Respiratory infection number 2

Question 1

With respect to non-TB mycobacterium, what are some of the common slow growers we see in Aus, and what about the fast growers?

Answer 1

Slow growers:

m. kansasii
M. avium complex, broken into M. avium and M. intracellulare

and college loves M. marinum

Rapid:
M. abscessus

Question 2

non-TB mycobacterium causes 4 distinct infection syndromes.

what are they?

Answer 2

1. fibrocavitating disease - usually in a male smoker and drinker - usually an upper lobe disease
   - easy to isolate from sputum
2. fibronodular disease
   - “Lady Windermere disease”
   - thin tall women, maybe with CTD
   - non-smoking women
   - seems to impact lingula and lower lobe (c.f. cavitating disease)
   - in this disease, there is only INTERMITTENT shedding, therefore only intermittently pos sputums
   - causes nodular bronchiectasis
3. disseminated in immunosuppressed.
4. soft tissue/skin, particularly in diabetics who inject themselves

Question 3

what is the treatment for Non-TB mycobacterium?

Answer 3

Rifampicin
Clarithromycin or Azithromycin

Ethambutol
Amikacin/streptomycin

sensitivity testing is ONLY useful for clari

Question 4

what is nocardia and where do we get it from?

what are the risk factors?

Answer 4

this is a gram pos rod, that is found in the soil

it is usually spread via skin, but after gardening injury and that sort of thing.

steroids are an important risk factor, but up to 40% no RF identified

Question 5

what are the clinical syndromes from nocardia?

Answer 5

can cause just about anything

one or more nodules/masses
lobar consol
bronchiectasis
cavitations
pleural disease
LN

can also cause disseminated and CNS disease (ring enhancing lesion)

Question 6

how do we treat nocardia infection?

Answer 6

TMP/SMX is mainstay of treatment

if very unwell, amikacin also added

Question 7

describe the source of cryptococcosis

are they capsulated or not?

Answer 7

c. neoformans is common in north america and europe.
we do have it in australia, in bird droppings

c. gattii is in the Red gum trees

this organism is capsule poor when it invades, but it reconstitutes inside man

the only fungus that invades humans

Question 8

what is the clinical population and what is the findings?

Answer 8

often immunosuppressed, but can be in immunocompetent host

variable presentation

often chest pain, sputum and cough

can be small nodules or up to 10cm lesions!

it can present as an EOSINOPHILIC PNEUMONIA

Question 9

what does the gram stain show in cryptococcal meningitis?

Answer 9

the classical thing is India Ink stain

this is an ink used in writing that attaches to gelatinous capsules

if you’ve read the other slides in this lecture, you’ll find that crypto is the only encapsulated fungi that invades humans

Question 10

how to treat cryptococcal resp infection?

Answer 10

all should be treated because there is a risk of meningeal spread

fluconazole for 3 - 6 months

Question 11

aspergillus is found where? how do we get it?

how does the body respond to its infection?

Answer 11

it is a fungus that is in the dust

normally the alveolar macrophages are capable of killing this bug, so something is usually required to be abnormal, such as a cavity

aspergillus invades across tissue planes, and this can lead to serious business, like that mycotic aneursym at the Whitt.

Question 12

how do we treat aspergillus infection?

Answer 12

voriconazole for invasive

itraconazole is less expensive and used for less savage

if there is an aspergilloma, then surgery may be necessary

Question 13

what is ABPA?

how does it cause disease? (and what is that disease?)

Answer 13

this is a complex hypersens reaction in patients WITH ASTHMA

it is repeated episodes of broncial obstruction, inflammation and mucoid impaction

this then leads to bronchiectasis, fibrosis and eventually resp compromise

it occurs in atopic individuals on exposure to fungal spores

we get formation of IgE and IgG Abs

the IgE is what we measure

There is colonisation with the aspergillus BUT THERE IS NO INVASION c.f. the other asper infections

Question 14

what are some of the diagnostic features that we see for ABPA?

Answer 14

history of asthma
skin test reactive to aspergillus antigens
precipitating Ab to aspergillus

serum IgE >1000
peripheral blood eosinophil > 500

lung infiltrates plus proximal (hilar) bronchiectasis is HIGHLY SUSPICIOUS

can get elevated specific IgE and IgG

Question 15

how do we treat ABPA?

Answer 15

steroids are effective but signif SE

inhaled control the asthma, but no evidence in acute ABPA

itraconazole = steroids can be reduced, but no role for monotherapy

usually we monitor serum IgE and FBC (for eosinophils)

overall, can get ‘roid dependent and that’s a bad thing

Question 16

how do we treat not-TB pulmonary abscesses?

(not empyema)

what are the bugs we are treating?

Answer 16

anaerobes are the bad boys.

some aerobes can also cause trouble, such as strept (pyogenes and milleri - not pneumococcus) and staph

antibiotics classically have been penicillin and metro

in the US they now use clinda because of betalactamase risk

in hospitalised patients, we worry about pseudomonas and staph aureus and enterobacter, so we add vanco (for MRSA, although US uses linezolid) and moxiflox for pseudomonas

Question 17

what is the treatment of PCP?

does an ABG provide any role?

Answer 17

the treatment is cotrimoxazole

if demonstrably hypoxic, then the addition of steroids is useful