S.Pyogenes Flashcards

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1
Q

What shape is S.Pyogenes?

A

Round shaped

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2
Q

What is the lancefield classification?

A

Group A Strep

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3
Q

How does S.Pyogenes stain

A

Gram positive

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4
Q

What type of anaerobes are S.Pyogenes

A

Facultative anaerobe;

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5
Q

What result does S.pyogenes give in catalase test

A

Catalase negative

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6
Q

What type of hemolysis does S.Pyogenes show in blood agar?

A

Beta hemolysis. This is because of streptolysins produced by S.Pyogenes

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7
Q

How can you distinguish between S.Pyogenes and S.Agalctiae

A

Bacitracin is added to the agar. S.Pyogenes is bacitracin sensitive so the colony will die off where as for S.agalactiae, they remain intact.

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8
Q

What are the components of the S.Pyogenes capsule

A

Adherence proteins, Streptococcus fibronectin binding protein and M protein which attach to skin or pharyngeal mucosa

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9
Q

How does hyaluronidase work?

A

Destroys hyaluronic acid

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10
Q

How does hyaluronidase work?

A

Destroys hyaluronic acid. A cement substance that keeps cells of the connective tissue tightly linked. This results in local inflammation and enables bacteria to enter the blood stream where it releases streprolysin O and S which cause hemolysis

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11
Q

Name the super antigens produces by S.Pyogenes

A

Streptococcal pyrogenic Extotoxin A and C (SpeA and Spec)

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12
Q

How do S.Pyogenes super antigens work?

A

They interact with Class 2 MHC molecule on the surface of the macrophage forming a super antigen MHC complex. This then stimulates 30% of the entire T-cell population stimulating release of many inflammatory cytokines, causing a cytokine storm which leads to Toxic shock syndrome, a widespread systemic vasodilation making blood pressure drop and causing poor perfusion of other organs

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13
Q

What disease does S.Pyogenes cause in the lungs?

A

Pneumonia and lung abscesses.

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14
Q

What disease does S.Pyogenes cause in the heart?

A

Clumps called vegetations on the heart valves causing Infective endocarditis

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15
Q

What disease does S.Pyogenes casuse in the CNS?

A

Brain abscesses or meningitis

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16
Q

Which areas of the body are peacefully colonized by S.Pyogenes?

A

Skin
Mucosa of pharynx
Vagina
Rectum

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17
Q

Who is under greater risk of infection by S.Pyogenes?

A
Infants
Elderly
Hiv patients
Diabetics
Maliginancies
18
Q

How does S.Pyogenes enter the blood stream?

A

It can enter through a breach in the skin

19
Q

What is the most common disease caused by S.Pyogenes

A

Strep pharyngitis, inflammation of the pharyngeal mucosa and tonsils

20
Q

Explain what happens when S.Pyogenes invades the epidermis, Upper dermis, Lower dermis, and muscle fascia respectively

A

Epidermis: Impetigo, superficial skin lesions that look like honey clusters

Upper dermis: Erysipelas, skin infection

Lower Dermis: Cellulitis, acute, painful quick spreading infection of lower dermis and subcutaneous tissue

Muscle fascia:Necrotizing fasciitis, when muscle fascia and subcutaneous tissue are destroyed by necrosis

21
Q

Explain Post infectious sequaelae

A

Complications that arise after bacteria has been eliminated from the body

22
Q

Explain post streptococcal glomerulonephritis

A

Acute inflammation of the kidneys glomerulis usually seen after impetigo. Usually happens after 2 to 4 weeks after initial infection due to type 3 sensitivity reaction. This means the streptococcal antigens that remained in the blood bind to antibodies forming antibody antigen complexes that are deposited in the basement membrane of the glomerulus. This can activate the complement system attracting neutrophils to glomeruli resulting in kidney damage

23
Q

What are the symptoms of Pharyngitis?

A

Fever, panful swallowing and swollen red tonsils that may have pus on them

24
Q

What are the symptoms of Impetigo

A

Itchy honey coloured scabs on skin that can become fluid filled blisters.

25
Q

What are the symptoms of Erysipelas?

A

Warm painful lesions on the skin with raised edges

26
Q

What are the symptoms of Necrotizing fasciitis?

A

Fever and the skin over affected part becomes painful and purple coloured

27
Q

What are the symptoms of scarlet Fever?

A

Fever, bright red skin rash, tongue may have a sandpaper feel

28
Q

What are the symptoms of Acute rheumatic fever?

A

Joints inflammation
Heart damage causing heart murmers. Subcutaneous nodules seen on elbows knees and forearm. Erythema marginatum, a rash with thick red margins. Sydenhams chorea, rapid involuntary movement of the face and hands.

29
Q

What are the symptoms of post streptococcal glomerulonephritis?

A

Mainly facial edema and dark red urine because glomerular damage allows red blood cells to pass in the urine

30
Q

How do you diagnose strep pharyngitis?

A

It can be done with rapid strep test or RST which looks for bacterial antigens in a throat swab. This however may give a false positive so a culture from a throat swab may be required

31
Q

How do you diagnose skin infections and systemic infections?

A

For skin infections, cultured can be made from the fluid inside the blisters or from debrided tissue. Blood cultures can be done for systemic infections

32
Q

What is the treatment for strep pyogenes?

A

Penicillin

33
Q

What is an alternative treatment?

A

Cephalosporins such as ceftriaxone and macrolides such as azithromycin

34
Q

What titre can be used to detect recent S.Pyogenes infection?

A

Anti-streptolysin O titre

35
Q

Which virulence factor of S.Pyogenes converts plasminogen to plasmin

A

Streptokinase

36
Q

A 30-year-old man comes to his primary care physician for evaluation of progressive fatigue and dyspnea for several months. He does not smoke, drink alcohol
, or use illicit drugs. Family history is unremarkable. He traveled to South America one year ago but does not recall any subsequent illnesses. Temperature is 37.0 °C (98.6 °F), pulse is 75/min, and blood pressure
is 131/80 mmHg. On physical examination, the patient appears visibly dyspneic. A systolic murmur
is auscultated over the cardiac apex. Pulmonary auscultation reveals diffuse rales over both lung
fields. The patient undergoes cardiac biopsy. What is the most likely etiology of this patient’s clinical condition?

A

Acute rheumatic fever. An early sequela of untreated group A streptococcal throat infection that usually occurs two weeks following untreated group A Streptococcus
(GAS) pharyngitis. Clinical manifestations include arthritis, carditis, chorea, erythema marginatum, and subcutaneous nodules. Cardiac involvement typically involves all layers of the heart (pancarditis).

Damage to cardiac valves often becomes chronic and progressive, leading to mitral (most common), aortic, and, rarely, tricuspid valve damage. Rheumatic heart disease may manifest years after the initial episode of GAS pharyngitis. Regurgitation is the most common complication, but it may progress to stenosis. Pathogenesis involves antibody production and subsequent T cell response against myosin that shares similar epitopes with the M protein virulence factor of the bacteria (type II hypersensitivity)

37
Q

A 34-year-old man presents to the emergency department for evaluation of pain in the right lower extremity. The patient was running on the beach without shoes over the past weekend and sustained a small laceration to the bottom of the foot. Over the past 24 hours, he has been experiencing severe pain and swelling of the foot to the point that he is unable to bear weight. He is otherwise healthy and does not
smoke
, consume
alcohol
, or use illicit substances. Temperature is 38.6°C (101.5°F),
pulse
is 109/min, respirations are 22/min, and
blood pressure
is 131/72 mmHg. On physical examination, a 3 cm x 3 cm area of erythema is noted on the underside of the right foot. The patient is exquisitely tender to palpation over the entire aspect of the right foot extending to the mid
tibia
. A radiograph of the right foot is obtained and demonstrates the following finding

A

This patient has right foot cellulitis
, pain out of proportion to physical exam findings, and radiograph demonstrating air in the soft tissue
. Together, these findings are consistent with necrotizing fasciitis
, which must be treated emergently with surgical debridement of devitalized tissue.

Necrotizing fasciitis
is a rare but serious infection of deep soft tissues
that results in rapid, progressive destruction of muscle
fascia and overlying subcutaneous fat
. Typically, bacteria (usually anaerobes or Streptococcus pyogenes
) with appropriate toxin-carrying capabilities enter through broken skin
and spread along the myofascial plane. Pyrogenic
exotoxins induce cytokine
production, contributing to tissue destruction and subsequent production of methane and CO2
. Ultimately, this process causes bullae
formation, crepitus
, and gas
within soft tissue
.

Necrotizing fasciitis
carries a high rate of morbidity and mortality. Therefore, prompt recognition and treatment are paramount. Clues to the diagnosis include pain out of proportion to physical exam findings, erythema without sharp margins, as well as skin
bullae
and necrosis
. Definitive treatment includes debridement of devitalized tissue for source control, as well as empiric antibiotics
that include either carbapenem
or piperacillin-tazobactam
plus vancomycin
and clindamycin
. This combination is effective against both Gram positive and anaerobic pathogens. Furthermore, clindamycin
helps inhibit bacterial toxin production.

38
Q

A 9-year-old girl comes to the office because of 2 days of sore throat and fevers of 38.9°C (102°F). Physical exam shows an erythematous pharynx with a white, creamy
exudate covering the left tonsil. Palpation of the neck shows an extremely tender left submandibular lymph node. Throat cultures are taken and show beta-hemolytic colonies on blood agar. Susceptibility analysis show
growth is inhibited by bacitracin
. What is the mostly likely causal organism?

A

Streptococcal pharyngitisis the most common form of pharyngitis and caused by group A Streptococcus (GAS), or Streptococcus pyogenes. GAS is a gram-positive cocci with a hyaluronic acid capsule. It is beta-hemolytic, meaning that growth on sheep blood agar plates will show a golden clearning around each colony due to complete breakdown of heme. GAS
is additionally bacitracin-sensitive, a feature that distinguishes it from Group B Streptococcus. GAS
pharyngitis is characterized by an exudative pharyngitis accompanied by fever, vomiting, tender cervical lymph nodes, palatal petechiae, and scarlatiniform rash. It can be diagnosed with throat culture. Penicillin is the first-line treatment.

39
Q

A 7-year-old girl is brought to the urgent care clinic by her mother after she developed a rash on her shoulders, neck, and upper chest in the past 24 hours. The rash followed a fever and a severe sore throat for 2 days duration. The mother states that other children in the patient’s class have had similar symptoms. Physical examination of the patient shows a flushed and ill-appearing child with erythematous macules on her shoulders and chest. Throat examination shows a white tongue with inflamed papillae (see image below) and tonsillar inflammation. What is the most likely agent causing the patient’s symptoms considering it is susceptible to bacitracin?

A

The patient in this question is showing symptoms of scarlet fever, a illness caused by Group A Streptococcus. Scarlet fever tends to be preceded by febrile streptococcal pharyngitis for a couple of days before the onset of an erythematous maculopapular rash that begins on the upper trunk and spreads to the extremities. Other significant symptoms include a “strawberry” tongue—a whiteish appearance with red, inflamed papillae, and a flushed face. Scarlet fever
can lead to acute poststreptococcal glomerulonephritis
as well as rheumatic fever. Many classes of gram positive organisms may be distinguished by their sensitivity to particular agents. Among the beta-hemolytic, catalase-negative organisms, one can tell apart group A streptococcus (S. pyogenes) from group B streptococcus (S. agalactiae) by Bacitracin
treatment in culture. Group A is sensitive to it, while Group B is resistant.

40
Q

How do the M proteins work?

A

M proteins are a virulence factors which break down complement proteins and delay breaking down. This prevents phagocytosis