Microbial Diseases of The Respiratory System: Micropara-Respiratory Infectionby DR Sonnie Talavera

24
Microbial Diseases of the Respiratory

System
MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

upper respiratory system
 The consists of the nose, pharynx, and associated

structures, such as the middle ear and auditory
tubes.
 Coarse hairs in the nose

 ciliated mucous membranes ( nose and throat )
 Lymphoid tissue, tonsils, and adenoids

lower respiratory system
 consists of the larynx, trachea, bronchial tubes,

and alveoli.
 ciliary escalator
 alveolar macrophages.
 Respiratory mucus contains IgA antibodies.

NORMAL MICROBIOTA OF THE
RESPIRATORY SYSTEM
 The normal microbiota of the nasal cavity and

throat can include pathogenic microorganisms.
 The lower respiratory system is usually sterile

because of the action of the ciliary escalator.

Upper Respiratory System
 Upper respiratory normal microbiota may include
pathogens
MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figure 24.1

Microbial Diseases of the
 Laryngitis: S. pneumoniae, S. pyogenes, viruses
 Tonsillitis: S. pneumoniae, S. pyogenes, viruses
 Sinusitis: Bacteria
 Epiglottitis: H. influenzae Hib vaccine

MICROBIAL DISEASES OF THE UPPER
RESPIRATORY SYSTEM
 These infections may be caused by several

bacteria and viruses, often in combination.
 Most respiratory tract infections are self-limiting.
 H. influenzae type b can cause epiglottitis.

Streptococcal Pharyngitis (Strep
Throat)
 GAS- Streptococcus
pyogenes
 Resistant to phagocytosis
 Streptokinases lyse clots
 Streptolysins are
cytotoxic
 Diagnosis by indirect
agglutination/ EIA

Throat)
 group A beta-hemolytic streptococci-
Streptococcus pyogenes.
 Symptoms of this infection are inflammation of

the mucous membrane and fever; tonsillitis and
otitis media may also occur.

Throat)
 Rapid diagnosis is made by enzyme immunoassays.
 Penicillin is used to treat streptococcal pharyngitis.
 Immunity to streptococcal infections is type-

specific.
 Strep throat is usually transmitted by droplets.

Scarlet Fever
 Streptococcus pyogenes
 Pharyngitis
 Erythrogenic toxin
produced by
lysogenized S.
pyogenes by a phage.

Scarlet Fever
 Strep throat, caused by an erythrogenic toxin-

producing S. pyogenes, results in scarlet fever.
 starts general malaise and swelling of neck
 Symptoms include a red rash, high fever, and a

SPOTTED STRABERRY like red, enlarged tongue.

Diphtheria
 Corynebacterium diphtheriae: Gram-positive rod
pleomorphic club shape

Diphtheria
 Clinical
 Start as sore throat and fever followed by general
malaise and swelling of neck
 Diphtheria (leather) tough grayish membrane of fibrin,
dead tissue, and bacteria
 Diphtheria toxin produced by lysogenized C.

diphtheriae (highly virulent toxin)

Diphtheria

Diphtheria

Vao day nghe bai nay di ban

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Diphtheria
 A membrane can block the passage of air.
 Exotoxin inhibits protein synthesis, and heart,
kidney, or nerve damage may result (fatal)
 minimal dissemination of the exotoxin in the

bloodstream.
 Antitoxin - neutralize the toxin
 Antibiotics- Penicillin and Erythromycin can stop

growth of the bacteria.
Diphtheria
 Prevented by DTaP and Td vaccine (Diphtheria
toxoid)
 Cutaneous diphtheria: Infected skin wound leads to
slow healing ulcer

Corynebacteria (Genus Corynebacterium)
• Aerobic or facultatively anaerobic
• Small, pleomorphic (club-shaped), gram-positive

bacilli short chains (“V” or “Y” configurations) or in
clumps resembling “Chinese letters”
• Cells contain metachromatic granules
• Lipid-rich cell wall contains meso -diaminopimelic

acid
OTITIS MEDIA
infection of the middle ear, primarily in infants and

young children
three manifestations
• acute otitis media
• chronic otitis media
• otitis media with effusion
A. Symptoms - fever, pain in the ear, dulled hearing.

Otitis Media
 S. pneumoniae (35%)
 H. influenzae (20-30%)
 M. catarrhalis (10-15%)
 S. pyogenes (8-10%)
 S. aureus (1-2%)
 RSV
 Affects 85% of children before age 3, and estimated
8 million cases/ year

Otitis Media
 Treated with broad-spectrum antibiotics

Amoxicillin
 Incidence of S. pneumoniae reduced by vaccine
Otitis Media
 Earache, or otitis media, can occur as a

complication of nose and throat infections.
 Pus accumulation causes pressure on the eardrum
causes inflammation and pain.
 Often in children because of shorter and more
horizontal eustachian tube

B. DIAGNOSIS –
1. clinical presentation of fever and pain, especially

following an URT infection such as a cold
2. otoscopic examination to see inflammation and/or fluid

(pus); also loss of mobility with air pressure
6.
• swelling and blockage

• cyclic pattern of damage
• discomfort - pressure and blocked nasal passages
Common cold
 Rhinoviruses (50%)
 Coronaviruses (15-20%)

The Common Cold
 Any one of approximately 200 different viruses

can cause the common cold; rhinoviruses cause
about 50% of all colds.
 Immunity is based on the ration of Ig A antibodies

The Common Cold
 Symptoms
 Sneezing
 nasal secretions
 congestion.
 Sinus infections, lower respiratory tract infections,
laryngitis, and otitis media can occur as
complications of a cold.

The Common Cold
 Colds are most often transmitted by indirect

contact.
 Rhinoviruses grow best slightly below body
temperature.
 The incidence of colds increases during cold
weather
 Antibodies are produced against the specific
viruses.

Microbial Diseases of the
Lower Respiratory System
 Bacteria, viruses, and fungi cause
 Bronchitis
 Bronchiolitis
 Pneumonia

 The ciliary escalator keeps the lower respiratory
system sterile.

Pertussis (Whooping Cough)
 Bordetella pertussis: Gram-
negative coccobacillus
 Capsule
 Tracheal cytotoxin of cell
wall damaged ciliated cells
 Pertussis toxin produces
systemic disease
 Prevented by DTaP
vaccine (acellular Pertussis
cell fragments)
Epidemiology of Bordetella pertussis
Infection
 Man is only natural host; obligate parasites of man
 Disease is highly communicable (highly infectious)
 Children under one year at highest risk, but prevalence
increasing in older children and adults
Whooping cough
Inhalation of aerosols
Adhere to ciliated epithelial cells

(FHA, Pili)
Toxin production
Damage to mucosal cells Act on neurons

(TCT, Ptx, Acase, LPS?) (Ptx, Acase, LPS)
Paroxysmal cough
Whooping cough
 Symptoms
 Severe coughing, spasms, inspiratory whoop
 Lymphocytosis
 Stages of disease
 Catarrhal -> Paroxysmal -> Convalescent
 Spread--highly contagious
 Inhalation or direct contact with secretion
 Usually self-limiting
 Neurological sequelae
 Secondary respiratory infections
 Secondary aspiration pneumoniae
 leading cause of death

.Initial stage of Paroxysmal

pertussis (second) stage
Convalescence
accumulation (third) stage
resembles a
cold and is of mucus in the
can last for
called the trachea and months
catarrhal stage. bronchi causes
deep coughs

Clinical Progression of Pertussis
,
or death
Inflammation of respiratory mucosal memb.
Most infectious, but

generally not yet
diagnosed
Laboratory Culture, Prevention &
Treatment of Bordetella
 Nonmotile
 Fastidious and slow-growing
· Requires nicotinamide and charcoal, starch, blood, or albumin
· Requires prolonged growth
· Isolated on modified Bordet-Gengou agar
 Treatment with erythromycin

 Laboratory diagnosis is based on isolation of the

bacteria on enrichment and selective media,
followed by serological tests.
 Regular immunization for children has decreased

the incidence of pertussis.

TUBERCULOSIS
Situationer
 Leading causes of death world wide

 Up to a half of world’s population infected,
95% in developing countries
 8 million people get TB every year
(WHO fact sheet 2007)

 Philippines ranks 4th for # of TB cases worldwide,
highest # per head in SEA
 2/3 of Filipinos with TB
(DOH, 2007)
PTB
 Mycobacterium tubercle, acid fast bacilli

 Airborne/droplets
 Pott’s disease – thoracolumbar
 Milliary TB – kidney, liver, lungs
Rex Karl S. Teoxon, R.N, M.D 44

Morphology
 Mycobacterium tuberculosis
 Thin straight rods, 0.4 x 3 µm
 Acid-fast organisms
Mycobacterial cell wall components
 Lipids (mycolic acids)

 Proteins
 Polysaccharides
TB symptoms
1. Cough with two weeks or more

2. Sputum expectoration
3. Fever
4. Significant weight loss
5. Hemoptysis
6. Chest and/or back pains
SIGNS AND SYMPTOMS
 Wt loss, night sweats, low fever, non productive to

productive cough, anorexia, Pleural effusion and
hypoxemia, cervical lymphadenopathy

Tuberculosis
 Mycobacterium
tuberculosis: Acid-fast rod;
transmitted from human
to human.
 M. bovis: <1% U.S. cases,
not transmitted from
human to human.
 M. avium-intracellulare
complex infects people
with late stage HIV
infection.
Tuberculosis
Mycobacterium tuberculosis
 Acid fast-lipid, wax
 Slow growth (nutrient permeability)
 Resist to detergent and common antibiotics
 A leading cause of death by infectious
disease
 50% population infected, 3m death/yr
 Reemergence in 1980 (AIDS, homeless, immigrants)
 Diagnose
 PPD test
 Chest X-ray
 Sputum smear (for acid-fast bacilli)
 Sputum culture
Diagnosis
 Sputum culture
 Slow, 13 hour generation time, takes weeks
 Acid-fast staining
 Skin test (PPD)
 DNA hybridization
 PCR (16s rRNA)
 Bacteriophage
PPD – ID
macrophages in skin take

up Ag and deliver it to T
cells
T cells move to skin site,

release lymphokines
activate macrophages and

in 48-72 hrs, skin becomes
indurated
- > 10 mm is (+)
DIAGNOSIS
Chest x ray - cavitary

lesion
Sputum exam
Sputum culture

Stages of disease
 Primary infection
 Asymptomatic to flu-like
 3-5% develop TB
 Tubercle (granulomatous response)
 Reactivation (active TB)
 Years later, 10% experience
 LRT disease (pneumonia)
 Disseminated miliary TB
 Almost everywhere
 AIDS and antibiotic resistance
Stages of pathogenesis
 Encounter - respiratory droplet

 Entry - direct inhalation into LRT (ID=10)
 SPREAD - alveoli, but can spread
throughout body seeding many tissues
 Multiplication
 Grows in phagosome of macrophage
 Strict aerobe
 Very slow in culture (24 hr doubling time)
 Evade defenses
 Inhibits phagolysosomal fusion
Tuberculosis
 Tuberculosis is caused by Mycobacterium

tuberculosis.
 Large amounts of lipids in the cell wall
account for the bacterium’s acid-fast
characteristic as well as its resistance to
dryingnd disinfectants.

Tuberculosis
 M. tuberculosis
may be ingested
by alveolar
macrophages; if
not killed, the
bacteria
reproduce in the
macrophages.

Tuberculosis
 Lesions formed by
M. tuberculosis are
called tubercles
 Dead macrophages
and bacteria form
the caseous lesion
that might calcify
and appear in an X
ray as a Ghon’s
complex.
Tuberculosis
 Liquefaction of the caseous
lesion results in a
tuberculous cavity in which
M. tuberculosis can grow.

Tuberculosis
 New foci of
infection can
develop when a
caseous lesion
ruptures and
releases bacteria
into blood or
lymph vessels;
this is called
miliary
tuberculosis.
M. tuberculosis
 Damage
 Host response to bacteria (cell-mediated immunity)
 Glycolipids (Freund adjuvant)
 Spread to new hosts

 Contagious by droplet, resistant to drying
 Vaccine - BCG
 Causes people to become PPD+, not very effective
 Infect AIDS
 Treatment
 Unusual set of antibiotics (isoniazid, ethambutol, rifampin)
 High mutation rate
Tuberculosis
 Miliary tuberculosis is characterized by weight

loss, coughing, and loss of vigor.
 Chemotherapy usually involves 3 or 4 drugs taken
for at least 6 months; multidrug-resistant M.
tuberculosis is becoming prevalent.

Tuberculosis
 Positive tuberculin skin test

 an active case of TB
 prior infection
 vaccination
 immunity to the disease
 Induration and reddening at
inoculation site within
48hours.
 Most accurate- Mantoux test

Tuberculosis
 Laboratory diagnosis is based on the presence of
acid-fast bacilli and isolation of the bacteria,
which requires incubation (3-6weeks) of up to 8
weeks (Lowenstein-Jensen Agar)

PPD Tuberculosis Skin Test Criteria
PPD = Purified Protein Derivative from M. tuberculosis

Chest X-Ray of Patient with
Active Pulmonary Tuberculosis
Tuberculosis
 Mycobacterium bovis
 causes bovine tuberculosis
 transmitted to humans by unpasteurized milk.
 affect the bones or lymphatic system.
 BCG vaccine -a live, avirulent culture of M. bovis
 M. avium-intracellulare complex infects patients in

the late stages of HIV

Tuberculosis
 Treatment of tuberculosis: Prolonged treatment
with multiple antibiotics.
 Vaccines: BCG, live, avirulent M. bovis; not widely
used in United States.

Tuberculosis

MANAGEMENT
 short course – 6-9 months

 long course – 9-12 months
 DOTS- direct observe treatment short course
 Case finding
 Home meds (members of the family)
 Referrals
 Follow-up short course – 6-9 months
 long course – 9-12 months

MANAGEMENT
 Follow-up
* 2 wks after medications – non communicable
3 successive (-) sputum - non communicable
rifampicin - prophylactic

CATEGORIES OF TB
 category I (new PTB) - (+) sputum
 category II (relapse)
 category III (PTB case) - (-) sputum

TREATMENT:
 CATEGORY 1 - NEW PTB, (+) SPUTUM
GIVE RIPE 2 MONTHS, MAINTENANCE OF RI 4
MONTHS
 CATEGORY 2 - PREVIOUSLY TREATED WITH
RELAPSES
GIVE RIPES 1ST 2 MONTHS, REPS 1 MONTH,
MAINTENANCE RIE 5 MONTHS
 CATEGORY 3 - NEW PTB (-) SPUTUM FOR 3X
GIVE RIP 2 MONTHS, MAINTENACE RI 2 MONTHS
* IF RESISTANT TO DRUGS GIVE ADDITIONAL

MONTH/S AS PRESCRIBED
MDT side effects
 r-orange urine
 i-neuritis and hepatitis
 p-hyperuricemia
 e-impairment of vision
 s-8th cranial nerve damage

AFB SMEAR REPORTING GUIDELINE,
DOH
NATIONAL TUBERCULOSIS CONTROL PROGRAM (2001)
Emilio M. Ramirez, MD
National Tuberculosis Control
Program (2001)
 prevent transmission of tubercle bacilli to a
healthy person
Goal: Reduce TB mortality and prevalence through
early case detection and treatment
Target: identify at least 70% of new smear (+) cases,

cure at least 85% TB patients discovered
Strategy: DOTS (directly observed treatment short

course chemotheapy)
Sputum Collection Schedule for
DIAGNOSIS
SPOT EARLY SPOT
MORNING
First specimen -
collected at the time
Day of consultation or as
soon as TB
1 symptomatic is
identified.
Second specimen Third specimen

Collected in the morning Collected at the time
Day by the TB symptomatic the TB symptomatic
when he/she is due to comes back to the
2 submit the specimen to health facility to
the health center. submit the second
specimen.
Ideal sputum specimen?
MACROSCOPIC
Yellowish
Mucopurulent
Cheesy material
When to collect another set of 3 sputum
specimens?
 When the diagnosis for the sputum microscopy
examination is doubtful.
 When the patient fails to complete his sputum

collection within two weeks from the time of the
previous collection.
Ideal sputum specimen?
MICROSCOPIC
greater than 25
wbc/LPO, 5 wbc/OIO
Presence of alveolar
macrophage, dust
cells
AFB STAINING
DIRECT SMEAR EXAMINATION
(Flow Chart)
SMEARING
SPREADING
DRYING
FIXATION
STAINING
INITIAL STAINING
HEATING
WASHING
DECOLORIZATION
WASHING
COUNTER-STAINING
WASHING
DRYING
MICROSCOPIC OBSERVATION
RECORDING & REPORTING

DIRECT SMEAR PREPARATION
LABELING THE SLIDES
 Write down the identification number of the sputum

specimen on the end of a clean glass slide.
SMEARING
SPREADING
 With a coconut midrib, fish

out one (1) loopful of
purulent, solid particles of
the sputum.
 Spread the sputum evenly

on the slide, approximately
2 x 3 cm
in size.
A Good Smear
Poor/too thick Good Poor/too thin

SMEARING
DRYING
 Allow the smear to dry completely at room temperature.

Do not dry it under the sun or over the flame.
 Place used midribs in a bottle with alcohol and sand mixture or Lysol,
or in a plastic containers and burn them later.
SMEARING
FIXATION
 Fix the smear by passing it through the flame of an alcohol lamp 2 to

3 times, about 2-3 seconds each.
Heat the back of smeared surface of the slide. Never scorch the
smear.
STAINING
FIXATION
 Fix the smear by passing it through the flame of an alcohol lamp 2 to

3 times, about 2-3 seconds each.
Heat the back of smeared surface of the slide. Never scorch the
smear.
STAINING
INITIAL STAINING
 Arrange the slides on the staining bridge consecutively.
 Pour carbol fuchsin solution covering the whole surface of the

slide.
STAINING
HEATING OF THE SLIDE
 Heat the slide using an alcohol lamp or spirit cotton in a stick ‘till
steam comes off from the stain.
Do not boil and do not allow the stain to dry. Leave it for five
minutes.
STAINING
WASHING OF THE SLIDE
 Tilt the slide to drain off excess stain.
 Wash the staining solution off with a gentle

stream of running water.
STAINING
DECOLOURIZATION
 Tilt the slide to drain off excess rinse water.
 Cover the whole slide with 3% hydrochloric acid-ethanol and

leave it until solution runs clear.
Staining
WASHING OF THE SLIDE
 Wash the slide with a gentle stream of running water.
 Tilt the slide to drain off excess rinse water.

Staining
COUNTERSTAINING
 Pour 0.1% methylene blue to cover the whole surface of the smear
and leave for 5-10 seconds.
 Tilt the slide to drain off excess methylene blue.

Staining
WASHING AND DRYING
 Wash the slide with a gentle stream of running water.
 Tilt and place the slide on the slide rack to dry in the air.
Don’t place under the sun to dry.
SMEAR READING
3 cm
 PROPER SCANNING
Horizontal Scanning
Vertical Scanning
 IMPROPER SCANNING
Zigzag Scanning
AFB OBSERVATION
Single/parallel form Coccoid form
Clump form Scratches on the slide

MICROSCOPIC OBSERVATION OF AFB IN PROPERLY AND
IMPROPERLY STAINED SMEAR
PROPER STAINING INSUFFICIENT HEATING
UNDERDECOLORIZED INTENSELY COUNTERSTAINED

National Standard Reporting Scale (2001)
No AFB seen in 300 visual fields 0
AFB/ 100 visual fields (x1000) 1-9 n+
AFB/ 100 visual fields (x1000) 10-99 +1
AFB/ OIF in at least 50 visual fields 1-10 +2
AFB/ OIF in at least 20 visual fields 10> +3

INTERPRETATION OF LAB RESULTS
POSITIVE - if all or at least two of the

three specimens are positive
NEGATIVE - if all (3) specimens are

negative
DOUBTFUL - if one of the three

specimens is positive
(sputum examination
should be repeated)
Bacterial Pneumonias
 Typical pneumonia is caused by S. pneumoniae.
 Atypical pneumonias are caused by other

microorganisms.
 Lobar pneumonia
 bronchopneumonia

Pneumonias
Sign/ symptoms
 High fever
 DOB
 Chest pain
 Productive cough

Pneumomoccal Pneumonia
 Streptococcus
pneumoniae:
Gram-positive
encapsulated
diplococci
 Diagnosis is by
culturing
bacteria.
 Penicillin
Fluoroquinolones
is drug of choice.
Pneumococcal pneumonia
(Streptococcus pneumoniae)
 Gram-positive diplococcus
 Encapsulated (>80 serotypes)
 Susceptible population
 Elderly
 Previously ill
 Phagocytic dysfunction (e.g., asplenic, sickle cell)
 Also cause meningitis, otitis media
 Sensitive to optichin; autolysis by bile
Pneumococcal Pneumonia
The bacteria can be

identified
 alpha-hemolysins,
 inhibition by optochin,
 bile solubility
 serological tests.

Identification
Not optochin sensitive
optochin sensitive
114
Pneumococcal Pneumonia
 Symptoms
 Fever
 breathing difficulty
 chest pain
 rust-colored sputum.
 A vaccine consists of
purified capsular material
from 23 serotypes of S.
pneumoniae.
Stages of pathogenesis
 Encounter - humans only, by respiratory droplet
 Entry - colonization of the oropharynx, aspiration
into lung (pneumonia)
 Spread (extracellular)
 Pneumonia - blood culture can be positive
 Meningitis - penetration of mucous membrane
 Otitis media- eustachian tube to middle ear
 Multiplication
 Grows well in serous fluid in alveoli space
 Evade defenses
 Capsule--antiphagocytic
 sIgA protease
Haemophilus Influenzae Pneumonia
 Gram-negative coccobacillus
 Alcoholism, poor nutrition, cancer, or diabetes are
predisposing factors.
 Second-generation cephalosporins

Mycoplasmal Pneumonia
 Mycoplasma pneumoniae causes mycoplasmal

pneumonia; it is an endemic disease.
 Young adults and children

 Symptoms persist for 3 weeks and longer (low
fever, cough and headaches)
 PRIMARY ATYPICAL/ WALKING PNEUMONIA

Mycoplasmal Pneumonia
 M. pneumoniae produces
small “fried-egg”
colonies after two weeks’
incubation on enriched
media containing horse
serum and yeast extract.
 Diagnosis is by PCR or
serological tests.

Atypical (walking) pneumonia Mycoplasma
pneumonia
 Lacks peptidoglycan
 -lactam resistant
 Disease primarily in young adults
 Encounter - inhalation from human
 Entry - restricted to mucosal surface
 Terminal adhesin protein (P1)
 Multiplication - require sterols
 Damage
 Inflammation
 Damage and desquamation of ciliated epithelium
 Treatments
 Erythromycin, doxycycline, tetracyline
Model for mycoplasma pathogenesis in the lungs
Legionellosis
 The disease is caused by the aerobic gram-

negative rod Legionella pneumophila.
 High fever 40.5C, cough and general pneumonia
symptoms
 The bacterium can grow in water, such as air-
conditioning cooling towers, and then be
disseminated in the air.

Legionnaire's disease/Pontiac Fever
Legionella pneumophila
 Gram-negative rod
 Stains irregularly
 Silver stain
 Disease
 Pontiac Fever - flu-like in anyone (1968)
 Fever muscular ache and cough(self limiting)
 Legionnaire's disease - pneumonia
 Primarily in middle aged to older men who heavy
smoker and drinker or chronically ill
 1976 American Legion Convention in Philadelphia
( toll 182 cases/29 death)
L. pneumophila
Legionellosis
 This pneumonia does not appear to be

transmitted from person to person.
 Bacterial culture, FA tests, and DNA probes are
used for laboratory diagnosis.
 Prevention : Copper Ionizing procedure
 Treatment : Erythromycin, some macrolides like
Azithromycin

Psittacosis (Ornithosis)
 Chlamydophila psittaci – gram negative

intracellular bacteria and is transmitted by
contact with contaminated droppings and
exudates of fowl.
 Elementary bodies allow the bacteria to survive
outside a host.
 s/sx: fever, headache , chills, some with delirium
and disorientation

Psittacosis (Ornithosis)
 Commercial bird handlers are most susceptible to

this disease.
 The bacteria are isolated in embryonated eggs,
mice, or cell culture; identification is based on FA
staining.
 Tx: Tetracycline

Chlamydial Pneumonia
 Chlamydophila pneumoniae causes pneumonia; it

is transmitted from person to person.
 Atherosclerosis-deposition of fats on arteries
 s/sx resemble mycoplasma pneumonia
 Tetracycline is used for treatment.

Q Fever
 Obligately parasitic, intracellular Coxiella burnetii

causes Q fever or X fever
 The disease is usually transmitted to humans
through unpasteurized milk or inhalation of
aerosols in dairy barns, cattle tick bites
 Laboratory diagnosis is made with the culture of
bacteria in embryonated eggs or cell culture.

Q Fever
 Wide range of clinical symptoms

 60% asymptomatic
 s/sx: High fever, muscle ache, headache and
coughing
 Hepatitis and endocarditis (persist for months)
 Tx: Doxycycline , Chloroquine

Melioidosis
 Melioidosis, glanders disease (horses) caused by

Burkholderia pseudomallei
 transmitted by inhalation, ingestion, or through
puncture wounds.
 Symptoms include pneumonia, sepsis, and
encephalitis.
 Tx: Ceftazidime

Disease Symptoms
Streptococcal pharyngitis Pharyngitis and tonsillitis

Scarlet fever Rash and fever
Diphtheria Membrane across throat

Whooping cough Paroxysmal coughing
Tuberculosis Tubercles, weight loss, and coughing
Pneumococcal pneumonia Reddish lungs, fever

H. influenzae pneumonia Similar to pneumococcal pneumonia
Chamydial pneumonia Low fever, cough, and headache
Legionellosis Fever and cough

Disease Symptoms
Psittacosis Fever and headache
Q fever Chills and chest pain
Epiglottitis Inflamed, abscessed epiglottis
Melioidosis Delayed-onset pneumonia

Diagnostic
Gram-positive cocci
Catalase-positive Staphylococcus aureus

Beta-hemolytic Streptococcus pyogenes
Alpha-hemolytic S. pneumoniae

Gram-positive rods
Not acid-fast Corynebacterium diphtheriae
Acid-fast Mycobacterium tuberculosis
Gram-negative cocci Moraxella catarrhalis

a. Streptococcus pneumoniae
b. Haemophilus influenzae -
c. Moraxella catarrhalis -
Gram-negative rods
Aerobes
Coccobacilli Bordetella pertussis
Rods
Grow on nutrient agarBurkholderia pseudomallei
Require special media Legionella pneumophila
Facultative anaerobes
Coccobacilli Haemophilus influenzae
Intracellular
Elementary bodies Chlamydophila psittaci
No elementary bodies Coxiella burnetii
Wall-less Mycoplasma pneumoniae

Viral Pneumonia
 A number of viruses can cause pneumonia as a

complication of infections such as influenza.
 The etiologies are not usually identified in a
clinical laboratory because of the difficulty in
isolating and identifying viruses.

Respiratory Syncytial Virus
(RSV)
 RSV is the most common cause of pneumonia in
infants 2-6months
 Life threatening- tx Ribavirin and Palizumab
 Coughing, wheezing last more than a week, fever
by bacterial infection

Influenza
 Hemagglutinin (H)
spikes used for
attachment to host
cells.
 Neuraminidase (N)
spikes used to release
virus from cell.

Influenza
 Antigenic shift
 Changes in H and N spikes
 Probably due to genetic recombination between
different strains infecting the same cell
 Antigenic drift
 Mutations in genes encoding H or N spikes
 May involve only 1 amino acid.
 Allows virus to avoid mucosal IgA antibodies.

Influenza Serotypes
 A: Causes most epidemics, H3N2, H1N1, H2N2
 B: Moderate, local outbreaks
 C: Mild disease

Influenza
 Deaths during epidemic - secondary bacterial

infections.
 Multivalent vaccines for the elderly and other
high-risk groups.
 Amantadine and rimantadine are effective
prophylactic and curative drugs
 Zanamivir and oseltamivir

SARS
 Coronavirus
 Severe acute respiratory syndrome
IP: 2-7 days
MOT: respiratory droplet/person to person

contact
146
RISK FACTORS
 history of recent travel to China, Hong Kong, or

Taiwan or close contact w/ ill persons with a hx of
recent travel to such areas, OR
 Is employed in an occupation at particular risk for
SARS exposure, i.e. healthcare worker with direct
patient contact or a worker in a laboratory that
contains live SARS, OR
 Is part of a cluster of cases of atypical pneumonia
without an alternative diagnosis
147
SIGNS AND SYMPTOMS
 fever, chills, rigors, myalgia, headache, diarrhea,

sore throat, rhinorrhea
 2-7 days after onset of illness - shortness of breath
and/or dry cough
148
DIAGNOSIS
 viral culture
 PCR
 serologic testing
Mgmt: supportive
149
Common cold Coronaviruses Sneezing, excessive nasal

secretions, congestion
Viral pneumonia Several viruses Fever, shortness of

breath, chest pains
Influenza Influenzavirus Chills, fever, headache,

muscular pains
RSV Respiratorysyncytial Coughing, wheezing

virus
Amantadine is used to treat influenza. Palivizumab, for life-threatening RSV.

FUNGAL DISEASES OF THE LOWER
RESPIRATORY SYSTEM
 Fungal spores are easily inhaled; they may
germinate in the lower respiratory tract.
 The incidence of fungal diseases has been
increasing in recent years.
 The mycoses in the sections below can be treated
with amphotericin B.

Histoplasmosis
 Histoplasma capsulatum, dimorphic fungus

Histoplasmosis
 Resembles Tuberculosis
 Histoplasma capsulatum causes a subclinical
respiratory infection that only occasionally
progresses to a severe, generalized disease.

Histoplasmosis
 Transmitted by airborne conidia from soil and thru bird
droppings
 Diagnosis by culturing fungus
 Treatment: Amphotericin B or Itraconizole

Coccidioidomycosis
 Coccidioides immitis- dimorphic fungi

Coccidioidomycosis
 Valley Fever or San Joaquin Fever

 s/sx- fever, coughing and weigth loss
 Most cases are subclinical, but when there are
predisposing factors such as fatigue and poor
nutrition, a progressive disease resembling
tuberculosis can result.

Coccidioidomycosis
 Transmitted by
airborne arthrospores
 Diagnosis by
serological tests or
DNA probe
 Treatment:
Amphotericin B
 Also Ketoconazole,
Itraconazole

Pneumocystis Pneumonia
 Pneumocystis jiroveci (P.
carinii) is found in
healthy human lungs.
 Pneumonia occurs in
newly infected infants
and
immunosuppressed
individuals.
 Treatment:
Timethoprim-
sulfamethoxazole
MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figure 24.22a
Pneumocystis Pneumonia
 P. jiroveci causes disease in immunosuppressed

patients.
 Site - lining of alveoli
 DOC Trimetophrim -Sulfamethoxazole

Pneumocystis

Blastomycosis
 Blastomyces dermatitidis, dimorphic fungus
 Found in soil
 Can cause extensive tissue destruction, cutaneous
lesions
 Treatment: Amphotericin B

Blastomycosis (North American
Blastomycosis)
 The infection begins in the lungs and can spread
to cause extensive abscesses.

Other Fungi Involved in
Respiratory Disease
 Opportunistic fungi can cause respiratory disease
in immunosuppressed hosts, especially when
large numbers of spores are inhaled.

Opportunistic Fungi Involved in
Respiratory Disease
 Aspergillus
 Rhizopus
 Mucor
Mucor indicus
MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figures 12.2b, 12.4

Microbial Diseases of The Respiratory System: Micropara-Respiratory Infectionby DR Sonnie Talavera

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24

Microbial Diseases of the Respiratory

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 The consists of the nose, pharynx, and associated

 Coarse hairs in the nose

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 consists of the larynx, trachea, bronchial tubes,

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 The normal microbiota of the nasal cavity and

 The lower respiratory system is usually sterile

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figure 24.1

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 These infections may be caused by several

 Most respiratory tract infections are self-limiting.

 H. influenzae type b can cause epiglottitis.

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figure 24.3

 Symptoms of this infection are inflammation of

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 Penicillin is used to treat streptococcal pharyngitis.

 Immunity to streptococcal infections is type-

 Strep throat is usually transmitted by droplets.

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figure 24.4

 Strep throat, caused by an erythrogenic toxin-

 starts general malaise and swelling of neck

 Symptoms include a red rash, high fever, and a

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 Diphtheria toxin produced by lysogenized C.

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figure 24.6

Vao day nghe bai nay di ban

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 minimal dissemination of the exotoxin in the

 Antitoxin - neutralize the toxin

 Antibiotics- Penicillin and Erythromycin can stop

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

• Small, pleomorphic (club-shaped), gram-positive

• Cells contain metachromatic granules

• Lipid-rich cell wall contains meso -diaminopimelic

infection of the middle ear, primarily in infants and

A. Symptoms - fever, pain in the ear, dulled hearing.

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figure 24.7

 Treated with broad-spectrum antibiotics

 Earache, or otitis media, can occur as a

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

1. clinical presentation of fever and pain, especially

2. otoscopic examination to see inflammation and/or fluid

• swelling and blockage

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 Any one of approximately 200 different viruses

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 Colds are most often transmitted by indirect

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

 Bacteria, viruses, and fungi cause

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera Figure 24.2

Adhere to ciliated epithelial cells

Damage to mucosal cells Act on neurons

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera