SbbPerson

No DAT. There are no other details to the question. 
 
 I’m just trying to get people’s opinion on the question. Thank you 

Good luck with your course if you don't read around the subject.  I am certain you will pass with flying colours.

I have never heard of your references. The main texts for my course includes AABB technical manual by Fung, Harmening's Modern blood banking and transfusion services, and AABB's Standards for blood banking. I am only a part time SBB student, I work full time as a Medical Technologist. This is my final semester. You don't need to show me references I never heard of,  I am certain you are right.  Mom's with PARTIAL D (NOT WEAK D, WE DON'T TEST WEAK D FOR MOMS) can be typed as Rh positive, but still may form Anti-D when exposed to Rh positive red cells from baby(Modern Blood banking and transfusion services, Harmening, 7th Ed. p. 160). 

Yes, you are completely right Malcolm and others.  My experience is limited to common positive DAT results for OB patients, which is the ABO mismatch. Those positives are usually 1+ or weaker. That's why we always do a microscopic if we get a macroscopic negative.  I forgot that Rh mismatch DATs can go from 2+ to 4+ positive, because I hardly ever come across those.  Thank you. 

We do weak D testing on all cords bloods that test negative with Anti-D. Regardless if the mom is Rh positive or negative. 

I am a worker from/in the UK, but if TRM.40780 says, "Maternal RhIG candidacy assessment must include the identification of weak-D phenotype newborns", that is exactly what it means.  It doesn't say "should" instead of "must", and it doesn't say, "until you give up because you are bored, because you have never found one"!
Yes, such types are rare, but they do happen, and they can cause the mother to produce an anti-D (of sorts).  These antibodies are not usually particularly clinically significant in terms of further pregnancies - but the word "usually" is the important one in that sentence.
The only thing I would say is, WHEN you do detect a newborn who tests as weak-D positive, don't forget to test the mother too; she may also express the same weak-D type (but, depending upon your laboratory's policy, may not have been tested as expressing this type during the pregnancy), and, if she does, she doesn't need the anti-D immunoglobulin (which, remember, is a human-derived blood product, which may contain a novel blood-borne virus type about which we know nothing - YET).

Sorry, you must be fed up with me.  I know I am like a dog with a bone, but, although IgG is a monomer antibody, it does have a valency of two, which is why, occasionally, it can cause agglutination visible to the naked eye.  Notably, some examples of IgG anti-D cause agglutination at 37oC with D--/D-- red cells, with no potentiator.

Strange.  The Direct Antiglobulin Test has been around since 1946, and this is the first time that I have heard that IgG antibodies will NEVER cause agglutination to the naked eye.  IgG ABO antibodies cause agglutination visible to the naked eye all the time, as do many examples of IgG anti-M and other specificities.
Sorry, but I rather think you could be wrong here.

Apologies for not answering earlier.
No, I did not mean 12 cells in the screening cell panel.  I meant putting up 12 different antibody screens (12 different patients) each using a three-cell screening panel.  Putting up = testing

Sorry, that was a very old post, those tools are no longer available.

We, too, encounter Anti-M often using Gel.  Apparently, Gel is just acidic enough to enhance this pest.  
Because the enhancement is more about pH than temperature, whenever we suspect Anti-M, we revert to other methods to help determine it's 'etiology'.  Prewarming Gel does not change the pH issue so we don't do that. We can't trust that negative results in prewarmed Gel are truly due to a cold Anti-M or that the positive results aren't due solely to the acidity.  (Besides, if testing is done using a Blood Analyzer (e.g. Vision, Eflexis), the cards are pre-warmed anyway.)
So, we test the plasma using Prewarmed Tube Testing (e.g. PEG which has similar sensitivity for most antibodies sans the low pH).  If positive with that, it's a Warm Anti-M. 
We also test at Room Temperature using Pooled Screening Cells.  If positive, then it's a cold Anti-M. 
If negative with both Prewarmed Tube and RT Pooled O Cells, it's 'Anti-M (Detected using Gel Only)' ... just due to the pH drop, no clinical significance. 
Likewise, positive with both, it's an Anti-M with a broad thermal amplitude.
Do what you like with the results.
PS.  Testing positive with Anti-M reagent does not mean the patient can't make Anti-M (Patient may be Mg Pos).  Someone please correct/confirm that or am I working on old reagent data?  (Like we don't see Anti-T or Aquired-B anymore because the reagents are 'purer'.)

sorry for the late reply.  
What I meant is that one tends to put up a batch of antibody screens.  In the time taken to put up say 12 screens the cells can cool down enough for a cold anti-M in the plasma to latch on.  On the other hand, panels tend to go up one at a time (1 patient at a time) so cells have less chance of cooling down. (Always assuming the screening cells and the pane are from the same manufacturer and being tested in the same method)

I can't say that I am in the least surprised about this, given the patient's ethnicity.  There is a frequency of the D antigen of 99% in most Asian populations.

Why would the red cells of an individual who is Jk(a-b-) not react with Ulex europeaus?

What is the patient's Rh type?

I agree with Malcolm,  definitely looks like anti-H.

And we need to remember: patient is from Mumbai.

What you are identifying is almost certainly a strong anti-H in an Oh individual.  However, if the individual requires a transfusion, you will need to perform differential allo-adsorption (or something similar) to identify any other underlying clinically significant atypical antibodies (you can ignore any underlying Lewis antibodies, which are commonly also present).

Result:
Patient red cells + Ulex europepeaus = Negative 

Looks like it could be an Oh individual.
Try testing the red cells of the patient with Ulex europeaus.

I might add that the patient was Filipino. 

It could also be that insufficient RhIg was given in the first place.  How should I put this, umm, not all women are of the same size, and this makes a difference.

Yes, I am sure they probably order those other tests you mention. But the topic of this thread is on "why titers are not ordered on subsequent pregnancies". 

Just looking for any help  for taking the BB Exam.   anyone here who has taken it recently.
 
Thanks for the help!

Yes indeed different pH, different suppliers may explain such a behavior (some anti-M are enhanced with acidification of plasma).
In addition, Anti-M often shows dosage effect but I believe you have antigen M double dose cells on your panel too. 
What are the phenotype of the 2 cells reacting in screening and the one not reacting? Is your patient antigen M negative?   
It also exists the anti-M1 (the M1 antigen belongs to the MN CHO collection) that reacts with some M positive cells and stronger with M/N positive cells (M1 is expressed on M positive cells) and it can be, though rarely, produced by antigen M positive patients.