Transcript meca auto

STAPHYLOCOCCUS &
STREPTOCOCCUS
STAPHYLOCOCCUS
• Important properties
• They are gram positive, spherical grape like
clusters, some strain produce capsule , non
fastidious, capable of aerobic and anaerobic
respiration
• can ferment carbohydrate and produce lactic
acid and not gas
• Resistance to drying, to heat (can withstand)
up to 50⁰C for 30 minutes
• Some are members of the normal flora of the
skin and mucous membrane
•
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•
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The main species of clinical importance are
Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus saprophyticus
S. aureus is coagulase positive
This characteristic differentiate it from other
staphylococcus species
S. epidermidis Is a normal body flora
• It causes infection associated with
implanted appliances and devices especially
in very young, very old and, can adhere to a
critical heart valve, vascular catheters,
shunts, and prosthetic joints may cause
tissue destruction mediated by degradative
enzymes.
• S. saprophyticus is common cause of urinary
tract infections in young women.
Staphylococcus aureus
• They are gramme positive coccus, cells in
clusters reflecting ability to divide in more
than one plane.
• Some strain produce capsules, non fastidious
• Capable of aerobic and anaerobic respiration
Diagnosis/ Laboratory
identification
• White or golden colonies of blood agar.
Catalase positive, coagulase positive, most
strains ferment mannial anaerobically.
Diseases
• Boils, skin sepsis, postoperative wound
infection, scalded skin syndrome, catheter
associated infection, foodborne infection,
septicemia, endocarditis, toxic shock
syndrome, osteomycetis pneumonia.
Two types S. aureus diseases
Pyogenic
infections
Toxic mediated
infections
Abscess, boils,
carbuncles
Endocarditis,
osteomyelitis
Pneumonia
No. 1 Food poisoning
Wound infections
Toxic shock
syndrome
Scalded skin
syndrome
EPIDEMIOLOGY
Sources of infection
1. Infected lesions
large number of staphylococcus are
disseminated from large infected
wounds, burns, secondary infected
lesions and in sputum coughed from the
lung of patients with bronchopneumonia
2.Direct contact
• small discharge lesions on the hands
of doctors and nurses are special
danger to their patients.
• airborne dissemination may also
occur
• cross infection is important method of
spread staphylococcal disease
particularly in hospital.
• Scrupulous and hand washing is
essential in preventing spread
3.Food handlers
may similarly introduce enterotoxin producing
food poisoning strains into food
4. Health carriers
• Staphylococcus aureus grows harmlessly on
the nostrils in many health persons and the
perineum is also commonly colonized.
Organisms are spread from these sites into
the environment by the hands,
handkerchiefs, clothing and dust consisting
of skin squames and cloth fibres
During the first day or two of life
babies become colonized in the nose
and skin by staphylococcus acquired
from their mother, nurse or
environment
• Nasal carriage in babies as in older
person is usually long lasting
• Transmission from babies to nursing
mothers cause mastitis
5. Animals
• may disseminate S. aureus which
cause infection to humans e.g. milk
from diary cow with mastitis cause
staphylococci food poisoning
MODE OF INFECTION
• Acquisition of infection can be exogenous
(from external source) or endogenous
(from internal source) or minor lesion
elsewhere in the patients own body.
• Staphylococcus do not grow outside the
body except occasionally in moist nutrients
material such as meat, milk and dirty water
• Body surface of human being and animals
are the main reservoir
• Although not spore forming they
remain alive in dormant state for
several months when dried in pus,
sputum, bed cloths or dust.
• They are killed by heat ( e.g. in moist
heat at 65 0C for 30 minutes) also by
exposure to light and common
disinfectants
PATHOGENESIS
• Staphylococcus cause diseases by
producing toxin and by multiplying in
tissue and causing inflammation
• The typical lesion of staphylococcus is
an abscess a localized region with pus
surrounded by inflamed tissue.
• The abscess undergo central necrosis
and usually drain to the outside (e.g.
boils ) but the organism may
disseminate via the blood stream as
well
Toxins and enzymes produced by
Staphylococcus aureus
 1. Enterotoxin: causes food poisoning
characteristics by prominent vomiting, and
non blood diarrheal it act as a super antigen
within the gastrointestinal tract to stimulate
the release of large amounts of interleukuin
1 (IL-1) and IL- 2from macrophage and
helper T cells
• Vomiting is caused by cytokins released
from lymphoid
Toxin conti….
• 2. Toxic shock syndrone toxin: caused toxic
shock especially . TSST causes shock by
stimulating the release of IL-1, IL-2 and turmor
necrosis factor (TNF)
Toxin cont……
• 3. Exfoliation: causes scalded skin, syndrome
in young children
• 4. Several toxins can kill the leucocytes and
cause necrosis of the tissue in vivo.
• The enzymes: coagulase, fibrinolysin,
hyaluronidase, protease, nucleuases, and
lipase.
• Coagulase, by clotting plasma serves to wall of
the infected site thereby retarding the
migration of neutrophils into the site.
• Staphylokinase is a fibrinolysis that can lyse
thrombin,
S. aureus (Pyogenic diseases)
• 1. Skin infection are very common.
• 2. Septicemia from localized lesion esppecially
wound infection.
• 3. Endorcaditis
• 4. Osteomycetis and urthritis especially to
children
• 5. Postsurgical wound infection
• 6. Pneumonia can occur in postoperative
patients
• 7. Abscesses
S. aureus (mediated diseases)
• 1. Food poisoning: vomiting and diarrhea
• 2. Toxic shock syndrome : fever, hypotension,a
diffuse, macular, sunburn like rash
• 3. Scalded skin syndrome; fever, large bulle,
Disease caused by exotoxin release:
1. Gastroenteritis (food poisoning)
Staphylococcus can grow in food and
produce an exotoxin
• When this food containing the
pre-formed toxin is eaten the
toxin stimulates peristalsis of the
intestine with ensuring nausea,
vomiting, diarrhoea abdominal
pain and occasionally fever.
• Incubation period is 1-8hrs
2.TOXIC SHOCK SYNDROME
• The syndrome involves the sudden onset of
high fever, nausea, vomiting and watery
diarrhoea (enterotoxin like) followed in a
few days by a diffuse erythematous (red)
rashes, myalgias, and hypotension with
cardiac and renal failure in most severe
cases.
• NB: Beta hemolysis (β-hemolysis), sometimes called complete
hemolysis, is a complete lysis of red cells in the media around and
under the colonies)
• The toxic shock syndrome is also
associated with septic shock.
• The patient may suffer severe organ
system damage (such as acute
respiratory distress syndrome or
acute renal failure)
• Infected sutures in surgical wounds,
cutaneous and subcutaneous infections
following child birth or abortion can all be foci
from which Staphylococcus aureus can release its
TSST-1 exotoxin
• Tampons when left in place for a long time
in some way stimulate the Staphylococcus aureus
to release the exotoxin TSST-1 which penetrate
vagina mucosa
TREATMENT
• Treatment include remove the tampon or
drainage of an infected wound along with
supportive care
• Antibiotic may help by killing the bacteria and
preventing more exotoxin from being
produced
• However antibiotic is not curative since it is
the exotoxin, not the bacteria which cause the
clinical manifestation
3.STAPHYLOCOCCAL SCALDED SKIN
SYNDROME
• This disease is similar in pathogenesis to
toxic shock syndrome
• S. aureus strain which produce exfoliatin
toxin establishes a localized infection
and releases a diffusible toxin that exerts
distance effects.
• Unlike toxic syndrome it usually affect
neonates with local infection of umbilicus or
older children with skin infection.
1. Infant and young children develop toxic
epidermal necrolysis (i.e Ritter’s disease)
which is characterized by large areas of
denuded skin and generalized bullae
formation.
• The syndrome is referred to as the
scalded baby syndrome because of the
moist red areas of denuded skin.
2. Older children and adult develop
localized bullae which are also red and
moist in appearance
• The syndrome is known as Lyell’s disease and
more common known as scalded skin syndrome
• Healing occurs without scaring in the absence of
secondary bacteria infection
3. Older children and adult also may develop a
scarlatina- like rash.
• The syndrome mimic streptococcal scarlet fever
except that the tongue and palate are not
involved
NOTE!
• The doctor must rule out a drug allergy
since this can present similarly and may
result in death if the use of the
offending drug is not halted
DISEASE RESULTING FROM DIRECT ORGAN
INVASION BY THE BACTERIA
1. PNEUMONIA
• S. aureus is a rare but severe cause
of community-acquired bacterial
pneumonia
• Pneumonia is more common in
hospitalized patients
• It usually follows a viral influenza
(flu) upper respiratory illness with
abrupt onset of fever, chills, and
lobar consolidation of the lung with
rapid destruction of the lung
parenchyma resulting in cavitations
(holes in the lungs)
• This violent destruction pneumonia
frequently causes effusions and empyema
(pus in the pleural space)
2.Meningitis,Cerebritis,Brain abscess
• The patient can present with high fever, stiff
neck, head ache, coma, and focal
neurological signs
3. OSTEOMYELITIS
• This is a bone infection which usually
occur in boys under 12 years of age
• The infection spreads to the bone
hematogenously
• presenting locally with warm swollen
tissue over the bone and with systemic
fever and shakes
4. ENDOCARDITIS
• Acute bacteria endocarditis is
caused by S. aureus.
• It is characterised by relatively
short time of less than 6 weeks
1. The infected
heart valve typically is
coated with numerous vegetation
composed of plateletes, bacteria and
other amorphous cellular debris;
perforation of the heart valve results
from the many extracellular enzymes
and products of S. aureus.
• Pieces of vegetation known as infective
emboli may dislodge into the circulation and
establish a focus of infection in any organ
system
• Emergency surgical replacement of the
heart valve usually is necessary to prevent
death from cardiac insufficiency.
• antimicrobial therapy is of minimal
value because the agents are unable to
penetrate the vegetation.
• Sub acute endocarditis is caused by S.
epidermidis. It has a time course of more
than 6 weeks and typically follows thoracic
surgery.
• Vegetation is not a prominent feature of
sub-acute endocarditis and intravenous
antimicrobial therapy generally eliminates
the infection
OTHER DISEASES CAUSED BY
STAPHYLOCOCUS
• Septic arthritis
• Skin infections
• Bacteraemia/sepsis
• Urinary tract infection
DIAGNOSTIC LABORATORY TESTS
• SPECIMENS
• One or more of the following specimens
should be collected to confirm a diagnosis
• Pus from abscess, wounds, burns
• Sputum from cases of pneumonia
• Faeces or vomits from patients with
susceptible food poisoning or the remaining
of implicated food
A. BLOOD
from patients with suspected bacteraemia, e.g.
septic shock, osteomyelitis or endocarditis
• Mid stream urine from patients with
suspected cystitis or pyelonephritis
• Anterior nasal and perineal swabs
(moistened in saline or sterile water) from
suspected carriers
B. SMEARS
• Typical Staphylococci are seen in stained smears
of pus or sputum. It is not possible to distinguish
saprophytic S. epidemidis from S. aureus
C. CULTURE
Specimen planted on blood agar plates give rise to
colonies in 18 hrs at 370 but haemolysis and
pigment production may not occur until several
days
S. aureus but not other staphylococci
ferment mannitol
Specimen contaminated with other flora can
be cultured on media containing 7.5% NaCl
the salt inhibit growth of other normal
flora but not S.aureus
• Mannitol salt agar is used to screen for
nasal carriers of S.aureus
D. CATALASE TEST
• A drop of hydrogen peroxide soln is placed on a
slide and small amount of the bacterial growth is
placed in the soln the formation of bubbles( the
release of oxygen) indicates a positive test
• the test can also be done by pouring hydrogen
peroxide soln over a heavy growth of bacteria on
an agar slant and observing for appearance of
bubbles
E. COAGULASE TEST
• Citrated rabbit or human plasma diluted 1:5 is
mixed with an equal volume of broth culture or
growth from colonies on agar and incubated at
370C
• a tube of plasma mixed with sterile broth is
included as control
• If clots form 1-4 hrs the test is positive Coagulase
positive staphylococcus are considered pathogenic for
humans.
F. SUSCEPTIBILITY TEST
• Susceptibility test should be done routinely on
staphylococcal isolates from clinically significant
infections.
• Resistance to penicillin G can be predicted by a
positive test for -lactimase.
• Nafcillin resistance correlates with the presence of
mecA the gene that code for a penicillin-binding
protein (PBP2a)
• The gene can be detected by polymerase chain
reaction
G.SEROLOGIC AND TYPING TESTS
• This have little practical value.
• Molecular typing technique have been
used to document the spread of
epidemic disease producing clones of
S.aureus
TREATMENT
• Most person harbours staphylococcus on
the skin and nose or throat.
• Even if skin can be cleared of
staphylococcus re-infection by droplets will
occur almost immediately.
• Because pathogenic organism are
commonly spread from one lesion to other
areas of the skin by fingers and clothing
scrupulous local antisepsis is important to
control infections
• Serious multiple skin infections ( acne,
furunculosis occurs most often in
adolescents
• Similar skin infection occur in patients
receiving prolonged corticosteroids.
• Tetracycline are used for long term
treatment
• Abscesses and other closed suppurating
lesions are treated by drainage and
antimicrobial therapy
• Is difficult to eradicate pathogenic
staphylococcal from infected persons
because the organism rapidly develop
resistance to many antimicrobial
• And drug cannot act in central
necrotic part of a suppurative lesion
• It is also difficult to eradicate the S.
aureus carrier state
• Acute haematogenous osteomyelitis
responds well to antimicrobial drugs
• In chronic and recurrent osteomyelitis ,
surgical draining and remover of dead bone
is accompanied by long term administration
of appropriate drugs
• but eradication of infecting staphylococcus
is difficult
• Bacteremia, endocarditis, pneumonia and
other severe infections due to S. aureus
required prolonged intravenous therapy
with a -lactimase-resistance penicillin
Vancomycin is often reserved for use with
nafcillin resistant staphylococci.
• If the infection is found to be due to non 
lactamase producing S. aureus penicillin G is
the drug of choice
• S. epidermis infections are difficult to cure
because they occur in prosthetic devices
where the bacteria can sequester
themselves in a biofilm.
• Because of the frequency of drug resistance
strains staphylococcus isolates should be
tested for antimicrobial susceptibility to help
in the choice of systemic drugs
• Methicillin–resistant Staphylococcus
aureus (MRSA) strains are an
increasingly infection control problem
and therapeutic challenge.
• These strains are resistant to all 
lactam agents and often
aminoglycosides and fluoroquinolones
• MRSA commonly colonize broken skin but
can cause the full range of staphylococcal
infections.
• These are predominantly hospital pathogens
in debilitated patients such as those in
intensive care units where the combination
of multiple causes of antibiotics and use of
invasive devices contribute greatly to the risk
of acquisition
• MRSA are becoming more common
in community especially in long stay
institutions
• Glycopeptides (vancomycin or
teicoplanin) are the agents of choice in
the treatment of systemic infection
Prevention
• No effective immunization with toxoids or
bacterial vaccine
• Cleanliness, frequent hand washing, aseptic
management of lesion control spread of S.
aureus
• Cefazolin is often used to perioperatively to
prevent staphylococcal surgical – wound
infection
STREPTOCOCCUS
These are bacteria belonging to the family
Streptococcae
Some members are human pathogens whereas
others are indigenous flora of the oropharynx
and gastrointestinal tract.
Properties
Gram positive spherical (cocii)
Arranged in pairs or chains
All are catalase - negative
The most important species pathogens
for humans include
Streptococcus pyogenes
Streptococcal agalactiae
 streptococcal faecalis
 the viridans streptococcus
Streptococcus pneumonia
Most important characteristic for identification of
Streptococcus is the type of hemolysis:
Alfa hemolytic streptococci form green zone around
their colonies as a result of incomplete/partially lysis
of blood cells in the blood agar)
Beta hemolytic form a clear zone around their
colonies (i.e. complete lysis of the red cell occurs)
Gamma hemolytic are unable to hemolyze the RBCs
they are therefore known as non- hemolytic
Historically the Lancefield antigens have
been used as a major way of
differentiating streptococci
However there are so many different
types of streptococci that we now don’t
rely on Lancefield antigens and more on
combination of tests such as hemolysis,
antigenic combinations, biochemical
reactions, growth characteristics and
genetic studies
BETA HEMOLYTIC STREPTOCCOCI
(Streptrococci pyogenes-GAS)
• Arranged into groups of A- U (known as
Lancefield groups)
• Group determined by precipitation tests with
antisera or by immunofluorescence
Group A ; (Streptococcus pyogenes)
• The most important human pathogens
• Many strain with hyaluronic acid capsule that is
ant phagocytic.
• Causes pharyngitis, and common in skin
infection
Group B: (S. agalactiae)
Colonize the genital tractof some
women and can cause neonatal
meningitis and sepsis.
They are usally bacitracin –resistant.
Hydrolyse (breakdown) hippurate an
important diagnostic criteria
• Group D (enterococcus eg: Enterococcus
faecalis and Enterococcus faccium) and
no enterococcus (S bovis)
• Enterococcus are member of the normal
flora of the colon.
• Causes urinary and cardiovascular
infections.
• Very hard organism not killed by
Penicyine G
•
• Nonenterococcus group D streptococci such as
B. bovis can cause above infection but are less
hardy organism eg; they are inhibited by
6.5%NaCl and killed by penicillin G.
• Groups C,E,F,G,H, and K-U Streptococci
infrequently cause human diseases.
NON – BETA – HEMOLYTIC
STREPTOCOCCI
• Some produce no hemolysis other produce
alpha-hemolysis.
• Principle organism S pneumoniae and the
viridans group of streptococci.
• S. pneumoniae are bile-solulbe and inhibited
by optochin
TRANSMISSION
Most streptococci are part of the normal flora of
human throat, skin, and intestines but produce
disease when they gain access to tissue or blood
Viridian streptococci and S. pneumonia are found
chiefly in the oropharynx
S.pyogenes is found on the skin and the oropharynx
in small numbers
S. agalactiae occurs in the female genital tract
 Enterococci and anaerobic streptococci are located
in the lower intestinal tract
PATHOGENESIS
• Group A cause diseases by three mechanism
• 1 pyogenic inflammation which is induced locally at
the site of the organism in tissue.
• 2. Exotoxin production which can cause widespread
systemic symptoms in areas of the body where there
are no organism.
• Immunological which occurs when the antibody
against a component of the organism cross- react
with normal tissue or forms immune complexes that
damage normal tissue
• The immunologic reactions cause inflammation
eg.inflamed joints of rheumatic fever.
PATHOGENESIS conti……
Group A Streptococci produce three important
inflammation – related enzymes
1.
2.
Hyaluronidase: degrade hyaluronic acid which is
the ground substance to subcutaneous tissue. Is
known as spreading factor because it facilitates
the rapid spread of S.pyogenes in skin infections:
Streptokinase (fibrinolysin); activate plasmogen
to form plasmin which dissolves fibrin in clots,
thrombi, and emboli. Lyse thrombi in the
coronary arteries of heart attack patients.
• Dnase (streptornase): depolymerizes DNAin
exudates or necrotic tissue.
• Other toxin and hemolysis produced by group
A streptococci includes:
– Erythrogenic toxin causes rash of scalrlet fever
– Streptomysin O is hemolysis.
– Streptolysin S is hemolysis
– Pyrogenic exotoxin- shock syndrome
– Exotoxin B
Virulence Factors - GAS
• Capsule: anti-phagocytosis & specific attachment to specific tissues
• M - protein in cell wall: anti-phagocytosis & specific attachment to
specific tissues
• Streptolysin O and S: leukocidins vs neutrophils & macrophages
• Streptococcal pyrogenic exotoxins (SPE): “superantigens” directly
stimulate T-cells (~1000X more than a normal immune response)
and cause them release high levels of the cytokines that are
responsible for fever and shock
• SPE is also responsible for various tissue destruction, including skin
lesions, and perhaps scarlet fever
• Hyaluronidase: dissolves the hyaluronic acid that holds cellular
basement membranes together (Hyaluronidase is therefore a
“spreading factor”)
CLINICAL
FINDINGS
S. pyogenes (group A streptococcus) is
the most common bacterial cause of
sore throat
Pharyngitis is characterized by
inflammation exudate, fever,
leucocytosis and tender cervical lymph
nodes
If untreated spontaneous recovery
occurs in 10 days
However it may extend to
otitis, sinusitis and meningitis
If the infecting streptococci produce
erythrogenic toxin and the host lacks
antitoxin scarlet fever may result
Rheumatic fever may occur following
pharyngitis
GAS can enter skin defects to
produce cellulites, erysipelas,
lymphangitis or bacteremia
They can enter the uterus after
delivery to produce endometritis and
sepsis( puerperal fever)
Streptococcal pyoderma (impertigo) is a
superficial infection of abraded skin that
forms pus or crusts
It is communicable among children
especially in hot humid climates
Glomerulonephritis may occur following
skin infections
Infective endocarditis is commonly
caused by viridans streptococci that
intermittently enter the blood stream
from the oropharynx (as a result of
poor dentition or after dental surgery)
Signs of endocarditis are anaemia,
fever, heart murmur and embolic
events
Post Streptococci Disease
These are disorders in which a local
infection with group A streptococci is
followed weeks later by
inflammation in an organ that was
not infected by streptococci
Acute Glomerulonephritis
Occurs 2-3 weeks after skin infection by
certain group A streptococcal types
 in children clinical feature include edema of
the face, ankles and smoky urine (owing to
red cell in the urine
Most patient recover completely
Re-infection with streptococci rarely leads to
recurrence of acute glomerulonephritis
The disease is initiated by antigen
antibody complexes in the glomerular
basement membrane and soluble
antigens from streptococcal membranes
may be the inciting antigen
It can be prevented by early eradication
of nephritogenic streptococci from skin
colonized sites but not by administration
of penicillin after onset of the symptoms
Rheumatic fever
Occurs from 1-4 weeks after any type of group
A streptococcal infection usually pharyngitis
Characterized by fever, migratory poly-arthritis
and carditis may develop
The carditis causes myocardial and valve
damage
Rheumatic fever is due to an immunologic
reaction. It is an auto immune disease
If streptococcal infection is treated within 8 days
after onset rheumatic fever is prevented.
After a heart damaging attack of rheumatic fever
re-infection must be prevented by long term
prophylaxis
LAB DIAGNOSIS
 Stained smear from the skin lesions or
wounds that reveal streptococci are
diagnostic
Culture of the swabs from the pharynx
Serologic
ASO titers are high soon after group A
streptococcal infections
TREATMENT AND PREVENTION
All group A streptococci are susceptible to
penicillin G but neither rheumatic fever nor
AGN patients benefit from penicillin treatment
after onset.
Endocarditis caused by most viridans
streptococci is curable by prolonged penicillin
treatment.
prevention of rheumatic fevers involve
prompt treatment of group A streptococcal
pharyngitis with penicillin
Streptococcus pneumonia
Pneumococii cause
pneumonia,
bacteremia,
meningitis,
and infections of the upper
respiratory tract such as otitis and
sinusitis
PROPERTIES
They are spherical cocci
arranged in pairs (diplococii) or short chains
Pneumococci possess polysaccharide capsule which
is the virulent factor
Transmission
Pneumococci are not considered to be
communicable since a proportion 5-50% of the
healthy population harbor virulent organism in the
oral pharynx.
Resistance is high in healthy young people and
disease result most often when predisposing factors
are present
Predisposing factors
1. Alcohol or drug intoxication or other
cerebral impairment that depress the
cough reflex and increase aspiration
of secretions
2. Abnormality of the respiratory tract
(e.g viral infection)
3. Pooling of mucus, bronchial obstruction
and respiratory tract injury due to
irritants (which disturb the movement of
mucocilliary)
4. Abnormal circulatory dynamics( e.g
pulmonary congestion and heart failure)
5. Chronic diseases( e.g sickle cell anemia,
hyposplenism, debility, malnutrition, and
nephrosis)
PATHOGENESIS
 Pneumolysin: anti-phagocytosis; it also
interferes with the action of tracheal
cilia – results in a croup-like cough
They produce IgA protease that may enhance the
organisms ability to colonize the mucosa of the
upper respiratory tract
Pneumococi multiply in tissue and cause
inflammation.
When they reach alveoli there is outpouring of
fluid and red and white cells resulting in
consolidation of the lung.
CLINICAL FINDINGS
Pneumonia begins with sudden chills
Fever, cough and pleuritic pain
Sputum is red or brown “rusty” color
Bacteremia occur in 15-25% of cases
Spontaneous recovery may begin in 5-10 days
accompanied by development of anticapsular
antibodies
 Pneumonia are a prominent cause of otitis
media, sinusitis, purulent bronchitis and
bacterial meningitis
 Lab diagnosis
 On blood agar pneumococci form small
alpha hemolytic colonies
 The colonies are bile soluble and growth is
inhibited by optochin
TREATMENT
Most pneumoccoci are susceptible to penicillin and
erythromycin
People at risk are
elderly ( people >65)
 immune compromised and
debilitated persons
Until recently the drug of choice was ampicillin in
enterococcal UTIs & non-urinary infections - this
resistance is increasing
PREVENTION
immunization with polyvalent 23 type
polysaccharide vaccine
Oral penicillin is given to young children
with hypo-gammaglobulinemia or
splenectomy because they are prone to
pneumococcal infections and respond
poorly to the vaccine
Group B streptococcal disease
S. agalactae type III cause neonatal
menengitis and type Ia cause neonatal
pneumonia
Immunity to group B streptococci is
induced by production of antibody
against the type specific antigens
Transplacental passage of maternal
antibodies to capsule of type three
protects the neonate against meningitis
GROUP D STREPTOCOCCUS
Include S. faecalis and S. faecium
(the enterococci)
Is common inhabitant of the human
gastrointestinal tract and is opportunistic or
secondary invader to damaged tissue.
The enterococci cause urinary tract infections
particularly in debilitated or immunosupressed
patients
Viridans sreptococci
 S. salvarius, S. sanguis, S. mitis and S. mutans
Two major types of human disease is caused by
viridans streptococci
1.Dental caries has been associated
with the presence of S.mutans
S.salvarius S.sanguis and S. mitis in
humans, rats and monkeys
S. mutans appear to be the most virulent spp
its pathogenesis seems to be due to ability to
adhere to the tooth surface
it produces large amounts of dextran from
sucrose but not from other carbohydrates
resulting into large plague formations
Capsule allows the bacterium (mainly S. mutans & S.
sobrinus) to adhere firmly to the teeth. Adherent
bacteria produce acid fermentation products that
dissolve the enamel of the teeth
2. Bacteria
edocarditis results
from the ability of most viridans
streptococci to adhere to
human heart valve.
They are the leading cause (#1 strep) of
bacterial native - valve and prosthetic valve
endocarditis – not pre-empted by
streptococcal pharyngitis
BLOOD ARGAR
Sheep’s blood has 3 advantages over other animal
blood:
1. Haemophilus species will not grow on SBA due to the
presence of NADase which neutralizes extracellular NAD
(“V” factor).
Hemolytic Haemophilus colonies on blood from other
animals is easily confused with beta hemolytic
Streptococcus species
2. Sheep’s blood gives a distinctly clear beta hemolysis that is
obviously different from alpha hemolysis – not necessarily
true of reactions on other animal bloods
3. Human blood can contain growth inhibiting antibodies, etc
that prevent recovery of organisms from samples
S. aureus G+VE STAIN
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