MICROBIOLOGY PPT LECTURE NOTES | Karya Tulis Ilmiah

(1)

(2)

soil

, it is occasionally

found in

intestinal flora of humans

and animals



C.

tetani

is the cause of

tetanus

,or

lockjaw

. When spores are introduced

into wounds by contaminated soil or

foreign objects such as nails or glass

(7)

BIOCHEMICAL CHARACTERISTICS

 MorphologyMorphology: long and slender; : long and slender; peritrichous flagella,no capsule, peritrichous flagella,no capsule,

terminal located round

terminal located round

spore(drum-stick apperance),

its diameter greater than

vegetative cell

vegetative cell..

 CultureCulture:obligate anaerobic; :obligate anaerobic;

Gram(+); swarming occures on Gram(+); swarming occures on

blood agar, faint hemolysis. blood agar, faint hemolysis.

 Biochemical activities:Biochemical activities:does not does not ferment any carbohydrate and

ferment any carbohydrate and proteins.

proteins.

 ResistanceResistance: tolerate boiling for : tolerate boiling for 60 min.alive several ten years in 60 min.alive several ten years in

soil. soil.

 ClassificationClassification and Antigenic and Antigenic Types:

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

There are no serotypes

2-5 x 0.3-0.5um

(8)

Pathogenicity

 No invasiveness; toxemia No invasiveness; toxemia

(exogenous infection

(exogenous infection ））

 produces two exotoxins: produces two exotoxins:

tetanolysin, and

tetanospasmin

tetanospasmin(a kind of (a kind of neurotoxin, toxicity strong)

neurotoxin, toxicity strong)

 The actions of The actions of

tetanospasmin

tetanospasmin are are

complex and involve three

components of the

nervous system:

nervous system: central central motor control

motor control, , autonomic autonomic function

function, and the , and the

neuromuscular junction neuromuscular junction..

 retrograde transport retrograde transport to (CNS)

to (CNS)

 delitescencedelitescence ：： a few a few days to several

days to several

weeks

 The two animal The two animal species most species most

susceptible to this susceptible to this

toxemia are horses toxemia are horses

and

(9)

Clostridium tetani

-

Tetanospasmin

 disseminates systemically disseminates systemically

 binds to ganglioside receptors binds to ganglioside receptors

• _{inhibitory neurones in CNS}_{inhibitory neurones in CNS}

 glycine glycine

• neurotransmitter_{neurotransmitter}

 stops nerve impulse to muscles stops nerve impulse to muscles  spastic paralysisspastic paralysis

痉挛性麻痹

 severe muscle contractions and severe muscle contractions and spasms

spasms

(10)

(11)

Clinical Manifestations

 The initial symptom is cramping and The initial symptom is cramping and

twitching of muscles around a wound. The

twitching of muscles around a wound. The

patient usually has

patient usually has no feverno fever but sweats but sweats profusely and begins to experience pain,

profusely and begins to experience pain,

especially in the area of the wound and

around the neck and jaw muscles

around the neck and jaw muscles (trismus)(trismus)

.

 Portions of the body may become extremely Portions of the body may become extremely

rigid, and

rigid, and opisthotonosopisthotonos

角弓反张

(a spasm (a spasm in which the head and heels are bent

in which the head and heels are bent

backward and the body bowed forward) is

common.

 Complications include fractures, bowel Complications include fractures, bowel

impaction, intramuscular hematoma, muscle

ruptures, and pulmonary, renal, and cardiac

ruptures, and pulmonary, renal, and cardiac

problems

(12)

Clinical Manifestations

DISEASE

DISEASE _{CLINCAL MANIFESTATIONSA}_{CLINCAL MANIFESTATIONSA}

Generalized

Generalized Involvement of bulbar and paraspinal Involvement of bulbar and paraspinal

muscles(trismus or lockjaw, risus sardonicus,

difficulty swallowing, irritability,

opisthotonos);involvement of autonomic

nervous system(sweating, hyper thermia,

nervous system(sweating, hyper thermia,

cardiac arrhythmias, fluctuations in blood

pressure)

Cephalic

Cephalic Primary infection in head,particularly Primary infection in head,particularly

ear;isolated or combined involvement of cranial

nerves, particularly seventh cranial nerve; very

nerves, particularly seventh cranial nerve; very

poor prognosis

Localized

Localized Involvement of muscles in area of primary Involvement of muscles in area of primary injury; infection may precede generalized

injury; infection may precede generalized

disease; favorable prognosis

Neonatal

Neonatal Generalized disease in neonates; infection Generalized disease in neonates; infection typically originates from umbilical

typically originates from umbilical 脐带

stump;very poor prognosis in infants whose

stump;very poor prognosis in infants whose

mothers are nonimmune

(13)

(14)

Epidemiology

 1 1 million cases of tetanus occur annually in the million cases of tetanus occur annually in the

world,with a mortality rate ranging from20% to world,with a mortality rate ranging from20% to

50%. But rare in most developed countries. 50%. But rare in most developed countries.

 In some In some developing countriesdeveloping countries, tetanus is still , tetanus is still

one of the ten leading causes of death, and one of the ten leading causes of death, and

neonatal tetanus accounts for approximately neonatal tetanus accounts for approximately

one-half of the cases worldwide. one-half of the cases worldwide.

 In less developed countries, approximate In less developed countries, approximate

mortality rates remain 85% for neonatal mortality rates remain 85% for neonatal

tetanus and 50% for nonneonatal tetanus. tetanus and 50% for nonneonatal tetanus.

 In the United States, intravenous drug abusers In the United States, intravenous drug abusers

have become another population with an have become another population with an

increasing incidence of clinical tetanus increasing incidence of clinical tetanus

 In untreated tetanus, the fatality rate is In untreated tetanus, the fatality rate is 90%90%

for the newborn and

(15)

Immunity

 Humoral immunityHumoral immunity(antitoxin)(antitoxin)

 There is little, if any, inate immunity There is little, if any, inate immunity

and the disease does not produce and the disease does not produce

immunity in the patient. immunity in the patient.

 Active immunity follows vaccination Active immunity follows vaccination

with tetanus

(16)

Diagnosis

 Diagnosis is primarily by Diagnosis is primarily by the clinical the clinical

symptoms (above).

symptoms (above). The wound may not The wound may not be obvious.

be obvious.

 C tetani can be recovered from the C tetani can be recovered from the

wound in only about one-third of the

cases.

 It is important for the clinician to be It is important for the clinician to be

aware that toxigenic strains of C tetani

aware that toxigenic strains of C tetani

can grow actively in the wound of an

immunized person.

 Numerous syndromes, including Numerous syndromes, including rabies rabies

and meningitis,

and meningitis, have symptoms similar to have symptoms similar to those of tetanus and must be considered

those of tetanus and must be considered

in the differential diagnosis.

(17)

•

infant

•

DPT (diptheria, pertussis, tetanus)

•

tetanus toxoid

– antigenic_antigenic

– _{no exotoxic activity}_{no exotoxic activity}

Vaccination

(18)

Control



The offending organism must be

removed by local

debridemen

清

创术



toxoid



TAT

; Metronidazole (For more

serious wounds)



AIDS

patients may not respond

to prophylactic injections of

tetanus toxoid

(19)

C. perfringens

•

soil, fecal contamination

•

gas gangrene

–

swelling of tissues

–

gas release

(20)

Toxins

toxin

toxin Biological Biological Feature

Feature Types of ToxinsTypes of Toxins A

A BB CC DD EE



 lecithinase_{vascular permeability;}lecithinase_{vascular permeability;}; increase the ; increase the hemolytic; produces hemolytic; produces necrotizing activity necrotizing activity + + +₊ +₊ +₊ +₊ 

 Necrotizing activity, Necrotizing activity,

induces hypertension

induces hypertension

by causing release of

catecholamines.

－

－ +₊ +₊ －_－－_－



 increase the increase the

permeability of permeability of gastrointestinal wall gastrointestinal wall －－ －_－ －_－ +₊ －_－ 

 Necrotizing activity; _{increase the vascular}Necrotizing activity; _{increase the vascular}

permeability

(21)

Toxins

 Many of these toxins have lethal, Many of these toxins have lethal,

necrotizing, and hemolytic properties; necrotizing, and hemolytic properties;

 The alpha toxin produced by all types of The alpha toxin produced by all types of C. C.

perfringens,

perfringens, is a lecithinase that lyses is a lecithinase that lyses erythrocytes, platelets, leukocytes, and erythrocytes, platelets, leukocytes, and endothelial cells. And its lethal action is endothelial cells. And its lethal action is

proportionate to the rate at which it splits proportionate to the rate at which it splits

lecithin to phosphorylcholine and lecithin to phosphorylcholine and

diglyceride. diglyceride.

 The theta toxin has similar hemolytic and The theta toxin has similar hemolytic and necrotizing effects.

necrotizing effects.

 DNAase, hyaluronidase, a collagenase are DNAase, hyaluronidase, a collagenase are also produced

(22)

Enterotoxin

 Many strains of type A produce Many strains of type A produce

enterotoxin, which is a heat-labile protein enterotoxin, which is a heat-labile protein

and destroyed immediately at 100 ℃. and destroyed immediately at 100 ℃.  Trypsin treatment enhances the toxin Trypsin treatment enhances the toxin

activity threefold. activity threefold.

 The toxin is produced primarily by type A The toxin is produced primarily by type A strains but also by a few type C and D

strains but also by a few type C and D strains.

strains.

 It disrupts ion transport in the It disrupts ion transport in the

ileum(primarily) and jejunum by inserting ileum(primarily) and jejunum by inserting

into the cell membrane and altering into the cell membrane and altering

(23)

(24)

•

Tissue degrading enzymes

–

lecithinase [



toxin]

–

proteolytic enzymes

–

saccharolytic enzymes

•

Destruction of blood vessels

•

Tissue necrosis

•

Anaerobic environment created

•

Organism spreads

Pathogenesis

(25)

Without treatment death

occurs within 2 days



effective antibiotic therapy



debridement



anti-toxin

(26)

Gas gangrene

 Gas gangreneGas gangrene is a life-threatening disease with _{is a life-threatening disease with}

a poor prognosis and often fatal outcome.

 Initial trauma to host tissue damages muscle and Initial trauma to host tissue damages muscle and

impairs blood supply----lack of oxygenation

 Initial symptomsInitial symptoms : : fever fever and pain in the infected and pain in the infected

tissue.; more local tissue necrosis and systemic

toxemia. Infected muscle is discolored (purple

mottling) and edematous and produces a

mottling) and edematous and produces a foulfoul- -smelling exudate; gas

smelling exudate; gas bubblesbubbles form from the form from the products of anaerobic fermentation.

(27)

Gas gangrene



As capillary permeability increases,

the accumulation of fluid increases,

and venous return eventually is

curtailed.



As more tissue becomes involved, the

clostridia multiply within the

increasing area of dead tissue,

releasing more toxins into the local

(28)

Food poisoning

 Enterotoxin producing strainsEnterotoxin producing strains..



These bacteria are found in

mammalian

faeces and soil

.



Small numbers of the bacteria may

also be found in foods and they may

propagate rapidly to dangerous

concentrations if the food is

(29)

Food poisoning

 more than 10more than 10₈₈ vegetative cells are vegetative cells are

ingested and sporulate in the gut, the ingested and sporulate in the gut, the

toxins can act rapidly in the body, toxins can act rapidly in the body,

causing severe diarrhea in 6-18 hours, causing severe diarrhea in 6-18 hours,

dysentery, gangrene, muscle infections dysentery, gangrene, muscle infections  The action of The action of C. perfringensC. perfringens enterotoxin enterotoxin

involves marked hypersecretion in the involves marked hypersecretion in the

jejunum and ileum, with loss of fluids jejunum and ileum, with loss of fluids

(30)

Cellulitis, Fasciitis



Cellulitis, Fasciitis

 Fasciitis : a rapidly progressive, destructive Fasciitis : a rapidly progressive, destructive process in which the organisms spread

process in which the organisms spread through fascial plan es.

through fascial plan es.

 Fasciitis causes suppuration and the Fasciitis causes suppuration and the formation of gas

formation of gas

 Absense of muscle involvementAbsense of muscle involvement

(31)



Necrotizing Enteritis

 Rare, acute necrotizing process in the Rare, acute necrotizing process in the jejunum

jejunum

 Abdominal pain, bloody diarrhea, shock, and Abdominal pain, bloody diarrhea, shock, and peritonitis

peritonitis

 Mortality: 50%Mortality: 50%

 Beta-toxin-producing Beta-toxin-producing C. perfringensC. perfringens type C type C

(32)

Who is at risk?



Surgical patients

; patient after

trauma with soil contamination.



People who ingest contaminated

meat products

(without proper

refrigeration or reheating to

inactivate endotoxin)

(33)

Epidemiology



C. perfringens

type A:

the intestinal

tract of humans and animals, soil and

water contaminated with feces. forms

spores under adverse environmental

conditions and can survive for

prolonged periods.



Type B to E strains

colonize the

intestinal tract of animals and

(34)

Epidemiology



Type A

: gas gangrene, soft tissue

infections and food poisoning

(35)

•

lecithinase production

Laboratory identification

Double Hemolysis Circles

(36)

(37)

Biological Features

 AnaerobicAnaerobic

 Gram-positiveGram-positive  rod-shapedrod-shaped

 sporeformersporeformer

 produces a protein neurotoxic.produces a protein neurotoxic.  soil, sediments of lakes, ponds, soil, sediments of lakes, ponds,

decaying vegetation. decaying vegetation.

 intestinal tracts of birds, mammals intestinal tracts of birds, mammals

(38)

---A, B, C1, D, E, F, and G. ---type A. 62%

---Not all produce toxin. ---C and D not

---G plasmid encoded.

Division

(39)

---spores heat resistant. canning.

anaerobic environment ---Botulism

eating uncooked foods spores

---GI, duodenum, blood stream, neuromuscular synapses.

Transmission

(40)

---bacterial protease

---light chain,A,50 kDa; heavy chain,100kDa. ---disulfide bond.

---A potent toxin

Virulence factors

(41)

Botulinum toxin

 binds peripheral nerve receptorsbinds peripheral nerve receptors • _{acetylcholine neurotransmitter}_{acetylcholine neurotransmitter}  inhibits nerve impulses inhibits nerve impulses

 flaccid paralysisflaccid paralysis

 death death

• _respiratory_respiratory

(42)

Botulinum toxin



Bioterrorism

• not an infection_{not an infection}

• resembles a chemical attack _{resembles a chemical attack}

(43)

---4: foodborne, infant, wound, undetermined. ---Certain foods; wound not.

---Foodborne botulism, consumption. ---Infant botulism, 1976, under 12m.

---ingestion, colonize and produce toxin in the intestinal tract of infants.

honey. ---increased.

---internationally recognized.

Epidemiology

(44)

---18-36 hours:

---weakness, dizziness,dryness of the mouth.

---Nausea,vomiting.

---Neurologic features: blurred vision,

inability to swallow, difficulty in speech,

descending weakness of skeletal muscles,

respiratory paralysis.

Clinical syndromes

(45)

Botulism

(

肉毒中毒

)

 food poisoningfood poisoning • _rare_rare

• _fatal_fatal

 germination of spore germination of spore

 inadequately sterilized canned inadequately sterilized canned

food food

• home_home

(46)

Infection with

C. botulinum



Neonatal botulism

• uncommon_uncommon

• the predominant form of _{the predominant form of} botulism

botulism

• _{colonization occurs}_{colonization occurs}

 no normal flora to competeno normal flora to compete

(47)

Wounds

•

extremely rare

(48)

Immunity

---specifically neutralized, specifically neutralized, antitoxinantitoxin. . ---toxoided, make good antigens.

---toxoided, make good antigens. ---does not develop, amount toxic. ---does not develop, amount toxic.

---Repeated occurrence. ---Repeated occurrence.

---Once bound, unaffected by antitoxin. ---Once bound, unaffected by antitoxin.

---circulating toxin ,neutralized , injection of ---circulating toxin ,neutralized , injection of

antitoxin. antitoxin.

---treated immediately with antiserum. ---treated immediately with antiserum.

---multivalent multivalent

toxoid,unjustified,infrequency. toxoid,unjustified,infrequency.

experimental vaccine.

(49)

Diagnosis

---by

clinical symptoms

alone

---differentiation difficult.

---

most direct and effective:

serum or

feces.

---most sensitive and widely used:

mouse neutralization test. 48h.

(50)

Treatment

 Individuals known to have ingested food Individuals known to have ingested food with botulism should be treated

with botulism should be treated immediately with antiserum.

immediately with antiserum.

 antibiotic therapy (if infectionantibiotic therapy (if infection))

• Vaccination will not protect hosts from _{Vaccination will not protect hosts from} botulism, however passive

botulism, however passive

immunisation with antibody is the immunisation with antibody is the

treatment of choice for cases of treatment of choice for cases of

(51)

Prevention

---

proper food handling and preparation.

--- spores survive boiling (100 degrees at

1 atm) 1h.

---toxin heat-labile, boiling or intense

heating, inactivate the toxin.

(52)

C. difficile

• _{After antibiotic use}_{After antibiotic use}

• Intestinal normal flora --greatly decreased_{Intestinal normal flora --greatly decreased}

• _{Colonization occurs}_{Colonization occurs} • _{Enterotoxin secreted}_{Enterotoxin secreted}

(53)

Pseudomembranous Colitis

 Pseudomembranous colitis (PC) results Pseudomembranous colitis (PC) results

predominantly as a consequence of the predominantly as a consequence of the

elimination of normal intestinal flora elimination of normal intestinal flora

through antibiotic therapy. through antibiotic therapy.

 Symptoms include Symptoms include abdominal abdominal pain with pain with

a

a watery diarrheawatery diarrhea and leukocytosis. and leukocytosis. "

"PseudomembranesPseudomembranes" consisting of " consisting of fibrin, mucus and leukocytes can be fibrin, mucus and leukocytes can be

observed by colonoscopy. observed by colonoscopy.

 Untreated pseudomembranous colitis Untreated pseudomembranous colitis

can be fatal in about

(54)

Therapy

 Discontinuation of initial antibiotic Discontinuation of initial antibiotic

(e.g. ampicillin) (e.g. ampicillin)

 Specific antibiotic therapy (e.g. Specific antibiotic therapy (e.g.

(55)

• _{no oxidative phosphorylation}_{no oxidative phosphorylation} • fermentation_fermentation

• _{killed by oxygen}_{killed by oxygen}

• _{lack certain enzymes}_{lack certain enzymes}

– _{superoxide dismutase}_{superoxide dismutase} * OO₂₂--+2H_+2H++ H_H

2

2OO2 2

– catalase _catalase

* HH₂₂OO₂₂ H H₂₂0 + O0 + O₂₂

– _peroxidase_peroxidase

* HH₂₂OO₂₂ H H₂₂00/NAD to NADH/NAD to NADH

Obligate

(56)

Strict anaerobe infectious

disease

 Sites throughout body Sites throughout body

 Muscle, cutaneous/sub-cutaneous Muscle, cutaneous/sub-cutaneous

necrosis necrosis

(57)

(58)

Bacterial Flora of the Body

Site

Site Total BacteriaTotal Bacteria RatioRatio (per/ml or gm)

(per/ml or gm) Anaerobes:Aerobes Anaerobes:Aerobes

Upper Airway Upper Airway

Nasal Washings

Nasal Washings 101033-10-1044 3-5:13-5:1

Saliva

Saliva 101088-10-1099 1:11:1

Tooth Surface

Tooth Surface 10101010-10-101111 1:11:1

Gingival Crevice

Gingival Crevice 10101111-10-101212 1000:1 1000:1

Gastrointestinal Tract Gastrointestinal Tract

Stomach

Stomach 101022-10-1055 1:11:1

Small Bowel

Small Bowel 101022-10-1044 1:11:1

Ileum

Ileum 101044-10-1077 1:11:1

Colon

Colon 10101111-10-101212 1000:11000:1

Female Genital Tract Female Genital Tract

Endocervix

Endocervix 101088-10-1099 3-5:13-5:1

Vagina

(59)

Problems in identification of

anaerobic infections

• _{air in sample (sampling, transportation)}_{air in sample (sampling, transportation)} – no growth_{no growth}

• _{identification takes several days or longer}_{identification takes several days or longer} – _{limiting usefulness}_{limiting usefulness}

• often derived from normal flora _{often derived from normal flora}

(60)

Virulence Factors

1.

1. Anti-phagocytic capsuleAnti-phagocytic capsule

• Also promote abscess formation_{Also promote abscess formation}

2.

2. Tissue destructive enzymesTissue destructive enzymes

• B. fragilis_{B. fragilis} produces variety of enzymes produces variety of enzymes (lipases, proteases, collagenases) that

(lipases, proteases, collagenases) that

destroy tissue

destroy tissue  Abscess Formation Abscess Formation

3.

3. Beta-lactamase productionBeta-lactamase production

• B. fragilis _{B. fragilis} – protect themselves and other – protect themselves and other species in mixed infections

species in mixed infections

4.

4. Superoxide dismutase productionSuperoxide dismutase production

• Protects bacteria from toxic O_{Protects bacteria from toxic O}22 radicals as radicals as

they move out of usual niche

(61)

Characteristics of Anaerobic Infections

1.

1. Most pathogenic anaerobes are Most pathogenic anaerobes are

usually commensals usually commensals

• Originate from our _{Originate from our}own floraown flora

2.

2. Predisposing ConditionsPredisposing Conditions

• Breeches in the mucocutaneous barrier _{Breeches in the mucocutaneous barrier}

 _ displace normal floradisplace normal flora

(62)

Characteristics of Anaerobic

Infections

3.

3. Complex FloraComplex Flora

 Multiple speciesMultiple species

• Abdominal Infection _{Abdominal Infection} Avg Avg

of 5 species

of 5 species  3 anaerobic3 anaerobic  2 aerobic2 aerobic

• Less complex then nl flora_{Less complex then nl flora} • Fecal flora 400 different _{Fecal flora 400 different}

species

 Those predominant in stool Those predominant in stool

are not infecting species are not infecting species

• Veillonella, Veillonella,

Bifidobacterium

Bifidobacterium  rarely rarely pathogenic

pathogenic

• Species uniquely suited to _{Species uniquely suited to}

cause infection

predominate

4.

4. Synergistic Mixture Synergistic Mixture of Aerobes

of Aerobes & & Anaerobes

Anaerobes

 E. coliE. coli  Consume O Consume O

2

• Allow growth _{Allow growth} of of anaerobes

anaerobes

 Anaerobes Anaerobes _ promote promote

growth of other

bacteria by being

(63)

Clues to Anaerobic Infection

1.

1. Infections in continuity to mucosal Infections in continuity to mucosal

surfaces surfaces

2.

2. Infections with tissue necrosis and Infections with tissue necrosis and

abscess formation abscess formation

3.

3. Putrid odorPutrid odor

4.

4. Gas in tissuesGas in tissues

5.

5. Polymicrobial floraPolymicrobial flora

6.

6. Failure to grow in the lab Failure to grow in the lab

BIOCHEMICAL KITS

BIOCHEMICAL KITS

• e.g. API SYSTEM_{e.g. API SYSTEM}

GAS CHROMATOGRAPHY

(64)

Bacteroides fragilis

• _{Major disease causing strict anaerobic}_{Major disease causing strict anaerobic}

after abdominal surgeryafter abdominal surgery

non-spore-former

•_{Prominent capsule}_{Prominent capsule}

–_{anti-phagocytic}_{anti-phagocytic} –_{abscess formation}_{abscess formation}

•_Endotoxin_Endotoxin – _{low toxicity}_{low toxicity}

– _{structure different than other}_{structure different than other}

(65)

•

Enterobacteriaceae

(facultative anaerobes)

–

commonly cause disease

–

low numbers gut flora

•

Strict anaerobes

MICROBIOLOGY PPT LECTURE NOTES | Karya Tulis Ilmiah

Category

Clostridium Species

pathogens. Nonetheless, they are pathogens. Nonetheless, they are

production of numerous exotoxins. production of numerous exotoxins.

Clostridium Tetani

tetani

BIOCHEMICAL CHARACTERISTICS

terminal located round

Pathogenicity

tetanospasmin

Clostridium tetani

spasms

Clinical Manifestations

twitching of muscles around a wound. The

around the neck and jaw muscles

角弓反张

in which the head and heels are bent

ruptures, and pulmonary, renal, and cardiac

Clinical Manifestations

Generalized

nervous system(sweating, hyper thermia,

nerves, particularly seventh cranial nerve; very

stump;very poor prognosis in infants whose

Epidemiology

world,with a mortality rate ranging from20% to world,with a mortality rate ranging from20% to

mortality rates remain 85% for neonatal mortality rates remain 85% for neonatal

Immunity

and the disease does not produce and the disease does not produce

Diagnosis

symptoms (above).

aware that toxigenic strains of C tetani

in the differential diagnosis.

infant

toxoid

soil, fecal contamination

induces hypertension

Toxins

Enterotoxin

Tissue degrading enzymes

Organism spreads

Gas gangrene

As more tissue becomes involved, the

These bacteria are found in

propagate rapidly to dangerous

Cellulitis, Fasciitis

Necrotizing Enteritis

; patient after

Epidemiology

spores under adverse environmental

Epidemiology

Double Hemolysis Circles

Biological Features

decaying vegetation. decaying vegetation.

Division

Botulinum toxin

Epidemiology

food food

Infection with

botulism

Wounds

Diagnosis

Prevention

heating, inactivate the toxin.

predominantly as a consequence of the predominantly as a consequence of the

Therapy

disease

necrosis necrosis

Bacterial Flora of the Body

Problems in identification of

Characteristics of Anaerobic Infections

1. Most pathogenic anaerobes are Most pathogenic anaerobes are

Characteristics of Anaerobic

of Aerobes & & Anaerobes

Clues to Anaerobic Infection

1. Infections in continuity to mucosal Infections in continuity to mucosal

BIOCHEMICAL KITS

after abdominal surgeryafter abdominal surgery

Enterobacteriaceae