Ph 162A Lec 24: Zoonoses

Front 1

what is zoonoses?

Back 1

diseases caused by microorganisms, whose reservoir is animals (nonhuman animals)
**can transmit disease to humans

**the transmission mechanism can be direct contact w/ animal feces or through insect vectors
**The organisms usually completes its entire life cycle w/in the animal, and the human is an accidental host

Front 2

Name the four zoonotic diseases we are going to learn?

Back 2

1. Bubonic Plague (black death)
2. Lyme disease
3. toxoplasmosis
4. rabies

Front 3

[Bubonic Plague (black death)]

Back 3

**in the 14th century-- outbreak in Europe killed 20-30 million people (responsible for killing a third of the world's population)
**second largest one was in 1855, a pandemic started in China and ended in the U.S, San Francisco.

**today about 2000 cases a year and less then 10 cases in the U.S

Front 4

[Bubonic Plague (black death)]

Etiology

Back 4

Yersinia pestis-- a gram-negative coccobacillus.

**note: infectious dose is extremely low, it only takes one organism for a person to become infected and develop the plague

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[Bubonic Plague (black death)]

reservoir

Back 5

rodents

note: in the U.S the most prevalent rodent that spreads infections to humans is squirrels

Front 6

[Bubonic Plague (black death)]

Transmission

Back 6

**insect vectors-- comes from the fleas that the rodents have, the fleas transmit the disease to humans

note: Yersinia will also kill the rodent, and this can be important to the spread because when the rodent dies, the fleas on that rodent need to find a new host. For that reason, the people at high risk for getting plague

Front 7

[Bubonic Plague (black death)]

Pathology and Clinical Manifestations

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**the bacteria multiply in the lymph at the site of the bite and then travel to the lymph nodes causing tremendous enlargement and swelling of that node know as bubo.
--bubo has dark regions on it, and this is caused by hemorrhages within the lymph nodes. It is blood under the skin.
--the term “bubonic plague” comes from this bubo.

** In more severe cases, the bacteria can actually get into the bloodstream, you will get breakage and leaking of the blood vessels. ------That hemorrhaging of the blood vessels causes an accumulation of blood under the skin, so you get this dark coloration of the skin.
-- nickname as “black death” of “black plague.”
**Bubonic plague can become pneumonic plague when it enters the bloodstream and considered pneumonic plague when it spreads to the lungs, --->this occurs rapidly once it enters the bloodstream.
--When it enters the lungs, it becomes much more virulent to an individual-->the person will start coughing up bloody mucous---> that rapidly progresses into a bloody froth that the person is coughing up.
--when a person is coughing this bloody mucous, they are spreading the bacteria through aerosolized droplets. So when the plague is pneumonic, it can spread from person to person.

Note: Pneumonic plague is extremely serious. If untreated, it has a 100% mortality rate. Death can be extremely rapid, occurring within a few hours of the onset of symptoms. On the chest X-ray of someone who has pneumonic plague, there is a haziness that is indicative of pneumonic plague.

Front 8

[Bubonic Plague (black death)]

Diagnosis

Back 8

**smear of material taken from the bubo
--on the stain you'll see a very typical type of bipolar staining of the Yersinia
--smears can also be reacted to the antibodies specific for Yersinia

Front 9

[Bubonic Plague (black death)]

Treatment

Back 9

note: in the Middle Age, a popular way of treating plague was by lancing the buboes

Treatment: antibiotics, aminoglycocides, as well as tetracycline are very effective
--they inhibit the bacterial protein synthesis
--need to treated early b/c if it spreads to the lungs treatment is not going to be as effective

Front 10

[Bubonic Plague (black death)]

Prevention (7)

Back 10

1. killed vaccine
2. f you are exposed to bubonic plague prophylactic antibiotics are given
3. surveillance of rodent populations-- screening them to see if they are infected
4. rodent extermination
5. avoid getting close or touching friendly rodents
6. insect repellent to prevent flea bites
7. inspection of ships and harbor areas to prevent transport of infected rats to new locations

Front 11

[Lyme Disease: the process of how Lyme disease was discovered]

When was Lyme disease first discovered? and who reported the cases?

Back 11

note: Lyme disease was relatively recently discovered, with the initial investigation starting in 1975.

**1975—2 mothers reported to officials of the Connecticut State Health Department: The first mother reported that 12 children in the town of Old Lyme had come down with juvenile rheumatoid arthritis. The second mother in the same town reported an epidemic of arthritis within her family, which is also extremely unusual.

Front 12

[Lyme Disease]

1975-1977-- public health epidemiologists found a set of signs and symptoms associated w/ the arthritis: what are they?

Back 12

1. A single red lesion on the skin that gradually expanded and cleared to a normal color in the center
2. Fever, chills, headache, stiff neck
3. Four weeks after initial lesion, arthritis appeared in 1 or few joints
***At this point, they had symptoms for this arthritic disease.

Front 13

[Lyme Disease]

This disease was called Lyme disease because

Back 13

it was initially recognized in the town of Old Lyme.

Front 14

[Lyme Disease]

1977-1979: Why were people in this area getting this disease (what was know at this time)? what was the identified tick they think it was?

Back 14

**there was this correlation between the ticks and Lyme disease
-- A number of individuals remember being bitten by ticks at the site of the red lesion. The tick that they identified was Ixodes scapularis.
--People also found that in times of greater tick season, they found more of this arthritic disease

Front 15

[Lyme Disease]

1980-- How did they found out that this Lyme disease was a bacterium and not a virus?

Back 15

a doctor decided to go ahead and try treating his patients with penicillin and tetracycline. When he gave his patients antibiotics, they greatly improved. This improvement after antibiotic treatment suggested that perhaps the agent was not a virus, but a bacterium.

Front 16

[Lyme Disease]

1980-82-- over the next two years, the bacterium that was identified was called____

Back 16

Borrelia burgdorferi-- a spiral-shaped bacterium ** named after Willy Burgdorfer

note: He isolated the bacteria from a tick and he inoculate the bacteria to the rabbits-- the rabbits would develop that bull’s eye lesion

Front 17

[Lyme Disease]

As people continued to learned more about lime disease, they found that there were more vectors to it. What are these other vectors?

Back 17

1. In California (the west coast)-- the vector is
**Ixodes pacificus (a tick)
**wood rat (discovered by Richard Brown and Robert Lane of UCB)
2. East Coast
** Ixodes scapularis
** deer
**field mouse

Front 18

[Lyme Disease]

What make lyme disease emerge as a new disease? why did we not see any of this before 1975?

Back 18

There are changes in the ways that we interact w/ animals. There were less hunting of deer, so the deer population increased--> and you also have humans live closer proximity to the animals that were in the reservoir

Front 19

[Lyme Disease]

Where else can you find Lyme disease other then the U.S?

Back 19

Europe, Canada

note: this also affects dogs, cows, and horses

Front 20

[Lyme Disease]

Why there are far more Lyme disease on the east coast than on the west coast?

Back 20

on the west coast, you have the western fence lizard-- it was determined that tick that spreads Lyme disease feeds on the western fence lizard. However, when it feeds on the lizard, the lizard does not get infected, and the tick actually clears the infection. The reason for this is that there is a protein within the lizard’s blood that kills the spirochete.

Front 21

[Lyme Disease]

Diagnosis

Back 21

**sign-- the bull's eye lesion
**serological tests for the spirochetes (not accurate)

Front 22

[Lyme Disease]

Treatment

Back 22

**amoxacillin and doxycycline-- very effective especially if treated early

Front 23

[Lyme Disease]

Prevention (5)

Back 23

1. have skin covered with when walking through underbrush
2. stick to cleared trail when hiking
3. use insect repellant
4. pregnant women should be especially careful
5. Vaccine-- for dogs

Front 24

[Toxoplasmosis]

etiology

Back 24

Toxoplasma gondii-- a protozoan (sporozoan)

Front 25

[Toxoplasmosis]

reservoir

Back 25

**cat-- is the definitive host for this protozoan
**humans, birds, rodents, ungulates-- made serve as the intermediate host

note:
**definitive host = is the the host in which the parasite reaches maturity and if applicable this is where the parasite will reproduce sexually
**intermediate host = host harbors the parasite only for a short period of time

Front 26

[Toxoplasmosis]

Transmission

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fecal-oral route:

**animals can consume the cat's excrement and if we under cook meat, we can become infected
**children eating dirt
**organ transplants

Front 27

[Toxoplasmosis]

life cycle

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**have complex life cycle but here is a general overview:

**the cat becomes infected, the Toxoplasma goes through a particular developmental step to form an oocyte---> That is passed in the cat’s feces. These oocytes are the infectious forms of Toxoplasma.

Front 28

[Toxoplasmosis]

Clinical Manifestations
**why is it more serious to fetuses and small children?

Back 28

**majority of infections are sasymptomatic
**swollen lymph nodes, a slight fever, or rash
**in small children and immunocompromised individuals the disease can be more serious---> can cuase ENCEPHALITIS = infection of the brain
**the disease is most serious in fetus-- infection may result in spontaneous abortion or marked damage to the CNS including hydrocephaly (this is the accumulation of cerebrospinal fluid in the brain), blindness, mental retardation, and motor disturbances.

Front 29

[Toxoplasmosis]

Diagnosis

Back 29

1. direct smear-- usually done by spinal fluid
--organism has dark spots for the nuclei
2. Measurement of antibodies to the the organism (the ELISA is the most sensitive)

Front 30

[Toxoplasmosis]

Treatment

Back 30

sulfonamides and pyrimethanmine -- these drugs inhibit folic acid synthesis

note: this is effective b/c protozoans need much more higher levels of folic acid to survive than we do

Front 31

[Toxoplasmosis]

Prevention (4)

Back 31

1. Don't have a cat
2. Keep cats from defecating where children play; e.g sandboxes, gardens
3. Cook all meat thoroughly
4. Pregnant women should be especially careful

Front 32

[Rabies]

etiology

Back 32

rabies virus-- an RNA virus (helical, enveloped)

**this disease is extremely deadly

Front 33

[Rabies]

reservoir

Back 33

**dogs and cats are the main reservoir in developing countries

**skunks, bats, raccoons, and foxes are the main wildife reservoirs in the USA-- b/c most cats and dogs are vaccinated

Front 34

[Rabies]

When an animal is infected w/ rabies it is called a ______

Back 34

rabid animal

Front 35

[Rabies]

Transmission

Back 35

transmitted from the saliva of the infected animal-- the virus is shed into the saliva, and when the animal bites another animal or human, it spreads the virus

note: bats can spread the virus through their feces

Front 36

[Rabies]

Incidence

Back 36

Rabies is found worldwide

**annually there are about 30-50 deaths-- death usually occur in children under the age of 15

note: It is very rare in the U.S

Front 37

[Rabies]

Pathology

Back 37

the virus will replicate in the tissue around the bite. And then from there, the virus moves to the nerves, and it can travel up the nerve tracts into the brain. Once there, the virus destroys nerve cells.

Front 38

[Rabies]

Clinical Manifestations

Back 38

**usually begins about 2-8 weeks after the initial bite

--starts w/ fever as well as nausea and vomiting, then you begin to see agitation as well as spasms of the throat muscle--> making it difficult to swallow--> where you get an accumulation of saliva---> eventually you get delirium and coma, and then death

notes: other symptoms include fear of water and rage.

Front 39

[Rabies]

diagnosis

Back 39

**First catch the animal that bites you--> killed it and section the brain to see if it has rabies
--you can do a staining and look for Negri bodies, you can also used fluorescent antibodies

--this is the only way to show if the person is infected by rabies by catching the animal that bit them

Front 40

[Rabies]

Host immune response

Back 40

**does not have a good immune response to this virus
--b/c onset of disease is so rapid that there isn't time to mount a good immune response

Front 41

[Rabies]

treatment

Back 41

**passive immunization-- administer antibodies specific to the virus.
** a person can be vaccinated so that they can have active immunity to the virus.
-- The vaccine is a killed preparation of viral glycoproteins.

note: Since the incubation time for this virus is somewhat long (it takes about two weeks for the rapid onset of symptoms), this gives time for someone to mount an immune response and for the vaccination to be effective.

Front 42

[Rabies]

Prevention (3)

Back 42

1. vaccination of dogs and cats
2. vaccination of people with professional risk
3. vaccination combined w/ quarantine of imported animals

Front 43

E. coli-- many serotypes and designations: name 3 serotypes and their pathogenecity

Back 43

1. EPEC-- an enteropathogenic-- no enterotoxins, found in raw meat
*does not form toxins, does little harm

2. EIEC-- enteroinvasive-- food source unkw.

3. EHEC: enterohemorrhagic-- serotype O157:H7 produces verotoxin and shiga like toxin

*very deadly causes bloody diarrhea

Front 44

What are the critical factors that makes E. coli virulence?

Back 44

*pathogenicity island
*production of an enterotoxin called Shiga toxin
*as few as 10 cells can cause infection

Front 45

Transmission of E. coli 0157:H7

Back 45

*animals to humans
--contaminated foods
--direct animal to human contact
*vegetable to human
*Person-to-person

Front 46

E. coli 0157:H7 pathology/clinical

Back 46

*Severe bloody diarrhea and abdominal cramps
--resolves in 5-10 days

*can contract HUS (hemolytic uremic syndrome)--> result in destruction of red blood cell and kidney failure

Front 47

diagnosis/ and treatment for E. coli 0157:H7

Back 47

*diagnosis-- positive stool sample

*Treatment: most people get better w/in 5-10 days w/o treatment.
--antibiotics are not recommended b/c they can further stress in the kidney
--avoid anti-diarrheal medication as it will stop the flushing of the bacterium from the body
--HUS requires extensive care

Front 48

Prevention of E. coli

Back 48

1. sensitive to heat-- heat meat to 160 F
2. wash fruits and vegetables well
3. avoid raw milk and unpasteurized diary and juice products
4. wash hands after using bathroom and visiting patting zoos