Mycobacterial neuritis in a cat

A 2-year-old spayed female domestic shorthair cat was referred for evaluation of rapidly progressive lameness of the right hind limb, which was paralyzed. Histologic examination of biopsy specimens revealed pyogranulomatous inflammation affecting the sciatic, common peroneal, and tibial nerves, and slender, beaded, acid-fast bacilli within macrophages, nerve fibers, and degenerate axons. A diagnosis of mycobacterial neuritis was made and the cat was treated with clofazimine and enrofloxacin for extended periods. Treatment was partially effective; the goal of returning normal function to the limb was not achieved, but disease progression was halted and the cat remained a viable pet.     

A case of feline leprosy caused by Mycobacterium lepraemurium originating from the island of Kythira (Greece): diagnosis and treatment

A 2-year-old, 4 kg, healthy, domestic shorthair female cat presented with ulcerated subcutaneous nodules on the commissures of its mouth. The cat was negative for feline leukaemia virus and feline immunodeficiency virus. Skin mycobacteriosis was diagnosed after detection of numerous acid-fast bacilli in Ziehl Neelsen-stained smears from the ulcers. Feline leprosy was suspected following preliminary polymerase chain reaction results: positive for Mycobacterium genus but negative for Mycobacterium tuberculosis and Mycobacterium avium complexes. Mycobacterium lepraemurium was later identified following DNA sequence analysis of the 5' end of the 16S rRNA gene and the 16S-23S internal transcribed spacer region. Microscopic lesions consisted of pyogranulomas containing mainly large foamy macrophages with 10-100 intra-cellular acid-fast bacilli per field. The cat was cured after surgery and a 14-week course of clofazimine (30 mg daily) and clarithromycin (50 mg twice daily).     

Subcutaneous granuloma caused by Mycobacterium avium complex infection in a cat

A localised subcutaneous swelling developed on the nasal bridge of a cat receiving chemotherapy for alimentary tract lymphosarcoma. Cytological and histological examination of representative samples of the lesion demonstrated pyogranulomatous inflammation and abundant acid-fast bacilli. A Mycobacterium sp was cultured from tissue excised from the lesion. Extensive testing at three reference laboratories indicated the strain was a member of the Mycobacterium avium complex. The infection was treated successfully by cytoreductive surgery and a 6 weeks course of orally administered clofazimine.     

A syndrome of hepatogenous photosensitisation, resembling geeldikkop, in sheep grazing Tribulus terrestris

Two outbreaks of photosensitivity disease occurred in weaner sheep in south western New South Wales during early autumn 1982. In each instance there was a history of access to the annual herb, Tribulus terrestris and both the clinical and pathological findings were consistent with geeldikkop, a major disease in the Republic of South Africa. The prevalence rates of clinical cases were 21 and 37%, while the case fatality rates approached 70%. Clinical signs were dominated by jaundice and photosensitisation. Ochre and khaki discolouration were present in the liver and kidneys, respectively. Histopathologically, the most characteristic lesion was the presence of acicular, cholesterol-like clefts in the lumens of bile ducts and in the cytoplasm of hepatocytes and Kupffer cells. Similar structures were also evident in the lumens of nephrons in association with segmental hyperplasia of the neighbouring tubular epithelium. The possible pathogenesis of the hepatogenous photosensitisation and its resemblance to geeldikkop are discussed.     

Crystal-associated cholangiohepatopathy and photosensitisation in lambs

Four outbreaks of hepatogenous photosensitisation occurred in weaned lambs in north eastern Victoria during the summers of 1985 and 1986. Attack rates varied between 7% and 43% and case fatality rates between 60% and 71%. Clinical signs included photosensitisation and jaundice. Serum biochemistry suggested hepatobiliary and hepatoparenchymal damage with impaired renal function. At necropsy livers were an ochre colour and kidneys a mottled brown to khaki. Histopathologically, needle-shaped to lenticular clefts were observed in and around bile ducts and in hepatocytes, hepatic sinusoidal macrophages and renal tubules. Optically active rhomboidal crystals were present in bile sediments. Panicum schinzii was identified as a possible cause in 2 of the 4 outbreaks. The clinical disease was reproduced in 2 of 6 lambs grazed on a toxic paddock. The disease was indistinguishable from geeldikkop except for the fact that Tribulus terrestris was not present on any of the 4 farms.     

WHITE LIVER DISEASE IN LAMBS

An outbreak of white liver disease in lambs in Western Australia is described. The disease affected 2- to 3-month-old lambs and was characterised by liver damage, severe ill-thrift, depression, serous ocular discharge, photosensitisation, and a high mortality rate. Transient central nervous system signs occurred. A positive response to vitamin B₁₂ therapy was demonstrated.     

Measurement of phylloerythrin (phytoporphyrin) in plasma or serum and skin from sheep photosensitised after ingestion of Narthecium ossifragum

AIM: To establish a method for measuring phylloerythrin in plasma or serum and skin from lambs photosensitised after ingestion of the plant, Narthecium ossifragum, which induces an hepatogenous photosensitisation similar to the disease known as facial eczema in sheep. METHODS: For two successive summers, lambs were grazed on uncultivated pastures containing N. ossifragum. Clinical photosensitisation was deemed to have occurred when symptoms such as restlessness, scratching, oedema and reddening of the skin were observed. Sixteen lambs that exhibited signs of photosensitisation were included in this study in the first year and five in the following year. A total of 16 clinically healthy lambs served as controls. Fluorescence emission and excitation spectra of phylloerythrin were measured in plasma or serum samples from the 21 photosensitised and 16 non-photosensitised lambs. In the first year of the study, skin samples were collected post mortem from the ear, lip, neck, nose, leg, belly, udder, back, vulva and perineal region, from all photosensitised and from seven non-photosensitised lambs, and examined by fixing them between two glass plates (each of 1 mm thickness) and placing them at a fixed angle in front of a fluorescence spectrofluorometer. RESULTS: All plasma or serum samples obtained from the photosensitised lambs exhibited strong phylloerythrin-like fluorescence of identical spectra; maximum fluorescence was at 650 and 711 nm, and maximum excitation at 425 nm. Emission spectra obtained from plasma or sera from non-photosensitised sheep grazing the same N. ossifragum-containing pastures exhibited either no or only minor fluorescence. Phylloerythrin concentration in plasma or serum exceeded 0.3 microg/ml before clinical photosensitisation occurred, whereas the concentration in samples from clinically healthy lambs was <0.05 microg/ml. Fluorescence from skin samples from the photosensitised lambs showed emission peaks at 650, 670 and 711 nm, whereas the phylloerythrin emission peaks at 650 and 711 nm were not observed in skin from clinically healthy lambs. CONCLUSION: Plasma concentrations of phylloerythrin in healthy sheep were <0.05 microg/ml. Clinical signs of photosensitisation were not observed until the concentration of phylloerythrin in plasma exceeded 0.3 microg/ml. This is the first reported spectroscopic method for analysis of phylloerythrin and the only one which does not involve exposure of the analyst to hazardous chemicals. It has the additional benefit of distinguishing between hepatogenous and primary photosensitisation.     

Adrenal-associated changes in experimental sporidesmin poisoning of sheep

Sporidesmin-dosed hoggets which developed photosensitisation were shown to have enlarged adrenal glands and premature involution of the thymus. These sheep also developed high concentrations of plasma cortisol after the onset of photosensitisation. Sporidesmin-dosed sheep which did not show photosensitisation showed less or no adrenal associated changes.     

Adrenal-associated changes in experimental sporidesmin poisoning of sheep

Sporidesmin-dosed hoggets which developed photosensitisation were shown to have enlarged adrenal glands and premature involution of the thymus. These sheep also developed high concentrations of plasma cortisol after the onset of photosensitisation. Sporidesmin-dosed sheep which did not show photosensitisation showed less or no adrenal associated changes.     

Pithomycotoxicosis (facial eczema) in ruminants in the Azores, Portugal

Outbreaks of pithomycotoxicosis (facial eczema), a hepatogenous photosensitisation caused by the mycotoxin sporidesmin, have affected ruminants in the Azores Islands of Portugal after warm, humid periods during late summer and autumn. Twenty-two outbreaks were recorded in cattle between 1999 and 2001, affecting 11.4 per cent of the animals in the affected herds, and in 2000 there was an outbreak in one sheep flock in which more than 20 per cent of the sheep died. The clinical signs included decreases in milk production, weight loss, photosensitisation and its sequelae, including death. The animals had high activities of gamma glutamyltransferase in their serum, and icterus and severe liver disease, including biliary hyperplasia and fibrosis, were found postmortem. The characteristic spores of the toxigenic saprophytic fungus Pithomyces chartarum were found on grass; all 381 isolates of the fungus were toxigenic for sporidesmin by elisa, and the results were confirmed by high-performance liquid chromatography analysis. Cattle from farms at greatest risk of pithomycotoxicosis were protected by supplementing their concentrate feed with zinc oxide, or using a slow-release intraruminal zinc bolus.     

Suspected photosensitisation in lambs grazing birdsfoot trefoil (Lotus corniculatus)

Suspected photosensitisation occurred in three groups of lambs grazing birdsfoot trefoil (Lotus corniculatus c.v. Grasslands Goldie). In one group, sucking lambs aged about 10 weeks, grazing birdsfoot trefoil, developed skin lesions while lambs of a similar age and from the same flock grazing lucerne (Medicago sativa) or a mixed sward of both species showed no signs of photosensitisation. Affected lambs had lesions on their backs and ears. In a few animals the tips of the ears were shortened by 2-3 cm. In the affected lambs, serum liver enzymes (gamma-glutamyltransferase, glutamate dehydrogenase), bilirubin and serum Vitamin B12 levels were within the normal range. At necropsy, no significant pathological changes were detected in the liver and histological changes in the skin were consistent with primary photosensitisation. In the second group, three of 80 weaned lambs grazing the same birdsfoot trefoil at a restricted intake were affected in the same manner as the first group. In the third group, 15 animals from 28 sets of sucking twin lambs were also affected. In only two sets of twins were both lambs affected. None of the ewes grazing with the lambs in the first or third groups showed any clinical signs of photosensitisation.     

Hepatogenous photosensitisation in fallow deer (Dama dama) in New Zealand

An outbreak of hepatogenous photosensitisation occurred in fallow deer and was diagnosed as facial eczema on the basis of liver lesions and plasma enzyme changes over 56 weeks. Clinical signs of photosensitisation were not as obvious as they are in sheep and cattle. The condition occurred over autumn and in the following spring. Six of 23 deer died or were destroyed. Concentrations of plasma total bilirubin, total bile acids and cholesterol increased, as well as the activities of aspartate transaminase, glutamic dehydrogenase, lactic dehydrogenase, alkaline phosphatase and gamma glutamyltransferase. Albumin:globulin ratios declined due to moderate increases in globulin and minor reductions in albumin. Many of the plasma enzyme activities did not return to normal after autumn and increased to even higher values during the spring outbreak of photosensitisation. Minor plasma biochemical changes were also detected in non-photosensitive deer in the same herd.     

Competition of a sporidesmin-producing Pithomyces strain with a non-toxigenic Pithomyces strain

Sporidesmin, a mycotoxin produced by some strains of Pithomyces chartarum, is responsible for the hepatogenous photosensitisation disease facial eczema, which causes severe losses in agricultural revenue in New Zealand. A sporidesmin-producing strain of P. chartarum, isolated in New Zealand, was grown in co-culture with a South African strain that does not produce the mycotoxin. Competition occurred between the two strains when grown both on agar plates and on dried ryegrass, with a significant decrease in the total amount of sporidesmin produced. Biological control of toxigenic P. chartarum can thus occur under laboratory conditions, raising the possibility of similar control in the field situation.     

Hepatogenous photosensitisation in Scottish sheep casued by Dicrocoelium dendriticum

Dicrocoeliosis was identified as the probable predisposing cause of weight loss and hepatogenous photosensitisation affecting half of a group of 14month-old ewe lambs on a farm on the Inner Hebridean island of Coll. Oral dosing of the ewe lambs with 15mg/kg albendazole only achieved a 79.2% reduction in Dicrocoelium dendriticum egg count, 21day post treatment. Thus, this report of dicrocoeliosis differs from the disease that occurs elsewhere, both in the severity and nature of its clinical signs, and in the response of the parasite to anthelmintic drug treatment. These differences could indicate the existence of a genetically divergent D. dendriticum population, which may have evolved within the unique and isolated biotope afforded by the machair on the island of Coll. Better understanding of these factors is a prerequisite for effective and sustainable disease control.     

Bovine congenital erythropoietic protoporphyria in a crossbred limousin heifer in Ireland

An unusual case of an 11-month-old, black Limousin-cross heifer, with an 8-month history of episodic seizures and photosensitisation, was referred by a veterinary practitioner to the Farm Animal Section of the UCD Veterinary Hospital, School of Veterinary Medicine, University College Dublin, Ireland, in August 2014. Following an investigation, a diagnosis of Bovine Congenital Erythropoietic Protoporphyria (BCEPP) was made. To the authors’ knowledge this is the first report of such a case in Ireland. BCEPP should be considered as a differential diagnosis in young animals displaying periodic seizures and/or photosensitisation.

Electronic supplementary material

The online version of this article (doi:10.1186/s13620-015-0044-3) contains supplementary material, which is available to authorized users.     

Effects of low dose rates of sporidesmin given orally to sheep

Aim: To examine clinical and subclinical effects of sporidesmin administered orally to sheep at very low daily dose rates for periods of 3 to 48 days.

Methods: Two experiments were conducted. In Experiment A, sporidesmin-A was administered orally to groups of 16 sheep at daily dose rates of approximately 0.0042, 0.0083 and 0.0167 mg/kg bodyweight for 48 days. In Experiment B, the highest of these doses was administered orally for 3, 6, 12, 24 or 48 consecutive days. Parameters of production, clinical findings, organ weights and pathological findings were recorded.

Results: In Experiment A, severe liver lesions and photosensitisation were evident as early as 18 days after commencement of daily low-dose administration of sporidesmin, and were associated with significant bodyweight loss. Significant bodyweight loss also occurred in non-photosensitised sporidesmin-treated sheep. Bodyweight reductions were associated with reduced carcass weights and skin weights in treated animals. Sporidesmin administration was also associated with reduced bodyweight gains and pathological changes of the liver, kidney, hepatic lymph nodes, thymus, adrenal gland, heart and spleen. In Experiment B, only moderate changes occurred in a few sheep in the groups dosed with sporidesmin at 0.0167 mg/kg for 3 or 6 days, but major changes were frequently recorded in animals dosed at this rate for 12 days or longer. These comprised changes in the liver and other organs, and photosensitisation typical of the disease, facial eczema. Results are discussed in relation to animal welfare and economic issues associated with this disease.

Conclusions: Sporidesmin caused significant clinical and sub-clinical disease and reduced animal production at relatively low daily dose rates. The effects of repeated daily low-dose administration of sporidesmin appear to be cumulative. There was considerable variation in susceptibility between individual animals.These results emphasise the considerable production losses and animal welfare effects associated with sporidesmin toxicity in sheep.     

Disseminated Mycobacterium avium infection in young cats: overrepresentation of Abyssinian cats

Disseminated Mycobacterium avium-intracellulare complex (MAC) infection was diagnosed in 10 young cats (1-5 years of age) from Australia or North America between 1995 and 2004. A further two cats with disseminated mycobacteriosis (precise agent not identified) were recognised during this period. Of the 12, 10 were Abyssinian cats, one was a Somali cat and one was a domestic shorthair cat. None of the cats tested positive for either FeLV antigen or FIV antibody. The clinical course of these infections was indolent, with cats typically presenting for weight loss, initially in the face of polyphagia, with a chronicity of up to several months. Additional clinical features included lower respiratory tract signs and peripheral lymphadenomegaly. A marked diffuse interstitial pattern was evident in thoracic radiographs, even in cats without overt respiratory involvement. Hair clipped to perform diagnostic procedures tended to regrow slowly, if at all. Diagnosis was generally made by obtaining representative tissue specimens from mesenteric lymph nodes, liver or kidney at laparotomy, or from a popliteal lymph node. The primary antecedent event was most likely colonisation of either the alimentary or respiratory tract, followed by local invasion and eventual lymphatic and haematogenous dissemination. Nine cases were treated using combination therapy with agents effective for MAC infection in human patients. Two cats are still undergoing initial therapy and have responded. Of the remaining seven, all responded during long courses (5-14 months) of clarithromycin combined with either clofazimine or rifampicin, and a fluoroquinolone or doxycycline. Of these, three cats remain well (with durations between 2 months and 2 years following therapy); two developed recurrent disease (at 3 months and 2 years, respectively, following therapy) and have restarted therapy. The remaining two cats improved 1 year and 5 months, respectively, after diagnosis but ultimately succumbed. The two cats in which therapy was restarted have improved dramatically. Certain lines of Abyssinian and Somali cats likely suffer from a familial immunodeficiency that predisposes them to infection with slow-growing mycobacteria such as MAC.     

Effects of low dose rates of sporidesmin given orally to sheep

AIM: To examine clinical and subclinical effects of sporidesmin administered orally to sheep at very low daily dose rates for periods of 3 to 48 days. METHODS: Two experiments were conducted. In Experiment A, sporidesmin-A was administered orally to groups of 16 sheep at daily dose rates of approximately 0.0042, 0.0083 and 0.0167 mg/kg bodyweight for 48 days. In Experiment B, the highest of these doses was administered orally for 3, 6, 12, 24 or 48 consecutive days. Parameters of production, clinical findings, organ weights and pathological findings were recorded. RESULTS: In Experiment A, severe liver lesions and photosensitisation were evident as early as 18 days after commencement of daily low-dose administration of sporidesmin, and were associated with significant bodyweight loss. Significant bodyweight loss also occurred in non-photosensitised sporidesmin-treated sheep. Bodyweight reductions were associated with reduced carcass weights and skin weights in treated animals. Sporidesmin administration was also associated with reduced bodyweight gains and pathological changes of the liver, kidney, hepatic lymph nodes, thymus, adrenal gland, heart and spleen. In Experiment B, only moderate changes occurred in a few sheep in the groups dosed with sporidesmin at 0.0167 mg/kg for 3 or 6 days, but major changes were frequently recorded in animals dosed at this rate for 12 days or longer. These comprised changes in the liver and other organs, and photosensitisation typical of the disease, facial eczema. Results are discussed in relation to animal welfare and economic issues associated with this disease. CONCLUSIONS: Sporidesmin caused significant clinical and sub-clinical disease and reduced animal production at relatively low daily dose rates. The effects of repeated daily low-dose administration of sporidesmin appear to be cumulative. There was considerable variation in susceptibility between individual animals. These results emphasise the considerable production losses and animal welfare effects associated with sporidesmin toxicity in sheep.     

Competition of a sporidesmin-producing Pithomyces strain with a non-toxigenic Pithomyces strain

Sporidesmin, a mycotoxin produced by some strains of Pithomyces chartarum, is responsible for the hepatogenous photosensitisation disease facial eczema, which causes severe losses in agricultural revenue in New Zealand. A sporidesmin-producing strain of P. chartarum, isolated in New Zealand, was grown in co-culture with a South African strain that does not produce the mycotoxin. Competition occurred between the two strains when grown both on agar plates and on dried ryegrass, with a significant decrease in the total amount of sporidesmin produced. Biological control of toxkenic P. chartarum can thus occur under laboratory conditions, raising the possibility of similar control in the field situation.     

Current ideas on the pathophysiology and treatment of lantana poisoning of ruminants

Lantana poisoning in ruminants results from the ingestion of toxic varieties of the plant Lantana camara, which contain the triterpene acids lantadene A and lantadene B. Poisoning results in intrahepatic cholestasis and the consequences of the liver injury include jaundice, photosensitisation and ruminal stasis. The decreased ruminal motility causes toxic material to be retained in the rumen and continuous absorption of toxins from the rumen maintains the disease. Lantana poisoning can best be treated by preventing further absorption of toxins. This can be achieved by giving a large quantity of activated charcoal into the rumen together with a large volume of a multiple electrolyte solution to stimulate ruminal motility and rehydrate the animal. Treatment for photosensitive dermatitis should also be given.