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Eastern Equine Encephalitis (EEE)
AGENT
RNA virus, genus Alphavirus (group A), family Togaviridae
RECOGNITION
Syndrome:
Human:
1. Most commonly seen in persons under 15 and over 50 years
of age.
2. In adults, sudden onset of high fever, headache, vomiting,
and lethargy,
3. progresses rapidly to include CNS signs, such as neck
stiffness, convulsions, spasticity, delirium, tremors, stupor,
and coma.
4. In children, typically manifested by fever, headache, and
vomiting for 1-2 days, apparent recovery, then fulminant
encephalitis.
5. Retardation or other permanent neurologic Sequelae are
frequent among survivors of all age groups.
Animal:
1. Equine infection is characterized by a biphasic febrile course,
2. neurologic signs appearing during the second period of
fever;
3. permanent brain damage is common in animals that survive.
4. Outbreaks also occur in commercially raised pheasants,
chukars, bobwhite quail, ducks, turkeys, and emus.
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Incubation period: 7-10 days in humans, 18-24 hours in
horses.
Case fatality rate: About 65%-80% in humans, 75%-90% in
horses.
Confirmatory tests:
Virus isolation from brain tissue or serologic tests (HI, CF, IFA,
SN) of paired sera.
Occurrence:
1. Restricted to Americas: eastern and central United States and
adjacent Canada, parts of Central and South America and
Caribbean islands.
2. Most epidemics occur between late August and the first
killing frost, and generally begin 1-2 weeks after epidemics
in horses, Cases are seen year-round in Florida and other
hyperendemic areas.
Transmission:
1. Mosquitoborne.
2. In the eastern United States, mosquitoes of the genus
Culisetu are major vectors.
3. Aedes is important on the Atlantic coast and in the
Southwest, where Coquilletidia may also be involved.
4. In tropical America C d a and Aedes species are the main
vectors, whereas other species of C d a maintain the virus in
endemic foci. Birds, especially Passeriformes, are the
reservoirs.
5. The mosquitoes feed on infected birds, as well as horses and
man, spreading infection.
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6. In pheasants the initial infection is mosquito borne, but can
be spread from bird to bird by pecking and cannibalism.
7. Because humans and horses develop only low-level viremia,
these species do not play a role in maintaining infection in
nature.
8. The term “equine” encephalitis refers only to the species
from which the virus was first isolated.
CONTROL AND PREVENTION
Individual/herd
For humans:
1. prevention of mosquito bites through use of protective
clothing and chemical repellents,
2. installation of mosquito netting and screens to exclude
mosquitoes from dwellings.
3. A vaccine is available from U.S. Army Medical Research
Institute for Infectious Disease, Ft. Detrick, Frederick, MD,
and is recommended for researchers and other persons who
are frequently and intensively exposed.
4. Immune serum should be administered after accidental
exposure to the agent.
5. A multivalent inactivated vaccine is available for horses and
birds.
Local/community:
Education of public as to mode of spread and control; control of
mosquitoes in area.
National/international: None.
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Venezuelan Equine Encephalitis (VEE)
AGENT
RNA virus, genus Alphavirus (group A), family Togaviridae,
endemic and epidemic strains
RECOGNITION
Syndrome:
Human:
1. A range of clinical signs from nonspecific fever to influenza-
like signs to encephalitis, but is usually a mild to severe
respiratory infection.
2. Usually rapid onset of fever, malaise, chills, retro-orbital and
muscular pain, headache, nausea, vomiting, and diarrhea.
3. Acute illness lasts 1-4 days or more, and length of
convalescence is proportional to the duration of fever.
4. Recovery is rapid and complete when febrile course is short,
but patients experience profound weakness with prolonged
fever, and convalescence may take several weeks.
5. Permanent sequelae seldom develop.
6. Encephalitis similar to other mosquitoborne encephalitides is
more often seen in children.
7. Meningitis is rare.
Animal:
1. VEE produces clinical signs only in the Equidae,
2. although many vertebrate species have been infected with
VEE virus.
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3. In some equines the disease is mild, with fever of a few days’
duration, anorexia, and depression.
4. Viremia may be low-titer, and affected animals recover
without sequelae.
5. The encephalomyelitic form, however, is more typical and
more severe, producing a viremia of high titer.
6. It has a sudden onset of high fever, depression, anorexia and
weight loss, grinding of teeth, and diarrhea or constipation.
7. Neurologic signs, including imbalance, stupor, falling,
excitation, circling, and convulsions, are frequent.
Incubation period: 1-6 days for humans; 1-3 for equines.
Case fatality rate:
Usually 0.2%-1% in humans, but may be higher in absence of
adequate medical care. Up to 80% in equines.
Confirmatory tests:
Direct isolation of virus from blood or nasopharyngeal washings
during the first 72 hours of illness; serologic testing of paired sera,
or detection of specific IgM.
Occurrence:
1. Americas only.
2. Endemic from the southern United States through the
Caribbean and Central America, to northern South America.
3. Outbreaks occur mainly in northern and western South
America, but have spread through Central America into the
United States.
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Transmission:
1. Mosquitoborne.
2. Endemic serotypes are maintained by a rodent-mosquito
cycle
3. humans are exposed only when they enter foci of the virus,
such as swampy areas within rain forests.
4. Culq Aedes, Mansonia, Psorophora, Haemagogus, Sabehs,
and Anopheles mosquitoes may be infected with these virus
types, whereas the main reservoirs are rodents.
5. Marsupials may also be involved, and one subtype is
maintained in birds.
6. In the virus type that causes human epidemics, horses
function as the major amplifiers.
7. Psorophora, Aedes, Mansonia, and Anopheles are the vectors
in epidemic disease, as well as biting flies Culicoides and
Simulium.
CONTROL AND PREVENTION
Individual/herd:
1. Use of protective clothing and repellents to prevent mosquito
bites,
2. avoidance of areas in which mosquitoes are active.
3. A live attenuated vaccine, available from USAMRIID,
should be used to protect individuals at high risk.
4. Horses may also be immunized.
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Local/community:
Mass immunization of horses and prevent movement from affected
areas to non-affected areas. Institute mosquito vector control
programs.
Western Equine Encephalitis (WEE)
AGENT
RNA virus, genus Alphavirus (group A), family Togaviridae
RECOGNITION
Syndrome:
Human:
1. In adults, sudden onset with fever, headache, neck and back
stiffness, lethargy, vision disturbances, and vertigo; mental
confusion is common.
2. In children, neurologic signs are preceded by fever,
headache, and malaise; convulsions, vomiting, and neck
stiffness often follow, and flaccid and spastic paralyses are
more frequent than in adults. Fever persists for 7-10 days.
3. Adults usually recover without permanent Sequelae, but
children often have mental retardation, spastic paralysis, and
recurrent convulsions.
Animal:
1. only horses and emus develop clinical illness,
2. although not all affected animals will develop encephalitis.
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3. Neurologic signs, e.g., restlessness, unsteady gait, lack of
coordination, and somnolence, appear after fever and viremia
have ceased.
4. Neurologic Sequelae, usually abnormal reflexes, are common
among animals that survive.
Incubation period:
25-10 days in humans, 1-3 weeks in horses.
Case fatality rate:
In humans, 3%-14%; in horses, usually 20%-30%, but
Confirmatory tests:
Virus isolation from brain tissue, or serologic tests can be as high
as 50%. (CF, HI, SN, or FA) on paired sera.
Occurrence:
1. Usually appears in summer, most cases occurring in young
adults and children under 1 year of age,
2. in the Americas from Canada to Argentina; rarer in humans
than in horses.
3. Equine cases occur almost every year in the western United
States.
4. In hyperendemic areas, serologic evidence of infection
among horses is high.
Transmission:
1. Mosquitoborne.
2. Wild birds, especially Passeriformes, are reservoirs, and
develop a viremia that can infect mosquitoes.
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3. In the western United States, mosquitoes of the genus Culex
are the usual vectors, and Aedes is involved in some areas.
4. The infection is maintained by transmission from a viremic to
a susceptible wild bird, which constitutes the endemic and
amplifying link in the circulation of the virus.
5. Snakes possibly may play a role in maintaining the virus
through the winter.
6. Both man and horses are accidental hosts and are not
involved in the basic cycle.
CONTROL AND PREVENTION
Individual/herd Same as EEE.
Local/community: Same as EEE.
National/international: None.
Rabies
AGENT
RNA virus, genus Lyssuvirus, family Rhabdoviridae. Strain
differences in virulence as well as reservoir host-related (i.e., bat,
fox, etc. source) glycoprotein surface antigens.
RECOGNITION
Syndrome:
Human:
1. Onset is characterized by apprehension, headache, low-grade
fever, malaise, and vague sensory changes, discomfort, and
irritation in the area of a previous animal bite.
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2. Optic and auditory hyperesthesia develop.
3. Paresis or paralysis follows, and spasmodic contractions of
deglutitory muscles when attempting to swallow cause the
patient to avoid liquids (“hydrophobia”) and to stop
swallowing saliva.
4. Delirium and convulsions usually precede death from
respiratory failure.
Animal:
1. In dogs, rabies may occur as either a furious or paralytic
(“dumb”) form.
2. The furious form begins with agitation, restlessness, and
excitability.
3. Aggression follows, with the dog attempting to bite objects,
other animals, humans, and itself.
4. Profuse salivation occurs, because spasms of deglutitory
muscles prevent swallowing; the vocal cords are affected,
altering the normal vocal sound.
5. Terminally, convulsions and paralysis develop. Paralytic
form begins with paralysis of the muscles of the head and
neck, causing difficulty in swallowing.
6. Paralysis of the extremities follows, then general paralysis
and death.
7. Cats usually develop the furious form, whereas cattle
generally develop the paralytic form. In wild foxes, skunks,
and raccoons, the furious form is more common than
paralytic.
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Incubation period:
Variable, dependent on amount of Virus received, site, and
severity of bite wound. In humans, 5 days to a year or more, but
usually 2-8 weeks; dogs, 10-60 days; cattle, 25-2150 days; wild
animals usually 10-180 days.
Case fatality rate:
Almost 100% in all species.
Confirmatory tests:
Direct FA (corneal impressions, lingual scrapings, or frozen skin
sections from the nuchal area can be tested while the subject is
alive). If human exposure, need test results within a day. Virus
isolation from brain or salivary glands.
Occurrence:
1. Worldwide, except for Australia, New Zealand, New Guinea,
Japan, most of Oceania, some Caribbean islands, Uruguay,
Great Britain, Ireland, the Netherlands, Noway, Sweden,
Spain, and Portugal.
2. In endemic regions, two cycles may occur: urban and
sylvatic.
3. Urban rabies, which accounts for most human cases, is
transmitted by dogs; sylvatic rabies circulates among wild
carnivores and bats, with some infection of dogs, cats, and
livestock.
4. Worldwide, over 30,000 people die of rabies each year, most
in developing nations.
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Transmission:
1. Most cases result from the bite of an infected animal; the
virus is abundant in saliva.
2. A few human cases have resulted from corneal transplants
when rabies was the unsuspected cause of death of the donor.
3. Airborne transmission may occur in bat caves.
CONTROL AND PREVENTION
Individual/herd
1. All dogs and cats should be vaccinated.
2. In areas where vampire bats transmit rabies, valuable cattle
and horses may be vaccinated.
3. Although most vaccines are now inactivated, be sure any live
(attenuated) vaccines are used only in the specific species
intended because they may be virulent for others.
4. Dogs and cats that have bitten a person should be quarantined
and observed for at least 10 days; if signs of rabies appear the
animal should be killed and its brain examined by FA
microscopy.
5. Wild animals that have bitten persons should be killed
immediately and examined.
6. If they have escaped, assume they are rabid.
7. Any unvaccinated animal that is bitten by a rabid animal
should be destroyed or quarantined for 6 months.
8. In the event of a bite from a known or suspected rabid
animal, immediate and thorough cleansing of the wound is
essential.
9. Flush with a strong stream of water and wash with soap or
detergent, then a disinfectant, such as alcohol, tincture of
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iodine, or quaternary ammonium compounds, should be
applied.
10. The area around the wound should be infiltrated with
antiserum, and suturing should be avoided or delayed to
allow bleeding and drainage.
11. For individuals without pre-exposure immunization, post-
exposure prophylaxis consists of an injection of rabies
immune globulin (RIG), half infiltrated around the wound
site and half injected intramuscularly.
12. This is followed by administration of vaccine, preferably
human diploid cell vaccine (HDCV) in a 5-dose course.
13. If the exposed person has had a full pre-exposure course of
HDCV, RIG is not necessary and give only 2 doses of
HDCV. Persons at risk, such as animal control personnel,
veterinarians, field zoologists, etc., should receive pre-
exposure prophylaxis and periodic boosters based on
antibody response. HDCV is preferable, but is expensive and
not generally available in all countries.
Local/community:
1. Educate the public as to the need to vaccinate dogs and cats.
2. Enforce animal control laws and eliminate stray animals.
3. Avoid animals acting strangely and report them to animal
control authorities.
4. Control vampire bats.
5. Oral vaccines are effective in free ranging carnivore (e.g.,
fox, dog) populations.
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National/international:
1. Health certification and proof of vaccination should be
required for importation of dogs.
2. For rabies-free areas, enact and enforce laws requiring
prolonged quarantine of dogs and other carnivores to be
imported.
California (Lacrosse) Encepha1itis
AGENT
RNA virus, genus Bunyavirus (group CAL), family Bunyaviridae
RECOGNITION
Syndrome:
Human:
1. Onset is characterized by fever, cephalgia, nausea and
vomiting, and nuchal rigidity.
2. Lethargy, convulsions, and other neurologic signs develop in
severe cases on about day 3 and persist for approximately a
week.
3. Subclinical infection is much more common than clinical
cases.
Animal:
1. No known clinical disease in animals.
2. Incubation period About 5-15 days.
Case fatality rate: Low.
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Confirmatory tests: Serologic tests (HI, CF, SN) are used.
Occurrence:
Occurs mainly in children under 15 years of age, predominantly in
the eastern and central United States, primarily in summer.
Transmission:
1. Mosquitoborne.
2. Chipmunks and squirrels are reservoirs and amplifiers of the
virus.
3. The main vector is Aedes triseratus, a forest-breeding
mosquito in whose eggs the virus overwinters, thus serving
as a reservoir.
CONTROL AND PREVENTION
Individual/herd:
1. Avoid mosquito bites by use of protective clothing and
chemical repellents, especially in wooded areas.
2. Screen dwellings and use mosquito netting around beds.
Spray campsites with insecticides.
Local/community: None.
National/international: None.
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Louping ill
AGENT
RNA virus, genus Flavivirus (group B), family Togaviridae;
closely related to Russian spring-summer encephalitis
RECOGNITION
Syndrome:
Human:
1. Usually has a biphasic course, the first phase lasting up to 12
days and being characterized by fever, headache, malaise,
and retro-orbital pain.
2. These signs abate for about 5 days before onset of the second
phase in which variable neurologic signs occur and the
disease may be mistaken for meningoencephalitis or
poliomyelitis.
3. Convalescence is often prolonged.
Animal:
1. In sheep, may be a biphasic febrile illness, although many
recover after the first phase.
2. If the virus invades the CNS, however, encephalomyelitis
results, producing motor incoordination, tremors, a hopping
gait, and, finally, prostration. Immunosuppressed animals are
more likely to develop encephalomyelitis.
3. Also seen occasionally in cattle, horses, and deer. Red grouse
are severely affected, with high mortality occurring in chicks
less than 2 months old.
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Incubation period:
tow to 8 days in humans; a few days to several weeks in animals.
Case featality rate:
Almost none in humans; in sheep, up to 50% with
encephalomyelitis.
Confirmatory tests:
For humans, virus isolation from blood (first phase) or CSF
(second phase). In animals with encephalomyelitis, isolate virus
from brain. Serologic tests (SN, CF, HI) useful.
Occurrence:
1. Restricted to Ireland, Scotland, Wales, and northern England.
2. Rare in humans;
3. in sheep, outbreaks qccur mainly in spring, early summer,
and autumn.
Transmission:
1. The vector is the tick ixodes ricinus, and sheep are the main
reservoir.
2. Tick larvae and nymphs are infected when they feed on
viremic sheep; the virus is transmitted transstadially to adult
ticks.
3. Inhalation by abattoir workers or accidental inoculation in the
laboratory have been the main routes of human infection,
perhaps because I. ricinus rarely bites humans.
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CONTROL AND PREVENTION
Individual/herd:
Tick control. An inactivated vaccine is available for
Local/community: None.
National/international: None.
Colorado Tick Fever (CTF)
AGENT
RNA virus, genus Orbivirus, family Reoviridae
RECOGNITION
Syndrome:
Human:
1. Sudden onset of fever, chills, headache, retro-ocular pain,
and myalgia.
2. Typically, characterized by a few days of illness followed by
a few days of remission, then recurrence of illness, which
may worsen over several cycles.
3. Young children may occasionally develop hemorrhages,
encephalitis, or myocarditis, but the disease is generally
milder in adults.
Animal: No clinical signs occur in animals.
Incubation period: 3-6 days.
Case fatality rate: Very low.
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Confirmatory tests:
Virus isolation, detection of antigen in erythrocytes by FA, or
serologic tests (CF, SN), however antibodies do not appear for at
least 2 weeks after onset.
Occurrence:
1. Throughout the range of vector ticks in the mountainous
western United States and Canada, but more than 80% of
cases from Colorado and Wyoming.
2. Occurs in spring and summer when ticks are active.
Transmission:
1. To humans by the bite of adult Dermucentor undersoni ticks,
2. The main reservoirs are least chipmunks and golden-mantled
ground squirrels, which are hosts to the immature stages of
the ticks.
CONTROL AND PREVENTION
Individual/herd:
1. Prevent tick bites by avoiding tick-infested areas whenever
possible.
2. When entering tick-infested areas, protective clothing should
be worn and chemical repellents used, and the body should
be inspected periodically.
3. Any attached ticks should be carefully removed to avoid
crushing and to avoid leaving mouth parts in the wound.
Local/community: None.
National/international: None.