Experimental Infection Of Dogs Research Articles

Elevation of the concentration of acute phase proteins in dogs infected with Trypanosoma brucei

Plasma concentrations of the acute phase proteins (APP), C-reactive protein (CRP) and haptoglobin (Hp), increased markedly following experimental infection of dogs with Trypanosoma brucei. The highest concentrations of CRP were observed immediately after peaks of parasitaemia. Treatment with curative doses of the trypanocidal drug suramin caused a rapid decrease in CRP. Relapse infections after subcurative treatment were followed by a reappearance of high plasma CRP concentrations. Haptoglobin remained elevated during the course of the disease. Curative treatment with suramin caused a gradual but slow decrease in Hp while subcurative treatment caused no significant changes. Thus, the estimation of CRP was useful in determining the presence of active infection and the success of chemotherapy. High Hp levels in severely anaemic dogs indicated that intravascular haemolysis does not contribute significantly to the anaemia associated with T. brucei infections in dogs. These conclusions need confirmation from a larger experiment.

Experimental infection of dogs with Campylobacter jejuni.

Three groups of conventional puppies were inoculated orally with Campylobacter jejuni biotype 2 which had been isolated from the small intestine of a dog with enteritis. Mild enteric disease was observed in one group. There was superficial intestinal colonization by the organism but penetration of intestinal epithelial cells was not apparent. C jejuni was isolated from the blood and viscera of inoculated dogs which showed no histological evidence of disease.

Experimental infection of the baboon (Papio cynocephalus) with Echinococcus granulosus of camel, cattle, sheep and goat origin from Kenya.

In different areas of the world, strains of Echinococcus granulosus have been described which appear to vary in their infectivity, and laboratory primates have been used as indicators of their infectivity to man. This phenomenon was evaluated in Kenya for hydatid material of human, camel, cattle, sheep and goat origin. Viable eggs, produced by experimental infections in dogs with larval material from all the above intermediate hosts, were fed separately to four baboons (Papio cynocephalus) in each case. Baboons were autopsied between 373 and 501 days following infection and the liver, lungs, heart, spleen and kidneys were thoroughly inspected. Hydatid cysts were recovered from two baboons in each of the camel, sheep and goat groups, three baboons in the cattle group and none of the baboons in the human group. Fertile cysts were found in the cattle and goat groups and it is suggested that the baboon could be used as an experimental model for this parasite.

Observations on Echinococcus multilocularis in the definitive host.

Six dogs were found to be susceptible to experimental infections with a European isolate of Echinococcus multilocularis from southern Germany. Two cats were only poorly susceptible. Adult worms were not evenly distributed throughout the small intestine and the majority of parasites were found in the posterior region. The mode of attachment of E. multilocularis in the dog was similar to that for E. granulosus with the adult worm extending its rostellum deep within a crypt of Lieberkühn. In cats only few worms were found to have penetrated deeply between the villi. E. multilocularis was found to possess a modified group of rostellar tegumental cells, morphologically and functionally identical to those described in E. granulosus and previously referred to as the "rostellar gland". By studying development in vivo and in vitro, the time required for the production of shelled eggs was demonstrated to be only 28 days. Concurrent experimental infections in dogs with E. multilocularis and E. granulosus revealed that both species will develop together in the same host. Their development was not retarded in any way by the presence of the other and both species were able to coexist in the same area of the intestine.

COLLATERAL PULMONARY CIRCULATION IN DOGS EXPERIMENTALLY INFECTED WITH DIROFILARIA IMMITIS: ITS ANGIOGRAPHIC EVALUATION*

Collateral pulmonary circulation was evaluated angiographically 11 months after experimental infection of dogs with either 25 or 100 infective larvae of Dirofilaria immitis. In both groups, collateral pulmonary circulation developed from bronchial arteries and esophageal branches of the left gastric artery. Of the four dogs receiving 25 larvae, one had no detectable collateral circulation, one developed collateral pulmonary circulation from the bronchial arteries only, and two had collateral pulmonary circulation from the bronchial arteries and esophageal branches of the left gastric artery. Of the three dogs receiving 100 larvae, all had collateral pulmonary circulation from the bronchial arteries and the esophageal branches of the left gastric artery. Bronchial artery collateral pulmonary circulation was more extensive in the 100‐larvae dogs than in the 25‐larvae dogs. Collateral pulmonary circulation from the left gastric artery esophageal branches was similar in both dog groups. Angiographically detectable collateral pulmonary circulation developed within the first year of heaertworm infection. In some respects, the extent of collateral pulmonary circulation development was related to the severity of heartworm infection.

ウェステルマン肺吸虫人工感染犬の糞便内EPGおよびEPDの変動とその診断的意義

ウェステルマン肺吸虫人工感染犬の糞便内EPGおよびEPDの変動とその診断的意義

Experimental infection of dogs with Sarcocystis from wapiti.

Ten domestic dogs became infected with Sarcocystis when fed simple portions of heart, esophagus and diaphragm from a two-year-old female wapiti (Cervus canadensis). The prepatent period was 14 days in all exposed dogs; the patent period ranged from 8 to 20 days. Neither the 10 control dogs, nor two dogs fed sporocysts collected from the infected dogs passed sporocysts within the study period. Sporocysts averaged 16.5 by 11.1 micron in size.

Experimental infection of dogs and monkeys with two rabies serogroup viruses, Lagos bat and Mokola (IbAn 27377). Gross pathologic and histopathologic changes.

Dogs and monkeys were inoculated intracerebrally or intramuscularly with Lagos bat virus or Mokola virus, two viruses serologically and morphologically related to rabies virus. All animals inoculated intracerebrally died, but some animals inoculated intramuscularly survived. One monkey inoculated intramuscularly with Lagos bat virus survived with a hemiparesis. In both dogs and monkeys that died there was a nonsuppurative meningoencephalomyelitis and ganglionitis. Lesions were more extensive than those reported after infection with street rabies virus. Intracytoplasmic inclusions, morphologically indistinguishable from Negri bodies, were seen in the central nervous system of monkeys, but not dogs, that died. With fluorescent-antibody microscopy, granular aggregations of viral antigen were observed in the cytoplasm of many neurons in the central nervous system. In some animals, the retina and ciliary body of the eye had focal inflammatory changes.

Experimental infection of dogs and monkeys with two rabies serogroup viruses, Lagos bat and Mokola (IbAn 27377): clinical, serologic, virologic, and fluorescent-antibody studies.

Experimental infection of dogs and monkeys with two rabies serogroup viruses, Lagos bat and Mokola (IbAn 27377): clinical, serologic, virologic, and fluorescent-antibody studies.

The role of domestic animals in the epidemiology of plague. I. Experimental infection of dogs and cats.

Dogs and cats are susceptible to experimental plague. Both species demonstrate bacteremia due to Yersinia pestis, formerly known as Pasturella pestis, as a result of the infection and thus may serve as the source of an infectious blood meal for fleas. The suppurating lesions developed by the cat indicate that there may be some risk of mechanical plague infection for those handling such animals. Despite this, the risk of infection of human beings due to contact with cats and dogs infected with plague is considered minimal. For the first time it has been experimentally established that, irrespective of the mode of infection, cats and dogs develop antibodies of high titer to the specific Fraction I antigen of Y. pestis. Such antibodies persist for at least 300 days in the sera of cats and dogs. The frequency with which such specific antibodies to Y. pestis can be detected in the sera of dogs that live in epidemic and natural plague foci indicates that serologic tests of canine sera for antibody to the plague bacterium should be an integral part of every survey and surveillance program.

Experimental Infection of Dogs with Two Strains of Venezuelan Equine Encephalomyelitis Virus

Summary Dogs infected with unmodified VEE developed fever, viremia, and leukopenia. Seven of the dogs infected failed to manifest frank clinical signs of illness. The remaining three dogs became somewhat aggressive toward the other dogs and less receptive to handling; no other frank signs of illness were observed. The infection was fatal for two of the three. Microscopic examination of the brains of these two animals failed to reveal evidence of encephalitis even though virus was recovered. The attenuated strain caused an inapparent infection detectable only by serologic methods. The infection resulted in immunity to subsequent challenge with unmodified virus.

EXPERIMENTAL INFECTION OF DOGS WITH JAPANESE B ENCEPHALITIS VIRUS.

Dogs aged 20 to 210 days were inoculated intracerebrally with Japanese B encephalitis virus, G1 strain, of the 242nd to 247th mouse brain passages.

Observations on the development of Toxocara canis (Werner, 1782) in the dog.

1. Evidence from previous literature shows that puppies are commonly infected with larvae ofToxocara canisat birth and that prenatal infection can be produced by feeding embryonated eggs to pregnant bitches.2. Observations on fifty-eight dogs in Brisbane showed that all of twenty-nine puppies 1–6 months old were infected, while only three out of twenty-nine dogs over 6 months old were infected.3. In naturally infected puppies, 1–3 weeks old, it was found that at birth third-stage larvae were present in the lungs. Third-stage larvae continued to appear in the lungs for the first week of life; their length was 0·6–1·3 mm.4. Third-stage larvae were found in the stomach on the day after birth; at 3 days after birth fourth-stage larvae were found in the intestine.5. It appeared likely that the second moult occurs in puppies before birth, and that the third moult takes place at a length of 1·0–1·3 mm. in the lungs and stomach within the first week of life.6. By the beginning of the second week, fourth-stage larvae were fully grown and had commenced the fourth moult at a length of 5–7 mm.7. Throughout the second and third weeks, adults grew rapidly, reaching a length of about 67 mm. by the end of the third week, but no eggs had appeared in the faeces at this time.8. Experimental infection of mice with eggs showed that the larvae were distributed to the somatic tissues, few reaching the alimentary tract. The larvae did not progress beyond the second stage in the tissues of mice.9. Experimental infection of dogs with eggs showed that in dogs over 5 weeks old the larvae were distributed to the somatic tissues and did not reach the alimentary tract. The larvae did not progress beyond the second stage, though some of them showed signs of commencing the second moult. In contrast, 1 to 3-week-old puppies infected in the same way were found to harbour larvae in the alimentary tract. Though some of these larvae were probably derived from a naturally acquired prenatal infection, it was evident from the progress of development that the experimental infection resulted in the presence of second-stage larvae in the liver and lungs and that these larvae underwent the second moult, commenced development as third-stage larvae in the lungs, migrated into the stomach and developed to the adult stage in the intestine.10. Experimental infection of dogs and foxes with mice harbouring second-stage larvae in the tissues showed that, in some instances, development of larvae proceeded in the alimentary tract. No evidence of somatic migration was found in dogs infected in this way, but in foxes second-stage larvae were found in the lungs.11. The structure and development of the second, third and fourth stage is described in detail and found to resemble closely the development ofT. catilarvae (Sprent, 1956). Second-stage larvae from dog tissues had a length of 0·34–0·44 mm. and the second moult occurred at a length of 0·37–0·44 mm. Third-stage larvae varied in length from 0·46 to 1·36 mm., and the third moult occurred at a length of 0·98–1·3 mm. Fourth-stage larvae measured 1·2–6·3 mm., though moulting fourth-stage larvae were observed up to a length of 7·4 mm. Sexual differentiation occurred during the fourth stage and was evident at a length of about 1·5 mm.12. The migratory behaviour of the larvae ofT. canisandT. catiis compared and discussed in relation to their wide range of hosts. It is concluded that differences in migratory behaviour are adaptations to prevailing modes of nutrition and it is suggested that the somatic migration occurring in dogs is an adaptation to the non-predatory habits of this particular host.

OBSERVATIONS ON EXPERIMENTAL INFECTION OF DOGS WITH ECHINOCOCCUS

Observations on the maturity of Echinococcus granulosus adults, their longevity in situ, the physical aspects of immature, mature, and senile segments eliminated in the faeces, and on the pathogenicity of the adult worm were made during the course of experimental infection of dogs.