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

Foundations in Microbiology

Chapter

18

PowerPoint to accompany

Fifth Edition

Talaro

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

2

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

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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.

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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.

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Staphylococcus aureus

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

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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

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• Hemolysins (– 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

Major Virulence Factors of S. aureus - Toxins

Virulence factor- any characteristic or structure of the microbe that contributes to the disease state

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S. aureus

Blood agar plate growing Staphylococcus aureus

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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

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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

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S. aureus skin infections

Sectional view of boil or furuncle

A furuncle

A carbuncle

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S. Aureus osteomyelitis in a long boneImportant systemic infections:

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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

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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

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Staphylococcus aureus test

S. aureus present

Other Staphylococcus species

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

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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

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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

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Streptococcus

Characteristic long intertwining chains

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Streptococci• Lancefield classification system based on

cell wall Antigens – 14 groups (A,B,C,….)

• Another classification system is based on hemolysis reactions

-hemolysis – A,B,C,G & some D strains-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

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Streptococcus pneumoniae displaying -hemolysis

Hemolysis patterns on blood agar may be used to separate streptococci into major subgroups

Table 18.2

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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

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-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

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-hemolytic S. pyogenesAntigens:• 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

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Cutaway view of group A Streptococcus

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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

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Streptococcal skin infections

Streptococcal impetigo, or pyoderma

Streptococcal erysipelas

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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

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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

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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

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Group D, C and G: EnterococciEnterococcus faecalis, & E. faecium

• Normal colonists of human large intestine

• Cause opportunistic urinary, wound, and skin infections, particularly in debilitated persons

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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 antibodiesPositive-the C-carbohydrate on group A streptococci causes clumpingNegative-milky smooth reaction

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• Group A & B are treated with penicillin

• Sensitivity testing needed for enterococci

• No vaccines available

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Viridans streptococci group

-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

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• 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

Viridans streptococci group

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Valve leaflet

Effects of stretococcal colonization on the heart

Nodular vegetations on the surface constantly release bacteria into the circulation

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• S. mutans produces slime layers that adhere to teeth, basis for plaque

• involved in dental caries

Viridans streptococci group

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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

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Diagnosing Steptococcus pneumoniae

Small diplococci

Gram stain of sputum from a pneumonia patient

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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

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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

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The course of bacterial pneumonia

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Pneumococcal otis media

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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

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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

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Neisseria

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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

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Neisseria gonorrhoeae

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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

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Gonorrheal damage to the male reproductive tract

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Gonorrheal damage to the female reproductive tract

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Gonorrhea in newborns

• Infected as they pass through birth canal

• Eye inflammation, blindness

• Prevented by prophylaxis after birth

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Gonorrhea diagnosis

Gram stain of urethral pus from a patient with gonorrhea

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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

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Neisseria meningitidis

Dissemination of the meningococcus from a nasopharyngeal infection

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Neisseria meningitidis

One clinical sign of meningococcemia

Table 18.4