Hilary / Reisinger - Endotoxin Shock/SIDS - (ecoli info)

[Guest guest]

Here is the information referenced in her position paper and

in the last email I forwarded to you all...

http://users.erols.com/drrobert.sids/Endotox.html

ENDOTOXIN SHOCK AND ITS RELATIONSHIP

TO SUDDEN DEATH AND OTHER CLINICAL

SYNDROMES OF YOUNG MAMMALS:

A UNIFYING CONCEPT

BY

ROBERT C. REISINGER, D.V.M., M.S.

1971

SUDDEN DEATH SYNDROME

There are striking similarities between the Sudden Death Syndrome (SDS) of

the human infant and the young of other mammalian species. The young calf,

piglet, foal, rabbit and monkey are similarly afflicted, (17, 33, 34, 45,

66, 67, 92, 98) as are the young of other, perhaps all, mammalian species.

It is postulated, that the final cause of death, an endotoxemia, is the

same in all. This endotoxemia may be precipitated by a variety of adverse

contributing factors, including viruses and various environmental

stressors.

The basis of this hypothesis is the well-documented, but generally ignored

fact that endotoxin is absorbed from the gastrointestinal tract of all

mammalian species (28, 29, 30, 33, 51, 61, 64, 66, 67, 98). Absorbed

endotoxin is normally detoxified in the liver. Endotoxemia results when one

or more of many and varied " adverse contributing factors " interferes with

normal liver functions, and/or results in increased endotoxin production

within an increased absorption from the gastrointestinal tract so the

detoxication is incomplete.

If incomplete detoxification occurs free endotoxin is carried via the

inferior vena cava into the right side of the heart and by the pulmonary

artery into the lungs. Lesser amounts are carried into the left side of the

heart and by the way of the arterial circulation into all parts of the

body, but in decreasing amounts. Extremely small quantities of endotoxin

absorbed over several hours time exert adrenergic action in the lungs, and

reduction of thrombocytes and fibrinogen. Alternating vasoconstriction and

dilatation, and increased capillary permeability, with drastically

decreased thrombocytes and fibrinogen levels, result in varying amounts of

edema and hemorrhage by diapedesis, primarily in the lungs, where the

greatest concentration of endotoxin occurs, and death (8).

Infants, who have succumbed to the sudden Death Syndrome have varying

degrees of edema and hemorrhage of the lungs and unclotted blood in the

heart and large vessels (2, 7). Decrease of platelets and fibrinogen

following initial vasoconstriction and then dilatation and increased

permeability of capillaries, all of which are known reactions to endotoxin

(29, 30, 72, 73) can cause such changes.

The intestinal microflora of the normal breast-fed infant consists largely

of Bacteroides and Lactobacillus spp., which may in the early weeks of life

constitute 90 percent or more of the total bacterial organisms in the feces

(35, 36, 58, 83). Relatively few toxin producing Escherichia coli are

present in the digestive tract of the normal breast-fed infant, usually

totaling no more than one percent of the total bacteria in the feces.

Substitution of breast feeding by bottle feeding with cow's milk results in

a dramatic and immediate hundred fold or greater increase in E. coli, so

that they may equal or exceed numbers of Bacteroides and Lactobacilli, and

a rise in pH from approximately 5.8 for the breast-fed infant to 7.4 in

infants fed cow's milk. Also, because of it's high casein and high calcium

content, cow's milk forms larger and firmer curds and takes longer to pass

through the bowel (99). Thus, cow's milk interferes with two basic defense

mechanisms of the infant's digestive tract - acidity and adequate

intestinal motility. Human milk has a lactose:protein-ratio of 6:1 and

cow's milk a lactose:protein-ratio of 1.5:1 (54). Various commercial infant

feeding formulas available in this country have lactose:protein-ratios from

5:1 to 2:1 (26). Experiments in the human infant and other mammalian

species have demonstrated that, to establish or maintain a predominantly

lactobacilli intestinal microflora it is essential that a quantity of

lactose sufficient to produce approximately the same quantitative

lactose:protein ratio, that exists in human milk be present (35, 99).

Theobald and n Orcutt (80) described the mechanism of diarrhea

in calves as " a great increase in the number of E. coli in the lowest third

of the small intestine with a spreading of the invasion towards the

duodenum as the disease gains headway. Under these conditions, a general

intoxication results......

Escherichia coli in the digestive tract has not been in general regarded as

significant. This significance appears when the quantitative factor,

obtained before natural death, is determined. " Thus, and Orcutt

explained and documented the key importance of quantitative and location

factors in the role of E. coli in the diarrhea syndrome of calves and the

fact that such changes occur antemortem.

Theobald and Ralph B. Little (81) described the action of E. coli

filtrates inoculated intravenously in the calf and cow. Their description

of the resulting pathology - primarily edema, congestion and hemorrhages

affecting the lungs and other organs, is very similar to the pathology

described by Adelson (2) and others (7) in the Sudden Death Syndrome.

Reisinger (66, 67) confirmed the findings of and co-workers regarding

the role of E. coli in the pathogenesis of calf diarrhea. He also reported

that two of his series of 65 calves died suddenly and unexpectedly, without

evidence of diarrhea or struggle, within several hours after having been

observed to appear healthy and normal. " -- in most of the early deaths,

grossly evident inflammation of the intestinal tract was conspicuous by

it's absence, and the most consistent gross pathological finding was

varying amounts of edema of the mesenteric lymph glands. " Septicemia was

not necessary for death to occur, but as many as 100-500 million E. Coli

organisms per ml of intestinal contents were demonstrated in the upper

ileum and jejunum which in the healthy animal contain few or none of these

organisms.

Gay (33) has described the " enteric-toxemic form of colibacillosis "

associated with sudden death of calves up to one month of age. In his

experience, " the calf usually died before scouring (diarrhea) was evident. "

Arnold and Brody (4) found the normal pH of the duodenum and upper jejunum

of dogs to be between 5.5. and 6.3. " The slightly acid reaction of the

content of this part of the intestinal tract is to a large extent dependent

upon the gastric secretory function, and under these conditions the

contents of the upper half of the small intestine are practically free of

bacteria. When the reaction is neutral or slightly alkaline (pH 7 to 8) the

bacterial flora resembles that of the cecum, i.e., there is a predominance

of the coli-aerogenes type of flora. This can be produced by injecting

alkaline-buffered solutions into the lumen of the duodenum, by feeding

alkaline salts, or by elevation of the temperature of the animals (dogs). "

Digestion and absorption of carbohydrates, fats and proteins occurs

primarily in the upper portion of the small intestine (10, 76). This

portion of the digestive tract normally contains few or no toxin-producing

organisms (20, 66, 67, 80) -- if toxin is produced in appreciable amounts

in this portion of the digestive tract, the individual is either ill or

dead, depending on the amount and rate of toxin absorption and relative

resistance or susceptibility to the toxin. (12, 25, 43, 53, 66, 67, 80).

Dubos et al. (24) in a review relating to the composition, alteration and

effects of the intestinal flora suggest that the enterobacteria and

especially E. coli, the Proteus and Pseudomonas bacilli, the enterococci

and the clostridia are accidental inhabitants of the intestine rather than

part of it's normal flora. They have developed and maintained a colony of

mice (NCS) practically free of E. coli in which the largest percentage of

intestinal flora cultivable both aerobically and anaerobically consists of

organisms commonly classified as Lactobacillus and Bacteroides spp. NCS

mice grow faster, are more resistant to lethal effects of endotoxin and

have less exacting nutritional requirements than control mice. However,

administration per os of even small quantities of penicillin brings about a

sudden disappearance of lactobacilli from the fecal flora of NCS mice

accompanied by an explosive and lasting increase in enterococci and gram

negative enterobacilli. E. coli, which is not normally found in the stool

cultures of the NCS mice, became abundant following treatment with

penicillin. These findings are similar to those of De Somer et al. (21) in

the guinea pig which also normally has a primarily gram positive intestinal

microflora. Schaedler and Dubos (74) found that in the mouse " the

composition of the bacterial flora could be rapidly and profoundly altered

by a variety of unrelated disturbances, such as sudden changes in

environmental temperature, crowding in cages, handling, administration of

antibacterial drugs, etc. The first effect of the change was a marked

decrease in the numbers of lactobacilli and commonly an increase in the

numbers of gram negative bacilli and enterococci. When tested three weeks

after these disturbances some NCS animals, normally relatively resistant,

were found to have become susceptible to the lethal effect of endotoxin. "

Dubos et al. (24) reported that the numbers of lactobacilli recovered from

stools of mice fed diets of natural materials were much larger than in

those mice fed a casein semi-synthetic diet.

Dubos et al. (24) and Ravin et al. (64) have shown, that endotoxin is being

continually absorbed into the circulatory system of animals which have

appreciable numbers of E. coli in their digestive tracts. Fine and

co-workers (28, 29, 30) have stated that endotoxins are always at hand

ready to destroy peripheral vascular integrity, and to kill the moment the

endotoxin detoxifying power is lost. They have shown that irreversible

shock resulting from prolonged blood loss is due to the inability of the

damaged reticuloendothelial system to adequately detoxify endotoxin being

continually absorbed from the intestinal tract. They have also shown that

blocking the reticuloendothelial system of the rabbit with thorotrast (a

sterile colloidal suspension of 25% thorium dioxide in dextrins) makes this

animal exquisitely susceptible to the effects of endotoxin.

Rabbits so blockaded can be killed with one one-hundred-thousandth of the

normally lethal dose of endotoxin (28). Guinea pigs, whose intestinal

tracts usually contain very few coliforms, are consistently killed with

penicillin or the tetracyclines, which destroy the normal gram positive

flora and allow overgrowth of E. coli (21).

Viruses, various immunization procedures,and any of the many and varied

other stressors which may interfere with, or occupy, the RE system may make

the infant even more normally sensitive to the effects of endotoxin.

Administration of Diphteria-Pertussis-Tetanus toxoid (DPT) can cause

temporary liver disfunctions in infants similar to those resulting from

viral hepatitis (14), and inoculations of killed Bordetella pertussis

organisms makes some strains of mice 200 times more sensitive to histamine

(1) and 3 to 5 times as sensitive to Brucella and Salmonella endotoxins for

approximately 14 days (1, 3).

These facts are well documented and when assembled make a reasonable

pattern supporting the critical importance of the effects of these various

stressors, particularly in the young infant absorbing relatively more

endotoxin from the intestinal tract than the more mature, and having less

resistance to it.

An infant absorbing abnormally large quantities of endotoxin from the

intestinal tract may be " up to the mouth " , almost drowning in endotoxin and

yet appear apparently normal until the critical threshold is reached. He is

able to handle relatively large amounts of endotoxin within limits as long

as his reticuloendothelial system is functioning properly and detoxifying

adequately. However, when viruses or other stressing factors interfere with

the detoxifying process or actions of the RE system, and/or interfere with

the normal defense mechanisms of the digestive system to the extent that

tremendously increased amounts of endotoxin are being produced in and

absorbed from the digestive tract, he is overwhelmed. The result may be a

less acute syndrome manifested by diarrhea and the symptoms associated

therewith, or by the peracute form manifested by the Sudden Death Syndrome.

In both conditions the mechanisms, are the same - they differ only in

degree.

Since we can never hope to protect an infant from the many viruses and

other environmental stressors with which in the normal course of events he

must come in contact, the most practical approach to prevention of the SDS

would seem by appropriate diet to maintain him as coliform-free as possible

during the period of greatest risk - at least through the first six months

of age. This can best be done by breast feeding.

OTHER CLINICAL MANIFESTATIONS OF ENDOTOXIN SHOCK:

UNIFYING CONCEPT

It is postulated that endotoxemia is the ultimate cause of a large

proportion of cases of not only Sudden Death Syndrome, but also of Hyaline

Membrane Disease, Infant Diarrhea, Pneumonias of " Obscure " Etiology and

Toxemia of Pregnancy. Each of these syndromes is a varying manifestation of

endotoxin action resulting from exposure to varying amounts of endotoxin

over varying periods of time in hosts of varying susceptibilities.

There is an abundance of experimental and clinical evidence in other

mammalian species, as well as in man, to indicate the occurrence and

importance of endotoxin absorption. While recognizing the need for further

research in this area, perhaps of equal importance is the need to

objectively examine presently available evidence. It is difficult to

believe that all positive evidence developed in the past is invalid. It is

equally difficult to believe that endotoxin absorption, proven so important

in the pathogenesis of many diseases of various other mammalian species,

does not occur in man. The stakes are too high to continue to ignore this

possibility. For if endotoxin absorption is an important factor in the

pathogenesis of human disease, knowledge of this fact makes amenable to

prevention and treatment of many important diseases now considered obscure.

With the extensive background of information and evidence available,

controlled clinical studies may offer the most logical and fruitful area

for confirmation and development of further information. Only when persons

engaged in the many different areas of disease studies begin to consider

it's possible involvement will the full role of endotoxin absorption begin

to be adequately assessed. All that is " known " in medicine, and all that is

unknown, should be reassessed from the standpoint of this possible

involvement.

Since it will probably never be possible to prevent, or even to know, all

of the many " adverse contributing factors " which may result in or

contribute to the state of endotoxemia, the best hope for prevention and

therapy of the various diseases in which endotoxemia is involved would seem

by appropriate dietary and chemotherapeutic means to limit amounts of

endotoxin produced in and absorbed from the digestive tract.

REFERENCES

1. ABERNATHY, S. and SPINK, Wesley W.: Studies on the Role of

Histamine in the Increased Susceptibility to Bacterial Endotoxins Induced

by Pertussis Vaccine. J Immunol 77: 418-422, 1956.

2. ADELSON, Lester: Specific Studies of Infant Victims of Sudden Death. In

Sudden Death in Infants, U.S. Public Health Service, Pub. No. 1412, 11-40,

1965.

3. ANDERSON, Else Krag: Studies on Reproducibility in Detecting a Decline

in Protection During Immunization on the Resistance of Mice to Heterologous

Infection. Acta Path Microbiol Scand 40: 235-247, 1957.

4. ARNOLD, Lloyd and BRODY, Louis: The Gastro-Duodenal Bactericidal

Mechanism. Amer J Hyg 6: 672-683, 1926.

5. ARTENSTEIN, Malcolm S., CADIGAN, Jr., Francis C. and BUESCHER,

L.: Clinical and Epidemiological Features of sackie Group B Virus

Infections. Ann Intern Med 63: (4) 597-603, October 1965.

6. BAKER, J.A.: A Filterable Virus Causing Enteritis an Pneumonia in

Calves. J Exp Med 78: 435-445, 1943.

7. BECKWITH, J. Bruce and BERGMAN, Abraham B.: The Sudden Death Syndrome of

Infancy. Hosp Pract 2: (11) 44-54, November 1967.

8. BELLER, Fritz K. and GRAEFF, Henner: Deposition of Glomerular Fibrin in

the Rabbit After Infusion with Endotoxin. Nature 215: (5098) 295-296, July

15, 1967.

9. BOHNHOFF, Marjorie, MILLER, C. Philipp and MARTIN, R.:

Resistance of the Mouse's Intestinal Tract to Experimental Salmonella

Infection. II. Factors responsible for it's loss following streptomycin

treatment. J Expt Med 120: (5) 817-828, November 1964.

10. BOOTH, C.C.: Sites of Absorption in the Small Intestine. Fed Proc 26:

(6) 1583-1588, November-December 1967.

11. BRANDLY, C.A. and McCLURKIN, A.W.: Epidemic Diarrheal Disease of Viral

Origin of Newborn Calves. Ann NY Acad Sci 66: 181-185, 1956.

12. BULLEN, J.J. and SCARISBRICK; R.: Enterotoxaemia of Sheep: Experimental

Reproduction of the Disease. J Path Bact 73: 495-509, 1957.

13. CALVES PROVIDE CLUES TO HUMAN 'CRIB DEATHS'. JAMA 199: (6) 38, February

6, 1967.

14. CAPPS, B., BENNETT, Alfred M., MILLS, H., ETTINGER,

H., DRAKE, Miles E. and STOKES, Jr., ph: Infectious Hepatitis

in Infants and Small Children. Amer J Dis Child 89: 701-716, 1955.

15. CELL DIVISION FREQUENCY: MICROORGANISMS. Table 75, p. 97. Handbook of

Biological Data. National Academy of Sciences - National Research Council,

(ed.) S. Spector, W.B. Saunders Co., Philadelphia and London, 1956.

16. CHIRIGOS, A., National Cancer Institute, National Institutes of

Health, U.S. Public Health Service, Department of Health, Education and

Welfare, Bethesda, MD. Personal Communication, 1968.

17. CHOPRA, S.L., BLACKWOOD, A.C., and DALE, D.G.: Enteritis of Early

Weaned Pigs. II. Pathogenesis. Canad J Comp med 28: 272-278, November 1964.

18. COOMBS, Robin: An Experimental Model for Cot Deaths. In Sudden Death in

Infants, pgs. 55-74, U.S. Department of Health, Education and Welfare,

Public Health Service, National Institute of child Health and Human

Development, Bethesda, land, October 1965.

19. CRAMBLETT, Henry G. and SIEWERS, C.M.F.: The Etiology of

Gastroenteritis in Infants and Children, with Emphasis on the Occurence of

Simultaneous Mixed Viral-Bacterial Infections. Pediatrics 35: (6), 885-898,

June 1965.

20. CREGAN, Judith and HAYWARD, J.: The Bacterial Content of the

Healthy Human Small Intestine. Brit Med J 1: (4824), 1356-1359, June 1953.

21. DE SOMER, P., DE VOORDE, H., EYSSEN H. and VAN DIJCK, P.: A Study on

Penicillin Toxicity in Guinea Pigs. Antibio Chemother V: (9), 463-469,

September 1955.

22. DI SANT'AGNESE, A.: The Stomach and Intestines: Intestinal

Malabsorption, p. 720-730. IN Textbook of Pediatrics, 8th Edition, (ed.)

Waldo E. , W.B., W.B. Saunders Co., Philadephia and London, 1964.

23. DOW, D., JARRETT, W.F.H. and McINTYRE, W.I.M.: A Disease of Cattle in

Britain Resembling the Virus Diarrhea-Mucosal Disease Complex. Vet. Rec 68:

620-623, 1956.

24. DUBOS, René, SCHAEDLER, W. and COSTELLO, : Composition,

Alteration and Effects of the Intestinal Flora. Fed Proc 22: 1322-1329,

November-December 1963.

25. DUDGEON, Leonard S.: A Study of the Intestinal Flora under Normal and

Abnormal Conditions. J Hyg 25: 119-141, 1926.

26. EDWARDS, Allan E., HILL, A., TREADWELL, Terry: Improvements in

the Magnetometer Technique of Measuring Gastric Motility. Psychophysiology

4: 116-118, 1967.

27. EINHEBER, A.: Discussion of Paper by Dr Fine. Fed Proc 20: 170-172,

1961.

28. FINE, J., RUTENBURG, S., SCHWEINBURG, F.B.: The Role of the

Reticulo-Endothelial System in Hemorrhagic Shock. J Exp Med 110: 84)

547-569, October 1959.

29. FINE, : Septic Shock. J Amer Med Ass 188: 427-432, 1964.

30. FINE, : Current Status of the Problem of Traumatic Shock. Surg

Gynec Obstet 120: 537-544, March 1965.

31. FOLEY, E.: Toxemia of Pregnancy in the Guinea Pig. J Exptl Med 75:

539-546, 1942.

32.GANAWAY, J.R. and ALLEN, A.M.: Obesity Predisposes to Pregnancy Toxemia

(Ketosis) of Guinea Pigs. Lab Anim Sci 21: 40-44, 1971.

33. GAY, C.C., McKay, K.A. and BARNUM, D.A.: Studies on Colibacillosis of

Calves. II. A clinical evaluation of the efficiency of vaccination of the

dam as a means of preventing colibacillosis of the calf. Canad vet J 5:

297-308, November 1964.

34. GAY, C.C.: Escherichia Coli and Neonatal Diseases in Calves. Bac Rev

29: (1) 75-101, March 1965.

35. GERSTLEY, , HOWELL, and NAGEL, Beth Reynolds: Some

Factors Influencing the Fecal Flora in Infants. Amer J Dis Child 43:

555-565, 1932.

36. GYLLENBERG, Helge and ROINE, Paavo: The Value of Colony Counts in

Evaluating the Abundance of " Lactobacillus " Bifidus in Infant Faeces. Acta

Path Microbiol Scand 41: 144-150, 1957.

37. HALBERG, Franz: Temporal Coordination of Physiologic Function. Cold

spring Harbor Symposia on Quantitative Biol XXV: 289-292, 1960.

38. HANDBOOK OF INFANT FORMULAS. J.B. Roerig Division, Chas. Pfizer & Co.,

Inc., New York, 1967, pp. 41.

39. HEATHFIELD, K.W.G., PILSWORTH, R., WALL, B.J. and CORSELLIS, J.A.N.:

sackie B5 Infections in Essex, 1965, with Particular Reference to the

Nervous System. Quart J Med 36: (144) 579-595, 1967.

40. HOSHINO, Hirotoshi: Hemodynamic Studies on Liver in Toxemias of Late

pregnancy. J Jap Obst & Gynec Soc (English Edition) 6: (1) 42-44, January

1959.

41. JOHNSON, W.C. and MEYER, J.: A Study of Pneumonia in the Stillborn and

Newborn. Amer J Obst & Gynec 9: (2) 151-176, 1925.

42. JOHNSTONE, J.M. and LAWY, H.S.: Role of Infection in Cot Deaths. Brit

med J 1: 706-709, March 1966.

43. KOHLER, E.M.: Studies of Escherichia Coli in Gnotobiotic Pigs. V.

Evaluation of the Effects of Oral and Parenteral Administration Immune

Serum. Canad J Comp Med 31: 283-289, November 1967.

44. MARONPOT, R.R. and WHITEHAIR, C.K.: Experimental Sprue-Like Small

Intestinal Lesions in Pigs. Canad J Comp Med 31: (12) 309-316, December

1967.

45. McCLURKIN, A.W.: The Characterization of a Virus Causing Calf

Pneumonia-Enteritis and Nature of the Disease. PhD Thesis, University of

Wisconsin, Madison, 1956.

46. McGAFFEY, Hazel L.: Acidosis May be Clue to Crib Death. JAMA 206: (7)

pg. 1440, November 1968.

47. McGAFFEY, Hazel L.: Sacred Heart Hospital, Idaho Falls, Idaho. Personal

Communication, 1969.

48. McKAY, G.: Disseminated Intravascular Coagulation. An

Intermediary Mechanism of Disease. Hoeber Medical Division, Harper & Row

Publishers, New York, ton and London, 1965, 493 pp.

49. McKAY, Jr., and SMITH; Clement A.: Diseases of the Newborn Infant: Full

Term and Premature, p. 397-398. IN Textbook of Pediatrics, 8th Edition,

(ed.) Waldo E. , W.B. Saunders Co., Philadelphia and London, 1964.

50. MARKLEY, K., SMALLMAN, E. and THRONTOB, S.W.: Demonstration of a

Circulating Endotoxic Hapten in Burned Mice. Proc Soc Exp Biol & Med 137:

584-589, 1971.

51. MARKLEY, Kehl, SMALLMAN, and EVANS, : Mortality due to

Endotoxin in Germfree and Conventional Mice after Tourniquet Trauma. Amer J

Physiol 212: (3) 541-548, March 1967.

52. MARKLEY, Kehl: The Role of Bacteria in Burn Mortality. Ann NY Acad Sci

150: (3) 922-930, August 1968.

53. MEYER, Ludwig Ferdinand and NASSAU, h: Physiology and Pathology of

Infant Nutrition. C. , Publisher, Springfield, Illinois,

1955, 548 pp.

54. MILK, CHEMICAL COMPOSITION: MAN, COW, GOAT. Table 34, p. 50 in Handbook

of Biological Data. National Academy of Sciences - National Research

Council, (ed.) S. Spectore, W.B. Saunders Co., Philadelphia and

London, 1956.

55. MILK, CHEMICAL COMPOSITION: VARIOUS ANIMALS. Table 35, p. 50 in

Handbook of Biological Data. National Academy of Sciences - National

Research Council, (ed.) S. Spector, W.B. Saunders Co., Philadelphia

and London, 1956.

56. MOFFET, Hugh L., SCHULENBERGER, Helen K., and BURKHOLDER, Ernest R.:

Epidemiology and Etiology of Severe Infantile Diarrhea. J. Ped 72: (1)

1-14, 1968.

57. NEWTON, Walter L., STEINMAN, Harry G. amd BRANDRISS, W.:

Absence of Lethal Effect of Penicillin in Germfree Guinea Pigs. J Bact 88:

(2) 537-538, August 1964.

58. OLSEN, : Studies on the Intestinal Flora of Infants. Ejnar

Munksgaard, Copenhagen, 1949, 147 pp.

59. O'REILLY, M.J.J. and WHILEY, Margaret K.: Cot Deaths in Brisbane, 1962

to 1966. Med J Aust 2: 1084-1087, December 1967.

60. PATHOLOGY, Fifth Edition, (ed.) W.A.D. , The C.V. Mosby

Company, Saint Louis, 1966.

61. PHYSICIANS INTERNATIONAL PRESS: Rapid E. Coli Invasion May Cause Sudden

Infant Death. Pediat Newsl: (6) 23-24, June 1967.

62. POTTER, Edith L.: Pathology of the Fetus and Infant. Year Book Medical

Publishers, Inc., Chicago, Second Edition, 1961.

63. RAMOS-ALVAREZ, M and OLARTE, J.: Diarrheal Diseases of Children. Amer J

Dis Child 107: (3) 218-231, March 1964.

64. RAVIN., ROWLEY, D., JENKINS, C and FINE J.: On the Absorption of

Bacterial Endotoxin From the Gastro-Intestinal Tract of the Normal and

Shocked Animal. J Exp Med 112: 783-792, 1960.

65. READ, A.E., McCarthy, C.F., AJDUKIEWICZ, A.B. amd BROWN, G.J.A.:

Encephalopathy After portacaval anastomosis. The Lancet II: (7576)

999-1001, November 1968.

66. REISINGER, C.: Studies on the Pathogenesis of Infectious

Diarrhea of Newborn Calves. M.S. Thesis, University of Wisconsin, Madison,

1957.

67. REISINGER, C. Pathogenesis and Prevention of Infectious Diarrhea

(Scours) in Newborn Calves. J Amer Vet Med Assoc 147: (12) 1377-1386,

December 1965.

68. REISINGER, C.: Parainfluenza 3 Virus in Cattle. Ann NY Acad Sci

101: Article 2, 576-582, November 1962.

69. ROBBINS, Frederick C.: The Response of Young Infants to Viral

Infections, p. 93-100. IN Sudden Death in Infants, U.S. Public Health

Service Pub. No. 1412, 1965.

70. ROGERS, J.B., VAN LOON, E. and BEATTIE, M.: Familial Incidence of a

Toxemia of Pregnancy in the Guinea Pig. J Exptl Zool 117: 247-258, 1951.

71. ROONEY, R., BRYANS, T. and DOLL, E.R.: Colitis " X " of

Horses. JAVMA 142:(5) 510-511, March 1963

72. ROSEN, Fred S.: The Endotoxins of Gram-negative Bacteria and Host

Resistance. New Eng J mEd 264: (18) 919-923, 1961.

73. ROSEN, Fred S.: The Endotoxins of Gram-negative Bacteria and Host

Resistance. (Concluded) New Eng J Med 264: (19) 980-985, 1961.

74. SCHAEDLER, W., and DUBOS, René J.: The Fecal Flora of Various

Strains of Mice, it's Bearing on their Susceptibility to Endotoxin. J Exp

Med 115: 1149-1160, 1962.

75. SEVERE PNEUMONIA IN YOUNG CHILDREN: IN British Medical Journal (Leading

Article) No. 5256, pg. 267, London, November 2, 1968.

76. SHEEHY, W. and FLOCH, H.: The Small Intestine; It's

Function and Diseases, p. 44-85. Hoeber Medical Division, Harper & Row,

Publisher, New York, ton and London, 1964.

77. SMITH, Clement A.: The Physiology of the Newborn Infant. C.

, Publisher, Springfield, Illinois, 1959, 497 pp.

78. SMITH, Clement A.: The Physiology of the Newborn Infant. C.

, Publisher, Springfield, Illinois, 1959, 497 pp.

79. SMITH, H.W. and CRABB, W.E.: Faecal Bacterial Flora of Animals and Man;

It's Development in the Young. J. Path Bact 82: 53-66, 1961.

79. SMITH, Theobald and LITTLE, R.B.: The Significance of Colostrum to the

Newborn Calf. J Exp Med 36: 181-199, 1922.

80. SMITH, Theobald and ORCUTT, n L.: The Bacteriology of the

Intestinal Tract of Young Calves with Special Reference to the Early

Diarrhea ( " Scours " ). J Exp Med 41: 89-106, 1925.

81. SMITH, Theobald and LITTLE, R.B.: Studies on Pathogenic Bacterium coli

from Bovine Sources. I. The pathogenic action of culture filtrates. J Exp

Med 46: 123-131, 1927.

82. SMITH, T.: Focal Interstitial Nephritis in the Calf Following

Interferences with the Normal Intake of Colostrum. J Exp Med 41: 413-425,

1925.

83. SNYDER, Marshall L.: The Bacterial Flora of Meconium Specimens

Collected from Sixty-Four Infants within Four Hours After Delivery. J

Pediat 9: 624-632, 1936.

84. STARK, R., ABRAMSON, and ERKAN, Vildan: Intra-vascular

Coagulation and Hyaline-Membrane Disease of the Newborn. Lancet 1180-1181,

June 1, 1968.

85. STEELE, R. and LANGWORTH, J.T.: The Relationship of Antenatal and

Postnatal Factors to Sudden Unexpected Death in Infancy. Canad Med Ass J

94: 1165, 1966.

86. SUDDEN DEATH IN INFANTS, p.1-165. U.S. Department of Health, Education

and Welfare Public Health Service, National Institute of Child Health and

Human Development, Bethesda, land, October 1965.

87. SUTTON, R.N.P. and EMERY, J.L.: Sudden Death in Infancy: A

Microbiological and Epidemiological Study. Arch Dis Childh 41: 674-677,

1966

88. TISSIER, Henry and DREYFUS, Suzanne: Sur les Streptocoques de la Flore

Intestinale des Nourrissons au sein. C R Soc Biol 92: 476-477, 1925.

89. URBASCHEK, B. and VERSTEYL, R.: Increase of the Effect of Histamine by

E. coli Endotoxin on the Smooth Muscle. Nature 207: (4998) 763-764, August

1965.

90. VALDES-DAPENA, Marie: Sudden and Unexpected Death in Infancy: A Review

of the World Literature 1954-1966. Pediatrics 39: 123-138, 1967.

91. VALDES-DAPENA, Marie, BIRLE, Leonard J., McGOVERN, A., McGILLEN,

F. and COLWELL, F. Herbert: Sudden Unexpected Death in Infancy: A

Statistical analysis of certain socioeconomic factors. J. Ped 73: (3)

387-394, September 1968.

92. WATANABE, Morimatsu, chief, 2nd Research Division (Virus), national

Institute of Animal Health (Kachukueisei Skikenjo) Kodaira-City, Tokyo,

Japan: Personal Communication, 1963.

93. WEINTRAUB, H., AMBRUS, Clara M. and AMBRUS, n L.: Studies on

Hyaline Membrane Disease. IV. Diagnostic and Pronostic Problems. Pediatrics

38: (2) Part I, 244-253, August 1966.

94. WILLIAMS OBSTETRICS, 13th Edition (ed.) Nicholson J. Eastman and Louis

M. Hellman, Appleton-Crofts Inc., New York, 1966.

95. WILSON, Sir Graham S.: The Hazards of Immunization. University of

London The Athlone Press, 1967, 324 pp.

96. WOODS, G.T., HANSON, L.E., SWENSON, G.H. and RHOADES, H.E.: Acute

Infectious Bovine Rhinotracheitis and Salmonellosis in a Dairy Herd. JAVMA

152: (10) 1530-1535, May 1968.

97. YORK, J. and BAKER, A.: A New Member of the

Psittacosis-Lymphogranuloma Group of Viruses that Causes Infection in

Calves. J Exp Med 93: (6) 587-604, June 1951.

98. YUILL, T.M. and HANSON, R.P.: Coliform Enteritis of Cottontail Rabbit.

J Bact 89: (1) 1-8, January 1965.

99. ROINE, Paavo, GYLLENBERG, Helge and ROSSANDER, Marjatta: Rat

Experiments with an Artificial Human Milk. 14th Internat Dairy Congr 1:

Part II, 414-423, 1956.

--------------------------------------------------------

Sheri Nakken, R.N., MA wwithin@...

Well Within's Earth Mysteries & Sacred Site Tours

http://www.nccn.net/~wwithin

Bookstore - http://www.nccn.net/~wwithin/bookstor.htm

International Tours, Homestudy Courses, ANTHRAX & OTHER Vaccine Dangers

Education, Homeopathic Education

KVMR Broadcaster/Programmer/Investigative Reporter, Nevada City CA

CEU's for nurses, Books & Multi-Pure Water Filters

------------------------------------------------------------------------

Special Offer-Earn 300 Points from MyPoints.com for trying @Backup

Get automatic protection and access to your important computer files.

Install today:

1/5667/10/_/472772/_/961361237/

------------------------------------------------------------------------

--------------------------------------------------------

Sheri Nakken, R.N., MA

Vaccination Information & Choice Network, Nevada City CA & Wales UK

$$ Donations to help in the work - accepted by Paypal account

vaccineinfo@...

(go to http://www.paypal.com) or by mail

PO Box 1563 Nevada City CA 95959 530-740-0561 Voicemail in US

http://www.nccn.net/~wwithin/vaccine.htm

ANY INFO OBTAINED HERE NOT TO BE CONSTRUED AS MEDICAL OR LEGAL ADVICE. THE

DECISION TO VACCINATE IS YOURS AND YOURS ALONE.

Well Within's Earth Mysteries & Sacred Site Tours

http://www.nccn.net/~wwithin

International Tours, Homestudy Courses, ANTHRAX & OTHER Vaccine Dangers

Education, Homeopathic Education

CEU's for nurses, Books & Multi-Pure Water Filters