Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
Influenza
Otitis
Sinusitis
Laringitis
Bronkhitis
Pneumonia
Tuberkulosis paru
BAKTERI PENYEBAB INFEKSI
SALURAN NAFAS
S. aureus
S. pyogenes
S. pneumoniae
C. diphteriae
N. gonorrhoeae
N. meningitidis
H. influenzae
K. pneumoniae
M. tuberculosis
Mycoplasma pneumoniae
Chlamydia psittaci
B. pertusis
P. aeruginosa
STAPHYLOCOCCUS
Morfologi sel
Bentuk bulat
Tersusun: bergerombol / tersebar / dua-dua / tetrat
Tidak membentuk spora
Morfologi koloni
Bahan pemeriksaan
Cat Gram
Staphylococcus Streptococcus
Staphylococcus
I. Cat Gram
II. Katalase
III. Koagulase
(+) (-)
S. aureus Non SA
Novobiosin
S
(S. epidermidis) R
(S.saprophyticus)
Laboratory Diagnosis: Specimen
Collection and Handling
Samples must be taken from the actual site of
infection
Prevent delay in transport of collected material
from infected sites
Transport in appropriate collection device that
would prevent drying and minimize growth of
contaminating organisms
Identification of Staphylococcus in
Samples
Frequently isolated from pus, tissue
exudates, sputum, urine, and blood
Cultivation, catalase, biochemical testing,
coagulase
Laboratory Diagnosis:
Direct Smear Examination
Microscopic Examination
Gram-positive cocci
pairs and clusters Insert Figure 10-1
Numerous
polymorphonuclear cells
(PMNs)
Laboratory Diagnosis:
Cultural Characteristics
Colony morphology
Smooth, butyrous,
white to yellow,
creamy
Grow well @ 18-24
hours
S. aureus may produce
hemolysis on blood
agar
S. aureus
Laboratory Diagnosis: Cultural
Characteristics
Coagulase-negative
staphylococci
Smooth, creamy, white
Small-to medium-
sized, usually non-
hemolytic
S. saprophyticus
Smooth, creamy, may
produce a yellow
pigment
Identification Tests: Catalase
Principle: tests for enzyme catalase
2 H2O2 2 H2O + O2
Bakteremia
Bila terjadi bakteremia
Endokarditis
Osteomilitis hematogen akut
Meningitis
Infeksi pulmo
TERAPI
Antibiotika gol. Penisilin dan yang lain.
Penisilin yang -laktamase : Sefalosporin, Vankomisin,
Metisilin (metilisin : S. aureus 10-20%; S. epidermisis 75%)
Staphylococcus sudah banyak yang resisten terhadap
Tetrasiklin, Penisilin, Eritromisin
Other infections
Respiratory (less often)
pneumonia
Bacteremia
Osteomyelitis/arthritis
Endocarditis
Pseudomembranous enterocolitis
Other Staphylococci
Coagulase-negative staphylococcus; frequently
involved in nosocomial and opportunistic infections
S. epidermidis lives on skin and mucous
membranes; endocarditis, bacteremia, UTI
S. hominis lives around apocrine sweat glands
S. capitis live on scalp, face, external ear
All 3 may cause wound infections by penetrating
through broken skin.
S. saprophyticus infrequently lives on skin,
intestine, vagina; UTI
Clinical Concerns and Treatment
95% have penicillinase and are
resistant to penicillin and ampicillin.
MRSA methicillin-resistant S. aureus
carry multiple resistance
Abscesses have to be surgically
perforated.
Systemic infections require intensive
lengthy therapy.
Prevention of Staphylococcal Infections
Universal precautions by healthcare
providers to prevent nosocomial infections
Hygiene and cleansing
Coagulase-Negative Staphylococci
Habitat: skin and mucous membranes
Common human isolates
S. epidermidis
S. saprophyticus
S. haemolyticus
Coagulase-Negative Staphylococci:
Staphylococcus epidermidis
Virulence factor: slime Helps to prevent
phagocytosis
Mode of transmission: implantation of medical
devices such as catheters, shunts, and prosthetic
devices
Infections are acquired nosocomially
Serious infections among immunosuppressed
patients may occur
Coagulase-Negative Staphylococci:
Staphylococcus saprophyticus
Habitat: skin and mucosal membranes
of the genitourinary tract
Common cause of urinary tract
infections in young, sexually active
females
When present in urine cultures, may
be found in low numbers, but
significant
STREPTOCOCCUS
Morfologi dan Identifikasi
Streptococcus terdiri dari 20 spesies, berdasarkan :
* Karakteristik koloni
* Tipe hemolisa pada agar darah
* Reaksi biokimia
* Reaksi spesifik antigen pada dinding sel
Sifat-sifat
Bakteri berbentuk bulat
bersifat Gram positip
tersusun berderet seperti rantai
sebagian bersifat fakultatif anaerob
Streptococcus
Hemolisa
Bile soluble Basitrasin
Bile esculin
(0,04 U)
(-) (+)
Lisis (-) S
(S. viridans) (grup D)
(S. pneumoniae)
(Strep. Grup A)
R
optochin
NaCl 6, 5%
S
(S. pneumoniae) (+) (-)
R
Enterococci) Non
(Strep. Non pnm)
Gram stain of Streptococcus pyogenes in a clinical specimen
Colonies of Streptococcus pyogenes on blood agar exhibiting beta (clear)
hemolysis
Sheep blood agar with colonies of beta-hemolytic group A
streptococcus
Hemolysis on blood agar
The type of hemolytic reaction displayed on blood
agar has long been used to classify the
streptococci.
Beta -hemolysis is associated with complete lysis of
red cells surrounding the colony,
whereas alpha-hemolysis is a partial or "green"
hemolysis associated with reduction of red cell
hemoglobin.
Nonhemolytic colonies have been termed gamma-
hemolytic.
1. KARBOHIDRAT
Sebagai dasar penggolongan grup (dari gula amino)
Grup A : ramnosa asetil glukosamin
B : ramnosa glukosamin polisakarida
C : ramnosa-N asetilgalaktosamin
D : gliserol asam teikoat mengandung d-alanin
dan glukosa
F : glukopiranosil-N-asetilgalaktosamin
2. SUBSTANSI T
tidak berhubungan dengan virulensi
tidak tahan asam dan panas.
Antigen permukaan yang lain protein R
3. PROTEIN M
* Faktor virulensi utama pada S. pyogenes grup A.
* lebih dari 80 tipe protein M.
* ada 2 kelas utama protein M (I dan II)
Antibodi terhadap M I bereaksi silang dengan
jaringan otot jantung merupakan determinan
virulensi pada demam rematik
4. NUKLEOPROTEIN
Diperoleh dengan mengekstraksi Streptococcus
dengan basa lemah.
Ekstrak tsb juga mengandung substansi P
Patogenesis dan Penyakit
A. Penyakit yang disebabkan oleh invasi S. pyogenes
infeksi cepat menyebar melalui saluran limfa darah
1. Erysipelas (bila infeksi melalui kulit): pembengkakan kecoklatan
dan cepat menyebar
2. Puerperal fever (masuk uterus setelah melahirkan
endometritis septicemia
3. Sepsis karena infeksi streptococcus pada luka / post operasi
2. Demam rematik
* Terjadi kerusakan pada klep dan otot jantung
* Antigen membran strain grup A otot jantung manusia
Electron micrographs of Streptococcus pyogenes
Production of Disease
Pneumococci produce disease through their ability to multiply in the tissues. They produce
no toxins of significance. The virulence of the organism is a function of its capsule, which
prevents or delays ingestion by phagocytes. A serum that contains antibodies against the
type-specific polysaccharide protects against infection. If such a serum is absorbed with the
type-specific polysaccharide, it loses its protective power.
Predisposing factor :
(1) Viral and other respiratory tract infections that damage surface cells; abnormal accumulations of
mucus (eg, allergy), which protect pneumococci from phagocytosis; bronchial obstruction (eg,
atelectasis); and respiratory tract injury due to irritants disturbing its mucociliary function.
(2) Alcohol or drug intoxication, which depresses phagocytic activity, depresses the cough reflex, and
facilitates aspiration of foreign material.
(3) Abnormal circulatory dynamics (eg, pulmonary congestion, heart failure).
(4) Other mechanisms, eg, malnutrition, general debility, sickle cell anemia, hyposplenism, nephrosis,
or complement deficiency.
Pathology
Pneumococcal infection causes a fibrinous edema
fluid into the alveoli, followed by red cells and
leukocytes, which results in consolidation of
portions of the lung. Many pneumococci are
found throughout this exudate, and they may
reach the bloodstream via the lymphatic drainage
of the lungs.
mononuclear cells actively phagocytose the
debris, and this liquid phase is gradually
reabsorbed. The pneumococci are taken up by
phagocytes and digested intracellularly.
Diagnostic Laboratory Tests
Blood is drawn for culture; CSF and sputum are collected for
demonstration of pneumococci by smear and culture. Serum
antibody tests are impractical. Sputum may be examined in
several ways.
Stained Smears
A Gram-stained film of rusty-red sputum shows typical organisms,
many polymorphonuclear neutrophils, and many red cells.
Capsule Swelling Tests
Fresh emulsified sputum mixed with antiserum causes capsule swelling
(the quellung reaction) for identification of pneumococci.
Culture
The culture is created by sputum cultured on blood agar and incubated
in CO2 or a candle jar. A blood culture is also taken.
Immunity
Immunity to infection with pneumococci is type-specific and depends
both on antibodies to capsular polysaccharide and on intact phagocytic
function. Vaccines can induce production of antibodies to capsular
polysaccharides
Treatment, prevention, control
Since pneumococci are sensitive to many antimicrobial
drugs, early treatment usually results in rapid recovery,
Penicillin G is the drug of choice, others : vancomycin.
Epidemiology,
Pneumococcal pneumonia accounts for about 60% of all
bacterial pneumonias, the healthy carrier is more important in
disseminating pneumococci than the sick patient.
It is possible to immunize individuals with type-specific
polysaccharides. Such vaccines can probably provide 90%
protection against bacteremic pneumonia. A polysaccharide
vaccine containing 23 types is licensed in the United States.
This vaccine is appropriate for elderly, debilitated, or
immunosuppressed individuals.
Mycobacterium tuberculosis
MDR-TB a serious
global health threat
Calcification
Ca++ salts deposited
Cavity formation
Center liquefies & empties into bronchi
PPD Tuberculosis Skin Test Criteria
KULTUR
Media Middlebrook padat / cair
Lowenstein-Jensen (media telur, + hijau malasit)
Tumbuh lambat (doubling time >24 jam)
Gol saprofit tumbuh cepat, pada 22-33oC ,
kurang tahan asam, pigmen lebih banyak
Dinding sel hidrofobik tumbuh menggerombol
Tahan kekeringan
DIAGNOSIS
1. Evidence of infection
a. Chest x-ray - hilar lymphadenopathy
calcification of primary focus/LN
b. Delayed hypersensitivity response to purified protein derivative
(PPD) MANTOUX /HEAF TEST
2. Evidence of active disease
a. Sputum for AFB using Ziehl-Neelsen technique
positive
3. Evidence of active disease
a. Indirect evidence of infection (Mantoux)
b. Direct evidence of infection PCR / culture
c. Histo-pathological evidence
Diagnosis of Tuberculosis
Acid fast staining
Eight Week Growth of Mycobacterium
tuberculosis on Lowenstein-Jensen Agar
KOMPONEN DINDING SEL
LIPID
asam mikolat
Kompleks asam mikolat + dipeptida muramil (dari
peptidoglikan) terbentuknya granuloma
wax
fosfolipid menginduksi nekrosis kaseasi
cord factor (trehalose-6,6-dimikolat) fungsi:
menghambat migrasi leukosit
granuloma kronis
sebagai ajuvan
PROTEIN: protein / protein-wax reaksi tuberkulin
POLISAKARIDA: dapat bereaksi dengan antibodi penderita
Lipid-Rich Cell Wall of Mycobacterium
Mycolic acids
BCG
AIDS
patients
Pathogenesis
Inhaled aerosols
Engulfed by alveolar macrophages
Bacilli replicate
Macrophages die
Infected macrophages migrate local lymph nodes
Develop Ghons focus Primary complex
Cell mediated immune response
Primary complex
Asymptomatic
HEALS
1 1 Primary complex
Asymptomatic
HEALS
2
3
Acute pulmonary disease REACTIVATION
Systemic spread Post-primary
Aymptomatic /symptomatic tuberculosis
TIPE LESI
1. Eksudatif (tes tuberkulin dapat positip)
Terjadi inflamasi akut pada jaringan paru (pneumonia)
eksudat diabsorbsi nekrosa
berkembang tipe produktif
2. Produktif
Bila berkembang granuloma kronis, terdiri:
Sel giant multi nukleus berisi bakteri dibagian tengah
dikelilingi lapisan epitel
Lapisan terluar: fibroblas, limfosit, monosit
bagian ini berkembang ditengah terjadi nekrosis
kaseasi (lesi ini disebut TUBERKEL)
Tuberkel pecah ke bronkus terjadi kaviti (penyembuhan
oleh fibroblas /
kalsifikasi)
PENYEBARAN BAKTERI DI DALAM INANG
PERTUMBUHAN INTRASELULER
Bakteri dalam sel monosit, retikuloendotelial, sel giant
menyebabkan:
kesulitan pengobatan
infeksi persisten
Granulomas: organized aggregates of immune cells that surround
foci of infected tissues; limits further dissemination of M.
tuberculosis
Diagram
of a
Granuloma
NOTE: ultimately a
fibrin layer develops
around granuloma
(fibrosis), further
walling off the
lesion.
Typical progression
in pulmonary TB
involves caseation,
calcification and
cavity formation.
Infection of M. tuberculosis: three
stages
Risk Factors for Tuberculosis
Congregate settings (prisons)
Overall health/immune system status
Poverty and unemployment
Homelessness
Alcoholism and drug abuse
HIV coinfection
Steroid (immunosuppressive use)
Genetic predisposition?
Strain virulence?
OBAT ANTI TUBERKULOSIS
Mekanisme aksi
INH (isoniasid) menghambat biosintesa asam mikolat
Rifampisin menghambat awal sintesa RNA
Etambutol menghambat penempatan asam mikolat
Gol. Aminoglikosida menghambat sintesa protein
Gol. Quinolon menghambat replikasi DNA
Tuberculosis Control
Priority of TB control is to identify and treat
infected patients (active or latent)
Successful cure of infectious patients will reduce
transmission
Patients with active infection become
noninfectious within two weeks of starting
treatment; latent????
Successful treatment of active infection takes 6
months (DOTS); latent???
Need to diagnose and treat latent infection
BORDOTELLA PERTUSIS
Sifat-sifat :
Obligat aerob, batang pendek, Gram negatif
Memfermentasi glukosa dan laktosa asam, tanpa gas
Tidak memerlukan faktor X dan V
Pemeriksaan lab.:
1. Direct Fluorescent Antibody (FA) test
2. Kultur
3. Serologi dapat dilihat setelah minggui ke 3
Imunitas :
Terbentuk antibodi yang mencegah
perlekatan bakteri pada sel epitel saluran
nafas
Patogenesis :
H. influenzae tidak berkapsul flora normal saluran.
H. influenzae tipe b infeksi supurativ saluran nafas
(sinusitis, Laringotrakheitis, otitis)
pada anak kecil meningitis
Pada beberapa orang > 3-5 tahun darahnya bersifat
bakterisidal terhadap H. influenzae
H. influenzae sering menyebabkan meningitis
terutama pada anak-anak. Di AS 10.000/ tahun
93% oleh H. influenzae sertipe b, biotipe 1.
Spesies lain :
H. haemolyticus infeksi saluran nafas atas
H. parainfluenzae endokarditis
H. aegypticus konjungtivitis
H. vaginalis (Corynebacterium vaginalis) vaginitis
H. ducreyi menyebabkan chancroid (pembengkakan
kelenjar limfa pada genital)