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Lecture 20 Flashcards

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1
Q

genus bacillus

A

Gram +, endosperm forming, motile, rods, aerobic or facultative, catalase positive, soil and saprophytes

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2
Q

Bacillus anthracis 2 virulence

A

Block rods, central endospores, immunogenic and antiphagocytic polypepticle capsule
Makes anthrax exotoxin

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3
Q

Anthrax exotoxin

A

Bacillus anthracis
Edema, cell death, tissue destruction

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4
Q

Bacillus anthracis life cycle

A

Animals become infected via spores then spores germinate into vegetative cans inside the host

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5
Q

Bacillus anthracis made of infection

A

Animals and humans come into contact with shores and they germinate inside the host to form vegetative cells which release the anthrax exotoxin

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6
Q

3 types of anthrax

A

Cutaneous, gastrointestinal, inhalation anthrax

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7
Q

Cutaneous anthrax

A

Most common least dangerous, spores enter through cuts in the skin, inoculation site forms raised lesion called papule, papule erupts to form painless black lesion called eschar

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8
Q

Gastrointestinal anthrax

A

Rare but deadly, ingest spores via contaminated meat, causing acute inflammation of GI tract, nausea, fever, vomiting, blood, severe diarrhea

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9
Q

GI anthrax survival rate

A

50% if untreated, 60% if treated

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10
Q

Inhalation anthrax

A

Deadliest form, 99% mortality if untreated, spores inhaled into lungs, engulfed by macrophages and transported to lymph modes, causes pulmonary edema, internal hemorrhaging, shock, rapid death

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11
Q

Anthrax treatment

A

Antibiotics

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12
Q

Anthrax vaccine

A

Subunit vaccine for high risk groups

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13
Q

Bacillus cereus

A

Air and dust-borne, multiplies readily in cooked foods, can survive short heating, spores germinate and release enterotoxins at room temperature

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14
Q

Which cooked foods does bacillus cereus multiply on

A

Rice, potatoes, and meat dishes

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15
Q

Entorotoxins

A

Released by B. cereus cause food intoxication which leads to acute vomiting, nausea, abdominal cramps, and diarrhea
Symptoms disappear after 24 hours

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16
Q

Genus clostridium

A

Gram +, endospore forming rods, anaerobic, catalase negative

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17
Q

Genus clostridium found

A

As saprobes in the environment and some are commensals with humans and animals

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18
Q

Clostridium morphology

A

Terminal ovoid or round spores

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19
Q

Clostridium genus makes some of the

A

Most potent exotoxins that are some of the most poisonous substances on earth

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20
Q

Clostridium species cause

A

Wound and tissue infections, food intoxication

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21
Q

Clostridium perfringens

A

Large rectangular, spore forming, found in soil/dust/human animal feces

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22
Q

Clostridium perfringens endospores not

A

Usually seen in clinical specimens

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23
Q

Clostridium perfringens entrance and causes

A

Contaminated meat especially reheated stews and gravies
Causes food intoxication

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24
Q

Clostridium perfringens symptoms

A

Sub-acute watery diarrhea, severe abdominal cramping, no vomiting

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25
Other form Clostridium perfringens
Spores introduced through anaerobic wounds germinate and release gas and alpha toxin
26
Alpha toxin
Released by clostridium perfringens, causes RBCs to rupture, edema, and tissue destruction
27
C. Perfringens and muscles
Does Myonecrosis (muscle death), during this process muscle carbohydrates are fermented and gas is released into the tissue causing gas gangrene
28
Gas gangrene symptoms
Edema, large bullae, crepitus (skin makes noises), tissue necrosis, fever, and shock Rapidly fatal if untreated
29
Gas gangrene treatment
Debridement (surgical removal of tissue), amputation, large doses of antibiotics, and hyperbaric oxygen therapy
30
Clostridium difficile found
Normal resident of colon usually present in 4-15% of population
31
Clostridium difficile is a common
Nosocomial infection
32
C. Diff overgrowth associated with
Antibiotic use
33
C. Diff overgrowth causes
Antibiotic-associated/pseudomembrane colitis
34
First and second most common GI diseases in industrialized countries
1. Salmonellosis 2. Clostridium difficile Half a million infections in the US each year
35
C. diff superinfection releases and causes
Exotoxins released causing diarrhea, inflammation, and intestinal damage giving rise to pseudomembranous colitis
36
Severe cases C. Diff
Death from intestinal perforation
37
C. Diff highest risk group
Nursing homes
38
C. Diff treatment
Removal of antibiotics in uncomplicated cases, stranger antibiotics in severe cases, and fecal transplantation
39
Clostridium tetani found
Resident of soil and GI tract of some animals
40
C. tetani resembles
Tennis racket or drumstick, terminal endosperm
41
C. tetani enterance
Spores enter through wound, deep implantation to germinate in anaerobic tissue Usually deep muscles
42
C. tetani vegetative cells release
Teranospasmin the tetanus toxin which blocks muscle relaxation
43
Spastic paralysis
Tetanospasmin is released into tissue and absorbed by peripheral nerves and carried to target neurons in spinal column, inhibits muscle relaxation causing muscles to contract uncontrollably
44
Trismus
Spastic paralysis begins in jaw, trismus is jaw muscle spasms causing lock jaw
45
Risus sardonicus
Facial muscle spasms producing wry, mask-like grin
46
If spastic paralysis untreated
Paralysis descends, rigid back, death from paralysis of respiratory muscles
47
Clostridium tetani treatment
TIG tetanus immune globulin the antitoxin immunotherapy Respirator and tracheostomy may be needed
48
Tetanus vaccine
DTap vaccine containing teanus toxoid Booster recommended every 10 years
49
Clostridium botulinum found
Soil, water, intestinal tract of animals
50
Clostridium botulinum under anaerobic conditions
Vegetative cell releases the most potent microbial toxin, botulinum toxin
51
Botulism
Intoxication associated with eating canned or preserved foods
52
3 types of botulism
Botulinum food poisoning, infant botulism, wound botulism
53
Botulism infection process
Ingested or secreted botulism toxin travels to the neuromuscular junctions of skeletal muscles, blocks release of acetylcholine and keeps the muscle from contracting leading to flaccid paralysis
54
Botulinum food poisoning results from
The improper canning of food especially homemade canned vegetables, smoked meats, cheese spreads Spores germinate in can producing botulinum toxin
55
Botulinum food poisoning incubation
1-2 days
56
Botulinum food poisoning affects
Muscles supplied by the cranial nerves first causing eyelid drooping, double vision, loss of facial expression, dry mouth, difficulty chewing and swallowing, followed by flaccid paralysis
57
Flaccid paralysis
Floppy, relaxed
58
Infant botulism occurs in
Infants less than one year old, most common form in US
59
Infant botulism entrance
Infant ingested spores in dust or honey
60
Infant botulism infection process
Immature GI tract allows spore germination and growth of vegetative cells
61
Infant botulism symptoms
Constipation, generalized weakness, weak crying, poor feeding, lethargy, loss of head control (floppy baby syndrome) and possible respiratory arrest
62
Wound botulism
Spores enter a wound or puncture
63
Wound botulism symptoms
Similar to food botulinum muscles of face supplied by cranial nerves
64
Botox
Injects super-diluted botulinum toxin into wrinkled areas to create controlled muscle weakening Wears Off, repeat every 4-6 months
65
Clostridium botulinum treatment
Antitoxin must be administered early for greatest effectiveness, patients managed with respiratory and cardiac support systems
66
Botulism prevention
Proper canning techniques, adequate pressure cooking achieves sterilization, throw away bulging cans, botulinum toxin inactivated at 100°C
67
Listeria monocytogenes
Gram +, rod, facultative anaerobe
68
Listeria monocytogenes can grow in
Acidic conditions, high salt, wide temp range including cold growth
69
Listeria monocytogenes found
Soil and water mainly Animals, plants, and food are secondary sources of infection
70
Listeriosis
Infection from listeria causing gastroenteritis leading to food poisoning from refrigerated foods usually unpasteurized milk or cheeses, deli meats, or unwashed produce
71
Listeria can
Cross the placenta or infect babies during delivery causing neonatal septicemia and meningitis
72
Corynebacterium diphtheriae
Gram positive bacilli, irregular shaped and pleimorophic Club-shaped Non-motile, grows best with oxygen
73
Corynebacterium found
Plants and animals and colonize the skin and mucous membranes of humans
74
C. Diphtheriae reservoir
Humans only through respiratory spread
75
C. Diphtheriae etiologic agent
Diphtheria
76
Diphtheria most common
Children from 1-10 yrs old non-immunized
77
1st stage corynebacterium dip
Local, primary infection in the upper respiratory tract
78
2nd stage corynebacterium dip
Toxin production and toxemia
79
Virulence of corynebacterium dip due to
Diphtheria exotoxin only produced by lysogenic strains
80
Diphtheria exotoxin causes
Exudative pharyngitis which evolves into a thick pseudomembrahl
81
Pseudomembrane components
Dead cells, fibrin, bacteria, lymphocytes, gray pigment
82
Pseudomembrane can cause
Suffocation by obstructing the air way
83
Diphtheria toxin can diffuse
Into neck tissue causing edema so the patient appears bull-necked
84
Diphtheria spread
Toxin doesn't invade deeper than epithelial but disseminated Then damages heart causing myocarditis
85
Diphtheria treatment
Antibiotics and diphtheria antitoxin
86
Mycobacteria genus
Gram +, irregular shaped bacilli, long filamenteus Acid-fast bacilli (afb) Strict aerobe
87
Mycobacteria grow
Well on simple nutrients/media but slower compared to other bacteria
88
2 mycobacteria species of medical importance
Mycobacterium tuberculosis Mycobacterium leprae
89
Mycobacterium TB virulence
No exctoxins/enzymes, cord factor (waxes) prevent destruction by phagocyte lysosomes
90
Cord factor contributes
To serpentine cord formation
91
Mycobacterium TB transmission
Fine respiratory droplets
92
TB stats
1/4 world population infected, 1-2 million deaths a year, leading killer of HIV infected worldwide
93
Primary tubereulosis
10 cells, bacilli phagocytized by alveolar macrophages multiply intracellularly Weeks later cell-mediated immune response form tubercles
94
Secondary tuberculosis
Tubercles with masses of bacilli expand and drain into the bronchial tubes and upper respiratory tract Symptoms worsen violent cough, green or bloody sputum, low fever, night sweats, weight loss, fatigue, chest pain
95
Extrapulmonary tuberculosis
Deactivation of bacilli allows them to disseminate rapidly to extrapulmonary sites like kidneys, bones, brain genital tract High mortality
96
Treatment for all TB stages
Multidrug therapy lasting from 6-24 months
97
TB vaccine
Only outside the US, live attenuated BCG vaccine
98
Mycobacterium leprae
Causes leprosy, HanSen's bacillus, strict parasite, can't culture Slowest growing of all species
99
Mycobacterium leprae infection
Direct contact transmission, not very contagious, multiplies in macrophages of skin and spreads to nerves
100
2 forms of leprosy
Tuberculoid leprosy Lepromatous leprosy
101
Tuberculoid leprosy
Superficial infection with shallow skin lesions containing few bacilli Damage to nerves causes loss of pain perception Easily treated
102
Lepromatous leprosy
Deeply modular infection causing severe disfigurement to face and extremities

Microbio (14 decks)

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