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Microbiology > 22-Streptococci > Flashcards

22-Streptococci Flashcards

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Biology 101 flashcards
1
Q

How can you differentiate between staph and strep?

A

Catalase reaction. Strep is catalase negative.

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2
Q

What is the hemolytic pattern of S. pyogenes?

A

Beta

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3
Q

What is the hemolytic pattern of S. agalactiae?

A

Beta

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4
Q

What is the hemolytic pattern of S. pneumonia?

A

Alpha

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5
Q

What is the hemolytic pattern of S. mutans?

A

Alpha

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6
Q

What is the hemolytic pattern of Enterococcus faecalis?

A

Alpha

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7
Q

What is the cause and presentation of Supporative Pharyngitis?

A

S. pyogenes

reddened pharynx with creamy-yellow exudates generally present; primarily children (5-15) via communicable. Specific diagnosis: bacteriologic or serologic tests. VF’s are hemolysins.

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8
Q

What is the cause and presentation of Scarlet Fever?

A

S. pyogenes

diffuse erythematous rash beginning on the chest and spreading over the extremities. Area around mouth is spared (Circumoral pallor), initial yellow-whitish coating on tongue is shed –> red and raw tongue (Strawberry Tongue), rash blanches when pressed and is best seen on the abdomen and in skin folds (Pastia lines). Results from a complication of streptococcal pharyngitis. VF is Spe toxins.

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9
Q

What is the cause and presentation of pyoderma (impetigo)?

A

S. pyogenes

Follow in insect bites, abrasions a localized skin infection with vesicles progressing to pustules; skin lesions are described as being Old Varnished or Honey Crusted. Seen during summer months in kids with poor hygiene.

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10
Q

What is the cause and presentation of Erysipelas?

A

localized skin infection with pain, inflammation, lymph node enlargement, and systemic symptoms (chills, fever, leukocytosis).

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11
Q

What is the cause and presentation of Cellulitis?

A

S. pyogenes

localized skin infection that involves the subcutaneous layer, local inflammation, and systemic signs

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12
Q

What is the cause and presentation of Necrotizing Fasciitis?

A

S. pyogenes

deep infection of skin that involves destruction of muscle and fat layers

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13
Q

What is the cause and presentation of Streptococcal Toxic Shock Syndrome (STSS)?

A

S. pyogenes

)- multiorgan systemic infection resembling staphylococcal toxic shock, however most of these patients are bacteremic and with fasciitis. Seen in patients with HIV, infection, cancer, diabetes mellitus, heart or pulmonary disease, and varicella-zoster infection, IV drug users and alcohol abuse. VF is M protein, mucopolysaccharide hyaluronic acid capsules, and Spe toxin.

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14
Q

What is the cause and presentation of Supporative bacteremia?

A

S. pyogenes

typically found in people with STSS and NF; however it is not usually seen in people with localized infections.

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15
Q

What is the cause and presentation of Rheumatic fever?

A

S. pyogenes

inflammatory changes of the heart (pancarditis), joints (arthralgia to arthritis), blood vessels, and subcutaneous tissue; results as a complication of streptococcal pharyngitis. Seen in young school age children during the fall and winter.

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16
Q

What is the VF of S. pyogenes that causes Rheumatic Fever?

A

M proteins

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17
Q

What is the cause and presentation of Acute Glomerulonephritis?

A

S. pyogenes

acute inflammation of the renal glomeruli with edema, hypertension, hematuria, and proteinuria. VF is M protein.

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18
Q

What are the 4 diseases assocaited with S. agalactiae?

A

Early-onset Neonatal Disease
Late-onset Neonatal Disease
Infections in Pregnant Women
Infections in men and non-pregnant women

19
Q

What is the cause of Abcess formation in deep tissue?

A

S. angiosus

20
Q

What is the cause and presentation of Pharyngitis?

A

S. dysgalactiae

disease resembles S. pyogenes which is sometimes complicated with glomerulonephritis, but it never produces rheumatic fever

21
Q

If a pt presents with acute onset with severe chills and sustained fever; productive cough with blood-tinged sputum; lobar consolidation (localized in the lower lobes of the lungs), what can be the causitive bacteria?

A

Pneumonia from S. pneumoniae

22
Q

What are the VF’s of S. pneumoniae?

A

VF’s are capsule, sIgA protease, and pneumolysin

23
Q

What is the cause and presentation of sinusitis?

A

S. pneumoniae

infection of paranasal sinuses; preceded by a viral infection of the upper respiratory tract

24
Q

What is the cause and presentation of Otitis media?

A

S. pneumoniae

infection of the ear; preceded by a viral infection of the upper respiratory tract. Typically seen in young children.

25
Q

What is the cause and presentation of meningitis?

A

S. pneumoniae

severe infection involving the meninges with headache, fever and sepsis; acquired through bacteremia, infections of the ear or sinuses, or head trauma. High mortality and severe neurologic deficits in survivors.

26
Q

What is the structure and function of the M protein for S. pyogenes?

A

M Protein is the major type-specific protein associated with virulent strains. It is composed of two polypeptide chains complexed in an alpha helix. The protein is anchored in the cytoplasmic membrane, extends through the cell wall, and protrudes above the cell surface. M proteins are subdivided into class I (share exposed antigens; only one to cause Rheumatic Fever) and II (do not have exposed shared antigens) molecules.

emm gene encodes the M protein. M protein is an adhesion, therefore it allows the S. pyogenes to interact with specific host cell receptors (ex: invade into epithelial cells  persistent infection and invasion into deep tissue).

27
Q

What clinical presentation do the Strep. Pyogenes Erythrogenic (SPE) toxins give rise to?

A

This family of exotoxins is believed to be responsible for many of the clinical manifestations of severe streptococcal disease. All Spe’s produce a fine, blanching, “sandpaper” rash on arms and upper trunk

28
Q

What is the purpose of the ASO test?

A

• Patients with a S. pyogenes disease produce antibodies to streptococcal enzymes such as strepolysin O. The ASO test measures the antibodies against streptolysin O and is therefore useful in confirming rheumatic fever or acute glomerulonephritis from a streptococcal pharyngeal infection. These Ab’s appear 3-4weeks after initial exposure to the organism.

29
Q

What is the mechanism of action and presentation of the effects of Streptokinase A and B virulence factors?

A

mediate the cleavage of plasminogen, releasing the protease plasmin that in turn cleaves fibrin and fibrinogen, resulting in lysis of clots and fibrin deposits thereby facilitating the rapid spread of the organism in infected tissues

30
Q

What is the mechanism of action and presentation of the DNase (A to D) virulence factors?

A

depolymerize free DNA present in pus, as a result this reduces the viscosity of the abscess material and facilitates the spread of the organism

31
Q

What is the mechnism of action of the C5a virulence factor?

A

disrupts the inflammation process by degrading C5a, thereby inhibiting the recruitment and activation of phagocytic cells.

32
Q

What are the lab tests needed to identify S. pyogenes?

A

PYR +

Beta hemolytic

Bacitracin sensitive

33
Q

What are the lab tests needed to identify S. agalactiae?

A

cAMP +

Beta hemolytic

bacitracin sensitive

hippurate hydrolysis +

34
Q

What are the lab tests needed to identify S. pneumoniae?

A

Alpha hemolytic

bile esculin soluble (-)

optochin sensitive

35
Q

What are the lab tests needed to identify Enterococcus sp?

A

Gamma or alpha hemolytic

bile esculin + (doesnt dissolve when exposed to bile)

PYR +

36
Q

How do neonates get colonized with their mothers S. agalactiae?

A

• Group B streptococci colonize the lower GI tract and genitourinary tract, as a result 60% of infants born to a colonized mother become colonized with their mothers’ organisms. Other risk factors for neonatal colonization are pre-mature delivery, prolonged membrane rupture, and intrapartum fever.

The colonization with subsequent development of disease in the neonate can occur in utero, at birth, or during the first few months of life. Infections in men and non-pregnant women (these people are typically older and have debilitating underlying conditions) are skin and soft-tissue infections, bacteremia, urosepsis (UTI w/ bacteremia), and pneumonia

37
Q

What are the clinical symptoms of early-onset neonatal disease?

A

within 7 days of birth, infected newborns develop signs and symptoms of pneumonia, meningitis, and sepsis; acquired in utero or at birth, commonly from mother because it is normally found in lower GI and GU tract. VF is polysaccharide capsule; interferes with phagocytosis.

38
Q

What are the clinical symptoms of late-onset neonatal disease?

A

more than a week after birth, neonates develop signs and symptoms of bacteremia with meningitis; commonly leads to permanent neurologic damage. Acquired in utero or at birth (ex: from mother or another infant) because this organism is normally found in lower GI and GU tract. VF is polysaccharide capsule; interferes with phagocytosis

39
Q

What are the symptoms of S. agalctiae infections in pregnant women?

A
40
Q

What is the mechanism of action of the polysaccharide capsule of S. pneumoniae?

A

which allows the organism to survive phagocytosis because of the phagocytic protection afforded and the pneumolysin-mediated suppression of the phagocytic cell oxidative burst.

41
Q

What is the mechanism of action of the Secretory IgA (sIgA) in S. pneumoniae?

A

Secretory IgA traps bacteria in mucin by attaching itself to the bacteria at the antigen-binding site and to mucin at the Fc region, the bacterial protease prevents this interaction thereby making it more difficult to be removed from the respiratory tract.

42
Q

What is the mechanism of action of pneumolysin in S. pneumoniae?

A
  • binds cholesterol in the host cell membrane and creates pores which destroy ciliated epithelial cells and phagocytic cells.
43
Q

What is CRP and what is it used to detect?

A

• C polysaccharide ( found in S. pnuemoniae) precipitates C-reactive protein (CRP; a serum globulin fraction [its made by the liver]) in the presence of calcium. CRP is present in low concentrations in a health person but is elevated in patients suffering from acute inflammatory diseases. Therefore, by monitoring levels of CRP you can predict inflammation.

Microbiology (35 decks)

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