Pleuropulmonary Infections r4q1w

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) 37C 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

ages, 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  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

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

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prodrome: malaise, diffuse myalgias, headache, fever, rigors

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cough, dyspnea, chest pain

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diarhea ( in 40% of the patients )

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hematuria & protein uria

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is not transmitted by person to person

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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