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,

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

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

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.

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.

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.

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).

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.