Malignant Catarrhal Fever Flashcards

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1
Q

what type of disease is MCF, and what causes it? where is it a problem? fatality?

A

 MCF is a severe lympho- proliferative disease caused by a group of herpesviruses collectively referred to as malignant catarrhal fever viruses.
 Highly fatal disease of: Cattle, deer, bison, buffalo, and other ruminants
 Major problem in zoos

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2
Q

how many viruses in the MCF group? How many associated with clinical disease?

A

Ten genetically and antigenically related viruses have been identified and constitute the group of MCF viruses.
Six of these viruses are associated with clinical disease, and the remaining four viruses have not yet been associated with disease

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3
Q

**previousy the most important type of MCF, outside Africa, in cattle? what about in africa

A
  • Outside Africa: Ovine herpesvirus type 2
    > now called ovine gammaherpesvirus 2
  • In Africa: Wildebeest
    > Alcelaphine gammaherpesvirus 1 (prev. alcephine herpesvirus type 1)
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4
Q

African MCF strain? what is a related one?

A

 Alcelaphine herpesvirus type 1 (wildebeest-associated γ- herpesvirus)

Not imortant probably:
Alcelaphine herpesvirus type 2 is a closely related γ- herpesvirus from other species of African antelope (Hartebeest).

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5
Q

Sheep-associated form of MCF, and its relative:

A

 (Syn: “American MCF”, “European MCF”) Ovine HerpesVirus-2 (OHV-2)
NOT yet isolated by conventional virology Antigenically related to AlHV-1

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6
Q

epidemiology of African MCF? where can this virus be isolated from?

A

Wildebeest → cattle and other susceptible species (calving season)

  • AHV-1 isolated from: asymptomatic wildebeests, from nasal and lacrimal secretions of wildebeest calves and fetus.
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7
Q

Geographic Distribution of AHV-1 and OHV-2 ? carried by what?

A

AHV-1 primarily in Africa
 Carried by wildebeest, hartebeest, topi
 Also in zoologic and wild animal parks

OHV-2 worldwide
 Carried by domestic and wild sheep and goats

 Positive bison have been found in U.S. and Canada
> often misdiagnosed in bison

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8
Q

animal transmission of AHV-1 (cell-associated)
- how does it spread? by what animals?

A

 Rarely transmitted
 Stress induces shedding cell-free virus
> Nasal secretions via aerosol
> Contaminate feed, water
> Arthropods
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 Neonatal wildebeests 4 days to 4 months
> Shed in lacrimal, nasal secretions, feces
<><>
 Same species horizontal transmission is rare (i.e. cow-to-cow)
> Dead end hosts

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9
Q

MCF “Wildebeest-derived” Form
- outbreaks morbidity, mortality?

A

 Outbreaks of WD-MCF occur in Africa
7% morbidity; up to 100% mortality
Outbreaks of WD-MCF have occurred in Oklahoma City
and San Diego zoos
 Threat to the North American cattle industry?

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10
Q

OHV-2 transmission? what animals and how?

A

 All ages of sheep infectious
 Spread to cattle during lambing
 Lambs infected by 4 months
 Goat spread unknown

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11
Q

MCF Sheep-associated” form
- outbreaks? mortality?

A

 Usually sporadic cases
 Outbreaks of MCF are rare
 High mortality rate (90-95%)

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12
Q

MCF incubation period, pathophysiology

A

 Incubation 3-10 weeks (but as long as 150 days)
 Lymphoid hyperplasia
> Atypical proliferation of sinusoidal cells
> Cerebro-meningeal changes due to vasculitis (encephalitis)
 Widespread vascular epithelial and mesothelial lesions
> Morphologically associated with lymphoid cells
 Synovitis (tibio-tarsal join)
> lymphoid vasculitis

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13
Q

MCF clinical signs for peracute, acute, and mild forms

A

 Peracute to mild form: wide variety of clinical signs
 Peracute:
> 1-3 days. Fever, dyspnea, and acute gastroenteritis,
> Some cases no signs are seen (acute deaths)
 Acute:
> 3-7 days, high mortality rate
 Mild form:
> mild fever, mild erosions on oral and nasal mucosae, persistent bilateral ocular leukomata (white eye)

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14
Q

MCF clinical pathology - WBC changes, joint fluid, CSF

A

 Leukopenia due to neutropenia (inconsistent)
 Leukocytosis occur in later stages
 Joint fluid: Cloudy, increased protein and mononuclear cells
 CSF: increased protein and WBC count mainly due to mononuclear cells

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15
Q

MCF diagnosis

A

 History of exposure
 Clinical signs
 Gross and histological lesions
 Virus isolation (nasal swabs, blood, spleen, lymph nodes). Do not freeze them.
 Cytopathic effect on thyroid cell cultures (4-20 days post infections)
 Laboratory Tests
> Histopathology
> PCR (blood or tissue)
> Serology (IF)

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16
Q

can we isolate MCF virus?

A

Virus isolation: not practical
 Instability of cell-associated AHV-1
 OHV-2 does not replicate in cell culture

17
Q

clin path and serology tests for MCF? whiich are useful?

A

Virus isolation: not practical
 Instability of cell-associated AHV-1
 OHV-2 does not replicate in cell culture
<><>
Virus neutralization
 Serologic test:
 AHV-1 antibodies in wildebeest
 Immunofluorescence in ruminants
 OHV-2 antibodies in sheep, cattle using IF
 CI-ELISA for screening
 ELISA, complement fixation, virus neutralization
<><>
 PCR

18
Q

MCF necropsy findings

A

 Nasal mucosa: hyperemic to hemorrhagic
 Oral mucosa: necrotic papilla, large areas of necrosis and ulceration
 Esophagus: Focal ulceration
 Forestomachs and intestines:
> Thickened, edematous, ulceration and hemorrhage
 Lymphadenopathy

19
Q

MCF Prevention and Control

A

 Separate infected and carrier animals from susceptible species
> Sheep and goats are carriers
 Avoid exposing cattle, bison, deer during
parturition
 Zoological parks:
> Introduce seronegative animals only
 No vaccine available

20
Q

MCF in humans and human transmission?

A

 MCF has not been documented as causing disease in humans
 Caution at lambing time
> Equipment used could spread infection to susceptible animals
 Virus quickly inactivated by sunlight
> Minimizes risk of fomite spread

21
Q

Hemorrhagic Bowel Syndrome - occurence? incidence and mortality?

A

 Sporadic in occurrence
 A typical case incidence rate is 2-3%, with some farms experiencing an outbreak form
 Mortality may approach 85-100% of cases due to peracute nature

22
Q

HBS - Hemorrhagic Bowel Syndrome other names? etiology?

A

 JHS: Jejunal hemorrage syndrome
 BBS: Bloody bowel syndrome
 Etiology (still in debate):
> Cl. perfringens
> Mycotoxins

23
Q

Clinical Signs of “HBS”? incubation?

A

 Short incubation period – hours rather than days
 Severe sweats
 Bruxism (teeth grinding)
 Sternal recumbency
 Lethargy (extreme depression)
 Enophthalmia (sunken eyes)
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 Slight bloating may be evident
 Pale mucous membranes
 Fluid “slosh” in lower right abdomen
 Distended gut loops per rectal palpation
 SUDDEN DEATH

24
Q

HBS post mortem findings

A

 Severe segmental small intestinal inflammation
 Segmental hemorrhaging and clotting forming a functional plug
> Necrosis +/-
> Impaction

25
Q

HBS diagnosis?

A

 Surgery or PM:
> Appearance of characteristic lesions and clinical signs
 Isolation of Clostridium perfringens type A from the lesion site in high numbers. Overgrowth occurs fast.
 Fecal culture?

26
Q

HBS treatments? prognosis? treatment success rate?

A

 Prognosis is extremely poor
* Surgical intervention
 Some areas of segmental clots may be massaged out to resolve the case
 Intestinal resection & anastamosis is usually required to remove affected tissue
Success Rate ~ 5-10%

27
Q

rinderpast organism

A

 Family Paramyxoviridae
 Genus Morbillivirus
 Other members of the family include
 Peste des Petits Ruminants virus
 Measles virus
 Canine distemper virus
 Phocid distemper virus of sea mammals
 Relatively fragile virus

28
Q

rinderspest economic impact

A

 Destroys entire populations of cattle
 Leads to famine in cattle-dependent areas
 1982-1984 outbreak: $500 million
 $100 million spent annually on vaccination

29
Q

Rinderpest Eradication Massive Vaccination Program

A

basically eliminated disease (in middle east, north africa where it was found) from 1980-2007