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Microbiology 1.6 Dr.

Fontanilla
Case A & B Plenary June 26 2013

OUTLINE  the condition can manifest anytime between age of 24mos. until young
I. Case A (CVID) adulthood
a. Primary VS Secondary Immunodeficiency
b. CVID
c. Common causes of infection in the case Common causes of the infection present in the case
d. Types of primary immunodeficiency  Pneumonia (focused during the discussion)
e. Secondary causes of hypogammaglobulinemia o Etiologic Agents of Pneumonia (in children)
f. Management for CVID  Encapsulated Bacteria
II. Case B (Hepatitis B Profile)  Streptococcus pneumonia
III. Editor’s Quick Tip -Gram(+) cocci in chains
 Haemophilus influenza
OBJECTIVES -Gram(-) coccobacilli
1. None that I know..   Klebsiella pneumonia
-Gram (-) bacilli
CASE A SUMMARY
EDITOR’S NOTES…PLS REMEMBER
 The patient presented with the following:
o History of recurrent pneumonia and sinusitis  All cocci are Gram(+) except: Neisseria, Branhamella,
o URTI (Upper Respiratory Tract Infection) Veilonella and Moraxella
o Community acquired pneumonia by S.pneumonia  All bacilli are Gram(-) except: Mycobacterium,
o Diagnosed with common variable immunodeficiency (CVID) Corynebacterium, Nocardia, Clostridium, Lactobacillus,
Actinomyces ,Bacillus, Listeria ,and Erysipelotrix
Primary VS Secondary Immunodeficiency o PNEUMONICS: My COR-Ny but COLorful L-A-B LifE.
 Primary Immunodeficiency
o Related to genetics Types Primary Immunodeficiency
o Usually hereditary  Antibody Deficiency disorder
o Includes defect in function and suppression of the processes of o Agammaglobulinemia, includes:
immunity i. CVID
 It doesn’t automatically mean a decrease in number or -have subclasses w/regard to deficiency (IgG/ IgG subclass)
activity
 It is a decrease in function ii. X-linked Autosomal Recessive Agammaglobulinemia(XLA)
o It is a decrease in the ability to regulate immune -most common agammaglobulinemia
response. This is the reason that the inability to respond -marked by tyrosine kinase deficiency
to an infection and allergic reaction are considered as -thus, failure of early maturation of B-cells
immunodeficiencies
iii. Autosomal Agammaglobulinemia
o Problems can arise anywhere from an immature cell to a mature
committed cell iv. Class-Switch Recombination Defect (CSR)
-described as: ↓IgG but Normal or ↑ IgM
 Secondary Immunodeficiency o Clinical Characteristics
o acquired from substances or environmental factors  generally the result of the lowered levels and/or function of
o there is an underlying identified cause (drugs, other diseases or antibodies
other infection)  recurrent infections: e.g. of the upper respiratory tract, the
sinuses(sinusitis), skin, CNS (meningitis), and GI (diarrhea)
Common Variable Immunodeficiency (CVID)  Note that the problem arise due to the lack of IgA
 a genetic disease that mostly exhibits an autosomal dominant pattern on the epithelial surfaces and other Igs wherever
in adherence to Mendelian genetics they should be-there is no more barrier to
o if the god don’t favour your existence, you may even inherit this infection
disease in an autosomal recessive pattern *Recurrent Sinusitis (maxillary sinus) may lead to otitis media.
 manifested by low levels of most Ig classes From here the infection can progress to the CNS to result to
o usually affecting: IgG, IgA and sometimes IgM meningitis
 Mostly IgG
o humoral immune system is affected
 it is either from the lack of B lymphocytes or the lack of functional B  Cell Mediated Immunity Disorder
lymphocytes owing to dysfunctional differentiation and maturation o From problems with T-cells
o sometimes, the disease pathology is rooted on abnormal antibody  Recall that T-cells develop in thymus. Afterwards, they
function (so the problem can be of deficient IgG levels and go to the periphery
response)  The disorder here is in the differentiation and
 IgG dysfunction is usually attributed to the impairment maturation of the T-Lymphocytes
of B cell receptors (BCRs)  Defect may be partial or total
 diagnosis is made by checking IgG titers and correlating the said  Partial
laboratory evidence with history -only limited T-cell defects to predispose
 thus, there is an increased susceptibility to infections patients to frequent infection

Group # | Renan Notes Page 1 of 2


Microbiology Laboratory

-note that these include immune EDITOR’S QUICK TIP


dysregulation (NO supression) and allow  Just remember this picture and you’ll get the sequence of events in
autoimmune conditions to occur Hepa B Ag-Ab production
-Examples: DiGeorge Syndrome, Wiscott-
AldwichSyndrome, Common Viral Infection

 Total
-Not compatible with life.
-this people die very very very early..(King
Renan said.. )

Secondary Causes of hypogammaglobulinemia


 Neoplasms
o Most common cause
o Most often lymphoid(Lymphoma, Leukemia, Chronic Lymphocytic
Leukemia and multiple Myeloma)
 Treatment for Neoplasms
 Certain Environmental Chemical

Management for CVID


Image2. From MT notes
1. Immunoglobulin replacement Therapy (usually IgG)
2. Antibiotics are given to deal with infections

CASE B (HEPATITIS PROFILE)

Image 1.From Dr.Llanera’s PPT


Hepatitis B
 Sequence of events in Ag and Ab:
1. Ag either surface(HBsAg )or envelop Ag(HBeAg)
-Presence of IgG in titer could mean that you are a chronic
carrier
2. Body now produces Ab-IgM against HBcAg(Core Ag)
-in Hepatitis infection, IgM class increases first
3. Later now it is anti-HBs IgG that rise

*Some People don’t Seroconvert especially if 40y/o above

ICS TIPS given during the discussion


a. What is the anatomic structure involved?
-gross and histological
b. What are the biochemical and physiological processes
involved? (eg. Defect in feedback mechanism)

Group # | Renan Notes Edited By: Michael Sy  Page 2 of 2