Foundations in Microbiology PowerPoint to accompany Foundations in Microbiology Fifth Edition Talaro Chapter 18 Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Cocci of Medical Importance Chapter 18

Cocci of Medical Importance Gram + and gram - are among most significant infectious agents of humans. Also prevalent members of the normal flora of skin, oral cavity, and intestine. Pyogenic cocci- infections with these bacteria tend to stimulate pus formation. Most common infectious species belong to 4 genera: Staphylococcus, Streptococcus, Enterococcus, and Neisseria

General characteristics of the Staphylococci Spherical cells arranged in irregular clusters Gram positive Common inhabitant of the skin & mucous membranes Lack spores and flagella May have capsules 31 species Most important human pathogens are: S. aureus*, S. epidermidis (and close relatives, S. capitis, and S. hominis) and S. saprophyticus.

Staphylococcus aureus grows in large, round, opaque colonies optimum temperature of 37oC facultative anaerobe withstands high salt, extremes in pH, & high temperatures produces many virulence factors Implicated in nearly 80,000 deaths nationwide.

Staphylococcus aureus This genus owes its name to the grapelike clusters it forms.

Major Virulence Factors of S. aureus - Enzymes coagulase – coagulates plasma and blood; produced by 97% of human isolates; diagnostic Hyaluronidase- digests connective tissue of the host Staphylokinase- digest blood clots Dnase- breaks down DNA Lipases- digests oils, allowing bacteria to more easily colonize skin Penicillinase- inactivates penicillin

Major Virulence Factors of S. aureus - Toxins Hemolysins (a, b, g– lyse RBCs Leukocidin- lyses neutrophils and macrophages Enterotoxins- induce, nausea, vomiting and diarrhea exfoliative toxin- causes desquamation of the skin toxic shock syndrome toxin- induces fever, vomitting, rash, and organ damage Virulence factor- any characteristic or structure of the microbe that contributes to the disease state

S. aureus Blood agar plate growing Staphylococcus aureus

S. aureus Present in most environments frequented by humans Readily isolated from fomites (an inanimate object) Carriage rate for healthy adults is 20-60% Carriage is mostly in anterior nares, skin, nasopharynx, intestine

S. aureus diseases Ranges from localized to systemic localized infections- abscess, folliculitis (inflammation of hair follicles), furuncle (boil), carbuncle (deeper lesion, aggregation of furuncles cluster) Systemic infections: osteomyelitis- pathogen establishes in the highly vascular part of the bone Bacteremia- bacteria that escaped infection site and are transported to kidneys, liver, spleen and heart lining toxigenic diseases – food intoxication, scalded skin syndrome (SSS), toxic shock syndrome

S. aureus skin infections A furuncle Sectional view of boil or furuncle A carbuncle

S. Aureus osteomyelitis in a long bone Important systemic infections: S. Aureus osteomyelitis in a long bone

Effects of S. Aureus toxins on the skin Staphylococcal scalded skin syndrome (SSSS) results when exfoliative toxin produced by local infections Segment of skin affected by SSSS

Other Staphylococci S. epidermidis – lives on skin & mucous membranes; endocarditis, bacteremia, UTI S. hominis – lives around apocrine sweat glands S. capitis – live on scalp, face, external ear All 3 may cause wound infections S. saprophyticus – infrequently lives on skin, intestine, vagina; UTI

Staphylococcus aureus test Other Staphylococcus species S. aureus present S. aureus present

Fig. 18.7 Identifies Staphylococcus isolates-can separate 19 species PHS= phosphatase production, URE= urea hydrolysis, GLS= glucosidase production, MNE= mannose fermentation, MAN= mannitol fermentation, TRE= trehalose fermentation, SAL= Salicin fermentation, GLC= glucuronidase production, ARG= arginine hydrolysis, NGP= galactosidase production

Table 18.1

Clinical concerns of Staph 95% have penicillinase & are resistant to penicillin & ampicillin MRSA – methicillin-resistant S. aureus – carry multiple resistance Abscesses have to be surgically perforated Systemic infections require intensive lengthy therapy

General Characteristics of the Streptococci Gram-positive spherical/ovoid cocci arranged in long chains Non-spore-forming, nonmotile Can form capsules & slime layers Facultative anaerobes Do not form catalase, but have a peroxidase system Most parasitic forms are fastidious & require enriched media Small, nonpigmented colonies Sensitive to drying, heat & disinfectants 25 species

Streptococcus Characteristic long intertwining chains

Streptococci Lancefield classification system based on cell wall Antigens – 14 groups (A,B,C,….) Another classification system is based on hemolysis reactions b-hemolysis – A,B,C,G & some D strains a-hemolysis – S. pneumoniae & others collectively called viridans Antigen- any cell particle or chemical that induces a specific immune response by B cells or T cells

Hemolysis patterns on blood agar may be used to separate streptococci into major subgroups Streptococcus pneumoniae displaying -hemolysis

Table 18.2

Human streptococcal pathogens S. pyogenes- primary pathogen of group A, has a variety of virulence factors, including surface antigens, toxins, and enzymes S. agalactiae- neonatal and wound infections viridans streptococci- - hemolytic S. pneumoniae- bacterial pneumonia Enterococcus faecalis- endocarditis and UTI

b-hemolytic S. pyogenes Main representative of group A Most serious streptococcal pathogen Strict parasite Inhabits throat, nasopharynx, occasionally skin Produces cell surface antigens and virulence factors C-carbohydrates, M-protein (fimbrae), streptokinase, hyaluronidase, DNase, hemolysins (SLO, SLS), pyogenic toxin

b-hemolytic S. pyogenes Antigens: C-carbohydrates- specialized polysaccarides or teichoic acids found on cell wall surface, protect bacterium from being dissolved by the lysozyme defense of host M-protein (fimbrae)-spiky surface projection, resist phagocytosis and improves adherence Enzymes and extracellular toxins: Streptokinase-digests clots Hyaluronidase- digests binding substance in connective tissue DNase- digists DNA hemolysins (SLO, SLS)- streptolysins that cause -hemolysis and damage cells and tissues pyogenic toxin-key toxin in dev of scarlet fever, causes bright red rash and fever by effecting temperature regulating center

Cutaway view of group A Streptococcus

S. pyogenes Humans only reservoir- 5-15% of population carriers Transmission – contact, droplets, food, fomites Skin infections –pyoderma, impetigo, erysipelas Systemic infections – strep throat, pharyngitis, scarlet fever Sequelae -rheumatic fever, glomerulonephritis

Streptococcal skin infections Streptococcal impetigo, or pyoderma Streptococcal erysipelas

Streptococcal pharyngitis or strep throat The appearance of the throat in pharyngitis and tonsillitis-pharynx and tonsils become bright red and swollen, pus nodules on tonsils

Heart disease due to Rheumatic Fever-group A streptococcal infection can extend to the heart

Invasive Group A Streps and “flesh-eating” syndrome or necrotizing fasciitis Caused by virulent strains of Streptococcus pyogenes

Group B: S. agalactiae Regularly resides in human vagina, pharynx & large intestine can be transferred to infant during delivery & cause severe infection Most prevalent cause of neonatal pneumonia, sepsis, & meningitis 15,000 infections & 5,000 deaths in US Pregnant women should be screened & treated wound and skin infections & endocarditis in debilitated people

Group D, C and G: Enterococci Enterococcus faecalis, & E. faecium Normal colonists of human large intestine Cause opportunistic urinary, wound, and skin infections, particularly in debilitated persons

Streptococcal tests Bacitracin disc test- only Streptococcus pyogenes is sensitive to minute bactiracin conc. Group A streptococci are negative for SXT sensitivity and the CAMP test Rapid, direct test kit for diagnosis of group A infections, throat swab introduced to latex beads and monoclonal antibodies Positive-the C-carbohydrate on group A streptococci causes clumping Negative-milky smooth reaction

Group A & B are treated with penicillin Sensitivity testing needed for enterococci No vaccines available

Viridans streptococci group a-hemolytic Large complex group Most numerous & widespread residents of the oral cavity & also found in nasopharynx, genital tract, skin Not very invasive, dental or surgical procedures facilitate entrance

Viridans streptococci group Bacteremia, meningitis, abdominal infection, tooth abscesses Most serious infection – subacute endocarditis – blood-borne bacteria settle & grow on heart lining or valves Persons with preexisting heart disease are at high risk & receive prophylactic antibiotics before surgery or dental procedures

Effects of stretococcal colonization on the heart Valve leaflet Nodular vegetations on the surface constantly release bacteria into the circulation

Viridans streptococci group S. mutans produces slime layers that adhere to teeth, basis for plaque involved in dental caries

Streptococcus pneumoniae Causes 60-70% of all bacterial pneumonias small, lancet-shaped cells arranged in pairs and short chains Culture requires blood or chocolate agar Growth improved by 5-10% CO2 Lack catalase & peroxidases – cultures die in O2

Diagnosing Steptococcus pneumoniae Small diplococci Gram stain of sputum from a pneumonia patient

S. pneumoniae All pathogenic strains form large capsules – major virulence factor Specific soluble substance (SSS) varies among types 84 capsular types have been identified using Quellung test or capsular swelling reaction Causes pneumonia & otitis media Vaccine available for high risk people

S. pneumoniae 5-50% of all people carry it as normal flora in pharynx Very delicate, does not survive long outside of its habitat Pneumonia occurs when cells are aspirated into the lungs of susceptible individuals Pneumococci multiply & induce an overwhelming inflammatory response Treated with penicillin

The course of bacterial pneumonia

Pneumococcal otis media

Family Neisseriaceae Gram-negative cocci Residents of mucous membranes of warm-blooded animals Genera include Neisseria, Moraxella, Acinetobacter 2 primary human pathogens Neisseria gonorrhoeae Neisseria meningitidis

Neisseria Gram-negative, bean-shaped, diplococci Reside in the mucous membrane of humans and animals none develop flagella or spores capsules on pathogens pili Strict parasites, do not survive long outside of the host Aerobic or microaerophilic Oxidative metabolism produce catalase & cytochrome oxidase Pathogenic species require enriched complex media and CO2

Neisseria

Neisseria gonorrhoeae Causes gonorrhea, an STD Virulence factors: pili, other surface molecules, IgA protease Strictly a human infection In top 5 STDs Infectious dose 100-1,000 Does not survive more than 1-2 hours on fomites Infection is asymptomatic in 10% of males and 50% of females

Neisseria gonorrhoeae

gonorrhea Males – urethritis, yellowish discharge, scarring & infertility Females – vaginitis, urethritis, salpingitis (PID) mixed anaerobic abdominal infection, common cause of sterility & ectopic tubal pregnancies Extragenital infections – anal, pharygeal, conjunctivitis, septicemia, arthritis

Gonorrheal damage to the male reproductive tract

Gonorrheal damage to the female reproductive tract

Gonorrhea in newborns Infected as they pass through birth canal Eye inflammation, blindness Prevented by prophylaxis after birth

Gonorrhea diagnosis Gram stain of urethral pus from a patient with gonorrhea

Neisseria meningitidis Virulence factors – capsule, pili, IgA protease 12 strains; serotypes A, B, C, cause most cases Prevalent cause of meningitis Disease begins when bacteria enter bloodstream, pass into cranial circulation, multiply in meninges; very rapid onset; endotoxin causes hemorrhage and shock; can be fatal Treated with penicillin, chloramphenicol Vaccines exist for group A and C

Neisseria meningitidis Dissemination of the meningococcus from a nasopharyngeal infection

Neisseria meningitidis One clinical sign of meningococcemia

Table 18.4