Respiratory tract infections Flashcards
URTIs
sinusitis
pharyngitis
laryngitis
tracheitis
upper airway obstruction
acute onset (usually):
croup (laryngotracheobronchitis)
epiglottitis
neck abscess (e.g. peritonsillar, retro-pharyngeal)
syphilitic gumma (soft, non-cancerous growth resulting from tertiary syphilis)
slow onset (usually): enlarged tonsils or adenoids
unlikely to produce significant obstruction:
TB
fungal infections
typical pneumonia
high fever tachycardia pleuritic pain severe SOB painful cough, rusty sputum CXR: lobar or broncho-pneumonia strep pneumoniae, staph aureus
atypical pneumonia
fever often moderate relative bradycardia usually no pleurisy consolidation variable cough may be late, often no sputum, rarely haemoptysis Mycoplasma pneumoniae Chlamydophila ( Chlamydia) pneumoniae Legionnaires disease ( Legionella pneumophila) Respiratory viruses, including the following: Influenza A and B Rhinovirus Respiratory syncytial virus Human metapneumovirus
mycoplasma pnuemoniae
epidemics every 4y, lasting for <1y
extrapulmonary features:
diarrhoea, vomiting, abdo pain, abnormal LFT, otalgia, pharyngitis
myalgia
pericarditis, myocarditis
haemolytic anaemia (cold agglutinins - high volumes of antibodies, usually IgM, directed against erythrocytes)
erythema multiforme
nosocomial pneumonia
oropharyngeal colonisation common - pseudomonas
predispositions - antacids, ABx, biofilms
ventilator associated - pseudomonas aeruginosa, staph aureus
clinical diagnosis of pneumonia
in absence of CXR:
- cough, 1 or more LRTI Sx, fever
- new focal signs O/E
- no other explanation for illness
with CXR:
- cough, 1 or more LRTI Sx, fever
- new radiographic infiltrates
- no other explanation for illness
CURB-65
Confusion Urea >7mmol/l Resp rate >29 BP < 60mmHg diastolic, or < 90mmHg systolic age > 65
for severity also consider hypoxaemia (<8kPa/<90%),
involvement of 2 lobes and any pre-existing disease
Tx of pneumonia
oxygen
ABx
analgesics
consider ITU
ABx therapy for pneumonia
for CAP, cover pneumococcus and atypical pathogens:
amoxicillin and clarithromycin
for severe use piperacillin-tazobactam
fro suspected staphylococcus add flucloxacillin
for nosocomial use pip-taz
acute bronchitis or bronchiolitis
common
cough, usually sputum, orten upper airway Sx
no consolidation on CXR
usually viral, seldom needs admission
infective exacerbation of COPD
increased volume or change on the character of sputum
increased freq and severity of cough
increased dyspnoea
CXR usually unchanged
bronchiectasis
irreversible dilation of the proximal medium-sized bronchi
poor tracheobronchial clearance
chronic airways infection
associations with bronchiectasis
CF
immunodeficiency, esp. hypogammaglobulinaemia
rheumatological disease esp. RA
IBD, esp. UC
bronchial obstruction and infection esp. TB
lung abscess associations
pulmonary infarction, malignancy, tumour
pneumonia - staph, klebsiella, strep pyogenes
patients who are unconscious or who are undergoing anaesthesia
pre-hospital vomiting while drunk
haematogenous spread - endocarditis, septic phlebitis
diagnosis of lung abscess
may present after pneumonia
commonly non-specific, weight loss, fever
later on, fingers may show clubbing
sputum cultures may be unreliable
Tx of abscess
ABx for 8 weeks or longer (choice depends on suspected cause)
usually start with broad spectrum
ABx will not cure the abscess
empyema
pus in pleural space
40% of bacterial pneumonias have effusion
9% of pneumonia in hospitalised patients will lead to empyema
spread of infection from lungs to mediastinum
exudative effusion: protein >30g/l, pH <7.20
1 year mortality up to 20%
Tx of empyema
if pus or pH <7.20, insert chest drain
ABx will not cure empyema
influenza
1918 ‘swine flu’ A/H1N1 killedn >25m people in 6/12
severe pneumonia - primary influenzal, secondary strep/staph
encephalitis lethargica
influenza virus
RNA virus from the family Orthomyxovirus
types A & B pathogenic for humans
epidemics chiefly type A
antigenic variation of influenza
antigenic drift: RNA replication is error prone
influenza Tx
oseltamivir (tamiflu)
zanamivir (relenza)
amantidine
prevention: annual immunisation for: over 65 chronic resp disease heart disease renal failure cancer DM immunosuppression nursing homes etc
TB
mycobacterium tuberculosis (M bovis, M africanum) symbiosis lasts many years (sometimes whole lifetime) converging evolutionary interests of the parasite and host intracellular parasite, replicates inside phagocytes
9.4 m active TB tb each year (55% in asia)
1.3m deaths a year
highest rates in the UK amongst indians, paki, bangladeshi
a disease of poverty and people who are hard to reach
cycle of TB
exposure leads to infection (not in everyone)
of these, 95% will develop latent TB, 5-10% of which will end up with secondary (active) TB (reactivation or reinfection)
the other 5% will develop primary TB, which either resolves or becomes latent TB`
clinical presentations of TB
primary vs post-primary (reactivated) TB
most clinical manifestations are due to host response, not the actual bacteria
lungs are the main site of primary TB infection
reactivated TB in manly at the lung apices
at first, non-specific Sx: weight loss, fatigue, night sweats
tissue necrosis, cavitation, enlargement of tubercles (bones)
cough, haemoptysis, SOB, chest pain occur late
now the patient becomes infectious
later on–> bronchiectasis and fibrosis
in the 15% of extrapulmonary TB:
lymph nodes, pleura, skeletal, meningeal, pericardial, miliary
more likely in immunosuppressed e.g. HIV
diagnosis of TB
CXR
histology - caseating granuloma
microscopy and culture (usually sputum) for definitive diagnosis
contact tracing (NB compulsorily notifiable)
for latent TB skin testing, IGRA
IGRA - interferon-gamma release assays
quantiFERON-TB gold, T-spot.TB
sensitivity is better than skin tests, though not enough to rule out TB
IGRA often negative in active TB
cannot distinguish between latent and active TB
false positives may occur with other bacteria
screening for TB
london has the highest rates in western europe
10% are drug resistant. increasingly MDR-TB
cough >4 weeks ? have you been street homeless
screening tests: PPD (mantoux) + IGRA
latent TB
1-2 billion worldwide (mostly sub-saharan africa and south asia)
55% increase in UK between 1993-2010
immune response keeps mycobacteria inside a granuloma so they cannot be detected directly
immune control may be weakened later by immunosuppression e.r under nutrition, HIV, prednisolone
10-15% lifetime chance of progression to active disease (>50% within 5 years of initial infection in children)
diagnosis of latent TB
no active TB on CXR, exam or bacteriology AND mantoux >6mm without BCG OR IGRA positive with or without BCG
microscopy for TB
sputum or other specimen (bronchial lavage, CSF; gastric washings in children)
at least 3 sputa
stain (usually ziehl-neelsen (acid fast stain) or auramine)
‘smear positive’ means alcohol and acid fast bacteria seen in sputum (e.g. mycobacteria, not necessarily in M TB)
Tx of TB - RIPE
initial phase: Rifampicin (hepatotoxic) Isoniazid (hepato & neuro toxic) Pyrazinamide (hepatotoxic) Ethambutol (neurotoxic, esp. to retina, colour vision is the first to deteriorate)
continuation phase:
rifampicin and isoniazid for 4 months (10 months in meningitis or spinal infection)
Tx of latent TB
treat in HIV or healthcare worker and >66y
rifampicin and isoniazid for 3 months
OR
isoniazid or rifampicin for 6 months
immunoprophylaxis of TB
bacillus calmette-guerin neonatal BCG in UK for baby at high risk offers some protection against severe TB unreliable in adolescents not for HIV infected as it is a live vaccine
non-TB mycobacteria (NTM)
environmental saprophytes in soil and water
thrive in chlorinated water, concentrated by heating
not transmitted person-person
clinical features determined by interaction with host
pulmonary NTM infection
diagnosis is difficult because the cultures can be false positive and false negative in non-cavitating infection
pulmonary NTM infection is increasing, mostly M avium, M kansasii and M malmoense
various manifestations e.g cavitation, bronchiectasis, nodules or masses, hypersensitivity pneumonia
Tx NTN infection
only treat if causing deterioration
NTM often drug resistant
usually requires multiple ABx
surgery may be more effective (esp. in M abscessus)
leprosy
mycobacterium leprae, very slow growing
mostly in india, brazil, indonesia, bangladesh. nigeria
mostly resp acquisition
early diagnosis and Tx prevent disability
spectrum of disease from tuberculoid (TL, paucibacillary) in people with strong immune defences to lepromatous (LL, multibacillary) in those with weak immunity
leprosy manifestations
skin: sparse hypoaesthetic maculkes in TL (tuberculoid leprosy) or multiple nodules full of bacilli in LL (lepromatous leprosy)
neuropathy (localised in TL, generalised in LL)
