Soil Pathogens

Question 1

Anthrax

Answer 1

-A disease that primarily affects livestock (particularly cattle) by can infect
humans.
-It is caused by Bacillus anthracis, a capsulated gram-positive bacterium that produces endospores upon exposure to the environment enabling survival,
in the soil for decades.

Question 2

Discovery of anthrax

Answer 2

Robert Koch isolated B. anthracis in 1877 and
established that it was the pathogen responsible for
Anthrax. He used this disease to formulate his
famous postulates.

Question 3

three forms of human anthrax

Answer 3

Cutaneous anthrax
Gastrointestinal anthrax
Pulmonary anthrax

Question 4

Cutaneous anthrax

Answer 4

Cutaneous anthrax is contacted when
spores are introduced into broken skin
through mechanical damage or flies

Question 5

Gastrointestinal anthrax

Answer 5

Gastrointestinal anthrax infects intestinal
lesions (animals eat spiky or hard
vegetation which damages the mucosa of
the gut).

Question 6

Pulmonary anthrax

Answer 6

the inhalation of spores
in dust

Question 7

Livestock contraction of anthrax

Answer 7

Livestock (or herbivores in the wild) are often infected by grazing on contaminated (spore-containing) soil, carnivores can contract the disease by eating infected animals

Question 8

Human source of anthrax

Answer 8

Humans commonly contract anthrax from the handling of contaminated animal products (hides, wool,
meat) as a result, cutaneous anthrax is the most common form of the disease in humans.

Question 9

Major virulence factor of anthrax

Answer 9

Capsule because it prevents killing by macrophages

Question 10

Cutaneous anthrax mortality rate

Answer 10

Cutaneous anthrax has a lower mortality rate than gastrointestinal and pulmonary anthrax
(approx. 20%) as the infection is initially a local one. If untreated it will spread, and the
individual will die from toxaemia (dissemination of toxins in the blood).

Question 11

Gastrointestinal anthrax has a mortality rate of

Answer 11

25-60%

Question 12

Pulmonary anthrax can have a mortality rate of

Answer 12

45-90%

Question 13

Antharx plasmids

Answer 13

pXO2 encodes for its capsule which is essential for immune evasion.
PXO1 encodes for its toxins: protective antigen (PA), edema factor (EF), and lethal factor
(LF).

Question 14

Anthrax toxin mechanism

Answer 14

Anthrax toxins are a variant of the A-B toxin system:
1) PA is responsible for the transport of EF and LF into cells. It binds to cell receptors then it is
cleaved by furin, a protease on the surface of the cell to generate a 63kDa protein
fragment. 5 fragments form a heptamer, which form a pore-like structure in the
membrane of the cell.
2) The pore heptamer complex facilitates the transport of EF into the cell. This causes an
increase in cAMP and altered calcium signalling. This alters ion and water transport, which
in turn alters osmolarity within the cell.
3) The pore heptamer complex also facilitates the transport of LF into the cell. This damages
the MAPK signalling pathway and causes apoptosis.

Question 16

Overall effect of anthrax toxin

Answer 16

Ultimately, the toxins kill immune cells and damage blood vessels leading to fluid
accumulation in tissues, cell death and the release of inflammatory cytokines. Death is from
shock, tissue damage and hypovolemic shock.

Question 17

Anthrax treatments

Answer 17

If diagnosed in time, anthrax can be treated with antibiotics however, if sufficient
toxins have already been produced in the infected individual, antibiotics are
ineffective.
A vaccine is available and was originally developed by Pasteur. This has significantly
reduced the incidence of anthrax, which was once a significant cause of livestock
mortality.

Question 18

Anthrax militray usage

Answer 18

The high mortality rate of pulmonary anthrax has led to it being developed as a
bioweapon by Japan and Russia and the UK during and after the second world war.
In 2001 anthrax ‘powder’ was sent to government offices in envelopes in the USA,
leading to several deaths. Bruce Ivins was later found to be responsible for these
bioterrorism attacks.

Question 19

Tetanus and Gas Gangrene description

Answer 19

Two potentially life-threatening diseases caused by soil-borne clostridia, which are spore-forming
gram-positive anaerobes.

Question 20

Infiltration and effect of tetani

Answer 20

C. tetani gains access to the body through a soil-contaminated wound, typically a deep
puncture.
Result of C. tetani infection on people is lockjaw. Paralysis extends to rest of body

Question 21

Tetanus treatment

Answer 21

Tetanus is preventable; the existing vaccine is completely effective, usually lasts for 10
years

Question 22

Tetanus toxin mechanism

Answer 22

a) Muscle relaxation is normally induced by glycine (G) release from inhibitory interneurons. Glycine acts on the motor
neurons to block excitation and release of acetylcholine (A) at the motor end plate. (b) Tetanus toxin binds to the
interneuron to prevent release of glycine from vesicles, resulting in a lack of inhibitory signals to the motor neurons,
constant release of acetylcholine to the muscle fibers, irreversible contraction of the muscles, and spastic paralysis.

Question 23

Gas gangrene (myonecrosis)

Answer 23

A potentially fatal infection of deep soft tissue mainly caused by Clostridium perfringens,
where the bacterium enters deep wounds through trauma.
Wounds formed as a complication of diabetes can also become gangrenous. Individuals
with vascular damage and immune impairment are most susceptible.

Question 24

Grangene disease mechanism

Answer 24

The clostridial organisms produce alpha and theta toxins that cause extensive tissue
damage. The infection can spread quickly, and within a matter of several hours, the patient
may develop overwhelming shock, sepsis, and death.

Question 25

Grangene disease treatment

Answer 25

Aggressive early treatment with antibiotics and hyperbaric oxygen is usually required.
Amputation of dead tissue may be necessary.

Question 26

Alpha toxin

Answer 26

Lecithinase (or phospholipase) that breaks down cell membrane resulting in cell death and tissue
necrosis. This toxin is also hemolytic and cardiotoxic.

Question 27

Beta toxin

Answer 27

Necrosis of tissue

Question 28

Delta toxin

Answer 28

Hemolysin

Question 29

Epsilon toxin:

Answer 29

Acts to increase cell membrane permeability; permease.
Iota toxin: Necrosis of tissue

Question 30

Kappa toxin

Answer 30

Collagenase, gelatinase, necrosis of tissue. Especially leads to destruction of blood vessels and
connective tissue.

Question 31

Lambda toxin

Answer 31

Protease

Question 32

Mu toxin

Answer 32

Hyaluronidase

Question 33

Nu toxin

Answer 33

Deoxyribonuclease, hemolytic and necrosis of tissu

Question 34

Phi toxin

Answer 34

Hemolysin, cytolysin

Question 35

Waterborne diseases

Answer 35

Many pathogens can be transmitted via contaminated water whether this is water used for drinking,
cooking washing etc. or recreational water (pools, ponds lakes etc.)
Eg: Cholera, Legionelles

Question 36

Cholera

Answer 36

Cholera is a potentially fatal gastrointestinal diarrheal disease caused by Vibrio cholerae, a
gram-negative highly motile (flagellated) bacterium

Question 37

Cholera transmission

Answer 37

Cholera is typically transmitted through
ingestion of (fecal) contaminated water or seafood such oysters or shellfish that have beenexposed to water containing the bacterium.
Vibrio cholerae accumulates in or interacts with phytoplankton and zooplankton which are eaten by shellfish.

Question 38

location cholera epidemics

Answer 38

Cholera epidemics were once common throughout the world but now, cases are
restricted to developing countries in Africa, Southeast Asia, the Indian subcontinent, and
Central and South America, where proper water treatment is lacking.
The discovery of the source of a major cholera outbreak in London in the 1850’s (the
Southwark and Vauxhall’s Broad-Street water pump) by physician, John Snow, is
regarded as a triumph of epidemiology.

Question 39

Cholera mechanism of infection

Answer 39

Once ingested, V. cholerae cells are mostly destroyed by stomach acid. Those cells that
survive move to the small intestine and migrate through the mucus layer covering the
epithelium and attach to epithelial cells of the small intestine where they begin to
proliferate and produce the cholera toxin.

Question 40

Cholera infection symptoms

Answer 40

This results in the production of large amounts of watery diarrhoea (called rice water),
which facilitates the expulsion of progeny bacterial cells from the host into new water
sources.
The enterotoxin causes fluid losses of up to 20 litres (20 kilograms or 44 l b) per person per
day, causing severe dehydration.
The mortality rate from untreated cholera is 25–50 percent

Question 41

Cholera toxin mechanism

Answer 41

The cholera toxin is a potent A-B toxin. The A
subunit, upon cellular entry, ADP-ribosylates the enzyme Adenylate cyclase, which causes a large increase in cAMP. This prevents Na ion uptake and the hypersecretion of anions and water from the cell

Question 42

Cholera treatment

Answer 42

Treatment usually requires oral or in severe cases, intravenous hydration therapy with
electrolyte replacement, together with antibiotics.
A vaccine is available.

Question 43

Legionnaire’s disease (LD) cause

Answer 43

A Non-Communicable Water-borne disease
The causative agent is Legionella pneumophila, a gram-negative bacterium known to be a major waterborne
pathogen in residential water systems such as hot-water tanks, hot tubs and the cooling water systems of air conditioners. It often exists in biofilms in which it is protected from the chlorine present in potable waters.
It also infects and ‘shelters’ within amoeba, which exist within biofilms.
Infected amoeba are reservoirs for Legionella pneumophila.

Question 44

LD route of infection

Answer 44

The pathogen is inhaled as aerosolized droplets into the lungs, where it is taken up by
resident macrophages.
Those usually at risk are the elderly and people with compromised lung function or those that smoke.

Question 45

LD mechansim of infection

Answer 45

The interaction of virulent legionellae with phagocytic cells can be divided into several
steps:
* binding of microorganisms to receptors on the surface of eukaryotic cells
* penetration of microorganisms into phagocytes
* escape from bactericidal attack
* formation of a replicative vacuole (a compartment within the cell where bacterial
replication occurs)
* intracellular multiplication and killing of the host cell.

Question 46

LD effect

Answer 46

This results in a severe, often fatal pneumonia, that is not spread to others.

Question 47

LD treatment

Answer 47

Legionellosis can be treated with
antibiotics, in particular rifampin
and erythromycin, and
intravenous administration of
erythromycin is the treatment of
choice for life-threatening cases.

Question 48

Nororvirus

Answer 48

(Norwalk Agent)
(non-enveloped, positive sense RNA virus)
A common viral cause of gastrointestinal illness.

Question 49

Norovirus symptoms

Answer 49

Symptoms are vomiting, diarrhoea, and malaise, it is rarely fatal.

Question 50

Norovirus cell type

Answer 50

The virus specifically attacks tuft cells found in the intestinal epithelium. These are a specialized class of chemosensory cells that detect specific molecules made by bacteria and protozoans within the intestine

Question 51

Norovirus transmission (where its found)

Answer 51

-Noroviruses are easily transmitted from person to person or to food by a faecal-oral route.
-Most common sources of waterborne norovirus outbreaks are well water or recreational waters that have been
contaminated with sewage.
-Often the culprit when mass common-source gastrointestinal illnesses strike people on cruise ships or in longterm care facilities or other group setting.