Diagnosis and control of acute attack of toxoplasmosis in dogs

From September to December 1997, some dog farms in Jiangsu and Anwei broke out successively with acute death, sudden acute pulmonary edema, dyspnea and foam-like fluid with blood in oral competition. According to the changes of autopsy, histopathological examination and toxicology, virology and bacteriological analysis, it was diagnosed as an acute outbreak of canine toxoplasmosis. The report is as follows.

1. The incidence of the disease: a dog farm in Nanjing jointly raised more than 100 German shepherds, another dog farm raised more than 10 German shepherds, and a dog farm in Anhui raised more than 10 wolf dogs. All three dog farms have special personnel to vaccinate rabies, canine distemper, canine parvovirus, canine infectious hepatitis and other infectious diseases every year, and the well carries out deworming according to the prescribed deworming plan. The dog has been in good condition for several years without any infectious diseases. However, from September to December 1997, 24 sick dogs showing symptoms of the disease occurred in the three dog farms, and 22 dogs died, including 15 adult dogs and 7 4-month-old dogs, with a mortality rate of 91,6%.

2. The dogs with clinical symptoms show two types of clinical symptoms: one is the sudden death of sick dogs. Eight of the 22 sick dogs died suddenly without any previous symptoms. The other is acute pulmonary edema. Among the 24 dogs, 16 dogs showed sudden shortness of breath, abdominal breathing, extreme dyspnea, foamy fluid with blood flowing from the mouth, dark red conjunctiva and filling of conjunctival vessels, and the body temperature of the diseased dogs did not change significantly at 38 ℃.

3. The autopsy changes of acute dead dogs showed scattered bleeding in the lungs, large hematoma of liver depression, dark red splenomegaly, crisp quality, knife mud, and mild gastrointestinal congestion. The autopsy changes after the death of dogs with acute pulmonary edema were pulmonary edema, trachea filled with foam-like fluid with blood, liver depression, hematoma, crisp mass, splenomegaly, dark red bleeding infarction, crisp quality, knife mud, gastrointestinal mucosal congestion and bleeding. there are a small amount of ringing water and coughing water.

4. Diagnosis and differential diagnosis

4.1 Toxicological examination was suspected to be a rodent poison poisoning disease according to the clinical symptoms of the diseased dog, but no poison was found after repeated toxicological examination of the stomach contents of the diseased dog.

4.2 histopathological examination the liver, spleen, kidney, lung and other tissue masses of dead dogs were taken for histopathological examination. The main changes were stagnation of hepatic central vein and hepatic sinusoid, red-stained edematous fluid between hepatocytes and perivascular edema. Toxoplasma gondii Tachyzoites were found in the edematous fluid. Capillary congestion in the alveolar wall, interstitial vascular edema, red blood cells, red-stained edema in the alveolar cavity and Toxoplasma gondii Tachyzoites in the alveolar cavity. Splenic pulp edema, erythrocytosis, splenic corpuscle enlargement, central necrosis and disintegration of red-stained edematous fluid.

4.3 Virological examination through virological examination of blood, serum and feces of diseased dogs, there was no canine parvovirus (hemagglutination inhibition test, fecal electron microscope), canine infectious hepatitis virus (serum neutralization test), canine distemper virus (immunofluorescence) and other viruses.

4.4 Bacteriological examination A gram-negative bacteria was found in the parenchyma organs of diseased dogs, but the pathogenicity test of dogs with pure culture was successful. According to the comprehensive analysis of the results of toxicology, virology, histopathology and bacteriology, the disease was diagnosed as acute attack of toxoplasmosis in dogs.

5. After the occurrence of the disease, we treated the dogs with clinical symptoms by intravenous injection of hypertonic grape diuretic and alcohol clear inhalation to reduce pulmonary edema, but the curative effect was not satisfactory. Only 2 of the 16 dogs with acute dyspnea survived. The dogs were screened by casein immunoassay, and the carriers were pre-treated with sulfa DB (60mB/kg weight, 2m / d, 3 times a day for 1-2 weeks). Carry out large-scale rodent control work in dog areas, cull wild cats, clean pools, change drinking water, and pay attention to the diet hygiene of dogs. After medication and other treatment, new sick dogs were not found.

6 summary and discussion

6.l Toxoplasmosis is a protozoa infection caused by Toxoplasma gondii [ToxoPlnsmn.80n]. More than 30 years ago, natural toxoplasmosis in dogs was first reported in Italy. It was also reported in other countries that most adult dogs showed recessive infection. In Japan, the infection rate of Toxoplasma gondii is 10%-30%, 30% of puppies get sick, and 50% die, mainly due to reduced resistance and reduced immunity caused by stress reactions such as malnutrition, bacterial or viral infection, cold, capture, etc. Canine toxoplasmosis was reported in China in 1937, and the prevalence of canine toxoplasmosis in police dogs has also been reported in recent years. According to the detection of toxoplasmosis in Guangdong and Guangxi by enzyme-linked immunosorbent assay, the infection rate of toxoplasmosis in police dogs is 3.33%-5.63%. However, the occurrence of acute fulminant canine toxoplasmosis has not been reported.

6.2 fulminant canine toxoplasmosis is sporadic and can be infected in both large and small dogs. All the diseased dogs found in the three farms showed discontinuous jumping morbidity and death. except for similar symptoms, the sick dogs had no regularity in the time of onset and age. This phenomenon may be related to whether the diseased dog is infected with a sufficient amount of Toxoplasma gondii trophozoites.

6.3 fulminant canine toxoplasmosis has sudden onset, severe symptoms and high mortality. Dogs with acute attack of toxoplasmosis often die suddenly or show sudden acute pulmonary edema, dyspnea and nose and mouth bleeding. He died within 48 hours after showing this symptom. The therapeutic effect of sick dogs with dyspnea is very poor. It often ends in death, and it is difficult to recover even with sulfonamides sensitive to Toxoplasma gondii. This may be because the mass reproduction of Toxoplasma gondii trophozoites has seriously damaged the normal physiological function of important organs such as lungs and livers of dogs, especially the occurrence of acute pulmonary edema, which directly causes difficulty in breathing and asphyxiates dogs to death.

6.4 the key to the prevention of this disease is to prevent dogs from coming into contact with Toxoplasma gondii trophozoites, especially to prevent the feces of feral cats and mice carrying the worm from polluting the water source. According to statistics, the acute attack of canine toxoplasmosis may be caused by a single ingestion of wildcat feces or long-term drinking of water contaminated by rat feces. The outbreak of canine toxoplasmosis in three dog farms may be an important inducing factor. Therefore, the hygiene of dog diet is very important, and preventing dogs from eating Toxoplasma gondii trophozoites is the key to effectively control the disease.