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Bacteria

Bacteria

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Published by: kohinoor815256 on Nov 21, 2008
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04/28/2013

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EXOTOXIC MODELCORYNEBACTERIUM DIPHTERIAE
Received its name from the hide-like pseudomembrane that forms on the tonsils, palate, or pharynx
Even though the exotoxin can cause fatty degeneration of heart muscle and nervous system, young childrenoften die because their Airway is occluded.
Exotoxins
o
Secreted proteins from microorganisms
o
Take form of A-B toxin where B interacts with a cell receptor as a ligand. A is then released,internalized and causes damage to the cell.
I.GENUS CORYNEBACTERIUMA.CHARACTERISTICS
Club Shape Rods
Gram Positive
 Non-spore forming
 Non-acid fast
Aerobic or Facultative anaerobic
Catalase Positive
 Non-motile
B.CHEMOTAXONOMICALLY
Cell walls contain:
Meso-diaminopimelic acid
Arabino-galactan polymer 
Short chain mycolic acids
C.CORYNEBACTERIUM SPP.
World Wide
D.CLOSELY RELATED GENERA
Rhodococcus, Nocardia, Mycobacterium
1
 
II.CORYNEBACTERIUM DIPHTERIAEA.PATHOGEN
Occurs naturally only in humans but we can infect farm animals
Produces Characteristic METACHROMATIC Granules that Stain Bluish Purple withMethylene blue.
Grows with Snapping division which results in Angular and Palisade arrangements thatlook like Chinese Letters.
B.CYCLE OF INFECTION
1.Respiratory tract diphtheria is most common in temperate climate2.Cutaneous diphtheria are seen in tropical areasa.Spread by Touch and Fomites b.Transmitted to cows by infected milker’s fingersc.Unpasteurized milk can then transmit the infection
C.PATHOGENESIS
1.Classic AB exotoxic diseasea.B domain binds to cell receptor and forms membrane channel for A b.A binds to Elongation Factor 2 (EF-2) and causes it to be ADPrebosylated and made inactive. Thus, the cell can no longer make proteins.2.Toxin Productiona.Low iron stimulates toxin production3.Biological Toxin Effectsa.Local pharyngeal membrane formation b.Heart, nerves, and kidney are most sensitive
D.CLINICAL MANIFESTATIONS
1.Pharyngitis2.Bullneck due to neck swelling which leads to difficult air passage3.No lymphadenopathy4.Open mouth and look for membrane, which is 1-3mm thick and is curling away fromthe tonsils, palate, uvula, or pharynx.5.Foul breath associated with necrosis and the greenish or blackened membrane arehallmarks****
E.DIAGNOSIS
1.Elick Test and Schick Test
F.TREATMENT
1.Erythromycin or penicillin2.Maintenance of open airway
G.PREVENTION
1.DPT in children2.Td in adults (booster every 10 years)
2
 
ENDOTOXIC MODELNEISSERIA MENINGITIDIS
ENDOTOXINS
o
Integral parts of microbial cell wall and are normally released only when the cell dies
o
Characteristic of Gram Negative Bacteria
I. NEISSERIA MENINGITIDISA.CELLULAR MORPHOLOGY
o
Small Gram Negative Diplococcus
o
Bean Shaped
o
 Non-motile
B.PHYSIOLOGY
o
Aerobic or facultative
o
Oxidase Positive
o
Grow on Chocolate Agar 
o
Sensitive to drying
C.ANTIGENIC CHARACTERISTICS
o
Capsular Polysaccharide
o
Surface antigens include proteins for iron uptake from transferrin
D.VIRULENCE FACTORS
o
Pili – Attach to cells of mucous membrane of pharynx or nasopharynx
o
Capsule – Anti-phagocytic
o
Endotoxin – Causes shock and necrosis
o
IgA protease
E.CYCLE OF INFECTION
o
Enters through Upper Respiratory Tract
o
Invade and enter bloodstream to infect skin, eyes, joints, lungs, and meninges.
F.DISEASES
o
Causes mild to acute pharyngitis
o
Skin affected with Petechial Rash** along the nuchal rigidity are early signs of meningitis.
o
Spinal fluid is turbid.
o
Sequellae: Nerve Deafness
Skin Damage
CNS Damage
Death without treatment
G.LABORATORY IDENTIFICATION
o
Thayer Martin Agar (Chocolate agar plus vancomycin)
H.MORBIDITY AND MORTALITY
o
Highest disease rate among children
o
Mortality is less than 10% with early diagnosis and treatment
I.TREATMENT
o
Before Lab diagnosis treat with Cephalosporin or Ampicillin
o
After lab diagnosis teat with Penicillin
J.RELATED ORGANISMS
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