PLEUROPULMONARY

INFECTIONS
Ania Kurniawati PD, dr. Mkes
Bagian Mikrobiologi FK-UNJANI

PLEUROPULMONARY
INFECTIONS
Etiology:
Pyogenic cocci: Strept. Pneumoniae/Pneumococcus
Strept. Pyogenes
Staph. Aureus
Gram negative: Klebsiella pneumoniae
rod
Escherichia coli
Proteus
Haemophilus influenzae
Pseudomonas aeruginosa
atypical
Mycoplasma pneumoniae
pneumonia Legionella pneumophila
Pneumococcus causing 80% of all
bacterialpneumonia

Pneumococcal Pneumonia
General characteristic `Strept. pneumonia
is a gram positive, shaped diplococcus
is differentiated from other streptococci by:
sensitivity

to optochin; bile
fermentation of inulin
possesses a type specific polysacharide capsule
with more than 80 different antigenic types
is part of the normal oropharynyeal flora in 4070% of human beings

IDENTIFIKASI GENUS SREPTOCOCCUS

Bahan
Pemeriksaan
Sediaan langsung
LAD, 24 jam,
(Gram)
37C
Tes Katalase : (-)
Hari 2
Hari
1

Tipe
hemolisis
Hari 3

(alpha)
S.pneumonia
e
-Tes Optokhin (+)

(Beta)
S.
hemolyticus /
S.viridans

-Tes Optokhin (-)

-Tes Inulin (+)

-Tes Inulin (-)

-Tes Klrtn empedu

-Tes Klrtn empedu

Tes
basitrasi
n
Sensitif
Grup A

(Gamma)
Tidak ada
tes khusus

Pathogenesis & Pathology :

is probably do not to direct inhalation of the

organism into the lung but to aspiration of upper

respiratory secretions
aspiration of only small quantity can infect the lung
seldom occurs as a primary infections
is uncommon among healthy people
75% of patient with pneumococcal pneumonia have
underlying disease ( infants, elderly, immuno
suppressed person & chronic alcoholic are most
vulnerable )

Pathogenesis & Pathology :

Is likely to occur in people who handle upper

respiratory secretion poorly:

increased volume of secretion the to viral
infection
impaired laryngeal reflexes ( coma, sleep )
pneumonia is likely to occur in patient whose

pulmonary antibacterial defenses are impaired:

COPD ( Chronic obstructive pulmonary
disease)
CHF ( Congestive Heart Failure )

Clinical Manifestations
prodromal symptoms: rhinorrhea; pharyaqitis; cough
abrupt occurrence of fever ( 1020 F ) pleuritic chest

pain, chills.
the sputum is typically rusty in color do to
alveolar hemorrhage
necrosis of the lung tissue rarely occur pneumococcus do not posses necrotizing extracellural
enzyme
destruction of lung tissue by leucogtic proteases is
apparently prevented by protease inhibitor
-1anti trypsin
-2 macro globalin

Diagnosis
Confirmation of the etiologic agent may require

examination of several type of specimens

blood: of patient with pneumococcal pneumonia have
demonstrable bacteremia
sputum: transtracheal aspiration
bronchoscopy
aspirated directly from the lung
expectorated
pleural fluid
control:

treatment: penicillin
prevention: Polyvalent vaccine

Streptococcus Pyogenes
Pneumonia (group A - hemol Strep.)
Attribute of Pathogenicity

Possesses M prot, a potent virulent factor

fimbria.
Has a nonantigenic, antiphagocytic hyaluronic
acid capsule.
Erythrogenic toxins is produced by lysogenic
strain.
Produces two hemolysin S and O.
Possesses multiple enzyme system.

Clinical Disease
1. Streptococcal pharyngitis
2. Scarlet fever
3. Post infectious disease :
- rheumatic fever
- GNA
4. Skin infection : impetigo, cellullitis,
erisipelas,
fascitis.

Streptococcus Pyogenes
Pneumonia
less than 5% of bacterial pneumonia

as complications of viral infections

Clinical manifestations:

- shaking chills, fever, pleura, chest pain

- pleura effusion ( 30-50% )
Diagnosis:

isolation of Strept. pyogenes from blood or pleural fluid

Treatment: Penicillin, Erythomycin

Staphylococcal
Pneumonia
A. General caracteristic of S. aureus
Gram (+), cluster-forming coccus
Nonmotile, nonsporeforming facultative

anaerobe
Fermentation of glucose produces mainly
lactic acid
Ferments mannitol (distinguishes from
S.epidermidis)

Catalase (+)
Coagulase (+)
Normal flora of human : nasal

passages, skin, and mucous

membranes
Pathogen of human : suppurative
infections, food poisoning, toxic
shock syndrome

B. Clasification
1. Staph. are catalase (+) whereas
Strept.
()
2. S. aureus (-hemolytic and coagulase
(+) is distinguished from the coagulase
(-) Staph., which are nonhemolytic.

C. Virulens factors :
1. Surface protein
2. Invasins (leukosidin, kinase, hyaluronidase)
3. Surface factors (carotenoids, catalase

production)
4. Immunological disguises (Protein A,
coagulase, clotting factor)
5. Membrane-damaging toxins (hemolysins,
leukotoxin, leukocidin)
6. Exotoxins (TSST, ExfoliatinToksin)

Virulence determinants of S.aureus

Staphylococcal Pneumonia
occurs in:
among hospitalized patient
person who inject unsterile materials into their vein
Clinical manifestations:

- shaking chills, high fever

- pleura effusion, cavitation
Complication:
abscess, empyema
pyopneumo thorax
destroyed lung
Diagnosis: culture from: blood, pleura fluid
Treatment: Methicillin, oxacillin, Vancomcin

Common Gram Negative Bacillary

pneumonias

Etiology: Gram negative bacilli

Klebsiella pneumonia
community
Escherichia coli
acquired
Proteus
pneumonia
Haemophilus influenza
Pseudomonas aeruginosa
acquired
pneumonia

hospital

Pathogenesis & Pathology:

is uncommon among healthy individual
10% of bacterial pneumonia due to these organism
affected patient with serious underlying disease
result from aspiration of upper respiratory secretion
colonization of gram.negative bacilli in the oropharynx only 2-6% of healthy people approaching
50% in patient with acute or chronic illness

Clinical manifestation
usually acute infections
common symptoms:

chills, fever, cough productive of purulent or

bloody sputum, chest pain
K.pneumonia mucoid sputum + blood
hypotension, shock, delirium
pleural effusion, empyema, cavition of the

lung

Diagnosis:
culture from blood ( 25% positive ), pleural

fluid, transtracheal aspiration, bronchoscopy

Complication & sequelae:

abuot 50%

die

the cause of death are multifactorial:

the underlying disease; shock; lung necrosis;
acute
respiration failure

Treatment:

- piperacilin & amikacin

Pneumonia due to H.influenza

occur predominantly among children < 3 years
may also occurs in adults
are lobar or diffuse broncho pneumonia

both types occur mainly in patient with serious

illness
chronic obstructive lung disease
similar to pneumococcal pneumonia:
the ouset of chills; pleuritic chest pain; purulent sputum

pleura effusion is common

cavitation may develop, but is not common

Diagnosis
smears of sputum: gram-negative bacilli & PMN
culture: require special attention

Chocolate agar with X & V factor require for growth

& primary isolation of H.influenza

demonstration of capsular antigen by

counterimmuno electrophoresis
Treatment:

ampicillin
chloramphenicol

Mycoplasma pneumonia
Etiology: mycoplasma pneumonia
formerly: Eaton agent
PPLO
are the smallest free living organism capable of
replicating in cell.free-media
they lack of cell wall

= L from bacteria

may be coccobacillary or filamentous

require cholesterol
is a mucous membrane pathogen that does not invade
tissues

Mycoplasma pneumonia
is an acute infection of the lower respiration tract

that exhibits the following characteristic :

1. Usually involves the dependent lobes of the lung
2. Last 14-21 days in untreated cases
3. Stimulates formation of specific antibodies
during
convalesce
4. Stimulates the production of cold aglutinin
5. Respond to treatment with erythromycin
6. Almost heals without sequelae

Pathogenesis & Pathology

spreads by in infection droplets from person to

person
M.pneumoniae attaches to neuraminic acid

residues on cilliated epithelial cells

stops cilliary activity destruction of cilia & cell

surfaces
attachment may be mediated by glycoprotein

in the membrane of the mycoplasma

the infection is superficial intracellular

organisms have not been observed by electron

microscopy

Clinical Manifestation:
cause primary atypical pneumonia
slow outset of fever; headache, malaise, not

productive cough
over several weeks; interstitial or broncho

pneumonic pneumonia develops

ro; reveals segmental lobar pneumonia
has its highest incidence in children 5-15 years
account of all cases of pneumonia in teenagers

Attribute of pathogenicity:
1. posses a LPS, different from that of

gram.negative bacteria
2. has a glycolipid traction that may play

role in autoimmune-like reaction

3. release hydrogen peroxide, which may

damage epithelial cells

Laboratory Diagnosis:
clinical specimens includes:
nasopharyngeal secretion
acute & convalescence sera
CFT
cold aglutinin reaction
culture is performed on PPLO agar

colonies not form for 2-3 weeks

exhibits a characteristic fried egg appearance
giemsa stain of culture organism reveals small
pleumorphic bacteria

DNA probe are under development

Treatment: erythromycin

tetracycline

Legionellosis = legionnairs`
disease & Pontiac fever
is an acut bacterial infections of humans
caused by member of the genus legionela:

L.pneumophila; L.micdadei; L.bozemanii

e.t.c (+ 10 sps)

1. legionnairs` disease: a multisystem

illness characterized by pneumonia & a high

case fatality ratio
2. Pontiac fever: a non-pneumonic, self
limited acute nonfatal, febrile illness
occurs both sporadically and in epidemic

Etiology:
genus legionella are faintly staining; thin
pleomorphic gram negative bacilli
do not grow on most commonly used
bacteriologic media
can be stained with:

wolbach modification of giemsa stain or

modification of the dierterle silver

impregnation stain

 Is a facultative intracellular parasite in tissue

these organism are typically found within

macrophages or free in the alveoli
is catalase positive, weakly oxydase positive
the organisms have been isolated from:

respiratory secretion; pleural fluid; lung tissue

water within heat rejection systems ( cooling

towers; evaporate condensers

rivers, lakes, ponds
shower heads

Attributes of pathogenicity
grow intra cellular
produce : cytotoxine
-lactamase
endotoxin

Clinical Manifestations:
Legionairs` disease:
is acquired by innhalation of organism from
environmental sources
predominantly in middle age & elder men is
most
common in smokers in the present of an organ
transplant T-cell defect & chronic lung disease
has abroad range of manifestations from a mild
to
fulminant multisystem disease

Incubation periode 2-10 days ( x : 5,5 days )

prodrome: malaise, diffuse myalgias, headache,

fever, rigors

cough, dyspnea, chest pain

diarhea ( in 40% of the patients )

hematuria & protein uria

is not transmitted by person to person contact

case fatality rate 10-20% death usually is result

of pulmonary insufficiency of shock

Clinical Manifestations:

Pontiac fever
is an acute; self limited, febrile illness
incubation periode: 5-66 hours ( x : 36 h )
starts abruptly:
diffuse myalgia, headache, fever, tachipneu;
tachicardia

chest x-rays do not reveal pulmonary infiltrate

Diagnosis
definitive diagnosis requires isolation of the organism
from clinical specimens
is often diagnosis by direct fluorescent antibody
staining or by demonstration of dieterle` silver stain
may be grown and identified on buffered charcoal
yeast extract agar ( CYE agar )
may also be identified by an increase in antibody titer
Treatment: erythromycin
rifampin ( immunocompromised patient)
Prevention: decotaminated of cooling towers;
shower head; rebulicer with hyperchloriration
desinfectants or heat