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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.

Clostridium botulinum A German physician and poet, Justinus Kerner called botulinum toxin in 1820 as the "Sausage Poison" (sausage poison), since these bacteria grow in the lead poisoning due to poor handling of processed meat. He was the first to put forward the idea of ​​using botulinum toxin as a tool terapi.Tahun 1895 Emile Van Ermengem first time to isolate the bacteria Clostridium botulinum which produces botulinum toxin. Then in 1944 Edward Schantz Clostridium botulinum and isolated breed poison and then 1949 Burgen group discovered that botulinum toxin inhibits neuromuscular transmission.
Currently a purified botulinum toxin used for beauty treatment, therapy crossed eyes (strabismus), (blepharospasm) and muscle pain (myofascial) in athletes.
Clostridium botulinum 

 
  Fig 2. C. botulinum

Botulinum bacteria are found everywhere, in soil, sediment towing, intestines and feces binatang.Clostridium botulinum is an anaerobic bacteria, gram positive, spore-forming, rod-shaped and relatively besar.Spora bacteria can be inhaled or ingested, or be able to wound infection Thus terbuka.Walaupun berbahaya.Botulism bacteria and spores do not, the state of paralysis, caused by a toxin produced by bacteria, which means the victim was not infected but botulism poisoning. This toxic substance known is probably the most acutely toxic, with a lethal dose of 200-300 pg / kg, which means when exceeding 100 grams could kill every human on earth. (As a rat poison Strychine picture, sometimes referred to as a highly poisonous toxin has a LD50 of 1 mg / kg or 1 billion pg / kg). There are seven strains of botulism, each produces a potent neurotoxin protein. Type A, B, E and F cause botulism in humans. Type C-alpha causes botulism in domestic poultry and liar.Tipe C-beta and D cause botulism in cattle. Seven types of botulism, strain G, was isolated from soil samples, but rare and has not shown a relationship that cause human or animal botulism. Type A and some type B and type F protein decomposition odor of animals and cause food to rot, and rotten meat. Type E and some type B, C, D and F are not proteolytic (protein digesting animals they do not). When it appears, the type of botulism can not be detected with a strong odor. Clostridium bacteria are bacteria resistant and can withstand heat of boiling the spores are destroyed lama.Untuk, food must be heated to a temperature of 120oC or more, as in the use of pressure cooker. Toxins produced by bacteria can be destroyed by heat. To destroy the toxin is derived from food, the food must be heated to 85 ° C or more for five minutes, or boil for at least 10 minutes.
Vector Clostridium is widespread throughout dunia.Botulinus present in the form of bacteria and spores in soil, sediments at sea, the surface of fruits and vegetables, in the intestines of mammals and fish and in gill and vixcera of shellfish, crabs. Because botulinum spores, contained in soils and sediments on the seabed, these spores can end up in the intestines of animals and fish that eat grass, then enter the human food chain. Almost in a few foods with a low pH (4.6 or less) can support the growth of bacteria and then produce it racun.Selain berkecambahnya factors that can support the spores is a state without oxygen - anaerobic, low pH can not destroy or inactivate toxins that have been produced. Salt levels below 7%, sugar content below 50%, temperatures between 4 ° C - 49oC or room temperature, high humidity levels, at least competitive with the bacterial flora. Both human adults and infants, usually inhale the spores, but less affected by this efeknya.Hal be due to the immune system that destroys the spores before they can grow and produce racun.Botulism in infants caused by swallowing the bacteria, rather than swallowing poison. There are three types of poisoning by way of contracting: Almost all events (90%) occurred due to poor food cans are preserved. Botulism due to food (foodborne botulism) is usually caused by contaminated meat (including seafood), and canned vegetables. Botulism in infants (Infant botulism) is a form of botulism the most umum.Disebabkan by inhaling the spores along with particles of dust that mikroskopis.Bagaimanapun source, children under one year do not have a good immune system and have not had an important protein in the intestines to destroy spores bakteri.Spora germinate and produce toxins (the colon) that attach to the motion around the nerves, causing paralysis and, in extreme cases, death. Botulism in the wound (wound botulism) is a rare form of botulism the most. Can occur when bacteria to wound infection (such as laceration or breakdown of bone formation) and produce toxin in vivo. Spores grown locally (in the wound) and toxins circulate through the blood vessels to reach other parts of tubuh.Jalan spores enter the wound may be small, and looks are not important.
Symptom Symptoms usually occur after eating a day, although the symptoms can be seen after 10 hari.Sebagian weak and lame, in general complain of fatigue, dry mouth and difficulty swallowing.
Mechanism Botulinum bacteria will be dangerous when active metabolic and producing botulinus toxin. In case of spores, botulinum is harmless. Heat can allow spores to germinate and active and heat can also kill other bacteria that become rivals with Clostridium Botulinum in a Host. Botulinum toxin structure and function have similarities with both tetanus.Kedua toxin is botulinum neurotoxin but the toxin affects the peripheral nervous system because it has afiniti to neurons at the neuromuscular junction. The toxin is synthesized as a single polipeptid chain (150.000 daltons) are less toxic. Nonetheless after the cut by a protease, it generates two chains: a light chain (subunit A, 50.00 dalton) and heavy chain (subunit B, 100,000 daltons) which duhubungkan by dwisulfida bond.
 A subunit is the most toxic toxin is botulinum type endopeptidase diketahui.Toksin which prevented the release of acetylcholine at a meeting between the muscle by the nerve (myoneural junction). It is specific to the nerve endings edge / periphery to the place where the motor neurons to stimulate muscles. This toxin acts such as tetanus toxin and solve synaptobrevin, interfere with the formation (and release) that contains vesicles of acetylcholine. Exposed cells that fail to release neurotransmitter (acetylcholine). If the muscle does not receive the signal rather than the nerve, he will not contract (contract). It causes paralysis (paralysis) motor systems. During the growth of C. Botulinum produces at least seven different toxins, including neurotoxins, enterotoxins, and haemotoxin, including several known poisons most berpotensial.Dalam certain cases, a single strain can produce more than one type of poison. Botulinum toxin primarily affects the nervous system around, in particular: a) Ganglionic synapses b) Post-ganglionic parasympathetic synapses c) the myoneural junction, the end of the nerve where the nerve joins the muscle and nerve terminal where the toxin blocks the movement (the motor nerve terminals)
Neurotransmitters in the body is sending a message to the chemical used by cells - nerve cells to communicate with each other and which are used by nerve cells to communicate with muscles. Botulism toxins cause flaccid paralysis characteristic by breaking one of the three proteins required for neurotransmitter release this blockade acetikolin release and the ability of nerve cells to communicate.
 With terblokadenya nerve terminal by poison, nerves can not send signals to the muscles to berkontraksi.Pasien experiencing weakness or paralysis, usually starting with a face / face and throat, chest and diaphragm and chest muscles lengan.Ketika exposed to its influence, breathing becomes difficult, hampered or fully lumpuh.Di some cases, patients died from asphyxia / chest tightness. Botulinum toxin acts by binding presynaptically to the location that is known to have high affinity in the cholinergic nerve terminals and reduce the release of acetylcholine, causing effects otot.Mekanisme nerve blockade is used as the basis for the development of this toxin as a therapeutic tool. Recovery occurs when the proximal axonal sprouting and muscle reinnervation occurs with the formation meeting of nerve - muscle (neuromuscular junction) is new. Botulinum toxin type and location of the target: A. BTX-A and BTX-E broke the synaptosome-associated protein (SNAP 25), a presynaptic membrane protein required for the incorporation of neurotranmitter containing vesicles. 2. BTX-B,-D BTX, and BTX-F broke the vesicle-associated membrane protein (Vamp), also known as synaptobrevin. 3. BTX-C acts by breaking syntaxin, a membrane protein targets.