staphylococcus

Antibiotic sensitivity pattern(ABSP)

(Very imp. In Pt. Management) Mechanisms 1. B lactamase production - plasmid mediated - Has made S. aureus resistant to penicillin group of antibiotics - 90% of S. aureus (Gp A) - B lactamase stable penicillins (cloxacillin, oxacillin, methicillin) used 2. Alteration of penicillin binding proteins (PBP) - (Chromosomal mediated) - Has made S. aureus resistant to B lactamase stable penicillins - 10-20% S. aureus Gp (B) GH Colombo/THP resistant to all Penicillins and Cephalasporins) - Vancomycin is the drug of choice

Staphylococcal food poisoning

- Due to production of enterotoxins - heat stable enterotoxins acts on gut - produces severe vomiting following a very short incubation period - Resolves on its own within about 24 hours

Structure and Physiology of staphylococcus

- Gram-positive cocci - Nonmotile - facultative anaerobes - Cells occur in grapelike clusters because division occurs along different planes and daughter cells remain attached to one another - Salt-tolerant: allows them to tolerate the salt present on human skin(5-25%NaCl) - Tolerant of desiccation: allows survival on environmental surfaces (fomites)

Prevention of staphylococci

- Hand antisepsis is the most important measure in preventing nosocomial infections - proper cleansing of wounds and surgical openings, aseptic use of catheters or indwelling needles, an appropriate use of antiseptics

Novobiocin Susceptibility

- Measure Zone of Inhibition - More than 17 mm = Sensitive - Less than 17 mm = Resistant

Staphylococcus epidermidis

- Skin commensal - Has predilection for plastic material - Ass. With infection of IV lines, prosthetic heart valves, shunts - Causes urinary tract infection in cathetarised patients - Has variable ABS pattern - Treatment should be aided with ABST

Stapylococcus saprophyticus

- Skin commensal - Imp. Cause of UTI in sexually active young women - Usually sensitive to wide range of antibiotics

Pyogenic Cocci

- Staphylococcus • Gram positive • Catalase +ve - Streptococcus • Gram positive • Catalase -ve - Neisseria • Gramnegative • Diplococci

Toxins of staphylococcus

- Staphylococcus aureus produces toxins more frequently than S. epidermidis 1. Cytolytic toxins - Disrupts the cytoplasmic membrane of a variety of cells - Leukocidin can lyse leukocytes specifically 2. Exfoliative (epidermolytic) toxins - semi superantigen proteases - split desmoglein 1 of the intercellular bridges in epidermis - produced by about 5-10% of S. aureus - causes generalized desquamation of the staphylococcal scalded skin syndrome (SSSS). 3. Toxic shock syndrome toxin-1 (TSST-1) - Superantigen - associates with fever, shock, desquamative skin rash of toxic shock syndrome in humans. 4. Enterotoxins - Superantigens - at least 10 soluble toxins produced by about 50% of S. aureus. - Heat-stable (100 C, 30 min.) and resistant to the gastric acid and gut enzymes. - Enterotoxins are produced in carbohydrate and protein foods. - Causing emesis, a characteristic of staphylococcal food poisoning

Treatment of disease caused by staphylococcus

- Vancomycin & Methicillin is the drug of choice to treat staphylococcal hospital and non - hospital acquired infections - Methicillin Is a semisynthetic form of penicillin and is not inactivated by -lactamase - MRSA: MRSA (ORSA): methicillin (oxacillin)-multiresistant S. aureus, resulting from acquisition of mecA, which encodes a novel PBP (PBP2') that is not bound by b-lactams. MRSA strains are usually also resistant to tetracyclines, erythromycins and aminoglycosides. - VIRSA: vancomycin intermediate resistant S. aureus two vancomycin-resistant strains (VRSA), have been isolated in USA since 2002.

Staphylococcal Diseases

1. Noninvasive Disease - Food poisoning from the ingestion of enterotoxin-contaminated food 2. Cutaneous Disease - Various skin conditions including - scalded skin syndrome - impetigo - folliculitis - furuncles 3. Systemic Disease

Differential Characteristics

1- Catalase 2H2O2 O2 + 2H2O Streptococci vs. Staphylococci 2- Coagulase Fibrinogen Fibrin 7

Staphylococcal infections

1- Due to direct effect of organism - Local lesions of skin - Deep abscesses - Systemic infections 2- Toxin mediated - Food poisoning - toxic shock syndrome - Scalded skin syndrome

Super toxins ( super antigens)

1- Exfoliative 2- toxic shock 3- Euterotoxine

Factors predisposing to Staph. aureus infections

1- Host factors - Breach in skin - Chemotaxis defects - Opsonisation defects - Neutrophil functional defects - Diabetes mellitus - Presence of foreign bodies 2- Pathogen Factors - Catalase (counteracts host defences) - Coagulase - Hyaluronidase - Lipases (Imp. in disseminating infection) - Β- lactamase (ass. With antibiotic resistance)

Laboratory Diagnosis

1- Specimen - Detection of Gram positive bacteria in grapelike arrangements isolated from pus, blood, or other fluids 2- Culture - (MSA, Chapman Stone Agar, Staph 110, Baird-parker Agar, V.J.Agar, CHROMagar ,Staphylococcus agar And TPY Agar & Broth) 3- Biochemical Reactions 4- Phage Typing - Epidemiological Typing Of Staph. aureus By Examining Differences In Lytic Patterns Based On Susceptibilities To The 23 Lytic Bacteriophages In The International Set(from 1975) For Human Staph. aureus Isolates 5- Antibiogram - in-vitro testing for the sensitivity of an isolated bacteria strain to different antibiotics( It is by definition an in vitro sensitivity_ . Frequently it follows the strain identification and represents the final goal of a bacteriolgy analysis. - There are 2 antibiogram methods: diffusimetric (most used and easy to do) and quantitative. - diffusimetric method - based on the diffusion property of the antibiotic from the impregnated paper disks.

Species of staphylococcus

1- Staph. Aureus - major pathogen for humans - cause suppuration - cause abscess formation - cause scalded skin syndrome - cause toxic shock syndrome - cause food poisoning. 2- Staph. Epidermidis - cause infection from prosthetic devices. 3- Staph. Saprophyticus - cause urinary tract infections (UTI) in young women. 4- Staph. Capitis - endocarditis, UTI, and opportunistic infections. 5- Staph. Haemolyticus - Cause endocarditis, UTI, and opportunistic infections. 6- Micrococcus spp. - opportunistic infections. 7- Stomatococcus - endocarditis, opportunistic infections. 8- Alloiococcus otitidis - chronic middle ear infection

Colony Characteristics on Sheep Blood Agar of Staphylococcus

1- Staphylococcus aureus - large (6-8 mm) - smooth - slightly raised (low convex) - cream to yellow to orange colonies with -hemolysis 2- Staphylococcus epidermidis - smaller (2.5-6 mm) - White - non-pigmented colonies without hemolysis after 3 days of incubation

Pathogenicity of staphylococcus ( virulence factors of Staphylococcus)

1- Structures that enable it to evade phagocytosis 2- Production of enzymes 3- Production of toxins

Systemic diseases of staphylococcal

1- Toxic shock syndrome-TSS - toxin is absorbed into the blood and causes shock 2- Bacteremia - presence of bacteria in the blood 3- Endocarditis - occurs when bacteria attack the lining of the heart 4- Pneumonia - inflammation of the lungs in which the alveoli and bronchioles become filled with fluid 5- Osteomyelitis - inflammation of the bone marrow and the surrounding bone

Classification of bacteria

1- does not dependent on 60SrRNA 2- depends on phenotypic and genetic factors

Differences between normal flora & biomicrotinic flora

1- normal flora - bacteria that always present in the surface 2- normal microtinic flora - include normal flora + pathogenic bacteria in which able to cause disease when immunological resistance of the disease are decreased

Enzymes of staphylococcus

1. Coagulase - Triggers blood clotting 2. Hyaluronidase - Breaks down hyaluronic acid, enabling the bacteria to spread between cells 3. Staphylokinase - Dissolves fibrin threads in blood clots, allowing Staphylococcus aureus to free itself from clots 4. Lipases - Digest lipids, allowing staphylococcus to grow on the skin's surface and in cutaneous oil glands 5. -lactamase - Breaks down penicillin - Allows the bacteria to survive treatment with -lactam antimicrobial drugs

Structural Defenses Against Phagocytosis (staphylococcus) ( virulence factors resistance phagocytosis)

1. Protein A coats the cell surface - Interferes with humeral immune responses by binding to class G antibodies - Inhibits the complement cascade 2. Clumping Factor (Bound coagulase) - Converts the soluble blood protein fibrinogen in insoluble fibrin molecules that form blood clots - Fibrin clots hide the bacteria from phagocytic cells 3. Synthesize loosely organized polysaccharide slime layers (often called capsules) - Inhibit chemotaxis and phagocytosis by leukocytes - Facilitates attachment of Staphylococcus to artificial surfaces

Family of staphylococcus

Micrococcaceae

Genus of staphylococcus

Micrococcus and Staphylococcus