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CAM201 Microbiology > URTI II > Flashcards

URTI II Flashcards

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1
Q

Sinusitis

A

Inflammation and infection of the paranasal sinuses.

Paranasal sinuses are usually sterile under normal conditions, unlike the nasal passages (which are heavily colonised by bacteria)

Mechanisms that usually ensure the sterility of sinuses are thought to include:

  • Local immune response (IgG, A, M and E; complement; and enzymes and proteins like lysosomes ad lactoferrin, for example)
  • Mucociliary clearance
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2
Q

Epidemiology sinusitis

A

Appears to aprallel the epidemiology of the common cold.

Occurs in:

  • 0.5-13% of viral URTI cases lead to bacterial sinusitis
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3
Q

Pathogenesis of sinusitis

A

The pathogenesis of sinusitis appears to depend upon a combination of the following events:

  • The narrow alibre of the sinus ostia; and other factors that further contribute to ostia blockage/obstruction
  • Dysfunction of the mucociliary apparatus
  • Viscosity of the sinus secretions
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4
Q

Factors that predispose to sinus ostial obstruction

A

Mucosal swelling

  • Viral URTI
  • Allergic inflammation
  • CF
  • Immune disorders
  • Immotile cilia
  • Tobacco smoke
  • Facial trauma
  • Overuse of nasal decongestants
  • Nasal intubation

Mechanical obstruction

  • Choanal atresia (nasal passage blockage)
  • Deviated septum
  • Nasal polyps
  • Foreign bodies
  • Tumor(s)
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5
Q

Sinusitis microbiology

A

The most common types of organisms affecting all age groups appears to be:

  • Streptocccus pneumoniae
  • Haemophilus influenzae
  • Other Streptococcus species (S. pyogenes etc)
  • Mixed anaerobes
  • Moraxella catarrhalis
  • Staphylococcus aureus
  • Fungi
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6
Q

Clinical manifestations of sinusitis

A

The pathogenesis of sinusitis and viral URTI are similar. The clinical manifestations overlap greatly.

Uncomplicated viral URTI usually has a typical course of 5-10 days.

  • Symptoms lasting >10 days without improvement is usually consistent with an acute bacterial infection.
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7
Q

Acute sinusitis

A
  • Persistent nasal discharge (thick, thin, serous, mucoid, or purulent [yellow/green])
  • Cough (wet or dry, particularly in the daytime)
  • Development of a high fever (>38.5) lasting 3-4 consecutive days
  • Patient might then appear to begin feeling better but then relapse with:
    • Fever
    • Exacerbation of nasal discharge and congestion, and cough
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8
Q

Chronic sinusitis

A
  • Symptoms lasting for at least 12 weeks
  • Mucopurulent drainage
  • Nasal congestion/obstruction
  • Facial pain on pressure (i.e. from build up of pus)
  • Hyposmia (loss of sense of smell)
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9
Q

Complications of chronic sinusitis

A

These are rare.

  • Orbital cellulitis
  • Orbital abscess
  • Brain (intraparenchymal) brain ascess
  • Meningitis
  • Venous sinus thrombosis
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10
Q

Diagnosis of sinusitis

A

Made on clinical grounds in most patients.

Symptoms and signs in the diagnosis of sinusitis might include:

  • Maxillary toothache
  • No improvement with decongestants
  • Cough
  • Sore throat
  • Headache
  • Purulent secretion
  • Sinus tenderness (facial pain)
  • Fever

Imaging (CT scans) are often reserved for patients presenting with rare complications, or for whome surgery is being considered.

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11
Q

Sinusitis treatment

A

Antimicrobial treatment

  • Amoxycillin
  • Augmentin
  • Cefaclor

Adjunctive treatment?

  • Large volume saline irrigation
  • No significant improvement with corticosteroid or antihistamines in clinical trials

Surgical intervention (complications of acute sinusitis)

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12
Q

Define acute otitis media

A

Defined as the presence of middle ear fliuid that is accompanied by inflammation of the mucosa that lines the middle ear space.

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13
Q

Epidemiology of otitis media

A

Often occurs secondary to viral URTI.

Peak incidence is in the first 3 years of life; highest rates in 6 to 24 months of age

Incidence declines with age, but then increases for school aged children (5 to 6 years of age)

Relatively rare in adults: but if suffered AOM in childhood can present with:

  • Hearing loss
  • Cholesteatoma
  • Chronic perforation of the tympanic membrane

Incidence also appears to be higher in boys that girls.

Can be recurrent and particularly severe in:

  • Indigenous people (Australian aborigines)
  • Children being breast fed for <3 months
  • Children with anatomical abnormalities (cleft palate, cleft uvula, sub-mucous cleft) and defects in physiological defenses (patulous eustachian tube)
  • Children placed in large daycare centres
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14
Q

Otitis media pathogenesis

A

The eustachian tube usually performs the following:

  • protection of the ear from nasopharyngeal secretions
  • Drainage of middle ear secretions into the nasopahrynx
  • Ventilation of the middle ear (equilibrate air pressure with that in the external ear canal)

AOM is thought to occur via the following pattern of events

  • Congestion of the mucosa of the URT (commonly precipitated by viral URTI)
  • Swelling of the mucosa of the austachian tube progressing to obstruction at its narrowest section (isthmus)
  • Accumulation of secretions behind the obstruction, providing a medium for bacterial growth
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15
Q

Microbiology of AOM

A

Bacteria involved in AOM include

  • Streptococcus pneumoniae
  • Haemiphilus influenzae
  • Moraxella catarrhalis
  • *Strepcoccus pyogenes *(now uncommon cause)
  • *Staphylococcus aureus *(uncommon cause, associated with placement with tympanostomy tube)

Viruses include

  • Respiratory syntial virus (RSV)
  • Influenza virus
  • Enteroviruses
  • Coronaviruses
  • Rhinoviruses
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16
Q

Clinical manifestations of otitis media

A

Specific symptoms and signs

  • Ear pain
  • Ear drainage
  • Hearing loss
  • Presence of fluid in the middle ear (assessed by otoscopy) dampens mobility of the tympanic membrane
  • Erythema of tympanic membrane

Non-specific signs and symptoms

  • ​Fever
  • Lethargy
  • Vertigo
  • Irritability
  • Tinnitus
  • Nystagmus
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17
Q

Otitis media complications

A

Mastoiditis

Fluid in the middle ear can lead to inflammation and oedema of the mastoid air cells, resulting in swelling, redness and tenderness ove rthe mastoid bone.

Serous and then purulent exudate collects in the cells.

Necrosis of the mastoid bone is then caused by the pressure of the purulent exudate on the bony septa

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18
Q

Otitis media treatment

A

Antimicrobial treatment should usually be active against common agents (S. pneumoniae; H. influenzae; and M. catarrhalis (may not be required* in the absence of fever and vomiting): If present then:

  • Amoxycillin (oral)
  • Cefaclor (orally; if hypersensitive to penicillin)

In cases of chronic suppurative OM:

  • Dexamethasone + framycetin + gramicidin ear drops; 3 drops, 6- hourly until middle ear is free of discharge for ~3 days (treatment should be no more than 7 days)

Surgical management

  • Tympanostomy tube (grommet)
  • Myringotomy
  • Removal of adenoids (only in some patients)
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19
Q

Pneumococcal vaccine

A

Form of prevention of otitis media.

23 valent Pneumococcal polysaccharide vaccine

Greatly reduces Pneumococcal infections in:

  • Aboriginals & Torres Strait Islanders
  • Elderly
  • Children
  • Immunosuppressed
20
Q

Otitis externa

A

Infection of the external auditory canal, as a result of maceration of the superficial layers of the epithelium (similar to other skin and soft tissue infections)

Infections usually subdivided into four categories:

  • Acute localised otitis externa
  • Acute diffuse otitis externa
  • Malignant (necrotising) otitis externa
21
Q

Clinical manifestations of otitis external

A

Also called furunculosis.

  • Pustule or furuncle associated with hair follicles.
  • Skin of the canal is usually erythematous, edamatous, and might be filled with pus and skin debris.
  • Staphylococcus aureus is the most frequent pathogen
22
Q

Clinical manifestations of acute diffuse otitis externa

A
  • Ear itches, and becomes increasingly painful
  • Skin of the canal is erythematous and edematous
  • Usually occurs in hot weather and with water (swimmer’s ear)
  • Pseudomonas aeruginosa is the most frequent pathogen (and less commonly fungi, Candida species, for example)
23
Q

Malignant otitis externa

A
  • Necrotising infection that spreads from the squamous epithelium of the ear canal to the adjacent areas of soft tissue, blood vessels, cartilage, and bone of the external canal and base of skull.
  • Severe pain and tenderness of the tissues aorund the ear and mastoid.
  • Potentially life threatening (can spread to the base of the skull, meninges and brain)
  • *P. aeruginosa *is almost always the cause
24
Q

Laboratory diagnosis of otitis externa

A

Ear swap sent for microbiology, cuture and abx sensitivity testing.

25
Q

Acute localised otitis externa treatment

A
  • Cleaning of ear and abx (usually di/flucloxacillin) usually curative
  • Incision and drainage of pustule may be necessary to relieve pain.
26
Q

Acute diffuse otitis externa treatment

A
  • Dexamethasone + framycetin + gramicidin ear drops; 3 times daily for 3-7 days (no more than 7 days)
  • For fungal infections (Candida, for example): flumethasone + clioquinol ear drops; twice daily for 3-7 days
27
Q

Malignant otitis media diagnosis and treatment

A

Canal should be cleansed, necrotic tissue removed and ear drops with antipseudomonal abx combined with topical corticosteroids should be instilled into the external canal.

Consult infectious disease physicial and otolaryngologist.

Systemic )antipseudomonal) abx include combinations of

  • Ceftazidime, piperacillin + tazobactam PLUS an aminoglycoside (gentamicin)
28
Q

*Bordatella pertussis *microbiology

A
  • Small gram-negative bacillus; grows aerobically at 35 degrees and does not ferment carbohydrates.
  • Strictly human pathogen
  • It is a fastidious organism, and grows best in media supplemented with blood, charcoal or starch.
29
Q

Pathogenesis of whooping cough

A

Bordatella pertussus attaches to cilia in the respiratory tract, causing ciliary stasis.

30
Q

Clinical presentation of whooping cough

A

Varies depending on patients age; degree of immunity and rspiratory co-infection.

In young children, classicially divided into:

  • Catarrhal stage
  • Paroxysmal stage
31
Q

Catarrhal stage

A

After an incubation period of 7-10 days, can range from 5-21 days

  • Signs and symptoms of URTI and rhinorrhea
  • Non-purulent conjunctivitis
  • Occasional cough
  • Low grade fever
  • Typically lasts 1-2 weeks
32
Q

Paroxysmal stage

A
  • Fits of coughing (10 to 15 coughs in a singe expiration) which at teh end might be associated with inspiratory whoop (inspiration against partially closed glottis)
  • Coughin spasms more frequent at night
  • Force of cough produces mucus plugs and usually post-tussive vomiting
  • Typically lasts 1 to 6 weeks
  • Then symptoms wane, and patiet enters the convalescent stage
33
Q

Clinicla and laboratory diagnosis of whooping cough

A

Clinical defined as a patient with a cough lasting >14 days with at least one of the following:

  • Paroxysmal cough
  • Inspiratory whoop
  • Post-tussive vomiting

Confirmation requires a positive laboratory finding by:

  • Culture (nasopharyngeal aspirate, swab, bacteria on charcoal again)
  • PCR
  • Serology (detect antibodies made against PT, lipopolysaccharide and adenylate cyclase enzyme, for example).
34
Q

Whooping cough treatment

A

Antibiotics

  • Azithromycin
  • Clarithromycin
  • Erythromycin
35
Q

Whooping cough prevention

A
  • DTPa vaccine (at 2, 4, 6 months; at 4, 15 years of age)
  • Vaccination rates 90-100%
  • Contacts of pertussis cases should be identified and alerted and prophylaxis recommended, including to:
    • Household members
    • Women in their last month of pregnancy
    • Childcare centres
    • Healthcare workers in maternity hospitals
36
Q

Epidemiology of croup

A

Also known as acute laryngoytracheobronchitis

Age specific viral infection causing inflammation of the subglottic area accompanied by:

  • dyspnoea
  • Characteristic stridor

Predominantly affects your children:

  • Children 3mnths - 3 years of age
  • Peak incidence second year of life
  • 5% of children have recurrent croup (3 or more cases)
37
Q

Microbiology and pathophysiology of croup

A

Usually occurs with the appearance of the common cold viruses, including:

  • Parainfluenzae types 1-3, rhinovirus, enteroviruses, RSV, influenza virus, adenovirus and bocavirus.
38
Q

Clinical presentation of croup

A

Affected children generally have a prodrome (12 to 48 hours) or URT infection signs, including:

  • Rhinorrhea
  • Cough
  • Fever (occasionally)

Then they develop:

  • Hoarseness
  • Characteristic cough
    • ‘Brassy tone’ akin to seal’s bark
    • Not productive
    • Increased at night, mild during the day, then worse again at night.

Most cases of croup last <3-4 days; barking cough resolves within 2 days.

39
Q

Diagnosis of croup

A

Diagnosed on clinical presentation. There is usually no need to identify causative agent (unless in severe cases associated with Influenza virus).

40
Q

Croup treatment

A

Largely supportive (at home) but in severe cases, dexamethasone (orally or intramuscular) can be considered.

41
Q

Epiglottitis epidemiology

A

Cellulitis of the epiglottis may cause abrupt and complete airway obstruction (hence, represents a medical emergency)

Typical patient used to be young child (2-4 years of age) but widespread use of *Haemophilus influnzae *type B (Hib) vaccine has dramatically decreased the incidence in this populatio.

Presentation is also in adults 9presenting with severe sore throat)

  • 2:1 male predominance
  • Majority of patients usually have good health but some having underlying disease and immune response insufficiency
42
Q

Causes of epiglottitis

A

Some causative infectious agents:

  • Haemophilus influenzae type B
  • H. parainfluenzae
  • Streptococcus pneumoniae
  • S. pyogenes
  • Herpes virus

Other causes

  • Hot water ingestion or inhalation
  • Smoking illicit drugs
  • Blind finger sweep
  • laryngeal mask
  • Tonsillectomy complication
  • Gastroesophageal reflux
  • Caustic ingestion
  • Chloramines in pool water
43
Q

Epiglottitis clinical presentation in pediatric patients

A
  • History of fever (6-12 hours)
  • Irritability
  • Dysphonia
  • Dysphagia
  • Prefer to sit leaning forwatd with drooling (of oral secretions)
  • Respiration is tentative
  • Inspiratory stridor
  • Hoarseness

`

44
Q

Epiglottitis clinical presentation in adult patients

A
  • Severe sore throat
  • Dyspnoea
  • Odynophagia
  • Stridor
45
Q

Epiglottitis diagnosis

A
  • Examination of the epiglottis should only ever be performed where preparations have been made to secure the airway immediately
    • Examining children, in particular, for airway obstruction is not recommended because mortality increases by 25% in those observed.
  • Blood cultures positive for *Haemophilus influenzae *type B
  • Samples of the epiglottis for cuture can be taken but only after an artificial airway has been secured.
46
Q

Treatment of epiglottitis

A

Focused on maintaining the airway

Control of infection (empirical therapy):

  • Ceftriaxone, or cefotaxime (IV) usually over a 5-10 day period
  • Patients usually show signs of recovery 12-48 hours after initiation of abx therapy

CAM201 Microbiology (7 decks)

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