L11 Pt. 2 (Maunsell) Flashcards
Transmission of MCF
- direct contact
- subclinically affected sheep and wildebeest are major reservoirs
- increased shedding during lambing/calving season
- cattle = dead end hosts
- highly contagious to cattle and bison
- very young calves usually NOT affected
Incubation period of MCF
3-10 weeks
Pathophys. Of MCF
Massive infiltration with lymphoid cells –> widespread vasculitis and epithelial necrosis
CS of MCF (peracute)
- high fever
- sudden death w/o other signs
CS of generalized form of MCF
- fever
- oral erosions and scabs, severe KCS w/ corneal opacity leading to blindness
- mucopurulent nasal d/c
- weakness
- dyspnea and stertor
- anorexia
- agalactia
- may slough hooves, horn, skin
- CNS signs if viral encephalitis
CS of Alimentary form of MCF
- severe diarrhea
- fever
- oral and esophageal erosions
Dx of MCF
- reportable!
- dx based on exposure, CS
- necropsy: ulcerated epithelia (oral and esophageal), swollen liver, diffuse hemorrhages, marked vasculitis w/ mononuclear perivascular cuffing, lymphoid hyperplasia, and lymphoid infiltrates assoc. with epithelial necrosis
- serology
- PCR confirms suspected cases and tests peracute cases
Tx/Control of MCF
- supportive
- poor prognosis
Control: keep cattle away from sheep, wildebeest, hartebeest and topis which can be carriers
Bluetongue virus etiology
- orbivirus transmitted by Culicoides spp.
- clinical dz in sheep most commonly
- reservoir = subclinically infected ruminants
- cattle develop high viremia often w/o CS and can be infective for 7-13 weeks
- endemic in tropical and subtropical regions
- epidemics occur in seasonally-affected areas
Where does bluetongue virus occur in the US?
South and California
Florida: endemic in cattle; sporadic dz in sheep and very occasionally cattle; most commonly seen in naive sheep imported from northern states
Transmission of Bluetongue
- transmission through skin, replicates in lymphoid tissue, viremia at day 3, clinical signs at day 6-7
- once in blood, infection of and replication in vascular endothelium –> widespread vasculitis, endothelial necrosis, thrombosis, hemorrhage
CS of Bluetongue
-fever
-nasal d/c
+/- dyspnea, laminitis/coronitis, swelling and edema of lips, gums, dental pad, tongue; necrotic ulcers of lips, anus, vulva
-sudden death or chronic wasting with PROLONGED recovery
Bluetongue: fetal infection
- abortion at any gestation
- infection at 60-120 days gestation causes congenital dz w/ excessive gingival tissue, agnathia (absence of jaws), arthrogryposis (joint contractures), ataxia, head pressing, hydranencephaly
Dx of Bluetongue
- viral isolation (gold standard)
- PCR
- competitive ELISA
- AGID not sensitive
Pathology of bluetongue
- generalized edema, hyperemia, hemorrhage, necrosis of skeletal and cardia muscle
- hemorrhage at base of pulmonary a.
- thrombosis and vascular damage
Tx/control of bluetongue virus
Tx: supportive (nursing care, rumen support, fluids, abx to prevent secondary infections)
Control: vector control/exposure, MLV vaccines
Anthrax etiology
- Bacillus anthracis (G+ rod)
- reportable, zoonotic
- 1ary habitat = soil
- vegetative and spore state
- ruminants and cervids most susceptible
Distr. of anthrax
- worldwide
- US: Texas and some areas of great plains have favorable soil conditions
- late summer, early fall most common for dz in US
Transmission and incubation period of anthrax
Ingestion or inhalation of spores
Incubation period: 1-7 days
Pathophys. Of anthrax
- enters body, primary replication in the regional LN, leads to bacteremia, septicemia, toxemia dissemination to all major organs
- death by toxic shock, multiple organ failure
- capsule protects against complement and phagocytosis
3 syndromes of anthrax
1) cutaneous
2) pulmonary
3) GI
Cutaneous syndrome of anthrax
- in people that work with animal hides and hair
- malignant pustule followed by necrotic ulcer
Pulmonary syndrome of anthrax
- people or animals that inhale spores
- rapidly fatal
- develop localized pulmonary infection that disseminates
GI syndrome of anthrax
-disseminates after oral ingestion (humans, animals)
CS of peracute syndrome of anthrax in cattle
1-2 hours:
- fever, muscle tremors, dyspnea, congesion of mm
- collapse w/ bloody discharge
- rapid death
CS of ACUTE syndrome of anthrax in cattle
48 hours:
- high fever
- tachycardia
- anorexia, ruminal stasis
- severe depression
- congested mm
- abortion
- blood-stained milk
- bloody discharge
- edema
- collapse and death
Anthrax of pigs
- usually from being fed infected carcasses
- same CS as cattle
- edema of head and throat, obstructed airway, bloodstained froth, petechia on skin
Anthrax pathology
- absence of rigor mortis
- blood from orifices
- saw horse posture
- ecchymoses
- bloodstained serous fluid in body cavity
- splenomegaly
- spleen looks like jelly
Dx of anthrax (skipped slide)
- NMB stain on blood smear
- direct blood or tissue smears or by culture
- rapid sample collection necessary
Control and prevention of anthrax
- carcass management
- vaccinate all clinically normal, potentially exposed animals
Malignant Catarrhal Fever affects which species
Domestic cattle, buffalo, wild ruminants, pigs
