By the end of this unit, students should demonstrate competency in the following topics on Streptococci:
Provide theory and methodologies involved in understanding the mechanisms of virulence and pathogenicity of viral and bacterial pathogens.
Discuss the diagnostics principles for the isolation and identification of bacteria using molecular, culture-based, biochemical, and serological methods.
Explain various diseases caused by bacterial and their immunological impact.
Classification of Streptococci
Based on oxygen requirement:
Aerobes
Facultative Anaerobes
Obligate Anaerobes
Based on hemolysis on blood agar:
Alpha (α) Hemolytic: Viridans group. Classified into species by physiological and biochemical properties.
Beta (β) Hemolytic: Serological classification based on group-specific C carbohydrate antigen. Contains 20 Lancefield groups (A-G, K-L, M-N, O-T, U-V). Group A example - Streptococcus pyogenes.
Gamma (γ) Hemolytic: Enterococcus group; classified into species by physiological and biochemical properties.
Morphology of Streptococci
Physical Characteristics:
Cocci that are spherical or oval in shape, measuring approximately 0.5–1.0 μm in diameter.
Arranged in chains due to division in one plane; daughter cells typically do not separate.
Some strains possess a capsule primarily made of hyaluronic acid.
Cultural Characteristics
Streptococci require specific nutrients and are fastidious:
On blood agar: Colonies appear small, circular, with a clear zone of hemolysis.
In liquid media: Exhibit granular turbidity and a powdery deposit, typically observed in glucose or serum broth.
Biochemical Reactions
Key Characteristics:
Catalase negative (unlike staphylococci).
Not soluble in 10% bile (unlike pneumococci).
Positive for Pyrolidonyl-Beta-naphthylamide (PYR) test.
Failure to ferment ribose assists in distinguishing S. pyogenes from other streptococci.
Resistance
Susceptibility Factors:
Easily destroyed by heat (e.g., 54°C for 30 min).
Rapidly inactivated by antiseptics.
Resistant to crystal violet and other selective media such as crystal violet, nalidixic acid, and colistin sulphate.
Streptococcus does not develop antibiotic resistance.
Antigenic Structure
Components:
Capsule that inhibits phagocytosis.
Cell wall composed of three layers:
Outer layer: protein and lipoteichoic acid.
Middle layer: group-specific carbohydrate.
Inner layer: peptidoglycan.
Presence of hair-like pili that project through the capsule, composed of M protein and covered with lipoteichoic acid, promoting attachment to epithelial cells.
Toxins and Virulence Factors
Streptococcal Pyrogenic Exotoxins (SPE):
Three types (A, B, and C) act as superantigens, analogous to staphylococcal enterotoxins and TSS toxin.
They function as T cell mitogens that provoke a massive release of inflammatory cytokines, leading to symptoms such as fever, shock, and tissue damage.
Pathogenicity
Disease Classification:
Suppurative: Direct pus-producing infections.
Non-Suppurative: Includes sequelae from post-streptococcal infections.
Common Disease Causers by S. pyogenes: Pyogenic lesions that exhibit a tendency to spread.
Suppurative Streptococcal Diseases
Various infections include:
Respiratory Infections:
Primary site of invasion is the throat, causing sore throat (tonsillitis and pharyngitis).
Can lead to suppurative complications such as otitis media, mastoiditis, quinsy, Ludwig’s angina, and suppurative adenitis.
Skin and Soft Tissue Infections:
Characterized by conditions such as Erysipelas and Impetigo.
S. pyogenes commonly causes suppurative infections in wounds or burns, often resulting in cellulitis or lymphangitis.
Erysipelas
Description:
A diffuse infection that affects the superficial lymphatics.
Affected areas become red, swollen, and markedly demarcated from surrounding healthy skin, typically observed in older patients.
Impetigo
Characteristics:
Caused primarily by higher numbered serotypes of S. pyogenes.
Common presentations include throat infections and infections of scabies lesions, which can lead to acute glomerulonephritis in children from tropical regions.
Subcutaneous Infections
Range from cellulitis to necrotizing fasciitis, wherein mixed aerobic and anaerobic infections are common.
Necrotizing fasciitis may involve S. pyogenes M types 1 and 3, with associated pyrogenic exotoxin A contributing to severe soft tissue destruction often termed as ‘flesh-eating disease’.
Genital Infections
Details:
Composed of both aerobic and anaerobic streptococci, which are normally found in the female genital tract.
S. pyogenes is implicated in puerperal sepsis.
Historical significance: Ignaz Semmelweis emphasized handwashing in 1847 to prevent outbreaks of puerperal fever, a condition more recently recognized to stem from endogenous infections with anaerobic cocci.
Non-Suppurative Diseases
Sequels:
Two notable sequelae include acute rheumatic fever and acute glomerulonephritis.
Onset occurs between 1 to 3 weeks following an initial streptococcal infection, often without detectable organisms at the time of sequelae.
Acute Rheumatic Fever
Key Features:
The primary lesion involves carditis characterized by connective tissue degeneration of heart valves and inflammatory myocardial lesions marked by Aschoff nodules.
Typically follows persistent or repeated throat infections of streptococci alongside a robust antibody response.
Glomerulonephritis
Etiology:
Linked to a select few ‘nephritogenic’ strains of S. pyogenes, especially observable in tropical regions following skin infections.
Antigenic cross-reactions may occur between glomerular membrane antigen and cell membranes of nephritogenic streptococci, contributing to immune complex diseases.
Epidemiology
Source:
S. pyogenes resides primarily in the human upper respiratory tract, present in both patients and asymptomatic carriers.
Transmission Factors:
Spread occurs via direct contact, contaminated hands, dust, or fomites.
Higher incidence in children aged 5–8 years, predominantly in winter for temperate regions, while tropical regions show no seasonal variations.
Crowding is a critical factor leading to the transmission of infections, especially in closed communities.
Laboratory Diagnosis
Acute Infections:
Diagnosed confirmed via culture methods.
Non-Suppurative Complications:
Diagnosed through antibody demonstration.
Specimen Collection
Appropriate specimens include throat swabs, pus, or exudates.
Sera samples are utilized in cases of rheumatic fever or glomerulonephritis.
Microscopy and Culture
Microscopy:
Gram-stained films from pus can provide presumptive identification. Stained smears from the throat are usually non-diagnostic.
Culture Conditions:
Collect samples for immediate plating or transportation in Pike’s medium.
Specimens should be plated on sheep blood agar incubated at 37°C under 5–10% CO₂ or anaerobically.
Identification Techniques
Hemolytic streptococci grouped via the Lancefield technique employing specific antisera.
Rapid diagnostic methods include detection of group A streptococcal antigen and bacitracin sensitivity to confirm S. pyogenes.
Serology
For rheumatic fever and glomerulonephritis: Retrospective diagnosis relies on antistreptolysin O titration (ASO) where a titer over 200 indicates a previous streptococcal infection.
Prophylaxis
Rheumatic Fever:
Long-term penicillin administration is recommended for children showing early signs of rheumatic fever to avert reinfection and potential heart valve damage.
Not deemed effective for glomerulonephritis as it follows a singular streptococcal infection.
Treatment Approaches
All beta-hemolytic Group A streptococci are susceptible to penicillin G.
Alternatives for those allergic to penicillin include erythromycin or cephalexin.
Tetracyclines and sulphonamides are not recommended as treatment options.
Antimicrobials are ineffective against established glomerulonephritis and rheumatic fever.
Group B Streptococci
Notable pathogens affecting cattle often causing bovine mastitis.
Streptococcus agalactiae is a significant human pathogen responsible for:
Neonatal infections: including meningitis, arthritis, osteomyelitis, conjunctivitis, respiratory infections, peritonitis, omphalitis, and endocarditis.
Adult infections: resulting in conditions like puerperal sepsis and pneumonia.
Neonatal Infections
Most commonly classified as:
Early Onset Type: Occurs within a week of birth, presenting primarily as meningitis and septicemia.
Late Onset Type: Develops between the second and twelfth weeks of life, often presenting as septicemia.
Other Group B Infections in Neonates
Additional risks include arthritis, osteomyelitis, conjunctivitis, respiratory infections, peritonitis, omphalitis, and endocarditis.
Group B Infections in Adults
Common infections associated with Group B Streptococci include puerperal sepsis and pneumonia.
CAMP Test
Definition:
Demonstrated by accentuated zones of hemolysis showing when S. agalactiae is placed perpendicular to a streak of S. aureus on blood agar, named the Christie, Atkins, and Munch-Peterson (CAMP) test.
Group C Streptococci
Primarily animal pathogens belonging to species such as S. equisimilis.
Cause conditions such as:
Upper respiratory tract infections
Deep infections: endocarditis, osteomyelitis, brain abscesses, pneumonia, and puerperal sepsis.
Noteworthy source of streptokinase used in thrombolytic therapy for patients.
Enterococcus Species
Considered enterococci or fecal streptococci, distinguished from streptococci by:
Growth on MacConkey medium forming tiny pink colonies.
Resistance to heat (able to withstand 60°C for 30 minutes).
Characteristic morphology: pairs of oval cocci arranged at angles to each other; non-hemolytic.
Characteristics of Enterococci
Present in the intestines and gastrointestinal tract.
Frequently isolated from urinary tract infections (UTI) and wound infections.
Can cause serious conditions such as endocarditis, septicemia, and intra-abdominal abscesses.
Antimicrobial Resistance in Enterococci
Intrinsically resistant to cephalosporins and exhibit low-level resistance to aminoglycosides.
In strains showing high-level resistance to aminoglycosides, vancomycin is considered the drug of choice.
Vancomycin-resistant enterococci (VRE) have emerged, primarily due to alterations in the D-alanyl-D-alanine chain in the cell wall, contributing to resistance mechanisms.
Viridans Group
Composed of streptococci resident in the mouth and upper respiratory tract exhibiting alpha-hemolysis on blood agar.
Predominantly cause diseases in individuals with pre-existing cardiac lesions, leading to bacterial endocarditis.
May follow dental procedures or tooth extractions, causing transient bacteremia, and can implant on damaged prosthetic valves.
Prophylactic antibiotics are recommended prior to dental procedures to prevent infective endocarditis.