Spore-forming Gram-positive Bacilli Flashcards
1
Q
are found in the soil
A
Spores
2
Q
remain viable in soil for decades. Although spores are naturally in soil from around the world, the organisms are not regularly cultivated from soils.
A
Spores
3
Q
Animals, esp. livestock (?), become infected while grazing on grass contaminated with spores which germinate.
A
goats, sheep, cattle, horses
4
Q
The vegetative cells multiply and elaborate toxins, which spread in the body cause fatal (?). When the organisms are returned to the soil in animal excrement or carcasses, they sporulate and become a long-term reservoir of infection.
A
septicemia and toxemia
5
Q
Transmission to humans is by
A
direct inoculation, ingestion, or inhalation of spores
6
Q
Most common form of anthrax in humans, accounting for more than 95% of cases, but the least dangerous form
A
Cutaneous Anthrax (malignant pustule)
7
Q
Acquired by inoculation of spores through cut or abrasion of the skin, either from soil or infected animal products
A
Cutaneous Anthrax (malignant pustule)
8
Q
begins with a small, itchy lesion resembling an insect bite; in 1-2 days, it develops into a non-painful papule that changes rapidly into a vesicle, then a pustule filled with blue-black edema fluid.
A
Cutaneous Anthrax (malignant pustule) : Signs and symptoms: Skin infection
9
Q
blackened crater, typically 1-3 cm in diameter, surrounded by edem.
A
“black eschar”
10
Q
Cutaneous Anthrax (malignant pustule) : Signs and symptoms
A
Lymphangitis and lymphadenopathy
11
Q
Cutaneous Anthrax (malignant pustule) : Signs and symptoms
A
fever, malaise, and headache may occur.
12
Q
is fully developed. Eventually, it dries, loosens, and separates; healing is by granulation and leaves a scar. It may take many weeks for the lesion to heal and the edema to subside.
A
Eschar
13
Q
Can lead to sepsis, the consequences of systemic infection—including meningitis—and death in 20% of untreated cases.
A
Cutaneous Anthrax (malignant pustule)
14
Q
Extremely rare in humans (accounts for less than 1% of cases)
A
Gastrointestinal Anthrax (violent enteritis)
15
Q
Acquired from ingestion of the organism’s spores from contaminated or uncooked meat.
A
Gastrointestinal Anthrax (violent enteritis)
16
Q
Characterized by an acute inflammation of the intestinal tract.
A
Gastrointestinal Anthrax (violent enteritis)
17
Q
Death occurs in 60% of untreated cases.
A
Gastrointestinal Anthrax (violent enteritis)
18
Q
Gastrointestinal Anthrax (violent enteritis) : Signs and symptoms:
A
- Initially, nausea, loss of appetite, vomiting, and fever
- Followed by abdominal pain, vomiting of blood, and severe (often bloody) diarrhea.
19
Q
Acquired by inhalation of airborne spores while handling animal products
A
Pulmonary or Inhalation Anthrax (Woolsorter’s disease)
20
Q
it develops in handlers of raw animal hair, wool or hides
A
Pulmonary or Inhalation Anthrax (Woolsorter’s disease)
21
Q
The incubation period in inhalation anthrax may be as long as 6 weeks.
A
Pulmonary or Inhalation Anthrax (Woolsorter’s disease)
22
Q
The fatality rate in inhalation anthrax is high in the setting of known exposure
A
Pulmonary or Inhalation Anthrax (Woolsorter’s disease)
23
Q
it is higher when the diagnosis is not initially suspected.
A
Pulmonary or Inhalation Anthrax (Woolsorter’s disease)
24
Q
- First symptoms are flu- or common cold-like symptoms including a sore throat, mild fever, and muscle aches.
- Followed by coughing, chest discomfort, shortness of breath, and tiredness — which are manifestations of toxemia, marked hemorrhagic necrosis, edema of the mediastinum, and substernal pain. Sepsis occurs, and there may be hematogenous spread to the gastrointestinal tract, causing bowel ulceration, or to the meninges, causing hemorrhagic meningitis.
A
Pulmonary or Inhalation Anthrax (Woolsorter’s disease):
Signs and symptoms
25
has been considered as an agent for bioterrorism. It has been classified as Category A (highest priority) biological agent because it is easily disseminated, can cause high mortality, and can generate public panic.
B. anthracis
26
Occurs after the intravenous injection of drugs contaminated with spores
Injectional anthrax
27
May result to soft tissue infections, may result in death of shock, coma, organ failure, and necrotizing fasciitis.
Injectional anthrax
28
Found in virulent strains of B. anthracis.
Capsule
29
Consists mainly of a polypeptide, poly-D-glutamic acid
Capsule
30
Instrumental in the adherence of the organism to host’s cells and tissue and is an anti-phagocytic factor.
Capsule
31
Antibodies formed against the capsule do not protect against the disease.
Capsule
32
Plasmid-encoded protein complex made up of 3 components
Anthrax exotoxins
33
binds to specific cell receptors, and after proteolytic activation, it forms a membrane channel that mediates entry of EF and LF into the host’s cell.
Protective antigen (PA)
34
It is so called because it induces protective antitoxins
Protective antigen (PA)
35
is an adenylate cyclase.
Edema factor (EF)
36
Together with PA, it forms a toxin known as edema toxin.
Edema factor (EF)
37
This most likely impairs host defenses and is responsible for the fluid accumulation seen in anthrax.
Edema factor (EF)
38
combines with PA to form lethal toxin, responsible for cytolysis of macrophages.
Lethal factor (LF)
39
This is a major virulence factor and cause of death in infected animals and humans. When injected into laboratory animals (eg, rats), the lethal toxin can quickly kill the animals.
Lethal factor (LF)
40
Control soil contamination is key to preventing anthrax, measures include:
(1) disposal of animal by burning or by deep burial in lime pits (2) decontamination (usually by autoclaving) of animal products (3) protective clothing and gloves for handling potentially infected materials
(4) active immunization of domestic animals with live attenuated vaccines
41
Vaccination is recommended for the following high-risk groups:
(1) laboratory workers handling the B. anthracis routinely
(2) persons who handle potentially infected animals/animal products (e.g., hides and furs) esp. in high incidence areas
(3) military personnel deployed to areas with high risk for exposure
42
The first-generation human vaccine to be licensed for use in the United States
BioThrax
43
a cell-free formulation prepared from a culture filtrate of a toxigenic, nonencapsulated, avirulent strain of B. anthracis , which contains PA, LF, and EF, with PA being the major component.
BioThrax
44
It consists of 3 subcutaneous injections given 2 weeks apart, followed by 3 additional SC injections given at 6, 12, and 18 months; annual booster injections are recommended thereafter to maintain protective level of immunity.
BioThrax
45
Two vaccines using highly purified recombinant (?) have been manufactured in the United States and the United Kingdom.
PA (rPA)
46
is recommended in the setting of potential exposure to B. anthracis as an agent of biologic warfare
Chemoprophylaxis
47
Similar to B. anthracis, but B. cereus are motile with peritrichous flagella, and are non-encapsulated.
Bacillus cereus
48
Spores are found in the soil (also considered as an airborne and dust-borne contaminant that multiplies very readily in cooked foods such as rice, potato, and meat dishes)
Bacillus cereus: HABITAT
49
Transmission to humans is by ingestion or direct inoculation.
Bacillus cereus: TRANSMISSION
50
Food poisoning
| •Has two distinct forms:
Emetic form
| Diarrheal form
51
Associated with eating fried rice, and occasionally, pasta dishes that are contaminated with the organism’s toxin.
Emetic form
52
Has incubation period of 1–6 hours
Emetic form
53
Manifestations include nausea, vomiting, abdominal cramps, and occasionally diarrhea (clinically resembles staphylococcal food poisoning)
Emetic form
54
Recovery occurs within 24 hours after the onset.
Emetic form
55
Associated with meat dishes and sauces contaminated with spores
Diarrheal form
56
Has an incubation period of 8-16 hours
Diarrheal form
57
Manifestations include profuse diarrhea with abdominal pain and cramps; fever and vomiting are uncommon (clinically resembles C. perfringens food poisoning)
Diarrheal form
58
Recovery occurs within 12 hours after the onset.
Diarrheal form
59
Occurs when the organisms are introduced into the eye by foreign bodies in association with trauma.
Eye Infections
60
Clinical presentation may be in the form of severe keratitis, endophthalmitis, and panophthalmitis.
Eye Infections
61
B. cereus has also been associated with localized infections and with systemic infections, including:
endocarditis, meningitis, osteomyelitis, and pneumonia.
62
are released during spore germination, and may be preformed in the food or produced in the intestine.
Enterotoxins
63
Responsible for the clinical presentation of the emetic form of the disease.
Heat-stable enterotoxin
64
Produced when spores survive cooking rice, and keeping the rice warm results in germination of spores and enterotoxin formation
Heat-stable enterotoxin
65
this pre-formed toxin remains in the food despite reheating.
Heat-stable enterotoxin
66
Responsible for the clinical presentation of the diarrheal form of the disease. •Produced after ingestion of the B. cereus spore-contaminated vegetables,
Heat-labile enterotoxin
67
Produced after ingestion of the B. cereus spore-contaminated vegetables, meat, and cream sauces.
Heat-labile enterotoxin
68
Acute diarrheal disease caused by B. cereus may be prevented by?
proper cooking and refrigeration of foods prepared in bulk to prevent proliferation of vegetative forms of the bacteria and formation of the enterotoxin.
69
may be gram-variable on prolonged incubation.
Gram-positive bacilli
70
Spores are larger than the diameter of the organism in which they are formed; may be placed centrally, subterminally, or terminally.
Spore-forming
71
Sporangia are swollen.
Spore-forming
72
Most are motile with peritrichous flagella EXCEPT
C. perfringens, C. innocuum, C. ramosum
73
Groups of anaerobes based on aerotolerance test: Each colony type from the anaerobic isolation plate is subcultured to an aerobic (5% to 10% CO2) and anaerobic blood agar plate for overnight incubation.
Anaerobic
74
NOT capable of growth on agar surfaces exposed to O2 levels above 0.5%.
Strict obligate anaerobes
75
e.g., C. heamolyticum, C. novyi type B, C. tetani, C. botulinum, Clostridioides (formerly Clostridium) difficile
Strict obligate anaerobes
76
- Can grow when exposed to oxygen levels ranging from about 2% to 8% (average, 3%) e.g., C. perfringens
Moderate obligate anaerobes
77
Show limited or scant growth on agar in room air or in a 5% to 10% CO2 incubator, but grow best under anaerobic conditions.
Aerotolerant anaerobes
78
e.g., C. histolyticum, C. tertium and C. carnis
Aerotolerant anaerobes
79
Catalase (-)
CLOSTRIDIUM SPECIES
80
Can be part of the normal flora of the GI tract; these are clinically relevant as the cause of both endogenous and exogenous infections.
CLOSTRIDIUM SPECIES
81
causes 80% of gas gangrene (myonecrosis)
C. perfringens
82
also associated with food poisoning, necrotizing skin infection, or bacteremia.
C. perfringens
83
Other causes of Gas Gangrene / Histotoxic Group
C. novyi, C. septicum, C. histolyticum, C. sordellii, C. sporogenes, C. bifermentans.
84
causes tetanus (commonly known as lock jaw)
C. tetani
85
a disease characterized by spastic paralysis.
C. tetani
86
causes botulism (foodborne, infant, wound, intestinal)
C. botulinum
87
a disease characterized by flaccid paralysis; listed by the Centers for Disease Control and Prevention (CDC) as a potential agent of bioterrorism.
C. botulinum
88
Other botulinum neurotoxin-producing species:
C. baratii, C. butyricum, C. argentinense.
89
cause bacteremia or other infections.
C. clostridioforme group, C. ramosum, C. innocuum, C. tertium
90
causes antibioticassociated diarrhea (AAD) to pseudomembranous colitis (PMC) and associated complications
Clostridioides (formerly Clostridium) difficile
91
normal colonizers of the GIT in 3% of healthy adults.
Clostridioides (formerly Clostridium) difficile
92
Formerly Clostridium welchii
Common name: Welch's bacillus
93
Spores are found in the soil, and the intestinal tract of animals and humans
Clostridium perfringens: HABITAT
94
Transmission occurs by direct inoculation of organisms’ spores through breaks in the skin, or by ingestion.
Clostridium perfringens: TRANSMISSION
95
Characterized by extensive necrosis of muscle and connective tissue
Gas gangrene (or anaerobic myonecrosis)
96
Acquired by wound contamination with spores of C. perfringens (or other clostridia within the same histotoxic group, such as C. septicum); most cases occur following trauma (e.g., gunshot) or surgical procedures (e.g. septic abortion)
Gas gangrene (or anaerobic myonecrosis)
97
Initial trauma to host tissue damages muscle and impairs blood supply resulting in hypoxia or anoxia. This lack of oxygenation allows spore germination and growth of anaerobic clostridia, and elaboration of exotoxins.
Gas gangrene (or anaerobic myonecrosis)
98
Initially, generalized fever, pain, edema, and blood-tinged exudate in the infected tissue.
Gas gangrene (or anaerobic myonecrosis): Signs and symptoms
99
Tissue becomes discolored, purple, then black, general tissue destruction and bubbles caused on the skin by gas formation in underlying tissue.
Gas gangrene (or anaerobic myonecrosis): Signs and symptoms
100
Tissue becomes filled with bubbles of gas, as CO2 and H2 accumulate during the growth of the organisms.
Gas gangrene (or anaerobic myonecrosis): Signs and symptoms
101
Occurs by ingestion of vegetative cells of C. perfringens in contaminated food.
Perfringens food poisoning
102
Signs and symptoms occur in 8 to 16 hours up to 24 hours after ingesting the suspected food.
Perfringens food poisoning
103
- Crampy abdominal pain
- Foamy, foul-smelling diarrhea
- Nausea
- Fever and vomiting re uncommon
Perfringens food poisoning: Signs and symptoms
104
Recovery is rapid and death is extremely rare.
Perfringens food poisoning
105
An inflammation of both the small intestines and the colon
Necrotizing Enterocolitis (or necrotizing bowel disease)
106
Acquired from contaminated food — food-borne, or it may be transmissible by inanimate objects.
Necrotizing Enterocolitis (or necrotizing bowel disease)
107
Characterized by the sudden onset of abdominal cramps and abdominal distention, vomiting, bloody diarrhea, shock related to fluid and electrolyte problems and acute inflammation with focal to widespread necrosis of the intestinal mucosa.
Necrotizing Enterocolitis (or necrotizing bowel disease)
108
Referred to by other names in some countries, such as “fire in the bowel" (Germany) or “pig bel" (Papua, New Guinea).
Necrotizing Enterocolitis (or necrotizing bowel disease)
109
Results when C. perfringens gains access to necrotic products of conception retained in the uterus, commonly after an incomplete abortion with inadequately sterilized instruments.
Endometritis
110
Necrosis of uterine tissue and bacteremia with massive intravascular hemolysis due to toxin then follow.
Endometritis
111
Clostridium perfringens produces multiple exotoxins that have different pathogenic significance in different animal species
Exotoxins
112
A necrotizing, hemolytic exotoxin
Alpha toxin (lecithinase, phospholipase C)
113
Hydrolyzes lecithin and sphingomyelin, thus disrupting the cell membranes of various host cells, including erythrocytes, leukocytes, and muscle cells.
Alpha toxin (lecithinase, phospholipase C)
114
Oxygen-labile cytolysin; contributes to rapid tissue destruction --- has pore-forming activity similar to streptolysin O
Theta (θ) toxin
115
Alters capillary permeability and is toxic to heart muscle.
Theta (θ) toxin
116
Responsible for the symptoms of food poisoning with C. perfringens
Enterotoxin
117
Released during sporulation of the organisms in the intestines
Enterotoxin
118
Inserts into enterocyte membranes to form pores leading to alterations in intracellular calcium and membrane permeability. This leads to loss of cellular fluid and macromolecules.
Enterotoxin
119
are liberated into the surrounding tissue, causing more local tissue necrosis and systemic toxemia.
Collagenase, protease, and lipase
120
one of the most effective ways to prevent clostridial wound infections along with prophylactic antibiotic therapy.
Immediate and rigorous cleansing and surgical of deep wounds, compound fractures, and infected incisions
121
Immediate and rigorous cleansing and surgical of deep wounds, compound fractures, and infected incisions, is one of the most effective ways to prevent clostridial wound infections along with prophylactic antibiotic therapy.
PREVENTION AND CONTROL of Clostridium perfringens
122
Prevention of food poisoning involves good cooking hygiene and adequate refrigeration.
PREVENTION AND CONTROL of Clostridium perfringens
123
Debridement (removal) of diseased tissue eliminate the conditions that promote the spread of gangrenous infections. This surgical treatment is supplemented by large doses of broad-spectrum antimicrobial agents in the intestines or body cavity, where only limited amount of tissue can be removed.
PREVENTION AND CONTROL of Clostridium perfringens
124
Surgical removal or amputation of the affected site in cases wherein there is extensive myonecrosis.
PREVENTION AND CONTROL of Clostridium perfringens
125
is being used to treat patients with clostridial wound infections and diabetic ulcers. This hyperbaric therapy involves breathing higher levels of oxygen. The increased oxygen content of the tissues presumably blocks further bacterial multiplication and toxin production, thereby promoting healing.
large decompressor chamber
126
Common names: Drumstick bacillus, lollipop bacillus, tennis racquet bacillus, tack head bacillus
Clostridium tetani
127
Spores are found in the soil, and in the intestinal tract of humans or animals
Clostridium tetani: HABITAT
128
Transmission occurs by wound contamination with spores from the soil (or soiled objects) or feces
Clostridium tetani: TRANSMISSION
129
Tetanus
| Gk. tetanos means?
to stretch
130
Acquired by spore contamination of wound; Necrotic tissue and poor blood supply in the wound favor spore germination and growth of anaerobic clostridia, and elaboration of exotoxins.
Tetanus
131
Some common types of wounds that can lead to tetanus infection include cuts from a rusty can, tattoos, animal bites, splinters, surgical wounds, injection drug use, body piercing, or lacerations.
Tetanus
132
The incubation period varies from 4 to 10 days, and shorter incubation period signifies a more serious condition.
Tetanus
133
whereby muscles contract uncontrollably
muscular spasm
134
is an early effect of the disease due to the rigid contraction of the masseter muscle of the face, resulting to difficulty in opening the jaw.
Trismus (or lockjaw)
135
is described as sustained trismus. The patient looks eerily as though he is smiling.
Risus sardonicus (sarcastic grin)
136
caused by involvement of spinal musculature
Opisthotonus
137
is characterized by continuous back spasms causing extreme arching of the back, flexion of the arms, and extension of the legs. Contractions are intermittent and extremely painful and may be forceful enough to break the vertebrae.
Opisthotonus
138
Respiratory failure ensues, and without treatment, results in high mortality rate up to how many %?
70%
139
is due to fecal contamination of the umbilical cord, or use of contaminated instruments (e.g., umbilical stumps).
Tetanus neonatorum (neonatal tetanus)
140
showing spastic paralysis of the paravertebral muscles, which locks the back into a rigid, arched position. Also note the abnormal flexion of the arms and the legs.
Baby with neonatal tetanus
141
A potent, heat-stable, plasmid-mediated neurotoxin and one of the most poisonous substances; only a small amount is required to initiate symptoms.
Tetanospasmin
142
Released by vegetative cells at the site of infection, and spread throughout the body by the blood stream. (The bacilli remain at the site of infection.)
Tetanospasmin
143
Binds to receptors on the presynaptic membranes of motor neurons, then travels along the nerves to the central nervous system (CNS).
Tetanospasmin
144
Binds to gangliosides, blocking the release of inhibitory neurotransmitters (glycine and γaminobutyric acid -- GABA), so muscles are released from inhibition and begin to contract uncontrollably --- spastic paralysis.
Tetanospasmin
145
is irreversible, so recovery requires the generation of new axon terminals.
Binding of the toxin
146
a) After traumatic injury, bacilli infecting the local tissue secrete tetanospasmin, which is absorbed by the peripheral axons and is carried to target neurons in the spinal column.
(b) In the spinal cord, the toxin attaches to the junction of regulatory neurons that inhibit inappropriate contraction. Released from inhibition, the muscles, even the opposing members of a muscle group, receive constant stimuli and contract uncontrollably.
(c) Muscles contract spasmodically, without regard to regulatory mechanisms of conscious control. Note the clenched jaw, typical of risus sardonicus.
The events in tetanus
147
that causes local tissue necrosis at sites of vegetative growth, thereby lowering oxygen tension in tissue.
hemolysin
148
Routine active immunization with tetanus toxoid, usually combined with diphtheria toxoid and pertussis vaccine (DPT) for primary immunization in childhood, and DT for adults, can completely prevent tetanus.
Five doses of DT are recommended, to be given at the ages of 2, 4, 6, and 18 months, and once again between the ages of 4 and 6 years. Thereafter, a booster of adulttype tetanus diphtheria toxoid should be given every 10 years.
PREVENTION AND CONTROL of Clostridium tetani
149
A patient with symptoms of tetanus should immediately receive antitoxin therapy with human tetanus immune globulin (TIGH). It neutralizes the circulating toxin, but is ineffective against toxin already fixed in the central nervous system. Active immunization with tetanus toxoid should accompany antitoxin prophylaxis.
PREVENTION AND CONTROL of Clostridium tetani
150
Prevention of tetanus also depends on aggressive wound care. Surgical debridement is vitally important because it removes the necrotic tissue that is essential for proliferation of the organisms.
PREVENTION AND CONTROL of Clostridium tetani
151
Antibiotic (penicillin) strongly inhibits the growth of C. tetani and stops further toxin production.
PREVENTION AND CONTROL of Clostridium tetani
152
Common name: Canned good bacillus
Clostridium botulinum
153
Spores are found in the soil, and vegetation.
Clostridium botulinum: HABITAT
154
Transmission is by ingestion preformed toxin or spores in food, or by wound contamination with spores.
Clostridium botulinum: TRANSMISSION
155
L. botulis = sausage: the disease was earlier associated with spoiled sausage
Classical Botulism or Food-borne botulism
156
Acquired by ingestion of preformed toxin, often traced to improperly canned (also vacuum-packed) food.
- The foods most often implicated are home-canned, low acid foods such as vegetables, fruits, condiments and fish.
- Most cases are due to inadequate sterilization, failing to kill the spores during the canning process. Canning creates an environment with little or no air which favors anaerobic germination of spores into vegetative cells that produce exotoxins.
Classical Botulism or Food-borne botulism
157
Signs and symptoms:
| -Onset is 12 to 72 hours after ingestion, depending on the size of the dose (amount of toxin ingested).
Classical Botulism or Food-borne botulism
158
Signs and symptoms:
-Initial neuromuscular symptoms involve the muscles of the head: ‣diplopia (double vision)
‣dysphagia (difficulty in swallowing), dysphonia (difficulty in speech) ‣dizziness, but there is no sensory or mental lapse.
Classical Botulism or Food-borne botulism
159
Later symptoms are descending muscular paralysis; cardiac arrhythmias and blood pressure instability are also evident; death results from respiratory paralysis unless there is proper respiratory intensive care, including mechanical ventilation.
Classical Botulism or Food-borne botulism
160
Commonly occurs in infants between the ages of 3 weeks and 8 months is now the most commonly diagnosed form of botulism.
Infant botulism
161
Acquired by ingestion of spores C. botulinum in honey, also from the soil, household dust, or another source; spores yield vegetative bacteria, which multiply and produce exotoxin in the infant’s colon.
Infant botulism
162
Signs and symptoms include constipation, poor muscle tone, lethargy, and feeding problems and may have ophthalmic and other paralyses similar to those in food-borne botulism, and respiratory arrest.
Infant botulism
163
Has accounted for a small number of sudden infant death syndrome (SIDS), also known as "crib death".
Infant botulism
164
Occurs when spore of C. botulinum enter a wound or a puncture, germinate and produce botulinum toxins.
Wound botulism
165
The symptoms are similar to those of food borne botulism.
Wound botulism
166
Cases have increasingly been reported in injecting drug users.
Wound botulism
167
Among most potent exotoxins known (together with tetanospasmin)
Botulinum toxin (botulin)
168
Heat-labile, phage-mediated neurotoxin
Botulinum toxin (botulin)
169
Of seven (7) types --- serotypes A to G
Botulinum toxin (botulin)
170
Is absorbed into the blood circulation, and binds to receptors of presynaptic membranes of motor neurons of the cranial nerves initially, followed by the peripheral nervous system.
Botulinum toxin (botulin)
171
Blocks the release of excitatory neurotransmitter acetylcholine at the peripheral nerve endings, including neuromuscular junctions, resulting in lack of muscle contraction ---flaccid paralysis.
Botulinum toxin (botulin)
172
are associated with botulism in man, with type F as the least common.
Botulinum toxin Types A, B, E, and F
173
are associated with botulism in birds and mammals.
Botulinum toxin Types C and D
174
produced by what is now reclassified C. argentinense; it is not clear to what extent these organisms cause botulism in humans.
Botulinum toxin Type G
175
The botulinum toxin in controlled doses can be used to temporarily minimize wrinkles.
Cosmetic injection of botulinum toxin (botox)
176
depends on educating the public about the proper methods of preserving and handling canned foods. Home canners should be aware of the types of foods and conditions that are likely to cause botulism.
Prevention of botulism
177
The administration of large doses of horse C. botulinum antitoxin is said to be useful in neutralizing free toxin.
PREVENTION AND CONTROL of Clostridium botulinum
178
A recommended prevention measure for infant botulism is to avoid giving honey to infants less than 12 months of age, as botulinum spores are often present. In older children and adults the normal intestinal bacteria suppress development of C. botulinum
PREVENTION AND CONTROL of Clostridium botulinum
179
Formerly Clostridium difficile
Clostridioides difficile
180
It is part of the normal gastrointestinal flora in 2–10% of humans, sometimes at higher rates among hospitalized persons and infants.
Clostridioides difficile: HABITAT
181
Disease is acquired endogenously.
Clostridioides difficile: TRANSMISSION
182
Develops as drug-resistant C. difficile super infect the intestine when the normal flora has been disrupted by antibiotics.
Antibiotic-associated diarrhea (AAD) and Pseudomembranous colitis (PMC, a.k.a. Antibioticassociated colitis)
183
The predominant symptom is diarrhea commencing late (usually 5 - 10 days) into the antimicrobial therapy or even after the therapy has stopped.
Antibiotic-associated diarrhea (AAD) and Pseudomembranous colitis (PMC, a.k.a. Antibioticassociated colitis)
184
The diarrhea may be mild and watery or bloody and accompanied by abdominal cramping, leukocytosis, and fever. The colon is inflamed and gradually sloughs off loose, membrane-like patches called pseudomembranes consisting of fibrin and inflammatory cells.
Antibiotic-associated diarrhea (AAD) and Pseudomembranous colitis (PMC, a.k.a. Antibioticassociated colitis)
185
If the condition is not arrested, cecal (cecum) perforation and death can result.
Antibiotic-associated diarrhea (AAD) and Pseudomembranous colitis (PMC, a.k.a. Antibioticassociated colitis)
186
An endoscope view of an inflamed colon caused by a C. difficile infection. The white plaques represent mucus and dead cells that have built up on the colon walls.
Pseudomembranous colitis
187
Cause necrosis of the intestinal epithelium; both act in the cytoplasm of enterocytes which results in the disruption of intercellular tight junctions followed by altered membrane permeability and fluid secretion.
Polypeptide toxins: Toxin A (enterotoxin) and Toxin B (cytotoxin/ cytopathic toxin)
188
Within hours of contact with enterocytes cell rounding and neutrophilic infiltration also appear.
Polypeptide toxins: Toxin A (enterotoxin) and Toxin B (cytotoxin/ cytopathic toxin)
189
Because infected persons shed large number of spores in their stools, increased precautions are necessary to prevent spread of the agent to other patients who may be on anti-microbic therapy.
PREVENTION AND CONTROL of Clostridioides difficile
190
Some new techniques include vaccination of C. difficile toxoid and restoration of normal flora by means of a mixed culture of lactobacilli and yeasts.
PREVENTION AND CONTROL of Clostridioides difficile
191
Mild, uncomplicated cases respond to withdrawal of antibiotics and replacement therapy for lost fluids and electrolytes.
PREVENTION AND CONTROL of Clostridioides difficile
192
is a microbial insect pathogen however, it is also capable of causing disease in humans occasionally — food poisoning, eye and other local infections.
B. thuringiensis
193
Commercial preparations containing endospores and crystalline toxin (Bt) of this bacterium are sold in gardening supply shops to be sprayed on plants.
Bacillus thuringiensis
194
The genes responsible for production of the Bt has been extracted and combined with those of plants to produce genetically - modified plants that are pest resistant (e.g. Bt corn).
Bacillus thuringiensis
195
Are not easily distinguishable from B. cereus as to microscopic appearance, colonial characteristics, and identification tests.
Bacillus thuringiensis
196
- Crystal formation is used to differentiate B. thuringiensis from B. cereus.
- After growth on sporulation agar or on nutrient agar for at least 48 hours, B. thuringiensis produces cuboid or diamond-shaped crystals adjacent to the spore (parasporal crystals).
- The crystals, which consist of naturally produced insecticidal toxin, are demonstrated with phase contrast microscopy or staining with malachite green.
Bacillus thuringiensis
197
Common name: hay bacillus
Bacillus subtilis
198
is a harmless air contaminant.
B. subtilis
199
When present in large numbers can cause lung and blood infections in people with weakened immunity.
Bacillus subtilis
200
Gram-positive bacilli typically in chains, individual cells are less than 1µm wide, sporangia are not swollen, and spores are ellipsoidal.
Bacillus subtilis
201
Nonmotile, non-encapsulated.
Bacillus subtilis
202
Colonies on 5% sheep BAM: Large (2-7 mm), flat, dull, with "frosted-glass" or "ground-glass appearance"; may be pigmented (pink, yellow, orange, or brown); may be β-hemolytic.
Bacillus subtilis
203
Colonies on PEMBA: Cream to light yellow with no zone of egg precipitation.
Bacillus subtilis
204
Because it is a common laboratory contaminant; identification is not recommended unless isolated from a sterile site (e.g., blood) or found in large numbers in pure culture.
Bacillus subtilis
