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GSSE > Infectious diseases > Flashcards

Infectious diseases Flashcards

1
Q

Where does the majority of the bodys normal flora exist

A

Large intestine >10 to the power of 14

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2
Q

Where are the other sites of the bodys flora

A

Skin
Oral cavity

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3
Q

What type of bugs occupy the skins normal flora

A

Majority are obligate anaerobes

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4
Q

What are the 4 types of common flora

A
  1. bacteria (i.e. prokaryotic cells)
  2. fungi (e.g. yeast Candida albicans and malassezia furfur)
  3. viruses (e.g. herpes group)
  4. possibly parasites (e.g. intestinal amoebae)
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5
Q

Why is the skin not an ideal environment for many microbes

A
  1. resident microbial flora
  2. dryness
  3. acid pH (~5.5)
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6
Q

What type of environemnt in the body fo flora microbes predominate?

A

High humidity/ nutrient rich areas

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7
Q

What microbiral flora is found in the upper intestinal tract

A

Enterococcus faecelias

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8
Q

What anaerobes are predominantly found in the mouth

A

Porphyromonas, Prevotella and Peptostreptococcus genera

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9
Q

What antibiotics are anaerobes in the mouth susceptible to

A

are susceptible to amoxycillin/clavulanic acid (coamoxyclav) combinations.

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10
Q

What abx are good for bite wounds and why

A

Augmentin (anaerobes in mouth are sensitive to this)

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11
Q

Is candida albicans a common skin commensal?
What circumstances allow it to colonise?

A

No
Excess hydration (i.e nappy rash) can allow to it transiently colonise

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12
Q

What is an important difference between gram positive and gram negative cell walls.

A

Gram positive has a thick cell wall with NO outer membrane.
Gram negative has a thin cell wall with an outer membrane

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13
Q

What are the 3 important features of the outer membrane of the gram negative cell wall

A

LPS (lipopholysaccaride which is made up of the following)

  1. lipid A classical endotoxin responsible for toxicity
  2. polysaccharide core
  3. terminal repeating units of ‘O’ somatic antigenic side chains, both important taxonomically
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14
Q

What is the function of the gram negative outer membrane

A
  • Prevents leakage of periplasmic proteins
  • Protects the cell (in enteric bacteria) from bile salts and hydrolytic enzymes of host environment
  • Proteinaceous pores (porins) -> allow passage of LMW solutes (large antibiotic molecules penetrate it slowly)
  • may act as a barrier to the entry of antimicrobials, as most antibiotics are not lipid soluble, so can’t get through OM
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15
Q

What does the cell wall of gram positive bacteria consist of

A
  • Peptidoglycan containing strands of tecihoic acid, proteins and CHO (depending on the species)
  • Not protected by an outer membrane (therefore susceptible to degradation by lysozyme)
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16
Q

How does the cell wall of mycobacteria differ from both gram positive and gram negative bacteria

A

contains large amounts of lipid , responsible for intracellular survival, adjuvant effect and survival in presence of acid

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17
Q

What happens when Gram negative LPS is injected intravenously

A
  1. produce arteriolar dilatation
  2. activate complement through the alternate pathway
  3. injure endothelial cell membrane
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18
Q

Under optimal conditions how fast can bacteria divide

A

10 to the power of 8 progeny in less than 24 hours

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19
Q

How do bacteria divide and how often

A

Binary fission every 10-20 minutes in vitro

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20
Q

What conditions do aerobic bacteria divide in

A

need air (i.e. oxygen as the hydrogen acceptor) to grow and divide

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21
Q

What conditions do anaerobic bacteria divide in

A

Only grow in the abscence of O2

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22
Q

What happens to obligate anaerobes exposed to oxygen

A

sensitive to oxygen, gets killed after brief exposure

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23
Q

What conditions do facultative anaerobes grow in

A

Anaerobe or aerobically

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24
Q

What conditions do microaerophilic microbes grow in

A

grow best under slightly reduced oxygen levels

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25
Q

What 3 ways are genes transferred between cells

A

Transformation
Transduction
Conjugation

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26
Q

Explain how transformation works and which bacteria is is common in

A
  • recipient cell takes up DNA released from donor cell
  • common in pneumococci, meningococci
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27
Q

Explain how transduction works and which bacteria it is common in

A

DNA transferred from donor cell to recipient via a virus (bacteriophage) vector
- common in staph

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28
Q

Explain how conjugation works and which bacteria it is common in

A

transfer always from donor to recipient via the fertility (F) factor, typically a plasmid or transposons (movable
segments of DNA)

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29
Q

What is a plasmid

A

Extra-chromosomal fragment of DNA
usually circular

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30
Q

5 reasons why plasmids are important

A
  1. may be a/w virulence
  2. are important in the transfer of drug resistance
  3. readily transmissible between related and unrelated bacterial strains
  4. often carry genes responsible for virulence and antibiotic resistance (e.g. resistance or R plasmids)
  5. whole or parts of plasmids may incorporate into chromosomal DNA
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31
Q

4 facts about genes for antibiotic resistance

A
  1. are often found in plasmids
  2. may be incorporated into cosmids
  3. often occur in circular DNA molecules
  4. are useful markers in recombinant DNA technology
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32
Q

What are the 2 types of toxins in bacteria

A

Endotoxin
Exotoxin

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33
Q

Which are more potent, endotoxins or exotoxins and why

A

exotoxins, they have a more specific site of action

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34
Q

Where do exotoxins produce their effect

A

Locally (may be severe eg gas gangrene)
OR distant from site of entry e.g Tetatnus

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35
Q

Which bacteria secrete exotoxins (be specific)

A
  • Corynebacterium diphtheria
  • clostridium difficile
  • staph. aureus )staph enterotoxins)
  • pseudomonas aeruginosa (one of the few gram negatives to excrete a significant exotoxin)
  • tetanus toxins
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36
Q

Are exotoxins proteins or lipids

A

Proteins

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37
Q

Are endotoxins proteins or lipids

A

Lipids
Lipid A portion of LPS!

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38
Q

When are exotoxins secreted

A

During growth of may gram positive bacteria

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39
Q

Are exotoxins immunogenic

A

Yes, the invoke an adaptive immune response. Stimulate the production of antibodies which provide a good measure of immunity.

40
Q

What bugs are endotoxins typically found in

A

Gram negative, e.g E.coli and pseudomonas

41
Q

What normally causes shock in patients with gram negative septicaemia

A
  1. bacterial endotoxins
  2. bacterial LPS
  3. products of complement activation
42
Q

Are endotoxins more inflammatory or immunogenic

A

inflammatory
Initiate a series of events, promote cytokines and TNF with subsequent vascular endothelial damage

43
Q

How do exotoxins differ from endotoxins

A
  • Convertible into toxoids
  • Cell wall associated
44
Q

List the 5 ways that tissue responds to inflammation

A
  1. Exudative inflammation
  2. Necrotising inflammation
  3. Granulomata’s infalammtion
  4. Interstitial mononuclear
  5. Cytopathic-cytoproliferative
45
Q

What causes exudative inflammation

A

Pyogenic infection
* by extracellular G+ve cocci and G-ve rod
* secondary to increased vascular permeability & leukotaxis of neutrophils attracted by bacterial peptides
* sizes of exudative lesions vary from small abscesses to entire lobe of lung

46
Q

What causes necrotising inflammation

A
  1. uncontrolled viral infection, e.g. fulminant HBV infection,
  2. secreted bacterial toxins (e.g. those of clostridium perfringes)
  3. contact-mediated cytolysis of host cells by protozoa (e.g. Entamoeba histolytica)
47
Q

What causes granulomatos inflammation

A

intracellular organisms

48
Q

What causes interstitial mononuclear inflammation

A

viruses, intracellular bacteria, spirochetes, intracellular parasites, helminthes
- includes mostly lymphocytes, e.g. chancre of primary syphilis, or macrophages (e.g. granulomas of mycobacteria),
depending on the characteristics of the organism and the host

Chronic inflammation

49
Q

What is cytopathic-cytoproliferative infections characterised by and what might they show

A
  • characterized by virus-mediated damage to individual host cells in the absence of host inflammatory response
  • may show
    a. inclusion bodies, e.g. CMV
    b. polykaryons, e.g. measles viruses
    c. Blisters, e.g herpes
    d. Warty changes, e.g. papillomaviruses
50
Q

Describe the shape staph aureus

A

Gram positive cocci, grapelike clusters

51
Q

Common sites for staph aureus infection

A

skin, pharyngitis, pneumonia, endocarditis
major cause of infection in persons with severe burns and surgical wounds

52
Q

Virulence factors associated with staph aureus

A
  • surface proteins,involved in adherence to host cells
  • enzymes that degrade host proteins (coagulase)
  • toxins that lyse host cells and cause
    a. scalded skin syndrome (toxins)
    b. food poisoning (enterotoxins)
    c. shock (endotoxin and toxic shock syndrome toxin ! which is a superantigen)
53
Q

What type of infection does staph aureus cause (i.e type of effect on tissue)

A

pyogenic

54
Q

What antibiotic is the only reliable emperiic treatment for MRSA, + what other abx may be useful for some strains

A

Vancomycin
Fusidic acid

55
Q

Abx of choice for SA septicemia when MRSA is not an issue

A

Flucloxacillin

56
Q

What antibitiocs are used for MSSA

A
  • Cefalexin
  • Augmentin
  • Flucloxacillin
  • Cefuroxime
57
Q

What do strep looks like

A

gram positive cocci in pairs or chains

58
Q

How are strep classified

A

According to their surface antigens

59
Q

What does S. pneumoniae cause

A

major cause of community acquired pneumonia and causes adult bacterial meningitis

60
Q

What does S pyogenes cause

A

produces pharyngitis, Scarlet fever, impetigo, rheumatic fever, glomerulonephritis

61
Q

What does S agalactiae cause

A

causes neonatal sepsis and UTI

62
Q

What does enterococcus faecalis and S viridians cause

A

endocarditiis

63
Q

What does S mutans cause

A

dental caries

64
Q

list 5 streptococcal virulence factos

A
  1. Rodlike surface M-proteins and a polysaccharide capsule that prevent bacteria from being phagocytosed
  2. A pneumolysin that lyses host cells and waste host complement
  3. Exotoxins that produce the rash in scarlet fever
  4. proteases that degrade chemotactic peptides and immunoglobulins
  5. lactic acid that demineralises tooth enamel
65
Q

2 side effects of streptococcus pneumonia

A
  • blood shunting through affected lung
  • Does NOT commonly cause residual fibrosis in affected area of lung
66
Q

Does pneumococcal pneumonia cause necrosis and explain why

A

Pneumococcal pneumonia causes inflammation without significant lung necrosis BECAUSE
Pneumococci include chemotaxis, but elaborate no major toxins

67
Q

What organism causes lobar pneumonia, who does it affect and does it leave functional abnormalities

A

Strep pneumoniae
On resolution leaves a few functional abnormalities
Disease of healthy young adults

68
Q

What is strep pneumonias main virulance factor and what impact does this have

A

Capsule
Allows bacteria to escape phagocystosis (therefore bacteremia is common)

69
Q

What type of bacteria is Nesiseria gonorrhea

A

encapsulated, G-ve diplococcus

70
Q

What infections does Neisseria gonorrhea cause

A
  • urethritis, pharyngitis, or proctitis
  • may cause urethral strictures and chronic infections of the epididymis, prostate and seminal vesicles
  • may infect the fallopian tubes (salpingitis) ! tubo-ovarian abscesses and scars, sterility, and ectopic pregnancy
71
Q

How does N gonorrhea cause disease

A

binds to host epithelial cells via pili, which show antigenic variation based on intragenomic recombination and on
recombination after incorporation of exogenous DNA from lysed gonococci

72
Q

Which organism is developing increasing resistance to vancomyinc

A

Eneterococcus faecilias

73
Q

What is becoming an increasingly important nosocomial pathogen

A

Eneterococcus faecilias

74
Q

E coli is a major causative agent of what 3 things

A
  1. haemorrhagic colitis
  2. bacteraemic episodes in the early stages of peritonitis
  3. osteomyelitis of IV drug abusers
75
Q

Where is pseudonomas widely distributed

A

Hospitals
Burns units

76
Q

Is pseudonomas readily contained by host defences

A

yes

77
Q

important pathogen following faecal leakage during colonic surgery

A

Gram negative anaerobes

78
Q

Important pathogens in lung abscesses following aspiration

A

Gram negative anaerobes

79
Q

Frequently associated with oxygen tolerant microbes

A

Gram negative anaerobes

80
Q

What type of organism is PJP

A

unicellular protozan (fungus)

81
Q

Who gets PCP

A

Immunocompromsied people

82
Q

When does PCP attach in HIV patients

A

CD4 <200

83
Q

Are antibodies to PCP helpful

A

No

84
Q

What type of infection does PCP cause?

A

infection causes a diffuse or patchy pneumonia, which alveolar spaces filled with a foamy stuff ! mainly proliferating
parasites and cell debris

85
Q

What type of inflammatory reaction is seen and not seen in PCP

A

mainly fluid and protein with perhaps hyaline membranes, but few cells
granulomatous reaction is not seen

86
Q

Who carries Hydatid disease

A

Sheep/dogs in autralasia
zoonosis

87
Q

How do humans become infected with Hydatid disease

A
  • tape worm segments (proglottids) containing eggs (ova) are in the dog’s faeces
  • Human disease results from ingestion or inhalation of ova of the tapeworm (Echinococcu granulosus) which resides in the dog intestine
88
Q

How do dogs become infected with Hydatid

A

Dogs, but NOT humans, become infected by eating sheep offal (e.g. liver, lungs) containing hydatid cysts

89
Q

How do you treat Hydatid disease

A

the only really effective treatment of hydatid disease in humans, is surgical removal of cysts
Chemotherapy (e.g. mebendaole type drugs) is generally ineffectively

90
Q

What infections are typically associated with lymph nodes

A
  1. toxoplasmosis
  2. secondary syphilis
  3. pulmonary tuberculosis in childhood
91
Q

how is HIV trasmitted

A

Blood

92
Q

What does HIV show tropism to

A

CD4 bearing cells

93
Q

Why cant a vaccine be made for HIV

A

Genetic variation between isolates

94
Q

What is hookworm disease

A

Hookwroms live in small intestine of humans, where they are attached to the mucosa
they suck blood and large numbers feeding in such a manner can produce a microcytic, hypochromic anaemia, esp. in
malnourished hosts

95
Q

What is the important hookworm in south east asia

A

Ankylostoma duodenale

96
Q

How do humans become infected with hook worms

A
  • Eggs containing developing larvae are shed in the faeces
  • in the soil, these develop into free-living juveniles which after some weeks develop into filariform larvae which invade man
    by penetrating the exposed skin, usually on the feet
  • after migration via the blood to the lungs, these larvae break into the alveolar spaces to migrate to the glottis and are
    swallowed
  • upon arriving in the small intestine, they develop into adults
  • larval passage through the lungs can induce a mild transient atypical broncho-pneumonia accompanied by eosinophilia

GSSE (15 decks)

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