Cattle and Sheep Infectious Diseases: GI Disease Pathogens, Johhne's Flashcards
(43 cards)
What bacterial diseases affect the GI of cattle?
ESCAPAO
Escherichia coli
Salmonellosis
Clostridial diseases
Actinomycosis
Paratuberculosis
Actinobacillosis
Oral and laryngeal necrobacillosis
What viral diseases affect cattle GI?
BVD
Winter Dysentery
Bovine papular stomatitis
Rinderpest- notifiable
What is the aeitology of actinomycosis?
Describe the epidemiology
What are the clinical findings?
What is the clinical pathology?
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
How is actinomycosis treated?
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
What is the aeitology of actinobacillosis?
Describe its epidemiology
What are its clinical findings?
What is its clinical pathology?
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
How is actinobacillosis treated?
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
What are the alternative names for oral and laryngeal necrobacillosis?
Oral- necrotic stomatitis
Laryngeal- Calf diptheria
What is the aetiology of oral/laryngeal necrobacillosis?
Describe its epidemiology
What are its clinical findings?
What is its clinical pathology?
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
How is oral and laryngeal necrobacillosis treated?
Antimicrobial for 5+ days with or without debridment
Can also give dexamethasone
Tracheostomy may be required it severe necrotic laryngitis
What is EHEC and why is it of concern?
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
Describe the aetiology of salmonellosis
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
Describe the epidemiology of salmonellosis
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
What are the three types of carriers of salmonellosis?
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
What are the risk factors of clinical salmonellosis?
Intensification of husbandry
Changes that could cause stress
Heavy grazing of land spread with slurry
Contaminated feedstuffs
What are the clinical signs of GI salmonellosis?
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
What is the clinical pathology of salmonellosis and how is it treated?
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
What are the 5 different isolates of clostridium perfringens and what classifies each?
Classified into 5 types- A-E depending on thier ability to produce the four major toxins
Where is clostridium perfringens normally found?
What can cause an increased chance on infection of clostridium perfringens?
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
Why is is difficult to confirm diagnosis of clostridium perfringens and how can it be treated?
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
What are the clinical signs and findings of clostridium perfringens A?
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
How does C. perfringens type B and C present?
Acutely- haemorrhagic diarhoea, abdominal pain and toxaemia
Predominant in very young animals, particularly fast-growing, well nourished
What is haemorrhagic bowel syndrome?
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%
What is the aetiology of BVD?
Describe its epidemiology
What is the pathogenesis?
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
What are the different presentations of BVD?
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