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Module 20: Global Vet Med > Equine Diseases of the Northern Hemisphere > Flashcards

Equine Diseases of the Northern Hemisphere Flashcards

1
Q

what is the most important viral respiratory disease of equids

A

equine influenza A

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2
Q

how is equine influenza A transmitted

A

Direct/indirect contact, aerosols

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3
Q

is there a carrier state for equine influenza A

A

no carrier state

requires circulation

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4
Q

what is the incubation period of equine influenza A

A

1-5d

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5
Q

what type of virus is equine influenza A

A

RNA

H3N8 strain circulating

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6
Q

what is responsible for attachment of virus to host cells in equine influenza A

A

hemagglutinin

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7
Q

what breaks down mucus bonds in the resp mucous in equine influenza A

A

neuraminidase

allows access of virus to underlying epithelial cells

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8
Q

what is the role of hemagglutinin (HA) and neuraminidase (NA) in equine influenza A virus

A

they both undergo antigenic drift which alters the antigenicity

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9
Q

what are the subdividisions of eqiune influenza A

A

clade 1 and 2

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10
Q

what are the signs of equine influenza A

A

Typically URT signs, extreme pyrexia

  • 39-40ºC

Lymphadenopathy

Nasal discharge

  • Serous

Acute signs decrease after 7 days, with harsh cough for 3-4 weeks

Can result in secondary bacterial pneumonia

Swollen legs/vasculitis/myositis/myocarditis may occur

Life threatening dysrhythmias

  • Should be evaluated for myocardial polypeptides, muscle enzyme before return to training
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11
Q

how is equine influenza A diagnosed

A

History, clinical signs, high morbidity rate

Viral isolation

  • Useful for strain surveillance — vaccine implications

Paired serology

Rapid antigen detection tests (ELISA)

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12
Q

what is the morbidity and mortality rate of influenza A

A

High morbidity

High mortality rate in foals and elderly

Reduced morbidity with improved immune status (ex. prior infection/vaccine)

Age is predictor of disease risk

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13
Q

how long does immunity last post infection in equine influenza A

A

1 year

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14
Q

what are the risk factors of equine influenza A

A

Prolonged journey is risk factor for horses developing equine influenza in UK (ex. importation from Europe)

New horses should be quarantined for 4 weeks after arrival

AHT maintains map of confined cases, and strain types

Lapse of vaccination

Prior vaccination does not prevent but reduces severity

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15
Q

what are the vaccination requirements of equine influenza A

A

Essential to know strain of circulating virus

Maintain up-to-date vaccine reservoir

OIE supplies information on circulating strains

Vaccines for international market should contain both clade 1 and clade 2 viruses of the Florida sub lineage

ProteqFlu has both clade 1 and clade 2 strains

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16
Q

what are the compulory vaccine for equine influenza A

A

FEI:

  • 1st vaccine at 4 months
  • 2nd after 21-92 days
  • 3rd after 150-215 days
  • Thereafter 6 monthly booster required

BHA:

  • As above, compulsory annual booster given on or prior to anniversary

Individual horse societies/events vary in rules

ProteqFlu vaccine

  • Canary pox vector
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17
Q

how is equine influenza A treated

A

Symptomatic

Particularly severe in naive individuals

Prolonged rest, NSAIDs, fluid therapy if severe

  • Post-viral syndrome and viral myocarditis relatively common
  • Sufficient nursing and rest duration vital in recover
  • May take 6 weeks for complete recovery to occur

Antibiotics may be required

  • Secondary bacterial infections common
  • May progress to interstitial pneumonia
  • Disease of high morbidity, particularly if vaccination has lapsed
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18
Q

what are the diseases that equine herpesvirus causes

A

EHV1:

  • Respiratory disease, abortion, neurological signs

EHV2:

  • Respiratory disease, keratitis, conjunctivitis

EHV3:

  • Coital exanthema

EHV4:

  • Respiratory disease, (abortion)

EHV5: Respiratory disease

  • Nodular pulmonary fibrosis?
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19
Q

what are the signs of equine herpesvirus respiratory tract infection

A

pyrexia (39-40C)

lymphadenopathy

URT signs but short duration

serous nasal discharge

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20
Q

what is the importance of EHV infections

A

common

performance limiting

contagious

spread from young to broodmares and neurotropic strains

abortion, neurological disease less common but high mortality

latent infections and recrudescence

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21
Q

why is important to know about the latency and recrudescence of EHV infections

A

disease prevetion

detection

disease transmission

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22
Q

how is EHV1 and 4 transmitted

A

Infection via inhalation or recrudescence of latent infection

Virus circulates in young horse population

Pregnant mares and visiting youngstock should be kept separate

Direct (nose to nose contact) or indirect (contaminated buckets, clothing, blankets contact with nasal discharges of infected horses)

Virus can travel via aerosol for short distances

Virus may also be transmitted by contact with aborted fetuses, placental fluids, or placentas form infected horses

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23
Q

what is the incubation period of EHV1 and 4

A

2-10 days

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24
Q

how long does shedding last of EHV1 and 4

A

up to 14d from onset of pyrexia

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25
Q

how is EHV1 and 4 controlled

A

3 week quarantine period of incoming horses

Separation of horses into suitable age groups

Consider vaccination to reduce circulating virus but does not prevent infection

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26
Q

how is EHV resp infection diagnosed

A

qPCR on fresh tracheal was specimen or nasopharyngeal swab

Serology not useful as virus is ubiquitous

May be useful to test several individuals

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27
Q

what is the disease progression of EHV resp infections

A

Self limiting in 3-7 days

May be secondary infections or vasculitis

Major risk due to abortion or neurological signs in susceptible individuals

Young animals should be quarantined for sufficient period to reduce likelihood of viral shedding

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28
Q

how are EHV resp infections treated

A

Symptomatic treatment only required

NSAIDs

Soft feed

Stable rest

Occasionally require treatment of vasculitis and limb edema, uveitis

Will remain carriers of infection and therefore concurrent disease or corticosteroids could induce recrudescence in future

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29
Q

what does rhodococcus equi infection affect

A

foals of 2-3 months most susceptible

waning colostral immunity

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30
Q

how is rhodococcus equi transmitted

A

Inhalation of contaminated dust

  • Intestinal lesions due to contaminated sputum
  • Parasites may introduce R. equi into tissues
  • Hematogenous spread rare

Increase by crowding, poor ventilation, dust

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31
Q

how does rhodococcus equi become endemic on stud farms

A

Will have high burden in the soil and will spread to successive foal crops

May be a significant annual problem

A proportion of foals will harbour infection, develop pulmonary abscesses and then have natural regression of these abscesses

Others develop clinical signs and require treatment to prevent/reduce mortality

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32
Q

what is the pathogenesis of rhodoccocus equi infection

A

Survives intracellularly in macrophages (difficult for antibiotics to reach)

  • Causes degeneration and necrosis of cells then further bacterial release

Polisaccaride capsule resists phagocytosis

VapA virulence factor

Exoenzyme virulence factors — phospholipase

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33
Q

what is the mortality and morbidity of rhodococcus equi

A

morbidity 10-15%

mortality >50%

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34
Q

what is the incubation period of rhodococcus equi

A

variable incubation period

clinical signs only apparent after few weeks

most presenting at 2-4 months old

35
Q

what are the clinical signs of rhodococcus equi infection

A

initial pyrexia

Bronchopneumonia

  • Polypnea, coughing, wheezing
  • Abdominal effort, cyanosis
  • May be nasal discharge, lacrimation

Ulcerative colitis +/- mesenteric LN abscess

  • Weight loss, poor thrift, poor haircoat
  • Low grade colic, lethargy and inappetance

Rarer clinical signs

  • Polysynovitis, joint sepsis, or osteomyelitis
  • Specific organ disruption ex. hepatic encephalopathy
  • Uveitis and hypopyon
36
Q

how is rhodococcus equi diagnosed

A

May be cultured from transtracheal aspirate (TTA) or blood

  • Negative culture does not rule out infection as intracellular organism

Neutrophilia and high fibrinogen levels

Metabolic acidosis if struggling with oxygenation

Positive serology indicates exposure only

Usually clinical diagnosis made on evaluation of diagnostic imaging together with clinical pathology

  • Cavitating abscesses may be present
  • Compression of trachea may cause stertor
37
Q

how is rhodococcus equi treated

A

Combination of erythromycin & rifampin most common

  • Need a lipophilic antimicrobial to penetrate the immune cells
  • Erythromycin may cause diarrhea, hyperthermia and tachypnea

Long term course of 4-9 weeks required

38
Q

what is used to guide duration of therapy of rhodococcus equi infection

A

Ultrasonographic appearance and resolution of acute phase response used to guide duration of therapy in addition to clinical response

Consensus guidelines according to lesion classification (U/S)

39
Q

what antibiotics may have greater efficacy in rhodococcus equi

A

Drug resistant R. equi huge problem in endemic areas (ex. Kentucky)

Newer macrolides have greater efficacy:

Azithromycin

Clarithromycin

Tulathromycin

40
Q

what is the prognosis for racing of rhodococcus equi infections

A

Good for continued athletic function if recover

41
Q

what is the intestinal presentation of rhodococcus equi infection

A

Settle in the abdomen in the lymph nodes

Failure to grow adequately

Diarrhea

May or may not be concurrent involvement of thorax

Difficult to treat, large abdominal abscesses and can adhere omentum and parts of bowel and major organs

42
Q

how are rhodococcus equi infections treated

A

Old stud farms

Heavy population

Hot, dry, dust

Infected foals isolated

Early recognition:

  • Observe foal lagging behind
  • Measure WCC and fibrinogen
  • Ultrasound screening repeated during first month of life
  • Hyperimmune plasma at 48 hours and 3-4 weeks thought previously to decrease incidence but individual variation in susceptibility and strain pathogenicity
43
Q

what is the causative agent of equine protozoal myeloencephalitis (EPM)

A

sarcocystis neurona

also incriminated – neopsora hughesi

44
Q

where is equine protozoal myeloencephalitis (EPM) reported

A

USA

canada

france?

seroprevalence >>> disease

45
Q

what are the risk factors for equine protozoal myeloencephalitis (EPM) infection

A

age (<1.5yo and >13)

season

presence of definitive hosts

watering/feeding management

adverse health events

46
Q

what is the definitive host of equine protozoal myeloencephalitis (EPM)

A

opossum

fecal excretion of infective sporocysts onto pasture

47
Q

what are the intermediate hosts of equine protozoal myeloencephalitis (EPM)

A

raccoon

armadillo

skunk

develop sarcosysts in muscle

48
Q

what are the incidental hosts in equine protozoal myeloencephalitis (EPM) life cycle

A

horses

49
Q

what does equine protozoal myeloencephalitis (EPM) cause in horses

A

multifocal distribution of lesions

expulsion of parasite –> asymptomatic

CNS lesions –> EPM

50
Q

what are the clinical signs of equine protozoal myeloencephalitis (EPM)

A

Highly variable

Often insidious

Most have spinal cord lesions

  • Ataxia & paresis often asymmetrical

5-10% have muscle atrophy

<5% have brain/brainstem lesions often persistent, but may wax and wane

  • Inflammatory response to the cyst in the nervous tissue

Multifocal disease possible

EPM = differential for many chronic neurological disorders in endemic areas (herpes virus)

51
Q

how is EPM diagnosed

A

Problematic due to widespread seroconversion

Relies on compatible signs and interpretation of relevant but non-definitive

Signalment, history, clinical signs

Exclusion of Ddx

Immunoblots (westner blot) — serum/CSF antibody ratio

  • High sensitivity, low specificity

Response to treatment

52
Q

how is EPM treated

A

Anti-protozoals

  • Ponazuril (toltrazuril sulfone)
    • Anti-coccidial, crosses BBB
    • Prolonged course of medication required
  • Sulphonamine-pyrimethamine

Ancillary therapy

  • NSAIDs
  • Corticosteroids/DMSO?
  • Vitamin E
  • Protect the myelin sheath
  • Immuno-modulators
53
Q

what is the % of horses that imrpove and relapse after EPM infection

A

60-70% improve

Relapse rate —> 10-20%

54
Q

how is EPM prevented

A

difficult

aim to limit exposure of forage and pasture to definitive host

55
Q

what is the causative agent of potomac horse fever

A

Neorickettsia risticii

56
Q

how is potomac horse fever treated

A

Fluid therapy

  • Colitis

Tetracyclines (doxycycline, OTC)

  • 7 day course

Tetracyclines may correct pyrexia within 48 hours

57
Q

how is potomac horse fever prevented

A

Vaccination highly successful in reducing incidence

Avoidance of risk factors

Stabling to avoid ingestion of infected trematodes at risk times of year

58
Q

what type of bacteria causes equine monocytic ehrlichiosis (aka potomac horse fever)

A

neorickettsia risticii

intracellular gram negative coccus

59
Q

where is equine monocytic ehrlichiosis (aka potomac horse fever) distributed

A

USA, canada, europe

60
Q

what is the vector of equine monocytic ehrlichiosis (aka potomac horse fever)

A

Virgulate (rod shaped) trematode of freshwater snails

Methods of transmission is unknown

Possible ingestion of immature stages in aquatic insects

61
Q

what is the pathogenesis of potomac horse fever

A

Infects monocytes

  • Obligate intracellular organism

Predilection for colon tissue, macrophages, crypt cells, mast cells

  • Loss of microvilli
  • Reduced electrolyte transport
  • Watery diarrhea
  • Dose dependent effect
62
Q

what is the prediliction site for potomac horse fever

A

colon tissue, macrophages, crypt cells, mast cells

63
Q

what are the clinical signs of potomac horse fever

A

Typhlocolitis

  • Biphasic fever (up to 41ºC)
  • Edema
  • Anorexia
  • Diarrhea
  • Endotoxemia
  • Laminitis

Sub-clinical disease

Abortion

  • Usually at 7 months
  • Maladjusted foals
64
Q

how is potomac horse fever diagnosed

A

history, signs

serology (IFAT or ELISA)

fecal PCR

65
Q

what are ddx for diarrhea in young foals

A

Clostridium difficile

Rotavirus infection

Strongyloides westeri — high burdens (epg >2000) leads to diarrhea

Strongylus vulgaris — cause verminous arteritis and colic signs

Cryptosporidia — more likely to occur in more intensive stud farms

Giardia

Parascaris equorum becomes significant in foals >3 months

Antibiotic induced diarrhea also common as in adults

66
Q

what are the viral causes of diarrhea in foals

A

rotavirus

67
Q

what are the epidemiological features of rotavirus

A

highly contagious

short incubation period

rapid spread

68
Q

what are the signs of rotavirus in foals

A

depressed and anorexic

69
Q

what age does rotavirus affect

A

2 days to 6 months

70
Q

how is rotavirus diagnosed

A

fecal antigen testing and electromicroscopy

71
Q

what are ddx for rotaviral infection in foals

A

adenovirus

coronavirus

parvovirus

bacterial causes of diarrhea

72
Q

what is the morbidity of rotavirus in foals

A

high

effective barrier nursing

disinfection required

vaccination in subsequent years

73
Q

how is foal diarrhea treated

A

Fluid therapy most important

  • IV or oral
  • Electrolytes, glucose
  • Hyperimmune plasma for Rotavirus infection

Intestinal protectants

  • Bismuth subsalicyclate
  • Activated charcoal
  • Bio-sponge

Anti-ulcer therapy

Antibiotics if pyrexic with secondary infection

Probiotics

74
Q

how is foal diarrhea prevented

A

Vaccination of mare at 8, 9, and 10 months of pregnancy to increase production of antibodies in colostrum to protect foals

75
Q

what causes proliferative enteropathy of foals

A

lawsonia intracellularis

76
Q

what age of horse does lawsonia intracellularis affect

A

weanlings

77
Q

what type of bacteria is lawsonia intracellularis

A

obligate intracellular gram negative organism

78
Q

where does lawsonia intracellularis invade

A

GI cyrpt cells

loss of villi and malabsorption

79
Q

at what time are horses affected by lawsonia intracellularis

A

around time of loss of colostral antibody protection

4-7 months

80
Q

what are the clinical signs of lawsonia intracellularis

A

Fever

Lethargy

Peripheral edema *

Diarrhea

Until final stages of condition

Colic

Weight loss

Profound hypoproteinemia

  • Albumin falling to 10 g/l (ref 30-33 g/l) in some cases
  • Foal may collapse due to hypotension
  • Better prognosis with earlier diagnosis and treatment
81
Q

how is l intracellularis diagnosed

A

Clinical signs and signalment

Extreme hypoalbuminemia

Fecal PCR

  • Intermittent shedding
  • Pool fecal samples or submit sequential samples for analysis

Serology

  • Seroconversion in high proportion of adults, but seropositivity in foal with clinical signs is suggestive of active infection

US appearance of small intestine

  • Cartwheel appearance
  • Narrowed lumen
82
Q

how is l intracellularis treated

A

Oxytetracycline

  • 4-6 weeks required
  • Doxycycline also effective

Colloidal oncotic support

  • Hetastarch or plasma

Full recovery can be made with early diagnosis and sufficient duration of treatment

83
Q

how is l intracellularis preveted

A

difficult

Wildlife reservoir

Vaccination of mares

Licensed equine vaccine

Module 20: Global Vet Med (21 decks)

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