Signalment: 18-month-old male Quarterhorse equine.
History: The horse was recumbent and had muscle fasciculation when found in the pasture. The horse was euthanized and the brain submitted for examination.
Gross Pathology: None.
Contributor's Diagnosis and Comments: Neuroaxonal dystrophy, chronic, multifocal, severe, brain.
The lesions are characteristic of locoweed poisoning. The winter rains of 1995 produced a bumper crop of locoweed in southeastern Arizona. Late spring and summer rains failed, however, resulting in minimal forage production. Horses and cattle in the area, when not given supplemental feed, resorted to consuming the dried-out locoweed. We received a number of submissions with the same nervous system signs and lesions during this period.
AFIP Diagnosis: Brain: Vacuolation, neuronal, diffuse, moderate, with minimal multifocal axonal sheath swelling and scattered spheroids, Quarterhorse, equine
Conference Note: Locoweed poisoning (locoism) occurs following ingestion of certain toxic plants: Swainsona spp. of Australia and the Astragalus and Oxytropis spp., the locoweeds of North America. Locoweed are not palatable but may be consumed when normal forage becomes unavailable. Once poisoned, most animals are unlikely to eat locoweed again; however, in some instances, chronic ingestion of locoweeds result in habituation where animals will seek out the plant in preference to other forage.
The clinical signs of locoweed toxicosis include depression, a staggering gait, muscular incoordination, rough hair coat, and nervousness, especially when startled. Affected animals may seek solitude, become hard to handle, and experience difficulty in eating and drinking. Other adverse effects include emaciation, abortion, birth defects and suppressed fertility.
Swainsonine, an indolizidine alkaloid, is the toxic principle. As a potent inhibitor of lysosomal a-mannosidase, swainsonine induces a form of a-mannosidosis which is microscopically and ultrastructurally identical to genetic a-mannosidosis of man, cattle (Angus, Murray Grey, Tasmanian Grey, and Galloway), and cats (Persian). As a consequence of a-mannosidase inhibition, there is storage of water-soluble oligosaccharides that contain mannose and N-acetyl-glucosamine within the vesicles of a variety of cells, particularly neurons, macrophages, and pancreatic exocrine cells. In the later stages of the disease, axonal degeneration is evident, particularly in the cerebellar roof nuclei and posterior brain stem.
Locoweed poisoning is biochemically distinct from the genetic disease because swainsonine also inhibits Golgi mannosidase 2, an enzyme involved in the posttranslational trimming modifications of the glycan moiety of glycoproteins. As a result, abnormal proportions of different types of glycoproteins are produced, and stored oligosaccharides are larger than those in the genetic disease.
Contributor: Arizona Veterinary Diagnostic Laboratory, 2831 N. Freeway, Tucson, AZ 85075.
1. Dorling PR, Huxtable CR, and Vogel P: Lysosomal storage in Swainsona spp. toxicosis: an induced mannosidosis. Neuropathol Appl Neurobiol 4:285-295, 1978.
2. Malynezux R and James L: Loco intoxication: indolizidine alkaloids of spotted locoweed (Astragalus lentigenosus). Science 216:190-191, 1982.
3. Jubb KVF, Kennedy PC, Palmer N: (eds) Pathology of Domestic Animals, Volume 1, Academic Press, pg. 319, 1993.
International Veterinary Pathology Slide Bank: None
Signalment: 10-year-old Holstein cow.
History: Cow from a dairy herd having multiple animals afflicted with lameness and decreased milk production.
Gross Pathology: Affected animals had one or several well-circumscribed ulcerated and/or papillated (wart-like) erythematous, painful skin lesions of the interdigital space or the heel bulb or both of more than one limb.
Laboratory Results: None
Contributor's Diagnosis and Comments: Bovine papillomatous digital dermatitis (BPDD). Cause: Spirochetal organisms?
In the skin biopsies examined, there was a papillomatous epidermal hyperplasia with the presence of neutrophils, necrotic cells and bacterial colonies in the outer zones of the hyperplastic epidermis. Epidermal ulceration was also observed. The use of a silver stain (Warthin-Starry) revealed the presence of large numbers of filamentous spiral bacteria having the morphology of spirochetes within the viable and necrotic outer zones of the hyperplastic epidermis. There were mild perivascular inflammatory infiltrates without significant fibrosis in the superficial dermis. The etiology of BPDD is unknown, but appears to be infectious. The presence of large numbers of spirochetal organisms which appear to be invasive in the lesions suggests that this microbe may have a primary role. Evidence for viral or mycotic etiologies has not been found. BPDD has become a common cause of lameness in dairy cattle throughout Europe, the United Kingdom, the United States and Canada. Environmental and management conditions which weaken foot tissues might predispose cows to develop this condition.
AFIP Diagnosis: Skin, interdigital: Dermatitis, chronic-active and eosinophilic, diffuse, moderate, with marked pseudoepitheliomatous hyperplasia and myriad argyrophilic spirochetes, Holstein, bovine.
Conference Note: The conference participants agreed with the contributor's diagnosis. A Gram's stain demonstraeted the presence of a mixed bacterial population with a predominance of thin, long and undulating Gram-negative spirochetes. The specific identification and role of the spirochete in bovine digital dermatitis have yet to be determined. A recent article indicated that the spirochete isolated from cases of papillomatous digital dermatitis had characteristics most consistent with the genus Treponema.
The lesions of papillomatous digital dermatitis are differentiated from those of interdigital Fusobacterium necrophorum infection ("foot rot") in that they are confined to the dermis and do not produce the deep necrosis associated with "foot rot". BPDD occurs as solitary, circumscribed, red, exudative, painful, 2 cm to 4 cm diameter lesions on the heel bulb. Chronic lesions may take on a verrucose or hairy appearance simulating a fibropapilloma.
Contributor: Department of Pathology and Microbiology, Faculty of Veterinary Medicine, University of Montreal, P.O. Box 5000, St. Hyacinthe, Quebec, CANADA J2S- 7C6.
International Veterinary Pathology Slide Bank: None.
Signalment: Greater than 1-year-old male haddock (Melanogrammus aeglefinus).
History: Captured in Autumn 1995 by hook and line in Bay of Fundy. Held until death on May 21, 1996 in a 4m2 fiberglass tank receiving pumped sea water. Water was slightly supersaturated with gases. Fish never treated, necropsied after death. Fed mixed raw fish diet with vitamin supplements.
Gross Pathology: Hemorrhaging noted at base of fins and along ventral surface of body. No mention of eye lesions.
Laboratory Results: Bacteriology negative. Smear of ventral surface hemorrhage revealed short gram-negative rods. Lateral skin scraping revealed tiny short gram-negative rods. A single nematode found in gill wet mount. IFAT of kidney tissue for Renibacterium salmoninarum was negative.
Contributor's Diagnosis and Comments: Gas embolism of the choroid gland, subacute to chronic, multifocal, severe, with thrombosis, pressure necrosis and histiocytic inflammation.
The lens, which was removed from this section, showed evidence of lenticular epithelial liquefaction consistent with cataract formation. With regard to etiology, the history indicated two possible causes for development of gas bubbles with the choroid reté: a) rapid decompression following capture and b) low level chronic gas supersaturation of the holding tank water. It is possible that both scenarios contributed to the lesions.
The accompanying kodachrome slide depicts the eye of another with nearly identical lesions.
AFIP Diagnosis: Choroid gland (rete): Emphysematous change, diffuse, severe, with retinal detachment and degeneration, and multifocal granulomatous inflammation, hemorrhage and necrosis, haddock (Melanogrammus aeglefinus), piscine.
Conference Note: Exophthalmos caused by the presence of gas bubbles ("gas bubble disease") within and behind the eye is a commonly reported cause of morbidity and mortality in fish. The disease is usually diagnosed by the detection of gas bubbles within tissues of affected animals in combination with the demonstration of gas supersaturation of the water. "Gas bubble disease" (GBD) is frequently compared to decompression disease ("the bends") of man. The pathogenesis of GBD differs in that it reflects a chronic exposure to low level supersaturation, whereas, in decompression disease, the pressure differences are greater and changes occur over a relatively short period of time. Fish equilibrate with the dissolved gas, usually nitrogen, that then comes out of solution into the bloodstream, forming gas emboli in a variety of tissues, especially those with large capillary beds, such as the gills and eyes. In fry, the yolk sac is commonly affected. In acute cases, small gas bubbles initially form in the choroid gland of the posterior uvea, which later increase markedly in size. In subacute and chronic cases, localization of gas bubbles in retrobulbar and periocular sites are frequent. During the acute phase of GBD, ocular lesions are limited to anatomical displacement of tissue and local degeneration of compressed tissues. Subacute sequelae include the formation of anterior synechia, cataract, and suppurative panophthalmitis. During chronic stages, large retrobulbar gas bubbles cause severe exophthalmia and distortion of the globe with stretching of the optic nerve and retinal vessels. Damage to the blood vessel supplying the eye often leads to thrombosis and perivasculitis.
Contributor: Atlantic Veterinary College, University of Prince Edward Island, 550 University Avenue, Charlottetown, PEI, Canada C1A 4P3.
International Veterinary Pathology Slide Bank: None.
Signalment: Tissue from a 12-week-old feeder pig.
History: Tissues were representative samples from a 960 head finishing barn which was operated in an "all-in all-out" flow pattern. These pigs were placed in this barn 10 days previously. The barn was dry and warm (72 F. with no appreciable moisture or condensation), yet the pigs were huddled and piling in the center of the pens. A marked increase in coughing was observed and numerous pigs had been treated with a variety of injectable antibiotics with little to no clinical improvement. Several pigs had died in the last 4 days, some of which were not recognized as sick by the caretaker.
Gross Pathology: The lungs were diffusely dark red, wet, rubbery, and failed to collapse. Moderate amounts of red-tinged fluid was free in the thoracic cavity, and similar appearing red-tinged edema fluid and froth were in the trachea and bronchi. The pulmonary pleura was faintly roughened by adherent fibrin.
Laboratory Results: The lungs were florescent antibody (FA) positive for swine influenza, and swine influenza virus was isolated. All examined lungs were negative for pseudorabies on FA and virus isolation. PRRS virus was not isolated, Pasteurella multocida and Streptococcus suis type II were isolated from some of the lungs cultured.
Contributor's Diagnosis and Comments: Diffuse acute fibrinosuppurative alveolitis with multifocal coalescent alveolar and bronchiolar necrosis.
Alveolar spaces are commonly filled with fibrin, neutrophils, macrophages or proteinic edema fluid with multiple, often coalescent, foci of alveolar septal necrosis, and septal microvascular thrombosis. Clusters of necrotic inflammatory cells are often in alveolar spaces. In less severely affected areas, alveolar septal thickening due to pneumocyte hypertrophy is evident. Bronchi and bronchioles display varying degree of epithelial necrosis, hypertrophy or hyperplasia, with occasional foci of squamous metaplasia in some sections. Peribronchiolar and perivascular lymphocytic infiltrates are evident in some sections. Microvascular congestion is prominent throughout the sections.
These animals had rather characteristic clinical signs of swine influenza, but the severity was somewhat unusual. Microscopically, the necrotic character of the lesion suggested pseudorabies virus as a possible diagnosis especially since some of the animals showed concurrent necrotizing tonsillitis (probably a result of Streptococcus suistype II). A variant of swine influenza which has recently been described causes proliferative and necrotizing pneumonia similar to the lesions seen in these cases. An acute fibrinohemorrhagic pneumonia caused by Streptococcus suis has also been recently described in which fibrinoid alveolar septal necrosis similar to that seen in these cases is a prominent feature. The extremely high morbidity and acute nature of the outbreak along with histologic features suggest swine influenza virus as the primary etiologic agent, but a dual infection with Streptococcus suis cannot be ruled out based upon the histologic lesions.
AFIP Diagnosis: Lung: Pneumonia, bronchointerstitial, fibrinonecrotic, acute to subacute, diffuse, moderate, with type II pneumocyte hyperplasia and multifocal vasculitis, crossbred pig, porcine.
Conference Note: Swine influenza is an acute contagious disease caused by type A orthomyxoviruses. Disease occurs in the form of explosive outbreaks with high morbidity but low mortality. The disease is often confined to young pigs and outbreaks occur mainly during the winter months. The classic disease is caused by the viral subtype H1N1, which contains distinct antigenic variants which may circulate concurrently in pig populations in different parts of the world. Subtype H1N1 is the primary agent of swine influenza in North America. Subtype H3N2 is prevalent in Europe.
The swine influenza viruses are zoonotic. There is circumstantial evidence that the classical swine subtype, H1N1, was acquired from humans in the 1918 pandemic, and the subtype H3N2 was also acquired from humans after its emergence in 1968 as Hong Kong flu. Humans are also thought to be susceptible to some antigenic variants circulating in swine.
Spread of swine influenza virus is rapid and via the inhalation
of infected aerosolized droplets. Viral replication is usually
limited to the epithelium of the trachea and bronchi and begins
in epithelial cells as soon as 2 hours post-infection. By 8 hours,
there is loss of cilia, extrusion of mucus, and vacuolar degeneration.
Within 24 hours, there is epithelial necrosis and sloughing with
emigration of leukocytes, chiefly neutrophils, into the airway
lumina. Extension of virus infection to alveolar epithelial cells
causes alveolar flooding by serofibrinous exudate and neutrophils.
Although a pure swine influenza virus infection can cause deaths,
most mortalities are the result of secondary bacterial infections
caused by such agents as with Haemophilus spp. or Pasteurella
multocida. Swine lungworms of the genus Metastrongylus are believed
to be responsible for the transmission of swine influenza virus
Contributor: College of Veterinary Medicine, Mississippi State University, Box 9825, Mississippi State, MS 39762.
International Veterinary Pathology Slide Bank:
Laser disc frame #19834, 19950-51, 20006.
Captain, VC, USA
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
* The American Veterinary Medical Association and the American College of Veterinary Pathologists are co-sponsors of the Registry of Veterinary Pathology. The C.L. Davis Foundation also provides substantial support for the Registry.