Chapter 21 Toxoplasmosis and Other Systemic Protozoal Infections

The protozoa that infect dogs and cats can be classified broadly into those that disseminate and cause systemic disease and those that primarily live in the intestinal tract. This chapter describes toxoplasmosis, the most important systemic protozoal infectious disease in North America, and other emerging systemic protozoal infections—neosporosis, hepatozoonosis, and leishmaniasis. These and other systemic protozoal infections are summarized in Table 21-1, including trypanosomiasis, babesiosis, cytauxzoonosis, encephalitozoonosis, acanthamebiasis, and pneumocystosis.

Table 21-1 SYSTEMIC PROTOZOAN INFECTIONS OF THE DOG AND CAT

Protozoa that parasitize erythrocytes, such as Babesia spp. and Cytauxzoon felis, are discussed in Chapter 22. Enteric protozoal infections (coccidiosis, giardiasis, tritrichomoniasis, amebiasis, and balantidiasis) are discussed in Chapter 69.

TOXOPLASMOSIS

Etiology

Toxoplasma gondii is an obligate intracellular protozoan parasite with worldwide distribution. The feline species is the definitive host for this coccidium, but most warm-blooded animals can be infected as intermediate hosts, including dogs and humans. Only cats complete the coccidian life cycle with intestinal replication and passage of oocysts in the feces.

• Serologic surveys estimate that over 30% of cats and humans are seropositive and presumed infected.

• Seroprevalence in cats increases with age, and it is higher in male and domestic shorthaired cats.

Routes of Transmission

Warm-blooded vertebrates can be infected by ingestion of any of the three life stages of the parasite (see the next section) or transplacentally.

Ingestion of Tissue Cysts

Cats are mainly infected through the ingestion of meat and animal tissues (carnivorism) that contain dormant Toxoplasma cysts (bradyzoites). Sources include uncooked meat (or meat scraps scavenged from garbage) or hunted prey (mice, birds).

• Ingestion of raw or undercooked meat (especially pork) is an important source of toxoplasmosis in dogs and humans.

• Ingestion of tachyzoites passed in milk can cause lactogenic infection in nursing kittens. Ingestion of tachyzoites in raw (unpasteurized) milk, especially from goats, is a rare source of infection.

Ingestion of Fecal Oocysts

Food, water, and soil contaminated with cat feces containing sporulated Toxoplasma oocysts are potentially important sources of infection for intermediate hosts such as humans, dogs, livestock, and rodents.

• Compared with carnivorous feeding, this is a relatively minor source of infection in the primary host, the cat.

• Oocysts can be transported from defecation sites in soil by cockroaches, flies, and earthworms.

Transplacental Infection

When a pregnant animal or human becomes infected during gestation, Toxoplasma tachyzoites can cross the placenta and infect the unborn fetus, resulting in severe or fatal disease (see under “Public Health Considerations”).

• For this reason, toxoplasmosis has major public health significance in humans.

• In dogs and cats, congenital toxoplasmosis is uncommon, but it is a potential cause of abortion, stillbirth, and neonatal mortality.

Stages of Infection

The three stages of Toxoplasma infection are (1) intestinal replication (cats only), (2) acute dissemination and intracellular replication, and (3) chronic tissue encystment.

Intestinal Replication and Oocyst Shedding

This is also called the sporozoite stage. When cats ingest the meat of an infected intermediate host, the encysted Toxoplasma bradyzoites are liberated by the cat’s digestive enzymes and invade the intestinal epithelial cells. Replication within the intestinal epithelium results in fecal excretion of millions of oocysts beginning 3 to 10 days after exposure and continuing for 1 to 3 weeks. Except for occasional transient diarrhea, clinical signs are usually absent until after oocyst shedding is over and the cat enters the next stage of infection.

• Infection by oocyst ingestion is a less important source in cats, but when it does occur, subsequent shedding of oocysts is delayed for 3 weeks or more and is much less pronounced.

• Excreted oocysts are oval-shaped, 10 × 12 μm in size, and unsporulated (uninfective). To become infectious, oocysts first must sporulate, which takes 1 to 5 days in the environment.

• These sporulated oocysts are environmentally resistant and can remain infectious in the environment for months to years.

Key Point

Intestinal replication and fecal excretion of Toxoplasma oocysts, which can contaminate soil, water, and food and can infect other animals, only occurs in cats, the definitive host.

• Intestinal immunity lasting up to 6 years after the first exposure prevents significant oocyst production upon reinfection.

Dissemination and Intracellular Replication

This is also called the tachyzoite stage. Simultaneous with intestinal replication in cats, or after infection by ingestion or transplacental transfer in non-feline species, Toxoplasma disseminates to extraintestinal tissues via blood and lymph. These rapidly multiplying tachyzoite forms can parasitize almost any cell in any tissue. The tachyzoites eventually rupture and destroy infected cells, releasing organisms to infect new cells and thus producing foci of necrosis and inflammation.

• In a small percentage of animals, these lesions become extensive enough to cause overt clinical disease, with the signs dependent on which tissues are damaged most severely.

• In most animals, this rapid replication stage is brief, and, as immunity develops and before signs occur, aggregates of these organisms encyst and become dormant.

Chronic Tissue Encystment

This is also called the bradyzoite stage. Coincident with the onset of immunity, slowly multiplying bradyzoite forms develop and form large (10 to 50 μm) tissue cysts, especially in muscle, brain, and visceral organs.

• There is minimal host response to these cysts, and they can persist in this dormant form for the life of the chronic carrier animal.

• Encysted Toxoplasma usually do not cause any clinical signs except in rare instances when cysts rupture within the central nervous system (CNS) or eye or when the infection is reactivated to an acute stage because of loss of host immune competence.

Key Point

In carnivores such as the cat, the principal source of infection is ingestion of Toxoplasma organisms encysted in the meat of chronically infected food-producing animals, small mammals, and birds.

Clinical Signs

Clinical toxoplasmosis is recognized more frequently in cats than in dogs, but the spectrum of signs is similar for both species. Clinical signs depend on the location and extent of tissue damage that results from extraintestinal dissemination and rapid intracellular replication of tachyzoites. The most commonly affected organs are lung, eyes, liver, and pancreas, as well as CNS and skeletal muscle. Organ-specific clinical signs are usually accompanied by anorexia, depression, and fever (often >104°F and unresponsive to antibiotics).

• Clinical signs can occur at the time of initial infection (acute or primary toxoplasmosis) or from reactivation of encysted infection (chronic or secondary toxoplasmosis) caused by an underlying immunosuppressive condition.

• Clinical toxoplasmosis is most severe and often fatal in neonatal kittens infected transplacentally or through milk.

Key Point

Most animals with toxoplasmosis are asymptomatic and have only serologic evidence of infection. Up to 30% of cats in the United States have Toxoplasma antibody titers and are presumed infected, with the highest prevalence in free-roaming and feral cats that hunt for their food.

Ocular Signs

Ocular toxoplasmosis (uveitis) is one of the most common forms of the disease. Blindness may result.

• Anterior uveitis causes aqueous flare, keratic precipitates, hypopyon, glaucoma, and lens luxation (see Chapter 136).

• Chorioretinitis causes retinal detachment, hyporeflective lesions in the tapetal fundus, and white fluffy infiltrates in the non-tapetum (see Chapter 138).

Respiratory Signs

Acute necrotizing interstitial and alveolar pneumonia is common and can cause progressive dyspnea.

Neuromuscular Signs

• Encephalomyelitis can cause behavior changes, seizures, ataxia, circling, tremors, paresis or paralysis, and cranial nerve deficits, depending on location of the lesions within the CNS.

• Myositis can cause hyperesthesia, stiff gait, muscle atrophy, and weakness.

Hepatic and Digestive Tract Signs

• Diffuse necrotizing hepatitis and cholangiohepatitis can cause anorexia, vomiting, diarrhea, jaundice, and ascites.

• Pancreatitis can cause anorexia, vomiting, abdominal pain, and jaundice.

• Enterocolitis can cause vomiting and diarrhea.

• Mesenteric lymphadenitis can cause palpable abdominal lymph nodes.

Cardiac Signs

Myocarditis can cause cardiac arrhythmias, sudden death, or heart failure.

Reproductive Signs

Transplacental infection can cause birth of stillborn kittens or kittens that die of neonatal toxoplasmosis of the lung, liver, and CNS.

Laboratory and Radiographic Findings

Abnormalities found on routine diagnostics are varied and nonspecific.

Hematology and Serum Chemistries

• Hematologic findings are variable and may include leukopenia with degenerative left shift (in acute disease) or neutrophilic leukocytosis, mild non-regenerative anemia, lymphocytosis, or eosinophilia.

• Hepatitis can cause elevated serum bilirubin, liver enzymes, and bile acids.

• Pancreatitis can cause increased pancreatic lipase immunoreactivity in cats or serum amylase and lipase dogs.

• Myositis can cause elevated muscle enzymes (e.g., creatine kinase [CK] and aspartate aminotransferase [AST]).

Radiography

• Pulmonary toxoplasmosis can cause generalized coalescing, patchy alveolar and interstitial lung infiltrates, and mild pleural effusion.

• Involvement of abdominal viscera can cause peritoneal effusion and hepatomegaly.

Cerebrospinal Fluid Analysis

• Cerebrospinal fluid (CSF) protein may be normal or increased.

• CSF nucleated cell count is usually mildly increased with a predominance of small mononuclear cells.

• CSF can also be evaluated by serology and polymerase chain reaction (PCR) (see the next section).

Key Point

Clinical toxoplasmosis can be an opportunistic disease associated with immunosuppression; thus, consider underlying concurrent infections such as feline immunodeficiency virus, feline leukemia virus, and feline infectious peritonitis in cats and canine distemper in dogs. Immunosuppressive drugs (glucocorticoids, cyclosporine, or antitumor therapy) may also predispose to clinical toxoplasmosis.

Diagnosis

The diagnosis of clinical toxoplasmosis is usually based on the combination of clinical findings and serologic and PCR testing of blood, CSF, and aqueous humor. PCR assays and serologic tests for immunoglobulin M and G (IgM and IgG) are available to the practicing veterinarian through the Veterinary Diagnostic Laboratory (College of Veterinary Medicine, Colorado State University, Fort Collins, CO 80523) and other reference labs.

• Visual identification of tachyzoites in cytology or biopsy specimens is only possible in a small fraction of the animals with toxoplasmosis, but in those cases it establishes a definitive diagnosis.

• Visual identification of T. gondii oocysts in the feces of clinically healthy cats is possible during the brief intestinal replication stage, but this is not useful for diagnosis of clinical toxoplasmosis.

Serology

Enzyme-linked immunosorbent assay (ELISA) methods are generally most reliable for determining Toxoplasma-specific antibody titers. Positive IgG and IgM antibody titers document previous or current infection. The IgM titer reflects the early immune response and has the best correlation with clinically active toxoplasmosis.

Key Point

The presence of antibodies against T. gondii indicates previous or current infection but does not prove clinical disease as a result of infection; thus, only use serology in conjunction with other clinical information.

Immunoglobulin M Antibody Titer

The IgM titer rises initially 1 to 2 weeks after exposure, typically coinciding with the onset of signs; it peaks after 3 to 6 weeks and dissipates by 12 weeks in most cats, thus paralleling clinical disease activity.

• Interpretation: IgM titer ≥ 1:64 suggests active or recent infection.

• The IgM titer may persist up to 1 year in some cats when there is reactivation of chronic infection or delayed antibody class shift from IgM to IgG caused by concurrent feline immunodeficiency virus infection or glucocorticoid therapy.

Key Point

The serum IgM Toxoplasma antibody titer is the serologic test of choice for presumptive diagnosis of active or recent infection.

Immunoglobulin G Antibody Titer

The IgG titer rises initially 2 to 4 weeks after exposure and persists for years to life; thus, a single positive IgG titer does not distinguish previous infection from current active infection.

• Interpretation: A fourfold rise in the IgG titer in paired specimens over a 2- to 3-week period is indicative of active infection. Both specimens must be measured together in the same test run to avoid assay variation.

Key Point

A single, high serum IgG Toxoplasma antibody titer is not diagnostic of active infection, no matter how high the titer level.

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