Avidity tets of antibodies IgG & IgM

Doctor , Please do not equate presence of  IgM means acute maternal / foetal infection Are U in dilemma when Lab reports come as  IgG titer is high & so also IgM (in Rubella or say CMV)  and you as care provider seriously consider termination or drug therapy ?? Is it a recent infection or past infection white no active tr is warranted?? ???    Obstetricians are often confused once IgG titer is high & raised IgM-more so if there is demonstrable foetal anomaly Sonologically at a later date:--It is difficult to confer some abnormalities of foetus, God forbid if appear later in this case, that whether such abnormalities (if at all appear in this case) - were due either to CMV or to Rubella with certainty:

Reasons are:--Firstly, in our country CMV IgG antibodies are as high in 95% +ve of all women of child bearing age. Though presence of IgG antibody do not guarantee against re-infection.

 Secondly :-One cant equate cong malformations due to  re-infection as re-infection rate is quite high in our country and in such cases a low IgM antibodies have less predictive value( in re-infection cases-I mean).What, then  is solution? Therefore, molecular methods of diagnosis are more relevant.

Please do not equate presence of  IgM means acute maternal / foetal infection:- Mere presence of high titers of IgG Rubella /IgG CMV in pregnancy do not always mean that the  concerned foetal abnormities (if at all occur at all)  were due to acute  viral infection acquired in the pregnancy. At best one can suspect acute viral infection, if IgM is very high. Because in most cases prepregnancy serological status remain unknown to us. Such high titers of antibody might have present earlier i.e. prior to pregnancy. Only an avidity case can prove whether the viral infection was recent or not.

What is meant by avidity test of antibodies? The terms avidity or “functional affinity” imply to quantify the net antigen –binding force/ capability of population of antibodies. IgG antibody affinity is now commonly done in many centres if India nowadays. This will diagnose the and differentiate between reactivation, re-infection, or primary infection. The high avidity rules out recent infection of less than 4 months even if IgM abs is present.  Therefore low avidity is not an absolute indication of recent infection. High avidity with 10% positive predictive value to rule out acute infection.

 Honestly speaking diagnosis of acute CMV in preg. Is very difficult to substantiate: -- One should remember acute primary/ secondary- reinfection of mother by CMV do not equate to “foetal transmission” not to speak of “foetal affection “. And institute anti-viral therapy. But in this case as so many soft markers were present there was no hesitation indeed laities are. The transplacental migration rate of primary CMV in first trimester is only 30-40% but rare transplacental migration if pri infn occur in 2/3 rd trimester.

 Confirmation of CMV possible by PCR mainly not by antibody testing only:-Many of us will insist on amniocentesis to confirm presence of CMV virus by PCR. But then again intrauterine transmission of virus does not always mean affection of foetus. Usg is of little help to confirm presence of virus and then discuss the options to the couple.

Prevalence of CMV in pregnancy:--An estimated 0.4 to 2.3% of all live born infants will exhibit CMV virus in their cord blood. CMV is the most common viral infection cause of cong. viral infection. Most of the malady appear later say after one year-e.g. microcephaly, chorioretinitis, poor I Q., cognitive deficits do appear in infancy.

Viral infection & pregnancy loss: - In addition to CMV –the other virus responsible for foetal loss is Parvovirus B19 which is least considered in D/D of foetal demise. In some courtiers I V. administration of human immunoglobulin to pregnant mother with primary CMV infection have been shown to help protect foetus to a great extent.

Maternal infection in pregnancy does not mean all foetuses will be affected:--Diagnosis of CMV: - Transmitted by foetal leukocytesà affects placenta; tissueà shedding into liq. --> swallowed by the foetus-> foetal viraemiaà amniocentesisàvirus can be detected by PCR.

How important is H/O previous confided CMV infection? Does previous immunity is enough to prevent reinfection in pregnancy? Surprisingly, many believe that preexisting immunity to CMV do not mitigate the outcome of congenital infection of CMV. I do not know how far this is true. The problem is that most affected foetus appears sonograpghically normal though serial scanning can help. But by the time abnormal findings are evident, say 32 weeks, then termination can’t be offered neither foetal therapy will work.

The usg findings are not unique to CMV infection only:--Limitations of USG in diagnosing CMV:-Though hepatosplenomegaly, pleural effusions, FGR, intracranial calcification, Ventriculomegaly, microcephaly, cardiomagaly, pericardial effusion, echogenic bowel ,hydrops sometimes do appear due to acute CMV but all such sonological markers  are nonspecific USG markers of CMV.    Therefore in your case detailed investigation on foetal renal agenesis, cardiomagaly, pl. effusion is warranted preconception ally.