9 - Lower Respiratory Tract Infections (LRTI)

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Lower Respiratory Tract

Infections (LRTI)
LRT includes the pharynx, trachea, bronchial branches
Bacterial Agents
Mycobacterium tuberculosis
Mycoplasma pneumoniae
Legionella pneumophila
Legionnaire’s disease or Pontiac Fever
doesnt require tx
Chlamydia psittaci
Psittacosis
affects birds
aka parrot fever, ornithosis
can infect ppl but mild sx
can progress to pneumonia
1st line = Macrolide
2nd line = Tetracycline
DOC ang Tetracycline unless contraindicated w Macrolide ang

px
Chlamydia pneumoniae
one of the causes of community-acquired pneumonia
Lower Respiratory Tract Infections (LRTI) 1

1st line = Macrolides — Azithromycin
once a day dosing
Coxiella burnetti
Q fever
animal reservoir
ppl can be infected
tx
1st line = Doxycycline
Streptococcus pneumoniae
Mycoplasma
very small, pleomorphic (cocci to filaments)
smallest replicating organisms (0.3 to 0.8 mcm)
have no cells walls, but have sterols in their membranes
require numerous growth factors to grow
fastidious
The absence of a cell wall makes them:
insensitive to penicillin and cephalosporins — beta-lactams
They cannot be visualized by Gram stain

acid-fast staining is used
They are pleomorphic and can assume a variety of shapes
How to visualize colonies of mycoplasma
Diene’s Stain
blue stain cuz may methylene blue
if you have a visible colony:
get a coverslip and wash w alcohol and dry it → put Diene’s stain
→ taob and dikit sa MO → view under dry lenses (LPO, HPO)
a nonspecific stain that imparts a contrasting appearance to

Mycoplasma on agar
Results — “ fried egg” colony morphology
dark blue center and light blue periphery, appearing highly

granular.
Characteristics of M. pneumoniae
aerobic organism
may take up to 3 weeks to produce detectable colonies
Antigenic structures
since these organisms do not have a cell wall, the antigenic determinants
are membrane glycolipids and proteins.
antibodies bind here

antibodies produced against these antigens may cross-react with human
tissues — auto-antibodies
M. pneumoniae may be detected by cross-reacting antibodies against

human-type “O” red cells
Virulence Factor — make MO more pathogenic
M. pneumoniae adheres tightly to and fuses with the membranes of

respiratory epithelial cells by a specialized terminal protein attachment
factor
This action inhibits cilia, and over the course of a few weeks, the cilia and the
epithelial cells are disrupted
no cilia = no brushing action
No known exotoxins are produced
causes a respiratory disease referred to as “atypical pneumonia” or walking

pneumonia
the common cause of community-acquired pneumonia

📌 Why “walking pneumonia”?
at the start of the illness, the px will have flu-like sx
can do daily activities
no need for hospitalization but already infectious
Pathogenesis of Atypical Pneumonia
H2O2 = superoxide
high levels of H2O2 → oxidative damage → death of the cell
a free radical
can cause cancer and aging of the skin
antioxidants = reduce free radicals
Ciliostasis

paralysis of the cilia
Chest X-Ray picture of atypical pneumonia
Diffuse bronchopneumonia
May also show peribronchial pneumonia, atelectasis, nodular infiltrates, and

hilar lymphadenopathy
not used for diagnosis cuz cant know the cause
Complications of M. pneumoniae
Pneumothorax
presence of gas in the pleural cavity
Intravascular coagulopathy
abnormal clotting of the blood
Arthritis
Myocarditis
Erythema multiforme
deposition of IgM on the skin → rashes
Guillain-Barre syndrome
the immune system produces antibodies that cross-react to the PNS

→ px becomes paralyzed
PNS governs involuntary muscles — e.g. breathing, heart muscles

Meningoencephalitis
like meningitis — inflammation of the brain and spinal cord
Laboratory Diagnosis
lack of standard in diagnosis
2 most frequent lab tests for M. pneumoniae
Complement Fixation (CF) and Enzyme immunoassay (EIAs)
marami sakit nadidiagnose — non specific
Treatment
Tetracycline or erythromycin significantly reduces the duration of signs

and symptoms and hastens the resolution of chest film findings
Azithromycin is preferred over erythromycin due to its better side-effects

profile and once-a-day dose
Prevention and Control
Currently no recommended specific control measures for M. pneumonia

outbreaks in closed communities

Prophylactic treatment of contact with azithromycin showed a decrease in
the attack rate in an institution and development of the illness
No vaccine available
Streptococcus pneumoniae
grows as lancet-shaped diplococci or in chains
diplococci like N. gonorrhoeae
facultative anaerobe
grows readily in BAP, needs to be transported quickly because of the fastidious

nature
alpha-hemolytic (partial lysis) on BAP
beta-hemolytic = complete lysis
gamma-hemolytic = no lysis
Colonies are often mucoid or umbilicated
sticky and viscous and parang may navel

Catalase negative
catalase is an enzyme present in lysosomes — a lysozyme
breaks down H2O2 → H2O and O2
O2 = formation of bubbles
no bubbling (left side)
most Streptococcus sp. are catalase (+)
Bile salt soluble
susceptible to bile
Susceptible to optochin
chemical toxic to some MO but not to some
Only strains of Streptococcus pneumoniae with capsules (encapsulated) are

virulent
As with other encapsulated organisms, its capsule is antiphagocytic
The capsular polysaccharide basis for typing, 90 serotypes identified

Mode of Transmission
Human to human by extensive contact with secretion harboring the

organism
Environments that enhance transmission — high risk for pneumococcal

infections
Day care centers
Prisons
Homeless centers
Military barracks
Aspiration of the endogenous oral organism
Pathogenesis of pneumococcal pneumonia

Predisposing conditions to pneumococcal pneumonia
Antecedent viral respiratory diseases
measles
influenza
others
Conditions that interfere with bacterial clearance
COPD
Alcoholism
CHF
Diabetes mellitus
Chronic renal disease
Immunocompromised
Clinical manifestations of pneumococcal pneumonia

Abrupt onset of shaking chill followed shortly by fever and productive rusty
sputum
Markedly ill, maybe cyanotic
Tachypneic, tachycardic
Laboratory diagnosis of S. pneumoniae
5% CO2 → parang candle jar method → anaerobic environment cuz

facultative anaerobe siya
remove some of the O2 by burning the candle to produce CO2
if onting sample lang nakuha mo, paparamihin sa lab animal yung MO
peritoneal washing → where MO is extracted
Quelleng (Neufeld) test to identify S. pneumoniae
Antibody to capsular antigen causes capsular swelling
biochemical reaction wherein the Ab-Antigen complex causes swelling of the

capsule → (+) rxn to Quelleng Test

Treatment of pneumococcal pneumonia
antibiotic therapy w supportive care (symptomatic tx) = mainstay tx
Organisms susceptible to Penicillin
Penicillin
Amoxicillin
Erythromycin
Organisms with intermediate resistance to penicillin
Amoxicillin
Cefuroxime
Clindamycin
Organisms highly resistant to penicillin
Cefpodoxime
Cefotaxime
Vancomycin

Tx depends on the variable situation of the px
Prevention with Pneumococcal Vaccines
PPSV23 (Pneumovax 23)
23-valent polysaccharide vaccine recommended for:
Aged ≥ 65 y
Aged 2 - 64 y with chronic disease (eg. cardiovascular, pulmonary, DM,

etc)
Aged 2 - 64 y residents of nursing homes/other-long-term-care facilities
Aged 2 - 64 y immunocompromised
mas maraming serotypes sa immunocompromised
PCV13 (Prevnar 13)
The first pneumococcal conjugate vaccine was licensed for use in the
US in 2000. Include purified capsular polysaccharides of seven serotypes

of S. pneumoniae
7 serotypes = pinakavirulent even sa immunocompetent
In 2010, a 13-valent pneumococcal conjugate vaccine (PCV13, Prevnar

13) was licensed in the United States. Contains the same 7 serotypes of
S. pneumoniae as PCV7 plus serotypes 1, 3, 5, 6A, 7F, and 19A.
Tuberculosis
Robert Koch isolated Mycobacterium tuberculosis in 1882
Characteristics
Obligate aerobe
lungs ang location ng M. tuberculosis
but TB can be in the bones and kidney
Can grow intracellularly
Generally, grow very slowly (chronic illness)
Bacillus
Weakly gram-positive cell wall
Mycolic acids as part of complex cell wall
Protects against desiccation
Protects against destruction by phagocytes
Requires acid-fast staining
Virulence Factor
M. tuberculosis does not produce toxins
many determinants of pathogenicity relate to its unique cell wall components

and the organism’s ability to survive phagocytic cells
CORD FACTOR
virulent strains of M. tuberculosis appear in culture as serpentine cords of

bacilli whereas avirulent stains do not display this morphology

a cell wall factor that connects cells (chains), resists phagocytosis,
toxic to host cells
acid-fast organism — red
Resistant to drying, acid, alkali, complement, and antibodies
Sensitive to UV, phenol, sodium hypochlorite, heat
Remains viable in dark areas for monthsSS
Pathogenesis of Latent TBI and TB Disease

carried via airborne droplets
Latent TB
immune system inhibits the replication of the MO
you have the MO but no sx and not infectious
when immunocompromised, immune cells will break down → active TB
Disseminated Tuberculosis
in some individuals, the initial infection w M. tuberculosis is not contained, and a

disseminated infection involving many organs results
spread from the lungs to the kidney, bone, heart

Reactivation Tuberculosis (Adult TB)
following primary exposure, the TB bacilli usually die as a result of host

defenses
in some individuals, a small number of organisms remain alive but are

contained in granulomas
Latent or treated TB → bumalik
these organisms may serve as a source for the reactivation of disease at a later
time
reactivation TB is usually seen in older individuals and in those who develop

impaired cell-mediated immunity

Diagnosis of TB
Sputum microscopy is the gold standard diagnosis for TB

Symptoms of Tuberculosis
Cough for 2 weeks or more
Sputum expectoration
Fever
at night and early in the morning cuz dun dumadami MO
Significant weight loss
Hemoptysis
blood in the sputum
Chest and/or back pain
may H2O sa baga so dun nagraradiate
Skin Test: PPD — Purified Protein Derivative
delayed-type hypersensitivity
Positive skin test in:
Primary infections
BCG immunization
Negative skin test in the presence of :
Severe malnutrition
Other diseases
Immune deficiency
cant produce Ab so no rxn to ID skin test

ID injection → >10mm diameter → (+) result
exposed or vaccinated (Bacillus Calamette Guerin — BCG vacc) → Ab

against M. tuberculosis is present
Ab is present → inflammation
Chest X-Ray is not a basis for diagnosis
can be over or under-read
many lung diseases mimic TB lesions
Sputum Microscopy using the Ziehl-Neelsen Stain
sensitive when there are approximately 10,000 bacilli per mL of the sputum

pag mas mababa pede mag negative
exam done on three samples
Important:
method of collection
quality of sputum
amount of sputum
3 samples para may confirmatory
8 weeks incubation cuz matagal mag grow ang MO
sputum collection
1st sample on consultation
2nd sample collected at home, in the morning
induce coughing if needed with steam inhalation
no food, toothbrush, mouthwash

should be submitted immediately
3rd sample second visit when 2nd sample is submitted
Evaluation of sputum microscopy for diagnosis
First set of 3 sputum samples
One sample (+) doubtful, collect 2nd set of three
Two samples (+) positive
All 3 samples (-), collect 2nd set of three
case holding
Second set of 3 sputum samples
One sample (+) , case is positive
All samples negative, do chest X-ray
Sputum microscopy is the recommended diagnostic tool and in following up

on treatment
For diagnosis:
3 sputum samples
For follow –up of treatment
Two consecutive negative smears, one month and 2 months after

treatment
to check the effectiveness of tx or if px is compliant
di nakakahawa if under tx
Culture in solid medium
Lowenstein-Jensen medium
Sensitive when there are at least 100 bacilli per mL of sputum

Drug Sensitivity for M. tuberculosis
Prevention and control measures
Case Finding
Sputum microscopy
Passive case finding
centralized reporting of TB px
Treatment

DOTS
standard program followed for TB tx
Case holding
susundan ung course of tx ng px
Immunization
BCG — Bacillus Calmette Guerin
live attenuated vaccine form of Mycobacterium bovis used to

prevent tuberculosis and other mycobacterial infections
Usually a part of the routine newborn immunization schedule.
Health Education
TB Life Cycle
Index Case = unang case ng suspected/exposed px
90-95% of immunocompetent indivs → healthy subjects

spontaneous remission = treated even w/o tx (strong immune system)
Directly Observed Therapy Short-course (DOTS)
5 Distinct Elements
Political Commitment — support of the government (LGUs)
Tool for diagnosis — sputum microscopy
Steady Drugs Supply
Surveillance & monitoring system
Direct observation of treatment
treatment partner
monitors px during the intensive phase
Standardized TB treatment regimens

Short Course Therapy

back to 0 if you missed and pede magdevelop ng resistance
FIxed Drug Combinations
HR isoniazid + rifampicin
HRZ isoniazid + rifampicin + pyrazinamide
HRZE isoniazid + rifampicin + pyrazinamide + ethambutol
Drug Resistance
Drug-resistant TB disease can develop in two different ways
Primary — infected with a resistant microorganism
Secondary — acquired resistance
inconsistent drug intake
di tinapos course of tx
nainfect ule
MDR TB is caused by organisms resistant to both isoniazid and rifampin,

which are the two most effective anti-TB drugs.

alternative = streptomycin and an injectable drug
XDR TB is a relatively rare type of drug-resistant TB. XDR TB is resistant to

both isoniazid and rifampin, plus any fluoroquinolone and at least one of
three injectable second-line drugs (i.e., amikacin, kanamycin, or
capreomycin)
tailor-fit medication is required
antibiotics are given thru IV or IM daily
Whooping Cough
CA — Bordetella pertussis
DPT vaccine can prevent diphtheria, tetanus, and pertussis — 3 in 1 vaccine
Spread
person-to-person airborne droplets
attach to, multiply in, the ciliated respiratory mucosa
SIGNS AND SYMPTOMS
Incubation period — 1-3 weeks
Catarrhal illness (mucus production)
Dry non-productive cough which becomes paroxysmal
series of short coughs producing copious mucus followed by “whoop”
Complications
CNS, anoxia, exhaustion, secondary pneumonia due to invasion of the

damaged respiratory tract by other pathogens
anoxia = insufficient O2 in organs
Dx
throat swab or on ‘cough plates’
Treatment
Supportive care

Hospitalization for children
Macrolides are the drug of choice
Prophylaxis (Erythromycin) is also recommended to control the spread of

infection
Vaccine
given to 8, 12, or 16-week-old babies — 6 or 5 in 1 vaccine in 3 doses
Acute Bronchitis
It is an inflammatory condition of the tracheobronchial tree
can progress to chronic lalo sa mga smokers
Causative agents
usually from smoking, dust, allergy
Viruses (influenza and adenovirus)
Secondary bacterial infections
S. pneumoniae
H. influenzae
SIGNS AND SYMPTOMS
cough — most prominent presentation
Treatment
Symptomatic
value of antibiotic is uncertain but usually recommended
Acute Exacerbations of Chronic Bronchitis
Characteristics:
frequency and severity of cough
Chest congestion and discomfort

Excessive mucus secretion
Causes
cigarette smoking
inhalation of dust or fumes
Chronic Bronchitis
Bronchitis
inflammation of the bronchial tube → difficulty in breathing
Causative Agents
Bacterial infection does not appear to initiate the disease but most frequently S.
pneumoniae and H. influenzae are isolated
Treatment:
Antibiotics may be helpful but efficacy is difficult to assess
Bronchiolitis

Causative agents
75% is due to respiratory syncytial virus (RSV)
25% viral
Occasional M. pneumoniae
Restricted to childhood, usually < 2 years of age
Restricted passage of air to and from the alveoli
Aspergillosis
Causative agent
Aspergillus fumigatus
Diseases
Allergic bronchopulmonary aspergillosis
Aspergilloma
Disseminated disease in an immunocompromised patient
Allergic bronchopulmonary aspergillosis
Allergic response to the presence of antigen in the lungs and occurs in

patients with asthma
fungi spores na naglodgesa aircon na matagal na di nililinis — aeroallergen →

spread sa air
Aspergilloma
It colonizes a cavity and grow to produce a mass-like fungal ball
immunocompromised px
fungal growth in the lungs → WBC and Ab attack it → lung abscess
abscess = accumulation of pus

Disseminated disease in the immunocompromised patient when the fungus
invades from the lungs
Treatment
Invasive aspergillosis is difficult to treat due to the limited number and

toxic nature of antifungal agents
itraconazole, amphotericin B
Cystic Fibrosis
Most common lethal inherited disorder among Caucasians
px produce thick mucus that cannot be expelled
nabloblock arteries and blood vessels in the lungs and pancreas
the mucus becomes the breeding ground for pathogens → pneumonia na

mahirap itreat
Lifespan = 30s to late 30s
Characteristics
pancreatic insufficiency
abnormal sweat electrolyte concentration
production of very viscid bronchial secretion
Invaders of Cystic Fibrosis

S. aureus
Causes respiratory distress and lung damage
P. aeruginosa
Colonizes lungs of almost all patients
H. influenzae
respiratory exacerbations
Treatment
Antibacterial therapy can reduce symptoms of infection and improve quality of

life
Infections particularly P. aeruginosa and P. cepacia are impossible to

eradicate and frequently a cause of death
Heart-lung transplantation
Lung Abscess
A supporative infection of the lung
Also referred as “necrotizing pneumonia”
Predisposing Cause
Aspiration of respiratory or gastric secretions due to altered consciousness
foreign material harboring MO — liquid, food, gastric juice — enters the

lungs due to the malfunction of the epiglottis → lung abscess, pleural
effusion (tubig sa baga)
Causative agents
Anaerobes i.e Bacteroides fragilis and Fusobacterium capsulatum
Symptoms:
Patient may be ill for at least two weeks before presentation of foul smelling
and large amounts of sputum
Diagnosis

chest radiograph
Treatment
broad spectrum antibiotics due to polymicrobial flora, such as
Clindamycin (600 mg IV on 8 h) and then 300 mg PO on 8 h or

combination ampicilin/sulbactam (1.5-3 gr IV on 6 h)
combination of penicillin and clavulanate or combination of penicillin and

metronidazole
Treatment may need 2 – 4 months to prevent relapse
Parasitic Infection of LRTI

it enters the body as a larva (microscopic stage of its life cycle)
Parasites
Nematodes such as Ascaris and hookworm
Schistosome larvae
Entamoeba histolytica — rarely involves the lungs
SIGNS AND SYMPTOMS
chest pain

DOB
can cause bronchopneumonia when large numbers of parasites are present
Treatment
Anthelminthic — Praziquantel

9 - Lower Respiratory Tract Infections (LRTI)

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9 - Lower Respiratory Tract Infections (LRTI)

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🫁

Lower Respiratory Tract

Legionnaire’s disease or Pontiac Fever

aka parrot fever, ornithosis

can infect ppl but mild sx

can progress to pneumonia

1st line = Macrolide

2nd line = Tetracycline

DOC ang Tetracycline unless contraindicated w Macrolide ang

one of the causes of community-acquired pneumonia

Lower Respiratory Tract Infections (LRTI) 1

once a day dosing

ppl can be infected

1st line = Doxycycline

very small, pleomorphic (cocci to filaments)

smallest replicating organisms (0.3 to 0.8 mcm)

have no cells walls, but have sterols in their membranes

require numerous growth factors to grow

The absence of a cell wall makes them:

insensitive to penicillin and cephalosporins — beta-lactams

They cannot be visualized by Gram stain

Lower Respiratory Tract Infections (LRTI) 2

They are pleomorphic and can assume a variety of shapes

How to visualize colonies of mycoplasma

blue stain cuz may methylene blue

if you have a visible colony:

a nonspecific stain that imparts a contrasting appearance to

Results — “ fried egg” colony morphology

dark blue center and light blue periphery, appearing highly

may take up to 3 weeks to produce detectable colonies

antibodies bind here

Lower Respiratory Tract Infections (LRTI) 3

M. pneumoniae may be detected by cross-reacting antibodies against

Virulence Factor — make MO more pathogenic

M. pneumoniae adheres tightly to and fuses with the membranes of

no cilia = no brushing action

No known exotoxins are produced

causes a respiratory disease referred to as “atypical pneumonia” or walking

the common cause of community-acquired pneumonia

Lower Respiratory Tract Infections (LRTI) 4

at the start of the illness, the px will have flu-like sx

can do daily activities

no need for hospitalization but already infectious

Pathogenesis of Atypical Pneumonia

high levels of H2O2 → oxidative damage → death of the cell

can cause cancer and aging of the skin

antioxidants = reduce free radicals

Lower Respiratory Tract Infections (LRTI) 5

Chest X-Ray picture of atypical pneumonia

May also show peribronchial pneumonia, atelectasis, nodular infiltrates, and

not used for diagnosis cuz cant know the cause

presence of gas in the pleural cavity

abnormal clotting of the blood

deposition of IgM on the skin → rashes

the immune system produces antibodies that cross-react to the PNS

PNS governs involuntary muscles — e.g. breathing, heart muscles

Lower Respiratory Tract Infections (LRTI) 6

like meningitis — inflammation of the brain and spinal cord

lack of standard in diagnosis

2 most frequent lab tests for M. pneumoniae

Complement Fixation (CF) and Enzyme immunoassay (EIAs)

marami sakit nadidiagnose — non specific

Tetracycline or erythromycin significantly reduces the duration of signs

Azithromycin is preferred over erythromycin due to its better side-effects