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Biodefense
Reference Library
Foreign
Animal and Zoonotic Disease Center
Zoonotic
Disease Online Course
Presented
by
Stephen M.
Apatow, Director
of Research and Development
Humanitarian
Resource Institute
Biodefense Reference Library
Foreign
Animal and Zoonotic Disease Center
[Vitae][Email]
ZOONOTIC
DISEASES
RICKETTSIAL
Q-FEVER
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
Q
fever
Office
International des Epizooties
Q
fever: Manual of standards Diagnostic Tests and Vaccines 2000
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Query
fever, Balkan influenza, Balkan grippe, pneumorickettsiosis, abattoir
fever)
AGENT:
Coxiella
burnetii Multiplies only in living cells. Stains red with Gimenez &
Macchiavello stains and purple with Giemsa. Infections in lab workers
have
been recognized for many years. Serious laboratory hazard in research
facilities
where infected "asymptomatic" ewes are used for projects.
RESERVOIR
AND INCIDENCE
Found
worldwide in wild and domestic animals in two self perpetuating cycles:
1. Wild animals, with numerous tick hosts 2. Domestic animals - sheep,
goats, cattle. Widespread in sheep in the U.S. Dogs, cats, and chickens
can also be infected. Enzootic infection among domestic animals is the
main reservoir of infection for humans.
TRANSMISSION:
Organism
shed in urine, feces, milk, and especially birth products of domestic
ungulates
that generally do not show clinical disease (usually sheep and goats).
Organism is resistant to drying and can persist for months while
providing
extensive environmental contamination. Aerosol is a major means of
transmission.
Contact with infected tissues: placenta of the infected ewe contains
109
organisms per gram of tissue. Amniotic and fetal tissues are highly
infective.
Soiled linen may infect personnel in the laundry. One organism is
considered
to be enough to cause infection in humans. Ingestion.
DISEASE
IN MAN:
Two weeks
to one month incubation. Febrile illness or subacute endocarditis. No
skin
eruption or rash, which distinguishes it from other Rickettsial species
infections. Severe frontal headache with retro-orbital pain, profuse
sweating,
myalgia, and nausea. Pulmonary involvement in half the cases.
Asymptomatic
in many cases. Most cases resolve in two weeks but may be protracted or
relapsing in the elderly. Chronic endocarditis, particularly in persons
with preexisting valvular disease, is difficult to treat and the case
fatality
rate may be as high as 60%.
DIAGNOSIS:
Leukopenia
with a diagnostic rise in specific CF antibodies to Coxiella phase 2.
The
Weil-Felix test (a test specific for typhus and other rickettsial
diseases)
is negative. Liver function tests are often abnormal. In Q fever
endocarditis,
there is a titer of 1:200 or more by CF or IFA with phase 1 antigen.
Isolation
of the organism from blood or sputum is rarely attempted due to
zoonotic
concerns.
TREATMENT:
Treatment
with tetracyclines can suppress symptoms and shorten the clinical
course
but does not always eradicate the infection. Even in untreated
patients,
the mortality rate is usually low, except with endocarditis. Treatment
of endocarditis consists of protracted (often for years) of antibiotic
therapy; valves often need replacement.
PREVENTION/CONTROL:
Use male
or nonpregnant female sheep for research, when possible. Q-Fever free
sheep
- limited practicality because requires intense surveillance program
and
frequent testing. Also, serologic status is not a useful indicator of
whether
the animal is shedding virus. Personnel education and control. Physical
separation of infected animals from humans are current methods
ofcontrol.
Restrictions on movement of animals within thefacility (with
considerations
of air handling). Label all potentially infected material and sterilize
or disinfect it. Protective clothing, masks, gloves, & shoe covers.
Intensive medical surveillance and health education program. Treatment
of acute disease in humans with tetracycline. Experimental vaccine for
sheep has shown promise. Delayed hypersensitivity skin test is
available
for high risk personnel.
SUITABLE
DISINFECTANTS
FOR Q-FEVER:
1:100
dilution of chlorine bleach containing 5-25% hypochlorite. 5% hydrogen
peroxide. 1:100 Lysol.
EHRLICHIOSIS
Centers
for Disease Control and Prevention: Viral and Rickettsial Zoonoses
Branch
ehrlichiosis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Tick-borne
fever)
AGENT:
An intraleukocytic
rickettsia, E. canis (many species of Ehrlichia exist. Previously only
E. sennetsu was known to infect man). Occurs intracytoplasmically,
singly
or in compact clusters (morulae) in circulating leukocytes.
RESERVOIR
AND INCIDENCE
First
recognized in dogs in 1935. Epizootic occurred in military working dogs
in Vietnam 1968-1970. Now known to have worldwide distribution. 11 to
58%
of dogs in U.S. are serologically positive. First reported case of E.
canis
in man in 1987. Several cases since then.
TRANSMISSION:
tick vector,
Rhipicephalus sanguineus, Brown Dog Tick. It is presumably transmitted
to humans by tick bite.
DISEASE
IN DOGS:
Incubation
period 10 to 14 days. Fever, lymphadenopathy, edema of legs and
scrotum,
epistaxis. Acute disease followed by a subclinical carrier stage.
DISEASE
IN MAN:
Similar
to Rocky mountain spotted fever, but no rash. 12 to 14 day incubation
period
and prodrome consisting of malaise, back pain and nausea, the patient
develops
sudden fever, bradycardia, and headache. Leukopenia and absolute
lymphopenia
as well as thrombocytopenia occur frequently.
DIAGNOSIS:
Not easy
to identify in peripheral blood smears but can attempt to identify
organisms
in leukocytes. An IFA assay that may be used to diagnose infection is
available
thru CDC and requires acute and convalescent sera.
TREATMENT:
Tetracycline.
PREVENTION/CONTROL:
Control
ticks.
ROCKY
MOUNTAIN SPOTTED FEVER
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
Rocky
Mountain spotted fever
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(American
Tick Typhus, Tick-borne Typhus Fever)
AGENT:
Rickettsia
rickettsii.
RESERVOIR
AND INCIDENCE
Dogs,
wild rodents and rabbits. Reported from most of continental U.S.,
highest
incidence in S. Atlantic and South Central States. 2/3 of human cases
are
reported in children.
TRANSMISSION:
Ixodid
ticks (especially Dermacentor) or their host species. Most rickettsias
are obligate intracellular parasites of the gut cells of invertebrates
and can only survive briefly outside living cells. Crushed ticks or
mites
and their feces may infect through broken skin. Transmission from tick
bite occurs only after several hours of attachment.
DISEASE
IN ANIMALS:
Subclinical
only.
DISEASE
IN MAN:
Fever
has a sudden onset, with chills, headache, severe muscle pains,
photophobia
and meningism for four weeks. A red, morbilliform rash develops within
3-5 days of onset of fever and with hemorrhages spreading on limbs.
Enlarged
liver and spleen, myocarditis, renal tubular necrosis and
bronchopneumonia
occur. Damage to endothelial cells of blood vessels by invasion of
rickettsias
causes thrombi and hemorrhages. Focal liver necrosis, hemorrhages in
genitalis
and gangrene of the scrotum may occur. The case fatality rate in
untreated
cases is 15-20%, but with prompt treatment is about 5%.
DIAGNOSIS:
Rickettsiae
can sometimes be isolated in special laboratories from blood obtained
in
the first few days of illness. A rise in antibody titer during the
second
week of illness can be detected by specific CF, IFA, and
microhemagglutination
tests or by the Weil-Felix test. Antibody response may be suppressed if
antimicrobial drugs are given very early.
TREATMENT/PREVENTION/CONTROL:
Treatment
of human disease with tetracycline or chloramphenicol. Control ticks on
newly arrived animals.
RICKETTSIALPOX
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Vesicular
Rickettsiosis, Kew Gardens Spotted Fever)
AGENT:
R. akari.
RESERVOIR
AND INCIDENCE
House
mouse is reservoir host; most commonly seen in rodent infested urban
dwellings
ie New York City and other Eastern U.S. cities. Rats and moles can also
harbor the organism. Not identified as a natural disease in laboratory
rodents.
TRANSMISSION:
Mite,
Allodermanyssus sanguineus, transmits to mice or to man. Lab infections
in humans via respiratory route have occurred but lab infections due to
mite bite have not been reported.
DISEASE
IN ANIMALS:
Not known
in wild animals. In experimental mice death follows pneumonia.
DISEASE
IN MAN:
Illness
lasting about a week is associated with an eschar which develops at the
site of the mite bite, regional lymphadenopathy and fever. A vesicular
rash over the body and limbs develops within 1-4 days.
DIAGNOSIS:
Leukopenia
and a rise in antibody titer with rickettsial antigen in CF tests.
However,
the Weil-Felix test is negative.
TREATMENT:
Tetracycline.
PREVENTION/CONTROL:
Eliminate
wild mice from animal facilities Control mites.
MURINE
TYPHUS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
murine
typhus
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Flea-borne
Typhus
Fever, Endemic Typhus Fever, Urban Typhus)
AGENT:
Rickettsia
typhi.
RESERVOIR
AND INCIDENCE
Natural
pathogen of rats and mice. Other mammals including cats, and their
ectoparasites
have been found infected. Outbreaks continue to occur in U.S.,
especially
Texas. Natural lab infections have not been reported but lab acquired
infections
in people handling experimentally infected mice have been
documented.
TRANSMISSION:
Transmitted
by flea or lice (Xenopsylla cheopis, Nosopsyllus fasciatus) to rodents
or man. Humans are infected by contamination of flea bites, broken skin
or conjunctiva by flea feces. Domestic animals may transport the flea
vector
to humans. Inhalation of contaminated dust may be a route of
infection.
DISEASE
IN ANIMALS:
The agent
localizes in the brain and various organs but with no known
lesions.
DISEASE
IN MAN:
There
is a gradual onset of fever with severe headache, rigors, generalized
pains
and dry cough (sometimes developing to bronchopneumonia) of about 2
weeks.
A macular rash appears by about 5 days, first appearing on the trunk
and
lasting about six days. CNS manifestations are possible. Damage is
caused
to vascular endothelia by invasion of rickettsia, possibly leading to
thrombosis
and hemorrhage. In untreated case, the case fatality rate is 1-2%.
DIAGNOSIS:
CF or
IFA.
TREATMENT:
Tetracycline
or chloramphenicol.
PREVENTION/CONTROL:
Control
wild rodents. In endemic areas control fleas while exterminating
rats.
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