Streptococci gram-positive cocci = chains of spherical cells Classification:

1. Streptococci gram-positive cocci = chains of spherical cells Classification: 1. growth characteristics on blood agar b-hemolytic lyse red blood cells (clear zone around colonies) a-hemolytic create green zone around colonies g-hemolytic have no zone around colonies 2. Cell wall polysaccharides (A-T) [Lancefield group] 3. Species (based on metabolic reactions) Streptococci only carry out fermentation (no respiration) oxygen-tolerant anaerobes (most pathogenic species)

2. Streptococcus pyogenes Group A strep b-hemolytic Lives on skin and mucous membranes Spreads asymptomatically

3. Streptococcal Sore Throat • spread by droplets of saliva or nasal secretions • clinical manifestations • 2 to 4 day incubation • pharyngitis, tonsillitis, malaise, fever, headache, and redness, edema, and lymph node enlargement in throat

4. Scarlet Fever • scarlatina • caused by S. pyogenes strain lysogenized by a bacteriophage that carries gene for an erythrogenic toxin

5. Scarlet fever… • spread by inhalation of infective respiratory droplets • clinical manifestations • after 2 days incubation, rash that spreads from upper body to remainder of body • sore throat, chills, fever, headache and strawberry tongue

6. Cellulitis and Erysipelas • cellulitis • diffuse, spreading infection of subcutaneous tissue • redness and swelling • impetigo • also caused by Staphylococcus aureus • superficial cutaneous infection commonly seen in children • crusty lesions and vesicles surrounded by red border • erysipelas • acute infection of dermal layer of skin • red patches that may occur periodically at same site for years

7. Invasive Streptococcus A Infections • caused by certain strains of S. pyogenes • carry genes for exotoxins • superantigens • tissue-destroying protease

8. Invasive infections… • clinical manifestations • necrotizing fasciitis • destruction of sheath covering skeletal muscle • myositis • inflammation and destruction of skeletal muscle and fat tissue • toxic shock syndrome (TSS) • precipitous drop of blood pressure, failure of multiple organs, and high fever

9. Poststreptococcal Diseases • occur 1 to 4 weeks after acute streptococcal infection • glomerulonephritis (Bright’s disease) • rheumatic fever

10. Glomerulonephritis • inflammatory disease of renal glomeruli • a type III hypersensitivity • clinical manifestations • edema, fever, hypertension, and hematuria • may spontaneously heal or may become chronic • treatment, prevention, and control • clinical history, physical findings, and confirmatory evidence of prior streptococcal infection • antibiotic therapy (to kill residual bacteria), otherwise no specific therapy • antibiotic therapy of acute infection

11. Rheumatic fever • autoimmune diseases involving heart valves, joints, subcutaneous tissues and central nervous system • clinical manifestations • vary widely, making diagnosis difficult • treatment, prevention, and control • symptomatic/supportive therapy • prompt treatment of acute streptococcal infection

12. Streptococci adhere to epithelial cells later gain entry to body Virulence factors = bacterial products or strategies that contribute to the ability of the bacterium to cause disease 1. Adhesins F1 and F2 proteins bind fibronectin Epa protein binds collagen M protein binds collagen and fibrinogen 2. Extracellular enzymes Streptolysin O lyses RBCs Streptolysin S lyses RBCs Streptokinase dissolves fibrin clots

13. 3. Antiphagocytic factors Hyaluronic acid capsule C5a peptidase M protein (binds Fc portion of IgG antibody) 4. Superantigens - toxins that nonspecifically stimulate large populations of T cells to produce cytokines SpeA (Toxic shock) SpeC 5. lipoteichoic acid (LTA) receptor = fibronectin activates cytokine production

14. Infection causes an inflammatory response Diagnosis often by sight culturing of organisms antigroup A carbohydrate antibody tests Acute Rheumatic fever previous stretococcal infection anti-streptolysin O (ASO test) anti-DNAase B test Treatment Penicillin

15. Streptococcal Pneumonia • endogenous infection • caused by one’s own normal microbiota • caused by Streptococcus pneumoniae • produces polysaccharide capsule and a toxin • rapidly multiplies in alveolar spaces • disease only occurs in individuals with predisposing condition

17. Streptococcal pneumonia… • clinical manifestations • abrupt onset of chills, hard labored breathing, chest pain, and rust colored sputum • treatment, prevention, and control • chest X-rays, bacterial culture and biochemical testing of isolate • antibiotic therapy (penicillin) • resistant strains have appeared • immunization and treatment of infected persons

18. Streptococcal diseases… • treatment, prevention, and control • most diagnosed using rapid diagnostic tests • most treated by antibiotic therapy (penecillin) • vaccine available only for streptococcal pneumonia • sanitation and personal hygiene measures

19. Bacillus anthracis gram-positive rod spore-forming agent of anthrax Important veterinary pathogen Bioterrorism agent for humans Cutaneous anthrax spores enter cut or lesion pustule develops with large surrounding area of swelling center of lesion becomes black (necrosis) ( called an eschar) 80% recovery

20. Gastrointestinal anthrax from eating contaminated meat fluid-filled vesicles in intestine (pain and bleeding) high mortality rate (even with antibiotics) Inhalation anthrax spores inhaled and taken up by lung macrophages spores germinate in macrophages no apparent lung disease but bacteria spread from lungs macrophages migrate to lymph nodes bacteria get into bloodstream (septic shock) high mortality rate (death within days) early antibiotic treatment can help (within 24 hr)

21. Virulence factors edema toxin A-B toxin A portion = adenylate cyclase (like Bordetella pertussis) Affects signaling, disrupts ion flow (and water) (edema) attacks most cell types lethal toxin A-B toxin attack and kills macrophages induces macrophages to produce high levels of cytokines triggers shock process B component the same for each toxin (PA=protective antigen) toxin genes are on a plasmid B. anthracis avoids ingestion after initial germination stage both toxins are antiphagocytic

22. Antiphagocytic capsule D-glutamate instead of polysaccharide Treatment antibiotics (ciprofloxacin) vaccine Pasteur developed a vaccine for farm animals

23. Listeria monocytogenes gram-positive rods motile (but not at 37oC) agent of septicemia, meningitis most deaths: fetuses, newborns, immunocompromised adults transmission bacteria are wide-spread intestinal tract of animals and humans sewage, soil, and water food-borne (not human-to-human contact) L. monocytogenes can multiply atrefrigeration temperatures need a large inoculum for disease long incubation time (avg. = 31 days)

24. bacteria enter cells via phagocytic vesicle rupture vesicle and move into cytoplasm replicates in cytoplasm of host cell Bacteria moves from cell to cell ActA protein polymerizes host cell actin at one pole of bacterial cell surface propels bacteria into host cell plasma membrane creates long membrane projections that pinch off into adjacent cell’s cytoplasm Listeriolysin O (LLO) pore-forming toxin (required for escape from phagosome) membrane damage (targets cholesterol) Phospholipases also damages membranes Metalloprotease (Zn-dependent)

25. Outbreaks of disease due to faulty food processing 10 -15% of adults are asymptomatic carriers Treatment usually not diagnosed early enough for antibiotics to be effective

26. Corynebacteria diphtheria gram-positive rods distinct club-shaped appearance agent of diphtheria thick mucopurulent nasal discharge, fever, cough local oropharyngeal inflammation tissue damage humans are only know reservoir colonization of throat by inhalation early symptoms non-specific malaise, low-grade fever, sore throat formation of pseudomembrane in respiratory epithelia fibrin, bacteria, inflammatory cells adheres to underlying tissue

27. diphtheria toxin (causes symptoms of diphtheria) carried in an integrated phage genome A-B toxin (diphteria toxin= 1 protein cut into 2 parts) ADP ribosyltransferase targets translation factor EF2 (halts protein synthesis) kills cells toxin spreads via circulatory system destroys tissue elsewhere in body cardiac, kidney, nervous tissues Transmission airborne (droplets) spreads in crowded, unsanitary conditions Treatment antitoxin antibiotics penicillin, erythromycin vaccination DPT vaccine directed against diphtheria toxin