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Biodefense Reference Library
Foreign Animal and Zoonotic Disease Center
One Medicine: One Health (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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