Dr. Allen Cherer is an accomplished neonatal care specialist with decades of medical experience.

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Avoiding the Delta Variant While Outdoors

For the majority of the pandemic, it has been recommended that people gather outdoors if they must gather at all, but that appears to be changing a little. The Delta variant of covid-19 has changed the playing field even among the vaccinated. Initially, we were advised to take as much of our daily lives outdoors as possible in order to reduce transmission of the virus. Makes sense, right? Well, with how the Delta variant has changed things, we thought we should put together a list of measures people can take to reduce their risk of exposure to the Delta Variant.

Mask Up!

First and foremost, the easiest thing a person can do to reduce transmission, regardless of whether or not they’re indoors, is to wear a mask. Surgical masks, respirators, and N95 masks have all been shown to reduce transmission by limiting the number of aerosolized particles that spread in our breath, sneezes, and coughs.

Get Vaccinated

Vaccinated people are 25 times less likely to fall significantly ill with the delta variant. Getting vaccinated is simple, free, and absolutely encouraged right now. It is the best way we can help reduce transmission and do our part to flatten the curve. By bolstering our immune systems through vaccination, we can ensure that our bodies will be better equipped to fight off the virus more effectively, and thereby lowering our risk of infecting someone else.

Social Distancing

Beth K. Thielen, MD, Ph.D., is an assistant professor of pediatrics at the University of Montana has encouraged people to continue socially distancing even when outdoors. The Delta Variant has been shown to spread even when outdoors, which has some medical professionals, like Dr. Thielen, rightfully suggesting that we revert to older, more established, and cautious preventative measures.

Conclusion

The increase in both breakthrough cases and outdoor infections indicates that we might need to exercise a little more caution with the new prominence of the Delta Variant. Doing our part to minimize transmission of the virus has become our civic duty as citizens not of our countries, but of humanity itself. The tips and recommendations here aren’t comprehensive by any means, but all of them offer a good rule of thumb to go by.

Reducing Costs and Saving Lives

Sick newborns often rely on a ventilator to supply oxygen, and are tethered by a plastic endotracheal tube (ETT).  Often-times, this tube accidentally pops out.  This represents the fourth most common complication experienced by newborns in NICUs.  It can cause oxygen deficiency (hypoxia), high carbon dioxide levels in the blood, trauma to their airway, intraventricular hemorrhage, code events, and more.  “Unplanned extubations” also have the potential to nearly double the time of a hospital stay and increase the cost of care by $36,000 per patient.  Because of this, the Children’s National Health System’s NICU spearheaded a quality-improvement initiative to reduce the prevalence of unplanned extubations.

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The P-Hack

It’s been said that statistics can be used to prove just about anything.  Take, for example, one study that I recently read about, which examined the link between vegetarianism among pregnant women and an increased risk of drug and alcohol abuse among their children.  The study examined over 5,000 women and their children, and finding that if their mothers ate little to no meat while pregnant, then the children were more likely to drink, smoke, and do drugs at 15.  It’s an interesting study, but at the same time, it’s one that could be part of a phenomenon that’s tragically common in the field of science, and is often used to push an agenda at the cost of objectivity.  I’m talking, of course, about “p-hacking”.

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Working Towards the Elimination of Perinatal Hepatitis B Infection

Hepatitis B virus (HBV) infection  is a serious illness in the newborn and young infant.  The virus,  first discovered in the mid-1960s, is transmitted through percutaneous (i.e., puncture through skin) or mucosal (i.e., direct contact with mucous membranes) exposure to infectious blood or body fluids. The  virus is highly infectious, can be transmitted in the absence of visible blood, and remains viable on environmental surfaces for at least seven days.  Once the virus enters the body, it is transported to the liver where it replicates.  Although one generally thinks of the acute illness as a self-limited one in the adult with characteristic signs and symptoms, HBV infection in the infant is almost exclusively asymptomatic and hence, unrecognized. The devastating aspect of the infection is that the infant and young child frequently fail to clear the virus, and the illness becomes chronic. As many as 80-90% of infected infants progress to chronic infection, and chronically infected persons as adults are at increased risk of cirrhosis, hepatocellular carcinoma, and liver failure with approximately 25% dying from these serious complications.

Before 1982, an estimated 200,000-300,000 persons in the U.S. alone were infected with HBV annually, including approximately 20,000 infants. No effective pre-exposure prophylaxis existed, and only post-exposure prophylaxis in the form of hepatitis B immune globulin (HBIG) was available. However, the first hepatitis B vaccine was approved in the United States in 1981 and proved to be a real game changer. The availability of the vaccine set the stage for remarkable progress in the elimination of HBV infection among all age groups. With the advent of an effective vaccine, incurable hepatitis B infection had become preventable. The vaccine saves lives!

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Unraveling Fragile X Syndrome

In 1943, Julia Bell and James Martin first described the sex-linked heritable condition now termed Fragile X Syndrome (FXS). In their paper, “A Pedigree of Mental Deficit Showing Sex-Linkage”, they described a single kindred in which eleven males spanning two generations  exhibited mental deficiency. After detailed investigation, the researchers concluded that the condition was heritable, sex-linked, and involved abnormal brain development. Since their initial description, much has been learned about Fragile X Syndrome, and yet the odyssey to lessen its impact on affected individuals and their families as well as future generations remains challenging.

 

Fragile X Syndrome is considered the most common cause of inherited intellectual disability. Although disease estimates are probably not precise for a number of reasons, the incidence among males is considered 1/4000 and among females 1/8000. In the 1990’s, the molecular basis for the disease was identified and found to lie within the FMR1 (Fragile X Mental Retardation 1) gene on the long arm of the X chromosome. Since that time, a whole new class of molecular disease has been characterized based on the presence of unstable and abnormal expansions of DNA triplets (trinucleotides). The normal FMR1 gene has CGG (cytosine-guanine-guanine) trinucleotide repeats  in the range of 7-54 in the 5’ untranslated region. The gene codes for FMRP (Fragile X mental retardation protein) which is responsible for the regulation of a number of cellular processes, not the least important of which is the development of brain synapses and the relaying of nerve impulses. In FXS, the CGG repeat expands to over 200. It is this abnormally expanded and hypermethylated  CGG segment that turns off (silences) the FMR1 gene and halts the production of FMRP. The loss or shortage (deficiency) of FMRP disrupts nervous system functions and leads to the signs and symptoms of FXS. Identifying trinucleotide repeats as the basis for disease has brought about a greater understanding not only of FXS but also a complex set of neurological diseases, such as Huntington’s Disease, the spinocerebellar ataxias, and myotonic dystrophy.

 

Since the FMR1 gene is located on the X chromosome and expansions of the CGG repeat  can include greater than the normal but less than the over 200 with the full mutation, a  number of different phenotypes are described based on the affected sex and the number of CGG repeats. In males, the mutation (> 200 trinucleotide repeats) often results in the full spectrum of FXS  signs/symptoms, including intellectual disability, speech/language and developmental delay, facial characteristics ( long face, large ears, broad forehead, joint laxity, macroorchidism) which become more apparent with age, and behavioral disorders (social anxiety, ADHD, autism). In females with the full mutation, the symptoms are often less frequent and severe most probably due to females having two X chromosomes (as opposed to males having a single X chromosome) and skewing of X inactivation among females.

 

The males and females with lesser repeats of the CGG segment (55-200) but greater than normal are said to have an FMR1 gene premutation primarily because expansion to the full mutation can occur in succeeding generations (genetic anticipation). Individuals with the premutation typically are intellectually normal. However, they may have lower than normal amounts of FMRP and consequently exhibit milder versions of the physical features and emotional problems  seen with the full mutation. On the other hand, two related disorders due to the premutation of the FMR1 gene are FXTAS (Fragile X-associated Tremor/Ataxia syndrome), a Parkinsonian-like syndrome occurring mostly in older males, and POI (Premature Ovarian Insufficiency) in females.

 

It is apparent that the spectrum of symptoms in individuals with the full mutation and with the premutation is extremely broad. In addition, the behavioral and developmental symptoms have significant overlay with autism and may be compounded by other neurologic disorders such as seizures. These  features make the clinical diagnosis of FXS difficult and often time-consuming. Fortunately, Fragile X Syndrome can be diagnosed with the blood FMR1 DNA test using Southern Blot analysis or Polymerase Chain Reaction (PCR). Clearly, it is imperative that any child who presents with global developmental delay, autism, and/or intellectual disability be tested for FXS with the FMR1 gene test.

 

Despite advances in the molecular understanding of FXS and its pathophysiology, treatment remains for the most part symptomatic and includes special education, behavioral therapy, and medication specific for ADHD, seizures, and neuropsychiatric problems. Molecules  aimed at targets in pathways that are dysregulated in the absence of FMRP continue to be developed and tested in order to offer effective drug therapies, but thus far overwhelming satisfaction has not been achieved. In the future, it is intriguing to envision the role of genome editing and CRISPR technology in the cure of this single gene disorder.

 

Tackling Rotavirus

National Infant Immunization Week Blog-a-thon with woman holding baby. #ivax2protect

Rotavirus gastroenteritis is the leading cause of diarrhea-associated hospitalizations and death in children younger than 5 years of age. Rotavirus illness is caused by a virus which enters the body by mouth and infects the intestines. It is a particularly hardy and contagious virus, capable of surviving on inanimate surfaces for long periods and spreading readily from child to child and also to adults. Large quantities of virus are shed in the stool both prior and following acute illness which is characterized by fever, vomiting, and watery diarrhea. Illness typically lasts 3-7 days; death may ensue due to severe dehydration. Since the infection is caused by a virus, antibiotics and antiparasitic drugs are ineffective, and care is primarily supportive. Prior to the development of effective vaccines, 80% of children in the U.S. would develop rotavirus gastroenteritis. Elsewhere in developing countries, the numbers were staggering with more than 500,000 deaths occurring annually in children under 5 years old.

The first rotavirus vaccine, RotaShield (Wyeth Laboratories) was licensed in the United States in 1998 but was withdrawn in 1999 due to a suspected association with intussusception, a type of bowel obstruction. In 2006, RotaTeq (GlaxoSmithKline) was FDA approved, followed by Rotarix (Merck) in 2008. Both are live, attenuated, oral vaccines requiring either a 3 dose or a 2 dose series and have shown significant efficacy in the range of 80-90% in middle and high income countries. Prior to 2006 when routine rotavirus vaccination was recommended, rotavirus gastroenteritis was estimated to result in 400,000 visits to physician’s offices, 200,000 visits to Emergency Rooms, 55,000 hospitalizations, and 20-60 deaths annually among children under 5 years of age in the U.S. for an estimated total cost close to $300 million. Since introduction of the vaccine, the impact has been striking; hospitalizations and rotavirus-related Emergency Room visits have decreased by 80%. In addition, by vaccinating infants, serious rotavirus infections among older children and adults have demonstrated similar declines, presumably through the so-called “herd effect” resulting from wide-spread immunization practice. In summary, clinical trials and experience of rotavirus vaccines in middle and high income countries have demonstrated high efficacy against serious rotavirus disease. Rotavirus vaccination works!

Despite the high efficacy rates of RotaTeq and Rotarix vaccines in middle and high income countries, clinical studies consistently demonstrate lower efficacy rates in the range of 37-61% with either vaccine in the lowest income nations where the burden of rotavirus infection is greatest. Such performance is typical of other live oral vaccines in similar populations. The reasons are not completely understood, but factors such as earlier onset of recurrent episodes of infectious diarrhea, different gut microbiome, the presence of neutralizing antibodies, poor nutritional status, and varying circulating rotavirus strains may play a role. Nevertheless, even a moderately effective vaccine can have a huge public health impact when introduced into a population where the burden of disease is great, especially when combined with the herd protection that occurs when most children in an area are vaccinated and immune.

In 2000, the Global Alliance for Vaccines and Immunization (Gavi) was founded as a public-private global health partnership with the intent to improve childhood immunization coverage in poor countries and increase access to new vaccines. By design, Gavi leverages not only financial resources but also expertise to make vaccines more available, affordable, and their provision more sustainable. The two current rotavirus vaccines obtained prequalification by the World Health Organization (WHO) in 2008 which followed with UNICEF procurement of the vaccines through the financial support of Gavi. These vaccines have been introduced in 42 Gavi-eligible countries and in 6 additional countries classified as low and middle income and have had a major impact on rotavirus-associated hospitalizations and deaths in all settings.

According to WHO estimates in 2013, approximately 215,000 children under 5 years of age die each year from vaccine-preventable rotavirus infections with almost half of them in 4 countries: India, Pakistan, Nigeria, and Democratic Republic of Congo. Ten countries account for almost 2/3 of all deaths. It is in this context that findings recently published in the New England Journal of Medicine related to a new vaccine against rotavirus are incredibly encouraging. The study reported by Isanaka et al. was conducted in Niger in Sub-Saharan Africa, a region with the highest rate of death associated with rotavirus disease and where the current cost of vaccines is probably unsustainable and where refrigeration and transportation are unreliable. The new vaccine, BRV-PV (Rotasil), is a live, oral rotavirus vaccine manufactured by Serum Institute of India and is lower in cost relative to existing vaccines and heat stable for as long as 6 months at 104 degrees F. and for 2 years at 98.6 degrees F. In a double-blind, placebo-controlled randomized trial including over 4000 healthy infants, the new vaccine was found to have a calculated efficacy rate of 67% with no apparent short term adverse events. Since existing vaccines are costly and require refrigeration, the new vaccine provides major advantages in resource-constrained countries where the burden of rotavirus is greatest. If further surveillance continues to yield good findings, the new vaccine promises to provide a giant step in the progress against rotavirus.

 

Congenital Cytomegalovirus Infection and Hearing Loss

ongenital Cytomegalovirus Infection and Hearing Loss

It has been over 50 years that the association between congenital Cytomegalovirus (CMV)  infection and hearing loss was described by Medearis et al. During that time, advances in understanding the pathogenesis and the natural history of the disease have been made. It is now acknowledged that CMV infection is not only the most common congenital viral infection in the world but also the leading non-genetic cause of childhood sensorineural hearing loss. The world-wide incidence of congenital CMV infection is estimated to range from 0.06% – 2.4% of all live births. As many as 10-15% of infected neonates are symptomatic at birth, presenting with a variety of signs/symptoms including growth failure, anemia, extramedullary hematopoiesis, thrombocytopenia, hepatosplenomegaly, intracranial calcifications, microcephaly, and chorioretinitis. Mortality is <5%, but as many as 50% of survivors will demonstrate  long-term sequelae, primarily sensorineural hearing loss and neurodevelopmental delay. On the other hand, the great majority of congenitally infected neonates are asymptomatic and may be totally unrecognized. They generally have a much better prognosis. Notably, however, approximately 10% of these asymptomatic infants will also manifest sensorineural hearing loss, often late in onset and progressive in nature, and some element of neurodevelopmental delay. Hence the global burden of congenital Cytomegalovirus infection is significant.

Cytomegalovirus is ubiquitous in humans and infects 50-85% of adults in the United States by 40 years of age. Virus excretion rates from urine and saliva in children from 1-3 years of age in child care centers are reported to range from 30-40% but can be as high as 70%. Generally, acquired infection  in adults and children is mild and inconsequential in terms of long-term sequelae. CMV, like Herpes Simplex and Varicella Zoster, belongs to the herpesvirus family. All three may cause congenital and perinatal infections. Transmission of the virus can occur vertically to the fetus during pregnancy with the highest risk of infection occurring during the first half of gestation. Maternal infection can occur following initial exposure, with reactivation of the virus following previous infection, or with reinfection with a different strain of the virus. Symptomatic infection occurs with similar frequency in newborns born to women with initial CMV infection (primary infection) and those born to women who were seropositive before pregnancy (non-primary infection). Then too, the severity of newborn disease and the rates of CMV-associated sensorineural hearing loss do not differ between primary and non-primary infection. Studies since 2003 have reported treatment benefit in terms of hearing  and neurodevelopmental outcome of intravenous ganciclovir for 6 weeks and subsequently in 2013 with its oral prodrug valganciclovir for 6 months. The American Academy of Pediatrics Red Book, 2015 edition, recommends antiviral treatment for those newborns with symptomatic congenital CMV infection with or without CNS involvement provided it can be initiated within the first month of life. The quandary, of course, arises when the definition of “symptomatic” is not clear. Suggestions have been offered, but none has been universally accepted. In addition, the Red Book specifically advises against antiviral treatment for those asymptomatic patients with congenital CMV infection, although a number of them are at risk for long-term sequelae.

In 2000, the Joint Committee on Infant Hearing endorsed Universal Newborn Hearing Screening (UNHS). Prior to that time, only at risk newborns for hearing impairment were screened, and it was estimated that close to 50% of all children with hearing loss were undiagnosed until 18 months to 3 years of age. It is generally accepted that in order to achieve linguistic and communicative competence, diagnosis and intervention must take place before 6 months of age. The aim of UNHS is to screen all newborns before 1 month of age and have confirmation of hearing loss in infants who do not pass through a complete audiologic evaluation by 3 months of age. A limitation of UNHS is not all cases of childhood hearing loss, especially those with late onset and/or progressive loss, will be detected. Clearly, newborns with congenital CMV infection, specifically those who are asymptomatic and have not been identified, may be missed altogether.

Based on the global nature and incidence of congenital CMV infection, the frequency of late onset hearing loss, and the benefits of early intervention, newborn screening for congenital  CMV infection has been explored  but has not yet been adopted. Dried blood spot  (DBS) PCR for CMV was initially encouraging but recent studies suggest poor sensitivity, and blood viral load does not appear to be sensitive or specific in predicting which infants will develop late onset hearing loss. Newborn saliva and urine PCR for CMV are best to identify congenital CMV infection, but  to date no specific biomarkers have been found to reliably predict which infants will develop late onset hearing loss. Ideally, maternal infection with CMV would be eliminated. An alternative would be to prevent transmission to the fetus or newborn. In the meantime, research continues to better identify and treat  those newborns with congenital infection and prevent the serious sequelae.

Supporting Universal Antenatal Pertussis Vaccination

Pertussis (Whooping Cough) is a serious health issue, especially in the very young infant. It is caused by a bacteria, Bordetella pertussis, and is transmitted person to person via aerosol droplets usually by coughing or sneezing. The illness typically begins with cold-like symptoms which may then progress to the characteristic paroxysms of cough terminating with an inspiratory whoop.

In young infants, the illness can proceed to cyanosis, severe respiratory fatigue, apnea, and even death. Although whole-cell and acellular vaccine formulations against B. pertussis  are available, primary immunization generally does not start until 6-8 weeks and as late as 3 months of age in some countries, leaving the  infant unprotected during a most vulnerable period.

The incidence of pertussis has steadily increased in the United States and elsewhere since the 1980s and especially since 2005. Since 2010, 10-50,000 cases of whooping cough have been reported each year in the United States with every state represented. More than 48,000 cases were reported in 2012, and in California alone, greater than 10,000 cases were reported in 2014. Although all ages are affected, the highest rates of disease and hospitalization occur in infants less than one year of age. The numbers have been accompanied by an alarming increase in the number of deaths, almost exclusively among infants less than 3 months of age.

One of the causes thought to explain the resurgence of pertussis is the rapid waning of the immunity induced by  current vaccines. Prior to the 1990s, a whole-cell vaccine was used and the immunity it induced was longer lasting. Since then, acellular pertussis vaccines have been used exclusively in the United States primarily due to less frequent adverse reactions.

However, these vaccines have been shown to induce immunity which wanes rapidly over a period of several years. As a result, pertussis immunization is required more frequently and the likelihood of non-protection is much greater, especially for older children  and adults. This is particularly alarming since such persons are often the caretakers and closest contacts of young infants. Thus, when considering prevention strategies for pertussis, it is critical to include approaches that prevent pertussis transmission to young infants.

In 2001, the Global Pertussis Initiative (GPI) was established in response to the resurgence of pertussis and in an effort to raise global awareness about pertussis and to develop evidence-based recommendations for vaccination strategies . Over the years, the GPI has focused particular attention on protection of the very young infant and has emphasized as a primary strategy maternal immunization during pregnancy which directly protects the infant through the passive transfer of pertussis antibodies from mother to fetus.

Numerous studies have demonstrated that a pregnancy booster (Tdap) provides the necessary protection to the very young from birth until infant-generated immunity is achieved from the primary series of pertussis immunizations. Based on studies that demonstrate robust maternal antibody production within 2 weeks of booster immunization and ready immunoglobulin transfer after 30 weeks’ gestation, current recommendations call for Tdap immunization between 28 and 38 weeks’ gestation.

Since maternal antibody levels decline significantly I year post immunization and are almost non-existent 2 years post immunization, the Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention (CDC) in 2012 recommended booster immunization during every pregnancy.

To date, research finds that vaccination against pertussis during pregnancy is well tolerated and not associated with any adverse obstetric, birth, or neonatal outcomes. Recently, a study from the United Kingdom evaluating antenatal booster immunization and efficacy in preterm births demonstrated with a mean gestational age of 29 weeks at time of immunization and birth at a mean gestation of 32 weeks, protective antibody  levels were found at the start of the primary immunization series.

Unfortunately, despite strong recommendations by the CDC, the American College of Obstetrics and Gynecology, the  American Academy of Family Physicians, and the American Academy of Pediatrics , pertussis immunization rates during pregnancy remain very low. Clearly, education of caregivers and patients  must be a goal. Until a new pertussis vaccine with longer duration of protection is available, large-scale pertussis outbreaks will continue and the burden of disease will continue to be particularly felt by the very young infant.

Tetanus Elimination: An Amazing Public Health Achievement

Neonatal tetanus is one form of a devastating illness with a very high mortality rate. The illness was recognized by Hippocrates as early as the 5th century BC. The causative bacterium and its exotoxin were identified in the late 1800s.

An effective toxoid vaccine was developed in 1924 and widely used during World War II to prevent tetanus induced by battle wounds. The illness itself is characterized by generalized rigidity and painful convulsive spasms of skeletal muscles.

The infectious agent, Clostridium tetani, is a spore-forming anaerobe found in the soil and in the gastrointestinal tract of animals. It generally enters the body through a break in the skin, such as a cut or a puncture wound with a contaminated object. The bacteria produce a potent biological toxin which is responsible for the clinical signs. The spores which cause tetanus are ubiquitous, so the only prevention is immunization.

Newborns typically receive passive immunity from their immunized mothers and are therefore protected. However, if mothers have not been immunized, not only are they at risk for developing tetanus but so are their unprotected babies. In many countries, deliveries take place in unhygienic circumstances putting both mothers and babies at risk for life-threatening infections.

Maternal and neonatal tetanus are among the most common lethal consequences of unclean (out of health care facilities and/or not assisted by medically trained assistants) deliveries.

In newborns, the site of infection is generally an unhealed umbilical cord stump, particularly when the cord is cut with a non-sterile instrument.
In 1988, the World Health Organization (WHO) estimated that 787,000 newborns died of neonatal tetanus.

The numbers are particularly staggering and alarming since deaths can be prevented by hygienic delivery and cord care practices and/or by immunizing mothers with tetanus vaccine that is both inexpensive and efficacious.

Subsequently, the WHO and partner organizations such as UNICEF and UNFPA initiated a public health campaign with the goal to eliminate maternal and neonatal tetanus. Tetanus cannot be eradicated such as polio and small pox due to the worldwide distribution of spores in the environment.

The goal, however, to eliminate the disease sets a target of less than 1 case/1000 live births. Persistent and painstaking efforts throughout all 6 WHO Regions to enhance vaccination of pregnant women and children as well as to increase skilled birth attendance and to educate regarding clean umbilical cord practices have achieved remarkable success.

As of 2013, the WHO estimated that 49,000 newborns died from neonatal tetanus, a 94% reduction from that of the late 1980s. As recently as May 2016, the WHO reported that the South-East Asia Region, an area comprising 25% of the global population, had successfully eliminated maternal and neonatal tetanus. India, a member nation of the South-East Asia Region had previously met the goal in 2015.

While progress continues to be made, by June 2016, 19 countries have not reached elimination status. Activities to achieve the goal are ongoing in these countries, with many likely to achieve maternal and neonatal tetanus elimination in the near future.

Despite the resounding success of the campaign, efforts can not cease and must continue to maintain and enhance high population immunity with tetanus vaccination during infancy, for women of childbearing age, and during adolescence through school immunization programs.

Additionally, achieving high coverage of skilled birth attendance and promoting appropriate umbilical cord care are essential goals necessary to maintain maternal and neonatal tetanus elimination.

The Zika Virus and Microcephaly

Zika virus is an arthropod-borne flavivirus discovered in Africa in 1947. When infected by the virus, most persons are asymptomatic or demonstrate generally mild, self-limited illness characterized by fever, rash, arthralgia, and conjunctivitis. The first widespread outbreak of the Zika virus was recognized on Yap Island, Federated States of Micronesia, in 2007, followed by outbreaks in Southeast Asia and the Western Pacific, including a large outbreak in French Polynesia in 2013-14.

Since the identification of the Zika virus infection in Brazil in May, 2015, the virus has spread rapidly throughout the Americas, and as of February 2016, thirty-one countries and territories had reported cases.

A bite of the Aedes aegypti mosquito is the main route of exposure, but sexual, maternal-fetal, and intrapartum transmission have all been documented. To date, all cases reported in the continental United States have been travel-associated, whereas in the U.S. territories (American Samoa, Puerto Rico, and U.S. Virgin Islands), the vast majority of cases have been locally acquired vector-borne.

Although infection with the Zika virus generally leads to mild disease, its emergence in the Americas has coincided with a marked increase in babies being born with microcephaly, a neurological disorder present at birth and defined as head circumference at least 2 SD smaller than the mean for sex, age, and ethnicity and with head circumference at least 3 SD smaller being deemed severe. Congenital microcephaly is a condition associated with a reduction in brain volume and is often caused by genetic or environmental factors that affect fetal brain development.

Prenatal viral infections, such as rubella and cytomegalovirus, hypertensive disorders, and maternal alcohol have also been associated with the condition. Cases have been reported after intrauterine infection with West Nile virus (also a flavivirus) and Chikungunya virus. Given the widespread nature of the Zika virus epidemic in the Americas, the temporally associated increase in microcephaly cases in Brazil, and the retrospective findings of a cluster of microcephaly and neurologic disorders associated with the Zika virus in French Polynesia, the WHO declared Zika virus a Public Health Emergency of International Concern on February 1, 2016.

In order to reduce the risk of microcephaly, recommendations included avoidance of travel to affected countries by pregnant and childbearing aged women, use of condoms with partners returning from affected countries, and pregnancy delay.

In order to better quantify the risk of microcephaly associated with the Zika virus infection, a retrospective study based on data from the completed Zika virus outbreak in French Polynesia in 2013-14 was reported in The Lancet by Simon Cauchemez, PhD, and colleagues from the Institut Pasteur.

Based on four datasets providing information on all cases of microcephaly, weekly number of consultations for suspected Zika infection, seroprevalence for Zika virus antibodies, and the number of births during the outbreak, the researchers developed a mathematical and statistical model to illustrate the association between the Zika virus and microcephaly and demonstrated the risk for microcephaly to be greatest during the first trimester of pregnancy.

According to the analysis, it is estimated that the risk for microcephaly for mothers with the Zika virus infection during the first trimester is about 1%. Although the risk appears low compared to other intrauterine viral infections (e.g., rubella, cytomegalovirus), the incidence of the Zika virus infection is very high during outbreaks (eg, 66% in French Polynesia and 73% in the island of Yap). Therefore, despite the relatively low fetal risk, infection with the Zika virus is an extremely important public health matter.

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