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Listeriosis is a serious food-borne disease with increasing frequency in humans and ruminants. Despite the facts that in both hosts, listeriosis can occur as rhombencephalitis and ruminants are a reservoir of Listeria monocytogenes (LM) strains pathogenic for humans, little work has been done on the pathogenesis in ruminants. This study investigates the neuropathogenesis of listeric encephalitis in over 200 natural cases in cattle, sheep and goats by analyzing anatomical distribution, severity, bacterial load and temporal evolution of the lesions. Our results suggest that LM gains access to the brainstem of all three species via axonal migration not only along the trigeminal nerve, but also along other nerves. The ensuing encephalitis does not remain restricted to the brainstem. Rather, LM spreads further from the brainstem into rostral brain regions likely by intracerebral axonal migration. Significant differences in severity of the lesions and bacterial load were found between cattle and small ruminants, which may be caused by species-specific properties of antibacterial immune responses. As histopathological lesions of human rhombencephalitis caused by LM strongly resemble those of ruminants, the disease likely has a similar pathogenesis in both hosts.

Present investigations were carried out on 10 dead animals including eight in lambs, one in goat kid and one in calf during subtropical summer at a local farm. The weather was hot and humid with rain occurring during the period. The history suggests an association of weather and concentrate/lush green diet/fodder with occurrence of the disease. The most consistent clinical signs reported were no interest in feeding, herding in a corner with head down, diarrhea of low degree and temperature around 102 degrees F. At postmortem examination, the most consistent findings were swollen soft kidneys, hydropericardium, congested and edematous lungs, congested liver, myocardial hemorrhages and ballooning of intestines. The histopathological examination revealed the most striking changes in kidney of vacuolation in renal tubular epithelial cells and increased Bowman's space in the glomeruli. The histopathological examination of liver revealed congestion. Lungs revealed congestion and edema. The urine from urinary bladder collected showed high glucose. The deaths in these animals were probably due to enterotoxaemia type D.

Magnesium is an essential mineral with many physiologic and biochemical functions. Surprisingly, Mg homeostasis is not regulated by a hormonal feedback system, but simply depends on inflow (absorption) from the gastrointestinal tract and outflow (endogenous secretion, requirement for milk production, uptake by tissues). Any surplus (inflow greater than outflow) is excreted via urine. Conversely, if the outflow (mainly milk secretion and endogenous loss) exceeds inflow, hypomagnesemia occurs because of the lack of hormonal mechanisms of homeostasis. The major reason for insufficient inflow is a reduced absorption of Mg from the forestomachs. Recent studies from our laboratory and data from the literature permit the proposal of a putative transport model for the secondary active transport of Mg across the rumen epithelium. This model includes two uptake mechanisms across the luminal membrane (PD-dependent and PD-independent) and basolateral extrusion via a Na/Mg exchange. The well-known negative interaction between ruminal K concentration and Mg absorption can be explained on the basis of this model: an increase of ruminal K depolarizes the potential difference of the luminal membrane, PDa, and as the driving force for PD-dependent (or K-sensitive) Mg uptake. Because Na deficiency causes an increase of K concentration in saliva and ruminal fluid, Na deficiency should be considered a potentially important risk factor. The data obtained from in vitro and in vivo studies on the association of Mg transport, changes of ruminal K concentration, and PDa are extensive and confirm the model, if the ruminal Mg concentrations are below 2 to 3 mM. It is further proposed by the model that the PD-independent Mg uptake mechanism is primarily working at high ruminal Mg concentration (above 2 mM). Mg absorption becomes more and more independent of ruminal K with increasing Mg concentration, which can be considered as an explanation for the well-known prophylaxis of hypomagnesemia by increasing oral Mg intake. Fermentation products, NH4+ and SCFA, influence Mg absorption. The possible meaning regarding the pathogenesis of hypomagnesemia is not quite clear. A sudden increase of ruminal NH4+ should be avoided, because high NH4+ concentrations transiently reduce Mg absorption. The most prominent signs of hypomagnesemia are excitations and muscle cramps, which are closely correlated with the Mg concentration in the CSF. It is suggested that the clinical signs are caused by spontaneous activation of neurons in the CNS at low Mg concentrations, which leads to tetany. Prophylactic measures are discussed in context with the known effects on ruminal Mg absorption.

Disease caused by Mycobacterium paratuberculosis involves a complex interaction of lymphoid and phagocytic cells of the peripheral and mucosal immune responses. For resistance to develop, animals must generate an effective cellular immune response to primary infections as well as multifocal exogenous and endogenous reinfections. If an effective immune response does not develop, infected animals transgress through a complex immunologic spectrum in which the immunologic reactions themselves are responsible for the disease manifestations.

Leptospirosis is a zoonotic disease caused by members of the genus Leptospira. Veterinarians' perceptions of leptospirosis as a disease of domestic animals has undergone considerable modification in the past decade or so because they have increasingly appreciated the role of the host-maintained leptospires as causes of reproductive wastage in their respective host species kept under modern intensive management systems.

Electrodiagnostic visual testing (electroretinogram [ERG] and visual-evoked potential [VEP]) was performed on 5 ruminants (3 lambs, 1 kid, and 1 steer) with thiamine-responsive polioencephalomalacia (PEM) and on 2 sheep with listeriosis. The lambs and kid had typical clinical signs of PEM, especially blindness. In these animals, the ERG was normal but the VEP was abnormal. Follow-up recordings in the kid and 1 lamb indicated an improvement in VEP recordings accompanying a gradual return of vision after thiamine treatment. Possible subtle changes in VEP peak latencies could not be assessed because of lack of normative VEP data for sheep and goats. All animals had complete return of vision (owner-assessed). The steer did not have signs of blindness, and the ERG and VEP were normal. Changes in VEP accompanying permanent PEM blindness are not known. One sheep with suspected listeriosis had lack of menace response and palpebral and corneal reflexes, but had intact vision. The ERG and VEP were normal. The second sheep with suspected listeriosis had intact menace response and vision, but became acutely blind and died; the ERG was normal, but VEP amplitudes were depressed.

The sympathetic nervous innervation of the head was surgically transected in the horse, cow, sheep and goat. The site of transection was preganglionic in all 4 species and ganglionic-postganglionic in 2 additional horses. The Horner's syndrome, manifested as a result of the iatrogenic lesion, varied with the species. Ptosis was the most constant sign in all species. Unilateral sweating over the face and proximal neck, particularly at the base of the ear, was the most prominent feature in the horse. The cow revealed distension of vasculature and cutaneous heat of the pinna, and a reduced production of beads of sweat over the nostril on the affected side. The goat and sheep exhibited little more than slight ptosis of the upper eyelid of the affected side as the most prominent sign. The ophthalmologic manifestations of Horner's syndrome seen in these large animals were not readily apparent and could easily be overlooked upon clinical examination.