Infectious Disease: Transmission via Direct Contact Flashcards

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1
Q

Nonsporulating Gram Positive Bacteria:

- Staphylococcus ?

A
  • aerobic, cocci
  • resistant to reduced water potential
  • tolerate high salt
  • many species are pigmented
  • staphylococcus aureus (yellow)
  • methicillin resistant Staphylococcus aureus (MRSA)
  • catalase positive
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2
Q

Staphylococcus aureus is part of the normal flora of about 20% of people, True or false?

A
  • true
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3
Q

Staphylococcus aureus:

- describe the disease inflicted by it

A
  • staphylococci: usually harmless inhabitants of the upper respiratory tract and skin
  • disease: Pyogenic infection aka pus forming. Acne, boils, pimples, impetigo, pneumonia, osteomylitis, carditis, meningitis and arthritis
  • some caused by staphylococcal superantigens
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4
Q

Explain the structure of a boil.

A

pus contents: mixture of white blood cells being broken down
-fibrilligen forming fibrin
L> protective response via preventing spread to epidermis but protects the infection from immune system

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5
Q

Explain toxic shock syndrome,

A
  • causes: Staphylococcus aureus, Streptococcus pyogenes
  • Symptoms: high fever, rash, vomiting, diarrhoea, death (70%)
  • rare, associated with local infection: complication of surgery and associated with tampons
  • Toxic shock syndrome toxin: TSST-1, superantigen
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6
Q

Explain the virulence factors of Staphylococcus aureus.
L> Toxins
L>Coagulase
L>Superantigens

A
  • toxins: haemoylsins (cell lysis), leukocidin (destroys leukocytes)
  • Coagulase: converts finrin to fibrinogen, localised clot
  • superantigens: eg toxic shock syndrome antigen, elicit a very strong immune response, stimulate T cells to grow and divide, T cells produce cytokines, excessive inflammatory response
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7
Q

What is direct contact?

A
  • with person or with blood or excreta
    L> Staphylococcus aureus, Helicobacter pylori, Hepatitis Viruses
  • sexually transmitted infections : Treponema pallidum, Chlamydia trachomatis
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8
Q

Methicillin-Resistant S. aureus (MRSA)

L> discuss B-lactans

A
  • B-lactan antibodies (eg penicillin) target transpeptidases (PBPs)
  • MRSA have a PBP that is not inhibited by penicillins : continue to make cell wall in presence of penicillin
  • ## B-lactans are ineffective in MRSA
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9
Q

Methicillin-Resistant S. aureus (MRSA)

L> alts to B-lactans?

A
  • more toxic
    -more expensive
    -more difficult to administer
    L> eg. vancomycin : acts on cell wall in a completely diff way.
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10
Q

Spirilla: Campylobacter and Helicobacter
L> discuss their adverse effects on hosts
and uniting characteristics

A

-motile
-microaerophilic
L> require O2 at lower than atmospheric concentrations (3-15%)
- most species are pathogenic to animals or humans
- Campylobacter: entertitis (bloody diarrhoea)
-Helicobacter: causes gastritis, peptic ulcers, can survive the acidic conditions of the stomach,

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11
Q

Helicobacter pylori

L> whats up with this lil broski?

A
  • gram negative, highly motile, spiral shaped bacterium
  • associated with gastritis, duodenal ulcers and gastric cancers
  • colonizes gastric epithelium
  • orally transmitted person to person, in families (usually)
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12
Q

Helicobacter pylori linked with what!??

L> Aussies ?

A
  • peptic ulcers
  • conventional thinking: bacterium can’t live in human stomach (pH1) and the ulcers are caused by stress.
  • 1979: Robin Warren seen it in a stomach biopsy…unintentionally left their plates incubating for five days and growth was found
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13
Q

Helicobacter pylori linked with peptic ulcers:
- What did Marshall discover in 1985?
L>treatment?

A
  • he drank a beaker of H. pylori
    L> developed nausea, vomiting
    L> endoscopy found gastritis and the presence of H.pylori
    L> AKA ULCERS ARE NOT CAUSED BY STRESS
    -antibiotics are effective in the treatment gastritis
    L>prevention of relapse of ulcers
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14
Q

Helicobacter pylori virulence factor??

A
  1. Flagellar motility and chemotaxis: needed to reach mucosa (needs to get out of gastric lumen into mucosa bc it will protect it from the acid..produces urease which neutralizes acid
  2. Urease: neut acids, scavenges nitrogen, ammonia damages mucosa
  3. Toxins, CagA and VacA: damage epithelium
  4. Enzymes: mucinase, proteases: helps work through the epithelium
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15
Q

Hepatitis

L> What type of disease? Symptoms?

A
  • liver disease: destruction of liver cells leads to cirrhosis
  • hepatitis viruses are phylogenetically diverse
  • can also be caused by bacteria
  • Symptoms: fever, Jaundice (excess billrubin released by the liver causing yellowing of the skin)
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16
Q

Hepatitis C

L> virus??

A
  • HCV hepacivirus
    L>ssRNA positive sense, enveloped
    -Transmission: parenterally (blood transfusion, dirty needles), STD
17
Q

What is the difference between viral capsid and bacterial capsule ?

A
  • bacterial capsule: usually polysaccharide, protects the bacterium from: host immune system, desiccation. Outermost layer of bacterium.
18
Q

What are the symptoms of Hep C

A
  • mild symptoms
  • chronic hepatitis
  • chronic liver disease and cirrhosis
  • liver cancer
19
Q

Pathogenesis of Hep CCCCCCCCCCCCCCCCCC

A
  • non cytopathic, can remain host associated but prevent cell death
  • damage to tissues caused by immune response
  • cancer may result from constant tissue repair
20
Q

Organisms causing sexually transmitted diseases - describe theeeem.

A
  1. are often gram positive bacteria they are resistant to drying
  2. are generally sensitive to environmental stresses such as drying, heat and light
  3. are usually viruses bc they can only be transmitted by close contact
21
Q

Syphilis - what’s up with that?

A
  • serious disease
    -can be passed to fetus = congenital syphilis
    -primary chancre is unsightly
    L> patients seek medical intervention (patients seek medical attentions..aids in diagnosis)
  • susceptible to penicillin : Benzathine penicillin G…longer course required for tertiary syphilis
22
Q

What causes syphilis?

A
  • T. pallidum
23
Q

What are T. pallidum’s virulence factors?

A
  • outer membrane proteins promote adherence
  • corkscrews into host tissue
  • surface coated with host proteins tissue destruction and lesions are primarily result of host’s immune response
24
Q

What are the factors affecting the incidence of gonorrhoea and syphilis?

A
  • often transmitted together
  • syphilis: lower incidence than gonorrhoea, chancre is an obvious symptom, can be cured by penicillin
  • Gonorrhoea: higher incidence, often asymptomatic, antibodies are strain specific - don’t prevent further infection. Oral contraceptives alter conditions in urogenital tract
25
Q

Chlamydia - give a description of it’s basic characteristics.

A
  • gram negative type cell walls
    L> does not strain with gram stain, outer lipopolysaccharide membrane
  • lacks peptidoglycan
    -Obligate parasites: poor metabolic capacities, require biosynthetic intermediates and probably ATP
    L> some of the simplest biochemical capacities of all known bacteria
26
Q

Chlamydial infections —-> GO.

A
  • currently one of the leading sexually transmitted diseases
  • non specific urethritis, associated with reactive arthritis
  • other strains cause trachoma (blindness)
  • key virulence factor ( type III secretion system)
27
Q

Chlamydial Urethritis: Clinical Features?

A
  • incubation: 1-4 weeks
  • Men: 25% asymptomatic, 75% urethritis with a mucopurulent discharge, usually less severe than in gonorrhoea
  • Women: usually asymptomatic, 30% vaginal discharge, 10-20% urethritis
28
Q

Chlamydial Urethritis
L> Complications?
L> Treatment?

A
  • pelvic inflammatory disease, conjunctivitis and pneumona in neonates, reactive arthritis
  • Treatment: azithromycin as a single dose or with doxycycline for 7 days or erythromycin for 14 days