Page 1548 - Small Animal Internal Medicine, 6th Edition

1520 PART XIV Infectious Diseases

imidacloprid/50% permethrin may lessen transmission in have been detected (Bresciani et al., 2007), but clinical
sandfly-endemic areas (Otranto et al., 2007). In one study, disease in naturally infected cats has not been reported. N.
VetBooks.ir the authors suggested that 65% permethrin applied every 2 caninum seropositive, nondomestic felids also have been
reported (Spencer et al., 2003; Sedlák et al., 2014). Neospora
to 3 weeks would be efficacious (Molina et al., 2012). Many
vaccines have been studied and are available for use with
result of abortion in cattle. Strategies for control of the infec-
dogs in some countries (Dantas-Torres, 2006; Fernández caninum infection can lead to great economic losses as a
Cotrina, et al., 2018; Palatnik-de-Sousa, 2012). For blood tion in cattle have been reviewed (Dubey et al., 2007a).
donor programs, high-risk breeds (e.g., Foxhounds) or dogs
from endemic areas should be screened for Leishmania spp. Clinical Features
infection by serology or PCR assays, and positive dogs Ascending paralysis with hyperextension of the hindlimbs in
should be excluded from the program (Wardrop et al., 2016). congenitally infected puppies is the most common clinical
manifestation of the disease. Muscle atrophy occurs in many
cases. Polymyositis and multifocal CNS disease can occur
NEOSPOROSIS alone or in combination. Cerebral ataxia and atrophy is a
recently recognized clinical syndrome associated with neo-
Etiology and Epidemiology sporosis (Garosi et al., 2010). Clinical signs can be evident
Neospora caninum is a coccidian previously confused with soon after birth or may be delayed for several weeks. Neo-
Toxoplasma gondii because of similar morphology. The natal death is common. Although disease tends to be most
sexual cycle is completed in the gastrointestinal tract of severe in congenitally infected puppies, dogs as old as 15
canids and results in the passage of oocysts in feces. Oocyst years have been clinically affected. In one dog presented
shedding can continue for several months in some dogs primarily for respiratory disease, cough was the principal
(McGarry et al., 2003). Sporozoites develop in oocysts within sign. Myocarditis, dysphagia, ulcerative dermatitis, pneumo-
24 hours of passage. Tachyzoites (rapidly dividing stage) and nia, and hepatitis occur in some dogs. Whether clinical
tissue cysts containing hundreds of bradyzoites (slowly disease in older dogs is from acute, primary infection or
dividing stage) are the other two life stages. In one study, exacerbation of chronic infection is unknown. Administra-
dogs fed sporulated oocysts were infected and seroconverted tion of glucocorticoids with or without cyclosporine may
but did not shed oocysts (Bandini et al., 2011). Dogs are activate bradyzoites in tissue cysts, resulting in clinical
infected by ingestion of bradyzoites but not tachyzoites. illness. Disease is caused by intracellular replication of N.
Infection has been documented after ingestion of a number caninum tachyzoites. Infection of CNS structures generally
of different infected bovine tissues. Dogs can also become causes mononuclear cell infiltrates, which suggests an
infected from ingesting intermediate hosts such as white- immune-mediated component to the pathogenesis of disease.
tailed deer, and the organism has been detected in the tissues Intact tissue cysts in neural structures are generally not asso-
of free-ranging chickens (Gondim et al., 2004; Gonçalves ciated with inflammation, but ruptured tissue cysts induce
et al., 2012). Thus free-roaming dogs appear to be at increased inflammation. Untreated disease generally results in death.
risk of infection. Transplacental infection has been well doc-
umented; dams that give birth to infected offspring can Diagnosis
repeat transplacental infection during subsequent pregnan- Hematologic and biochemical findings are nonspecific.
cies. Because repeated transplacental infections occur, Myositis commonly results in increased creatine kinase and
puppies from a bitch who previously birthed infected puppies aspartate aminotransferase activities. Cerebrospinal fluid
are at an increased risk. Canine neosporosis has been (CSF) abnormalities include increased protein concentration
reported in many countries around the world. Seropreva- (20-50 mg/dL) and a mild, mixed pleocytosis (10-50 cells/µL)
lence of infection has varied from 0% to 100% depending on consisting of monocytes, lymphocytes, neutrophils, and,
the country and lifestyle of the dog (Dubey et al., 2007a). In rarely, eosinophils. Interstitial and alveolar patterns can be
one paper from Australia, the canine prevalence rate noted on thoracic radiographs. Magnetic resonance imaging
increased over a 20-year period (Sloan et al., 2017). Oocysts of seven dogs with cerebellar disease showed marked bilater-
are rarely reported in fecal surveys; in one study of 24,677 ally symmetric cerebellar atrophy surrounded by an area
dog samples, oocysts consistent with N. caninum were T2-weighted hyperintense and T1-weighted hypointense
detected in 0.3% (Barutzki and Schaper, 2011). DNA of N. signal (Garosi et al., 2010).
caninum has been amplified from feces of coyotes as well Definitive diagnosis is based on demonstration of the
(Klein et al., 2018). The pathogenesis of the disease is pri- organism in CSF or tissues. Tachyzoites are rarely identified
marily related to the intracellular replication of tachyzoites. on cytologic examination of CSF, imprints of dermatologic
Although organism replication occurs in many tissues, lesions, and bronchoalveolar lavage. Mixed inflammation
including the lungs, in dogs clinical illness is primarily neu- with neutrophils, lymphocytes, eosinophils, plasma cells,
romuscular. Administration of glucocorticoids may activate macrophages, and tachyzoites was noted on transthoracic
bradyzoites in tissue cysts, resulting in clinical illness. aspirate of one dog with lung disease. N. caninum tissue cysts
Encephalomyelitis and myositis develop in experimen- have a wall thicker than 1 µm; T. gondii tissue cysts have a
tally infected kittens, and seropositive, naturally exposed cats wall thinner than 1 µm (Fig. 98.4). Oocysts can be detected