Homemade Diaper Cream (Great for Eczema Too)

My favorite all purpose natural body cream is CJ’s Butter Cream. You can use it as diaper cream (cloth diaper friendly) or for dry, patchy skin (even eczema).

Here’s the thing though – it’s expensive. Although well worth the $18 price tag, I thought I would give it a whirl and see if I could do better!

I use shea butter as a base since this is the base used for the CJ Butter Cream (and I love it so much).



But I also use shea butter because of its great benefits. (Did you know that shea butter is edible?) Shea butter is an anti-inflammatory, emollient and humectant. It even has the ability to absorb ultra-violet radiation – pretty awesome, huh? 

Shea butter has even been studied to be effective for relief of nasal congestion, lowering cholesterol levels and for blood thinning! Check it out here


I could write an entire post about shea butter – but let’s move on instead…

Here are the ingredients used

1/2 cup          Shea butter-unrefined (anti-inflammatory, moisturizer)

1/4 cup          Coconut oil (antiviral, antifungal, anti yeast)

                       

1 tbsp             Beeswax pellets (anti-inflammatory)

2 tbsp             Vegetable glycerin (humectant, moisturizer)

3 drops           Calendula oil

Fragrance (if preferred)

The Mechanics of It

I used a double boiler method.

I melted a few heaping tablespoons of shea butter (1/2 cup).



I added my coconut oil.

Once you have the shea butter and oil melted, you can add the beeswax. I used a white organic beeswax. I used about 2 tablespoons or so.



Once the beeswax is melted, remove from heat and add your vegetable glycerin.

Vegetable Glycerin can be purchased online
and is rather cheap. I get mine here.

Once that is completely mixed, I poured the liquid in a small glass mason jar. I added the calendula oil (mine contains vitamin E as well) and fragrance (I used “fruit slices”, you can opt for no fragrance if you choose).

The liquid is still pretty hot in this picture, but you
see the cooling already beginning at the edges-
add your fragrance now.

Let this cool, uncovered overnight - it will continue to firm up as it cools.

Remeber - a little goes a long way!

Protecting Babies By Getting Your Tdap Booster? Ponder This.

Pertussis.

A scary word for parents and grandparents across the country.

I’ve had friends and even close family members seek out and receive an aP (pertussis/whooping cough) vaccine in the hopes of protecting the babies in their life.

One question arises, “Why does the general public believe that getting this vaccine will prevent transmission of the B. Pertussis toxin?”.

I think there exists a great misconception of information regarding the disease and vaccine regarding the effectiveness on transmission of pertussis (whether it be intentional or not).

Let’s start at the beginning – according to the manufacturer.

It is unknown whether immunizing adolescents and adults against pertussis will reduce the risk of transmission to infants[1]

There are currently no data which demonstrate a reduction of transmission of pertussis after immunization with BOOSTRIX.[2]

…booster immunization of adults with acellular pertussis vaccines was not found to increase bactericidal activity over preimmunization levels.[4]

Why not be extra-safe and get the vaccine anyways? 

Vaccinated adolescents and adults may serve as reservoirs for silent infection and become potential transmitters to unprotected infants (3-11)….even young, recently vaccinated children may serve as reservoirs and potential transmitters of infection."[5]

(According to the phenomenon coined as “original antigenic sin”) DTaP vaccinated kids might be more contagious when they catch pertussis compared to unvaxed kids after they catch pertussis.[6]

Here, we ask how aP vaccination affects competitive interactions between Bordetella species within co-infected rodent hosts and thus the aP-driven strength and direction of in-host selection. We show that aP vaccination helped clear B. pertussis but resulted in an approximately 40-fold increase in B. parapertussis lung colony-forming units (CFUs).[7]

Further, we show that aP vaccination impedes host immunity against B. parapertussis—measured as reduced lung inflammatory and neutrophil responses. Thus, we conclude that aP vaccination interferes with the optimal clearance of B. parapertussis and enhances the performance of this pathogen. Our data raise the possibility that widespread aP vaccination can create hosts more susceptible to B. parapertussis infection.[7] 

The benefit of the vaccine must be there, we must get it to promote herd immunity…

The efficacy of Tdap vaccination in controlling school or institutional outbreaks has not been evaluated[8][9]

Hold on a second. By giving the vaccine to children (at 2 mo, 4mo, 6mo, 15mo, 4-6yrs, adulthood, and 65 +), the incidence of pertussis has definitely declined... right? 

The overall incidence of pertussis has been increasing steadily since 2007 and has now surpassed peak rates observed during 2004-2005.[10]

Despite high vaccination rates, the number of reported cases of pertussis in the United States has increased steadily since the 1980s.[3]

Chart from the CDC-see reference 10

All Pertussis (aP) vaccines tend to modify duration and severity of disease rather than completely preventing illness.[12]

Pertussis is considered an endemic disease, characterized by an epidemic every 2–5 years. This rate of exacerbations has not changed, even after the introduction of mass vaccination – a fact that indicates the efficacy of the vaccine in preventing the disease but not the transmission of the causative agent (B. pertussis) within the population [13]

I don’t understand. Why isn’t this vaccine effective against the transmission of the pertussis?

Yes, that is the question!

And it looks like the science community is aware of this fault and is attempting to resolve it. Although, all while still fronting that the vaccine is effective at reducing transmission. 

Despite detailed molecular analysis of several virulence-associated factors of B. pertussis, significant gaps remain in our understanding of the pathogenesis of this infection and disease. For instance, we know next to nothing about the cause of pertussis cough or its specific characteristics, and we do not know which bacterial factors contribute to the cough pathology. One of the challenges in understanding this pathology is that there are no small animal models that reproduce the specific characteristics of B. pertussis infection and disease in humans.[14]

Serologic studies of patients in the clinical efficacy trials of the acellular pertussis vaccines did not yield a correlation between antibody levels and protection against pertussis….. The mechanisms of vaccine-induced immunity remain elusive and determination of whether these products are working as initially predicted will require further study.[15]

The research continues to grow regarding the shifting epidemiology and evolutionary changes in Bordatella agent. To understand the current research, let’s do a quick de-briefing.

The current vaccines contain antigenic components for 3 pertussis antigens (proteins found in the bacteria); Filamentous hemagglutinin which protects against filamentous hemagglutinin adhesion, a virulence factor that allows bacterial colonization of the respiratory tract; Pertactin, another virulence factor that functions as an auto-transporter for B. pertussis adherence to lung epithelium and pertussis toxin; and the pertussis toxin itself (PT).

Unfortunately, the vaccine is omitting a vital toxin. The adenylate cyclase toxin (CyaA or also known as ACT).

Two of the most important virulence factors of B. pertussis are the secreted toxins pertussis toxin (PT) and adenylate cyclase toxin (ACT). The emerging picture revealed by the recent literature is that these toxins play a major role in suppression and modulation of host immune and inflammatory responses.[14]

Adenylate cyclase toxin has not been included as a component of newer generation acellular pertussis vaccines, despite the observations that ACT is an important virulence factor for B. pertussis[14]

Current research from a study in 2010 is continuing to add to the base knowledge we have. Some believe that administering a detoxified ACT vector along with the DTaP vaccine, the yielded results will add to the ability to halt transmission. 

detoxified ACT is being developed as a possible vaccine vector molecule, so immune responses to the vector itself would be important. Two recent reports addressed the issue of the use of detoxified ACT as a pertussis vaccine component. In one, co-administration of detoxified ACT with acellular pertussis vaccine to mice significantly enhanced protection against B. pertussis, with adjuvant effects on both Th1 and Th2 immune responses [134]. [14]

Unfortunately, there is unwanted side effects with this (of course) …

In the other, however, detoxified ACT was found to block CR3 transiently and inhibit complement-dependent phagocytosis by human neutrophil-like cells [135], a potentially unwanted side effect[14].

Hmm, so now what?

Whether this investigation will progress further to human clinical trials will probably depend upon a major push towards development of newer acellular pertussis vaccines [14]

On February 22, 2011, the U.S. Supreme Court ruled (in Bruesewitz v. Wyeth) that vaccine makers are immune from lawsuits charging that the design of a vaccine is defective.[16]

 
Pause for Disclosure

I want to say upfront, that I understand that more would be gained by finding a well-written, objective review article about B. pertussis-specific immunology instead of trying to understand the complexities with a disjointed article presentation.

I am all for an expert on the subject to do the work for me, but unfortunately, I was unable to find one.

Conclusion

What I take away from what I have read over the last few weeks regarding transmission and the DTaP vaccine is that there is still much to learn and it doesn’t seem like anyone knows exactly what is going on (which the scientific community admits to!) with the pertussis bacteria and how it relates to immune response, repeat immune response, and transmission.

What is the most disturbing is that mothers, fathers, grandparents, and children are wholeheartedly depending on this vaccine without any reservation.

The pertussis vaccines do not prevent transmission.

They do, however, prevent or suppress the symptoms (making the individual asymptomatic), and leads to subclinical infection.

I clearly have my reservations and I am skeptical of the promises TV commercials and well advertised web pages claim, especially after taking the time to learn about it myself. I hope this information opens up an internal dialogue in your mind – questioning, learning, assessing.

Reference:

[1] Adacel Patient Brochure (Sanofi Pasteur) page 5

[2] Boostrix  Production Information (GlaxoSmithKline Biologicals SA) page 3

[3] Weiss, A., Patton, A., Millen, S., Chang, S.j., Ward, J., Bernstein, D. Acellular pertussis vaccines and complement killing of bordetella pertussis. American Society for Microbiology (Infection and Immunity). Vol 72(12): 7346-7351. Dec 2004.

[4] Weingart, C., Keitel, W., Edwards, K., Weiss, A. Characterization of bactericidal immune responses following vaccination with acellular pertussis vaccines in adults. American Society for Microbiology (Infection and Immunity). Vol80(5). May 2012

[5] I. Srugo, D. Benilevi, R. Madeb, S. Shapiro, T. Shohat, E. Somekh, Y. Rimmar, V. Gershtein, R. Gershtein, E. Marva, and N. Lahat. Pertussis Infection in Fully Vaccinated Children in Day-Care Centers, Israel. Emerging Infectious Diseases. Vol 6(5): 526-529. Sept/Oct 2000

[6] James D. Cherry, Dorothy X. L. Xing, Penny Newland, Kashmira Patel, Ulrich Heininger, and Michael J. Corbel. Determination of Serum Antibody to Bordetella pertussis Adenylate Cyclase Toxin in Vaccinated and Unvaccinated Children and in Children and Adults with Pertussis. Clinical Infectious Diseases. Vol 38 (4): 502-507. 2004

[7] Gráinne H. Long, Alexia T. Karanikas, Eric T. Harvill, Andrew F. Read and Peter J. Hudson. Acellular pertussis vaccination facilitates Bordetella parapertussis infection in a rodent model of bordetellosis. Proceedings of the Royal Society (Biological Sciences). Vol 277 (1690):2017-2025. Jul 2010

[8] CDC. Preventing tetanus, diphtheria, and pertussis among adolescents: use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2006

[9] CDC. Preventing tetanus, diphtheria, and pertussis among adults: use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccine. Recommendations of the Advisory Committee on Immunization Practices (ACIP) and recommendation of ACIP, supported by the Healthcare Infection Control Practices Advisory Committee (HICPAC), for use of Tdap among health-care personnel. MMWR 2006;55(No. RR-17):1–37.

[10] CDC-Surveillance & Reporting Trends. Pertussis (Whooping Cough). Last Updated Sept 2011

[11] Wendelboe, Aaron M. MSPH; Van Rie, Annelies MD, PhD; Salmaso, Stefania PhD; Englund, Janet A. MD. Duration of Immunity Against Pertussis After Natural Infection or Vaccination. The Pediatric Infectious Disease Journal. Vol 24(5):S58-S61. May 2005

[12] The Science and Fiction of Pertussis Vaccines. Pediatrics. Vol 104;No 6. Dec 1999

[13] Ori Hochwald, Ellen Bamberger and Issaac Srugo. The Return of Pertussis: Who is Responsible? What Can Be Done? Israel

[14]Vaccine Research Initiative. Vol 8: 301-307. May 2006[14]Nicholas Carbonetti. Pertussis toxin and adenylate cyclase toxin: key virulence factors of Bordetella pertussis and cell biology tools. Future Microbiol. Vol 5: 455-469. Mar 2010

[15] Hewlett, Erik. Pertussis: current concepts of pathogenesis and prevention. Pediatric Infectious Disease Journal. Vol 16(4): S78-S84. Apr 1997

[16] Aaron Kesselheim. Safety, Supply, and Suits — Litigation and the Vaccine Industry. The New England Journal of Medicine. Vol 364: 1485-1487. Apr 2011

Chickenpox Party-RSVP?

 

The infamous chicken pox party.
 
Even if you choose to vaccinate per the CDC’s recommended schedule (see 2013 update here), there is a likely chance you are aware of what a pox party is.
 
Here is the history, the rational and why I choose not to RSVP.
 
 
Welcome to the Party
 
 
“Chicken Pox Party” (aka Pox Party) - This term refers to when parents intentionally expose their otherwise healthy child to the varicella virus in hopes they contract the disease to promote natural immunity.
 
A person does not necessarily have to have a party. Some parents attempt to collect some type of infected material such as saliva, the elusive licked lollipop, or piece of clothing from the infected child/person.
 
However, it is unlikely that these particular methods will transmit the chickenpox virus effectively or reliably. This is because the varicella virus cannot survive for very long on the surface of such items. 
 
 
History
 
 
Forms of controlled inoculation are not new at all. Small pox and rubella are a few examples of diseases that where purposely transmitted in children earlier in history.
 
 
Chicken pox parties, in particular, were popular in the 1980’s prior to the national vaccination program included in the CDC’s list as of 1995. These gatherings would normally consist of family members or groups of children that play together/live near each other. These “pox parties” were among people that the families knew well.
 
 
The Purpose
 
 
If you decline the varicella vaccine for your child or if you aren't exposed to the wild-type strain, there is a risk (as with any disease), that your child may contract the disease later in life.
 
The purposeful infection of chickenpox is typically organized by parents on the main premise that contracting chicken pox at a younger age is less severe than if the disease is caught in adulthood.
 
It is well documented that complications in chickenpox are more likely to occur adults then in children. Considering that adults (13 yrs of age or older) only account for 5 percent of chickenpox cases each year, they account for a disproportionate number of deaths (55 percent).[1]
 
(On a side note, other diseases listed as being more severe later in life are measles and influenza. Flu-party anyone?)
 
 
 
RSVP, Regrets Only Please
 
While I can comprehend and appreciate the reasoning of a chickenpox party, I would not seek out and partake in one.  While we have chosen to decline this vaccine, there are several reasons why I would also decline this invite.
 
 
 
Reason 1
 
You cannot predict who will have a moderate or severe reaction.
 
Although it may be less common, children still have the potential to have a reaction from the varicella virus. Holding the full intention in making your healthy child sick with this virus, what if something did happen? 
 
 
Reason 2
 
A child depends on their parents completely to keep them safe and healthy. How is intentionally making your child sick fulfilling this obligation? Even if it is in hopes of the rare occasion they may contract chickenpox in adulthood and have a terrible, life-altering reaction from it.
 
 
One of the arguments people present concerning the use of vaccines is that they are unnatural. For me, a part of seeking out a disease to intentionally make a child sick carries something to be said about being unnatural as well.  
 
 
Reason 3
 
Is the significant risk real in adulthood?
 
 
Prior to the introduction of the varicella vaccine in 1995, there were approximately 4,000 annual cases of adult chicken pox resulting in 50 deaths from the disease.[2][3]
 
After the vaccine was introduced, there are approximately 1 in 2,254 annual cases in the United States (that’s 0.04 percent).[4]
 
 
Complications from adult chickenpox are still fairly rare considering 90 percent of cases occurring children younger then 10 years of age. This risk in adulthood largely accounts for adults with eczema, compromised immune systems, and those taking steroid medications.[5]
 
 
Bacterial superinfection of the skin is the most common serious complication of chickenpox in adults (but is still very rare).[6][7]
 
In my opinion, this does not give me a reason to deliberately seek out an infectious disease and hope my daughter contracts it in her youth. Moving from a 0.04 percent of potential risk to 100 percent potential risk doesn’t add up for me.
 
Reason 4 
 
 
The effectiveness of both the vaccine and wild-type chickenpox in youth to defer future attacks in adulthood relies heavily on the incidence of wild-type chickenpox within the community to act as boosters throughout life. This is noted in the package insert for the chickenpox vaccine as well as other peer-reviewed journals.
 
This means that if chickenpox is not common and you have been exposed to the virus while in your childhood (either by vaccine or naturally), you risk developing it again in adulthood or even suffering from the more severe disease of shingles.
 
Would this mean that once you have successfully given your child chickenpox, they would be reliant on attending chicken pox parties throughout their lives or require booster vaccines? That’s not something I would want.
 
 
Reason 5
 
Shingles.
 
By infecting a child with chickenpox intentionally, a parent is also placing their child at risk of suffering from shingles later in life.
 
Don’t get me wrong, this is a concern for children who contract chickenpox naturally and via vaccine administration.[8]
 
Here is the concern with Shingles:
 
The nationwide-mass varicella vaccination program has the medical community bracing for a major increase of herpes-zoster (shingles). This is, again, due to the lack of wild-type boosting properties of chickenpox that has been lost over the last decade.[8][9]
 
The highest increase of shingles has been seen among those 25 to 44 years and over 65 years of age. [8]
 
Shingles is a very painful rash that can turn into agonizing blisters. The painful (not itchy) rash can disrupt sleep and eating habits which has the potential in resulting in a condition called postherpetic neuralgia (PHN) which causes severe pain even when the rash clears. 
 
 

Are There Benefits?

 
 
Sure there are, and don’t get me wrong, I’m definitely not a proponent for the varicella vaccine. If I had to choose one over the other I would choose the wild-type strain naturally contracted.
 
 
However, we are in a precarious situation. Since the wild-type strain of chickenpox is extremely limited. When a parent exposes a child to the virus (which will lay dormant in their nervous system) in hopes of them having a more mild reaction then they would in adulthood - we are setting them up in an environment that does not offer boosters throughout life.
 
Again, they would then have two choices in adulthood - seek out more wild-strain chicken pox parties or get a booster vaccine (Chickenpox or shingles).
 
Another possible benefit of exposure in childhood would be that a woman gains the ability to pass on antibodies to her newborn which is more susceptible to adverse reactions from the virus (something that has not been documented on happening in vaccine induced immunity).
 
 
Conclusion
 
Every part of my being is passionate with making my daughters as healthy and happy as possible...the act of intentionally getting them sick “just in case” doesn’t seem to coincide with that (for me).
 

If my daughters became infected with chickenpox (or measles or whatever) naturally, I would welcome the implications that comes with it (natural immunity, stronger immune response, etc), but I couldn't devise a plan to purposefully infect my little ladies with disease. Nah, couldn’t do it.

References

 
[1] Schoenstadt, A. Adult Chickenpox-Diagnosing and Treating Adult Chickenpox. MedTV Website. Oct 2006
 
[2] Adult Chicken Pox on Disease.com Website
 
[3]   Schoenstadt, A. Chickenpox and Death. MedTV Website. Oct 2006
 
[4] Prevalence and Incidence of Chickenpox. Right Diagnosis website. Source statistic for calculation
 
[5] Infectious Diseases-Chickenpox. Medicalook Website
 
[6] Shingles and chickenpox (Varicella-zoster virus) – complications. University of Maryland Medical Center website.
 
[7] Nnama, H. (reviewed by D Fisher). Compications from Adult Chickenpox. Jul 2010
 
[8] Schmid, D. S., Jumaan, A., Impact of Varicella Vaccine on Varicella-Zoster Virus Dynamics. Clinical Microbiology Reviews. Vol 23 (1): 202-217. Jan 2010
 
[9] Brisson, M., Gay, N. J., Edmunds, W.J., Andrews, N.J. Exposure to varicella boosts immunity to herpes-zoster:implications for mass vaccination against chickenpox. Vaccine. Vol 20 Issues 19-20: 2500-2507. Jun 2002
 

 

A Critical Look at Rhogam and Rhesus Disease

There are a lot concerns that surface when a woman finds out she is expecting. If you happen to be a RhD-Negative mother then you have one more to add to the list.

When I was pregnant with both of my daughters I sought out information, and frankly, I was always left feeling like there must be more.

I gathered this information in the desire to help other mothers out there understand what it means to be RhD-Negative, what the Rhogam shot is and what it isn’t, and lend my personal experience.



Blood Type

To be able to understand what the RhIg (Rhogam) shot does and to determine if it is necessary in your circumstance, we must begin with this brief lesson.

A blood type is a classification used to express if someone has either the presence or absence of a specific antigenic substance on the surface of their red blood cells. These red blood cells are the most common type of blood cells in our system and is the principle means of delivering oxygen to the body.

There are a total of 30 human blood group systems according to the International Society of Blood Transfusion (ISBT). [1]

If you are a RhD-Negative mother then your blood cells lack a specific protein found on the surface of red blood cells called a Rhesus D (RhD) antigen. This is never a concern during a woman’s lifetime, until she becomes pregnant.

When a woman is pregnant it is probable that the baby will have a different blood type from her own and there is no concern with this unless the mother is RhD-Negative and the father is RhD-Positive. (if the father is RhD-Negative the concern is alleviated)

You can determine the likelihood of having a RhD-Positive child by reviewing the father’s parents blood type.

Your partner carries two copies of the gene that generates the D antigen (one from his mother and one from his father). If your partner has two copies of the D antigen (homozygote DD) which would happen if both his mother and father are RhD-Positive, then the child will definitely inherit one copy of the D antigen and will be RhD-Positive.[2]  (see chart to illustrate)

If, however, your partner only carries one copy (heterozygote Dd) there is a  50 percent chance your baby will be RhD-Negative like the mother. If this is the case, the baby will lack the RhD antigen and there is no apprehension on hazard to the process of sensitization.[2]

Two interesting points to note. There is a rather new technique developed in England where is it possible to determine the baby’s blood type by performing a genetic test on the mother’s plasma. Apparently, there is free-floating DNA from the baby in the mother’s blood.[3]

Another tidbit, an individual will most likely have the same blood type for life, but in rare occasions such as particular infections, malignancy or autoimmune disease the blood type will change due to the addition or suppression of an antigen (pretty interesting stuff ehh?).

 

Red Cell Alloimmunization (aka Sensitization)

**Now listen up - enough of the refresher, time to take notes!**

Let us assume, for the sake of 100% safety, that the baby is RhD-Postive.

When a woman is pregnant her blood is contained separate from the baby. The mother’s blood will run alongside of the placenta and the nutrients are absorbed and transfer to the baby through a membrane separating the blood (as known as the “placental barrier”). There is, however, a very valuable antibody (IgG) which is able to pass through this placental barrier which provides humoral immune protection to the baby (colostrum contains a high percentage of IgG). If the mother’s blood has never encountered the baby’s blood, then this antibody trucks along doing its job like normal – protecting the baby. However, it does carry potential concern for RhD-Negative moms.

Mother's blood does not mix with baby's - however,
benefical IgG antibodies freely move past the placental
barrier provided humoral immune protection.

**Initially, if in the event when the blood of a RhD-Negative mother and RhD-Positive infant mix, the mother’s body produces the IgM (not IgG which passes through the placenta) antibody in response to the red blood cells that appear foreign to her body (because they lack the RhD antigen). It is crucial to note that the IgM protein can not cross the placenta. It is in subsequent pregnancies, a repeat encounter with the Rh D antigen which stimulates the rapid production of the IgG anti-D. This antibody is then transported across the placenta and enters the baby’s circulation marking the red blood cells to be destroyed. [2][4][5][6]



When sensitization occurs, mother will produce IgM antibodies.
Remember, IgM will NOT cross the placenta - so the CURRENT
pregnancy is NOT AT RISK



Let me pause here and reiterate that sensitization occurs in the first pregnancy but the risk is only to the subsequent pregnancies. [2][4][5][6][7]

It is in subsequent pregnancies, a repeat encounter with the Rh D
antigen which stimulates the mother to rapidly produce IgG anti-D
which passes through the placenta.

How Sensitization Can Occur

Nearly 90% of sensitized cases occur during child birth (for example: when the placenta is forcibly detached from the uterine wall).[8]

Medical interventions during pregnancy that breach the uterine wall increase the risk of sensitization such as amniocentesis and chorionic villus sampling (CVS).  




Obviously, injury trama may result in the mixing of blood between the mother and baby. This is seen occurring in approximately 10% of cases.[8]

Other risk factors include miscarriage, abortion, ectopic pregnancy, external version (adjusting a breech baby), or a blood transfusion.

There is a vary rare sensitization model that can occur in blood type O Rh-Negative mothers (this is what I actually have). An immune response against A and B antigens has the potential to occur since they are widespread in our environment which could lead to the production of IgM antibodies early in life. Very rarely, IgG antibodies are produced.

You can have a doctor test your blood to determine if you have been sensitized at anytime in your life or throughout your pregnancy. A simple blood test is performed.

Rhesus Disease (or hemolytic disease of newborn, HDN)

The Disease

HDN is an alloimmune condition (alloimmune conidtions are seen in such instances when a person gets a skin graph or possibly after a blood transfusion). When the mothers IgG anitbodies pass through the placental wall, the antibodies break down the infants red blood cells and the baby may become anemic (anemia is when an individual has a low red cell blood count).

This disease can range from mild to severe.

Elavated bilirubin may develop as well after the birth since the mother is no longer aiding the baby in eliminating this waste product. Bilirubin is the yellow by-product of the breakdown of red blood cells – this is seen when you get a bruise and the yellow coloring develops, also is responsible for the yellow color of urine and for the coloring of jaundice.

Because of this, infants that suffer from HDN may show symptoms of jaundice which increases within 24 hours after birth.

If the case is severe enough, the liver, spleen and other organs increase in size because they are producing an over load of red blood cells to compensate the ones being destroyed. Disfunction of the liver may result.

Treatment

After the birth, treatment is dependent upon the severity of the condition. Ten percent of babies that suffer from Rh disease will have a severe case. In some cases Rh disease is so mild that it doesn't require treatment.

 

photo-therapy for jaundice

Postnatal Treatment- Phototherapy may be performed on infants showing jaundice in mild cases. A blood transfusion may occur for moderate to severe disease. Sodium bicarbonate may be given to correct acidosis.

Antenatal Treatment– Ultrasound will be performed during the pregnancy to monitor increasing blood flow. Early delivery may be recommended (usually around 36 weeks gestation). Blood transfusions in utero may also be performed.

Prevalence

According to the March of Dimes, Rh disease affects 4,000 infants each year and a mother with a RhD-Negative blood type has approximately 0.7 percent chance of giving birth to a baby that suffers from the disease. (This is without the anti-D injection aka Rhogam).[7][9][10]

If you receive the injection your chances decrease by 0.02 percent.) [7][9][10]

Rho(D) Immune Globulin

This medicine is recommended by the American College
of Obstetricians and Gynecologists (ACOG) to mothers with RhD-Negative blood and is routinely administered at 28 weeks gestation and within 72 hours after childbirth. It is also given in following a traumatic event such as a car accident or a fall.[11]

Anti-D Injection



Interesting to note that the half life of this injection is 23 to 26 days; if you receive the injection at 28 weeks then you would be susceptible again to become sensitized at 31 weeks pregnant. [11] [12]

  

The solution consists of IgG antibodies (from mothers that have been sensitized) that bind to and destroy the fetal RhD-Positive red blood cells.


Yes, you read that correct. The solution contains the very antibodies that we are attempting to avoid-the IgG antibodies that pass through the placental wall and enter the blood system of the fetus.


You see, according to the March of Dimes, it is not known exactly how RhIg works. In theory, the smaller does of IgG will elude the full force of the mother’s immune response to mount an attack on her child’s red blood cells. This will in turn avoid a mother becoming sensitized. Some of the IgG antibodies from the medicine will be transferred to the fetus and destroy a few red blood cells but it is believed to be not as many as if the mother was sensitized herself. [7] [10]



woman getting Rhogam shot



This medication has been given a Category C drug rating from the FDA. This means that animal reproduction studies have demonstrated an adverse effect on the fetus (or safety research is lacking) and that there are no adequate, well controlled studies in humans, but doctors believe the potential benefits may warrant use of the drug in pregnant women despite potential risks. There is a chance of fetal harm if the drug is administered during pregnancy.[13]


The RhIg is a derived from several human plasma pools. By using a method developed in the 1950’s, the plasma is filtered to eliminate bacterial and viral contaminates.

RhIg does have the potential to trigger an allergic reaction and carries the possibility to infect the mother with Creutzfeldt-Jakob disease (a degenerative neurological disorder that is incurable and fatal).
Live vaccines (such as the influenza vaccine) may interact with this injection according an article in Gold Standard (this may be within a 3 months time frame).[14]

Another vaccine currently recommended to pregnant mothers is the Tdap booster. I have not found any completed research regarding the effects of the combination use of Rhogam and this vaccine.

The medicine is not approved for use in children.

My Story

happy, confident and pregnant!



At 28 weeks pregnant with my first child I was written a prescription for the anti-D injection (Rhogam) by a real jackass of an OBGYN (lets just say he instructed me to get the shot while doubting me if I was sure if my husband was indeed the father of my baby…in front on my husband no less).


At that time, I was just beginning to learn more about vaccines and such. Most of what I was attempting to learn about at that point in time was how bad the epidural was going to hurt (since who actually gives birth naturally these days if they don’t have to, right?...ahhhh, to be young and naïve again).


From what I read, it didn’t make sense to get the shot until after the birth. I decided to decline the prenatal shot and decided to administer the injection after the birth only in the case if my daughter was born Rh positive. My daughter was born at 2 am  with type O negative blood, just like her mama and no shot was given.


With my second daughter, I declined both the prenatal and postnatal shot since me and my husband both decided that we did not want anymore children. She was born au natural in the living room.


If we did decide to have more children, I would have my blood tested to make sure I was not sensitized. If I was, then I would consider any risks (0.07 risk of Rhesus disease if the mother is sensitized). [7][9]


In hindsight, I am glad that I declined this medicine in my particular situation and circumstance. I also feel lucky to have the blood type that I do because it has provided my the opportunity to learn this information and spread it to those women in my similar situation.


This subject is close to my heart and I anticipate that it will help spread information regarding what educated options we have as RhD-Negative mothers.

Thank you for reading and sharing!!

Reference

[1] Table of blood groups. HUGO Gene Nomenclature Committee. Retrieved 2008-09-12.http://ibgrl.blood.co.uk/isbt%20pages/isbt%20terminology%20pages/table%20of%20blood%20group%20systems.htm.

[2] Causes of Rhesus Disease. NHS Choices. Nov 2011

[3] Hill, M. Blood test could save babies. BBC News. Oct 2002

[4] Bethesda

, D. Blood Groups and Red Cell Antigens (Chapter 4 Hemolytic disease of the newborn). National
Center for Biotechnology Information (US). 2005

[5] Beischer, N., Colditz, P., Mackay, E. Obstetrics and the Newborn (Third Edition). W.B. Saunders Company, Ltd., Philadelphia

, PA 1997. p226

[6] Letsky E.; Leck

I., Bowman J.Rhesus and other haemolytic diseases (Chapter 12-Antenatal & neonatal screening). Oxford University Press. 2000

[7] March of Dimes Website. Printable Articles about Birth Defects – Rh disease

[8]Bowman J et al . Rh-immunization during pregnancy: antenatal prophylaxis. Canadian Med Ass Journal . Vol 118: 623–627. 1978

[9] Lubusky M., Prochazka M., Krejcova L., Vetr M., Santavy J. and Kudela M. Prevention of Rh (D) alloimmunization in Rh (D) negative women in pregnancy and after birth of Rg (D) positive infant, Mendeley. Vol 71 Issue 3 Pgs 173-179. 2006

[10] Moise K. Management of Rhesus Alloimmunization in Pregnancy. Obstetrics & Gynecology (ACOG)

. Vol 112 No 1. Jul 2008

[11] The Official RhoGAM Website. Page Title: “Aligned with ACOG/AABB Standards

[12]Mintz PD. Rh Immune Globulin. Transfusion Therapy: Clinical Principles and Practice (2nd Edition). AABB Press. 2005.

[13] American Pregnancy Association Website. Page Title: “FDA Drug Category Ratings”

[14] Brigham and Women’s Hospital (Affiliate of Harvard Medical School) Website. Encyclopedia Section – Page Title: “Rho
(D) Immune Globulin Solution for Injection

Blood type picture from: Precious Passage Website (Rh Incompatibility) http://www.preciouspassage.com/d/rhIncompatability

Photo-therapy picture from: http://www.norwanie.blogspot.com  

Rhogam injection picture from : http://www.theanellos.com  

IgM is produced when mother becomes
sensitized.