Case Studies Mcqs (All Four)

Front 1

Case Study 4: HIV

Laboratory diagnosis of HIV infection:
1) Cellular immunity to HIV is routinely assayed for the diagnosis of HIV infection.
2) Current tests for HIV antibody are prone to fake positive results because of low specificity.
3) Testing for HIV p24 angiten reduces the seronegative window period and thereby provides an earlier diagnosis than HIV antibody tests.
4) Detection of IgG class anti-HIV in the baby's blood at birth is used to diagnose vertical transmission.
5) HIV antibodytests become unreliable after the onset of immune deficiency.

Back 1

3) Testing for HIV p24 angiten reduces the seronegative window period and thereby provides an earlier diagnosis than HIV antibody tests. Before the person makes antibody, there's a lot of virus in the blood. p24 is an important structural part of the virus.

1. Not really used as perhaps dangerous for operators, takes a long time, assaying cellular immunity is quite difficult (have to use tissue culture), not the way to diagnose infection. Done in research lab.
2. False as although original tests not specific because they were based on cultured virus (which often had HLA in it so there was cross-containmination), but now HIGHLY SENSITIVE AND SPECIFIC.
4. False because IgG crosses the placenta. Tells us if baby is at risk or not, but no more than that as it just reflects what the mother has.
5. False becauses tests are so sensitive, you can still use them.

Front 2

Case Study 4: HIV

Transmission of HIV infection:
1) Globally, homosexual intercourse and injecting drug abuse are the major routes of HIV infection.
2) Materno-foetal transmission of HIV typically occurs during the first three months of pregnancy.
3) Gential herpes infection (HSV-2) in women increases the risk of acquiring HIV by sexual intercourse.
4) Male circumcision does not affect transmission of HIV.
5) Recombinant factor VIII is no longer used to treat haemophiliacs because of the risk of HIV infection.

Back 2

3) Gential herpes infection (HSV-2) in women increases the risk of acquiring HIV by sexual intercourse. Because the person may have nasty inflamed ulcers so it is easier for the virus to get in.

1. False, it's HETEROSEXUAL transmission is most important.
2. False, main way HIV transmits is AT BIRTH. Some transmission in utero but not that early on. Rare however so can use antiretroviral drugs at birth.
4. False, for males who are circumcised, transmission of HIV is less. Not clear why but must have something to do with the foreskin.
5. Factor VIII made from human material, human plasma is no longer used. Recombinant factor VIII is made using genetic engineering - no risk of HIV transmission that way.

Front 3

Case Study 4: HIV

Antiretroviral therapy:
1) Resistance genotyping involves culture of HIV in lymphocytes.
2) Nevirapine, a nucleoside analogue, inhibits HIV reverse transcriptase.
3) Use of HAART can lead to immune reconstitution inflammatory system.
4) Monitoring the response to antiviral drugs is achieved by regular measurement of HIV proviral DNA in plasma.
5) Since the advent of HAART, HIV infection can sometimes be cured.

Back 3

3) Use of HAART can lead to immune reconstitution inflammatory system. HAART reduces viral replication so level of virus in blood is very low, so immune system can reconstitute itself to some extent. It deals with all the infections it has previously been unable to deal with.

1. False we don't do that because it would take a long time, require high security facilities. We use gene rescue, use PCR. Then virtual phenotyping because we know from the sequence what the changes will be.
2. Nevirapine acts ALLOSTERICALLY on the reverse transcriptase, it doesn't act competitively on the enzyme. Example of NNRTI. Non-nucleoside reverse transcriptase inhibitor.
4. Wrong, plasma has no cells in it so can't find proviral DNA there. Antiviral drugs help stop viral replication but doesn't remove the proviral DNA - it will always be there. Wrong thing to look at. Look at RNA in plasma.
5. False.

Front 4

Case Study 4: HIV

Primary HIV infection may involve:
1) An increase in the CD4:CD8 ratio.
2) An increased incidence of lymphoid neoplasia and/or progressive multifocal leucoencephalopathy.
3) Fever, granulomas and a rash.
4) Cerebral toxoplasmosis.
5) A glandular fever-like illness and/or encephalitis.

Back 4

5) A glandular fever-like illness and/or encephalitis (inflammation of the brain). HIV can also be fairly SILENT and not be recognized at all.

1. Ratio DECREASES as CD4 cell number decreases.
2. Accurate if you are talking about AIDS, primary infection is what happens at first encounter with the virus. Those things happen only when person is very immunocomprimised. Developing lymphoid neoplasia (cancer) takes a long time.
3. Can have fever and rash with primary infection but don't get granulomas (TB).
4. Appears in AIDS, parasite toxoplasma growing uncontrolled in the brain.

Front 5

Case Study 4: HIV

Kaposi's sarcoma:
1) Is now becoming a common disease throughout the world.
2) Was first described in elderly men in equatorial Africa in the early 1980's.
3) KSHV, the cause of epidermic Karposi's sarcoma is an RNA virus also known as human herpesvirus type 8 or HHV8.
4) Is irreversible in immunosuppressed organ transplant patients.
5) Internal organs may be involved in HIV-associated Karposi's sarcoma although it is primarily a cutaneous tumour.

Back 5

5) Internal organs may be involved in HIV-associated Karposi's sarcoma although it is primarily a cutaneous tumour. In a person with HIV, it can become life-threatening by invading the internal organs.

1. Not a common disease throughout the WORLD but COMMON in PEOPLE WITH HIV. It is an AIDS INDICATOR.
2. Found in MEDITERRANEAN and JEWISH people, not in central Africa.
3. NOT a RNA virus. HERPESVIRUSES ARE DNA VIRUSES. They don't vary a lot like RNA viruses, just well-adapted to man.
4. False - does not have to be irreversible if you remove the immunosuppression.

Front 6

Case Study 3: Malaria

Malaria:
1) Infection is mainly spread by male Anopheles mosquitoes.
2) The parasite enters via veins in the human host.
3) The highest incidence of infection is in South America.
4) On average, over 5,000 cases of malaria are reported in the UK every year.
5) Virulence factors include toxin production, expression of variant cytoadherence factor PfEMP-1.

Back 6

5) Virulence factors include toxin production, expression of variant cytoadherence factor PfEMP-1 (it goes for B cell receptors, erythrocyte membrane protein, present on mature stages of the parasite).

1. False!
2. Parasites go through the skin.
3. No, Subsaharan Africa or in Southeast Asia, depending on type.
4. No, around 2000.

Front 7

Case Study 3: Malaria

Which one of the following is NOT involved in tissue damage?
1) Release of IL-10
2) Release of TNF
3) Obstruction of capillaries
4) Haemolysis of erythrocytes
5) Haemozoin pigment

Back 7

1) Release of IL-10. An interleukin, cytokine. It is an antiinflammatory cytokine.

2. TNF -a inflammatory cytokine.
3. Obstruction in all major organs, lead to ischaemic changesi n the body, get tissue damage.
4. Haemolysis is the direct result of high levels of TNF. Only pathology seen in malaria that is not related to sequestration. Cause fragility of the red cell membranes so they lyse.
5. Haemozoin is a breakdown product of HAEM which is TOXIC to the parasites. Parasites break haem down into haemozoin that goes straight into the food vacuole. When parasite gets phagacytosed by macrophages, some of that haem is released into the circulation where it has an effect on erythroid process in the bone marrow. Results in failure to produce erythrocytes. One of the mechanisms of anemia during malaria.

Front 8

Case Study 3: Malaria

Host cell response and avoidance:
1) Antibody plays no role in protection.
2) The parasite is unable to vary its antigens.
3) T-cells can kill infected liver cells.
4) Plasmodium is always only present inside cells.
5) Secretory IgA antibody plays a major role in protection.

Back 8

3) T-cells can kill infected liver cells. Cytotoxicity. Cytotoxic t cell recognizes antigen in association with MHC class I.

1. False. Antibody acts on sporozites, in all the blood stages.
2. False. It varies its antigens to avoid recognition by the immune system, in response to immune pressure.
4. False.
5. No, because it is a systemic infection.

Front 9

Case Study 3: Malaria

Diagnosis, treatment and avoidance:
1) Has to be diagnosed using PCR.
2) Can be prevented using penicillin.
3) Is mainly controlled by vaccination.
4) Is always treated with chloroquine.
5) Prophylatic drugs include proguanil.

Back 9

5) Prophylatic drugs include proguanil.

1. Blood films by microscropy is gold standard, however advantage of PCR is it is sensitive, so can detect low levels of parasite, if you are trying to distinguish between the species of parasite.
2. No.
3. No. We have no vaccine for malaria currently.
4. No, due to drug resistance. Can be used in combination with other drugs.

Front 10

Case Study 2: Tuberculosis

The Organism.
The single best defining feature of Mycobacterium tuberculosis is that it:
1) Has a Gram-positive cell wall structure.
2) Can be cultured quickly using solid and liquid media.
3) Is an aerobe.
4) Is an "acid-fast" bacterium.
5) Shares cell wall antigens with other bacteria.

Back 10

4) Is an "acid-fast" bacterium.

1. False - Gram staining is for ordinary bacteria that do not have waxy mycolic acid on their surfaces. TB does not take up the gram stain. However, if you treated the cells with heat or alcohol, you might get a little bit but not the usual way of staining the bacteria.
2.
3. It is an aerobe but not a strict aerobe - can survive anaerobically in its dormant or latent form when it is not growing readily.
5.

Front 11

Case Study 2: Tuberculosis

Spread, entry and virulence factors.
The single best defining feature of Mycobacterium tuberculosis is that it:
1) Phagocytosis of M. tuberculosis involves a single receptor.
2) Infection can be transmitted via urine.
3) The main virulence factors of M. tuberculosis are the cell wall mycolic acids and lipoarabinomannan.
4) It can reside inside neutrophils.
5) The oral-faecal routie is the the principal route of infection.

Back 11

3) The main virulence factors of M. tuberculosis are the cell wall mycolic acids and lipoarabinomannan. One of the main receptors for binding to phagocytes is the mannan receptor. Lipoarabinomannan is thought to be one of the principle molecules for binding to mannan receptors on the surfaces of phagocytes.

1. Wrong - multiple receptors.
2. Very rarely - may happen. Not the best answer.
4.
5. Very rarely - may happen. Not the best answer.

Front 12

Case Study 2: Tuberculosis

Tissue damage mechanisms, clincial presentation and complications.
The single best defining feature of the pathology of Mycobacterium tuberculosis is that it:
1) Antibodies provide protection against M. tuberculosis.
2) The main virulence factors of M. tuberculosis are the cell wall mycolic acids and lipoarabinomannan.
3) M. tuberculosis can infect lungs without causing lesions.
4) M. tuberculosis is ingested by monocytes.
5) Causes inflammatory bowel disease.

Back 12

2) The main virulence factors of M. tuberculosis are the cell wall mycolic acids and lipoarabinomannan. The mycolic acids are responsible for its transmission and stability within the environment.


1.
3. If it goes into the lung, there are several outcomes. Firstly, using the innate system, we can kill all the TB bacteria and clear the infection. Secondly, we mount an antibody response that doesn't clear all the bacteria. Those bacteria are then surrounded and form the lesions that you normally see wth lung infection. Thirdly, if you have an immunosuppressed system where you don't necessarily form the lesion, you can get infection of the lung without lesions - can lead to other diseases (miliary?) where it can be disemminated to other parts of the body. So correct as well.
4.Can be ingested by monocytes but that's not usually the case.
5. Possible, but not much known.

Front 13

Case Study 2: Tuberculosis

Host response and avoidance.
1) NK cell recognition of infected macrophages.
2) The involvement of Th1 cells.
3) Activation of infected macrophages by IFN-gamma produced from Th2 cells.
4) The recruitment of regulatory T-cells into the granuloma.
5) MHC class II presentation of M. tuberculosis antigens to CD8+ cytotoxic T cells.

Back 13

2) The involvement of Th1 cells.

3. IFN-gamma is produced from Th2 cells and it can activate the macrophage and by doing so, it can inhibit intracellular growth of the pathogen and possibly stimulate bacterial killing. However, in contrast the IFN-gamma is thought to reduce the binding of the bacterium on the surface of the macrophage by reducing the number of receptors on the surface. It is part of the immune response but not the major part.
5. MHC class II presents M. tuberculosis antigens but MHC class II doesn't react via the CD8, reacts with CD4.

Front 14

Case Study 2: Tuberculosis

Diagnosis, treatment and avoidance.
The single most important fact related to diagnosis and treatment of tuberculosis is that:
1) Acid fast bacilli can be detected by microscopic examination of sputum smears that are negatively stained.
2) Diagnosis of tuberculosis is a clinical decision.
3) Standard antimicrobial treatment is a combination of rifampicin + isoniazid + pyrazinamide +/- ethambutol.
4) Molecular diagnostics by the polymerase chain reaction detect M. tuberculosis proteins.
5) Total treatment time depends on the clinical presentation of the disease.

Back 14

3) Standard antimicrobial treatment is a combination of rifampicin + isoniazid + pyrazinamide +/- ethambutol. Because it is located in a place where drugs can't get in very effectively, because it lies dormant, because it divides very slowly, we have to give drugs over a prolonged period of time to catch all the organisms. Therefore if we gave a single drug, the organism will acquire resistance before we kill all of them and therefore we would be unable to treat it. Longtime therapy over six months and during that time you would get resistance to individual drugs. Despite these efforts, there are still organisms that are showing resistanc to multiple drugs - to all of those.

1. Wrong because of NEGATIVELY STAINED.
2. Without the microscopy, we don't actually begin treatment for TB. Not solely based on symptoms.
4. PCR is not USED FOR PROTEINS. We do use it though to speed things up, particularly if we find no bacilli in the sputum.
5. Not relevant as it is not the severity of the disease that determines treatment type, it's the fact that if you have it, there is a fixed treatment.

Front 15

Case Study 1: Streptoccal sore throat

Streptococcus pyogenes:
1) Is a Gram negative organism.
2) Posses a hyaluronic acid capsule.
3) Is a group C b-haemolytic streptococcus.
4) Lacks peptidoglycan in its cell wall.
5) Has an outer lipopolysaccharide layer.

Back 15

2) Posses a hyaluronic acid capsule.

1. Wrong.
3. Lancefield - group A.
4. Wrong.
5. Doesn't have one because it is NOT GRAM-NEGATIVE.

Front 16

Case Study 1: Streptoccal sore throat

Entry, spread and virulence factors.
Streptococcus pyogenes:
1) Is only found in the oro-pharynx.
2) Is spread only by direct contact.
3) Is not a significant agent of nosocomial infections.
4) Infection always results in symptoms.
5) May possess ‘superantigens'.

Back 16

5) May possess ‘superantigens'.

1. Wrong.
2. Wrong.
3. IT IS both nosocomial and community.
4. Wrong.

Front 17

Case Study 1: Streptoccal sore throat

Infection with Streptoccocus pyogenes can result in:
1) Yellow fever.
2) Diphtheria.
3) Damage to heart valves.
4) Gomerulonephritis within 24 hours of infection.
5) Polycythemia.

Back 17

3) Damage to heart valves.

4. It does cause kidney problems but not usually within the first twenty four hours - not that quick. More chronic problem.

Front 18

Case Study 1: Streptoccal sore throat

The host-pathogen relationship involves:
1) Bacterial stimulation of TNF production by host macrophages.
2) Constriction of local blood vessels.
3) Activation of complement component C5 by C5 peptidase.
4) The M carbohydrate of Streptococcus pyogenes.
5) Inhibition of bradykinin production.

Back 18

1) Bacterial stimulation of TNF production by host macrophages. TNF is Tumour Necosis Factor.

3. The enzyme is CONVERTASE. Streptococci themselves produce the C5 peptidase that degrades C5, reducing complement. C5 peptidase is a streptococci enzyme.
4. The M structure is PROTEIN.

Front 19

Case Study 1: Streptoccal sore throat

In Streptococcus pyogenes infection:
1) Diagnosis can be made by culture of the virus.
2) The possession of specific antibodies are valuable in the diagnosis of a sore throat.
3) Acute infections are treated with acyclovir.
4) Clindamycin is used in cases of necrotising faciitis.
5) Most individuals are protected by routine vaccination.

Back 19

4) Clindamycin is used in cases of necrotising faciitis.

1. Wrong.
2. Doesn't rely on antibodies because bacteria that may have been killed will still leave behind antibodies so it doesn't reflect ACTIVE INFECTION. Can be used alongside microbiological culture methods. Not as valuable.
3. NOT A VIRUS. Acyclovir is an antiviral.
5. Not against this particular organism.