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24 Microbial Diseases of the RespiratorySystem

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

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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


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lower respiratory system

consists of the larynx, trachea, bronchial tubes,

and alveoli.

ciliary escalator

alveolar macrophages.

Respiratory mucus contains IgA antibodies.


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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.


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Upper Respiratory System

Upper respiratory normal microbiota may includepathogens

Figure 24.1


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Microbial Diseases of theUpper Respiratory System

Laryngitis: S. pneumoniae, S. pyogenes, viruses

Tonsillitis: S. pneumoniae, S. pyogenes, viruses

Sinusitis: Bacteria

Epiglottitis: H. influenzae Hib vaccine


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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.


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Streptococcal Pharyngitis (Strep

Throat) GAS- Streptococcus

pyogenes

Resistant to

phagocytosis Streptokinases lyse clots

Streptolysins arecytotoxic

Diagnosis by indirectagglutination/ EIA

Figure 24.3MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

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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.


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Throat) Rapid diagnosis is made by enzyme

immunoassays.

Penicillin is used to treat streptococcalpharyngitis.

Immunity to streptococcal infections is type-specific.

Strep throat is usually transmitted by droplets.


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Scarlet Fever

Streptococcus pyogenes

Pharyngitis

Erythrogenic toxin

produced bylysogenized S.

pyogenes by a phage.


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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.


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Diphtheria

Corynebacterium diphtheriae: Gram-positive rodpleomorphic club shape


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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)


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Diphtheria


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Diphtheria


Vao day nghe bai nay di ban

http://nhattruongquang.0catch.com

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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 thebloodstream.

Antitoxin - neutralize the toxin

Antibiotics- Penicillin and Erythromycin can stopgrowth of the bacteria.


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Diphtheria

Prevented by DTaP andTd vaccine (Diphtheriatoxoid)

Cutaneous diphtheria: Infected skin wound leads to

slow healing ulcer


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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 -diaminopimelicacid

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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.

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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


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Otitis Media

Treated with broad-spectrum antibioticsAmoxicillin

Incidence of S. pneumoniae reduced by vaccine


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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


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B. DIAGNOSIS

1

. clinical presentation of fever and pain, especially followingan URT infection such as a cold

2. otoscopic examination to see inflammation and/or fluid(pus); also loss of mobility with air pressure

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6.

swelling and blockage

cyclic pattern of damage discomfort - pressure and blocked nasal passages

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Common cold

Rhinoviruses (50%) Coronaviruses (15-20%)


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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


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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.


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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 specificviruses.


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MicrobialDiseases of the

Lower Respiratory System

Bacteria, viruses, and fungi cause

Bronchitis Bronchiolitis

Pneumonia


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Lower Respiratory System

The ciliary escalator keeps the lower respiratorysystem sterile.


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Pertussis (Whooping Cough)

Bordetella pertussis: Gram-negative coccobacillus

Capsule

Tracheal cytotoxin of cell

wall damaged ciliatedcells

Pertussis toxin producessystemic disease

Prevented by DTaPvaccine (acellularPertussis cell fragments)


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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

Epidemiology of Bordetella pertussis

Infection

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Whooping cough

Inhalation of aerosols

Adhere to ciliated epithelial cells

(FHA, Pili)

Toxin production

Damage to mucosal cells

(TCT, Ptx, Acase, LPS?)

Act on neurons

(Ptx, Acase, LPS)

Paroxysmal cough

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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

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Infants incapable of coughing produces irreversible brain

damage

Gasping of air in between coughs causes the whooping

sound( several times a day for 1-6 weeks)

Ciliary action is compromised

Mucus accumulate- desperate attempt to cough out

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.


Initial stage ofpertussis

resembles acold and iscalled thecatarrhal

stage.

Paroxysmal(second) stage

accumulationof mucus in the

trachea andbronchi causes

deep coughs

Convalescence(third) stage

can last for

months

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Clinical Progression of Pertussis

Most infectious, but

generally not yet

diagnosed

Inflammation of respiratory mucosal memb.

,or death

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Laboratory Culture, Prevention &

Treatment of Bordetella

Treatment with erythromycin

Nonmotile Fastidious and slow-growing

y Requires nicotinamide and charcoal, starch, blood, or albumin

y Requires prolonged growthy Isolated on modifiedBordet-Gengou agar

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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.


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TUBERCULOSIS

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Situationer

Leading causes of death world wide

Up to a half of worlds population infected,95% in developing countries

8 million people getTB every year

(WHO fact sheet 2007)

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Philippines ranks 4th for # ofTB cases worldwide,

highest # per head in SEA

2/3 of Filipinos withTB

(DOH, 2007)

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Rex Karl S. Teoxon, R.N, M.D 44

PTB

Mycobacterium tubercle, acid fast bacilli

Airborne/droplets Potts disease thoracolumbar

MilliaryTB kidney, liver, lungs

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Rex Karl S. Teoxon, R.N, M.D45

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Morphology

Mycobacterium tuberculosis

Thin straight rods, 0.4 x 3 m

Acid-fast organisms

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Mycobacterial cell wall components

Lipids (mycolic acids)

Proteins

Polysaccharides

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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

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0

SIGNS AND SYMPTOMS

Wt loss, night sweats, low fever, non productive to

productive cough, anorexia, Pleural effusion and

hypoxemia, cervical lymphadenopathy

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Tuberculosis

Mycobacteriumtuberculosis: Acid-fast rod;

transmitted from human

to human.

M. bovis:

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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

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Diagnosis

Sputum culture

Slow, 13 hour generation time, takesweeks

Acid-fast staining

Skin test (PPD)

DNA hybridization

PCR (16s rRNA)Bacteriophage

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PPD ID

macrophages in skin takeup Ag and deliver it to Tcells

T cells move to skin site,release lymphokines

activate macrophages and

in 48-72 hrs, skin becomesindurated

- > 10 mm is (+)

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DIAGNOSIS

Chest x ray - cavitary

lesionSputum exam

Sputum culture

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Stages of disease Primary infection

Asymptomatic to flu-like 3-5% develop TB Tubercle (granulomatous response)

Reactivation (active TB) Years later, 10% experience

LRTdisease (pneumonia) Disseminated miliary TB

Almost everywhere AIDS and antibiotic resistance

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Stages of pathogenesis

Encounter - respiratory droplet

Entry - direct inhalation into LRT(ID=10)

SPREAD - alveoli, but can spreadthroughout 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

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Tuberculosis

Tuberculosis is caused by Mycobacterium

tuberculosis.

Large amounts of lipids in the cell wall

account for the bacteriums acid-fastcharacteristic as well as its resistance to

dryingnd disinfectants.


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Tuberculosis

M. tuberculosis

may be ingested

by alveolar

macrophages; ifnot killed, the

bacteria

reproduce in the

macrophages.


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Tuberculosis Liquefaction of the caseous

lesion results in a

tuberculous cavity in which

M. tuberculosis can grow.


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Tuberculosis

New foci ofinfection can

develop when a

caseous lesion

ruptures andreleases bacteria

into blood or

lymph vessels;

this is calledmiliary

tuberculosis.


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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 setof antibiotics (isoniazid, ethambutol, rifampin) High mutation rate

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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.


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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)


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PPD Tuberculosis Skin Test Criteria

PPD = Purified Protein Derivative from M. tuberculosis

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Ch t X R f P ti t ith

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Chest X-Ray of Patient with

Active Pulmonary Tuberculosis

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Tuberculosis

Mycobacterium bovis

causes bovine tuberculosis

transmitted to humans by unpasteurized milk.

affect the bones or lymphatic system.

BCG vaccine -a live, avirulent culture ofM. bovis

M. avium-intracellulare complex infects patients in

the late stages of HIV


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Tuberculosis

Treatment of tuberculosis: Prolonged treatmentwith multiple antibiotics.

Vaccines: BCG, live, avirulentM. bovis; not widely

used inUnited States.


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Tuberculosis


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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

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MANAGEMENT

Follow-up* 2 wks after medications non communicable3 successive (-) sputum - non communicable

rifampicin - prophylactic

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CATEGORIES OF TB

category I (new PTB) - (+) sputum

category II (relapse)

category III (PTB case) - (-) sputum

TREATMENT:

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TREATMENT:

CATEGORY 1 -NEW PTB, (+) SPUTUM

GIVE RIPE 2 MONT

HS, MAINT

EN

AN

CE OF RI 4MONTHS

CATEGORY 2 - PREVIOUSLYTREATEDWITH

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 RESISTANTTO DRUGS GIVE ADDITIONAL

MONTH/S AS PRESCRIBED

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MDT side effects

r-orange urine

i-neuritis and hepatitis

p-hyperuricemia

e-impairment of vision

s-8th cranial nerve damage

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AFB SMEAR REPORTING GUIDELINE,DOH

NATIONALTUBERCULOSIS CONTROL PROGRAM (2001)

Emilio M. Ramirez, MD

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National Tuberculosis Control

Program (2001)

prevent transmission of tubercle bacilli to a

healthy person

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Goal: ReduceTB mortality and prevalence throughearly 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)

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Sputum Collection Schedule for

DIAGNOSIS

SPOT EARLY

MORNING

SPOT

Day

1

First specimen -

collected at the timeof consultation or assoon as TBsymptomatic isidentified.

Day

2

Second specimen

Collected in the morningby the TB symptomaticwhen he/she is due tosubmit the specimen tothe health center.

Third specimen

Collected at the timethe TB symptomaticcomes back to thehealth facility tosubmit the secondspecimen.

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Ideal sputum specimen?

MACROSCOPIC

- Yellowish

- Mucopurulent- Cheesy material

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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 sputumcollection within two weeks from the time of the

previous collection.

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Ideal sputum specimen?

MICROSCOPIC

- greater than 25

wbc/LPO, 5 wbc/OIO

- Presence of alveolar

macrophage, dust cells

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AFB STAINING

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DIRECT SMEAR EXAMINATION(Flow Chart)

SMEARINGSMEARINGSPREADING

DRYING

FIXATION

STAININGINITIAL STAINING

HEAT

IN

GWASHING

DECOLORIZATION

WASHING

COUNTER-STAINING

WASHING

DRYING

MICROSCOPIC OBSERVATION

RECORDING & REPORTING

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DIRECT SMEAR PREPARATION

LABELING THE SLIDES

Write down the

identification number ofthe sputum specimen on

the end of a clean glass

slide.

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SMEARING

SPREADING

With a coconut midrib, fish

out one (1) loopful ofpurulent, solid particles ofthe sputum.

Spread the sputum evenly

on the slide, approximately2 x 3 cm

in size.

G d S

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A Good Smear

Poor/too thick Good Poor/too thin

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SMEARING

DRYING

Allow the smear to drycompletely at room

temperature.Do not dry it under the sun orover the flame.

Place used midribs in a bottlewith alcohol and sandmixture or Lysol,

or in a plastic containers andburn them later.

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SMEARING

FIXATION

Fix the smear by passing it

through the flame of analcohol lamp 2 to 3 times,about 2-3 seconds each.

Heat the back of smeared

surface of the slide.Neverscorch the smear.

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STAINING

FIXATION

Fix the smear by passing it

through the flame of analcohol lamp 2 to 3 times,about 2-3 seconds each.

Heat the back of smeared

surface of the slide.Neverscorch the smear.

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STAINING

INITIAL STAINING

Arrange the slides on the

staining bridgeconsecutively.

Pour carbol fuchsin

solution covering thewhole surface of the slide.

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STAINING

HEATING OF THE SLIDE

Heat the slide using an

alcohol lamp or spirit cottonin a stick till steam comes offfrom the stain.

Do not boil and do not allow

the stain to dry. Leave it forfive minutes.

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STAINING

WASHING OF THESLIDE

Tilt the slide to drainoff excess stain.

Wash the staining

solution off with agentle stream ofrunning water.

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STAINING

DECOLOURIZATION

Tilt the slide to drain off

excess rinse water.

Cover the whole slide with3% hydrochloric acid-

ethanol and leave it untilsolution runs clear.

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Staining

WASHING OF THE SLIDE

Wash the slide with a

gentle stream of runningwater.

Tilt the slide to drain off

excess rinse water.

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Staining

COUNTERSTAINING

Pour 0.1% methylene blue to

cover the whole surface ofthe smear and leave for 5-10seconds.

Tilt the slide to drain offexcess methylene blue.

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Staining

WASHING AND DRYING

Wash the slide with a gentle

stream of running water.

Tilt and place the slide on theslide rack to dry in the air.

Dont place under the sun to

dry.

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SMEAR READING

PROPER SCANNING

Horizontal Scanning

Vertical Scanning

IMPROPER SCANNING

Zigzag Scanning

3 cm

AFB OBSERVATION

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AFB OBSERVATION

Single/parallel form

Clump form

Coccoid form

Scratches on the slide

MICROSCOPICOBSERVATIONOF AFB IN PROPERLY AND

O S S

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IMPROPERLY STAINED SMEAR

PROPER STAINING INSUFFICIENT HEATING

UNDERDECOLORIZED INTENSELY COUNTERSTAINED

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National Standard Reporting Scale (2001)

No AFB seen in 300 visual fields0

1-9 AFB/ 100 visual fields (x1000)+n

10-99 AFB/ 100 visual fields (x1000)1+

1-10 AFB/ OIF in at least 50 visual fields2+

>10 AFB/ OIF in at least 20 visual fields3+

INTERPRETATION OF LAB RESULTS

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INTERPRETATION OF LAB RESULTS

POSITIVE - if all or at least two of the three specimens

are positive

NEGATIVE - if all (3) specimensare negative

DOUBTFUL - if one of the three

specimens is positive(sputum examination

should be repeated)

Bacterial Pneumonias

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Bacterial Pneumonias

Typical pneumonia is caused by S. pneumoniae.

Atypical pneumonias are caused by other

microorganisms.

Lobar pneumonia

bronchopneumonia


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Pneumonias

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Pneumonias

Sign/ symptoms

High fever

DOB

Chest pain

Productive cough


Pneumomoccal Pneumonia

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Pneumomoccal Pneumonia

Streptococcuspneumoniae:Gram-positiveencapsulateddiplococci

Diagnosis is byculturingbacteria.

Penicillin

Fluoroquinolones

is drug of choice.


Pneumococcal pneumonia

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Pneumococcal pneumonia(Streptococcuspneumoniae)

Gram-positive diplococcus Encapsulated (>80 serotypes)

Susceptible population Elderly

Previou

sly ill

Phagocytic dysfunction (e.g., asplenic, sickle cell)

Also cause meningitis, otitismedia

Sensitive to optichin; autolysisby bile

Pneumococcal Pneumonia

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The bacteria can be

identified

alpha-hemolysins,

inhibition by optochin,

bile solubility

serological tests.


IdentificationIdentification

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114

Not optochin sensitive

optochin sensitive


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Symptoms

Fever

breathing difficulty

chest pain

rust-colored sputum.

A vaccine consists of

purified capsular materialfrom 23 serotypes ofS.

pneumoniae.



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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

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Haemophilus Influenzae Pneumonia

Gram-negative coccobacillus

Alcoholism, poor nutrition, cancer, or diabetes are

predisposing factors.

Second-generation cephalosporins


Mycoplasmal Pneumonia

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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



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M. pneumoniae producessmall fried-eggcolonies after twoweeks incubation on

enriched mediacontaining horse serumand yeast extract.

Diagnosis is by PCR orserological tests.


Atypical (walking) pneumonia Mycoplasma

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Atypical (walking) pneumonia Mycoplasmapneumonia

Lackspeptidoglycan F-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

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y p p g g

Legionellosis

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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

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L g / FLegionella 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 hil

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L. pneumophila

Legionellosis

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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)

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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



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s ttacos s (O t os s)

Commercial bird handlers are most susceptible to

this disease.

The bacteria are isolated in embryonated eggs,

mice, or cell culture; identification is based on FAstaining.

Tx:Tetracycline


Chlamydial Pneumonia

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y

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

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Q

Obligately parasitic, intracellular Coxiella burnetii

causes Q fever or X fever

The disease is usually transmitted to humans

through unpasteurized milk or inhalation ofaerosols in dairy barns, cattle tick bites

Laboratory diagnosis is made with the culture of

bacteria in embryonated eggs or cell culture.


Q Fever

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Q

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

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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

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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


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Disease Symptoms

Psittacosis Fever and headache

Q fever Chills and chest pain

Epiglottitis Inflamed, abscessed epiglottis

Melioidosis Delayed-onset pneumonia


Diagnostic

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g

Gram-positive cocci

Catalase-positive Staphylococcus aureus

Beta-hemolytic Streptococcus pyogenes

Alpha-hemolytic S. pneumoniae


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Gram-positive rods

Not acid-fast Corynebacterium diphtheriae

Acid-fast Mycobacterium tuberculosis

Gram-negative cocci Moraxella catarrhalis


a. Streptococcus pneumoniae

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b.Haemophilus influenzae -

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c. Moraxella catarrhalis -

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Gram negative rods

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Gram-negative rods

Aerobes

Coccobacilli Bordetella pertussisRods

Grow on nutrient agar Burkholderia 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

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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 inisolating and identifying viruses.


Respiratory Syncytial Virus

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(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, feverby bacterial infection


Influenza

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Hemagglutinin (H)spikes used for

attachment to host

cells.

Neuraminidase (N)spikes used to release

virus from cell.


Influenza

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Antigenic shift Changes in H andN 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

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A: Causes most epidemics, H3

N2, H1

N1, H2

N2

B: Moderate, local outbreaks

C: Mild disease


Influenza

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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

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146

Coronavirus

Severe acute respiratory syndrome

IP: 2-7 days

MOT: respiratory droplet/person to personcontact

RISK FACTORS

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147

history of recent travel to China, Hong Kong, orTaiwan or close contact w/ ill persons with a hx ofrecent travel to such areas, OR

Is employed in an occupation at particular risk forSARS exposure, i.e. healthcare worker with directpatient contact or a worker in a laboratory thatcontains live SARS, OR

Is part of a cluster of cases of atypical pneumonia

without an alternative diagnosis

SIGNS AND SYMPTOMS

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148

fever, chills, rigors, myalgia, headache, diarrhea,

sore throat, rhinorrhea

2-7 days after onset of illness - shortness of breath

and/or dry cough

DIAGNOSIS

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149

viral culture

PCR

serologic testing

Mgmt: supportive

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UpperRespiratory System

Common cold Coronaviruses Sneezing, excessivenasal secretions,

congestion

LowerRespiratory System

Viral pneumonia Several viruses Fever, shortness ofbreath, chest pains

Influenza Influenzavirus Chills, fever, headache,muscular pains

RSV Respiratorysyncytial virus Coughing, wheezing

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


FUNGAL DISEASES OF THE LOWER

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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

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Histoplasma capsulatum, dimorphic fungus


Histoplasmosis

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Resembles Tuberculosis

Histoplasma capsulatum causes a subclinical

respiratory infection that only occasionally

progresses to a severe, generalized disease.


Histoplasmosis

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Transmitted by airborne conidia from soil and thru bird

droppings Diagnosis by culturing fungus

Treatment: Amphotericin B or Itraconizole


Coccidioidomycosis

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Coccidioides immitis- dimorphic fungi


Coccidioidomycosis

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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 poornutrition, a progressive disease resembling

tuberculosis can result.


Coccidioidomycosis

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Transmitted by

airborne arthrospores

Diagnosis by

serological tests or

DNA probe

Treatment:

Amphotericin B

Also Ketoconazole,

Itraconazole


Pneumocystis Pneumonia

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Pneumocystis jiroveci(P.

carinii) is found in

healthy human lungs.

Pneumonia occurs in

newly infected infantsand

immunosuppressed

individuals.

Treatment:Timethoprim-

sulfamethoxazoleFigure 24.22aMICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

Pneumocystis Pneumonia

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P. jirovecicauses disease in immunosuppressed

patients.

Site - lining of alveoli

DOC Trimetophrim -Sulfamethoxazole


Pneumocystis

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Blastomycosis

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Blastomyces dermatitidis, dimorphic fungus

Found in soil

Can cause extensive tissue destruction, cutaneouslesions

Treatment: Amphotericin B


Blastomycosis (North American

Blastomycosis)

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Blastomycosis) The infection begins in the lungs and can spread

to cause extensive abscesses.


Other Fungi Involved in

Respiratory Disease

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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

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Aspergillus

Rhizopus

Mucor

respimicro

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