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
What is *S. uberis*
* 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
What is the pathogenesis of *S. uberis*
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
What are the subspecies of *S. equi?*
* 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
What is Strangles?
* 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
What is the pathogenesis of Strangles?
* 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
What are the clinical signs of Strangles?
* 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
What is ‘Bastard Strangles’
* 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
What is the prognosis of Strangles
* 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
How is Strangles diagnosed?
* Culture of nasal swabs for isolation of *S. equi*
* A PCR assay to detect *seM,* the gene that encodes for antiphagocytic surface protein
34
How is Strangles treated?
* 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
Is there a vaccine for Strangles?
* 2 types
* A live non-encapsulated, attenuated strain.
* Given intranasally
* Vaccine based on purified surface proteins
* Given intramuscularly
36
What is *S. equi* subsp. *zooepidemicus*
* 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
How does *S. equi zooepidemicus* affect pigs
* 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
How does *S. equi zooepidemicus* affect humans
* acquired mainly from contact with horses and pigs
* Causes: pharyngitis, glomerulonephrtis, skin/soft tissue infection, toxic shock syndrome, infectious arthritis
39
What is *S. canis*
* present on the anal mucosa
* Causes: infections of the genital, prostate, mouth, tonsils, nose, ears, uterus, mamary gland, lymph nodes etc.
40
What does *S. porcinus* cause
* Jowl abscesses or porcine strangles
* no longer reported
41
What is *S. suis*
* 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
What are the major Virulence Factors or *S. suis?*
* Capsular polysaccharide
* Sialic acid-rich
* antiphagocytic and aids in intracellular survival
* Surface exposed or secreted proteins
* hemolysin called “suilysin”
43
What are the different serotypes of *S. suis?*
* 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
What is suilysin?
* 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
What is the pathogenesis of *S. suis?*
* 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
What are the clinical signs of *S. suis* infection?
* 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
How is *S. suis* diagnosed?
* Based on clinical signs, age of animals, and gross lesions
* Confimation requires isolation of organism
* Serotyping is important
48
How is *S. suis* infection treated?
* 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
Are there Vaccines for *S. suis?*
* Commercial or autogenous bacterins
* results of protection have been inconsistent
* Vaccination given at ~3-4 weeks old
50
Is *S. suis* zoonotic?
* 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
*S. suis* infections in humans?
* 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
What is *Enterococcus?*
* 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
What does *Enterococcus* cause in animals and humans?
* wound infections of all animals
* mastitis in cattle
* UTI in dogs
* Ear infections in dogs
* **2nd most common nosocomial infection in humans!**
54
How do you treat *Enterococcus?*
* Intrinsically resistant to many antimicrobial agents
* Propensity to acquire and disseminate resistance genes via horizontal gene transfer
55
What is VRE?
* 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
