Clostridium perfringens презентация

common bacterial agent for gas gangrene. Some symptoms include blisters, tachycardia, swelling, and jaundice.

Biochemical properties: Catalase: Negative, Spot indole: Positive, Lecithinase: Positive, Lipase: Negative, Litmus Milk: Stormy Fermentation, Reverse CAMP plate: Positive, Gas Liquid Chromatography products: (Acetic, Butyric and Lactic Acids).

Clostridium perfringens
on blood agar

and exotoxins .
Alpha toxin ( lecithinase) :
• It is lethal and necrotizing; it lyses cell membrane lecithins, causing cell death. Can be detected by Nagler ‘s reaction.
2. Theta-toxin (oxygen-labile cytolysin) are important in the disease pathology, causes tissue destruction by several mechanisms .
3. Extracellular enzyme: as hemolysins , proteases, lipases, collagenase and hyaluronidase, contribute to the invasive process.
4. Enterotoxins: are produced by some strains of C. perfringens .

intestinal (bowel) gas gangrene (a) Macroscopic picture of the edematous intestinal wall with multiple submucosal and subserosal cysts (b) Histological picture of the intestinal mucosa with nonreactive necrosis (c) Gram stain of cysts with large, rod-shaped bacteria (d) Electron microscopic picture of a bacterium found in a submucosal cyst

Myonecrosis is a condition of necrotic damage, specific to muscle tissue. It is often seen in infections with C. perfringens or any of myriad soil-borne anaerobic bacteria. Bacteria cause myonecrosis by specific exotoxins. These microorganisms are opportunistic and, in general, enter the body through significant skin breakage. Gangrenous infection by soil-borne bacteria was common in the combat injuries of soldiers well into the 20th century, because of nonsterile field surgery and the basic nature of care for severe projectile wounds

suspect organism is cultured on an egg yolk media plate. One side of the plate contains anti-alpha-toxin, while the other side does not. A streak of suspect organism is placed through both sides.
An area of turbidity will form around the side that does not have the anti-alpha-toxin, indicating uninhibited lecithinase activity.
In addition, laboratories can diagnose the bacteria by determining the number of bacteria in the feces.
Within the 48 hours from when the disease began, if the individual has more than 106 spores of the bacteria per gram of stool, then the illness is diagnosed as C. perfringens food poisoning.  

 Nagler's reaction

Isolation of Clostridia from wound, pus, blood or faeces, along with toxin and serological assays aid in the diagnosis of clostridial infections. 

other Clostridium genus species, it is Gram-positive, and its appearance on a gram stain resembles tennis rackets or drumsticks.  C. tetani is found as spores in soil or in the gastrointestinal tract of animals. C. tetani produces a potent biological toxin, tetanospasmin, and is the causative agent of tetanus, a disease characterized by painful muscular spasms that can lead to respiratory failure and, in up to 10% of cases, death.

Seen here is a diagram depicting the bacterium, Clostridium tetani, which causes the tetanus infection known for its symptoms of muscle spasms and lockjaw. This bacterium is strongly durable due to its endospores, which can carry the infection's DNA even when the bacterium is dead. Pictured is the bacterium alone, with a spore being produced, and the spore alone.

role in Pathogenesis .
b.Tetanospasmin:
• A neurotoxin responsible for the symptoms of tetanus
• All C. tetani strains produce a toxin with identical immunological and pharmacological properties .
• The toxin is heat labile, destroyed at 56 °C in 5 minutes, and is oxygen labile .
• The toxin rapidly converts to toxoid in the presence of formalin .
• Toxin action : It blocks the release of inhibitory neurotransmitters, so it produces the generalized muscular spasms characteristic of tetanus.

common type, the spasms begin in the jaw and then progress to the rest of the body.  These spasms usually last a few minutes each time and occur frequently for three to four weeks. Spasms may be so severe that bone fractures may occur.  Other symptoms may include fever, sweating, headache, trouble swallowing, high blood pressure, and a fast heart rate. Onset of symptoms is typically three to twenty-one days following infection. It may take months to recover.  About 10% of those infected die.

a tetanus toxin inactivated with formaldehyde to be immunogenic but not pathogenic. The vaccine can be formulated as simple or adsorbed tetanus vaccine, combined tetanus and killed polio vaccine, or the older (diphtheria, tetanus, pertussis) (DPT) vaccine. Side effects are rare, but if they do occur, include fever, pain (sometimes long lasting) at the injection site, unexplained crying in infants, and irritability in older children or adults. Severe reactions are extremely rare and include anaphylaxis, seizures and encephalopathy. All infants are recommended to receive the vaccine at 2, 4, 6, and 15 months of age . A fifth booster dose should be given at 4–6 years of age. After that, it should be given every 10 years. However, if a bite, scratch, or puncture occurs more than five years after the last dose of vaccine, the patients should receive another dose of vaccine.

at 37°C.
• C tetani produces colonies with complete haemolysis on blood agar and swarming • Has terminal spherical spores
• Produces indole, but does not produce acid from glucose.
• Isolation of C.tetani must be confirmed by production of toxin and its neutralization by specific antitoxin

toxin can cause a severe flaccid paralytic disease in humans and other animals and is the most potent toxin known to humankind, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans.

designated A, B, C1, D, E, F, and G) .
• Types A, B, E and F are the most toxic for humans.
• Type A is the most potent exotoxin known (10 ng can kill a normal adult).
• Toxin is heat-labile

• Toxin binds to neuromuscular junctions of parasympathetic nerves and interferes with acetylcholine release, causing flaccid muscle paralysis.

3 ways:
Food poisoning :
• The botulinum toxin is ingested with food(specially home canned) in which spores have germinated and the organism has grown.

2.Wound botulism
• a rare disease, results from C. botulinum growing in the necrotic tissue of wound.

3. Infant botulism : germination of spores in the GIT.
• At its site of entry into the body , spores vegetate , cells replicate and release toxin, the toxin passes into the blood stream .
• Toxin binds to neuromuscular junctions of parasympathetic nerves and interferes with acetylcholine release, causing flaccid muscle paralysis.

food will inactivate the toxin, as it is heat-labile .
• Food containers that bulge may contain gas produced by C. botulinum and should not be opened or tasted.
• A multivalent toxoid produces good protective antibiody response
• Its use is unjustified due to the infrequency of the disease.

• Fecal samples are the best specimens for detecting toxin in food poisoning or infant botulism .
• Toxin is usually detected by its lethal effect in mice coupled with neutralization of this effect by specific antisera.