Streptococci Flashcards

1
Q

Overview of the Streptococcus genus, and how are species classified?

A

Many species (>30) of gram positive streptococci. There are five significant human pathogens of streptococci.

Most are facultative anaerobic.

Require blood agar or chocolate agar cultivation, will not grow on simple agar

Catalase neg

Are beta-alpha, or gamma (non) hemolyzing.

Classified by :

1) Hemolysis: alpha beta or gamma
2) Lancefield group: based on the “C” aminopolysaccharide in the cell wall.
3) Serotype: based on the “M” protein in the cell wall.
4) 16sRNA coding DNA sequence: there are 6 clusters, which have similar pathologies or ecologies.

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2
Q

What are the Lancefield groups?

How is a bacteria’s Lancefield group determined?

What are the bacteria of groups A, B, and D?

What are the two significant human streptococci that do not have Lancefield groups?

A

The group of bacteria that express a specific antigen epitope, can be identified by a specific antibody, lancefield groups go from A thru S.

The epitope is a specific amino-sugar moiety that is expressed by that bacterial group

The Lancefield group is determined by latex agglutination test with the lancefield antibodies.

Streptococcus pyogenes = A

Streptococcus agalactiae = B

Enterococcus faecalis and Streptococcus bovis = D

  • S. pneumoniae* has no lancefield antigens
  • Viridans streptococci* have no lancefield antigens.
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3
Q

Streptococcus genus morphology, cultivation

A

Gram positive cocci in chains

are “demandingrequire blood agar media

Remember that the Pie Genies demand blood! (and so do all their other streptococcus friends)

form small ~1 mm round colonies “needletip colonies

Catalase neg

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4
Q

General description, morphology, culture of Streptococcus pyogenes

A

Gram positive streptococcus (long chains of spheres) ~1uM diameter

demanding, requires blood agar.

Hyaluronic acid capsule

Wide beta hemolysis, ~1 centimeter, around the colonies

small colorless needletip colonies.

A - Lancefield group

Is PYR positive Pyrrolidonyl Arylamidase, can hydrolyze this substrate.

Expresses streptolysins S and O (hemolysins)

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5
Q

Streptococcus pyogenes virulence factors

A

Hyaluronic acid capsule

Lipoteichoic acid,

F-protein - Fibronectin binding protein, mediates cell attachment.

M-protein - inhibits C3 convertase, prevents opsonization

Streptolysins O and S (hemolysins, O-oxygen labile S-stabile in oxygen)

NADase

Hyaluronidase

Streptokinase - Converts Plasminogen to Plasmin, which then lyses fibrin clots.

Streptodornase (DNAse)

“C” carbohydrates R and T

Erythorogenic toxins - capillary toxin, scarlet fever toxin. SpeA, SpeB, SpeC.

SpeA and SpeC are Superantigens, and SpeB is a protease causing necrotising fasciitis.

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6
Q

How is streptococcus diagnosed

A

by determining the ASO titer (concentration of anti-Streptolysin O antibodies in the blood) of the blood. If it is abnormally high, then there is an active streptococcus infection or may indicate a post-streptococcal syndrome.

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7
Q

How is an ASO titer performed?

A

Antibody titers against streptolysin O in patients serum are a useful indicator of a recent S. pyogenes infection.
- serial dilutions of patient’s serum are prepared
- Streptolysin ‘O’ (antigen) added the tubes
- Incubation – for 15 minutes at 37 C
If antibody is present it neutralizes the streptolysin which is then no longer to free to lyse
RBCs
We can read the end titer corresponds to a serum dilution (for example 1/160-200 = 60-200
Todd units of antistreptolysin / ml is considered abnormally high)

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8
Q

What clinical disorders are caused by S. pyogenes

A

Streptococcus pyogenes causes

1) Purulent infections

Impetigo contagiosa - yellow/orange crusty skin infection, contagious on contact

Phlegmone - deep tissue infection of the subdermal adipose or fascia. often seen in the extremities

Erysipelas - red swollen superficial skin infection with well demarcated borders.

Puerperal fever - child bedfever, transmitted to mothers giving birth by doctors hands, demonstrated by Ignaz Semmelweis.

Follicular tonsillitis, pharnygitis, sinusitis - classic “Strep throat” with follicular exudate on the tonsils.

Meningitis

Pneumonia

Endocarditis

Necrotising Fasciitis - infection of the fascia layer which rapidly spreads, causing swelling and then subsequent death of the overlying tissue all the way down to the fascia. Must be treated by amputation of that muscle/fascia.

2) Toxin mediated infections

Scarlet fever - mediated by erythrogen toxin. Which destroys capillary endothelial cells causing RBC leakage and redness.

  • Widespread redness results after 2 days, called exanthema.
  • On the tongue, this causes papillary hypertrophy, resulting in strawberry tongue.

Toxic shock syndrome -

3) Post-streptococcal diseases

Rheumatic fever: Type 2 hypersensitivity (antibody mediated hypersensitivity RXN). Cardiomyocytes surface antigen is similar to M-protein on S pyogenes, and autoimmune antibodies continue to be produces and attack the heart muscle. Pancarditis (damage of the heart muscle), and endocarditis (damage of the valves) occur.

Acute Glomerulonephritis (GN): Type 3 hypersensitivity (immune complex mediated) Deposition of immune complexes in the glomeruli basal membrane, damage, inflammation glomerulonephritis

Polyarthritis: Also Type 3 reaction, Immune complexes in the joints.

Erythema nodosum: Type 3. Subcutaneous, adipose deposition of immunce complexes

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9
Q

What causes scarlet fever?

How many times can Scarlet fever be acquired?

How many times can tonsillitis follicularis be acquired?

A

Caused by erythrogenic toxin that is released after infection of S pyogenes by a bacteriophage stimulates the bacteria to produce the toxin.

During scarlet fever antibodies agaisnt the toxin are produced, so scarlet fever can only occur once

Scarlet fever is caused by many different serotypes/strains of streptococcus pyogenes, so the follicular tonsillitis or phayrngitis caused by them can occur many times.

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10
Q

What is the treatment for Streptococcus pyogenes?

Prevention?

A

Penicillins

Streptococci are almost always very susceptible to penicillin.

but as usual, antibiogram should be performed to confirm this.

If patient is allergic to penicillin, Macrolides (Erythromicin, 50S inhibits RNA translocation through ribosome)

For skin lesions or fasciitis, Local antiseptics and/or surgical removal

Prevention:

No specific prevention exists,

Post-streptococcal diseases are prevented by long-0term penicillin treatment.

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11
Q

Streptococcus a….

name, morphology, culture

A

Streptococcus agalactiae

Gram positive streptococci, chains of cocci, 1uM

Demanding, blood agar. A galactic baby demands blood.

Narrow beta-hemolysis (as opposed to S. pyogenes which is very wide)

tiny, needletip colonies

CAMP test + (like other group Bs)

Bacitracin resistant

Lancefield group B

Hippurate+, hydrolyzes Na-hippurate.

The #1 cause of meningitis in neonates.

Also common cause of Sepsis and Pneumonia in neonates.

Usually infected when the baby passes through the birth canal, and all pregnant women should be check at 35 weeks.

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12
Q

Streptococcus a…

Pathogenicity

Clinical diseases

Treatment

Prevention

A

Streptococcus agalactiae

Pathogenic colonization of the vagina

Can cause abortion during pregnancy

Can infect babies during birth: newborn pneumonia, ARDS, meningitis, or sepsis

Is the most common cause of meningitis in infants, and a leading cause of pneumonia and sepsis.

The mother is usually asymptomatic, therefore ALL pregnant women need to be screened during the third trimester, 35th week.

Penicillin/Ampicillin used for both treatment and prophylactic prevention.

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13
Q

Enterococcus genus

morphology, culture

A

Gram positive

Slightly elongated cocci, in short chains and in pairs

Lancefield Group D

Enterococcus do NOT demand blood, like the other streptococcus.

On simple Agar - small greyish, shiny colonies

On blood agar - small greyish, shiny, usually alpha hemolytic, but different strains may be beta- or non-hemolytic

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14
Q

What are the group D streptococci?

A

Enterococci and non enterococcal group D streptococci!

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15
Q

Diagnosing Enterococcus faecalis

A

Selective culturing on Bile Esculin Agar, aka E67 agar, produces black colonies

Catalase neg

PYR positive, can hydrolyze PYR, generates color change

Esculin Positive, can hydrolyze esculin, generates color change.

Grows in 6.5% agar

mild cold tolerance, ​grows at 45 C

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16
Q

What is the habitat/reservoir of Streptococcus faecalis?

How is it transmitted?

What are the clinical diseases?

Prevention?

A

It is normal flora of the GI (entero)

It is transmitted as a nosocomial infections often in the found in hospital ICU’s

Usually from the patients own GI population getting into an area it shouldn’t.

From urinary or GI tract wounds.

Can cause:

After GI perforation: sepsis, peritonitis.

After a surgery can cause infection of any area the wound opens into -> meningitis, endocarditis, bactermia,.. etc.

17
Q

Virulence factors of Enterococcus faecalis?

A

There are no well defined virulence factors, as they are normally commensal organisms of the GI and considered beneficial normally.

18
Q

Streptococcus faecalis

Treatment

Prevention

A

Treatment: Antibiogram

Enterococcus very often has many resistances

Intrinsic resistance to cephalosporins, monobactams

Intrinsic mild resistance to aminoglycosides

Acquired resistance to fluoroquinolones and vancomycin.

usual treatment in serious infections is Vancomycin and Aminoglycosides.

In addition to all of the antibiotics, E faecalis is the most resistant non-spore forming bacteria,

highly heat, dessicant, and salt resistant

Prevention:

No specific prevention available other than attempting to use good aseptic/sterile technique during surgery and recovery periods.

19
Q

What is the Streptococcus viridans group of bacteria?

A

S. Mutans, Mitis, Milleri, Salivarius, Sanguis. Anginosus

A heterogenous collection of Alpha-hemolytic streptococci of short chains or pairs. alpha hemolytic –> viridans

They are Anaerobic and some are microaerophilic. (two A’s Alpha-hemolytic and Anaerobic streptococci)

They are normaflora of the oral cavity and GI tract. Are responsible for abscess in the gums, and dental caries with poor oral hygeine

Streptococcus viridans in the blood stream can cause subacute endocarditis. So people with dental caries and gingivitis are at risk for endocarditis.

20
Q

How is Streptococcus viridans differentiated from Streptococcus pneumoniae?

A

By demonstrating Optochin Resistance

Pneumococcus (Streptococcus pneumoniae) is sensitive to optorchin and Viridans is resistant.

Or by bile solubility

Pneumococcus will be lysed and killed by 2% bile salt in the agar, while S viridans are bile resistant

Or by Inulin fermentation

Pneumococcus can ferment inulin

21
Q

What clinical diseases are caused by Streptococcus viridans?

What is the treatment?

A

Dental caries, Gingivial abscess

Endocarditis

Sepsis

Treatment: long term (6 weeks) beta-lactam plus aminoglycoside

Penicillin or vancomycin plus gentamicin.

22
Q

Which specific bacteria are responsible for dental caries?

A

Streptococcus mutans of the viridans group

in conjunction with Lactobacillus bacteria species

S mutans and Lactobacilli are members of the oral normaflora. but in poor hygeine grow too much.

  • S mutans* secretes extracellular polysaccharides that coat the teeth and provide growth environment for more bacteria, it also produces lactic and other acids from sugars in the oral cavity
  • Lactobacillus* also produces more lactic acid and contributes.

Both are able to live fine in low pH values, and thus keep living even inside of the low pH lesion that is eroding the teeth.

23
Q

Streptococcus pneumoniae

Morphology

Culture, diagnosis

A

aka Pneumococcus

Gram positive “lance- or flame-shaped” diplococci, pairs of oval shaped bacteria

Demanding, cultured on blood or chocolate agar.

Gray, shiny colonies with alpha-hemolysis (green)

Colonies undergo autolysis as they age, forming ring shaped “umbilibus”

Some strains have capsules and have a large mucinous apearance to the colonies.

Bile salt soluble (lyses if they’re present in the agar)

Optorchin antibiotic sensitive

Quellung reaction positive

Alpha hemolytic

Has no lancefield group class

But, microscopically, it looks like a pair of lance shaped diplococci. (alpha night tournament)

24
Q

Streptococcus pneumoniae

Habitat and infection methods

A

~5-10% of the population carry it in the respiratory tract and nasopharynx

Transmitted by contact with respiratory droplets from a person carrying it.

25
Q

Streptococcus pneumoniea

diagnosis

treatment

prevention

A

Diagnosis

Clinical sample is taken, throat swab, pus sample, blood culture.

Stain: gram positive flame shaped diplococci

Culture: on blood agar, alpha hemolysing gray shiny colonies with autolysis. Strep pneumo knight demands blod.

Antibody Serology tests and Quellung reaction test for capsul

Bile salt soluble/sensitive, Optochin sensitive

Treatment:

Penicillin, after antibiogram of course

only 5-10% of pneumococci are totally penicillin resistant and about 20% are moderately resistant.

if penicillin resitant, Macrolides and Cephtriaxone (3rd gen cephalosporin)

Prevention:

There is a obligatory vaccine for newborns against 13 of the most common capsule serotypes. 13 valent polysaccharide conjugated vaccine.

Recommended for

newborns since 2014

adults over 65

patients with chronic disease, COPD, heart failure

patients after splenectomy (because severely immunocompromised)

26
Q

Pneumococcus virulence factors (7)

A

Polysaccharide capsule

  • there are about 90 strains expressing different capsules this determines the antigenic serotype of the pneumococcus.
  • the capsule prevents C3b binding and opsonization of bacterial membrane.

Capsule serotyping by agglutination of antibody tagged latex beads is used to diagnose Pneumococcus strain.

Pneumolysin: RBC lysis

Hyaluronidase

DNAse

Proteinases

Neuraminidase: cleave sialic acid groups from glycoproteins, involved in cell lysis and in biofilm formation.

IgA protease: Destroys IgA antibodies.

27
Q

Clinical diseases caused by Streptococcus pneumoniae

A

Sinusitis,

Lobar Pneumonia

Endocarditis, angina

Meningitis, Peritonitis

Bacteremia, Septic arthritis

Ulcus serpens corneae - creeping ulcer of the cornea after a small puncture wound of the cornea

Otitis media - middle (media) ear (otitis) inflammation

28
Q

What are the major post-streptococcal diseases?

What causes them?

A

1) Rheumatic fever: Caused by M-protein, the virulence factor in S. pyogenes cell wall which inhibits opsonization factors.

M-protein is very immunogenic, and causes antibodies against cardiac muscle myosin. M-protein Mimics Myocardial Myosin and Mostly Mitral Valves.

Starts only after Pharyngitis infections and not skin infections.

JONES:

J: joints, arthritis

O: actually heart shaped-O, valve damage and murmur, myo- and peri-carditis

N: nodules, subcutaneous nodule formation

Erythema: Erythema marginata, well defined erythema rash

S: Sydenham’s chorea. uncontrollable rapid movements of the hands and face.

2) Post-streptococcal Glomerulonephritis: Type 3 hypersens. reaction, from the immune complexes.

Dark brown urine “cola colored urine”, and facial edema.

Occurs 2 weeks after onset of the Strep infection.

Can occur after either pharyngitis or a skin infection.

Early treatment of the pharyngitis prevents Rheumatic fever but does NOT prevent PSGN.

29
Q

What is the main Group “A” streptococcus?

What is the main Group “B” streptococcus?

How are they differentiated?

A

By expression of their Lancefield antigens,

So an infection can be determined by serology and latex agglutination of the appropriate antigens. ie, by ASO antigen titration of the serum.

Or

by Bacitracin sensitivity.

Group A strep: sensitive to Bacitracin.

Group B: Bacitracin Resistant.

30
Q

Which Streptococci have No lancefield group?

How are they differentiated?

A

S. viridans and S. pneumonia

(the alpha knights)

S. pneumo is Optochin sensitive and viridans is resistant

Strep. pneumo is bile soluble and won’t grow on bile.

31
Q

Streptococcus pneumonia

Clinical diseases

A

Is the #1 cause of all these diseases:

MOPS:

meningitis

Otitis media

Pneumonia

Sinusitis

also: Ulcerus cornea serpens

Signs:

Rust colored sputum and lobar pneumonia

32
Q

What are some of the specific species in the S. viridans group?

A
  • S. mutans - major one for dental carries*
  • S. Oralis* - Subacute Endocarditis
  • S. Sanguis -* Subacute endocarditis
  • S. bovis* - GI malignancies
  • S. anginosus microaerophilic*
  • S. milleri* - microaerophilic, both part of normal GI flora.
33
Q

What are the major oral bacteria responsible for dental caries?

A

S. mutans

It produces water-soluble extracellular polysaccharides from sucrose. It is able to initiate and maintain microbial growth and to continue acid production at low pH values. It rapidly metabolizes sugars to lactic and other organic acids.

Lactobacillus spp.

Lactobacilli are able to grow in low pH environments and to produce lactic acid. Some Lactobacillus strains synthesize extracellular polysaccharides.