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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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