Académique Documents
Professionnel Documents
Culture Documents
This exam must be uploaded to Canvas as a Google Doc no later than Monday, November 6th
at 11:30 AM. Due to the generous time allotted for completion, any exam received after this
deadline is subject to a 50% grading penalty.
Please completely and directly answer the following questions as a work group. In class notes,
supplemental postings to Canvas, and your textbook are excellent resources to help get you
started, but you will need to perform outside research to provide quality answers for most of
these questions. Your outside sources must be:
Scholarly and credible; this includes other textbooks, journal articles, content from reputable
organizations (CDC, WHO, Pasteur Institute, etc.). Use of non-credible sources will be factored
in to your grade.
Properly cited via in-text citations and a formatted reference page (APA or Council of
Science Editors format preferred). No direct quotes are permitted in your answers; all material
should be appropriately paraphrased.
Please feel free to consult with me at any time if you have any questions about guidelines,
formatting, or clarification of material. Given the nature of this exam, I am unable to tell you
ahead of time if you have enough material to answer the question, if your answer is correct, etc.
I also strongly suggest that you develop a teamwork contract as soon as possible to help you
fairly divide the workload across your group (provided on next page).
Please note that plagiarism will not be tolerated in this assignment. Your answers will be
submitted to TurnItIn.com and evaluated for similarity to source material and to material
submitted by other students. Suspected instances of plagiarism will be reported to Academic
Affairs and will result in severe grading penalties and loss of groupwork privileges.
IMPORTANT NOTE ON GRADING: Demonstration of group effort and peer Team Member
Performance Evaluations will be taken into consideration for individual exam grades. In order to
track individual effort, each group must complete the Teamwork Contract on the next page and
perform all work within this Google Doc. In order to earn the privilege of the group exam score,
each student must 1) fulfill all obligations as listed on the Teamwork Contract and 2)
demonstrate a level of effort expected for students in a 200-level course. Failure to contribute
equally to the group effort will result in grading penalties.
Teamwork Contract (developed in part from Team Dynamics by Kolb and Francoeur)
Mission Statement:
Who is your point person to contact instructor, submit assignments, etc.?
Alexandra Barbera
How will you ensure members are meeting their personal objectives?
We will ensure the members are meeting their personal objectives by meeting as a
group and discussing progress.
1. Answer the following questions regarding the adaptive immune system.
a. CASE STUDY. You are a physician assistant working in a primary care office. One of
your patients is a 10-year old boy who is in the office because his parents are concerned about
his recurring gastrointestinal and upper respiratory tract diseases. Over the last few years, the
child has suffered repeated bouts of diarrhea and various upper respiratory infections. After
youve confirmed that the child has received all childhood vaccinations with no reported side
effects, you are suspicious that the child may have some underlying cause for his repeated
bouts of illness. Both parents are healthy, and the boy is their only child. You do learn that the
boy has two uncles living in California who also have severe recurring bouts of sinus infections
You suspect that your patient may have some underlying disorder of the immune system, so
you order some lab tests to determine the amount of IgG antibodies the boy has against
childhood vaccines and a complete blood cell count. Upon reviewing the lab test results, you
learn that the boy has normal IgG and IgM levels but no detectable levels of IgA. You consult
with the family, deciding that the best course of action is to treat the boys future infections as
they occur. You do not recommend that the boy undergo therapy to replace the missing IgA.
i. (2 pts) Why did you need to know if the boy received all of his childhood vaccines?
In active immunization, like the type of immunization given during childhood, the
body is injected with an inactive or dead antigen (1). The immune system uses these
pathogens to form antibodies and T cells that are specific to that antigen and keep
record of how to attach and destroy it (1). If the child had never received his vaccines,
his body would have had no way of making an antibody for the pathogens he is being
vaccines?
IgM is the first antibody that is produced by the body in response to an infection
while IgG is produced after the fact to specifically target a certain antigen (2) . By a
clinician looking at the levels of IgG and IgM they are able to distinguish whether the
patient has previously had this type of infection in the past. This is able to be done
because high levels of IgM indicate that the infection is new because this is the bodys
general first response to new antigens, however if there are high levels of IgG this
indicates that the body has already had a run in with this disease because it is able to
activate its already formed memory B-cells to differentiate into antibody secreting
plasma B-cells creating a specific antigen response that would be IgG in this scenario
(1).
iii. (2 pts) What important information did you gather from learning that the two uncles have
The information pertaining to the two uncles having similar disease symptoms
allows the practitioner to lean towards the idea that this immune disorder was inherited
rather than developed during his lifetime. Primary immunodeficiencies have a genetic
basis and present in childhood (1). Because the patient is a child and has been
pathogens being enteric bacteria and viruses (1). These pathogens usually infect the
gastrointestinal tract, nasal and eyes (1). The uncles presented with GI and sinus
infections. The uncles symptoms correlate with that of selective IgA deficiency which can
be assumed that their condition is also that of a primary immunodeficiency. The fact that
the 10-year-old boy and the uncles have similar symptoms characteristic of primary
immunodeficiencies, specifically IgA deficiency, support the idea that the disease was
iv. (2 pts) How does the IgA deficiency correlate with the sites where infections are
occurring?
IgA is secreted onto mucous membranes to fight off pathogens that try to enter
the body (1). The upper respiratory and gastrointestinal tracts are two major portals of
entry to the body and are lined with mucous membranes, so a deficiency of IgA would
directly correlate with an inability for these parts of the body to fight off infection(1).
Additionally, bacteria with polysaccharide capsules can not be neutralized by the innate
immune system because they cannot be phagocytized (2). Therefore the only way to
fight off these kind of infections is for the bacteria to be targeted by either complement,
v. (2 pts) Why would any attempt to replace the missing IgA antibodies be unsafe?
There have been correlations between B cell defects that affect maturation and
IgA deficiencies found in patients that have family members also suffering from IgA
deficiencies (3). IgA replacement therapy is unsafe because it can trigger anaphylaxis in
a patient that has IgG (3). IgG can act as an anti-IgA antibody that would attack the
foreign IgA. That is why this immunoglobulin replacement therapy is only considered for
patients that dont have IgG or IgE antibodies that would attack IgA (3).
b. (4 pts) IgM and IgG play major roles in the humoral immune response. Why do you
suppose a two antibody response system is used for the human immune system?
A two antibody response is used in the humoral immune system to help the body
buy time to elicit a proper response. The IgM antibody is the first immunoglobulin
bypass T-cell activation of B-cells (2) . This immunoglobulin type is a very generalized
antibody that has 10 antigen binding sites that look for certain pathogen factors such as
bacterial capsules and polysaccharides (2) . IgM is also helpful in the first response
because it is able to initiate the complement pathway starting the inflammation process
allowing the body to begin to control infections (2) . Overall this process buys the body
time to begin the process of isotype switching and this is where B-cells once activated by
the proper T-cell mass produce specific antibodies to rival the infection. In this case IgG
antibodies are being produced, which are the most abundant antibodies found in the
blood plasma (2) . IgG immunoglobulin, once produced, assists with inflammation and
opsonization of foreign microbes in body tissues. The IgG antibody is the more specific
antibody to that microbe while IgM is the more general response for the body.
c. (4 pts) Why do T cells need to bind to both antigen and to MHC receptors?
T cells only bind to antigens that are already present on the surface of another
cell, these cells are known as antigen-presenting cells (APCs). The surface proteins on
the APCs are called major histocompatibility complexes (MHCs). MHCs help to
distinguish between antigens that are created by the body and those that are foreign (1).
Another important structure that is vital to T cell binding are the T cell receptors (TCRs).
These are distinctly different because they are antigen binding molecules that strictly
bind peptides and do not bind with a free-floating antigen (1). In order for TCRs to bind
to an antigen, the antigen must be attached to the MHC with an APC. It is necessary for
T cells to bind to both antigen and to MHC receptors to elicit an immune response.
Without T cell activation, the infection can spread and become devastating.
d. (5 pts) You are treating a patient who has AIDS. This patient has a low TH cell count.
Why does this patient have difficulty in making antibodies? How does this patient make any
antibodies at all? Do you recommend that this patient be vaccinated against influenza? Explain.
When treating a patient with AIDS it is important to understand that this individual
has well below normal levels of T-cells (below 200). T-cells are made in two initial
versions, CD4 and CD8, T-cells that display the antigen CD8 deal with cell mediated
immunity while T-cells that present the CD4 antigen work with antibody secreting
immunity (1). CD4 T-cells or helper T-cells come in five different versions making low
helper T-cells very important to an individual. The first type of helper T-cell, TH O, is the
base that can then be made into the other forms such as TH1, TH2, TH17, or regulatory
T-cells commonly known as Tregs (1). Each T-cell version is produced depending on the
type of immunity the body wants to use. When trying to figure out what version T-cell is
needed the body relies on cytokine production and depending on the type of cytokine
present tells the body what version of T-cell needs to be formed (1). If an AIDS patient
has a low number of helper T-cells they will have trouble being able to produce the
necessary versions of T-cells that stimulate B-cell activation and antibody production.
With this being known the patient is now vulnerable to microbes/viruses that normally
would not be a problem for a healthy individual and these microbes are known as
opportunistic pathogens. Even though the helper T-cells levels are low, affecting their
ability to produce antibodies, they are still able to produce some antibodies because
there are still some left in the body. Since there are still some Helper T-cells that are able
to illicit a response it is advised that these patients are vaccinated against influenza. With
their immune system being in such a vulnerable state it is suggested that an inactivated
influenza virus is used. For certain patients who have severe versions HIV like AIDS it is
advised that before receiving the flu shot the patient undergoes p
re-exposure
chemoprophylaxis, which is a common antiviral drug that will help with regulating the spread
receive the nasal-spray version of the flu vaccine because this vaccine does not use a dead
version of the disease but rather a weakened alive version that may still cause problems in
immunosuppressed patients (4). Immunocompromised patients should be given the flu shot
because it can help the bodys weakened immune system prepare for the influenza virus. If
an immunocompromised patient is not vaccinated ahead of time and they contract the
influenza virus they stand very little chance of fighting that virus off and it could possibly
e. (4 pts) You are required to obtain a tuberculosis test in order to work at the hospital. You
This test injects 0.1 mL of tuberculin purified protein derivative into the inner
forearm skin using a tuberculin syringe (5). The injection should initially produce a pale
raised area of the skin (5). The site is observed 48 hours to 72 hours later to determine if
there is a reaction (5). The purpose of the test is to determine the degree of
hypersensitivity the body has towards the antigen (6). The bodys T cells that have
lymphokines to cause a local reaction after 24 hours at the site of injection (6). No
reaction after 48 hours concludes that the person does not have the disease, or not
enough time has passed for the body to react with the test (6).
ii. You complete the test, and unfortunately the test comes back positive. What does this
A positive test can mean a variety of things, but one thing is known for sure:
additional tests need to be conducted. A red and peeling test site may be due to a type
vaccination for tuberculosis (1). The size and the type or reaction can also play a factor
in what the test result means. If the site of injection appears to have bubbles or tissue
necrosis, the patient is likely infected with tubercle bacilli (6). If the size of the reaction is
five millimeters, the person may have previously had and recovered from tuberculosis,
that is ten millimeters of reaction is seen in people from high-risk countries, people
Fifteen millimeter reactions can be seen in any person including those with the BCG
test result may also have TB in the latent form and not an active tuberculosis infection
(6). The test may also display a false positive if the test was not administered correctly or
the patient had been infected with a mycobacterium species that did not cause
tuberculosis (6). Additional tests, such as a chest x-ray, sputum analysis or blood test
tuberculosis is in the form of a blood test. An Interferon Gamma Release Assay (IGRA)
is a blood test that measures how strong a patients immune system reacts to the
tuberculosis bacterium (7). There are two IGRA tests currently approved by the United
States Food and Drug Administration that are available. These tests are the
QuantiFERON-TB Gold In-Tube (QFT-GIT) test and T-SPOT.TB (T-Spot) test (7). In
these tests, blood is collected into special tubes and sent to the lab and analyzed (7).
IGRA tests are effective because infected patients white blood cells will release
interferon-g when mixed with M. tuberculosis antigens (8). The QFT-GIT test measures
the IFN-g concentration while the T-Spot test measures the number of IFN-g producing
cells (8). The tuberculosis antigens used in both tests are ESAT-6 and CFP-10, as well
as, TB7.7. in QFT-GIT tests (8). Positive results indicate that the patient has been
infected, but more tests would need to be conducted to determine whether he/she had
latent or active tuberculosis for the correct treatment plan (7). Negative results indicate
that neither a latent or active tuberculosis infection is likely (7). Advantages of IRGA tests
are that it only requires a single visit, results within 24 hours, and the BCG vaccination
does not cause a false positive like a skin test would (8). These tests do not determine if
the tuberculosis is latent or active and should not be taken in addition to the skin test (8).
was a low risk patient, a skin test would be recommended. If a patient is at high risk for
infection a blood test may be recommended if their skin test came back negative (9). A
blood test would be recommended for those who received the BCG vaccine as a
false-positive reaction would occur in a skin test (9). Skin tests are recommended for
patients less than five years old (8). Another factor involves the availability of the tests
as well as their respective costs. If one test was more readily available or cost effective,
a. (4 pts) Discuss the concept of immune tolerance. Why is this system necessary? What
Immune tolerance happens when T cells are essentially deleted from the
thymus when T cells react too strongly to an antigen (1). T cells first enter the thymus to
are allowed to live. This is due to the weak relationship between the TCRs and the MHC
(1). In negative selection, abnormal T cells are deleted. They are deleted because they
react too strongly to the MHC proteins (1). This system is necessary because if they
werent deleted, they would start to attack the MHC proteins regardless of the antigen
bound to it (1). When there is no self immune tolerance, the body will begin to attack
itself. When the body starts to attack its own self, it is called an autoimmune response
(1).
b. (5 pts) You are an obstetrician treating a female patient who is carrying a fetus that
developed hemolytic disease of the newborn. The patients blood type is A+, but she once
received a transfusion of AB+ blood while on a volunteer service trip abroad. The blood type of
pregnant and gives birth to an Rh+ baby (1). Similar to the way that you do not have an
allergic reaction the first time you are exposed to an allergen, the first Rh+ child that a
mother gives birth to will not experience incompatibility disease (1). Only the subsequent
Rh+ children will be in danger because when the first childs blood enters the mother's
blood during birth, the mothers immune system produces IgG antibodies and memory B
cells against Rh+ blood cells (1). It is these IgG antibodies that will be produced by
memory B cells, cross the placental barrier, and lyse the blood cells of the Rh+ babies
ii. Fully explain why the fetus developed this condition even though another type B+ fetus
When the mother received a transfusion of AB+ blood, her immune system
recognized the B antigen as foreign (1). This recognition triggered the production of
anti-B IgG antibodies and memory B cells. The other mother has not been exposed to
any kind of type B blood cells before, so her immune system does not have the memory
B cells that are producing the IgG antibodies but rather just generic IgM anti-B
antibodies. In order for a fetus to develop this condition, the mothers blood would have
had to have been exposed to the incompatible blood type before so that the mother
would have memory B cells ready to produce IgG antibodies upon a second exposure,
because IgG can cross the placenta(1). The other mother, who has not had a
transfusion, would also have anti-B antibodies but they would be mostly the IgM variety
During development your T cells are being educated to not attack self cells, by
Some of the T cells in your own body can recognize the MHC complexes on foreign cells
from a donor human (1). These allotypic MHC proteins appear to be a self cell that is
infected with a pathogen (1). This triggers Cytotoxic T cells to come and destroy the
tissues that are presenting these allotypic MHC proteins as if they were ridding the body
iv. What is the molecular basis for the four ABO and Rh blood groups?
The ABO blood group utilizes four carbohydrate antigens in which the sequence
of oligosaccharides on the red blood cell surface (10). The antigens are produced by the
ABO gene in three main allelic forms (10). These forms are A, B, AB, and O types that
arise from the H antigen precursor (10). The A and B antigens antigens arise because of
amino acids (10). The A transferase that makes the A antigen is the O allele of the ABO
gene codes for an inactive glycosyltransferase leaving the initial H antigen intact (10).
People that have Type B blood have the anti-A antibody in their blood and people with
type A blood have the anti-B antibody(1). In the presence of an incompatible blood type,
the antibodies bind to the antigens on the incompatible red blood cells and destroy the
cell (1). This is the reason why people with type A and B blood cannot donate blood to
the other type (1). Type AB blood has neither antibody but both antigens so they can
only give blood to another AB+ blood type (1). Type O blood had both antibodies but
neither antigen so they are the universal donor but can only receive blood from other O-
(1).
A person becomes sensitized to the Rh factor if they are Rh- and their blood
encounters Rh+ blood for the first time (10). This can happen during a blood transfusion
and cause hemolytic transfusion reaction (10). It can occur during pregnancy and cause
hemolytic disease of the newborn, particularly in a mothers second pregnancy since her
blood was exposed to the Rh factor during the first birth (1). Other than these two major
instances this exposure can occur any time Rh+ blood contaminates Rh- blood. The
pathophysiology of this exposure is that the Rh- blood is making anti-Rh factor
antibodies that attack and lyse the red blood cells containing the Rh protein and cause a
c. (4 pts) You are treating a patient who works at a mushroom farm. The patient suddenly
developed swollen lymph nodes, hives, and edema after several months of working at the farm.
i. What is your diagnosis for this patient? Fully explain the condition.
This patient has a type I hypersensitivity. The average time of a reaction onset is
2-30 minutes after exposure (1). This would explain the sudden onset of swollen lymph
nodes, hives and edema. In his time working at the farm, he would have been exposed
to the antigen once before which would have sensitized him to the antigen by producing
antigen specific IgE antibodies, without causing symptoms (1). The second exposure to
the antigen is what would have actually caused the hives, edema and swollen lymph
nodes when coming in contact with IgE-coated mast cells (1). The severity of the
route of entry, and the number of sensitised mast cells present (1). The allergen, or
antigen, in this case is unknown, but may be a variety of things can cause a type I
hypersensitivity reaction. Allergy skin testing can be performed in order to determine the
The antigen itself in the first mediator in the reaction process. The antigen comes
into contact with the second mediator, IgE, which coats mast cells (1). The mast cell
degranulates because cAMP levels are lowered, and releases histamine, prostaglandins,
leukotrienes, and chemotactic factors (1). The hives the patient is experiencing is due to
cause itching, and loosen endothelial junctions of blood vessels to cause vasodilation
and permeability (1). The dilation and permeability of the blood vessels causes fluid
accumulation in the tissues resulting in raised welts, or hives (1). The leukotrienes and
prostaglandins also play a role in vasodilation and permeability (1). The combined effect
of these three mediators causing the permeability of blood vessels increasing fluid
accumulation in the tissues has the potential to cause edema in the patient (1). Swollen
lymph nodes occur during type I hypersensitivity due to the detection of an antigen. This
causes the antibodies that bind to the antigen to begin to line along the walls of the
lymph vessels, which further causes the inflammation in the nodes (11).
(1). The skin test is an accurate and quick procedure that can be done in the clinical
setting (1). Extracts of the allergens are placed on the skin and then pricked to determine
if there is a reaction (1). The reaction results in a wheal, or a red and itchy bump on the
skin if there is a sensitivity to the antigen and if there is no reaction, there is no sensitivity
iv. Other workers at the farm do not seem to be affected with these signs and symptoms.
Other workers at the farm did not exhibit these signs and symptoms. This could
The other workers may not have a hypersensitivity to that particular antigen so even if
they were exposed, the antigen would have no effect on them. The exact reason of this
difference is not clear, but a genetic predisposition could be accountable (1). Other
reasons include the number of sensitized mast cells present and the allergen entry (1).
More sensitised mast cells would result in the symptoms appearing more severe. The
other workers may have the sensitivity, but if only a few mast cells are present and
undergo degranulation, the reaction might not be as severe enough to notice. The entry
of the allergen into the body can also determine how severe the reaction is (1). If the
allergen enters the bloodstream by injection or ingestion, more mast cells are able to be
triggered to degranulate as compared to only touching the skin in one area (1). If the
patient failed to wear protective gear, such as gloves, and had a small abrasion or the
allergen was inserted by something such as a needle prick or splinter, the allergen could
enter the bloodstream and cause a more widespread and severe reaction.
Works Cited
1. Aliabadi Z, Foster J, Slonczewski. Microbiology The Human Experience. New York (NY):
2. Janeway CA, Travers P, Walport M. Immunobiology: the immune system in health and
4. Influenza (Flu). Centers for Disease Control and Prevention. 2017 Oct 3 [accessed 2017
5. Tuberculosis Skin Testing. Centers for Disease Control and Prevention. 2016 May 11
https://www.cdc.gov/tb/publications/factsheets/testing/skintesting.htm
6. Nayak S, Acharjya B. Mantoux test and its interpretation. Indian Dermatology Online
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481914/
7. Testing for Tuberculosis. Center for Disease Control. 2011 Nov [accessed 2017 Nov 5].
https://www.cdc.gov/tb/publications/factsheets/testing/TB_Factsheet.pdf
8. Interferon-Gamma Release Assays (IGRAs)- Blood Tests for TB Infection. Centers for
Disease Control and Prevention. 2015 Aug 17 [accessed 2017 Nov 5].
https://www.cdc.gov/tb/publications/factsheets/testing/igra.htm
https://www.mayoclinic.org/diseases-conditions/tuberculosis/diagnosis-treatment/drc-203
51256
10. Dean L. Blood Groups and Red Cell Antigens. Bethesda, MD: National Center for
11. Ehrlich SD. Serum sickness. University of Maryland Medical Center. 2015 [accessed