Lecture 9 - Bluetongue, Salmonellosis, Paratuberculosis Flashcards
BLUETONGUE (BT) is a
non-contagious viral disease of ruminants
transmitted by midges (Culicoides spp),
caused by Orbivirus,
characterized by fever, oral lesions, cyanotic tongue and coronitis.
BLUETONGUE (BT) is a non-contagious viral disease of ruminants transmitted by
midges (Culicoides spp),
caused by Orbivirus,
characterized by fever, oral lesions, cyanotic tongue and coronitis.
BLUETONGUE (BT) is a non-contagious viral disease of ruminants transmitted by midges (Culicoides spp), caused by
Orbivirus,
characterized by fever, oral lesions, cyanotic tongue and coronitis.
BLUETONGUE (BT) is a non-contagious viral disease of ruminants transmitted by midges (Culicoides spp), caused by Orbivirus, characterized by
fever, oral lesions, cyanotic tongue and coronitis.
BTV
Bluetongue virus
What genus and family does BTV belong to?
Genus Orbivirus,
family Reoviridae
What type of virus is BTV?
RNA virus
How many serotypes does BTV have?
26
In what circumstances is BTV inactivated?
Inactivated in pH <6 and >8
Disinfectants: sodium hypochlorite (bleach), 3% sodium hydroxide (lye).
Virus does not persist once cold weather kills the Culicoides vectors.
Why does BTV not persist once cold weather hits?
Virus does not persist once cold weather kills the Culicoides vectors (biting midges).
Host range of BTV.
Host range: all ruminants
Primary host – sheep
Other infected – cattle, goats, deer etc.
Primary host of BTV
Sheep, though affects all ruminants.
Morbidity of BTV in sheep.
Sheep are the primary host.
Severity of dz varies by breed, virus strain and environmental stress.
Morbidity <100%
Mortality of BTV in cattle & goats.
CATTLE & GOATS
Death is rare
Morbidity of BTV in cattle & goats.
CATTLE & GOATS
Morbidity <5%
Mortality of BTV in sheep.
Sheep are the primary host.
Severity of dz varies by breed, virus strain and environmental stress.
Mortality 0-30%
Recent distribution of BTV.
Transmission of BTV. (3)
Biting midges – Culicoides spp
In utero
Mechanical (iatrogenic by blood e.g. needles and instruments)
Excretion of BTV.
Venereal possible?
Is excreted in semen but venereal transmission is uncommon.
The incubation period for bluetongue is
5 to 10 days.
The vast majority of infections with bluetongue are
clinically inapparent aka asymptomatic.
Clinical signs of BTV in sheep. (4)
Oral lesions and ulceration.
Tongue – swollen, protruding, cyanotic (= ‘blue-tongue’).
Reproductive failure.
Coronitis – inflammation of coronary band leading to lameness.
What might the image depict?
coronitis and consequent lameness due to bluetongue disease
Clinical signs of BTV in cattle & goats. (5)
Usually subclinical.
Vesicles or ulcers in the mouth.
Erosions, crusts around nose and teats.
Coronitis.
Reproduction failure.
Post mortem lesions of BTV in sheep. (5)
Face and ears edematous
Dry, crusty exudate on nostrils
Coronary bands hyperemic
Internal hemorrhaging
Hydranencephaly, cerebellar dysplasia
Post mortem lesions of BTV in cattle. (2)
Skin: edematous, ulcerated, dry, thick folds
Mouth: vesicles, ulcers, necrosis
Post mortem lesions of BTV in newborns and fetuses. (3)
Hydranencephaly
Cerebellar dysplasia
Cerebral cysts
DDx for BTV. (6)
FMD (both have lameness and oral lesions)
Vesicular stomatitis (both have oral lesions)
Peste des petits ruminants
Malignant catarrhal fever
Bovine virus diarrhea
Infectious Bovine Rhinotracheitis
Material for diagnosis of BTV. (3)
Blood
Spleen, liver, red bone marrow, heart blood, LNs.
Aborted and congenitally infected newborns: pre-colostrum serum.
Lab analyses for diagnosis of BTV. (4)
Virus isolation
Immunological tests
PCR
Serology (ELISA, AGID)
What is the only vesicular disease of horses?
vesicular stomatitis, a viral disease
(can also affect cattle and pigs but not really as much anymore, mostly a horse thing in America)
Treatment of BTV.
no treatment, is viral disease
Prevention & control of BTV in Disease free areas: (3)
Quarantine and restriction of movements,
serological survey.
Vector control.
Prevention & control of BTV in Infected areas: (1)
vector control
Vaccination toward BTV.
Live attenuated vaccines are serotype specific.
Can be transmitted to unvaccinated animals and could reassort with field strains with a potential risk of new viral strains?
Killed vaccines also available.
Another name for Salmonellosis.
paratyphoid
SALMONELLOSIS is a disease of
multiple animal species,
caused by Salmonella spp.,
associated with septicemia, diarrhea and abortions.
SALMONELLOSIS is a disease of multiple animal species, caused by
Salmonella spp. bacteria,
associated with septicemia, diarrhea and abortions.
SALMONELLOSIS is a disease of multiple animal species, caused by Salmonella spp. bacteria, associated with (3)
septicemia, diarrhea and abortions.
Describe salmonella species.
Gram–, facultatively anaerobic rods.
What family and genus do Salmonella spp. belong to?
Family Enterobacteriaceae, genus Salmonella
over 2500 serovars!
Salmonella serotypes are typically divided into
typhoidic and non-typhoidic.
(s.typhimurium & s.enteridis)
over 2500 serovars!
Most zoonotic salmonella spp. belong to what species?
Salmonella enterica subsp. enterica (subspecies I)
Serovars referred by name, e.g. S. enterica subsp. enterica serotype Enteritidis or Salmonella ser. Enteritidis or Salmonella Enteritidis
Shortname S. enterica subsp. I, refers to?
Full name is: S. enterica subsp. enterica (subspecies I)
S. enterica subsp. II is short for…?
Short for: S. enterica subsp. salamae (subsp. II)
S. enterica subsp. IIIa is short for?
S. enterica subsp. arizonae (subsp. IIIa)
S. enterica subsp. IIIb is short for?
S. enterica subsp. diarizonae (subsp. III b)
S. enterica subsp. IV is short for?
S. enterica subsp. houtenae (subsp. IV)
S. enterica subsp. VI is short for..?
S. enterica subsp. indica (subsp. VI)
Serovars in other S. enterica subspecies and S. bongori are referred to by
antigenic formulas,
e.g. Salmonella serotype IV 45:g,z51:
- The subspecies/species designation (I, II, IIIa, IIIb, IV or VI for S. enterica subtypes; V for S. bongori).
- O (somatic) antigens followed by a colon.
- H (flagellar) antigens (phase 1) followed by a colon.
- H antigens (phase 2, if present).
Salmonella species are classified into serovars (serotypes) based on (3)
the lipopolysaccharide (O),
flagellar protein (H), and
sometimes the capsular (Vi) antigens.
There are more than 2500 known serovars.
Within a serovar, there may be strains that differ in virulence.
Can salmonella survive in the environment?
Very resistant in the environment
Likes wet and warm
stability of salmonella
Susceptible to many disinfectants (e.g. 70% ethanol).
In food:
Cooking meat min. internal temperature:
Roast and steaks 63 °C
Ground beef 71 °C
Poultry parts 77 °C , whole poultry 82 °C
Pasteurizing milk at 71.1 °C 15 min
Host range of salmonella.
mammals, birds, reptiles and amphibians
NB! ZOONOSIS!
fish and invertebrates Can also be infected.
Salmonella is particularly prevalent in which animals? (3)
poultry, swine and reptiles
Some salmonella serovars have a narrow host range, such as: (3)
S. cholerasuis – pigs,
S. Abortusovis – sheep,
S. pullorum – poultry
Clinical cases of salmonella are typically seen in what animals? (3)
cattle, pigs and horses
Morbidity of salmonellosis.
Morbidity 1-90% – varies between species;
higher in reptiles and birds.
Mortality of salmonellosis.
Mortality <100% – severe cases and young animals more likely to succumb.
Distribution of salmonella.
worldwide
“Salmonella ser. Enteritidis and Salmonella ser. Typhimurium, are found worldwide. Others are limited to specific geographic regions.”
Prevalence of salmonellosis in…?
turtles
chickens
dogs
horses
cattle
Turtles: estimates range from 36% to more than 80-90%. Some authorities consider most or all reptiles to be Salmonella carriers.
Chickens: isolated from 41% of turkeys tested in California and 50% of chickens examined in Massachusetts.
Dogs: isolated from 1-36% of healthy dogs and 1-18% of healthy cats.
Cattle: found in 6% of beef cattle in feedlots.
Horses: 2-20% of horses are thought to be healthy shedders.
Foods associated with salmonella outbreaks. (5)
poultry 29%
eggs 18%
veg, fruit, nuts 13%
pork 12%
beef 8%
Excretion of salmonella.
feces
(Route: fecal-oral)
Transmission of salmonella. (5)
Direct contact
Contaminated feed, water
Fomites
Insect vectors that move contamination from once place to another (no bites).
Vertical transmission in birds and mammals
(in utero transmission also in humans!).
Route: fecal-oral
How is salmonella shed?
in feces
Shedding of the pathogen for weeks or even years!
Reptiles shed continuously or intermittently.
Passive carriers – constantly reacquiring the pathogen from environment.
IP of salmonellosis.
highly variable!
Horses – acute severe infections: 6-24h.
In many cases, infections become symptomatic only when stressed.
Pregnant, lactating or young animals most susceptible.
But Often asymptomatic.
Clinical signs of salmonellosis in animals in general.
Often asymptomatic.
Clinical disease when animal is stressed (transport, parturition etc.).
In reptiles: clinical disease uncommon but can be Subcutaneous abscesses, septicemia, osteomyelitis, osteoarthritis.
Clinical signs of salmonellosis in RUMINANTS, PIGS AND HORSES.
Acute enteritis.
Most common form in adults and in calves over a week old.
Diarrhea (watery to pasty), dehydration, depression, abdominal pain and anorexia.
Fever; decrease in milk yield; death from dehydration, toxemia.
Lasts usually for 2-7 days.
Horses die within 24-48h due severe enteritis.
Salmonellosis: Subacute enteritis
Typically seen in Adult horses, cattle and sheep.
Diarrhea (or persistent soft stool) and weight loss.
Salmonellosis: Chronic enteritis
Typically seen in Adults, older calves, growing pigs.
Emaciation, fever, inappetence, scant feces.
Salmonellosis: Septicemia
May be seen in Young animals (<6 months).
Depression, fever, CNS signs or pneumonia, especially in calves and pigs.
Dark discoloration of skin (ears and ventral abdomen) seen in pigs.
Death within 1-2 days.
Lesser known signs of salmonellosis.
Abortions, with or without clinical signs.
Associated serovars:
S. Dublin – cattle
S. Abortusovis – sheep
S. Abortusequi – horses
Abortion may be the first clinical sign in cows with subacute enteritis.
Joint infections/gangrene in calves, affecting the limb extremities, tips of the ears and tail.
Clinical signs of salmonellosis in dogs and cats. (4)
Acute diarrhea – recover 3-4 weeks.
Septicemia.
Cats: chronic febrile illness.
Abortions, weak offspring.
Clinical signs of salmonellosis in birds.
Very young birds.
Anorexia, lethargy, diarrhea, thirst, CNS signs.
IP of salmonellosis.
Gastroenteritis 12h – 3 days,
enteric fever 10-14 days.
All serovars can produce all forms –
reptile associated is the most severe.
Clinical signs of gastroenteric salmonellosis in humans.
- Nausea, vomiting, cramping abdominal pain and diarrhea (may be bloody); headache, fever, chills, myalgia.
- Severe dehydration: infants, elderly.
- Symptoms resolve in 1 to 7 days; deaths are rare.
- Sequela: Reiter’s syndrome (2%) (reactive arthritis).
Clinical signs of enteric fever (typhoidic) salmonellosis in humans.
is systemic salmonellosis. Mostly caused by S. Typhimurium.
- Clinical signs non-specific: GI disease; fever, anorexia, headache, lethargy, myalgias, constipation (!).
- Meningitis, septicemia which can be fatal.
Post mortem lesions of salmonella. (3)
Non-specific
Most common: intestinal lesions
- Lower ileum and large intestine
Mesenteric LN – edematous and hemorrhagic
DDx for salmonellosis in cattle. (4)
E. coli: Enterotoxigenic and verotoxigenic
Cryptosporidiosis
IBR
BVD
etc.
DDx for salmonellosis in sheep. (4)
Enteric colibacillosis
Septicemia due to Haemophilus sp
Pasteurella
Coccidiosis
DDx for salmonellosis in pigs. (4)
Enteric colibacillosis
Clostridium difficile
Swine dysentery
Campylobacteriosis
DDx for salmonellosis in horses. (3)
E.coli
Actinobacillus equuli
Streptococci infection
DDx for salmonellosis in poultry. (2)
Coliform enteritis (caused by e.coli)
Yersinia pseudotuberculosis
Material for diagnosis of salmonellosis. (3)
Feces
Blood, tonsils!
Placental, vaginal exudate, fetal stomach
Lab analyses for diagnosis of salmonellosis. (3)
Isolate organism – e.g. Biochemical test
Serology – e.g. ELISA, agglutination tests
(Also for herds or flocks)
PCR
Treatment of salmonellosis.
Abs – for septicemia, not for enteric disease.
Fluid replacement and NSAIDs.
Prevention & control of salmonellosis.
Prevent fecal contamination (food, water).
In herds/flocks: Buy new animals from tested sources, isolate new animals. Or, All in – all out.
During outbreak: Isolate carriers, treat or cull. Retest treated animals!
Cleaning and disinfection.
Preventing clinical dz: good hygiene, minimize stressful events, colostrum and vaccination.
Alt. name for PARATUBERCULOSIS.
Johne’s Disease
Causative agent of Johne’s Disease.
Mycobacterium avium subsp. paratuberculosis
PARATUBERCULOSIS is a
contagious disease of ruminants,
caused by Mycobacterium avium subsp. paratuberculosis.,
characterized by irreversible wasting, diarrhea and death from cachexia.
PARATUBERCULOSIS is a contagious disease of ruminants, caused by
Mycobacterium avium subsp. paratuberculosis., characterized by irreversible wasting, diarrhea and death from cachexia.
PARATUBERCULOSIS is a contagious disease of ruminants, caused by Mycobacterium avium subsp. paratuberculosis., characterized by
irreversible wasting, diarrhea and death from cachexia.
Describe the causative agent of paratuberculosis.
Agent: Mycobacterium avium subsp. Paratuberculosis
Obligate gram pos. acid-fast rod
Member of a MAI (M. avium-Mycobacterium intracellulare) complex of organisms.
Two main types.
(Type II or C strains, and Type I or S strains)
What are the two main types of agent for paratuberculosis.
Type II or C strains – cattle, goats, camelids, wildlife (also non-ruminant).
Type I or S strains – sheep and other small ruminants.
Stability of Mycobacterium avium subsp. Paratuberculosis.
Resistant to environmental conditions.
Can survive on pastures >1 year.
Viable bacteria in bovine urine <1 week, feces 8-11 months.
Water (pond, tap or distilled water) 9-19 months.
Sunlight helps to inactivate.
Resistant to most disinfectants.
Host range of John’s disease.
mammals and birds
Clinical cases in domesticated and wild ruminants.
Humans: may be involved in Crohn’s disease (chronic enteritis of humans).
Distribution of John’s disease.
worldwide
Morbidity of John’s disease.
Morbidity 20-50%
<50% of the animals may be infected asymptomatically leading to production losses (e.g. 15% less milk).
Mortality of John’s disease.
Mortality 1%
Vaccines for salmonella?
for poultry, and one for pigs.
are per os vaccines.
Distribution of Johne’s disease recently.
Not lately in Europe but about 3 years ago there was an outbreak in Norway (2019 ish?).
Transmission of Johne’s disease.
Fomites such as contaminated feed and water. Insects via contamination.
In utero; horizontal transmission.
Route: fecal-oral
Chronic carriers may shed the rest of their lives!
Excretion of Johne’s disease.
Excretion: feces; colostrum, milk, udder and the male and female reproductive tracts.
Asymptomatic carriers may shed the bacteria intermittently.
Chronic carriers may shed the rest of their lives!
IP of Johne’s disease.
4 months to 15 years.
Calves generally become infected soon after birth but rarely show clinical signs before they are two years old.
Clinical signs of Johne’s disease in sheep and goats.
Wool is often damaged and easily shed.
Diarrhea is less common than in cattle.
Clinical signs of Johne’s disease in cattle.
Diarrhea and wasting away.
Most cases seen in 2-6 year old animals.
Initially: weight loss, decreased milk production or roughening of the coat; appetite and temp. are normal, diarrhea is thick.
As progresses: diarrhea more constant and severe over weeks or months; intermandibular or ventral edema.
Progressive disease: affected animal become increasingly emaciated and usually die (result of dehydration and severe cachexia).
Post mortem lesions of Johne’s disease.
Characteristic: thickened, often corrugated, wall in the distal small intestine (severe cases: from duodenum to rectum).
LNs – enlarged an edematous.
DDx for Johne’s disease.
GI parasites
Peritonitis
Renal amyloidosis
Lymphosarcoma
Kidney failure
Chronic salmonellosis and other chronic infectious dz
Copper deficiency
Starvation
Material for diagnosis for Johne’s disease.
Feces
Intestinal mucosa and wall
LNs (ileal, mesenteric and ileocecal)
Blood serum; milk
Lab analyses for diagnosis of Johne’s disease.
Microscopy (Ziehl-Neelsen staining)
Culture
Serology (CF, ELISA)
(Humoral immunity 10-17 months after infection)
PCR and DNA probes
Treatment for Johne’s disease.
no satisfactory treatment.
Combinations of ABs maybe?
Susceptible to relatively few drugs.
Prevention & control of Johne’s disease.
New animals quarantined and tested before introducing them to a herd.
Vaccination.
When in herd:
Prevent young animals from becoming infected
Decrease exposure in the herd
Test and slaughter
Good management practices
Describe vaccination of Johne’s disease.
Vaccine: live attenuated – decreases the severity of symptoms and bacterial load but does not prevent shedding of agent!
