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Strep A Rapid Test---Dipstick or Cassette


Streptococcus pyogenes is non-motile gram-positive cocci, which contains the Lancefield group A antigen that can cause serious infections such as tonsillitis, pharyngitis, scarlet fever.respiratory infection, impetigo, endocarditis, meningitis, puerperal sepsis, and arthritis. Left untreated, these infections can lead to serious  complications, including rheumatic fever and peritonsillar abscess. Traditional identification procedures for Group A Streptococci infection involve the isolation and identification of viable organisms using techniques that require 24 to 48 hours or longer.The Strep A Rapid Test is a rapid test to qualitatively detect the presence of Strep A antigen in throat swab specimens, providing results within 10 minutes. The test utilizes antibodies specific for whole cell Lancefield Group A Streptococcus to selectively detect Strep A antigen in a throat swab specimen.
  • Easy to use
  • Easy to interpret results 
  • Rapid - results in approximately 5 minutes
  • In-built controls to monitor:
    • Antibody functionality - indicated by presence of the Positive On Board Control
    • Non-specific binding - indicated by presence of the Negative On Board Control
  • Highly sensitive and specific
Test Procedure:
1 Remove the test strip from the sealed foil pouch and use it as soon as possible.
2 Hold the Reagent A bottle vertically and add 4 full drops (approximately 240 ul) to an extraction test tube. Hold the Reagent B bottle vertically and add 4 full drops (approximately 160ul) of Reagent B. Mix the solution by gently swirling the extraction test tube.

High performance:
--High Sensitivity: 97.6%

--High Specificity: 99.3%

--Reliable results		 3 Immediately add the throat swab into the extraction test tube of yellow solution. Agitate the swab by rotating it at least 10 times. Leave the swab in the extraction test tube for 1 minute. Then express the liquid from the swab head by rolling the swab against the inside of the tube and squeezing the tube as the swab is withdrawn.  Discard the swab.
AN1009C   Strep A Rapid Test Cassette
AN1009S   Strep A Dipstick		 4 With arrows pointing toward the specimen, immerse the test strip vertically into the extracted specimen solution and then start the timer. If the procedure is followed correctly, the extraction solution should not pass the arrow on the test strip when the strip is immersed. See the illustration below.
5 Leave the strip in the extraction tube and wait for the red line(s) to appear.  Read the result at 5 minutes.

More about Strep A
S. pyogenes, also known as Group A Streptococcus (GAS), is the causative agent in Group A streptococcal infections, including streptococcal pharyngitis ("strep throat"), acute rheumatic fever, scarlet fever, acute glomerulonephritis and necrotizing fasciitis. If strep throat is not treated, it can develop into rheumatic fever, a disease that affects the joints and heart valves. Other Streptococcus species may also possess the Group A antigen, but human infections by non-S. pyogenes GAS strains (some S. dysgalactiae subsp. equisimilis and S. anginosus Group strains) appear to be uncommon.

Group A Strep infection is generally diagnosed with a Rapid Strep Test or by culture.

Streptococcus pyogenes is a spherical gram-positive bacteria that grows in long chains and is the cause of Group A streptococcal infections. S. pyogenes displays streptococcal group A antigen on its cell wall. S. pyogenes typically produces large zones of beta-hemolysis (the complete disruption of erythrocytes and the release of hemoglobin) when cultured on blood agar plates and are therefore also called Group A (beta-hemolytic) Streptococcus (abbreviated GAS).

Streptococci are catalase-negative. In ideal conditions, S. pyogenes has an incubation period of approximately 10 days.

Serotyping
In 1928, Rebecca Lancefield published a method for serotyping S. pyogenes based on its M protein, a virulence factor that is displayed on its surface. Later in 1946, Lancefield described the serologic classification of S. pyogenes isolates based on their surface T antigen. Four of the 20 T antigens have been revealed to be pili, which are used by bacteria to attach to host cells. Over 100 M serotypes and approximately 20 T serotypes are known.

Pathogenesis
See also: Group A streptococcal infection
S. pyogenes is the cause of many important human diseases ranging from mild superficial skin infections to life-threatening systemic diseases. Infections typically begin in the throat or skin. Examples of mild S. pyogenes infections include pharyngitis ("strep throat") and localized skin infection ("impetigo"). Erysipelas and cellulitis are characterized by multiplication and lateral spread of S. pyogenes in deep layers of the skin. S. pyogenes invasion and multiplication in the fascia can lead to necrotizing fasciitis, a potentially life-threatening condition requiring surgical treatment.

Infections due to certain strains of S. pyogenes can be associated with the release of bacterial toxins. Throat infections associated with release of certain toxins lead to scarlet fever. Other toxigenic S. pyogenes infections may lead to streptococcal toxic shock syndrome, which can be life-threatening.

S. pyogenes can also cause disease in the form of post-infectious "non-pyogenic" (not associated with local bacterial multiplication and pus formation) syndromes. These autoimmune mediated complications follow a small percentage of infections and include rheumatic fever and acute poststreptococcal glomerulonephritis. Both conditions appear several weeks following the initial streptococcal infection. Rheumatic fever is characterised by inflammation of the joints and/or heart following an episode of Streptococcal pharyngitis. Acute glomerulonephritis, inflammation of the renal glomerulus, can follow Streptococcal pharyngitis or skin infection.

Infection with group A streptococci has been proposed to be a risk factor in the development of obsessive-compulsive disorders (OCD) and/or tic disorders in children. This hypothesis is known as Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections and is usually known by its abbreviation PANDAS. There is controversy in the medical field over the reality of this disease, as studies have failed to prove or disprove its existence. PANDAS became popular in the late 1990s and continues to be a highly researched and controversial topic in the field of pediatric neuroscience.

This bacterium remains acutely sensitive to penicillin. Failure of treatment with penicillin is generally attributed to other local commensal organisms producing β-lactamase or failure to achieve adequate tissue levels in the pharynx. Certain strains have developed resistance to macrolides, tetracyclines and clindamycin.

Virulence factors
S. pyogenes has several virulence factors that enable it to attach to host tissues, evade the immune response, and spread by penetrating host tissue layers.A carbohydrate capsule composed of hyaluronic acid surrounds the bacterium, protecting it from phagocytosis by neutrophils. In addition, the capsule and several factors embedded in the cell wall, including M protein, lipoteichoic acid, and protein F (SfbI) facilitate attachment to various host cells.M protein also inhibits opsonization by the alternative complement pathway by binding to host complement regulators. M protein found on some serotypes are also able to prevent opsonization by binding to fibrinogen. However, the M protein is also the weakest point in this pathogen's defense as antibodies produced by the immune system against M protein target the bacteria for engulfment by phagocytes. M proteins are unique to each strain, and identification can be used clinically to confirm the strain causing an infection.

S. pyogenes releases a number of proteins, including several virulence factors, into its host:

Streptolysin O and S
These are toxins which are the basis of the organism's beta-hemolytic property. Streptolysin O is a potent cell poison affecting many types of cell including neutrophils, platelets, and sub-cellular organelles. It causes an immune response and detection of antibodies to it; antistreptolysin O (ASO) can be clinically used to confirm a recent infection. Streptolysin O is cardiotoxic.
Streptococcal pyogenic exotoxins (Spe) A and C
SpeA and SpeC are superantigens secreted by many strains of S. pyogenes. These pyogenic exotoxins are responsible for the rash of scarlet fever and many of the symptoms of streptococcal toxic shock syndrome.
Streptokinase
Enzymatically activates plasminogen, a proteolytic enzyme, into plasmin which in turn digests fibrin and other proteins.
Hyaluronidase
It is widely assumed that hyaluronidase facilitates the spread of the bacteria through tissues by breaking down hyaluronic acid, an important component of connective tissue. However, very few isolates of S. pyogenes are capable of secreting active hyaluronidase due to mutations in the gene that encode the enzyme. Moreover, the few isolates that are capable of secreting hyaluronidase do not appear to need it to spread through tissues or to cause skin lesions.Thus, the true role of hyaluronidase in pathogenesis, if any, remains unknown.
Streptodornase
Most strains of S. pyogenes secrete up to four different DNases, which are sometimes called streptodornase. The DNases protect the bacteria from being trapped in neutrophil extracellular traps (NETs) by digesting the NET's web of DNA, to which are bound neutrophil serine proteases that can kill the bacteria.
C5a peptidase
C5a peptidase cleaves a potent neutrophil chemotaxin called C5a, which is produced by the complement system.C5a peptidase is necessary to minimize the influx of neutrophils early in infection as the bacteria are attempting to colonize the host's tissue.
Streptococcal chemokine protease
The affected tissue of patients with severe cases of necrotizing fasciitis are devoid of neutrophils.The serine protease ScpC, which is released by S. pyogenes, is responsible for preventing the migration of neutrophils to the spreading infection. ScpC degrades the chemokine IL-8, which would otherwise attract neutrophils to the site of infection. C5a peptidase, although required to degrade the neutrophil chemotaxin C5a in the early stages of infection, is not required for S. pyogenes to prevent the influx of neutrophils as the bacteria spread through the fascia.

Diagnosis
Usually, a throat swab is taken to the laboratory for testing. A Gram stain is performed to show Gram positive, cocci in chains. Then, culture the organism on blood agar with added bacitracin antibiotic disk to show beta-haemolytic colonies and sensitivity (zone of inhibition around the disk) for the antibiotic. Then, perform catalase test, which should show a negative reaction for all Streptococci. S. pyogenes is cAMP and hippurate tests negative. Serological identification of the organism involves testing for the presence of group A specific polysaccharide in the bacterium's cell wall using the Phadebact test.

Treatment
The treatment of choice is penicillin and the duration of treatment is well established as being 10 days minimum. There is no reported instance of penicillin-resistance reported to date, although since 1985 there have been many reports of penicillin-tolerance.

Macrolides, chloramphenicol, and tetracyclines may be used if the strain isolated has been shown to be sensitive, but resistance is much more common.