systemic bacteriology Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

describe cocci

A
  • Many cocci are Gram-positive bacteria
  • Do not produce spores
  • Not motile
  • Produce exotoxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does catalase do ?

A

breaks down hydrogen peroxide into water and oxygen. 2 H2O2 = 2 H2O + O2 (gas bubbles). in bacteria catalase protects from intra-phagocyte killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

if the addition of 1-3 Peroxide to bacteria produces bubbles it indicates that?

A

it is catalase positive bacteria ( staphylococcus )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe staphylococci

A

are Gram-positive cocci (0.8-
1.5 µm diameter) arranged in grape-like clusters, primarily aerobic, facultative
anaerobic, do not form spores, and are nonmotile
Some staphylococci produce capsules, many are able to produce biofilms
Unlike streptococci, staphylococci produce catalase
Optimal temperature 30-37 °C and pH 7-7.5
Colonies grow well in 18-24 hours, are round, smooth, butyrous
On blood agar, S. aureus forms white colonies that tend to turn a buff-golden color
with time and may produce β-hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

staphylococcus are usually part of which microbiota?

A

skin, mucosal surfaces, upper respiratory airways and the intestinal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what separates S. aureus from other less virulent staphylococci species?

A

the presense of coagulase ( converts fibrinogen to fibrin )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

_________ % of healthy individuals are carriers of S.aureus

A

15-50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Protein A is covalently linked to PG
binds to Ig Fc to do what?

A

block phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

S. Aureus enzymes?

A

Coagulases (bound or free)
Hyaluronidase “spreading factor” of S. aureus
Nucleases cleave DNA and RNA
Serin-Proteases
Staphylokinase (fibrinolysin, allows the spread of infection)
Lipases
Esterases
β-lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

S. Aureus exotoxins?

A

Cytolytic (cytotoxins; cytolysins):
Alpha toxin hemolysin (pore-forming)
Beta toxin Sphingomyelinase
Gamma toxin Hemolytic activity
Delta toxin Cytopathic for: RBCs, Macrophages, Lymphocytes,
Neutrophils, Platelets
Enterotoxic activity
PV (Panton-Valentine) Leukocidin active against neutrophils and platelets
Staphylococcal Superantigen Toxins:
Enterotoxins stable to boiling and digestive enzymes
Exfoliative toxin epidermolytic toxin, acts on desmosomes
Toxic Shock Syndrome toxin (TSST)
Pyrogenic exotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is TSST?

A

toxic shock syndrome toxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is an abscess?

A

is a collection of pus that has built up in a tissue of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Staphylococcal disease can be differentiated in:

A

1) Due to the direct effect of the
microorganism: local- skin, deep abscesses, systemic infection

2) toxin-mediated: food poisoning, toxic shock syndrome, scalded skin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

clinical manifestations of the skin due to the S. aureus :

A
  • folliculitis
  • boils (furuncles) develop in hair follicles
  • styes (infection at the base of the eyelash)
  • carbuncles, multiple boils become carbuncle
  • impetigo (bullous & pustular)
  • wound infections
  • scalded skin syndrome (neonates and
    children under 4 years)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

examples of diseases that are mediated by exfoliative toxins?

A

Staphylococcal scalded skin syndrome (SSSS) and bullous impetigo
- Bullous impetigo: localized cutaneous infection characterized by vesicle on an
erythematous base
- SSSS: disseminated desquamation of epithelium in infants; blisters with no
bacteria or leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

deep infections due to S. aureus?

A
  • Direct / by blood
  • Can be single/multiple
  • Breast, kidney, brain abscesses
  • Osteomyelitis
  • Septic arthritis
  • Staphylococcal pneumonia: secondary to some other insult to
    the lung, such as influenza, aspiration, or pulmonary edema.
    Necrotizing pneumonia has been associated with strains
    producing the PV leukocidin
  • Endocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is bacteremia ?

A

presence of bacteria in the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

______________is the second most common
cause of bacteremia

A

S. aureus, the first is E. coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

toxin-mediated diseases?

A

Staphylococcal food poisoning, Toxic shock syndrome ( in women using intravaginal tampons )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the examples of coagulase-negative Staphylococci?

A

S. epidermidis
S. saprophyticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

The colony is adhered to a surface and coated with _____________________

A

polysaccharide layer (or slime layer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

S. saprophyticus is a common cause of ____________________

A

urinary tract infections in young,
sexually active females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

CONS( coagulase-negative staphylococci) can produce a ______________ that
bonds them to catheters and protects them from
antibiotics and immune cells -> infections of
catheters and shunts

A

polysaccharide slime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

___________ Agar can be used as a
selective and differential medium for
the isolation and identification of
staphylococci

A

Mannitol Salt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

the presence of
______________ at high concentration
(7.5%) results in the partial or
complete inhibition of bacterial
organisms other than staphylococci

A

sodium chloride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

mannitol fermentation differentiates
____________, which forms yellow colonies
surrounded by yellow medium, from
coagulase-negative staphylococci that
form red colonies and cause no color
change of the surrounding medium

A

S. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

examples of Beta-lactam group of antibiotics?

A

penicillin, cloxacillin, ampicillin, amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

For methicillin-resistant S. aureus (MRSA)
the main alternatives are _____________ and
___________ for deep-seated infections (endocarditis,
osteomyelitis, bacteremia, pneumonia) with
macrolides and tetracyclines restricted to more
superficial skin and soft tissue infections

A

vancomycin, daptomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

describe streptococci?

A

gram-positive bacteria, arranged in chains of over 30 cells, do not form spores, non-motile, facultative anaerobes, some from capsules, human are the main reservoir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are Group A Streptococci?

A

GAS, or Streptococci Pyogenes, typically appear in small colonies with a large zone of hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are group B Streptococci?

A

GBS, or Streptococci agalactia, typically appears in large colonies with a small zone of hemolysis

32
Q

what are the examples of Beta Hemolytic streptococci?

A

S. Pyogenes and S. agalactia

33
Q

what are the examples of Alpha Hemolytic Streptococci?

A

Streptococcus mitis, Streptococcus
oralis, Streptococcus pneumoniae

34
Q

streptolysins O and S cause _________?

A

Beta hemolysis

35
Q

extracellular products of S. Pyogenes?

A

– Streptolysin S: oxygen stable
– Streptolysin O: oxygen labile (a pore-forming cytotoxin, able to
lyse leukocytes, tissue cells, and platelets)
– DNAses (four, A to D) – NADase
– Streptokinase: dissolves clots – Hyaluronidase – C5a peptidase degrades complement component C5a
– Neuraminidase
SPE, Streptococcal Pyrogenic Exotoxins, act as superantigens
(produced by 10% of GAS) – SpeB also has direct enzymatic activity digesting tissue and
extracellular matrix proteins (cysteine protease) – SpeA and SpeC: erythrogenic toxins associated with scarlet fever

36
Q

__________ results from minor trauma such as insect bites in skin transiently colonized with
GAS. In streptococcal toxic shock, StrepSAgs producing GAS in a superficial lesion spread into
the bloodstream. Note both toxin and bacteria are circulating.

A

impetigo

37
Q

Streptococcus pyogenes disease:

A
  • Asymptomatic colonization (less than 1%)
  • Pharyngitis
    – Scarlet fever
  • Pyoderma, impetigo
  • Invasive skin and soft tissue infections (SSTI): erysipelas,
    cellulitis, necrotizing fasciitis, myositis, peripartum sepsis
  • Toxic Shock Syndrome
  • Bacteremia
  • Sequelae: rheumatic fever, glomerulonephritis
38
Q

Characteristics of Streptococcal Pharyngitis?

A
  • Highest incidence: ages 5-15; adults also infected
    – Person-to-person transmission via droplets or secretions;
    proximity and crowding worsen
    – Food- and water-borne outbreaks occur
  • Acute onset: sore throat, fever, malaise
    – Enlarged, hyperemic tonsils, exudates
    – Tender cervical lymph nodes
  • Self-limiting in about one week
    – Treat to hasten resolution, stop spread, reduce sequelae
    Suppurative complications: peritonsillar abscess, retropharyngeal
    abscess, lymphadenitis, mastoiditis, meningitis, brain abscess,
    thrombosis of intracranial venous sinuses
39
Q

Scarlet fewer characteristics?

A
  • Classically associated with pharyngitis, but may occur after
    infections at other sites
  • Requires GAS strain producing erythrogenic toxins
  • Rash typically on 2nd day
    – Face flushed except for circumoral pallor
    – Enanthem: small, hemorrhagic spots on hard and soft
    palate
    – Exanthem: upper chest to torso, extremities; face, palms,
    soles spared; diffuse blush with points of deeper red that
    blanch; Pastia’s lines (skin folds deeper red)
    – Tongue: coated to red strawberry tongue
40
Q

characteristics of S. Agalactia?

A
  • β-hemolysis is due to a pore-forming cytolysin (may be absent)
  • Capsule is the most significant virulence factor (nine antigenic
    types: Ia, Ib, II-VIII, all containing sialic acid)
  • Pili and surface proteins as adhesion factors
  • Colonizes genital and lower gastrointestinal (GI) tracts of 10-
    40% of women; also found in oropharynx, upper GI
  • Pass to baby during birth
41
Q

__________ (during labor) antimicrobial prophylaxis with intravenous
penicillin has been shown to reduce transmission and disease

A

intrapartum

42
Q

neonatal infections:

A
  • Early-Onset
    – 12 hours of age average
    – Bacteremia (85%), pneumonia (10%), meningitis (5-10%)
    – Risk factors: heavy maternal carriage (untreated), delivery at less than
    37 weeks, intra-partum fever, intra-amniotic infection, rupture of the
    amniotic membranes ≥18 hours before delivery
  • Late-Onset
    – Median 36 days (7-89)
    – Bacteremia
43
Q

what is serotype?

A

A serotype or serovar is a distinct variation within a species of bacteria or virus or among immune cells of different individuals

44
Q

Virulence factors of S. Pneumonia

A

– Capsule composed of polysaccharide polymers
* Antiphagocytic
* More than 90 serotypes
* Both antigenic and type-specific
* Serotypes 3 and 7 are the most virulent
* 90% of cases of bacteremic pneumococcal pneumonia
and meningitis are caused by 23 serotypes – Pneumolysin (released by autolysins, peptidoglycan
degrading enzymes)
* Membrane-damaging toxin
– Surface proteins (among which Choline-binding proteins)

45
Q

-The S. Pneumonia is a common cause of community-acquired:

A

pneumonia, meningitis, otitis media, sinusitis and bacteremia

46
Q

__________________: the major anti-phagocytic surface element of pneumococci
and the major protective antigen

A

Polysaccharidic capsule. For the treatment Purified capsular polysaccharides from
the most common serotypes are used in
a polyvalent vaccine

47
Q

diseases caused by S. Pneumonia?

A
  • Respiratory tract infections
    – Lobar pneumonia (commonest cause of Community
    Acquired Pneumonia)
    – Empyema
    – Otitis media (6 months – 3 years)
    – Mastoiditis
    – Sinusitis
    – Acute exacerbation of chronic bronchitis
  • Meningitis
  • Conjunctivitis
  • Peritonitis (primary)
  • Bacteremia (15 % of pneumonia)
  • Septicaemia
48
Q

Symptoms of the lobar pneumonia:

A

– Sudden onset
– Fever
– rigor
– Cough, rusty sputum
– Pleural pain
– Signs of lobar consolidation
– Polymorphonuclear leukocytosis
– Empyema, pericarditis

49
Q

symptoms of Meningitis:

A

– High Mortality (20%)
– Primary
– Complicate infections at another site (lung)
– Bacteremia usually coexists
– Bimodal incidence (< 3 years - > 45 years)

50
Q

layers of Meninges?

A

Outer: Dura mater
Middle: Arachnoid
Inner: Pia mater

51
Q

Predisposing factors to Streptococcus pneumoniae infection:

A

– Aspiration of upper airway secretions (endogenous)
– Disturbed consciousness, general anaesthesia, convulsions,
cerebral vascular accident, epilepsy, head trauma
– Prior viral infection of the lower respiratory tract
– Preexisting respiratory diseases, smoking
* Chronic bronchitis, bronchogenic malignancy
– Chronic heart disease
– Chronic renal disease (nephrotic syndrome )
– Chronic liver disease (cirrhosis)
– Diabetes mellitus
– Old age (extreme of age)
– Malnutrition, alcoholism
– Hypogammaglobulinaemia
– Asplenia, hyposplenism (<tuftsin)
– Homozygous sickle cell disease
– Coeliac disease
– Multiple myeloma, leukemia, lymphomas
– Neutropenia
– HIV

52
Q

Viridans Streptococci-associated diseases:

A

Endocarditis
Often with previous valvular pathology
Proportion increases with time after valve replacement
Subacute: often weeks
Fever, malaise, anorexia
Low-grade bacteremia (1-30 Colony Forming Units per mL blood)
Bacteremia
Account for 2.6% of all positive blood cultures
After toothbrushing, 25-50% of people have bacteremia
If transient, may consider limited clinical significance
More common and profound in oncologic patients
Meningitis
Rare: 0.3 to 5% of culture-positive meningitis
Pneumonia
Very rarely the sole pathogen

53
Q

Characteristics of Enterococci
genus Enterococcus:

A
  • distantly related to other streptococci, present the Lancefield
    group D antigen
  • colonize the gastrointestinal tract (gut microbiota),
    responsible for – urinary tract infection
    fecal contamination
    – opportunistic (nosocomial) infections
    particularly endocarditis
  • most common species E. faecalis, E. faecium
  • can grow in 6.5% NaCl and in presence of 40% bile salts, from
    10°-45°C; hydrolyze esculin
54
Q

Enterococci Challenges of Treatment:

A
  • Intrinsically resistant to many antibacterials with acquisition
    of additional resistance
  • inherent relative resistance to most β-lactams
  • complete resistance to all cephalosporins
  • high-level resistance to aminoglycosides
    Enterococci also have particularly efficient means of acquiring
    plasmid and transposon resistance genes from themselves
    and other species
55
Q

Streptococcus pneumoniae characteristics:

A

Morphology and Characteristics:
Colonies on blood agar
*Gram-positive, encapsulated: Ovoid or lancet-shaped, 1-2 μm, usually in pairs (diplococci)
*Non-motile, non-spore forming: Do not produce catalase and oxidase, are facultative
anaerobes
*Environment: Fragile in the environment, require enriched media (blood or chocolate agar)
and 5-10% CO₂ atmosphere
*Alpha Hemolysis: Some strains are mucoid
*Bile Solubility: Soluble in bile due to autolytic enzyme activation

56
Q

Streptococcus pneumoniae Virulence factors:

A

– Capsule composed of polysaccharide polymers
* Antiphagocytic
* More than 90 serotypes
* Both antigenic and type specific
* Serotype 3 and 7 are most virulent
* 90% of cases of bacteremic pneumococcal pneumonia
and meningitis are caused by 23 serotypes – Pneumolysin (released by autolysins, peptidoglycan
degrading enzymes)
* Membrane damaging toxin– Surface proteins (among which Choline-binding proteins)

56
Q

Epidemiology of S.pneumoniae infection:

A

-Airborne transmission
Carrier Rates in Children and Adults: 5-10% of healthy adults
and 20-40% of healthy children are colonized
-The organism is a common cause of community-acquired pneumonia,
meningitis, otitis media, sinusitis and bacteremia

-Disease is most common in
the elderly and young children

57
Q

Do S. pneumonia colonies appear Alpha or beta-lytic?

A

Alpha

Colony morphology varies: colonies
of capsulated strains are generally
large, round, and mucoid, while
colonies of non-capsulated strains
are smaller and flat on blood agar.
All colonies undergo autolysis as
they age, that is, the central portion
of the colony dissolves, leaving a
small depression in the center of the
colony

57
Q

Antimicrobial Susceptibility for S. Pneumonia :

A

Pneumococci were uniformly susceptible to penicillin until a few decades ago when
decreased susceptibility to all β-lactams began to emerge
Resistant strains have mutations in one or more transpeptidases, penicillinase is not
produced. Resistance rates now exceed 10% in most locales and may be greater than 40% in some areas. Resistance to macrolides is increasing and is more likely with penicillin-resistant
strains.

58
Q

S.pneumoniae: virulence factors 1:

A
  1. Capsule
    *Description: The capsule is a
    polysaccharide layer that
    surrounds the bacterial cell.
    *Role: It prevents phagocytosis by
    immune cells, helping the
    bacteria evade the host’s immune
    system.
    *Impact: This is the most
    important virulence factor of
    Streptococcus pneumoniae.
    It represents the major
    protective antigen

*More than 90 serotypes.
*Significance: Both antigenic and type-specific; serotypes 3
and 7 are particularly virulent.
*Impact: 90% of cases of bacteremic pneumococcal
pneumonia and meningitis are caused by 23 serotypes.

58
Q

S.pneumoniae: virulence factors 4:

A
  1. Surface Proteins
    *Choline-binding proteins: These
    proteins bind to choline residues on
    the bacterial cell wall and help in
    adherence to host cells.
    * Example: PspA
    (Pneumococcal surface
    protein A) interferes with
    complement deposition and
    protects the bacteria from
    phagocytosis.
    *Adhesins: These proteins help the
    bacteria attach to host tissues,
    facilitating colonization.
    * Example: CbpA (Choline
    binding protein A) is
    important for adherence to
    the nasopharyngeal
    epithelium.
59
Q

Clinical symptoms of Meningitis?

A

– High Mortality (20%)
– Primary
– Complicate infections at another site (lung)
– Bacteremia usually coexists
– Bimodal incidence

59
Q

S.pneumoniae: virulence factors 5,6:

A
  1. IgA1 Protease
    *Description: IgA1 protease is an
    the enzyme that cleaves IgA antibodies.
    *Role: It helps the bacteria evade the
    immune system by destroying IgA
    antibodies, which are important for
    mucosal immunity.
    *Impact: This facilitates colonization
    and invasion of mucosal surfaces.
  2. Hyaluronidase
    *Description: Hyaluronidase is an
    enzyme that breaks down hyaluronic
    acid in the extracellular matrix.
    *Role: It aids in the spread of the
    bacteria through tissues by degrading
    the extracellular matrix.
    *Impact: This contributes to the
    invasive potential of Streptococcus
    pneumoniae.
59
Q

S.pneumoniae: virulence factors 2,3:

A
  1. Pneumolysin
    *Description: Pneumolysin is a pore
    forming toxin.
    *Role: It damages host cell
    membranes, leading to cell lysis and
    tissue damage.
    *Impact: It can inhibit immune cell
    function and activate the
    complement system, causing
    inflammation.
  2. Autolysin (LytA)
    *Description: Autolysin is an enzyme
    that breaks down the bacterial cell
    wall.
    *Role: It helps in releasing
    pneumolysin and other virulence
    factors during bacterial cell death.
    *Impact: This can lead to increased
    inflammation and tissue damage in
    the host.
60
Q

S.pneumoniae: virulence factors 7

A
  1. Neuraminidase
    *Description: Neuraminidase is an
    enzyme that cleaves sialic acid
    residues from host cell surfaces.
    *Role: It exposes binding sites for
    bacterial adhesion and can help in
    the spread of the bacteria.
    *Impact: It plays a role in colonization
    and invasion of host tissues.
60
Q

S.pneumoniae: pathogenesis of
infection:

A
  • Pneumococcal disease occurs when
    organisms colonizing the nasopharynx
    and oropharynx spread to the lungs
    (pneumonia), paranasal sinuses
    (sinusitis), ears (otitis media), or
    meninges (meningitis)- Spread of S. pneumoniaein blood
    (bacteremia) can occur with all of these
    diseases
61
Q

Clinical features of Lobar pneumonia?

A

– Sudden onset
– Fever
– rigor
– Cough, rusty sputum
– Pleural pain
– Signs of lobar consolidation
– Polymorphonuclear leukocytosis
– Empyema, pericard

61
Q

Predisposing factors to Streptococcus pneumoniae infection:

A

– Aspiration of upper airway secretions (endogenous)
– Disturbed consciousness, general anesthesia, convulsions,
cerebral vascular accident, epilepsy, head trauma
– Prior viral infection of the lower respiratory tract
– Preexisting respiratory diseases, smoking
* Chronic bronchitis, bronchogenic malignancy
– Chronic heart diseases
– Chronic renal disease (nephrotic syndrome )
– Chronic liver disease (cirrhosis)
– Diabetes mellitus
– Old age (extreme of age)
– Malnutrition, alcoholism
Specific deficiencies in host defense
– Hypogammaglobulinaemia
– Asplenia, hyposplenism (<tuftsin)
– Homozygous sickle cell disease
– Coeliac disease
– Multiple myeloma, leukemia, lymphomas
– Neutropenia
– HIV

61
Q

Diseases of S. pneumoniae:

A
  • Respiratory tract infections
    – Lobar pneumonia (the most common cause of Community-Acquired Pneumonia)
    – Empyema
    – Otitis media (6 months – 3 years)
    – Mastoiditis
    – Sinusitis
    – Acute exacerbation of chronic bronchitis
  • Meningitis
  • Conjunctivitis
  • Peritonitis (primary)
  • Bacteremia (15 % of pneumonia)
  • Septicaemia
61
Q

Diagnosis of S.pneumoniae infection:

A
  • Direct diagnosis only-
    Specimens: sputum, cerebrospinal fluid (CSF), blood
  • Microscopy of CSF :
    Gram stain is a rapid way to diagnose
    pneumococcal meningitis (but moderate sensitivity: 60-80%)
  • Detection of pneumococcal antigens in CSF and urine
    Pneumococcal capsule polysaccharide is excreted in urine:
    useful specimen in the suspicion of pneumococcal pneumonia

Nucleic Acid–Based Tests:
PCR assays have been developed for
identification of S. pneumoniae isolates in CSF

  • Culture from sputum, blood, CSF:
    on blood agar plates.
    S.pneumoniae is susceptible to the antibiotic optochin
62
Q

Prevention of S. Pneumonia related diseases:

A

Two pneumococcal vaccines prepared from capsular polysaccharides are available.
The first pneumococcal polysaccharide vaccine contains purified polysaccharides extracted
from the 23 serotypes of S. pneumoniae most commonly isolated from invasive disease. It
shares the T-cell-independent characteristics of other polysaccharide immunogens and is
recommended for use only in those older than 2 years.
The second vaccine, in which capsular polysaccharide is conjugated with proteins, stimulates
T-dependent TH2 responses and is effective beginning at 2 months of age. The 13-valent
conjugate vaccine is the standard for childhood immunization.

63
Q

Pneumococcal Conjugate Vaccine (PCV):

A

*Examples: PCV13 (Prevnar 13)
*Coverage: Protects against 13 serotypes of Streptococcus
pneumoniae.
*Target Group: Recommended for all children under 5 years
old, adults over 65, and individuals with certain medical
conditions.

T-celldependent immunity
Longer termimmunity
Immunologicalmemory

63
Q

Pneumococcal Polysaccharide Vaccine (PPSV):

A

*Examples: PPSV23 (Pneumovax 23)
*Coverage: Protects against 23 serotypes of Streptococcus
pneumoniae.
*Target Group: Recommended for adults over 65 and
individuals aged 2-64 with specific health conditions

T-cell independent
immunity
Shortertermimmunity
No immunologicalmemory

64
Q

Viridans Streptococci:

A
  • 5 groups– anginosus group– mitis group– mutans group– salivarius group– sanguinis group
  • Members of oral microbiota of animals and humans
  • Low virulence; no toxins
    Streptococcus sanguinis, S. mutans, S. mitis, S. salivarius, S. oralis, and
    S. gordonii are usually present in dental plaque biofilm
    Streptococcus mutans is now regarded as the dominant organism for
    the initiation of caries, but multiple members of the plaque biofilm
    participate in the evolution of the lesions, including other streptococci
    (S. salivarius, S. sanguinis, S. sobrinus)
64
Q

Viridans Streptococci-associated diseases:

A

1) Endocarditis:
Often with previous valvular pathology
Proportion increases with time after valve replacement
Subacute: often weeks
Fever, malaise, anorexia
Low-grade bacteremia (1-30 Colony Forming Units per mL blood)
2) Bacteremia:
Account for 2.6% of all positive blood cultures
After toothbrushing, 25-50% of people have bacteremia
If transient, may consider limited clinical significance
More common and profound in oncologic patients
3) Meningitis
Rare: 0.3 to 5% of culture-positive meningitis
4) Pneumonia
Very rarely the sole pathogen

64
Q

Enterococci
genus Enterococcus:

A
  • distantly related to other streptococci, present the Lancefield
    group D antigen
  • colonize the gastrointestinal tract (gut microbiota),
    responsible for– urinary tract infection
    fecal contamination– opportunistic (nosocomial) infections
    particularly endocarditis
  • most common species E. faecalis, E. faecium
  • can grow in 6.5% NaCl and in presence of 40% bile salts, from
    10°-45°C; hydrolyze esculin
64
Q

Enterococci: Challenges of Treatment:

A
  • Intrinsically resistant to many antibacterials with acquisition
    of additional resistance
  • inherent relative resistance to most β-lactams
  • complete resistance to all cephalosporins
  • high-level resistance to aminoglycosides
    Enterococci also have particularly efficient means of acquiring
    plasmid and transposon resistance genes from themselves
    and other species
    Vancomycin resistance emerging threat