Pathogenic Gram positive cocci bacteriolyg.ppt

bacteriology

1. CHAPTER II CHAPTER II
Medical important bacteriaMedical important bacteria
1

2. Objectives (summary)Objectives (summary)
Upon completion of this, the student will be
able to:Discribe medically important
bacteria:
General characteristics
Virulent factors
Pathogenicity and clinical manifestations
Lab diagnosis
Prevention & control
2

3. There are two most important genera of gram-positive
cocci
The Genus staphylococcus
The Genus Streptococcus
2.1.1. The Genus staphylococcus
The name staphylococci is derived from Greek term
staphyle ‘‘ mean’’ bunch of grapes’’ and cocci mean
spherical
Staphylococci make avery large contribution to
man's commonsal flora and also account for a high
proportion of his acute and chronic lesions.
2.1. Pathogenic gram positive cocci
3

4. Gram positive in reaction
Arranged in grape like irregular clusters
◦Single cocci, pairs, tetrads / rarely chains
◦All staphylococci produce catalase that break H
2
O
2

in to O
2 and H
2O
The genus contains 32 species and 15 subspecies
◦Contain 3 main Spp of Clinical importance:
S. aureus
S. epidermidis
S. saprophyticus
General properties /characteristics
4

5. Grow on many types of media
 Some are members of normal flora of:
Skin( S. epidermidis)& mucous member of
humans (S. aureus)
Others cause a variety of infections
Pathogenic staphylococci:
Hemolyze blood
Coagulate plasma ( e.g S .aureus)
Produce extra cellular enzymes/toxins
Cause food poisoning: Heat stable staphylococci
enterotoxin (S. aureus)
Resistance to some anti-microbial agents
5

6. 
Identification
A. Culture and its growth characteristics
Grow on most bacteriological media under:
Aerobic & micro aerophilic conditions
Grow rapidly at 35 - 37
0
C
Colonies on solid media are round, smooth &
raised
S. aureus forms gray to deep golden yellow
colonies on MSA
S. epidermis produces gray to white colonies
6

7. Produce catalase
Ferments carbohydrate (release of lactic acid & not gas)
Produce many extra cellular substances e.g enzyme and
toxin
Resistant to:
 Drying, Heat (50
0
C for 30 min)
 9% NaCl
Variably sensitive to many antibiotics
B - lactamase production (Due to plasmid genes)
 Resistant to Ampicillin Tetracycline, Amino glycosides
N.B: Plasmids are small and specialized genetic elements
that can carry and confer resistant genes to certain
bacteria
7

8. Antigenic and virulence Antigenic and virulence
characteristic characteristic
What is virulence factor?
Pathogenesis?????
◦Pathogenic virulence factors are the genetic,
biochemical, or structural features that enable an
organism to produce disease.
◦The clinical outcome of an infection depends on
virulence factor and effectiveness host defense
mechanisms
◦S. aureus expresses many potential virulence factors
8

9. 1.Cell wall virulence factors:
A.Protein A: is a major component of the S. aureus
cell wall.
It binds to the Fc moiety of IgG, exerting an
antiopsonin (and therefore strongly antiphagocytic)
effect.
However protein A is used in certain tests
 it binds to IgG and forms a "coagglutinate" with
antigen-antibody complexes.
The CNS do not produce protein A.
B. Fibronectin-binding protein (FnBP) and other
staphylococcal surface proteins promote binding to
mucosal cells and tissue matrices.
C.Teichoic acids: aid in attachment and stimulate the
inflammatory response when complexed with
peptidoglycan.
9

10. D. Polysaccharide capsule :
The capsule is antiphagocytic and poorly
immunogenic, which has made producing an
effective vaccine difficult.
and also helps to bind on foreign materials in our
body (catheter, prosthetic valves, grafts, joints, and
other materials)
Toxins
10

11. Toxins are poisonous substances that are produced
by certain microorganisms.
The capacity of microorganisms to produce toxins is
called toxigenicity.
Toxins are of two general types, based on their
position relative to the microbial cell:
◦exotoxins and endotoxins.
Exotoxins
◦Are produced inside some bacteria as part of their
growth and metabolism and are secreted by the
bacterium into the surrounding medium or released
following lysis
◦Bacteria that produce exotoxins may be gram-
positive or gram-negative
11

12. Endotoxins
◦Endoloxins differ from exotoxins in several ways
◦part of the outer portion of the cell wall of gram-
negative bacteria.
◦endotoxins are lipopolysaccharides (lipid A),
whereas exotoxins are proteins.
◦Endotoxins are released when gram-negative
bacteria die and their cell walls undergo lysis
Can be also released during bacterial multiplication
1.Cytolytic exotoxins: toxins attack mammalian
cell (including red blood cell) membranes, and are
often referred to as hemolysins.
12

13. 2. Superantigen exotoxins:
These toxins have an affinity for both the T cell
receptor and MHC Class II antigen complex
simultaneously, and stimulate enhanced T lymphocyte
response
T cell activation can cause toxic shock syndrome,
primarily by releasing extremely large amounts of T cell
cytokines, such as IL-2, interferon-gamma), and tumor
necrosis factor-alpha.
3. Enterotoxins:
six major antigenic types( A, B, C, D, E, and G) are
produced by approximately half of all S. aureus
isolates.
The toxin stimulates the vomiting center in the brain
by binding to neural receptors in the upper
gastrointestinal (GI) tract.
13

14. Enterotoxins are superantigens
more heat-stable than S. aureus;
 therefore, organisms are not always recovered from
incriminated food.
also resistant to stomach acid and to enzymes in the
stomach and jejunum.
4.Toxic shock syndrome toxin (TSST-1)
is the classic cause of toxic shock syndrome.
The toxin enters the bloodstream, causing a toxemia.
Blood cultures typically do not grow S. aureus.
TSST-1 is a super antigen and causes toxic shock by
stimulating the release of large amounts of IL-1, IL-
2,and tumor necrosis factor (TNF)
Toxic shock occurs in people who do not have
antibody against TSST.
14

15. Exfoliatin (exfoliative toxin, ET)
is also a superantigen.
It causes scalded skin syndrome in children.
acts as a protease that cleaves desmoglein in
desmosomes, leading to the separation of the epidermis
at the granular cell layer.
Several toxins can kill leukocytes (leukocidins) and
cause necrosis of tissues in vivo
◦Its cytotoxic effect is attributed to the formation of holes in
the cell membrane and the consequent loss of low-
molecular-weight substances from the damaged cell.
alpha toxin, which causes marked necrosis of the skin and
hemolysis.
Leukocidin: kills white blood cells by damaging cell
membranes.
15

16. Enzymes
Coagulase
Deposit fibrin on the surface of staphylococci as a
result Inhibits phagocytosis
Associated with pathogenicity
Catalase:is an important virulence factor
◦H202 is microbicidal and its degradation limits the
ability of neutrophils to kill.
Other enzymes
◦Hyaluronidase: Spreading factors i.e hydrolysis
hyaluronic acids in connective tissue
◦Staphylokinase: Cause fibrinolysis
◦Beta- lactamase: Disrupts the Beta -lactame rings
◦Proteinases, nucleases, and lipases
16

17. 17

18. Epidemiology:
 They are normal flora of the skin and mucosal
membrane.
Carriers serve as a source of infection to themselves and
others;
for example, by direct contact, by contamination of
fomites (objects such as a doorknob, which in turn can
be a source of infection) or food, which can then result
in food poisoning.
Generally, significant host compromise is required for S.
aureus infection,
Such as a break in the skin or insertion of a foreign
body (wounds, surgical infections, or central venous
catheters), an obstructed hair follicle (folliculitis), or a
compromised immune system
18

19. S. aureus disease may be due to
19

20. Food poisoning: Caused by enterotoxin
produced by S. aureus, characterized by
violent nausea, vomiting, and diarrhea with
out fever.
Staphylococcal gastroenteritis
Staphylococcal scalded skin syndrome:
Caused by exfoliative toxin produced by S.
aureus.
lesions of scalded s kin syndrome. It is
especially likely to occur in children
under age 2.
20

21. Toxic shock syndrome: Caused
by toxic shock syndrome toxin-1
produced by S. aureus
 Characterized by abrupt onset
of high fever, vomiting, diarrhea,
myalgia, rash, and hypotension
with cardiac and renal failure in
the most severe disease
occuring within 5 days after the
onset of menses in young
women who use tampons.
21

22. Bulbous impetigo: Crusted superficial
skin lesion
lesions of impetigo. This disease is
characterized by isolated pustules that
become crusted.
(e) Impetigo on the neck of 2-year-old
male.
22

23. (a) Superficial folliculitis in which
raised, domed pustules form
around hair follicles.
(b) In deep folliculitis the
microorganism invades the deep
portion of the follicle and dermis.
(c) A furuncle arises when a
large abscess forms around
a hair follicle.
Folliculitis: Infection of one hair follicle.
23

24. (d) A carbuncle consists of a
multiocular abscess around
several hair follicles.
Cellulitis: Infection of skin and
subcutaneous tissue.
Abscess formation: focal
suppuration
Mastitis: Infection of breast which
leads to inflammation, especially in
lactating mother.
Pneumonia: Infection of lung
parenchyma.
Empyema: Accumulation of pus in
pleural space
Osteomyelitis: Infection of bone
Endocarditis and meningitis:
Infection of heart tissue and
leptomeninges respectively
24

25. S. epidermidisS. epidermidis and and S .saprophyticusS .saprophyticus
 They are opportunistic pathogens.
 They are coagulase negative
 S. epidermidis is frequently associated with
endocarditis, bacteremia, wound infection and
urinary tract infection (UTI).
 S. saprophyticus is now recognized as an important
cause of UTI in sexually active females.
Coagulase-negative staphylococcal species are
important agents of hospital-acquired infections
associated with the use of implanted prosthetic
devices and catheters.
25

26. Potential specimens:
Pus
Tracheal aspirates
Blood
CSF
Lab. techniques
A. Smears
 Gram’s stain (Typical organisms)
 Not helps to distinguish among different Spp.
Lab. Dx
26

27. Figure: Gram positive cocci
27

28. B. Culture
Blood agar plates give typical colonies in 18 hrs at 37
0
C
Media containing 7.5% NaCl (MSA) inhibits the growth
of other bacteria, but not S. aureus
N.B. Hemolysis & pigment production can stay for several
days Nonhemolytic Staphylococcus Beta hemolytic
Staphylococcus
28

29. S.epidermidis and S. saprophyticus E.g. S. auerus
29

30. C. Catalase Test
◦A drop of H
2
0
2
(+) small amount of bacterial growth on
a slide
◦ Formation of bubbles (release of 02) ----- Positive test
D. Coagulase Test
◦Human / citrated rabbit / plasma diluted 1:5 (+)
equal volume of growth from colonies from broth
culture
◦Incubated at 370C
Positive test: If clots form in 1- 4 hrs
N.B. All coagulase positive staphylococci are considered
pathogenic to humans
30

31. E. Susceptibility Testing
◦Disk disffusion susceptibility testing
◦to penicillin detected by a pos. test for ß -
lactamase
F. Serological Testing
Anti-bodies to teichoic acid (Chronic infections)
.
31

32. Identification of an isolate as a staphylococcus relies
largely on microscopic and colony morphology, and
catalase positivity.
◦Bacteria stain strongly gram-positive, and are
frequently seen in grapelike clusters.
◦S. aureus is distinguished from the coagulase-
negative staphylococci primarily by coagulase
positivity.
◦In addition, S. aureus colonies tend to be yellow and
β-hemolytic,rather than gray and non hemolytic like
the coagulase-negative staphylococci.
◦S. aureus is also distinguished from most coagulase-
negative staphylococci by being mannitol-positive.
32

33. Table: Biochemical characteristic of Table: Biochemical characteristic of
staphylococcistaphylococci
33

34. Fig. Flow
diagram for
the
preliminary
identification
of human
Staphylococ
cus species
34

35. Treatment, Prevention & control
Treatment
always prescribe drugs after sensitivity testing.
90% S. aureus is resistant to penicillin( penicillase, beta-
lactamase)
Prevention and control
Source of infection is shedding human lesions,
human respiratory tract and skin contact
Treatment of nasal carriers with topical antiseptics
or Rifampicin and anti-staphylococcal drug.
There is no effective vaccine against S. aureus.
Infection control procedures, such as barrier
precautions and disinfection of hands and fomites,
are important in the control of nosocomial S. aureus
epidemics.
35

36. Q1.A 32-year-old woman became ill four days after the
onset of her menstrual period. She presented in the
emergency room of Nekemte hospital with fever
(104°F; normal = 98.6°F), elevated white blood cell
count (16,000/mm
3
; normal = 4,000 to 10,000/mm
3
),
and a rash on her trunk and extremities. She
complained of fatigue, vomiting, and diarrhea. She
had recently eaten at a fast-food at Dessalegn hotel,
but otherwise had prepared all her meals at home.
The patient described most likely has:
A. staphylococcal food poisoning.
B. scalded skin syndrome.
C. infection with a Staphylococcus saprophyticus.
D. chickenpox.
E. toxic shock syndrome.
36

37. Reading assignment II
Micrococcus
◦General characteristics
◦Virulence and pathogenicity
◦Laboratory diagnosis
37

38. Genus StreptococciGenus Streptococci
Properties
are gram-positive, nonmotile, and catalase-negative
are ovoid to spherical in shape, and occur as pairs or
chains
Most are facultative anaerobes, but grow fermentatively
even in the presence of oxygen.
blood-enriched medium is generally used for their
isolation
Capsular streptococcal strains give rise to mucoid colonies
They are widely distributed in nature and are found in
URT, GIT and GUT as normal microbial flora.
They are heterogeneous group of bacteria, and no one
system sufficient to classify them.
38

39. Currently Streptococci can be classified
based on
1. Clinical scheme as pyogenic, oral, and enteric
2. Hemolytic pattern as beta, alpha, and gamma
hemolytic on blood agar.
3. Serological property (antigenic composition of group
specific cell wall substance)
Streptococci produce group specific carbohydrates(C
carbohydrates) identified using group specific
antiserum:
Lancefield grouping A to H, K to M, & O to V
4. Biochemical (physiological) property.
sensitivity to Bacitracin and optochin, Growth in
6.5%NaCl , Bile solubility.
39

40. NB: Viridans streptococci
and anaerobic
streptococci are not
grouped under Lancefield
Classification.
40

41. Species Lance field group Hemolysis Biochemical property
S. pyogenes A beta Bacitracin sensitive
S. agalactiae B beta Bacitracin resistant
S. faecalis D Alpha or gamma Growth in 6.5%NaCl
S. bovis D Alpha or gamma No growth in 6.5%NaCl
S. pneumoniae no Alpha Bile soluble, inhibited by OPt
Viridian group no Alpha Not bile soluble, inhibited by
optochin
41

42. Group A streptococci (Group A streptococci (S. pyogenes)S. pyogenes)
The most pathogenic member of the genus.
occur as long chains when recovered from liquid
culture ,but
may appear as individual cocci, pairs, or clusters of
cells in Gram stains of samples from infected tissue.
It is present as a commensal in the URT
(nasopharynx) in a variable proportion of healthy
individuals and on the skin.
It produces different types of enzymes and exotoxins.
The pathogen is spread from person to person through
respiratory droplets.
42

43. Virulence factors:
capsule: (Hyaluronic acid), identical to that found in human
connective tissue, is antiphagocytic
lipotiechoic acid: binds to epithelial cells.
Cell wall: The cell wall contains a number of clinically
important components:
A.Fimbriae: contain the major S. pyogenes virulence factor,
the M protein.
M proteins are highly variable, especially the N-terminal
regions, resulting in over eighty different antigenic types
Schematic
representation
of the
streptococcal M
protein.
43

44. ◦M protein is the main antiphagocytic component of S.
pyogenes,
M-like protein: binds to immunoglobulin M and G
and alpha-2 micro globulin
Protein F (fibronectin-binding protein): mediates
attachment to fibronectin in the pharyngeal
epithelium.
Pyrogenic exotoxin A: is the toxin responsible for
most cases of streptococcal TSS.
◦It has the same mode of action as does
staphylococcal TSST
44

45. Hemolysins: Two types
A.Streptolysin-S: lyses leukocytes, platelets and
erythrocytes, stimulate release of lysosomal
enzymes.
It is non immunogenic.
not inactivated by oxygen (oxygen-stable)
B. Streptolysin-O: the same as to that of streptolysin S
but immunogenic and inactivated by oxygen
(oxygen-labile)

Antibody (ASO)develops after infection
Streptokinase: lyses blood clots (Fibrinolysin) and
facilitate spread of bacteria.
It is an active proteolytic enzyme which lyses fibrin
by catalytic conversion of plasminogen to plasmin.
Has been given intravenously for the treatment of
pulmonary edema and of arterial and venous
thrombosis
45

46. DNAse: depolymerises cell free DNA.
C5a peptidase: degrades complement component
C5a.
Hyaluronidase: Spreading factor
It degrades the ground substance of connective
tissue (hyaluronic acid) and aids in spreading
infectious micro-organisms
Erythrogenic toxin causes the rash of scarlet fever.
Its mechanism of action is similar to that of the TSST
of S. aureus
46

47. 47

48. Epidemiology
The only known reservoir for S. pyogenes in nature is
the skin and mucous membranes of the human host.
 Respiratory droplets or skin contact spread Group A
streptococcal infection from person to person,
especially in crowded environments such as classrooms
or children's play areas.
Clinical significance
S. pyogenes cause disease in three mechanisms;
inflammatory mediated, exotoxin mediated, and
immunologic mechanism.
48

49. S. pyogenes causes three types of diseases:
(1) pyogenic diseases such as pharyngitis, cellulitis, acute
Otitis, Impetigo and erysipelas

.
Lesions of erysipelas, caused by group A
beta-hemolytic streptococcal toxins.
49

50. (2) toxigenic diseases such as scarlet fever and toxic
shock syndrome,and
 (3) immunologic diseases such as rheumatic fever
and acute glomerulonephritis
Acute glomerulonephritis occurs usually following
a streptococcal infection of the skin.
There is inflammation of the kidney due to
deposition of immune complex in the glomerulli.
◦It clinically manifests with generalized body edema,
elevated blood pressure, protein and blood in the
urine, blood urea nitrogen retention and low
complement level.
50

51. Acute rheumatic fever
◦(This autoimmune disease occurs 2 to 3 weeks after the
initiation of pharyngitis.
◦ It is caused by cross-reactions between antigens of the
heart and joint tissues, and the streptococcal
antibody).
◦It clinically presents with fever, malaise, migratory non-
supprative polyarthritis, carditis, erythema
marginatum and subcutaneous nodules
51

52. Necrotizing fasciitis due to group A
streptococci.
Necrotizing fasciitis (Streptococcal gangrene):
Extensive and rapidly spreading necrosis of skin
and subcutaneous tissue.
NB. S. pyogenes is the
most common bacterial
cause of sore throat.
52

53. Laboratory diagnosis
Depending on the form of the disease, specimens for laboratory
analysis can be obtained from throat swabs, pus and lesion
samples, sputum, blood, or spinal fluid.
Culture & growth characteristics
Most grow an solid media
Media should be supplemented with blood / tissue
fluids
Strains with capsular materials produce mucoid
colonies
Growth & hemolysis are aided by incubation in
10% CO2
Most hemolytic strep. cocci grow best at 370C
Most strep cocci are facultative anaerobes
53

54. S. pyogenes forms characteristic small, opalescent
colonies surrounded by a large zone of beta hemolysis
on sheep blood agar.
◦[Note: Hemolysis of the blood cells is caused by
streptolysin S, which damages mammalian cells
resulting in cell lysis.]
◦This organism is highly sensitive to bacitracin.
◦Serologic tests detect a patient's antibody titer to
streptolysin-O (ASO test) after group A streptococcal
infection.
Serology
◦Rapid latex antigen kits for direct detection of group A
streptococci in patient samples are widely used.
◦Specimens from patients with clinical signs of pharyngitis
and a negative antigen detection test should undergo
routine culturing for streptococcal identification.
54

55. Group B beta-Hemolytic Streptococci (Streptococcus
agalactiae)
◦S. agalactiae is found in the vaginocervical tract of
female carriers, and the urethral mucous membranes
of male carriers, as well as in the GI tract, and oral
cavity as normal flora
◦Transmission occurs from an infected mother to her
infant at birth, and venereally (propagated by sexual
contact) among adults.
In neonates it causes two forms of diseases
1.Early on set:
Results from vertical transmission of the
microorganism from mother to infant in the uterus or
during passage through the birth canal.
55

56. It has high mortality as a result of
neonatal sepsis or pneumonia.
2. Late onset:
Can be acquired from mothers, hospital personnel,
etc.
Meningitis is the most frequent complication of
late on set.
•Group B streptococci can also cause endocarditis, Group B streptococci can also cause endocarditis,
arthritis, osteomyelitis and sexually transmitted arthritis, osteomyelitis and sexually transmitted
diseases.diseases.
•The predisposing factors include diabetes, premature The predisposing factors include diabetes, premature
labor, and prolonged rupture of placental membrane.labor, and prolonged rupture of placental membrane.
•It causes septic abortion in pregnant womenIt causes septic abortion in pregnant women
56

57. Laboratory diagnosis
◦Samples of blood, cervical swabs, sputum, or spinal
fluid can be obtained for culture on blood agar.
◦Group B streptococci are β-hemolytic, with larger
colonies and less hemolysis than group A.
◦Most isolates remain sensitive to penicillin G and
ampicillin, which are still the antibiotics of choice.
57

58. Streptococcus Pneumoniae
(Pneumococcus)
◦S. pneumoniae are gram-positive, nonmotile,
encapsulated cocci.
◦They are lancet-shaped, and their tendency to occur
in pairs accounts for their earlier designation as
Diplococcus pneumoniae.
◦ In tissue, pus or sputum pneumococci are typically
arranged in pairs (diplococci) each coccus some what
elongated, and pointed at one end but rounded at the
other (lanceolate) and the two members of a pair
point away from each other.
–Has an autolytic enzyme
–Possess a capsule of polysaccharide that permits typing
with specific antisera (more than 80 serotypes)
58

59. A. Epidemiology
S. pneumoniae is an obligate parasite of humans, and
can be found in the nasopharynx of many healthy
individuals.
It is extremely sensitive to environmental agents.
Pneumococcal infections can be either endogenous or
exogenous.
◦For example, endogenous infection involves the
spread of S. pneumoniae residing in the
nasopharynx of a carrier who develops impaired
resistance to the organism.
59

60. Pathogenesis
◦capsule of S. pneumoniae is the most important virulence
factor.
◦ Cell-associated enzymes, pneumolysin, and autolysin
contribute to its pathogenicity
Autolysin: This peptidoglycan hydrolase is present in cell wall,
and is normally inactive.
◦However, it is readily triggered (for example, by surface-active
agents, beta-lactam antibiotics, or aging), resulting in cell lysis.
Autolysin is thus responsible for the release of intracellular
virulence factors (notably, pneumolysin).
Pneumolysin:
◦is an important virulence factor by virtue of its ability to attack
mammalian cell membranes, causing lysis once it is released
by autolysin from the interior of the bacterium.
60

61. Clinical pictures
◦Pneumococci cause pneumonia, meningitis,
endocarditis, Otitis media, bacteremia and infection of
the upper respiratory tract.
The following factors lower host resistance and
predispose to pneumococcal infection;
Alcohol or drug intoxication or other cerebral
impairment that can depress the cough reflex and
aspiration or secretion.
Abnormality of the respiratory tract
Chronic disease such as sickle cell anemia and
nephrosis
Trauma to the head that causes leakage of spinal fluid
through the nose predisposes to pneumococcal
meningitis.
61

62. Age-specific rates of community-acquired
pneumonia caused by specific pathogens.
62

63. Laboratory diagnosis
Specimens for laboratory evaluation can be obtained
from a nasopharyngeal swab, blood, pus, sputum, or
spinal fluid.
Lancet-shaped, gram-positive diplococci are observed
on a Gram stain of the sample.
α-Hemolytic colonies appear when S. pneumoniae is
grown on blood agar overnight under aerobic
conditions at 37°C.
Growth of these bacteria is inhibited by low
concentrations of the surfactant, optochin, and the
cells are lysed by bile acids.
Capsular swelling is observed when the pneumococci
are treated with type-specific antisera (the Quellung
reaction).
63

64. Laboratory tests useful in the identification of
Streptococcus pneumoniae.
A. Optochin disk test.
B. Quellung reaction.
C. Lysis by bile acids.
Treatment, prevention and
control
drugs of choice are penicillin,
erythromycin and cotrimoxazole.
immunization with polyvalent
polysaccharide vaccine provides
long lasting immunity( at least 5
years ).
64

65. Enterococci
◦Enterococci contain a C-carbohydrate that reacts
with group D antisera.
◦ Therefore, in the past, they were considered group
D streptococci.
◦Today, DNA analysis and other properties have
placed them in their own genus, Enterococcus.
◦The clinically most important species are E. faecalis
and E. faecium.
◦Enterococci can be alpha, beta, or nonhemolytic.
◦enterococci are not very virulent, but they have
become prominent as a cause of nosocomial
infections as a result of their multiple antibiotic
resistance.
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66. A. Epidemiology
◦Enterococci are part of the normal fecal flora.
◦However, they can also colonize oral mucous
membranes and skin, especially in hospital settings.
◦ These organisms are highly resistant to environmental
and chemical agents, and can persist on fomites.
B. Diseases
◦Enterococci seldom cause disease in normal, healthy individuals.
◦ However, if host resistance is lowered or the integrity of the GIT
or GUT has been disrupted (for example, by instrumentation),
enterococci can spread to normally sterile sites, causing
◦urinary tract infections, bacteremia-sepsis, subacute bacterial
endocarditis, biliary tract infection, or intra-abdominal abscesses.
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67. C. Laboratory identification
◦Enterococci are distinguished from the non Group D streptococci
by
ability to survive in the presence of bile, and
 hydrolyze the polysaccharide esculin.
◦Unlike nonenterococcal group D streptococci,
 enterococci grow in 6.5 percent NaCl, and yield a positive
pyrazin amidase (PYR) test.
◦E. faecalis can be distinguished from E. faecium by their
fermentation patterns, which are commonly evaluated in clinical
laboratories.
D. Treatment
◦Enterococci are naturally resistant to beta-lactam antibiotics and
aminoglycosides, but are sensitive to the synergistic action of a
combination of these classes
E. Prevention
◦Judicious use of antibiotics is an important factor in controlling
the emergence of enterococcal infections.
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68. Reading assignment III
1. Nonenterococcal Group D Streptococci
2. Viridans streptococci
◦General characteristics
◦Virulence factor and pathogenesis
◦Clinical manifestation
◦Lab. diagnosis
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