Memorial web site for Elisa Jane Scovill, daughter of Christine Maggiore

Commentary on the death of Eliza Jane Scovill: Is an Amoxicillin adverse reaction the 47th AIDS-defining indicator disease?

By Dr Andrew Maniotis

Abstract:

Eliza Jane Scovill was a 3 1/2 year-old child who died in a hospital emergency room 36 hours after imbibing amoxicillin. She had never been exposed to amoxicillin or any other beta-lactams before. An autopsy was performed and “no cause of death” was found by the Los Angeles County coroner’s office where her case had been referred. Approximately one week after the autopsy, the coroner’s office learned of her parents’ unorthodox views on HIV and AIDS and the testing history of the mother (inconclusive, positive, inconclusive, positive, negative, positive, and now consistently positive). Rather than ordering a second analysis, another medical examiner (James K. Ribe) not originally assigned to the case was "brought in to help resolve the case," and revised autopsy findings were released claiming Eliza Jane died of Pneumocystis carinii pneumonia and “HIV encephalopathy.” I present information in this commentary that indicates Eliza Jane's symptoms during her crisis period, the similarities of these symptoms to amoxicillin package inserts, and descriptions of delayed reactions in the medical literature, do not support an "AIDS" diagnosis. The fact that she had 10,800 lymphocytes/µl at the time of her death as measured by the hospital indicates that she had more than the normal numbers of lymphocytes, casting doubt on any diagnosis of Pneumocystis carinii pneumonia, a disease indisputably associated with immune suppression. The facts of the case, and the reaction of AIDS proponents to these facts, are discussed in the context of rational versus empirical approaches in medicine with the hope that other children and families might be spared from a similar tragic, experience.

SEQUENCE OF EVENTS SURROUDING THE DEATH.

As described by her parents, pre-school teachers, pediatricians, neighbors, and family friends, Eliza Jane Scovill lived a happy, and healthy life for 3 ½ years, free of illness (medical records note only a diaper rash in 2001, a cold the same year, and chicken pox in 2002) or medical interventions. On April 30, 2005, Eliza Jane presented to one of her two local pediatricians with a cough and upper respiratory infection.

In the weeks that followed, three pediatricians examined her and noted that Eliza Jane's lungs were clear on April 30^th (Dr Paul Fleiss), May 5^th (Dr Jay Gordon) and May 8^th (Dr Philip Incao). They noted that she appeared to be healthy, except for fluid in her ear, for which non-pharmaceutical remedies were prescribed. On May 14th, in a follow-up to the May 8^th visit, Dr. Incao found that her lungs were clear, but noted redness in addition to fluid in her right eardrum. He prescribed 400mg of amoxicillin twice a day to the beta-lactam-naïve child (1).

After the second dose of amoxicillin on May 15, she vomited several times, and she became agitated. Her mother noticed that the child’s face became pale. Following the fourth dose, Eliza Jane's father stated that Eliza Jane was not looking well, seemed to be deteriorating, and was cold to the touch. She was agitated and ran a low fever. During a call to Incao to report these symptoms, the child fell unconscious and stopped breathing. Her parents called 911 and no pulse could be felt by the emergency technicians that arrived at the home or by the admitting physicians at the emergency room at Valley Presbyterian Hospital (VPH) where she was taken by ambulance (1, 2).

Upon admission to the ER at Valley Presbyterian Hospital (VPH), her abdomen was noticeably protruded (2). On May 16th, 2005, thirty-six hours after imbibing the first dose of amoxicillin, and after having had consumed four doses of amoxicillin (1.6 gm), and an undisclosed antibiotic at the hospital given during attempts at CPR, Eliza Jane died of cardiopulmonary arrest, despite numerous attempts to revive her (2).

The reason why such a young and formerly healthy child’s heart should stop suddenly could not be explained by the hospital. The case was referred to the Los Angeles County Coroner’s office. On May 18^th an autopsy was performed. The medical examiner phoned the family following the autopsy to report that no cause of death was apparent (Christine Maggiore, personal communication).

CORONERS LEARN ABOUT ELIZA JANE'S MOTHER.

Sometime between the family’s communication with the ME the week of May 25 regarding the release of the child’s body to a mortuary and a memorial service held on May 29, the coroner’s office became aware that Eliza Jane's mother wrote a book challenging conventional thinking on "HIV" and "AIDS" and is an outspoken critic of the HIV = AIDS paradigm. More than a decade earlier, starting in 1992 in a series of standard “HIV tests,” Eliza Jane's mother, Christine Maggiore, tested inconclusive (first test), positive (second test), inconclusive (third test), positive (fourth test), negative (fifth test), and positive (sixth test). (3). According to the doctor who ordered the third, fourth and fifth tests, Maggiore did not fit into an “AIDS risk group." Since 1994, Maggiore has been interviewed numerous times by television and other media about her experiences and viewpoints regarding "HIV" and "AIDS."

To better understand her own positive diagnosis, Maggiore researched and wrote a well-referenced book on the subject of HIV and AIDS and about her experiences in coping with her asymptomatic and inconsistent diagnosis (3). She also founded a non-profit organization, Alive & Well AIDS Alternatives, to help others gather factual information about an HIV positive or AIDS diagnosis. Last year, Maggiore's partner of 9 years, Robin Scovill, who is Eliza Jane's father and an award winning film-maker (Special Jury Prize at the AFI Los Angeles International Film Festival for his documentary "The Other Side of AIDS") tested sero-negative three times.

Scovill’s documentary is comprised of a series of interviews with a variety of scientific and medical experts including Dr Kary Mullis, the Nobel Laureate who invented PCR (polymerase chain reaction) used to determine "HIV viral load." Other scientists, including Dr. Peter Duesberg, a member of the National Academy, also are interviewed in the film about the safety, efficacy, and mechanisms of action of antiretroviral and protease inhibitors, as well as the accuracy of "HIV" test kits one scientist in the film helped develop. A physician with the US military, a Professor of Nursing, and several people who have been “living with HIV" for years without anti-retrovirals or the development of any AIDS-defining illnesses, are also interviewed about their experiences. Although the documentary includes several leaders in the AIDS community who present and defend current views regarding "HIV/AIDS," the film helps define an empirical direction in thinking about how the physiology and biochemistry of everyone differs in the context of "HIV/AIDS," and information is presented in the interviews regarding how different individuals have learned to cope with their "HIV/AIDS" death sentence.

REACTION OF THE HIV/AIDS ESTABLISHMENT TO THE WORK OF CHRISTINE MAGGIORE, ROBIN SCOVILL, AND OTHERS WHO QUESTION ORTHODOX DOGMAS AND PUBLIC HEALTH POLICY.

Most of the HIV/AIDS establishment as well as some in the Gay community, and the pharmaceutical industries that make "AIDS drugs," have increasingly regarded the questions, efforts, empirical, and homeopathic ideas of Christine Maggiore, Robin Scovill, and other “HIV/AIDS” question-askers as a threat to the rationalist, reductionist, and allopathically-focused "HIV/AIDS” practices and public health policies, as well as perhaps, an economic threat to pharmaceutical profits. By law, it is mandated that "HIV/AIDS" is a reportable disease. Those who raise issue with "HIV/AIDS dogma” or public health policies are often regarded and treated as enemies of the medical and scientific community. For instance, "HIV/AIDS" critics have been called "Holocaust deniers," “flat-earthers,” "irresponsible," and "criminal." From the beginning of the AIDS era, the AIDS establishment, backed by the federal government and Epidemic Intelligence Service, has attacked those who question any of the accepted AIDS axioms or dogmas with increasing hostility, censorship, and legal consequences. Recently in Maine, Oregon, Massachusetts, and Canada, the children of parents who test "HIV-positive" and who refuse "AIDS medications” for their children, have been taken away by the state. Parents in some instances have faced legal retribution. In New York at Incarnation Children's Center (ICC), an NIH and GlaxoSmithKline-funded trial was conducted in which it is documented that some children who refused to take their medications, or were too young to easily manage were force fed antiretrovirals through G-tubes surgically implanted in their stomach (4, 5). Upon threat of court martial and military prison, since 1990-91, military inductees were forced to be immunized with an ineffective "anthrax" vaccine, and perhaps other experimental vaccines (such as AIDSVAX), that are known to contain dangerous autoimmune syndrome-inducing adjuvants (because the vaccines don't work), during Operation Desert Storm (6). Apparently, during the early 1990's, this experimental program was overseen by Dr. Edmund Tremont, a powerful figure in the AIDS establishment.

The sudden and antibiotic-associated death of child of a mother who had previously questioned "HIV/AIDS dogma” and public health policies regarding "HIV/AIDS" has presented a formidable medical, social, and political conundrum for some in the HIV/AIDS establishment. However, Christine Maggiore is not alone. There are now thousands of scientists including several Nobel Laureates, National Academy members, physicians, scholars, journalists, and people living with "HIV/AIDS" throughout the world, who do not believe that scientific, medical, or epidemiological evidence supports the hypothesis that "HIV causes "AIDS," that “AIDS” is a transmissible syndrome, or that "HIV" is an exogenous retrovirus that has been correctly isolated (see http://aras.ab.ca/rethinkers.htm; http://www.virusmyth.net/aids/statement/).

They believe instead that profound immunosuppression is caused by a myriad of factors and that it is incorrect to group these syndromes under a single disease entity, "HIV/AIDS." The consequences of this view suggest that different treatment strategies are needed for the spectrum of the 46 previously known “AIDS-indicator diseases,” rather than the toxic and dangerous pharmaceutical or vaccination approaches currently in place.

In the aftermath of the tragic death of Eliza Jane, and many other high profile cases that were said to have died of "AIDS," the AIDS establishment could have chosen one of two paths to improve Public Health policies regarding “HIV/AIDS patients.” 1) Initiate a non-pharmaceutical company backed scientific investigation with an open and critical look at the accuracy of the so-called "HIV tests," the efficacy and safety of the so-called “life saving AIDS medicines (regardless of the fact that not one of their package inserts claims that they are “life saving” or even that they have been tested for safety or efficacy) and begin an investigation as to the scientific credibility, accountability, ethics, and motives of leading AIDS researchers who were accused of fraud and scientific misconduct at the beginning of the AIDS era (7), and investigate AIDS program leaders such as Edmund Tremont, who openly admitted to changing safety reports in Nevirapine drug trials last year because he "knew better" than other AIDS scientists and drug-trial safety officers about "AIDS" (8). Or, 2) the tragedy of Eliza Jane’s death could present a golden opportunity for some in the "HIV/AIDS" establishment to even more vigorously attack those who ask questions regarding the current "HIV/AIDS" paradigms, axioms, and policies, by mounting a politically motivated, highly publicized, quasi-religious, and Inquisition-style Salem witch hunt for Christine Maggiore and Robin Scovill, because they have dared to question AIDS dogma, and therefore have threatened, the "HIV=AIDS" establishment.

REVISION OF AUTOPSY FINDINGS.

Predictably, and in retaliation for asking questions, or for never consistently testing "HIV-positive," and perhaps at the most vulnerable moment in the lives of any parents, the public health officials were somehow made aware that a reappraisal of Eliza Jane's “indeterminate” autopsy findings by the LA coroner's office was in order, to determine if the parents should be prosecuted, and their other child aged 8, taken away by The State to be "HIV" tested, and perhaps fed antiretrovirals.

The new autopsy analysis was performed by Dr. Chanikarn Changsri of the LA coroner's office, and Dr. Maurice A. Verity, a neuropathology consultant from UCLA who was asked to 'help her' interpret 'the new neuropathology findings'. Also, another LA coroner, Dr. James Ribe, was summoned in to oversee Dr. Changsri's and Dr. Verity's report. Dr. Ribe has been under investigation by the LA Appellate Court, and other legislative bodies, for his seriously flawed and fraudulent autopsy findings in at least 5 well-documented cases that led to child abuse and murder convictions of parents. For example, in 1996, an autopsy report he wrote led to the life time convictions of the Jacobo parents for findings he felt consistent with child sexual abuse and murder, but which after reappraisal, appeared consistent with a inherited vitamin deficiency, which has led to the release of the father but not the mother, who is still in prison for life (Case No 95-09550). Other examples of Ribe's alleged criminal misconduct can be found at http://www.justiceforej.com/ribeflipflops.html.)

Four months after the autopsy and case reassessment was ordered, on September 15, 2005, Dr. Changsri, Dr. Verity, and Dr. Ribe concluded in their autopsy report and press release to the LA times, that Eliza Jane actually died of end-stage AIDS-related Pneumocystis carinii pneumonia (PCP), and that the child suffered from p24-positive brain encephalopathy due to the ravages of "HIV," despite her almost twice normal lymphocyte count of 10,800 lymphocytes/µl.

Trauma, physical abuse, or chemicals known to render the acute symptoms consistent with the 36 hour temporal sequence of Eliza Jane's death were eliminated through scans at VPH hospital, and at autopsy (1,2). On May 16, 2005, blood analysis at VPH showed that her lymphocyte count was high. The analysis showed that she had 10,800 lymphocytes/µl (normal=2000-8000 lymphocytes/µl) (2). Her hemoglobin and hematocrit counts were low (hemoglobin=6.3 g/dl instead of 12-16g/dl, and hematocrit=21% instead of 37-48%, respectively). (2). Her neutrophils were measured at 12% (normal=45-74%) (2). Her monocyte percentage was in the normal range at 8% (normal is 4-10%) and her platelet count (214 k/µl) was in the normal range (130 k/µl -400 k/µl) (2). The revised autopsy revealed that she had pericardial and pleural effusion and ascites attributed to PCP pneumonia, that her lungs, heart, liver, and kidneys were significantly increased over the expected average weight for her age (184%, 131%, 121%, 146% of normal), that her liver was significantly enlarged and the hepatocytes showed micro-and macrovesicular steatosis. that there were non-specific microscopic lesions in the brain consisting of microglia, multinucleated giant cells, and p24 protein staining, and that her bone marrow showed atrophy, as did her thymus and spleen. These findings differed significantly from "no cause of death" detected by the coroners before they had become aware of the mother's viewpoints on "HIV/AIDS."

ENTER THE MEDIA.

The new finding of PCP pneumonia and "HIV”-encephalopathy were immediately made available to the LA Times by the coroner's office without the consent of the parents. The findings, in addition, were presented by the LA Times and more recently, by ABC Primetime, to insinuate heretical wrong doing on the part of the parents and pediatricians. In the first of many inflammatory articles that came out coincident with the release of the revised autopsy report of Dr. Changsri, Dr. Verity, and Dr. Ribe, entitled "A mother's denial: a daughter's death,” The LA Times went into great detail alluding to how Christine Maggiore barbarously gave birth to her two children at home, refused the Holy Waters of infant vaccines, and unconscionably breast fed her children. It described how one of her three pediatricians defended his daughter, who was a accused of being a Madame involved in prostitution, and worse, how Christine never had the children tested (9), to see if they would test as she had: positive (the first one), indisputably positive (the second one), inconclusive (the third one), positive (forth one), negative (fifth one), and positive (sixth one).

PARENTS AND PEDIATRICIANS UNDER INVESTIGATION, AND THREATS TO REMOVE CHARLIE FROM THE FAMILY.

Predictably, and due to the coroner's revised findings and recommendations, the parents were placed under investigation by The Department of Children and Family Services, the LA police department, and the media. The pediatricians are now being investigated by the State Medical Board. To protect the unity of their family, Christine Maggiore and Robin Scovill immediately arranged to have their 8-year old son Charlie "HIV"-tested multiple times by their pediatricians, and presented with consistently negative results. The 8-year old is still living at home with them.

INDEPENDENT DIFFERENTIAL DIAGNOSIS.

An independent investigation of the coroners' and UCLA consultant's report was solicited from Dr. Mohammed Al-Bayati. Dr. Al-Bayati is a board certified toxicologist and UC Davis-trained comparative pathologist, and is an expert regarding "AIDS." He was asked to perform a differential diagnosis of Eliza Jane's medical records, the coroner's report (1) and the hospital records (2) to determine if indeed the findings of Changsri, Verity, and Ribe were consistent with a toxic adverse reaction to amoxicillin, an AIDS-related syndrome, or attributable to some other cause.

Dr. Al-Bayati is uniquely qualified to perform a differential diagnosis of this case because he has published extensively on drug effects on organs and organ systems, and is an expert in comparative pathology and toxicology. He has done extensive work on the differential diagnosis of unusual deaths of children, such as shaken baby syndrome. He has developed test kits for chemical toxins such as pesticides, and has submitted 7 publications on AIDS to the widely read and highly respected British Medical Journal (BMJ), that were accepted as Letters for publication. He has published pioneering studies on the experimental toxicology of the immune system network that can be found on Medline.

Notably, he has extensively researched and written a book about AIDS (10). It is a concise masterpiece in the differential diagnosis of AIDS. The book provides new information regarding the epidemiology of AIDS in risk groups, the causes and pathogenesis of AIDS in drug users, describes how changes in the lymphoid organs and adrenal glands appear in patients with AIDS, how cohorts of subjects were presumptively selected for the first AZT trials without positive "HIV" tests being obtained for the majority of cases, how opportunistic diseases in AIDS patients are caused by the use of drugs, how the immune network is sensitive to certain toxins, how hemophilia patients acquire AIDS via immunosuppressive agents, how malnutrition causes AIDS, and especially how current leaders of the AIDS establishment, such as Dr. Anthony Fauci, warned in the 1970's, that over prescription of glucocorticosteroids cause profound immune suppression before "HIV," "a variant of a known human cancer virus," was announced by media press release, "as being the probable cause of AIDS" by Robert Gallo, Margaret Heckler, and the Federal Government (11, 12). Dr, Al-Bayati's differential diagnosis regarding Eliza Jane's death was accepted by Medical Veritas, a journal with an editorial board comprised of 11 physicians and 11 scientists.

Dr. Al-Bayati’s differential diagnosis concluded that the death was consistent with an amoxicillin adverse reaction, and not end-stage "AIDS" (13). His report also concluded that Dr. Changsri, Dr. Verity, and Dr. Ribe had performed an unscientific and incorrect analysis of the autopsy data, and failed to provide any coherent explanation for the findings consistent with end-stage AIDS causing the girl's death. For a comparison of Dr. Al-Bayati's analysis of the Eliza Jane Scovill case, I refer the reader to http://JusticeForEJ.com-where Dr. Harold E. Buttram's review of Dr. Al-Bayati's differential diagnosis can be found. It should be mentioned that Dr. Harold E. Buttram, MD, FAAEM is a Fellow of The American Academy of Emergency Medicine and is a very well known pediatrician. He has served on 80 similar cases, and he completely concurs with Dr. Al-Bayati’s differential diagnosis.

It is clear that the events surrounding Eliza Jane's death are as much about the medical facts of the case, as they are about the viewpoints and activities of the parents regarding AIDS, and the reaction of the public health service and media to these viewpoints. Because of this complex mixture of medical, social, and political factors in the case as I have described them so far, one may cogently ask, "Is it even possible at this point to render a scientifically justified understanding of the death of Eliza Jane amidst the firestorm of politicized, quasi-religious fervor surrounding a potential antibiotic adverse reaction, or an "AIDS" diagnosis, in a child of a mother that doesn't consistently test "HIV-positive?" I believe that the available facts, interpreted in light of the temporal sequence of events leading up to Eliza Jane's death, and in light of what is now known about adverse reactions to amoxicillin, and "AIDS," that the true cause of Eliza Jane's death can not be due to "HIV/AIDS," or any "AIDS-defining illness."

ADVERSE REACTION TO AMOXICILLIN.

Nobody can claim to be an expert on adverse reactions to drugs: the science that studies them is at its infancy. However, it is widely appreciated that adverse reactions for all kinds of pharmaceutical interventions are under-reported, or aren’t reported at all. No physician or hospital wants to be responsible for the tragic event that a prescription, meant to alleviate suffering, caused an adverse reaction or death of a patient. Yet the history of drug and vaccine trials show that responses to these and other medical interventions are always associated with unpredictable adverse responses, as the physiology of every human is different. When adverse reactions do occur, they may be difficult or impossible to pigeonhole as a stereotypical series of complications. Nevertheless, and despite under reporting, beta-lactam adverse reactions are frequently reported. Most doctors indeed ask, "are you or is your child allergic to penicillins or other antibiotics," before they are prescribed.

The World Health Organization puts the figure of adverse reactions to this class of drugs at around 0.7%-10%, depending on the nation studied (14).

In a 2000 case report, da Fonseca reported that (15):

"Penicillin is the drug that most often leads to allergic reactions and anaphylaxis. The incidence of adverse events triggered by penicillins is believed to be between 1% and 10%. Up to one-tenth of these episodes are life-threatening, with the most serious reactions occurring in patients with no history of allergy."

Investigators who study allergic reactions, such as Gomes et al., reported that: (16):

"The prevalence of self-reported drug allergy was 7.8% (181/2309): 4.5% to penicillins or other betalactams, 1.9% to aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) and 1.5% to other drugs. In the group 'allergic to beta-lactams', the most frequently implicated drug was penicillin G or V (76.2%) followed by the association of amoxicillin and clavulanic acids (14.3%)."

"Women were significantly more likely to claim a drug allergy than men (10.2% vs. 5.3%). The most common manifestations were cutaneous (63.5%), followed by cardiovascular symptoms (35.9%). Most of the reactions were immediate, occurring on the first day of treatment (78.5%).

Out of 2409 spontaneous adverse event reporting from 1991-1996 in Bulgaria:

" 29% of the adverse drug reaction reports concerned the patients in the age groups of 0-5 year old, and amoxicillin is a drug with a majority of reports for the period" (17).

A group in Spain reported similar findings where amoxicillin caused the most adverse reactions (18).

So-called delayed reactions with amoxicillin are also frequent, and are a subject of intense investigation. For example, there is a developed literature on the subject with titles such as: "Diagnosing nonimmediate reactions to penicillins by in vivo tests" (19), "A diagnostic protocol for evaluating nonimmediate reactions to aminopenicillins" (20), "Diagnosis of nonimmediate reactions to betalactam antibiotics" (21), "Role of delayed cellular hypersensitivity and adhesion molecules in amoxicillin-induced morbilliform rashes" (22), "Nonimmediate reactions to betalactams: prevalence and role of the different penicillins" (23), "In vitro T-cell responses to beta-lactam drugs in immediate and nonimmediate allergic reactions" (24), "Skin test evaluation in nonimmediate allergic reactions to penicillins" (25), "Two cases of toxic epidermal necrolysis caused by delayed hypersensitivity to beta-lactam antibiotics" (26), "Immediate and delayed hypersensitivity from penicillin (27), "Incidence of beta-lactam-induced delayed hypersensitivity and neutropenia during treatment of infective endocarditis" (28).

Nevertheless, in their allopathic training, most medical students are only taught that "a true amoxicillin allergic reaction" is rapid and stereotypic, would present as tachycardia and produce its symptoms within seconds or minutes instead of hours or days, and would be rapidly reversible by administration of epinephrine. This misinformation ignores the developed literature on delayed hypersensitivity reactions indicated above. The weight of Eliza Jane's heart as reported by the ME at autopsy was 131% of normal. This evidence of ventricular hypertrophy (or edema) is best attributed to loss of pressure due to loss of fluid over a period of hours from the capillaries in heart, and subsequent widely observed compensation by the heart muscle to pump more fluid. It also ignores the likelihood that electromechanical dissociation (EMD), may have been responsible for the slowed rhythms of her heart and the pulseless state that were noted by the ER staff (rather than tachycardia), in association with hypotensive multiple organ failure accompanying massive edema (loss of fluid from the vasculature into the organs and tissues). If there is significant loss of blood volume from the vasculature, because 40% of it has leaked out into the tissues due to the toxic effects of amoxicillin, and if the vasculature continues to be permeable, as indicated by the measurements of Eliza Jane's abnormal organ weights, then as long as the antibiotic was present, and inducing a series of reactions leading to vascular permeability, it wouldn't matter if the heart was restarted or even working normally, or how much IV solution she was infused with. This hypothesis is supported by the fact that although the ER treatments of epinephrine transiently stimulated the heart to beat on several occasions, before she was given more antibiotics of an undisclosed type at the hospital, and presumably more IV's, the multiple boluses of epinephrine couldn't stabilize her heart for very long, or restore normal blood pressure or normal pulse. The IV fluids repeatedly administered could have killed her by continuing to swell her heart as they leaked out, causing EMD, and drowning her lungs (and kidneys) with extravasated proteins and fluids leaked from the vasculature. However, the fact that her abdomen and liver were protruding by the time she arrived at the ER may have meant that she had already leaked too much fluid from her own vasculature to ever recover normal vascular blood volume, even before the multiple IV's were administered, principally from the delayed adverse reaction to the amoxicillin itself (2):

"On May 14th, in a follow-up visit, one of the physicians found that her lungs were clear, but noted redness in addition to fluid in her right eardrum. He prescribed 400mg of amoxicillin twice a day to the beta-lactam-naïve child" (1).

"After the third dose of amoxicillin, she vomited several times, and she became agitated. Her mother noticed that her face became pale, her arms changed color and were cold to the touch. She became lethargic and ran a low fever. Then she fell unconscious and stopped breathing, and no pulse could be felt by the emergency team or by the admitting physicians" (2).

"The Los Angeles City Fire Department RA 239 was dispatched on May 16^th at 0003 and arrived at Eliza Jane's home at 0006 (1,2). Upon the paramedic's arrival, Eliza Jane was found pulseless and apneic on the floor. She was cyanotic with cold extremities and asystolic on the cardiac monitor."

"Eliza Jane was presented at the emergency room of Valley Presbyterian Hospital at 0026 on May 16^th. On arrival, she was pulseless, had no spontaneous respiration, and appeared very pale. Her pupils were mid position and fixed."

"The treating physician examined Eliza Jane and found that her abdomen and her liver were distended. Her extremities were cold and poorly perfused with non-palpable pulses. Her oral mucous membranes were pink and there was a lesion on her lower lip."

"At 0105 her heart rate began to slow down into the 40-60 b/min range and she did not have a papable pusle. CPR was restarted. She was bagged with 100% O2 and given high dose epinephrine 1.3mg, atropine 0.26 mg, and sodium bicarbonate 13 mEq. Her heart rate began to increase, it came up to 113 b/minute, and she had a palpable pulse."

"At 0137, no blood pressure could be obtained and Eliza Jane was started on dopamine drip at 5 microgram/kg per hour. Her blood pressure reached to 41/28 and was taken to CT scan. While in CT scan, she had another episode of asystole and she was given atropine, and sodium bicarbonate. She developed a pulse again and was transferred to the Pediatric ICU."

"At the PICU, her heart rate reached approximately 120b/min but she did not have a pulse. She was given fluid boluses, as well as being placed on dopamine 10 microgram/kg/hour and dobutamine 10 microgram/kg per hour. She did not have a pulse and her blood pressure was not obtainable in spite of these treatments. She was also started on antibiotics."

The type of antibiotic given in the PICU is not disclosed, but is of concern, given that Eliza Jane presented with classic signs, and a package-insert-perfect description of an adverse reaction to amoxicillin, rather than end-stage AIDS, as stated by the Medical Examiner's office.

Amoxicillin package inserts (29) describe most if not all the reactions manifested by Eliza Jane in their warnings (I have underlined the adverse events manifested by Eliza Jane as described by her parents, the hospital, and the coroner's report).

"1. Beta lactam antibiotics

Anaphylactic reactions manifested by urticaria, flushing, pruritus, laryngeal edema, and cardiovascular collapse may occur within minutes or, less frequently, hours after administration of beta lactam antibiotics (ie, drugs that have a common beta lactam ring structure)."

SIDE EFFECTS AND SPECIAL PRECAUTIONS

Gastro-intestinal side effects including diahrroea, nausea and vomiting may occur quite frequently. Pseudomembranous colitis has also been reported.Super-infection is relatively common. Doses should be reduced in severe renal failure.

Nausea and vomiting occurred after Eliza Jane's second dose of amoxicillin. Eliza Jane's kidneys were measured at 146% of normal, without significant damage exhibited microscopically, consistent with massive edema and recent injury.

"The most feared adverse events attributed to beta-lactam antibiotics are IgE type I immediate or accelerated reactions. These develop within minutes to hours of drug administration and cause hypotension, laryngeal edema or bronchospasm. Such reactions occur when patients with preformed beta-lactam-specific IgE antibodies, which are bound to tissue mast cells and circulating basophils, are exposed to the drug or tissue protein complex, resulting in the release of inflammatory mediators."

"Unpredictable reactions occur independent of the dose and route of administration and reflect such factors as drug intolerance, allergy, and other idiosyncratic responses. These reactions seem to preferentially affect certain body systems, most commonly blood, skin, and liver."

Eliza Jane's bood work was abnormal to the extent that she was profoundly anemic and exhibited a low hematocrit (Her hemoglobin and hematocrit counts were low (6.3 g/dl instead of 12-16g/dl, and 21% instead of 37-48%, respectively). (2). Her neutrophils were measured at 12% (normal=45-74%) (2). Her monocyte percentage was in the normal range at 8% (normal is 4-10%) and her platelet count (214 k/µl) was in the normal range (130 k/µl -400 k/µl) (2).

And as indicated on the amoxicillin package insert:

"Additional unique life-threatening reactions caused by beta-lactam antibiotics are referred to as "late" reactions. They include such events as hemolytic anemia, Stevens-Johnson syndrome, and exfoliative dermatitis."

Her liver findings were abnormal as well: Eliza Jane autopsy showed liver changes consistent with an immune reaction to amoxicillin, which in some cases of acute toxicity has been noted to resemble pregnancy-fat-like-accumulation and steatosis (30-33).

It is also now emphasized during the early training of many clinicians, as well as in the literature (16), that the effects of amoxicillin on the liver are usually only found when used with another drug, clavulanate, but this misinformation is not supported by the primary literature in Medline: there are many reports that indicate the rate of acute reactions occur in multiple cohorts of patients who were studied for amoxicillin versus amoxicillin-clavulanate reactions, and both appear quite frequently, judging by the number of reports. Perhaps the most comprehensive report that surveys the growing literature on the subject of amoxicillin versus amoxicillin/ clavulanate is presented by Berg et al, and in connection to both fatal and non-fatal adverse reactions to amoxicillin/amoxicillin clavulanate, which they claim typically occur after antibiotic therapy was discontinued, and serves to reinforce the idea that none of these drugs can be considered as safe, even after they are withdrawn (34).

Eliza Jane was never administered any skin allergy tests for amoxicillin, which may have been a wise thing to do, for a bata-lactam-naïve child of an immunologically hyper-reactive mother. Even so, there have even been references to amoxicillin-induced death when cutaneous sensitivity tests to the beta-lactam drugs are given at allergy testing doses (which are extremely small doses) to determine if someone is allergic to these drugs, before giving them a full dose (35).

One group of allergists have even postulated the technical term "flare-up" to describe these kind of delayed reactions as a Type IV mechanism, and described the difficulty in typifying these kinds of reactions. As stated by Reig Rincon de Arellano I et al., (36).

" We suggest that this phenomenon of Flare up occurs by a Type IV mechanism mediated by T-cells without participation of IgE antibodies. The betalactam hypersensitivity mechanism which has usually been described is an IgE mediated reaction, but there are other not very well known mechanisms that are responsible for the delayed reactions."

Also, adverse drug reactions often present with a myriad of unusual symptoms, and they may be difficult to recognize as adverse reactions, rather than as some complication of the illness for which they were prescribed. Among some clinical trial investigators within the "AIDS" Establishment for example, awareness is increasing that the "HIV"-targeted antiretrovirals and protease inhibitors hasten death and morbidity in patients through the induction of profound immune suppression, profound anemia, mitochondrial damage, muscle wasting, dementia, liver damage, renal damage, heart damage, birth defects, carcinogenesis, and many other toxin-induced syndromes listed on the package inserts of AZT, 3TC, other NRTI's [Nucleoside Reverse Transcriptase inhibitors, Non-nucleoside Resverse Transcriptase Inhibitors, non-specific “DNA chain terminators” such as 3Tc, ddI, and others, and protease inhibitors (37-65)]. Many “AIDS specialists,” will not give these highly immunotoxic HAART drugs to patients whose T-cells are above 200 cells/ml. Instead, they prescribe the immunosuppressive cocktails only to patients whose immune systems are already showing evidence of failing, consistent with the new recommendations of the AIDS establishment (see: Yeni PG et al. Antiretroviral treatment for adult HIV infection in 2002: updated recommendations of the International AIDS Society-USA Panel. JAMA. 2002 Jul 10; 288(2): 222-35, which stated:

"The available data from cohort studies, with one exception, have not been able to define a CD4 stratum above 200 cells/microliter at which patients benefit from initiation of therapy"..

In the case of Eliza Jane, and in light of this growing “awareness” and compassion on the part of some members of the AIDS establishment who appear to be retreating more and more from their old battle-cry “Hit ‘em hard and early,” it is surprising that at least some members of the AIDS establishment that are aware of the Eliza Jane Scovill case have failed to attribute the death of Eliza Jane to an amoxicillin adverse reaction, rather than to end-stage "AIDS."

The symptoms in the 36 hours preceding the death of Eliza Jane's are consistent with a delayed sensitivity reaction followed by edema in multiple critical organs. The coroner should have focused on amoxicillin first and foremost, because it was the last (known) agent given before she arrested (as specified before, another antibiotic was given but was not disclosed in the hospital report). Furthermore, the acute symptoms presented were consistent with a delayed adverse reaction to amoxicillin, according to the drug's package inserts, the clinical marketing experience, the data entered by the ER staff when they tried to revive her (2), and her parent's descriptions of her symptoms immediately preceding her collapse (1).

NO EVIDENCE OF IMMUNE SUPPRESSION IN ELIZA JANE.

Is there only one mechanism that can scientifically account for the complexity of AIDS? The term "AIDS," stands for Acquired Immune Deficiency Syndrome. To distinguish AIDS from other known forms of immune suppression, the term AIDS is used to describe persons who are said to exhibit immune suppression specifically because of the negative direct and indirect biochemical activity of "HIV" on lymphoid cells in the body, causing profound immune suppression. The suppression could be reflected in decreases in total or specific immune cell subsets, or, perhaps in a decline in function of existing immune cells. Therefore, to establish an "AIDS" diagnosis, "AIDS" immune suppression is determined by detecting a loss of CD4+ lymphocytes, and more specifically in AIDS cases, the finding of an inverted ratio of CD4+CD8+ T-cell lymphocytes. Eliza Jane's absolute CD4+ cell count wasn't measured by the coroner, nor was her CD4+/CD8+ ratio. However, her absolute lymphocyte count was measured at the hospital (2), which was 10,800 lymphocytes/µl). More than anything else, this number of cells strongly argues against her being an ARC or end-stage AIDS victim, and excludes her as someone suffering from immune suppression of any kind. Because lymphocyte counts in AIDS patients are lower than 1000 cells/microliter, by definition, there is no possible way Eliza Jane could be considered to be an AIDS victim or victim of immune suppression.

To address the issue of why absolute lymphocytes versus CD4/CD8 ratios weren't measured before the coroners were made aware of Christine Maggiore's (inconsistent) "HIV-positive status," and before the coroners changed their initial “indeterminate” cause of death, and deemed Eliza Jane an "AIDS statistic," it is clear that there was no reason for anyone to assume that in Eliza Jane's case, they were dealing with an immune suppressed individual. Her acute symptoms during her 36-hour death appeared to be due to a hyper-immune reaction to a prescribed drug. However, despite the coroner's failure to provide a CD4+/CD8+ ratio in support of the "AIDS diagnosis," it should be emphasized that the accuracy of total lymphocyte counts in predicting death due to "AIDS-associated indicator diseases" is considered equal or even superior to measuring the CD4/CD8 ratio. Therefore, and despite the fact that CD4/CD8 ratios were NOT obtained (by those attributing her death to AIDS after the revised autopsy report was filed some 4 months after the death), absolute lymphocyte numbers were obtained at the hospital, and according to "AIDS experts," they are just as predictive of AIDS-related death in children, if not more so. In a recent study of 3917 children, it was reported that (66):

“For children older than 2 years, the 12-month risk of death and AIDS increased sharply at values less than 1500-2000 cells per microliter, with little trend at higher values.” (Eliza Jane's count was 10,800 cells/microliter).

“Mortality risk was substantially higher at thresholds of total lymphocyte count recommended by WHO than at corresponding thresholds of CD4-cell percentage. When the markers were compared at the threshold values at which mortality risks were about equal, total lymphocyte count was as effective as CD4-cell percentage for identifying children before death…”

In the context of lymphocyte numbers, and despite disagreement in "AIDS science" about what mechanism explains why low lymphocyte numbers are seen in end-stage "AIDS patients," most AIDS researchers still agree that low, rather than high lymphocyte numbers have something to do with full-blown "AIDS." For example, even David Ho and David Douek- principal AIDS-Establishment advocates who continue to advocate and use Kary Mullis's PCR test to detect “viral load” (and which Mullis the Nobelist who created the test continues to unconditionally deny as being able to do so), chaired a meeting at the12th International Conference on Retroviruses and Opportunistic infections, where a consensus emerged that "HIV" attacks the gut {stupid}. A few statements from a Science article describing the meeting may be helpful:

“It’s the gut, stupid. That was one of the clearest take-home messages from the 12^th Conference on Retroviruses and Opportunistic Infections, where 3900 researchers from 72 countries converged to discuss some of the most fundamental questions riddling the field” (67).

"Despite 20 years of research on "HIV," debates still rage about the path from infection to immunological mayhem. There is abundant evidence that HIV preferentially infects and decimates CD4+ white blood cells, and researchers have long argued that direct killing alone accounts for the profound CD4 loss that is the hallmark of AIDS. That prompted David Ho, chair of this year's meeting, to once wear a button saying, "It’s the virus, stupid." Another camp contends that HIV infects a relatively small number of CD4 cells, and indirectly causes the death of uninfected innocent bystanders by activating them, a process leading to their death" (67).

“Just as the inflammation caused by hepatitis destroys the liver, chronic inflammation of the lymph nodes –which Douek dubbed “immunitis-destroys their architecture, leading to massive buildup of collagen, causing fibrosis” (67).

Yet other "AIDS experts," and indeed the original proponents of "LAV" ("HIV)" suggested the idea that HIV" virus-like particles, surrogate markers, and lymphocyte and lymph node pathogenesis associated with these particles might merely constitute the break-down material from excessive cell activation. It was suggested by the work of different groups of investigators (Bess, Gluschankof, and others), that the virus-like particles represent a laboratory Petri dish artifact of phytohemmaglutinnin (PHA-a plant lectin that oxidizes lymphocytes) and interleukin 2 (IL2)-stimulated peripheral blood mononuclear cells (PMBCs) to secrete vesicles through a phenomenon known as blebbing.

In a series of papers published at the beginning of the AIDS era (68 ,69,70), Montagnier and his colleagues reported that electron microscopy of the "umbilical cord lymphocytes that were "infected" with patient 1's lymphocytes exhibited immature particles with dense crescent (C-type) budding at the plasma membane, and they characterized them as "a typical type-C RNA TUMOR virus." In 1984, this same group reported "HIV" to be a type D retrovirus, and later "HIV" was reported to be a lentivirus. Montagnier's Patient 1 from which these cells were derived, according to his 1983 paper, also had acquired herpes, 2 cases of gonnorhea, 1 case of syphilis, cytomegalovirus, and Epstein-Barr virus before his "LAV" diagnosis. (See Montagnier L. Historical accuracy of HIV isolation. Nat Med 9, 1235, 2003, for a recent debate about whether or not a retrovirus was "isolated" in 1983 that could cause cytopathic effects on T-cells).

The in vitro evidence from this group that first discovered "LAV" ("HIV") suggested that "the mitogen-induced creation of "HIV" was consistent with the hypothesis that:

"Mitogenic stimulation and activation, in control cultures in the absence of HIV, can induce the same cytopathic effects as sera or cells derived from "AIDS" patients."

In other words, Montagnier and his colleagues showed that HIV is neither necessary nor sufficient for the induction of the cytopathic effects observed in HIV infected cultures.

Other groups also provided evidence that the artificial stimulation of cultures with mitogens, and not viral replication, led to cell death (71). The DAIDS 1997 official "HIV" culturing manual, under quality control, Section VI, implores:

Although Dr. Gallo and others have claimed that in a stadium full of "HIV-negative" people, not one molecule of "HIV" will be present, the DAIDS (Division of AIDS) culturing manual says that if "HIV-infected" cells from human blood express more than 30 units of “HIV-specific” p24 protein on 2 or 3 separate tests (30 pg/ml), one is considered “HIV-positive,” and if one sleeps with somebody without telling them they have these 30 or more units, one can be tried for attempted murder, one can’t obtain health insurance, one might be fired from his or her job, one might commit suicide, if pregnant one may be frightened into aborting her baby. If your cells express less than 30 units of this protein 2 or 3 separate times (pg/ml), then one is considered non-"HIV-infected" and is home free-one can donate blood, sleep with anyone he or she wants, without telling them his or her “less than 30 status,” etc. How could this be possible if there isn't one molecule of "HIV" in a stadium full of "HIV-negative" people? Its an arbitrary measurement of a molecular signature that may have nothing to do with a virus or immune suppression that is arbitrarily being measured at more than 30 units for an "infected" person, and less than 30 units for a non-infected person (72). The certainty of these kinds of data are what have prompted the Public Health Service, The Media, the AIDS Establishment, and indeed, all those who defend and support the "HIV=AIDS" hypothesis to attack an inconsistently positive woman, and her family during the tragic period of loss of a daughter?

Articles published in The New England Journal of Medicine claim, in addition, that "HIV" infects and destroys heart muscle even in the absence of HAART (73, 74), and causes wasting in skeletal muscle, and disrupts other non-cycling cells, or cells that even lack nuclei (such as platelets in thrombocytopenia, or red blood cells in anemia)? Yet if "HIV" specifically destroys only cycling cells such as lymphocytes, macrophages, or other cycling cells, it could not possibly affect these other, non-cycling cells. What has been confused for "HIV's" terrible long-term effects have been confused, in many cases, with the toxic effects of medication regimens.

It was also pointed out by Luc Montagnier, and in a series of papers by other AIDS experts based in Australia known as The Perth Group, (68, 69, 70, 75, 76, 77, 78) that:

"....replication and cytopathic effect of LAV ("HIV") can only be observed in activated T4 cells. Indeed, LAV infection of resting T4 cells does not lead to viral replication or to expression of viral antigen on the cell surface, while stimulation by lectins or antigens of the same cells results in the production of viral particles, antigenic expression and the cytopathic effect."

Importantly, and after much research into the circumstances required for the in vitro induction of "HIV" viral-like particles, p24, and other "HIV"-associated surrogate markers being induced by IL2 and PHA, or in vivo by perhaps other inducers such as chronic drug use, transfusions, and hemophilia medications and treatments, Papadopulos-Eleopulos et al., concluded that the most likely explanation for the appearance of "HIV" virus-like particles and surrogate markers in both infected and non-infected AIDS cultures and AIDS patients was explained by oxidation due to artificial (pathological) stimulation of lymphocytes with various oxidizing agents, and that these agents could induce the production of "retroviral-like particles" and their surrogate markers from normal uninfected cells (75-78):

"Since both AIDS cultures and AIDS patients are exposed to mitogens (activating agents), many of which are oxidizing agents, the production of viral-like particles, reverse transcriptase, antigen/antibody reactions (WB), and "HIV-PCR- hybridization"may be due simply to oxidative stress which stimulates expression of latent "retroviral" sequences….."(78).

According to this hypothesis, "retroviral-like particles" or their surrogate markers (p24, reverse transcriptase, nucleic acids thought to be specific for "HIV") are not transmitted to the host from outside through infection (they aren't in fact 'exogenous'), but instead, are evoked and derived 'endogenously,' from oxidized cells that produce them when they are stressed.

Gallo and his colleagues also reported that (79):

"The expression of HTLV-III was always preceded by the initiation of interleukin-2 secretion, both of which occurred only when T-cells were immunologically [PHA] activated."

In other words, the immunological stimulation with PHA is required for IL-2 secretion, and during this artificial stimulation of lymphocytes, "viral-like particles" or "retroviral sequence" expression in the absence of any type of infection, is induced, and is accompanied by cell death in some experiments. Thus, relatively early during the AIDS era, it was known that HIV is not necessary or sufficient for the appearance of the cytopathic effects seen in T-cell cultures, yet for some unknown reason, up till 1991 very little (or no) data was presented regarding the effects of the activating agents themselves on T-cell survival or dynamics in culture.

Other investigators involved in the AIDS Vaccine Program, SAIC, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland, also published reports stating that PHA (phytohemmaglutinin) and IL2 (interleukin-2) stimulated healthy cells produce "viral like particles" and HIV 'specific' proteins only when stimulated with PHA and IL-2. They also claimed that microvesicles were a source of contaminating cellular proteins found in purified HIV-1 preparations, as the title of their paper, " Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations," suggests (80).

This would also be consistent with what is hypothesized more generally about retroviral sequence expression.

For example, other AIDS researchers from The Department of Microbiology, University of Minnesota, Minneapolis, even as early as 1992, claimed that “HIV” gene sequences can be evoked from non-infected humans, chimps, and monkeys (81):

"Endogenous retrovirus-related sequences exist within the normal genomic DNA of all eukaryotes, and these endogenous sequences have been shown to be important to the nature and biology of related exogenous retroviruses and may also play a role in cellular functions. To date, no endogenous sequences related to human immunodeficiency virus type 1 (HIV-1) have been reported. Herein we describe the first report of the presence of nucleotide sequences related to HIV-1 in human, chimpanzee, and rhesus monkey DNAs from normal uninfected individuals."

This concept is consistent with what other investigators have discovered about retroids-genetic elements that are abundant in the human genome that code for endogenous sequences of great similarity to "HIV's" (82).

Yet another indication of the probable endogenous nature of "LAV," "HIV," "Type C tumor virus," or "lentivirus," or whatever you want to call “HIV's” molecular signature, the failure of the “HIV/AIDS” vaccine (AIDSVAX) pogrom, followed by the failure of the STEP trial, and because of at least 60 other documented failed "HIV' vaccine pogroms, demonstrates perhaps best of all that materials isolated from "AIDS" patients to be used as antigens in healthy people as a vaccine are not antigenic in that “HIV-positivity” was not shown to be consistently invoked in the vaccinated experimental arms of any trial to date, because these components were not recognized by the immune system as foreign, or exogenous. If "HIV" components were antigenic, then everyone vaccinated (or even some of those vaccinated) should at least temporarily test "HIV" positive. It was even announced by Dr. Robert Gallo himself last year that (83):

"A sound Rationale (is) needed for Phase III HIV vaccine trials"

In this Science article, the AIDSVAX trials were criticized by Gallo and his co-authors because they were from the beginning, a colossal waste of time, money, but most of all, as Gallo warns in the last sentence of the letter to Science, the trials are potentially damaging for the credibility (and future funding) of the "HIV=AIDS" paradigm.

"The decision about whether or not to proceed with mounting a phase III HIV-1 vaccine trial needs to take into account the likelihood of success and the consequences of failure, the value of what can realistically be learned, the human and financial costs involved. As a whole, the scientific community must do a better job of bringing truly promising vaccine candidates to this stage of development and beyond." (83).

It would seem at this point that Robert Gallo and the AIDS establishment, "must do a better job" of establishing a credible disease hypotheses in connection with either cancer or immune suppression, and they should start doing "this better job" by providing evidence that they have isolated an exogenous virus according to routine standards of microbial isolation worked out by Pasteur and his two lab assistants at low budget for rabies, anthrax and chicken cholera more than 130 years ago, and then perhaps show that "HIV" has a consistent effect on cells, or show that it is even associated with a disease syndrome or has an effect on T-cells according to the standards of routine tissue culture or animal models in which "AIDS-indicator diseases" can be shown to occur.

In the 1991 paper published in Virology by Montagnier's group, additionally showed that (70):

" in acutely HIV infected CEM cultures in the presence of mycoplasma removal agent, cell death (apoptosis) is maximum at 6-7 days post infection, whereas maximal virus production occurred at Days 10-17."

This is important not only because effect appears to be preceding cause (you'd expect maximal virus production to correspond to the time when the maximum of cell death is measured at day 6-7, but here cell death at 6-7 days precedes maximal virus production which is at 10-17 days, after the majority of cells are "killed"). Indeed, I was always taught that viruses require cells for their replication, because viruses are non-living things, but these results suggest that a lot of replication of virus is occurring on days 10-17 after the majority of cells are supposedly killed by "the virus" on days 6-7. The statement is also important because it suggests that mycoplasma removal agent affected the outcome of these experiments, since mycoplasmas are responsible somehow for the effects that are observed in these experiments, and not "HIV." Among experts of cell culturing, mycoplasma infections act like a putative "AIDS-causing retrovirus" might have been expected to act, because cells become "weakened" over time, but are not killed by mycoplasma infections.

Yet in some cultures, Montagnier's group also stated that:

"In chronically infected CEM cells and the monocytic line, U937, no apoptosis was detected although "these cells produced continuously infectious virus."

If this is true, then why should continuously productive lymphocytes producing infectious "HIV" induce any cellular pathology in humans?

This non-pathogenic effect noted in persistently infected T-cell cultures was also noted in 1985 by Hoxie et al. in a paper published in 1985 in Science entitled:

"Persistent noncytopathic infection of normal human T ymphocytes with AIDS-associated retrovirus (84).”

A lack of pathological effect on T cells in vitro noted by Montagnier et al. and Hoxie et al. would not be inconsistent with one of Gallo's initial claims regarding one of the characteristics of the first "AIDS" defining disease, Kaposi's Sarcoma, where he proclaimed that:

"The association of Kaposi's sarcoma with AIDS deserves special mention. This otherwise extremely rare malignancy occurs predominantly in a restricted group, that is, the homosexuals, and can occur in the absence of any T-cell defect in the patients" (85).

Although opportunistic infections are still currently considered to be a hallmark of "AIDS" by the AIDS establishment, it hasn't been that long since the other hallmark AIDS-indicator disease, Kaposi's Sarcoma, was considered to be caused by "HIV," but which is no longer considered to be caused by "HIV (86) (currently, there are 46 previously known diseases that have become AIDS-indicator diseases: 6 AIDS-indicator cancers (Kaposi's sarcoma is no longer considered an AIDS-defining illness so actually it is 5 cancers currently), 10 generalized AIDS-indicator syndromes (such as a long-lasting fever or headache), 16 opportunistic AIDS-indicator microbial and parasitic infections, 5 AIDS-indicator viral infections such as Herpes, the 7 AIDS-indicator birth or perinatal syndromes such as heart defects, and 4 new AIDS-defining illnesses).

Perhaps a few years from now, as AIDS disease definitions continue to change, it is possible that all of the 16 opportunistic infections that have been considered "AIDS-indicator diseases, as well as the 5 cancers, 10 generalized AIDS-indicator syndromes (such as a long-lasting fever or headache), 5 AIDS-indictor viral infections such as Herpes or HPV, the 7 AIDS-indicator birth or perinatal syndromes such as heart defects among babies of drug-addicted women, and the 4 recently added AIDS-defining illnesses including "exacerbation of Alzheimer's dementia," will be no longer considered "AIDS-indicator diseases," in the same manner that Kaposi's sarcoma, which was one of the original two, is no longer considered as one? Conversely, if the AIDS establishment continues to add more and more previously known syndromes to the definition of AIDS, are we expected to now accept the idea that an amoxicillin adverse reaction now be added to these 46 AIDS-indicator diseases, and constitute the 47th AIDS-defining syndrome? In this scenario, it would mean that if a patient possesses a p24-positive signal in any tissue while experiencing an amoxicillin adverse reaction, then, that person is an AIDS patient (even in persons such as Eliza Jane with 10,800 lymphocytes/µl), whereas an amoxicillin adverse reaction minus a p24-positive signal would simply be classified as your "ordinary" amoxicillin adverse reaction.

This cursory survey of various "AIDS" hypotheses regarding cytopathogenicity presented here shows that one mechanism cannot possibly explain the complexity of "AIDS." Different investigators, and indeed even the same investigators have published different outcomes of experiments that point to different hypotheses regarding the pathogenesis of "HIV," or indeed, have published that no pathogenic behavior is seen with "persistently infected cultures" at all. According to these hypotheses, "HIV/AIDS" is induced by cellular or environmental stressors, and not due to an exogenous infectious, transmissible microbe. Different investigators have suggested that "the AIDS-indicator diseases" are caused by either direct or indirect lymphoid depletion in the Peyer's patches of the gut, (although no evidence for this hypothesis was given in the Science article in the same patient over time-especially in AIDS drug-naïve patients. Instead, in this article, anyone who would doubt this claim are referred to as “stupid,” by Ho and other "HIV=AIDS" advocates) (67). Yet the first work on lymphadenopathy and “LAV” by Montagnier claimed that lymphadenapathy (or GRID as it was then considered-Gay Related Immune Disorder) was associated with a typical type-C RNA TUMOR virus." Other work has claimed that "HIV" is not an exogenous virus at all, but a mitogen-or toxin-evoked expression of endogenously generated viral-like particles and "HIV-sequences" probably due to oxidative stress. Still other work has claimed that there is NO apoptosis observed in cultures that produce "continuously-infectious retrovirus" which implies that "HIV" has no effect on T-cells in vitro or in Humans. Montagnier’s group also published that a co-factor like mycoplasma infection may play the important role in T-cell pathogenesis because the addition of mycoplasma removal agent exhibits dynamics and timing of cell death in such a way that the (apoptotic) effect of "HIV" (cell death) precedes the proposed cause (high viral expression), and Robert Gallo himself asserted that homosexual patients can develop the first hallmark AIDS-indicator disease, Kaposi's Sarcoma, without any detectable T-cell defect whatsoever according to Gallo, which is effect without any cause in this case (although Kaposi's is no longer considered to be caused by "HIV" but caused by HHV8) (86).

NO EVIDENCE FOR PNEUMOCYSTIS CARINII PNEUMONIA (PCP) IN ELIZA JANE.

If anything, Eliza Jane had a perfect or even hyperactive immune system because of her lymphocyte count of 10,800 lymphocytes/µl (see above). Therefore, the conclusions of the ME are unjustifiable regarding the conclusion that she had end-staged PC pneumonia.

PCP is a disease that presents with a daunting complexity of findings in "ARC" or end-staged "AIDS" patients. PCP is thought to be ubiquitous in humans, and presents in humans with a daunting array of different phenotypes that are still being investigated, as the study of PCP is at its infancy.

However, there is no controversy about PCP being associated with immune suppression before or during the history of the AIDS era. All information to date indicates that PCP occurs only in individuals that are immunocompromised from a variety of natural or iatragenic causes. Some of these causes include long-term corticosteroid treatments, organ transplantation and immunosuppressive anti-rejection treatments, cancer chemotherapy, transfusions, or it is seen along with other concurrent long-term infections such as TB.

Eliza Jane's lymphocyte count, above all, demonstrates that she was not immune suppressed: she had never received corticosteroids, transplants, or chemotherapy, she did not have cancer, and her lung findings were inconsistent with a developed pneumonia of any kind. The microscopic examination of Eliza Jane's lungs revealed no evidence of inflammation, which in an immunocompromised host such as an advanced "AIDS" patient may not be present, but in a patient with 10,800 lymphocytes/µl, an inflammatory response and fibrosis after a long-term or even a short-term infection would be likely. Yet, the ME did not observe any inflammatory response or fibrosis in the alveoli or in the interstitial tissue to justify a diagnosis of Pneumocystis carinii pneumonia or any other form of pneumonia (1).

Another mistake that underscores the unscientific re-analysis by the ME, regards the 'finding' of Pneumocystis organisms in the lung associated with "foamy casts," and arriving at a conclusion, in the absence of indicators of inflammation or fibrosis in an immunocompetent patient, that these organisms were pathogenic in EJ's case, and that they had caused the foamy casts. Foamy casts have not been causally connected to the presence of P. carinii in the lung-foamy casts are frequently seen in emergency rooms accompanying a sudden, often fatal, hypotensive cardio-pulmonary event.

Because PCP was the centerpiece of the coroner's AIDS diagnosis, there should have been a rigorous characterization of quantity of P. carinii in the ME report. First of all, the ME did not count P. carinii in 1 ml of fluid, or in tissue. They just looked at a slide with a stain on it-the ME only did a qualitative, and not quantitative analysis for the presence of P.carinii. Therefore, we have no idea how many organisms of P. carinii there were in the tissue. In the absence of inflammation, fibrosis, or quantification, the conclusion cannot be drawn that Eliza Jane had a large, established, or even widespread infection with P. carinii.

Nor can we know if the particular micro-organisms or strain of P. carinii detected in her lung was of any harm to her at all, or that they were responsible for forming the foamy casts. It is widely known that P. carinii cannot be cultured, and therefore, any potential cytopathic effect these organisms may have on living cells has not been established to date. As mentioned above, foamy casts are not specific to P. carinii, and are seen in cardiopulmonary collapse with high frequency. P. carinii is nearly ubiquitous in humans, and only rarely becomes a problem in a subpopulation of immunocompromised hosts. No one in their right mind would assume that the presence of the organism, especially in the absence of pneumonia or absence of fibrosis in an immunocompetent host (or the absence of shortness of breath-her pediatricians in the weeks leading up to her death noted that her lungs were clear-(1, 2) equals a lethal case of PCP.

Animal models of the disease have been attempted, and show, for example, that P. carinii in "SIV"-infected Macaques is accompanied by a massive influx of neutrophils in the lung (87). As stated above, the ME saw no inflammatory response in the foamy exudates of Eliza Jane, and in fact, she was neutropenic (Neutrophil %=12: Normal=45-74%). Although "SIV" isn't "HIV," "SAIDS" is not like "AIDS," and macaques aren't nearly as related phylogenetically or socially to humans as are chimps, there is no literature on PCP in chimps, because chimps do not develop AIDS, even after injection with end-stage AIDS-patient sera. In fact, it is known that chimps are completely left unharmed by “HIV” "isolates, or "AIDS-patient sera," because in the past 23 years since they were first inoculated with AIDS patient's sera, not one of them has developed “AIDS,” as they continue to sit in their 27 million dollar retirement homes (88).

In theory, at least, it would be expected that a microbial pathological infection in a non-immunocompromised host, such as Eliza Jane, would present with an inflammatory response (which wasn't present according to the coroner), and/or with fibrosis (which also wasn't present in the lung according to the coroner). In support of the fact that polysaccharide residues that form fibrous structures in diseased tissues are a principal hallmark of chronic disease, and a principal cause of resistance within pathological communities of microorganisms, similar to what we observe in malignant tumors (and their metastases) containing vasculogenic mimicry patterns (89-96), it has been long established that like malignant tumors harboring fibrotic extracellular matrix patterns, that multicellular colonies of micro-organisms also produce biofilms made of cells suspended in polysaccharaide matrices that are highly impervious to antibiotics, metals, radiation, as well as extreme changes in pH, oxygen tension, and heat. These biofilms that form fibrosis are important in human pathology because:

As reviewed by Harrison et al. (97):

"The Centers for Disease Control and Prevention estimates that up to 70 percent of the human infections in the Western world are caused by biofilms. This includes diseases such as prostatitis and kidney infections, as well as illnesses associated with implanted medical devices such as artificial joints and catheters and the dental diseases—both tooth decay and gum disease—that arise from dental plaque, a biofilm. In the lungs of cystic fibrosis patients, Pseudomonas aeruginosa frequently forms biofilms that cause potentially lethal pneumonias. There is a long list of biofilm related ailments."

"In almost all instances, the biofilm plays a central role in helping microbes survive or spread within the host. That’s because the slimy matrix acts as a shield, protecting pathogenic bacteria from antibodies and white blood cells, the sentinels of the immune system. Biofilms are also notorious for their ability to withstand extraordinarily high concentrations of antibiotics that are otherwise lethal in smaller doses to their planktonic counterparts. In fact, a biofilm can be 10 to 1,000 times less susceptible to an antimicrobial substance than the same organism in suspension."

Therefore, there is no evidence that a pathological PCP infection was established in the lungs of Eliza Jane, if indeed the particular strain of P. carinii was at all pathogenic in her. Thus, the observation of the ME, that an undetermined quantity of a ubiquitous organism found in the lungs of healthy persons (P. carinii) amidst foamy casts in the lungs of Eliza Jane, can most likely be attributed to detection of a ubiquitous organism awash in proteins leaked from the vasculature, that became pooled, and highly oxygenated near the time of her death, as a result of sudden system-wide vascular permeability caused by an amoxicillin delayed adverse reaction. Association is not causation, and as we warn medical students, the following scenario must always be foremost in the mind of a pathologist working up a differential diagnosis, or before advancing a new hypothesis regarding an association between cause X, and a disease syndrome Y:

"In New York City, during the summer, the sidewalks get hot from the sun and crack more frequently than they do in the winter. Also during the summer there is a higher rate of infant mortality. Therefore, cracking sidewalks cause a higher infant mortality rate in New York during the summertime."

The presence and mere association of P. carinii in foamy casts in lung tissue does not mean that the P. carinii organisms induced the foamy casts, or pneumonia, or death, especially in the absence of inflammation, neutrophils, or fibrosis, and in the presence of 10,800 lymphocytes/microliter.

The UCLA neuropathologist's brain findings of "HIV-encephalopathy" failed to take into account the well known non-specificity of p24 antigen even among living people, not to mention deceased persons. With respect to the certainty of diagnosing "HIV/AIDS," the CDC and the medical literature lists flu, flu vaccination, hepatitis B, hepatitis B vaccination, high levels of circulating immune complexes, high antibody affinity for polystyrene used in different test kits, anti-carbohydrate antibodies, anti-collagen antibodies, lipemic serum, non-specific detection of free ribonucleoproteins, hypergammaglobulinemia, HLA antibodies (to Class I and II leukocyte antigens), having more than one child (multiparous pregnancy is the technical term), herpes simplex I and II, exposure to alpha interferon therapy, arthritis, systemic lupus erythematosus, alcoholic and other forms of hepatitis, leprosy, scleroderma, connective tissue disease, dermatomyostitis, tuberculosis, some malarial infections, hemophilia, hemodialysis hyperbilirubinemia, the presence of some malignant neoplasms, mycobacteriaum avium, organ transplantation, other retroviruses, multiple transfusions, Q-fever with associated hepatitis, primary billiary cirrhosis, primary sclerosing cholangitis, renal failure, Stevens-Johnson syndrome, chronic drug addiction or alcoholism, or visceral leishmaniasis (and about 40 other) as factors that have been shown to generate false positive "HIV" tests. There are some of 70 known risk factors for testing "HIV" false-positive (a complete list can be found in Reference 3 page 11).

50 % of dogs also show structural proteins such as p24 thought to be specific for “HIV” and never develop AIDS (98). Also goats, and cow milk also induced the expression of the p24 antigen (99). Also the thymus glands of "HIV-negative" children are known to express p24 and other so-called “HIV-specific” markers (100).

From the beginning of the AIDS era, the non-specificity of p24 and other surrogate markers for "HIV" have been widely appreciated, even by proponents of the "HIV=AIDS" hypothesis and members of the AIDS establishment. Thus, the need for a gold standard for diagnosis and disease staging in "HIV/AIDS" is particularly acute. From the beginning of the AIDS era, the literature indicates that because the proper isolation and purification of an exogenous "HIV" virus itself has not been possible (86, 101, 102).

Josephson et al. (103) reported the results of a Western Blot study, in which they claimed:

"Despite the fact the the majority of p24-and p24/25-indeterminate specimens exhibited specific antibody reactiviy with HIV core antigen, there was no evidence linking this reactivity to HIV infection. On the contrary, based on available data and limited patient information, we predict that HIV infection was not the cause in most cases."

With these kinds of considerations, then, how can people claim to have isolated pure proteins or nucleic acid sequences from an exogenous retrovirus, and use this material to generate reagents to test pathological specimens, when the viral particles they supposedly comprise cannot itself be isolated according to the discoverer of "HIV" (LAV), or shown to induce a consistent cytopathogenic effect on cells in vitro (104-112)?

Then what are the test kits used for if not as tests to selectively bias or confirm those individuals whom AIDS establishment folks believe live with behavioral risk factors or who belong to a certain demographic membership? Although the kits were originally used to protect the blood supply, the evidence I will present below demonstrates that selective bias is the principal reason for the existence and widespread use of the tests currently. Suffice it to say for now, as grave as an "HIV" or "AIDS" diagnosis and subsequent death sentence is, one might expect there should be widely publicized attempts to alert the public about the lack of a gold standard (standard virus isolation). Or one might minimally expect, if the test kits predict progression to an "AIDS-defining illness," and regardless of whether you believe the evidence shows that "HIV/AIDS" is an endogenous or exogenously acquired syndrome, that at least one test kit type or brand available of the more than 31 on the market, by itself, can serve as a gold standard to identify individuals who carry specific proteins, antibodies or nucleic acids of the "HIV" endogenous/exogenous "virus-like particle" itself.

I believe the evidence supports the probability that Eleni Papadopulos-Eleopulos et al., Dr. de Harven, and others were correct to propose that these kinds of qualifications also present us with an intractable paradox regarding any recommendation that advocates universal testing, or believing recommendations from studies which identify cohorts in clinical trails on the basis of these tests (or statistical surveys based on antibody tests), or results gained from drug treatment trials. Nor will the proliferation of recent rapid test kits that claim to have been validated by comparing positive or negative (or indeterminate) outcomes against the more widely used and non-validated test kits such as Abbott's, Epitope's, or Roche's increase the certainty of "HIV" diagnosis, if, or until, a gold standard is developed against which all kit results can be validated, which is true virus isolation itself.

GIANT MULTINUCLEATED CELLS IN THE BRAIN.

It was claimed by the coroner that giant multinucleated cells were observed microscopically in the Brain of Eliza Jane. Dr. Al-Bayati's report presented information explaining how it is generally believed these cells form from the fusion of immune cells (glial cells) due to a variety of factors. For example, during an acute reaction to a drug that causes systemic vascular permeability and leakage of non-resident proteins in the perivascular areas of the brain, it is not far fetched to suppose that glial cells would try to absorb the insult, and in the process, become fused together to form giant multinucleated cells visible upon microscopic examination. Not much is known regarding adverse reactions to amoxicillin.

Adopting the orthodox view of "HIV" encephalapathy for a moment, and that giant cells are created via fusion of cells by "HIV" (rather than extravasated proteins leaked from the vasculature due to the insult of amoxicillin), it should be asked exactly how does "HIV" induce cell fusion of brain glial cells or macrophages? At the cellular level, if you believe "HIV" is an exogenous virus and dispute the evidence that "HIV" viral-like particles, or "HIV" sequences are evoked endogenously via oxidation as I have presented evidence in support of, it is still not established in the experimental literature if "HIV," or whatever you call it, can fuse cells of any kind together, especially at the titers that are thought to be present in end-stage "AIDS" patients (quite low to the point of not being detectable by many accounts). Again, it was Gallo’s group that first published data claiming that "HIV" induces a "syncytial cytopathic effect" (cell fusion) in vitro (113), amidst their claims that the cytopathic effects of "HIV," when they are observed in T-cell cultures, are most likely caused by the many activating (oxidizing) agents to which the cultures (or some "AIDS" patients) are exposed. Yet these data were derived from a cancer cell line instead of normal peripheral lymphocytes, established from a patient with mature T4-cell leukemia, and this could account for this phenomenon (79).

"The virus positive cultures consistently showed a high proportion of round giant cells containing numerous nuclei", (syncytia)."

However, it subsequently became widely appreciated that the HT line used by Gallo is in fact the HUT78 cancer cell line (114, 115, 116).

If cancer cells are used to generate "HIV infections" in vitro, then what relevance does this have in explaining the behavior of normal lymphocytes, or when one identifies giant multinucleated cells in vivo in a person without cancer?

It should be acknowledged, in addition, that leukemia cells or even normal lymphocytes treated with toxic factors such as PHA or stimulated to produce IL2 which are both toxic oxidizing agents to normal peripheral T-cells, may promote either normal or cancer cells to undergo endoreplication (leading to supernumerary nuclei), and is not representative of the environment of normal lymphocytes, glial cells, or normal cells in Petri dishes, or in humans. But tissue culture artifacts are fun to study-sometimes even fantastic claims can be advanced in first-line journals, by simply watching cells with multiple nuclei move, as long as HIV is somewhere involved (118). However, the cellular mechanisms for cell fusion, are known, and even "exogenous HIV," if it could be shown to exist, doesn't provide the necessary fusigenic properties or conditions for fusion thought to exist in end-stage "AIDS" patients, if only because "HIV" has traditionally been impossible to "isolate" even from end-stage "AIDS" patients, let alone in sufficient titer, if it were an exogenous virus like Sendai virus, that can induce cell fusion.

INVOLUTED THYMUS AND SPLEEN ATROPHY.

Eliza Jane’s thymus and spleen weights were measured as being 8g and 40 g, which are 32% and 85% of their normal expected weight for her size (1). There was fibrosis detected in the thymus, which according to the coroner, was involuted. The spleen was also said to exhibit a reduction in the white pulp in the coroners report (1). An infection such as a severe earache, or 3 week-long upper respiratory infection, adrenalin overdose, or stress to the system of any kind can induce the formation of an involuted thymus containing fibrosis, or apparent atrophy of the spleen. In his report, Dr. Al-Bayati provides well substantiated references and arguments in his report that a at least 130 different illnesses or syndromes of less than 5 day duration can cause stress and release cortisol, causing the thymus to "involute, and that the degree of involution is dependent upon the duration of the illness" (13). In this context, it is of interest that even the non-specificity of "HIV" markers such as p24 have also been documented in the context of thymus involution in "HIV-negative" persons (119):

" …There were no major differences between thymus tissue in AIDS patients and in the other patients studied. This argues against the claim expressed in the literature that the epithelial microenvironment incurs particular HIV-1-induced injury in AIDS. This conclusion is substantiated by immunohistochemistry for HIV-1 gag and env proteins, and by hybridohistochemistry for gag/pol and env mRNA of HIV-1. Positive cells were observed only in low numbers, both inside the epithelial parenchyma and in the (expanded) perivascular areas. An interesting finding was the labeling of subcapsular/medullary epithelium in normal uninvoluted thymus by a number of antibodies to HIV-1 gag p17 and p24 proteins. Compatible with this labeling was the staining of epithelial stalks in hyperinvoluted thymuses irrespective of disease category. The previously reported cross-reactivity between HIV-1 core protein and thymosin alpha 1 cannot fully explain this observation, because the epithelium in the hyperinvoluted state is negative for thymosin alpha 1. This study confirms and extends previous reports on the endogenous presence of epitopes of retroviral antigens in thymic epithelium."

Although the possible effects of her prior upper-respiratory infection and earache on thymus atrophy and spleen atrophy should not be ignored or dismissed as contributory, it should here again be emphasized, that Eliza Jane’s lymphocyte count of 10,800 lymphocytes/µl precludes her from even being considered immune suppressed. Perhaps what could account for these findings of both an atrophied thymus and spleen, as well as fat accumulation in the liver (as this was also detected), is the use of amoxicillin. In preclinical mammalian studies of young rodents, for example, it was established that a short course of amoxicillin therapy specifically can affect the size and morphological characteristics of the thymus, spleen, and form fat in the liver at the same time, and can even cross the blood brain barrier to affect these simultaneous changes in the weights of these three organs (120). Few studies, however, have specifically looked at changes in these organs in the context of amoxicillin adverse reactions in humans (since they typically aren’t even reported or suspected, and are typically dismissed).

A related hypothesis, however, could explain these simultaneous changes, as well as the increase in measured lymphocyte count of 10,800 lymphocytes/µl in a non-immunosuppressed individual showing atrophy of the thymus and spleen. Eliza Jane’s excessive lymphocyte numbers measured at the hospital had to have come from somewhere. A likely place was from either the thymus or the spleen or both. In this regard, there is a developed literature on how beta-lactams activate lymphocytes. Thus, it is possible that the excess number of lymphocytes measured in her peripheral circulation were derived from her thymus and spleen, or one or both of these organs (in the context of a post-upper-respiratory infection or earache), during the 36 hour amoxicillin delayed reaction she appears to have experienced.

For example, her elevated 10,800 lymphocytes/µl count obtained at the hospital on the day of her death is consistent with the possibility that after she imbibed the first dose of amoxicillin, her immune system went into high gear, judging by the parent's and emergency response team's descriptions of her acute symptoms (2). It might also be mentioned that consistent with the acute amoxicillin-induced lymphocyte increases, vascular permeability, and tissue destruction, studies have shown that T-cells are reactive in delayed amoxicillin hypersensitivity reactions. In this regard, there is a developed literature that documents how amoxicillin potentiates T-cells to kill other cells specifically in delayed hypersensitivity reactions:

"beta-Lactam drugs may induce both cellular and humoral allergic reactions, and there is evidence that T cells play an important role in the pathogenesis of these reactions. The aim of this work was to assess the sensitivity and specificity of the lymphocyte transformation test (LTT) as an in vitro diagnostic tool, in patients with either an immediate or a nonimmediate reaction to penicillin G and/or amoxicillin." (24).

The authors of this work concluded by stating that:

"The LTT should be considered a useful in vitro diagnostic tool to identify subjects allergic to penicillins, especially patients with nonimmediate reactions where the LTT has a better diagnostic value than skin tests.

In a similar context, Yawalkar et al., (121) concluded that:

"In conclusion, a substantial part of the T cells in drug-induced epicutaneous test reactions are drug specific and are composed of a heterogeneous cell population. Drug-specific T cells producing interleukin-5 may contribute to eosinophilia, whereas cytotoxic CD4+ T cells may account for tissue damage. These data underline the role of T cells in delayed-type cutaneous adverse drug eruptions and drug-induced epicutaneous test reactions."

NO FAILURE TO THRIVE AND NOT AIDS-ASSOCIATED WASTING SYNDROME IN ELIZA JANE.

Her 5th to 10th percentile weight gain from January to March in 2005 contradicts the possibility that AIDS-related wasting syndrome or failure to thrive contributed to the death, as has been suggested by members of the AIDS establishment in their ill-informed and terse dismissal of Dr. Al-Bayati’s differential diagnosis (See: http://catallarchy.net/blog/wp-content/images/A_report_on_Eliza.pdf ). By “wasting,” or “failure to thrive,” it is generally indicated that people are losing weight, instead of gaining weight.

DISCUSSION AND CONCLUSIONS:

From classical times, medical treatments have been predicated on either a rationalist or empiricist philosophy (122). Rationalists, as a group, tend to regard and approach disease as a localized entity and attack "it" directly by attempting to reduce or reverse its cause or primary symptoms. Radiation, mainstream chemotherapy, and targeted immune therapy are principal examples of a rationalist approach. Antiretroviral therapy or HAART are also examples of the rationalist approach, which employs Ehrlich's "law of contraries," to target a supposed exogenous invader, "HIV," that is thought to be responsible for 46 (47 if you now want to include amoxicillin adverse reactions) different syndromes that were previously known before "HIV" was announced by government proclamation as being the sole cause of "AIDS."

Empiricists tend to regard and approach disease as an imbalance in the living organism, which they attempt to restore by aiding the body in re-establishing its lost balance in ways that increase "resistance," or which non-specifically alert the organism via a "danger signal." Microbial immune therapy, antiangiogenesis therapy, and hyperthermic therapy are examples of an empirical approach. AIDSVAX, the GP120-based "HIV" vaccine is also an example of an empiricist approach, as it employs "the law of similars, to provide the organism with a similar substance (and not target the hypothesized cause directly), to alert the organism to subdue the exogenous invader, which is "HIV." Also, reconstitution of the immune system through nutrition therapy would be considered a form of empiricist therapeutics for immune suppressed individuals. It should be emphasized that people are not considered to have an AIDS-defining illness if they have suffered from chronic starvation, as these individuals are known to possess a helper T-cell ratio in the AIDS-defining range or even lower (< 250 cells/ml), and can present with as much as a 90% reduction in their normal T-cell number, that is reversible upon supplying the proper nutrition and nutritional supplements (123, 124), as Fauzi et al. have shown in a recent study using vitamin supplements in the absence of HAART (125).

Both approaches are "scientific”, depending of course on how an experiment or trial is conducted (whether it is terminated prematurely as most, if not all of the FDA AZT and other retroviral trials have been), or if there are consistent results generated, such as testing "HIV positive," "HIV positive," and "HIV positive." In science, a finding that repeats 2 times might be a fluke, while 3 points define a straight line, and constitute a minimum requirement to establish 'consistency,' or even 'a trend.' Rationalists also perform their medical experiments on an " average" or idealized patient harboring some "average" symptoms of "a disease," to the extent that even adverse or idiosyncratic reactions to medications such as amoxicillin are believed to fall into stereotypic responses, while empiricists perform their medical experiments in an attempt to restore the apparent imbalance manifested by person-specific, individualized symptoms that may appear different in each patient.

But if Eliza Jane had too many lymphocytes at the hospital to even consider her an immunosuppressed victim, if "HIV" isn't an exogenous virus, if the cell biology of "HIV" doesn't make any sense (if in different labs "it" causes T-cells to apoptose, if "it" doesn't cause T-cells to apoptose, if "it" causes T-cells to fuse, if "it" doesn't do anything to T-cells except induce them to make "viral-like particles" and cause cells to pump out their endogenous molecules packaged in membrane surrounded vesicles that are surrogate markers without showing cytopathic effects, if "it" cannot be photographed from purified bands on a sucrose gradient, if "it" cannot be shown to cause AIDS in chimps our phylogenetically closest relative, or even cause transference of “HIV seropositivity in serodiscordant human couples, like Robin Scovill, if "it" can't be shown to have consistent biochemical activity in vitro, and if there are 70 or more syndromes or situations, including 50% of dogs, or sheep, goats or worms, or Christine Maggiore, that test positive where "HIV" surrogate markers can be obtained in the absence of any evidence of immune suppression or any other of the 46 "AIDS-indicator diseases," then neither the rationalist or empiricist approach makes sense, or will produce results, as neither have over 22 years, in the treatment of profoundly immune suppressed individuals that are called "AIDS patients."

If this is a wrong representation of the facts, why would the Head of the Virus Reference Laboratory of the British Public Health Laboratory Service, Dr Philip Mortimer, write that:

“It may be impossible to relate an antibody response specifically to HIV-1 infection” (126)?

I do not believe that similarities of adverse reactions on the amoxicillin package inserts, and the succession of Eliza Jane's 36 hour series of symptoms warrant the incarceration of Christine Maggiore, Robin Scovill, the removal and state-remand of Charlie, their "HIV-negative" son, or can justify the public humiliation and inquisition-style witch hunt initiated by the coroners office, the LA Times, or ABC Primetime at a time at what is perhaps the greatest tragedy a family can face.

The evidence suggests that all adverse reactions of Eliza Jane were consistent with adverse reactions listed on amoxicillin package inserts, and the succession of Eliza Jane's 36 hour series of symptoms support the hospital records, and her prior medical records which do not suggest an "AIDS" diagnosis in any way, shape, or form. The false charges of potential parental negligence and the erroneous claims of Eliza Jane as a child with AIDS are outside the realm of scientific thinking. The coroner’s incompetence and extreme negligence prompted local authorities and the media to debate removal and state-remand of Charlie, Christine and Robin's "HIV-negative" son. According to Ms. Maggiore (personal communication), Charlie had to be subjected to no less than 4 negative “HIV” tests before The State would allow the boy to be allowed without harassment back into the unsupervised charge of his mother and father, to grieve the loss of his baby sister. In this horrible, inquisition-style witch-hunt, an innocent family was abused by a derelict ME and coroner and press who are fully responsible for significantly adding to this family's nightmare. We cannot even trust that the slides showing PC pneumonia and "HIV" encephalopathy belong to Eliza Jane, as Dr. Ribe is under investigation for "fixing" at least 5 other cases. Therefore, we are left with the lymphocyte count obtained upon admission to the hospital and reports regarding Eliza Jane's apparent good health preceding her crisis period. In turn, it should be appreciated that high lymphocyte counts are inconsistent with PCP or encephalitis or immune suppression of any kind. Eliza Jane's fatal symptoms appeared immediately after her imbibing amoxicillin.

John Moore of Weil Medical College is the greatest AIDS denialist of them all-despite his "HAIL MARY Experiments," he betrayed a deep-seated AIDS denialism at the 2006 International AIDS conference:

Dr. John Moore of Weil Medical College, one of the featured speakers in this year's International Toronto AIDS Conference is an enigmatic character. In a talk he gave at the 2006 conference about his work, which involves inseminating rhesus macaques up to 5 times after smearing a microbicide cream in their vaginas to prevent “SIV,” he claimed that these “HAIL MARY" experiments (a term used in American football when the quarterback wildly throws a pass and "prays" somebody will catch it) hold great promise and could solve the “AIDS apocalypse in Africa and elsewhere. He claimed that multiple inseminations are necessary in order to model the frequent sexual activity that goes on amongst the "filthy humans" that populate these 3^rd World Nations. Not being Catholic or a football fan, I didn’t quite understand at first what was meant by the term “HAIL MARY experiments.” To rigorously prove his “SIV-fighting” spermicide worked, I gathered that HAIL-MARYING HIS monkeys and inseminating them 4-5 times represented the fact that his microbicide “absolves” the monkeys of contracting “SIV,” as one would if a Catholic perhaps were “absolved of sin” after saying “HAIL MARY” numerous times as penance? I didn't know it was a football term.

Although “SIV” has always been a better model of “HIV” than “HIV,” a critic might suggest Moore try Human “HIV,” perhaps with dogs, cows, goats, sheep, or non-infected monkeys, chimps, and humans that have naturally occurring “HIV” sequences (18). Although none of these animals acquire AIDS from “HIV,” neither do his monkeys since he is inseminating them with “SIV.”

Because I learned so much about religion in science at his scientific talk, I listened to another talk Dr. Moore gave in a session at the Toronto Conference regarding “AIDS and Responsible Journalism." It was here that I noticed, however, that AIDS denialism appears to have infected even some of his thinking, and despite his warnings about extreme AIDS denialists in a recent Amazon.com book review where he said that AIDS denialists are:

"scientists whose careers fizzled out; but others are zealots with extreme political views (both on the far-right and the far-left) who find AIDS denialism politically convenient; and some are deeply troubled individuals with disturbing behavior patterns who deserve pity and professional help."

Allow me to give one example illustrating Moore's denialism. In his AIDS denialism, Dr. Moore described the case of Christine Maggiore, and the recent tragic death of her daughter, Eliza Jane. Dr. Moore then suggested that Ms. Maggiore and her partner, Robin Scovill, had been irresponsible and negligent parents regarding the raising of their children, and that a responsible press ought to mercilessly and unabashedly punish the parents for Ms. Maggiore's minimizing or ignoring her possible “HIV-positive” status, for her alleged subsequent infecting and killing her daughter with "HIV," and for both parents refusal to give either of their children or themselves (any more) "HIV" tests, or HAART, in the 3 years preceding the child's tragic amoxicillin-induced death.

However, a little research into the matter would have clearly revealed the depth of this type of AIDS denialism and stigmatization (to quote Malinda Gates warning against stigmatization) that was distastefully, and I would say, angrily advanced, by Dr. Moore. But that is how AIDS denialism works on even some of the best minds, which, as Moore himself has said, "deserve pity and professional help." Like "the virus that causes AIDS" itself, AIDS denialism can infect even the most faithful "HIV=AIDS" promoters, which is why I guess they say AIDS denialism it is so insidious. For instance, Moore's ill-informed suggestion to the AIDS and Responsible Journalism session, that a Salem Witch Trial for Ms. Maggiore and her family be intensively pursued, was nothing less than unparalleled arrogance and a publicly-presented savage abuse of their human rights, their rights as U.S. citizens, stigmatization, and, most woefully perhaps, his tantrum bent the logic of the "HIV=AIDS” paradigm. Dr. Moore's effort to malign these parents using his scientific credentials and considerable skill and reputation to motivate the press to use its influence to pelt the Maggiore-Scovill Family with insults, threats, and other unimaginable forms of torment in the aftermath of the tragic death of the little girl, constitutes an extreme form of AIDS denialism (this was after all an AIDS and Responsible Journalism Session).

Before maligning Ms. Maggiore and Robin Scovill on stage before the entire world, a little research of Eliza Jane's hospital admission data that was published in the respected journal, Medical Veritas, and in the Coroner's report posted all over the Internet would have demonstrated to Dr. Moore instantly that Eliza Jane could not have died of AIDS. In this scenario, if Eliza Jane had AIDS, it would mean that A ("HIV") may cause an increase in B (immune system increase), which leads to C (AIDS-indicator diseases). Despite Gallo's, Montagnier's, "HIV" test kit makers, vaccine makers, drug makers, and other AIDS denialist constructions and distortions of the correct "HIV=AIDS" hypothesis, this form of AIDS denialism is perhaps the most insidious and horrifying of all, not only because it threatens both the freedom and Human rights of those accused of being "HIV-positive," but particularly, because it distorts the “HIV= AIDS paradigm completely in the wrong direction.

In this scenario,

A (“HIV”)------leads to B (10,800lymphocytes/microliter)-----leads to C (PCP, “HIV”

encephalopathy).

To address the issue of why absolute lymphocytes versus CD4/CD8 ratios weren't measured before the coroners were made aware of Christine Maggiore's (inconsistent) "HIV-positive status," and before the coroners changed their initial “indeterminate” cause of death, and deemed Eliza Jane an "AIDS statistic," it is clear that there was no reason for anyone to assume that in Eliza Jane's case, they were dealing with an immune suppressed individual. Her acute symptoms during her 36-hour death appeared to be due to a hyper-immune reaction to a prescribed drug, and an earache. However, despite the coroner's failure to provide a CD4+/CD8+ ratio in support of the "AIDS diagnosis," it should be emphasized in this context as well that the accuracy of total lymphocyte counts in predicting death due to "AIDS-associated indicator diseases" is considered equal or even superior to measuring the CD4/CD8 ratio (94). Therefore, and despite the fact that an "HIV" test or CD4/CD8 ratios were NOT obtained (by those attributing her death to AIDS after the revised autopsy report was filed some 4 months after the death), absolute lymphocyte numbers WERE obtained at the hospital, and according to "AIDS experts," are just as predictive of AIDS-related death in children, if not more so. In a recent study of 3917 children, it was reported that:

“For children older than 2 years, the 12-month risk of death and AIDS increased sharply at values less than 1500-2000 cells per microliter, with little trend at higher values.” (Eliza Jane's count was 10,800 cells/microliter).

“Mortality risk was substantially higher at thresholds of total lymphocyte count recommended by WHO than at corresponding thresholds of CD4-cell percentage. When the markers were compared at the threshold values at which mortality risks were about equal, total lymphocyte count was as effective as CD4-cell percentage for identifying children before death…”

In the context of lymphocyte numbers, and despite occasional and minor discord in "AIDS science meetings amongst the very smartest "HIV=AIDS" promoters about the precise molecular mechanism that explains why low lymphocyte numbers are seen in end-stage "AIDS" patients (is it really "the Gut" stupid, how quickly does "HIV" cause heart disease, or infect neuronal macrophages, kidneys, liver, etc.), "HIV=AIDS" scientists are as certain today that low, rather than high lymphocyte numbers have something to do with full-blown "AIDS," as they are about gravity being caused by those little graviton particles.

By attributing Eliza Jane's death to AIDS, Dr. Moore has in effect, "denied the cause of gravity," because if Eliza Jane had "HIV" and 10,800 lymphocytes/microliter at the time of her death, then A ("HIV") would have had to have to led to a massive stimulation or overproduction of B (immune cell numbers-10,800 lymphocytes/microliter), instead of a decrease in B (to a 1000 or less meeting the WHO surveillance definition shown above), to induce C (the PC pneumonia and "HIV" encephalopathy that was missed by the first coroners but determined 4 months later by Dr. Ribe-who is now under intense investigation for lying in other reports that have led to the life-time convictions of innocent parents). To assume that "AIDS" is caused by too many lymphocytes, is taking "HIV=AIDS" completely in the wrong direction. AIDS is a disease showing too few lymphocytes, not too many, like cancer.

Thus in maligning Ms. Maggiore and her family before the world stage, John Moore, perhaps in a weak moment, betrayed his deep-seated AIDS denialism to the Toronto Conference, to the shame of all of humanity.

For these and a myriad other reasons, it is wrong to assume Eliza Jane died of "AIDS,"or to continue to vilify or attempt to coerce or harass Christine Maggiore, Robin Scovill, and their 8 year-old son, Charlie.

Addendum:

AUGUST 15 - 21, 2003

Web of Deceit

Murder conviction overturned because D.A. withheld evidence

by Jim Crogan

A state appellate court has overturned the murder conviction of Jose Salazar for killing an infant girl in 1996, ruling that the L.A. County District Attorney’s Office deliberately concealed information from the defense about a deputy coroner’s mistakes, his altered findings and changed testimony in other homicide cases.

The case against Salazar had focused on the timing of the child’s injuries. Since that timeline was in dispute, and no forensic evidence or eyewitness tied him to the crime, the appeals court determined that the introduction of Deputy Coroner James Ribe’s credibility problems would likely have produced a different verdict.

The unanimous decision was handed down last week. The three-judge panel also ordered the case returned to the trial court. But the District Attorney’s Office has not yet said if it will retry the case. The 2nd Appellate District underscored its anger at the D.A.’s Office by publishing the opinion, meaning it can be cited as a precedent by defense attorneys, and naming names of the offending parties.

Gail Harper, Salazar’s appellate attorney, said the oral arguments in June signaled victory. “The judges patiently listened to me. Then they challenged the deputy attorney general, representing the D.A., to explain why sanctions shouldn’t be issued for this deliberate Brady violation.”

Under the U.S. Supreme Court’s 1963 Brady v. Maryland decision, prosecutors must turn over potentially exculpatory evidence to defense attorneys. Withholding such favorable evidence violates a person’s right to a fair trial. “The D.A.’s Office has this ‘win at any cost’ attitude. Publishing it and naming names is the only way you get these folks’ attention,” Harper says. “They don’t give a damn about their legal obligations. I hope attorneys in other Ribe cases are lining up to file appeals.”

Salazar was sentenced to 15 years to life for killing Adriana Krygoski. He volunteered to watch her while the babysitter went shopping. He was the boyfriend of the sitter’s daughter and lived with them. Witnesses testified that the child had two visible head bruises when her mother dropped her off, but otherwise appeared to be healthy. The toddler then hit her head on a coffee table while Salazar’s girlfriend was with her.

When the infant awoke from her nap, she started vomiting. Salazar said he tried to help, but eventually called 911. At the hospital, doctors discovered two skull fractures. Ribe testified that the injuries were consistent with violent shaking or hitting a flat surface. The injuries, he said, would have rendered Adriana “instantaneously” unconscious. Without treatment, death would have followed within a few minutes or a few hours. The defense’s medical expert strongly disagreed, arguing that the injuries could have occurred hours earlier. But Ribe’s timeline focused suspicion on Salazar.

Prosecutors intentionally withheld information about Ribe’s inconsistent testimony in other child-death cases, particularly the 1995 beating death of 2 1/2-year-old Lance Helms. The issues in that case closely match those in Salazar’s.

In the Helms case, Ribe testified that death occurred within “30 to 60 minutes” of his injuries. The boy’s mother, Eve Wingfield, was with him when he died. Wingfield’s public defender then persuaded her to plead guilty to a lesser charge of child abuse. Ribe later changed his mind and told detectives the boy died immediately after the beating. The LAPD reopened the case in 1996 and charged Helms’ father. David Helms was convicted of murder, and Wingfield was released. An appeal is pending, and Harper says the appellate court requested she investigate potential Brady violations in that case.

The appellate court also highlighted other Ribe cases. At the 1996 trial of Roberto Cauchi, for the torture-murder of a child, Ribe changed his earlier preliminary-hearing testimony, introducing unexpected evidence of sexual abuse and “shaken baby” syndrome. In the 1996 gunshot-murder trial of Sean Hand, Ribe changed his preliminary testimony about the wounds and time of death. In the 1996 trial of Charles Rathbun, Ribe changed his conclusion on the cause of Linda Sobek’s death from inconclusive to strangulation. In the 1996 “shaken baby” death trial of Destiny Jacobo, Ribe admitted missing two bruises and changed his conclusions about the time of death. In the 1997 stabbing-death trial of Lorrie Tuccinardi, Ribe changed his testimony about the wounds. At a 1997 preliminary hearing for Edith Arce and Rene Urbano, in a child-murder case, Ribe testified that he changed his mind about a bruise, saying it came from a blow, not a bedsore.

Appellate Judge J. Gary Hastings wrote, “The duty of disclosure [exculpatory material by prosecutors] does not end when the trial is over.” Hastings also detailed the efforts taken by Deputy D.A. Jennifer Turkat, who prosecuted Salazar; her supervisor, Alan Yochelson; his supervisor, Roger Gunson; and the D.A.’s Office to stonewall Salazar’s defense, Harper, and even Deputy D.A. Dinko Bozanich, the prosecutor of the Arce/Urbano case.

Ultimately, it was Bozanich, a veteran prosecutor, who exposed this web of deceit. In 1999, he gave Harper an affidavit on his investigation into Ribe and the D.A.’s repeated failure to disclose exculpatory evidence. In his opinion, this revealed “intolerable and unethical practices at the highest levels of our office.”

Harper says it was Bozanich’s stand that helped her discover the truth. And Gigi Gordon, a veteran defense attorney and acknowledged Brady expert, says, “Dinko is the real hero here. He broke the code of silence inside the D.A.’s Office.”

Bozanich says he only did what prosecutors must do ethically. “What happened here sends an awful message to young prosecutors and the public,” he explains. “When prosecutors do something wrong, sanctions should follow.” Bozanich says it’s evidence of a “just win, baby” philosophy that developed during Gil Garcetti’s tenure. “I’m sorry to say, nothing has changed under Steve Cooley.”

But Lael Rubin, a special counsel to D.A. Cooley who helped establish his office’s Brady Policy and Alert System for prosecutors to check out witnesses, insists things are better. “If the office had our Brady policy in place prior to December 2000, this case would have been handled very differently.”

But the Cooley administration has been in office for two years, and it could have told the court that Garcetti’s position was a mistake. Yet it didn’t. “We just got the Salazar decision this week,” responds Rubin.

And what of the Brady Alert System? Is Ribe’s name included? “No, I don’t think so,” she answers. “Our system is not totally complete.”

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