A common disease, chorioamnionitis, is now subject to revision.
This disease is another example of a so-called maternal-fetal infection misdiagnosed as germ causation, a cover story for Medical radiation damage.
The supposed infection leads to FIRS (fetal inflammatory response syndrome). That is, it is said to be an inflammatory response to the presence of infection, e.g., GBS (Group B Streptococcal), E. coli, and/or mycoplasma bacteria. The disease is associated with preterm birth, and a risk factor for other disorders such as microcephaly.
It is often diagnosed by the presence of maternal fever and increased heart rate in mother or child. Notice in the following, the caring rationale for skipping the bacterial test. Tita (2010):
...chorioamnionitis is diagnosed solely based on clinical signs since access to uncontaminated amniotic fluid or placenta for culture is invasive and usually avoided.
A diagnosis of chorioamnionitis due to fever alone could bring a treatment of intravenous antibiotics to the mother and fetus, or newborn. Dr. Audra Robertson explains:
Chorioamnionitis usually develops when bacteria that are part of the normal vaginal flora ‘ascend’ [upward] into the uterine cavity. The amniotic fluid and placenta, as well as the baby, become infected. E. coli, group B streptococci… Chorioamnionitis affects between 1 and 10% of women at term and up to 33% of patients preterm… In most cases, your doctor can diagnose chorioamnionitis due to fever in the mother and an increased heart rate in both the mother and her baby.
“Infection”, ascertained by signs of inflammation such as fever, is the official cause of chorioamnionitis — and the declared most common cause of microcephaly.
Retrospective study indicates the commonest etiologies for prenatal microcephaly are in utero infection.
The inflammation is real. But the “infection”, I argue, is a false assumption, with chorioamnionitis actually being a symptom of DUS (diagnostic ultrasound) damage. Any germs, if possibly found, would be common symbionts, friendly microbial scavengers and helpers, etc. Under toxic stress they could prevail because of micro-ecological imbalances.
Fever, infection, etc., are symptoms reminiscent of Zika virus infection: Chorioamnionitis and other “infectious maternal diseases” such as puerperal fever*, initiation of autism, and Zika virus positives, all are commonly diagnosed near the 20th week of gestation, i.e., all correlate with the common DUS schedule. Allanson (2010):
Chorioamnionitis is a common cause of second trimester pregnancy loss, usually due to ascending infection. This study investigates the prevalence and bacteriology of chorioamnionitis in cases of spontaneous pregnancy loss in previable gestations (16-22 weeks).
Robert W. Bendon, MD
Dr. Bendon is an obstetrical pathologist with vast experience and knowledge, a world-class authority. He is a straight-laced Medical official, as is apparent from his extensive article on chorioamnionitis. He begins with the standard definition.
Chorioamnionitis is an ascending infection of the intrauterine cavity during pregnancy. The concept is that microorganisms, primarily bacteria, ascend from the vagina through the cervix into the intrauterine cavity where they initiate an inflammatory response in the mother and fetus.
Dr. Bendon’s article is a wealth of mainstream science, from which I can assemble a critical view, as follows.
He describes chorioamnionitis as virtually aseptic, i.e., no infection found.
The majority of microscope slides showing chorioamnionitis do not demonstrate microorganisms.
Yes, you read correctly. And as follows, even the most powerful germ detection technique, PCR, fails to find an infection source in the endometrium (inner uterine membrane)!
The role of vaginal flora and its potential interaction with the cervix remain incompletely understood aspects of chorioamnionitis. Is chorioamnionitis initiated by microorganisms chronically in the endometrium? Not surprisingly, pathogenic microorganisms, E. coli and Group B streptococci, were not found in genetic amniocenteses by the PCR technique.
We can assume that chemical and radiation causation is being avoided.
Only infectious causes of chorioamnionitis have been plausibly proposed, but it remains a frustrating fact that even very sensitive molecular techniques [PCR, etc] have failed to find bacteria in the amniotic fluid in all cases of chorioamnionitis…
When microbes are found, they are often not very dangerous.
Surprisingly the microorganisms were often not very pathogenetic, with ureaplasma being the most common either alone or in culture with other organisms.
Maternal defenses are strong.
The cervix is filled with mountainous ridges raining down viscous mucus, drone like antibodies, chemical warfare, and white cell snipers... The evidence is against this mad rush of microorganisms reaching the uterus.
Bendon carefully walks along the threshold of blasphemy. Without saying “poison”, he indirectly supports a toxicological view.
...even if we accept that all chorioamnionitis has an infectious etiology, it does not necessarily follow that the organism detected in the amniotic fluid is actually the organism that initiated the inflammatory response...
Diagnoses could include signs of inflammation that indicate tissue injury, not necessarily infection.
Bendon describes mediators of inflammation as evidence of inflammation.
As a pathologist, I identify chorioamnionitis by the presence of neutrophils, a white cell that is relatively easy to identify with routine H&E sections, and is a recognized marker of acute inflammation. Neutrophils are normally circulating in the blood, but enter the tissue in response to acute inflammatory signals (chemotaxis) secreted by lymphocytes and macrophages or from tissue injury…
Bendon writes, “neutrophils [are a] marker of acute inflammation” — however, it is known that neutrophils also move substantially towards non-acute injury. Thus there is a stronger toxicological context, one that could even more certainly include DUS as a good explanation for neutrophil presence.
Without a toxicological review, CDC advises that maternal fever is reason enough to presume the presence of pathogens,
In an effort to avert neonatal infections, maternal fever alone in labor may be used as a sign of chorioamnionitis and hence indication for antibiotic treatment…
Administering antibiotic poisons for a disease that could be caused by poisons is a common, profitable, iatrogenic, and deadly protocol.
...antibiotics have not prevented preterm labor even in patients with positive endometrial culture or plasma cells on endometrial biopsy at the start of the study and may have increased the incidence of adverse outcome...
Note: "...antibiotics... may have increased the incidence of adverse outcome..."
Note: Chorioamnionitis can lead to “poor cardiorespiratory, neurological, and renal outcomes”, per Galinsky (2013).
Should not such outcomes be expected from radiation damage (DUS) and toxic synergists (intravenous antibiotic treatment for chorioamnionitis)?
Here is industry’s complicated and absurd causative chain.
Maternal germs ascend to®
That is similar to claiming that fever is the cause of disease symptoms, rather than itself a symptom.
Industry’s paradigm remains unresolved because both valid microbial and toxicological reviews are missing. The paradigm is backwards. It contradicts the evidence, seeking to put causation on the mother. Was she filthy with germs? Was she innately weak, unable to mount a sufficient or correct response to germ invasion?
The DUS paradigm, on the other hand, agrees with the evidence.
Critics, with DUS causation evidence, can better interpret the test for inflammatory mediators, i.e., neutrophil presence. They can view that presence as a marker, a positive test result for DUS synergistic damage.
DUS damage is always present. Capable pathogens are not usually present.
...we seldom see microorganisms in the tissue sections of chorioamnionitis...
DUS causation theory is sensible, scientific, and simple, yet avoided by Modern Medicine.
DUS has been empirically demonstrated to readily damage the chorioamnion region, so of course, inflammation or neutrophil presence could occur after DUS. Tests are supposedly for inflammation, however, they test for inflammatory mediators such as neutrophils, as indicators of inflammation.
DUS causation is supported by a rare Western human study, Carrera (1990): Carrera studied DUS chorionic damage with two sub-studies, one in vivo that results positive, and one in vitro lab study that results negative. Carrera is dismissed by Marinac (2002), who asserts that Carrera utilized high DUS intensity and infers Carrera’s human study was unethical. Andreassi (2004) lists Cerrera’s negative results and omits Carrera’s positive results that indict DUS. Carrera is not very strong, yet the study should be presented as evidence.
JZhang (2002) is a modern Chinese in vivo study published in English that documents human chorioamnion damage due to DUS. There appears to be no public discussion of this study, except as begun with my ultrasound book. The study is perhaps masked from the public by its title, which indicates an overly technical focus on DUS’s relation to biochemical pathways leading to chorioamnion cellular apoptosis, rather than, simply stated, DUS damage to fetal region. But obfuscation is required for publishing. JZhang brilliantly obfuscates, fulfilling the oppressive rules while providing tremendous evidence against DUS.
There are many other Chinese in utero human studies that describe DUS damage in the chorionic region in a total of approximately 600 maternal-fetus pairs. See DUS Book I.
Here is the sensible and direct DUS causation chain, a natural view:
DUS damages chorioamnion and fetus®
DUS exposure to various areas is a matter of chance, operator habits, and shading from adjacent organs, as organs of various densities shade each other from the radiation.
DUS radiation flows directionally like a flashlight beam. Knowing this, then does not Bendon’s following text serve as an analogy for DUS damage?
The intensity of the fetal response may be less or even more intense than the maternal response. An area of the membrane may be markedly more intense than another.
Bendon describes inflammation intensity and location. That can be critically interpreted in terms of proximity to the DUS transducer. See below, where I use brackets and bolding to reveal what he is saying as if he were describing DUS radiation.
Daily histologic examination of placentas confirms that there is a wide range of difference between maternal [nearer to DUS] and fetal [farther from DUS] response in individual placentas.
It is unusual for the fetal response [farther from DUS] to be more intense than the maternal [nearer to DUS]. In general the more intense the maternal response, the more intense will be the fetal response [as if DUS were toxic radiation].
DUS causation of microcephaly could be described similarly, whereby DUS would be radiating the forebrain, the front of the fetus, a common radiological examination view. In fact, microcephaly usually consists of forebrain, eye and hearing damage. Pilu (1999):
When microcephaly is present, the most affected part is usually the forebrain.
Even if one assumes germ causation, one could theorize that DUS damage would create microbial ecological imbalance, not necessarily direct germ pathogenesis. If industry must pursue germ pathogenesis then it could consider that DUS damage in the chorion region would also open up pathways for microbial migration. Industry does not want to go there.
Chorioamnionitis and FIRS should be considered as natural responses to DUS damage.
Bendon’s becomes extra-verbal when he nears the possibility of environmental causation.
The failure to prove an infection is not evidence that it is not present. The possibility that a subset of chorioamnionitis is not infectious cannot be excluded, but no plausible alternative mechanism has been proposed.
He does not write “environmental” or “toxicological”, which fall under his phrase, “not infectious”. He moves into an unusually intricate phrasing with five negatives and four diminishments, i.e., “failure… not… not… possibility… subset… not… not… excluded… no… alternative”. This, I have found, is the common semantic form utilized by professionals for politically sensitive material. They tend to sink into these semantic netherlands.
In the netherland, Bendon calls non-infectious chorioamnionitis a “subset”, but that is logically improbable, if not impossible. He already stated that the general case is not found infectious. He already established infection as the minor subset. His entire article on chorioamnionitis is limited to the minor subset of chorioamnionitis — as if the official actionable view of chorioamnionitis that advises intravenous antibiotics is the general case. The official view politically dominates but in terms of available data, it is a logical subset of the general view, in terms of available data.
Bendon is a fine intellect, willing to consider DUS possibilities. I believe he understands the sensitivity of this topic, and that he can only discuss it within the netherland. As expected, despite being quite helpful with my challenges, he maintained the official view during our conversation.
My comment awaited moderation for several days, then was rejected.
I emailed Bendon again. No reply.
*Thanks to OregonMatt at POM forum. His comment under Steve Kelley's smart post, got me thinking about toxic cause for the maternal disease, "puerperal fever". This disease appears to be very similar to chorioamnionitis, but occurring during the 10 days following birth, rather during gestation, and so it is listed here. Thanks for his editorial review.
 Alan T. N. Tita and William W. Andrews, “Diagnosis and Management of Clinical Chorioamnionitis,” Clinics in Perinatology 37, no. 2 (June 2010): 339–54, https://doi.org/10.1016/j.clp.2010.02.003.
 Audra Robertson, MD, “Chorioamnionitis: Could This Infection Spell Disaster?” (Department of Obstetrics and Gynecology, Brigham and Women’s Hospital, Boston, MA, March 15, 2012), http://www.healthline.com/health/pregnancy/infections-chorioamnionitis.
 L. Dahlgren and R. D. Wilson, “Prenatally Diagnosed Microcephaly: A Review of Etiologies,” Fetal Diagnosis and Therapy 16, no. 6 (December 2001): 323–26, doi:53935.
 Ben Allanson et al., “Infection and Fetal Loss in the Mid-Second Trimester of Pregnancy,” The Australian & New Zealand Journal of Obstetrics & Gynaecology 50, no. 3 (June 2010): 221–25, doi:10.1111/j.1479-828X.2010.01148.x.
 Robert Bendon, MD, “Chorioamnionitis,” Obstetrical Pathology, December 3, 2012, http://obstetricalpathology.wordpress.com/chorioamnionitis/.
 Zaccaria Ricci et al., “Whole Blood Assessment of Neutrophil Gelatinase-Associated Lipocalin versus pediatricRIFLE for Acute Kidney Injury Diagnosis and Prognosis after Pediatric Cardiac Surgery: Cross-Sectional Study*,” Pediatric Critical Care Medicine: A Journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies 13, no. 6 (November 2012): 667–70, doi:10.1097/PCC.0b013e3182601167.
 CDC, “Prevention of Perinatal Group B Streptococcal Disease.”
 Robert Galinsky et al., “The Consequences of Chorioamnionitis: Preterm Birth and Effects on Development,” Journal of Pregnancy 2013 (March 7, 2013), doi:10.1155/2013/412831.
 Paola Carrera et al., “Sister Chromatid Exchanges in First-Trimester Chorionic Villi after in Vivo and in Vitro Exposure to Diagnostic Ultrasound,” Prenatal Diagnosis 10, no. 3 (March 1990): 141–148, doi:10.1002/pd.1970100302.
 Marinac-Dabic, Danica; Krulewitch, Cara J.; Moore, Roscoe M. Jr, “The Safety of Prenatal Ultrasound Exposure in Human Studies,” Epidemiology 13, no. 3 (May 2002): S19–22.
 Maria G. Andreassi, “The Biological Effects of Diagnostic Cardiac Imaging on Chronically Exposed Physicians: The Importance of Being Non-Ionizing,” Cardiovascular Ultrasound 2, no. 1 (November 22, 2004): 25, doi:10.1186/1476-7120-2-25.
 JiaYin Zhang et al., “Long Dwell-Time Exposure of Human Chorionic Villi to Transvaginal Ultrasound in the First Trimester of Pregnancy Induces Activation of Caspase-3 and Cytochrome C Release,” Biology of Reproduction 67, no. 2 (August 1, 2002): 580–83, doi:10.1095/biolreprod67.2.580.
 Gianluigi Pilu, Philippe Jeanty, “Microcephaly,” The Fetus, July 27, 1999, http://sonoworld.com/fetus/page.aspx?id=127.