Malignant Catahrral Fever MCF

MALIGNANT CATARRHAL
FEVER (MCF)
Benha University
Faculty of Veterinary Medicine
Shawky Ahmed Moustafa

2020
MALIGNANT CATARRHAL
FEVER (MCF)
Malignant catarrhal fever, is an infectious
disease of ruminants. It is also referred
to as malignant catarrh, malignant head
catarrh, and gangrenous coryza.
❖ It is a worldwide sporadic, fatal,
multisystemic disease of domestic cattle and
wild ruminants (deer, buffalo, antelopes) that
is caused by a gammaherpesvirus
❖ Characterized by lymphoproliferation,
vasculitis, and erosive-ulcerative mucosal and
cutaneous lesions predominantly affecting the
respiratory and gastrointestinal systems.
Etiology
caused by genus rhadinovirus (γ-herpesviruses)
 Wildebeest derived MCF is caused

by Alcelaphine herpesvirus type
1(AHV-1)
 Sheep associated MCF is caused

by Ovine herpesvirus-2 (OVH-2)
Malignant Catarrhal Fever

Etiology
and
 White-tailed deer herpesvirus
 Caprine herpesvirus type 2
 All are Lymphotropic Cell-associated Gamma

family herpesviruses
Malignant Catarrhal Fever

General Discussion
•Gamma herpesvirus; genus rhadinovirus
•Causes lymphoproliferation, vasculitis, and
erosive to ulcerative mucosal lesions.
•In affected cattle, the virus DOES NOT
induce herpetic necrosis, and there are no
inclusion bodies or syncytial giant cells.
•Affects numerous species of cervids and
bovids.
•Usually sporadic; occasional outbreaks
•Mortality approaches 100%.
Four forms
1. Wildebeest-associated (WA-
MCF):Alcelaphine herpesvirus-1; primarily
in Africa, but also in zoos and wild animal
parks
2. Sheep-associated (SA-MCF): Ovine
herpesvirus-2; worldwide; one of most
serious diseases in farmed deer in New
Zealand, Australia, and Britain
3. White-tailed deer herpesvirus (MCF-WTD):
Newly recognized form that is highly
virulent in White-tailed deer; closely related
to the above viruses; reservoir unknown
4. Caprine herpesvirus-2 in association with
naturally occurring malignant catarrhal
fever in captive Sika deer
Host Range
The disease can
occur in cattle,
domesticated
buffaloes, a wide
range of captive
antelopes and deer,
and free-living deer.
Reservoir ruminant species
Blue Wildebeest
Black Wildebeest
Pathogenesis
➢ Virus is usually cell-associated in adults,
probably with lymphocytes.
➢ Wildebeest are infected for life and transmit

AHV-1 to their calves without showing clinical
signs; the calves are infected within the first
2-3 months and shed cell-free virus in nasal
and ocular secretions and feces
➢ In Africa, Wildebeest calves are considered

the main source of infection to cattle; adult
wildebeests that are stressed or receiving
corticosteroids also may shed cell-free virus
Pathogenesis
➢ Virus is transmitted by inhalation of
aerosolized cell-free virus, ingestion of
contaminated feed or water, and possibly by
contact with infected placentas or
mechanically by arthropods.
➢ Incubation period: Usually 2-8 weeks
➢Mucous membranes of the upper

respiratory tract or tonsils are likely routes of
entry
➢ Primary viral replication occurs in small and

medium-sized lymphocytes
Pathogenesis
➢ T-lymphocyte proliferation is likely
secondary to infection of large granular
lymphocytes, which have T-suppressor cell and
natural killer cell activity.
➢ Viral infection and dysfunction of these cells
causes lymphoproliferation (suppressor
dysfunction) and necrosis (killer cell dysfunction)
➢ The mechanism of vasculitis is proposed to be
immune-mediated, but demonstration of
immunoglobulin and complement has been
inconsistent
➢ Cattle appear to shed only cell-associated virus;
transmission among cattle is rare
Clinical Findings
• Fever, nasal/ocular discharge, edema of
eyelids and palpebral conjunctivae, corneal
opacity, diarrhea, lymphadenopathy, dermatitis, oral
erosions and CNS signs
•Four clinical forms:
• 1. Peracute: 1-3 day course with fever and
possible hemorrhagic diarrhea
• 2. Intestinal: 4-9 day course with fever,
lymphadenopathy, diarrhea
• 3. Head and eye: Typical form, longer duration
than above with depression, high fever, profuse
mucopurulent nasal discharge, dyspnea, ocular
discharge, blepharospasm
• 4. Mild: In experimental cases that recover
Clinical Signs
Ocular and
nasal discharge
Clinical Signs
Painful Conjunctivitis
Severe panophthalmitis,
hypopion, corneal erosions
are more frequent in cattle
Gross Findings
➢ Lymph nodes : Enlarged, edematous
➢ Mucosal surfaces: Hyperemia and edema,
erosions and ulcerations.
➢ Gastrointestinal tract: Extensive mucosal
erosions from oral cavity to rectum (especially in
deer), edema, hemorrhage.
➢ Respiratory: Serous to mucopurulent nasal
discharge, crusted muzzle, edematous lungs, gray-
yellow pseudomembranes that cover laryngeal and
pharyngeal erosions
Gross Findings
➢ Eye: Corneal edema, conjunctivitis,
corneal opacity (edema), ocular mucopurulent
discharge, +/- corneal ulceration, blepharedema,
chemosis and hypopyon
➢ Kidney: infarcts or multiple raised 2-4mm white

necrotic lesions, ecchymotic hemorrhages,
renomegaly
➢ Liver: Slightly enlarged and mottled with white

foci.
Gross Findings
➢ Spleen: Enlarged with prominent
lymphoid follicles
➢ Skin (base of horns and hooves, loins and

perineum): Hyperemia to exanthema with crust
formation and shedding of hoof wall
➢ CNS: Meninges wet, possibly with petechial

hemorrhages
➢ Deer: Predominantly hemorrhagic

gastrointestinal and myocardial lesions
Microscopic Findings
➢ Vessels (Necrotizing vasculitis): Perivascular
and intramural infiltrates of lymphocytes and

lymphoblasts; fibrinoid necrotizing vasculitis in all
tissues
➢Lymphocytic infiltrate in kidneys, liver
(periportal), GI mucosa, dermis, meninges, heart,
etc.
➢ Kidney: Infarcts, foci of nonsuppurative
(lymphocytic) interstitial nephritis.
➢Lymph node: Active proliferation of
lymphoblasts, especially in T cell-dependent
areas of interfollicular and paracortical zones;
Severe edema, ectatic lymphatics, lymphocytic
and reticuloendothelial cell proliferation
➢ eye: Lymphocytic uveitis and ophthalmitis;
corneal edema, secondary to vasculitis, is
responsible initially for the opacity
➢ Spleen: Variation between lymphoid
cell hyperplasia in the periarteriolar sheaths to
atrophy and depletion of lymphocytes
➢ CNS: Perivascular edema, nonsuppurative
meningoencephalomyelitis, lymphocytic
perivascular cuffing
➢ GI: Edema, congestion, mucosal erosions,
abomasal ulcers and submucosal eosinophilic
inflammation
➢ Oral and pharyngeal mucosa: Epithelial
necrosis, lymphocytic stomatitis and pharyngitis
➢ Skin: Exudative lymphocytic dermatitis,
edema, epithelial necrosis
Bovine, muzzle. Multiple shallow erosions are filled
with dried nasal exudate.
Bovine, muzzle. The muzzle is hyperemic, multifocally covered by
adherent mucopurulent exudate, and contains many shallow erosions
Bovine, muzzle. There is diffuse superficial
necrosis of the muzzle
Bovine, oral mucosa. There is a gingival
Corneal edema in malignant catarrhal fever.
Bovine, hard palate. There are multiple
coalescing mucosal erosions
Ulcerative lesions in the hard palate of
a bison with malignant catarrhal fever.
Bovine, skin. There are numerous
raised plaques (multifocal dermatitis).
Bovine, prescapular lymph nodes: Moderately (left)
to markedly enlarged (right) due to MCF.
Bovine, prescapular lymph node. There are foci of hemorrhage
(and necrosis) in the cortex, and the medulla is edematous.
Bovine, spiral colon. There are multiple
mucosal hemorrhages.
Focal nonsuppurative interstitial nephritis.
T lymphocyte hyperplasia, cell necrosis
Severe necrotizing vasculitis
Perivascular lymphoid infiltration
Necrotizing vasculitis : inflammatory infiltrate markedly expands and disrupts the
tunica media and adventitia, admixed with cellular and karyorrhectic necrotic debris
lymphocytic interstitial nephritis
Erosive tracheitis in malignant catarrhal fever.
Accumulations of lymphocytes in
portal triads in malignant catarrhal fever.
Extensive cuff of mononuclear cells, and fibrinoid
necrosis in the wall of a small arteriole in the kidney.
Malignant catarrhal fever
in an ox. Infiltration of
lamina propria by
lymphocytic cells with
developing ulcer over
papilla in the tongue.
Colitis with collapse
of glands in
Malignant catarrhal
fever.

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MALIGNANT CATARRHAL

Shawky Ahmed Moustafa

 Wildebeest derived MCF is caused

 Sheep associated MCF is caused

Malignant Catarrhal Fever

 All are Lymphotropic Cell-associated Gamma

Malignant Catarrhal Fever

➢ Wildebeest are infected for life and transmit

➢ In Africa, Wildebeest calves are considered

➢ Incubation period: Usually 2-8 weeks

➢Mucous membranes of the upper

➢ Primary viral replication occurs in small and

➢ Kidney: infarcts or multiple raised 2-4mm white

➢ Liver: Slightly enlarged and mottled with white

➢ Skin (base of horns and hooves, loins and

➢ CNS: Meninges wet, possibly with petechial

➢ Deer: Predominantly hemorrhagic

and intramural infiltrates of lymphocytes and

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