HLTB21H3 Lecture 5: Plagues and people lecture 5.docx

32 views5 pages

champagnegoldfish804

17 Mar 2012

School

Department

Course

Professor

For unlimited access to Class Notes, a Class+ subscription is required.

Document Summary

Phthsis or consumption - used at the peak of the disease in london, england homer 800 bc. Tb present in human population since antiquity. Evidence of tb in egyptian mummies in 2400 bc. Term tuberculosis was not used earlier on. Phtsis- as described by hippocrates, is the form of tb known as pulmonary tb. 460 bc hippocrates; disease was due to evil air but did not consider it contagious. Aristotle (384-322 bc) suggested that tb may be due to bad and heavy breath . Pulmonary form of tuberculosis , selector , loubous (skin), enlargements in the lymph nodes called schofula. Tb was documented in egypt, india, and china as early as 5000, 3000, and 2300 years ago respectively. Tb was limited to animals in prehistoric times (8000-4000 bc) due to domestication of animals the disease was able to spread to humans more quickly.

Related Questions

1) Quantitatively the largest class of immunoglobulins in humanserum is: a) IgG b) IgA c) IgM d) IgD e)IgE

2) A viral vaccine for the common cold probably would not bebeneficial because: a) A pure culture cannot be frown in tissuecultures b) A multiplicity of viral agents is responsible for thecommon cold c) Immunity is of brief duration d) All of the above e)None of the above

3)A point to note in relation to tuberculosis is: a) It isalways acute b) It is always chronic c) The outcome of the strugglebetween the tubercle bacillus and the hist may not be decided formany years d) The disease is always confined to the lungs e) Noneof the above

4) Characteristics associated with virulent staphylococciinclude: a) Coagulase positive b)Fermentation of mannitol c) Betatype hemolysis on blood agar d)all of the above e) only A and C

5) The basic lesion produced by staphylococci is : a)abscessb)ulcer c)varicose veins d)Impetigo e)none of the above

6)The most common method for the transmission of serum hepatitisis: a) direct injection b) Respiratory secretions c) Fomities d)Contaminated water e) None of the above

7)The direct cause of the symptoms of tetanus is: a)Endotoxinb)Exotoxin c)Toxic effect of the cell d)Hemolysins e)none of theabove

yellowsea-lion832

1. Human papilloma virus serotypes 1 and 2 (HPV-1 & HPV-2) both cause benign skin warts. Explain the likely outcome of the following two scenarios and explain in detail why you expect these outcomes. In both scenarios, a person is infected with HPV-1 in January 2012, develops a skin wart which resolves (disappears) without treatment by December 2012. Scenario 1: The same person is re-infected with HPV-1 in January 2013. Scenario 2: the same person is infected with HPV-2 in January 2013.

2. Why do herpes simplex virus type 1 or 2 (HSV-1 or HSV-2) infections recur at or near the site of the original infection? Why is HSV-1 or HSV-2 infection not eliminated from the body when the symptoms of the initial infection subside? Explain both answers in detail.

3. Describe the mechanisms responsible for antigenic drift and antigenic shift in influenza virus. Which mechanism is responsible for the yearly changes in influenza virus and which may create strains of influenza virus that result in pandemics?

4. What organism causes syphilis? How can it be treated and prevented? Describe the stages of syphilis including the order in which they appear and the symptoms of each stage.

5. Name and describe in detail the three stages of disease caused by HIV infection in the order in which they occur. What defines the beginning and end of each stage and what events occur to cause the transitions from each stage to the next?

6. Name and describe the five modes of action of antibacterial drugs. Give an example of a drug that works by each mode of action and state whether it is broad or narrow spectrum and/or suited for treatment of Gram negative or Gram positive infections.

7. Explain the mechanism of action of the antiviral drug acyclovir. Why does it not harm uninfected cells?

8. Name and describe one of the seven most common neglected tropical diseases. Describe the organism that causes the disease, the symptoms, drugs used to treat it and the approximate number of people affected. Why is it necessary to treat the entire population in a geographic region rather than just those suffering symptoms in order to prevent new infections?

9. Describe and explain the causes of rheumatic fever. Why is it important for patients to complete the dose of antibiotics prescribed for "strep throat"?

10. What organism causes Lyme disease? How is it transmitted to humans and why is it most prevalent in parts of New England and the northern Midwest? Describe the possible long-term sequelae of Lyme disease.

11. Describe the five stages of the pathogenesis of tuberculosis. Which stages are seen in asymptomatic infected individuals and which are found in people that have active infectious tuberculosis?

12. Describe the six stages of rabies virus infection and pathology including the common sources of infection in the USA. Explain why fatal disease can be prevented by vaccination after infection.

13. Describe the four mechanisms by which bacteria can become resistant to antibacterial drugs. Describe two ways bacteria may be genetically modified to achieve drug resistance naturally.

Tasmanian devils (Sarcophilus harrisii), the worldâs largest carnivorous marsupials, are facing extinction. Not from hunting, or habitat loss, but from within; a transmissible cancerous derivative of Schwann cells, responsible for devil facial tumour disease (DFTD). First seen in 1996, the disease has spread widely though the population, and is now estimated to be present in 80% of the population. With the grim prognosis of ~100% mortality in 12-18 months, animals that once went through multiple breeding cycles are now lucky to reproduce once before death, resulting in a 70% decline in their population over the past decade. The cancer is transmitted by biting (a common ritual used by these animals to establish and maintain social position), with cancer cells from one animal (the biter) being implanted in the wound inflicted on the other animal. Equally common in both sexes, the disease itself is more prevalent in animals higher on the social scale, presumably reflecting higher levels of social interaction (biting). The cancer is usually first evident as facial tumors, from which metastasis to cervical lymph nodes occurs, often followed by dissemination to other organ systems. Cause of death is by organ failure or by malnutrition in those with facial tumors large enough to prevent feeding. Based on what we have covered regarding the Major Histocompatibility Complex, you would expect the passage of a cancer from one individual to another* to be a rare event (to see just how rare, read the accompanying popular press piece from the New York Times). Here are some things that you already know: *Yes, some viruses can cause cancer (example: Hepatitis B virus and liver cancer), and you can transmit a virus from one individual to another; but that is not the same thing as passing the cancer itself. v Almost all nucleated cells express high levels of class I MHC proteins on their surface. v Class I MHC proteins collect peptides produced from endogenous proteins and display them at the cell surface. v Different Class I MHC proteins bind and display different peptides. v Developing cytotoxic T-cells that recognize self-antigens are eliminated. v Mature cytotoxic T-cells conduct surveillance by scanning the peptides displayed by class I MHC proteins. v Mature cytotoxic T-cells that recognize an antigen on a cell will kill that cell (recall that cytotoxic T cell activity is important in rejection of tissue transplants).

Before the questions:
v Tasmanian Devils are not immunosuppressed.
v Tasmanian Devil cytotoxic T-cells are not broken, they can kill cells.
So neither of those should be part of your answers.
This is an ongoing research topic with large gaps in our knowledge; we really donât fully understand how this works
and so there is no âcorrectâ answer. Your job is to provide a logical argument, with some research and details to
support your contention. Note that in questions 1 & 2 class I MHC should be part of your answer, but not in
question 3.

Questions:
1.) Acquiring DFTD is basically like receiving a transplant that is not rejected. How can that be? Suggest a possible
way this could occur. Be sure to explain why you think this would work, and then explain how you would test
that model to determine if it were correct. (10 point question).
2.) Canine Transmissible Venereal Tumor (CTVT) is the other know transmissible cancer in mammals. Unlike
DFTD, CTVT does not usually result in death. Do a little research on this disease and summarize how it is
different from DFTD. Provide an explanation as to why one is lethal and the other is generally not. (10 point
question).
3.) Recently, researchers at Washington State University determined that some Tasmanian devils had developed
resistance to this cancer. By scanning partial genome sequences of resistant and susceptible animals (a
complete devil genome has yet to be assembled) they identified a set of genes where mutations appeared to
enhance resistance. Speculate as to the function of the proteins these genes encode, and explain why that
might provide for resistance (note: they were NOT MHC genes).

Mainly need guidance/ideas for #1's 1 and 3!

HLTB21H3 Lecture 5: Plagues and people lecture 5.docx

Document Summary

Get access

Related Documents

HLTB21H3 Chapter Notes - Chapter 13: Andrean High School, Tuberculosis, Mycobacterium Bovis

HLTB21H3 Lecture 4: Lecture 4 notes

HLTB21H3 Lecture Notes - Lecture 4: Mycobacterium Tuberculosis, Miliary Tuberculosis, Hermann Brehmer

Related Questions