What really killed the four infants during the NSW pertussis epidemic in 1996-97?
By Dr Viera Scheibner (Principal Research Scientist- Retired)
“none so blind as he who will not see.”
Medical Journal of Australia (vol 168, 16 March 1998: 281-283) published a short report on ‘Infant pertussis deaths in New South Wales 1996-1997 by Williams, Matthews, Choong and Ferson. The authors of this article wrote “Since 1996, south-eastern Australia has been experiencing a pertussis epidemic which has resulted in the deaths of several infants, including four from NSW in the 12 months to July 1997. All were less than six weeks of age and died from overwhelming cardiovascular compromise “despite intensive care support”. “The failure of management in three different pediatric intensive care units to save their lives reflects the inadequacy of technology in such cases, and, as all were too young to have been vaccinated against pertusiss, emphasises the need to prevent pertussis transmission through good herd immunity”. They continued that this excessive infant mortality from a preventable disease demonstrates the need for better pertussis immunity in the community and for erythromycin treatment of all suspected cases and family contacts, especially infants. Importantly, the article also revealed that the four deaths, plus the death of a Victorian infant which was also attributed to pertussis, represents a mortality of about 0.03 per 100,000 population per year after indexing to the Australian population. “In contrast, in the United States throughout the 1980s and early 1990s, pertussis mortality varied between 0.0005 and 0.002 per 100,000 population per year. Even in peak years, this was at least 15-fold less than the Australian mortality reported here.”
[The above statement in interesting in that also in other situations, such as polio vaccine-caused paralysis in Romania (Strebel et al. 1995), the difference between the admitted US rate and the Romanian rate was around 14- to 15-fold (compared with other countries, 5 to 17 times higher). In my understanding, this simply reflects the level of plain misinformation on the part of the US health authorities; the widely quoted number of vaccine-induced paralysis: 12, extrapolated from Romania and other countries, should actually be at least 12,000 and even that figure is grossly minimised].
Williams et al. (1998) then, predictably, offered an explanation that “the recent sustained high level of pertussis in Australia (and the resulting infant deaths) is incomplete vaccination coverage”, this being 87% for the primary course at ages two, four and six months, only 60% for the 18-months booster and 20% for the booster at school entry. They consider vaccine failure as a possible, but less likely explanation.
At the time, the media were saying that these young infants contracted whooping cough from “some unknown unvaccinated children who suffered whooping cough.”
Let’s now have a look how these four NSW infants contracted whooping cough and what really caused their deaths.
Based on the facts described in the above article, the cases 1,2, and 4 represented infants aged 5 weeks, 16 days and four weeks, all obviously too young to have been vaccinated.
All contracted whooping cough from their fully or partly vaccinated siblings and/or fully vaccinated mothers who suffered whooping cough for a number of weeks at the time of these babies’ birth.
The case 3 was a five-week old male whose 11-year old sibling, with “immunisation status uncertain” (meaning that he still could have vaccinated) suffered paroxysmal cough for three weeks at the time of the deceased baby’s birth.
The above clearly debunks the misinformation that none of the above babies contracted the disease from “some unknown unvaccinated child”; they all contracted whooping cough from well-known fully/partly (and one most probably) vaccinated family members.
None of the babies were very ill on admission to hospitals. The highest temperature was 37.6 C and none suffered paroxysmal cough. They were doing well initially, until they were administered intravenous antibiotics cefotaxime, erythromycin and/or ceftriaxone. All initially did quite well, but quite obviously started deteriorating and died after the administration of the above antibiotics.
Baby 1 (five-week-old male twin), admitted to a Sydney teaching hospital, experienced 48 hours of lethargy, poor feeding, tachypnoea, and cough and temperature 36.5 centigrades; in hospital, he was administered intravenous cefotaxime (from day 3) and erythromycin (from day 5) and while remaining stable over the first five days with satisfactory breast feeding and occasional coughing, on day 5, his respiratory distress (not mentioned within the first five days of the admission) increased and he developed “severe pulmonary hypertension and cardiovascular compromise and died [allegedly] 72 hours after admission to Sydney Children’s Hospital”. Whichever way I look at it, the authors had the timing of death wrong, since the baby was on intravenous antibiotics which would hardly have been administered in his home. Nevertheless, it is clear that until the administration of IV erythromycin on hospital day 5, the baby was doing fine and died at least 120 hours after the initial presentation.
Baby 2 was a sixteen-day-old 3.7kg female admitted to a Sydney teaching hospital with two days of poor feeding, cough, tachypnoea and fever (37.6 centigrades, hardly a high fever) who was administered intravenous cefotaxime (from Day 1) and intravenous erythromycin (from Day 2), and over 18 hours after the antibiotic aministration, developed progressive tachypnoea with respiratory distress, tachycardia, hypercapnia unresponsive to different ventilatory regimens. Circulatory compromise also developed and was not ameliorated with infusion of adrenaline or inhalation of nitric oxide administered to treat presumed pulmonary hypertension. Systemic hypotension and severe metabolic acidosis developed, and the infant died following an asystolic arrest “48 hours after initial presentation”. Again, the authors got lost in their maths. The baby died at least 90 hours after the initial presentation.
Baby 3, five-week-old male admitted in a country base hospital, with three days of cough and treated with ampicillin. He was pale and lethargic, with a minimally elevated temperature (37 centigrades) and was put on intravenous cefotaxime and within minutes required bag-and-mask ventilation for several minutes. Ten hours after admission his respiratory distress worsened, he was intubated and transferred to the Women’s and Children’s Hospital in Adelaide and “the infant died 25 hours after initial presentation”. Again, the authors’ maths suffered dementia.
Baby 4, a four-week-old male admitted to a country district hospital, initially experienced 48 hours of cough without fever, and sudden onset of respiratory distress. In hospital, the baby was put on supplemental oxygen, intraosseous resuscitation fluids and intravenous ceftriaxone. Within hours of this ‘management, the infants’ respiratory difficulty increased, and he developed poor perfusion requiring artificial ventilation together with further substantial colloid and inotrope support of the circulation. Six hours after transfer to the New Childrens’ Hospital in Sydney, “despite escalation of inotrope therapy, the infant remained hypotensive and poorly perfused, with a severe mixed respiratory and metabolic acidosis (pH 6.99)”…, culminating in cardiac arrest.
Bordetella pertussis was isolated from all babies, and at least some mothers and siblings who suffered whooping cough at the crucial time.
The article does not give any information on possible administration of paracetamol.
It must be obvious to an objective observer that all these babies contracted whooping cough from their vaccinated mothers, and/or siblings who suffered whooping cough at the crucial time, and, clearly, started deteriorating and died shortly after being administered intravenous antibiotics. They would have been better off staying at home and given nothing, particularly those who were breastfed. It is also obvious (this word is a rarity in medicine) that they developed whooping cough because of the lack of transplacentally-transmitted immunity since their mothers were vaccinated in their childhood. The vaccination obviously failed to protect the mothers and siblings.
Why the authors failed to recognise these material facts is anybody’s guess; however, the obsessive preoccupation with vaccination and unproven safety of antibiotics are close to home.
The toxicity of antibiotics of the kind used in the above cases is well established. Tragically, but, in my opinion, not coincidentally, a year later, Medical Journal of Australia (MJA 1998; 169: 116) published a retrospective review of antibiotic-associated serum sickness in children presenting to a paediatric emergency department in Victoria (Parshuram and Phillips 1998). These authors retrospectively examined the records of 537 children who attended the Royal Children’s Hospital emergency departments between May 1994 and July 1996 and who had a coded diagnosis of serum sickness, erythema multiforme, urticaria, anaphylaxis or drug reaction. Those who developed symptoms within 5-21 days of the start of taking medication, were considered to have medication-associated serum sickness.
There is little excuse for Wiliams et al.’s (1998) misdiagnosis, since serum sickness (or serum sickness-like) reactions to penicillin and more modern (broad spectrum) antibiotics since penicillin (cephalosporins) have been well known since their introduction in the eighties (Stricker and Tijssen (1992); Martin and Abbott (1985), Levin (1985). Moreover, since the mass use of any antibiotics, deaths in their recipients have been published. Coleman et al. (1955) wrote that “Severe immediate reactions to the administration of penicillin, some ending in fatalities, are occurring with increasing frequency”.
“None so blind as he who will not see”.
Williams GD, Matthews NT, Choong RK, and Ferson M. 1998. Infant
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Strebel PM, Ion-Nedelcu N, Baughman AL, Sutter RW, and Cochi SL.
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Parshuram CS, and Phillips RJ. 1998. Retrospective review of antibiotic
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department. MJA; 169: 116.
Stricker BH, and Tijssen JG. 1992. Serum sickness-like reactions to
cefaclor. J Clin Epidemiology; 45: 1177-1184.
Levine L. 1985. Quantitative comparison of adverse reactions to cefaclor in
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Coleman M, Stamford C, and Siegel BB. 1955. Studies in penicillin
hypersensitivity II. The significance of penicillin as a contaminant. J