Salmon poisoning disease (SPD) is an acute, infectious disease of canids, in which the infective agent is transmitted through the various stages of a fluke in a snail-fish-dog life cycle. The name of the disease is misleading because no toxin is involved. Elokomin fluke fever (EFF) is an acute infectious disease of canids, ferrets, bears, and raccoons that resembles SPD but has a wider host range. In humans, Neorickettsia sennetsu causes a disease known as Sennetsu ehrlichiosis; this has not been reported as a cause of illness in dogs.
SPD is caused by N helminthoeca and is sometimes complicated by a second agent, N elokominica, which causes EFF. The vector for these Neorickettsia agents is a small fluke, Nanophyetus salmincola. Dogs and other animals become infected by ingesting trout, salmon, or Pacific giant salamanders that contain encysted metacercariae of the rickettsia-infected fluke. In the dog's intestine, the larval flukes excyst, embed in the duodenal mucosa, and introduce the rickettsiae. The fluke infection itself produces little or no clinical disease. A recent report of SPD in 2 captive Malayan sun bears underscores the need to consider this etiology in non-native exotic species with compatible exposure and clinical histories.
The life cycle is maintained by the passage of infected fluke ova in the feces of the host. Miracidia develop from these ova and infect the snail Oxytrema plicifer to form rediae. Rediae develop into cercariae that are released from the snail, penetrate the salmon or trout, and develop into infective, encysted metacercariae. The cycle is completed when a dog eats the fish and becomes infected with the rickettsiae. Transmission by cage-to-cage contact, rectal thermometers, or aerosols is rare.
There are no age, sex, or breed predilections; however, the disease prevalence is higher when the availability of fish is greater. Infected fish are found in the Pacific Ocean from San Francisco to the coast of Alaska, but SPD is more prevalent from northern California to Puget Sound. It is also seen inland along the rivers of fish migration. Apparently, the snail is the geographically limiting factor.
In SPD, signs appear suddenly, usually 5–7 days after eating infected fish, but may be delayed as long as 33 days, and persist for 7–10 days before culminating in death in up to 90% of untreated animals. Body temperature peaks at 104–107.6°F (40–42°C) 1–2 days later, then gradually declines for 4–8 days and returns to normal. Frequently, animals are hypothermic before death. Fever is accompanied by depression and complete anorexia in virtually all cases. Persistent vomiting usually occurs by day 4 or 5. Diarrhea develops by day 5–7; it often contains blood and may be severe. Dehydration and extreme weight loss occur. When severe, the GI signs are clinically indistinguishable from those of canine parvoviral infection. Generalized lymphadenopathy develops in ∼60% of cases. Nasal or conjunctival exudate may be present and mimic signs of distemper. Neutrophilia is common, but a marked, absolute leukopenia with a degenerative left shift may occur. Thrombocytopenia is reported in 94% of the cases. Serum chemistry values are normal.
Clinically, EFF is a milder infection than SPD. Severe GI signs are less commonly seen in EFF infections, and lymphadenopathy may be a more pronounced finding. Case fatality rates with EFF are lower, occurring in ~10% of untreated cases.
Infection appears to chiefly affect the lymphoid tissues and intestines. There is enlargement of the GI lymph follicles, lymph nodes, tonsils, thymus, and to some extent, the spleen, with microscopic necrosis, hemorrhage, and hyperplasia. A variable but often severe hemorrhagic enteritis, which seems to arise from damaged lymph follicles, is seen throughout the intestine with SPD, but is less commonly observed with EFF. Microscopic foci of necrosis also appear apart from the follicles. Flukes embedded in the duodenum account for little tissue damage. Nonsuppurative meningitis or meningoencephalitis has been identified in some dogs.
Fluke ova are found on fecal examination in ∼92% of cases, which supports the diagnosis. The ova are oval, yellowish brown, rough-surfaced, and ∼87–97 × 35–55 μm, with an indistinct operculum and a small, blunt point on the opposite end. During the first day or two, few ova may be passed. Intracellular organisms have been demonstrated via lymph node aspiration in ∼70% of the cases. Other causes of fever of unknown origin, generalized lymphadenopathy, vomiting, and diarrhea are differential diagnoses. When diarrhea and exudative conjunctivitis occur, distemper should be considered.
Prevention and Treatment
Currently, the only means of prevention is to prevent the ingestion of uncooked salmon, trout, steelhead, and similar freshwater fish. In animals that recover, a profound humoral immune response persists, but there is no cross-resistance between N helminthoeca and N elokominica. Various sulfonamides given PO or parenterally are effective, as are chlortetracycline, oxytetracycline, and chloramphenicol. Animals usually succumb because of dehydration, electrolyte and acid-base imbalances, and anemia. Therefore, general supportive therapy to maintain hydration and acid-base balance, while meeting nutritional requirements and controlling diarrhea, is often essential. Judicious use of whole blood transfusions may be helpful.
Last full review/revision March 2012 by Jennifer H. McQuiston, DVM, MS