Zika virus is a global public health emergency, declares WHO

Continuing my comments on men in white overalls spraying with DDT left right and centre, I’d like to remind readers of Rachel Carson’s “Silent Spring. New York: Houghton Mifflin: 1962)”.

In her book, Rachel Carson described a great number of harmful effects of spraying with DDT (and other similar toxic compounds) on the environment and its wildlife, as well as people and their food.

Dr Cristobal S. Berry-Caban (DDT and Silent Spring: Fifty years later. J Military and Veterans Health ; 19(4) October 2011) in the review article described how “One day in January 1958, Rachel Carson received a long, angry letter from her friend Olga Huckins, describing the deadly effect of DDT spraying for mosquito control over the Huckins’ private two-acre bird sanctuary at Powder Point, in Duxbury, Massachusetts. Not long afterwards Carson was a house guest at Powder Point when, late in the afternoon, a spraying plane flew over. The next morning she went through the estuary with the Huckins in their boat. She was sickened by what she saw - dead and dying fish everywhere, crayfish and crabs dead or staggering as their nervous systems appeared destroyed. She then realised that she would write about DDT.”

Even though the process was very slow (DDT was first synthesised in 1874), it was ultimately (in 1930s) established that DDT was insecticide. During WWII it was established that DDT had tremendous possibilities against several noxious insects, such as lice, mosquitoes and flies and ultimately against the malaria parasites, typhus and dysentery . This was found useful by the military. However, some cautioned that DDT must not be allowed to get into food or be ingested accidentally.

Berry-Caban also quoted Fred Bishop (1946. Present position of DDT in the control in insects of medical importance, Am J Publ Health. June; 36(6): 593-606), an American naturalist, who warned that the indiscriminate DDT spraying can upset the balance of nature and that 90% of all insects are beneficial.

Rachel Carson in her book (Silent Spring) wrote that DDT killed insects for weeks and months and not only the targeted ones but countless more, and remained toxic in the environment even after it was diluted by rainwater. She concluded that DDT had irrevocally harmed birds and animals and contaminated the entire world’s food supply. Additionally, the most devastating were the delayed kills, and the inhibition of reproduction, threatening entire species of birds and animals with extinction.

Carson pointed to the most damaging unintended effects of indiscriminate use of DDT: the extinction of birds and animals depending on certain insects and population explosion in other pests, with repercussions for humans because of DDT soaking into the soil and poisoning drinking water, and causing cancer.

The overuse of DDT in agriculture resulted in malaria –spreading mosquitoes developing resistance to DDT and other pesticides, similar to the well-documented bacterial resistance to sulpha drugs and antibiotics and, ultimately, to a vaccine-driven resistance of bacteria, viruses and other microorganisms.

Carson confirmed the phenomenal capacity of insects to adapt to new poisons; anything that kills a large proportion of an insect population ends up changing the insects’ genetics, favouring those that are most adaptable to new conditions. Susceptible populations can be rapidly replaced by the resistant ones. The survival intelligence of mosquitoes is demonstrated by an observation of strains of mosquitoes that can metabolise DDT into harmless by-products and others whose nervous systems became immune to DDT. There are even mosquitoes that learnt to avoid the toxic effects of DDT by resting between meals on the exterior walls of the houses not sprayed by DDT, avoiding the interior walls sprayed by DDT.

The little critters are arguably a 'superior intelligence'.

This all sounds elementary but nevertheless it indicates that humans, sadly, do not always learn from previous experience.

Might it be worthwhile to reconsider releasing GM male Aedes aegypti (AA) mosquitoes into the environment as a means of vector control of dengue? This question has become relevant in the coincidence of the release of the GM AA mosquitoes into the environment with the Zika outbreak in Brazil.

Because of their high rate of turnover, mosquitoes are capable of random genetic changes within a very short time. Not only would you get several generations in a year (20+ generations per year) but they also produce several eggs per batch – about 200 eggs per batch by AA female mosquitoes.

Let us put aside the genetic modification of the AA mosquitoes and say that the only thing done was to rear normal AA mosquitoes in the lab and release the 20th generation AA mosquitoes into the environment. If you rear ordinary mosquitoes in a lab, you would end up in a short time with generations of mosquitoes with profoundly different genetic make up from the mosquitoes you started with. When we release the lab-bred mosquitoes into the environment, we say we are releasing them into the wild. But mosquitoes in the environment are the normal mosquitoes because they live in the normal environment. So rather the lab-bred mosquitoes may well be the WILD type.

What genetic changes would male lab-bred non-GM mosquitoes bring to the normal mosquito population when released into the environment? Here we can think of several possibilities

- Female AA mosquito lives 2 to 3 weeks. Indoors - warm and moist, the female mosquito can live up to 2 months. So we know that environment determines how long the female mosquito would hang around to transmit whatever it is transmitting. Can we say that the lab-bred mosquitoes would over 20 generations assume a longer adult life to be passed on to female offspring on mating with mosquitoes not bred in the lab? And would that not increase the infection period?

- Normal AA eggs can withstand desiccation and dry conditions for very long times awaiting rains or wet conditions to advance to the next stage. Considering the 5-star hotel conditions in which generations of lab mosquitoes are bred, would it be far fetched to assume that resulting eggs in the environment would have different resistance or tolerance to the weather?

- Normal AA mosquitoes are mostly daytime mosquitoes. Would the lab-bred conditions alter day-night activity cycles of the mosquitoes in the environment?

- Male AA mosquitoes don’t bite, don’t transmit disease. Would the feeding habits and diet in lab conditions alter this?

We cannot rule out with certainty these possibilities that would alter the efficiency of AA mosquitoes in infecting humans nor the infectiousness and pathogenicity of the viruses – Dengue, chikungunya and Zika, in absolute and relative terms, carried by the AA mosquitoes

Particularly when we consider that:

- Tetracycline in chicken derived feed given to male AA mosquitoes in the lab is responsible for the failure to achieve 100% sterilization rates in any cohort of mosquitoes

- Tetracycline in the environment, into which the genetically modified mosquitoes are released, reverses the sterility of some (15% reported once) of the male GM AA mosquitoes.

These considerations become important under the current circumstances and release of male GM AA mosquitoes, where the Zika virus - the least infectious and pathogenic of the three viruses carried by AA mosquitoes - has assumed the most important status.

Dear Editors

In response to Dr Viera Scheibner (PhD) 's question, Hercule Poirot (if he existed) would had reminded us of his previous quibb "Sensationalism dies quickly, fear is long-lived" (Death in the Clouds).

Some food for thought:

While Zika virus (first discovered 70 years ago) is known to be endemic in certain areas for decades, the causal link to fetal microcephaly is still not proven despite claims of 4000 newly diagnosed neonates with microcephaly over the last 3 months in Brazil (so far 270 cases are confirmed and 462 excluded, of the 700-odd reviewed)

"In 2014, only about 150 cases were reported in Brazil in a year — a surprisingly small amount for a large country with nearly 3 million births a year. The United States, with about 4 million births a year, has an estimated 2,500 cases of microcephaly a year, said Margaret Honein, a CDC epidemiologist."

http://www.usnews.com/news/world/articles/2016-01-27/brazil-270-of-4-120...

So is the increase real or just better awareness? Surely not all 2500 documented cases of microcephaly in the USA annually is due to Zika infection?

These are reasons to be concerned, but not to panic.

Microcephaly in Brazilian babies

Could maternal fever be a major contributing factor?

The chronology of events reveals some interesting observations.

According to Marco Caceres (http://www.thevaccinereaction.org/2016/02/tdap-vaccinations-for-all-preg...) in October 2014 the Brazilian Ministry of Health’s Epidemiological Surveillance Center “Prof. Alexandre Vranjac” (CVE) in Sao Paulo announced a mandatory vaccination of pregnant women between the 27th and 36th week of pregnancy, from December 2014 with TDaP vaccine From early May 2015 a great number of babies were born with microcephaly . Most of the cases occurred in Pernambuco where most of TDaP vaccines were distributed.

Tens of thousands of pregnant women have been vaccinated with GlaxoSmithKline’s (U.K.) vaccine brand name Refortrix, or more commonly known as Boostrix, and which has been licenced in Brazil for more than a decade, and Adacel produced by Sanofi Pasteur (France). According to the package insert for Boostrix, “Animal fertility studies have not been conducted with Boostrix. There are no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, Boostrix should be given to a pregnant woman only if clearly needed.”

And, according to CDC,“Pregnant women should get a dose of TdaP during every pregnancy, regardless of whether a woman has already received one dose of TdaP to protect the newborn from pertussis… Tdap may safely be given at the same time as other vaccines.”

In December 2015, the Brazilian Government declared an emergency after 2,400 Brazilian babies were found to be born with “shrunken’heads (microcephaly) and damaged brains since October 2015.

The WHO came up with an answer: a little known Zika virus first described in the 1940s in Zika forests of Uganda, and allegedly spread by mosquitoes (Aedes aegypti) in the same way as is the West Nile virus.

The Zika virus has been known to infect people in Africa, South and Central Americas and Asia for more than 70 years without causing any birth defects. .

The Zika virus theory is largely based on the Zika virus allegedly found in a baby with microcephaly following an autopsy of the dead child and amniotic fluid of two mothers whose babies had the condition. No explanation has been given as to why suddenly it could be causing all these cases of microcephaly within the short period of time after, and not before, the mass vaccination of all pregnant women about 10 months before the first cases have appeared. The Brazilian government has accepted that as the cause.

Even if we disregard some of the above information as the cause of microcephaly in Brazilian babies, one effect of all vaccines is irrefutable: fever.

Product inserts of all vaccines, including the ones given to the Brazilian expectant mothers as above, list fever as a ubiquitous reaction.

According to “antimicrobe” (http://www.antimicrobe.org/e42.asp) hyperthermia in pregnancy causes a wide range of fetal structural and functional defects, with the central nervous system (CNS) being most at risk. While there is a greater incidence of neonatal morbidity and mortality with transmitted infections, not all maternal infections lead to transmission to foetus, nor does transmission to the fetus lead to disease or sequelae.

Somatic cell proliferation is adapted to, and proceeds optimally at the normal body temperature range of the species, and the deleterious effects of higher levels on mitotic cell proliferation and survival are widely recognised.

A hyperthermic episode during pregnancy can result in embryonic death, abortion, growth retardation, and defects of development. Maternal pyrexia, resulting from both microbial infection as well as non-infective causes such as epidural anaesthesia, could therefore augment the deleterious effects of hypoxia of the fetal brain, possibly by increasing the cerebral metabolism rate and demand for oxygen. Systemic fetal hypotension, endethelial injury and leukocyte aggregation may contribute to local tissue ischemia, especially in vulnerable areas, and many of these mechanisms could lead directly to cell death.

The above may also have an indirect neurotoxic effect by sensitising the brain and lowering the threshold at which hypoxia triggers apoptosis. The proinflammatory cytokines such as granulocyte colony-stimulating factor, tumour necrosis factor alpha, interleukin 1beta, C-reactive protein and interferon gamma, have a variety of effects. These include direct toxic effect on neurons and vulnerable oligodendrocyte precursor populations, gliosis with release of nitric oxide and mitochondrial dysfunction, as well as microglial activation in the brain. Animal studies reveal the direct correlation between increasing maternal temperature during gestation and the susceptibility to a variety of neurotoxic factors.

Graham et al. (1998. Teratogen update: gestational effects of maternal hyperthermia due to febrile illnesses and resultant patterns of defects in humans. Teratology; 58: 209-221.) demonstrated heat to be as significant that hyperthermia was the first teratogen in animals that was subsequently proven to be teratogenic in humans. They wrote, “These problems range from embryonic death and abortion to teratogenically induced anomalies, and are heavily dependent on the dose and timing of the exposure.

The range of defects induced by hyperthermia in experimental animals includes: anencephaly/exencephaly, encephalocele, microencephaly, talipes, arthrogryposis, abdominal wall defects and limb reduction defects. “

Perhaps, the traditional strict policy to not prescribe and administer any fever producing medication during pregnancy still applies.

Competing interests: No competing interests
Dr Viera Scheibner (PhD)
Scientist.author retired
n/a
Blackheath NSW Australia