DISEASES Flashcards
E. Coli
PATHOPHYSIOLOGY: K99+ E. coli causes osmotic diarrhea. The bacteria adhere to the gut mucosal cells and release a toxin that causes hypersecretion of water into the gut lumen. This fluid is lost as the villi cannot reabsorb the fluid due to osmotic pressure in the lumen. This leads to rapid dehydration. The villi largely remain intact and calves are rarely acidotic.
PREVENTION: Cleanliness, colostrum, vaccination of dam
Colisepticaemia and meningitis
PATHOPHYSIOLOGY: The disease is almost always a combination of failure or partial failure of passive transfer and exposure to an overwhelming quantity of bacteria from the environment. Entry is usually via the oropharynx, upper respiratory tract or intestines. If complete FPT then it is thought that septicemia is the likely outcome. If partial FPT then bacteremia is believed to be the more likely outcome (possible settling out in joints leading to joint ill, endocarditis, clouding in the anterior chamber of the eye, meningitis).
TREATMENT: Enrofloxacin, NSAIDs
PREVENTION: Colostrum, cleanliness, maternal vaccination
Rotavirus
PATHOPHYSIOLOGY: The virus replicates in the epithelial cells of the small intestine leading to desquamation of the absorptive mature cells at the tips of the villi. The secretory cells in the crypts remain and continue to secrete fluid to the lumen. This leads to loss of potassium, sodium, and bicarbonate with the water. Cells that release disaccharidases are lost and therefore sugars are not broken down and absorbed. They remain to the colon and are fermented leading to organic acids and H+ ion release. Metabolic acidosis is caused by a combination of loss of bicarbonate and increased absorption of H+ ions. Potassium moves from the intra-cellular to extra-cellular space as H+ ions are taken in to cells to buffer the acidosis. However, potassium is lost into the lumen so there are no clinical signs associated with hyperkalaemia, rather a hypokaelaemia results
TREATMENT: IV with bicarb, oral fluid therapy, NSAIDs, meloxicam
PREVENTION: Colostrum, maternal vacciantion, cleanliness
Cryptosporidiosis
PATHOPHYSIOLOGY: Following ingestion the oocysts invade the brush border of the microvilli. There is swelling, stunting and fusion of the villi. Loss of villous absorptive area leads to reduced absorption of fluid and other metabolites from the gut lumen.
TREATMENT: Self-limiting, correct dehydration
PREVENTION: Cleanliness, do not graze lambs and calves on the same pasture
Coccidiosis
PATHOPHYSIOLOGY: Eimeria zuernii, E. bovis, and E. alabemensis, and in lambs are E. crandalis and E. ovinoidalis. The oocysts take 2-4 days to become infective and need high humidity and warmth. The oocysts that infect lambs can either be from the ewes or have overwintered from the previous year’s crop. Liberated sporozoites enter the intestinal epithelial cells, multiply, and cause the cells to lyse. The merozoites released can invade neighbouring cells leading to further damage. E. zuernii and both ovine species mainly cause pathology in caecum and colon. The pre-patent period can be 3-4 weeks in ruminants, hence the age affected (time to mulitply oocysts in environment). Absorption of ingesta and fluid is affected by the damage and feed conversion efficiency can become diminished in the long term leading to severe loss in productivity. Calves and lambs do develop immunity without clinical signs when exposed to small number of oocysts
TREATMENT: Sulphonamides, NSAIDs, oral fluids
PREVENTION: prevent humid conditions, prevent build up of faeces
IBR
Infectious bovine Rhinotracheitis
caused by Bovine Herpes Virus-1 (BHV1), results in a purulent tracheitis. Be suspicious of involvement where there is significant tracheal noise on clinical exam, hypersalivation and/or serous (progressing to mucopurulent) oculo-nasal discharge. May also cause conjunctivitis and corneal oedema. Cattle become latently infected, with viral recrudescence at times of stress including at calving, hence increasing the likelihood of the dam infecting the calf. Encephalitis has been reported in neonatal calves born to seronegative dams, hence beware in endemically infected herds buying in from naïve sources.
BRSV
Bovine Respiratory Syncytial Virus
a paramyxovirus that causes a necrotising bronchiolitis and interstitial pneumonia, whilst emphysematous lesions may develop in caudodorsal lung lobes. Dyspnoea can be severe, some authors suggest the use of corticosteroids if dyspnoea is life threatening. Beware as corticosteroids are contra-indicated in the face of other pathogens, particularly IBR. Early vaccines resulted in vaccine enhanced disease, potentially due to the vaccine stimulating a TH2 and IgE response at the expense of a cellular TH1 response.
PI3
Parainfluenza Virus Type 3
a paramyxovirus that causes a relatively mild bronchiolitis, but compromises monocyte and alveolar macrophage function, leading to bacterial infection.
BoCV
Bovine Coronavirus
– not currently clear whether BoCV is an important cause of BRD in the UK, however it was the sole pathogen isolated in 16% of 593 pneumonia affected lung samples tested by the Moredun Research Institute.
BVD
Bovine Viral Diarrhoea
– a pestivirus and not a respiratory pathogen per se. Persistently infected calves (PIs) are the most important epidemiological unit as they shed large amounts of virus that infect other calves, causing leukopaenia and resulting in immunosuppression that predisposes to BRD. Effective control through the testing and removal of PIs is essential to a satisfactory BRD control programme
Mannheimia haemolytica
gram negative, small rod, facultative anaerobe. Results in a necrotising, fibrinous pleuropneumonia. There are 12 capsular serotypes of which A1 is the most important. It is often isolated as a commensal of the upper respiratory tract and the switch to a pathogenic phenotype may be density dependent as virulence factors such as leukotoxin are expressed during rapid growth. It is the primary aetiological agent in shipping fever, an acute pneumonia seen more commonly in North America in older cattle 7-14 days following transport.
Pasteurella Multocida
gram negative, rods or coccoid rods, facultative anaerobe. Results in a necrotising, fibrinous pleuropneumonia. Another commensal of the upper respiratory tract and potentially zoonotic. Switch to pathogenicity is poorly understood, may simply be an opportunist, but it is not uncommon to find this as the only organism in an outbreak.
Histophilus somni
gram negative, small rod, facultative anaerobe. Range of pathogenicity amongst strains, with some being considered commensals, whilst others can cause severe septicaemia. Range of pathology including myocarditis, pleurisy, bronchopneumonia, polyarthritis and thromboembolic meningoencephalitis (TEME, also known as “sleeping sickness”).
Mycoplasma bovis
lacks a cell wall (hence beta-lactam antibiotics are ineffective), very small pleomorphic cells, facultative anaerobe. Causes an exudative bronchopneumonia. Can survive intracellularly, hence must select antibiotics with good intracellular penetrance. Experimental infection of cattle results in mild disease, but co-infection with IBR or H. somni severe. Can cause a range of clinical signs and can be transmitted to calves via milk, hence advise pasteurisation if waste milk is being used to rear calves in dairy herds with endemic M. bovis infection.
