ORGANISM MOT PATHOPHYSIOLOGY CLINICAL MANIFESTATIONS TREATMENT PREVENTION

AND CONTROL
Streptococcu Spread from Virulence factors Diseases caused by S. pyogenes are  s.pyogenes remains S. pyogenes is so
s pyogenes person to attributable to different factors, which are as sensitive to widespread that the
person. follows: PENICILLIN. The scope for preventive
treatment of choice measures is limited.
- It is most Attributable to INVASION in pharyngeal or skin
commonly infections with S.  There is no
1. Erysipelas pyogenes is protective vaccine.
spread by - If the portal of entry is the skin, therefore a 10 day Skin infections can
the direct erysipelas results with massive best be avoided by
course of oral or
contact of brawny edema & a rapidly parenteral following hygiene
mucus from advancing margin of infection penicillin. measures and
a sick, 2. Cellulitis generally
infected - Streptococcal cellulitis is an acute,  Erythromycin improving
person to a rapidly spreading infection of the should be given to standards of
healthy skin & subcutaneous tissue patients who are living in tropical
person. - It follows infection associated with allergic to and subtropical
mild trauma, burns, wounds or penicillin, but countries.
Strains of Str. pyogenes express a large arsenal surgical incisions resistance has been
of viruence factors and, hence, their pathogenicity - Pain, tenderness, swelling & observed.  Treatment with
and the clinical signs that they induce are very erythema occur Cellulitis is antibiotics should
diverse. The viru- lence factors are involved in differentiated from erysipelas by 2  Alternatively, be started as
adherence, evasion of host immunity and tissue clinical findings, lesion is not treatment with a five quickly as
damage. raised and ine between the to 10 day course of possible. The
involved & uninvolved tissue is an oral occurrence of
indistince cephalosporin or infection in
Adhesion. Interaction with host fibronectin, a
3. Necrotizing fasciitis (streptococcal macrolide has hospitals demands
matrix protein on eukaryotic cells, is considered
gangrene) shown good results. special hygiene
the principal mechanism by which Str. pyogenes
- Extensive & very rapidly spreading measures. An early
binds to epithelial cells of the pharynx and skin.
necrosis of the skin, tissue & fascia  In cases of severe start of a 10 day
The interaction between the streptococcal F
Group A streptococci that cause systemic infection course of antibiotics
protein and host cell fibronectin also mediates
necrotizing fasciitis have (septicaemia, shortens the
internalization of the bacteria into host cells.
sometimes been termed flesh- streptococcal toxic infectivity period
eating bacteria shock syndrome, and reduces the
M proteins. The ability of Str. pyogenes to resist
4. Puerperal fever necrotising fasciitis), likelihood of late
phagocytosis by polymorphonuclear leucocytes
- If the streptococci enter the uterus a dose of sequelae after
is to a high degree due to the cell surface-exposed
after delivery, puerperal fever clindamycin is pharyngitis.
M protein. Acquired resistance to infection by
develops which is essentially a recommended in Asymptomatic
Str. pyogenes is the result of antibodies in
septicemia originating in the addition to carriers are not
secretions and sera to the M protein molecule.
infected wound (endometritis) parenteral penicillin. treated.
However, as a result of genetic polymorphism in
5. Bacteremia or Sepsis
the gene encod- ing the M protein, the most
- Infection of traumatic or surgical  Contacts do not
distal part of the protein shows extensive
 wounds with streptococci results in have to adhere to
variability among strains. As a consequence, bactermia which can rapidly be special measures;
individuals may suffer from recurrent Str. pyo- fatal they should be
genes infections with strains expressing different - S. pyogenes bacteremia can also informed about
versions of the M protein. More than 80 different occur with skin infections such as the risk of
types of M protein have been identified by cellulitis & rarely pharyngitis infection and
serological means. possible
Attributable to LOCAL INFECTION symptoms, so that
All these proteins can bind various serum proteins if they become ill
of the host, including fibrinogen, plasminogen, 1. Streptococcal Sore Throat they can seek
albumin, IgG, IgA, the pro- teinase inhibitor 2- - Most common infection caused by medical advice.
macroglobulin, and some regulatory factors from β-hemolytic S. pyogenes. Infection
the complement system (factor H and C4b- of the upper respiratory tract does
binding protein). not usually involve the lungs but in
severe cases, Pneumonia may
Capsule. Some strains of Str. pyogenes form a occur. Frequently characterized by
capsule composed of hyaluronic acid. Such sore throat, fever, malaise,
strains grow as mucoid colonies on blood agar
headache, tonsillar abscesses &
and are highly virulent in animal models. While
capsule production is rare among isolates from tender anterior cervical lymph
uncomplicated pharyngitis, a significant proportion nodes
of isolates from severe infections have a capsule. 2. Streptococcal pyoderma
Like other bacterial capsules it has an - Local infection of superficial layers
antiphagocytic effect. of skin especially in children is
called impetigo. Consists of
The capsule is identical to the hyaluronic acid of superficial vesicles (blisters) that
the connective tissue of the host and is not break down and eroded areas
immunogenic. The bacteria may, in this way, whose denuded surface is covered
disguise themselves with an immunological ‘self’ with pus & later is encrusted
substance.
Other DISEASES
C5a peptidase. The C5a peptidase, which is
found also in human pathogenic strains of Str. 1. Streptococcal Toxic Shock
agalactiae, is presented on the surface of all Syndrome
strains of Str. pyogenes. It specifically cleaves, - Infection tend to occur after minor
and thereby inactivates, human C5a, one of the trauma in otherwise healthy
principal chemoattractants of phagocytic cells. persons with several presentations
of soft tissue infection such as:
Streptolysins. Str. pyogenes produces two ◌ Necrotizing fasciitis
distinct haemolysins, termed streptolysins O ◌ Myositis
(oxygen-labile) and S (serum-soluble), both of ◌ Infections at other sites
which lyse erythrocytes, polymorphonuclear - Characterized by shock,
leucocytes and platelets by forming pores in bacteremia, respiratory failure &
 multiorgan failure. Death occurs
their cell membrane. in about 30% of patients
2. Scarlet Fever
Streptolysin O may play a role in the - Caused by pyrogenic exotoxins A-
pathogenesis of post-streptococcal rheumatic C in association with S. pyogenes
fever. Serum antibodies can be demonstrated pharyngitis or with skin or soft
after streptococcal infection, particularly after tissue infection
severe infections.
NON-SUPPURATIVE Sequelae
Streptolysin S is responsible for the -haemolysis
around colonies on blood agar plates. It can also 1. Acute Glomerulonephritis
induce the release of lysosomal contents with - Sometimes develops 1-4 weeks
subsequent cell death after engulfment by after S. pyogenes skin infection
phagocytes. In contrast to streptolysin O it is not (pyoderma, impetigo) or pharyngitis
immunogenic. particularly nephritogenic
principally with M types 12, 4, 2 &
Pyrogenic exotoxins. Most strains of Str. 49
pyogenes produce one or more toxins that are - Glomerulonephritis may be initiated
called pyrogenic exotoxins because of their ability by antigen-antibody complexes on
to induce fever. Three, SPE A, SPE B and SPE the glomerular basement
C, have been extensively charcterized, but there membrane
are several others. Purified SPE A causes death 2. Rheumatic Fever
when injected into rabbits, and is the most toxic of - Most serious sequel of S.
the three, but SPE B also causes myocardial pyogenes because it results in
necrosis and death in experimental animals. damage to heart muscle & valves.
- Certain strains of group A
streptococci contain cell membrane
Hyaluronidase. Str. pyogenes and several other
antigens that cross-react with
pyogenic streptococci use a secreted
human heart tissue antigens
hyaluronidase to degrade hyaluronic acid, the
(molecular mimicry). Signs and
ground substance of host connective tissue.
symptoms include fever, malaise,
This property may facilitate the spread of infection
migratory nonsuppurative
along fascial planes. During infections, particularly
polyarthritis, evidence of
those involving the skin, serum anti- body titres to
inflammation of all parts of the
hyaluronidase show a significant rise.
heart (endocardimyocardium,
pericardium)
Streptokinase. Streptokinase, also known as
fibrinolysin, is another spreading factor. It is
expressed by all strains of Str. pyogenes and co-
operates with a surface- expressed plasminogen-
binding site on the bacteria. Once host
plasminogen is bound to the bacterial surface, it is
activated to plasmin by streptokinase. Thus, in
contrast to Staph. aureus, which aims at hiding
 behind a wall of coagulated plasma (fibrin), Str.
pyogenes employs host plasmin to hinder build-up
of fibrin barriers. As a result, soft tissue infections
due to Str. pyogenes are more diffuse, and often
rapidly spreading, in contrast to the well localized
abscesses that typify staphylococcal infections.

Lipoproteinase. This enzyme is also called

opacity factor, as it induces opalescence in
growth media containing serum. The exact
biological significance is not known but there is a
strong correlation between the production of this
enzyme and particular M types, and it is produced
mainly by strains causing skin infections.

Deoxyribonucleases (DNAases). At least four

dis- tinct forms of DNAases, designated A, B, C
and D, are produced by Str. pyogenes. DNAase B
is the most common form. The enzymes hydrolyse
nucleic acids and may play a role as spreading
factors by liquefying viscous exudates.

Spread is The virulence factors of S. saprophyticus Clinical features. Common symptoms of  Staphyloccus The single most
through direct include: inflammation and infection of the lower saprophyticus important factor that
contact. tract, such as hematuria and pyuria, were infections are treated can reduce the
Lipoteichoic Acid. It is associated with seen more often among patients with with Penicillin and incidence of
adherence to urothelial cells by means of a colonization of S. saprophyticus. In addition, are resistant to
infections due to
surface-associated protein, S. saprophyticus was the cause of 13% of Novubiocin.
Hemagglutinin. This structure binds to upper UTIs, an incidence higher than that
coagulase-negative
fibronectin, a hemolysin; reported for other bacteria. In addition, some  Penicillin-resistant staphylococci as S.
Slime. The production of extracellular slime also observations were showed that significantly may be given with saprophyticus is
contributes to its virulence. more patients infected with S. saprophyticus cephalosporins or strict adherence to
complained of dysuria, urinary frequency, and glycopeptides hand washing, both
back pain than did patients infected with E. alternatively. prior to and after
coli. examining patients.

Meticulous surgical
technique is
paramount to limit
intra-operative
bacterial
contamination,
particularly in
procedures where
foreign bodies such
as prosthetic valves
and joints are being
introduced. Strict
attention to

Coagulase-negative
staphylococci are part
of the normal nasal
and cutaneous flora
so they will never be,
nor should they be
fully eradicated.
There may be
healthcare-related
clones, much like
some clones of S.
aureus, that are move
virulent and
eradication of such
clones may be
desirable when there
are proven methods
for effective
decolonization.