Ruminants integument & mixed II Flashcards
Bovine ulcerative mammillitis is a contagious disease of cattle, caused by Herpesvirus, and that is characterized by
ulcerative condition of teat and udder skin.
Causative agent of Bovine ulcerative mammillitis
genus
family
DNA type
Bovine herpesvirus 2 and 4
(BHV-2, BHV-4)
Genus Simplexvirus,
family Herpesviridae
DNA virus
Survival of Bovine herpesvirus 2 & 4 in the environment.
Resistant in the environment
Disinfectant: iodophor
Survives cold weather well (spike in cases)
BHV-2 can cause two distinct syndromes in cattle:
Bovine herpes mammillitis (lesions and ulceration on the skin of the udder and teats)
Pseudo-lumpy skin disease (generalized superficial skin lesions)
Host range of Bovine herpes mammillitis
cattle
Most common in animals within the first 2 weeks after calving, particularly in heifers.
Two patterns of Bovine herpes mammillitis outbreaks:
The whole herd is affected
or
Only ones affected are the heifers
Morbidity of Bovine herpes mammillitis
morbidity high on first infection of the herd; 18-96%
Mortality of Bovine ulcerative mammillitis
negligible
Transmission of Bovine ulcerative mammillitis
Excretion: saliva, nasal and vaginal discharge, milk, semen, urine and feces, epithelia.
Direct contact
Blood-sucking insect vectors
Fomites
Route: via skin abrasions, mucous membranes
IP of Bovine ulcerative mammillitis
IP: 5-10 days
Clinical signs of Bovine ulcerative mammillitis.
Lesions confined to the skin of the teats and udder.
After vesicle rupture: sloughing of the skin
Edema, hyperemia, erosions
In severe cases: untreatable mastitis or gangrene.
Material for diagnosis of Bovine ulcerative mammillitis (3)
Vesicle fluid
Swabs from early ulcers
Blood
Lab analyses for diagnosis of Bovine ulcerative mammillitis (3)
Culture
Electron microscopy
Serology
Tx of Bovine ulcerative mammillitis
no specific treatment
Aim should be to develop scabs that can withstand machine milking (e.g. with ointments).
Prevention & control of Bovine ulcerative mammillitis
No specific prevention or control methods.
Isolation of affected animals and strict hygiene in the milking parlor are practiced but have little effect on the spread of the disease, nor does milking heifers first.
To prevent spread: iodophor disinfectant
Clostridial myositis or blackleg is a contagious disease of cattle, caused by Clostridium chauvoei, and characterized by
myositis of skeletal muscles.
Causative agent of blackleg disease.
Clostridial myositis caused by gram positive Clostridium chauvoei.
Spore-forming
Survival of Clostridium chauvoei in environment.
Spores are highly resistant to environmental changes and disinfectants.
Spores persist in soil for many years.
Host range of blackleg.
cattle, sheep
6 month olds to 2 year-olds
Risk factors: rapidly growing cattle and high plane nutrition.
In humans: rare cases (veterinarians)
Seasonality of blackleg
during warm months
Mortality of blackleg.
Mortality – case fatality <100%
Transmission of blackleg.
Soil-borne infection
Route: alimentary probably
In sheep: associated with wound infection
IP of Clostridium chauvoei
IP: 1-5 days
Clinical signs of clostridial myositis / blackleg
Severe lameness with pronounced swelling (and crepitation) of the upper part of affected leg.
First: hot and painful
Later: cold and painless
Depression
Complete anorexia and ruminal stasis
High fever
High pulse rate
Death within 12-36 h after the appearance of clinical signs!
Post mortem signs of clostridial myositis / blackleg
Affected muscles are dark red to black and dry and spongy, have a sweetish odor, and are infiltrated with small bubbles but little edema.
Lesions may be seen in any muscle (even in the tongue, heart or diaphragm).
Material for diagnosis of Clostridial myositis.
Muscle samples
Lab analyses for diagnosis of Clostridial myositis. (3)
Culture
Biochemical identification
PCR
Tx of blackleg.
Tx: penicillin and surgical debridement of affected muscle groups
Tx if animal is not moribund
Prevention of blackleg
Vaccination
In Estonia: Covexin 10 vaccine against many Clostridia spp.
Control of Clostridium chauvoei during outbreak.
Unaffected should be vaccinated and given penicillin profylactically.
Movement of cattle away from affected pasture.
Carcasses should be destroyed by burning or buried deeply in a fenced-off area to limit heavy spore contamination of the soil.
Necrobacteriosis can cause 2 forms of disease:
Necrotic laryngitis & footrot
Necrotic laryngitis is a contagious disease of young cattle, caused by Fusobacterium necrophorum, and characterized by
fever, cough, inspiratory dyspnea and stridor.
Necrotic laryngitis is also known as:
calf diphtheria
Causative agent of Necrobacteriosis: necrotic laryngitis and footrot.
genus
family
gram?
Gram negative Fusobacterium necrophorum,
family Fusobacteriaceae
Non-sporeforming anaerobe
Fusobacterium necrophorum is a Normal inhabitant of
the alimentary, respiratory and genital tracts of animals – opportunistic pathogen!
Host range of necrotic laryngitis.
cattle, horses, goats, pigs, and sheep
Primarily occurs in 3-18 month-olds
In humans: zoonootic!
Seasonality of necrotic laryngitis.
Reported all year around; more prevalent in fall and winter.
Mostly sporadic
Prevalence in feedlot calves: 1-2%
suspected portal of entry for F. necrophorum
Laryngeal contact ulcers
transmission of necrotic laryngitis
direct contact and fomites
Route: via mucous membranes
Clinical signs of necrotic laryngitis
Moist, painful cough
Severe inspiratory dyspnea,
loud inspiratory stridor
Ptyalism
Bilateral purulent nasal discharge
fever, anorexia, depression, hyperemia of the mucous membranes due to endotoxins.
If untreated – death in 2-7 days due to toxemia and upper airway obstruction.
Long term sequelae: aspiration pneumonia, permanent distortion of the larynx.
Post mortem signs of necrotic laryngitis.
Lesions on vocal processes and medial angles of arytenoid cartilages.
Acute lesions: edema and hyperemia surrounding a necrotic ulcer in the laryngeal mucosa.
Chronic cases: necrotic cartilage associated with a draining tract surrounded by granulation tissue.
Diagnosis of necrotic laryngitis.
Clinical signs usually sufficient to establish diagnosis.
Larynx should be visualized to confirm the diagnosis.
Tx of necrotic laryngitis.
Tx: ABs (Oxytetracycline or procaine penicillin)
NSAIDs
IV fluids if dehydrated
Tracheostomy if severe inspiratory dyspnea.
Prognosis:
Good if Tx started early and aggressively.
Chronic cases – require surgery (60% success rate).
Prevention & control of necrotic laryngitis.
No specific control measures
Maybe beneficial: control measures for common respiratory pathogens
Good animal husbandry!
Footrot is a highly contagious disease of ruminants, caused by Fusobacterium necrophorum, and is characterized by
interdigital phlegmons which is also the alt. name for foot rot - “interdigital phlegmon”.
phlegmon refers to a localized area of acute inflammation of the soft tissues.
Causative agent of footrot.
gram neg. Fusobacterium necrophorum
Three subspecies and number of genotypes which affect different tissues.
Other organisms that may be involved in footrot in addition to F.necrophorum: (5)
Bacteroides melaninogenicus
Dichelobacter nodosus
Escherichia coli
Staphylococcus aureus
Trueperella pyogenes
Survival of footrot agents in the environment.
Can survive in soil for 10 months.
Host range for footrot.
ruminants
On average, footrot accounts for what % of foot diseases?
<15% of foot diseases
Sporadic: May be endemic in intensive beef units or in cattle at pasture.
Transmission of footrot.
Excretion: feces!
Portal of entry – injury to the interdigital skin
Transmission is highest in humid and muddy conditions.
IP: for footrot
IP: one week
Clinical signs of footrot.
More commonly hindlimbs are affected.
In calves: more than one foot at a time.
Fever, anorexia
Lameness
Reddening of the interdigital tissue and swelling of the foot, toes are spread.
skin of the interdigital space fragments with exudate production and foul odor
can spread to joints
Footrot is Typically diagnosed by
the distinctive lesions and odor.
Bacterial culture can be done but is rarely necessary.
Tx of footrot.
Cleaning and disinfection
ABs – penicillin, oxytetracycline, sulfonamides
Recovery in 3-4 days
Prevention & control of footrot.
Foot baths
Regular foot trimming
Housing:
Minimize interdigital trauma
Adequate draining of feces etc. dry floors.
Feeding: zinc supplements work well.
