Biology 261

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Biology 261
2011-12-05 07:42:05
Chapter 33

Chapter 33
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  1. Antigenic shift:
    • a major change in a protein
    • coat antigen resulting from the total replacement of an RNA segment.
  2. Antigenic drift:
    • limited mutations ceate
    • slightly altered antigens.
  3. Cirrhosis:
    • breakdown of normal liver
    • architecture resulting in fibrosis.
  4. Congenital syphilis
    • syphilis contracted by an
    • infant from its mother during birth.
  5. Hepatitis
    • a liver inflammation
    • commonly caused by an infectious agent.
  6. Meningitis:
    • inflammation of the
    • meninges (brain tissue), sometimes caused by Neisseria meningitides and
    • characterized by sudden onset of headache, vomiting, and stiff neck, often
    • progressing to coma within hours.
  7. Rheumatic fever:
    • an inflammatory autoimmune
    • disease triggered by an immune response to infection by Streptococcus pyogenes.
  8. Scarlet fever:
    • characteristic reddish rash
    • resulting from an exotoxin produced by Streptococcus pyogenes.
  9. Toxic shock syndrome (TTS):
    • acute systemic shock
    • resulting from a host response to an exotoxin produced by Staphylococcus
    • aureaus.
  10. Tuberculin test:
    - a skin test for previous infection with Mycobacterium tuberculosis.
  11. What are the common pathogens associated with the upper and lower respiratory tracts?
    - Legionella pneumophila (Legionnaire’s disease)

    - Streptococcus pyogenes (group A Streptoccus)

    - Streptococcus pneumoniae
  12. What diseases are associated with Streptococcus pyogenes. How is it diagnosed?
    - Streptococcal pharyngitis (strep throat)

    - Produce a toxin that lyses red blood cells in culture media (B-hemolysis)
  13. Describe diseases caused by Streptococcus pneumoniae? How are streptococcal infections treated?
    • Contains capsule, invades alviolar tissues.

    • If untreated mortality may reach 30%, with aggressive treatment it is ~5-10%

    • Detection: gram-positive
    • diplococci from either patent sputum or blood.

    • Immunity is strain-specific. More than 90 strains is known

    • Vaccine is available.

    • • Streptococcus infections are treated by penicillin, erythromycin, cephalosporin, fluoroquinalone,
    • ceftriaxone, cefotaxime, vancomycin.
  14. What is the pathogenesis of diphtheria? What bacterium causes diphtheria? How is diphtheria treated?
    • Produces neuraminidase, diphtheria toxin encoded by the bacteriophage b.

    • Untreated infection (in 25% cases) leads to heart, kidneys, liver and adrenal glands.

    •50,000 cases worldwide/5,000 fatal

    • Diagnostics: culture from throat, nasal passages.

    • Effective vaccine (DTP - diphtheria, tetanus, pertussis) is available.

    • Treatment: antibiotics (penicillin, erythromycin, gentamicin) and antitoxin.
  15. What are the virulence factors of Bordetella pertusis? How is it diagnosed? Why do we observe an increasing number of whooping cough cases in the US?
    • Most typically among children under age 19. Violent cough, which may last up to six weeks.

    • Adherence to cells of upper respiratory tract through filamentous hemagglutinin antigen.

    • Exotoxin induces synthesis of cAMP. Endotoxin induces cough.

    • 50 million cases world wide and 300,000 deaths

    • Diagnosis: fluorescent antibodies, isolation of colonies on blood-glycerol-potato extract agar, hemolysine positive colonies are tested by a latex agglutination test.

    • Vaccine is available but lasts less than 10 years.

    • Treatment with antibiotics is used but rarely successful.
  16. Why is Mycobacterium tuberculosis such a widespread respiratory pathogen? What are the two type of infection caused by M. tuberculosis?
    What is the most common treatment of tuberculosis? What is the mechanism of action of isoniazid?
    • Presently 14,000 new cases and 700 deaths in the US annually, worldwide 1,6 million deaths per year.

    Two kind: primary and post primary (or re-infection).

    • During primary infection, tubercles, aggregates of macrophages, are formed in lungs. In individuals with low resistance, acute pulmonary infection may occur.

    • Post primary is the result of re-infection or reactivation of existing bacteria.

    • Diaganostics: tuberculine test followed by chest X-ray.

    • Chemotherapy is a major factor in controlling the disease: streptomycin, isoniazid, rifampin.

    • Usual treatment is with rifampin and isoniazid for 2 month daily and then biweekly doses for 9 months.
  17. What are the two forms of leprosy and how is it
    • Cannot be cultured, but can grow in armadillo.

    • Diagnosis: acid-fast staining.

    • Lepromatous or multibacillary form - bacteria are detected easily.

    • Tubercular (tuberculoid) or paucibacillar form - no bacteria can be detected.

    • Treatment with rifampine, dapsone, and clofazimine for 1 year.

    • In the US fewer than 100 cases per year; 12 million people worldwide, 750,000 new infections.
  18. What diseases do pathogenic mycobacteria other than
    M. tuberculosis and M. leprae cause?
    • Mycobacterium bovis – symptoms of tuberculosis but entry though gastrointestinal tract.

    • M. kansasii

    • M. avium – pneumonia in AIDS patients

    • M. chelonae

    • M. scofulaceum

    • M. ulcerans – Buruli ulcer
  19. What are bacteria and viruses that cause
    meningitis? How could bacterial meningitis be diagnosed? What would you expect to see on a gram stain
    and what type of media and environment would you grow it in?
    • Meningitis is an inflammation of meninges or membranes that line central nervous system.

    • Can be bacterial, viral or aseptic.

    • Occurs as epidemics in closed populations. Up 30% of people carry N. meningitidis is their respiratory system. Spread via the airborne root. Mortality can reach 3%

    • • Meningococcemia is another disease caused by N. meningitidis, mortality from which can be caused in up 10%
    • of cases.

    • Diagnosis by isolation of a culture on MTM (modified Thayer-Martin) medium.

    • Treatment: penicillin G, chloramphenicol, cephalosporin, rifampin.

    • A vaccine exists but is not long
    • lasting

    • Staphylococcus

    • Streptococcus

    • Haemophilis influenzae

    • Viruses: herpes simplex virus, lymphocytic chorimeningitis virus, enteroviruses, mumps virus.
  20. How measles, mumps, rubella and chicken pox are
    controlled? Why do we observe a dramatic decrease in the number of cases measles; mumps, rubella and chicken pox?
    • Measles (rubeola) virus is a paramyxovirus

    • Infection last 7-10 day,

    • Complications: secondary bacterial infections and measles encephalomyelitis.

    • Mumps virus is a different paramyxovirus.

    • Complications: encephalitis and sterility.

    • Rubella virus is a togavirus.

    • Complications: fetal abnormalities

    • Efficient vaccine is available all three.

    • Chickenpox (varicella) is a herpes family virus.

    • Effectively controlled by a vaccine.
  21. Define and compare the symptoms of influenza and common
    colds. What are the viruses, which cause common colds?
    • Caused by rhinoviruses from picornovirus group (70% of cases), coronaviruses (15%).

    • • Adenoviruses, coxsackie viruses, orthomyxoviruses, respiratory syncytial virus are responsible for
    • remaining 10%
  22. How antigen drift and shift allow the influenza virus to
    avoid host immune defenses? Where does influenza originate and how is it
    • An RNA containing orthomyxovirus.

    • • Has segmented genome - 8 different RNA molecules or “chromosomes”. The result is re-assortment of genes
    • between different strains called antigen shift.

    • The rate of mutations (antigen drift) is very high.

    • Disease is highly seasonal.

    • Epidemics every 2-3 years, pandemics 10 to 40 years apart.

    • Can be controlled by immunization.

    • Treatment: amanthadine and remanthadine inhibit replication; Tamilfu - neuraminidase.
  23. What are the diseases commonly caused by
    • Acne, boils, pimples, impetigo, pneumonia, osteomyelitis, carditis, meningitis, arthritis.

    • Many of these are suppurative or pus-forming diseases.

    • S. aureus produces four different hemolysins, enetrotoxin, coagulase, leukocidin, catalaze.

    • • Some S. aureus strains are implicated in toxic shock
    • syndrome (TSS), which is caused by toxic shock syndrome toxin.

    Enterotoxin A causes food poisoning

    • The structure of a boil. (a) Staphylococci initiate a localized infection of the skin and become walled off
    • by coagulated blood and fibrin through the action of coagulase. (b) The rupture of the boil releases pus and bacteria.

    • Treatment with antibiotics leads to spread of antibiotic resistant strains. MRSA – methicillin- resistant S. aureus.

    • Prevention is problematic since many people are asymptomatic carriers. No long term immunity.
  24. What type of disease does H. pylori cause and how is it diagnosed and treated?
    • Gastritis, peptic ulcers, gastric cancer.

    • Spread from individual to individual and ingested with food. Can be recovered from cats.

    • Colonizes gastric mucosa.

    • Cytoxotin VacA, urease, lipopolysaccharide are important in tissue destruction and ulceration.

    • • Definitive diagnosis is isolation of a pure
    • culture. There are a breath test for urease and immunological test for antibodies in blood and antigen in stool.

    • Treatment with two antibiotics
    • metranidazole or clarithromycin and tetracycline or amoxicillin + plus antiacid
  25. Describe the different types of hepatitis
    viruses and how they are spread? Are
    there vaccines for any of them? Why do we observe decline in the number of cases
    of hepatitis A and B? How are different types of hepatitis diagnosed, prevented
    and treated?
    • Hepatitis is a liver inflammation.

    • Symptoms: fever, jaundice, hepatomegaly.

    • May eventually lead to cirrhosis or hepatocarcinoma.

    • Hepatitis A is transmitted from person to person or through ingestion of contaminated food (most commonly seafood) or water.

    • Hepatitis B is transmitted parenterally through blood transfusion, hypodermic needles, sexual intercourse.

    • Hepatitis D is a defective virus, must be co-infected with hepatitis B virus.

    • • Hepatitis C is also transmitted parenterally. 85%
    • individuals develop chronic hepatitis, 20% chronic liver disease and cirrhosis

    • Hepatitis E transmits via an enteric route.

    • Hepatitis G causes mild disease or asymptomatic.

    • Diagnostics:

    • • enzyme-linked immunoassay for viral antigens or antibodies for hepatitis B virus, immunoblot,
    • immunoelectron microscopy and immunofluorescence.

    • Prevention and treatment:

    • Hepatitis A and B - vaccination

    • Maintaining pathogen free food

    • Postexposure treatment with human immunoglobuline, interferon a, ribavirin, gancyclovir, foscarnet, lamivudine.
  26. Why are STDs difficult to diagnose, treat and
    control? What factor has contributed to increased incidence of gonorrhea? How
    is gonorrhea treated? What would you expect to see if you did a gram stain of
    the discharge from someone with gonorrhea?
    • Variety of bacteria, viruses, protozoan, fungi.

    • Very sensitive to drying, therefore transmission is only possible sexually.

    • Difficult to treat, effectively diagnose and limit the spread.

    – First, difficult to trace infection route, particularly in teenagers.

    – Second, many STD have minor symptoms

    – Third, a social stigma attached to STD prevent from seeking early treatment.


    • • Neisseria gonorrhoeae: gonorrhea and eye infection of
    • newborns.

    • Treated with penicillin, cefixime, ceftiaxone, doxycycline, azithromycin.

    • Still a prevalent
    • disease because:

    – No acquired immunity

    – Usually asymptomatic in women

    – Use of oral contraceptives creates conditions favorable for colonization.
  27. What type of organism causes syphilis and how is
    it diagnosed? What are the symptoms and stages during syphilis progression?
    • Infections through breaks in skin, as well as congenital syphilis.

    • Primary lesion is called chancre.

    • Secondary stage is characterized by skin rash.

    • Tertiary stage from mild infection of skin or bone to paralysis.

    • Diagnostics: detection of antibodies against T. pallidum.

    • Treatment with penicillin G.
  28. What are the diseases caused by Chlamydia trachomatis?
    • Intracellular parasite, immunological detection.

    • Most prevalent STD in the US

    • ~4 million of new cases a year, only 900,000 reported.

    • Transferred via sexual intercourse and to newborns from mothers.

    • Chlamydial nongonococcal urethritis can lead to testicular and prostate inflamation.

    • • Other diseases: trachoma
    • - eye infection, arterial plaques and cardiovascular disease non-STD strains.

    • Lymphogranuloma venereum can lead to proctitis.

    • Inapparent infections are also common.
  29. Describe the difference between herpes
    infections? Can herpes be cured? What is the drug used to control herpes
    • •Herpes simplex virus 1 causes cold sores and fever blisters.
    • Transferred through direct contact or saliva. Up to 90% of human population can
    • be carriers.

    • Herpes simplex virus 2 causes blisters in anogenital area and mouth. Can lead to cervical cancer in women.

    • Treatment – acyclovir and its analogs.
  30. How can one get infected with trichomoniasis and
    how is it treated?
    • STD but also through contacts with toilet seats, sauna benches and paper towels.

    •Infects vagina, urethra, prostate and seminal vesicles.

    • In most cases is asymptomatic in men.

    • Diagnosed by microscopic observation.

    • Treatment: metronidazole.
  31. What type of cell does HIV infect? Describe the
    progression of an HIV infection. What are the criteria used to diagnose AIDS?
    How does HIV kill CD4 T lymphocytes?
    • • More than 950,000 cases of AIDS have been reported in the US, 530,000 died. 476,000 to 1.4 million are
    • HIV positive.

    • 50 million people are infected worldwide.

    • HIV-1 (99% of all cases) and HIV-2 (1%).

    • • Retrovirus: genome 9749 nucleotides in each of the two identical
    • “chromosomes”.

    • Affects immune system,nwhich lead to opportunistic infections.

    • • AIDS: tests positive fornanti-HIV antobodies, <200/mm3 of CD4 T lymphocytes, and either CD4 T lymphocyte/total lymphocytes of less 14%
    • or one of opportunistic infections or one of associated cancers is
    • present.

    Some AIDS associated infections

    • Candida albicans, systemic candidiasis

    • Cryptococcus neoformans, cryptococcosis

    • Histoplasma capsulatum, histoplasmosis

    •Pneumocystis carinii, pulmonary pneumocytosis

    • Cryptosporidium sp., cryptosporidiosis

    •Toxoplasma gondii, toxoplasmosis

    • Mycobacterium spp. infections
  32. What are the roles of gp120, CCR5, CD4, CXCR4 in spread of
    AIDS virus?
    • HIV first binds to macrophage APC (next two pictures).

    • After that a new form of gp120 receptor is made, which recognizes CXCR4 and CD4 receptors of T helper cells.

    • HIV does not immediately lyse or kill host cells. T cell containing HIV stop dividing and eventually dies.

    • • Infected T cell can bind to up to 50 other T
    • lymphocytes, forming syncytia, which shortly die.

    • T helper cells stop producing chemokines, which inactivates healthy lymphocytes.

    Interaction of HIV with a target cell through specific binding of HIV gp120 to the CD4 receptor and a coreceptor on target cells such as macrophages or T cells. The coreceptor shown is the membrane-spanning chemokine receptor CCR5 found on macrophages. A similar coreceptor, CXCR4, is found on CD4 T cells.
  33. How is HIV detected in infected individuals?
    • Antibodies in blood by ELISA followed by immunoblot. Antibodies develop within 6 weeks to a year.

    • RT-PCR estimates viral load.
  34. Can AIDS be cured and how is it treated? Name the
    three classes of drugs used to treat HIV.
    • Nucleoside reverse transcriptase inhibitors

    • Non-nucleoside reverse transcriptase inhibitors

    • Protease inhibitors

    • Fusion inhibitors

    • • Current treatment is s
    • cocktail of drugs (Highly Active Antiretroviral Therapy - HAART)

    • • Problems with AIDS
    • therapy: drug toxicity and resistance mutations.
  35. What are the two major problems with anti-HIV
    therapy? Is a vaccine for HIV available? What is the most effective way to
    control the spread of AIDS?
    • Nucleoside reverse transcriptase inhibitors

    • Non-nucleoside reverse transcriptase inhibitors

    • Protease inhibitors

    •Fusion inhibitors

    • Current treatment is a cocktail of drugs (Highly Active Antiretroviral Therapy - HAART)

    • Problems with AIDS therapy: drug toxicity and resistance mutations.