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Bacteriology and Mycology > Streptococcus > Flashcards

Streptococcus Flashcards

1
Q

Streptococcus

A
  • Pyogenic
  • Gram positive
  • Cocci
  • At least 98 species
    • only a few cause diseases
  • Part of normal flora of Upper Respiratory Tract and Lower Genitourinary Tract
  • Do not persist in the environment
  • Catalase negative
  • More fastidious (need more nutritious culture medium)
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2
Q

How are streptococci species classified?

A
  • Based on:
    • Hemolysis
    • Serology
    • Habitat and biological activity
    • Organ or tissue tropisms
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3
Q

How does Serology Classification work?

A
  • “Lancefield Classification”
  • Based on the carbohydrate, called Substance “C”, on cell surfaces of streptococci
  • 20 serogroups, A-V (but no I or J)
  • Subdivided into serotypes based on 3 protein antigens, M, R, T
  • Group A (GAS): Human pathogen only
  • Groups B, C, D: Human and Animal
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4
Q

How does classification based on Habitat and Biological activities work?

A
  • Pyogenic group:
    • Cause pyogenic infections in humans and animals.
    • Generally Beta hemolytic
  • Oral or Viridans grroup:
    • Primarily commensals on mucous membranes.
    • Alpha hemolytic; causing greenish discoloration
    • Many produce lactic acid from sugar fermentation, could cause dental caries
  • Lactic group:
    • Present in milk/milk products
    • moved to genus Lactococcus
  • Enteric group:
    • present in intestinal contents
    • Some now in genus Enterococcus
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5
Q

How are streptococcus classified based on adaptations to specific organs or organ systems?

A
  • S. agalactiae, S. dysgalactiae, S. uberis infect the udder and cause mastitis
  • S. equi, S. canis, S. porcinus infect the lymphatics and lymph nodes of the head and neck
  • S. pneumoniae infects the lower respiratory tract
  • S. suis survives in or on the mononuclear cells in the blood and are transported to CNS, lungs and joints
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6
Q

What Virulence Factors do Streptococcs spp. have?

A
  • Adhesins
    • Bind to a variety of extracellular matrix proteins of the host (Fibrinogen, Fibronectin, Collagen, Antibodies, etc)
    • Coating of streptococcal cells with host proteins results in masking of sites for complement activation and thus decrease opsonization
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7
Q

What Surface Proteins do Strepococcus spp have?

A
  • M protein
  • FbsA protein
  • FOG protein
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8
Q

What does M protein do?

A
  • Binds to fibrinogen and imparts an antiphagocytic property and enhances adherence to host epithelial cells
  • S. pyogenes, S. equi
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9
Q

What is FbsA protein

A
  • A Ig-binding protein
  • S. agalactiae
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10
Q

What is FOG protein

A
  • Similar protein to FbsA
  • S. dysgalactiae, subspecies equisimilis
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11
Q

What types of capsules do streptococcus species have?

A
  • S. pyogenes & S. equi produce capsules composed of hyaluronic acid
    • poorly antigenic and is antiphagocytic
  • S. agalactiae, S. porcinus, & S. canis have capsules composed of polysaccharide
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12
Q

What are the cell wall components of Streptococci?

A
  • Peptidoglycan and lipoteichoic acid
    • Interact with macrophages to release proinflammatory cytokines
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13
Q

What Hemolysins does Streptocccus have?

A
  • Streptolysin O (SLO): Oxygen labile
    • Pore-forming toxin
    • Suilysin is the SLO of A. suis
  • Streptolysin S: Oxygen stable
    • Responsible for beta hemolysis
    • Cytolytic to macrophages, leukocytes, platelets, etc.
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14
Q

What is Streptokinase

A
  • Activates plasminogen to form plasmin
  • Gene is located on a prophage
  • Plasmin is a proteolytic enzyme that acts on host proteins, including fibrin (dissolves blood clots)
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15
Q

What other enzymes does Streptococcus have?

A
  • Hyaluronidase
  • DNAse
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16
Q

What is the Pathogenesis of Streptococcus?

A
  • Primarily cause pyogenic infections that affect the skin, respiratory tract, reproductive tract, and mammary gland
  • Organisms may enter the blood to cause septicemia
  • Toxemia and immune-mediated lesions are common sequel of the disease
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17
Q

What species of Stretococcus cause Mastitis in cattle?

A
  • S. agalactiae
  • S. dysgalactiae
  • S. uberis
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18
Q

What causes Stangles?

A

S. equi subspecies equi

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19
Q

S. agalactiae

A
  • Chronic contagious mastitis
  • Septicemia and meningitis in human newborns: Human and bovine strains are different
  • 9 serotypes based on capsular antigen
    • occurrence varies by geographical location
  • Obligate parasite of the epithelium and tissues of mammary gland
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20
Q

What is the pathogenesis of S. agalactiae?

A
  • Mode of infection: via the teat
  • Capsule: Antiphagocytic activity
  • Surface proteins are involved in adhesion, invasion, and inhibition of phagocytosis
  • 22.5-kDa protein called CAMP factor
    • Potentiates the action of staphylococcal beta toxin
    • Has cytotoxic activity against mammary tissue
  • Death of PMNs and release of lysosomal enzymes cause tissue damage and inflammation
  • Fibrin plug formation in the smaller milk ducts lead to involution of secretory tissue and loss of milk production
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21
Q

What is a CAMP test?

A
  • Christie-Atkins-Munch-Peterson test
  • will differentiate staph and S. agalactiae
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22
Q

What is the treatment for S. agalactiae

A
  • highly susceptible to penicillins
  • Herds are mass treated, “blitz treatment”
  • Milk from all lactating cows are cultured and cows with positive culture are treated
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23
Q

What is S. dysgalactiae

A
  • Subspecies dysgalactiae
    • alpha hemolytic
    • Acute and subclinical mastitis in cows
  • Subspecies equisimilis
    • Beta hemolytic
    • Disease in other animals:
      • Abscesses in horses
      • Arthritis, meningitis, endometritis, mastitis, in pigs cattle, dogs and birds
24
Q

What is the pathogenesis of S. dysgalactiae?

A
  • Usually requires injury of the teat or udder (insect bites0
  • Opportunistic infections
  • Associated with other bacteria:
    • Trueperella (arcanobacterium) pyogenes
25
Q

What is S. uberis

A
  • Commensal of cattle:
    • Tonsillar, intestinal, mucosal and epithelial cells
  • Responsible for 20-30% of cases of clinical mastitis in the US.
  • Many are opportunistic invaders of the mammary gland of older cows under conditions of heavy environmental soiling with feces
26
Q

What is the pathogenesis of S. uberis

A
  1. Entry through the teat canal
  2. Organisms attach and proliferate and induce influx of neutrophils
  3. Edema and vacuolation of secretory cells
  4. Necrosis of the alveoli
  • Severity varies
27
Q

What are the subspecies of S. equi?

A
  • 2 subspecies:
    • Equi & zooepidemicus
    • Both are beta hemolytic
    • Differ in host specificity, pathogenicity and can be differentiated by genetic typing
  • Subsp. equi is an equine pathogen, causes Strangles
  • Subsp. zooepidemicus is a mucosal commensal and an opportunistic pathogen with a wide host range
28
Q

What is Strangles?

A
  • Highly contagious disease of horses caused by S. equi subsp equi
  • Disease is a purulent pharyngitis and lymphadenitis of the upper respiratory tract with involvement of the regional lymph nodes (Mandibular, submandibular, and retropharyngeal)
  • Disease is observed primarily in young horses
29
Q

What is the pathogenesis of Strangles?

A
  • Mode of infection:
    • Feed, water, o fomites directly contaminated by nasal discharge or pus from an abscess
  • S. equi enters via mouth or nose and attaches to cells in the crypts of the tonsils
  • Primary attachment sites are lymph nodes around the tonsils with colonization of guttural pouch and cranial sinuses
  • Incubation period is 3-14 days
30
Q

What are the clinical signs of Strangles?

A
  • Fever, lassitude, nasal discharge, slight cough, difficulty in swallowing, swelling of the mandibular lymph nodes
  • Pressure of the enlarged retropharyngeal lymph nodes and associated edema on the airway may cause respiratory difficulty, hence “strangles”
31
Q

What is ‘Bastard Strangles’

A
  • Generally Strangles involves the URT including guttural pouches and associated lymph nodes
  • Occasionally metastasis may result in abscess formation in other locations such as lungs, brain, and abdomen
32
Q

What is the prognosis of Strangles

A
  • Most cases recover quickly and uneventfully
  • ~75% develop a strong immunity to Strangles following recovery
  • ~25% become susceptible to a second attack of the infection within months
33
Q

How is Strangles diagnosed?

A
  • Culture of nasal swabs for isolation of S. equi
  • A PCR assay to detect seM, the gene that encodes for antiphagocytic surface protein
34
Q

How is Strangles treated?

A
  • Majority of horses require no treatment other than rest and soft moist and palatable feed
  • During an outbreak, antibiotic treatment in early cases phase of infection may prevent abscessation
  • Penicillin is the antibiotic of choice. Other antibiotics include cephalosporins and macrolides
  • Once an external lymph node is affected, antibiotic therapy is not given because it only prolongs inevitable enlargement and eventual rupture of lymph node abscess
35
Q

Is there a vaccine for Strangles?

A
  • 2 types
  • A live non-encapsulated, attenuated strain.
    • Given intranasally
  • Vaccine based on purified surface proteins
    • Given intramuscularly
36
Q

What is S. equi subsp. zooepidemicus

A
  • A opportunistic commensal in the URT of horses and pigs
  • Infections occur in many animals species, including humans
  • In horses, respiratory disease (rhinitis, bronchitis, pneumonia) and endometritis are most commonly seen
  • Causes Mastitis in cattle and goats
37
Q

How does S. equi zooepidemicus affect pigs

A
  • unil 2019 S. equi zooepidemicus was confined to Asia
  • It is now an emerging swine pathogen in the US
  • Causes weakness, lethargy, fever, and rapidly escalating mortality in pigs
  • Splenomegaly and lymphadenopathy may be observed at necropsy
  • High mortality (up to 50%)
38
Q

How does S. equi zooepidemicus affect humans

A
  • acquired mainly from contact with horses and pigs
  • Causes: pharyngitis, glomerulonephrtis, skin/soft tissue infection, toxic shock syndrome, infectious arthritis
39
Q

What is S. canis

A
  • present on the anal mucosa
  • Causes: infections of the genital, prostate, mouth, tonsils, nose, ears, uterus, mamary gland, lymph nodes etc.
40
Q

What does S. porcinus cause

A
  • Jowl abscesses or porcine strangles
  • no longer reported
41
Q

What is S. suis

A
  • important swine pathogen
  • Causes wide range of clinical syndromes in pigs and other domestic animals
  • Zoonotic
  • Pigs carry pathogen on their tonsils and transmission is by the respiratory and oral routes
  • Predisposing factors are important and include stress and lowered immunity
  • May also be transmitted by fomites (feed and water troughs)
42
Q

What are the major Virulence Factors or S. suis?

A
  • Capsular polysaccharide
    • Sialic acid-rich
    • antiphagocytic and aids in intracellular survival
  • Surface exposed or secreted proteins
  • hemolysin called “suilysin”
43
Q

What are the different serotypes of S. suis?

A
  • Based on antigenicity of capsular polysaccharide
  • 35 different serotypes have been identified
    • most frequent are 2, 3, ½, 4, and 8
  • Distribution varies geographically
  • Capsular type 2 is most prevalent in NA and Europe
44
Q

What is suilysin?

A
  • A pore-forming, 64 kDa protein that is cytotoxic to neutrophils
  • Homologous to Pneumolysin (S. pneumoniae), Streptolysin O (S. pyogenes), and Listeriolysin (Listeria monocytgenes)
45
Q

What is the pathogenesis of S. suis?

A
  • Pigs generally 5-10 weeks old
  • After entry of the organism into tonsils, bacteremia or septicemia with seeding of the organism into joints, meninges, and lungs
  • Bacteria may be carried by macrophages to joints and meninges
  • Meningoencephalitis requires sustained bacteremia
  • Lungs can also be infected directly from the upper respiratory tract
    • Often precedes entry into the CNS
  • S. suis is most frequently isolated organism from lesions of endocarditis in pigs
46
Q

What are the clinical signs of S. suis infection?

A
  • Rise in rectal temperature (up to 108.5F)
  • During bacteremia/septicemia, usually fluctuating fever, loss of appetite, depression, shifting lameness
  • Proportion of pigs develop neurological signs because of meningitis (incoordination, unusual stances, inability to stand, opisthotonous (arched back), leading to convulsions
47
Q

How is S. suis diagnosed?

A
  • Based on clinical signs, age of animals, and gross lesions
  • Confimation requires isolation of organism
  • Serotyping is important
48
Q

How is S. suis infection treated?

A
  • Antibiotics including ampicillin, ceftiofur, gentamicin, tiamulin, and a combination of trimethoprim and sulfonamide
    • Parenteral treatment with antibiotics in pigs with early recognition may maximize pig survival
49
Q

Are there Vaccines for S. suis?

A
  • Commercial or autogenous bacterins
  • results of protection have been inconsistent
  • Vaccination given at ~3-4 weeks old
50
Q

Is S. suis zoonotic?

A
  • Most cases occur in people in close contact with pigs or handling unprocessed pork
  • Occupational Disease
    • Pig farmers, butchers, abattoir workers, meat inspectors, swine veterinarians.
  • Serotype 2 is most common
51
Q

S. suis infections in humans?

A
  • Occurs through breaks in the skin
  • Usually produces meningitis
    • Frequent complication is deafness
  • Additionally: endocarditis, cellulitis, peritonitis, arthritis, pneumonia, uveitis, and endopthalmitis
  • Rare in the US
    • most in China and Vietnam
  • 2005 outbreak in Sichuan, China
    • followed by local outbreak in swine, >600 backyard pigs euthanized
    • 215 human cases, 39 deaths
52
Q

What is Enterococcus?

A
  • initially, characterized as Group D Streptococci
  • Normally found in GI tract of animals and humans
  • Medically important: E. faecalis & E. faecium
  • Low virulence- opportunistic pathogens
53
Q

What does Enterococcus cause in animals and humans?

A
  • wound infections of all animals
  • mastitis in cattle
  • UTI in dogs
  • Ear infections in dogs
  • 2nd most common nosocomial infection in humans!
54
Q

How do you treat Enterococcus?

A
  • Intrinsically resistant to many antimicrobial agents
  • Propensity to acquire and disseminate resistance genes via horizontal gene transfer
55
Q

What is VRE?

A
  • Vanomycin Resistant Enterococci
  • Antibiotic resistant enterococci
  • Major problem in human hospitals due to limited options for treatment
  • VRE in animals are of public health concern

Bacteriology and Mycology (35 decks)

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