -- and in New York City, at least as many variations in susceptibility.

Blaming trichloroethylene and the soda-lime absorber raises questions because trichloroethylene ("trilene") was only used twice during a 4 month period, insofar as shown in Table I. Generally, at Middlesex, trichloroethylene was used in 13% of the 600 inhalation anaesthesia performed in Theatre I where a closed circuit machine was used and all of the encephalitis cases occurred. The chemicals which were usually associated with the soda-lime absorber and encephalitis (per Table I) were: 1) cyclopentane and/or ether, and 2) oxygen -- but not including the last day. These 3 chemicals are individually considered to be safer than trichloroethylene, so trichloroethylene was suspected because it can produce toxic phosgene in contact with soda-lime. However, the 13% frequency of usage questions its culpability, but if culpable, reinforces its dangers (and the dangers of organochlorines generally) when present at very low dosages in mixture with other chemicals: ether, oxygen, aromatic nitros, cyclopentane, and a catalyst. The similar argument might be made for nitrous oxide, which was also used twice. Aromatic nitros can be highly neurotoxic.

Only oxygen and the absorber could actually be associated 100% of the time with encephalitis. However, in all but one case (case #6) cyclopentane and oxygen were present. In case #6, ether was substituted for cyclopentane. The most dramatic cases (associated with the shortest periods, as low as 5 minutes of anaesthesia) occurred in the presence of only these two chemicals and the soda-lime absorber. The New York City victims had several months of exposure to record-high air-neurotoxins.

The events at Middlesex Hospital Cyclopentane serendipitously serve as a comprehensive laboratory study for the chemically analogous events which occurred environmentally in NYC, the summer of 1999. Cyclopentane (analogous to basic automobile emissions), pure oxygen (somewhat analogous to ozone), nitrous oxide (nitrogen oxides which form aromatic nitros), ether (analogous to MTBE), and the minor role of trichloroethylene (solvents, pesticides), result in a strong analogy for the air toxics over the New York Region during the summer of 1999, by recognizing in Table I, the minimal presence of trichloroethylene, which this study held as primary suspect.

I have summarized the Middlesex study in the following table:

Comparative Summary of Middlesex vs. New York City, 1999
C o m p o n e n t C o m m e n t
Middlesex NYC 1999 Middlesex NYC 1999
Cyclopentane A large variety of volatile automobile emissions 12 cases  
Ether MTBE (methyl tertiary butyl ether) 7 cases MTBE in RFG gasoline increased as of 1995, record high pollution in 1999, unprecedented bird deaths in 1999.
Oxygen (O2) Oxygen and ozone 13 cases (all) Ozone is said to be a neurotoxin
Pentothal   8 cases (C11H17N2O2SNa) No direct analogy
Trichloroethane Many various organo- and fluoro- hydrocarbons (solvents, pesticides) 2 cases. Possibly lingered in the mechanical system and the soda-lime absorber. Thus if culpable, the effects must have been due to very low dosage. In the presence of soda-lime, it can form dichloroacetylene which in turn can oxidize to phosgene, both reaction products being neurotoxic. Organochlorines are common solvents.
Nitrous Oxide NO2, NO1, and NOx 2 cases Combines photochemically to produce aromatic nitros, which are powerful neurotoxins.
  Sulfur oxides   Toxic
  Carbon particulates   Stressor
  Carbon monoxide   Neurotoxic
  Carbon dioxide    
  Other: e.g., organophosphate pesticides, etc.   Powerful neurotoxins
Soda-lime absorber (catalyst) Sunlight (catalyst) All cases. See 'trichloroethane' above, for formation of other neurotoxins, which were suspected to have caused fatal encephalitis and to have 'lit up' viruses (much faster than normal incubation periods). Dangerous levels of neurotoxic, photochemical smog.

The Middlesex authors note that attempts had been made since the 1920s to incriminate herpes virus for neurological disease, without success, yet as stated in the Harvard reference (above), modern studies have deemed its association with encephalitis as causal.

The Middlesex study: Virus tests in the brain tissue (animal inoculation studies, some of which included unfiltered tissue puree) were negative, however, in 1944, limited methods were available to find viruses as PCR technique did not exist. With PCR, possible findings might have been WNV, SLE, Kunjin virus, HIV, or bad genes. If the scientific standards found in the current AIDS or WNV paradigms were applied, then these patients could have been found endangered by mosquitoes, unsafe sex, or genetic susceptibility to neurotoxins.

Because of the prevalence of herpes in the U.S. (65-70%), herpesvirus would likely be found in a high percent of encephalitis victims in New York City. In light of the Middlesex study, 100% of all encephalitis victims in New York City might test positive for herpesvirus. I suggest a search for herpesvirus in all encephalitis patients. CDC virologist, Lanciotti, has stated that to his knowledge, during 1999, only viruses within the arbovirus paradigm were tested for.

Recent studies have consistently associated herpesvirus and a herpes-retrovirus with several forms of CNS disease (See book by The Virus Within).

Explaining Herpes

Isn't chickenpox or herpesvirus contagious?  Answer:  Apparently, but studies show symptoms are brought about by poisoning.  Symptoms can be explained as beneficial, i.e., cathartic or metabolic responses to poisoning.   The observed contagion could be response symptoms shared or catalyzed between individuals,  like yawning or menstruation.  All can be explained by behavioral and hormonal sciences.  Behavioral inertia in hormones and enzymes, and/or triggering (cellular level suggestions) of protective capabilities in a poisoned environment, could explain transmission.  The virus paradigm is too narrow (cog and gear, the pathogenic external enemy) to explain anything, too protective of industry and oblivious to the needs of health. The virus itself was isolated and properly characterized as claimed of Weller and Stoddard (1952).  Behavior memory, learning theory, is the best explanation for what is actually a catharsis and defense against poisoning.


All Rights Reserved -- Jim West