Staphylococcus lecture bls 209

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Pathogenic Gram-Positive Cocci (Staphylococci) VMP 231 Hoza, A.S

Transcript of Staphylococcus lecture bls 209

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Pathogenic Gram-Positive Cocci (Staphylococci)

VMP 231

Hoza, A.S

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Stain purple when gram-stained

Can be categorized into 2 major groups

Genera of cocci-shaped organisms- Staphylococcus, Streptococcus, and Enterococcus

Genera of bacilli-shaped organisms- Bacillus, Clostridium, Listeria, Corynebacterium, Mycobacterium, Nocardia, and Actinomyces

Gram-Positive Pathogens

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Normal members of every human’s and animal microbiota

Can be opportunistic pathogens

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Gram-positive cocci, nonmotile, facultative anaerobes

Cells occur in grapelike clusters because cells division occurs along different planes and the daughter cells remain attached to one another

Salt-tolerant: allows them to tolerate the salt present on human skin

Tolerant of desiccation: allows survival on environmental surfaces (fomites)

Structure and Physiology

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Two species are commonly associated with staphylococcal diseases in humans/ANIMALS

Staphylococcus aureus-The more virulent strain that can produce a variety of conditions depending on the site of infection

Staphylococcus epidermidis-Normal microbiota of human skin that can cause opportunistic infections in immunocompromised patients or when introduced into the body

Structure and Physiology

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“Staph’ infections result when staphylococci breach the body’s physical barriers

Entry of only a few hundred bacteria can result in disease

Pathogenicity results from 3 features

Structures that enable it to evade phagocytosis

Production of enzymes

Production of toxins

Pathogenicity

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1. Protein A coats the cell surface

Interferes with humoral 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

Structural Defenses Against Phagocytosis

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3. Synthesize loosely organized polysaccharide slime layers (often called capsules)

Inhibit chemotaxis of and phagocytosis by leukocytes

Facilitates attachment of Staphylococcus to artificial surfaces

Structural Defenses Against Phagocytosis

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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

Enzymes

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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

Enzymes (cont.)

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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 toxins

• Causes the patient’s skin cells to separate from each other and slough off the body

Toxins

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3. Toxic-shock-syndrome toxin

Causes toxic shock syndrome

4. Enterotoxins

Stimulate the intestinal muscle contractions, nausea, and intense vomiting associated with staphylococcal food poisoning

Toxins (cont.)

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                                                                                                              III.   

Virulence factors of Staphylococcus aureus

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3 categories

Noninvasive Disease

• Food poisoning from the ingestion of enterotoxin-contaminated food

Cutaneous Disease

• Various skin conditions including scalded skin syndrome, impetigo, folliculitis, and furuncles

Staphylococcal Diseases

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Systemic Disease

• Toxic shock syndrome-TSS toxin is absorbed into the blood and causes shock

• Bacteremia-presence of bacteria in the blood

• Endocarditis-occurs when bacteria attack the lining of the heart

• Pneumonia-inflammation of the lungs in which the alveoli and bronchioles become filled with fluid

• Osteomyelitis-inflammation of the bone marrow and the surrounding bone

Staphylococcal Diseases

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Diagnosis

Detection of Gram-positive bacteria in grapelike arrangements isolated from pus, blood, or other fluids

Treatment

Methicillin is the drug of choice to treat staphylococcal infections

• Is a semisynthetic form of penicillin and is not inactivated by -lactamase

Diagnosis, Treatment, and Prevention

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Diagnosis

Specimen

Smear

Culture

Film

Biochemical Reactions

Antibiogram

Typing

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Prevention

Hand antisepsis is the most important measure in preventing nosocomial infections

Also important is the proper cleansing of wounds and surgical openings, aseptic use of catheters or indwelling needles, an appropriate use of antiseptics

Diagnosis, Treatment, and Prevention (cont.)

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Antibiotic sensitivity pattern

Very variable and not predictable

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)

• β lactamase stable penicillins (cloxacillin, oxacillin, methicillin) used

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2. Alteration of penicillin binding proteins

• (Chromosomal mediated)

• Has made S. aureus resistant to β lactamase stable penicillins

• 10-20% S. aureus Gp (B) GH Colombo/THP resistant to all Penicillins and Cephalasporins)

• Vancomycin is the drug of choice

Antibiotic sensitivity pattern

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Tested in lab using methicillin

Referred to as methicillin resistant S. aureus (MRSA)

Emerging problem in the world

Drug of choice - vancomycin

No effective antibiotics discovered -We might have to discover

Antibiotic sensitivity pattern