Respiratory Infections

Front 1

Coryza (the common cold)

Back 1

Rhinoviruses of the most common cause and there are over 100 serotypes. It is also caused by parainfluenza viruses, adenoviruses, corona viruses and enteroviruses. These viruses may predipose an individual to secondary bacterial infections (sinusitis, otitis, bronchitis, pneumonia) which can be very severe.

Front 2

Pharyngitis/tonsillitis

Back 2

It is caused by viruses (adenoviruses) or bacteria (strep pyogenes).

Front 3

Infectious mononucleosis (Glandular fever)

Back 3

This syndrome causes pharyngitis, lymphadenopathy, fever and malaise. The individual will have atypical mononuclear cells in their peripheral blood. It is most commonly caused by the Epstein-Barr virus and other causes are cytomegalovirus, toxoplasmosis and HIV seroconversion.

Front 4

Croup

Back 4

A particular type of cough that occurs in young children. It's caused by viruses (paraflu and RSV). Inspiratory stridor occurs due to narrowed airways.

Front 5

Epiglottitis

Back 5

It is bacterial and potentially life threatening due to swelling and inflammation which may block the airways.

Front 6

Genome of influenza viruses

Back 6

They have segmented negative ssRNA genome. 8 segments of RNA encode 11 proteins. Segment 4 encodes haemagglutinin and segment 6 encodes neuraminidase which are two surface proteins. The 3 subtypes are based on internal proteins and matrix.

Front 7

Flu-like illness

Back 7

There must be 2 key components

- respiratory tract symptoms such as rhinitis, cough or shortness of breath

- systemic symptoms such as headache, fever and myalgia.

Front 8

Influenza virus

Back 8

It is caused by a pneumotropic virus that infects cells living in the respiratory tract down to the alveoli. The infection is lytic and strips off respiratory epithelium so there are no mucus secreting cells and cilia. It stays in the lungs and produces interferons which circulate in the blood.

Front 9

Antigenic drift

Back 9

This involves random spontaneous mutation in viral genes (e.g.encoding HA and NA) resulting in a 1-2% sequence change. This allows the virus to escape herd immunity. It occurs in type A and B influenza.

Front 10

Antigenic shift

Back 10

This involves genetic reassortment between human and non-human viruses leading to new subtypes. There are >20% differences, hence the emergence of new pandemic strains against which the population has no pre-existing immunity.

Front 11

Respiratory syncytial virus

Back 11

This is an enveloped paramyxovirus. It's negative ssRNA encodes 9 polypeptides including 2 surface proteins: F and G. It's highly seasonal and common. Causes lower respiratory tract infection in children. High hospitalisation rate but low mortality rate unless patient has congenital heart or lung disease or immunodeficiency. Requires rapid diagnosis and control measures.

Front 12

Community aquired pneumonia (CAP)

Back 12

The presence of symptoms/signs of lower respiratory tract infection and new pulmonary shadowing on chest X-ray. Major cause of morbidity and mortality. More common in males, the elderly, alcoholics and people with chronic disease.

Front 13

Streptococcus pneumoniae

Back 13

The most common cause of CAP in those who don't COPD. The capsular polysaccharide os the major virulence factor. Resistance to penicillin is becoming common.

Front 14

Haemophilus influenzae

Back 14

Capsulated is a primary cause of CAP in children who haven't been vaccinated. Non-capsulated is an important cause of disease in COPD.

Front 15

Mycoplasma pneumoniae

Back 15

It causes >40% of CAP in the 17-44 age group. It can cause epidemic CAP and has characteristic extra-pulmonary features. It has a long prodrome. There will be patchy consolidation on CXR.

Front 16

Chlamydophila pneumoniae

Back 16

A recently recognised pathogen that causes upper respiratory tract infection in infancy and CAP in the elderly.

Front 17

Legionella pneumophila

Back 17

A cause of both sporadic and outbreak CAP that can cause severe disease particularly in the immunocompromised and smokers. Serogroup 1 causes nearly all of it and doesn't respond to standard therapy. There is multilobar involvement on CXR, hyponatraemia and focal neurological disease.

Front 18

Investigations done in CAP

Back 18

- Confirm diagnosis and assess severity through temperature, full blood count, urea, electrolytes, liver function tests, CXR scans and arterial gases

- Define the aetiological agent

- Identify complications

Microbiological investigations include sputum and blood analysis and cultures, and urinary antigens.

Front 19

Criteria for severe CAP

Back 19

3 or more out of:

- confusion: a mini-mental test score or 8 or less

- urea>7mmol/L

- respiratory rate >30 per minute

- blood pressure: systolic <90, diastolic <60

- 65 of older

Front 20

Hospital acquired pneumonia (HAP)

Back 20

Occurs more than 48 hours after admission to hospital or within 10 days of previous admission. It is the second most common infection acquired in hospital. Caused by E.coli, Klebsiella spp, proteus spp, S. pneumoniae, and S. aureus.

Front 21

Staphylococcus aureus

Back 21

It may cause CAP during an influenza outbreak. Methicillin resistant staphylococcus aureus (MRSA) risk is assessed by previous MRSA infection, long term urinary catheter, treated as inpatient within the last 6 months, resident of a nursing home with skin breaks and undwelling line.

Front 22

Infections in cystic fibrosis

Back 22

The airways of CF patients are chronically infected with bacteria (S. aureus and P. aeruginose). Symptoms are persistent and progressive but subject to intermittent acute exacerbations.

Front 23

Tuberculosis incidence and causes

Back 23

Infects 1/3 of the global population with 8 million new cases a year and causes more than 2 million deaths.HIV has caused the recent increase in cases and an estimated 11% of new cases occur in HIV+ patients. Its caused by M. tuberculosis, M. bovis, M. microti and M. africanum.

Front 24

Tuberculoid leprosy

Back 24

It is common. There is a strong cellular immune response, a few bacilli lesions and depigmented anaesthetic lesions.

Front 25

Lepromatous leprosy

Back 25

It is uncommon. There is weak cellular immune resonse, many bacilli in lesions and thick granulomatous lesions.

Front 26

Mycobcaterium tuberculosis

Back 26

Obligate aerobes that grow in tissues with a high oxygen content. Faculative intracellular pathogens usually infect mononuclear phagocytes. Slow growing. It is hydrophobic due to having a high lipid content in the cell wall and is therefore less permeable to usual bacterial stains. Known as acid-fast because once stained, cells resist decolourisation

Front 27

Tuberculosis spread

Back 27

It is spread by airborne droplet nuclei which can remain airborne after coughing for several hours. These droplets are inhaled, lodge in the alveoli and the organism is taken up by alveolar macrophages where they replicate slowly and spread via the lymphatic system to the hilar lymph nodes.

Front 28

Tuberculosis infection

Back 28

In most individuals cell-mediated immunity develops 2-8weeks after infection. Activated T lymphocytes and macrophages form granulomas that limit further replication and spread but bacterial cells remain (viable) in the centre of necrotic caseating granulomas. Most individuals are asymptomatic.

Front 29

Clinical features of TB

Back 29

Fever, weight-loss, night sweats, cough, shortness of breath, haemoptosis and chest pain. Pulmonary disease and extrapulmonary disease is more common in HIV+. Most serious is TB meningitis and space occupying lesions (tuberculomas). Other sites of infection: skin, soft tissues, bones, joints, genitourinary tract and disseminated disease.

Front 30

Zhiel-neelson stain

Back 30

A staining technique introduced by Robert Koch 1882. It is crucial for TB diagnosis and control. It is cheap, rapid, simple, robust and has moderate specificity and sensitivity.

Front 31

Treatment of TB

Back 31

Initial phase: 2 month of rifampacin, isoniazid, ethambutol and pyrazinamide.

Continuation phase: 4 months of rampacin and isoniazid.

If resistance is suspected then 5 drugs may be used initially and for confirmed resistant strains longer courses are required with second line agents.

Front 32

Prevention of TB

Back 32

Open pulmonary disease is non-infectious after 2 weeks of effective treatment. Contact tracing and detecting of latent infection is done with tuberculin skin test, chest radiography and in vitro interferon gamma release disease. Contacts are traced if there's evidence of an infection. TB is a formally notifiable disease.