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Respiratory SCE > Pulmonary Infection > Flashcards

Pulmonary Infection Flashcards

1
Q

What is babesiosis and what is used to treat it ?

A

Babesiosis is a microscopic parasites transmitted by tick bite and results in malaria like illness with most common complication being non cardiogenic pulmonary oedema and even ARDS.

Diagnosed in peripheral blood smear which shows a tetrad or ring pattern in the RBCs and indicates babesiosis

Tx is with atovaquone and clari/azithro or a combination of clindamycin and quinine

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2
Q

What is Lemierre’s syndrome ?

A

A rare complication of bacterial pharyngitis/tonsillitis and involves an extension of the infection into the lateral pharyngeal spaces of the neck with subsequent septic thrombophlebitis of the internal jugular vein(s) with septic embolisation to the lung and subsequent cavitation /abscess . Can get empyema/ascites

Tx - Betalactamase resistant abx

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3
Q

What is the most common pathogenic cause of Lemierre’s ?

A

Fusobacterium Necrophorum

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4
Q

What is the CURB-65 score and what does it comprise of?

A

30 day mortality risk

Confusion (AMTs ≤ 8) , Urea > 7, RR ≥ 30 , BP (SBP <90 or DBP ≤ 60mmHg) ; Age ≥ 65

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5
Q

What are the 30 day mortality risks for each of the CURB-65 severity scores (Low, Moderate, High)?

A

Low Risk (0-1) : 3%
Moderate Risk (2) : 9%
High Risk (3-5): 15-40%

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6
Q

When should CXR and be CRP be repeated in hospital as per BTS guidelines ?

A

If not improving after 3/7 of treatment

Failure or CRP to fall by 50% at 4 days is useful finding suggesting failure of tx / development of lung abscess /effusion

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7
Q

What is the empirical abx for low severity CAP?

A

Amoxicillin 500mg TDS

(Alternate: Clarithromycin, Doxycycline)

(If can’t tolerate oral then IV amox or IV Ben Pen)

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8
Q

What is the empirical abx for moderate severity CAP?

A

Amoxicillin 500mg TDS (+ Clarithromycin 500mg BD)

(If can’t tolerate PO then IV amox + clari , Ben-Pen + Clari)

(Alternative: Doxycycline, Levofloxacin / Moxifloxaxin)

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9
Q

What is the empirical abx for high severity CAP?

A

Co-amoxiclav and Clari

(If pen allergic 2nd generation cephlasporin- Cefuroxime and Clari ; 3rd generation cephlasporin - Ceftriaxone and Clari)

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10
Q

How long do BTS/NICE recommend for abx in pneumonia

A

Low/ Moderate: BTS 7/7 , NICE 5/7
High: BTS/NICE: 7-10 /7

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11
Q

What to do if failure of empirical treatment in CAP?

A

Low Severity: Add macrolide

Mod Severity: Change to Doxycycline/ Fluoroquinolone

High Severity: Add Fluroquinolone

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12
Q

What is PVL-SA Pneumonia?

A

Panton Valentine Leukocidin (PVL) Staph Aureus (SA) is a rare cause of high severity pneumonia and can be associated with rapid lung cavitation and multi organ failure

If strongly suspected:
IV Linezolid 600mg BD, IV Clindamycin 1.2g QDS and Rifampicin 600mg BD

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13
Q

What is the preferred abx for S.Pneumoniae?

A

Amoxicillin 500mg- 1g TDS PO (Ben Pen 1.2g QDS IV if need IV)

Alternative: Clarithromycin or Cefuroxime, Cefotaxime, Ceftriaxone)

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14
Q

What is the preferred abx for M.Pneumoniae (C.Pneumoniae)?

A

Clarithromycin 500mg BD PO/IV

(Alternative Doxycycline or Fluoquinolone)

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15
Q

What is the preferred abx for C.Psittaci?

A

Doxycycline 200mg PO stat , then 100mg OD

(Alternate - Clari)

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16
Q

What is the preferred abx for Legionella ?

A

Fluoroquinolones PO/IV

(Alternative: Clarithromycin)

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17
Q

What is the preferred abx for H.Influenzae?

A

Non-Beta Lactamase producing: Amoxicillin

Beta Lactamase producing : Co-Amoxiclav

(Alternatives: Cefuroxime, Cefotaxime, Ceftriaxone, Fluroquinolone)

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18
Q

What is the preferred abx for Gram -ve enteric bacilli?

A

Cefuroxime, Cefotaxime, Ceftriaxone

(alternative: Fluroquinolone or Imipenem or Meropenem)

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19
Q

What is the preferred abx for Pseudomonas Aeruginosa?

A

Ceftazidine 2g TDS plus Gentamicin /Tobramycin

(alternate : Ciprofloxacin 400mg BD IV or Piperacillin 4g TDS plus Gent/Tobra

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20
Q

What is the preferred abx for S.aureus?

A

Non MRSA: Flucloxacillin 1-2g IV QDS +/- Rifampicin

MRSA: Vancomycin or Linezolid or Teicoplanin +/- Rifampicin

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21
Q

What is the preferred abx for Aspiration?

A

Co- Amoxiclav

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22
Q

What micro tests needed in different severity CAP?

A

Low Severity: None unless complicated, co-morbid or failing to improve

Moderate Severity: BC , Sputum (if expectorating and no prev abx; but only gram stain if complicated), Strep Pneumoniae urinary antigen , Legionella antigens (BTS - no, NICE - yes) , Mycoplasma if outbreak

High severity: BC, Sputum culture + gram stain, S.Pneumoniae antigen , Legionella antigen , Mycoplasma, Chlamydophillia

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23
Q

NICE recommends stopping abx treatments for pneumonia after 5 days unless evidence for need of longer course, which is provided by what?

A

Fever in the past 48 hours (>37.8)
HR>100, RR> 24, BP <90 , Sats <90

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24
Q

What do we need to be aware of with prescribing fluroquinolones ?

A

Stop if any sign of adverse features (tendonitis) , prescribe with caution over 60 yo and try to avoid co-administration with steroids

Aortic aneurysm and dissection

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25
Q

What is the preferred macrolide in pregnancy?

A

Erythromycin

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26
Q

What is the main bacterial infection causing CAP?

A

S.Pneumoniae

(M.Pneumoniae occurs in outbreaks every 4 years)

(NB bacteria most common cause of CAP but viral accounts for 13%)

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27
Q

Does testing for pneumococcal and legionella in moderate to high severity CAP make a difference?

A

In moderate to high severity CAP abx prescribing guided by Pneumococcal /Legionella antigen testing was not significantly different to a strategy that used broad spectrum abx without antigen testing for outcomes of mortality, clinical response and hospital admission

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28
Q

Why avoid doxycycline in pregnancy?

A

Avoid in pregnancy and breast feeding as deposits in growing bone/teeth

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29
Q

What is the strongest independent risk factor for invasive pneumococcal disease in immunocompetent patients ?

A

Smoking

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30
Q

What are common bacteria causing CAP in COPD?

A

H.Influenzae and M. catarrhalis

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31
Q

What causes hypoxia in pneumonia?

A

VQ mismatch

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32
Q

Outline S.Pneumoniae

A

Commonest cause of bacterial CAP
High fever and pleuritic chest pain in young adults, in the elderly can be atypical
Austrian Syndrome: Meningitis , Endocarditis and Pneumonia caused by S.Pneumoniae (now very rare but mortality 60%)

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33
Q

What are the main viral causes of CAP?

A

Human Rhinovirus
Influenza A/B

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34
Q

Outline Legionnaire’s Disease

A

Legionnaire’s is Pneumonia is caused by Legionella pneumophilia .

Increased risk if: increased age, male, smoking, EtOH XS, immunosuppression, HIV, exposure to contaminated water (hot tubs, air con units)

Often associated with: altered mental state, neuro/GI sx, abnormal LFTs, high CK and low sodium

Tx: 10-14 days Fluoroquinolones (Cipro +/- Azitrhom) inform HPU

Pontiac Syndrome: self limiting , non pneumonic form of Legionnaires assoc with fever

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35
Q

Outline features associated with M.Pneumoniae

A

Affects younger patients
Prominent extra pulmonary involvement:
- haemolysis
- cold agglutins
- hepatitis
- skin
- joint problems

May cause primary small airways involvement : tree in bud on CT

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36
Q

Outline Staph Aureus

A

More common in winter months often recent/concurrent influenza

Risk of MRSA (if hospital or abx last 90/7 recent influenza, hemodialysis. c previous MRSA, CCF)

PVL SA: necrosis , cavitation and multi organ failure ; tx Linezolid + Clindamycin + Rifampicin

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37
Q

Outline Coxiella Burnetti (Q fever)

A

Dry cough, fever , headache , animal sources (sheeps/goats)

Tx: 14 days Doxycycline /Clarithromycin

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38
Q

What is VAP and what causes it?

A

Ventilator Associated Pneumonia , occurs in ICU patients who have received mechanical ventilation for >48 hours

EARLY VAP (before 5/7) :
Strep Pneumoniae
H. Influenzae
Methicillin Sensitive Staph Aureus

LATE VAP (after 5/7);
Pseudomonas Aeuroginosa
Acinetobacter Baumanii
MRSA
Gram -ve Bacilli

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39
Q

Who is at high risk of developing MDR pathogens in HAP/VAP?

A
  • Admitted to unit with high rates of MDR pathogens
  • Prior abx use
  • Recent prolonged hospitalization >5 days
  • Previous colonization of MDR pathogen
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40
Q

What is a HAP?

A

Hospital Acquired Pneumonia, new radiographic infiltrates with evidence of infection and >48 after hospital admission. Accounts for 15% of hospital infections.

Caused by aspiration of infected upper airway secretions from the inhalation of bacteria from infected equipment or haemotogenous spread

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41
Q

What are the different organisms commonly causing HAP?

A

S.Pneumoniae/H.Influenzae : following trauma

S.Aureus: incr in ventilated neurosurgical patients

P.Aeruginosa: I&V > 8days , COPD, prolonged abx

Acinetobacter: I&V and previous broad spectrum abx

Anaerobic bacteria: Recent abdominal surgery

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42
Q

Is CURB-65 validated in HAP?

A

No

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43
Q

In VAP undergoing bronchs what are the significant cut offs for bacteria?

A

Protected Specimen Brush (PSB) : >1000 cfu/ml

BAL >10,000 cfu/ml

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44
Q

What are the stages of aspiration pneumonia ?

A

Chemical Pneumonitis: occurs within 1-2 hours, low grade fever and CXR changes with 2 hours ; need abx as acid damaged lung high risk

Bacterial infection

Mechanical obstruction

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45
Q

What causes lung abscess ?

A

Bacterial inoculum reaches the lung parenchyma (often dependent area) , pneumonitis , followed by necrosis over 7-14 days. Cavitation occurs when the parenchymal necrosis leads to communication with the bronchi’s and entry of air and expectoration of necrotic material leads to air-fluid level. Bronchial obstruction leads to atelectasis with stasis and subsequent infection which can predispose to abscess formation

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46
Q

How do we normally treat lung abscess ?

A

Co-Amox and Clindamycin (commonly
IV for 1-2 weeks, followed by PO for 4-6 weeks)

Rarely beed surgery , but more likely if:

  • large diameter >6cm
  • resistant organism
  • haemorrhage
  • recurrent disease
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47
Q

Describe key points for Nocardia

A

Clinical/ Imaging: Lobar consolidation (cavities in 30%), CNS (5-40%) and skin abscess (10%)

Who: Immunocompromised (often post transplant)

Micro: Gram +ve , Acid fast, filamentous rod

Tx: 6 MONTHS Septrin , Amikacin, 3rd generation cephalsporin (Ceph)

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48
Q

Describe key point for actinomyces

A

Clinical/ Imaging: Patchy consolidation may mimic TB/Cancer as also involves LN; suspect if lung and soft tissue infection of H&N

Who:Dental work /aspiration . Immunocompromised or COPD w poor dental hygeine

Micro: Gram +ve filamentous bacteria with yellowish sulphar granules

Tx: Penicillin for 6 months

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49
Q

Describe key points for anthrax

A

Clinical/ Imaging: Flu like illness cutaneous oedema and necrotic ulceration. Meningitis (fatal), hemorrhagic pleural effusion

Who: Inhalational (worse prognosis) vs cutaneous

Micro: Gram +ve spore forming bacillus

Tx: Cipro + Clinda +/- anti toxin +/- IVIG
Inform ID and public health

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50
Q

Describe key points for tularaemia

A

Clinical/ Imaging: fever and dry cough , tender ulcer and regional lymphadenopathy - ulceroglandular tularaemia

Who: Type A worse than B; rural - farmer/hunter

Micro: Gram -ve

Tx: 10-14 days Cipro ; Streptomycin / Gentamicin

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51
Q

Describe key points for meliodosis

A

Clinical/ Imaging: Cavitstion/empyema /nodular consolidation

Who: Returning travelers from Asia/Australasia with CAP/ subacute chronic TB like picture

Micro: Gram -ve bacillus

Tx: 3 months treatment : IV Ceftazidine/ IV meropenem /IV Imipenem (Septrin)

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52
Q

Outline leptospirosis

A

Clinical/ Imaging: Asymptomatic > multi organ failure, Weil’s disease is fever, myalgia , conjunctival haemorrhage , rash, jaundice /hepatic failure , renal failure , cosgulopathy and thrombocytopenia , shock , myocarditis / cardiac arrhythmias

Who: Vets/farmers/sewage workers

Micro: zoonosis

Tx: 7 days Penicillin/Ceftriaxone / doxycycline

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53
Q

What is the definition of MDR TB?

A

Resistance to at least Isoniazid and Rifampicin
Or
Rifampicin

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54
Q

What is the definition of pre-extensively drug resistant TB?

A

Resistance to isoniazid and Rifampicin and either a Fluroquinolone or second line injectable agent but not both

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55
Q

What is the definition of extensively drug resistant TB - XDR-TB?

A

Resistance to isoniazid and Rifampicin and Fluoroquinolone and any one of the remaining first line drugs for MDR-TB

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56
Q

What is the risk of an aspergilloma forming in a cavity >2cm in diameter?

A

15-20%

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57
Q

What are the discharge criteria for patients with pneumonia ?

A

Patients should not have more than one of the following:
T>37.8
HR>100
RR>24
Sats <90%
BP <90
Poor oral intake
Abnormal mental state

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58
Q

What are features of mucomycosis and how do we treat ?

A

Black lesions in mouth and CT demonstrating bilateral nodular lesions and cavitations. Seen post COVID . Tx with Amphotericin

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59
Q

What respiratory support do we offer patients with COVID not responding to FiO2 40% ?

A

CPAP

Do not routinely offer HFNO, unless unable to tolerate CPAP etc

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60
Q

What therapeutics can we give to patients with COVID-19 who do not need supplemental O2 but high risk of progressing ?

A

Nirmatrelvir/ritonavir (PO)

Molnupiravir (within 5/7 , can have 5/7 treatment , not for preggos, PO)

Sotrovimab (if >40kg, if Nirmatrelvir/ritonavir unsuitable)

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61
Q

Who gets Remdesevir in COVID-19?

A

Consider course (upto 5/7) in those who have COVID-19 and are in hospital needing low flow supplemental O2

(Don’t use on those req HFNO/CPAP/NIV / I&V)

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62
Q

What course of steroids do patients receive with COVID?

A

Dexamethasone 6mg PO OD for upto 10 days (unless discharged)

For those who need supplemental
O2 (nb can also be Pred 40mg and Hydrocortisone 50mg TDS)

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63
Q

Who gets Toculizumab in COVID-19?

A

Can have if having systemic steroids and needing supplemental O2

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64
Q

Who gets Barcitinib in COVID 19?

A

Need O2 and having /have completed steroids and no evidence of infection (NB c/I in pregnancy and breast feeding) . May be considered in ppl that can’t have Toci or if clinical deterioration despite Toci

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65
Q

What are the complications of COVID and how do we combat them?

A

AKI - can be common associated with increased mortality, monitor ppl with CKD for at least 2 years after AKI

Acute MI- increased Trop and BNP, ECG changes

VTE- prophylactic LMWH req low flow/high flow O2. Continue with prophylactic dose for 7 days including after discharge . Tx dose if on CPAP /HFNO/I&V

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66
Q

What are the signs of failure of CPAP/HFNO/NIV

A

Limited response within 6 hours
Lack of improvement in 3/7
Unchanged /increased work of breathing
Not tolerating CPAP /NIV

Remember days on CPAP impact on suitability for ECMO

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67
Q

What are the considerations for pregnant women with COVID-19?

A
  • Can prone up until 28 weeks (with appropriate padding)
  • Can use Tocilizumab /Sarulimab in those with CRP>75 or admitted to ICU (can use Ronapreve IV or Sotrovimab) ONLY give remdesevir if worsening
  • Steroids ;
  • if req for pre term delivery Dex 12mg x2 in 24 hours then Pred
  • if not req for Pre term delivery Pred 40mg OD and then hydrocortisone
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68
Q

What is Aspergillus?

A

Ubiquitous fungus causing variety of clinical syndromes.

Aspergillus Fumigatus is the most common species in pulmonary syndromes

Aspergillus Flavus more common cause of allergic rhinosinusitis , post operative aspergillosis and fungal keratosis

Aspergillus Terreus: common cause of IA in some places and Amphotericin B resistant

Aspergillus Niger: occ causes IA/aspergillus bronchitis but more common colonises respiratory tract

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69
Q

Will everyone exposed to aspergillus develop clinical syndrome?

A

No , it depends on patients immunocompromise.
If severe immune dysfunction (ie HSCT) can develop IA , if not as severe
Immune dysfunction - subacute IA

If underlying lung disease:
CPA
Aspergilloma
Aspergillus Bronchitis

If immune hyperactivity
ABPA
SAFS

70
Q

What is invasive aspergilloma?

A

Invasion of lung tissue by hyphae as demonstrated on histology

Clinical presentation often rapid , days - weeks

Neutropaenia classical risk factor (thrombocytopenia tends to parralel) . Angioinvasion in Neutropaenia hosts leading to dissemination in skin, brain , eyes

HIGH RISK : Allogenic stem cell transplant, prolonged Neutropaenia following chemo

71
Q

Which non neutropaenic patients get IA?

A

Most commonly associated with steroid use, prior to hospital.

Recognised in solid organ transplants (particularly heart , and lung + heart),
AIDS, COPD , Critically unwell, Liver failure , Chronic granulomatous disease

With non neutropaenic patients you don’t tend to get angioinvasion

often delayed dx, weeks to progress, subacute

72
Q

What is the most common fungal infection in lung transplant patients ?

A

Aspergillosis (44%)

Trachebronchial disease most common - ulceration /pseudomembranous noted at bronchoscopy

73
Q

Do lung transplant patients get prophylaxis for aspergillosis?

A

Yes : inhaled Amphotericin or oral Voriconazole /Itraconazole . Most impt factor is pre or post transplant infection, post transplant independent risk factor for mortality

74
Q

What are the risk factors for aspergillus infection in lung transplant ?

A
  • Induction with Alemtuzumab / Thymoglobulin
  • Single lung transplant
  • CMV infection
  • Hypogammoglobulinaemia
  • Rejection with use of mAb
75
Q

Who gets IA?

A

Neutropaenic
Non Neutropaenic (But IC)
Lung transplant
Critically unwell
Normal host - if extensive exposure

76
Q

How do we diagnose IA?

A

Fungal cultures
Galactomannan
PCR

Resp samples better than blood samples for all tests other than B-D Glucan

77
Q

How useful is BAL Galactomannan?

A

May be useful prognostic factor >2 associated with worse outcomes in non Neutropaenic whereas with HSCT serum GM useful prognosticator

78
Q

What are the radiological signs of
IA?

A

Cavitation
Pleural bases areas of apparent infection
Non specific necrosis

79
Q

How do you treat IA?

A

Voriconazole (can be problem in renal failure due to accumulation but often will still use)

12 weeks for non neutropenic subjects and repeat CT scan

Monitor levels

80
Q

Who gets CPA?

A

Those with underlying respiratory pathology , worldwide previously treated TB most common

Also: COPD/ Bronchiectasis /Sarcoid / Prev lung cancer / ABPA/ PTX

81
Q

What are the NTMs often associated with Aspergillus?

A

M.Avium
M.Kansasii
M.Xenopi
M. malmoense

82
Q

If sarcoid patient starts getting haemoptysis what should we think of ?

A

CPA!

83
Q

What is the classical presentation of CPA?

A

Middle Aged, male, constitutional symptoms (WL, malaise, night sweats, fatigue), chronic productive cough , breathless, chest discomfort , haemoptysis (denotes presence of aspergilloma)

84
Q

What are the radiological fx of CPA?

A

Lung cavitation , infiltration, nodules , varying degrees of lung or pleural fibrosis

85
Q

What is the critical test for CPA?

A

Aspergillus Specific IgG (or precipitans) supported by evidence of Aspergillus in sputum culture or PCR or biopsy/aspiration

86
Q

What is chronic cavitatory pulmonary aspergillosis ?

A

Slowly evolving, single or multiple lung cavities usually thick walled and with or without fungal ball (aspergilloma) and with concomitant pleural fibrosis

87
Q

What is an aspergilloma?

A

Rounded conglomeration of fungal hyphae, fibrin, mucus and cellular debris that arise in the pulmonary cavity and late presentation of CPA

NB if present , azole resistance is higher

88
Q

What is the risk in developing an aspergilloma in cavity >2cm?

A

15-20%

89
Q

How do we classify aspergillomas ?

A

Simple Aspergilloma : If stable over months

Complex Aspergilloma

90
Q

What is an aspergillus nodule?

A

Usually incidental finding on CT. Difficult to differentiate from cancer , often dx after excision biopsy

91
Q

How do we treat CPA?

A

Itraconazole
(2nd line Voriconazole , posiconazole)

92
Q

What are the side effects of Itraconazole?

A

Peripheral oedem
HF
HTN

Liver toxicity
Neuropathy

93
Q

What are the side effects of Voriconazole ?

A

Photosensitisation, if continued can develop pre-cancerous lesions

94
Q

If patients with CPA fail or intolerant to Azole therapy what treatments can be given?

A

Amphotericin B or Echinocandins
For 3-4/52 followed by maintenance with azole

95
Q

How might we manage simple/complex aspergilloma?

A

Surgically in patients with adequate respiratory reserve - lobectomy

Usually pre and post op anti fungal therapy to stop spread of fungal disease into pleural cavity

96
Q

What is the mortality of
CPA?

A

27% over 30 months
50% over 5 years

97
Q

What is the most common allergic bronchopulmonary mycosis?

A

ABPA

98
Q

What is ABPA?

A

Hypersensitivity to Aspergillus reflected by high Aspergillus specific IgE or positive Aspergillus skin test . It manifests as poorly controlled asthma but also with fevet , haemoptysis , malaise and expectoration of mucus plugs - impt to recognise as can lead to development of bronchiectasis if left untreated

99
Q

What is the treatment for ABPA

A

Corticosteroids and taper accordingly

100
Q

48 yo female with asthma presents with difficult to control symptoms , Asp Specific IgE is sent and is negative , how would you approach?

A

Consider sending total IgE , ?sensitization to other fungi other than A. Fumigatus then dz with Allergic bronchopulmonaru mycosis

101
Q

48 yo female presents with poorly controlled asthma, Asp. Fumigatus specific IgE is positive and total IgE is 1200 . How would you approach?

A

Review:
- Asp Precipitans
- Asp IgG
- Skin test
- Eosinophils

If 2/4 positive then HRCT

If normal HRCT: ABPA seropositive
If bronchiectasis HRCT: ABPA- Bronchiectasis

102
Q

48 yo female presents with poorly controlled asthma, Asp. Fumigatus specific IgE is positive and total IgE is 800 . How would you approach?

A

Dx with severe asthma with fungal sensitization

103
Q

48 yo female presents withcontrolled asthma, as part of screening Asp. Fumigatus specific IgE is sent which is positive and total IgE sent which is 600 . How would you approach?

A

Repeat total IgE in 1-2 years, if rising then can have :
Asp Skin test
Eos count
Asp IgG
Asp Precipitans

104
Q

Treatment for IA

A

Voriconazole

105
Q

Treatment for CPA

A

Itraconazole

(TDM 2-3 weeks after commencement and then 6/12)

Usually treatment for 12 months and reassess

106
Q

Treatment for ABPA

A

Corticosteroids

(2nd line Itraconazole)

107
Q

What fungal infection very common with liver transplant ?

A

Candidiasis

108
Q

What is needed to diagnose NTM?

A

Two sputum samples collected on separate days positive for mycobacterium culture with in keeping imaging.

If concerned but non productive - induced sputum

If sputum negative and concerned - CT directed Bronch

109
Q

What is used to treat Mycobacterium Avium Complex (MAC) PD?

A

Rifampicin , Ethambutol , Macrolide (Clari/Azithro)

** If severe , add in injectable aminoglycoside (Amikacin /Streptomycin)
** If Clari resistant - Rifampicin, Ethambutol and Isoniazid / Quinolone + Injectsble

110
Q

How long should treatment continue for NTM patients ?

A

For minimum of 12 months following culture conversion

111
Q

What is used to treat Mycobacterium Kansasii PD?

A

Rifampicin + Ethambutol + Macrolide/ Isoniazid

If Rifampicin resistant then 3 drug regimen guided by susceptibility testing

112
Q

What is used to treat Mycobacterium Malonese PD?

A

Rifampicin + Ethambutol + Macrolide

If severe disease (ie AFB +ve , microbiological evidence of cavitation /severe sx) add in injectable aminoglycoside

113
Q

What is used to treat Mycobacterium Xenopi- PD?

A

Rifampicin + Ethambutol + Macrolide + Quinolone / Isoniazid

If severe add in aminoglycoside

114
Q

What is used to treat Mycobacterium Abcessus PD?

A

INDUCTION:

4 week IV course of:

IV Amikacin + IV Tigecycline + IV Imipenem + PO Clarithromycin /Azithromycin

(if Macrolide resistance IV Amikacin , IV Tigecycline and IV Impipenem)

Duration of abx influenced by severity of disease

CONTINUATION:
Nebulised amikacin + PO Macrolide + Clofazamine / Linezolid /Minecycline / Doxycycline

(If Macrolide resistant , Amikacin + 2/4 of above)

115
Q

How often check sputum in NTM patients?

A

Every 4-12 weeks during treatment for 12/12

116
Q

When do we image NTM patients?

A

Beginning and end of treatment , any deterioration in between

117
Q

What is the treatment for Nocardia?

A

6 months of Ceph/Septrin

118
Q

Outline Mycoplasma

A

Dry cough, fever, pericarditis ,headache , rash, LFT derrangement, haemolysis , cold agglutinins

Tx: 7 days Dox / Clari

119
Q

What is the treatment for actinomyces ?

A

6 months penicillin

120
Q

What is the tx for Melioidosis?

A

3 months Ceph > Septrin

121
Q

What is the treatment for Coxiella ?

A

2 weeks Clarithromycin / Doxycycline

122
Q

What is the treatment for Legionella ?

A

10-14 days Cipro +/- Azitrho

123
Q

What is the treatment for Tularaemia ?

A

10-14 days Cipro

124
Q

What is the treatment for Mycoplasma?

A

7 days Doxy/Clari

125
Q

What is the treatment for Leptospirosis ?

A

7 days Pen /Doxy

126
Q

What are the most common infections for Primary Antibody deficiency patients ?

A

Otitis media, Sinusitis , Pneumonia

127
Q

What is the most common cause of Pneumonia in Primary Autoimmune deficiency patients ?

A

S. Pneumoniae
H. Influenzae type B
H. parainfluenzae
M. Pneumoniae
P. Aeruginosa
S. Aureus

Often concomitant viruses with RSV and enterovirus

128
Q

Why are PAD patients more susceptible to M. Pneumoniae,?

A

Increased susceptibility to Ureaplasma urealyticum

129
Q

In addition to usual infections PAD pts get what are CVID and XLA also at risk of ?

A

PCP
Mycobacterium Hominis
Mycobacterium avium
Adenovirus

130
Q

What proportion of Haematopoietic Stem Cell Transplants (HSCT) get pulmonary complications ?

A

1/3

Respiratory failure continues to be one of the leading causes of ICU admission for those undergoing HSCT, mechanical ventilation is a predictor of poor outcome

131
Q

What are the stages following HSCT?

A

Pre-Engraftment Phase <30 days

Immediate Post Engraftment Phase 30-100 days

Late Post Engraftment Phase > 100 days

132
Q

What are the is the host immune system defect in pre engraftment (0-30 days) phase ?

A

Neutropenia , Mucositis

133
Q

What is the host immune defect in the immediate post engraftment phase (30-100 days)?

A

Impaired Cellular Immunity

134
Q

What is the host immune defect in the late post engraftment phase ? (>100 days)

A

Impaired cellular and humoral immunity

135
Q

What infections do patients get in the pre engraftment phase ?

A

Gram -ve
Gram +ve (including Staph and Strep)
Candida
Aspergillus
HSV
CRV- RSV , influenza , Adenovirus

136
Q

What infections do patients get in the immediate post engraftment phase ?

A

Gram +ve (Strep, Staph)
Aspergillus
Candida
CRV (RSV, Influenza and adenovirus )

Towards the latter half
PCP
CMV
Aspergillus

137
Q

What infections do patients get in the late post engraftment phase ?

A

Encapsulated Bacteria
Nocardia
Aspergillus
PCP
HZV
CMV
CRV - RSV, Influenza , Adenovirus

138
Q

What are the non infectious resp complications in the pre-engraftment stage following HSCT?

A

CHF
PERDS
VOD
Diffuse Alveolar Haemorrhage
Idiopathic Pneumonia syndromes

139
Q

What are the non infectious resp complications in the immediate post -engraftment stage following HSCT?

A

VOD
Diffuse Alveolar Haemorrhage
IPS

Later :
COP
PTLPD

140
Q

What are the non infectious resp complications in the late post -engraftment stage following HSCT?

A

Bronchiolitis Obliterans
COP
PTLPD

141
Q

What is the strongest predictor of pulmonary complications following HSCT?

A

Low Karnofsky score
Underlying malignancy

142
Q

What types of HSCT more likely to have infective complications ?

A

Allogenic due to prolonged immunosuppressive therapy and GVHD

Plus the chemo regimen Rituxan and Purine analogues impair B cell function and T cell response

143
Q

What is GVHD?

A

Complication in which the newly transplanted donor haematopoietic bone marrow attacks the recipients body

144
Q

What is the most commonly isolated resp virus in HSCT patients ?

A

RSV ; higher mortality than Influenzae / parainfluenza

145
Q

Who more likely to get Invasice pulmonary aspergillosis in HSCT?

A

Allogenic (5-30%) autologous (1-5%)

146
Q

Who gets azole prophylaxis in HSCT?

A

Neutropaenic >2 weeks

Immunosuppressive tx for GVHD

147
Q

Outline Zygomycetes in HSCT

A

Includes Mucor and Rhizopus
Prevalence 1.9% in Allogenic

Tx : Amphotericin B / Surgical resection

148
Q

Outline Fusarium in HSCT

A

0.5-2% Allogenic

Survival 13%

149
Q

Outline Scedosporium in HSCT

A

Fungal
Needs surgical resextion

150
Q

Outline PERDS in HSCT

A

Peri Engraftment Respiratory distress syndrome

Incidence: Autologous > Allogenic

Onset: Early / acute, within 96 hours

Clincial: Temp 38.3 , >25% surface area erythrodermatous rash, pulmonary infiltrates , hepatic dysfunction, renal insufficiency, transient encephalopathy

Excellent response to steroids

Good prognosis

151
Q

Outline DAH in HSCT

A

Incidence : Autologous = Allogenic

Onset: Early / Acute

Clinical : Progressively bloodier BAL from > subsegmental lobes or > 20% haemosiderin laden macrophages , absence of infection

Moderate response to steroids

Poor prognosis , usually die of multi organ failure and sepsis

152
Q

Outline IPH in HSCT

A

Incidence : Allogenic > Autologous

Onset: Late / Subacute

Clinical feature: Progressive resp failure with absence of infection confirmed by BAL and then second 2-14 days later . Biopsy showing diffuse alveolar damage or interstitial pneumonia

Poor response to steroids

Usually die of resp failure

153
Q

What makes prognosis worse in BO in HSCT?

A

Rapidly deteriorating FEV1
> 60
Progressive GVHD

154
Q

How make dx of BO in HSCT?

A
  1. Allogenic HSCT
  2. Chronic GVHD
  3. Airflow obstruction FEV1/FVC<70 and FEV1 < 75%
  4. Air trapping or small airway thickening on HRCT
  5. absence of infection
  6. Biopsy
155
Q

What are the risk factors for developing BO in HSCT?

A

Older age
Non related donor
Total body irradiation >12Gy
Acute GVHD

156
Q

Outline BO in HSCT

A

Incidence :0-48%

HSCT: Allogenic

Onset: Late (1 year)

Sx: wheeze , cough , dyspnoea

Radiology: Normal: hyperinflated, air trapping, bronchiectasis (mosaic lung attenuation)

PFTs: Obstructive , normal TLCO

Dx: clinical , radiology , physiology

Histo: fibrotic plugs obliterating bronchiocoeles with inflammation and scarring

Tx: steroids and immunosuppression

Outcomes : poor

157
Q

Outline COP in HSCT

A

Incidence : <2%

HSCT: Allogenic and autologous

Onset: usually first 100 days

Sx: sob , cough , fever

Radiology: patchy consolidation, ground glass, modular opacities

PFTs: Restrictive , reduced TLCO

Dx: biopsy

Histo: granular plugs of bronchiocoeles extending into the alveoli

Tx: steroids

Outcome : good response
Outcomes :

158
Q

Outline PTLPD in HSCT

A

Uncommon but serious

Over proliferation of EVV infected lymphocytes

present 6/12 after HSCT with enlarged lymph nodes, liver and spleen

Tx: reduce immunosuppression and administer anti B cell monoclonal ab therapy

159
Q

What are the classical image changes seen in NTM?

A

Centrilobular Nodules
Tree in Bud
Middle lobe bronchiectasis / consolidation /cavitation

160
Q

What does LAT (legionella urine test) detect ?

A

Legionella Pneumophilia Serotype 1

161
Q

How long does it take for fatigue to improve post Pneumonia?

A

6 months

162
Q

Who gets endemic mycoses ?

A

Those with : AIDs , Lymphoma, steroid use

Relies on diminished T cell immunity

163
Q

Outline Histoplasmosis

A
  • Bird/Bat droppings in soil
  • Ohio, USA
  • Often asymptomatic can be acute /chronic /disseminated
  • CXR: target lesion, BHL
  • Dx with smears of culture infected material
  • Tx: Mild/Mod: Itraconazole; severe Amphotericin B
164
Q

Outline Blastomycosis

A
  • Inhalation of infected spores from soil, common in canoers; USA
  • Asymptomatic/Acute /Chronic / Disseminated- can effect bone /skin
    -Dx on staining
  • NB if BAL beware lidocaine as reduced growth
  • Tx - Mild/Mod : Itraconazole , severe - Amphotericin B
165
Q

Outline Coccidiomycosis

A
  • USA, infected soil, desert post rain
  • Asymptomatic /Acute (high Eos) /Chronic / Disseminated
  • Variable on CXR can be consolidation, lymphadenopathy, effusion
  • Dx on staining
    -Tx Fluconazole if severe Amphotericin B
166
Q

Outline Paracoccidiomycoses

A
  • South America / Mexico
  • Asymptomatic /Acute (<30years , fever, night sweats , cytopenia, hepatosplenomegaly)
  • Culture on sputum /BAL
  • Tx with Itraconazole , severe Amphotericin B
167
Q

Outline Pencilliosis

A

SE Asia
Tx : Amphotericin B

168
Q

Outline Adiaspiromycosis

A
  • Worldwide, Immunocompromised
  • Cough, fever , chest pain
  • CXR - focal consolidation , reticular shadowing
  • Dx often req lung biopsy
  • Tx : Amphotericin B
169
Q

What are the predominant infections in antibody deficiency patients ?

A

Otitis media (usually children)
Sinusitis
Pneumonia

Infective pathogens usually:
S.Pneumoniae
H.Influenzae
M. Catarrhalis

Concomittant virus with RSV

170
Q

What is the most common manifestation of Primary Autoimmune Deficiency?

A

Pneumonua

S.Pneumoniae, H. Influenzae Type B, H. Parainfluenzae, M.Pneumoniae (increase due to increase incidence of Ureaplasma Urealytica)

171
Q

What infections do CVID/XLA patients get ?

A

PCP
Mycobacterium Hominis
MAI
Adenovirus

Respiratory SCE (15 decks)

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