Canine tungiasis: High prevalence in a tourist region in Bahia state, Brazil.

Tungiasis is a parasitic skin disease neglected by authorities, health professionals, and the general population. Its occurrence is significantly associated with poverty. A cross-sectional study was conducted to describe the prevalence of tungiasis, associated clinical signs and risk factors of the canine population at a tourist site in the city of Ilhéus, Bahia (northeast Brazil). All village households were visited and dogs inspected after authorization by owners. A semi-structured questionnaire was administered. Of the 114 dogs included in the study, 71 (62.3%) were infested; all of them had lesions on their pads. An ectopic lesion on the nose was observed in one dog (1.4%). The number of manipulated lesions outnumbered the number of vital and avital lesions with an average of 88.3%. Edema (95.8%) and hyperkeratosis (85.9%) were the most prevalent clinical signs. Behavioral disorders such as excessive licking (6/71; 8.5%), disobedience (1/71; 1.4%) and prostration (2/71; 2.8%) were reported. In the multi-variate analysis, semi-restricted condition of the dogs (adjusted OR=8.58; 95% CI=2.47-29.76) and the presence of sand on the compound (adjusted OR=14.23, 95% CI=2.88-70.28) were significantly associated with infestation. We concluded that, infestation with Tunga spp. is highly endemic in the canine population of the village. The low level of restrictions on dogs and the presence of sand in areas most frequented by the animals are perpetuating factors of infestation in the community, subject to integrated and multidisciplinary intervention measures.

[Leishmania infantum induced bone lesions in a dog]. / Leishmania-infantum-bedingte Knochenläsionen bei einem Hund.

A 3-year-old Labrador Retriever originating from Spain was presented with a left-sided hind limb lameness for several months. The orthopedic examination revealed a pain response when palpating the left tarsal joint. Radiographic and computed tomographic studies showed polyostotic, aggressive osteolytic bone lesions with mild erosive arthritis. The diagnosis of canine leishmaniasis was confirmed by bone biopsy and the detection of the pathogen by PCR. Three weeks after initiation of therapy with allopurinol, the dog presented no signs of lameness. Eight months after start of therapy, radiographic examination revealed moderate regression of the osteolytic bone lesions.

Chagas disease in a Texan horse with neurologic deficits.

A 10-year-old Quarter Horse gelding presented to the Texas A&M University Veterinary Teaching Hospital with a six month-history of ataxia and lameness in the hind limbs. The horse was treated presumptively for equine protozoal myeloencephalitis (EPM) based on clinical signs but was ultimately euthanized after its condition worsened. Gross lesions were limited to a small area of reddening in the gray matter of the thoracic spinal cord. Histologically, trypanosome amastigotes morphologically similar to Trypanosoma cruzi, the agent of Chagas disease in humans and dogs, were sporadically detected within segments of the thoracic spinal cord surrounded by mild lymphoplasmacytic inflammation. Ancillary testing for Sarcocystis neurona, Neospora spp., Toxoplasma gondii and Leishmania spp. was negative. Conventional and real time polymerase chain reaction (PCR) of affected paraffin embedded spinal cord were positive for T. cruzi, and sequencing of the amplified T. cruzi satellite DNA PCR fragment from the horse was homologous with various clones of T. cruzi in GenBank. While canine Chagas disease cases have been widely reported in southern Texas, this is the first report of clinical T. cruzi infection in an equid with demonstrable amastigotes in the spinal cord. In contrast to previous instances of Chagas disease in the central nervous system (CNS) of dogs and humans, no inflammation or T. cruzi amastigotes were detected in the heart of the horse. Based on clinical signs, there is a potential for misdiagnosis of Chagas disease with other infectious diseases that affect the equine CNS. T. cruzi should be considered as a differential diagnosis in horses with neurologic clinical signs and histologic evidence of meningomyelitis that originate in areas where Chagas disease is present. The prevalence of T. cruzi in horses and the role of equids in the parasite life cycle require further study.

[Monoxenous and heteroxenous parasites of fish manipulate behavior of their hosts in different ways].

Adaptive host manipulation hypothesis is usually supported by case studies on trophically transmitted heteroxenous endoparasites. Trematodes and cestodes are among efficient manipulators of fish, their common intermediate hosts. In this review paper, new data on modifications of host fish behavior caused by monoxenous ectoparasitic crustaceans are provided together with a review of effects caused by heteroxenous parasites. Differences in modifications of host behavior caused by heteroxenous and monoxenous parasites are discussed. Manipulation by heteroxenous parasites enhances availability of infected fish to predators--definitive hosts of the parasites. Fine-tuned synchronization of modified anti-predator behavior with a certain phase of the trematode Diplostomum spathaceum development in the eyes of fish, their second intermediate host, was shown. Modifications of behavior are habitat specific. When juvenile salmonids are in the open water, parasites impair their cooperative anti-predator behavior; in territorial bottom-dwelling salmonids, individual defense behavior such as sheltering is the main target of manipulation. It was shown that monoxenous ectoparasitic crustaceans Argulus spp. decreased motor activity, aggressiveness and increased shoal cohesiveness of infected fish. Such a behavior facilitates host and mate searching in these parasites, which often change their hosts, especially during reproduction. Reviewed experimental data suggest that heteroxenous parasites manipulate their host mainly through impaired defense behavior, e.g. impairing shoaling in fish. Alternatively, monoxenous parasites facilitate shoaling that is profitable for both parasites and hosts. Coordination of modified host behavior with the parasite life cycle, both temporal and spatial, is the most convincing criterion of the adaptive value of host manipulation.

Proliferative sparganosis in a dog.

CASE DESCRIPTION: A 21-month-old spayed female Border Collie was examined because of progressive right forelimb lameness, signs of pain, and subcutaneous edema. The dog lived in a fenced yard in Tampa, Fla, that contained a small area of marshy terrain. CLINICAL FINDINGS: The subcutis and intermuscular fascia contained multiple cystic cavities filled with larval cestodes (plerocercoids or spargana) and cloudy red fluid. Parasites were identified morphologically and by DNA sequence analysis as pseudophyllidean cestodes, most likely Sparganum proliferum. The dog developed a progressively worsening fever, dyspnea, mature neutrophilia, and hypoproteinemia. Septic pleuritis and peritonitis complicated the later stages of the disease. TREATMENT AND OUTCOME: Treatment with praziquantel, fenbendazole, and nitazoxanide failed to control the proliferation and dissemination of larval cestodes. The dog was euthanatized after 133 days of treatment. At necropsy, numerous parasitic tissue cysts were present in the subcutis and intermuscular fascia; these cysts were most abundant in the soft tissues of the forelimbs and cervical musculature. The pleural and peritoneal cavities contained multiple larval cestodes and were characterized by neutrophilic inflammation and secondary bacterial infection. CLINICAL RELEVANCE: Findings indicated that clinical signs associated with proliferative sparganosis in dogs may be rapidly progressive and that the condition may be refractory to antiparasitic treatment. Veterinarians should be aware of this zoonotic, water-borne agent.

Intraarticular Dirofilaria immitis microfilariae in two dogs.

Dirofilaria immitis microfilariae were found in the synovial fluid of two dogs. One dog had clinical and cytological evidence of polyarthritis at the time of presentation. The second dog presented with severe effusion in a single joint and was later diagnosed with synovial sarcoma of the affected joint. These patients were not protected with heartworm prophylaxis and lived in heartworm endemic areas. Though there is documentation of D. immitis microfilaria in the synovial fluid of several clinically normal research dogs with cytologically normal synovial fluid, to our knowledge these are the first documented cases of intraarticular microfilaria in a dog with cytologically confirmed polyarthritis. Based on these unique cases, D. immitis infection should be considered a differential diagnosis in patients with polyarthropathies. Interpretive caution must be used when intraarticular microfilaria are present, as concurrent etiologies may also be present.

Clinical and radiographic study of bone and joint lesions in 26 dogs with leishmaniasis.

Twenty-six dogs with parasitologically confirmed leishmaniasis and abnormalities of gait were studied to determine the most common radiological patterns of bone and joint lesions. The clinical findings included either lameness, joint pain and crepitation, soft tissue swelling and/or muscle atrophy. Bone lesions were observed radiographically in 12 of the 26 dogs; the radius and ulna were affected in seven, the tibia in six and the femur in six. Joint lesions were observed radiographically in 15 of the 26 dogs; the carpus and stifle were affected in all 15, and the tarsus in nine. There was a tendency for the bones and joints to be affected bilaterally. The radiographic patterns observed were different in the long bones and the joints. In the long bones, the most common pattern was periosteal and intramedullary proliferation, involving the diaphyses and related to the nutrient foramen; in the joints, two patterns, either non-erosive or erosive polyarthritis with soft-tissue swelling, were observed. The changes observed in the synovial fluid were associated in most cases with osteolytic lesions. However, Leishmania organisms were identified in the synovial fluid from joints without bony radiographic changes.

[Neospora caninum as a cause of lameness symptoms in young dogs]. / Neospora caninum als oorzaak van verlammings-verschijnselen bij jonge honden.

At the age of three weeks, two Labrador retriever puppies, out of a litter of nine, suffered from diarrhoea and muscular weakness. One puppy died within two days. The other was killed after a tetraparalysis had developed. Two weeks later a third puppy was killed because of a paretic hind leg. At the age of five months another dog had to be euthanized because of progressive hind limb ataxia. Pathological examination revealed polyradiculoneuritis, multifocal encephalomyelitis and polymyositis. In the lesions, particularly in the nerve roots, free and clustered protozoal tachyzoites were found. In the central nervous system tissue cysts were seen. By use of immunohistochemistry the protozoal organisms were identified as Neospora caninum, a newly recognized protozoan in the dog. Fresh bovine heart, that had been fed to the puppies, is regarded as the possible source of infection.

Pre-erythrocytic development and associated host responses to Haemoproteus meleagridis (Haemosporina: Haemoproteidae) in experimentally infected domestic turkeys.

Two generations of pre-erythrocytic schizogony occurred in skeletal and cardiac muscle of domestic turkeys infected with sporozoites of Haemoproteus meleagridis. First generation schizonts reached maturity approximately five days post-inoculation (DPI) and developed in capillary endothelial cells and myofibroblasts. The schizonts ranged from 12 to 20 microns in diameter and produced long (5-6 microns), slender merozoites. Early second generation schizonts were first detected in capillary endothelial cells between 5 and 8 DPI. They were cylindrical and ranged in size from 5 to 8 microns in diameter and up to 28 microns in length. Second generation schizonts which reached maturity by 17 DPI were surrounded by a thick, hyaline wall and were packed with numerous spherical merozoites less than 1 micron in diameter. Mature megaloschizonts were fusiform, ranged from 30 to 113 microns in diameter, and extended as much as 465 microns along the long axis of muscle fibers. Merozoites developed as buds from cytomeres that formed between 8 and 14 DPI. Infected turkeys developed a moderate to severe myositis within 5 DPI and were lame in one or both legs. The myositis was associated with the necrosis of scattered groups of muscle fibers. Muscle fibers surrounding mature megaloschizonts were swollen and hyaline. Megaloschizonts were surrounded occasionally by fibroblasts and infiltrates of mononuclear cells. The morphology and site of development of mature megaloschizonts of Haemoproteus meleagridis are contrasted with those of other avian haemosporidians.