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The Cocci of Medical Importance

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1 The Cocci of Medical Importance
Chapter 18 The Cocci of Medical Importance

2 General Characteristics of the Staphylococci
Nonmotile, gram-positive cocci arranged in irregular clusters Facultative anaerobes Fermentative Salt-tolerant Catalase-positive Pyogenic if stimulate pus formation


4 Staphylococcus aureus
Skin infections: Local abscess occurs at site of invasion of hair follicle, gland Manifestations: Folliculitis – inflammation of hair follicle Furuncle - boil Carbuncle – deeper lesion aggregation of a cluster of furuncles Bullous impetigo – epidermal swellings that peel away

5 Staphylococcus aureus
Toxic disease: Food intoxication due to enterotoxin Staphylococcal scaled skin syndrome Toxic shock syndrome Toxemia in women due to infection of vagina Associated with tampon usage

6 Staphylococcus aureus
Osteomyelitis Bacteria spread in the circulation from some other infection site, enter the artery, and lodge in the small vessels in bony pockets of the marrow Growth of the cells causes inflammation and damage that manifest as swelling and necrosis

7 Principal coagulase-Negative Staphylococci
Staphylococcus saprophyticus Urinary pathogen Staphylococcus epidermidis Normal resident of skin and follicles An opportunist One of the most common causes of nosocomial infections Mainly in surgical patients with indwelling medical devices or implants

8 Treatment for Staph infections
S. aureus has multiple resistance to antibiotics, especially penicillin, ampicillin, and methicillin Abscesses require debridement and removal of pus Staphylococci have extreme resistance to harsh environmental conditions Staph infections are frequently complicated by their tendency to form biofilms on medical devices

9 General Characteristics of the Streptococci Genera
Gram-positive cocci in chains of various lengths Nonmotile Non-spore forming Encapsulated Catalase negative

10 Streptococcus Genus - Streptococcus
Streptococcus pyogenes (Group A streptococci) Streptococcus agalactiae (Group B streptococci) Group D streptococci Enterococci Enterococcus (Streptococcus) faecalis Enterococcus (Streptococcus) faecium Enterococcus (Streptococcus) durans Non-enterococcal Group D Streptococcus bovis Streptococcus equinus Viridans streptococci Streptococcus pneumoniae

11 Classification scheme for streptococci
Based on hemolytic properties Types of hemolysis Beta (clear, complete) Alpha (green, incomplete) - also called viridans; green color = production of a hemoglobin reducing agent Alpha prime = large zone of alpha hemolysis encircled by a narrow zone of beta Gamma (none) - commonly called non-hemolytic strep Reasons for being unreliable criteria Some strains become hemolytic after 24 hrs incubation Type hemolysis cell dependent - sheep blood used in U.S.

12 Classification scheme for streptococci
Based on antigenic properties Lancefield grouping = carbohydrates in cell wall (C group carbohydrates) Found in all strep except viridans Classifies into 13 groups (designated A-O) Methods for detection have been time consuming and difficult - new easier methods now available Definitive method of classification Most common groups encountered = A, B, C, D, F, and G

13 Virulence Factors for S. pyogenes (Group A streptococci)
Anatomical M protein - associated with pilli and lipoteichoic acid; play role in attachment; over 70 different types known; immunity to streptococcal infection M type specific Capsule - composed of hyaluronic acid; antiphagocytic

14 Virulence Factors for S. pyogenes (Group A streptococci)
Toxins and other biologically active extracellular products Hemolysins - streptolysins Streptolysin O - oxygen labile Binds cholesterol in cell membranes of rbc's wbc's, and platelets - lysis causes degranulation of wbc's with release of hydrolytic enzymes - further damages tissue Reversibly inactivated by oxygen - demonstrated in vitro in deep (anaerobic) colonies Antigenic - antibodies = antistreptolysin O (ASO) Streptolysin S - oxygen stable Mostly cell bound No neutralizing Ab yet described rbc's; inhibit chemotaxis & phagocytosis

15 Virulence Factors for S. pyogenes (Group A streptococci)
Deoxyribonucleases (DNases) - degrade DNA and to a lesser extent RNA in pus - facilitates spread of infection Hyaluronidase - spreading factor; sometimes find both hyaluronic capsules and hyaluronidase in same organism Erythrogenic toxin (also called streptococcal pyrogenic exotoxins) Responsible for rash of scarlet fever and appear to play role in toxic-like syndrome

16 Virulence Factors for S. agalactiae (Group B streptococci)
Anatomical - capsule; antigenic and antiphagocytic

17 Virulence Factors for S. pneumoniae
Anatomical - capsule is polysaccharide; 84 different types known; some types cross-react with polysaccharides produced by other bacteria and with human blood group B isoantigen; antiphagocytic

18 S. pyogenes (Group A streptococci) Diseases
Suppurative infections - invasive properties related to capsule and M proteins; virulence with streptolysins (pyogenic) Pharyngitis - common in children; usually self-limiting; can lead to non-suppurative sequelae Puerperal infection (childbed fever) - infection of endometrium at or near delivery; life threatening; may spread to other sites in body

19 S. pyogenes (Group A streptococci) Diseases
Impetigo (Indian fire) - localized skin infection; common in children Erysipelas - involves skin and subcutaneous tissue; spreads rapidly

20 S. pyogenes (Group A streptococci) Diseases
Toxic disease Scarlet fever Caused by infection with erythrogenic strains in sensitive individuals Localized infection with systemic manifestations Characterized by red rash over most of body (strawberry tongue)

21 S. pyogenes (Group A streptococci) Diseases
Delayed Non-Suppurative Complications Acute rheumatic fever (ARF) Symptoms - fever and inflammation of joints, heart, subcutaneous tissue and CNS beginning 1-5 weeks after Group A pharyngitis; may cause serious and permanent damage to heart Follows only respiratory strept. infection Can be prevented by treatment of pharyngitis within 9 days of onset of infection

22 S. pyogenes (Group A streptococci) Diseases
Delayed Non-Suppurative Complications Acute glomerulonephritis (AGN) Symptoms - edema, hypertension, hematuria & proteinuria; usually benign but may lead to renal failure and death Follows either respiratory or cutaneous infections; requires infection with certain M type strains called nephritogenic Typically occurs 6-10 days after onset of pharyngitis or days after cutaneous infection; not prevented by rapid therapy

23 S. agalactiae (Group B streptococcal) Diseases
Infants - leading cause of pneumonia, sepsis and meningitis during first 2 months of life Most develop in immediate perinatal period (within 7 days of birth) Most result from contamination from female genital tract where organism is normal in ~ one-third women Degree of vaginal & cervical colonization in mother directly related to likelihood & severity of disease in infant

24 S. agalactiae (Group B streptococcal) Diseases
Children and adults Infections associated with gynecologic manipulation/surgery Rare cause of upper respiratory infections, meningitis, bacteremia and endocarditis

25 Group D (enterococci and non-enterococcal strains) Diseases
Urinary tract infections - associated with manipulations, malignancies, biliary tract disease & GI disorders Wound and soft tissue infections Endocarditis - bacteremia associated with lon-term indwelling intravenous catheters S. bovis (non-enterococcal sp.) linked to neoplasms of GI tract, esp. colon; recovery from adult blood cultures should prompt GI tract evaluation

26 Viridans streptococci Diseases
Sub-acute bacterial endocarditis (SBE) Organism normally present in oral cavity showered into blood = transient bacteremia Presence of previously damaged heart valves = SBE May be fatal Some species associated with brain abscesses, meningitis, liver abscesses & appendicitis

27 S. pneumoniae Diseases Pneumonia
Most common cause of community-acquired pneumonia Organisms part of normal upper respiratory tract – begins with aspiration More common in persons with chronic lung conditions including smokers, defects in phagocyte function or humoral immunity or those with ethanol intoxication

28 The Course of Bacterial Pneumonia
As the pneumococcus traces a pathway down the respiratory tree, it provokes intense inflammation and exudate formation The blocking of the bronchioles and alveoli by consolidation of inflammatory cells and product is shown

29 S. pneumoniae Diseases Meningitis
One of three leading causes of meningitis More common in later life Signs and symptoms similar in all forms of meningitis Upper respiratory infections - sinusitis, otitis media Other - endocarditis, arthritis, peritonitis

30 S. pneumoniae Diseases Upper respiratory infections - sinusitis, otitis media The direct connection between the pharynx and middle ear via the eustachian tube makes this possible

31 Epidemiology of Streptococcus
Natural habitat Group A, pneumococci and viridans strept - upper respiratory tract of humans Group A, B, and D - vaginal Group B and D – intestine Transmission Direct contact with mucosa or secretions Aerosols - droplet produced by coughing, sneezing, talking Indirect - fomites (shared inanimate objects) Insects, esp. Flies Food-borne

32 Epidemiology of Streptococcus
Control and prevention Hand washing C section (Group B) Vaccines - M protein antigens for Group A strep & capsular antigens for pneumococci Treatment - penicillin (drug of choice) except enterococci which require combination of penicillin or vancomycin with an aminoglycoside

33 General Characteristics of the Neisseria Genera
Gram-negative diplococci that have capsules and fimbriae Oxidase-positive Non-spore forming Nonmotile Fastidious Do not survive long in the environment Common residents of mucous membranes

34 Neisseria Family Acinetobacter - only oxidase negative genera
Kingella - only catalase negative genera Moraxella including M. catarrhalis (former called Branhamella catarrhalis) Neisseria N. gonorrhoeae (common name = gonococcus or GC) N. meningitidis (common name = meningococcus) N. lactamica Other Neisseria = N. sicca, N. subflava, N. mucosa, N. flavescens, N. cinerea, and N. elongata

35 Virulence Factors for N. gonorrhoeae
Anatomical Pili - mediate adherence; antigenically variable Endotoxin - mediates local and systemic damage including petechiae and DIC Biologically active extracellular products IgA1 protease - role unknown; may facilitate invasion Beta lactamase - destroys penicillin; not found in all strains

36 Virulence Factors for N. meningitidis
Anatomical Pili - mediate adherence; selective for non-ciliated columnar epithelium Capsules - polysaccharide; antigenic; subdivides meningococci into 9 groups (epidemic groups = A, B, and C); antiphagocytic Endotoxin - mediates tissue damage; causes petechiae and DIC

37 Clinical Manifestations of N. gonorrhoeae
Pathogenesis Attach via pili to epithelial cells on contact, enter and multiply within cells (intracellular parasites) Spread via direct extension; cause acute, localized inflammatory response - further spread facilitated by pilus-mediated attachment to sperm; may also spread hematogenously

38 Clinical Manifestations of N. gonorrhoeae
Genital infections are of epidemic proportions (approx. 1M cases/yr. in US) Genital infections (gonorrhea) - commonly called “clap”; occurs after genital intercourse Different for man v. woman

39 Clinical Manifestations of N. gonorrhoeae
Genital Gonorrhea in the Male Primary site - urethra Symptoms begin 1-14 days post infection; purulent urethral discharge and dysuria; rarely mild or absent Local extension uncommon but possible leading to prostatitis & epididymitis

40 Clinical Manifestations of N. gonorrhoeae
Genital Gonorrhea in the Female Primary site - endocervix Symptoms begin 2-7 days post infection; vaginal discharge, dysuria, abdominal pain and menstrual abnormalities; usually mild or absent Local extension common leading to pelvic inflammatory disease (PID) and sterility

41 Clinical Manifestations of N. gonorrhoeae
Rectal infections - occurs after rectal intercourse or after contamination of rectal area with infected vaginal secretions in females; symptoms may manifest as rectal bleeding but usually asymptomatic Pharyngeal infections - follows oral/genital sex; generally asymptomatic but may produce sore throat and cervical adenitis

42 Clinical Manifestations of N. gonorrhoeae
Pelvic inflammatory disease (PID) Local extension of cervical infection; causes endometritis, salpingitis & peritonitis Symptoms = fever and lower abdominal pain Sterility caused by scarring of fallopian tubes – may follow single attack; occurs in up to 20% of women with gonorrhea Disseminated gonococcal infections (DGI) Follows hematogenous spread from any site Symptoms = rash (petechial, maculopapular or pustular), arthritis (large joints), endocarditis, and meningitis

43 Clinical Manifestations of N. gonorrhoeae
Conjunctivitis and ophthalmia neonatorum (ON) May occur at any age by contamination of conjunctiva (ON - of newborn during vaginal birth from infected mother) Symptoms = severe, acute, purulent conjunctivitis; may lead to blindness Common cause of blindness in newborns until use of silver nitrate or penicillin drops instituted as standard treatment for all newborns

44 N. Meningitidis - also called meningococcus
Pathogenesis Pili mediate attachment of organisms to non-ciliated columnar epithelial cells in nasopharynx where organisms multiply and spread by direct extension to adjacent cells -may damage adjacent ciliated cells via release of endotoxin Enter blood via cervical lymph nodes (meningococcemia) to spread hematogenously throughout the body Cross blood-brain barrier and infect meninges

45 Clinical Manifestations of N. meningitidis
Meningitis (acute, epidemic meningitis) Most common form of meningococcal infection Peak incidence = 6 months - 2 years and 5-18 yrs. (common in military recruits) Symptoms = fever, headache, stiff neck, paralysis; coma and death occurs if not treated If present, petechial rash diagnostic for MC

46 Clinical Manifestations of N. meningitidis
Meningococcemia and petechial rash Occurs with or without meningitis Rash caused by thrombocytopenia and endotoxemia may also be accompanied by DIC Waterhouse-Friderichsen syndrome Occurs in fulminant meningococcemia Characterized by DIC with bilateral hemorrhagic destruction of adrenal glands due to endotoxemia

47 Clinical Manifestations of M. Catarrhalis
Occurs in individuals with compromised respiratory tract function; Normally part of upper respiratory flora Lower respiratory infection - acute bronchitis and pneumonia Also cause on rare occasion endocarditis, meningitis, conjunctivitis and septicemia Other = Otitis media and maxillary sinusitis

48 Epidemiology of Neisseria
Habitat - strict human parasites; mucous membranes M. Catarrhalis and all Neisseria except N. gonorrhoeae part of normal flora - high normal carrier rate All except N. gonorrhoeae norm in upper respiratory tract Routes of transmission N. gonorrhoeae - most by direct venereal (sexual) routes; rarely involves fomites N. meningitidis - respiratory droplets; requires close contact and a susceptible (non-immune) host M. catarrhalis - endogenous; droplet

49 Epidemiology of Neisseria
Prevention and Control N. gonorrhoeae - “safe” sex; case-contact tracking/treatment N. meningitidis - chemoprophylaxis (rifampin) if exposed; vaccines to susceptible individuals; vaccines directed against polysaccharide capsular antigens available - used primarily in military recruits Treatment N. gonorrhoeae - penicillin for non-resistant strains; spectinomycin or ceftriaxone for PPNG (penicillinase producing Neisseria gonorrhoeae) N. meningitidis - penicillin (ampicillin) M. catarrhalis - most strains produce penicillinase; may use erythromycin or tetracycline

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