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Ross LAM I > 1 - Infectious Diseases > Flashcards

1 - Infectious Diseases Flashcards

1
Q

What is the etiology of equine strangles? Which horses does it typically infect?

A

Streptococcus equi ssp equi

Young horses mainly affected

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2
Q

How is strangles transmitted?

A

Direct and indirect nose/mouth contact or via contaminated fomites

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3
Q

How do horses become chronic carriers of strangles?

A

Chondroids may form in guttural pouch after infection, continue to carry infectious organism

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4
Q

Relative to disease course, when are horses shedding Strep equi? (disregarding chronic carriers)

A

Nasal shedding begins 4-7 days post infection, ceases 3-6 weeks after acute phase

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5
Q

What clinical signs are associated with strangles?

A

Depression/reduced appetite/fever precede nasal shedding
Serous then mucopurulent nasal discharge
Purulent lymphadenitis of the URT (LNs are firm and painful, rupture and drain ~1-2 weeks)

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6
Q

What complications are associated with strangles?

A 
Asphyxiation
Pneumonia (rare)
Guttural pouch empyema
Bastard strangle - dissemination and abscessation elsewhere
Purpura hemorrhagica
Immune-mediated myositis
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7
Q

How is strangles diagnosed?

A

Culture (S. equi NEVER commensal)
PCR (more sensitive)
Strep-M protein ELISA - for Bastard/purpura only

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8
Q

How is strangles treated in cases with early clinical signs and NO LN abscessation?

A

Procaine penicillin BID, NSAIDs

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9
Q

How is strangles treated in cases with abscessed LNs?

A

AVOID abx unless URT obstruction

Enhance maturation and drainage of LNs

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10
Q

What treatment can be given to horses exposed to strangles?

A

Penicillin may prevent disease

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11
Q

How is strangles treated in cases with complications?

A

Abx therapy for metastatic abscession
Local flushes in cases of pouch empyema
Penicillin and steroids for purpura

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12
Q

How are carriers identified in strangles cases?

A

Most horses stop shedding 4-6 weeks post-infection
Use nasal/GP washes (culture/PCR) to determine suitability to return to herd
If positive look for GP chondroids and retest q30 days

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13
Q

What vaccination options are there for strangles? What complications are associated with each?

A
  1. Killed (IM) - local swelling, injection site abscesses, purpura hemorrhagica
  2. Live attenuated (IN) - nasal discharge, lymphadenopathy, deep abscesses, limb edema, purpura
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14
Q

Which strains of equine herpesvirus are most important and which disease presentations do they cause?

A

EHV-1: abortion storms and EHM

EHV-4: rhinopneumonitis

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15
Q

Describe the rhinopneumonitis form of EHV.

A

Spread via aerosol, direct contact, fomites
Young animals most often affected
Signs (if any) 2-10 days post-exposure
Mostly upper respiratory signs (biphasic fever, nasal discharge, +/- cough, pharyngitis, tracheitis)
Recovery 2-3 weeks if no complications

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16
Q

Describe the abortive form of EHV.

A

Sporadic/storm abortions in last 4m of pregnancy
HIGH levels of virus in fetal fluids/placenta
Foals may be born alive but in bad shape
Mare’s future fertility not affected

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17
Q

Describe the myeloencephalopathy (EHM) form of EHV.

A

Gene mutation in viral DNA polymerase - more aggressive replication and higher risk of neuro disease
*Can occur in ANY strain of EHV

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18
Q

How is EHV diagnosed?

A

Must prove viremia + CS
1. Virus isolation and rtPCR - best choice
<10 days after infection, *nasal swabs + whole blood
2. CSF may show xanthochromia, RBCs, elevated protein
3. Serology with 4x rise in titer
4. Necropsy
5. Histopath - vasculitis, intranuclear inclusions
6. Immunohistochem on formalin-fixed tissue

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19
Q

How is EHV treated?

A

Symptomatic tx
Antivirals - Acyclovir IV or Valacyclovir PO
Neuro complications - NSAIDs, DMSO, corticosteroids

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20
Q

What isolation and quarantine protocols should be followed in EHV cases?

A

Isolate with >35 ft separation

Quarantine for 4 weeks after last case, 2 weeks if PCR test negative 2-4 times

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21
Q

Which drug can be used as an immunomodulator to reduce upper respiratory disease in EHV cases?

A

Zylexis

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22
Q

What vaccination options are there for EHV?

A

For herd control only:
Prestige II/V (killed for EHV-1/4)

Also indicated for pregnant mares:
Rhinomune (MLV for EHV-1)
Calvenza
Prodigy (killed for EHV-1)

For pregnant mares only:
Pneumabort K

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23
Q

What is the etiology of infectious bovine rhinotracheitis?

A

Bovine herpesvirus 1

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24
Q

How is IBR transmitted?

A

Inhalation, ingestion, and venereally

Virus is shed in respiratory, ocular, and genital secretions

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25
Q

What are the primary sites of infection of IBR?

A

Respiratory tract
Conjunctiva
Reproductive tract

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26
Q

Which strain of bovine herpesvirus causes encephalitis?

A

BHV - 5

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27
Q

How does IBR manifest in neonatal calves?

A

Pneumonia and gastroenteritis

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28
Q

What clinical signs are associated with standard IBR infection?

A

Cough, increased resp rate
Fever, inappetance
Nasal lesions (hyperemia)

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29
Q

What are the variant forms of IBR and what clinical signs do they have?

A
  1. Conjunctival form (Winter Pink Eye) - exudate of both eyes
  2. Urogenital form - focal pustular lesions
  3. Encephalitic form - calves under 6 months, generalized encephalitis
  4. Neonatal systemic form - calves infected late in gestation, severe respiratory and intestinal inflammation/necrosis
  5. Abortion - last trimester, retained placenta, autolyzed fetus
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30
Q

What necropsy findings are consistent with IBR? Standard, encephalitic, and neonatal systemic forms?

A
  1. Extensive respiratory diphtheric membrane
  2. Meningoencephalitis with intranuclear inclusion bodies
  3. Turkish towel lesion - entire forestomach has diphtheric membrane
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31
Q

How is IBR diagnosed?

A

Virus isolation by tissue culture
PCR
Viral Ag in immunofluorescence or IHC (post-mortem)

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32
Q

What are the differentials for abortion caused by IBR?

A

BVD
Lepto
Neospora

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33
Q

What are the differentials for conjunctivitis caused by IBR?

A

Bacterial keratoconjunctivitis

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34
Q

What are the differentials for neurologic dz caused by IBR?

A

Histophilus
Listeria
Rabies
toxic/metabolic dz

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35
Q

What are the differentials for neonatal dz caused by IBR?

A

FPT and bacterial septicemia
Neonatal diarrhea and septicemia
BVD

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36
Q

How is IBR treated and prevented?

A

Supportive care
Vaccination:
1. Killed vax (IM) - do not require refrigeration
2. MLV (IN) - approved in pregnant cows
3. MLV (IM) - may be approved in pregnant cows by label claims only

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37
Q

How long does passive (colostral) immunity for IBR last?

A

4-6 months (long!)

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38
Q

Which hosts does Bluetongue virus infect?

A

Cattle - natural hosts, rarely develop dz

Sheep - clinical disease

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39
Q

T/F: Bluetongue is a reportable virus.

A

TRUE (in many states)

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40
Q

What the pathogenesis of Bluetongue?

A

Infects endothelial cells
Widespread vasculitis
Edema and necrosis of epithelial and mucosal surfaces

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41
Q

What clinical signs are associated with Bluetongue?

A 
SHEEP
Edema of face, lips, muzzle, ears
Serous to mucopurulent nasal discharge
Oral erosions and ulcerations
Coronitis and lameness/laminitis

Fetal infection disrupts organogenesis and causes teratogenesis, abortion, or weak lambs

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42
Q

How is Bluetongue diagnosed?

A

Viral isolation from blood/tissues (most definitive)

RT-PCR or serology

43
Q

What are the ddx for oral lesions caused by bluetongue?

A

FMD
Vesicular stomatitis
Orf
Sheep pox

44
Q

How is Bluetongue treated and controlled?

A

Supportive care

MLV vaccine

45
Q

What is the etiology of Malignant Catarrhal Fever?

A

North American form - ovine herpesvirus 2

African form - alcelaphine herpesvirus 1 and 2

46
Q

Which hosts does Malignant Catarrhal Fever affect?

A

No disease in natural hosts (sheep and wildebeest)

Highly fatal dz in non-host adapted ruminants (cattle)

47
Q

What is the pathogenesis of Malignant Catarrhal Fever?

A

Replication in lymphoid tissue
Spread to endothelial cells throughout body
Widespread necrotizing vasculitis with lymphocytic cuffing

48
Q

What clinical signs are consistent with Malignant Catarrhal Fever?

A

Keratoconjunctivitis, edema, ocular discharge
Mucopurulent nasal discharge
Oral ulcerations, salivation
Diarrhea, dysentery
Skin lesions of muzzle / teats and claws/horns may be sloughed
Progressive neurological signs
Death within 3-7 days

49
Q

What are the ddx for Malignant Catarrhal Fever?

A

BVD / mucosal disease
Bluetongue (rare in cattle)
Vesicular stomatitis
FMD

50
Q

T/F: Malignant Catarrhal Fever is reportable

A

False, but state/federal agencies should be notified d/t similarity to FMD

51
Q

How is Malignant Catarrhal Fever diagnosed?

A

Viral isolation (nasal swabs, blood, PM tissues)
PCR (blood, PM tissues)
Serology

52
Q

How is Malignant Catarrhal Fever treated?

A

Supportive care

Grave prognosis

53
Q

What is the etiology/epidemiology of sporadic bovine lymphosarcoma?

A

Affects young cows. Etiology unknown

54
Q

Describe calf/juvenile lymphosarcoma

A

Affects cattle under 1 year.

CS similar to adult enzootic form (generalized, symmetric lymphadenopathy)

55
Q

Describe thymic (adolescent) lymphosarcoma

A

Affects cattle 6-24 months

CS are d/t space-occupying masses in the neck/thorax

56
Q

Describe cutaneous lymphosarcoma

A

Affects cattle 1-3 years

Multiple raised, circular, ulcerated masses

57
Q

What is the etiology/epidemiology of enzootic bovine lymphosarcoma?

A

Adult form (over 2 years), caused by bovine leucosis virus (BLV)
Transmitted horizontally by blood-sucking insects, direct contact with infected cattle, or iatrogenically
Low rate of vertical transmission transplacentally or by ingestion of milk/colostrum

58
Q

What are the main CS associated with enzootic bovine lymphosarcoma?

A

Decreased milk production, weight loss, reduced appetite
External lymphadenopathy, internal abdominal lymphadenopathy
Abomasal/cardiac involvement
Exopthalmos
Posterior paresis/paralysis

59
Q

How is enzootic bovine lymphosarcoma diagnosed?

A

CBC - lymphocytosis
*Histo or cytologic demonstration of neoplastic cells
Serology confirms BLV infection but not lymphosarcoma

60
Q

How is enzootic bovine lymphosarcoma treated and controlled?

A

No tx recommended - 60 day prognosis
No vaccines

Serologic testing followed by

  1. Culling of all seropositive cattle
  2. Segregation of infected from uninfected cattle
  3. Control efforts to prevent further iatrogenic spread
61
Q

T/F: Equine Herpes Myeloencephalopathy (EHM) is reportable

A

TRUE

62
Q

T/F: BVDV is very stable in the environment and hard to disinfect

A

FALSE

63
Q

How is BVDV transmitted?

A

Isolated in most body fluids

PI cattle and acutely infected cattle are major sources

64
Q

Describe the standard pathogenesis of BVD

A

Primary replication in resp tract and tonsils
Dissemination to lymphoid tissue and epithelial surfaces
Lymphoid depletion and epithelial erosions

65
Q

How does the pathogenesis of BVD occur in non-PI immunocompetent animals with NCP?

A

Replication is inhibited by immunity (passive or acquired), subclinical or mild infection most common
May cause infertility, acute disease, or thrombocytopenia

66
Q

How does BVD occur in transplacental infection at 1-50 days of gestation?

A

Conception failure and early embryonic death

67
Q

How does BVD occur in transplacental infection at 50-125 days of gestation?

A

Abortion and fetal mummification OR

immunotolerant PI calf

68
Q

How does BVD occur in transplacental infection at 125-150 days of gestation?

A

Congenital abnormalities (cerebellar hypoplasia and ocular defects)

69
Q

How does BVD occur in transplacental infection at 150-270 days of gestation?

A

Fetus mounts immune response (seropositive pre-colostrum) and clears virus OR
Virus causes organ damage leading to late term abortion

70
Q

Describe the acute mucosal disease associated with BVD

A

Occurs in cases of superinfection (PI animals with NCP and CP)
Case fatality near 100% (5-7 days post-infection)
Depression, complete anorexia, rumen stasis, profuse watery diarrhea, oral lesions, skin erosions

71
Q

Describe a case of acute BVD

A

Cattle 6-24 months
Erosive gastroenteritis and oral lesions
NOT typically fatal

72
Q

Describe hemorrhagic/bleeder syndrome associated with BVD

A

Thrombocytopenia (under 25,000) and PLT dysfunction d/t viral infection of PLTs causing massive hemorrhage
Case fatality ~25%

73
Q

Which form of BVD is the most common in endemic herds?

A

Reproductive disease

Infertility, repeat breeders, abortion, stillbirths, congenital abnormalities

74
Q

Which form of BVD is typical of beef calves newly entering the feedlot?

A 
Respiratory disease (d/t immunosuppressive effects of virus)
Fibrinous pneumonia
75
Q

What is the significance of getting pre-colostral titers for BVDV?

A

If calves are negative pre-colostrum, virtually no chance of PI animal in herd

76
Q

Which diagnostic method for BVDV uses ear notch samples?

A

IHC staining for Ag

Useful to dx PI animals

77
Q

Which two infectious diseases of cattle have long (~6 months) colostral protection?

A

IBR and BVD

78
Q

How is BVD treated and prevented?

A

Abx and supportive therapy

MLV (IM) vaccine

79
Q

Which leptospirosis serovars affect ruminants (esp cattle)

A

Hardjo - host adapted to cattle (long-term herd infections)

Pomona - cattle are incidental hosts

80
Q

What clinical signs are associated with leptospirosis in ruminants?

A

Acute (lambs/calves) - hemolytic anemia
Subacute - drop in milk, slack udders, blood-stained milk, abortion (second half)
Chronic - transient milk drop followed by wave of abortions

81
Q

How is leptospirosis in ruminants diagnosed? What diagnostic challenge is there?

A

Fluorescent Ab staining / PCR testing of urine
IHC or PCR of kidneys in aborted fetuses
Serology (MAT) - cannot use paired titers because already convalescent at time of abortion, use established serovar-based cutoffs

82
Q

How is leptospirosis treated and prevented in ruminants

A

Cetiofur / oxytetracycline

Vaccination

83
Q

Which leptospirosis serovars are significant in the equine?

A

Pomona and Bratislava

84
Q

What clinical signs are associated with leptospirosis in horses?

A

Abortion
‘Moon blindness’ (recurrent uveitis/periodic opthalmia)
In foals - renal, hepatic, lung damage, hemolytic anemia

85
Q

How is leptospirosis treated and prevented in the horse?

A

Abx - IV K penicillin, TMS, cephtiofur, tetracycline
For uveitis - Topical and systemic steroids, cyclosporine, NSAIDs

Vaccine available - new and not very efficacious

86
Q

Which ruminant pathogen discussed can be isolated from NORMAL cattle?

A

Histophilus somni

87
Q

Who does H. somni affect? When is it seen?

A

Feedlot cattle 4-12 months. Outbreaks ~4 weeks after arrival

88
Q

Describe the pathogenesis of H. somni

A

Colonization of respiratory/urogenital mm
Pneumonia/endometritis
Septicemia and vasculitis

89
Q

What clinical signs are associated with H. somni infection?

A 
Pneumonia
Septicemia (high fever and sudden death)
TME (thrombotic meningioencephalitis) 
Myocarditis (exercise intolerance)
Pericarditis (jugular distension and brisket edema)
Pleuritis
90
Q

How is H. somni diagnosed?

A

Primarily at necropsy

Serology - rapid seroconversion but titers fall rapidly

91
Q

How is H. somni treated and prevented?

A

Most abx susceptible - ceftiofur and enrofloxacin DOC
Vaccines (bacterins) have many complications
Abx in feed during first 60 days on feedlot

*On arrival metaphylaxis effective for shipping fever but NOT H. somni

92
Q

How is Mycoplasma bovis transmitted?

A

Ingestion of mastitic milk
Direct nose to nose contact
Aerosol of respiratory secretions

93
Q

How does Mycoplasma bovis present clinically?

A

Mastitis
Pneumonia and polyarthritis
Otitis media/interna

94
Q

What age of cattle are most susceptible to Mycoplasma bovis?

A

Calves

95
Q

How is Mycoplasma bovis diagnosed?

A

Necropsy
IHC stains on histopath
Culture of M. bovis (M. spp is not significant)

96
Q

How is Mycoplasma bovis treated and prevented?

A

Tulathromycin, enrofloxacin, gamithromycin, florfenicol
(Macrolides NOT effective, though good for most Mycoplasma)
Metaphylaxis on feedlots

97
Q

How is Brucellosis (B. abortus) transmitted to humans?

A 
Humans:
-Unpasteurized dairy products (NOT in cooked meat)
-Occupational exposures
Cattle:
-Ingestion
-Semen
98
Q

Describe the pathogenesis of B. abortus

A

Entry through mm of oral cavity, conjunctiva, skin, or nasal cavity
Localization in regional LN, proliferation
Bacteremia

99
Q

How is B. abortus diagnosed?

A

Third trimester abortion w/o other clinical signs

Serology / culture

100
Q

How is B. abortus controlled?

A

Vaccination

Surveillance by Market Cattle ID (blood sampling at slaughter) and Brucellosis Ring Test (milk)

101
Q

What is the etiology of tuberculosis?

A

Mycobacterium bovis

102
Q

How is tuberculosis transmitted?

A

Bronchial secretions, milk, meat

103
Q

Describe the pathogenesis of tuberculosis

A

Primary focus at point of infection (lung/intestine)
Calcification of focus and regional LNs
Enlarging lesion and metastatic spread

104
Q

How is tuberculosis diagnosed and monitored?

A

Intra-dermal caudal fold test (CFT)

Ross LAM I (4 decks)

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