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Medical Microbiology and Virology > 20 Lower respiratory tract infections > Flashcards

20 Lower respiratory tract infections Flashcards

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1
Q

What are causes of laryngitis/ tracheitis

Lower respiratory tract continuous with upper. But lower tend to be more severe. Similar organisms

A 
Parainfluenza - most common
Influenza
Rhinovirus
RSV
Adenovirus

Diptheria
H Influenzae
S Aureus
GAS

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2
Q

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?

A

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

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3
Q

Incubation period of diptheria

Route of spread

A

2-5 days

Droplet spread
Direct contact - cutaneous

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4
Q

Structure of diptheria toxin

How does diptheria toxin work

A

Fragment A - toxic fragment
Fragment B - binding

Toxin binds to cells, and uptaken by cells. Fragment A inactivates ribosomal protein synthesis, causing apoptosis.

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5
Q

Investigations diptheria

Treatment diptheria

A

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

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6
Q

How to deal with contacts exposed to diptheria

A

Nasopharyngeal swab - assess if asymptomatic carrier
Erythromycin prophylaxis
Diptheria immunisation

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7
Q

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

A

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

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8
Q

Pertussis incubation period

Symptoms

Diagnosis

A

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

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9
Q

Treatment of whooping cough

Prevention

A

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

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10
Q

Causes of acute bronchitis

Causes of acute exacerbation of chronic bronchitis

A

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

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11
Q

Why does bronchiolitis usually occur in children <2

Causes of bronchiolitis

A

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

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12
Q

How is RSV transmitted

Incubation period

When to outbreaks occur

How does in attach to enpithelial cells

A

Droplet

4-5 days

Winter
Outbreaks often spread in hospitals

G proteins to attach to cells
Fusion protein to penetrate cell membrane

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13
Q

Investigations for bronchiolitis

Treatment

A

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

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14
Q

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

A

Inhalation of aerosolized material or aspiration normal flora
Via bloodstream

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15
Q

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)

A

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

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16
Q

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
A 
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
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17
Q

Causes of CAP

  • following viral infection
  • HIV positive
  • lung cancer
A

Post - viral
Strep pneumoniae
Staph aureus

HIV positive
PCP
Mycobacterium species
CMV

Lung cancer -
Moraxella cattharalis

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18
Q

Causes of CAP

  • cooling tower exposure
  • abbatoir worker/ vet/ farmer
  • animal hide importers, wool sorters
A
  • legionella
  • coxiella burnetti
  • brucella species
  • coxiella burnetti
  • bacilus anthracis
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19
Q

Causes of CAP

  • exposure infected birds
  • exposure infected sheep/ goat/ cattle
  • exposure to bats/ bat droppings
A
  • chlamydia psitacci
  • coxiella burnetti
  • brucella species
  • histoplasma capsulatum
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20
Q

Causes of CAP

  • hotel air conditioning
  • California/ New Mexico/ Texas travel
  • SE Asia, South/ Central America
A
  • legionella
  • coccidioides immitis
  • Burkholderia pseudomallei - melioidosis
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21
Q

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
A

Immunocompromised

  • PCP
  • CMV
  • Mycobacterium species
  • Nocardia
  • Aspergillus

Ventilator

  • Pseudomonas aeruginosa
  • Staph aureus
  • Enterobacteriaceae - Klebsiella, E. Coli, proteus, Enterobacter, Serratia
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22
Q

Causes of CAP

  • Cystic fibrosis
A

CF -
Staph aureus
Haemophilus
Pseudomonas

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23
Q

Symptoms of typical/ atypical pneumonia

A

Cough
SOB
Pleurisy
Fever

Diarrhoea
Renal/ liver dysfunction

Meningitis - pneumococcal can spread via blood

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24
Q

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

A

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

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25
Q

Serological tests for atypica pneumonia

Legionella

Mycoplasma

Chlamydia pneumonia/ psittaci

Coxiella burnetti

A

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

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26
Q

Antibiotic selection for CAP

A

First choice - Amoxicilin

Secondary to viral infection - co-amoxiclav

Aspiration - co-amoxiclav and gentamicin

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27
Q

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

A

Strep pneumoniae - amox/ clarithromycin

Staph aureus - flucloaxacillin

Haemophilus - co-amoxiclav/ cefuroxime

Klebsiella - gent/ cipro

Atypicals - doxycycline

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28
Q

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

A
  • 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
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29
Q

Structure parainfluenza

How many types

A

(-) 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

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30
Q

What are four types of influenza, and how easily does it spread

A

Type A - epidemics, occasionally pandemics. Birds resevoir host

Type B - epidemics, no animal hosts

Type C - minor URTI

Type D - infects cattle usually

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31
Q

Describe structure of influenza virus and role of each part

A

(-) 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

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32
Q

How are influenza A strains named

A

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)

33
Q

Why is influenza able to evolve whilst spreading through host species

A
  • 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
34
Q

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

A

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

35
Q

Describe how influenza infects and causes damage

A

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

36
Q

Complications of influenza

A

Pneumonia -Secondary bacterial infection can occur with staphylococci (most common), pneumococci,
haemophilus

CNS infection - due to immunopathological complications rather than CNS invasion by virus

37
Q

Diagnosis of influenza

A

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

38
Q

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

A
  • Egg-grown virus, purified and formalin inactivated
  • live attenuated egg grown virus
  • H/N reactogenic purified antigens
39
Q

What antiviral agents are there for influenza

Future is to develop antiviral agents focussing on entry, replication and maturation.

Early detection/ diagnosis is key

A

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

40
Q

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

A
  • 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
41
Q

What is pathogenesis of SARS-CoV

A
  • 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
42
Q

Diagnosis SARS

Treatment SARS

A

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

43
Q

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

A

Developing country
Unvaccinated
Malnutrition - vitamin A deficiency (impaired vaccine response)

Fever
Rash - maculopapular
Runny nose
Conunctivits
Cough
Koplik's spots
44
Q

Diagnosis of measles

Treatment of measles pneumonia

MMR vaccine helps prevent

A

Clinical diagnosis
IgM and viral RNA sequencing

Ribavirin some effect
Antibiotics
Vitamin A replacement

45
Q

Which patients get CMV pneumonia, and what is pathogenesis of this

A
  • 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
46
Q

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

A

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
47
Q

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

A

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)

48
Q

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

A
  • 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
49
Q

What are the different types and sub-species of M. Avium complex (MAC)

A

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
50
Q

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

A

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

51
Q

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

A

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

52
Q

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

A

6 weeks culture

Gene Xpert MTB-RIF - can detect TB and rifampicin resistance genes

53
Q

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.

A 
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

54
Q

Definition of MDR-TB

Definition of extremely drug resistant TB (XDR-TB)

A

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

55
Q

Fungal infections commonly seen in immunocompromised patients

What are two most common fungal pathogens

A

Aspergillus fumigatus/ flavus

Pneumocystic jirovecii

56
Q

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

A
  • 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
57
Q

Common anti-fungals used for aspergillosis

A

Amphotericin B
Voriconazole
Caspofungin

58
Q

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?

A

Trophozoite
Precyst
Cyst - spores released when cysts rupture

Co-trimoxazole
Pentamidine

59
Q

Protozoa can also cause infection.

Which species can cause infection:

  • nematodes
  • microfilaria
A
  • 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
60
Q

Protozoa can also cause infection

  • How does schistosomiasis cause respiratory symptoms
  • Echinococcus
  • Paragonimus
A
  • 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
61
Q

Treatment of:

  • acute bronchitis
  • chronic bronchitis (COPD)
A
  • acute bronchitis - nil
  • chronic bronchitis (COPD)
    Doxycyline
    Amoxicillin
    Clarithromycin

Severe -
Co-amoxiclav
Levofloxacin
Co-trimaxazole

62
Q

What are parts of curb65

Treatment for mild pneumonia (0-1) is from:
Doxycyline
Amoxicillin
Clarithromycin

A 
Confusion
Urea >7
RR >30
BP <90
Age >65
63
Q

Treatment moderate pneumonia (curb65 2)

Treatment severe pneumonia (curb65 >3)

A

Moderate -
Amoxicillin plus clarithromycin
Doxycycline
Levofloxacin

Severe -
Co-amoxiclav plus clarithromycin
Cefuroxime plus clarithromycin (pen allergy)
Levofloxacin

64
Q

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?

A

Tazocin
Ceftazidime plus metronidazole
Co-trimoxazole

65
Q

Treatment of aspiration pneumonia

Treatment of empyema/ lung abscess

A

Co-amoxiclav
Cefuroxime plus metronidazole

Co-amoxiclav/ tazocin/ cephalosporins/ meorpenem show good pleural penetration

66
Q

Treatment of bronchiectasis

Usually 2 weeks IV, 4 weeks oral (6 weeks total)

A 
If non-severe - amox/ doxy/ clari
Inhaled colistin if pseudomonas
Nebulised tobramycin
Ceftazidime for eradication
Azithromycin prophylaxis
67
Q

Investigations in patient with recurrent infections

A

Immunoglobulins
Functional antibodies
Complement
HIV/ HTLV

68
Q

Treatment of PCP

Treat for 21 days

A

Co-trimoxazole plus steroids if severe

Alternatives -
Clindamicin plus primaquine
Dapsone plus trimethoprim
Pentamidine

Check G6PD prior to starting dapsone or primaquine

69
Q

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

A

ceftriaxone - higher penicillin resistance in other countries

PCP unlikely given good HIV treatment

70
Q

Mycobacterium tuberculosis complex is made up of many species - what are they?

A 
M tuberculosis
M bovis
Bacilus Calmette-Guerin
M africanum
M canetti
M caprae
71
Q

What percentage of patients with latent TB experience reactivation?

A

10%

Higher risk if immunosuppressed

72
Q

What is gold standard test for TB?

A

TB culture is gold standard. Can take 3-6 weeks

Microscopy is important. But low PPV in UK as low prevalence

73
Q

What is GeneXpert, and how does it work?

A

Detects pulmonary TB

Nested PCR which detects MTB-DNA, and sequences rpo gene for rifampicin resistance on sputum smear

Takes 70mins

74
Q

BCG vaccine derived from in vitro attenuation of M bovis.

What benefits does it confer?

A

No protection against pulmonary TB

Prevents disseminated TB/ TB meningitis in children

75
Q

Patient with HIV and TB - when to start ART after starting TB treatment?

A

Risk of IRIS as immune system reactivates.

Treatment for IRIS is NSAIDS/ steroids

ART within two weeks if CD4 <50

76
Q

There are >180 non-tuberculous mycobacteria (NTM). Found in soil/ water, and are ubiquitous.

What are examples?

A 
M avium intracelulare complex (including M chimaera)
M marinum
M ulcerans (buruli ulcer)
77
Q

What are risk factors for NTM infection?

A

Immunosuppression - HIV/ transplant
Chronic lung disease

But can also occur in immunocompetent host

78
Q

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

A

Leprosy - lepromin test, similar to Tuberculin test. Tests hosts reaction to Dharmendra antigen

79
Q

Patient with rising LFTs just started TB medication. When to stop therapy?

A

ALT 3x ULN with symptoms (nausea/ jaundice)

ALT 5x ULN asymptomatic

Repeat bloods in one week, and re-introduce drugs slowly

Medical Microbiology and Virology (60 decks)

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