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Ebola Hemorrhagic Fever (EHF)
AGENT
RNA virus, genus Filovirus, family Filoviridae
RECOGNITION
Syndrome:
Human:
1. Clinically similar to Marburg disease.
2. Sudden onset,
3. the first signs being headache, fever, myalgia, and nausea,
4. followed a few days later by development of a maculopapular
rash, sore throat, diarrhea, and vomiting.
5. Hemorrhage, ranging from mild to life-threatening, may
begin early in the clinical course and usually takes the form
of epistaxis, melena, hematemesis, and bloody diarrhea, and
blood may seep from needle punctures.
6. Death results from hemorrhage, shock, or renal and/or
hepatic failure.
7. In survivors of severe disease, convalescence is slow and
often accompanied by desquamation of the skin.
8. Subclinical infections and mild illness may occur.
Animal:
Febrile illness in experimentally infected primates similar to
humans.
Incubation period: 2-21 days.
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Case fatality rate:
1. 50%-90% in humans;
2. 100% in experimentally infected primates.
Confirmatory tests:
1. Virus isolation is very hazardous.
2. Serologic tests include IFA, ELISA, and Western blot.
Occurrence:
1. Major outbreaks with high fatality rates in humans occurred
from 1976 to 1979 in Sudan and Zaire.
2. Antibodies to EHF have been detected elsewhere in Africa,
suggesting that subclinical infection also occurs.
3. Fatal infection with an ebola-like virus occurred among
monkeys in a research laboratory in Washington, D.C., in
1989.
4. This virus was evidently imported in crab-eating monkeys
from the Philippines, and has not been associated with human
illness, although several animal handlers exposed to the
monkeys developed antibodies.
Transmission:
1. By direct contact with blood and other bodily fluids of
affected patients;
2. EHF virus persists in semen for many weeks after clinical
recovery.
3. Nosocomial outbreaks
have resulted from use
of
contaminated syringes and needles.
4. Spread by aerosol is also possible.
5. No nonhuman reservoir or vector has been implicated.
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CONTROL AND PREVENTION
Individual/herd:
1. Infected persons should be kept in strict isolation
2. those involved in their care wear gloves, masks, and
protective clothing.
3. All excreta, sputum, blood, and other secretions should be
sterilized by autoclaving before disposal,
4. as should objects that come in contact with a patient or the
patient’s blood (laboratory glassware, etc.).
5. Sexual intercourse with male survivors should be avoided
until it is established that semen is free of virus.
6. In case of accidental exposure via needle stick or other
penetration of the skin, oral ribavirin should be administered.
7. There is no vaccine.
Local/community:
1. If an outbreak occurs, the public should be alerted to the
communicability of EHF
2. need for extreme caution when caring for patients.
3. Handling of the deceased should be kept to a minimum and
cremation is preferable to traditional burial.
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Rift Valley Fever (RVF)
AGENT
RNA virus, genus Phlebovirus (ungrouped), family Bunyaviridae
RECOGNITION
Syndrome:
Human:
1. Sudden onset of chills, muscular and back pain, headache,
nausea, and fever lasting for a week or more.
2. Most cases are mild and uncomplicated, with recovery
complete in about 3weeks.
3. Of the severe forms there are three manifestations:
hemorrhagic RVF, RVF with meningoencephalitis; and
RVFwith retinitis.
4. Most fatalities occur among those with the hemorrhagic
form, which begins with fever for 2-4 days, then progresses
to jaundice and hemorrhages, including hematemesis,
melena, hemorrhagic gingivitis, and dermal petechiae and
purpura; hepatic necrosis may be found postmortem.
5. The meningoencephalitic form follows the initial febrile
period after 5-15 days, causing disorientation, hallucination,
and vertigo, with meningitis and pleocytosis common.
6. In the retinal form, patients experience loss of visual acuity
5-15 days after onset of fever, often with bilateral retinal
lesions.
7. Permanent loss of central vision is common among
individuals with severe lesions.
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Animal:
1. Sheep, goats, cattle, and buffalo are most frequently affected.
2. In some outbreaks, only lambs are affected, whereas in
others, adults are affected.
3. In newborn lambs the disease is rapid, without definite signs,
and highly fatal.
4. Pregnant ewes often abort; among nonpregnant adults,
vomiting may be the only sign of illness.
5. Cattle may abort, and often have a fever of short duration as
well as anorexia, hypersalivation, and diarrhea.
6. Dogs and cats may also be affected, with abortion in pregnant
females.
Incubation period
In humans, 2-7 days; in animals, 1-2 days.
Case fatality rate:
1. Human, about 3%;
2. 18%-20% in ruminants.
3. High mortality in puppies and kittens.
4. May reach 95% among newborn lambs.
Confirmatory tests:
1. Human infection in acute phase can be diagnosed by isolation
of virus from blood.
2. Serologic testing (SN, CF, HI, IFA, gel diffusion, and
ELISA) of paired sera.
3. Rapid diagnosis by seeding cell culture and performing FA
test the next day.
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Occurrence:
1. Widespread throughout Africa,
2. most south of the Sahara.
3. Heavy rains in late summer and autumn, which allow the
vector population to increase, are precursors to epidemics,
4. although outbreaks also recorded in irrigated areas.
Transmission:
1. Generally mosquitoborne.
2. Species of at least six mosquito genera, including Aedes and
Culex, transmit RVF virus,
3. as do biting flies Cuficoides and Simulium, which are
mechanical vectors.
4. The reservoir is unknown, but may be rodents or bats.
5. Domestic sheep and cattle play a role in maintaining and
amplifying the virus.
6. Humans are highly susceptible, and usually are infected by
contact with tissues of infected animals, e.g. veterinarians
and persons slaughtering diseased livestock.
7. Aerosol transmission is a factor in human infection.
8. Because humans maintain a viremia for more than a week,
they may be involved in virus amplification.
Control and Prevention
Individual/herd
1. Inactivated or modified live vaccines may be used to protect
domestic animals.
2. The modified live vaccine may cause abortion and it cannot
be used in newborn animals.
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3. Because of the possibility of reversion to a virulent form, it
should not be used in nonendemic areas.
4. The risk of human infection during an outbreak can be
lessened by carefully handling diseased or dead animals, and
by use of protective clothing.
5. An inactivated vaccine is available to protect individuals at
high risk.
Local/community:
1. Because domestic livestock are the main amplifiers of the
virus, immunization programs may help prevent outbreaks.
2. Butchering of diseased animals should be prohibited.
National/International:
Restrict movement of animals from endemic areas.
Viral Hepatitis Type A (HA)
AGENT
Hepatitis A virus (HAV); RNA virus, genus Enterovius, family
Picornaviridae
RECOGNITION
Syndrome:
Human:
1. Sudden onset of fever, malaise, anorexia, and nausea.
2. Dark urine and jaundice may also develop.
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3. Generally more serious in adults, often subclinical in
children.
Animal:
1. Nonhuman primates are susceptible to HA infection,
although many are subclinical.
2. Clinical manifestations are variable, and can range from mild
respiratory involvement to nonspecific gastrointestinal signs.
3. Anorexia and persistent diarrhea may occur.
Incubation period
1. Human, 15-50 days
2. 3-4 weeks in nonhuman primates.
Case fatality rate:
<1.0% in humans.
Confirmatory tests:
Serologic testing to detect IgM anti-HAV in paired sera.
Occurrence:
1. Worldwide, most commonly among older children and young
adults
2. may be sporadic or epidemic.
3. In many developing nations, adults are immune because of
prior infection.
4. Humans and nonhuman primates are reservoirs.
Transmission:
1. Shed in feces, with the highest concentrations occurring late
in incubation period and early in illness.
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2. Among humans, transmission is primarily person-to-person,
usually by the fecal-oral route, and is facilitated by poor
hygiene.
3. Infected food handlers are often the cause of outbreaks
4. infections are common at day-care centers with diapered
children.
5. Intravenous drug users are frequently infected, as are sexual
and other intimate contacts of acutely ill.
6. Contaminated water or food also may be sources.
7. Clams, oysters, and other filter-feeders from contaminated
waters are often a source.
8. Nonhuman primates are infected via ingestion of
contaminated food or water or coprophagy;
9. humans may become infected from exposure to infected
primates when hygienic precautions are not observed.
CONTROL AND PREVENTION
Individual/herd
1. Food handlers should practice careful hygiene and wash
hands frequently.
2. Travelers to endemic areas who may be at high risk should
receive pre-exposure IG.
3. While in endemic areas, avoid drinking unbottled water or
beverages with ice and eating uncooked shellfish or
uncooked fruits or vegetables.
4. Care in handling nonhuman primates is important to avoid
contact with excreta.
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Local/community:
1. Public education campaigns should be conducted to alert
people to the mode of spread of the virus and to emphasize
the importance of good hygiene, especially thorough hand
washing and the sanitary disposal of feces.
2. Proper sewage and water treatment systems should be
provided.
Viral Hepatitis Type B (HB)
AGENT
Hepatitis B virus (HBV); DNA virus, genus Hepudnavirus, family
Hepadnaviridae
RECOGNITION
Syndrome:
Human:
1. Insidious onset of anorexia, malaise, and gastrointestinal
signs, frequently progressing to jaundice.
2. Mild fever, arthralgias, and skin rashes may also occur.
3. Severity is variable, from subclinical to fulminant life
threatening.
4. Chronic infections can develop, particularly if infected in
infancy or early childhood
5. a long-term carrier state, often progressing to cirrhosis, may
result.
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6. Is a major cause of primary hepatocellular carcinoma, and
may be responsible for up to 80% of cases worldwide.
Animal:
1. Nonhuman primates are susceptible to infection
2. as antibodies have been detected in several species
3. but clinical disease is rare.
4. Infections in cynomolgus monkeys caused anorexia, lethargy,
and hepatomegaly
5. infected chimpanzees also developed jaundice.
Incubation period
1. In humans, 45-180 days, average 120 days
2. Over 180 days in chimpanzees.
Case fatality rate:
About 1.4% of reported human cases.
Confirmatory tests:
RIA or ELISA testing for HBV surface antigen (HBsAg) or other
markers.
Occurrence:
1. Worldwide, and variably endemic.
2. In the United States, western Europe, and Australia, HB is of
low endemicity.
3. In these areas, infection usually contracted in young
adulthood, and less than 1% of the population are chronically
infected.
4. Intravenous drug addicts, homosexual men, heterosexuals
with multiple partners, and health care personnel who have
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frequent and routine exposure to blood and other body fluids
are at greatest risk.
5. In China, Southeast Asia, Africa, Oceania, the Middle East,
and the Amazon Basin, HB is highly endemic.
6. Most HB in these countries is acquired at birth or during
childhood, and 8%-15% of the population are carriers.
7. In moderately endemic areas, 2%-7% of the population have
chronic infections.
8. High prevalence rates of HB antibodies have been found in
some species of nonhuman primates.
Transmission:
1. In humans, mainly by percutaneous or permucosal contact
with infective body fluids.
2. Contaminated needles and syringes contribute to spread
among drug addicts,
3. Is also transmitted by sexual activity.
4. In highly endemic areas, perinatal infection is frequent.
Control and Prevention
Individual/herd:
1. Vaccines are available and should be administered to
individuals at high risk.
2. Pregnant women should be screened for HBs Ag,
3. and newborn infants of those testing positive should receive
HB immunoglobulin (HBIG).
4. Persons exposed via percutaneous or permucosal contact
should receive HBIG and vaccine.
5. Blood donated to blood banks should be tested for HBsAg.
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6. Gloves should be worn when handling infected animals or
when there is likelihood of skin contact with infectious
material.
Local/community:
In hyperendemic and moderately endemic areas, vaccinate infants
and children.
Viral Hepatitis Type C (HC)
AGENT
Hepatitis C virus (HCV); unclassified RNA virus, possibly a
flavivirus
RECOGNITION
Syndrome:
Human:
1. Insidious onset of anorexia, gastrointestinal discomfort,
nausea, and vomiting;
2. jaundice develops less frequently than in HB.
3. Severity is variable, from subclinical to fulminating, although
rarely life threatening.
4. Chronic HC develops in about 50% of patients but does not
usually progress to cirrhosis;
5. clinical improvement is often seen within 2-3 years.
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Animal:
1. Chimpanzees may be infected with HCV, and typical liver
lesions produced, but clinical and biochemical changes may
not occur.
2. Incubation period: In humans, usually about 6-9 weeks.
Case fatality rate: Low.
Confirmatory tests:
1. Serologic testing.
2. Most with chronic HC have antibodies
3. but there may be a long period after onset of acute disease
before detectable antibodies develop.
Occurrence:
1. Worldwide.
2. In the United States, causes 20%-40% of community-
acquired acute viral hepatitis and about 90% of
posttransfusion hepatitis.
3. Groups at high risk include transfusion recipients, users of
illicit parenteral drugs, dialysis patients,
4. health care workers who have frequent contact with blood
5. persons who have had hepatitis in the past, and household
and sexual contacts of infected persons.
6. Spontaneous HC infections have not been reported in
nonhuman hosts.
Transmission:
1. Percutaneous exposure to blood or plasma from an infected
person,
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2. direct contact (e.g., transfusion)
3. contaminated needles and syringes, is most common.
4. Exposure by person-to-person contact and sexual activity
also may occur.
Control And Prevention
Individual/herd
1. Similar to HB.
2. Because of the lack of a sensitive test for HCV antibodies,
blood banks should discard any donated units with elevated
liver enzyme levels.
3. The value of administration of prophylactic IG to persons
exposed to HC has not been established.
4. Interferon may be useful in treating patients with chronic
disease.
5. No vaccine is available.
6. Gloves should be worn when handling infected chimpanzees
and when there is likelihood of skin contact with infectious
material.
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Viral Hepatitis Type D (HD)
AGENT
Hepatitis delta virus (HDV), a defective RNA virus that requires
the presence of HBV to replicate
RECOGNITION
Syndrome:
Human:
1. Always occurs either concurrently with acute HB, or
superimposed upon an existing chronic HB infection.
2. Clinical signs are similar to HB, and are usually of abrupt
onset.
3. Usually more severe in superinfections than in co-infections,
and often leads to chronic HD.
Animal:
Clinical signs develop when infect HBV-infected chimpanzees.
Incubation period
Uncertain in humans; 2-10 weeks in chimpanzees.
Case fatality rate: Similar to HB.
Confirmatory tests: Serologic testing (RIA, ELISA).
Occurrence:
Worldwide, mostly among populations with high HB prevalence.
Epidemics have occurred in Brazil, Venezuela, Colombia, and the
Central African Republic. In the United States, groups at highest
risk are hemophiliacs and others receiving blood or blood
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derivatives, users of parenteral street drugs, health care workers
who have frequent contact with blood or infected persons, and
male homosexuals, Spontaneous HD infection has not been
reported in nonhuman hosts.
Transmission: Same as HB.
CONTROL AND PREVENTION
Individual/herd:
1. Same as HB.
2. HDV cannot aim the absence of HB.
3. No vaccine is available for HD,
4. and neither IG nor HBIG protects against HDV
superinfection.
5. Gloves should be worn when handling infected animals or
when there is likelihood of skin contact with infectious
material.
Local/community:
1. In endemic areas, vaccination of infants and children against
HB will also reduce occurrence of HD.
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Viral Hepatitis Type E (HE)
AGENT
Not yet completely characterized
but serologically distinct from other hepatitis viruses.
RECOGNITION
Syndrome:
Human:
2. Similar to HA
3. with sudden onset of fever, malaise, anorexia, and nausea;
dark urine and jaundice are often present.
4. Chronicity does not develop.
Animal:
1. Clinical signs develop in experimentally infected
chimpanzees, cynomolgus macaques, owl monkeys,
tamarins, and marmosets.
2. Natural infections may occur.
Incubation period
usually 26-42 days in humans.
Case fatality rate:
1. Generally less than 1%
2. except may reach 20% among pregnant women in the third
trimester.
Confirmatory tests:
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Diagnosis by serologically excluding other hepatitis viruses,
especially HA.
Occurrence:
1. Epidemics have occurred in Asia, North and East Africa, and
Mexico.
2. Not endemic in the United States or western Europe, as cases
in these countries have been limited to travelers returning
from endemic areas.
3. Young to middle-aged adults, especially men, are most often
affected.
4. Children and the elderly seldom affected.
Transmission:
1. Fecal-oral route, with contaminated water the source of most
epidemics.
2. Poor hygiene can also result in person-to-person
transmission.
CONTROL AND PREVENTION
Individual/herd
1. In endemic areas:
a. avoid drinking unbottled water or beverages with ice
and eating uncooked shellfish or uncooked fruits or
vegetables.
b. Avoid fecal-oral exposure.
2. No vaccine is available.
Local/community:
a. Proper sewage disposal. 2-Chlorinate public water supplies.