Transcript Prezentace aplikace PowerPoint

STREPTOCOCCI
Streptococci
- facultative anaerobe
- Gram-positive
- chains or pairs
- catalase negative (staphylococci are catalase positive)
Streptococcus in chains
Streptococcus pneumoniae (diplococcus).
Groups of Streptococci
• Lancefield groups A-H, K-V
- rapid identification of many streptococcal pathogens
Hemolysis reaction - sheep blood agar
. Hemolysis alpha
– partial hemolysis
• green color
• Hemolysis beta
– complete clearing
– A and B
• Hemolysis gamma
– no lysis
Streptococcus pyogenes
Streptococcus pyogenes (Group A streptococcus)
suppurative infections
-Gram-positive, nonmotile, nonsporeforming coccus that occurs in chains or
in pairs of cells.
-Individual cells are round-to-ovoid cocci, 0.6-1.0 micrometer
in diameter (Figure 1).
-The metabolism of S. pyogenes is fermentative; the organism is a catalasenegative (facultative anaerobe)
Requires enriched medium containing blood in order to grow.
Group A streptococci typically have a capsule composed of hyaluronic acid
and exhibit beta (clear) hemolysis on blood agar.
Figure 1. Streptococcus pyogenes.
Virulence factors
Virulence factors of Group A streptococci include:
•M protein - inhibit phagocytosis, type specific, virulent strains,
- binds Fc end of IgG and IgA (masking)
•Hyaluronic acid capsule - inhibit phagocytosis
•Protein F - binds fibronectin (host cell protein)
•Lipoteichoic acid – adherence
•Invasins: streptokinase, streptodornase (DNase B), hyaluronidase
•Streptolysins: streptolysin S and O - lysis of Ery, Leu
•Exotoxins: pyrogenic ( = erythrogenic) toxin (superAg – cytokines)
- rash of scarlet fever
- systemic toxic shock syndrome.
Virulence factors
•Invasins: streptokinase, streptodornase (DNase B),
hyaluronidase
•Streptolysins: streptolysin S and O (ASLO test) - lysis of
Ery, Leu, Tr
•Exotoxins: pyrogenic ( = erythrogenic) toxin (superAg
– cytokines)
- rash of scarlet fever
- systemic toxic shock syndrome.
C5a peptidase -  recruiting and activation of phagocytes
Frequency
Streptococcus pyogenes is one of the most frequent pathogens of humans.
It is estimated that between 5-15% of normal individuals harbor the
bacterium, usually in the respiratory tract, without signs of disease.
As normal flora, S. pyogenes can infect when defenses are compromised or
when the organisms are able to penetrate the constitutive defenses.
When the bacteria are introduced or transmitted to vulnerable tissues, a
variety of types of suppurative infections (pus) can occur.
• Puerperal fever (sepsis after childbirth)
• Pharyngitis (strep throat)
• Scarlet fever (rash) – antibiotic therapy
• Impetigo (infection of the superficial layers of the skin)
• Cellulitis (infection of the deep layers of the skin).
• Erysipelas (a form of cellulitis accompanied by fever and
systemic toxicity) is less common today.
• Pharyngitis (strep throat)
•SIGNS AND SYMPTOMS OF SCARLET FEVER
•Sudden fever with sore throat.
•Flushed face with circumoral pallor.
•Tonsils - edematous, erythematous, and covered with an
exudates.
•Petechiae on the soft palate.
•Anterior cervical lymphadenopathy.
•On day 1 or 2, a white strawberry tongue.
•By day 4 or 5, a raspberry tongue.
•The body rash appears 12-24 hours after onset of illness.
Impetigo (isolated pustules)
•Isolated pustules that rupture and become crusted
•Incidence in children
•Probable mode of spread is contact
Penicillin preferred for treatment
Erysipelas (reddish patches)
•Infection of the dermal layer
•Reddish patches with raised margins
•Infection often begins on the face
•Often preceded by streptococcal pharyngitis
•High fever
Invasive group A beta-hemolytic streptococci
cause severe and rapid tissue destruction.
•Cellulitis - destruction of solid tissue
•Myositis - destruction of muscle
•Necrotizing Fascititis - destruction of fascia
(connective tissue covering of muscle)
Necrotizing Fascititis
Patients may also develop immune-mediated post-streptococcal
sequelae:
• acute rheumatic fever
• acute glomerulonephritis
Group B Streptococci
Group B Streptococci
Streptococcus agalactiae
Diseases:
- Neonatal infections (meningitis, pneumonia, bacteremia)
- Urinary tract infection, amnionitis, endometritis
- Wound infections
- Pneumonia
- Bacteremia, becteriemia
Epidemiology
- lower GIT, GUIT
- transient vaginal carriage – risk of neonatal colonization
- early - onset: bacteremia, pneumonia or meningitis –
neurological sequelae
- late - onset
Physiology and structure
• Gram-positive cocci
• short chains in specimens
• buttery-appearing colonies larger than group A
streptococci colonies
• narrow zone of beta-hemolysis (alpha or gamma rare strains)
• serotypes - epidemiology
Enzymes
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DNases
hyaluronidase
neuraminidase
proteases
hippurase
hemolysins
Detection of enzymes is important in identifying of the
organism.
Clinical Syndromes I
• Early Onset Neonatal Disease
• bacteremia
• pneumonia or meningitis
• mortality: < 5%
• Neurological sequelae: blindness, deafness, mental
retardation
Clinical Syndromes II
Late-Onset Neonatal Disease
• Bacteremia with meningitis
• Neurological complications
Infection in Pregnant Women
• Complications are rare
Infections in Men and Non-pregnant Women
• Older persons
Lab. diagnosis
• Ag detection – rapid detection of group B streptococcal
infection in neonates,
• Culture - large colonies,
- beta-hemolysis may be difficult to detect
- selective medium with ATB
• Identification: CAMP positive, hydrolysis of hippurate
Definitively identified by the demonstration
of the group-specific carbohydrates
Treatment, Prevention and
Control
• Susceptible to penicillin PNC
• High MIC – need 10 times higher concentrations than that
needed to inhibit group A streptococci.
• Tolerance to PNC (inhibition not killing)
• Serious infections - combination of PNC and aminoglycosides
• Vancomycin
• Resistance to erythromycin and tetracycline
• Prevention - intrapartum PNC
Other beta-hemolytic
Streptococci
Streptococcus equisimilis
• Cultivation. large colonies, large zone of beta hemolysis
• Diseases - like group A streptococci (pharingitis,
glomerulonephritis but not rheumatic fever)
Streptococcus anginosus
• Cultivation - smaller colonies, beta-hemolysis (narrow
zone)
• Epidemiology - oropharinx, GIT, GUIT – produce
diseases in which absces formation is prominent feature
• Diseases: abscess
VIRIDANS
STREPTOCOCCI
S. mutans, S. sanguis
• Cultivation – complex media (blood, vitamines)
- alfa or gamma hemolytic
• Epidemiology – oropharynx, GIT, GUIT
• Diseases
- Dental CARIES
- subacute endocarditis, suppurative
intraabdominal infections
• Treatment – susceptible to PNC,
moderately resistant strains: PNC + aminoglycoside
Streptococcus pneumoniae
Streptococcus pneumoniae
Structure: encapsulated, G+, pairs or short
chains
- C ubstance - teichoic acid
Culture: large, round, mucoid, unpigmented – species specific
hemolysis alfa (beta in anaerob. conditions)
complex media (BHI, TSA + blood products)
Pathogenesis and Immunity
Virulence factor
Biological effect
Colonization and migration
Protein adhesin
Secretory IgA protease
Pneumolysin
Binds to epithelial cells
Disrupts secretory IgA mediated clearence
Possibly destroys ciliated epithelial cells
Tissue destruction
Teichoic acid
Peptidoglycan fragments
Pneumolysin
Hydrogen peroxide
Phosphoryl chorine
Activates alternative C pathway
Activates alternative C pathway
Activates classic C pathway
Damage of cells
Invasion to host cells
Phagocytic survival
Capsule
Pneumolysin
Antiphagocytic
Supress oxidative burst
Colonization and Migration
Colonization - oropharynx
Infection - lungs, paranasal sinuses, middle ear, (brain)
Migration - prevented by mucus and removing from
airways
Tissue Destruction – recruitment of inflammatory cells >> teichoic
acid, peptidoglycan fragments, pneumolysin,
temperature > IL-1, TNF-alpha
Clinical Syndromes
• Pneumonia
Gram Stain of a film of sputum
from a case of lobar pneumonia
• Sinusitis and Otitis Media
• Bacteremia
Lab.Diagnosis
• Microscopical Examination – sputum Gram lancet shape,
diplococci, capsule, Quellung reaction
• Ag Detection
• culture – fastidious nutritional requirements
ATB therapy v.s. isolation of S.pneumoniae
Identification: - bile test – autolysis
- susceptible to optochin
Treatment
• PNC (recently increrased resistance)
• Cephalosporins, erythromycin
• Chloramphenicol (meningitis)
• Resistance to tetracycline
Enterococci
“enteric cocci”
fromerly group D Streptococci
Physiology and structure
- G+, in pairs or short chains (cannot be differentiated from
S. pneumoniae)
- facultatively anaerobic
- blood agar, large white colonies, nonhemolytic
- (but can be alpha or beta)
- growth in 6.5% NaCl, tolerate 40% bile salts, hydrolyse esculin
Enterococcal Virulence factors
Colonization factors
Biological Effect
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Aggregation substance
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Carbohydrate adhesins
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Adhesion to epithelia, exchanging
of plasmids
Binding to host cells
Secreted factors
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Cytolysin
Pheromone
Gelatinase
Antibiotic resistance
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Inhibits G+ MIO, tissue damage
PMNL, inflammation
Hydrolysis gelatin, collagen, Hb,...
Aminoglycosides, beta-lactam
ATB, vancomycin !!!
Epidemiology
- E.faecalis, E. faecium
- Commensal
- Large intestinum, GUIT
Clinical Syndrome
• Nosocomial pathogen (resistance to all conventional ATB)
• Infections: UTI, bloodstream (cathetrisation), polymicrobial
infections – intraabdominal abscesses
• Patients hospitalized for prolonged period + broad-spectrum
ATB
Lab. diagnosis
• Biochemical tests:
– resistance to optochin
– do not dissolve in bile
– hydrolise PYR ( pyrolidonyl-beta naphthylaminde)
Treatment, Prevention and
Control
• therapy – complicated
• therapy: combination of aminoglycoside +
AMP, VAN
• resistance aminoglycosides (>25%), AMP
(50%), PNC, VAN (>20%)
• Resistance – plasmid encoded