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Gas gangrene

الكلية كلية الطب     القسم  الاحياء المجهرية     المرحلة 3
أستاذ المادة حبيب صاحب نهر المزيداوي       4/8/2011 3:29:06 PM

Gas Gangrene and Related Clostridial Wound Infections:
Clinical Manifestations: Patients may present with a wound infection. Severity varies from invasion of live tissue with systemic toxemia to relatively benign superficial contamination of already necrotic tissue.


Structure: The clostridia that cause gas gangrene are anaerobic, spore-forming bacilli, but some species may not readily sporulate, e.g., C perfringens.


Classification and Antigenic Types:
Clostridial wound infections are typically polymicrobic. The primary pathogens are various clostridial species, including C perfringens, C novyi, C septicum, and others.


Pathogenesis: Wounds are contaminated by clostridia from the environment or the host s normal flora. The anaerobic tissue environment facilitates replication of clostridia and secretion of toxins.


Host Defenses: Host defenses are essentially absent. There is little, if any, innate immunity.


Epidemiology: Clostridial wound infections are found worldwide. Clostridia are ubiquitous in the soil and in the normal microbial flora of humans and animals.


Diagnosis: These infections are diagnosed by recognition of a characteristic lesion coupled with tissue Gram stains and bacterial culture.


Control: und infections are controlled by administration of antimicrobial agents (e.g., penicillin, chloramphenicol) coupled with tissue debridement (for more severe forms of clostridial wound infections).


Tetanus and Clostridium Tetani:
Clinical Manifestations: Tetanus is characterized by twitching of muscles around a wound, pain in neck and jaw muscles (trismus), and around the wound. Patients have no fever, but sweat profusely and exhibit muscle rigidity and spasms.


Structure: These organisms are bacilli with terminal spores.


Classification and Antigenic Types: C tetani is the only species. There are no serotypes.


Pathogenesis: The infection is initiated as a result of contamination of a wound with C tetani. The anaerobic tissue environment facilitates C tetani replication and secretion of exotoxins. A spasmogenic toxin, tetanospasmin, fixes to inhibitory neurons and blocks the release of neurotransmitters, glycine and gamma-aminobutyric acid.


Host Defenses: Host defenses are essentially absent. There is little, if any, inate immunity and the disease does not produce immunity in the patient. Active immunity follows vaccination with tetanus toxoid.


Epidemiology: C tetani is found worldwide. Ubiquitous in soil, it is occasionally found in intestinal flora of humans and animals.


Diagnosis: Diagnosis is primarily by the clinical symptoms (above). The wound may not be obvious. Furthermore, C tetani is recovered from only one-third of all implicated wounds.


Control: The administration of tetanus toxoid is a preventive measure. C tetani infection is treated with antimicrobial agents (metronidazole or penicillin) and by local wound debridement. Other measures include tetanus immunoglobulin and supportive therapy.


المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .