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)
2
Q
How are streptococci species classified?
A
- Based on:
- Hemolysis
- Serology
- Habitat and biological activity
- Organ or tissue tropisms
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
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
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
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
7
Q
What Surface Proteins do Strepococcus spp have?
A
- M protein
- FbsA protein
- FOG protein
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
9
Q
What is FbsA protein
A
- A Ig-binding protein
- S. agalactiae
10
Q
What is FOG protein
A
- Similar protein to FbsA
- S. dysgalactiae, subspecies equisimilis
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
12
Q
What are the cell wall components of Streptococci?
A
- Peptidoglycan and lipoteichoic acid
- Interact with macrophages to release proinflammatory cytokines
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.
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)
15
Q
What other enzymes does Streptococcus have?
A
- Hyaluronidase
- DNAse
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
17
Q
What species of Stretococcus cause Mastitis in cattle?
A
- S. agalactiae
- S. dysgalactiae
- S. uberis
18
Q
What causes Stangles?
A
S. equi subspecies equi
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
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
21
Q
What is a CAMP test?
A
- Christie-Atkins-Munch-Peterson test
- will differentiate staph and S. agalactiae
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
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
- Entry through the teat canal
- Organisms attach and proliferate and induce influx of neutrophils
- Edema and vacuolation of secretory cells
- 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
