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Module 21: Ruminant Production > Lepto, Salmonellosis, Malignant Catarrhal Fever > Flashcards

Lepto, Salmonellosis, Malignant Catarrhal Fever Flashcards

1
Q

is leptospirosis zoonotic

A

yes

worldwide

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2
Q

what type of bacteria is lepto

A

aerobic

gram negative

spirochete

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3
Q

what is the host adapted type of lepto to cattle in USA

A

L. borgpetersenii serovar Hardjo type hardjo-bovis (HB)

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4
Q

what is the host adapted type of lepto to cattle in UK

A

L. interrogans serovar Hardjo type hardjo-prajitno (HP)

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5
Q

what is the route of transmission of lepto

A

Shed in bodily fluids ex. urine, milk, vaginal discharge, semen

Penetrates mucus membranes (eye, mouth, nose, genital tract)

Persists in environment in moist conditions

Chronic carriers — often asymptomatic, intermittent shedding, often seronegative/low titres

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6
Q

what is the risk factors of lepto

A

Open vs closed herd (x2)

Bulls vs AI (x4)

Sheep co-graze with cattle (x6)

Cattle have access to waterways (x8)

Excretion in during grazing, decreases when house and fed silage (increased acidity of urine?)

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7
Q

what is the pathogenesis of lepto infection

A

Infection of non-immune animals

Bacteremia

Multiplication systemically, liver etc

Antibody from day 5

From day 7 limited to immunologically privileged sites:

  • Brain
  • Joints
  • Kidney tubules from which shed into urine for 18 months
  • Reproductive tract
  • Seminal vesicles in bull
  • Uterus, placenta and fetus in cow
  • Multiplies in fetus
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8
Q

what are the reproductive clinical signs of lepto

A

Infertility

  • Leptospires in uterus causing inflammation and embryo death

Low conception rates

Abortion

  • 6-12 weeks after infection
  • Usually last 3 months of gestation
  • Tends to affect young cattle more frequently
  • Live born calves weak and unviable

Stillbirths

Weak calves

Milk drop syndrome or ‘flabby bag’

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9
Q

what is milk drop syndrome or ‘flabby bag’ caused by lepto

A

Sudden onset fever and agalactia

All 4 quarters of udder soft and flabby producing quantities of yellow/orange secretion which may contain small clots

May affect 50% of cows at one time

Milk has high leukocyte count and therefore high SCC

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10
Q

what are the clinical signs of lepto in calves <2 months and >2 months

A

Often non-host adapted serovars

Calves under 2 months of age (nervous signs):

  • Meningitis, anorexia, severe depression
  • Opisthotonus, trismus, muscle tremors, paddling
  • Pyrexia (40.5-41.5ºC)

Calves over 2 months of age:

  • Anorexia and dullness
  • Rarely pallor, petechiation, jaundice, hemoglobinuria
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11
Q

how is lepto diagnosed

A

Direct methods:

  • Dark ground microscopy
  • Culture and ID (difficult)
  • PCR
  • Immunofluorescence/peroxidase in tissue

Indirect methods:

  • Serology ELISA
  • Blood
  • Milk
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12
Q

what occurs to antibodies in lepto infection

A

Antibody levels rise at first and may be associated with clinical signs

They then fall

Abortion can take place with low levels of antibody (up to 12 weeks after infection)

Antibody is present in the serum of carriers and vaccinated animals

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13
Q

how is lepto diagnosed on a herd basis

A

Serology:

  • Rising titre in paired samples taken 14 days apart
  • Individual samples with titres >1:100 indicates chronic or active infection

Abortion:

  • Fetal serology
  • Culture

Bulk milk ELISA now regularly used for surveillance

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14
Q

what are the aims in lepto treatment

A

To reduce the # of infected animals (pre-vacc?)

To minimize urinary status

To reduce spread of organism to other cattle and species including humans

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15
Q

how is lepto treated

A

Dihydrostreptomycin 25mg/kg (repeat after 7d)

  • Off data sheep
  • Problems with milk loss if a whole herd treatment

Other sensitive antibiotics:

  • Amoxycillin (15mg/kg)
  • Oxytetracycline (20mg/kg IM)
  • Tilmicosin (10mg/kg SC)
    • If the product is administered during the dry period or to pregnant animals, milk should not be used for human consumption until 36d after calving
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16
Q

how is lepto controlled

A

ID and removal of carrier animals

Vaccination

Test/treat/vaccinate replacements

Hygiene with special attention to water supply

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17
Q

how should vaccination be done in dairy herds against lepto

A

Close contact with workers

Raise replacements separately therefore heifers are naive

Complete vaccination course in heifers before breeding

Spring booster

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18
Q

how should vaccination be done in beef herds against lepto

A

Youngstock usually acquire some level of immunity

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19
Q

what are the 3 important types of salmonella

A

S. enterica Dublin

S. enterica Mbandaka

S. enterica Typhimurium

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20
Q

what is the most common isolated serovar of salmonella in british cattle

A

S dublin

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21
Q

what does S. enterica Mbandaka cause in adults

A

Diarrhea & malaise

Abortion

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22
Q

what is the main source of S. enterica Mbandaka in cattle

A

Infected feed origin

Mostly larger herds supplementing feed/housing all year

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23
Q

what does S. enterica Dublin mainly infect

A

calves

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24
Q

who does S dublin mostly affect

A

calves and adult cattle

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25
Q

does S dublin cause latent or persistent carriers

A

yes

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26
Q

what is S dublin associated with

A

abortion

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27
Q

how is salmonella transmitted

A

feco-oral route

28
Q

how is salmonella transmitted cattle to cattle

A

Carrier status important — asymptomatic, may shed intermittently especially in times of stress

Carriers can shed millions of bacteria per day in feces

Neighbouring herds, marts, shows, bulls

29
Q

how is salmonella transmitted through slurry

A

persists for months and in soil for a year

30
Q

how is salmonella transmitted through feed/water

A

watercourses and feedstuffs can be contaminated by other stock and wildlife

31
Q

what is the prevalence of salmonella

A

No routine monitoring

  • No one knows the scale of exposure
  • Rely on laboratory diagnosis from clinical cases
  • Requires material to be submitted

Under diagnosed

  • 75% dairy
  • 12% beef
  • 4% calf reares
32
Q

what are the risk factors for salmonella

A

Buying in cattle/co-grazing

High stocking density, group pens

Poor hygiene

Concurrent disease — fluke, BVDV?

Season

Age/stage — calves under 3 months, cattle in first 2 weeks of lactation

33
Q

what are the clincal signs of salmonella and what do they depend on

A

range of clinical signs

  • Acute or chronic enteritis
  • Abortion
  • Septicemia
  • Reduced productivity
  • Poor calf health

may be overlooked/underdiagnosed

severity may depend on infective dose and age/stage

34
Q

what are the signs of acute enteritis caused by salmonella in calves

A

>2 weeks and adults

High fever, severe diarrhea, sometimes bloody, anorexia, colic, abortion

Severe dehydration

35
Q

what is the mortality of acute enteritis caused by salmonella

A

up to 75%

36
Q

what are the clinical signs of chronic enteritis due to salmonella

A

May follow acute enteritis

Reduced weight gain, intermittent diarrhea, inappetence

37
Q

what can trigger clinical signs of chronic enteritis due to salmonella

A

Poor nutrition

Long transport times

Calving

Mixing

Crowding

38
Q

when is septicemia commonly seen due to salmonella

A

Mainly seen in neonatal calves (<2-3 weeks)

39
Q

what are the signs of septicemia due to salmonella

A

Depression, fever, lethargy, laboured breathing, nervous signs, rapid death (6-48hrs)

Dry gangrene of extremities after initial phase

Joint infections

40
Q

when is abortion commonly seen due to salmonella

A

Usually 5-8 months of pregnancy

41
Q

what are the clinical signs of abortion due to salmonella

A

+/- fever and anorexia

retained placenta and reduced lactation

42
Q

can salmonella cause abortion storms

A

up to 25% of herd

43
Q

what can salmonella also cause in calves

A

Pneumonia

Poor growth rates

Ill thrift

Meningitis

44
Q

how is salmonellosis diagnosed on an individual basis

A

fecal culture

PM

serology

45
Q

how is salmonella on an individual clinical case diagnosed using fecal culture

A

Fecal sample not swab

Pooling decreases sensitivity

Remember previous use of antibiotics will affect culture

46
Q

how is salmonella on an individual clinical case diagnosed on PM

A

Culture a range of tissues

In abortions, culture fetal stomach contents

47
Q

how is salmonella on an individual clinical case diagnosed using serology

A

Best results in calves 3-10 months

Poor seroconversion <12 weeks old

Cross reactivity

Retrospective due to time taken to seroconvert

48
Q

how is salmonella diagnosed on a herd level

A

carrier animals

culture

serology

49
Q

how are salmonella carrier animals diagnosed

A

shedding may be intermittent

3 serology tests over 8 months

50
Q

how can salmonella be diagnosed on a herd level using culture

A

slurry samples or feces of cases

51
Q

how can salmonella be diagnosed on a herd level using serology

A

Bulk milk tank

  • Good for continued monitoring (dairy)

Serology of all animals

Serology of a subset of animals

  • Calves
  • Those showing clinical signs
  • 10 youngest calves over 12 weeks
52
Q

how is salmonella treated

A

Early treatment is essential for septicemia salmonellosis

  • S dublin usually susceptible to antibiotics

Controversy regarding the use of antimicrobials for intestinal salmonellosis

  • Carrier status

Intestinal cases may cure clinical but not bacteriology

53
Q

how is salmonella controlled

A

In a negative herd:

  • Prevent entry using biosecurity

If already infected:

  • Biocontainment (and biosecurity)
54
Q

how is salmonella controlled using biosecurity

A

Maintain a closed herd or source new stock from high health status farms

Quarantine all in-coming stock for at least 4 weeks

Avoid shared equipment, bulls and grazing areas

Maintain good fences

Protect feed and bedding from vermin

Use mains water (not natural source)

Provide farm clothing for visitors or clean and disinfect boots/clothing before entering/leaving

Investigate abortions, scour cases or other illness as early as possible

Consider herd vaccination with Bovivac S (MSD)

55
Q

how is salmonella controlled using biocontainment

A

egregate and treat clinical cases

All buildings should have good drainage and waste removal

Clean and disinfect calving/maternity pens and buildings between occupancies

Remove calf from dam ASAP

Colostrum management

Do not feed milk from ill cows to calves

Only spread slurry on arable land

Strict personal hygiene

Zoonotic risk

  • Esp older people and children
  • Do not consume unpasteurized milk
56
Q

how is salmonella controlled using vaccines

A

bovivac S

the only licenced for bovine salmonellosis

contains both S typhimurium and S dublin

inactivated vaccine

57
Q

what is the causative agent of malignant catarrhal fever (MCF) in wildebeest

A

Causative agent of wildebeest-associated MCF (WA-MCF) is Alcelaphine HV-1 (AHV-1)

58
Q

what is the causative agent of malignant catarrhal fever (MCF) in sheep

A

Causative agent of sheep-associated MCF (SA-MCF) is ovine herpesvirus 2 (OvHV-1)

59
Q

who are the natural and dead end hosts of MCF

A

sheep and wildebeest are natural hosts

cattle, deer and pigs are dead end hosts

60
Q

how is MCF transmitted

A

Direct:

Aerosol

May be intermediate host (? flies)

Evidence for distance transmission

Windborne/mechanical?

61
Q

how do cases of MCF typically arise

A

Typically sporadic, multiple cases usually caused by close proximity of lambing ewes to housed cattle

Reactivation during calving/lambing

62
Q

what are the clinical signs of MCF

A

‘head and eye’ peracute, intestinal

Extreme dullness

Anorexia

Agalactia

Copious mucopurulent oculo-nasal discharge +/- blood

Drooling of saliva (‘ropes’)

Dyspnea and stertorous breathing

Loss of condition

Usually fatal

Survive ~1 week

Pyrexia (41ºC)

Congestion of scleral vessels, centripetal corneal edema, hypopyon

Corneal neovascularization

Diffuse oral ulceration with pain (loss of tips of oral papillae at commissures of lips) extending onto the rhinarium

Generalized lymphadenopathy + lymphocytosis

Dermatitis

  • Sweating, crusting lesions
  • Severe ulcerated lesions on the teats

Cystitis +/- pyuria

Altered fecal consistency

(sloughing of horns and horn of the digits)

63
Q

what is the pathology of MCF

A

Lesions in virtually every system

Hydropic degeneration

Vesicle formation and erosion in stratified squamous epithelium

Ulcers coalesce and can become very extensive

Vasculitis:

  • Perivascular cuffing with lymphoid cells

Paracortical expansion in lymphoid tissues

64
Q

how is MCF diagnosed

A

Antibodies in serum or from affected tissues

  • PCR for virus
  • Tissue
  • Whole blood

Exclude important ddx

  • Mucosal disease
  • FMD
  • Bluetongue
65
Q

how is MCF treated

A

euthanasia

66
Q

how is MCF controlled

A

avoid contact with sheep esp during lambing

Module 21: Ruminant Production (21 decks)

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