Bacterial Pathogens: Streptococci Quiz

Bacterial Pathogens: Streptococci

• Streptococci are gram-positive cocci, either in chains or diplococci
• Over 40 species exist
• Species are often restricted to a single host species
• Streptococcus species are grouped by common characteristics including hemolytic activity/surface antigens and fermentation properties

Haemolysis

• Haemolysis (horse blood agar) is used to distinguish different Streptococcus species
• Y haemolysis: no haemolysis
• β haemolysis: complete haemolysis (SLO & SLS)
• α haemolysis: partial haemolysis (hydrogen peroxide)

Grouping ofStreptococcal Species

• Species are grouped based on chain length, haemolysis, and Lancefield group(s)
• Lancefield groupings are based on variants of major cell wall polysaccharides extracted using hot HCl
• 21 groups have been identified, but have limited practical value
• M-protein subgroupings number approximately 120

Streptococci and Host Preference

• Specific streptococcal species have preferences for unique hosts, such as human (Str. pyogenes), horse (Str. equi, Str. equisimilis, Str. zooepidemicus)
• See table for full details

Equine Strangles

• Equine strangles is a highly contagious respiratory disease of horses, often occurring in young horses (<5 years old)
• Strangles is a prevalent condition with a widespread distribution, causing substantial farm disruptions and death in some cases
• Str. equisimilis, Str. zooepidemicus and Str. equi are the types of bacteria that cause equine strangles

Clinical Symptoms of Strangles

• Early Symptoms: abrupt onset of fever (103°F or higher), pharyngitis causing dysphagia (reluctance to eat), neck extension, listlessness, and depression; and pharyngitis, laryngitis, and rhinitis contributing to nasal discharge
• Later Symptoms: lymphadenopathy (a major clinical sign), submandibular and retropharyngeal lymph nodes swell
• swelling and pain (1 week post infection), serum oozing from skin, and tenacious creamy pus. Potential for tracheostomy needed due to upper respiratory blockage
• Bastard Strangles: strangles can spread to other areas, causing bacteremia and leading to abscesses in various lymph nodes and organs (thorax and abdomen)
• May also cause unusual immune reaction leading to hemorrhagic purpura, widespread damage to blood vessels, and swelling of legs and head. Can affect brain.

Pathogenicity Factors of Pyogenic (β-haemolytic) Streptococci

• Adherence: Many surface proteins allow binding to epithelium and host proteins such as fibronectin, Fg-binding proteins and IgG-binding protein, aiding uptake.
• Degradative Enzymes: Proteases and hyaluronidase degrade host substrates like fibrinogen and casein, aiding spread.
• Anti-opsonic & Anti-phagocytic Factors: Factors like capsule and M-proteins, PMN cytotoxin, and haemolysins prevent phagocytosis.
• Cell & Tissue Damage: Haemolysins (SLS), and other toxins damage cells.

Pathogenesis of Strangles

• S. equi enters the mouth and nose.
• Attaches to cells in crypt of the lingual and palatine tonsils
• Produces many MSCRAMMs (surface adhesins)
• Binding to extracellular matrix proteins

Pathogenicity Factors: Fibronectin-Binding Proteins

• Involved in adherence and invasions of cells.
• At least two different proteins.
• Bacteria difficult to detect on the mucosal surface a few hours post infection. But are visible inside epithelial cells.

M Protein and M-like proteins

• Hypervariable region with 124 different M types.
• Antiphagocytic effect due to factor H binding
• Bind to multiple proteins like fibrinogen, fibronectin, albumin, plasminogen and affect the immune system
• Involves the alternate complement pathway by binding to factor H. Blocking the pathway prevents opsonization and phagocytosis

M Protein and Fibrinogen Binding

• Fg, an abundant plasma protein is also found in the extracellular matrix.
• S. equi bacteria show better binding to equine Fg compared to human Fg
• Fg-binding contributes to anti-phagocytosis

ZAG protein

• Antibody binding to protein G, preventing opsonization

Streptolysin S

• Toxin causing cell death in PMNs/platelets/lysosomes

Superoxide Dismutase (SOD)

• Neutralises antibacterial oxygen radicals produced during phagocytic respiratory bursts in phagocytes.

Degradative Enzymes

• Cysteine proteases break down host components including fibrinogen, casein and gelatin
• Hyaluronidase breaks down hyaluronic acid, enabling spread through tissues

Streptococcal Pyrogenic Exotoxins (Superantigens)

• Activate cytokines and modulate the host's immune response
• Can lead to shock.
• Cause fever during early strangles infections

Diagnosis of Strangles

• Traditional methods include culturing samples from nasal swabs, washes or pus from abscesses on Columbia CAN (colistin, nalidixic acid blood agar)
• PCR testing is more sensitive

Epidemiology of Strangles

• Purulent discharges from horses
• Horse-to-horse contact
• Indirect transmission from contaminated housing, feed, etc.
• Outwardly healthy animals may shed bacteria after recovery. Guttoral pouch associated with long-term carriage, potentially leading to chondroids
• 10% of animals may become carriers.

Vaccination

• Natural infections often result in solid immunity for >5 years
• Vaccines may not be fully effective, due to various parameters
• Limited efficacy with certain bacterins and adjuvanted extracts, despite potential
• Multivalent M-protein is a candidate immunogen
• Attenuated live vaccines may be a possibility

Treatment

• Ampicillins/aminoglycosides frequently used, however aminoglycosides may produce complications
• Penicillin is a treatment of choice, though not completely effective.

Control of Strangles Outbreaks

• During infection: stop movement of horses in/out, quarantine infected and exposed horses, and provide antibiotic treatment
• After clinical recovery: take multiple nasal swabs at 1 week intervals, and maintain strict hygiene

Aetiology & Pathogenesis of Streptococcal Mastitis

• Specific streptococci have specific roles in mastitis, either as commensal organisms or causing severe complications
• Str.agalactiae: usually commensal, enters teats and ducts, leading to mild and chronic duct blockage
• Str.dysgalactiae: enters the mouth and ducts, leading to acute and permanent damage often in summer months
• Str.uberis: GI commensal, resulting in faecal contamination, leading to teat duct colonisation potentially becoming a severe environmental issue

Streptococcus suis

• Pig disease, often asymptomatic, but can lead to septicemia,meningitis or pneumonia
• Young pigs are most susceptible
• Intensive farming can lead to stress and immune response suppression
• Zoonotic infection of humans occurs, but has no evidence of human-to-human transmission