MBI 111 Exam 3 Questions | 2026/2027 | Answers Correct |
With Complete Solutions
pathogenesis of anthrax
- spores rapidly germinate on contact with tissue
- capsule inhibits phagocytosis
- organs fill with bloody black fluid
- high mortality
process of anthrax pathogenesis
produces 3-component toxin
- PA (protective antigen) binds to cell, transports factors into
cell
- LF (lethal factor) interferes with cell signaling
- EF (edema factor) causes tissue swelling
Cutaneous anthrax
boil-like lesions with black crusts
transmission of cutaneous anthrax
contact with contaminated animal products
incubation period for cutaneous anthrax
2-3 days
symptoms of cutaneous anthrax
papule
necrotic ulcer
,may have fever, malaise, headache
potential blood invasion
treatment of cutaneous anthrax
doxycycline, ciprofloxacin (must be given early)
there is a vaccine
gastrointestinal anthrax
rare in humans - lesions on intestinal wall
Transmission of gastrointestinal anthrax
ingestion of contaminated meat
incubation for gastrointestinal anthrax
3-5 days
Symptoms of gastrointestinal anthrax
lesions on intestinal wall
nausea, loss of appetite, vomiting and fever,
abdominal pain, vomiting blood, and bloody diarrhea potential
for blood invasion
almost 100% mortality
Pulmonary anthrax
(woolsorters' disease)
acquired by shearers, wool sorters, tanners- rapid and severe
blood infection
transmission of pulmonary anthrax
inhalation of spores
,incubation of pulmonary anthrax
1-6 days
symptoms of pulmonary anthrax
initially flu-like (no runny nose)
hemorrhagic pneumonia and respiratory failure
shock and death within 24h
potential for long-term memory damage in survivors
mortality of pulmonary anthrax
often fatal (45-80%), even if treated
95% if treated after 48 h infection
> 99% if untreated
Tetanus
Clostridium tetani
Transmission of Tetanus
wound entry by spores
spores germinate in anaerobic environment of trauma site
pathogenesis of tetanus
entirely toxin-mediated - not invasive, can pass through without
causing disease
produces tetanospasmin toxin, neurotoxin, potent at extremely
low doses, second most powerful after botulinum toxin
mechanism of tetanus
blocks release of inhibitory neurotransmitter (GABA) from
upstream neuron
, cannot inhibit muscle contraction
simultaneous spasms of agonist and antagonist muscles
spastic paralysis
binds irreversibly
requires regeneration of neuron to recover
symptoms of tetanus
within hours
muscle stiffness
lockjaw
arching of back and rib muscles, seizures in diaphragm
treatment of tetanus
antitoxin to neutralize toxin, penicillin to eliminate infection,
supportive measures, muscle relaxants, sedatives, respiratory
assistance
immunization of tetanus
DPT tetanus toxoid - formaldehyde-treated toxin
boosters every 10 years
gangrene
condition that develops when blood flow ceases to a local area,
usually by blockage with dead tissue, body part becomes dry,
shrunken, and purple-black, may spread as proteolytic enzymes
are released from dead cells
gas gangrene
occurs when soilborne bacteria invade dead anaerobic tissue
transmission of gangrene
With Complete Solutions
pathogenesis of anthrax
- spores rapidly germinate on contact with tissue
- capsule inhibits phagocytosis
- organs fill with bloody black fluid
- high mortality
process of anthrax pathogenesis
produces 3-component toxin
- PA (protective antigen) binds to cell, transports factors into
cell
- LF (lethal factor) interferes with cell signaling
- EF (edema factor) causes tissue swelling
Cutaneous anthrax
boil-like lesions with black crusts
transmission of cutaneous anthrax
contact with contaminated animal products
incubation period for cutaneous anthrax
2-3 days
symptoms of cutaneous anthrax
papule
necrotic ulcer
,may have fever, malaise, headache
potential blood invasion
treatment of cutaneous anthrax
doxycycline, ciprofloxacin (must be given early)
there is a vaccine
gastrointestinal anthrax
rare in humans - lesions on intestinal wall
Transmission of gastrointestinal anthrax
ingestion of contaminated meat
incubation for gastrointestinal anthrax
3-5 days
Symptoms of gastrointestinal anthrax
lesions on intestinal wall
nausea, loss of appetite, vomiting and fever,
abdominal pain, vomiting blood, and bloody diarrhea potential
for blood invasion
almost 100% mortality
Pulmonary anthrax
(woolsorters' disease)
acquired by shearers, wool sorters, tanners- rapid and severe
blood infection
transmission of pulmonary anthrax
inhalation of spores
,incubation of pulmonary anthrax
1-6 days
symptoms of pulmonary anthrax
initially flu-like (no runny nose)
hemorrhagic pneumonia and respiratory failure
shock and death within 24h
potential for long-term memory damage in survivors
mortality of pulmonary anthrax
often fatal (45-80%), even if treated
95% if treated after 48 h infection
> 99% if untreated
Tetanus
Clostridium tetani
Transmission of Tetanus
wound entry by spores
spores germinate in anaerobic environment of trauma site
pathogenesis of tetanus
entirely toxin-mediated - not invasive, can pass through without
causing disease
produces tetanospasmin toxin, neurotoxin, potent at extremely
low doses, second most powerful after botulinum toxin
mechanism of tetanus
blocks release of inhibitory neurotransmitter (GABA) from
upstream neuron
, cannot inhibit muscle contraction
simultaneous spasms of agonist and antagonist muscles
spastic paralysis
binds irreversibly
requires regeneration of neuron to recover
symptoms of tetanus
within hours
muscle stiffness
lockjaw
arching of back and rib muscles, seizures in diaphragm
treatment of tetanus
antitoxin to neutralize toxin, penicillin to eliminate infection,
supportive measures, muscle relaxants, sedatives, respiratory
assistance
immunization of tetanus
DPT tetanus toxoid - formaldehyde-treated toxin
boosters every 10 years
gangrene
condition that develops when blood flow ceases to a local area,
usually by blockage with dead tissue, body part becomes dry,
shrunken, and purple-black, may spread as proteolytic enzymes
are released from dead cells
gas gangrene
occurs when soilborne bacteria invade dead anaerobic tissue
transmission of gangrene
