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Infectious diseases I & II > Inf. diseases II - Horses 1/2 > Flashcards

Inf. diseases II - Horses 1/2 Flashcards

1
Q

VEE

A

Venezuelan Equine Encephalomyelitis

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2
Q

Venezuelan Equine Encephalomyelitis is an acute mosquito-borne disease, caused by Alphavirus, characterized by (3)

A

fever, neurological signs and death.

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3
Q

Causative agent of Venezuelan Equine Encephalomyelitis.
Genus, family, DNA type.

A

Genus Alphavirus,
family Togaviridae
RNA- virus

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4
Q

Subtypes of Venezuelan Equine Encephalomyelitis virus.

A

Six subtypes (I to VI)

Epizootic (or epidemic) and enzootic (or endemic) groups.

Subtype I subdivided in five serovars
(AB to F)

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5
Q

Venezuelan Equine Encephalomyelitis virus Subtype I subdivided into

A

Subtype I subdivided into five serovars
(AB to F)

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6
Q

Survival of Venezuelan equine encephalomyelitis virus.

A

Stable at pH 7-8, inactivated quickly by acidic pH.

Susceptible to radiant sunlight, moist or dry heat and drying.

Likes cool, moist & dark

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7
Q

Venezuelan equine encephalomyelitis virus subtypes to affect both horses and humans?
And which affect humans only?

A

Subtype I A through C cause disease in both horses and humans.

Subtype I D through F causes disease in only humans.

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8
Q

Host range of Venezuelan equine encephalomyelitis.

A

Equids

So Horses are definitive hosts.

The following are non-amplifiers but may be infected: Cattle, swine, dogs, chickens, cotton rats, opossums, gray foxes, bats, wild birds can be infected.

NB! ZOONOSIS! ppl too! humans are dead-end hosts.

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9
Q

Morbidity of VEE.

A

Venezuelan equine encephalomyelitis

Epidemic VEEV:
Morbidity 10-100%

Enzootic – usually no serious dz in horses.

Humans:
Morbidity >10%

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10
Q

Mortality of VEE.

A

Venezuelan equine encephalomyelitis

Epidemic VEEV:
Mortality 38-90%

Enzootic – usually no deaths in horses.
1990s outbreak mortality 30-50%

Humans:
Mortality ≤ 1%

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11
Q

Transmission of VEE.

A

Primary vector: multiple mosquito species.

Excretion: body fluids – epidemic

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12
Q

IP of VEE

A

IP: 1-5 days

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13
Q

Horses are most susceptible to what type of VEE?

A

Horses are most susceptible to epidemic VEE!

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14
Q

Clinical signs of VEE.
epidemic vs endemic

A

epidemic VEE:
Fever, anorexia, depression
Flaccid lips, droopy eyelids and ears
Incoordination, blindness
Neurological signs usually appear around day 5
Mortality: 50-90%

In utero transmission can cause abortion, stillbirth.

ENZOOTIC VEE: subclinical or mild, nonspecific signs.

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15
Q

IP of VEE in humans.

A

IP: 1-6 days

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16
Q

Clinical signs of VEE in humans.

A

Usually acute, often mild, systemic illness.

Fever, chills, headache, myalgia; coughing, vomiting, diarrhea.

CNS signs:
Encephalitis in 4% of kids
<1% of symptomatic adults

Pregnant women:
Fetal encephalitis, placental damage, abortion/stillbirth, congenital dz.

Death is rare
Recovery in 2 weeks

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17
Q

Post mortem signs of VEE in horses.

A

Nonspecific

Equids may have no lesions in CNS, or there may be extensive necrosis with hemorrhages.

May be some extracranial lesions but are too variable to be diagnostically useful.
- Pancreas, liver, heart

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18
Q

Material for diagnosis of VEE.

A

Blood
Brain
Pancreas

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19
Q

Lab analyses for diagnosis of VEE.

A

Virus isolation
PCR
Serology (PNR, ELISA, CF, HI)

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20
Q

Tx of VEE.

A

no treatment, only supportive care

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21
Q

Prevention & control of VEE.

A

Quarantine and restriction of movements
Vector control
Vaccination
(Attenuated (strain TC-83)
Inactivated (strain TC-83))

Can be used as a biological weapon – aerosolized VEEV.

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22
Q

Contagious equine metritis is a highly contagious, sexually transmitted disease of horses, caused by Taylorella equigenitalis, and is characterized by

A

an acute, self-limiting, suppurative metritis endometritis and infertility.

Notifiable disease

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23
Q

Causative agent of Contagious equine metritis.

A

gram negative Taylorella equigenitalis

Non-motile coccobacillus,
Notifiable disease

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24
Q

Sero or biotypes of Contagious equine metritis.

A

gram negative Taylorella equigenitalis with

One serotype, two biotypes:

streptomycin-sensitive (more common) and
streptomycin-resistant

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25
Q

Survival of Taylorella equigenitalis.

A

Do not survives longterm in a free-living form in the environment.

Can infect and replicate in free-living amoebae (at least one week).

Susceptible to most common disinfectants.

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26
Q

Host range of contagious equine metritis.

A

horses
donkeys under experimental conditions

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27
Q

Epidemiology of CEM.

A

contagious equine metritis

Infected horses do not become systemically ill or die.
Infection: ≤ 100%
Clinical disease:30-40%

28
Q

Excretion of CEM.

A

contagious equine metritis

Excretion (sometimes intermittent): semen, vaginal discharge, placenta.

Can be found in the urethral fossa and its associated sinus, the distal urethra, the exterior of the penis and prepuce, and occasionally in the pre-ejaculatory fluid of stallions.

Mares maintain the bacteria on the clitoris, particularly in the clitoral sinuses and fossa, but a few carry it in the uterus.

29
Q

Transmission of CEM.

A

contagious equine metritis

In utero (breeding or AI, transplacental infection).

Fomites

Contact of the external genitalia of the foal with aT. equigenitalis–positive placenta or clitoral area.

Route: venereal

Stallions can become carriers for many months or even years.

30
Q

IP CEM

A

contagious equine metritis

IP: 10-14 days (2-14 d)

31
Q

Clinical signs of contagious equine metritis.

A

Stallions are subclinical carriers. In rare cases - orchitis.

Mares:
Shortened estrus cycle.
Mucopurulent, grayish-white vaginal discharge.
Variable degrees of endometritis, cervicitis and vaginitis.

Infertility for a few weeks
Abortions (around 7 months’ gestation) are rare.

Some mares can carry T. equigenitalis for a time.

32
Q

Post mortem signs of CEM.

A

Lesions are not pathognomonic.

Endometritis with mucopurulent exudate.

Edema, hyperemia and a mucopurulent exudate on the cervix.
Mild multifocal salpingitis
Vaginitis

The lesions are most apparent approximately 14 days after infection.

33
Q

Diagnosis of CEM.

A

three testsat 3 – 7 day intervals

Antibodies from day 7 after infection; in some animals, undetectable for up to 2 to 3 weeks.

34
Q

Material for diagnosis of CEM.

A

Mares: swabs from the clitoral fossa, clitoral sinuses, cervical and endometrial swabs, placenta, aborted fetuses.

Stallions: swabs from the prepuce, urethral fossa, and penile sheath (external surface of the penis), pre-ejaculatory fluid

35
Q

Lab analyses for diagnosis of CEM.

A

Bacterial culture but difficult to grow.

PCR

Immunological methods (cross-reactions): slide agglutination, latex agglutination and immunostaining etc.

Serology is unreliable as a diagnostic tool, but it may be helpful as an adjunct screening test.

Carrier mares may or may not be seropositive. Stallions do not produce detectable antibodies to T. equigenitalis.

36
Q

Tx of CEM.

A

In carriers:
washing the external genitalia with disinfectants (e.g., chlorhexidine)
washing of the clitoral fossa and sinuses
local antimicrobial treatments (nitrofurazone, silver sulfadiazine or gentamicin ointment)

Systemic AB in some animals.

Even surgical excision of the clitoral sinuses.

37
Q

Prevention & control of CEM.

A

Surveillance/ testing
Quarantine of infected animals

Treatment and a moratorium(suspension) on breeding from infected animals.

Good hygiene

Vaccine is not available!

38
Q

Rhodococcus equi pneumonia is an infectious disease of foals, caused by Rhodococcus equi, and is characterized by

A

bronchopneumonia, pulmonary abscesses and lymphadenitis.

39
Q

Details about Causative agent Rhodococcus equi.

A

Gram+
Facultatively intracellular
Nearly ubiquitous in soil

40
Q

Host range of Rhodococcus equi pneumonia.

A

horses

Occasional pathogen of humans

41
Q

Epidemiology of rhodococcus equi pneumonia.

A

Most serious cause of pneumonia in foals 1-4 months of age.

Clinical disease is rare in horses >8 months of age.

Foals that produce little to no detectable 𝛾 interferon (IFN-𝛾) are at risk of developing pneumonia.

42
Q

Morbidity & mortality of rhodococcus equi pneumonia.

A

Often sporadic

On farms where dz is endemic: annual morbidity can be high.

Mortality: case-fatality without Tx 80%

43
Q

Transmission of rhodococcus equi pneumonia.

A

Excretion: feces

Dust
Indirect contact (manure)

Route: respiratory (inhalation)
Foals are infected during first weeks of life.

44
Q

Clinical signs of rhodococcus equi pneumonia.

A

Slowly progressive.
Acute to subacute clinical manifestations.

Pulmonary lesions:
Subacute to chronic suppurative bronchopneumonia.
Pulmonary abscessation
Suppurative lymphadenitis

Lethargy, fever, tachypnea
Diarrhea – in 1/3 of foals
Cough

Also might be seen: polysynovitis, intestinal and mesenteric abscesses, osteomyelitis.

45
Q

Post mortem signs of rhodococcus equi pneumonia.

A

Pyogranulomatous pneumonia

Lymphadenitis of the bronchial LNs

46
Q

Material for diagnosis of rhodococcus equi pneumonia.

A

Transtracheal lavage
Lung, LNs

47
Q

Lab analyses for diagnosis of rhodococcus equi pneumonia.

A

Bacterial culture – for definitive diagnosis
Cytology
Histology

48
Q

Tx of rhodococcus equi pneumonia.

A

Tx: ABs – combination of erythromycin and rifampin.

Length: 3-8 weeks

Supportive therapy – IV fluids, saline nebulization, NSAIDs, oxygen, prophylactic antiulcer medication.

49
Q

Prevention & control of rhodococcus equi pneumonia.

A

Early detection of clinical cases.
Enhancing passive immunity for neonatal foals.

Enhancing nonspecific immunity for neonatal foals.

Foals should be maintained in well-ventilated, dust-free areas, avoiding dirt paddocks and overcrowding.

Pneumonic foals should be isolated.

50
Q

EIA

A

Equine infectious anemia

51
Q

Equine infectious anemia is a contagious disease of equids, caused by retrovirus, and is characterized by

A

recurring clinical signs as fever, anemia, edema and cachexia.

52
Q

Causative agent of Equine infectious anemia.
genus
family
DNA type

A

Equine infectious anemia virus (EIAV)

Genus Lentivirus,
family Retroviridae
RNA virus

53
Q

Survival of Equine infectious anemia virus.

A

Readily destroyed by most common disinfectants.

Survives limited time on the mouthparts of insects.

54
Q

Host range of Equine infectious anemia virus.

A

Host range: all members of the Equidae.

Clinical cases in horses and ponies, also mules.

55
Q

Equine infectious anemia virus infections are
particularly common in what types of regions?

A

Infections particularly common in humid, swampy regions.

Found nearly worldwide

Absent in few countries, incl. Iceland, Japan

56
Q

The presence of EIAV in a herd goes often unnoticed until some horses (2)

A

develop chronic form of the dz or routine testing is done.

57
Q

Morbidity & mortality of EIAV.

A

In endemic farms seroprevalence rate <70%.

Deaths are rare in naturally infected horses.

58
Q

Transmission of EIAV.

A

Mechanical vectors: biting flies (family Tabanidae: horse flies, deer flies).

Blood transfusion
Contaminated needles, surgical instruments and teeth floats

In utero transmission

Route: mechanically on the mouthparts of biting insects

59
Q

EIAV persists in what cells?

A

blood leucocytes

Can be found in milk and semen

60
Q

IP of EIAV.

A

IP: a week to 45 days or longer.

Some horses remain asymptomatic until they are stressed.

61
Q

Clinical signs of EIAV.

A

Signs are often nonspecific.
Fever, transient inappetence

More severe cases: weak, depressed and inappetant.

Additional signs: jaundice, tachypnea, tachycardia, ventral pitting edema, thrombocytopenia, petechiae on the mucus membranes, epistaxis or blood-stained feces.

Anemia – more severe in chronic cases.

62
Q

Post mortem signs of EIAV.

A

Spleen, liver and abdominal LNs are enlarged.

In chronic cases: emaciation

Edema on the limbs and along the ventral abdominal wall.

Petechia on internal organs (spleen, kidney).

Mucosal and visceral hemorrhages, blood vessel thrombosis.

63
Q

Suspect EIAV when?

A

Individual animals: weight loss, edema and intermittent fever.

In herd: several horses have fever, anemia, edema, progressive weakness or weight loss, particularly when new animals have been introduced into the herd or a member of a herd has died.

64
Q

Material for diagnosis of EIAV.

A

blood

65
Q

Lab analyses for diagnosis of EIAV.

A

serology
RT-PCR
viral isolation (rare)

66
Q

Tx for EIAV.

A

No Tx
No vaccine

Infected horses are lifelong carriers – must be permanently isolated from other susceptible animals or euthanized.

Foals born to infected mares should be isolated from other equids until the foal is determined to be free of infection.

The risk of congenital infection is higher if the mare has clinical signs before she gives birth.

67
Q

Prevention and control of EIAV.

A

During outbreak:
Spraying to control insect vectors, insect repellents and insect-proof stabling.

Prevent iatrogenic transmission.

In countries with no previous infection: quarantines and movement control, tracing of cases and surveillance.

Infectious diseases I & II (33 decks)

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