2. Hantavirus Pulmonary
Syndrome (HPS)
The first recognized cases occurred in
May of 1993, in the four corners area of
the southwest USA.
– New Mexico, Arizona, Colorado, Utah
Through June 6, 2002 there have been a
total of 318 cases of HPS in the USA.
38% of all reported cases have resulted
in death
Cases have been reported in 31 states,
including most of the western ½ of the
country, and some eastern states
– Over half of the cases of HPS are found
outside the four corners area.
3. Hantavirus Pulmonary
Syndrome
Cases of HPS have
also been confirmed
from Argentina,
Bolivia, Brazil, Canada,
Chile, Panama,
Paraguay, and
Uruguay.
– HPS is classified as a
pan-American zoonosis
HPS has also been
linked with
hypertensive renal
disease in the inner
city
Carriers in the USA and
the virus they transmit:
Deer Mouse Sin Nombre virus -
most often
Cotton rat (Florida) Black canal
virus
Rice rat (Louisiana) Bayou
virus
White footed mouse (New
York) SNV
4. Bat viruses in Australia
All of the newly identified viruses are
Rhabdoviruses which are related to the
viruses that cause rabies and Lyssa
fever.
– Viruses in this family have a high fatality rate
often near 100%
Henda Virus (Equine Morbillivirus) -
infects humans, horses, cats and Guinea
pigs. Fruit bats are the natural reservoir.
– Fast response to outbreak in Australia
Australian bat lyssa viruses (Ballina
virus) - this is a close relative of rabies
Menangle virus - carried by fruit bats and
causes disease in pigs
5. Dog and Cat
Roundworms
(See assigned reading)
http://www.dpd.cdc.gov/dpdx/HT
ML/Toxocariasis.htm
(All 6 parts – “Causal agent”
through “Treatment”)
6.
7. Raccoon Roundworms
(Baylisascaris procyonis)
Common intestinal roundworm of raccoons
Eggs deposited in raccoon feces (infective in
thirty days)
Ingested by man or other animal
Aggressive migration (eyes, brain, other
tissue)
– Fatal nervous system disease, eye
disease in intermediate host (mice,
squirrel, chickens, quail, man etc.)
– Encyst and await ingestion by raccoon
scavenger.
9. Raccoon Roundworms
Transmission of Baylisascaris to
Humans
Eggs shed in raccoon feces, infective
in 30 days
Hatch after ingestion, penetrate
intestinal wall
Migrate to liver, lungs and muscle
Encyst in small fibrous nodules
causing no further problems or
Some enter the brain and eyes and
cause disease.
10. Raccoon Roundworms
Prevalence of Baylisascaris in
Raccoons
50- 89% of raccoons have the worm
One study of 520 raccoons 70% of all age
groups and 88% of juvenile raccoons
were infected.
Eggs are very resistant and can survive
three to five years.
Serious infection is rarely diagnosed;
<30 cases reported. Probably many
undiagnosed cases.
11. Raccoon Roundworm
Human infection
Ocular infection
– Primate research – multifocal retinal
hemorrhages, white spots, chorioretinitis,
inflammatory tracks, vascular sheathing, and
diffuse retinal degeneration
– Reaches eyes by 7 days post-ingestion
Diagnosis of Baylisascaris infection
– History of pica, raccoon exposure
– Serology (still experimental- ELISA & Indirect
immunofluroescent test).
– Difficult to diagnose in a living person but in
ocular cases there is often a diagnostic
lesion in the eye.
12.
13. Raccoon Roundworms
Control and/or Prevention of
Baylisascaris
Disinfectants for contaminated
areas (heat or lipid solvents)
Discourage raccoon ownership
(pets)
Regularly de-worm raccoons at
zoos, wildlife exhibits, etc.
Discourage raccoons from living
near people by removing sources
of food and/or shelter
14. Other Similar Roundworm
Species
Skunk roundworm (Baylisascaris
columnaris)
– Poorly understood
– Kills mice, rabbits, and woodchucks
by CNS migration
– Infection of man is unknown
15. Viral Hemorrhagic
Fever
Caused by a number of viruses – Lassa,
Marburg, Ebola, and Congo-Crimean
Hemorrhagic Fever
Most are transmitted by direct contact of
bodily fluids in the later stages of the
disease
– Vomiting, diarrhea, shock and hemorrhage.
– not transmissible via air.
– Caregivers often infected.
Ebola and Marburg are RNA viruses in
the filovirus family.
Electron
micrograph of
Ebola virus.
biosafety level four
(BSL-4) pathogens
16. Marburg
First occurred in Germany in 1967
when Laboratory workers were
exposed to infected monkeys from
Uganda.
Non-human primates can be
infected but they are not considered
to be the natural reservoir.
– The natural reservoirs for this virus is
unknown.
17. Ebola
First discovered in 1976 near the Ebola
river.
There are four known types of the Ebola:
Zaire, Sudan, Ivory Coast, and Reston
The Zaire and Sudan strains are associated
with disease in humans.
– Incubation period is up to 3 weeks.
– Initial clinical signs include fever, headache,
chills, myalgia, and malaise. Later abdominal
pain, vomiting, diarrhea and occasionally a
maculopapular rash are seen. Hemorrhagic
manifestations with disseminated intravascular
coagulation can be observed in fatal cases.
18. Zaire and Sudan strains (Continued)
– 50- 90% fatality has been
reported.
– Since its discovery in 1976, Ebola
has killed more than 800 people.
– Due to the high fatality of the
disease, the outbreaks have not
become large.
19. Zaire and Sudan strains (Continued)
Like Marburg, the natural reservoir is
unknown but human cases are often
preceded by large die-offs of non-human
primates. Epidemiologists, including
veterinarians, are currently investigating
many sources including plants as
possible vectors.
The last known cases of Ebola occurred in
The Republic of the Congo and Gabon in
late 2001 to 2002.
– As of 4/1/2002, these outbreaks took the lives of
96 people in 122 known cases (WHO).
20. Personal Safety Issues
Veterinarians chasing
around the jungle for Ebola
EIS Track record
“Outbreak” the movie
21. Ebola - Reston (“The Hot Zone”)
This strain of Ebola was discovered in Reston,
Virginia in 1989.
It was first identified in monkeys from the
Philippines.
Ebola-Reston is often fatal in monkeys, in four
known cases in humans however the virus
evokes an immune response but was
asymptomatic.
Four episodes of Ebola-Reston infection among
monkeys imported from the Philippines have
occurred in the USA and Italy.
Aerosol spread, while not documented in
humans, has been seen in non-human primates.
– Very scary!
22. Brucellosis
Undulant Fever, Mediterranean Fever, or Malta Fever.
Species of Brucella and the usual host.
– B. canis in dogs
– B. melitensis in goats and sheep
– B. suis in pigs
– B. abortus in cattle
B. melitensis is the most virulent in humans and
infection
is usually associated with unpasturized dairy
products
from Mediterranean countries or Mexico
Incidence of human infections:
1947 - 6300 cases a year
1990 – about 100 cases a year (but only 4 to 10%
are recognized and reported).
23. Brucellosis
Human cases:
– Incubation period- usually 30 days but can
be up to 5 months
– Symptoms - non-specific. Fever, chills,
headache, myalgia, arthralgia, anorexia,
fatigue, lymphadenopathy and
splenomagaly. The ratio to subclinical to
clinical cases is 1:1 to 12:1.
– Treatment - many different antibiotics -
Doxycycline Occupational exposures are
common. Occupational exposure is seen
among packing plant workers,
veterinarians, livestock producers, and
laboratory workers. Vets used to get strain
19 (vaccine)
– Exposures occur through breaks in the
skin, inhalation and conjunctival contact.
24. Brucellosis
Prevention:
– Reduce exposure by controlling the
disease in the animal population.
– Public health efforts to ensure the
proper pasteurization of dairy products.
Eradication Programs:
– Cattle Brucellosis program - the goal is
eradication. Most of the infected herds
are in Texas and the South Eastern
states.
– Swine Brucellosis program – Nearly
eradicated from US.
25. Bartonellosis
Two diseases: Cat Scratch Disease
and Bacillary Angiomatosis.
Cat Scratch Disease has been
described for 100 years. The agent,
slightly curved gram negative rods, was
identified in 1988.
The agent has been placed in the genus
Bartonella
– may be related to the agents which cause
Typhus, RMSF, tsutsugamushi, Q fever,
Brucella, and Richettsia quintana.
26. CSD
The disease is subclinical in cats.
Transmission to humans:
– Following cat bites, scratches, and
possibly bites
from cat fleas.
– Cat saliva over an area of compromised
skin integrity may also lead to infection.
– Kittens are more likely to infect people
because they scratch more often and
have a higher prevalence of Bartonella.
– Prevalence in cats of all ages can be 30
to 50%.
27. CSD
An estimated 22,000 cases occur in the
USA each year.
First a 2-3 mm macule occurs at the site
of exposure. The macule becomes
papular within a few days.
The duration of the disease is usually
several weeks
Regional lymphadenopathy may develop
with fever, fatigue, and headache.
Clinically it can look similar to tularemia
or bubonic plague.
28. CSD
14% of cases can progress to more
severe symptoms which can include
eye problems, encephalopathy,
arthritis, osteolysis, vascular system
lesions, hepatitis, or pneumonia.
Treatment:
– Uncomplicated cases resolve on their
own.
– Antibiotics are effective in more severe
cases.
29. Bacillary Angiomatosis
Mostly in HIV - infected and other
immuno-suppressed individuals.
Much more severe disease than is CSD.
– Vascular lesions may involve many organs,
with skin being the most common.
Prevention:
– Wash hands after handling cats.
– Do not encourage rough play with cats.
– Use flea control.
– Do not let cats lick areas of abraded skin or
open wounds.
– HIV patients may wish to avoid being
scratched by cats.
30. Are CSD and Bacillary Angiomatosis
caused by the same agent?
Despite the similarities in histochemical staining
properties and epidemiology, serious reservations
remained concerning a possible link between the
causative agents of CSD and BA.
The pathologic features of classical CSD
(granuloma) and BA (proliferative vascular lesions
without granuloma) are distinctly different.
The two diseases seem to respond differently to
antibiotic therapy.
– The majority of BA patients evaluated responded quickly
to single-agent therapy with either erythromycin or
doxycycline (14,23), whereas the symptoms and signs of
patients with CSD failed to show consistent rapid
resolution following antibiotic therapy.
31. Rat Bite Fever
The responsible agent is Streptobaccilus
moniliformis (more common in U.S.) or
spirillary RBF by Spirillum minus
Nasopharyngeal carriage rates in healthy
laboratory rats range from 10% to 100%;
carriage rates in wild rats range from 50% to
100%
Transmission is usually through a rat bite.
However, some cases have rat exposure but no
reported bite.
– Ingestion of food contaminated with rat feces
Children and laboratory workers are at high risk
to contract this disease.
Cases are rarely reported in the United States
and the true incidence of disease is unknown.
32. Rat Bite Fever
Clinical syndrome: 2-10 days after rat
bite.
Usually a mild protracted illness with a
fever, malaise, cough, maculopapular
rash, and occasionally arthritis.
– Human fatalities have been reported.
– Antibiotics are effective (Shot gun)
Susceptible to penicillin
diagnosed by blood culture only.
33. Lymphocytic Choriomeningitis Virus
(LCMV)
The main reservoir is the house mouse (Mus
musculus) but hamsters and domestic mice can
also be infected.
Infection in people:
– Often subclinical.
– “influenza-like symptoms” but sometimes
meningeal symptoms of a stiff neck, fever,
headache, malaise, and muscular pain.
– Incubation period - 1 to 2 weeks.
– Pregnant women may transmit the disease to
the unborn fetus resulting in fetal or neonatal
death, hydrocephalus, chorioretinitis, or
psychomotor retardation.
Usually a history of a febrile illness during
their pregnancy.
34. LCMV
Prevalence- a study in Baltimore showed
that 9% of house mice and 4.7% of
residents had LCMV antibody
Transmission:
– Contact with mouse nasal secretions, urine,
semen, milk, and feces
– Mouse and hamster bites.
– Humans become infected by inhaling
infectious aerosolized particles of rodent
urine, feces, or saliva, by ingesting food
contaminated with virus, by contamination of
mucus membranes with infected body fluids,
or by directly exposing cuts or other open
wounds to virus-infected blood.
35. LCM
Risk factors:
– Recreational activates in rural
environments.
– Habitation in older rodent-infected
homes.
– Acquisition of rodents for pets
– Laboratory exposure to unscreened
rodents (rare)
– Pregnant women risk exposure to their
unborn children.
36. LCMV
Epidemiology of LCMV in mice:
– Much studied, interesting epidemiology, when
LCMV is introduced to a non-infected colony.
– Adult mouse infection shows some morbidity,
but most recover and no longer shed the virus.
– Infections acquired in utero lead to a persistent
tolerant infection with heavy shedding
throughout their lives (similar to BVD in cattle).
– Over time, the infection was only transmitted
congenitally in that all mice had been infected
before they were born.
– It appeared that transovarian infection was the
rule, rather than the exception.
37. LCMV
Prevention:
– Control the mouse population in
houses.
– Don’t touch dead mice.
– Pregnant women should avoid
hamsters, and other rodents.
– Most all laboratory animal colonies in
the US are LCMV-free.