Diagnosis and Control Methods for Acute Onset of Toxoplasmosis in Dogs
From September to December 1997, certain kennels in Jiangsu, Anhui and other places successively experienced outbreaks of a disease characterised by acute death in dogs, sudden acute pulmonary oedema, difficulty breathing, and bloody foam-like fluid flowing from the mouth. Based on necropsy changes, histopathological examination, and toxicological, virological and bacteriological analyses, it was confirmed as an acute outbreak of canine toxoplasmosis. The report is as follows.
1. Incidence: A kennel in Nanjing kept more than 100 German Shepherd Dogs, another kennel kept more than 10 German Shepherd Dogs, and a kennel in Anhui kept more than 10 wolf dogs. All three kennels had dedicated personnel who vaccinated the dogs yearly against rabies, canine distemper, canine parvovirus, infectious canine hepatitis and other infectious diseases, and carried out deworming according to the prescribed deworming schedule. For several years the dogs' body condition had remained good, and no infectious disease had occurred. However, from September to December 1997, all three kennels successively had 24 dogs showing symptoms of this disease, of which 22 died, including 15 adult dogs and 7 four-month-old puppies, with a mortality rate of 91.6%.
2. Clinical symptoms: Affected dogs showed two types of clinical symptoms: one was sudden death of the affected dog. Of the 22 affected dogs, 8 died suddenly without any prior symptoms. The other was the acute pulmonary oedema type. Of the 24 affected dogs, 16 showed sudden tachypnoea, abdominal breathing, extreme difficulty breathing, and bloody foam-like fluid flowing from the mouth; the ocular conjunctiva was dark red, and the conjunctival blood vessels were engorged; the body temperature of the affected dogs was 38-39 degrees C, with no obvious change.
3. Necropsy changes: The necropsy changes of acutely dead affected dogs were scattered haemorrhagic spots in the lungs, congested and enlarged liver, enlarged spleen that was dark red, friable and had a knife smear, and mild congestion of the gastrointestinal tract. The post-mortem changes of affected dogs that died of acute pulmonary oedema were pulmonary oedema, the trachea filled with bloody foam-like fluid, congested and enlarged liver that was friable, enlarged spleen with dark red haemorrhagic infarcts, friable and with a knife smear, and congestion and haemorrhage of the gastrointestinal mucosa, with a small amount of fluid and foamy fluid.
4. Diagnosis and differential diagnosis
4.1 Toxicological examination: Based on the clinical symptoms of the affected dogs, poisoning by ANTU-type rodenticides was suspected, but after multiple toxicological examinations of the gastric contents of the affected dogs, no poison was found.
4.2 Histopathological examination: Tissue blocks of liver, spleen, kidney, lung and other organs from the dead affected dogs were taken for histopathological examination. The main changes were congestion of the central hepatic vein and hepatic sinuses, red-stained oedematous fluid between hepatocytes, perivascular oedema, and Toxoplasma tachyzoites found in the oedematous fluid. The alveolar wall capillaries were congested, the interstitial blood vessels were oedematous, the alveolar cavities contained red blood cells, red-stained oedematous fluid and macrophages, and Toxoplasma tachyzoites were present in the alveolar cavities. The splenic pulp was oedematous, with increased red blood cells, enlarged splenic corpuscles, and central necrosis and disintegration with red-stained oedematous fluid.
4.3 Virological examination: Through virological examination of the blood, serum and faeces of the affected dogs, no viruses such as canine parvovirus (haemagglutination inhibition test, faecal electron microscopy), infectious canine hepatitis virus (serum neutralisation test) or canine distemper virus (immunofluorescence method) were found either.
4.4 Bacteriological examination: Bacteriological examination of the parenchymal organs of the affected dogs found one strain of Gram-negative bacteria, but the pathogenicity test in dogs using the pure culture was unsuccessful. Based on a comprehensive analysis of the results of toxicological, virological, histopathological and bacteriological examinations, the disease was confirmed as an acute onset of canine toxoplasmosis.
5. Control measures: After the disease occurred, we treated the dogs showing clinical symptoms symptomatically, with intravenous hypertonic glucose for diuresis and alcohol inhalation to reduce pulmonary oedema, but the therapeutic effects were unsatisfactory; of the 16 dogs with acute difficulty breathing, only 2 survived. An enzyme-linked immunosorbent assay was used to screen the dog population, and those carrying the parasite were given sulfonamide DB (60 mg/kg body weight, 2-3 times/day, for 1-2 consecutive weeks) for preventive treatment. Large-scale rodent control was carried out in the dog areas, stray cats were culled, water pools were cleaned, drinking water was replaced, and attention was paid to the dogs' dietary hygiene. After medication and other treatments, no new affected dogs were found.
6. Summary and discussion
6.1 Toxoplasmosis is a protozoal infection caused by Toxoplasma gondii (Toxoplasma gondii). More than 30 years ago, Italy first reported natural toxoplasmosis in dogs (M06[1], 1910), and other countries have also reported it; adult dogs mostly show latent infection. In Japan, the infection rate of Toxoplasma in dogs is 10%-30%, 30% of puppies develop the disease, and 50% die, mainly because stress responses such as malnutrition, bacterial or viral infection, cold, and capture weaken resistance and lower immunity, thereby causing death in dogs. In China, canine toxoplasmosis was reported in 1937, and in recent years some have also reported the prevalence of canine toxoplasmosis in police dogs; according to enzyme-linked immunosorbent assay testing in Guangdong and Guangxi, the infection rate of toxoplasmosis in police dogs is 3.33%-5.63%, but the occurrence of acute fulminant canine toxoplasmosis has not yet been reported.
6.2 Fulminant canine toxoplasmosis is sporadic, and both large and small dogs can be infected and develop the disease. The affected dogs found in the three kennels all showed discontinuous, jumping-style onset and death; apart from showing similar symptoms, the affected dogs had no discernible pattern in terms of onset time and age. The appearance of this phenomenon may be related to whether the affected dogs were infected with a sufficient disease-causing dose of Toxoplasma trophozoites.
6.3 Fulminant canine toxoplasmosis has a sudden onset, severe symptoms and a high mortality rate. During acute onset of canine toxoplasmosis, affected dogs often die suddenly or show sudden acute pulmonary oedema, difficulty breathing, and bleeding from the mouth and nose. Death occurs within 4-48 hours after these symptoms appear. The treatment effect for affected dogs showing symptoms of difficulty breathing is very poor. They often end in death, and even treatment with sulfonamide drugs to which canine Toxoplasma is sensitive makes recovery very difficult; this may be because the massive proliferation of Toxoplasma trophozoites has severely damaged the normal physiological functions of important organs such as the lungs and liver of the dog, especially the occurrence of acute pulmonary oedema, which directly causes difficulty breathing and leads to the dog's death by suffocation.
6.4 The key to preventing this disease is to prevent dogs from coming into contact with Toxoplasma trophozoites, and particular attention should be paid to preventing faeces of parasite-carrying stray cats and rats from contaminating water sources. According to statistics, a dog eating stray cat faeces once or drinking water contaminated by rat faeces over a long period may cause acute onset of canine toxoplasmosis. This may be an important triggering factor in the fulminant canine toxoplasmosis in the three kennels this time. Therefore, ensuring the hygiene of the dogs' diet is very important, and preventing dogs from ingesting canine Toxoplasma trophozoites is the key to effectively controlling this disease.