Question

Could some one help me i have to write an essay about this and it need to be in detail

Please discuss the mechanism that pseudomonas aeruginosa, Staphylococcus aureus,Propionibacterium acnes and streptococcus progenies utilize to cause disease on skin and in the eyes. You must state what disease these microorganism cause. In addition, [lease list and explain the host immune defenses that the microbe would have to overcome to be successful at causing disease ( include a discussion what role personal hygiene plays in microbial skin and eye infections). Also, please list and explain what the microbes cold contain that would allow them to overcome these host immune response. Please explain how these infection could lead to more serious conditions such as endocarditis ( hint: Discuss the relationship between local and systemic infection and septicemia.) include a discussion what roles quorum seeing and sequential timing play in microbial skin and eye diseases.

Answer 1

Pseudomonas aeruginosa

- Gram-negative bacilli
- facultative aerobes - growth with and without O2
- motile
- opportunistic pathogen
- grows in a wide range of temperatures
- widely distributed
a. moist environments, like soil and water (hot tubs)
b. on fresh fruit and vegetables

It is the fourth most commonly isolated nosocomial pathogen accounting for approx.
- 10 % of all hospital-acquired infections.
- Patient-to-patient spread and direct patient contact with environmental reservoirs.
a. disinfectants,
b. respiratory equipment,
c. food,
d. sinks, taps

Pseudomonas aeruginosa become pathogenic in a host with altered host defences

1. disrupted mucous membranes and skin (ex: burns)
2. intravenous and urinary catheters
3. neutropenia (ex: cancer chemotherapy)

The mechanism of infection for p. aeruginosa

1. attaches to mucous membranes and skin
2. invades locally
3. produces a systemic disease

Pseudomonas aeruginosa attaches to epithelial cells. P. aeruginosa secretes many proteins into the host cells using Type III secretion system. Type III secretion system causes host cell death. Exotoxin A and subunit A-B exotoxin are the cytotoxic toxins are released by p. aeruginosa. The exotoxin work as A subunit inhibitors protein synthesis by inactivating EF-2 (elongation factor). Besides, Exotoxin A, the other exotoxin is secreted by Pseudomonas aeruginosa is LPS.

The LPS:

1. Can cause septic shock syndrome
2. Creates intrinsic resistance to antibiotics
3. Decreases permeability
4. Involved in drug efflux pumps1

Treatment:

1. need to start treating quickly (t correlates with the outcome)
2. remove infected catheters
3. drain abscesses
4. remove obstructions (where bacteria can live)
5. know antibiotic resistant patterns of the hospital (esp. ICU)
6. use combination antibiotics - anti-pseudomonal beta-lactam (ex: ceftazidime) PLUS aminoglycoside

Antibiotic therapy:

Combination therapy:
Anti-pseudomonal beta-lactam (ex: ceftazidime)
+
Aminoglycoside

Staphylococcus Aureus

Staphyle means a bunch of grapes (gram-positive, clusters) aureus means golden (grows golden on the plate). Metabolically versatile, facultative anaerobe, can grow over a wide temperature range, halophilic, antibiotic resistant.

Staphylococcus aureus from all other Staphylococcus species by, S. aureus is coagulase positive. Staphylococcus aureus most frequently colonizes in/on the nasal passages.

The types of skin infections caused by Staphylococcus aureus are Pimple or stye, boils and carbuncles, impetigo, scaled skin syndrome.

The virulence factors of Staphylococcus aureus possess Capsule, invasins, adhesins and toxins. The two general mechanisms that Staphylococcus aureus has used to become penicillin and later methicillin-resistant are Gene mutations and acquisition of resistance genes.

The typical treatment for a patient with a localized Staphylococcus aureus skin infection to receive Incision and drainage.

The typical treatment for a patient with a more serious Staphylococcus aureus infection to receiveTetracyclines and clindamycins.

Propionibacterium acnes

GPR. diphtheroid. 4 phylogenetic groups. similar to C. diphtheria in cell morphology/arrangement. Most common, non-spore forming, anaerobic GPR found in clinical specimens. Commensal: skin, mouth, urinary tract, large intestine. Slow growing aerotolerant anaerobe. Is difficult to ID because it is anaerobic. Produces propionic acid as by-product of fermentation. Catalase +. opportunistic; causes inflammatory disease states. Synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome.

P. acnes produce Propionic acid as a by-product of fermentation.

P. acnes virulence factors

1. biofilm former- associated with heart valves, prosthetic devices, CNS shunts.

2. numerous uncharacterized adhesins.

3. 5 CAMP factors.

4. secrete many degradative enzymes (triacylglycerol lipase (GehA) digests sebum, producing fatty acids).

5. Can resist phagocytosis and live in macrophage. 6. fatty acids and bacterial antigens lead to intense local inflammation

Acne vulgaris disease progression

1. P acnes resides in the anaerobic environment of sebaceous glands.

2. secretes lipases that break down sebum to generate fatty acids.

3. fatty acids induce keratinocyte growth, resulting in whiteheads and blackheads.

4. produce PMN chemotactic factors that attract PMNs into sebaceous glands.

5. pus formed: invading PMNs digest P. acnes.

6. P. acnes activates classical and alternative complement pathways.

7. fatty acids trigger local inflammatory responses.

Inflammatory responses to P. acnes:

P. acnes induces production and secretion of numerous pro-inflammatory cytokines by monocytes. IL8, IL1, TNF-alpha are mediated thru toll-like receptor 2 (TLR2), which recognizes P. acnes peptidoglycan. This results in the production of beta-defensin-2, and antimicrobial peptide. Inflammatory response and biofilm formation assists information of pimples (comedones)

Treatment:

1. antimicrobial drugs: doxycycline. recently, there has been increased resistance to doxycycline and erythromycin. must reach high local concentrations in sebaceous glands to be effective.

2. chemicals that cause exfoliation of dead skin cells (benzoyl peroxide).

3. anti-inflammatory drugs: oral and topical retinoids (acutane, a derivative of vitamin A/retinoic acid) is used to treat severe, cystic acne. 4. blue light therapy- destroys P. acnes by increasing ROS.

Strep. Pyogenes

Group A Strep
Gram+ cocci
β-hemolysis
No CATALASE
Facultative anaerobe
Have a peroxidase system
most serious streptococcal pathogen

Streptococcus pyogenes cause:

- Strep Throat (streptococcal pharyngitis)

- Streptococcal Impetigo (Pyoderma)

-Wound Infections

Cell-associated virulence factors

• Capsule (hyaluronic acid) - inhibits phagocytosis b/c too similar to human, streptokinase to break up blood clots, and DNase to digest DNA
• M-protein - Spiky projections, attach bacteria to cells, inhibits phagocytosis and suppresses complement.
• C Carbohydrates on surface protect from being dissolved.
• Lipoteichoic acid - attachment and cytotoxicity
• -Puerperal fever (infection of the uterus in childbirth.)

Toxins:

Erythrogenic or Pyrogenic Toxin (produced only by lysogenized Group A Streptococci): responsible for scarlet fever

Toxic shock syndrome toxin (similar to, but different from the staph exotoxin TSST-1)

Pathology 1

DIRECT INVASION/TOXIN
1. Pharyngitis:
A. Red, swollen tonsils and pharynx
B. Purulent exudate on tonsils
C. Fever
D. Swollen lymph nodes
2. Skin Infections:
A. Folliculitis
B. Cellulitis
C. Impetigo
D. Necrotizing fasciitis
3. Scarlet Fever: fever and a scarlet red rash on the body
4. Toxic shock syndrome

Pathology 2

ANTIBODY-MEDIATED
1. Rheumatic fever (may follow streptococcal pharyngitis):
A. Fever
B. Myocarditis: heart inflammation
C. Arthritis: migratory polyarthritis
D. Chorea
E. Rash: erythema marginatum
F. Subcutaneous nodule
∗ 10 - 20 yrs after infection, may develop permanent heart valve damage (likely after recurrent infections with streptococci).
2. Acute post-streptococcal glomerulonephritis: tea-coloured urine, following streptococcal skin or pharynx infection.

Treatment

1. Penicillin G
2. Penicillin V
3. Erythromycin
4. Penicillinase-resistant penicillin: In skin infections, where staphylococci could be the responsible organism.
∗ Following rheumatic fever:
A. Patients are placed on continuous prophylactic antibiotics to prevent repeat strep throat infections that could potentially lead to a repeat case of rheumatic fever.
B. If permanent heart valve damage has occurred, antibiotics are required when certain procedures are preformed (such as dental work), due to the high risk of bacterial endocarditis.
∗ For invasive Streptococcus pyogenes infections, such as necrotizing fasciitis or streptococcal toxic shock syndrome, consider adding clindamycin.