A. Corynebaterium diphtheriae
Corynebacterium diphtheriae is a pathogenic bacterium that causes diphtheria. Diphtheria
is a contagious infectious disease and meny moaned the upper airway in
the form of pseudo membrane and exotoxin transmission through air and
food.
Corynebacterium
diphtheriae is a creature of facultative anaerobic and gram-positive,
characterized by an encapsulated, not berspora, motionless, and a
rod-shaped 1 to 8 μm and width of 0.3 to 0.8 μm. These bacteria release diphtheria exotoxin. Diphtheria toxin is heat-resistant polypeptide not Dapa tmematikan at a dose of 0.1 mg / kg.
Modes of Transmission
The
bacteria is transmitted through saliva splashes of objects or coughing
patient or food that has been contaminated by bacteria. When it has entered the body, the bacteria release a toxin or poison. This
toxin will spread through the blood and the bias caused damage
throughout the body tissues, especially the heart and nerves.
Mechanism of Corynebacterium diphtheriae
In general, these bacteria are not invasive and rarely get into the bloodstream,
but the local breed on their mucous membranes or on dead tissue. The toxin produced can enter the bloodstream and spread throughout the body.
When
bacteria multiply and release toxins, leading to cell death, and with
fibrin, leukocytes (white blood cells), as well as other blood
components that form the lining of bias berwarrna white, yellow, or
rather gray. Along with terjadiny apembengkaan, it can cause airway obstruction, which can be fatal.
Bias
toxin reaches the heart, with a specific mechanism Dapa tmenghambat
protein synthesis in cardiac cells and damage mitokhondria. This is so may cause "fatty infiltration" followed by the occurrence of fibrosis, heart function will then tergannggu. Bias deaths occurred.
Toxins can also cause damage to the myelin sheath (nerve cell packing) and the nerve cells themselves are also damaged bias. Compared with the sensory nerves, motor neurons more damage, nerve function is further impaired
The disease process
A. Diarbsorbsi toxin into the mucous membranes and causes the destruction of the superficial epithelium and inflammatory response.
2. Epithelial
necrosis which have embedded in the exudate of fibrin and red blood
cells and white, forming a "pseudo membrane" which are often coated gray
tonsils, pharynx, or larynx. Any attempt to remove the pseudo capillary membrane will break and cause bleeding.
3. Regional lymph nodes in the neck are enlarged, and edema can occur is evident throughout the neck. Idifteria bacteria produce a toxin in the membrane continues to be active.
4. These
toxins cause damage diarbsorbsi and far away, especially parenchymal
degeneration, fatty infiltration, and necrosis of cardiac muscle, liver,
kidneys, and adrenal, sometimes followed by severe bleeding. These toxins cause nerve damage that often results in paralysis of the soft palate, the eye muscles, or ekstermitas.
Diphtheria Diphtheria wound or skin tropic areas was found. A membrane may form on infected wounds that are not dapatsembuh. However, absorbs toxins are usually small and negligible systemic effects. "Virulence"
diphtheria bacteria due to its ability to cause infection, growing
fast, and then quickly remove toxins are absorbed effectively. C. diphteriae
not need a genie to cause toksi local infection or skin for example, in
nasopharynx remain non toksi istren the genie does not cause local or
systemic toxic effects. C. menginfasi diphteriae not actively network in and practically never entered circulation.
Corynebacterium diphteriae
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