Chapter 5 R ESPIRATORY I NFECTIONS. I NFECTIONS OF THE R ESPIRATORY TRACT Most common entry point...
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Transcript of Chapter 5 R ESPIRATORY I NFECTIONS. I NFECTIONS OF THE R ESPIRATORY TRACT Most common entry point...
Chapter 5
RESPIRATORY INFECTIONS
INFECTIONS OF THE RESPIRATORY TRACT
Most common entry point for infections
Upper respiratory tract
nose, nasal cavity, sinuses, mouth, throat
Lower respiratory tract
Trachea, bronchi, bronchioles, and alveoli in the lungs
RESPIRATORY TRACT
PROTECTIVE MECHANISMS
Normal flora: Commensal organisms
Limited to the upper tract
Mostly Gram positive or anaeorbic
Microbial antagonist (competition)
Clearance of particles and organisms from the respiratory tract
Cilia and microvilli move particles up to the throat where they are swallowed.
Alveolar macrophages migrate and engulf particles and bacteria in the alveoli deep in the lungs.
Protective Mechanisms
OTHER PROTECTIVE MECHANISMS
Nasal hair, nasal turbinates
Mucus
Involuntary responses (coughing)
Secretory IgA
Immune cells
RESPONSE TOWARDS FOREIGN PARTICLES
Ventilatory flow
Cough
Mucociliary clearance mechanisms
Mucosal immune system
SELECTED BACTERIAL INFECTIONS
Pharyngitis
Group A Strep - Streptococcus pyogenes
(Many viruses also cause this)
Pneumonia - Streptococcus pneumoniae
Diphtheria - Corynebacterium diphtheriae
Tuberculosis - Mycobacterium tuberculosis
Whooping cough - Bordetella pertussis
DISEASE OF UPPER RESPIRATORY TRACT
1. Pharyngitis and related infections
2. Diptheria
EXAMPLES OF COMMON INFECTIONS
Laryngitis
Streptococcal Pharyngitis
Scarlet Fever
Sinusitis
Diptheria
Otitis media
Advance stages – bacterial superinfection, mastoiditis, meningitis and brain abscess
LARYNGITIS
Most commomly upper respiratory viruses
Diphtheria
- C. diphtheriae produces a cytotoxic exotoxin causing tissues necrosis at site of infection with associated acute inflammation. Membrane may narrow airway and/ or slough off (asphyxiation)
STREPTOCOCCAL PHARYNGITIS (STREP THROAT)
Caused by group A beta-hemolytic streptococci of S.pyogenes
Also causing impetigo, erysipelas and endocarditis on skin
Causing inflammation of the mucous membrane and fever; tonsilitis and otitis media may also occur
Rapid diagnosis using enzyme immunoassays.
STREP THROAT
Fever
Tonsillitis
Enlarged lymph nodes
Middle-ear infection
REDDENING OF THROAT
STREPTOCOCCUS PYOGENES
Gram positive streptococci
Carried and transmitted from the throat
In Respiratory secretions
GROUP A STREP
Capsule -resistant to phagocytosis
Enzymes damage host cells
M protein adhesinThe M protein has many antigenic varietiesand thus, different strain of S.pyogenes cause repeat infections
ENZYME IMMUNOASSAYS
SCARLET FEVER
Caused by S. pyogenes producing erythrogenic toxin
The bacteriophage disturb the normal characterristic of bacteria that involving genetic mutation
Also associate with pharyngitis and skin infection that caused by the same bacteria
It is nowadays become mild and rare disease
SCARLET FEVER
Caused by ErythrogenicToxin secreted by S. pyogenes
SCARLET FEVER The erythrogenic
toxin is coded by a gene
lysogenic bacteriophage
within the genome of
S. pyogenes Rash is an inflammatory reaction to the toxin
SINUSITIS
Commonly caused by S. pneumoniae, Moraxella catarrhalis / H. influezae
can also caused by S. aureus / S.pyogenes
The sinus cavity will swelling and prevent drainage that resulting pressure and severe pain
Pt usually produce mucus, bacteria and phagocytic cells that collect in the sinuses
CONT.
Chronic stages caused by Bacteriodes
Mostly occur above the root of upper teeth which infection derived from oral cavity
Treatment by applying moist heat on particular area / drop an ephedrine / raise head to help drainage
Best antibiotic - penicillin
SINUSITIS
DIPTERIA
Until 1935, it leading infection to children of US
Vaccine used for children is DTaP vaccine
Diptheria Toxoid antibodies Production (DTaP)
Spread thru air bourne and resistant towards drying
The greyish toungue contain fibrin, dead tissues and bacterial cells that block the air passage
0.01mg of highly virulence toxin - fatal
CORYNEBACTERIUM DIPHTHERIAE
Aerobic Gram + bacillus Toxin inhibits protein synthesis of
cells to which it binds Destroyed cells and WBC form
"pseudomembrane" which blocks airways
SEVERE STAGE
UNDER MICROSCOPIC OBSERVATION
CORYNEBACTERIUM DIPHTHERIAE
To produce toxin, C. dithpheriae must be infected with a bacteriophage carrying the toxin gene
GREY MEMBRANE
THE DIPHTHERIA OUTBREAK OF NOME, ALASKA, 1925
Heroic Alaska Dog Teams
AN “AB” TOXIN
B = binding subunit A = active subunit
which binds to and inhibits a eucaryotic ribosomal translation factor
Vaccine is diphtheria toxoid
OTITIS MEDIA
Uncomfortable common cold, that infecting nose or throat (otitis media)
85% infecting children below 3 yrs old
Best antibiotic from penicillin group
The antibiotics used were just reduction the duration of infection
CAUSES
S. pneumoniae
H. influenzae
S.pyogene
Moraxella catarrhalis
S.aureus
INFECTED
MIDDLE EAR
(OTITIS MEDIA)
DISEASES OF LOWER RESPIRATORY TRACT
1. Whooping cough
2. Tuberculosis
3. Pneumonia
WHOOPING COUGH
BORDETELLA PERTUSSIS
Gram negative cocco-bacillus
Capsule Adherence to ciliated
cells
Pertussis toxin is A-B toxin
PERTUSSIS (WHOOPING COUGH)
Cough
Violent coughing followed by whooping sound
Vaccine – it is made of
purified components
Not lifelong immunity – adult carriers
PNEUMONIA
BACTERIAL PNEUMONIABacterial, viral or fungal infection can cause
Inflammation of the lung with fluid filled alveoli
COMMUNITY ACQUIRED PNEUMONIA
Infection of the lung parenchyma in a person who is not hospitalized or living in a long-term care facility for ≥ 2 weeks
5.6 million cases annually in the U.S.
Estimated total annual cost of health care = $8.4 billion
Most common pathogen = S. pneumo (60-70% of CAP cases)
“NOSOCOMIAL” PNEUMONIA
Hospital-acquired pneumonia (HAP)
Occurs 48 hours or more after admission, which was not incubating at the time of admission
Ventilator-associated pneumonia (VAP)
Arises more than 48-72 hours after endotracheal intubation
“NOSOCOMIAL” PNEUMONIA
Healthcare-associated pneumonia (HCAP) Patients who were hospitalized in an acute care
hospital for two or more days within 90 days of the infection; resided in a nursing home or LTC facility; received recent IV abx, chemotherapy, or wound care within the past 30 days of the current infection; or attended a hospital or hemodialysis clinic
Guidelines for the Management of Adults with HAP, VAP, and HCAP. American Thoracic Society, 2005
PATHOGENESIS
Inhalation, aspiration and hematogenous spread are the 3 main mechanisms by which bacteria reaches the lungs
Primary inhalation: when organisms bypass normal respiratory defense mechanisms or when the Pt inhales aerobic GN organisms that colonize the upper respiratory tract or respiratory support equipment
PATHOGENESIS
Aspiration: occurs when the Pt aspirates colonized upper respiratory tract secretions
Stomach: reservoir of GNR that can ascend, colonizing the respiratory tract.
Hematogenous: originate from a distant source and reach the lungs via the blood stream.
PATHOGENS
CAP usually caused by a single organism
Even with extensive diagnostic testing, most investigators cannot identify a specific etiology for CAP in ≥ 50% of patients.
In those identified, S. pneumo is causative pathogen 60-70% of the time
STREPTOCOCCUS PNEUMONIA
Most common cause of CAP
Gram positive diplococci
“Typical” symptoms (e.g. malaise, shaking chills, fever, rusty sputum, pleuritic hest pain, cough)
Lobar infiltrate on CXR
Suppressed host
25% bacteremic
ATYPICAL PNEUMONIA
#2 cause (especially in younger population)
Commonly associated with milder Sx’s: subacute onset, non-productive cough, no focal infiltrate on CXR
Mycoplasma: younger Pts, extra-pulm Sx’s (anemia, rashes), headache, sore throat
Chlamydia: year round, URI Sx, sore throat
Legionella: higher mortality rate, water-borne outbreaks, hyponatremia, diarrhea
VIRAL PNEUMONIA
More common cause in children
RSV, influenza, parainfluenza
Influenza most important viral cause in adults, especially during winter months
Post-influenza pneumonia (secondary bacterial infection)
S. pneumo, Staph aureus
OTHER BACTERIA
Anaerobes Aspiration-prone Pt, putrid sputum, dental disease
Gram negative Klebsiella - alcoholics
Branhamella catarrhalis - sinus disease, otitis, COPD
H. influenza
Staphylococcus aureus IVDU, skin disease, foreign bodies (catheters,
prosthetic joints) prior viral pneumonia
STREPTOCOCCUS PNEUMONIAE
Pneumococcus
Encapsulated
Often secondary infection following influenza virus
BACTERIAL PNEUMONIAStreptococcus pneumoniae• 2/3 of all pneumonia• Risk Factors- old age, season, underlying
viral infection, diabetes, alcohol and narcotic use
• Variable capsular antigen• Purified component (capsule) vaccine
Others that cause pneumonia:Mycoplasma pneumoniaeLegionella pneumophila
TUBERCULOSIS
MYCOBACTERIUM TUBERCULOSIS
Acid-fast bacillus – complex cell wall with “cord factor”
Causes TB: lungs
bones, other organs
Airborne, (milk, v. rare)
MYCOBACTERIUM TUBERCULOSIS
Thick lipid coat
of “Mycolic fatty acids”
Grows very slowly
Resists killing by macrophages and grows in them
TUBERCULE FORMATION
A tubercle in the lung is a “granuloma”
consisting of a central core of TB bacteria inside an enlarged macrophage, and an outer wall of fibroblasts, lymphocytes, and neutrophils
TUBERCULOSIS
Primary
Lung tubercles, caseous, tuberculin skin reaction
Secondary (reactivation)
Consumption: Coughing and chronic weight loss
Dissemination
Extrapulmonary TB (lymph nodes, kidneys, bones, genital tract, brain, meninges)
TUBERCULOSISElimination requires long antibiotic treatment with “cocktail” of antibiotics because
of the resistance that develops.
MULTI-DRUG RESISTANTMYCOBACTERIUM
TUBERCULOSIS
TB SKIN TEST
HOW DOES TUBERCULOSIS DEVELOP?
There are two possible ways a person can become sick with TB disease:
The first applies to a person who may have had been infected with TB but is perfectly healthy. The person can get infected again if they have a another disease such as HIV or cancer or they may get infected if they use drugs/alcohol.
The other way it TB can develop, happens much more quickly. Sometimes when a person first breathes in the TB germs, the body is unable to protect itself against the disease. The germs then develop into active TB disease within weeks.
WHO GETS TUBERCULOSIS?
Anyone can get tuberculosis. Some people are at higher risks than others. The people who have more of a chance getting TB are:
People who share same breathing space
Poor people/homeless people
Prisoners
Alcoholics or Drug users
People with medical conditions (cancer, diabetes)
Specially people with aids
PRIMARY TUBERCULOSIS PNEUMONIA
This is an uncommon type of TB as pneumonia is infectious. People who have it, have high fevers and productive coughs. It occurs most often in extremely young children and the elderly. This type is also found in HIV and Aids infected people.
THE THREE STAGES
There are three stages in the disease of tuberculosis. These three stages are identified from mild to extreme danger which is death. The first mild stage can get cured easily as long as the patient gets medication on time and takes good care. The second stage is more dangerous and the patient has to be really careful and that is were the symptoms should be considered. The third stage is extremely dangerous and there is no cure which means death. The third stage is the stage were nothing should go wrong and the patient will slowly begin to vomit blood and eventually die.
WHO DISCOVERED TUBERCULOSIS?
In 1882, Robert Koch discovered TB and soon he found out that it was caused by a microorganism Mycobacterium tuberculosis. After discovering that this disease was infectious, he started to consider treatments. Many treatments were tried but none were discovered until the year of 1943 were the activity of streptomycin was discovered.
VIRUS INFECTIONS
Respiratory syncytial virus (“RSV”)
Influenza virus
Fungal Infections•Coccidiodomycosis (Valley Fever)
Coccidioides immitis
THE COMMON COLD
Also known as coryza
Caused by viral infection
Show symptoms as other cold but secretion might consist of pus and blood mucus
Leads to 2ndary infection – sinusitis, bronchitis and otitis media
In serious case – likely as whooping cough and respiratory
RESPIRATORY SYNCYTIAL VIRUS
Enveloped (membrane) RNA virus
Spread by respiratory droplets
Community outbreaks in late fall to spring
Upper respiratory tract infection – epithelial cells
May be fatal in infants
INFLUENZA VIRUS AN ENVELOPED RNA VIRUS
Structure
Influenza Virus
New human strains every year• Mutations
Pandemic strains Genetic Recombinant Viruses•1957 Asian Flu H2N2•1968 Hong Kong Flu H3N2•1977 Russian Flu H1N1
Bird FluDirectly from birds•?? H5N1
‘H’ AND ‘N’ FLU GLYCOPROTEINS
H – Hemagglutinin • Specific parts bind to host
cells of the respiratory mucosa• Different parts are
recognized by the host antibodies• Subject to changes
N - Neuraminidase • Breaks down protective
mucous coating • Assist in viral release
INFLUENZA
Epidemics and pandemics, mostly in winter Upper respiratory tract infection –
epithelial cells Multivalent killed virus vaccine with strains
from the previous year (Grown in embryonated eggs)
Bird flu (H5N1) pandemic in birds
COCCIDIOIDES IMMITIS Soil fungus in
American Southwest
Cause of Valley Fever
Highly infectious
COCCIDIOIDES IMMITIS LIFE CYCLE
COCCIDIOIDES IMMITIS
Valley Fever usually a flu-like illness
Can spread to bones, skin, meninges
100,000 new cases/yr in SW