Clinical signs associated with ingestion of black walnut tree (Juglans nigra) wood, nuts, and hulls in dogs: 93 cases (2001-2012).

OBJECTIVE: To identify clinical signs associated with oral exposure to black walnut tree (Juglans nigra) wood, nuts, or nut hulls in dogs and to compare clinical syndromes between dogs that ingested wood and dogs that ingested the walnuts or nut hulls. DESIGN: Retrospective case series. ANIMALS: 93 dogs. PROCEDURES: Records of dogs with oral exposure to black walnut wood, nuts, or nut hulls between November 2001 and December 2012 were retrieved from the Animal Poison Control Center database. Records were reviewed, and data regarding signalment; exposure; time of onset, type, and duration of clinical signs; serum biochemical abnormalities; treatment; and response to treatment were collected. Results were compared statistically between dogs that ingested wood and those that ingested nut components. RESULTS: 28 cases involved exposure to wood, and 65 involved exposure to nuts or hulls. Spontaneous vomiting was commonly observed (13/28 [46%] and 31/65 [48%] dogs that ingested wood and nut components, respectively). Neurologic or musculoskeletal signs were significantly more common in dogs that ingested wood (26/28 [93%]) than in those that ingested nuts or hulls (15/65 [23%]). Relative risk of developing neurologic signs after ingestion of wood was approximately 4 times that after ingestion of nuts or hulls. CONCLUSIONS AND CLINICAL RELEVANCE: Ingestion of black walnut wood by dogs resulted in a clinical syndrome in which neurologic or musculoskeletal signs were most frequently reported, whereas ingestion of black walnuts or their hulls was most commonly associated with vomiting. To our knowledge, this is the first report describing 2 different clinical syndromes associated with exposure to black walnut tree components in dogs.

"Pine mouth" syndrome: cacogeusia following ingestion of pine nuts (genus: pinus). An emerging problem?

We report a case of cacogeusia, specifically metallogeusia (a perceived metallic or bitter taste) following pine nut ingestion. A 36-year-old male presented with cacogeusia one day following ingestion of 10-15 roasted pine nuts (genus: Pinus). Symptoms became worst on post-exposure day 2 and progressively improved without treatment over 5 days. There were no other symptoms and physical examination was unrevealing. All symptoms resolved without sequalae. We contemporaneously report a rise in pine nut-associated cacogeusia reported online during the first quarter of 2009, and a significant rise in online searches related to pine nut-associated cacogeusia (or what the online public has termed "pine mouth") during this time. Most online contributors note a similar cacogeusia 1-3 days following pine nut ingestion lasting for up to 2 weeks. All cases seem self-limited. Patients occasionally describe abdominal cramping and nausea after eating the nuts. Raw, cooked, and processed nuts (in pesto, for example) are implicated. While there appears to be an association between pine nut ingestion and cacogeusia, little is known about this condition, nor can any specific mechanism of specific cause be identified. It is not known if a specific species of pine nut can be implicated. "Pine mouth" appears to be an emerging problem.

Acute selenium poisoning by paradise nuts (Lecythis ollaria).

Two previously healthy women developed nausea, vomiting, headache and dizziness for several days, a massive hair loss about 2 weeks later and a discoloration of the fingernails. Detailed diagnostic procedures did not reveal any pathological results. Therapeutic measures did not show any effect. Thallium and arsenic were within normal range in plasma. Delayed quantitative determination of selenium in blood, however revealed toxic values (in case I: 479 microg/L of serum, 8 weeks after ingestion, and in case II 300 microg/L of serum, 9 weeks after ingestion). In retrospect, a relation to the ingestion of paradise nuts could be established.

Ginkgo nut intoxication in a 2-year-old male.

This report describes a case of ginkgo nut intoxication in a 2-year-old male. The patient presented with vomiting and afebrile convulsion 4 hours after eating a large number of roasted gingko nuts. There was a large volume of ginkgo nuts in his vomited matter, and on admission the concentrations of 4-O-methoxypyridoxine in his serum and urine were elevated. The patient was diagnosed as having ginkgo nut intoxication, and diazepam and pyridoxal phosphate were administered intravenously. After the treatment, his symptoms were resolved. The neurotoxicity of ginkgo nuts should be recognized by pediatricians and parents who have infants.

Weakness, tremors, and depression associated with macadamia nuts in dogs.

The ASPCA National Animal Poison Center managed 29 cases of ingestion of commercially available macadamia nuts in dogs during a 5-y period. Clinical signs included, from most to least, weakness, depression, vomiting, ataxia, tremor, hyperthermia, abdominal pain, lameness, stiffness, recumbency, and pale mucous membranes. The onset of clinical signs was reported as < 12 h in 79% of the cases. The duration of clinical signs for the majority of cases was < 24 h. The amount of macadamia nuts ingested was estimated in 72% of the calls with a mean of 11.7 g/kg bw. In an attempt to reproduce the syndrome, 4 dogs were gavaged with 20 g macadamia nuts/kg bw in a water slurry. The experimentally dosed dogs developed weakness, manifested by the inability to rise 12 h after dosing, mild central nervous system depression, vomiting, and hyperthermia, with rectal temperatures up to 40.5 C. Mild elevations in serum triglycerides and serum alkaline phosphatase were detected. Lipase values peaked sharply at 24 h and returned to normal by 48 h after dosing. Other serum biochemical and electrolyte determinations were unremarkable. Serum lipoprotein electrophoresis determinations were unchanged from baseline. The mechanism of the syndrome is unknown. All field and experimental dogs recovered uneventfully within 1 to 2 d whether treated by a veterinarian or not.

Emic accounts of a mystery illness: the Groote Eylandt syndrome.

The Aboriginal people of Groote Eylandt, in the Northern Territory of Australia, are suffering from an unusual disease complex having neurological, psychiatric and teratological features, which admits no ready explanation. The island people at various times blame it on the spirits, or accuse enemies, or take some responsibility upon themselves. In this paper, 'emic' accounts of the illness (those current among the members of the society) are described in order to compare them with 'etic' accounts of those who study the society from the outside. Since emic views regulate people's behaviours toward illness, it is suggested these views should complement and inform etic views of researchers and therapists. This principle might apply to all mysterious or poorly understood illness.

Primary liver cancer and food-based toxins. A Swaziland review.

This review brings together evidence on the scientific unfolding of the relationship between primary liver cancer and food based toxins with particular reference to Swaziland. Growth of knowledge of the geographic patterns of the disease has been paralleled by development in other disciplines, notably agriculture and toxicology, of understanding of the occurrence and mode of action of natural hepatotoxins in the dietary environment of people in southern Africa. Areas for further enquiry are highlighted but the agriculturally advantageous side-effects of policies aimed to reduce mycotoxin ingestion in Swaziland are already unequivocal.

Acorn poisoning in cattle.

Ten cows in a suckler herd totalling 60 sickened after grazing parkland which was heavily covered with acorns. Two died. The main clinical signs were dullness, anorexia and constipation. The main pathological findings were severe nephrosis and some intestinal ulceration. After removal to an acorn-free pasture, the remaining eight animals made a full recovery.

The occurrence of aflatoxin in nuts and nut products imported to Finland for human consumption during the years 1974-1976.

An examination was made of 1050 lots of nuts and nut products, totalling 4.7 million kg, imported to Finland in the years 1974-1976. Of these, 44 lots (4.2%) were found to contain aflatoxin. The highest percentage of aflatoxin-containing lots, was observed in the case of sliced and crushed peanuts (29.4%). Of the positive samples, 20.5% contained 101-500 microgram aflatoxin per kg, 52.3% contained 6-100 microgram/kg and 20.5% contained less than or equal to 5 microgram/kg. Rest of the samples (6.7%) contained aflatoxin 501 microgram/kg or more. The most commonly detected toxin types were B1 and B2. The proportion of aflatoxin-containing lots showed a slight decrease during the 3-year research period. On the basis of the research results and the sampling plan used, and bearing in mind the acceptable quality level (AQL: 5 microgram/kg) employed in Finland, the reliability of approval and rejection decisions was discussed from the point of view of both the producer's and the consumer's risk.