GRAM POSITIVE RODS · 2 --Bacillus cereus: no capsule • food poisoning by enterotoxin Cases in...
Transcript of GRAM POSITIVE RODS · 2 --Bacillus cereus: no capsule • food poisoning by enterotoxin Cases in...
GRAM POSITIVERODS
Dr Hamed Al-Zoubi
Ass. Prof. / Department of Microbiology
Bacterial infections of GIT
• Corynebacterium
• Bacillus cereus and anthracis
• Clostridium
Corynebacterium
• Aerobic, non motile GPR, club shape, Chinese letters L V shapes
• 1 - C. diphtheria
• 2 - Others: low pathogenic ability e.g diphtheroids (skin, urogenital and commensals)
Corynebacterium
• C. diphtheria:
• Virulence and pathogenesis:
• Local invasion
• heat stable exotoxin
➢bacteriophage tox gene
➢A and B parts:
➢Inhibit EF2 and protein synthesis leading to cell necrosis and death
• Clinically:• Transmission by respiratory route , skin contact
• Incubation 1-10 days, infectivity 2-4 weeks if untreated or 4 days if treated
1 Local inflammation in nasal, oral, pharyngeal, laryngeal areas <thick adherent green psuedomembrane < airway obstructionand death
2 systemic:
• Toxin tropism to brain, heart and adrenal glands
• Paralysis, heart failure low platelets
6
This child has diphtheria resulting in a thick gray
coating over back of throat. This coating can
eventually expand down through airway and, if not
treated, the child could die from suffocation CDC
• Diagnosis:
➢Swab:Not from the membrane.. and tell the lab:
• Blood agar
• Loeffler medium for chromogenic granules
• Tensdale agar: has K tellurtite medium• reduction by bacteria
• tellurium precipitation
• black colonies
• Toxin detection ELEK test or PCR
• Treatment: start ASAP
antitoxin, penicillin plus gentamicin
• Prevention: toxoid vaccine DIPHTHERIA TETANUS AND PERTUSIS ( DTP) 2m,3m,4m,1y,6y
• BACILLUS: GPR, aerobic, spore centrally located
• 1- Anthracis• Non motile, glutamic acid capsule
• Plasmid toxin: increase vascular permeability and shock
• Zoonosis
• Inhalation: hemorrhagic pneumonia and sepsis
• Ingestion: bloody diarrhea and death
• skin scratch: vesicles that rupture leaving malignant black eschar
•Motile but
2 --Bacillus cereus :no capsule
• food poisoning by enterotoxin
✓Cases in which vomiting, occurring within 1-6 h of ingestion, is the main symptom.
• Caused by preformed toxin, which is a low molecular weight, heat- and acid-stable toxin that can withstand intestinal proteolytic enzymes (similar to s. aureus).
✓A diarrhoeal form of food poisoning, occurring 8-24 h after ingestion of spores
• caused by heat labile enterotoxins formed in the intestine.
• Bacillus diagnosis:• blood agar: (medusa head) grey wavy with
projections
•Gram stain:
String of pearls
Appears G neg
in old culture
•TREATMENT
•Anthrax: penicillin
•Cereus:
Symptomatic : fluids
If antibiotic needed: Cindamycin or erythromycin
•Prevention : Human vaccines for Anthrax
Cellualr antigen from culture supernatan
Anthrax genetically engineered antigen
Clostridi
um• Characteristics:
• Gram positive anaerobic rods (appear as gram negative in old cultures)
• Spore forming, dust water soil...
• Anaerobics
• May appear G neg in old culture
• C. Botulinum and Tetanus : neurotoxins
• C. Perfringens and Difficile: enterotoxins
Clostridium botulinum• Seven main types A-G: A, B and E are the commonest
• Each secretes antigenically distinct but functionally similar toxin (very potent)
• The toxin (heat labile):
1. Preformed in food that is badly preserved and processed (hygiene and heat) > food borne botulism (canned, smoked..)
2. Spores ingestion e.g Honey > germinate in the gut > toxin production > infantile or (intestinal) botulism
Clostridium
botulinumSpores:
• Oval and subterminal
Clostridium
botulinum
• Pathogenesis:
Neurotoxin production > stomach
absorption > circulation > neuromuscular
junction (NMJ) > inhibition of acetylcholine
release at the NMJ > flaccid descending
motor paralysis
Clostridium botulinum• Clinically (food borne and wound botulism ):
✓ Incubation period 12-48hrs in food borne
✓ Early: nausea, vomiting, weakness, dizziness but no fever
✓ Late: double vision, difficulty in swallowing, speaking and respiratory failure (descending motor paralysis)
• Infantile: weakness, altered cry, loss of appetite , loss of head control, Floppy child syndrome and sudden infant death syndrome
Clostridium
botulinum• Diagnosis:
• Isolating the organism or toxin from gastric aspirates, bloodorstool
• Detecting Toxin in the food
• n.b: toxin-antitoxin approach
• Alert the lab
Clostridium
botulinum✓ Treatment:
• Gastric wash
• Antitoxin (A, B, E)
• Supportive: ICU and respiratory support, wound cleaning and debridement
✓ Prevention:
• Proper cooking and heating of food?
• Avoid suspicious canned food
• Proper processing, preservation and canning of food
• vaccine
Clostridium perfringens:• It causes gas gangrene and food poisoning (HL)
• subterminal spores
• Toxins:
• Alpha toxin (phospholipase C, lecithinase): Degrades lecithin in mammalian cell membrane leading to cell lysis
• Other toxins: collagenase, proteinase, hyaluronidase
• Identification: Nagler agar: based on neutralisation of alpha toxin by a specific antitoxin
Clostridium tetani
• Widely distributed in theenvironment especially in the soil
• Gram positive, motile anaerobic rods (GNR in old culture)
• Spore forming: roundterminal (drumstick, tennisracket)
• Not commonly seen due to vaccine(DTP)
Clostridium tetani• Not commonly seen due to vaccine (DTP)
• Produce two plasmid coded exotoxins:
1. Tetnospasmin:
• Neurotoxin
• Heavy (binding ) and light chain (neurotoxic part)
• One antigenic toxin
2. Tetanolysin (haemolysin): pathogenesis not clearly known but ? RBCs haemolysis
➢ produced when spores germinate and vegetative cells grow in necrotic tissues. The organism multiplies locally and symptoms appear remote from the infection site
Clostridium tetani• Pathogenesis: Spastic paralysis
inhibition of the inhibitory
neurotransmitter gamma aminobutyric
acid (GABA) > loss of
inhibitory action on
motor and autonomic neurons> uncontrolled muscle contractions
Clostridium tetani /
pathogenesis
Clostridium tetani✓ Clinically (tetanus):
• Mode of transmission:
• Spores > wound contamination(low oxygen) > germination to bacilli that secrete the toxins
• Incubation period: 3days – 3 weeks
✓ Source:
• Infected wound and abscesses (~65%), eg, wood ormetal, thorns...)
• Chronic skin ulcers are the source in approximately 5% ofcases
• in the remainder of cases, no obvious source is identified (cryptogenic)
Clostridium tetani1. Local:
Muscles spasm and pain at/near injury site
2. Generalised:
• Trismus (locked jaw): may bite the tongue
• Opisthotonus: flexion and adduction of thearms, clenching of the fists, extension ofthe lower extremities
• spasm is stimulated by noise and light
• the patient is afebrile, has intact sensation
• Meningitis, seizures and coma
Clostridium tetani
Clostridium tetaniDiagnosis:
1. Clinical (very useful):
✓ Sign and symptoms
✓ Vaccination history
✓ History of a trauma
2. Wound smear staining: may help
3. Culture
4. Toxin-antitoxin test in mice
Clostridium tetani• Treatment:• Wound debridement
• Treat in In a dark quite room
• Sedation, Muscle relaxant (e.g diazepam) and artificialventilation
• Antibiotics:
✓ may be given to kill any vegetative forms
✓ metronidazole
• Tetanus immunoglobulin TIG
• Vaccination:
• Toxoid vaccine: formalin inactivated
• VACCINE as per vaccination program and a booster every 10 years
C. difficile• Secrete toxins A (enterotoxin) and B (cytotoxin).
> exotoxins that cause inflammation and mucosal damage.
• Most common cause of nosocomial diarrhea.
• Colonizes the colon of up to 3% of healthy adults and it increases to 15 – 25% of debilitated and antibiotic-treated hospitalized adults.
• present in environment.
• Spread primarily on hands of HCW.
Risk factors1. Antimicrobial exposure
2. Acquisition of C. difficile
3. Advanced age
4. Underlying illness
5. Immunosuppression
6. Tube feeds / Enema..
All are Modifiable but not
3. 1 & 2 are major
Clinical picture and Complications• Asymptomatic colonization
• Diarrhea (mild to severe)
• Colitis +/- pseudomembranes (endoscopy)
• Toxic megacolon (radiology)
• Colonic perforation/peritonitis
• Sepsis and acute abdomen withoutdiarrhea
Diagnosis• Clinically
• Enzyme-linked immunosorbentassay (ELISA) for toxins A and B
• Endoscopy (pseudomembranouscolitis)
Management• Resuscitate the patient; fluids, electrolytes
• Isolate the patient: Private room or cohorting
• Stop antibiotics and the just in case ones.
• Daily monitoring.
• ANTIBIOTICS: metronidazole / and or vancomycin
The End