Lecture 8 - Rift Valley fever, African horse sickness & Glanders Flashcards
RVFV
Rift Valley Fever virus
another name for Rift Valley Fever virus
Infectious Enzootic Hepatitis of Sheep and Cattle
RIFT VALLEY FEVER (RVF) is a
mosquito-borne viral disease of animals and humans,
caused by Bunyavirus,
characterized by a short incubation period,
fever, hepatitis, abortion, and death of young animals.
RIFT VALLEY FEVER (RVF) is a mosquito-borne viral disease of animals and humans, caused by
Bunyavirus,
characterized by a short incubation period,
fever, hepatitis, abortion, and death of young animals.
RIFT VALLEY FEVER (RVF) is a mosquito-borne viral disease of animals and humans, caused by Bunyavirus, characterized by
a short incubation period,
fever, hepatitis, abortion, and death of young animals.
RVFV belongs to what genus and family?
Genus Phlebovirus,
family Bunyaviridae
What type of virus is RVFV?
RNA-virus
How many serotypes does RVFV have?
One serotype, a lot of strains with variable virulence.
How is RVFV inactivated?
Inactivated pH ≤ 6.2
In what conditions can RVFV survive/persist?
Survives in freeze dried form, and aerosols at 23°C and 50-85% humidity.
Host range of RVFV?
Host range: various.
Sheep, goats and cattle are primary amplifying hosts.
Ruminants, monkeys, rodents may also be infected.
NB! ZOONOSIS! Humans too!
Morbidity of RVFV?
Morbidity varies between outbreaks: pre-existing immunity, pregnancy status and age influence.
Abortion rate in sheep 5-100%, cattle <10%.
Mortality of RVFV?
Newborn lambs and kids 70-100%
Calves and older lambs and kids 10-70%
Adult sheep 10-30% - most common in pregnant ewes that abort.
Adult cattle abortion rate <10%
RVFV epidemics occur when?
Cyclic epidemics: every 5-20 years.
The long intervals between outbreaks allow for development of a susceptible animal population that is severely affected by the following outbreak.
RVFV does not cause
persistent infection (carrier state)
Currently RVF is endemic throughout
most of Africa.
Transmission of RVFV. (3)
Biological vectors: mosquito bites – transcutaneous route.
Transovarial from adult insect to insect larvae. Virus survives in dried eggs and hatching is associated with heavy rainfall and flooding.
In utero transmission in animals.
Excretion of RVFV. (4)
oral fluids and nasal discharge, semen, milk
(but these are not significant modes of transmission, arthropod vectors are more important)
Transmission of RVFV to humans?
mainly direct contact with tissues of infected animals
Also in utero
Once a ruminant is infected with RVFV, it serves as an
amplifying host.
Infected livestock can be highly viremic and cause infection of other mosquitoes.
Name a reservoir and vector for RVFV.
Mosquitoes are both.
The most characteristic clinical signs of RVFV are: (2)
High mortality rates among newborns
Abortions in adults
Clinical signs of RVFV in adult cattle (4)
ADULTS are moderately susceptible.
Usually asymptomatic, some acute cases.
Abortions <85%.
Fever, dry and/or dull coat, anorexia, weakness, diarrhea, fall in milk yield.
Clinical signs of RVFV in calves (3)
CALVES are highly susceptible.
Fever
Loss of appetite
Weakness and depression
Bloody or fetid diarrhea
Icterus
Mortality 10-70%
Incubation period of RVFV?
<3 days (lambs: 12-36 h)
Clinical signs of RVFV in sheep & goats:
ADULTS & LAMBS that are >2 weeks old are highly susceptible.
Peracute disease: sudden death (20-30%).
Acute disease more often in adult sheep & goats.
Fever, anorexia, weakness, depression.
Increased RR, vomiting, diarrhea, mucopurulent nasal discharge.
Icterus in some animals.
In pregnant ewes: ‘abortion storms’ <100%
NB! Parturient material can contain virus!
Mortality in lambs >2 weeks old 20%
Clinical signs of RVFV in sheep & goats: neonates specifically.
NEWBORN & <2 week olds are extremely susceptible.
Biphasic fever – subsides just before death.
Anorexia, weakness, listlessness
Abdominal pain; rapid, abdominal respiration prior to death
Death in 24-36 hours
Mortality >90%
Clinical signs of RVFV in humans.
Often asymptomatic, or Influenza-like syndrome.
Fever, headache, muscular pain, weakness, nausea, epigastric discomfort, photophobia.
Recovery: 4-7 days
Complications: retinopathy, blindness, meningo-encephalitis, hemorrhagic syndrome with jaundice, petechiae, death.
Tx: supportive care
Incubation period of RVFV in humans.
2-6 days
Post mortem hepatic signs of RVFV. (3)
Hepatic necrosis, focal or generalised.
Liver enlarged, yellow, friable.
Petechial hemorrhages prominent:
Cutaneous & serosal.
Post mortem signs of RVFV other than hepatic. (4)
Enlarged lymph nodes.
Congestion and cortical haemorrhages of kidneys & gallbladder.
Haemorrhagic enteritis.
Icterus in calves!
DDx for RVFV.
Bluetongue
Enterotoxemia
Brucellosis (also abortions as a sign)
Vibriosis (bact.)
Trichomonosis (protozoa)
Nairobi sheep disease
Toxins
Bacterial septicemias (Pasteurella, Salmonella, Anthrax)
Rinderpest and PPR (enteritis and fever are similarities, and mucopurulent nasal discharge is in both PPR and RVFV)
Material for diagnosis of RVFV. (3)
Blood
Liver, spleen, kidney, lymph nodes, brain
Aborted fetuses
Laboratory analyses for diagnosis of RVFV. (4)
Culture
PCR (RNA)
Histopathology
Serology (virus neutralization, ELISA)
Treatment for RVFV in animals.
none
Prevention & control of RVFV. (5)
Vector control
Restriction of movements, quarantine
Vaccination
PPE to prevent exposure to infectious tissues or blood.
Milk: pasteurized or boiled
Meat & tissues: cooked thoroughly
Vaccination and RVFV.
Vaccination in endemic areas using live attenuated vaccine which gives better immunity but may cause abortions and birth defects in pregnant animals.
Inactivated vax also avail. Both options may be used during outbreaks.
RVFV as a biological weapon.
Aerosols or droplets – hypothesis:
50 kg of agent dropped 1 km downwind could affect
35 000 humans and cause 400 deaths if 1% mortality rate.
AHSV
African horse sickness virus
African horse sickness (AHS) is
an acute or subacute (non contagious), insect-borne, viral disease of Equidae,
caused by Orbivirus,
characterized by clinical signs and lesions associated with respiratory and circulatory impairment.
African horse sickness (AHS) is an acute or subacute (non contagious), insect-borne, viral disease of Equidae, caused by
Orbivirus,
characterized by clinical signs and lesions associated with respiratory and circulatory impairment.
African horse sickness (AHS) is an acute or subacute (non contagious), insect-borne, viral disease of Equidae,
caused by Orbivirus,
characterized by
clinical signs and lesions associated with respiratory and circulatory impairment.
What genus and family does AHSV belong to?
Genus Orbivirus,
family Reoviridae
What type of virus is AHSV?
RNA virus
How many serotypes does AHSV have?
Nine serotypes (1-9).
Some are cross-protective (e.g. 6 and 9).
Serotype 9 widespread in endemic regions.
Outbreaks occur with “new” serotypes.
How is AHSV inactivated?
Inactivated pH <6 and >12
In what conditions can AHSV persist/survive? (2)
Persist in frozen meat for sometime
Putrefaction does not inactivate - >2 years active
Host range of AHSV.
Equidae:
Horses, mules, donkeys.
Zebras are the reservoi.
Dogs; wild carnivores (e.g. hyenas) can catch it and become seropositive.
Reservoir of AHSV?
zebras
Carnivores that can be infected by AHSV?
Dogs; wild carnivores (e.g. hyenas) - seropositivity.
Typically become infected by eating infected meat.
The pulmonary form is reported to be the most common form in dogs. Fatal cases have been described in dogs that ate infected meat during epidemics. But not all infected dogs get sick at all.
The significance of seropositive animals is still unclear, and no animals other than equids are thought to be important in maintaining or amplifying AHSV.
Morbidity of AHSV?
Varies by viral strain, species, previous immunity and form of the dz.
Mortality of AHSV?
Horses:
Pulmonary form: <100%
Cardiac form: >50%
Mixed: 70 - >80%
Horsesickness fever: 0%
Mules 50% (epidemic)
Donkeys 5-10%
Excretion of AHSV.
semen, urine and nearly all secretions during viraemia.
But no studies have documented transmission via the above secretions so Not contagious by contact (needs a vector).
Viraemia in horses lasts 4-8 days (<21 days),
zebras < 40 days.
Recovered animals do not remain carriers.
Transmisson of AHSV.
By vectors, typically midges of the Cullicoides spp.
Occasionally also mosquitoes, ticks and possibly biting flies.
So, Not contagious by contact.
Recovered animals do not remain carriers.
Incubation period of AHSV.
depends on disease form
3 days to 2 weeks (usually < 9 days)
What are the forms of disease in AHSV? (4)
pulmonary form (peracute; high mortality),
cardiac form (subacute; also called edematous),
mixed form (acute), and
“horsesickness fever”
Clinical signs of pulmonary form of AHSV. (3)
Acute fever
Severe respiratory distress: posture, dyspnoe, spasmodic coughing, dilated nostrils with frothy fluid.
Nearly always fatal – death in few hours/days (< 1 week)
Upper left in image.
Clinical signs of cardiac/edematous form of AHSV. (3)
Fever
Swelling of the supraorbital fossa, eyelids, facial tissues, neck, thorax, brisket and shoulders
Death due cardiac failure
All in image but upper left.
Clinical signs of mixed form of AHSV.
Clinical signs of both pulmonary and cardiac forms.
Cardiac form subclinical, respiratory distress.
Common – not well recognized.
Clinical signs of horse sickness fever form of AHSV. (3)
Mild clinical signs.
Fever – morning remission, afternoon exacerbation.
Death is rare.
Clinical signs of AHSV in dogs. (3)
Most common: pulmonary form.
Fever, depression, dyspnea.
Death in few days.
Subclinical cases? – seropositive dogs exist.
Post mortem lesions of AHSV pulmonary form. (4)
Severe, diffuse pulmonary edema.
Hydrothorax, ascites.
Enlarged and edematous LNs.
Hyperemia and petechial hemorrhages in intestines.
Post mortem lesions of AHSV cardiac form. (4)
Yellow gelatinous infiltrate in subcutaneous an intermuscular fascia.
Head, neck shoulders; brisket, ventral abdomen, rump.
Hydropericardium.
Submucosal edema of cecum, large colon, rectum.
Post mortem lesions of AHSV mixed form.
A mix of pulmonary and cardiac form lesions.
DDx for AHSV.
Equine viral arteritis
Equine infectious anemia
Hendra virus infection
Purpura hemorrhagica
Equine piroplasmosis
Equine encephalosis virus
Anthrax
Toxins
Material for diagnosis of AHSV. (4)
Blood
Spleen, lung, Lymph nodes
Laboratory analyses for diagnosis of AHSV. (4)
Virus isolation in cell culture
Antigens (ELISA)
RT-PCR to detect viral RNA
Serology (ELISA, virus neutralization)
Treatment of AHSV.
none
only symptomatic care
Prevention & control of AHSV. (5)
Quarantine and restriction of movements.
Vector control and protection.
Monitor temperature of all equids (optimal twice daily).
Disinfection
Vaccination
Describe vaccination AHSV. (4)
Live attenuated vaccine available.
In endemic areas – monovalent, polyvalent.
Vax has Teratogenic effect though.
Vaccine strains can be transmitted by Culicoides vectors.
finnish for glanders
räkätauti (or malleus)
Glanders is caused by what pathogen?
Burkholderia mallei gram neg. bacteria
GLANDERS is a disease of
horses, mules and donkeys,
caused by Burkholderia mallei, and is
characterized by ulcerative nodules on the skin, nasal passages and lungs.
GLANDERS is a disease of horses, mules and donkeys, caused by
Burkholderia mallei, and is
characterized by ulcerative nodules on the skin, nasal passages and lungs.
GLANDERS is a disease of horses, mules and donkeys, caused by Burkholderia mallei, and is characterized by (3)
ulcerative nodules on the skin, nasal passages and lungs.
What bacterial family does Burkholeria mallei belong?
Family Burkholderiaceae
Note: Formerly know as Pseudomonas mallei
Describe Burkholderia mallei. (3)
Gram neg–, aerobic, facultatively intracellular.
Burkholderia mallei is inactivated by (3)
Inactivated by heat and sunlight; survival prolonged in wet or humid environments.
Under most conditions survives in the environment <2 weeks.
Susceptible to most common disinfectants (e.g. 70% ethanol).
Describe glanders in people.
very severe bacteriosis
Host range of glanders.
horses, mules, donkeys
Carnivores: especially felids.
NB! ZOONOSIS! Humans can catch it too.
Glanders is endemic to?
Endemic in parts of the Middle East, Asia, Africa and Central and South America.
(so no longer in europe and north america)
Diagnosed in Estonia the last time in 1945.
Glanders is more common in animals that are…
undernourished or otherwise in poor condition.
Mortality rate of glanders in animals?
Mortality rates are thought to be high – hard to estimate since animals are usually euthanized promptly.
Eventually fatal in most cases!
Mortality rate of glanders in humans?
In humans mortality is:
With treatment 40-50%,
without treatment up to 90->95% - pulmonary form.
20% even in only localized disease
<50% - chronic cases
Excretion of Burkholderia mallei. (2)
respiratory secretions, exudates from skin lesions
Transmission of glanders. (5)
Direct contact
Aerosols
Fomites (contaminated feed, water)
Venereal transmission
Vertical transmission
Route of entry of glanders (4)
via skin abrasions or mucous membranes, inhalation
Carnivores: ingestion of contaminated meat
Incubation period of Burkholderia mallei.
few days to few months
(most commonly 2-6 weeks)
Glanders presents in what forms (3)
Nasal, pulmonary and cutaneous forms.
Clinical cases are often a combination of forms, and may be acute, subacute, chronic or latent.
Horses: chronic glanders;
donkeys and mules: acute glanders.
Clinical signs of glanders nasal form. (3)
Nodules inside the nasal passages, star-shaped scars with purulent nasal discharge.
Regional (submaxillary) LNs enlarged.
Clinical signs of glanders pulmonary form. (3)
Nodules and abscesses in the lung; bronchopneumonia.
Mild to severe respiratory signs with fever or febrile episodes and progressive debilitation.
Clinical signs of glanders cutaneous form (also called “farcy”).
Nodules on the skin, along the course of lymphatic vessels that may rupture, ulcerate.
Most common on the inner thighs, limbs and abdomen.
Regional lymphatics and LNs enlarged.
Post mortem lesions of glanders. (4)
Nodules, granulomas and/or ulcers in various tissues.
Swollen lymphatics, with chains of nodules and ulcerated nodules in the skin.
LNs enlarged, congested and/or fibrotic.
Orchitis in males
Describe the Nodules, granulomas and/or ulcers found in various tissues in cases of glanders.
Firm, round, diameter ca 1cm, caseous or calcified center.
Surrounded by areas of inflammation.
Upper respiratory tract, lungs; other visceral organs (liver, spleen).
ddx for glanders
depends on the form the disease is presenting in
Material for diagnosis of glanders. (4)
Blood
Nasal swabs
Swab from lesions
LNs
Laboratory analyses for diagnosis of glanders. (4)
Culture
PCR
Serology (complement fixation, ELISA)
Smears
What is the mallein test?
an allergic hypersensitivity test used as a diagnosis for glanders.
The protein fraction of B. mallei is injected into the eyelid (intradermo-palpebral test), administered in eyedrops or injected subcutaneously at a site other than the eye.
Marked swelling occursin positive animals after 1-2 days. No swelling in animals not previously exposed/sensitized.
Can cause transient false positives in subsequent serological tests.
Treatment of glanders.
Tx: not recommended or even allowed in some countries.
But technically ABs, e.g. enrofloxacin.
Prevention & control of glanders. (4)
Euthanasia/slaughter of infected animsl (is mandatory in some countries).
Outbreaks in non-endemic regions: Quarantines, decontamination of premises.
In endemic areas: routine test and slaughter.
Import testing using serology
Note: Can be used as a biological weapon!
Vaccination for glanders.
no vaccine available
Glanders in humans.
