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
What are the primary sites of infection of IBR?
Respiratory tract Conjunctiva Reproductive tract
26
Which strain of bovine herpesvirus causes encephalitis?
BHV - 5
27
How does IBR manifest in neonatal calves?
Pneumonia and gastroenteritis
28
What clinical signs are associated with standard IBR infection?
Cough, increased resp rate Fever, inappetance Nasal lesions (hyperemia)
29
What are the variant forms of IBR and what clinical signs do they have?
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
30
What necropsy findings are consistent with IBR? Standard, encephalitic, and neonatal systemic forms?
1. Extensive respiratory diphtheric membrane 2. Meningoencephalitis with intranuclear inclusion bodies 3. Turkish towel lesion - entire forestomach has diphtheric membrane
31
How is IBR diagnosed?
Virus isolation by tissue culture PCR Viral Ag in immunofluorescence or IHC (post-mortem)
32
What are the differentials for abortion caused by IBR?
BVD Lepto Neospora
33
What are the differentials for conjunctivitis caused by IBR?
Bacterial keratoconjunctivitis
34
What are the differentials for neurologic dz caused by IBR?
Histophilus Listeria Rabies toxic/metabolic dz
35
What are the differentials for neonatal dz caused by IBR?
FPT and bacterial septicemia Neonatal diarrhea and septicemia BVD
36
How is IBR treated and prevented?
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
37
How long does passive (colostral) immunity for IBR last?
4-6 months (long!)
38
Which hosts does Bluetongue virus infect?
Cattle - natural hosts, rarely develop dz | Sheep - clinical disease
39
T/F: Bluetongue is a reportable virus.
TRUE (in many states)
40
What the pathogenesis of Bluetongue?
Infects endothelial cells Widespread vasculitis Edema and necrosis of epithelial and mucosal surfaces
41
What clinical signs are associated with Bluetongue?
``` 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
42
How is Bluetongue diagnosed?
Viral isolation from blood/tissues (most definitive) | RT-PCR or serology
43
What are the ddx for oral lesions caused by bluetongue?
FMD Vesicular stomatitis Orf Sheep pox
44
How is Bluetongue treated and controlled?
Supportive care | MLV vaccine
45
What is the etiology of Malignant Catarrhal Fever?
North American form - ovine herpesvirus 2 | African form - alcelaphine herpesvirus 1 and 2
46
Which hosts does Malignant Catarrhal Fever affect?
No disease in natural hosts (sheep and wildebeest) | Highly fatal dz in non-host adapted ruminants (cattle)
47
What is the pathogenesis of Malignant Catarrhal Fever?
Replication in lymphoid tissue Spread to endothelial cells throughout body Widespread necrotizing vasculitis with lymphocytic cuffing
48
What clinical signs are consistent with Malignant Catarrhal Fever?
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
What are the ddx for Malignant Catarrhal Fever?
BVD / mucosal disease Bluetongue (rare in cattle) Vesicular stomatitis FMD
50
T/F: Malignant Catarrhal Fever is reportable
False, but state/federal agencies should be notified d/t similarity to FMD
51
How is Malignant Catarrhal Fever diagnosed?
Viral isolation (nasal swabs, blood, PM tissues) PCR (blood, PM tissues) Serology
52
How is Malignant Catarrhal Fever treated?
Supportive care | Grave prognosis
53
What is the etiology/epidemiology of sporadic bovine lymphosarcoma?
Affects young cows. Etiology unknown
54
Describe calf/juvenile lymphosarcoma
Affects cattle under 1 year. | CS similar to adult enzootic form (generalized, symmetric lymphadenopathy)
55
Describe thymic (adolescent) lymphosarcoma
Affects cattle 6-24 months | CS are d/t space-occupying masses in the neck/thorax
56
Describe cutaneous lymphosarcoma
Affects cattle 1-3 years | Multiple raised, circular, ulcerated masses
57
What is the etiology/epidemiology of enzootic bovine lymphosarcoma?
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
What are the main CS associated with enzootic bovine lymphosarcoma?
Decreased milk production, weight loss, reduced appetite External lymphadenopathy, internal abdominal lymphadenopathy Abomasal/cardiac involvement Exopthalmos Posterior paresis/paralysis
59
How is enzootic bovine lymphosarcoma diagnosed?
CBC - lymphocytosis *Histo or cytologic demonstration of neoplastic cells Serology confirms BLV infection but not lymphosarcoma
60
How is enzootic bovine lymphosarcoma treated and controlled?
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
T/F: Equine Herpes Myeloencephalopathy (EHM) is reportable
TRUE
62
T/F: BVDV is very stable in the environment and hard to disinfect
FALSE
63
How is BVDV transmitted?
Isolated in most body fluids | PI cattle and acutely infected cattle are major sources
64
Describe the standard pathogenesis of BVD
Primary replication in resp tract and tonsils Dissemination to lymphoid tissue and epithelial surfaces Lymphoid depletion and epithelial erosions
65
How does the pathogenesis of BVD occur in non-PI immunocompetent animals with NCP?
Replication is inhibited by immunity (passive or acquired), subclinical or mild infection most common May cause infertility, acute disease, or thrombocytopenia
66
How does BVD occur in transplacental infection at 1-50 days of gestation?
Conception failure and early embryonic death
67
How does BVD occur in transplacental infection at 50-125 days of gestation?
Abortion and fetal mummification OR | immunotolerant PI calf
68
How does BVD occur in transplacental infection at 125-150 days of gestation?
Congenital abnormalities (cerebellar hypoplasia and ocular defects)
69
How does BVD occur in transplacental infection at 150-270 days of gestation?
Fetus mounts immune response (seropositive pre-colostrum) and clears virus OR Virus causes organ damage leading to late term abortion
70
Describe the acute mucosal disease associated with BVD
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
Describe a case of acute BVD
Cattle 6-24 months Erosive gastroenteritis and oral lesions NOT typically fatal
72
Describe hemorrhagic/bleeder syndrome associated with BVD
Thrombocytopenia (under 25,000) and PLT dysfunction d/t viral infection of PLTs causing massive hemorrhage Case fatality ~25%
73
Which form of BVD is the most common in endemic herds?
Reproductive disease | Infertility, repeat breeders, abortion, stillbirths, congenital abnormalities
74
Which form of BVD is typical of beef calves newly entering the feedlot?
``` Respiratory disease (d/t immunosuppressive effects of virus) Fibrinous pneumonia ```
75
What is the significance of getting pre-colostral titers for BVDV?
If calves are negative pre-colostrum, virtually no chance of PI animal in herd
76
Which diagnostic method for BVDV uses ear notch samples?
IHC staining for Ag | Useful to dx PI animals
77
Which two infectious diseases of cattle have long (~6 months) colostral protection?
IBR and BVD
78
How is BVD treated and prevented?
Abx and supportive therapy | MLV (IM) vaccine
79
Which leptospirosis serovars affect ruminants (esp cattle)
Hardjo - host adapted to cattle (long-term herd infections) | Pomona - cattle are incidental hosts
80
What clinical signs are associated with leptospirosis in ruminants?
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
How is leptospirosis in ruminants diagnosed? What diagnostic challenge is there?
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
How is leptospirosis treated and prevented in ruminants
Cetiofur / oxytetracycline | Vaccination
83
Which leptospirosis serovars are significant in the equine?
Pomona and Bratislava
84
What clinical signs are associated with leptospirosis in horses?
Abortion 'Moon blindness' (recurrent uveitis/periodic opthalmia) In foals - renal, hepatic, lung damage, hemolytic anemia
85
How is leptospirosis treated and prevented in the horse?
Abx - IV K penicillin, TMS, cephtiofur, tetracycline For uveitis - Topical and systemic steroids, cyclosporine, NSAIDs Vaccine available - new and not very efficacious
86
Which ruminant pathogen discussed can be isolated from NORMAL cattle?
Histophilus somni
87
Who does H. somni affect? When is it seen?
Feedlot cattle 4-12 months. Outbreaks ~4 weeks after arrival
88
Describe the pathogenesis of H. somni
Colonization of respiratory/urogenital mm Pneumonia/endometritis Septicemia and vasculitis
89
What clinical signs are associated with H. somni infection?
``` Pneumonia Septicemia (high fever and sudden death) TME (thrombotic meningioencephalitis) Myocarditis (exercise intolerance) Pericarditis (jugular distension and brisket edema) Pleuritis ```
90
How is H. somni diagnosed?
Primarily at necropsy | Serology - rapid seroconversion but titers fall rapidly
91
How is H. somni treated and prevented?
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
How is Mycoplasma bovis transmitted?
Ingestion of mastitic milk Direct nose to nose contact Aerosol of respiratory secretions
93
How does Mycoplasma bovis present clinically?
Mastitis Pneumonia and polyarthritis Otitis media/interna
94
What age of cattle are most susceptible to Mycoplasma bovis?
Calves
95
How is Mycoplasma bovis diagnosed?
Necropsy IHC stains on histopath Culture of M. bovis (M. spp is not significant)
96
How is Mycoplasma bovis treated and prevented?
Tulathromycin, enrofloxacin, gamithromycin, florfenicol (Macrolides NOT effective, though good for most Mycoplasma) Metaphylaxis on feedlots
97
How is Brucellosis (B. abortus) transmitted to humans?
``` Humans: -Unpasteurized dairy products (NOT in cooked meat) -Occupational exposures Cattle: -Ingestion -Semen ```
98
Describe the pathogenesis of B. abortus
Entry through mm of oral cavity, conjunctiva, skin, or nasal cavity Localization in regional LN, proliferation Bacteremia
99
How is B. abortus diagnosed?
Third trimester abortion w/o other clinical signs | Serology / culture
100
How is B. abortus controlled?
Vaccination | Surveillance by Market Cattle ID (blood sampling at slaughter) and Brucellosis Ring Test (milk)
101
What is the etiology of tuberculosis?
Mycobacterium bovis
102
How is tuberculosis transmitted?
Bronchial secretions, milk, meat
103
Describe the pathogenesis of tuberculosis
Primary focus at point of infection (lung/intestine) Calcification of focus and regional LNs Enlarging lesion and metastatic spread
104
How is tuberculosis diagnosed and monitored?
Intra-dermal caudal fold test (CFT)