You need to understand that by “contact” we only mean a small amount of blood, not 2 liters 😀 😀 If the mother is negative and the baby is positive, than all that is needed is one viable red blood cell to produce the specific response. If the situation is reversed, in the case of a contact it may kill a few red blood cells, but nothing alarming will happen

The blood of the baby and the blood of the mother NEVER mixes. What do you mean by saying a small rupture?

Ok, so what you need to understand is that the blood of the baby and that of the mothernever mix. It happens(though rarely) that they mix at childbirth. If what you are saying were to happen(but it doesn’t) the result would be death of the baby, the mother would be fine

If the blood mixes, the mother’s body threats the baby like its a foreign organ.

What I think is the matter of how many blood inside the baby. The diferences between mother’s and the baby’s blood in quantity maybe one of the factor that nothing happened when Rh+ mother have an Rh- baby

Maybe. But also think that, as I said before, the baby is like an organ of the mother. So the body prefers to kill the organ rather than killing the organism.

But, now I get a little doubt bout my statement above..I started to think that cells can reproduce in fast time…so soon or later they will be many also (not as man as mothers but I think it’s enough to create problems inside the mother’s womb)

It causes problems. If the baby dies inside the mother, she can even die.

Yes but not necessarily. Many babies are born dead

It is necessary. I’m not talking about dead born babies. Those babies die inside the mother, couldn’t be recognized and poison the mother’s blood.

So, the conclusion is the same then…if the mother and the baby have different Rh (whoever has Rh+ or Rh-) will cause death..is it like that?

No, Erytroblastosis fetalis only occurs if the mother is Rh- and the child id Rh+. We were talking about another situation there.

Oh, maybe it will happen in some occasion.. 😉 wow, if like that, this is serious problem…I should not marry western girl then, because it’s said that 85% of women in western area (america) are Rh- and I have Rh+ 😆

Preventing it is easy. A vaccine is used after the birth of the first baby. Don’t worry. Feel free to marry. 😉

Doesn’t the mother treat the child as a foreign object and send antibodies against it?

It is the situation for the second baby if the vaccine (as much as I know it is something that prevents antibody production.) is not used after the birth of the first baby. The first child is not under danger.

Ok, cool

Probably as IgMs are produced first , which cannot cross human placent [ i don’t know what happens about the other animals and how the babies are saved , does anybody know ???] So, even if the mothers body treates the baby as forign , it cannot make it die…
But please clear this one- why does ababy die when mother is Rh-ve and baby +ve???
Does the aglgutination formed in/near placenta / umbilical cord block nutient supply???
Please help… 😥

What is the effect of this phenomenon on natural selection [ today natural selection would not occur,as there are medicine to help, but if it were to happen then…] ???

hruusheekeish

Note that all the animal’s blood systems are not the same.

If it is the second baby, the mother can make the baby die. This is a the common result. But sometimes babies can born but there are some diseases at those babies.

At the first baby, there are no antibodies against Rh+, while birth, blood of the baby and the mother mixes and there are some antibodies produced, And those antibodies make the second baby die or born with some abnormalities. IgG can pass through placenta. Actually erythroblastosis fetalis can also be defined as the lysis of fetal RBCs by maternal IgGs .

[ I THINK ].But the mixing ammounts of maternal and baby’s blood are not enogh to make baby die even if all the fetal RBCs in that mixed blood blast . So, are you shure that these ammounts are large enough to make baby die…
Please help…

😳

hruusheekeish

Ok, here is exactly what happens if the mother is Rh- and the baby Rh+:
1st baby: No problem, the baby is healthy. But at birth the blood of the mother is mixed with that of the baby. It really does not matter how much blood is mixed, ONE red blood cell is enough to enter the mother’s circulatory sistem for her body to produce anti-Rh anitbodies.
2nd baby: If it is Rh+, than the antibodies created by the mother after she gave birth to the first baby will pass through the placenta and cause lysis…
Hope it is clear

It sure is… 😉 um, how about the 3rd? 4th? 5th?…….. 😆 😆

Same as the second

Please, try to understand my q.
🙄 See, the antibodies are present in the maternal blood and very less maternal blood mixes with the fetal blood . So, less feto- RBCs would be killed due to direct mixing of blood.
But i wonder if the antibodies may get flushed into the fetal blood-vessels near placenta due to pressure. If the pressure and offcourse the concentration of these Abs in maternal blood is large enough to have enough Abs flushed into fetal blood then fetus may die due to erythroblastosis. But all this is my hypothesis, is it correct??? 😕
Have u got my pt…
😥

Please help…

hruusheekeish

Man, blood does not mix, but some things, like nutrients and antibodies do cross the placenta

And the bold one mentioned above is the main problem whicg cause ErythroFeta.

So, enough no. of Abs get flushed into fetal blood due to pressure through the placental blood vessels and they lead to the erythroblastosis. But , one pt. is that the fetus must not be in a developemental stage to raise immunoresponse agaist the maternal Abs … otherwise less erythroblastosis will occur . Right???

hrushikesh

If you remember your anatomy 101, the immune sistem of the baby is not developed even at birth. The baby takes antibodies from the mother’s milk via pinocytosis vesicles

Some antibodies can pass. Not all.

What do you mean ‘some’? what kind of anti that can’t pass? the one that has huge molecule structure?

Huge molecule structures cannot pass. IMMSMR, IgG is the only one that can pass form mother to fetus by placenta.

Ow….placenta also have its limitation.. 😆 hey, you try to use ‘IMMSMR’ also…that’s good… 😆

I liked IMMSMR. 😉

Hey how about this..huge molecules can transport through endocytosis can’t they??do placenta do endocytosis?..anyway..next time if anyone doubt, just IMMSMR… 😆

I don’t think it can.

Hey Ozge, I’ve checked my book and I found it…yes, it’s true that only IgG can pass through placenta. The others (IgA, IgM, IgD, IgE) can’t pass. But IgM can be formed as the primary immune response.
IgA is the main immunoglobulin from secrets such as saliva, milk, etc…it protects the mukosa from bacterias and viruses.
IgE act as the fast response allergic because it’s contained in basophyll
IgD act as the certain antigen response…majority contained in B limphocyte.

hmms…why is it that only IgG can pass through?

small molecular weight.

I think its MW (molecular weight) is 400.000 AMQ (atom mass quantity)

It says that:
IgA :160,000* (Looks small too but it aggregates with higher molecular weights)
IgM: 900,000*
IgG: 150,000*
IgE: 200,000*
IgD: 185,000*

*: Daltons approximately

IgA gets in together with milk from their mom..so, no need placenta then.. 😆

Yeah. But I haven’t seen a mother suckling a fetus. 😆

Maybe after this diagram:
Embryo – fetus – [born] – baby

That’s when they get the IgA.. 😆

Good diagram. 😉

What is the mechanism for IgG to get into the fetus?
Probably it is forced into the blood of fetus though the fenistrations in the maternal capillaries , so the size , shape and molecular wt. all matter.

M I RIGHT???

hrushikesh

Or maybe they can be carried out through endocytocys and exocytocys….

From a bleeding during the delivery. So far it was stated that IgG come into fetus via maternal-fetal circulatory system and it was not true.

From what i know IgG do come into the fetus via the circulatory sistem… That is the reason why the child dies in the first part of pregnancy. If what you say were true, the child would live.
It is true that blood cells do get inside the body of the mother at the first baby via bleeding during delivery

Hey, I’ve read that beside IgG that comes to the fetus, There’s also IgM which can be activated if there’s any antigen infection.

In erythroblastosis foetalis, the first baby is usually safe and live, because first, the contact with IgG will be happened just right when it has just been delivered. Second, the level of that IgG is just in a little number. In the second and subsequent pregnancy the level will increase and yes it will pass through placenta.

victor: IgM is the ‘ancient’ immunoglubulin family. All that fetus has is IgM. In the development, further exposure to antigens, it will switch into IgG, IgE, or IgA depends on the purpose. IgM also appears in acute disease, after few hours or days it will switch into, mostly IgG. The clinical examination of IgM and IgG can be used to determine whether the patient is still in acute phase or chronic phase of her/his disease, respectively.

Hmm…it’s just like IgM is the master of all Igs…(maybe because of it’s pentamer valency 10 structure)

It is NOT a master, it is just an initial, an ancient type. IgM cannot do anything if it doesn’t switched into proper IgG, IgE, or IgA. Those three types are more professional on their own purpose.

Related to the IgE activity, why some people are more sensitive to alergens than other? Does this have to do whith the quantity or the activity of basophylls.
Some allergies can be kept under control with certain vaccins. Does anyone know if theis vaccins contain IgE?

I am not sure IgE is contained in basophil. Immunoglobulins are produced by B cells… 😉

Ok, sorry about that 🙁 .
But can you answer my question? Why some people are more sensitive to allergens?

Maybe produced by B-cells but complexed with basophils membrane.
Oh, yes, IgM also can be switched into IgD….so, that’s why immature B-cells contain many IgM….because they’re still not a professionals yet.. 😆

Naah, IgD never exists alone, and it’s not a switched version from IgM, IgD always present with IgM, because there is no switching point from IgM to IgD.

This is a simple schematic of the switching points:

—IgM—IgD—*—IgG—*—IgA—*—IgE—

* = switching point

IgM/D -/-> IgD
IgM/D —> IgG
IgM/D —> IgA
IgM/D —> IgE

victor: IgE is produced by plasma cell and being attached to cells which have a receptor for it, called FCεRI, such as mast cells, basophils, eosinophils 😉

Allergens actually are harmless antigens (innocuous), e.g. pollens, clothes, chitin, etc, but to certain people, they become harmful and even deadly things. Allergic reactions occur when an individual produces IgE in response to such innocuous antigen(s), and subsequently encounters the same allergen(s). Their ‘sensitive’ IgE, which mainly attach on mast cells membrane surfaces, recognize those antigens and then stimulate mast cells activation and degranulation.

And thus the release of some mediators of inflammation, including histamine.
And anti-histaminic drogs are the only drugs that can help….in a way 🙁

Do you realize that the topic of this thread is changed now? 😆

Yes, I do. I just got caried away I guess…. 😳 🙂

I think I contribute on this changing too 😆

I’ll change it back then. lol. Who coined the term “Erythroblastosis Fetalis”?

lol – sudden change back to the right track again lol

…As recently as 1946, erythroblastosis fetalis, or hemolytic disease of the newborn, affected between 0.5% and 1.0% of fetuses and newborns in the USA. It had a 50% mortality as well as significant neurologic morbidity in many survivors. Prior to 1936, four seemingly distinct neonatal syndromes had been identified: fetal hydrops; fetal erythroblastosis with massive red-cell proliferation in fetal organs; icterus gravis familiaris, a severe neonatal jaundice that often affected subsequent infants; and severe anemia in surviving infants who had not had edema or striking jaundice, which was simply called anemia of the newborn. Based on histological and hematological similarities and the familial occurrence, Diamond, Blackfan, and Baty put forth their unifying hypothesis that these four syndromes were all manifestations of an unknown single underlying disease process. They designated all of these neonatal syndromes “erythroblastosis fetalis”

For complete article, click HERE 😉

Good job, Who was the first person to be diagnosed with it?

Is it a homework? 🙄 😆

Don’t say homework b_d_ or it will become a business part??? 😆

I don’t think you can be diagnosed with rytroblastosic foetails, because that means you died at birth 😆

lol. just made something up.

The mother CAN NOT be Rh + and the baby Rh -, simply because the Rh neg allel is recessive! 😛

is the mother is Dd(Rh+) and the father is both Dd(Rh+) then 1/4 of children will be dd(Rh-). Do a punner square 😉

Even if an Rh° baby developed antibodies to his Rh+ mother at the time of birth there would not be enough time to produce a clinical effect in the mother. This would be the same with subsequent pregnancies, so the Rh+ mother would never develop an Rh incompatibility problem.

The Rh° babies will have been sensitized to Rh+ blood and might have a stronger reaction to it if transfused with it.

The antibody response is to the rh markers. If you are rh-negative, those markers are "foreign," so once exposed you produce antibodies to them. If you are rh-positive, exposure to rh-negative blood doesn’t give you something to make antibodies to.

I have to disagree about blood mixing, though. The tearing free of the placenta mixes exposes the mother to the fetus’ blood pretty reliably. There are also many instances of what would otherwise be minor exposures during pregnancy, as well as cases of maternal rejection of rh-positive fetuses in a first pregnancy.