legaljustice4john.com
The Shaken Baby Syndrome Myth
renamed "Abusive Head Trauma" or "Non-Accidental Injury"

WAS

SBS: EVERTHING IS BROKEN

* SBS began as an unproven theory and medical opinions, now discredited by biomechanical engineering studies
* No DIFFERENTIAL DIAGNOSIS done to eliminate other causes, abuse assumed without evidence
* Shaken Baby diagnostic symptoms not caused by shaking
* Child protective agencies snatch children, destroy families based on medical accusations without proof of wrong-doing
*Poor or deceptive police investigations, falsified reports, perjured testimony threaten legal rights, due process
* Prosecutors seek "victory", over justice; defense attorneys guilty of ineffective counsel, ignorance, lack of effort
* Care-takers threatened, manipulated, in order to force plea bargains, false confessions
* A fractured criminal justice system--a big piece for the rich, a small piece for the poor, and none for alleged SBS cases.

1. SBS "MYTH" WEBSITE SUMMARY 
2. ARTICLE ABOUT PEDIATRIC ACADEMY SBS FRAUD

3. SUMMARIZED HISTORY OF THE SHAKEN BABY SYNDROME THEORY
4. POLICE ASSAULT: PROTESTING FOR A POLYGRAPH --DJT


Related websites/ important people and projects ShakenBabySyndrome/Vaccines/YurkoProject
CHRISTINA ENGLAND: BOOK
"Shaken Baby Syndrome or Vaccine Induced Encephalitis-- Are Parents Being Falsely Accused?" by Dr Harold Buttram, with Christina England (WEBSITE)
Evidence Based Medicine and Social Investigation:
EBMSI conferences, resources and information Articles and Reports
VacTruth: Jeffry Aufderheide; The SBS conection and other dangerous or deadly side effects of vaccination 

Vaccinefraud.com/The true, suppressed history of the smallpox vaccine fraud and other books:
Patrick Jordan
On SBS:
Sue Luttner, must-read articles and information on Shaken Baby Syndrome: her resources link
The Amanda Truth Project: Amanda's mother speaks out at symposium
Tonya Sadowsky


SUBJECT: Dr Robert Reisinger DVM, MS

    Introduction

  1. "The Role of Environmental Factors in Infant Morbidity and Mortality"
  2. Bacterial Endotoxins in Pathogenesis of Toxemia of Pregnancy, Neonatal Encephalopathies, and Cot Death
  3. Sudden Death Syndrome of Young Mammals; A Unifying Concept.
  4. Sudden Infant Death Syndrome:A Final Mechanism of Cardiac and Respiratory Failure
  5. Discussion: Death caused by endotoxins, e-coli--the danger of feeding cow's milk to human infants
  6. Pathogenesis and Prevention of Infectious Diarrhea (Scours) of Newborn Calves
  7. Discussion: E-coli/endotoxins kill or harm infants
  8. Quotes: Disturbed immune function can cause ear infections, unconsciousness and death

Intro: Dr. Robert Reisinger was a noted veterinarian who did animal studies on the side effects of animal vaccines. He proved that vaccines cause a rise in blood histamine levels, which cause inflammation and potential hemorrhage as capillaries are made more permeable. Blood histamines are neutralized by Vitamin C, which in turn can cause vitamin deficiency, itself a hemorrhagic condition resulting from "capillary fragility",  evolving into bone disease, systemic damage and even sudden death.

http://www.ncbi.nlm.nih.gov/pubmed/15050101

Med Hypotheses. 2004;62(4):533-6.
Elevated blood histamine caused by vaccinations and Vitamin C deficiency may mimic the shaken baby yndrome.

Clemetson CA.

Department of Obstetrics and Gynecology, Tulane University School of Medicine, New Orleans, LA, USA. megcc2000@yahoo.com
Abstract

The findings of subdural hematoma and retinal hemorrhages in infants, without any documented history of major trauma, do not always indicate child abuse. A combination of ascorbate depletion and the injection of foreign proteins can cause a very high blood histamine level, leading to capillary fragility and venular bleeding. This can be prevented by the administration of vitamin C.

PMID:
15050101
[PubMed - indexed for MEDLINE]


1.

International Congress on SUDDEN INFANT DEATH SYNDROME

"The Role of Environmental Factors in Infant Morbidity and Mortality"

GRAZ-AUSTRIA May 24 to 27, 1995

SLEEPING POSITION, FORMULA FEEDING, ENDOTOXIN AND SIDS Robert C Reisinger, DVM, MS, 3810 Dustin Road, Burtonsville, MD 20866 U.S.A.

Formula fed infants have 1,000 to 10,000 times more E. coli in their g.i. tracts than do breast fed infants. Numerous viruses, avitaminosis A, C, B-6, etc., chilling, overheating, and various other environmental stressors may make the infant 10,000 times more susceptible to E.coli endotoxin (lipopolysaccharide) . . . Raising ambient temperature increases susceptibility to endotoxin . . . Formula feeding increases body heat . . . Being in the prone position increases body heat . . . Prone positioning thus may increase susceptibility of formula fed infants to SIDS . . . Prone positioning would not equally increase susceptibility of the totally breast fed infant to SIDS . . .

Sudden Death Syndrome (SDS) in young of other mammalian species, including the calf and rhesus monkey, is associated with greatly increased numbers of E.coli in the proximal ileum and jej unum . . . J. Bendig and H. Haenel have reported similar increased E.coli in the proximal intestinal tract of 24 of 29 SIDS cases . . . Absorption of increased amounts of endotoxin into the general blood circulation through a temporarily dysfunctional reticuloendothelial system causes decrease of phosphoenolpyruvate carboxykinase (PEPCK) in the liver, release of large amounts of serotonin from blood platelets, non-coagulability of blood, pulmonary edema and hemorrhage by diapedesis. . . Serotonin initiates in some cases the coronary chemoreflex (Bezold-Jarisch reflex) in which there is inhibition of sympathetic outflow and increased activity of the cardiac (efferent) vagus leading to profound bradycardia, hypotension and cardiac collapse . . . Minimal lethal dose of endotoxin given over hours of time is so small as to be undetectable by any clinical test presently in use.

Bendig, J. and Hacnel, H.: Gastrointestinal Microecology of Sudden Unexpected Death of InfantsNutrition, Proc. Eight Congress Nutr., Prague, Sept. 1969. (ed) Josef Masek, Prague, & Sir David P. Cuthbertson, Glasgow. Exccrptica Medica, pub., Amsterdam p.212-214-1970.

Reisinger, RC.: A final mechanism of cardiac and respiratory failure. Pub. in SIDS 1974. Proc. of Camps International. Symp. on SUD in Infancy. Pub: Canadian Found. for Study of Infant Deaths. 4 Lawson Blvd., Toronto M4V 1Z4. 77-X2-1974.

Reisinger, RC.: Pathogenesis and prevention of infectious diarrhea (scours) of newborn calves. J Amer Vet. Med. Assoc 147:1377-1386, 1965.

Reisinger, RC: Studies on the pathogenesis of diarrhea of newborn calves. M.S. thesis. U Wisconsin, Madison, 1957.

Reisinger, RC: Parainfluenza 3 virus in cattle. Ann NY Acad Sci 101: 576-582, 1962.

Woodruff, P.W.H., O'Carroll, D.L, Kuizumi, S., and Fine, J.: Role of Intestinal Flora in Major Trauma J. Inf. Dis. 128 Supl: S290-294, July 1973.

Wells, J.C.K, Davies, P.S.W.: Sudden Infant Death Syndrome. Archives of Disease in Childhood 1994 70:


2.

Abstract

ESPID--European Society for Study and Prevention of Infant Deaths

Oxford, England August 27-30, 1993

Bacterial Endotoxins in Pathogenesis of Toxemia of Pregnancy, Neonatal Encephalopathies, and Cot Death.

Robert C. Reisinger, DVM, MS 3810 Dustin Road, Burtonsville, MD 20866 U.S.A.

Toxemia of Pregnancy

Blood flow from pregnant uterus (or hydatidiform mole) raises pressure in the inferior vena cave lessening flow through hepatic veins with variable stasis of hepatic circulation. This results in loss of hepatic function to adequately detoxify bacterial endotoxins of intestinal origin. Signs and pathology associated with toxemia of pregnancy in human and other animals are consistent with endotoxemia. Following birth, spontaneous or induced abortion, there is rapid lessening of blood flow from the uterus, drop in pressure in inferior vena cave, normalized blood flow through the liver which is then able to detoxify the build-up of circulating endotoxin. If the preceding events occur in a timely manner, patients return to normal; if not, irreversible sequelae or death may ensue.

Neonatal Encephalopathy

Reisinger, R.C. Discussion on Endotoxemia. Inf. Dis. 128 (Supl): S303-305, July 1973.

Gilles, F.H. et al.: Neonatal endotoxin encephalopathy. AM Neurol. 2:49, 1977.

Cot Death

Endotoxemia is the major cause of Sudden Death Syndrome (SDS) in calves, foals, Rhesus monkeys, etc. The one published study in the human infant has yielded results similar to those found in other animals. (Bendig, J. and Haenel, H.: Gastrointestir.al Microecology of Sudden Unexpected Death of Infants. Nutrition, Proc. Eight Congress Nutr., Prague, Sept. 1969. (ed) Josef Masek, Prague, and Sir David P. Cuthbertson, Glasgow.: Excerptica Medica, pub., Amsterdam. p.212-214, 1970.)

Reisinger, R.C.: A final mechanism of cardiac and respiratory failure. Pub. in SIDS 1974. Proc. of Camps International. Symp. on SUD in Infancy. Pub: Canadian, Found. for Study of Infant Deaths. 4 Lawson Blvd., Toronto M4V 1Z4.

Reisinger, R.C.: Pathogenesis and prevention of infectious diarrhea (scours) of newborn calves. JAmer Vet Assoc 147:1377-1386, 1965.

Reisinger, R.C.: Studies on the pathogenesis of diarrhea of newborn calves. M.S. thesis. U Wisconsin, Madison, 1957.

Reisinger, R.C.: Parainfluenza 3 virus in cattle. Ann NY Acad Sci 101:576-582, 1962.

Woodruff,P.W.H., O'Carroll, D.I., Koizumi, S., and Fine, J.: Role of Intestinal Flora in Major Trauma. J. Inf. Dis. 128 Supl: S290-294, July 1973.
_______________________________________________________________________________________

3.
Abstract

ESPID--European Society for Study and Prevention of Infant Deaths

June 10-13, 1992, Lubeck/Travemunde, Germany

Sudden Death Syndrome of Young Mammals; A Unifying Concept.

Robert C. Reisinger, DVM, MS, 3810 Dustin Road, Burtonsville, MD 20866 U.S.A.

When accumulated knowledge regarding the Sudden Death Syndrome (SDS) of the human infant and of the young of other mammalian species is carefully examined, the preponderance of cases of Sudden Infant Death Syndrome (SDS) no longer constitute a mystery. SDS of other young mammals including the calf, foal, piglet, rabbit, and monkey, has been determined to be not ~ separate etiologic entity but a peracute manifestation of the respiratory-enteric disease complex, or complexes…. SDS is associated with a greatly increased numbers of E. coli in the proximal ileum and jejunum, as has been shown in diarrhea of various mammalian species, including the human infant. Studies in Germany (Bendig and Haenel) have shown similar increased E. coli in the proximal intestinal tract of 24 of 29 SIDS cases. Invasion of E. cold into these more absorptive portions of the small intestine results in absorption of increased amounts of lipopolysaccharides (LPS, or endotoxin) into the general blood circulation through a temporarily dysfunctional liver (RE system). Endotoxin causes decrease of phosphoenolpyruvate carboxykinase (PEPCK) in the liver, release of large amounts of serotonin from blood platelets, non-coagulability of blood, hyperkalemia, hyponatremia, acidosis, pulmonary edema and hemorrhage by diapedesis... Serotonin initiates in some cases the coronary chemoreflex (Bezold-Jarisch reflex) in which there is inhibition of sympathetic outflow and increased activity of the cardiac (efferent) vagus leading to profound bradycardia, hypotension and cardiac collapse . . . Triggering stressors include various viruses, chilling, overheating, lack of vitamins including A, C, B6, etc. . . Prevention includes feeding of breast milk only, to maximize immunologic defenses and minimize numbers of E. cold in the g.i. tract. The g.i. tract of the bottle-fed infant contains approximately 1,000 times the number of E. coli normal to the breast-fed infant.

Bendig, J. and Haenel, H.: Gastrointestinal Microecology of Sudden Unexpected Death of Infants. Nutrition, Proc. Eight Congress Nutr., Prague, Sept. 1969. (ed) Josef Masek, Prague, & Sir David P. Cuthbertson, Glasgow. Excerptica Medica, pub., Amsterdam. p.212-214-1970.

Reisinger, R.C.: A final mechanism of cardiac and respiratory failure. Pub. in SIDS 1974. Proc. of Camps International. Symp. on SUD in Infancy. Pub: Canadian Found. for Study of Infant Deaths. 4 Lawson Blvd., Toronto M4V 1Z4.

Reisinger, R.C.: Pathogenesis and prevention of infectious diarrhea (scours) of newborn calves. J Amer Vet Assoc 147: 1377-1386, 1965.

Reisinger, R.C.: Studies on the pathogenesis of diarrhea of newborn calves. M.S. thesis. U Wisconsin, Madison, 1957.

Reisinger, R.C.: Parainfluenza 3 virus in cattle. Ann NY Acad Sci 101: 576-582, 1962.

Woodruff, P.W.H., O'Carroll, D.I., Koizumi, S., and Fine, J.: Role of Intestinal Flora in Major Trauma. J. Inf. Dis. 128 Supl: S290-294, July 1973)
______________________________________________________________________________________

4.

SIDS 1974

proceedings of

THE FRANCIS E. CAMPS INTERNATIONAL SYMPOSIUM ON SUDDEN AND UNEXPECTED DEATHS IN INFANCY

edited by

ROBERT R. ROBINSON

consulting editors

ALAN H. FINLEY

SYDNEY SEGAL

J. HILLSDON SMITH

ROBERT STEELE
published by

THE CANADIAN FOUNDATION FOR THE STUDY OF INFANT DEATHS

Appendix P-3
Sudden Infant Death Syndrome:A Final Mechanism of Cardiac and Respiratory Failure
ROBERT C. REISINGER* Bethesda, Md., U.S.A

*Robert C. Reisinger, D.V.M., M.S. was associated with the National Cancer Institute, United States Public Health Service, Bethesda, Md. His present address is 3810 Dustin Road, Burtonsville, MD 20866. Phone 301-421-9377 or Fax 301-421-0854.

Absorption into the bloodstream over hours of time of small amounts of bacterial endotoxin not detoxified by a temporarily dysfunctional reticuloendothelial system results in removal of blood platelets and fibrinogen from the circulating blood.1 The result is release of relatively large amounts of serotonin from platelets into the blood plasma (in some experiments the increase of plasma serotonin is almost 100-fold). Serotonin initiates in some cases the coronary chemoreflex (Bezold-Jarisch reflex) in which there is inhibition of sympathetic outflow and increased activity of the cardiac (efferent) vagus, leading to profound brachycardia, hypotension, and cardiovascular collapse.2 The complex pathogenesis of endotoxemia, depending on time and dosage, also involves release of norepinephrine, epinephrine, corticosteriods, etc. However, if death occurs early in the course of this syndrome, it is due primarily to serotonin effect. Serotonin is associated with deep sleep and in certain circumstances strongly inhibits respiratory movements. . . Endotoxin also has a more direct effect on cellular respiration, since it interferes with oxidative metabolism of mitochondria in vitro as well as in vivo3. . . Between three and six hours, vascular capillary permeability has become more substantial, and varying amounts of edema and hemorrhage by diapedesis are apparent. After six to eight hours or more, fibrin-platelet clots have formed, and disseminated intravascular coagulation (DIC) is present in lungs, kidneys, and other organs and tissues.

In Some Animals and Human Infants

There are very few Escherichia coli in the more absorptive portion of the small intestine, the duodenum, jejunum and proximal ileum. This is true of all mammalian species so far studied, including the cow and calf, the human infant and adult4. Smith and Orcutt5 demonstrated that calves suffering diarrhea have tremendously increased numbers of E. coli in the intestinal tract. They described 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 . . . E. 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." Their original work has since been confirmed in calves by other workers4,6 who further reported that infrequently death may occur before diarrhea is evident, with similar overgrowth of E. coli in the absorptive portion of the small intestine. Two of these studies demonstrated a triggering effect of various viral infections, and further demonstrated that the viral infections are non-lethal in the absence of E. coli, or in the presence of relatively few E. coli, in the digestive tract.

In the enterotoximic form of diarrhea and sudden death syndrome the blood and internal organs are usually free of bacteria.

In the only appropriate study thus far reported of the gastrointestinal microflora of human infant victims of SIDS, Bendig and Haenel7 reported finding an abnormal microbial flora in the intestinal tract, including greatly increased numbers of E. coli in the proximal small intestine, of 24 out of 29 cases. "Only in three infants did there exist normal, eubiotic relations." Beller and Graeff1 have demonstrated in the rabbit that continuous i.v. injection of very small amounts (50 mµg/kg/hr.) of E. coli endotoxin up to 14 hours results in quiet death which occurs at varying lengths of time after injection has begun, although some few rabbits do not die. There is a decrease in platelets and fibrinogen, so that after six hours, the blood does not clot. Animals which die early have few or no lesions, those which die somewhat later show varying amounts of edema and petechial hemorrhage of the lungs. Disseminated intravascular coagulation is observed only in rabbits which die eight hours or longer after infusion began. This extremely relevant experiment beautifully demonstrates the varying susceptibility of individual animals at various times to endotoxin effect, and the variety of lesions which may be produced from very little or nothing to moderate to severe. The pathology is consistent to that reported in SIDS in the human, the calf and other mammalian species.5,6

If one considers the relatively obscure pathogenesis and reported pathology of other infant diseases including cerebral palsy, mental retardation, hearing and speech defects, retrolental fibroplasia, respiratory distress syndrome, etc., and accepts the reality of bacterial endotoxin absorption from the gastrointestinal tract, it is not difficult to see the possibility of endotoxin involvement in at least a portion of these syndromes. It is increasingly apparent that bacteria and bacterial toxins play an important role in the pathogenosis of many "viral" diseases.4,8 Canine distemper virus (CDV), an agent closely related to measles virus, is associated in dogs with a disease syndrome often characterized by encephalitis, pneumonitis and enteritis. Brain lesions and CNS sequelae following CDV infection in the dog are similar to those characteristic of cerebral palsy in the human. However, the only signs of disease in gnotobiotic dogs infected with CDV were mild transient fever and leukopenia. Very similar findings have been reported in gnotobiotic kittens infected with feline panleukopenia virus, an agent which causes a highly lethal enteritis in conventional kittens.

Dubos et al 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 anerobically 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 amounts of penicillin brings about a sudden disappearance of lactobacilli from 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 in the guinea pig which also normally has a primarily gram positive intestinal microflora, and dies from E. coli overgrowth when penicillin or the tetracyclines are administered. Schaedler and Dubos 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 relative resistant, were found to have become susceptible to the lethal effect of endotoxin."

Dubos et al 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 and Ravin et al 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 have stated that endotoxins are always at hand ready to destroy peripheral vascular integrity, and to kill when endotoxin detoxifying power is lost, and have reported that blocking the reticuloendothelial system of the rabbit with thorotrast (a sterile colloidal suspension of 25 per cent 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.

Administration of Diphtheria-Pertussis-Tetanus Toxoid (DPT) can cause temporary liver dysfunctions in infants similar to those resulting from viral hepatitis, and inoculation of killed Bordetella pertussis organisms makes some strains of mice 200 times more sensitive to histamine and three to five times as sensitive to endotoxins for approximately 14 days.

Infants and Calves

Deaths can occur within several hours after the feeding of an apparently healthy normal calf.4,10 Pathologic lesions at autopsy are absent or minimal, as in the crib-death syndrome in the human infant. Experimentally, the diarrhea syndrome can be precipitated by exposure to various viruses, cold and wet, avitaminous A, etc. – any "adverse contributing factor" that impairs optimal reticuloendothelial and/or gastrointestinal function. A feature of many cases of the calf-diarrhea syndrome is labored breathing (pneumonic signs without pneunionic lesions), but this disappears when, by appropriate antibiotic therapy, excessive numbers of E. coli are cleared from the digestive tract.

Death may occur in calves before diarrhea is evident. Writing of diarrhea in the human infant, McKay and Smith11 stated that "An occasional infant may go into shock and die from water and electrolyte loss into the intestinal lumen before a diartheal stool is passed." It is difficult to accept that lethal loss of water and electrolytes could occur without evidence of diarrhea, and bacterial endotoxin action is probably occurring in such cases.

The celiac crisis, "an acute medical emergency and a severe and immediate threat to the patient's life" is often triggered by upper respiratory infection. The child is prostrate, drowsy and dehydrated, and has the chemical and laboratory manifestations of acidosis.12

Severe pneumonias of unexplained etiology in young children have been referred to as "missed cot deaths", and the signs and course of the disease, as well as the described pathology, are compatible with known endotoxin effects.

Some factors common to many cases of SIDS, the respiratory-distress syndrome, and endotoxin shock are hyperkalemia, hyponatremia, acidosis, thrombocytopenia, noncoagulability of blood, early respiratory signs without appropriate lesions, pulmonary edema, hemorrhage by diapedesis, fast, weak pulse, and circulatory collapse. It is more illogical to consider these similarities as fortuitous than to realize the probability, or at least possibility, of a common cause or mechanism.

Milk

There is a great deal of evidence to indicate that the breast-fed baby is relatively healthier, suffers less allergy, respiratory, enteric and other disease, and less mortality than his bottle-fed counterpart.11,13-17

SIDS is preponderently a disease of the bottle-fed infant. Coombs18 stated that if SIDS were relatively as common in the breast-fed as in the bottle-fed infant he should have had 17 breast-fed cases in his series, whereas at that time he had not one. Johnstone and Lawry19 reported, "In the 46 cases where the type of feeding is definitely known all but two were fed on dried cow's milk. The two exceptions were aged four and eight days." Tonkin reported that in her series of 86 SIDS cases, only two were breast-fed. Since twenty-five percent of her control population were breast fed, she should have had 21 cases of SIDS in breast-fed infants, if the risk were the same in both breast-fed and bottle-fed. Steele20 reported SIDS to be significantly related to feeding other than at the breast.

The data of Rivera21, concerning feeding of infants in low income families attending a New York City clinic indicate that more than 30 per cent of two-month-old infants were fed evaporated milk formulas. and an additional 20 per cent or more were fed on fresh cow's milk. These data are interesting and probably significant when coupled with various reports of epidemiological studies in various countries indicating a significant increased incidence of SIDS in low income groups.

In rural Chile, infant mortality rose with income. It is reported that with higher income and better education, weaning was practiced earlier and more infants were fed by bottle only. The National Health Service of Chile attempts to provide all weanlings and preschool children with dried cow's milk.

There are important differences between bacterial flora, pH, and physical characteristics of the intestinal contents of human infants fed human milk and those fed cow's milk.13,22,23 Due to its high content of calcium and protein and its lower content of lactose, cow's milk fed to the human infant raises the E. coli count in the large intestine approximately 1,000-fold (from 106-107 /g to 109-1010 /g), raises the pH from acid (4.5-5.6) to alkaline (7.0-8.0), makes curds hard and coarse instead of soft and fine, and makes bowel movements relatively infrequent. Characteristics of a healthy human infant on human milk are a relative low coliform count, acid pH, soft, fine curds, and frequent bowel movements. Even if there were no SIDS, use of cow's milk or any other formula during the first six months of age is against all scientific reason to produce the optimally healthy child and the healthy adult he should become.

Although SIDS is primarily a disease of the bottle-fed infant, it does occur in fully breast-fed infants. Relatively long term studies on the fecal flora of breast-fed infants show that the numbers of E. coli may increase intermittently for variable periods of time, but they seldom achieve or maintain numbers characteristic of the cow's milk-fed infant. Thus the breast-fed infant is presumably at high risk for shorter periods of time.

Evidence accumulated in studies of the young of various mammalian species, including the human infant, indicates that the Sudden Infant Death Syndrome is not a disease entity, but a peracute, lethal manifestation of other disease syndromes, including gastroenteritis and respiratory disease.

The "endotoxin theory" does not detract from, but is additive to, several other theories postulated for SIDS, such as sudden vagal storms and other malfunctions of the autonomic nervous system, apnea. anoxia, allergy to cow's milk, overwhelming viral, bacterial, or mixed infection, etc.

It is not claimed that the "endotoxin theory" will explain all cases of SIDS, but it is believed that endotoxins, and other bacterial toxins, are directly involved in a high percentage of these cases.

REFERENCES

Beller FK, Graeff H: Deposition of glomerular fibrin in the rabbit after infusion with endotoxin. Nature 215:295-6, 1967.
Douglas WW: 5-Hydroxytryptamine and antagonists; polypeptides - angiotensin and kinins, in The Pharmacological Basis of Therapeutics, 4th edition, Edited by Goodman LS, and Gilman A, Macmillan, New York, 1970.
Greer GG, Epps NA, Vail WJ: Interaction of lipopolysaccharides with mitochondria. I. Quantitative assay of salmonella typhimurirnm lipopolysaccharides with isolated mitochondria. J Infect Dis 127:551-6, 1973.
Reisinger RC: Pathogenesis and prevention of infectious diarrhea (scours) of newborn calves. J Amer Vet Med Assoc 147:1377-1386, 1965.
Smith T, Orcutt ML: The bacteriology of the intestinal tract of young calves with special reference to early diarrhea ("scours"). J Exp Med 41:89-106, 1925.
Reisinger RC: Studies on the pathogenesis of infectious diarrhea of newborn calves. M.S. thesis, U Wisconsin, Madison, 1957.
Bendig J, Haenel H: Gastrointestinal microecology in sudden unexpected death of infants. Nutrition, Proc 8th Congress Nutrition, Prague 1969, Edited by Masek J, Osancova K and Cuthbertson DP, Excerpta Medica, Amsterdam, pp. 212-214, 1970.
Reisinger RC: Parainfiuenza 3 virus in cattle. Ann NY Acad Sci 101:576-582, 1962.
Schaedler RW, Dubos RI: The fecal flora of various strains of mice, its bearing on their susceptibility to endotoxin. J Exp Med 115:1149-60, 1962.
Smith T, Little RB: The significance of colostrum to the newborn calf. J Exp Med 36:181-199, 1922.
McKay RJ Jr, Smith CA: Diseases of the newborn infant: full term and premature, in Textbook of Pediatrics, 8th edition, edited by Nelson WE and Saunders WB, Philadelphia, pp. 397-8, 1964.
Di Sant'Agnese PA: The stomach and intestines: intestinal malabsorption, in Textbook of Pediatrics, 8th edition, edited by Nelson WE and Saunders WB, Philadelphia, pp. 720-730, 1964.
Bullen CL, Willis AT: Resistance of the breast-fed infant to gastroenteritis. Br Med J 3:338-343, 1971.
Davies PA: Problems of the newborn: feeding. Br Med J 4:351-354, 1971.
Gyorgy P, Dhanamitta S, Steers E: Protective effects of human milk in experimental staphylococcus infection. Science 137:338, 1962.
Wade N: Bottle feeding: adverse effects of a Western technology. Science 184:45-48, 1974.
Winberg J, Wessner G: Does breast milk protect against septicemia of the newborn? Lancet, pp. 1091-1094, May 29, 1971.
Coombs R: An experimental model for cot deaths, in Sudden Death in Infants, Nat Inst Child Health Human Dvlpt, Bethesda, Md., pp. 55-74, 1965.
Johnstone JM, Lawry HS: Role of infection in cot deaths. Br Med J 1:706-709, 1966.
Steele R, Langworth IT: The relationship of antenatal and postnatal factors to sudden unexpected death in infancy. Can Med Assoc J 94:1165, 1966.
Rivera J: The frequency of use of various kinds of milk during infancy in middle and lower income families. Amer J Pub Health 61:277, 1971.
Gyllenberg H, Roine P: The value of colony counts in evaluating the abundance of "Lactobacillus" Bifidus in infant faeces, Acta Path Microbiol Scand 41:144-150, 1957.
Roine P, Gyllenberg H, Rossandre M: Rat experiments with artificial human milk. 14th Internat Dairy Congr 1: Part II, pp. 414-423, 1956.

(A more complete list of references may be obtained from the author.)


5.

THE JOURNAL OF INFECTIOUS DISEASES • VOL. 128, SUPPLEMENT • JULY 1973

(c) 1973 by the University of Chicago. All rights reserved.

Summary of Discussion

Remarks of Dr. Robert C Reisinger

DR. REISINGER: I would like first to show you some things that you probably have learned but may have forgotten. This first slide (figure 1) is just to remind you that there are very few Escherichia coli in the more absorptive portion of the small intestine, the duodenum, jejunum, and proximal ileum. This is true of all mammalian species so far studied, including the cow and calf, the human infant and adult.

Figure 1. Distribution of Escherichia coli in the
intestinal tract of the normal calf.

The next slide (figure 2) shows what was demonstrated by Theobald Smith and Marion Orcutt in 1922, i.e.. that calves suffering diarrhea have tremendously increased numbers of E. coli in the intestinal tract. They described "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 . . . E. 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."

Figure 2. Distribution of Escherichia coli in the
intestinal tract of the scouring calf.

My work in Wisconsin, that of Gay in Canada, and that of Mebus in Nebraska confirmed that of Smith and Orcutt and further confirmed and demonstrated that the same mechanism of invasion of E. coli into the proximal small intestine may result in peracute deaths without septicemia and without diarrhea (SDS). Such deaths can occur within several hours after the feeding of an apparently healthy normal calf. Pathologic lesions at autopsy are absent or minimal. as in the crib-death syndrome in the human infant. Experimentally, the diarrhea syndrome can be precipitated by exposure to various viruses, cold and wet, avitaminous A, etc.—any "adverse contributing factor" that impairs optimal reticuloendothelial and/or gastrointestinal function. A classic feature of the calf-diarrhea syndrome is labored breathing (pneumonic signs without pneumonic lesions), but this disappears when, by appropriate antibiotic therapy, excessive numbers of E. coli are cleared from the digestive tract.

Bacterial endotoxins produced in the intestinal tract, which may be absorbed into the venous system, are transported directly into the liver. If for any reason these endotoxins are not inactivated in the liver, they obviously go via the inferior vena cave into the heart and lungs and, to a lesser extent (at least early in the syndrome), into the general arterial circulation.

Some factors common to many cases of SDS, the respiratory-distress syndrome, and endotoxin shock are hyperkalemia, hyponatremia, acidosis, thrombocytopenia, noncoagulability of blood, early respiratory signs without appropriate lesions, pulmonary edema, hemorrhage by diapesis, fast, weak pulse, and circulatory collapse. It is more illogical to consider these similarities as fortuitous than to realize the probability, or at least possibility, of a common cause or mechanism.

There are great differences between bacterial flora, pH, and physical characteristics of the intestinal contents of human infants fed human milk and these features in infants fed cow's milk. Due to its higher content of calcium and protein and its lower content of lactose, cow's milk fed to the human infant raises the E. coli count in the large intestine approximately 1,000-fold (from 106-107/g to 109-1010/g), raises the pH from acid (4.5-5.6) to alkaline (7.0-8.0), makes curds hard and coarse instead of soft and fine, and makes bowel movements relatively infrequent. Characteristics of a healthy human infant on human milk are a relatively low coliform count, acid pH, soft, fine curds, and frequent bowel movements. Even if there were no SDS, these adverse changes wrought by a diet of cow's milk any time during the first six months of age are against all reason in producing the optimally healthy child and the healthy adult he should become.

I believe that crib death, or SDS, is only the tip of the iceberg with regard to effects of absorption of bacterial endotoxin in the human infant. The vasoconstriction, vasodilation, disseminated intravascular coagulation, and other characteristic effects of endotoxin may well account for much of the pathology associated with many cases of cerebral palsy, mental retardation, learning and speech defects, retrolental fibroplasia, hyaline-membrane disease, etc. These latter diseases appear predominantly in infants with immature or otherwise impaired hepatic function, i.e., the immature infants of diabetic mothers, infants anoxic due to placenta praevia, infants whose birth is long and difficult, etc. In long and difficult births, there is also a prolonged in-utero opportunity for seeding of the infants' digestive tracts should infected amniotic fluid be swallowed.

Since absorption of endotoxin from the digestive tract is a confirmed fact in various mammalian species, the probability, or at least the possibility, of similar absorption from the intestinal tract of the human infant should be considered and investigated.
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6.

Reprint from thc JOURNAL of the American Vetrinary Medical Association, Vol. 1417, No. t2, Dec., I5, 1965, pp. I377-86. http://users.erols.com/drrobert.sids/Calves.html

Pathogenesis and Prevention of Infectious Diarrhea (Scours) of Newborn Calves

Robert C. Reisinger, D.V.M., M.S.

Summary

The pathogenesis of Escherichia coli diarrhea of newborn calves is the same today as when described so well by Theobald Smith and co-workers in the 1920's. There are multiple adverse contributing factors involved in precipitating this disease syndrome which vary from time to time and from area to area, but the pathogenesis of E. coli diarrhea of newborn calves remains the same. This will be true in later years when further research has given additional information as to the exact physiologic changes induced by presently known and as yet unknown adverse contributing factors, and to the various strains of E. coli involved. The newborn calf will not have changed (he will still be born into his world as naked on the inside as on the outside) and the pathogenesis of E. coli diarrhea in this animal will not have changed. The basic requirements necessary for prevention of diarrhea and death in problem herds and problem areas (which will be always with us) will remain the same, and will require (1) intelligent application of known husbandry and veterinary principles and method to ensure the birth of healthy calves into a favorable environment, (2) prompt feeding of colostrum, and (3) prompt and intelligent administration of appropriate drugs to offset both avoidable and unavoidable deficiencies which will arise from time to time in implementation of the first 2 requirements.

A visitor from another planet studying some of the literature on calf diarrhea published during the past several years might believe that the role of E. coli in the pathogenesis of this disease was just being discovered. Such is not the case. The classic work of Theobald Smith and co-workers from 1917 to 1930 52-62 clearly delineated the major aspects of the role of E. coli in the pathogenesis of diarrhea of newborn calves, including the protective role of colostrum. That work is as current and valid now as it was then. One reads reports of recent excellent studies which confirm various parts of this early work, although apparently the authors of such studies are often not aware that they are confirming previously reported experimental evidence. 9, 16 Others18 have questioned some of the findings because they differ from results of more recent but less extensive studies.61

While amply demonstrating the importance of the decisive role of E. coli in the pathogenesis of calf diarrhea Theobald Smith stated that there were other factors about which he knew very little which also played a part in this disease. In those days, technology did not include tools and methods to reveal obscure viral agents. Subsequent studies have revealed viral agents in some cases of calf diarrhea. 2,6,13,33-35,42,43,65 The observations56 regarding the significance of quantitative and location factors in assessing the role of E. coli in the digestive tract of the calf with diarrhea have been fully confirmed.43 In studies involving more than 60 calves,43 quantitative cultures were made of the abomasum, 6-inch representative portions of the small intestine 10, 20, 30, and 40 ft. posterior to the abomasum, and the cecum and rectum of calves 1 to 10 days old which had been (1) apparently normal, (2) scouring, or suddenly dead or moribund without signs of diarrhea, (3) treated with chloramphenicol, and (4) treated with oxytetracycline. Coliform identifications were made, utilizing the replica plating technique30 adapted64 for screening intestinal coliform bacteria. Experiments also revealed the predisposing or contributing role of viral agents and of environmental stressors correlated with E. coli in the pathogenesis of this complex disease. Studies on bovine shipping fever have established that this syndrome is also a disease of complex pathogenesis involving various viruses, bacteria, and environmental stressors.28,44,45

It has been observed that E. coli plays a similar role in pigs exposed to transmissible gastroenteritis (TGE) virus, by invading the upper intestinal tract of pigs exposed to TGE virus.63 Transmissible gastroenteritis virus can cause death of newborn pigs, even "germfree" ones. However, it appears that in many cases of TGE infection in somewhat more resistant pigs. (i.e., those several days old and with variable amounts of antibody) which could survive TGE virus infection alone, multiplication and migration of E. coli into the upper digestive tract can be the determining factor in producing serious disease and death. These observations are supported by workers who isolated enteropathogenic strains of E. coli from pigs with TGE.36,37 The usefulness of this method of assessing pathogenic strains was questioned since apparently another worker considered TGE a simple viral disease,18 rather than the complex disease which in reality it is.

An increase in coliform organisms and a decrease in gram-positive flora were reported in pigs with diarrhea.9 Exposure of young rabbits to cold resulted in intestinal E. coli overgrowth, enteritis, and death.66

A recent monograph18 furnishes an excellent and up-to-date review of the literature on diarrhea of newborn calves. There are several omissions of pertinent work ( some previously unpublished ), some of which we will attempt to supply. In some cases our conclusions differ with those reported in the monograph.18 The more important of these differences are mentioned.

The Disease

Infectious diarrhea (scours) of newborn calves (9 to 10 days of age) is characterized usually by watery white or yellowish diarrhea, rapid onset and course, and high mortality. In affected calves diarrhea begins typically within 36 to 72 hours after birth, and the calves die within 2 to 3 days. Some calves may die several hours after having appeared healthy, without having any diarrhea at all.

The disease may affect most calves born in a herd, or may occur as a sporadic infection affecting only one or several calves while the rest remain well. Epizootics usually occur during the colder seasons of the year, but may occur during any season.

On the same farm or ranch and under the same apparent conditions of management, diarrhea may appear one year and not the next. Severity of the disease is known to vary considerably from year to year on given premises, even in an isolated herd.

Despite the many and varied studies undertaken regarding its cause, pathogenesis, prevention, and treatment, infectious diarrhea is still the major cause of death and illness in newborn calves, and often the major cause of economic loss to the raiser of beef and dairy calves.

Pathogenesis

The following facts must be considered to adequately understand, prevent, and treat diarrhea in newborn calves:

1 ) The calf derives no maternal antibody from its dam while in utero.1,15,18,26,31,32,38,43,54

2) The calf is exposed to E coli, and to other bacteria and viruses, as soon as it is born. The calf is very often exposed to microorganisms, particularly E. coli, during its passage through the birth canal.14,18,43,56

     

3) These organisms begin to multiply in the calf immediately. Escherichia coli organisms capable of being pathogenic exist on every farm and ranch and in every animal.43,56 They are normally confined to the rectum, large intestine, and lower portion of the small intestine. 43,56 The abomasum and approximately the first 30 to 40 ft. of the small intestine (where most digestion and absorption of nutrients occur) are normally acid and provide a suitable environment for the "benign" lactobacilli and enterococci which normally inhabit them. When these bacteria are established they, by their competitive physical presence and production of acid, help to create and maintain an environment inhospitable to E. coli. Lactobacilli are apparently normal inhabitants of the udder, since they are in raw milk, and also of the vagina.

4 ) The colostrum contains antibodies against those organisms to which the dam has previously developed some immunity. Colostrum may contain 15 to 20 times the concentration of protective antibody contained in the blood serum of the dam.

5) During the first several hours (approx. 6 to 24) of life, the upper portion of the calf's small intestine is highly absorptive.18,26 This absorptive capability is not of an "on" and "off" nature, like an electric light switch, but is ever-decreasing. During this period, which nature apparently intended to allow absorption of the relatively large amount of antibodies contained in colostrum, toxins and other harmful substances can also be most readily absorbed.

6) Under "normal" conditions, a healthy calf partakes of colostrum within minutes after birth. Antibody begins immediately to be absorbed via the lymphatics into the general blood circulatory system and also spreads through the intestinal tract, limiting the growth and invasion of E. coli and other harmful agents. Lactobacilli from the colostrum and enterococci from the digestive tract of thc dam become established in the upper digestive tract, E. coli in the lower, and a healthy equilibrium is established (Fig. 1 ).

7) When colostrum is not taken by the calf immediately after birth, an alteration of this "normal" condition results. Escherichia coli organisms unhampered by colostral antibodies actively compete with enterococci, and the few lactobacilli which may have been collected by the calf on its way through the birth canal, for a place in the upper intestinal tract. If the calf is subjected to one or more additional adverse contributing factors (Table 1 and Fig. 3), the E. coli usually win and become the dominant flora in this absorptive portion of the intestine which is normally "off limits" to them (Fig. 2). As they go through the processes of multiplication and death, they release increasing amounts of highly potent and lethal endotoxin. Depending upon the potency and amount of toxin absorbed by the calf, varying degrees of illness, or death, ensue. Damages to intestinal epithelium may allow entry of E. coli organisms into the general circulation and internal organs. Some strains are more highly invasive than others, and can quickly gain entrance through apparently intact mucosa.18,22 In other cases, with less invasive but highly potent strains, toxin may be so quickly absorbed from the intestinal tract that illness and death result from toxemia without bacteremia--often so quickly that death results without observed illness.

In the course of extensive studies on calf diarrhea, pathognomonic lesions associated with peracute deaths in very young calves could not be demonstrated.34 Peracute deaths due to the "enteric-toxemic" form of E. coli proliferation in the small intestine, without bacteremia, have been reported in calves up to 6 months of age.21 It is apparent that in such cases, lacking pathognomonic lesions and with negative bacteriologic cultures of internal organs, unless various levels of the small intestine are examined quantitatively for E. coli the case will go undiagnosed, or be recorded as "sudden unexpected death" (SUD) of undetermined cause.

It is the multiplicity of number and degree of adverse contributing factors referred to which makes diarrhea of newborn calves such a complex and variable disease. These factors include (1) unavoidable rigorous weather conditions, and sometimes avoidable adverse management conditions, that result in exposure to cold, wind, and wet;43,66 (2) subnormal nutritional state derived from the dam, including avitaminosis A;4,25 (3) pathogenicity, concentration, and multiplicity of viral and bacterial agents to which the calf is exposed; (4) the time interval between birth and colostrum feeding;6,34,43 and others.

These adverse contributing factors are inter-related. When the total effect of adverse contributing factors, including those just described in (1), (2), and (3) is small, the "allowable time" before first colostrum feeding is large--conversely, as the total effect of adverse contributing factors becomes greater, the allowable time between birth and first colostrum feeding becomes smaller, until it approaches zero (Fig. 3). For example, the time factor will not be as critical for a calf born on clean grass on a warm sunny morning from a healthy dam as for a calf born into mud and manure on a cold windy night from a dam with avitaminosis A or otherwise diseased.

8) If a calf receives colostrum after the chain of adverse internal events is underway, it may (1) recover without clinical signs (even subclinical cases may result in stunted calves, preventing their achieving optimal potential), (2) become clinically ill and yet recover, or (3) die, depending upon the total effect of adverse contributing factors, and upon others, many yet unknown. Once the chain of adverse events has begun, E. coli alter conditions in the anterior intestine, to a greater or lesser degree, to their own requirements, and it becomes increasingly difficult for lactobacilli and enterococci to become established. Escherichia coli may multiply to the extent that as many as 100 million to 1 billion may be demonstrated per cubic centimeter of intestinal contents even in the upper portion of the small intestine. On a quantitative basis, there may then be insufficient E. coli antibody in the colostrum to adequately cope with this vast number of organisms. Usually at this stage one of the many strains of E coli present will have asserted itself over the others and become numerically predominant. It is in this manner that the most highly pathogenic strains of E. coli are "selected out," and become the predominant flora in a calf, or in an epizootic. Ability to multiply quickly in the host is usually an inherent mechanism of pathogenicity in bacterial organisms--hence, when opportunity allows, the most highly pathogenic strains flow into the breach and become the predominant flora. This is one logical explanation of why the incidence of calf diarrhea may increase and the disease become more severe as calving season progresses. Pathogenic strains are selected out and have grown perhaps even more pathogenic.

When one, or even several, highly pathogenic strains predominate, there may result a quantitative antigen-antibody imbalance. Colostrum normally contains antibodies to many different types of E. coli. When only one or several types predominate, antibody against these types, while present, may be quantitatively insufficient unless given most promptly after birth of the calf.

Prevention

In clearly visualizing the condition existing in the intestinal tract of the normal calf and in one with diarrhea, one can understand that any factor which serves to upset the equilibrium between upper and lower bowel may result in disease. Overfeeding can result in dilution of the normal acid condition of the anterior portion, ballooning of the bowel, sluggish peristalsis, and a resultant forward migration of E. coli. Chilling and wetting can result in lowered vitality and suppression of normal peristalsis with the same result. Such factors in older calves are not as highly or quickly lethal, since the intestinal tract in these animals is tougher and less absorptive than in the 1- and 2-day-old calf.

Prevention of diarrhea and death in newborn calves must be directed toward establishing as rapidly as possible the normal bacterial flora and normal physiologic state within the intestinal tract.

Colostrum.--The greatest single factor for accomplishing normalization is early feeding of colostrum, preferably within 15 minutes after birth.34,43 If fed within this time, the initial amount required is not great. Under experimental conditions 1/2 to 1 pint has proved sufficient. The key word is early.

"Prompt" feeding of colostrum has been, defined as "within 24 hours after birth''15 but this definition is not valid, at least not for this country. Studies in Wisconsin33,34,43 have shown that many calves born during the winter months would have diarrhea if not fed colostrum within the first 2 hours or less after birth. In some calves, the ability to absorb, from colostrum, antibody to a somatic antigen of E. coli may be lost as early as 6 to 8 hours after birth.

Prevent Overfeeding.--For the first several days of life, feeding milk equal to 10% of the body weight per day is ample. This may be fed in 2 equally divided meals--for example, two 4-lb, feedings for an 80-lb calf. In cool, damp weather, calves will not require additional water for these first several days.

In problem herds, a temporary muzzle may be constructed of a piece of meta1 or plastic mesh and a piece of baling wire, with a piece of binder twine tied behind the cars for thc strap, to prevent overeating of milk and ingestion of straw and filth. Individual calf pens are, of course, preferable and are becoming increasingly more popular.

Antibiotics.--There is no adequate substitute for early feeding of colostrum. Adhering to the recommendation for early feeding of colostrum will sometimes require truly Herculean efforts, but the results will be worth the efforts and work involved. However, it is realized that under even the best conditions it will not be possible to get colostrum promptly into 100% of the calves. In cases of delay, depending upon the total effect of the adverse contributing factors, it may be necessary to administer an appropriate antibiotic simultaneously with the colostrum. Since E. coli organisms are gram negative and the benign lactobacilli and enterococci are gram positive, an antibiotic more selectively active against the gram-negative bacteria than against the gram-positive ones is required.

Chloramphenicol is such a drug.8,ll,24,34,43 While it may reduce the numbers of lactobacilli and enterococci to some extent, it is very quickly and highly effective against E. coli. The recommended dosage is 500 mg. per orum administered at approximately 12-hour intervals until 2 or 3 doses have been given. This will keep the E. coli bacteria in check until the calf's intestinal tract has become more resistant and less absorptive. The effectiveness of chloramphenicol is due to quickly eliminating E. coli from the small intestine, and even from much of the large intestine. Aerobacter species become the predominant flora in these areas, so that after chloramphenicol treatment is stopped, the E. coli must compete with these to re-entrench in even its normal habitat.

Parenteral injection of chloramphenicol is recommended also, if E. coli septicemia is suspected or confirmed. It must be remembered, however, that necessary antibiotic levels for required prompt destruction of E. coli in the intestinal tract cannot be achieved by parenteral injection, and that calves can readily die from absorption of toxins from the intestinal tract even in the absence of bacteremia. Thus, parenteral administration is an adjunct to, and not a substitute for, oral dosage. It should also be recognized that calves may develop pneumonia even while being given oral doses of chloramphenicol adequate to prevent or control intestinal infection, and supportive parenteral administration of penicillin-streptomycin combinations or other appropriate therapy should be administered when indicated.

The tetracycline group of antibiotics should not be relied on for prevention or therapy of diarrhea of newborn calves. A1though probably effective at one time, they have been so widely used clinically and as feed additives that many strains of E. coli are now resistant to them.3,24,27,49,50

Contrary to some popular opinion and much illusionary advertising, there is no valid controlled experimental evidence to prove that feeding tetracycline supplements to calves decreases the incidence of diarrhea.

Calves allowed no colostrum but given 500 mg. of oxytetracycline twice daily from shortly after birth developed diarrhea and died slightly more quickly than similarly fed calves given no treatment at all.34,43 In the guinea pig, "the normal gram-positive intestinal flora is inhibited in its development soon after the administration of penicillin, chlortetracycline, and bacitracin. The gram-negative bacilli overgrow other organisms of the intestinal tract, secreting toxins that paralyze the normal intestinal peristalsis," with resulting illness and death.12 A similar condition appears to be elicited in certain instances in calves.

The writer's experience is specifically with chloramphenicol and the tetracyclines. Other antibiotics and chemotherapeutic agents' such as the nitrofurans,23,29,38,39,40 may be as effective in preventing diarrhea of newborn calves as is chloramphenicol.

The 3 criteria for selecting a preventive or therapeutic agent are: (1) it must act effectively against E. coli in the calf's digestive tract, not just in the uncomplicated environment of a bouillon tube or agar plate; (2) it must not destroy great numbers of the necessary lactobacilli and enterococci organisms; and (3) it must act quickly. Some drugs ineffective against diarrhea of newborn calves may be effective in treating older calves where the time factor is not so critical and the digestive tract is tougher and not so absorptive. But in preventing diarrhea and death in newborn calves, time is a highly critical factor.

One worker10 found a lower pH in feces of normal calves than in calves with diarrhea, and has had success in prevention and treatment of diarrhea with solutions of dilute acids. This is analogous to the farm remedy of "a coke bottle full (6 oz.) of vinegar," and of the extensive use of vinegar in human folk medicine in northeastern United States. This treatment may present excellent possibilities, since it would create an environment favorable to lactobacilli and unfavorable to E. coli. Furthermore, one would not expect development of resistant strains of E. coli, as must be anticipated with use of antibiotics.

Favorable results have been reported in some cases in calves and lambs following use of acidophilus milk.46,47 This excellent and painstaking work was apparently the basis for some of the lactobacilli powders commercially available today. Although undoubtedly of benefit in some cases, including cases in which prolonged use of broadspectrum antibiotics has destroyed all or most of the normal gram-positive flora in the small intestine, action of the dried cultures is apparently too slow to be of decisive benefit in critical cases, and use of liquid acidophilus milk is unavoidably cumbersome.

Artificial Immunization.--It is theoretically possible that, in some instances, colostrum from most cows within a herd may be lacking in specific antibodies against certain E. coli strains in the herd environment. This might be expected to occur when there have been additions to a segregated herd recently enough so that cows have not had time to be exposed to "imported" strains, and so develop antibodies against them. However, definitive evidence is lacking that this is so, and that absence of specific colostral antibody in the dam is a critical factor in cages and epizootics of calf diarrhea usually encountered.

Bacterins containing killed cultures of E. coli and other Coliform organisms have been used for many years, inoculated into both cows and calves in the hope of preventing calf diarrhea. None has yet been proved effective.18 Killed cultures of E. coli are notably poor inducers of antibody production. There are many different strains, most of which are potential pathogens, and they mutate quickly on artificial mediums.58 Even allowing for the possibility of an adequately antigenic autogenous bacterin prepared against certain strains in a particular herd, such a bacterin could hardly be expected to induce appreciable antibody production in time for the current calving season. The E. coli strains causing diarrhea during one calving season would not be expected to be the most prevalent troublemakers during the next. Furthermore, by the following calving season, the cows should have contacted the strains sufficiently in the environment to be naturally immunized against them.

In studies in Ontario, Canada, calves fed colostrum from unvaccinated cows were resistant to colisepticemia when challenged with an imported virulent strain, RVC 1787, even though some of these calves had no demonstrable agglutinins to RVC 1787 in their serum, and RVC 1787 has not been isolated from calves with naturally occurring cases of the disease in Ontario.22 Because "colostrum-fed calves are resistant to experimental infection with serotypes of E coli associated with colisepticemia regardless of the presence or absence in their serum of specific agglutinins against these serotypes," it was considered unlikely that lack of K agglutinins in colostrum or serum was an accurate indicator of lack of protective antibody.l8 Other workers found no relationship between bactericidal activity of the serum and resistance of the calf.23

The greatest proportion of diarrhea in newborn calves appears due, not to lack of specific antibody in colostrum, but to lack of promptness in its administration, coupled with a variety of adverse contributing factors.

Husbandry Practices.--Trite though it may sound, the ultin1ate prevention of diarrhea and death of newborn calves entails having a healthy, vigorous calf born to a healthy well-nourished dam under excellent environmental conditions--facts well demonstrated and documented in past ranching, farming, and research experience. This simple statement encompasses all phases of animal husbandry and veterinary medicine.

As stated before, if the total of adverse contributing factors becomes great enough, the allowable time for feeding colostrum approaches zero. It must be recognized that environmental conditions can become so impossibly inadequate they cannot be overcome. No presently known measures, nor any capable of being developed through the most thorough and adequate research, can prevail against them.

"Instead of having to endeavor to control disease under impossible conditions, it should, by proper planning, be possible to develop intensive management systems which are both favorable to the animal and adequately hygienic "5 For the rancher and dairyman to accept this statement, this philosophy, he must know why, and we have the responsibility to adequately explain why in specifics, not generalities. If, as is becoming increasingly the case, the cattleman chooses to have his cows bred so that they calve early in the year in hopes that he will have heavier calves to market as feeders, he must be given adequate and understandable facts, so that he may know beyond a shadow of a doubt exactly why, if unfavorable weather conditions prevail during calving season and there is not adequate shelter for his calves, his losses may well be high. At the same time he must be given information as to what he can best do under the circumstances to, as far as possible, reduce these losses. He must bc told beforehand that if the previous summer was dry and hot, and his hay is, therefore, weedy and low in vitamin A and other essential components and the calving season is co1d,windy and wet, and his cows have been brought into relatively small pastures or lots where proximity favors selection of particularly virulent strain" of E. coli and fosters spread of various viral agents, he had better be riding or walking night-herd (and day-herd) to see that calves get early colostrum and shelter, and in some cases promptly administered appropriate antibiotics. There is no easy way.

Workers have demonstrated a viral agent (calf pneumonia, enteritis virus) in the lungs of normal cattle, and reported that during the winter months this agent became concentrated in the relatively closed and humid atmosphere of dairy barns.6 Calves born into this atmosphere and not promptly given colostrum had diarrhea and usually died. Another worker confirmed the latter observation43 and further demonstrated that calves born outside during the winter months, not given colostrum and not dried, and placed inside a clean isolation unit maintained at approximately 45 F., had diarrhea and died. Large numbers of E. coli were found in their anterior intestinal tracts, and in one instance in spleen and heart blood. Calves treated similarly, except that they were promptly rubbed dry with absorbent cloth sacking rinsed in hot water and squeezed as dry as possible, remained healthy and had no diarrhea. It is postulated that these 2 situations are analogous to those which occur when a calf is born and its dam either (1 ) immediately wanders off for a variable time or (2) remains to nuzzle and lick the calf dry and allows it to partake of colostrum.

We are told that early calving is a question of economics. Some years ago we were told that winter racing for 2-year-old Thoroughbreds was a question of economics. There was very high attrition among these 2-year-olds. There was a complete numerical turnover of horses in training on the race track approximately every 3 years-- 27,000 horses were in training on all tracks, and about 9,000 Thoroughbred foals were registered each year. There was very little or nothing that we, as veterinarians, could do to stop this attrition. We were working against reason and nature with people who were trying to do something that could not be done. There has been a marked decrease in winter racing of 2-year-olds over the past several years. The reason is called economic. It was finally realized that a 4 1/2-furlong race contested by erratically running youngsters was not a particularly interesting spectacle or favorable wager for the bettors, and also that perhaps the economic cost in crippled youngsters was too high. So now the trend is reversing primarily due to what is called economics.

The veterinary profession has no authority to determine how any person will manage his livestock. This is determined by each individual's ideas or interpretations, as long as his individual "economics'' will stand it. But our profession does have the responsibility to explain to the rancher, dairyman, or other animal owner, as clearly and as objectively as possible, the probable health and disease results and consequences relating to various husbandry practices.

It is appropriate here to quote from the words of Theobald Smith, "The achievements of science are neutral, until applied by man for purposes constructive or destructive, good or evil."30A Research on diarrhea and death of newborn calves should be continued and expanded. But while we are seeking further answers, we must apply all available knowledge, which is considerable, to solving present problems.

References

1Aschaffenburg, R.: Nutritive Value of Colostrum for the Calf. 3. Changes of Serum Protein of the Newborn Calf Following Ingestion of Small Ouantities of Nonfatty Fraction. Brit. J. Nutr., 3, (1949): 200-204.

2Baker, J. A.: A Filterable Virus Causing Enteritis and Pneumonia in Calves. J Exptl. Med., 78 (1943): 435 445.

3Barr, F. S., Carman,P. E., and Clarkson, T. B.: Resistance of Calf Scour-Producing Organisms to Broad-Spectrum Antibiotics. Am. J. Vet. Res., 16, (Oct., 1955): 515-516.

4Boyer, P. D., Phillips, P. H., Lundquist, N. S., Jensen, C. W., and Rupel, I. W.: Vitamin A and Carotene Requirements for the Maintenance of Adequate Blood Plasma Vitamin A in the Dairy Calf. J. Dai. Sci., 25, (1943): 443-440.

5Brander, G. C: Factory Farming. Vet. Rec., 76, (Dec. 26, 1964): 1523-1524.

6Brandly, C A., and McClurkin, A. W.: Epidemic Diarrheal Disease of Viral Origin of Newborn Calves. Ann. New York Acad. Sci., 66, (1956): 181-185.

7Chapman, G. H.: A Culture Medium for Detecting and Confirming Escherichia coli in Ten Hours. Am. J. Pub. Health, 41, (1951): 1381.

8Chittenden, G. E., Sharp, E. A., Van Der Heide, E. C., Bratton, A. C., Glazka, A. J., and Stimpert, F. D.: The Treatment of Bacillary Urinary Infections with Chloromycetin. J. Urol., 62, (1949): 771.

9Chopra, S. L, Blackwood, A. C., and Dale, D. G.: Intestinal Microflora Associated with Enteritis of Early-Weaned Pigs. Canad. J. Comp. Med. & Vet. Sci., 27, (Dec., 1963): 290-294.

10Cowie, R S.: The Use of Dilute Acids in the Treatment of White Scour in Calves. Vet. Rec., 76, (Dec. 26, 1964): 1516-1518.

11Dalton, R. G., Fisher, E. W., and McIntyre, W. L. M.: Antibiotics and Calf Diarrhea. British Vet. Assoc.; Presented at the 78th Annual Congress of the Association held in Glasgow, Aug. 28 to Sept. 3, 1960.

12De Somer, P., De Voorde, H., Eyssen, H., and Van Dijck, P.: A Study on Penicillin Toxicity in Guinea Pigs. Antibiotics and Chemother., 9, (Sept., 1955): 463-469.

13Dow, D., Jarrett, W. F. H., and McIntyre, W. I. M.: A Disease of Cattle in Britain Resembling the Virus Diarrhoea-Mucosal Disease Complex. Vet. Rec. 68, (1956): 620-623.

14Dunne, H. W., Glantz, P. J., Hokanson, J. F., and Bortree, A. L.: Escherichia coli as a Cause of Diarrhea in Calves. Ann. New York Acad. Sci., 66, (1956): 121-135.

15Fey, H., Margadant, Anita, Nicolet, J., and Hunyady, G.: Colostrum Prophylaxis of Experimental Colisepsis in Calves. Schweiz. Arch Tierheilk., 105, (1963): 361-370.

16Fey, Hans: Patrogenesis of Colibacillary Septicemia in the Calf. Bull. Off. internat. Epizoot., 62, 1904

17Gasow, F., Oja, E., and Eads, F. E.: Chloromycetin in Treatment of Complications Due to Secondary Invaders of Canine Distemper and of Gastro-enteritis. North Am. Vet., 32, (1951): 841-842.

18Gay, C. C: Escherichia coli and Neonatal Disease of Calves Bact. Rev., 29, (March, 1965): 75-101.

19Gay, C. C: Bacteriological and Serological Studies of Colibacillosis in Calves with Special Reference to Vaccination as a Means of Prevention. M.V.Sc. Thesis, University of Toronto, Ont., 1962.

20Gay, C. C. McKay, K A., and Barnum, D.A.: Studies on Colibacillosis of Calves. I. The Antibody Acquired by Calves as the Result of Vaccination of the Dam. Canad. Vet. J., 5, (1964): 248-261.

21Gay, 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, (1964): 297-308.

22Gay, C. C, McKay, K A., and Barnum, D. A.: Studies on Colibacillosis of Calves. III. The Experimental Reproduction of Colibacillosis. Canad. Vet. J., 5, (1964): 314-325.

23Glantz, P. J., Dunne, H. W., Heist, C. E., and Hokanson, J. F.: Bacteriological and Serological Studies of Escherichia coli Serotypes Associated with Calf Scours. Pennsylvania State Univ. Agric. Esper. Sta. Bull. 645, (1959): 22.

24Glantz, P. J.: In Vitro Sensitivity of Escherichia coli to Antibiotics and Nitrofurans. Cornell Vet., 52, (Oct., 1962): 552-562.

25Hansen, R. G., Phillip, P. H., and Rupel, I. W.: The Effect of Vitamin Supplements Upon Survival of Newborn Calves. J. Dai. Sci., 29, (1946): 761-766.

26Hansen, R G., and Phillip, P. H.: Studies on Protein from Bovine Colostrum. I. Electrophoretic Studies on the Blood Serum Proteins of Colostrum. Free Calves and Calves Fed Colostrum at Variow Ages. J. Biol. Chem., 171, (1947): 223-227.

27Harry, E G.: The Ability of Low Concentrations of Chemotherapeutic Substances to Induce Resistance in E. coli. Res. Vet. Sci., 3, (1962): 85-93.

28Heddleston, K L, Reisinger, R. C, and Watko, L. P.: Studies on the Transmission and Etiology of Bovine Shipping Fever. Am. J. Vet. Res., 23, (May, 1962): 548-553.

29Henry, R T., and Blackburn, E. G.: Treatment of Calf Enteritis with Nifuraldezone Compound. Vet. Med., 52, (March, 1957): 122-124.

30Lederberg, J., and Lederberg, E.: Replica Plating and Indirect Selection of Bacterial Mutants. J. Bact., 63, (1952): 122-124.

30AALeikind, Morris C: Theobald Smith (1859-1934). A Centennial Appraisal. Proc. US. Livestock San. A., (1959): 52-60.

31Little, R. B., and Orcutt, M. L: The Transmission of Agglutinins of Bacillus abortus from Cow to Calf in the Colostrum. J. Exptl. Med., 35, (1922): 161-171.

32Lovell, R.: Intestinal Diseases of Young Calves with Special Reference to Infection with Bacterium coli. Vet. Rev. Annot., 1, (1955): 1-32.

33MeClurkin, A. W.: Transmission of Calf Pneumonia-Enteritis Caused by a Virus-like Agent. M.S. Thesis, University of Wisconsin, Madison, 1954.

34McClurkin, A. W.: The Characterization of a Virus Causing Calf Pneumonia-Enteritis and Nature of the Disease. Ph.D. Thesis, University of Wisconsin, Madison, 1956.

35Moll, Torbjorn: The Infectivity and Transmissibility of the Viral Agent of Pneumonia-Enteritis of Calves and the Clinical and Pathological Features of the Disease. Ph.D. Thesis, University of Wisconsin, Madison, 1952.

36Namioka, S., Urushido, M., and Sakazaki, R.: Escherichia coli Isolated from Transmissible Gastroenteritis of Pigs. Japan. J. Med. Sci Biol., 11, (1958): 141-151.

37Namioka, S., and Murata, M.: Studies on the Pathogenicity of Escherichia coli. R. The Effects of A Substance Obtained from Pseudo-eosinophilis of Rabhits on the Organism. Cornell Vet., 52, (1962): 289-296.

38Orcutt, M. L., and Howe, P. E.: The Relationship Between the Accumulation of Globulins and the Appearance of Agglutinins in the Blood of Newborn Calves. J. Exptl. Med., 36, (1922): 291-308.

39Osborne, J. Clark, Mochrie, R. D., and Batte, E. G.: Microbiological and Therapeutic Aspects in Calf Enteritis. J.A.V.M.A., 134, (Feb. 15, 1959): 173-177.

40Osborne, J. Clark: Microbiology, Serology and Therapy of Calf Enteritis. New Horizons in Chemotherapy. 3rd Regional Conference on the Nitrofurans in Veterinary Medicine. Held under the auspices of the Georgia Veterinary Medical Association and Eaton Laboratories, Div. of the Norwich Pharmacal Co., Norwich, New York, Atlanta, Ga., (Jan. 14, 1960): 8-13.

41Osborne, J. Clark, and Watson, D. F.: Furaltadone in the Prevention of Experimentally Induced Escherichia coli Enteritis in Young Calves. Vet. Med./Small Anim. Clin., 60, (Feb., 1965): 159-163.

42Paterson, A. B.: Virus Diseases in Calves. Vet. Rec., 74, (Dec. 8, 1962): 1384-1388.

43Reisinger, R. C.: Studies on the Pathogenesis of Infectious Diarrhea of Newborn Calved M.S. Thesis, University of Wisconsin, Madison, 1957.

44Reisinger, R. C., Heddleston, K L., and Manthei, C A.: A Myxovirus (SF-4) Associated with Shipping Fever of Cattle. J.A.V.M. A., 135, (Aug. 1, 1959): 147-152.

45Reisinger, R. C.: Parainfluenza 3 Virus in Cattle. Ann. New York Acad. Sci., 101, (Nov. 30, 1962): 576-582.

46Shaw, J. N., and Muth, O. H.: A Treatment for Scours in Calves. North Am. Vet., 17, (1936): 35-38.

47Shaw, J. N., and Muth, O. H.: Use of Acidophilus Milk in the Treatment of Dysentery of Young Animals. J.A.V.M.A., 90, (Feb., 1937): 171-175.

48Smith, H. W., and Crabb, W. E.: The Typing of E. coli by Bacteriophage, Its Application to the Study of the E. coli Population of the Intestinal Tract of Healthy Calves and of Calves Suffering from White Scours. J. Gen. Microbiol., 15, (1956): 556-574.

49Smith, H. W., and Crabb, W. E.: The Sensitivity to Chemotherapeutic Agents of a Further Series of Strains of Bacterium coli from Cases of White Scours: the Relationship Between Sensitivity Tests and Response to Treatment. Vet. Rec., 68, (May 12, 1956): 274-276.

50Smith, H. W., and Crabb, W. E.: The Effect of the Continuous Administration of Diets Containing Low Levels of Tetracyclines on the Incidence of Drug-Resistant Bacterium coli in the Feces of Pigs and Chickens: The Sensitivity of the Bact. coli to Other Chemotherapeutic Agents. Vet. Rec., 69, (Jan. 12, 1957): 24-30.

51Smith, H. W.: Observations on the Aetiology of Neonatal Diarrhoea (Scour) in Calves. J. Path. & Bact., 84, (1963): 147-168.

52Smith, T., and Little, R. B.: The Significance of Colostrum to the Newborn Calf. J. Exptl. Med., 36, (1922): 181-192.

53Smith, T., and Little, R B.: Cow Serum as a Substitute for Colostrum in Newborn Calves. J. Exptl. Med., 36, (1922): 453-468.

54Smith, T., and Little, R. B.: Absorption of Specific Agglutinins in Homologous Serum Fed to Calves During the Early Hours of Life. J. Exptl. Med., 37, (1922): 671-683.

55Smith, T., and Little, R. B.: Proteinuria in Newborn Calves Following the Feeding of Colostrum. J. Exptl. Med., 39, (1924): 303-312.

56Smith, T., and Orcutt, M. L.: The Bacteriology of the Intestinal Tract of Young Calves with Special Reference to Early Diarrhoea. J. Exptl. Med., 41, (1925): 89-106.

57Smith, T.: Focal Interstitial Nephritis in the Calf Following Interference with the Normal Intake of Colostrum. J. Exptl. Med., 41, (1925): 413-425.

58Smith, T., and Bryant, G.: Studies on Pathogenic B. coli from Bovine Sources. II. Mutations and Their Inununological Significance. J. Exptl. Med., 46, (1927): 133-140.

59Smith, T.: Studies on Pathogenic B. coli from Bovine Sources. III. Normal and Serologically Induced Resistance to B. coli and Its Mutant. J. Exptl. Med., 46, (1927): 141-154.

60Smith, T.: The Relationship of the Capsular Substance of B. coli to Antibody Production. J. Exptl. Med., 48, (1928): 351-361.

61Smith, T.: The Immunological Significance of Colostrum. I. The Relationship Between Colostrum, Serum, and the Milk of Cows Normal and Immunized Towards B. coli. J. Exptl. Med., 51, (1930): 473-481.

62Smith, T., and Little, R. B.: The Immunological Significance of Colostrum. II. The Initial Feeding of Serum from Normal Cows and Cows Immunized Towards B. coli in Place of Colostrum. J. Exptl. Med., 51, (1930): 483-492.

63Jatanabe, Morimatsu, chief, 2nd Research Division (Virus), National Institute of Animal Health (Kachikueisei Skikenjo), Kodaira-City, Tdeyo, Japan: Personal communication, 1963.

64Wiseman, R. F., and Sarles, W. B.: A Plating Technique for Screening Internal Coliform Bacteria. J. Bact., 71, (1956): 480-481.

65York, C J., and Baker, J. A.: A New Member of the Psittacosis-Lymphogranuloma Group of Viruses That Causes Infection in Calves. J. Exptl. Med., 93, (June 1, 1951): 587-604.

66Yuill, T. M., and Hanson, R. P.: Coliform Enteritis of Cottontail Rabbits. J. Bact., 89, (Jan., 1965): 1-8.
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7.

THE JOURNAL OF INFECTIOUS DISEASES • VOL. 128, SUPPLEMENT • JULY 1973

(c) 1973 by the University of Chicago. All rights reserved.

Summary of Discussion

Remarks of Dr. Robert C Reisinger

DR. REISINGER: I would like first to show you some things that you probably have learned but may have forgotten. This first slide (figure 1) is just to remind you that there are very few Escherichia coli in the more absorptive portion of the small intestine, the duodenum, jejunum, and proximal ileum. This is true of all mammalian species so far studied, including the cow and calf, the human infant and adult.

Figure 1. Distribution of Escherichia coli in the 
intestinal tract of the normal calf.

 

 

 

 

 

 

The next slide (figure 2) shows what was demonstrated by Theobald Smith and Marion Orcutt in 1922, i.e.. that calves suffering diarrhea have tremendously increased numbers of E. coli in the intestinal tract. They described "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 . . . E. 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."
My work in Wisconsin, that of Gay in Canada, and that of Mebus in Nebraska confirmed that of Smith and Orcutt and further confirmed and demonstrated that the same mechanism of invasion of E. coli into the proximal small intestine may result in peracute deaths without septicemia and without diarrhea (SDS). Such deaths can occur within several hours after the feeding of an apparently healthy normal calf. Pathologic lesions at autopsy are absent or minimal. as in the crib-death syndrome in the human infant. Experimentally, the diarrhea syndrome can be precipitated by exposure to various viruses, cold and wet, avitaminous A, etc.—any "adverse contributing factor" that impairs optimal reticuloendothelial and/or gastrointestinal function. A classic feature of the calf-diarrhea syndrome is labored breathing (pneumonic signs without pneumonic lesions), but this disappears when, by appropriate antibiotic therapy, excessive numbers of E. coli are cleared from the digestive tract.

Bacterial endotoxins produced in the intestinal tract, which may be absorbed into the venous system, are transported directly into the liver. If for any reason these endotoxins are not inactivated in the liver, they obviously go via the inferior vena cave into the heart and lungs and, to a lesser extent (at least early in the syndrome), into the general arterial circulation.

Some factors common to many cases of SDS, the respiratory-distress syndrome, and endotoxin shock are hyperkalemia, hyponatremia, acidosis, thrombocytopenia, noncoagulability of blood, early respiratory signs without appropriate lesions, pulmonary edema, hemorrhage by diapesis, fast, weak pulse, and circulatory collapse. It is more illogical to consider these similarities as fortuitous than to realize the probability, or at least possibility, of a common cause or mechanism.

There are great differences between bacterial flora, pH, and physical characteristics of the intestinal contents of human infants fed human milk and these features in infants fed cow's milk. Due to its higher content of calcium and protein and its lower content of lactose, cow's milk fed to the human infant raises the E. coli count in the large intestine approximately 1,000-fold (from 106-107/g to 109-1010/g), raises the pH from acid (4.5-5.6) to alkaline (7.0-8.0), makes curds hard and coarse instead of soft and fine, and makes bowel movements relatively infrequent. Characteristics of a healthy human infant on human milk are a relatively low coliform count, acid pH, soft, fine curds, and frequent bowel movements. Even if there were no SDS, these adverse changes wrought by a diet of cow's milk any time during the first six months of age are against all reason in producing the optimally healthy child and the healthy adult he should become.

I believe that crib death, or SDS, is only the tip of the iceberg with regard to effects of absorption of bacterial endotoxin in the human infant. The vasoconstriction, vasodilation, disseminated intravascular coagulation, and other characteristic effects of endotoxin may well account for much of the pathology associated with many cases of cerebral palsy, mental retardation, learning and speech defects, retrolental fibroplasia, hyaline-membrane disease, etc. These latter diseases appear predominantly in infants with immature or otherwise impaired hepatic function, i.e., the immature infants of diabetic mothers, infants anoxic due to placenta praevia, infants whose birth is long and difficult, etc. In long and difficult births, there is also a prolonged in-utero opportunity for seeding of the infants' digestive tracts should infected amniotic fluid be swallowed.

Since absorption of endotoxin from the digestive tract is a confirmed fact in various mammalian species, the probability, or at least the possibility, of similar absorption from the intestinal tract of the human infant should be considered and investigated.
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8.
QUOTES

"A ‘cold’, a viral infection, or anything that disturbs immune responses can result in subtle changes in the gram negative bacterial flora of the the gut, stimulating them to produce endotoxin. This is absorbed into the blood stream, not adequately detoxified, and results in inflammatory responses in the mucous membrane linings of the middle ear............ that endotoxin is the initial cause of the inflammatory response in acute otitis media............ Dr Robert Reisinger in America had first alerted me to this group of substances and their relationship to SIDS......The reason why proper breast-feeding provides a known and large amount of protection against otitis media becomes obvious. Breast-feeding tends to prevent the overgrowth of abnormal forms of intestinal organisms that tend, under certain conditions, to produce endotoxin........Finally, there are two substances that are known to be effective as rapid detoxifiers of endotoxin - Vitamin C and erythromycin -they are both in ‘Archie’s triple injection’. The relationship between SIDS, sudden unexplained shock, sudden unexplained unconsciousness, and otitis media is worthy of consideration. If endotoxin is the ‘cause’ of otitis and also the ‘cause’ of SIDS, sudden unexplained unconsciousness and unexplained shock — as I now know (at least there is a association), then otitis media should be found in a significant number of SIDS cases. That this is so is clearly demonstrated in a number of reported studies. "---Dr Kalokerinos MD (p311 Medical Pioneer)

"One bottle of formula is enough to change a baby’s gut dramatically, and it takes two weeks of breastfeeding to return the gut back to normal. (Personal communication, Dr Robert Reisinger) How can this happen? E Coli is the main culprit. This bacteria is a putrefactive protein loving bacteria. The protein content of human breast milk is lower than in any other mammal, and the protein content of formula or any other milk supplement has a direct influence on the numbers of E Coli in the gut . Not only does the acid gut and very low protein content of breastmilk provide a more hostile environment for E Coli, but breastmilk also contain neutralising factors against E Coli.
Several studies have shown that babies who died of SIDS have a high prevalence of E Coli in the flora of the gut. Some suggest that the E coli "have acquired a plasmid which confers toxigenicity" (Med J Aust, 1989, Vol 151, pg 538) But E. Coli is intrinsically toxic. The outer coating (lipopolysaccharide) is the toxic component, but the key to the toxicity level is the speed with which it can multiply, given the right circumstances. These factors include bottle feeding (which results inmore gram negative bacteria, and a protein and alkaline level favouring E Coli), stress, overheating, viruses, vitamin deficiencies AND the suppressive actions of vaccines on the reticuloendothelial system.
In 1974, Dr Robert Reisinger presented a paper at an International SIDS conference. He quoted many authors who found SIDS predominantly among bottle-fed babies. Included in the authors quoted (but not referenced) was Shirley Tonkin from New Zealand:
"Tonkin reported that in her series of 86 SIDS cases, only two were breast-fed. Since twenty-five percent of her control population were breast fed, she should have had 21 cases of SIDS in breast-fed infants if the risk were the same in both breast-fed and bottle-fed."
"Coombs stated that if SIDS were relatively as common in the breast-fed as in the bottle-fed infant he should have had 17 breast-fed cases in his series, whereas at that time he had not one."---Hilary Butler

The Robert Reisinger Memorial Trust

Dr Robert Reisinger was a medical researcher and veterinarian. For about 15 years Hilary often went to him as a resource person, mentor and tutor, and they worked together on a number of occasions helping parents understand the importance of gut flora, breast-feeding and the effect of vaccines on babies.

On his death in 2003, Dr Reisinger made provision in his will for the purposes of funding future research and writing, into sudden infant death syndrome, vaccines and various aspects of endotoxemia and shaken baby syndrome, recognizing that Hilary had been closely associated with him in these areas of his expertise, and that she would be the only one able to promote and continue the research.

One example of their collaboration is attached separately to this letter.

At the beginning of 2004, the RRMT was established for the charitable purposes of such medical research giving the trustees complete and exclusive authority to determine the medical fields and research which are related to vaccines, sudden infant death syndrome, shaken baby syndrome and endotoxemia, particularly as they relate to the health of mothers and children.

In particular Dr Reisinger wanted the focus to be a grass roots education with an emphasis on helping parents better understand important issues and enabling them to be in a more knowledgeable position to make informed choices about how they chose to parent their children.

The Robert Reisinger Memorial Trust (or RRMT),
25 Harrisville Road,
Tuakau. 1892,
South Auckland,
New Zealand. Phone : (0064) 92368990

"For about one generation several theories of interpretation of SIDS causes have been suggested. My research and conclusions point out, that STRESS may be the key word: receiving formula instead of breastmilk, sleeping alone, breathing tobacco laden air and vaccinations (especially pertussis alone or combined with diphtheria and tetanus in the DPT vaccine) are the main culprits. If a tendency to allergies is given (due to inadequate feeding, which causes the intestial wall to let pass too many allergens, and provoques a pathologic flora) or if the baby has been premature, immature, or in multiple births, all these factors of stress weigh heavier. We parents, mothers especially, can do our share to reduce these multiple stress to almost zero! As long as VACCINATIONS are not included in official SIDS research, there will be no progress and as many as 50-70% of cases will never be explained."---Colette Leick-Welter, Ph.D. (N. H.)

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Dr. Reisinger mentored researcher/writer Hilary Butler, author of "Just A Little Prick" about the dangers of vaccination:  book excerpt:

http://www.whale.to/vaccines/JALP_18_19newlores.indd.pdf

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Dianne Jacobs Thompson  Est. 2007
Also http://truthquest2.com (alternative medicine featuring drugless cancer treatments)
Author publication: NEXUS MAGAZINE "Seawater--A Safe Blood Plasma Substitute?"