Microbio Lecture 4
Gram Positive Cocci
Size: 10 µm
Staphylococcus aureus
Name Origin: "Staphule" means grape in Greek.
Exotoxins produced by staph aureus (a single one wont produce all):
Cytotoxins
Hemolysins
Enterotoxins (A-E, G-I)
an exotoxin that binds or affects the intestinal tract.
Exfoliative toxins (ETA, ETB)
Toxic shock syndrome toxin 1
Enzymes
Coagulase
Causes coagulation of fibrin.
Found in almost all pathogenic staphylococci.
Used in lab tests to differentiate from S. epidermidis, S. capitis, and S. saprophyticus.
Beta-lactamase (penicillinase)
Destroys penicillin.
Epidemiology and Infection
Carried in ~15% of the normal population.
Common carriage sites: anterior nares, axilla, perineum, and hands.
Problems:
85-90% of hospital strains are penicillin resistant.
Causes localized purulent infections (pustules, boils, styes, conjunctivitis, otitis, etc.).
Associated with pneumonia, osteomyelitis, septicaemia, endocarditis, food poisoning, toxic shock syndrome, and scalded skin syndrome.
Impetigo is caused by sta3ph aureus
Nosocomial Infections
Major cause of hospital-acquired infections from stitch abscesses, infected wounds.
Prevention:
Aseptic technique in ER and OR.
Education of health personnel.
Handwashing.
Staphylococcus epidermidis
Part of normal skin/mucous membrane flora.
Generally non-pathogenic; can cause infections in compromised patients, including:
Post-operative infections (brain, open heart, endocarditis, shunt infections).
Opportunistic pathogen.
Streptococci
Arranged in pairs or chains; "streptos" means twisted in Greek.
Subdivided into groups based on:
Hemolytic properties (alpha, beta).
Carbohydrate C antigen (Lancefield classification).
M-protein classification.
gamma hemolytic: do nothing to red blood cells
beta-hemolytic: completely destroy red blodd cells, leading to a clear zone around the colony on blood agar.
alpha-hemolytic: partially lyse red blood cells, resulting in a greenish discoloration around the colony on blood agar.
Streptococcus pyogenes
Group A, beta-hemolytic.
Causes:
Acute tonsillitis (strep throat), potentially leading to rheumatic heart disease.
Skin infections (impetigo, cellulitis).
Fever and septicemia.
Toxins
Streptolysins (O and S) that affect neutrophils and macrophages.
Streptococcal pyrogenic exotoxins (SPEs) involved in scarlet fever rash.
Enzymes
Hyaluronidase aids in bacterial spreading.
Virtually all strains are penicillin G sensitive.
Prevention:
Education of health personnel.
Aseptic obstetric procedures.
Early detection and treatment.
Flesh-eating disease (Necrotizing fasciitis)
Caused by Streptococcus pyogenes.
Mechanism:
Toxins hijack plasminogen, activate proteases to aid spreading.
Bacteriophage enables escape from neutrophil attacks.
Streptococcus agalactiae
Group B, commonly found in the vagina of healthy women.
Can cause neonatal infections:
Early septicemia (respiratory distress/shock at birth) with high fatality rates.
Delayed meningitic form (1-12 weeks post-partum).
Streptococcus faecalis (Enterococcus)
Group D, part of normal GI-tract flora.
Opportunistic infections in compromised individuals.
Viridens streptococci
Found in the oral cavity.
Can cause endocarditis in patients with damaged heart valves.
Streptococcus pneumoniae
Known as pneumococcus.
Features:
Polysaccharide capsule has antiphagocytic properties (90 distinct serotypes).
Found in the naso-pharynx of healthy individuals.
Can cause:
Lobar pneumonia
Meningitis
Prevention strategies:
Target groups include the elderly, alcoholics, and those in crowded living conditions.
Vaccination is recommended.
Neisseria meningitidis
Gram-negative diplococci.
Laboratory isolation:
Grown on chocolate agar at 5-10% CO2, 37°C.
Selective media (Thayer-Martin) when isolating from the nasopharynx.
Frequently found in healthy individuals.
Antiphagocytic polysaccharide capsule with 13 serogroups (A, B, C, X, Y, W135 most prevalent).
Transmission and Infection
Carriers can develop infection or spread to non-immune individuals.
Infects only humans; commonly in children or those in crowded settings.
Results in:
Meningitis
Septicemia
Waterhouse-Friderichsen syndrome (severe septicemia complication).
Meningitis Symptoms in Infants
Signs include:
Bulging soft spot, high temperature, extreme sleepiness, vomiting, irritability.
Fast breathing, changing skin color.
Recognize purple bruises or rash as urgent signs.
Historical Background
First described by Arthur Francis Voelcker in 1894.
Comprehensive review by Carl Friderichsen in 1918 led to the syndrome's naming.
Prevention and Treatment of Meningitis
Primary treatment involves penicillin.
Vaccination recommended for specific age groups (11-12 years, college students).
Conjugated vaccine for serogroups A, C, Y, and W135.
Vaccine for infants against serogroup C.
Neisseria gonorrhoeae
Gram-negative diplococci (0.6-1 µm).
Grown on Thayer-Martin plates in CO2.
Second highest reported STD in the US after chlamydia (~350,000 cases/year).
Clinical Manifestations
MEN:
Acute urethritis (90-95% cases).
WOMEN:
50% are asymptomatic; cervicitis.
Potential complications include PID (pelvic inflammatory disease) and sterility.
Neonatal infections can lead to gonococcal ophthalmia neonatorum (conjunctivitis).
Spread and Diagnosis
Can enter bloodstream leading to disseminated infections (meningitis, endocarditis).
Diagnosis:
MEN: microscopy of urethral discharge.
WOMEN: culture from endocervical and anal swabs.
Treatment and Resistance
Increasing penicillin resistance in certain regions.
Recommend ceftriaxone, cefixime, and combined treatments.
Simultaneous treatment of partners is essential; no vaccine available.