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36 Cards in this Set

  • Front
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Complications of Streptococcus pryogens

•Scarlet fever-Red rash usually on skin of back, chest or trunk


•Cellulitis-Necrotizing fasciitis flesh eating bacteria)


•Rheumatic heart disease- Heart valve damage resulting in a “murmur” or valve leakage


•Glomerulonephritis-Kidney damage leading to decreased kidney function or failure

Cellulitis

Necrotizing fasciitis flesh eating bacteria);

Rheumatic heart disease

Heart valve damage resulting in a “murmur” or valve leakage

Glomerulonephritis

Kidney damage leading to decreased kidney function or failure

Virulence Factors Staphylococcus aureus

•Toxin1–Associated with multi-system illness •ToxicShock Syndrome (TSS)•Occurs in males and females

Elek test

Test for toxigenic strains of Corynebacterium diphtheria

S. salivarius,S. vestibularis
-Gumdrop colonies on mitis salivarius agar (MSA)

-Produce fructose levans (linear polymer of fructose)


-Non-hemolytic


-Adhere to tongue, shed into saliva


-Fimbriae- adherance structures

Diphtheria

•Treatment-two fold


1-Antitoxin•Produced in horses•Patient may react to horse serum•Not effective once toxin inside host cells•


2-Antibiotics to stop the source of more Toxins

Staphylococcus epidermidis
Epidemiology Habitat:

Urinary tract infections, catheter-related sepsis, joint infections


Opportunistic


Major “Normal Flora” on skin

Staphylococcus saprophyticus

Epidemiology:


UTI


Adheres to epithelial cells in the UG tract Capable of causing disease in low numbers Leading cause of UTIs in young women

Virulence Factors of Group A Streptococcus pyrogens
Somatic factors – associated with cell surface components

-M protein – anti-phagocytic, inhibits complement binding


-Hyaluronic acid capsule – does not induce host response


-Group A polysaccharide and PG fragments – inflammation

Staphylococcus aureus
Infections

-Skin and wound infections (suppurative) – cuts, burns, surgery


-Food poisoning from enterotoxin production


-Exfoliative dermatitis from epidermolytic toxin


-TSS


-Secondary pneumonia


-Endocarditis, osteomyelitis, septic arthritis

Lancefield Grouping Scheme

Method which differentiates streptococci based on CW components extracted from various strains


-Group antigens = C carbohydrate (cell wall)


-Polysaccharides in CW


-Different sugar = different serologic group


-Type antigens = M proteins


-Associated with virulence


-Different M proteins = different types of infections

Rheumatic Fever
-Associated with post-streptococcal infection

-Antibodies formed against microbe cross-react with cardiac antigens


-Affects heart valve function


-Dental patients with a history of rheumatic fever are predisposed to sub-acute bacterial endocarditis (SBE)

Diphtheria

-Pseudomembrane formation -> obstruction


-Systemic effects from toxin – cardiac failure, paralysis


-Skin manifestations – chronic ulcers, pseudomembrane


-May become bloodborne

Group B Streptococcus(Streptococcus agalactiae)
Habitat and transmission

-Colonizes vaginal and rectal areas


Infections


-Invasive disease in newborns: Pneumonia, meningitis, sepsis


-Adults: Young women - after childbirth, abortion, endometriosis, wound infection


-Elderly – underlying disease, immunodeficiency

Clinical Infections of Neisseria gonorrhoeae

Disseminated


-Rare – bloodborne infections may cause septic arthritis, septicemia, pelvic inflammatory disease, and prostatitis


Other


-Anorectal


-Oropharyngeal


-Opthalmia neonatorum-conjunctivitis leading to blindness in the newborn

Hemophilus influenzae
Clinical infections

-Most common cause of Meningitis in children 3 to 6 months old– serotype b


Colonization, invasion, replication in mucous membranes


-Bloodstream invasion (bacteremia)


-Most frequent cause of Epiglottitis in children

Actinomycesis species
We are not fungi!!

Prokaryotic


Bacterial cell wall composition – no chitin


Do not produce aerial hyphae


Sensitive to bacterial antibiotics

Haemophilus sp.
“Blood lovers”

-X factor (hemin) found in RBCs


-V factor (NAD)


-X factor in SBA, but V factor hydrolyzed


-Chocolate agar – heating lyses RBCs, releases both factors


-Satellitism – other bacteria provide V factor


-Fastidious so antibiotics are added to media to prevent overgrowth by other organisms

Laboratory Diagnosis Haemophilus sp.
Specimen processing and isolation

-Found in many clinical specimens


-Die rapidly – need to be transported/processed ASAP


-CHOC agar:


33-37C


5-10% CO2


Bacitracin reduces overgrowth of respiratory NF


Vancomycin reduces overgrowth of genital NF


“Rough” colonies in 18-24h; mucoid colonies 36-48h

Pathogenicity Actinomyces
Actinomycosis

-8 Actinomyces species in the oral cavity


-Plaque, calculus, tongue, tonsils, other soft tissue


-Opportunistic infections frequently follow injury


-Chronic, granulomatous, soft tissue infection (draining abscess formation)


-Most infections monomicrobial; may be polymicrobial

Staphylococcus Virulence Factors
Somatic antigens:

Capsules and slime layers


-Protect pathogenic bacteria from phagocytosis by host


-Help pathogenic bacteria adhere to host cellsProtein A


-Competes with phagocytes for Fc region of IgG molecule


Clumping


-Coagulase - enzyme in CW that clumps plasma providing protection from host defenses

Clinical Infections Neisseria gonorrhoeae
Men

-Short incubation period (2-7d)


-95% symptomatic – urethritis (discharge, dysuria)


-Prostatitis, epididymitis


-50-75% women are astmptomatic

LumpyJaw Syndrome
Symptoms include:Purulent material sent for examination demonstrates sulfur granules containing gram positive filamentous bacteria. The causative agent is most likely a member of the genus: Actinomyces
Streptococcus mutans group
S. mutans, S. sobrinus, S. cricetus, S. rattus
Streptococcus mutans group
-Ferment many sugars, including sucrose, mannitol and sorbitol

-Lots of acid production-> decrease in pH-> caries


-Produce sticky, extracellular polysaccharides (dextrans, aka mutans) which hold plaque together


-Has few fimbriae for attachment, relies on plaque

General Characteristics Streptococci
Cocci arranged predominantly in chains

Gram positive


Catalase negative


Facultative or strict anaerobes

Staphylococcus Virulence Factors
Enzymes:

Coagulase – promotes fibrin formation; protects from host


Catalase – degrades H2O2 from host phagocytes


Hyaluronidase – degrades hyaluronic acid in connective tissue


Staphylokinase – degrades fibrin clot


DNAse and RNAse – degrades nucleic acids

The Oral Streptococci
General Characteristics:

-Gram positive cocci in chains


-Usually alpha hemolytic, may be beta or gamma


-4 main ‘species groups’


mutans group


salivarius group


anginosus group


mitis group

Lactobacilli Characteristics
Gram-positive coccobacillary forms

-Alpha or non-hemolytic


- Facultative anaerobes


These organisms ferment carbohydrates to form acids


- Acidogenic


And can survive well in acidic milieu


-Aciduric

Corynebacterium diphtheriae
Complex growth requirements – require 8 amino acids, not easily grown except on special media

Growth medium affects morphology and toxin production


3 distinct types of colonies observed:


-Gravis strains – short rods, gray/black colonies on tellurite agar


-Mitis strains – long, curved rods, shiny black colonies


-Intermedius strains – long rods, creamy colonies

General Characteristics Neisseria
Gram negative

DiplococciOxidase and catalase positive


Humid environment


Aerobic


Increased CO2 (5%)


Non-motile


32-36C


2 primary pathogens- Remainder are opportunistic

Neisseria gonorrhoeae
Virulence factors:

Capsule


Pili


Cell wall proteins


LPS


IgA protease

Ecology of Actinomyces Species
Surface properties and adherence

-Fimbriae help bacteria attach to host tissues


Type I – teeth


Type II – epithelial cells and other bacteria

Virulence Factors Staphylococcus
Antibiotic resistance:

Penicillin


-Plasmids carry gene for penicillinase


-This enzyme is also called Beta-Lactamase


-Plasmids are transferred by bacteriophage (transduction)


Methicillin, oxacillin – synthetic penicillins


Cephalosporins