Download Free Medical ANAEROBIC BACTERIA PowerPoint Presentation

ANAEROBIC BACTERIA PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Anaerobic Bacteria, which is titled "ANAEROBIC BACTERIA", to know about anaerobic bacteria, a micrbe that can only grow under anarobic condition.

Tags : Anaerobic Bacteria, micrbe, anarobic condition

Published on : Jul 01, 2021 | Views : 3650 | Downloads : 11

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

ANAEROBIC BACTERIA Dr- Fawzia Al-otaibi
Slide 2-

DEFENITION A MICRBE THAT CAN ONLY GROW UNDER ANAROBIC CONDITION SENSETIVE TO metronidazole (MTZ) FAIL TO GROW IN AIR 10 % O2
Slide 3-

ppt slide no 3 content not found
Slide 4-

Why can’t anaerobic bacteria survive in oxygen? The presence of oxygen leads to the production in cells of the superoxide radical (a negatively charged O2 molecule). Normally, the superoxide anion is lethal enough to kill almost any organism. Aerobic organisms and facultative anaerobes have the enzymes superoxide dismutase and catalase. These enzymes work together to convert superoxide to oxygen and hydrogen peroxide
Slide 5-

CLASSIFICATION A -NON SPORE FORMINGN {MOR COMMN} B - SPORE FORMING
Slide 6-

A - NON SPORING A –GRAM NEGATIVE BACILLI bacteroides fragilis ( resistant to penicillin) Prevotella spp Leptotricha buccalis fusobacterium spp f.nucleatum Viellonella sp. GRAM NEGATIVE COCCi
Slide 7-

B –GRAME POSITIVE COCCI Peptococci Peptostreptococci C –GRAME POSITIVE BACILLI Propionobacterium propionicum ,p.acne Bifidobacterium Euobacterium LACTOBACILLUS Actinomyces israelii D-MICROAEROPHILIC STREPT.
Slide 8-

BACTEROIDES GROUP = B. FRAGILIS, B. VULGARIS, B.THETAIOTAMICRON, B. UNIFORMIS ACCOUNT FOR 1/3 OF ALL ISOLATES RESISTANT TO 20% BILE RESISTANT TO MANY ANTIBIOTICS PENICILLIN, KANAMYCIN, VANCOMYCIN, COLISTIN – AND MANY MORE NO PIGMENTATION OF COLONIES OR FLUORESCENCE
Slide 9-

BACTEROIDES OTHER SP BACTEROIDES SPECIES OTHER THAN B. FRAGILIS GROUP BILE SENSITIVE RESISTANT TO KANAMYCIN ONLY SOME PIGMENTED
Slide 10-

SPORE FORMING GRAME POSITIVE BACILLI CL .perfringens CL .Septicum CL .novyi CL .Histolyticum CL .Difficile CL .Tetani CL .Botulinum
Slide 11-

IMPORTANCE Dominate the indigenous flora (colonization resistance) Commonly found in infection Easy to overlook special precautions Slow growth Mixed infection Difficult treatment
Slide 12-

PRESENCE AS NORMAL FLORA Skin Nose Mouth, throat Stomach Large intestine >1011 / gram colonic contents Vagina Endocervix Urethra
Slide 13-

MODEFIED BY Pathophysiologic states Antimicrobial agents ,H-Blockers ,antacids Hormonal changes Age
Slide 14-

EPIDEMIOLOGY Almost all infections are indigenous except Tetanus Infant ,wound botulism Gas gangrene { some cases } Bites C .difficile {nosocomial }
Slide 15-

HABITAT : These organism are normal flora in: Oropharynx Provetella melaninogenicus. Fusobacteria, Veillonella Gastrointestinal tract Found mainly in the large colon in large numbers Total number of anaerobes = 10 11 While all aerobes (including E. coli) = 10 4 examples are (1) Bacteroides fragilis Bifidobacterium species Female genital tract (mainly in the vagina)
Slide 16-

CHARACTER OF ANAEROBIC INFECTION Suppuration Abscess formation Tissue destruction{gangrene} Septic thrombophlebitis Some have unique pathology Actinomycosis Psedomembranous colitis Gas gangrene
Slide 17-

PREDISPOSING FACTORS Low O tension {Eh} Trauma, dead tissue , deep wound Impaired blood supply Presence of other organisms Foreign bodies
Slide 18-

ppt slide no 18 content not found
Slide 19-

ppt slide no 19 content not found
Slide 20-

A 43-year-old man with surgically proved pyogenic brain abscess in the right basal ganglion secondary to Eubacterium lentum (obligate anaerobe) infection. Axial contrast-enhanced T1-weighted MR image shows a ring-shaped cystic lesion and surrounding edema.
Slide 21-

Predisposing factors Antibiotic therapy Neoplasm Trauma Cholecystitis Obstruction Ulceration Diabetes mellitus Pylephlebitis Diverticula formation
Slide 22-

INFECTIONS BEGIN : DISRUPTION OF BARRIERS TRAUMA OPERATIONS CANCEROUS INVASION OF TISSUES DISRUPTION OF BLOOD SUPPLY DROPS OXYGEN CONTENT OF TISSUE DECREASE IN Eh POTENTIAL TISSUE NECROSIS
Slide 23-

LABORATORY DIAGNOSIS: When anaerobic infection is suspected; a) Specimens have to be collected from the site containing necrotic tissue. b) Pus is better than swabs. c) Specimens has to be send to the laboratory within 1/2 hour why? d) Fluid media like cooked meat broth are the best culture media. e) Specimens have to incubated anaerobically for 48 hours.
Slide 24-

ppt slide no 24 content not found
Slide 25-

ppt slide no 25 content not found
Slide 26-

ACTINOMYCOSIS Actinomyces are branching anaerobic or microaerophilic Gram positive bacilli Source of the infection is normal flora and the host usually normal host Primary site of the infection is mouth, lung, appendix, uterus with IUD (chronic infection) Infection can spread to the brain, liver, bone and blood Diagnosis by Gram stain with sulfur granules and growth of molar tooth colonies Treatment penicillin, clindamycin or tetracycline
Slide 27-

ppt slide no 27 content not found
Slide 28-

TREATMENT: Bacteroides fragilis is always resistant to penicillin. But penicillin can he used for other anaerobes Flagyl (metronidazole) is the drug of choice. Clindamycin can also be used.
Slide 29-

TETANUS TRIMUS LOCKJAW 1884 Strict toxigenic disease
Slide 30-

ppt slide no 30 content not found
Slide 31-

ppt slide no 31 content not found
Slide 32-

EPIDEMIOLOGY 1 Million/year > 60 yr .injection of drugs {young} ½ due to neonatal tetanus Cryptogenic t. {23%} Disease of non-immunized animals and humans {toxoid}
Slide 33-

SOURCE Animals feaces {horses} ,soil Contaminated wound {minor} Compound fracture Narcotic addicts Unsterile injections Burns , bites ,avulsions Umbilical stump Face , neck , upper extremities wounds are more dangerous
Slide 34-

TETANUS PATHOGENESIS EXTOXIN {TETANOSPASMIN} Presynaptic terminals of LMN Inhibitory impulses to MNs Persistent tonic spasm Clinical picture Generalized Localized Cephalic Neonatal{ >90%}mortality IP 3-21 days
Slide 35-

ppt slide no 35 content not found
Slide 36-

ppt slide no 36 content not found
Slide 37-

ppt slide no 37 content not found
Slide 38-

ppt slide no 38 content not found
Slide 39-

TRATMENT Supportive Airway Muscle relaxant Wound care Antitoxin Antibiotics :MTZ , PG TIG {500 UNITS} PREVENTION Complete active childhood immunization Appropriate wound management Type of wound Immunization history DIAGNOSIS Clinical Laboratory {minor role}
Slide 40-

C. Perfringens {C.Welchii} Histotoxic clostridia Gas gangrene Food Poisoning
Slide 41-

ppt slide no 41 content not found
Slide 42-

ppt slide no 42 content not found
Slide 43-

NATURAL HABITATS Soil and intestinal tracts of animals and humans { 103 108 } Widespread occurrence Vagina of 1-9 % healthy women
Slide 44-

CLINICAL SIGNIFICANCE Species most commonly isolated from clinical specimens Many clinical settings ranging from :- Simple contamination of wounds – traumatic or non traumatic myonecrosis C. Cellulitis Intra-abdominal sepsis Gangrenous cholecystitis Post-abortion infections – septicemia Bacteremia Brain abscess
Slide 45-

Gas gangrene Toxin mediated breakdown of muscle tissue Rapid progression { Uterus } Liquefactive necrosis of muscle , gas formation , toxemia Fulminant septicemia Intravascular hemolysis Hemoglobinuria Blood cultures positive in 15 % of patients
Slide 46-

ppt slide no 46 content not found
Slide 47-

ppt slide no 47 content not found
Slide 48-

ppt slide no 48 content not found
Slide 49-

ppt slide no 49 content not found
Slide 50-

PATHOGENESIS 5 – Toxins [ A – E ] Phospholipase C { alpha toxin } Acts on membranes of muscle cells , leukocytes and platelets . Play major role in the pathogenesis of C. myonecrosis Has necrotizing activity Other toxins :- collagenase , proteinase , DNAs
Slide 51-

Clinical picture Acute progressive pain , edema , skin discoloration Systemic – fever , tachycardia , hypotension , renal failure , crepitus , pulmonary edema , death
Slide 52-

ETIOLOGY C.perfringens { 80% } C.Novyi C.Septicum C.Histolyticum
Slide 53-

DIAGNOSIS CLINICAL SURGICAL MICRO. Gram stain :- G PB , absent leukocytes Culture { aerobic and anaerobic } Exudate , aspirates Tissue Blood Nagler reaction
Slide 54-

FOOD POISONING One of most common bacterial causes of food –borne illness Sporadic cases and outbreaks Almost all due to type A Improperly cooked meat or meat product Ingestion of vegetative cells [ 108 ] Afebrile Crampy abdominal pain - diarrhea within 7-15 h Enterotoxin [ SPORULATION ] Mild illness , recovery after 2-3 days
Slide 55-

TRATMENT Early and complete surgical excision of necrotic infected tissue { most important } High dose of :- Penicillin G IV Metronidazole Clindamycin Management of shock , hemolysis , anemia
Slide 56-

C . Difficile Pseudomembranous colitis Antimicrobial associated diarrhea Hospital acquired diarrhea
Slide 57-

Epidemiology Clostridium difficile causes antibiotic associated diarrhea (AD) and more serious intestinal conditions such as colitis and pseudo membranous colitis . Overgrowth of Clostridium difficile in the colon, usually after the normal flora has been disturbed by anti microbial chemotherapy
Slide 58-

EPIDEMIOLOGY Soil Human and animal feces Hospital environment {Reservoirs} Spores acquired – Environment Fecal – oral { colonized persons } Intestinal colonization rate Healthy neonates , young infant [ 50 %] Children > 2yrs , adults {3 % }
Slide 59-

CLINICAL PICTURE Mild diarrhea , asymptomatic carriage – Toxic megacolon ,bowel perforation and death Pseudomembranous colitis Bloody diarrhea , abdominal cramps, Fever , systemic toxicity Colonic mucosa – yellowish plaques Sever disease – neutropenic , inflammatory bowel disease .
Slide 60-

Control Measures Proper hand washing {contact precautions} Limiting use of antimicrobial agents Isolation of patients with diarrhea Disinfection of pt. rooms
Slide 61-

ppt slide no 61 content not found
Slide 62-

ppt slide no 62 content not found
Slide 63-

TREATMENT Discontinue antimicrobial therapy { clinical significant diarrhea or colitis Antimicrobial therapy : severe toxicity , persistent diarrhea Metronidazole for 7-10 days , oral , IV Oral vancomycin : {emergence of VRE } 10-20 % relapse rate Antimotility drugs : contraindicated
Slide 64-

Risk Factors Exposure to organisms Disturbed normal gut flora {proliferate – toxin} Repeated enema Prolonged NG tube GI surgery Bowel stasis Antimicrobials : penicillins , clindamycin , Cephalosporins
Slide 65-

PATHOGENESIS TOXINS TOXIN A [ Enterotoxin ] TOXIN B [ Cytotoxin ] , more potent Most strains produce both or no toxins
Slide 66-

DIAGNOSIS Endoscopy : pseudomembranes and Hyperemic rectal mucosa Stool : toxins { EIA } , Cell culture Confirm toxigenic strains Isolation of C. Difficile { not diagnostic } PCR
Slide 67-

C.BOTULINUM BOTULISM
Slide 68-

TRANSMISSION SPORES VEGETABLES , MEATS ,FISH CANNED FOOD PREFORMED TOXIN
Slide 69-

PATHOGENESIS TOXIN (PHAGE) MOST TOXIC SUBSTANCE GUT BLOOD PERIPHERAL NERVE SYNAPSES BLOKS RELEASE OF ACETYLCHLINE FLACCID PARALYSIS
Slide 70-

CLINICAL DESCENDING PARALYSIS DIPLOPIA DYSPHAGIA RESPIRATORY MUSCLE FAILURE NO FEVER WOUND , INFANT BOTULISM ( honey )
Slide 71-

ppt slide no 71 content not found
Slide 72-

Diagnosis : clinical (TOXIN ,FOOD SERUM ) PREVENTION STERILIZATION OF CANNED FOOD TREATMENT ANTITOXIN A , B ,E RESPIRATORY SUPPORT