19 Upper respiratory tract infections Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Introduction

A

We distinguish between upper and lower respiratory tract, even though it is a continuum. Some organisms have a preference (e.g nasopharynx - cornaviruses/ rhinoviruses)

Proximal to distal - Rhinitis, sinusitis, pharyngitis, laryngitis, tracheitis, bronchitis, bronchilotis, pneumonia

Some microorganisms are restricted to surface of epithelium. Some spread to other parts of body before returning to respiratory tract/ oropharynx/ salivary glands e.g mumps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are “professional “ invaders, and “secondary invaders”

A

Professional successfully infect the normal healthy respiratory tract, and can evade local host defences, e.g attachment mechanisms for respiratory viruses

Secondary invaders cause disease only only when host defences are already impaired e.g staph aureus after influenza

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Normal flora of respiratory tract

Common >50% people
Occasional <10% people

A
Streptococci
Neisseria spp
Moraxella
Corynebacterium
Bacteroides
Candida albicans
Haemophilus influenzae

Streptococcus pneumoniae
Streptococcus pyogenes
Neisseria meningitidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal flora of respiratory tract

Uncommon <1% people
Residents in latent state in tissues

A

Corynebacterium diptheria
Klbesiella pneumoniae
Pseudomonas
E. Coli

Pneumocystis jirovecii
Mycobacterium TB
CMV
EBV
HSV
VZV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathogens which gain access via upper respiratory tract through the surface

Short incubation period. Local defences breeched, and infection established before adaptive immune response active

A
Rhinoviruses
Influenza
Streptococci in throat
Chlamydia (conjunctivitis)
Diptheria
Pertussis
Candida albicans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathogens which gain access via upper respiratory via spreading through body

Little or no entry in respiratory system. Pathogen spreads throughout body, returns to surface for final multiplication and shedding. Adaptive immune system important in recovery, longer incubation (weeks)

A
Measles - respiratory tract
Mumps - salivary gland
Rubella
EBV - salivary gland
CMV - salivary gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Professional invaders

What are examples of pathogens which -

  • Adhere to normal mucosa (in spite of mucociliary system)
  • Ability to interfere with cilia
A

Respiratory viruses - influenza, rhinovirus
Strep pyogenes
Strep pneumoniae
Chlamydia

Bordetella pertussis
Mycoplasma pneumoniae
Strep pneumoniae (pneumolysin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Professional invaders

What are examples of pathogens which -

  • Resist destruction by alveolar macrophage
  • Damage local mucosa/ submucosal tissues
A

Legionella
TB

Corynebacteriym diptheriae (toxin)
Strep pneuomniae (pneumolysin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Secondary invaders

What are examples of pathogens which -

  • Infect after initial damage by respiratory virus
  • Infect when local defences impaired (e.g cystic
    fibrosis)
  • Infect in chronic bronchitis, local foreign body or tumour
A

Staph aureus
Strep pneumoniae

Staph aureus
Pseudomonas

Haemophilus influenzae
Strep pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Secondary invaders

What are examples of pathogens which -

  • Infect when immune response depressed
  • Infect when resistance depressed - elderly, alcoholism, CKD, liver disease
A

Pneumocystis jirovecii
CMV
TB

Strep pneumoniae
Staph aureus
Haemophilus influenzae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Respiratory viruses cause common cold. They induce flow of virus rich fluid (rhinorrhoea), and sneezing triggers release of virus particles into air - aerosol transmission.

Most respiratory viruses have surface molecules which allows them to bind to microvilli, so they are not washed away in normal respiratory secretions.

Once first cell is infected, virus progeny from spread to neighbouring cells and via surface secretions to new sites on mucosal surface. Damage to epithelial cells and release of inflammatory mediators such as bradykinin lead to cold type symptoms

How are most virus infections diagnosed?

A

Viral PCR used these days

Use throat swabs

Avoid nasopharyngeal aspirates, as risks aerosol production of pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the attachment mechanism for the following viruses and what disease can it cause

  • Rhinovirus (>100 types)
  • Enteroviruses including:
    Coxsackie virus A (24 types)
    Echoviruses (34 types)
    Enteroviruses (116 serotypes)
A

capsid protein binds to ICAM-1 (intercellular adhesion molecules expressed on wide variety of normal cells) - common cold

Capsid protein binds to ICAM-1
Common cold, hand foot and mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the attachment mechanism for the following viruses

  • Influenza (A, B, C)
  • parainfluenza (1,2,3,4)
  • RSV (A, B)
A

Haemagglutinin binds neuraminic acid containing protein on cell surface

Viral envelope proteins binds to glycoside on cell

G protein on virus attaches to receptor on cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the attachment mechanism for the following viruses and what disease does it cause

  • Coronaviruses (several types)
  • Adenovirus (41 types)
A

Viral envelope protein binds to glycoprotein receptors on cell - common cold, SARS, Middle East respiratory syndrome coronavirus (MERS CoV)

Penton fibre binds to cell receptor
Pharyngitis, conjunctivitis, bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Common viruses which cause acute pharnygitis 8

Viruses inevitably encounter the submucosal lymphoid tissue that form a defensive risk around the oropharynx.

A
Rhinoviruses
Coronavirus
Adenovirus
Influenza
Parainfluenza - more severe than common cold
Enteroviruses including Coxsackie A16 - small vesicles on hard palate/ tongue (hand, foot and mouth)
EBV
HSV1 - hard palate/ tongue vesicles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Common bacteria which cause acute pharyngitis

A

Streptococcus pyogenes - usually 5-10 years old
Neisseria gonorrhoeae - often asymptomatic
Corynebacterium diptheriae - can be severe
Haemophilus influenzae - epiglottitis
Borrelia vincentti - Vincent’s angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Routes of transmission for CMV

CMV humans are natural hosts

A
Saliva
Blood
Organ donor
Urine
Semen/ cervical
Breast milk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CMV causes silent infection, often asymptomatic.

Spreads to lymphoid tissues, then systemically via circulating lymphocytes and monocytes to involve lymph nodes/ spleen and epithelial cells of salivary gland/ kidney tubules/ cervix/ semen, where it is shed to outside world.

How does CMV cause disease

A
Inhibits T-cell response by interfering with MHC class I expression
Induces Fc receptors on infected cells to help spread

Causes no illness in children, mild disease in adults. Cell mediated immunity helps keep virus at bay, but cannot clear it, remains throughout life. Can cause disease one immunity impaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does CMV spread to foetus

A

Primary infection during pregnancy allows spread of virus from blood to placenta, then to foetus. 18% foetus symptomatic at birth. CMV second only to Down’s syndrome as cause of intellectual disability

20
Q

What are symptoms of CMV

A

In immunodeficiency such as HIV, bone marrow/ solid organ transplant

Interstital pneumonitis with infiltrating infected mononuclear cells
CNS
Retinitis
GI - colitis, hepatitis

21
Q

Diagnosis of CMV

Cannot diagnose clinically, as usually asymptomatic

A

CMV IgM/ IgG. Not very helpful in immunosuppressed patient.

Use CMV DNA level monitoring if CMV positive prior to immunosuppression

Pneumonitis - bronchoalveolar lavage for CMV DNA/ Antigen detection
Colitis - biopsy

22
Q

Treatment CMV

Treatment CMV pneumonitis

CMV vaccine has been trialled, as it is big cause of intellectual disability, and morbidity in immunosuppressed. CMV glycoprotein B vaccine helps generate antibodies to reduce future viraemia if becomes infected

A

Ganciclovir
Foscarnet

Anti-virals reduce viral replication, do not eliminate virus

CMV pneumonitis is immunopathological process, CMV specific or normal human immunoglobulin is given to help block Tc-cell response to pneumocytes expressing the target antigens. Also give anti-virals

23
Q

EBV humans are natural host. Virus is morphologically identical to other herpesviruses, but antigenically distinct.

What are the antigens?

How is it transmitted

A

Viral capsid antigen (VCA)
EBV associated nuclear antigen (EBNA)

Exchange of saliva - e.g kissing
Therefore peaks occur in children (sub-clinical), and 14-20 years old

24
Q

Explain local body spread of EBV infection from initial infection

What is incubation period

A

EBV replicates in local B lymphocytes after attaching to C3d (CD21) receptor, in oropharynx. Virus also infects oropharyngeal epithelial cells. Virus is shed from lymphocytes/ epithelial cells into salivary gland

B lymphocytes spread via blood to liver/ lymph nodes/ spleen

4-7 weeks

25
Q

What is immune response to EBV?

A

T cells respond to infected B cells. T-cells appear as atypical lymphocytes on blood film. T-cells destroy infected B cells to gradually clear the infection. This cause lymphadenopathy

Immune response usually weak, and produces no clinical symptoms in children.

IFN-gamma produced by T-cells and NK cells contribute to symptoms. Infected B cells produce polyclonal antibodies and other auto-antibodies, which can cause AIHA

26
Q

What are clinical features and severe complications

A
Fever
Sore throat
Petechiae on hard palate
Lymphadenopathy
Splenomegaly
Lethargy
Hepatitis

Severe complications -
aseptic meningitis
airway obstruction
haemophagocytic syndrome

27
Q

How does EBV remain latent

A

Acts against complement and IFN
Produces it’s on fake IL-10, which interferes with hosts normal IL-10
Prevents apoptosis of infected cells

28
Q

How to diagnose EBV

Treatment

A

Usually clinical diagnosis

VCA IgM/ VCA IgG in serum
EBNA IgG appears few weeks after symptoms

Atypical lymphocytes on blood film
Heterophil antibodies to horse/ sheep erythrocytes in monospot test

Antivirals not used in immunocompetent
Antivirals only work on lytic part of infection

29
Q

Which cancers are associated with EBV (4)

A

Burkitt’s lymphoma in Africa/ PNG. Restricted to certain areas, so clear that EBV alone does not cause lymphoma. Co-carinogen malaria, weaknes T-cell control of EBV infection, and possibly increases activation of B cells. This increased B-cell turnover can lead to neoplastic transformation

B-cell lymphoma - usually if primary EBV vaccination post-transplant. EBV DNA found in tumour cells, which also show translocation of c-myc oncogene

Post-transplant lymphoproliferative disorder - due to uncontrolled B-cell proliferation related to EBV

Nasopharyngeal carcinoma - SE asia. EBV DNA in tumour cells. Co-carcinogen may be ingested nitrosamines from preserved fish

30
Q

What are compliciations of strep pyogenes infection

A

Peritonsilar abscess - quinsy

Otitis media/ sinusitis/ mastoiditis

Scarlet fever - certain strains produce erythrogenic toxin , which localises in skin, and causes erythematous rash. Rash, sore throat, red cheeks, swollen tongue. Then get skin desquamination. Highly contagious

Impetigo/ erysipelas/ cellulitis

Pneumonia

Rheumatic fever - antibodies formed to antigens in streptococcal cell wall, cross-react with sarcolemma of heart. Myocarditis develops after 2-4 weeks. Duckett-Jones criteria for diagnosis

Rheumatic heart disease - repeated attacks strep pyogenes with different M types can damage heart valves. May need prophylaxis. Most common cause heart disease in resource poor settings

Glomerulonephritis - immuno complexes form which are deposited in glomeruli. Immune cells are recruited, and cytokines released, causes inflammation. Develop oedema/ HTN 1-2 weeks after sore throat

31
Q

Diagnostic criteria for rheumatic fever
Revised Duckett-Jones criteria

Acute RF -
2 major or
1 major plus 2 minor

A
Major -
Carditis
Arthritis
Chorea - jerky motion
Erythema marginatum - pink rings come and go
Subcutaneous nodules
Minor -
Polyarthalgia
Fever
Raised CRP/ ESR
Prolonged PR interval on ECG
32
Q

Diagnosis of strep pyogenes

Treatment

A

Throat swab
Blood culture

GAS are sensitive to penicillin

33
Q

Which bacteria cause Group A Strep

16% of schoolchildren carry GAS in throat during winter

A

Strep pyogenes
Strep anginosis
Strep dysgalactiae

34
Q

How does mumps spread?

What is it’s route through the body

When are patients with mumps infectious?

A

Airborne droplets/ salivary secretions

Multiply in epithelium of respiratory tract
Spread to local lymph nodes - multiplies there
Primary viraemia
Spread to salivary gland/ testes/ pancreas/ CNS/ kidneys - replication causes oedema and symptoms

Infected patient is contagious from 3 days before symtpom onset, to 6 days after symptom onset

35
Q

Age of peak incidence of mumps

Incubation period of mumps

Symptoms of mumps

Reinfection can occur after primary infection, or after MMR vaccine

A

5-14 years old

16-18 days

Painful/ swollen parotid glands
Fever
Orchitis
Pancreatitis

36
Q

Diagnosis of mumps

Treatment

Prevention

A

viral RNA throat swab/ CSF/ urine
Mumps IgM

Symptomatic treatment

MMR live attenuated vaccine

37
Q

Acute otitis media occurs due to purulent material building up leading to a bulging, red, tympanic membrane which may rupture and discharge.

Why is more common children?

Most common viral/ bacterial organisms

A

Eustachian tube is open more widely, and is shorter

RSV - most common
Strep pneumoniae
H Influenzae
M Catarrhalis
S pyogenes
38
Q

Signs of acute otitis media

Treatment

If acute attacks of otitis media are not properly treated, can develop chronic suppurative otitis media

A

Fever
Bulging tympanic membrane

Fluid may persists in ear after treatment (glue ear), can can cause hearing and learning difficulties

Analgesia
Antibiotics if systemic involvement - amox/ clari

39
Q

Causes of otitis externa

Treatment

A

External canal has bacterial flora similar to that of skin, so pathogens are usually different to otitis media

S Aureus
Candida albicans
Proteus
Pseudomonas

Neomycin/ chloramphenicol drops

40
Q

Causes of acute sinusitis

Treatment

A
Same as otitis media:
RSV - most common
Strep pneumoniae
H Influenzae
M Catarrhalis
S pyogenes

Viral cause most common by far. If duration more than ten days, likely to be bacterial in origin.

Amox/ co-amox/ clari empirically
Consider CT if considering complications

41
Q

Acute epiglottiitis seen in young children. Hib vaccine has reduced incidence

What is the most common cause

What is main complication

Treatment

A

H Influenzae capsular type B
Spreads from nasopharynx to expiglottis causing severe inflammation and oedema. Can look similar to diptheria

Airway obstruction - may need intubation

Antibiotics e/g cefotaxime

42
Q

Oraal cavity is continous with pharynx, but is different as has teeth, which specific bacteria attach to. 1 litre of saliva per day produced. Contains lysozyme, lactoperoxidase, antibodies to help find infection

When does candida albicans establish infection

Treatment oral candida

A

Prolonged antibiotic courses
Immunocompromised - HIV/ chemotherapy

Nystatin
Fluconazole

43
Q

Which bacteria cause dental caries
How does it gain competitive advantage

Bacteria form dental plaque on tooth surface by synthesising glucan (polysaccharide) which forms matrix between streptococci. Removed with brushing, but re-establishes after few hours.

Bacteria use dietary sugar to form lactic acid, which decalcifies teeth, and proteolytic enzymes to break down enamel and cause tooth cavity

90% people colonised with this bacateria, so may be regarded as most prevalent infectious disease in resource-rich countries

A

Step mutans

Produces bacteriocins which kill other bacteria
Reduces pH to 4.0 to kill other bacteria

44
Q

Gingival crevice forms between gums and tooth margin, can develop peridontal disease

Which bacteria cause peridontal disease

In disease, gingival crevice increases in size, and becomes a pocket of exudate. Activated macrophages release cytokines which activates peridontal fibroblasts and matrix metalloproteinases causing collagen degredation. Structures supporting teeth such as ligaments weaken, and tooth becomes looser. Gums bleed easily and then recede. Major cause of tooth loss

A

Actinomyces viscosus
Actinobacillus
Fusobacteriym
Bacteroids

45
Q

Treatment of:

  • Mastoiditis
  • Otitis externa
  • Otitis media
  • Quinsy
A
  • Mastoiditis - contact ENT
  • Otitis externa - no treatment
  • Otitis media - most cases viral, just analgesia. If chronic (>4 days) then amoxicillin or clarithromycin for 5 days
  • Quinsy - benzylpenicillin and metronidazole, clindamicin second line
46
Q

In sore throat/ pharyngitis, how do you decide who should get treatment

What is treatment

Beware EBV which when given penicillin can cause rash

A

Patients with 3 of 5 centor criteria (history of fever, purulent tonsils, cervical adenopathy, absence of cough, age) or history of otitis media may benefit more from antibiotics.

PenV
Clarithromycin
Co-amoxiclav if EBV

47
Q

Treatment of:

  • epiglottitis
  • acute sinusitis
  • chronic sinusitis
  • whooping cough
A
  • Epiglottitis - Cefotaxime
  • acute sinusitis - usually viral, nsaisds
  • chronic sinusitis - co-amoxiclav, clarithromycin, doxycyline
  • whooping cough - antibiotics have little effect in paroxysmal stage. Clarithromycin