Streptococcus pyogenes Streptococcus pyogenes.jpg S. pyogenes bacteria at 900x magnification Scientific classification Kingdom: Eubacteria Phylum: Firmicutes Class: Bacilli Order: Lactobacillales Family: Streptococcaceae Genus: Streptococcus Species: S. pyogenes Binomial name Streptococcus pyogenes Rosenbach 1884 Streptococcus pyogenes is a species of Gram-positive bacteria. These bacteria are aerotolerant and an extracellular bacterium, made up of non-motile and non-sporing cocci. As expected with a streptococci, it is clinically important in human illness. It is an infrequent, but usually pathogenic, part of the skin microbiota. It is the predominant species harboring the Lancefield group A antigen, and is often called group A streptococcus (GAS). However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen. Group A streptococci when grown on blood agar typically produces small zones of beta-hemolysis, a complete destruction of red blood cells. (A zone size of 2–3 mm is typical.) It is thus also called group A (beta-hemolytic) streptococcus (GABHS), and can make colonies greater than 5 mm in size.[1] Like other cocci, streptococci are round bacteria. The name is derived from Greek words meaning chain(Strepto) of berries (coccus) and pus(pyo)-forming(genes), because streptococcal cells tend to link in chains of round cells (see image) and a number of infections caused by the bacterium, produce pus. Streptococci are can be catalase positive or negative.[2] S. pyogenes can be cultured on blood agar plates. Under ideal conditions, it has an incubation period of 1 to 3 days.[3] An estimated 700 million GAS infections occur worldwide each year. While the overall mortality rate for these infections is 0.1%, over 650,000 of the cases are severe and invasive, and have a mortality rate of 25%.[4] Early recognition and treatment are critical; diagnostic failure can result in sepsis and death.[5][6]

1. By:Nimmy.A.Shibu
Group:4
STREPTOCOCCUS
PYOGENES

2. INTRODUCTION
• Streptococcus pyogenes is a species of Gram-positive bacteria.
• These bacteria are aerotolerant and an extracellular bacterium,
made up of non-motile and non-sporing cocci.
• pathogenic part of the skin flora.
• It is the predominant species harboring the Lancefield group A
antigen, and is often called group A streptococcus (GAS).

3. • Group A streptococci when grown on blood agar typically produces
small zones of beta-hemolysis, a complete destruction of red blood
cells.
• It is thus also called group A (beta-hemolytic) streptococcus
(GABHS).
• Streptococci are round bacteria.
• Streptococci are catalase-negative and Gram-positive.

5. METHODS OF TRANSMISSION
• Respiratory droplets.
• Hand contact with nasal discharge and skin contact with
impetigo lesions.
• The pathogen can also be found in its carrier state (anus,
vagina, skin, pharynx)
• Can also be spread from cattle to humans through raw milk and
contaminated foods (salads, milk, eggs)

6. POSTSTREPTOCOCCAL DISEASES
• Acute glomerulonephritis
• Rheumatic fever

7. GLOMERULNEPHRITIS
• Glomerular nephritis, is a term used to refer to several kidney
diseases.
• Characterised by inflammation either of the glomeruli or of the
small blood vessels in the kidneys.
• It may present with isolated hematuria and/or proteinuria (blood
or protein in the urine); or as a nephrotic syndrome, a nephritic
syndrome, acute kidney injury, or chronic kidney disease.
• They are grouped into non-proliferative or proliferative types.

8. SIGNS AND SYMPTOMS
• Glomerulonephritis refers to an inflammation of the
glomerulus, which is the unit involved in filtration in the
kidney. This inflammation typically results in one or
both of the nephrotic or nephritic syndromes.

9. NEPHROTIC SYNDROME
• The nephrotic syndrome is characterised by the finding of
edema in a person with increased protein in the urine and
decreased protein in the blood, with increased fat in the blood.
• Inflammation that affects the cells surrounding the glomerulus,
podocytes, increases the permeability to proteins, resulting in an
increase in excreted proteins.
• With decreased proteins in the blood, there is a decrease in the
oncotic pressure of the blood. This results in edema.
• This is worsened by the secretion of the hormone aldosterone
by the adrenal gland, which is secreted in response to the
decrease in circulating blood and causes sodium and water
retention.

10. NEPHRITIC SYNDROME
• The nephritic syndrome is characterised by blood in the
urine and a decrease in the amount of urine in the presence
of hypertension.
• This syndrome, inflammatory damage to cells lining the
glomerulus are thought to result in destruction of the
epithelial barrier, leading to blood being found in the urine.
• The renin-angiotensin system may be subsequently
activated, because of the decrease in perfusion of
juxtaglomerular apparatus, which may result in
hypertension.

11. NONPROLIFERATIVE
• This is characterised by forms of glomerulonephritis in
which the number of cells is not changed. These forms
usually result in the nephrotic syndrome. Causes
include:
a) Minimal change disease
Minimal change disease typically presents with edema, an
increase in proteins passed from urine and decrease in blood
protein levels, and an increase in circulating lipids.

12. b) Focal segmental glomerulosclerosis
Characterised by a sclerosis of segments of some glomerules. It is
likely to present as a nephrotic syndrome. This form of
glomerulonephritis may be associated with conditions such as HIV
and heroin abuse, or inherited as Alport syndrome.
c) Membranous glomerulonephritis
Cause either nephrotic or a nephritic picture. About two-thirds are
associated with auto-antibodies to phospholipase A2 receptor, but
other associations include cancers of the lung and bowel, infections
such as hepatitis B and malaria, drugs including penicillamine, and
connective tissue diseases such as systemic lupus erythematosus.

13. PROLIFERATIVE
• Proliferative glomerulonephritis is characterised by an
increased number of cells in the glomerulus. These
forms usually present with a triad of blood in the urine,
decreased urine production, and hypertension, the
nephritic syndrome. These forms usually progress to
end-stage kidney failure (ESKF) over weeks to years.

14. a) IgA nephropathy
It is characterised by deposits of IgA in the space between
glomerular capillaries.
b) Post-infectious
Occurs after infection with the bacteria Streptococcus pyogenes. It typically
occurs 1–4 weeks after a pharyngeal infection with this bacterium, and is
likely to present with malaise, a slight fever, nausea and a mild nephritic
syndrome of moderately increased blood pressure, gross haematuria, and
smoky-brown urine.
c) Membranoproliferative
characterised by an increase in the number of cells in the
glomerulus, and alterations in the glomerular basement membrane.
Type 1 MPGN is caused by circulating immune complexes. Type 2
MPGN is characterised by an excessive activation of the complement
system.

15. edemaGlomerulonephritis

16. PREVENTION&TREATMENT
• Glomerular nephritis:
-immunosuppressants:
mycophenolate mofetil
azathioprine
rituximab
ciclosporin
tacrolimus
-angiotensin-converting enzyme inhibitors&
angiotensin receptor blockers .
-Dietary changes and Stopping smoking

17. RHEUMATIC FEVER
• It is an inflammatory disease that can involve the heart,
joints, skin, and brain.
• The disease typically develops two to four weeks after
a streptococcal throat infection. It is believed to be
caused by antibody cross-reactivity.
• Rheumatic fever is an inflammatory disease that can
develop as a complication of inadequately treated strep
throat or scarlet fever. Strep throat and scarlet fever are
caused by an infection with streptococcus bacteria.

18. SIGNS AND SYMPTOMS
• The disease typically develops two to four weeks after a throat
infection.
• Symptoms include:
-fever, painful joints
-involuntary muscle movements,
-erythema marginatum
- heart failure
-atrial fibrillation and infection of the valves
-Polyarthritis, Arthralgia, Leukocytosis
-Sydenham's chorea, Carditis

19. PATHOPHYSIOLOGY
• Rheumatic fever is a systemic disease affecting the connective tissue
around arterioles, and can occur after an untreated strep throat
infection, specifically due to group A streptococcus (GAS),
Streptococcus pyogenes.
• It is believed to be caused by antibody cross-reactivity.
• S. pyogenes has a cell wall composed of branched polymers which
sometimes contain M protein, a virulence factor that is highly
antigenic.
• The antibodies which the immune system generates against the M
protein may cross-react with heart muscle cell protein myosin,heart
muscle glycogen and smooth muscle cells of arteries, inducing
cytokine release and tissue destruction.

20. • During a streptococcal infection, mature antigen-
presenting cells such as B cells present the bacterial
antigen to CD4+T cells which differentiate into helper T2
cells. Helper T2 cells subsequently activate the B cells to
become plasma cells and induce the production of
antibodies against the cell wall of Streptococcus.
However the antibodies may also react against the
myocardium and joints, producing the symptoms of
rheumatic fever.

21. rashrheumatic fever

22. PREVENTION & TREATMENT
• Rheumatic fever:
-Rheumatic fever can be prevented by effectively treating
strep throat with antibiotics.
-with anti-inflammatory medications such as
aspirin or corticosteroids.
- use of benzathine benzylpenicillin.
-treatment for heart failure: ACE inhibitors,
diuretics, beta blockers, and digoxin.

23. THANKYOU