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Respiratory diseases
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Microbiology Mapa Mental sobre Respiratory diseases, creado por maisie_oj el 20/04/2013.
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Respiratory diseases
Upper respiratory tract
Infections of the URT are most common
Pathogens that enter the repiratory tract can infect any other parts of the body
Gateway for infection
Structures of the URT
Nose - external part of the respiratory system
Nasal cavity - internal part of the nose, lined with ciliated mucous membranes and hairs (acts as a filter/trap for particles)
Pharynx - lined with ciliated mucous membranes that pushes contaminents into the digestive tract
Tonsils - aggregations of lymphoid tissue
Mucous - contains antimicrobial agents
Functions
Exchange of gases between the atmosophere and blood
URT - collects and filters air before delivering it to the lower respiratory tract (LRT)
LRT - Gas exchange
Infections of the URT (sinuses and ears)
Diptheria
Caused by: Cornybacterium diptheriae
Pathogen and virulence factors: virulent C. diptheriae produces diptheria toxin which inhibits polypeptide synthesis - causing cell death
Diptheria toxin inhibits protein synthesis (at the ribosome) and can cause heart, renal or nerve damage
Signs and symptoms: sore throat, oozing fluid that hardens into a pseudomembrane that can obstruct the airways
Pathogenesis + epidemiology: Spread via droplet infection or skin contact, causes symptomatic infection in both immuno- / non-immunocomprimised people
Still common in developing countries - 40-50% of untreated patients die
Diagnosis: based on clinical picture and presence of pseudomembrane
Rarely by microscopy: Gram positive rods (with clubbed ends) seen in two formations: V-sahpes (two bacteria) or palisade arrangement (multiple)
Pseudomembrane is diagnostic (= fibrin, dead cells and bacterial cells)
Treatment and prevention: antitoxin and antibiotics, immunization (vaccine = DTaP) is an effective prevention
Abx = Penicillin G, erythromycin or metronidazole
Cutaneous form (especially in people >30yrs) - infected skin wound results in a slow healing ulcer
Otitis media (infection of the middle ear) and sinusitis
Causes: various bacteria including; Strep pneumoniae (35%), Staph aureus (1-2%), Haemophilus influenzae (20-30%), Moraxella catarrhalis (10-15%)
Can occur as a complication of nose/throat infection
Signs and symptoms: (sinusitis) pain of the affected sinus with malaise; (otitis media) ear pain +/- fever
Lower respiratory tract
The LRT is usually sterile due to the action of the ciliary escalator
Microorganisms hoping to infect the respiratory tract are trapped in the sticky mucous membrane of the tract and moved towards the oesophagus
When bacterial infection of the LRT occurs, life-threatening illness can result
Bacterial pneumonia
Inflammation of the lungs accompanied by fluid filled alveoli and bronchioles
Can bedescribed by either the location of the infection or the causitive organism (e.g. lobar pneumonia, involving the entire lobe)
Most serious and frequent in adults
Primary atypical (mycoplasma) pneumonia
Cause: Mycoplasma pneumoniae
Virulence factors: adhesion protein
Signs and symptoms: fever, maaise, sore throat, excessive sweating
Epidemiology: droplet infection (nasal secretions)
Diagnosis: microscopy (mycoplasma bacteria - with capsule), PCR, cold agglutination test, clinical picture
Advaced techniques: PCR and serological testing (capsule)
Treatment: Abx = tetracyclin and erythromycin
Prevention: difficult as individuals can be infective without symptoms
Common causes of classical pneumonia: G+; Strep pneumoniae and Staph aerues; less common = G-; Haemophilus influenzae, Klebsiella pneumoniae etc.
Strep pneumonia = G+ diplococci (with capsule)
Klebsiella pneumonia
Cause: K. pneumoniae
Virulence factors: a capsule
Signs and symptoms: typical pneumoniae symptoms with thick bloody sputum and reccurent chills
Epidemiology: Immunocomprimised indicviduals at greatest risk
Diagnosis: microspcopy (G-, bacilli), culture (facultative anaerobe, lactose fermenting)
Treatment: Abx = aminoglycosides (kanamycin, amikacin, streptomysin) and cephalosporins
Prevention: good aseptic technique by healthcare workers
Other bacterial pneumonias
Causes: Strep pneumonia, Haemophilus influenza, Staph aureus, Yersinia pestis (plague) and Chlamydial spp.
Portal of entry: inhalation (Y. pestis can infect via blood as well)
Signs and symptoms: typical pneumonia symptoms, with frothy, bloody sputum in the case of Y. pestis
Incubation period: variable depending on the causitive organism (although Y. pestis can cause symptoms within hours)
Epidemiology: typically young children more susceptibile
Treatment: amoxicillin (Strep pneumoniae), flucloxacillin (S. aureus), doxycycline (H. influenzae and Chlamydial spp) and Streptomycin/gentamycin (Y.)
Prevention: good hygiene; vaccine available for H. influenzae
H. influenzae pneumonia
Gram negative coccobacillus
Predisposing factors: alcoholism, poor nutrition, cancer or diabetes
Signs and symptoms: similar to pneumococcal pneumonia (Strep pneumonia)
Diagnosis: isolation; special media for culture requirements (Chocolate agar with added factors; X ( haem) and V (NAD))
Treatment: cephalosporins
Legionellosis
Cause: Legionella pneumophila
G- rod
Found in water
Transmitted by aerosols (not human to human)
Signs and symptoms: potentially fatal; mutli system involvement (including; lungs, kidneys, liver, CNS and GIT)
Diagnosis: culture on selective media (CYE media with added iron and cysteine), poor Gram stainer (stains with silver)
Advaced: Sera agglutination test, fluorescent Ab's, ELISA or DNA probe (fluorescent probe for L. pneumoniae genes)
Epidemiology: The elderly, smokers and immunocomprimised individuals are highest risk
Treatment: Quinolones or macrolides
Prevention: reduction o bacterial presence in water sources
Pathogenesis: L. pneomoniae kills human cells causing tissue damage and inflammation
Require macrophage uptake -> reside within endosome and divide (inhibit lysosome fusal by injecting effector proteins into macrophage)
Effector proteins injected via a Type IV secretion system called Dot/ICM)
This causes the endocytotic vesicle to recruit ER membrane and form a protective vacuole in which it divides
Stimulates a massvie immune response in tissues - tissue death
Other LRT infections
Pertussis (whooping cough)
Cause: Bordetella pertussis
Virulence factors: various toxins
Pertussis toxin - inhibits Gi proteins (remain GDP-bound and therefore inacitve) meaning adenylate cyclase cannot be turned off - excessive cAMP
Can cause hypoglycaemia via constant release of insulin
Adenylate cycalse toxin
Dermonecrotic toxin
Tracheal cytotoxin
Causes ciliated cell damage
Signs and symptoms: Initially cold-like, followed by characteristic cough
Epidemiology: Highly contagious; droplet infection
Pathogenesis: 4 phases - incubation (7-10 days), catarrhal (mild respiratory symptoms), paroxysmal (chronic, uncontrollable coughing with whoops)...
... and convalescent (reduction and eventual ceasation of coughs)
Diagnosis: symptoms alone are diagnostic
Treatment: primarily supportive (self limiting)
Prevention: with DTaP vaccine
Inhalation anthrax
Cause: Bacillus anthracic
G+, rod-shaped and endospore forming
Virulence factors: capsule and anthrax toxin
Signs and symptoms: Resemble cold/flu, progress to severe coughing, shortness of breath, shock then death
Epidemiology: not person-person transmissible, but acquired through contact and inhalation
Diagnosis: based on identification of bacteria in sputum
Treatment: early, agressive treatment with Abx (doxycycline, erythromycin, vancomycin and penicillin)
Prevention: Anthrax vaccine available to military personnel, researchers and health care workers dealing with anthrax patients
Tuberculosis
Cause: Mycoplasma tuberculosis
Epidemiology: immunocomprimised people at greatest risk (leading killer of HIV patients)
Its global occurence and monitoring of MDR and XDR strains can be achieved by molecular identification
PCR of variable number tandem repeats (VNTR), RFLP etc.
Pathogenesis: M. tuberculosis remain viable for long periods of time in aerosol drops, there are three types
Primary - initial case of TB
Secondary - reestablished TB
Disseminated - systemic infeciton
1) Bacteria reaches the alveoli and is ingested by a macrophage, some survive and cause infection but no symptoms
2) Bacteria replicate in macrophages cause a chemotactic repsonse which recruits further macrophages - fomring a protective layer (tubercle)
Most macrphages can't kill the bacteria so release enzymes and cytokines that cause a chronic inflammtion (lung damage)
3) After a few weeks symptoms appear as many macrophages die, releasing more bacteria and creating a caseous centre (necrosis) to the tubercle
4) In the mature tubercle the caseous centre enlarges (liquefaction) and forms an airfilled centre in whic bacteria can divide outside of macrophages
5) Liquefaction continues, the tubercle ruptures - bacteria can access; bronchioles for local spread and the blood/lymphatics for systemic spread
Treatment; prolonged Abx treatment - "RIPE" (rifampicin, isoniazid, pyrazinamide and ethambutol)
Problem now: MDR and XDR TB
Prevention: BCG vaccine (live, attenuated M. bovis) - not widely used in the USA
Screening: tuberculin skin test - six needle test thing (can indicate a current or previous TB infection
Diagnosis from specimen (after referal to doctor with persistent cough, >7weeks)
Culture
Solid media (Jensen-lowenstein) - takes >8 weeks
If growth positive
Subculture (for biochemical typing and Abx sensitivity)
Microscopy
Molecular biological identification/typing
PCR (for drug resistence genes, and 16S ribosome)
Relatively high sensitivity (if smear and culture positive)
RFLP (restriction fragment length polymorphism) - using restriciton enzymes to cleave homologous DNA
Differences will be apparent by loss of cleavage sites (and therfore loss different specieis subtype DNA fragment lengths)
Viewed by agarose gel electrophoresis, transferring to membrane and hybridising with DNA probe (IS6110) - that binds to the conserved IS6100 sequence
DNA probes (Gen Probe) that hybridise with drug resistence/subspecies specific sequences
Liquid media (faster)
Smear sputum and stain with Zhiel Neelsen (acid fast) technique
Microscopy
PCR (fast) - using commercial kits (COBAS or AMPLICORE MTB)
About 1/3 of the world's population infected, with around 10,000,000 new cases each year and 3,000,000 deaths yearly
TB comprise 25% of all avoidable deaths in developing countries
Highest incidences in India and China
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