DISCUSSION OF CASE STUDY 3.2
Chris had pharyngitis, most likely caused by Streptococcus pyogenes or one
of a number of viruses. Taking throat swabs and culturing the bacterium
can confirm this. Antibiotic treatment is desirable to effect a rapid
cure and prevent the poststreptococcal sequelae, rheumatic fever and
glomerulonephritis.DISCUSSION OF CASE STUDY 3.3
All the symptoms are typical of whooping cough caused by Bordetella
pertussis.CHAPTER 4
DISCUSSION OF CASE STUDY 4.1
Immunoglobulin M is always first to be produced in an immune response
and is the predominant antibody of the primary response. The fact that
Maria had only IgM indicates that she has been exposed to this virus for the
first time and is likely to be infected. Such an infection may harm the baby,
particularly as Maria is in the first three months of gestation. Rubella infection
of an early fetus may cause fetal death or the development of congenital
rubella syndrome (CRS), which can cause mental retardation and impaired
sight and hearing. If IgG antibodies had been detected instead of IgM, this
would have indicated that Maria was immune to the virus and that the baby
is unlikely to be exposed to this microorganism. Maria should be counseled
as to the possible harm to her baby. The possibility of a therapeutic abortion
should be discussed.DISCUSSION OF CASE STUDY 4.2
Electrophoresis of the patient’s serum, followed by staining of the
electrophorogram, would show a thick band, referred to as a paraprotein, in
theF globulin region (Figure. 1.9). This would indicate myeloma, although
other tests would be needed to confirm the class of antibody being produced.
If this were an IgG myeloma, levels of IgG in the blood would be high, and a
highly sensitive assay would not be required. Radial immunodiffusion using
an antibody to IgG incorporated into the agar could be used to measure IgG
levels. Nephelometry would be quicker and could confirm the IgG secreting
nature of the myeloma.CHAPTER 5
DISCUSSION OF CASE STUDY 5.1
Repeated bacterial infections suggest a defect in humoral immunity. This
could be transient hypogammaglobulinemia, caused by a delay in the
production of antibodies. However, his small tonsils suggest the more
serious disorder, X-linked agammaglobulinemia (XLA). George needs to
have a full blood count and an assessment of his B lymphocyte count. His
immunoglobulin levels should also be measured to confirm a humoral
deficit. If B cell numbers are greatly reduced, then it is likely that he has XLA.
Molecular biological techniques would confirm mutations of the BTK gene.
If XLA is confirmed, George will need immunological replacement therapy
and antibiotics to control any bacterial infections.CASE STUDY DISCUSSIONS*(' W^dad\nd[Y^hZVhZ