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Streptococcus Flashcards

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1
Q

Give some of the general characteristics of Streptococcus.

A

Strepto= thread coccus= seed or berry

Gram-positive

Spherical (may be squared or lemon-shaped).

Streptococci form variable length chains when grown in broth.

Note: Most organisms previously classified as Group D streptococci, Viridans group streptococci, etc., have been placed in the genus Enterococcus

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2
Q

Describe the habitat for Streptococcus.

A

These organisms are widely distributed in nature, on skin, large numbers in intestines of all animals as normal flora, oral and nasal cavities.

Most are not disease producers.

Many require serum or blood (usually use blood agar to grow them)

37C is best, decreased O2 helps, increased CO2 helps. Most grow as facultative anaerobes.

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3
Q

Describe the biochemical characteristics of Streptococcus.

A

Catalase neg (all Staphs are pos), gas negative, sugars are fermented resulting in lactic acid production.

Patterns of sugar fermentation are routinely used to help identify.

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4
Q

What do the colonies of Streptococcus look like?

A

Distinctly smaller than those of staphylococci, translucent to transparent, usually no white or yellow pigments.

Picture is of S. pyogenes

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5
Q

Describe alpha, beta and non-hemolysis? How many hours after plating would you look for hemolysis?

A

Complete hemolysis around the colony at 18-24 hr = beta hemolysis (most pathogens were in the beta hemolytic group)

Incomplete= alpha hemolysis at 18 to 24 hr; The RBCs are still present in the media but the hemoglobin has been changed to methemoglobin which has a green color.

Note: If incubated longer than 24 hr, the red cells in the zone of alpha hemolysis often appear to completely lyse around the colonies.

Picture: Hemolyses of Streptococcus spp. (left) α-hemolysis (S. mitis); (middle) β-hemolysis (S. pyogenes); (right) γ-hemolysis (= non-hemolytic, S. salivarius)

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6
Q

What is the purpose of a Lancefield test?

How is it performed?

A

To group catalase-negative, coagulase-negative bacteria based on the carbohydrate composition of bacterial antigens found on their cell walls. (Streptococcus spp.)

Carried out by heating or treating the unknown Strep. strain with acid to destroy the protein antigens present on the cell wall.

The material is pelleted and the supernatant used in capillary tube precipitation tests against various group-specific antisera (antibodies).

Depending on which antibodies cause agglutination in the tube determines the “group” (A, B, C ect.)

Note: A more modern method the group-specific antisera are bound to Protein A in the cell wall of Staphylococcus aureus.

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7
Q

What is important with some, especially the Group A streptococci which have a capsule composed of hyaluronic acid?

A

This not only masks the organism but mimics host tissues.

Protects the bacteria from phagocytosis.

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8
Q

Name the 5 toxins associated with the Streptococcus genus.

A
  1. ) Streptolysin O
  2. ) Streptolysin S
  3. ) Streptokinase
  4. ) Streptodornase (DNase)
  5. ) Hyaluronidase
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9
Q

What are the effects of Streptolysin O toxin?

A

It is leukotoxic, attacks RBC and causes complete hemolysis, toxic to platelets and fibroblasts, very antigenic

Note: The measurement of anti-streptolysin-O (ASO) titers is considered to be a good indicator of recent streptococcus pyogenes infection in humans.

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10
Q

How is Streptolysin O toxin activated?

A

This toxin is a thiol-activated cytolysin (sequesters cholesterol in the cell membrane)

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11
Q

When culturing clinical material suspected of harboring a beta-hemolytic streptococcus, what is a good method to try and observe the activity of Streptolysin O toxin?

A

Inoculating a portion below the surface of the agar.

This will enhance the observation of the activity of this toxin.

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12
Q

Describe the Streptolysin S toxin.

A

It is serum stable; less toxic, non-antigenic, stable to O2, the one producing the hemolysis ordinarily seen.

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13
Q

What is the classification of the Streptokinase toxin and what is its mode of action?

A

Fibrinolysin

In addition to lysing fibrin, this enzyme is also able to cleave C3

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14
Q

What classification is the Streptodornase (DNase) toxin?

A

It is a nuclease.

All strains of Group A streptococci produce at least one nuclease that assists in liquefaction of pus and obtaining nutrients.

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15
Q

What is the mode of action for the Hyaluronidase toxin?

A

Breaks down hyaluronic acid in tissues and is considered to be a spreading factor.

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16
Q

S. pyogenes

What goup do they belong to?

What is their typical habitat?

What clinical signs would be observed with a S. pyogenes?

A

Group A (there are 84 types of this species based upon the M and T proteins)

Human pharyngeal and tonsillar areas.

Humans: strep throat, scarlet fever, sinusitis, heart valve lesions, glomerulonephritis, rheumatic fever,

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17
Q

In the news recently the S. pyogenes have been sensationlized for causing what specific disease that primarily affects the young and elderly?

A

So called Ainvasive Group A streps leading to “flesh-eating” (necrotizing fasciitis).

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18
Q

What is the major virulence factor of Group A (S. pyogenes) streptococci?

What is the purpose of this virulence factor?

Where is it found?

A

M-protein (bacteria lacking the M proteins are readily killed)

Antiphagocytic: Interferes with the deposition of C3b on the surface of the organism.

Fibrillar surface molecule.

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19
Q

What is another feature to help identify the Group A (S. pyogenes) Streptoccoci?

A

T-proteins (trypsin sensitive)

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20
Q

Antibody levels to _______ are usually highest in patients with rheumatic fever.

A

M-Associated protein (MAP): Antigenically related to myocardial tissue.

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21
Q

Describe the Erythrogenic toxins in S. pyogenes.

A

They are classed as superantigens and there are three major toxins, A, B and C.

Produce the rash and fever in scarlet fever; highly antigenic (only sees the rash during the first infection). The major importance of the toxins is in the production of fever rather than the production of a rash

The genes encoding these toxins are carried on bacteriophages and thus are not expressed unless the infecting strain is lysogenic for the phage

Note: Lysogenic means the bacterium is carrying the phage genome and replicating it along with its own

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22
Q

Define the term Lytic infection.

A

It means the bacteriophage has taken over the bacterial cell and is multiplying to high numbers and killing the bacterium.

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23
Q

Vaccines against Group A (S. pyogenes) Streps utilize which antigenic structure?

Are they effective?

A

M-proteins

There are effective against the specific M-Proteins but protection is highly specific to the M-protein. There are just too many M protein variations to immunize against all of the S. pyogenes.

Recovery does not confer immunity against other M-protein types but is fairly solid against homologous strains; carriers.

24
Q

Describe the treatment for a Group A (S. pyogenes) infection.

A

Penicillin class antibiotics. Beta hemolytic streptococci do not readily develop resistance

25
Q

S. equi subspecies equi (most refer to this as S. equi)

What group?

What type of hemolysis?

What species does it infect?

Describe the growth on medium.

A

Group C

Beta Hemolysis

Horses

One of the more fastidious streps; tends to die out on subculture. Colonies are mucoid from the heavy capsule.

26
Q

Describe the M-proteins of S. equi.

Would it be possible to make a viable vaccine?

A

It has essentially one M-protein of importance (there are one or two more of little importance) and it serves as an virulence factor (antiphagocytic).

Unlike S. pyogenes with 84 different M-proteins you could make a viable vaccine against S. equi because there is only one variant.

27
Q

Describe the cytotoxin of S. equi.

A

It is a powerful cytotoxin that damages phagocytic cells and results in a high rate of intracellular survival

28
Q

What is the term for an upper respiratory infection caused by S. equi?

Describe this disease and its process.

A

“Strangles”

Usually in horses less than 2 yr of age but can cause clinical disease in any age horse.

Often starts as an upper respiratory infection with a serous nasal discharge which turns purulent.

Abscessation of head and neck lymph nodes with painful swelling may interfere with breathing or cause nerve damage.

May become septicemic and cause death or it may cause “bastard strangles” (generalized abscessation) which often results in death.

29
Q

What is this an example of?

What organism causes this?

A

“Strangles”

S. equi

30
Q

Purpura can be caused by S. equis.

Describe this process.

What is the prognosis for animals diagnosed with purpura?

A

Often known as purpura hemorrhagica.

Delayed immune reaction. Horses have high serum IgA antibody titers. IgA apparently forms immune complexes with the M-Protein. Fever, edema, hemorrhages; the primary lesion is vasculitis and necrosis of blood vessel walls.

Poor prognosis: usually results in death

31
Q

True/False: S. equis can cause reproductive tract infections: Metritis.

True/False: It is not as common with S. zooepidemicus.

A

True

True

32
Q

What is the immunity against S. equis?

Is there a vaccine out for S. equis?

A

Good following infection. Protection against infection is provided by M-Protein-specific IgA on the surface of the nasal epithelium.

Yes: Several on the market.

33
Q

Describe the different methods of vaccination against S. equis and the effectiveness of each.

A

Modified live: It is given intranasally. In some horses it is capable of producing a low level of disease. Good protection.

Bacterins: not very effective and a lot of swelling occurs at the injection site.

M-Protein vaccines: Showed some promise at first but are generally not much better than the bacterins. Neither of the killed vaccines produces good levels of anti-M-Protein IgA on the nasal epithelium.

34
Q

What is the treatment for S. equi infection?

A

Penicillin. Works best prophylactically but environmental contamination and chronically infected horses complicate prophylaxis.

Lance abscesses that form.

35
Q

S. zooepidemicus (S. equi subspecies zooepidemicus is the proper nomenclature)

What group?

Hemolysis?

Describe the growth on culture.

What is its natural habitat?

A

Group C.

Wide zone of Beta hemolysis.

Colonies may be quite mucoid due to capsule production. The colonies collapse as they age and dry (often within 48 hours).

Commensal of the skin, upper respiratory mucosa, and tonsillar and associated pharyngeal lymphoid tissues of horses.

36
Q

Describe the pathogenicity of S. zooepidemicus.

A

Horses: Said to be the most common agent in wound infections; common secondary invader in respiratory disease; umbilical cord infections (omphalophlebitis), bacteremia, and polyarthritis.

Mare: Most common organism in uterine and cervical infections, can be carried in the semen.

Dogs: There are reports of a highly contagious hemorrhagic pneumonia in dogs. There is typically an acute onset of clinical signs including fever, dyspnea and hemorrhagic nasal discharge.

Other animals (alpacas, llamas): Occasional infections.

37
Q

Are immunizations commonly practiced with S. zooepidemicus?

A

Not normally practiced. Immunity is poor following infection

38
Q

S. dysgalactiae subspecies equisimilis.

What group?

Hemolysis?

A

Group C, G and L

Wide Beta hemolysis

Note: The mastitis pathogen in dairy cattle is classified as S. dysgalactiae subspecies dysgalactiae but that organism is alpha hemolytic and appears to be quite distinct.

39
Q

What is the pathogenicity of S. dysgalactiae subspecies equisimilis.

Is there a vaccine?

A

Associated with metritis and cervicitis in sows. Can also cause vegetative valvular endocarditis. The organism is found in secretions from the nose, oral cavity, vagina and prepuce. It can also be present in milk of sows.

Occasionally isolated from horses with a strangles-like disease.

Dogs: Occasional reproductive tract infections in females.

There are no vaccines for this pathogen

40
Q

S. canis

Group?

Hemolysis?

Describe the pathogenicity of S. canis.

A

Group G

Beta Hemolysis

Widely distributed in dogs. Tonsillitis, metritis, umbilical infections, septicemia, wound infections. The male genital tract appears to be a natural habitat. Can be found causing similar diseases in cats, especially wound infections.

There have been several reports of wound infections in humans and some reports of mastitis in dairy cattle.

41
Q

S. porcinus

Group?

Describe the pathogenicity for S. porcinus.

A

Group E, P, U and V

Jowl abscesses in swine (cervical lymphadenitis) used to be common in swine. It is rare in the U.S. today. The cervical abscesses do not interfere with feed conversion but dealing with the abscesses in the slaughter plant can be difficult. The heads are usually condemned.

42
Q

This is an example of what?

What pathogen is associated with it?

A

Jowl abscess.

S. porcinus

43
Q

What is the treatment for S. porcinus?

Is there a vaccine for it?

A

Tetracycline in the feed prevents it and is likely one of the factors that led to a much lower incidence of disease. However, FDA Guidance 209 bans the use of growth promoting levels of antibiotics in feeds and this could have an impact if the organism becomes more widespread.

A vaccine used to be available to control the disease but it was taken off the market for lack of interest. Simply removing the head was considered to be less than the cost of control.

44
Q

S. suis

Group?

Hemolysis?

Describe the pathogenicity of S. suis.

A

Group D: There are at least 35 capsular types described. Type 2 is most commonly associated with disease.

Alpha Hemolytic

Currently a very important disease of swine. Resides in the mothers birth canal and is transmitted to piglets at birth or shortly after. Produces a septicemia in young pigs that can progress to meningitis, arthritis, and possibly bronchopneumonia.

Occasionally reported from wild boars, horses, dogs, cats and birds.

45
Q

What are the virulence factors of S. suis?

A

Muramidase-released protein (MRP) and extracellular protein factor (EF)seem to be required for virulence in type 2 disease.

Suilysin (a cholesterol-binding hemolysin) is produced by about 70% of the isolates from pigs.

These strains were more likely to be isolated from cases of meningitis, septicemia and arthritis.

46
Q

What is the importance of S. suis being zoonotic?

How does this disease enter humans?

What are the symptoms and prognosis of this disease?

A

An outbreak occurred in Sichaun, China in 2005 where 215 cases were reported, all were backyard farmers who were directly exposed when they slaughtered pigs that had died of unknown causes or were killed for food because they were ill.

Enters via cuts, abrasions, through the conjunctiva and possibly other routes.

Septicemia with meningitis, pneumonia, arthritis, endocarditis and toxic shock syndrome all occur. Meningitis can lead to permanent hearing loss in about 50% of human cases. Streptococcal toxic shock syndrome occurred in 28% of these cases and 62% of those people died

47
Q

This is an example of what pathogen?

A

S. suis

Notice how the animal is uncoordinated and rolling around on the ground. Indicative of meningitis.

48
Q

S. agalactiae

Group?

Hemolysis?

Pathogenicity?

A

Group B

Narrow zone of Beta Hemolysis

Causes an acute localized mastitis with swelling, abnormal milk and decreased secretion (agalactia) and eventually chronic infection with induration. One of the more serious mastitis pathogens for cows. Also causes mastitis in sheep and goats.

Usually spreads via the milking equipment. It is an obligate intramammary pathogen.

49
Q

What are the best methods of controlling S. agalactiae?

A

Since it is an obligate intramammary pathogen it can be eliminated from the herd when aggressively pursued.

The general recommendation is to culture every cow, treat the positives, re-test and eliminate the non-responsive cows.

Good management practices such as dry cow therapy and elimination of chronically infected cows have helped to lessen the prevalence of this organism.

50
Q

Is there a vaccine available for S. agalactiae?

A

No bacterin is available.

Usually much easier and more economical to eliminate from the herd.

A good bacterin might be of some benefit in these herds but the organism does not produce good immunity even in natural infections.

51
Q

What is the treatment for an S. agalactiae infection?

A

The organism is quite susceptible to intramammary infusion of penicillin. Novobiocin+penicillin is also used

52
Q

Fun Fact: An organism that causes middle ear infections and septicemias in human infants and septicemias in pregnant women is also called S. agalactiae also referred to as “Group B Strep” but it is apparently not the same organism as the S. agalactiae that causes mastitis in cows.

A
53
Q

S. dysgalactiae subspecies dysgalactiae (SDSD)

Group?

Hemolysis?

Pathogenicity?

A

Group C

Alpha Hemolytic (greenish coloration)

Common cause of mastitis in dairy cows. Present on the skin and in the mouth and gains entry through the streak canal via wounds and sores involving the teat orifice producing an acute painful mastitis.

The organism is able to invade mammary epithelial cells.

54
Q

How does S. dysgalactiae resist the immune system?

A

This organism produces and AM-like protein@ similar to that of S. pyogenes. It also produces an Fc-receptor protein that interferes with phagocytosis and a fibronectin receptor.

55
Q

S. uberis

Group?

Hemolysis?

Pathogenicity?

A

Can’t be placed in a Lancefield group.

Alpha or non-hemolytic

It causes mastitis in cattle. The organism is common in the GI tract and bedding as well as being found on skin. Hygiene is important in control

56
Q

What are the three Strep. species that cause mastitis?

What test would you perform to differentiate them?

What would be the expected results for each species?

A
  1. ) S. agalactiae
  2. ) S. dysgalactiae
  3. ) S. uberis

You would perform a CAMP test.

Results for CAMP test:

S. agalactiae- CAMP positive

S. dysgalactiae- CAMP negative

S. uberis- 15% are CAMP positive 85% negative

57
Q

What is this image depicting?

A

A CAMP test.

Notice the arrow head shape indicative of a positive result.

Microbiology (6 decks)

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