Infection in BC Infection Infections in BC.ppt

Infection in BC Infection Infections in BC

1. WOUND SEPSIS
Gas gangrene & Tetanus

2. Clostridium
• Genus includes all anaerobic, gram-positive bacilli
capable of forming endospores (some aerotolerant)
• Organisms are ubiquitous, present in soil, water, and
sewage and as part of normal gut flora
• Human diseases and associated pathogen(s):
• Tetanus - C. tetani
• Botulism - C. botulinum
• Gas gangrene - C. perfringens

3. • Large, rectangular gram-
positive bacillus
• Non motile, however, rapidly
spreads on laboratory media
• Grows rapidly in tissues, is
hemolytic and metabolically
active
• Produces four major lethal
toxins that are used to subdivide
isolates into five types (A-E)
Clostridium perfringens

4. Bacterial Spores

5. Gas gangrene due to injury

6. Clostridial gas gangrene 10 hours post amputation

7. Human gas gangrene caused by Clostridium perfringens

8. Epidemiology
• Type A commonly inhabits the intestinal tract of animals
and humans; widely found in contaminated water
and soil
• Forms spores under adverse environmental conditions
that can survive for prolonged periods
• Types B to E do not survive in soil, but rather in gut of
animals and sometimes humans
• Type A causes gas gangrene, soft tissue infections and
food poisoning while type C causes necrotizing
enteritis

9. Lethal Toxins of C. perfringens
1)Alpha - produced by all types; is a lecithinase that
lyses erythrocytes, platelets, leukocytes and
endothelial cells
•Increases vascular permeability; massive
haemolysis bleeding, tissue destruction, myocardial
dysfunction
2)Beta - responsible for causing necrotic lesions in
necrotizing enteritis
3)Epsilon - protein activated by trypsin that increases
vascular permeability of gastrointestinal
wall
4) Iota - necrotic activity/increases vascular permeability

10. Gas gangrene is an infectious Gas gangrene is an infectious
disease emergency. Rapid onset disease emergency. Rapid onset
of myonecrosis, gas production of myonecrosis, gas production
and sepsis are the hallmarks of and sepsis are the hallmarks of
this disease. this disease.

11. 
Traumatic gas gangreneTraumatic gas gangrene (most (most
common infection type) occurs through common infection type) occurs through
direct inoculation of a contaminated direct inoculation of a contaminated
ischemic wound and occasionally after a ischemic wound and occasionally after a
surgical procedure. surgical procedure. Clostridium Clostridium
perfringensperfringens causes 80-95% of cases of causes 80-95% of cases of
gas gangrene gas gangrene

Spontaneous gas gangreneSpontaneous gas gangrene is caused is caused
by hematogenous spread of toxin-by hematogenous spread of toxin-
producing bacteria (often in patients producing bacteria (often in patients
who are immunocompromised or those who are immunocompromised or those
with diabetes). with diabetes).

12. Clinical Syndromes
• Myonecrosis (gas gangrene) - extensive muscle necrosis,
shock, renal failure, death; 2 days
• Soft tissue infections - similar to myonecrosis except no
muscle involvement
• Food poisoning - 8 to 24 hours, self-limiting
• Necrotizing enteritis
• Septicemia

13. 
Clostridium septicumClostridium septicum is the most is the most
common causative organism of common causative organism of
spontaneous gas gangrene. Exotoxin, spontaneous gas gangrene. Exotoxin,
not bacterial proliferation, is not bacterial proliferation, is
responsible for rapid spread of responsible for rapid spread of
infection. Exotoxin causes muscle infection. Exotoxin causes muscle
destruction and creates an anaerobic destruction and creates an anaerobic
environment conducive to further environment conducive to further
bacilli growth. Products of tissue bacilli growth. Products of tissue
breakdown (eg, creatine breakdown (eg, creatine
phosphokinase, myoglobin, potassium) phosphokinase, myoglobin, potassium)
cause secondary toxicity. cause secondary toxicity.

14. 
History: History:

Incubation period usually is less than 3 Incubation period usually is less than 3
days with rapid onset of symptoms.days with rapid onset of symptoms.

Infection can advance as much as Infection can advance as much as
1in/h.1in/h.

Pain commonly is out of proportion to Pain commonly is out of proportion to
physical findings.physical findings.

Progression to toxemia and shock can Progression to toxemia and shock can
be rapid.be rapid.

15. 
PHYSICALPHYSICAL

Local findingsLocal findings

CrepitanceCrepitance

Brawny edemaBrawny edema

Foul-smelling or sweet-smelling Foul-smelling or sweet-smelling
serosanguinous dischargeserosanguinous discharge

Brown or bronze skin discolourationBrown or bronze skin discolouration

Cutaneous bullaeCutaneous bullae

Ischemic-appearing muscle tissueIschemic-appearing muscle tissue

16. 
PHYSICALPHYSICAL

Systemic findingsSystemic findings

Fever, often low grade early in the Fever, often low grade early in the
diseasedisease

Tachycardia out of proportion to Tachycardia out of proportion to
feverfever

Altered level of consciousnessAltered level of consciousness

17. Risk factorsRisk factors

Patients who develop non traumatic gas Patients who develop non traumatic gas
gangrene usually are immuno gangrene usually are immuno
compromised.compromised.

Gas gangrene is associated with Gas gangrene is associated with
hematologic and gastrointestinal hematologic and gastrointestinal
malignancies.malignancies.

Additional risk factors include diabetes Additional risk factors include diabetes
mellitus, peripheral vascular disease, drug mellitus, peripheral vascular disease, drug
abuse and alcoholism.abuse and alcoholism.

  

18. Lab Studies:
Gram stain of bullae fluid or muscle tissue: Pleomorphic,
gram-positive bacilli with a paucity of leukocytes are
considered diagnostic.
CBC may reveal evidence of haemolysis and anemia
secondary to release of toxins.
Liver function tests: Hyperbilirubinemia
Electrolytes: Hyperkalemia can result from cell breakdown.
Renal panel: Kidney dysfunction
Arterial blood gas: Metabolic acidosis.
Coagulation panel: Coagulopathy and thrombocytopenia
 Myoglobin: Myoglobinemia and myoglobinuria

19. Prehospital Care Prehospital Care

OxygenationOxygenation

Intravenous (IV) fluidsIntravenous (IV) fluids

Rapid stabilization of patient Rapid stabilization of patient
because the disease may because the disease may
progress rapidlyprogress rapidly

20. Emergency Department Care: Emergency Department Care:

Resuscitation, supplemental oxygen and Resuscitation, supplemental oxygen and
aggressive volume expansion may be aggressive volume expansion may be
indicated.indicated.

Use vasoconstrictors only if absolutely Use vasoconstrictors only if absolutely
necessary; they can decrease perfusion necessary; they can decrease perfusion
to already ischemic tissue.to already ischemic tissue.

Administer antibiotics.( Sod Penicillin, Administer antibiotics.( Sod Penicillin,
Clindamycin, Metronidazole, Ceftriaxone)Clindamycin, Metronidazole, Ceftriaxone)

21. Emergency Department Care: Emergency Department Care:

Tetanus toxoid and immuno globulin Tetanus toxoid and immuno globulin
may be administered if indicated.may be administered if indicated.

Surgical debridement is the definitive Surgical debridement is the definitive
treatment.treatment.

Hyperbaric OxygenHyperbaric Oxygen

22. Clostridium tetani
• Small, motile terminal spore-forming bacillus
• Difficult to grow and identify because it is extremely
sensitive to oxygen toxicity and relatively
inactive metabolically

23. Pathogenesis
• Produces two toxins:
1. Tetanolysin - oxygen-labile hemolysin
2. Tetanospasmin - produced during stationary
phase of growth and released when the cell is
lysed
• A-B toxin synthesized as single peptide
and cleaved protease
• Carboxy-terminus of B chain binds
receptor on neuronal
membranes
• A chain internalized and moves to CNS

24. Tetanospasmin
• Acts by blocking the release of neurotransmitters for
inhibitory synapses, thus causing excitatory
synaptic activity to be unregulated (spastic
paralysis)
• Toxin binding is irreversible

25. Clinical Syndromes
• Generalized tetanus - involvement of masseter
muscles (lockjaw)
• Early signs include drooling, sweating,
irritability and persistent back spasms
• Localized tetanus - disease confined to musculature at
site of primary infection;
• Neonatal tetanus

26. No laboratory tests is specific
Diagnosis is clinical in presence of trismus,
dysphagia, generalized muscular rigidity, and/or
spasm.
Laboratory studies may demonstrate a moderate
peripheral leukocytosis.
Cerebral Spinal Fluid (CSF) studies usually are
within normal limits
Work upWork up

27. TreatmentTreatment

Treatment of muscle spasm, prevention Treatment of muscle spasm, prevention
of respiratory and metabolic of respiratory and metabolic
complications, neutralization of complications, neutralization of
circulating toxin to prevent the continued circulating toxin to prevent the continued
spread and elimination of the source. spread and elimination of the source.

Intubation / TracheostomyIntubation / Tracheostomy

Wound debridementWound debridement

NutritionNutrition

28. Treatment
•Metronidazole, Sod Penicillin
• Passive immunization with human tetanus
immunoglobulin
• Toxin bound to nerve endings is protected from
antibodies, thus must treat symptomatically until normal
regulation of synaptic transmission is restored
• Vaccination with tetanus toxoid vaccine
• Toxoid vaccine given in three doses and booster every
ten years

29. Risus Sardonicus - tetanus