Endemic Diseases (Lepto, Salmonellosis, Malignant Catarrhal Fever)

Module 21, week 4

Leptospirosis

Who does it affect? Zoonotic? Clinical Effects?

• worldwide distribution

• affects virtually all mammals - zoonotic disease

• broad range of clinical effects from mild, to subclinical, to multi organ failure and death - commonly headache, fever, lethargy, malaise

Leptospirosis

Etiology of Leptospirosis

• aerobic, gram negative spirochete

• fastidious, slow growing, corkscrew like motility

Leptospirosis

What are the cattle host-adapted types of Lepto

USA and much of the world: L. borgpetersenii serovar Hardjo type hardjo-bovis (HB)

Primarily in the UK: L. interrogans serovar hardjo type hardjo-prajitno (HP)

• Often referred to simply as Leptospira Hardjo

Leptospirosis

What is the transmission epidemiology of Lepto

• sheds in bodily fluids eg urine, milk, vaginal discharge, semen

• penetrates mucous membranes (eyes, mouth, nose, genital tract)

• persists in environment in moist conditions

• chronic carriers - often asymptomatic, intermitted shedding, often seronegative/low titres

Leptospirosis

What are risk factors for lepto epidimiology

• open vs closed herd x 2

• bulls vs ai x 4

• sheep co grace with cattle x 6

• cattle have access to waterways x 8

• excretion in during grazing, decreases when house and fed silage

Leptospirosis

Pathogenesis of Lepto

• where does the bacteria hide?

• infection of non immune animals

• bacteremia

• antibody from day 5

• from day 7 limited to immunologically privileged sites: brain, joints, kidney tubules which shed into urine for 18 months, repro tract, seminal vesicles in bull, uterus, placenta, fetus in cow, multiplies in fetus

Leptospirosis

What does the affected lepto kidney look like

small white foci in tubules

Leptospirosis

Clinical signs of Lepto

Infection with host adapted serovars (L hardjo)

• acute phase usually subclinical (apart from lactating cows)

• repro disease: infertility, low conception rates, abortion, stillbirths, weak calves

• infertility: uterus inflammation and embryo death

• abortion: 6-12 weeks post infection, usually lasts 3 months of gestation, tend to affect younger cattle more frequently

• milk drop: ‘flabby bag’, sudden onset of fever and agalactia, all 4 quarters of udder is soft and flabby producing yellow/orange secretion which may contain small clots, may affect >50% of cows at a time, milk has high leukocyte count therefore high SCC

Leptospirosis

Clinical signs in calves and youngstock (Rare)

often non-host adapted serovars - not the L hardjos

calves under 2 mo:

• meningitis, anorexia, severe depression

• opisthotonus (muscle spasm causing arching in head/neck), trismus (cant open mouth), muscle tremors, paddling

• pyrexia (40.5-41.5)

• ophthalmitis, hypopyon (accumulation of inflammatory cells, such as pus, setting in anterior chamber of eye), optic disc edema, congestion of retinal vessels

calves over 2 mo:

• anorexia and dullness

• rarely pallor, petichiation, jaundice, hemoglobinuria

Leptospirosis

How do we diagnose Lepto

Direct methods: dark ground microscopy (can see them), culture and identification (difficult), PCR, immunofluorescence/peroxidase in tissue

Indirect methods: serology ELISA on Blood or milk

Leptospirosis

Describe the antibody rise/drop of lepto 

• rise at first and may be associated with clinical disease

• then they fall

• abortion can take place with low levels of antibodies (up to 12 weeks after infection)

• antibody is present in the serum of carriers and vaccianted animals

Leptospirosis

How would you diagnose lepto on a herd basis

• easy on herd basis

• serology - rising tire in paired samples taken 14 days apart, individual samples with tires >1:100 indicates chronic or active infection

• abortion - fetal serology, culture

  • bulk milk ELISA now regularly used for surveillance

Leptospirosis

What are the 3 aims of lepto treatment

Aim:

• to reduce the number of infected animals

• to minimize urinary shedding

• to reduce spread of organism to other cattle and other species including man

Leptospirosis

What abx do we use to treat lepto

Dihydrostreptomycin 25mg/kg (repeat after 7 days)

• off data sheet - problems with milk loss if a whole herd tx

• also sensitive to other abx including amoxycillin, oxytetracycline, tilmicosin

Leptospirosis

4 aspects to control of lepto

• identification and removal of carrier animals

• vaccination

• test/treat/vaccinate replacements

• hygiene with special attention to water supply

Leptospirosis

What are the 2 types of vaccinations used for lepto

1. Leptavoid (MSD)

2. Spirovac (Zoetis) - more common

- Vaccine availability: issues with leptavoid-H, farmers advised to boost with spirovac

Leptospirosis

When do you vaccinate dairy cattle?

Dairy: if in close contact with workers, raise replacements separately therefore heifers are naive, complete vac before breeding, spring booster

Beef: young stock usually acquire some level of immunity

Salmonellosis

Who does it affect? Zoonotic?

• wide host range, various animals plus humans ZOONOTIC

• only a few are important in cattle

• serious economic health and public health implications

• can hide from the immune system

Salmonellosis

What are the 3 important types? Which is the most common isolated in british cattle?

S. enterica Dublin - most common

S. enterica Mbandaka

S. enterica Typhimurium

Salmonella Mbandaka

Who does it affect? Clinical signs? Origin? 

• adults: diarrhea and malaise, also abortion

• infected feed origin

• mostly larger herds supplementing feed/housing all year (SW)

• very rarely seen in humans

Salmonella Typhimurium

Who does it affect? Clinical signs?

• affects mainly calves

• various clinical signs

• carrier animals

Salmonella Dublin

Who does it affect? Clinical signs? Origin? 

• host adapted

• affects both calves and adult cattle

• latent or persistent carriers

• associated with abortion

• infrequent in humans, but potentially fatal

  • via infected livestock or unpasteurized milk

Salmonellosis

What are the 4 routes of transmission

1. cattle to cattle: usually a fecal oral route

2. slurry : persists in slurry for months, soil for a year

3. Fomites: farm visitors, animals, birds, vehicles, equipment

4. Feed/water: watercourses and feedstuffs can be contaminated by other stock and wildlife

Salmonellosis

What are the transmission risk factors 

• buying in cattle/co-grazing

• high stocking density, group pens

• poor hygiene

• concurrent disease - fluke, bvdv?

• season

• age/status - calves under 3 months, cattle in first 2 weeks of lactation though to be at a higher risk

Salmonellosis

Clinical signs

• range of clinical signs - may be overlooked/under-diagnosed, severity may depend on infective dose and age/stage

• acute or chronic enteritis

• abortion

• septicemia

• reduced productivity

• poor calf health

Salmonellosis - Acute Enteritis

Clinical signs of acute enteritis? Who does it affect?

• high fever, severe diarrhea, sometimes bloody, anorexia, colic, abortion

• severe dehydration

• fatalities can be up to 75%

• calves >2week and adults

Salmonellosis - Chronic Enteritis

Clinical signs of chronic enteritis? Who does it affect?

• may follow acute enteritis

• reduced weight gain, intermittent D+, inappetance

• stressors can trigger disease - poor nutrition, long transport times, calving, mixing, crowding

Salmonellosis - Septicemia

Clinical signs of septicemia? Who does it affect?

• mainly seen in neonatal calves (<2-3 weeks)

• depression, fever, lethargy, labored breathing, nervous signs, rapid death (6-48 hours)

• dry gangrene of extremities after initial phase

• joint infections

Salmonellosis - Abortion

When does it occur? CS? Abortion storms?

• usually 5-8 months of pregnancy

• ±/- fever and anorexia

• retained placenta and reduced lactation

• abortion storms: up to 25% of the herd

Don’t forget these things..

• poor calf health

• pneumonia

• poor growth rates

• illl thrift

• meningitis

Salmonellosis

How do we diagnose on an individual case basis?

• fecal culture: fecal sample NOT swab, pooling decreases sensitivity, remember previous use of abx will affect culture

• PM: culture a range of tissues, in abortions culture fetal stomach contents

• Serology:

  • best results in calves 3-10 mo

  • poor seroconverstion <12 weeks

  • cross reactivity

  • retrospective due to time taken to seroconvert

Salmonellosis

How do we diagnose on a herd level?

• carrier animals: shedding may be intermittent, 3 serology tests over 8 months?

• culture: slurry samples or feces of cases

• serology: BMT, serology of all animals, serology of a subset of animals (calves, those showing clinical signs, 10 youngest calves over 12 weeks)

Salmonellosis

How do we treat?

• early treatment is essential for septicemic salmonellosis - S Dublin usually sensitive to most abxs

• controversy regarding the use of antimicrobials for intestinal salmonellosis - carrier status

• intestinal cases may cure clinically but not bacteriologically

Salmonellosis

How do we control

• Negative herd = prevent entry (biosecurity)

• Positive herd = biocontainment (and biosecurity)

• Vaccination

Salmonellosis

Biosecurity measures to take

Salmonellosis

Biocontainment measures to take

Salmonellosis

Which vaccinations are licensed for salmonellosis

Bovivac S (MSD) is the only one. contains both S Typhimurium and S Dublin.

inactivated vaccine

Malignant Catarrhal Fever (Snotsiekte)

How is it transmitted

• efficiently between individuals of a natural host, inefficiently between other species

• direct, aerosol, may be IMH

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

• reactivation - calving/lambing time

• recrudescence is possible in recovered cattle

Malignant Catarrhal Fever (Snotsiekte)

Clinical Signs (brace yourselves ☹ it’s a lot)

• head and eye peracute, intestinal

• extreme dullness

• anorexia

• agalactia

• copious mucopurulent oculo-nasal discharge ±/- blood

• drooling of saliva

• dyspnea and stertorous breathing

• loss of condition

• usually fatal - survive- 1 week

• pyrexia 41C, 106F

• congestion of scleral vessels, centripetal corneal edema, hypopyon

• corneal neo-vascularization

• diffuse oral ulceration with pain extending onto the rhinarium

• generalized lymphadenopathy

• dermatitis

• cystitis +- pyuria

• altered fecal consistency

• SEE THE LECTURE FOR PICTURES

Malignant Catarrhal Fever (Snotsiekte)

Pathology

• 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

• SEE LECTURE FOR PICTURES

Malignant Catarrhal Fever (Snotsiekte)

Diagnosis? Treatment? Control?

Diagnosis:

• antibodies in serum or from affected tissues

• PCR for virus (tissue / whole blood)

• exclude important DDX - mucosal disease, FMD, Bluetongue

Treatment:

• euthanasia

• supportive therapy

Control

• avoid contact with sheep - lambing time