Probable hydrogen sulfide toxicity in pigs in Ontario
Felipe Reggeti, Josepha DeLay, Beverly McEwen, Sherry Smith, Dwayne Schrunk, Wilson Rumbeiha
In November 2017, a case of massive mortality was reported on a swine farm in Ontario; ~75% of the pigs in a 400-head grower barn died unexpectedly and over a short timespan following failure of the barn ventilation system. There were no previous health issues with these animals. Postmortem examinations and histopathology performed on 3 affected pigs revealed:
- Multifocal peri-bronchiolar interstitial hemorrhage and fibrin exudation with mild fibrinous alveolitis.
- Mild multifocal acute degenerative myopathy.
- Multiorgan congestion.
Histopathologic findings were not consistent with infectious diseases. Respiratory changes suggested direct irritation of the respiratory mucosa (e.g., noxious gases); mild myopathy was consistent with terminal seizure activity or muscle spasms. Because of massive sudden death and poor barn ventilation, carbon monoxide (CO) poisoning, hydrogen sulfide (H2S) intoxication, and/or hyperthermia were suspected. Carboxyhemoglobin was not detected in blood samples from affected pigs, making CO poisoning less likely. Thiosulfate was detected in ocular fluid from 3 exposed animals at 5.9 - 27.2 ppm. Comparatively, in the aqueous of 3 healthy unexposed control pigs, concentrations of this molecule were below the detection limit of the assay (< 1.0 ppm). Although hyperthermia could not be excluded entirely, the clinical presentation and postmortem findings were not supportive of this condition. Based on histopathologic findings and analytical toxicology data, exposure to H2S gas of manure pit origin was considered the most likely cause of death.
H2S is produced endogenously at very low concentrations, and it is physiologically beneficial; however, it can be a lethal xenobiotic gas at high concentrations. Cases of fatal H2S toxicity involving livestock and humans are annually reported as a result of improper manure disposal, but risk of occupational exposure is also present in the petrochemical industry, natural gas extraction plants,
storage) and others.
H2S is neurotoxic, and neurotoxicity is the cause of death following acute exposure. H2S inhibits complex IV of the cytochrome C oxidase mitochondrial enzyme, compromising energy metabolism and potentially causing acute death. However, H2S is quickly metabolized and eliminated from the body as sulfides, thiosulfates, sulfites, or sulfates following sub-lethal exposures. In veterinary medicine, the diagnosis of acute H2S poisoning is commonly supported by circumstantial conditions and exclusion of other causes of acute mortality; however, identification of H2S metabolites in body fluids provides an opportunity for objective evaluation of exposure.
Currently, researchers at Iowa State University are working on identification of H2S poisoning biomarkers, including thiosulfate levels in ocular fluids, serum, and urine. Although these studies are experimental at this time, preliminary results (including this case report) are promising for the development of validated diagnostic methods. Further, confirmation of H2S exposure by identification of its metabolites provides opportunities to better characterize the subtle anatomic and histologic changes that may occur in lethal and sub-lethal exposures. Thiosulfates are successfully used as biomarkers of H2S intoxication in human cases.
Veterinarians encountering animal cases of presumptive H2S intoxications are encouraged to contact us to provide support with the diagnostic investigation. Essential samples to collect for toxicology include frozen eyeballs, serum, and urine. Acute exposure to H2S may produce histologic lesions in brain in animals that do not immediately succumb to toxicity, although lesions were not identified in the current case. Postmortem examination with histopathology is strongly recommended to rule out other causes of unexpected death, and to identify compatible brain lesions, if present. AHL
Jiang J, et al. Hydrogen sulfide—mechanisms of toxicity and development of an antidote. Sci Rep 2016;6:20831.
Qiumei You, Jason Eidt, Hugh Y. Cai
By testing the DNA extract of a 10-fold serial dilution of M. hyosynoviae S16 culture, the analytical sensitivity of the TaqMan qPCR was determined to be 12 CFU M. hyosynoviae per PCR reaction, which was 10 to 100 time more sensitive than the SYBR Green qPCR in our hands. A small set of clinical samples was used to evaluate the M. hyosynoviae TaqMan qPCR in comparison with the published SYBR Green qPCR. Among the 38 samples tested, 2 were positive and 20 were negative by both assays; 14 samples were positive by the TaqMan qPCR while negative or inconclusive by the SYBR Green qPCR. It appears that the AHL TaqMan qPCR was more sensitive than the SYBR Green qPCR for the detection of M. hyosynoviae in clinical samples. As well, the TaqMan qPCR requires less labor and is easier to automate. AHL