Cattle and Sheep Infectious Diseases: GI Disease Pathogens, Johhne's

Question 1

What bacterial diseases affect the GI of cattle?

ESCAPAO

Answer 1

Escherichia coli
Salmonellosis
Clostridial diseases
Actinomycosis
Paratuberculosis
Actinobacillosis
Oral and laryngeal necrobacillosis

Question 2

What viral diseases affect cattle GI?

Answer 2

BVD

Winter Dysentery

Bovine papular stomatitis

Rinderpest- notifiable

Question 3

What is the aeitology of actinomycosis?

Describe the epidemiology

What are the clinical findings?

What is the clinical pathology?

Answer 3

Aetiology- actinomyces bovis, commensal of oral cavity

Epidemiology:
Sporadic, more common in cattle fed coarse feed that damages mucosa and gums

Clinical findings:
Hard immovable lump on maxilla or mandible, initially painless but becomes more painful and may ooze thick pus with yellow-white granules

Clinical pathology:
Gram-positive filamentous rods identified by staining granules in pus

Question 4

How is actinomycosis treated?

Answer 4

Debridment and antibacterial therapy

Oral or IV iodine is most commonly used with/without penicillin or oxytetracylcine

Advisable to cull animals with discharging lesoins to reduce infectious load

Removal or coarse roughage important

Question 5

What is the aeitology of actinobacillosis?

Describe its epidemiology

What are its clinical findings?

What is its clinical pathology?

Answer 5

Aetiology:
Actinobacillus ligniersii, commensal of upper alimentary tract

Epidemiology:
Sporadic occurence, but more common if grazing abrasive pasture plants that can cause damage to the alimentary mucosa

Clinical findings:
Difficulty with prehension and mastication, swelling and abscessation of tongue and drainaing lymph nodes in cattle and lips in sheep

Clinical pathology:
Purulent discharge typically contains ‘sulfur’ bodies, which are granular and consist of club-like rossettes with a central foci of gram negative bacteria. Culture required for difinitive diagnosis but isolation of pathogen can be dificult following antibiotic therapy

Question 6

How is actinobacillosis treated?

Answer 6

Oral or IV iodides are the mainstay of treatment and are typically more effective than treatment of actinomycosis

Streptomycin, penacillin or sulfonamides are also used

Question 7

What are the alternative names for oral and laryngeal necrobacillosis?

Answer 7

Oral- necrotic stomatitis

Laryngeal- Calf diptheria

Question 8

What is the aetiology of oral/laryngeal necrobacillosis?

Describe its epidemiology

What are its clinical findings?

What is its clinical pathology?

Answer 8

Aetiology:
Fusobacterium necrophorum- gram negative, non-spore forming anaerobic but aerotolerant organism, commensal of alimentary tract

Epidemiology:
Non-contagious, oral disease in calves often associated with oesphageal feeder injury

Clinical findings:
Fetid breath, necrotic lesions of oral mucosa (necrotic stomatitis) or larynx (calf diptheria), inspiratory dyspnea or stridor (high pitched lung sound)

Clinical pathology:
Bacteriology of swabs- anaerobic culture- usually necessary

Question 9

How is oral and laryngeal necrobacillosis treated?

Answer 9

Antimicrobial for 5+ days with or without debridment

Can also give dexamethasone

Tracheostomy may be required it severe necrotic laryngitis

Question 10

What is EHEC and why is it of concern?

Answer 10

Enterohaemorrhagic Escherichia coli is a sub-group of shiga-toxin producing serotypes of E.coli

Ruminants are the reservoir but do not typically develop clinical disease

Infection of humans through food/water/direct contact can cause mild to blood diarrhoea, haemorrhagic colitis, haemolytic uremic syndrome

Question 11

Describe the aetiology of salmonellosis

Answer 11

Gram-negative, rod-shaped bacilli
Facultative intracellular organisms that survive in the phagolysosome of macrophages
Most common serovars- S.typhimurium, S.Dublin, S. Mbandaka, S.Newport, S. Enteritdis, S.Montevideo

Infection primarily occurs orally and organisms replicate in the submucosa and peyer’s patches of the distal ileum, liver and onto blood stream

Question 12

Describe the epidemiology of salmonellosis

Answer 12

Transmission occurs via direct and indirect means
Common routes- contaminated feed and environment and during transport at shedding increased by stress
Intro of a carrier animal can commonly cause outbreaks

Can survive in the environment for 14 months- dry faeces for 6 years

Some adapted to colonise mammary gland, milk more commonly contaminated by faeces

Some serovars allow airborne spead

As an intracellular organism it can evade the immune system and either cause clinical disease or become a carrier

Question 13

What are the three types of carriers of salmonellosis?

Answer 13

Active carriers- constantly or intermittently in faces

Latent carriers- don’t shed but have organisms persisting within lymph nodes

Passive carriers- contantly acquire new infections but organisms do not spread to tissues- help disseminate the organism

Question 14

What are the risk factors of clinical salmonellosis?

Answer 14

Intensification of husbandry

Changes that could cause stress

Heavy grazing of land spread with slurry

Contaminated feedstuffs

Question 15

What are the clinical signs of GI salmonellosis?

Answer 15

Morbidity and mortality greatest in calves <12 weeks

Once established disease may manifest as septicemia, abortion, enteritis and localized tissue infections such as arthritis, osteitis and terminal dry gangrene

Question 16

What is the clinical pathology of salmonellosis and how is it treated?

Answer 16

Clinical pathology:
Bacterial culture needed for definitive diagnosis- complicated by intermittent shedding, Labs need 48+h to test for different serovars

Intestines can vary from mucoenteritis to necrotic and haemorrhagic

Mesenteric lymphnodes are typically enlarged, oedamtous and haemorrhagic

Treatment:

Antimicrobials controversial becasue of the selection for resistance and their use may prolong the duration of clinical recovery- oral and IV NSAIDS should be considered

Vaccines available for more common serovars- specific herd ones can be made
Killed vaccines can be given in late pregnancy to protect calves through passive transfer

Question 17

What are the 5 different isolates of clostridium perfringens and what classifies each?

Answer 17

Classified into 5 types- A-E depending on thier ability to produce the four major toxins

Question 18

Where is clostridium perfringens normally found?

What can cause an increased chance on infection of clostridium perfringens?

Answer 18

Normal inhabitants of the intestinal tract

Surplus carbohydrate or protein that exceeds the capacity of the intestine to absorb it are used for bacterial growth and toxin production- dieteary change or engorgement are risk factors

Question 19

Why is is difficult to confirm diagnosis of clostridium perfringens and how can it be treated?

Answer 19

Can smear feaces or intestinal content but commensal so subjective
Can test for toxin but not routinely offered

Treatment not effective as disease is often acute. However, hyperimmune serum and anti-toxins are available- oral and parental penicillin may prevent further pathogen proliferatoin

Question 20

What are the clinical signs and findings of clostridium perfringens A?

Answer 20

A- have been associated with haemorrhagic enterotoxaemia and haemolytic diseases of ruminanys, abomasal ulcer and jejunal haemorrhage syndrome
haemolytic disease

Presents acutely with severe depression, collapse, mucosal pallor, jaundice, hemoglobinuria, severe abdominal pain

Kidneys are swollen and dark brown and the liver pale and swollen with extensive necrosis of the SI

Question 21

How does C. perfringens type B and C present?

Answer 21

Acutely- haemorrhagic diarhoea, abdominal pain and toxaemia

Predominant in very young animals, particularly fast-growing, well nourished

Question 22

What is haemorrhagic bowel syndrome?

Answer 22

Highly fatal disease of cattle- intraluminal blood clot formation secondary to necrotizing haemorrhagic enteritis of the jejunum

Surgical removal of the blood clot, intraluminal and systemic penicillin and intensive fluid therapy

Prognosis <10%

Question 23

What is the aetiology of BVD?

Describe its epidemiology

What is the pathogenesis?

Answer 23

Aetiology- BVD has 2 subtypes, a pesti virus with noncytopathic and cytopathic biotypes

Epidemiology:

Found worldwide, found in all secretions, major source is persistently infected animals can also spread by fomites and airborne

Persistently infected animals remain clinically normal for several years and produce persistently infected offspring

Pathogenesis:

Transient immune suppression occurs in acutely infected animals, innate and adaptive immune cells infected

Question 24

What are the different presentations of BVD?

Answer 24

Subclinical BVD- immunocompetent non-pregnant cattle- mild transient disease with inappetance, depression, fever, leukopenia and mild diarrhoea

Diarrhoea of calves- pathogenesis uncertain

Peracute BVD- severe form of enteric disease that can be fatal, occuring in immunocompetent postnatal cattle, typically occurs following are PI into a naive herd- common signs- depression, anorexia, profuse watery diarrhoea, conjunctivitis

Question 25

How does BVD cause mucosal disease?

Answer 25

Foetal infection during day 45-120 may lead to PI in the calf

May remain healthy for upto 5 years

Causes lesions of MD characterized by small ulcers that only affect epithelial cells, death usually <2 weeks of clinical signs, some become chronically ill

Clinical signs:

• Fever
• Tachycardia
• Tachpnea
• Poor/absent rumen contractility
• Profuse, watery, foul-smelling diarrhoea
• Ulcers in mouth may become necrotic
• Mucopurulent nasal discharge

Question 26

How is BVD treated and prevented?

Answer 26

No treatment

Prevention- detection and eradication of PI animals- strict biosecurity

Question 27

What is the epidemiology, clinical signs, treatment and control of water dysentry?

Answer 27

Epidemiology- faeco-oral transmission, high morbidity, low mortality, occurs in winter months of housed cattle

Clinical signs- sudden onset of diarrhoea among majority of herd, fever, milk drop, inappetance, recovery within a few days

Treatment- none

Control- hygiene, reduce overcrowding

Question 28

What is the aetiology, epidemiology, clinical signs, treatment, and control of papular stomatitis?

Answer 28

Aetiology- bovine papular stomatitis virus, a parapox

Epidemiology- most common in young- zoonotic

Clinical signs- lesions on face, muzzle, mouth, udder, oesophagus and forestomach possible, may lead to ulceration and secondary infection

Treatment- supportive, resolve spontaneously

Control- hygiene, reduce overcrowding

Question 29

Describe the aetiology of paratuberculosis or Johne’s disease?

Answer 29

Mycobacterium avium subspecies paratuberculosis (MAP)

Slow growing acid-fast aerobic microorganism

Obligate intracellular pathogen, but can survive for 1+ year in the environment

There is a slow growing type S (for sheep) or faster growing type II C (for cattle)

Type I has stong host preference for sheep

Question 30

Describe the epidemiology of Johne’s disease

Answer 30

Disease worldwide

Incidence highest in animals kept intensively as is common in the dairy industry

For every clinical case there are 15-25 additional infected animals

MAP has a very high host range

Prevalence- 50%+ of European herds

Mode of transmission ingestion > transplancental

Newborn calves most susceptible- contaminated colostrum primary source

Incubation period longer then latent period

Some animals can excrete MAP in faeces without being infected- pass-through shedder

Question 31

What are the risk factors of Johne’s disease?

Answer 31

Age- resistance to infection increases with age, infection becomes more dificult in calves 4+ months of age

Genetics

Herd management- minimise calf-cow contact

Soil type- affects persistance in environment

Thermal resistance- recovery of viable MAP from milk after standard pasturization

Question 32

How does Johne’s disease affect the economics of farms?

Answer 32

Estimates from £100 to £200 a year

This is attributable to decreased milk production, premature culling, decreased fertility, decreased carcass value, reduced feed efficiency, delayed genetic improvment due to involuntary culling, replacement costs

Question 33

Describe the pathogenesis of Johne’s disease

Answer 33

Organism localises within the submucosa and mesenteric lymph nodes of the terminal small and large intestine
This triggers an inflammatory response with the acumulation of more macrophages and lymphocytes
Granuloma formation with multinucleated giant cells

Results in decreased absorption and ensuing chronic diarrhoea

Reduced protein absoption and increased leakage leads to protein losing enteropathy and consequenctly muscle wastage, hypoproteinaemia and oedema

Immune response- cell-mediated then humoral

Question 34

What is the clinical progresion of Johne’s disease?

Answer 34

Silent infectoin- no clinical signs, animals may shed, tests will not detect but faecal culture may be successful

Subclinical disease- no specific clinical signs, may show other abnormalities such as infertility, low sensitivity to faecal culture, negative to most serologic tests

Clinical disease- typically occur after 2 years of age, gradual loss of body weight, normal or increased appetite, drop in milk production

Advanced disease- typically not seen on farms as affected cattle culled, intermandibular oedema and ‘pipestream’ faces

Question 35

What are the different ways Johne’s disease can be detected?

Answer 35

Bacterial Cultrue

Microscopic examination

PCR

Culture of blood and milk

Tissue biopsy

ELISA

Question 36

How effective is bacterial culture for detection of Johne’s disease?

Answer 36

Culture requires incubation of 4-8 weeks for liquid culture media and 8-16 for solid culture media

Sensitivity varies with stage of infection:
70% in clinical to 25% infected
Specificity is high 98% pass through shedding explains the 2% false positives

Question 37

How effective is micoscopic examination for detection of Johne’s disease and what stain is used?

Answer 37

Ziehl-Neelson stain shows acid-fast bacteria

Results are available <1 hour

False positives possible

Question 38

How effective is PCR detection of Johne’s?

Answer 38

Majority of commercial tests use the IS900 sequence becasue it is present in multiple copies within the MAP genome because is it present in multiple copies

It is also present in environmental mycobacteria, reducing specificity

Question 39

How useful are culture of blood and milk and tissue biopsy for detection of Johne’s disease?

Answer 39

Culture of blood and milk- MAP found in the udders of 35% of clinically affected cows

Tissue biopsy- full thickness biopsy of ileum and associated lymph node- MAP not present in all samples

Question 40

Why are serologic tests not always useful?

Answer 40

Tests are based on humoral response to MAP and are typically only useful later in the course of the disease

An IFN-y assag can be used but has low specificity

Question 41

How useful are ELISA tests for Johne’s?

Answer 41

ELISA test for antibodies against MAP and has the highest sensitivity and specificity of the available tests- particularly in subclinical cases

Milk samples facilitate the detection of MAP infected animals

Sensitivity is highest in early of late in milk

Question 42

What are the necropsy findings of Johne’s disease?

Answer 42

Terminal small intestine, cecum and first section of the colon are typically affected

The intestine is three to four times thicker then normal with corrugated mucosa, promient lymphatics and enlarged lymphnodes

Question 43

What are the differential diagnoses of Johne’s disease?

Answer 43

Salmonellosis

Coccidiosis

GI helminths

Secondary copper deficiency