20 Lower respiratory tract infections Flashcards
What are causes of laryngitis/ tracheitis
Lower respiratory tract continuous with upper. But lower tend to be more severe. Similar organisms
Parainfluenza - most common Influenza Rhinovirus RSV Adenovirus
Diptheria
H Influenzae
S Aureus
GAS
Diptheria caused by corynebacterium diptheriae. Can colonise pharynx in normal people. Exotoxin producing strains cause disease. Diptheria can also cause cutaneous diptheria. Disease in resource-poor settings
Bacteria adheres using pili on cell wall to pharynx. Multiplies locally. Toxin destroys epithelial cells/ polymorphs, and necrotic ulcer forms
What are signs of diptheria infection?
Why is diptheria serious condition?
Exudate on pharynx causing “false membrane”
Bull neck - enlarged cervical nodes
Nasopharyngeal diptheria can cause hoarseness, stridor, and life threatening respiratory obstruction
Exotoxin can be absorbed systemically causing fever, myocarditis, polyneuritis due to demyelination
Incubation period of diptheria
Route of spread
2-5 days
Droplet spread
Direct contact - cutaneous
Structure of diptheria toxin
How does diptheria toxin work
Fragment A - toxic fragment
Fragment B - binding
Toxin binds to cells, and uptaken by cells. Fragment A inactivates ribosomal protein synthesis, causing apoptosis.
Investigations diptheria
Treatment diptheria
Nasopharyngeal throat swab - bacterial culture
Isolation
Airway management
Benpen/ erythromycin
Diptheria antitoxin - produced in horse serum
Diptheria vaccination - as antibody level post infection may not be high enough
How to deal with contacts exposed to diptheria
Nasopharyngeal swab - assess if asymptomatic carrier
Erythromycin prophylaxis
Diptheria immunisation
Bordetella pertussis causes whooping cough. Usually disease in children.
Bacteria attach and multiply on ciliated respiratory mucosa, but do not invade deeper structures. Has filamentous haemagglutinin and fimbriae which allow it to attach
Which toxins does it produce
Pertussis toxin - has A and B unit. Toxin upregulates cAMP causing dysregulated immune response
Tracheal cytotoxin - cell wall component directly kills tracheal epithelial cells
Inhibits phagocytosis
Inhibits chemotaxis
Inhibit antibody production
Pertussis incubation period
Symptoms
Diagnosis
7-10 days
Initial catarrhal illness
1 week later non-productive cough develops, which becomes paroxysmal. Paroxysyms characterised by series of short cough producing copious sputum, followed by “whoop”
Nasopharyngeal swab
Treatment of whooping cough
Prevention
Isolate - infective up to 3 weeks after symptom onset
Macrolide - erythro/ clarithro/ azithro - appears to reduce severity and duration, and infectivity of patient
Prophylactic antibiotics for close contacts
Immunisation with DPT (diptheria/pertussis/tetanus) vaccine. Targetted program at pregnant mothers, as maternal antibodies confer some protection to newborns
Causes of acute bronchitis
Causes of acute exacerbation of chronic bronchitis
Adenovirus
Coronavirus
Influenza - can cause post-influenza pneumonia with strep pneumoniae
Rhinovirus
Mycoplasma pneumoniae
Secondary infection with strep pneumoniae/ h influenzae common
Chronic bronchitis cough with excessive mucus secretion. Infection appears to be one component, along with smoking and inhalation of noxious substances. Multiple bacteria can cause it, but microbiology analysis difficult, as often some can be commensals and not cause disease. Multiple viruses can cause it, and can lead to secondary bacterial infection
Why does bronchiolitis usually occur in children <2
Causes of bronchiolitis
Bronchioles in young children very narrow, so when lining cells become inflamed, can cause airway obstruction. Severe in babies, with peak mortality at 3 months of age. Older children it is limited to URTI
RSV 75%
Parainfluenza
Influenza
Metapneumovirus
How is RSV transmitted
Incubation period
When to outbreaks occur
How does in attach to enpithelial cells
Droplet
4-5 days
Winter
Outbreaks often spread in hospitals
G proteins to attach to cells
Fusion protein to penetrate cell membrane
Investigations for bronchiolitis
Treatment
Viral throat swab
Supportive
Rehydration
Bronchodilators
Oxygen
Ribavirin - shown some efficacy
Palivizumab - monoclonal antibody can be used as prophylaxis in children <2 high risk airway disease. Given before and during RSV season
RSV pooled immunoglobulin can be given to high risk children
How do microbes gain access to lower respiratory tract
Microbes must be <5mm to reach alveoli
If impaired defences (HIV) or preceeding viral infaction, organisms which do not normally cause infectionm can cause infections in healthy individuals
Inhalation of aerosolized material or aspiration normal flora
Via bloodstream
What are four descriptive terms used for pneumonia
Pneumonia causes respiratory distress by interfering with gas exchange in the lungs, and causes systemic upset (sepsis)
Lobar pneumonia - distinct involvement of one lobe. Polymorphs form exudate in response to infection - causes solidification. Can spread between adjacted lobes
Bronchopneumonia - diffuse patchy changes due to consolidation in small airways
Interstitial pneumonia - invasion of interstitium usually seen in viral infections/ PCP
Lung abscess - necrotizing pneumonia with cavitation and destruction
Pneumonia more commonly causes by viruses in children. Adults tends to be bacteria
Causes of CAP
- typicals
- atypicals (because causes extrapulmonary features). Usually intracellular, so don’t show up on basic investigations
Typicals - Strep pneumoniae Haemophilus influenzae Moraxella cattarhalis Group A Strep Klebsiella Aspiration pneumonia
Atypicals -
Mycoplasma pneumoniae
Chalmydia pneumoniae
Legionella pneumophila
Atypical zoonotic -
Chladmydia psittaci
Coxiella burnetti
Tularaemia
Atypical viral - Adenovirus Influenza Parainfluenza RSV Measles SARS/ MERS/ COVID
Causes of CAP
- following viral infection
- HIV positive
- lung cancer
Post - viral
Strep pneumoniae
Staph aureus
HIV positive
PCP
Mycobacterium species
CMV
Lung cancer -
Moraxella cattharalis
Causes of CAP
- cooling tower exposure
- abbatoir worker/ vet/ farmer
- animal hide importers, wool sorters
- legionella
- coxiella burnetti
- brucella species
- coxiella burnetti
- bacilus anthracis
Causes of CAP
- exposure infected birds
- exposure infected sheep/ goat/ cattle
- exposure to bats/ bat droppings
- chlamydia psitacci
- coxiella burnetti
- brucella species
- histoplasma capsulatum
Causes of CAP
- hotel air conditioning
- California/ New Mexico/ Texas travel
- SE Asia, South/ Central America
- legionella
- coccidioides immitis
- Burkholderia pseudomallei - melioidosis
Hospital acquired pneumonia associated with more gram negatives. This is due to respiratory tract being colonised from lower GI tract - reflux/ PPI use
Causes of HAP
- Immunocompromised e.g post-organ transplant
- ventilator associated
Immunocompromised
- PCP
- CMV
- Mycobacterium species
- Nocardia
- Aspergillus
Ventilator
- Pseudomonas aeruginosa
- Staph aureus
- Enterobacteriaceae - Klebsiella, E. Coli, proteus, Enterobacter, Serratia
Causes of CAP
- Cystic fibrosis
CF -
Staph aureus
Haemophilus
Pseudomonas
Symptoms of typical/ atypical pneumonia
Cough
SOB
Pleurisy
Fever
Diarrhoea
Renal/ liver dysfunction
Meningitis - pneumococcal can spread via blood
When to take sputum sample and why
If sputum shows organism but no polymorphs, could just be commensal.
Immunocompromised patient may not have neutrophil response.
Atypicals bacteria (except legionella) will not show up on gram stain
May need chest physio/ bronchoscopy for sputum
What are rapid tests for pneumococcal
Take sputum first thing in morning - sputum pools in lungs, and prevents contamination with food
Antigen testing of sputum/ urine for antigen by agglutination of antibody-coated latex particles. Urine tests cannot test sensitivities on
Serological tests for atypica pneumonia
Legionella
Mycoplasma
Chlamydia pneumonia/ psittaci
Coxiella burnetti
Legionella - Urinary antigen test or rapid agglutination test
Mycoplasma - Complement fixation (CFT), IgM by latex agglutination or ELISA
Chlamydia - microimmunofluouresence of ELISA using species-specific antigens
Coxiella - Complement fixation test
Antibiotic selection for CAP
First choice - Amoxicilin
Secondary to viral infection - co-amoxiclav
Aspiration - co-amoxiclav and gentamicin
Antibiotics selection for specific organisms
- Strep pneumoniae
- Staph aureus
- Haemophilus
- Klebsiella
- Atypicals
Amoxicillin is often not active against many other causes of pneumonia, co combination therapy usually used as first line.
Can prevent strep pneumoniae with vaccine comprising polysaccharide capsular antigens. For splenectomy patients and those with chronic disease
Strep pneumoniae - amox/ clarithromycin
Staph aureus - flucloaxacillin
Haemophilus - co-amoxiclav/ cefuroxime
Klebsiella - gent/ cipro
Atypicals - doxycycline
Viruses can invade the lung via bloodstream as well as directly to respiratory tract. They can sometimes cause initial damage, which allows bacterial infection
What are common causes of viral pneumonia, and what clinical condition do they produce
- Influenza A/B - can cause secondary bacterial infection. Type A causes pandemics, Type B epidemcis. Antiviral available
- Parainfluenza types 1-4 - croup/ pneumonia children, URTI adults. No treatment
- Measles - secondary bacterial infection. Can cause primary infection immunocompromised.
- RSV/ metapneumovirus - bronchiolitis children, URTI adults
- Adenovirus - pharyngitis. Occurs in military - vaccine available. Cidofovir/ ribavirin can help
- CMV - interstitial pneumonia immunocompromised patients. Ganciclovir/ valganciclovir/ foscarnet/ cidofovir and immunoglobulin available
- HSV - interstitial pneumonia - immunocompromised
- Varicella-zoster - penumonia in children chickenpox
Structure parainfluenza
How many types
(-) SS-RNA
Surface spikes have haemagluttinin plus neuraminidase on one spike, fusion protein on other spike
Types 1-3 cause pharyngitis, croup, otitis media, bronchiolitis, pneumonia
Type 4 causes mild disease
What are four types of influenza, and how easily does it spread
Type A - epidemics, occasionally pandemics. Birds resevoir host
Type B - epidemics, no animal hosts
Type C - minor URTI
Type D - infects cattle usually
Describe structure of influenza virus and role of each part
(-) sense SS-RNA - 8 segments
Nucleoprotein
Polymerase
(these 3 help form ribonuceleoprotein)
Matrix protein
Lipid envelope
Haemagluttinin - approx 500 spikes - bind to host cell. H1-H16 different types
Neuraminidase - approx 100 spikes - release virus from cell. N1-N9
How are influenza A strains named
Full name includes:
antigenic type geographical origin first isolated strain number, year of isolation Sub-type of antigens H/N
e.g A/ Sydney/ 05/ 97 (H3N2)
Why is influenza able to evolve whilst spreading through host species
- Antigenic shift - when a cell is infected by two different strains influenza A, re-assembly of 8 unit RNA can occur, producing virus progeny with different combination of H/ N antigens Can rapidly spread through populations as no immunity as new strain
- Antigenic drift - small mutations to H/N occur over time, new subtype can infect previously immune population
WHO have influenza surveillance labs in 79 countries, to monitor for novel outbreaks.
Younger people at risk of pandemics, as elderly more likely to have some prior exposure to pathogen and have antibodies. H1N1 (swine flu) 2009 showed this.
Worry about H5N1 - bird flu
When does influenza transmission occur and how is it transmitted
Winter months - people spend more time in buildings with limited spaces, which favours droplet spread. Influenza natural host is birds
Droplet transmission
Avian influenza occur due to spread of poultry
Describe how influenza infects and causes damage
Virus enters via droplets, binds to sialic acid receptors in epithelial cells via H glycoprotein on virus envelope
Virus causes direct damage. -3 days later cytokines liberated from damaged cells and infiltrating leukocytes causes symptoms such as chills, malaise, fever, myalgia, runny nose, sore throat, cough
Complications of influenza
Pneumonia -Secondary bacterial infection can occur with staphylococci (most common), pneumococci,
haemophilus
CNS infection - due to immunopathological complications rather than CNS invasion by virus
Diagnosis of influenza
Often clinical diagnosis
Viral PCR throat swab - can do virus typing
Can do virus specific antibodies can be detected by complement fixation or ELISA. But take time for antibody titre to rise. So only really useful retrospectively for epidemilogical purposes
Influenza immunisation can help prevent infection. Can be trivalent of quadrivalent. Given to those at high risk or over 65
What types of vaccine in use
Vaccines are adapted depending on common strains. Gives protection of up to 70% for 1 year
Usually given as injection. Children given intranasal
- Egg-grown virus, purified and formalin inactivated
- live attenuated egg grown virus
- H/N reactogenic purified antigens
What antiviral agents are there for influenza
Future is to develop antiviral agents focussing on entry, replication and maturation.
Early detection/ diagnosis is key
Osteltamivir (oral) and zanamavir (inhaled) are neuraminidase inhibitors which act on influenza A/B, which inhibit virus replication
Useful if given within 48 hours of symptom onset, or as prophylaxis following exposure
Use of pooled hyperimmune plasma from survivors of previous pandemics (e.g spanish flu 1918). Trialled during H1N1 pandemic
Severe acute respiratory distress syndrome (SARS) and Middle east respiratory syndrome (Mers-CoV) both caused by coronavirus
Describe route of transmission and hosts of SARS
Describe route of transmission and host of Mers-CoV
Cross-species happens due to human eating habits changing, and human encroachment on animal territory. SARS has disappeared, MERS infections still ongoing
- Coronavirus in bats, zoonotic tranmission to palm civets and other animals traded in markets. Zoonotic transmission to humans
- Coronavirus in bats, zoonotic tranmission to camels. Zoonotic transmission to humans
- Once infections in humans, spread by droplet/ direct contact. Aim to prevent transmission with isolation/ masks. Virus can survive for up to 4 days outside body in saliva/ faeces
What is pathogenesis of SARS-CoV
- SARS uses protein spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors on host cell
- Receptor is down-regulated resulting in lung injury due to massive production of angiotensin 2. This bind angiotensin 2 receptor, that increases lung blood vessel permeability, and causes respiratory distress
Diagnosis SARS
Treatment SARS
Viral PCR throat swab/ sputum/ faeces
Ribavirin shown some effect
Steroids shown to reduce immune response
HIV antivirals (protease inhibitor) shown some benefit
Vaccine has been developed
What are risk factors for measles pneumonia
Virus replicates in lower respiratory tract, can cause damage leading to secondary bacterial pneumonia. Incubation period 10-14 days.
What are symptoms
Developing country
Unvaccinated
Malnutrition - vitamin A deficiency (impaired vaccine response)
Fever Rash - maculopapular Runny nose Conunctivits Cough Koplik's spots
Diagnosis of measles
Treatment of measles pneumonia
MMR vaccine helps prevent
Clinical diagnosis
IgM and viral RNA sequencing
Ribavirin some effect
Antibiotics
Vitamin A replacement
Which patients get CMV pneumonia, and what is pathogenesis of this
- Does not normally replicated in respiratory epithelium.
- If immunocompromised (bone marrow transplant), it can cause interstitial pneumonia
- Biopsy of lung tissue can show owl’s eye inclusion, where large numbers of viral particles accumulate in nucleus of infected cell
Cystic fibrosis most common lethal inherited disorder. Abnormal sodium channels caused production of viscous bronchial secretions. Patients have different lung flora
What organisms commonly invade lungs in cystic fibrosis
Pseudomonas aueriginosa - colonises most lungs by age 15-20. Often encouraged by anti-staph antibiotics given during childhood pneumonia. Forms mucoid material, which causes immunological response, leading to lung parenchymal damage. Rarely invades beyond lung. Inhaled antibiotics recommended for eradication
Staph aureus Burkholderia cepacia - difficult to erradicate Haemophilus influenzae Aspergillus fumigatus Non-tuberculous mycobacterium
Lung abscess is suppurative infection of lung. Most common cause is reflux of gastric secretions. Therefore cultures often have mixture of bacteria such as bacteroides and fusobacterium. Foul smelling sputum because of this
Treatment duration for lung abscess
May need treatment 2-4 months
Use metrodniazole for anaerobe cover, in addition to other agent
If treatment delayed, may lead to infection of pleural space (empyema)
Mycobacterium TB is one of top 10 causes of death globally
What species of mycobacterium cause these diseases
Slow growers: Bovine tuberculosis Leprosy Disseminated infection in AIDS Associated aquatic activity Skin infections
Rapid growers:
Opportunistic infection occuring during trauma or invasive procedures
Rapid growers grow culture in 7 days, slow growers over 7 days
- Bovine tuberculosis - M. bovis
- Leprosy - M. Leprae
- Disseminated infection in AIDS - M. Avium and M. Intracellulare (MAC)
- Associated aquatic activity - M. marinum
- Skin infections - M. Ulcerans
- Opportunistic infection occuring during trauma or invasive procedures - M. Fortuitum and M. Chelonae
What are the different types and sub-species of M. Avium complex (MAC)
M. Avium complex overarching term
- serotypes 1-6 and 8-11 are assigned M. Avium
- serotypes 7, 12-17, 19, 20, 25 are assigned M. intracellularle
Primary TB infection organisms are engulfed by alveolar macrophages, in which they survive and multiply. Creates what is known as a Ghon complex. Material within granulomas becomes necrotic. Non-resident macrophages are recruited, and they help carry TB to lymph nodes. This then stimulates the cell mediated immune response. Mycobacterium do not cause direct damage, damage is all due to immune response. Asymptomatic for long time. 90% cases go no further, 10% produce clinical disease.
How soon can TB be detected after primary exposure
What initial tests are available
4-6 weeks after infection by tuberculin skin test (Mantoux test). This injects small amount of purified protein derivative of M TB into skin . Local response shown in 48-72 hours - Type IV hypersensitivity reaction. Not useful in populations with BCG vaccination e.g healthcare worker
IFNgamma test IGRA (quantiferon) - cannot differentiate between latent/ active disease. Tests if lymphocytes produce response to two TB antigens ESAT-6 and CFP-10
Primary TB tubercles may heal spontaneously, become fibrotic or calcified. Can be there for entirety of life. Small percentage of people, particularly immunocompromised, mycobacterium are not contained within tubercle but invade bloodstream and cause disseminated disease (miliary TB) (lungs/ liver/ spleen)
What is secondary TB
Due to reactivation of dormant mycobacteriym, usually consequence of impaired immune function due to HIV or malnutrition, chemotherapy, steroids.
Usually apex of lung as more highly oxygenated, allows M TB to multiply more rapidly
TB can disseminate via lymphatics and bloodstream to other parts of body, causing necrosis and destruction.
Can also spread locally into bronchi or into pleura
Diagnosis via symptomcs, CXR, mantoux test. Ziehl-neelson stain
How long until culture result
What can be used for rapid test
6 weeks culture
Gene Xpert MTB-RIF - can detect TB and rifampicin resistance genes
What is basic treatment for TB and duration of therapy
Basic treatment following close cotnact TB exposure
Vaccination with BCG prevents infection disseminating, but does not prevent primary infection.
Rifampicin Isoniazid Pyrazinamide Ethambutol for 6 months
Extend to 12 months if CNS involvement
Extend to 18-24 months if MDR-TB
Rifampicin and isoniazid for 3 months
Definition of MDR-TB
Definition of extremely drug resistant TB (XDR-TB)
Resistance to rifampicin and isoniazid
Resistance to rifampin and isoniazid, plus any fluoroquinolone and at least one of three injectable second-line drugs (i.e., amikacin, kanamycin, or capreomycin
Never add a single drug to failing regimen, because agent will soon be llost
Fungal infections commonly seen in immunocompromised patients
What are two most common fungal pathogens
Aspergillus fumigatus/ flavus
Pneumocystic jirovecii
What diseases can aspergillus cause?
Aspergullus is ubiquitous in environment, and is not part of normal flora.
Invasive aspergillosis carries high mortality, and treatment difficult due to toxic nature of antigfungal drugs, plus lack of functional host defences
- Allergic bronchopulmonary aspergillosis (ABPA) - allergic response to presence of aspergillus antigen in lungs and occurs in patients with asthma/ CF
- Aspergilloma - in patients with pre-existing lung cavities or chronic lung disease. Aspergillus colonises a cavity and produced a fungal ball of tangled hyphae. Fungi do not invade lung tissue. But can be related to ABPA causing invasion
- Disseminated aspergillus - fungus spreads from lungs in immunocompromised patient
Common anti-fungals used for aspergillosis
Amphotericin B
Voriconazole
Caspofungin
Pneumocystis is fungus commonly found in immunocompetent patients and rodents. Disease occurs in immunocompromised patients. High mortality in HIV patients prior to invetion of antiviral therapy. Causes interstitial pneumonia
What are stages of PCP organism?
Treatment of PCP?
Trophozoite
Precyst
Cyst - spores released when cysts rupture
Co-trimoxazole
Pentamidine
Protozoa can also cause infection.
Which species can cause infection:
- nematodes
- microfilaria
- Nematodes - move through small intestine, break through capillaries around alveoli to enter bronchioles. Damage this causes can cause pneumonitis
Ascaris
Strongyloides
Hookworms - Microfilaria - Wuchereria/ Brugia appear in peripheral circulation with diurnal/ nocturnal periodicity, co-coinciding with feeding time of vectors. Outside of these times, larvae become sequestered in capillaries of lung. This i termed “tropical pulmonary eosinophilia”. History of several months of cough, dyspnoea, wheeze, eosinophilia. Antifilarial antibody tests are positive
Protozoa can also cause infection
- How does schistosomiasis cause respiratory symptoms
- Echinococcus
- Paragonimus
- schistosomiasis - larvae migrate through lungs
- Echinococcus - larvae of tapeworm move to lungs, form cysts which can reach reasonable size. and cause respiratory distress. Cysts can rupture and cause acute anaphylaxis
- Oriental lung fluke, acquired by eating crustaceans containing infective metacercariae. Migrate from intestine across body cavity and penetrate lungs. Adults develop within fibrous cysts which conttect bronchi to provide exit for eggs. Causes bronchopneumonia. Large cysts can be confused with lung cancer, TB and fungal lesions. Praziquantel is effective treatment
Treatment of:
- acute bronchitis
- chronic bronchitis (COPD)
- acute bronchitis - nil
- chronic bronchitis (COPD)
Doxycyline
Amoxicillin
Clarithromycin
Severe -
Co-amoxiclav
Levofloxacin
Co-trimaxazole
What are parts of curb65
Treatment for mild pneumonia (0-1) is from:
Doxycyline
Amoxicillin
Clarithromycin
Confusion Urea >7 RR >30 BP <90 Age >65
Treatment moderate pneumonia (curb65 2)
Treatment severe pneumonia (curb65 >3)
Moderate -
Amoxicillin plus clarithromycin
Doxycycline
Levofloxacin
Severe -
Co-amoxiclav plus clarithromycin
Cefuroxime plus clarithromycin (pen allergy)
Levofloxacin
Hospital acquired pneumonia occurs 48 hours after admission
Treatment for mild/ moderate same as CAP:
Amoxicillin plus clarithromycin
Doxycycline
Levofloxacin
What is treatment for severe?
Tazocin
Ceftazidime plus metronidazole
Co-trimoxazole
Treatment of aspiration pneumonia
Treatment of empyema/ lung abscess
Co-amoxiclav
Cefuroxime plus metronidazole
Co-amoxiclav/ tazocin/ cephalosporins/ meorpenem show good pleural penetration
Treatment of bronchiectasis
Usually 2 weeks IV, 4 weeks oral (6 weeks total)
If non-severe - amox/ doxy/ clari Inhaled colistin if pseudomonas Nebulised tobramycin Ceftazidime for eradication Azithromycin prophylaxis
Investigations in patient with recurrent infections
Immunoglobulins
Functional antibodies
Complement
HIV/ HTLV
Treatment of PCP
Treat for 21 days
Co-trimoxazole plus steroids if severe
Alternatives -
Clindamicin plus primaquine
Dapsone plus trimethoprim
Pentamidine
Check G6PD prior to starting dapsone or primaquine
HIV positive man returns from Spain. Fever, tachycardia. CXR shows consolidation. Good CD4 count, surpressed viral load.
What is treatment option?
co-amox + clari
ceftriazone
cotrimoxazole
ceftriaxone - higher penicillin resistance in other countries
PCP unlikely given good HIV treatment
Mycobacterium tuberculosis complex is made up of many species - what are they?
M tuberculosis M bovis Bacilus Calmette-Guerin M africanum M canetti M caprae
What percentage of patients with latent TB experience reactivation?
10%
Higher risk if immunosuppressed
What is gold standard test for TB?
TB culture is gold standard. Can take 3-6 weeks
Microscopy is important. But low PPV in UK as low prevalence
What is GeneXpert, and how does it work?
Detects pulmonary TB
Nested PCR which detects MTB-DNA, and sequences rpo gene for rifampicin resistance on sputum smear
Takes 70mins
BCG vaccine derived from in vitro attenuation of M bovis.
What benefits does it confer?
No protection against pulmonary TB
Prevents disseminated TB/ TB meningitis in children
Patient with HIV and TB - when to start ART after starting TB treatment?
Risk of IRIS as immune system reactivates.
Treatment for IRIS is NSAIDS/ steroids
ART within two weeks if CD4 <50
There are >180 non-tuberculous mycobacteria (NTM). Found in soil/ water, and are ubiquitous.
What are examples?
M avium intracelulare complex (including M chimaera) M marinum M ulcerans (buruli ulcer)
What are risk factors for NTM infection?
Immunosuppression - HIV/ transplant
Chronic lung disease
But can also occur in immunocompetent host
Man presents with multiple non-pruriginous hypopigmented macules on his limbs, with altered sensation.
What is diagnostic test?
Lepromin test
PCR
Skin biopsy
Slit smear
Leprosy - lepromin test, similar to Tuberculin test. Tests hosts reaction to Dharmendra antigen
Patient with rising LFTs just started TB medication. When to stop therapy?
ALT 3x ULN with symptoms (nausea/ jaundice)
ALT 5x ULN asymptomatic
Repeat bloods in one week, and re-introduce drugs slowly
