Infectious Disorders (Raf with Danielle additions) Flashcards
1
Q
What is the most common type of pulmonary infection in HIV?
A
- Bacterial pneumonia
- TB
2
Q
Echinococcus genus (hydatid organism)–>how is it passed on? What is the treatment?
A
- Passed to humans by contact with eggs in feces of definitive host (eg. fox, wolf) or close contact with canine or sheep
- Treatment: surgical resection, or percutaneous drainage with treatment with albendazole, which also potentially used after treatment. For Canadian variety, may ok to just use medical treatment and not surgical
3
Q
Post exposure prophylaxis for varicella?
A
Red Book algorithm
Immune or not?
Any contraindications to vaccine, which is ideally within 5 days?
If can’t get vaccine, are they within 10 day time frame for VZIG?
4
Q
What does and duration of prednisone is defined as immunosuppression?
A
> =2 mg/kg/day x 14 days
5
Q
What is the evidence for high flow in bronchiolitis?
A
CPS statement re: evidence in general:
- Extensive neonatal literature that there is decreased need for intubation and ventilation. (They don’t go into details about specific disease conditions)
- Pediatric studies have suggested reduced need for intubation, but studies were inadequately powered to show difference in mortality or length of icu stay. (They don’t specify these pediatric conditions)
Bronchiolitis:
NEJM 2018:
- Largest RCT to date
- Infants <12 months of age requiring oxygen for bronchiolitis were randomized to either receive low flow oxygen therapy or high flow at 2 L/kg/min
- Primary outcome: therapy escalation
- Secondary outcome: various including transfer to ICU, mortality, length of stay, intubation
- Finding: children on high flow were less likely to have an escalation in therapy compared to children on low flow, but there were no differences in any of the secondary outcomes, such as transfer to ICU
- Key critiques:
- The jump from high flow to further escalation is perceived as a bigger jump than from low flow to high flow, so this could explain the differencethey try and account for the difference in RR before escalation of therapy by doing a sensitivity analysis
- The presence of an ICU on site also affected decision for escalation of therapybut they also try and account for this with sensitivity analysis
6
Q
Radiographic signs for Echinococcus
A
1) Meniscus sign/crescent sign
2) Cumbo sign/onion peel (double air layer appearance/onion peel/double arch)
3) Water lily
4) serpent sign
5) cavity
6) well defined round opacity (due to uncomplicated cyst, no rupture)
4) U/S: same as CXR + honeycomb appearance, ball of wool sign, cyst wall calcification
7
Q
3 major forms for Echinococcus
A
Cystic (predominant form affecting lungs)
Alveolar
Polycystic
(two major organs affected are liver and lung. In children, lung is more commonly affected)
8
Q
Treatment for Echinococcus
A
U/S guided aspiration of cysts
Surgery
Drugs: Albendazole or Mebendazole
9
Q
Mechanisms of Acute Flaccid Paralysis causing lung disease
A
Atelectasis
Aspiration
Hypoventilation/respiratory muscle weakness
Secondary infection
Guillam Barre = autonomic neuropathy - cardiac failure - pulmonary edema
10
Q
Causes of Acute Flaccid Paralysis
A
Enterovirus: polio and non-polio enteroviruses, D68 (anterior horn cell) West Nile (anterior horn cell) Guillain Barre (axon demyelination) Adenovirus (anterior horn cell) Botulism (NM junction) Tetanus (NM junction) Spinal cord compression
11
Q
What are features of an airborne isolation room?
A
- negative pressure ventilation
- door closed at all times
- no opening of windows
- bathroom and hygeine area for patient
- handwashing sink for healthcare staff
- exhaust of air goes to outside of the building
- air has to go through HEPA filter before going to general circulation
- healthcare workers must wear N95 and be fit tested
12
Q
Infectious disorders that cause GBS?
A
Often prior infection, resulting in molecular mimicry:
- Campylobacter jejuni - most important
- Mycoplasma pneumonia
Viruses- CMV, EBV, HIV, Influenza
- post vaccination, such as influenza
13
Q
What organisms is a patient with CGD at risk of?
A
recurrent infections with catalase positive bacteria or fungi
The mnemonic “cats Need PLACESS to Belch their Hairballs” can be used to memorise the catalase-positive bacteria (and Candida and Aspergillus, which are fungi): nocardia, pseudomonas, PJP, listeria, aspergillus, candida, E. coli, staphylococcus, serratia, B. cepacia and H. pylori.[52] (so some common CF bugs like Pseudomonas and Burkholderia can actually be seen in CGD patients)
14
Q
Where are endemic fungi located in Canada?
A
BC: cryptococcus
Manitoba: blastomycoses
Ontario: blasto and histo
Quebec: blasto and histo
15
Q
What sorts of infections are patient with neutropenia at risk for?
A
Neutropenia:
- Decreased number of neutrophils: chemotherapy induced neutropenia
- Decreased function of neutrophils: CGD, steroids
- At risk for infection with bacteria and fungi
- Chemotherapy induced neutropenia: risk of infection with own bacteria such Strep, Staph. G - like E. coli, Klebsiella, Pseudomonas and Fungi like aspergillus
- CGD: see above
16
Q
What infections are patients with impaired humoral immunity at risk of?
A
- Mostly bacteria, in particular encapsulated (Strep pneumo, Neisseria, Haemophilus, GBS, salmonella) and some virus (like enterovirus)
17
Q
What infections are patients with cell mediated immunity problems at risk of?
A
Intracellular pathogens:
Viruses: CMV, VZV, EBV, community viruses (eg. RSV)
Fungi: PJP, aspergillus, endemic fungi
Intracellular bacteria like nocardia
Mycobacteria
Parasites: toxoplasma gondii and strongyloides
18
Q
Conditions needing airborne precautions?
A
Active pulmonary TB (specify that it is active and pulmonary) VZV Measles SARS - severe acute respriatory syndrome small pox
19
Q
Why is diphtheria deadly?
A
- Airway obstruction: diphtheria makes a toxin which destroys tissue and causes membranous pharyngitis–>these membranes can extend to larynx and can cause airway obstruction OR pharyngeal membrane can get dislodged and obstruct airway
- toxin also causes:
- myocarditis/cardiomyopathy
- sepsis
- secondary pneumonia
20
Q
If suspicious of diptheria, do you wait for laboratory confirmation before giving anti-toxin?
A
No.
Diphtheria antitoxin to neutralize circulating toxin (administer before lab confirmation).
· Antibiotics (penicillin, erythromycin x 14d) to eradicate the organism, stop toxin production and reduce transmission, but do not replace antitoxin.
21
Q
Most common cause of croup (D)
A
Parainfluenza
22
Q
Infectious causes of upper airway obstruction (D)
A
Viral croup Epiglottitis Bacterial Tracheitis Diphtheria Retropharyngeal abscess Peritonisllar abscess Infectious mono
23
Q
Non-infectious causes of upper airway obstruction (D)
A
FB Trauma Caustic burns Spasmodic Croup Angioneurotic Edema
24
Q
Common causes of Epiglottitis (D)
A
Historically - H. influenzae (type B)
Now: Strep (Group A, B, C, G), H. parainfluenzae, Staph aureus, Moraxella catarrhalis,
Pneumococcus, Klebsiella, Psuedomonas, Candida, viruses
25
Most common cause of Bacterial Tracheitis (D)
S. Aureus
26
Characteristic of Diphtheria infection (D)
Membrane formation - "Membranous Pharyngitis"
27
Predominant organisms for Peritonsillar Abscess (D)
Strep pyogenes
28
Definition of Bronchitis (D)
Inflammation of the bronchus
Dominant symptom = Cough.
29
Usual resolution time of bronchitis (D)
Acute respiratory illness resolution: w/n 10-days = 50%, w/n 25 days - 90%
30
What is the most important air pollutant in acute bronchitis? (D)
Tobacco smoke
31
Most common cause of cough in children (D)
Viral acute respiratory infection
32
Pointers to the presence of specific cough (D)
```
Auscultatory findings (crackles, wheezes)
Cardiac abnormalities
Chest wall abnormalities
Digital clubbing
Daily moist or productive cough
Dyspnea
Exertional dyspnea
Hemoptysis
Immune deficiency
Neurodevelopmental abnormality
Recurrent pneumonia
Respiratory noises (stridor, wheeze)
Systemic symptoms
```
33
Are OTC cough med recommended for bronchitis? (D)
No
34
Clinical definition of PBB (D)
1) Isolated chronic (>4 weeks) wet cough
2) Resolution of cough with antimicrobial therapy
3) Absence of pointers suggesting alternate diagnosis
35
How is PBB differentiated from acute bronchitis? (D)
duration of illness
36
Common features of PBB (D)
Children usually <5
Lack other systemic symptoms including sinus, ear disease
Parents may report "wheeze" however "rattle" of airway secretions more common
May be misdiagnosed as asthma
Tracheo/bronchomalacia may coexist (common finding)
CXR = peribronchial thickening = most common
Resolution only after prolonged antibiotic course
37
Most common bacteria for PBB (D)
non-typeable H.flu
S.pneumo
M.catarrhalis
*often preceded by viral respiratory illness
Colonization may be due to impaired cough (nmd), mucous plugging (asthmatics), airway lesions that impair clearance (tracheomalacia = common finding) or mucosal damage (aspiration)
38
Characteristics of Plastic Bronchitis (D)
Characterized by extensive bronchial cast formation → airway obstruction
39
2 types of Plastic Bronchitis (D)
Type-1: Inflammatory = fibrin w/ cellular infiltrates; occurs in inflammatory lung d/o
-Assoc w: Sickle cell (ACS), asthma, aspergillosis, pna, CF, pulmonary lymphatic dz, neoplastic infiltrates
Type-2: Acellular = mucin, w/ few cells; occurs in congenital cardiac defect (esp FONTAN) -NOTE: Cast may not totally fit one type
40
Definition of Bronchiolitis (D)
Wheezing illness assoc w/ URTI in children <2 years
Characterized by inflammation, edema, mucous prod, bronchospasm, necrosis of a/w epithelium
Most common RTI of infancy
41
Most common cause of bronchiolitis (D)
RSV
| HMPV = up to 19% (2nd place)
42
Mechanism of RSV causing bronchiolitis (D)
binds TLR-4 on aiway epithelium → fuses w/ membrane.
- Causes direct cell & ciliary damage. Indirect inflammation resp tract
- Viral replication → epithelial cell necrosis and ciliary destruction
- Cell destructn → inflam response → infiltration submucosa with PMNS, lymphs
- ↑ mucous productn + desquamated epithelium = mucous plugs → airway obstructn -Bronchiolar obstructn → air trapping / hyper-inflation & lobar collapse → V/Q abn
-Immunopathogenesis poorly understood - T-cells play some (unclear) role
43
“Typical” radiograph for bronchiolitis (D)
hyperinflation, flattened diaphragm, peribronchial thickening, airway was thickening and occasionally patchy atelectasis
44
Differential diagnosis of bronchiolitis (D)
-Upper a/w obstructn (adenoid hypertrophy)
-Laryngeal obstructn (croup, FB)
-Asthma
-Pneumonia
-Metabolic d/o (DKA, IEM, salicylate
poisoning)
-Congestive heart failure
-Parenchymal dz (CF, CLD, chILD)
45
Management principles of bronchiolitis (D)
- Cornerstone = SUPPORTIVE care
- Most managed at home
- Mod-severe resp distress (1-3%) = admission
- Guidelines exist (AAP, SIGN, CPS).
- not much evidence for medication of any sort
46
Suggested admission criteria for bronchiolitis (D)
- No clear criteria
- Consider admission when RR >60-70, Sats <90%, hx of apnea, lethargy or dehydration
- Factors influencing disposition: prematurity, v. young age, prev cardiopulm dz, immunodef, NMD
- Social situation a factor as well
- Cdn study assoc gestational age, HR, RR, Resp distress score, O2 w/ risk of severe bronchiolitis
47
RSV prevention strategies (D)
- Hand hygiene reduced nosocomial spread in hosp + at home.
- Virus capable of living on objects in the environment for hours
- No vaccine - difficult due to multiple strains - and infection does not confer long-term immunity -Passive immunity (Synagis/Palivizumab) recommended for high risk infants
- Palivizumab (Synagis) = agent of choice
48
Palivizumab - What is it and Is there risk of transferring infection? (D)
Palivizumab = a humanized murine monoclonal immunoglobulin G-1 directed against an epitope on the F glycoprotein of RSV
It is produced by recombinant DNA technology and directed against an epitope of the F glycoprotein of RSV.
Palivizumab binds to this glycoprotein and prevents viral invasion of the host cells in the airway. This reduces viral activity and cell-to-cell transmission, and blocks the fusion of infected cells
Standard dosing is 15 mg/kg administered intramuscularly every 30 days during RSV season for a maximum of five doses.
The most common reported adverse effects of palivizumab are local erythema, pain at the injection site, fever, and rash
Palivizumab is a recombinant product and has no potential for transmitting blood-borne infectious diseases. Moreover, it does not interfere with response to vaccines and does not affect the measles-mumps-rubella or other live virus immunization schedules.
49
National recommendations for those who should have RSV prophylaxis (D)
1) Children with hemodynamically significant CHD or CLD who require ongoing diuretics, bronchodilators, steroids or supplemental oxygen if they are <12 months of age at the start of RSV season.
2) In preterm infants without CLD born before 30 + 0 weeks’ GA who are <6 months of age at the start of RSV season
3) Infants in remote communities who would require air transportation for hospitalization born before 36 + 0 weeks’ GA and <6 months of age at the start of RSV season
Children with immunodeficiencies, Down syndrome, cystic fibrosis, upper airway obstruction or a chronic pulmonary disease other than CLD should not routinely be offered palivizumab. However, prophylaxis may be considered for children <24 months of age who are on home oxygen, have had a prolonged hospitalization for severe pulmonary disease or are severely immunocompromised.
50
Long term sequelae of bronchiolitis (D)
Bronchiolitis Obliterans
| possible development of asthma/wheezing illness later in life
51
Definition of pneumonia (D)
Inflammation of lung tissue due to an infectious agent, thereby stimulating a response resulting in damage to lung tissue
52
Common preceding infection for bacterial pneumonias (D)
Bacterial infections are commonly preceded by viral or Mycoplasma infections
Viral pathogens can impair cough, interrupt mucociliary clearance, and enhance bacterial adherence to cell wall
53
Most common causes of pneumonia birth to 1 mos (D)
GBS, or Gram-negative bacteria, RSV
54
Most common causes of pneumonia infants to 3 mos (D)
```
Multiple causes (Chlamydia trachomatis, viruses, Bordetella pertussis, or Ureaplasma urealyticum)
Also: S.pneumo, Haemophilus, S. Aureus
```
55
Most common causes of pneumonia children <5 (D)
Viruses are most common
| Most common bacteria are pneumococcus and atypicals (M. pneumoniae, C. pneumoniae), S. pneumo
56
Most common causes of pneumonia children older than 5 (D)
S. pneumoniae
M. pneumoniae
C. pneumoniae
57
Most prevalent bacteria causing CAP (D)
S. pneumoniae
58
Typical symptoms suggestive of typical bacterial pneumonia (D)
Fever, chills, abdominal and/or chest pain, cough (productive)
Symptoms consistent with atypical organisms (including M pneumonia) include = gradual onset, with headache, malaise, non-productive cough, low grade/absent
fever
Wheezing tends to occur with viral pneumonia, also with Mycoplasma pneumonia or Chlamydia pneumonias
59
Most sensitive sign and most specific signs associated with alveolar infiltrate on CXR in pneumonia (D)
Fever = most sensitive sign
| Grunting and retraction = most specific signs
60
Features that suggest a viral cause for pneumonia (D)
Bilateral interstitial infiltrates, atelectasis, signs of bronchiolitis (wheeze), generalized hyperinflation
61
When to do follow-up CXR in pneumonia? (D)
Round pneumonia
Lobar collapse
Clinical deterioration
62
Most common cause of pneumatoceles associated with pneumonia (D)
Staph aureus
Effusion and empyema are also common (90%)
63
Risk factors for antibiotic resistance (D)
Prior use of Abx, daycare attendance, travel, infection exposure, coexisting morbidities
64
Choice of antibiotic for CAP (D)
Penicillins can be used for most (penicillin, amoxicillin, or ampicillin)
Beta-lactams can be used in hospitalized patients
65
With pneumonia, in what time period would you expect children to get better with empiric antibiotic treatment? (D)
Typically children improve between 48-96 hrs after empiric treatment
- Recommended to not change antibiotics during this time, unless new information available (Ie. Culture results, pneumatocele development)
Consider empyema/abscess with ongoing fevers or pleuritic pain
With slow resolution consider the following:
o Right drug, right dose, resistant organisms, compliance
66
How does necrotizing pneumonia happen? (D)
Necrosis and liquefaction of consolidated lung disease
Majority confined to a single lobe, can have multilobar involvement
Pneumatoceles are common
Commonly see hemoptysis, high fevers, leucopenia, hypoalbuminemia, empyema
67
Complication of necrotizing pneumonia (D)
Radiolucent foci (solitary, multiple, multiloculated)
Bronchopleural fistula
Intrapulmonary abscess
68
Formation of pneumatoceles in necrotizing pneumonia (D)
Consequence of localized bronchiolar and alveolar necrosis = one way passage of air into the peripheral airways and alveoli
69
Common causes of necrotizing pneumonia (D)
Usually due to pneumococcus, Staphylococcus aureus, or Pseudomonas aeruginosa
70
How do pleural effusion and empyema in the setting of pneumonia happen? (D)
Occur when inflammatory response creates increase in pleura permeability, with accumulation of fluid into the pleural space
(Consequence of increased capillary permeability that occurs with lung injury = This favours migration of inflammatory cells into the pleural space)
71
What characterizes an empyema? (D)
When germs enter pleural space = appearance of pus
72
Stages of infectious pleural effusion (D)
```
Stage I (Exudative stage) = 3-5 days
Stage II (Fibropurulent stage) = 7-10 after first sign of acute disease
Stage III (Organizing stage) = Takes place in 2-3 weeks time
- Fibroblast infiltration of pleural cavity
```
73
Most common causes of infectious pleural effusions (D)
```
Streptococcus spp (predominantly S. pneumococcus)
S. aureus (most common for empyema)
H influenza
Mycobacterium spp
Pseudomonas aeruginosa
Anaerobes (more so with aspiration, especially with neurodevelopmental delay)
Mycoplasma pneumoniae
Fungi
```
74
Complications of infectious pleural effusion or empyema (D)
Bronchopleural fistula
Lung abscess
Perforation through chest wall (empyema necessitatis)
75
Most sensitive diagnostic test for pleural effusion (D)
U/S
76
What does bubbling in the underwater seal mean for a chest tube?
Bubbling represents pneumothorax
| Continuous bubbling represents bronchopleural fistula
77
Pathogenesis of lung abscess (D)
Inflammation of parenchyma, necrosis, cavitation abscess formation
78
Common causes of primary lung abscesses (D)
Typically due to Gram positive cocci (Pneumococcus, S. aureus, S. pyogenes) or by Pseudomonas or Klebsiella
79
Treatment for lung abscess (D)
IV Abx for 2-3 weeks, then 4-8 weeks of PO Abx
▪ Penicillin +/- clindamycin, or metronidazole
Consider interventional drainage/CT aspiration
80
Complications of lung abscess (D)
Empyema
Pyothorax
Pneumothorax
Bronchopleural fistula
81
Types of Influenza virus (D)
3 - A, B (8 segments), C (7 segments)
82
Morbidity concerns with influenza and small children (D)
School aged children - increased infection rate
| Higher rates of secondary bacterial infection and ventilatory need than younger children
83
Clinical Manifestations of Influenza infection (D)
Typical Influenza-like illness (ILI) = sudden onset, high fever, myalgia, cough, sore throat
84
Complications from Influenza (D)
Complications from influenza infection common in children
○ AOM - 30%
○ Croup and pneumonic infiltrates - common
○ Febrile sz, encephailits - may occur
○ Influenza B: Acute myositis - common, renal failure due to myoglobinuria - rare
○ 2° bacterial infection (S. pnemo, Staph) more common in older children
○ Asthma exacerbation - asthmatics
○ Even in healthy young adults - lung fxn abn may persist weeks
85
Types of Influenza vaccine (D)
Live attenutated vaccine (LAIV) = nasal spray
■ Licensed ages 2-49
■ LAIV superior in covered pediatric age group
■ Safe and more efficacious in older children w/ asthma - less wheezing
than TIV in the 14-days post vaccination
■ Younger children, mild-intermittent asthma - tolerate LAIV well
■ Severe, poorly controlled asthma = contra-indication
Trivalent inactivated subunit vaccine (TIV) = injection
■ Licensed age >6mo
○ Both contain A-H1N1, A-H3N2, and Flu B, updated annually
○ Quadrivalent (covering 2-B lineages) coming in the future
86
Antiviral agents (2) for Influenza (D)
Adamantanes (Amantadine, rimantidine) = M2 inhibitors
■ Effective vs. Influenza A only
■ M2 inhibitors: block ion channel M2 that facilitates fusion w/ cell
membrane
■ Viral resistance develops quickly
Neuraminidase Inhibitors (Oseltamivir/Tamiflu) = NA inhibitors
■ Neuraminidase needed to release virus particles from infected cells
■ Effective vs. Flu A and B
■ Oseltamivir = PO med, useful to treatment & prophylax children >1yr
● If given w/n 48-hrs of onset: ↓ length of illness, complicatns, spread
● Side-fx: Nausea, vomiting
■ Zanamivir = inhalation, similar effectiveness as tamiflu, children >5yrs
● Side-fx: Airway irritation, bronchospasm
● Most viruses resistant to Tamiflu, sensitive to Zanamivir
87
Recommendations for antiviral treatment of Influenza (D)
treatment only for those expected to have serious illness or complication, includes admitted pts
■ Most effective if initiated in first 48-hrs
■ Some suggest Rx all presenting early: ∵ hard to predict who gets sick and this may reduce spread, complication
■ Rapid diagnostic tests may guide Rx, but not necessary in flu epidemic w/ ILI in children >5yrs
■ Systematic early treatment may reduce 2° bact infection, complication rates
88
Known reservoir for Hantavirus (D)
Rodents
| Transmitted through inhalation of aerosols of rodent excreta
89
3 stages of Hantavirus Pulmonary Syndrome (D)
1) Febrile prodrome
2) Cardiopulmonary stage (rapid development of pulmonary edema)
3) Convalescence (1-2 weeks after resolution of edema)
90
Clinical manifestations of Legionnaires disease (D)
Necrotizing multifocal pneumonia with a fulminant course
o Begins with prodrome of myalgia, fatigue, anorexia, malaise, headache, chills,
vomiting, diarrhea
▪ Insidious or acute
▪ Followed by fever
o May see relative bradycardia
o Pleuritic chest pain, dry cough → turning to productive
91
Treatment of Legionnaires disease (D)
Azithromycin 5-10 days
92
Clinical manifestations of Chlamydophila pneumoniae (D)
Begins with non-specific prodrome of sore throat, malaise, headache, low grade fever, cough
o Typically long (2-6 weeks), biphasic
o May have URT symptoms
- Many will develop pneumonia or bronchitis
- Leads to elevation of IgE, with bronchial reactivity
o Exam often reveals non-exudative pharyngitis, with wheezes and crackles (fine or coarse)
- May be severe infection
o Pneumatocele, pleural effusion, pneumothorax, interstitial fibrosis, abscess
93
Complications of Chlamydophila pneumoniae (D)
Guillain Barre Syndrome, meningoencephalitis, myocarditis, endocarditis, AOM
94
Treatment of Chlamydophila pneumoniae (D)
Susceptible to macrolides, tetracyclines, quinolones
o Treat with 5 days of azithromycin, 10 days of clarithromycin, and 14 days of
erythromycin
o Adolescents can use doxycycline (14-21 days)
95
Clinical manifestations of Mycoplasma (D)
20% of cases are asymptomatic
- Typically manifest as pharyngitis, hoarseness
- Frequent fever, persistent cough. Less common to have rhinorrhea
- May have vomiting and diarrhea (20%)
- Physical Exam:
o Crackles (40-73%) and wheezing (35%)
- Duration of illness is ~ 2 weeks, cough can last for 1 month or longer
Children may have more severe disease, as do high risk groups:
o Sickle cell, immunodeficiency, cardiac disease
96
Complications associated Mycoplasma (D)
Associated with AOM, sinusitis, mucocutaneous eruption, myocarditis, pericarditis,
hemolytic anemia, arthritis, glomerulonephritis, and neurologic conditions (aseptic meningitis, encephalitis, cerebral ataxia, transverse myelitis, peripheral neuropathy, psychosis, and GBS)
97
Common CXR findings of Mycoplasma (D)
Most common findings were peri-hilar linear opacities (60%), reticulonodular infiltrates (40%), segmental or lobar consolidation (28%)
o Pleural effusion in ~ 8%
98
Treatment of Mycoplasma (D)
Treat with macrolides or tetracyclines for 10 days
| Macrolide is drug of choice for young children
99
3 pattens of inhalation Anthrax (D)
Dermatologic, gastrointestinal, and inhalational
100
Most common presentation of Anthrax (D)
Majority of infections are cutaneous
Inhalation = Associated with highest mortality (hemorrhagic mediastinitis, hemorrhagic pleural effusion, bacteremia)
101
Treatment of inhalation Anthrax (D)
Ciprofloxacin and Doxycycline are antimicrobials of choice
Recommended duration of therapy is 60 days (14 minimum)
Corticosteroids can be considered for adjunctive therapy
102
Post exposure prophylaxis for Anthrax (D)
3 doses of anthrax vaccine (children and adults)
o Ciprofloxacin and Doxycycline for confirmed/suspected aerosol exposure
▪ If organism proven susceptible, Amoxicillin can be used in children
o Continue antibiotics for 60 days (some say 100)
103
4 classic presentations for Histoplasmosis (D)
Infantile
Acute Histoplasmosis
Mediastinal Fibrosis
Recrudescent disease (Recurrent)
104
Clinical manifestations of pulmonary histoplasmosis (D)
Acute: Fever, cough, chest pain
▪ Tend to have fever for over 2 weeks duration
▪ Over 50% have wheeze, often unilateral
o May have mediastinal adenopathy, which is difficult to distinguish from lymphoma or tuberculosis
o Bronchial and/or vascular compression is best defined by CT
o May see pericarditis → enlarged cardiac silhouette
o May see residual calcification
105
Diagnosis of Histoplasmosis (D)
Serology: Immunodiffusion (measures H and M bands), complement fixation
H. capsulatum antigen assay
Tissue histology or culture (most reliable)
106
Treatment for Histoplasmosis (D)
Typically self limited without need for treatment
- Indications for treatment:
o Prolonged fever, radiographic evidence of large inoculum, bronchial compression
- Treatment:
o Oral itraconazole (5-10mg/kgday) x 4 to 6 weeks
o Can use Voriconazole, posaconazole - Disseminated disease
o Gold standard is amphotericin B (can use liposomal form) ▪ 30-35mg/kg over 2 to 3 months
107
Clinical manifestations of Coccidioiomycosis (D)
Pulmonary coccidiomycosis develops in about 1/3
o Incubation period of 7 to 21 days
o Develops chest pain, cough, fever
o 1⁄2 develop dyspnea, constitutional symptoms (fatigue, weight loss)
o May have rash
▪ Commonly a fine popular rash
▪ May also have other presentations including the “desert rheumatism”
● Fever, arthralgia, erythema nodosum
● Presence of erythema nodosum is correlated with low risk of
extrapulmonary dissemination
▪ May have rash similar to erythema multiforme (more in children than
adults)
o Nodules, calcifications, cavitary lesions and bronchiectasis are late findings
o May have hemoptysis (may be only symptom of pulmonary cavity)
108
Treatment for Coccidioiomycosis (D)
Only treat those at high risk for severe disease, or with disseminated infection
HIV, organ transplants, prolonged use of steroids, TNF inhibitors, pregnancy
Amphotericin B for severe disease
o Fluconazole is effective, well tolerated, and high bioavailability
▪ Excellent meningeal penetration
o Itraconazole is effective
▪ Best for bone disease
▪ Requires drug levels due to variable absorption
109
Clinical manifestations of Blastomycosis (D)
Alveolar infiltrate on CXR
- May present with a persistent pneumonia with productive cough (similar to histo)
- Skin lesions:
o Verrucous lesions & ulcerated lesions with friable granulation tissue
- Bone Lesions: osteolytic lesions
- GU tract: prostatitis or epididymitis in males
110
Treatment for Blastomycosis (D)
Treatment is recommended, although spontaneous recovery can occur
- Must treat if infection becomes chronic, or with extrapulmonary infection
- Amphotericin is drug of choice in life threatening disease
- Itraconizole is the optimal azole if less severe
- Duration of therapy is 6 months, with levels of itraconazole being followed
111
Risk factors for increased susceptibility for opportunistic fungi (D)
- Therapies causing reduced number and function of lymphocytes/phagocytes
- Broad spectrum antibiotics
- Disruption of normal mucosal barriers to infection
- Indwelling catheters and invasive procedures
- HIV/AIDS
112
Opportunistic fungal infections with lung pathology (D)
Aspergillosis – Invasive Pulmonary Disease
Candidiasis
Zygomycosis
113
Predisposing factors to Aspergillosis infection (D)
Neutropenia, corticosteroid therapy, cytotoxic chemotherapy, broad spectrum
abx, acute leukemia
Invasive Aspergillosis is a leading cause of death in those with BMT, even without neutropenia
▪ Leukemia patients have higher risk of Invasive Apergillosis due to higher
intensity of risk factors
▪ Lung and heart transplant recipients have higher risk of Invasive
Aspergillosis than other solid organ transplant recipients
▪ Highest risk in first 6 months post transplant
▪ Increased risk with CMV infection, smoking history, poor graft function, renal failure
HIV patients are at risk
Premature infants are at high risk
114
4 presentations of Invasive Aspergillosis (D)
Pulmonary
Disseminated
Tracheobronchitis
Rhinosinusitis
115
Clinical manifestations of Invasive Pulmonary Aspergillosis (D)
Most common form.
● Variable presentation
o Hemorrhagic infarction, lobar pneumonia, lung abscess, solitary or multiple pulmonary nodules, pleural based disease with effusion
● Non specific symptoms (Commonly fever, cough, dyspnea)
● Symptoms more common with disease are pleuritic chest pain with hemoptysis
116
Classic CT findings for Invasive Pulmonary Aspergillosis (D)
```
Halo sign (nodular density with surrounding ground glass)
Air Crescent sign (late finding of cavitation)
```
117
Treatment for Invasive Pulmonary Aspergillosis (D)
```
Voriconazole is now the treatment of choice
▪ Broad activity against Aspergillus
▪ IV and highly bioavailable oral forms
▪ Higher rates of success
▪ Higher rates of survival
▪ Lower toxicity
```
118
Clinical manifestations of pulmonary Cryptococcus in immunocompetent patients (D)
Despite the thought that it is an opportunistic infection (and it is), most common infection occurs as subclinical or mild pulmonary disease in normal host
o Symptoms: Cough, chest pain, fever
o Isolated pulmonary nodule may be only manifestation in immunocompetent
individual
▪ May have hilar lymphadenopathy
▪ May also have masslike and consolidative lesion in lower lobes
119
Clinical manifestations of pulmonary Cryptococcus in immunocompetent patients (D)
May still have mild or asymptomatic presentation
▪ Respiratory tract likely portal of entry
● Only 10% of patients with disseminated cryptococcosis have pulmonary symptoms at diagnosis
▪ Symptoms are quite variable:
● Subacute cough with fever, chest pain, weight loss
● May have rapidly progressive pulmonary disease (ARDS)
No typical radiographic pattern
● Pulmonary nodules, mass lesions, lobar consolidations, diffuse infiltrates, effusion
120
Diagnosis of pulmonary Cryptococcus (D)
Cultures may take up to one week
May also have opportunistic infections simultaneously (TB, NTM, CMV, Nocardia, PJP)
Histopathologic samples from biopsy is sensitive and specific
▪ Stains: Grocott-Gomori methenamine-silver nitrate
▪ India ink for CSF samples
121
Treatment for pulmonary Cryptococcus (D)
Asymptomatic patient with normal immune system and positive culture from respiratory tract:
- Fluconazole for 6-12 months
Normal host with mild-moderate symptoms:
- Fluconazole for 6-12 months (oral or IV)
- Itraconazole, voriconazole, or posaconazole are alternatives
Severe symptoms or imunocompromised:
- Treat as if CNS cryptococcal infection
- Amphotericin B & flucytosine for 2 weeks (or until CSF cultures negative)
- Then Fluconazole for 12 months
- If failure, may be due to subtype of Cryptococcus (var gattii)
- Fluconazole not used first line for severe due to worse outcomes
122
Characteristics of Pulmonary Candidiasis (D)
When pulmonary candidiasis occurs, usually secondary to disseminated disease, hematogenous spread, or aspiration of infected secretions
Higher risk in: neutropenic patients, Low Birth Weight, Premature infants of mothers with Candida chorioamnionitis
123
Clinical manifestations of Pulmonary Candidiasis (D)
Clinical manifestations/radiographic findings are non-specific
o Fever, cough, ill/septic appearance
o Multilobar consolidation, widespread pneumonia, nodular infiltrates
o Rarely get ARDS or effusions
124
Treatment of Pulmonary Candidiasis (D)
95% of C. albicans is susceptible to fluconazole
| ▪ Resistance is higher in other strains
125
Components of Humoral Immunity (D)
```
Immunoglobulins, complement, and other nonspecific antibacterial
Molecular species (e.g. defensins) important to innate pulmonary defenses.
```
126
Components of Cellular Immunity (D)
Includes phagocytic cells, particularly neutrophils, and lymphocytes.
127
Pulmonary infections usually seen within the early stage after organ transplant (pre-engraftment)
Bacterial infections
HSV stomatitis
Fungal infections (yeast, Aspergillus)
128
Pulmonary infections usually seen within the early stage after organ transplant (after 1 mos)
```
PJP
Viral infections (CMV, Varicella)
```
129
Pulmonary infections usually seen > 2mos following organ transplant (Engraftment to Late phase)
Co-pathogen (viral, fungal)
Late viral (Adeno, HHV-6, HMPV)
Mycobacterial disease
Atypical pneumonia (Legionella)
130
Presentation of CMV pneumonitis (D)
CMV pneumonitis can be diffuse, discrete parenchymal hemorrhagic nodules to diffuse alveolar damage or chronic interstitial pneumonitis.
Imaging reveals diffuse reticulonodular pattern that is less “alveolar” than PJP
Late CMV: Retinitis, BM failure and encephalitis.
131
Pathology of CMV pneumonitis (D)
Infected alveolar cells contain basophilic nuclear inclusions surrounded by a clear halo = owl eye appearance
CMV DNA by PCR in Urine, BAL, Blood.
132
Treatment of CMV pneumonitis (D)
Prevent: CMV-neg blood products, IVIg, Foscarnet and ganciclovir. Less intense myeloablative chemo.
TTT: valganciclovir (PO)/ganciclovir (IV)
133
Presentation of pulmonary VZV/HSV (D)
Fever, cough, dyspnea, chest pain, cutaneous vesicles and visceral involvement.
Can get secondary bacterial infections
CXR shows ill-defined, b/l scattered nodular densities first in periphery with later coalescence into more extensive infiltrates (pneumonitis)
134
Pathology of pulmonary VZV/HSV (D)
Micro: the infection involves alveoli, BV, bronchial wall.
EM: Intranuclear viral inclusions; hemorrhage/necrosis/alveolar edema in severely affected areas; hemorrhagic tracheitis and bronchitis
135
Treatment of pulmonary VZV/HSV (D)
Prevent: VZ vaccine
Prevent or decrease severity: VZ IG if given within first 48-72 hrs of exposure
Treatment: Acyclovir
136
Presentation of pulmonary Adenovirus (D)
Fever, pharyngitis, cough, conjunctivitis, pneumonia – necrotizing bronchitis and bronciolitis + GI/urologic problems or disseminated dz
CXR – nonspecific diffuse pattern (consider if failure to respond to typical tx)
137
Pathology of pulmonary Adenovirus (D)
Lung Biopsy or brusing → Adenoviral inclusions bodies.
Culture→ take time
DNA by PCR→ Blood or other fluid
138
Treatment of pulmonary Adenovirus (D)
Supportive tx including O2, treatment of bacterial superinfection, IVIG, assisted ventilation
Treatment: Cidofovir in select patients (needs more research to determine who)
139
Presentation of PJP (D)
Fever, cough, dyspnea, tachypnea
Early hypoxemia with mild respiratory alkalosis is common
CXR shows diffuse b/l infiltrates
140
Pathology of PJP (D)
2 forms in tissues: trophozoite (more common) and sporozoite
Stain best with Giemsa stains - cysts are spherical or cup- shaped
Alveoli are filled with trophozoites and protein-rich debris and altered permeability causes pulmonary edema and surfactant abnormality
141
Treatment of PJP (D)
Prevent and treat: Septra.
Second line: Pentamidine (side effects: hypotension, tachycardia, nausea, hypoglycemia, nephrotoxicity)
Also: Dapsone, Clinda + primaquine
If severe disease can add steroid.
142
Presentation of Aspergillus (D)
Aspergillus fumigates is the most common to cause pneumonia – can be acute or chronic necrotizing form (risk factors: prolonged neutropenia, chemo+steroid tx, broad-spectrum abx use)
HRCT:
- Air crescent sign (nodular lesions of necrosis surrounded by air)
- Halo sign (nodule surrounded by ground glass opacity often representing hemorrhage)
- Reverse halo sign (ground glass opacity surrounded by ring of consolidation)
143
Pathology of Aspergillus (D)
Septate hyphae with regular 45 degree dichotomous branching best observed with Methenamine silver staining
Biopsy→ High risk of bleed
Galactomanan (Blood or BAL)
144
Treatment of Aspergillus (D)
Amphotericin B, Itraconazole, Voriconazole, Ambisome, Caspofungin
145
Clinical presentation of Mucor (D)
Insidious segmental pneumonia that is slowly progressive despite antifungal tx
Persistent fever, chest pain, hemoptysis, weight loss
Can progress to cavitation and dissemination to brain and other sites secondary to hematogenous spread Death from pulmonary hemorrhage, mediastinitis, airway obstruction
Usually needs lung biopsy to confirm dx
146
Pathology of Mucor (D)
Nonseptate hyphae that branch at angles up to 90 degrees and have an appearance of “twisted ribbons”
147
Treatment of Mucor (D)
Amphotericin B / Vori and sometimes Posaconazole
| Possible surgical resection ASAP
148
Best imaging for lung abscess (D)
CT with contrast
149
TB question about management in children post exposure. (D)
All exposed children: symptom inquiry and TST
- If <5 years, close contact, symptomatic then also physical exam and CXR
- If <5 years of age, negative TST, no evidence of active TB, then TREAT prophylactically to prevent development of TB
o Even if TST is negative, it can take up to 8 weeks for TST to turn positive
o In <5 years, higher risk of progression to active TB
o If it’s likely a drug susceptible strain that the child was exposed to-->INH. If at 8 weeks, TST negative, child asymptomatic, >6 months, immunocompetent-->discontinue INH
o Optimal treatment for prevent of multi-drug resistant TB is not clear
- If TST is positive (>=5 mm) and no clinical or radiographic signs of active disease, then treat for latent TB
o (Recall that interpretation of TST is based on exposure status, among other clinical factors)
150
Management of neonate post TB exposure (D)
Evaluation for congenital TB: physical exam, CXR, cultures (gastric aspirate, blood culture), lumbar puncture, abdominal ultrasound, consider head ultrasound
- TST is usually negative and then becomes positive at 1-3 months of treatment
- Not much data on IGRA in infants
- If there is no congenital TB, then treat with INH at 10-15 mg/kg for 4-9 months
o 4 months if less infectious source, no evidence of conversion in older exposed contacts and repeat TST is negative
o 6 months if higher risk exposure (household or smear positive source case), repeat TST before discontinuing treatment
o If repeat TST is positive, then reassess the infant for TB disease. If no active TB, then continue prophylactic treatment for total of 9 months
151
A 6 year old girl has hemoptysis and known TB contact…
| What investigation do you do and how do you manage this patient? (D)
You are suspicious of TB
- Investigations:
- Physical exam
- CXR
- TST
- Gastric aspirate x 3 or induced sputum-->AFB smear and mycobacterial culture and drug susceptibility testing. If adolescent, then would get expectorated sputum.
- Consider: HIV testing, Xpert MTB/RIF (mycobacterial tuberculosis complex and rifampin resistance)
152
Classic triad for TB diagnosis in children (D)
(1) Recent close contact with an infectious case
(2) A positive tuberculin skin test (TST) or interferon-gamma release assay (IGRA)
(3) Suggestive symptoms and findings on chest radiograph or physical examination
153
TB drug management (D)
Empiric treatment:
- Start treatment promptly
- Use drug susceptibility testing or susceptibility results from probable source case to guide treatment
- Empiric treatment: INH, rifampin, ethambutol, PZA = RIPE
Treatment Modification after knowing susceptibility profile:
- Fully Susceptible, intrathoracic TB: RIP (rifampin, INH, PZA) x 2 months (initiation phase), then 4 months RI (continuation phase) for minimum total duration of 6 months
o Treat for 9 months if cavities on CXR or positive sputum culture after 2 months of treatment
154
Side effects of Isoniazid (D)
```
Hepatotoxicity
Peripheral Neuropathy (interferes with pyridoxine metabolism)
```
155
Side effects of Rifampin (D)
```
Hepatotoxicity
Hypersensitivity reactions
Memory Impairment
Drug interactions
Body fluid turns orange
```
156
Side effects of Pyrazinamide (D)
Hepatotoxicity
| Increased uric acid levels
157
Side effects of Ethambutol (D)
Optic neuropathy (decreased acuity, decreased visual fields, colour blindness)
158
What is Pyridoxine used for in TB management? (D)
To prevent Isoniazid neuropathy
Pyridoxine (vitamin B6): for children with milk and meat deficient diet, breastfed infant, nutritional deficiencies, children with symptomatic HIV, adolescents who are pregnant or breastfeeding
159
How will you decide when to stop TB treatment? (D)
- Based on planned duration of therapy: 6-9 months
- Worsening CXR findings
Monitoring during treatment:
- Clinical evaluation every month-->ask about symptoms of TB, drug side effects, monitor weight, may need to dose adjust treatment
- Adolescents or older children: follow up sputum for AFB smear and culture every month, until 2 consecutive cultures are negative. Smear and culture status at the end of 2 months (end of the intensive phase of treatment) is important for assessing risk of relapse and duration of the continuation phase; if culture still positive, then drug susceptibility testing should be done.
- CXR at 2 months into treatment to rule out extension of disease
o Persistent CXR findings is NOT a reason to change treatment
o Can have persistent lymphadenopathy or scarring for 2-3 years post treatment
o So, normal CXR is NOT needed to stop therapy
- Follow up x 1 year post treatment
Extrapulmonary TB such as CNS, Disseminated/military, bone and joint:
- Treatment duration of 9-12 months
Pulmonary TB in patients with HIV:
- optimal treatment duration is not known
160
Mother with cavitary TB; 2 year old with child with PPD (-). What and why? (D)
Children less than 5 years of age with a negative TST and no evidence of active TB by examination or radiology should be given "window" of preventive therapy to prevent the development of TB.
This is because it may take up to 8 weeks after infection for the TST to convert to positive, during which time the infection may progress to disease.
For children presumed to have been exposed to a drug-susceptible isolate, INH is recommended.
The INH may be discontinued if, after a period of 8 weeks after the last contact, the repeat TST is negative, and the child remains asymptomatic and is immunocompetent.
The optimal treatment of children in contact with patients with MDR-TB is uncertain Consultation with a TB specialist is recommended
161
Who is considered high priority contact group for TB? (D)
Household contacts plus close non-household contacts who are immunologically vulnerable, such as children under 5 years.
For smear-positive/cavitary/laryngeal TB, it is recommended that the initial contact follow-up include both high- and medium-priority contacts.
162
Who is considered medium priority contact group for TB? (D)
Close non-household contacts with daily or almost daily exposure, including those at school and work.
For smear negative respiratory TB cases, household members should always be assessed in the initial contact investigation, along with any other high-priority contacts. However, investigation should be expanded to medium-priority contacts (e.g. other close non-household contacts) only if there is evidence of transmission
163
Who is considered low priority contact group for TB? (D)
Casual contacts with lower amounts of exposure.
164
What is the most reliable indicator of infectiousness in TB? (D)
Sputum status
Cases of laryngeal TB are considered four to five times more contagious than smear-positive pulmonary cases, as they are likely to have a large number of bacteria due to extensive concurrent pulmonary disease
Cavitary disease on chest x-ray has been repeatedly linked to higher infectiousness, independent of smear status
Coughing is the least reliable indicator of infectiousness but is generally linked to it, particularly within households.
165
A 5 year old sat in an airplane containing a man with active pulmonary TB. Skin test is 0 mm. Chest x-ray and urine are normal. How would you treat? (D)
Treat with INH, then repeat the testing after 8-10 weeks after the child is no longer exposed to the index case.
Repeat the testing after 8-10 weeks and if testing is negative, patient is symptom free INH can be discontinued.
If the testing is positive a full course of treatment total of 9 months.
166
2 months later after a potential TB exposure, a 5yo is receiving steroids for nephritic syndrome, how would you treat? (D)
In nephritic syndrome the use of steroid will be for at least 2 weeks before tapering down which will affect the testing results ( PBG / IGRA ) so testing will not be reliable at that time.
Ideally for kids who are exposed to TB should be tested before giving the steroid, but in this case since the kid started on steroid already. The treatment of choice will be to treat him as latent TB
So to extend the INH course for a total of 9 months.
167
Native child with his mother are coming for clinic visit. He has a cough. Mention 3 measures/precautions for infection control. (D)
If possible, visits by people with suspected or confirmed respiratory TB disease should be postponed until no longer infectious.
If a visit cannot be postponed, it should be scheduled at the end of the day to minimize exposure to others, and, when possible, staff should be alerted of these visits to allow for prompt use of precautions
The patient should be provided with a mask before arrival or immediately upon reception to be worn until an Airborne infection isolation room(AIIR) becomes available. If unavailable, the patient should be temporarily assessed or treated in a single room with the door closed, away from vulnerable patients, and transferred as soon as medically feasible to a facility with AIIRs if admission is required.
HCWs caring for people with suspected or confirmed respiratory TB disease in outpatient clinics should wear a respirator (N95 or higher filter classes )
168
Etiology of Respiratory Papillomatosis (D)
HPV
169
2 life threatening complications of Respiratory Papillomatosis (D)
Airway obstruction
| Malignant transformation
170
Most common pathogen of bacterial tracheitis (D)
Staph aureus
171
Treatment for bacterial tracheitis (D)
Ceftriaxone + Vancomycin
Diagnostic rigid bronchoscopy
Intubation and ventilation
172
Patient with chronic granulomatous disease on Keflex prophylaxis, presenting with chest imaging findings of increasing hilar adenopathy and bilateral infiltrates - what is the likely etiology?
What therapeutic altering diagnostic test would you perform? (D)
Aspergillus
Bronch + BAL
173
What are two adverse effects of Palivizumab? (D)
```
Rare cases of anaphylaxis are the only recognized serious event
Fever
Rash
Injection site reaction
Antibody development
```
174
By what percentage does Palivizumab decrease hospital admissions because of RSV? (D)
Limited effect on hospitalizations on population basis
Reduction in hospitalizations of 80% in infants with prematurity (<36 weeks and without CLD), 40% in infants with prematurity and CLD, and 45% in children with CHD (but not with cyanotic heart disease)
175
What is the percentage risk of blood borne infections are caused by Palivizumab? (D)
0%
| Produced by recombinant DNA technology
176
What is Palivizumab? (D)
Humanized Monoclonal immunoglobulin G-1 directed against an epitope on the F glycoprotein of RSV (95% human/5% murine amino acid sequences)
177
Indications for Palivizumab? (D)
Prematurity <29+0 AAP (<30+0 CPS), <12mos at start of RSV season
o Prematurity >=29+0, depends on additional risk factors, e.g., CHD, CLD, other conditions
o Preterm infants with CLD in the first year of life (<32wks, >21% O2 for at least 28d after birth)
o Preterm infants with CLD in the second year if continued medical support (corticosteroid, diuretic or supplemental O2) is still required in the 6 mos before 2ndRSV season
o Infants with hemodynamically significant CHD (i.e., acyanotic heart disease on medication to control CHF and will require surgical procedure, moderate to severe pulmonary hypertension), <12mos. Cyanotic lesions in discussion with pediatric cardiologist.
o Anatomic pulmonary abnormality or neuromuscular disorder
o Immunocompromised
o Trisomy 21 only if associated CLD, airway clearance issues or prematurity <29 weeks
o Not recommended routinely in CF
o GA <36+0 in remote community needing air transportation to hospital
178
Pneumonia not improving - additional investigations? (D)
Ultrasound to characterize pleural effusion
Chest tube insertion for drainage of moderate to large pleural effusion drainage, chest tube to -20cmH20
Send fluid for Cell count and differential, Gram stain and bacterial culture, (pH, LDH, protein, glucose rarely change patient management)
Ensure antibacterial coverage of S. aureus and S. pneumoniae. Consider addition of MRSA coverage (e.g., Vancomycin and Ceftriaxone)
Consider addition of fibrinolytic (e.g., alteplase via chest tube BID for 3 days)
Continue chest tube until output <1cc/kg/day (per IDSA guidelines)
Supportive management including O2 to maintain SpO2>92% throughout, fluid management
Anticipate improvement in O2 requirement with source control, but involve PICU for additional respiratory support if progressive work of breathing or increasing O2 requirement
Continue IV antibiotics until chest tube removed and clinically improved (e.g, defervescence, resolution of respiratory distress and O2 requirement), then step down to oral antibiotic coverage for 2- 4 weeks (reassess based on clinical course)
179
What are the two most common bacterial organisms to cause a superinfection/pneumonia during an influenza infection? (D)
S. pneumo
| S. aureus
180
Chest tube inserted, but not draining adequately. Provide two therapeutic options to assist drainage of effusion (D)
External suction
Intrapleural fibrinolysis
Tube manipulation, ensuring no kinks etc. → tube replacement such as with larger tube or additional tube. Reposition if chest tube appears to be in wrong position on CXR.
VATS if not improved with above
181
Pertussis – 8 month old 7 days into paroxysms phase; in daycare Treatment? (D)
Erythromycin = first line x 14 days in neonates and infants
Respiratory isolation precautions should be implemented until 5 days of effective antibiotic treatment have been received
May return to daycare 5 days of effective antibiotic treatment
Azithromycin is the preferred treatment because it seems to be less associated with IHPS (idiopathic hypertrophic pyloric stenosis) than is erythromycin, although cases of IHPS have also been associated with azithromycin
Supportive care is the mainstay of management.
Any infant younger than 6 months with suspected pertussis should be admitted to the hospital to monitor for progression of the illness and associated complications and to educate family members before discharge.
182
Infants with pertussis should be monitored for what? (D)
The development of pulmonary hypertension.
183
Why treat pertussis/what does treatment accomplish? (D)
When given in the catarrhal or early paroxysmal stage of the illness, this will help the symptoms, eradicate the bacteria from the nasopharynx within a few days and terminate contagiousness of the patient
184
Who else gets treated for pertussis besides the index case? (D)
Prophylactic use of erythromycin (or clarithromycin or azithromycin) has been shown to protect from B.pertussis when given to close contacts and is most useful when given before the occurrence of the first secondary case.
Recommended antibiotic dosage and duration is the same as for treatment and should be given to all close contacts regardless of age and immunization status
Postexposure active immunization should be considered in unimmunized or incompletely immunized individuals by use of a dose of age-appropriate pertussis vaccine
Active immunization = most effective way to prevent pertussis → acellular pertussis vaccines (most recommend primary series of 2 or 3 vaccines in infancy and a reinforcing dose in the second year of life)
Treatment of infants with pertussis requires specific considerations. Infants younger than 6 weeks must be monitored for infantile hypertrophic pyloric stenosis (IHPS), which is associated with macrolide therapy, for 1 to 2 months after treatment.
185
Bug involved in Pertussis (D)
Bordetella pertussis → bordetella = small, aerobic, gram-negative coccobacilli
The typical incubation period is 7 to 10 days, but it may be as long as 21 days.
Organism is transmitted by aerosol droplets from infected to susceptible humans
186
3 stages of Pertussis
1. Catarrhal: lasts for 1-2 weeks, characterized by flulike symptoms (coryza, sneezing, lacrimation, conjunctival injection, malaise and nonspecific cough)
2. Paroxysmal: (in classical cases) marked by an increase in frequency and severity of coughing, with paroxysms as the most typical features → repetitive series of 5-10 or more hacking spells of cough occur during a single expiration → at the end of a paroxysm, a typical whoop (caused by a sudden rush of inspired air through the narrowed glottis) is noted. The paroxysms may happen up to several times per hour (day and night), triggered by various stimuli (eating, drinking, physical and emotional stress). Can last for days to weeks. (Not until this paroxysmal stage, that it’s more obvious that it’s pertussis).
3. Convalescent: marked by a decrease in frequency and severity of coughing spells
187
Child on D2 of treatment of staphylococcus pneumonia. CXR showed large RUL abscess. Mom wondering about surgery. Would you consider the surgery? (D)
Surgery = last resource after medical therapy has failed
188
What is the most appropriate action of treatment for Staph aureus lung abscess? (D)
Mainstay of treatment = IV antibiotics for 4-6 weeks
Ampicillin-sulbactam (or a cephalosporin with clindamycin for MRSA) = usual choices to cover most prevalent pathogens (use vanco for MRSA for clinda resistance)
Usually only treatment but IR or surgery can be considered → CT-guided aspiration or CT guided pigtail drainage catheters
189
Steps in lung abscess formation (D)
Begins with inflammation of the parenchyma → necrosis → cavitation → abscess formation
May be secondary to predisposing conditions (pulmonary aspiration) → neurodevelopmental delay, congenital malformations, immunodeficiency, endocarditis
Usually the most dependent segments of the lung (esp upper lobes, apical segments of the lower lobes) = affected
Associated with a pulmonary infection especially secondary to gram-positive cocci and gram-negative bacteria
190
Characteristic imaging finding of lung abscess (D)
CXR usually confirms the diagnosis → characteristic finding = cavity with thick walls and an air-fluid level
U/S is helpful in defining a lung abscess and to differentiate an abscess from a loculated empyema
Investigation of choice = contrast-enhanced CT (preferred to guide invasive drainage procedure)
191
10 YO boy previously healthy with fever and cough. CXR showed LLL pneumonia
Name 3 most appropriate investigations (D)
Sputum culture (IDSA guideline), though we don’t practically do this
Sensitive and specific tests for the rapid diagnosis of influenza virus and other respiratory viruses
CBC w/ differential
CRP / ESR / Procalcitonin
```
Electrolytes - in case of SIADH
Blood culture (10% yield)
```
192
Name most appropriate outpatient antibiotic treatment for CA pneumonia (D)
PO Amoxil
193
Name most appropriate inpatient antibiotic treatment for CA pneumonia (D)
IV Ampicillin
(to the fully immunized infant or school-aged child admitted to a hospital ward with CAP when local epidemiologic data document lack of substantial high-level penicillin resistance for invasive S. pneumoniae.)
194
CXR with LLL round pneumonia. 2 days History of fever and cough. What is most likely diagnosis? (D)
Strep. pneumo
195
Differential diagnosis of round pneumonia (D)
Other infections:
- Atypical pneumonia
- Tuberculosis
- Fungal infection / aspergilloma
- Abscess
Congenital:
- Congenital pulmonary airway malformation
- Sequestration
- Bronchogenic cyst
Cancer:
- Lymphoma
- Chest wall tumor
- Metastasis
- Neuroblastoma
- PPB
Other:
- Atelectasis
- Artifact
196
Would you do a follow up CXR for a round pneumonia? Why? (D)
Yes. Round pneumonias warrant a repeat CXR to confirm the resolution of the opacity, given the possibility of other serious differential diagnosis.
No follow-up radiographs are needed to evaluate a CAP with good clinical response EXCEPT for cases of round pneumonia, lobar collapse or whenever clinical deterioration may occur
Most round pneumonia should resolved within 30 days on CXR
Repeat imaging at 4-6 weeks
197
Why are round pneumonias generally only seen in children? (D)
Round pneumonias are more common in younger children due to lack of development of collateral ventilation, through the pores of Kohn and canals or Lambert.
198
Work-up for pneumonia/abnormal chest xray (D)
```
Blood work:
· CBC + diff
· Blood culture
· Electrolytes
. CRP /ESR / Procalcitonin
```
Imaging:
· Chest radiograph (PA and lateral)
· Consider bedside ultrasound
· CT should not be used routinely, unless other diagnosis is suspected (e.g. tumor)
· Look through previous CXR, if any, for location of
previous pneumonia
· Repeat CXR if indicated (e.g. round pneumonia)
```
Other:
· Sputum culture
· NPA for viral detection
· TST if indicated
· Sweat chloride if indicated
· Bronchoscopy/BAL if indicated
· Biopsy
```
199
CT scan showing left consolidated lung with pleural effusion. What is the diagnosis? (D)
1- Pleural Fluid ( Transudative or Exudative)
2. Empyema
3. Hemothorax
4. Chylothorax
5. Urinothorax
