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BDS2 BAMS > Respiratory Tract Infections > Flashcards

Respiratory Tract Infections Flashcards

1
Q

what is the main problem with respiratory tract infections?

A

secondary infections

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2
Q

how is the nasopharynx adapted for respiratory tract infections?

A

very adapted with innate and adaptive immunity to prevent infection

Saliva - absorb virus particles and bacteria, as well as having antimicrobial peptides present

Alveolar macrophages

Virus are very common and change rapidly so don’t develop immunity - hence why colds/coughs common

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3
Q

issue with viruses and host immunity

A

Virus are very common and change rapidly so don’t develop immunity - hence why colds/coughs common

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4
Q

3 most common upper respiratory tract infections

A

sinusitis (rhinosinusitis)

tonsilitis

pharygitis

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5
Q

sinusitis (rhinosinusitis)

A

inflammation of sinuses

nice environment for bacteria to grow

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6
Q

pharyngitis

A

red swollen throat

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7
Q

best way to treat upper respiratory tract infections

A

gargle with salt water or chlorohexidine

generally don’t need antibiotic

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8
Q

what type of infection are most URT infections?

A

viral

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9
Q

key bacteria that can infect URT

A

streptococcis pyogens

bordatalla pertusis

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10
Q

what % aetiology is viral for Tonsillitis/Pharyngitis?

A

70

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11
Q

what viruses can cause Tonsillitis/Pharyngitis?

A

rhinovirus (common cold)
adenovirus
parainflluenza
others

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12
Q

what causes glandular fever?

A

Epstein Barr Virus

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13
Q

what does Epstein Barr glandular fever effect?

A

Effects lymph nodes, out of work for up to 6 months potentially

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14
Q

how does a viral particle progress in the body

A
  • Virus attached to epithelia
  • Gets inside the cells
  • Divides rapidly
  • Causes cell to self-destruct
  • Virus shedding
  • Macrophages may come along to tidy things up
  • Disrupt viral membranes

If unchecked bacteria can take over

Fundamentally should recover in short period of time

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15
Q

what does the viral particle induce in the host?

A

physiological response

chemical mediators of inflammation –> vascular dilation –> nasal obstruction

increased vascular permeability –> serum transudation —> rhinorrhea

sensitisation and irritation of airways receptors –> cholinergic stimulation –> bronchoconstriction —> cough

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16
Q

what causes 25% of sore throats?

A

S.pyogens (group A)

resides in nasopharynx

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17
Q

what % of children are asymptotic carriers of S.pyogens (group A)?

A

15-20%

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18
Q

what is a pathogenic virus?

A

Viral strain adapted to causing disease e.g. S.pyogens (group A)

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19
Q

what is a cariogenic organism

A

S.mutans

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20
Q

whats dies Group A Strep Pyogens produces as Virulence factors?

A
  • pyrogenic exotoxins
  • streptolysins
  • hyaluronidase
  • M protein
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21
Q

what do exotoxins made by Strep Pyogens do?

A

Exotoxins break up cell membranes, blood cells and collagen fibres

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22
Q

what do M proteins made by Strep Pyogens do?

A

Surrounds the organism

Prevents desiccation

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23
Q

potential M protein secondary effects

A

M protein looks like self-protein
- antibody response to M protein

Attack cardiac tissue
- rheumatic fever (caused by antigens), myocarditis

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24
Q

possible complications of streptococcal sore throat

A
  • peri-tonsillar abscess
  • ottis media or sinusitis
  • scarlet fever (less common)
  • rheumatic fever
  • rheumatic heart disease
  • acute glomerulonephritis
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25
Q

rheumatic fever

A

indirect complication of streptococcal sore throat

antibodies to antigens in streptococcal cell wall cross-react with the sarcolemma of human heart

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26
Q

rheumatic heart disease

A

repeated attacks of streptococcus pyogenes infection can result in damage to heart valves

future attacks prevented by penicillin prophylaxis in childhood

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27
Q

asthma

A 
upper airways affected
fairly common
- Airways decrease
- Mucous build ups - plugs
- Cough to try and remove the mucous 
- Smoke and allergies can stimulate asthma

All culminate to cause bronchitis

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28
Q

bronchitis

A

inflammation of the tracheobronchial tree

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29
Q

acute bronchitis occurs when

A

usually during winter months

most often viral infection

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30
Q

chronic bronchitis is

A

Productive cough on most days during at least 3 months in each of 2 successive years.
- Affects 10-25% of population.

Predisposing = Smoking, infection, air pollution & allergies

Viral & bacterial agents

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31
Q

chronic bronchitis affects

A

10-25% of population

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32
Q

causes of chronic bronchitis

A

Predisposing = Smoking, infection, air pollution & allergies

Viral & bacterial agents

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33
Q

virus Vs bacteria upper respiratory infection causes

A

virus 90%

bacteria 10%

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34
Q

common viral infections of upper respiratory tract

A
  • rhinovirus
  • Influenza
  • adenovirus
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35
Q

common bacteria infections of upper respiratory tract

A
  • Bordatella pertussis
  • Mycoplasma pneumoniae
  • Chlamydia pneumoniae
  • Haemophilus influenzae
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36
Q

Bordatella pertussis of upper respiratory tract

A

hooping cough, can be fatal

  • Cough till sick
  • Produces an exotoxin - stimulate the upper bronchi
  • Lots of energy needed, may need incubated and hospitalised
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37
Q

treatment of upper respiratory tract infections

A

Decongestants, salt water gargle, NSAIDs, antibiotics where appropriate

Antibiotics if infection doesn’t clear
- Bacterial infection not viral

38
Q

prevalence of mycobacterium tuberculosis infection

A

New infection every second

1/3 of entire global population infected
- 1% of population infected every year

3 million deaths per year (lot unnecessarily)
- 8 Million symptomatic

Causes 25% of preventable deaths

Most pre-eminent fatal disease l Predicted by 2020:
- 1 billion infected, 200 Million, 35 Million Deaths

Ability of people to global travel means quick spread from hot spots (Africa, India, Pakistan)
Many are asymptomatic but carriers - risk

39
Q

why is mycobacterium tuberculosis infection so wide spread?

A

Ability of people to global travel means quick spread from hot spots (Africa, India, Pakistan)

Many are asymptomatic but carriers - risk

40
Q

why is mycobacterium tuberculosis successful at spreading?

A

lipid outer cell wall which protects it

  • Macrophages engulf but cannot do anything
  • Grows inside and then grows out of it
  • Builds tubercle in lung (ball)
    (Can be latent for many years)
  • But if immune system low, will grow again
  • Become liquid and get into lungs (systemic spread) and spread via cough
  • Causes body to shut down and die
41
Q

treatment and prevention of mycobacterium tuberculosis

A

Triple therapy - streptomycin, para-aminosalicylic acid & isoniazid

  • 3 different antibiotics, twice a day for 6 months (costly)
  • Long term

DOTS – Directly Observed Treatment Short course

  • Microscopy services
  • Drug supplies
  • Surveillance
  • Political commitment
  • Monitoring systems

95% cure rate

Prevents transmission

42
Q

what is a common difficulty in treatment of respiratory tract infections?

A

hard to diagnose

Bacterial or viral? Hard to tell as symptoms are similar

43
Q

transmission of TB

A

inhalation of aerosolised respiratory droplet nuclei from infected person with active pulmonary TB

  • low infectivity among casual contacts
  • higher infectivity among long-term contacts especially in crowded conditions or closed air environments
44
Q

high risk factors for TB

A
  • close contact with known active TB case
  • residency in prison or health care facilities
  • HIV infection
  • injection drug abuse
  • alcoholism
  • contact with persons from high prevalence TB countries (Africa, Asia, Latin America)
45
Q

symptoms of TB

A 
malaise
productive cough for more than 3 weeks
headache, fever
weight loss, night sweats
blood in sputum
46
Q

diagnosis of TB

A
  • acid-fast bacilli in sputum
  • isolation of mycobacterium tuberculosis from sputum
  • skin testing (tuberculin testing) with purified protein derivative to determine infection
  • chest radiograph
47
Q

preventive therapy of TB

A

BCG vaccine

48
Q

pneumonia

A

an inflammatory condition of the lung – especially affecting the microscopic air sacs (alveoli)

49
Q

what typically causes pneumonia?

A

Typically caused by an infections, but multi- factorial

- Bacteria, viruses, fungi and parasites (often combination)

50
Q

what do most people die of?

A

pneumonia

Tipped over the edge

  • Cancer, care homes, hospitalised
  • Lungs less efficient - infection deep in lungs can no longer cope
51
Q

clinical features of pneumonia

A
  • Sudden or insidious onset
  • Fever, rigors, malaise
  • Shortness of breath, rapid shallow breathing, cyanosis
  • Cough producing purulent sputum
  • Consolidation of lungs on clinical and radiographic examination

flu like
generally need hospitalised

52
Q

causes of community acquired pneumonia

A

Streptococcus pneumonia

Viruses

  • Mycoplasma pneumonia
  • Haemophilus influenzae
  • Legionella pneumophila
  • Chlamydia pneumonia
  • Moraxella (branhamella) catarrhalis
  • Pneumocystis carinii
53
Q

causes of hospital acquired pneumonia

A

Esp if incubated standard oral care not as good as it should be
- Mouth is source of infection

  • Staphylococcus aureus
  • Gram-negative bacilli e.g. pseudomonas spp.
  • Klebsiella pneumoniae
  • Escherichia coli
  • Legionella pneumophila
54
Q

what is the main causative agent in bacterial pneumonia?

A

streptococcus pneumonia

55
Q

how is likely to be affected by streptococcus pneumonia?

A 
Affect young (children and neonates), elderly and immuno-compromised
- Less now due to vaccine
56
Q

cases and mortality rate of adult pneumococcal pneumonia

A

50,000 cases of adult pneumococcal pneumonia/year - 9000 fatalities per year (21% mortality rate)

57
Q

under 5 pneumococcal pneumonia infection rate

A

1 in 200 UK’s under 5’s admitted with pneumococcal pneumonia

58
Q

what type of infection in streptococcus pneumonia?

A

Encapsulated Bacterial Infection
- Cause infection as good at avoiding immune system

Capsule surrounds things

  • Can’t be seen by complement
  • Immune system become frustrated
  • Organisms of inflammatory nature = gram positive more
59
Q

how is streptococcus pneumonia adapted to infect people?

A

encapsulated

pneumolysin binds to tissue and can be free in solution and can bind to Fc portion of antibody

has adhesins

  • pneumococcal surface protein
  • pneumococcal surface adhesin
  • surface protein A
  • choline binding protein A
60
Q

clinical management of pneumonia

A

Antibiotics (iv), plus hospitalization?

  • beta-lactams, erthyromycin, quinolones
  • Pre-antibiotic era – 35% mortality
  • Resistance

Vaccination

  • Based on 23 different serotypes
  • Polysaccharide antigens ineffective at promoting memory – T-cell independent
  • Conjugate vaccines of polysaccharides and proteins appear efficaceous, with proper clinical intervention
61
Q

increasing issue with pneumonia treatment

A

Antibiotic therapy is increasingly ineffective due to increasing resistance of isolates (beta-lactams, erthyromycin, quinolones)
- Better to prevent than treat

Take key proteins to make multivalent vaccine

But, deal with one organisms but other organisms take over their place to cause pneumonia
- they adapt faster than we develop

62
Q

concern with hospital and dental chair water supplies and lines

A

bacteria biofilm can grow easily
- aerosolise when use hand-piece = spread

can cause Legionnaire’s disease

  • Inhalation of aerosols from contaminated water
  • Aspiration of oropharyngeal colonised bacteria

dental chairs have their own water supply - replace daily
hospital water supply is hard to be completely sterile

63
Q

legionnaire’s disease symptoms

A

Initially flue like symptoms which progress to a sever pneumonia
- Sometimes confusion, renal failure and GI symptoms

64
Q

legionnaire’s disease diagnosis

A
  • Culture and identification or demonstration in tissue or body fluids by immunofluorescence or DNA probes
  • Measurement of antibody levels
  • Chest radiographs
65
Q

legionnaire’s disease diagnosis

A
  • Erythromycin is drug of choice

Unresponsive to penicillin

66
Q

hospital associated pneumonia

A

Incubated - tube has potential to transmit as organisms can attach and spread into lungs, can die

Think of oral cavity for vulnerable cared for individual
- Toothbrushing, chlorhexidine - often overlooked but can prevent infection

67
Q

case mortality for Legionnaire’s disease

A
  • 5% in treated patients
  • 20-30% in untreated otherwise healthy patients
  • 24% in treat immunocompromised patients
  • 80% in untreated immunocompromised patients
68
Q

dentures as sources of respiratory tract infections

A

Patients often do not remove their dentures
- Microorganisms attach to denture
- Harbour more than their natural teeth
Aspiration pneumonia risk

69
Q

influenza characteristics

A
  • Types A, B, C
  • Diameter 80 - 120 nm
  • Pleiomorphic, spherical, filamentous particles
  • Single-stranded RNA
  • Segmented genome, 8 segments in A and B
  • Hemagglutinin and Neuraminidase on surface of virion
70
Q

classification of influenza

A

Classified on the basis of hemagglutinin (HA) and neuraminidase (NA)

15 subtypes of HA and 9 subtypes of NA are known to exist in animals (HA 1-15, NA 1-9)

3 subtypes of HA (1-3) and 2 subtypes of NA (1-2) are human influenza viruses. HA 5, 7, 9 and NA 7 can also infect humans

complex

71
Q

method of influenza infection

A

virus adsorbs to a respiratory epithelial cell by hemaglutinin spikes and fuses with the membrane

the virus is endocytosed into a vacuole and uncoated to release its B nucleocapsid segments into the cytoplasm

nucelocapsids are transported into the nucleus. There the (-) RNA strand transcribed into a (+) strand that will be translated into viral proteins that make up the capsid and spikes

(+) RNA is used to sythesise glycoprotein spikes inserted into the host membrane

(+) RNA strands are used to synthesis new (-) RNA strands. These are assembled into nucleocapsids and transported out of the nucleus to the cell membrane

Release of mature virus occurs when viral parts gather at the cell membrane and are budded off with an envelope containing spikes

72
Q

source of influenza infection

A

patients and carriers.

73
Q

mode of influenza transmission in humans

A

aerosol

- 100,000 TO 1,000,000 VIRIONS PER DROPLET

74
Q

common aerosol transmission of influenza virus

A

large droplets (sneezing, coughing, contact with saliva)

75
Q

probably common influenza transmission

A
  • contact
  • direct
  • fomite
76
Q

rare influenza transmission

A
  • airborne over long distance
77
Q

incubation for influenza

A

18-72 hours

78
Q

symptoms of influenza

A

Central
– headache

Systemic
– fever (usually high)

Muscular
– (extreme) tiredness

Joints
– aches

Nasopharynx
– runny/stuffy nose; sore throat; aches

Respiratory
– coughing

Gastric
– vomiting

79
Q

prophylaxis for influenza

A

Masks

  • Effectiveness not shown for influenza
  • However, could reduce transmission associated with large droplets

Handwashing
Generally perceived to be useful (No studies specifically performed for influenza)
Easy to recommend

80
Q

immunoprophylaxis with vaccine

A 
Inactivated:
(1) whole-virus
(2) subvirion
(3) purified surface antigen 
(Only subvirion or purified antigen should be used in children. Any of the three can be used for adults)

Live attenuated:

81
Q

free influenza vaccine recipients

A

Women in 2nd or 3rd trimester of pregnancy during flu season.

Household members of persons in high-risk groups

Health care workers and others providing essential community services.

82
Q

antivirals for influenza

A

Adamantanes and neurominidase inhibitors

83
Q

epidemic

A

The occurrence of more cases of disease than expected in a given area or among a specific group of people over a particular period of time*.

84
Q

pandemic

A

An epidemic occurring over a very wide area (several countries or continents) and usually affecting a large proportion of the population.

Examples:

  • Cholera
  • AIDS
  • Pandemic Influenza
85
Q

antigenic variation

A

Influenza viruses tend to undergo changes from time to time.

Changes in the antigenic characteristics of influenza viruses determine the extent and severity of influenza epidemics

There are two types of changes:

  • antigenic shift
  • antigenic drift
86
Q

2 types of antigenic variation

A

antigenic shift

antigenic drift

87
Q

antigenic drift

A

denotes MINOR changes in hemagglutinin and neuraminidase of influenza virus

results from mutation in the RNA segments coding for either the HA or NA

involves no change in serotype; there is merely an alteration in amino acid sequence of HA or NA leading to change in antigenicity.

88
Q

what causes antigenic drift

A

results from mutation in the RNA segments coding for either the HA or NA

89
Q

what is the consequence of antigenic drift

A

involves no change in serotype;

there is merely an alteration in amino acid sequence of HA or NA leading to change in antigenicity.

90
Q

antigenic shift

A

denotes MAJOR changes in hemagglutinin and neuraminidase resulting from reassortment of gene segments involving two different influenza viruses

When this occurs, worldwide epidemics may be the consequence since the entire population is susceptible to the virus

91
Q

consequence of antigenic shift

A

worldwide epidemics may be the consequence since the entire population is susceptible to the virus

92
Q

1918 flu pandemic

A

May have killed as many people as the Black Death- bubonic plague
- The majority of deaths were from a secondary infection such as bacterial pneumonia

It killed between 2 and 20% of those infected; normal mortality rate is 0.1%

It mostly killed young adults with more than half of the deaths in people between 20 - 40 years old due to novel surface proteins on the virus.

It killed as many as 25 million in the first 25 weeks, whereas HIV/AIDS has killed 25 million in the first 25 years.

BDS2 BAMS (54 decks)

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