Miscellaneous Viral Diseases

Chapter 16 Miscellaneous Viral Diseases



Robert G. Sherding



INFECTIOUS CANINE HEPATITIS



Etiology


Infectious canine hepatitis (ICH) is caused by canine adenovirus type 1 (CAV-1), a virus related to but distinct from CAV-2 that causes canine infectious tracheobronchitis (kennel cough; see Chapter 12).



Incidence


Dogs, foxes, coyotes, wolves, other wild canids, and bears are susceptible to CAV-1. Because of widespread use of highly effective CAV vaccines, ICH is rare and is seen almost exclusively in unvaccinated dogs. Wild canids are a reservoir for the virus.



Transmission


CAV-1 is acquired through oronasal exposure. The virus is found in all tissues and is shed in all secretions during acute infection. It also is shed for at least 6 to 9 months in the urine after recovery. CAV-1 is highly resistant to inactivation and disinfection, thus enabling spread by fomites and possibly ectoparasites.



Pathogenesis



• After oronasal exposure, CAV-1 causes viremia and disseminates to all tissues, especially targeting hepatocytes and endothelial cells. Hepatocyte injury results in acute hepatic necrosis or chronic hepatitis.

• Endothelial injury can affect any tissue, but CAV-1 is noted particularly for its effects on corneal endothelium (corneal edema, anterior uveitis), renal glomeruli (glomerulonephritis), and vascular endothelium (disseminated intravascular coagulation [DIC]).


Clinical Signs



Peracute Infection


Acutely ill dogs become suddenly moribund and die within hours.



Acute Systemic Infection



• A 5- to 7-day course is characterized by a fever of 103 to 106°F (39.5–41°C), vomiting, diarrhea, abdominal pain, tonsillitis-pharyngitis, cervical lymphadenopathy and edema, cough (pneumonitis), and hemorrhagic diathesis (petechiae, ecchymoses, epistaxis, and melena).

• Central nervous system (CNS) signs (disorientation, depression, stupor, coma, and seizures) may occur as a result of hepatic encephalopathy, hypoglycemia, or non-suppurative encephalitis.


Ocular Infection


Ocular disease can develop during acute infection, after recovery from inapparent infection, or after modified live virus (MLV) CAV-1 vaccines (no longer commercially available). Ocular findings include the following:


• Corneal edema (cloudy cornea; also called hepatitis blue eye)

• Anterior uveitis (blepharospasm, aqueous flare, miosis)

• Secondary glaucoma


Chronic Hepatitis


In infected dogs with partial immunity, a persistent hepatic infection that causes chronic hepatitis, and hepatic fibrosis has been reported.



Diagnosis


Suspect ICH based on clinical signs in unvaccinated dogs, especially young puppies.



Routine Laboratory Evaluations


ICH may cause neutropenia/lymphopenia (early), neutrophilic leukocytosis (later), increased alanine transaminase (ALT) and alkaline phosphatase (ALP) levels, thrombocytopenia and coagulation abnormalities typical of DIC (see Chapter 23), proteinuria, and occasionally hypoglycemia. The abdomen may contain a non-septic exudate.



Definitive Diagnosis


ICH can be confirmed by serologic testing, virus isolation, immunofluorescent studies, or histopathology (centrilobular hepatic necrosis with intranuclear viral inclusions); however, a definitive diagnosis is not needed for instituting supportive treatment measures.



Treatment


Treatment is supportive until recovery from the acute stage of infection and hepatocellular regeneration can occur. This usually requires parenteral fluid therapy using potassium and dextrose-supplemented solutions (see Chapter 5), treatment for DIC using fresh plasma or whole blood transfusion (see Chapter 23), treatment for hepatic encephalopathy (see Chapter 91), and antibiotics for secondary bacterial complications such as pneumonia or pyelonephritis.



Prevention




Key Point


Vaccination is highly effective for preventing CAV-1 infection.



• MLV canine adenovirus vaccines can induce effective immunity against ICH; however, only CAV-2 vaccines are recommended. This is because CAV-2 vaccines produce highly effective immunity against both adenoviruses with minimal side effects, whereas CAV-1 vaccine viruses can localize in the kidney and produce mild nephritis and urine shedding of virus or may localize in the eyes and produce anterior uveitis (in approximately 0.4% of vaccinates). The cloudy cornea is usually transient but sometimes irreversible.

• Vaccinate puppies using CAV-2 at 6 to 8 weeks, 9 to 11 weeks, and 12 to 14 weeks of age. Give the first booster 1 year later and additional boosters every 3 years thereafter (see Chapter 7 for comprehensive vaccination recommendations).


CANINE ACIDOPHIL CELL HEPATITIS



Etiology


A transmissible form of hepatitis has been described in dogs in Great Britain. Although the etiologic agent has not been identified, evidence strongly suggests that it is a virus and that it is distinct from CAV-1 and CAV-2.



Clinical Signs


Clinical forms of the disease, which may represent stages of progression, include acute hepatitis, chronic hepatitis, cirrhosis, and occasionally hepatocellular carcinoma. Early signs, such as anorexia, vomiting, and occasional fever, are nonspecific. Later signs reflect progressive hepatic failure (ascites, hepatic encephalopathy).



Diagnosis


Laboratory findings are nonspecific and typical of those found in other types of acute and chronic liver disease. Increased serum ALT and ALP activities are the most consistent abnormalities. Diagnosis depends on liver biopsy to identify hepatitis associated with characteristic acidophil cells.



Treatment and Prevention


Specific measures for treatment and prevention are unknown; however, supportive treatment for liver failure in general and specific treatment used in other forms of hepatitis and cirrhosis may be applicable (refer to Chapter 71).



CANINE HERPESVIRUS



Etiology


Canine herpesvirus (CHV) infects only canids. Its biologic behavior is similar to herpesviruses of other species. Infected dogs remain latent carriers for life. CHV is inactivated relatively easily outside the host.



Incidence


CHV is widespread in the canine population; however, it causes clinical disease almost exclusively in newborn puppies during the first 3 weeks of life.



Transmission


Perinatal infection is acquired before, during, or soon after birth. Transmission can occur in utero, during passage through the birth canal, or by direct oronasal contact with infectious secretions from the infected mother, littermates, or fomites. Respiratory and venereal transmission may occur in adults.



Clinical Signs




Key Point


Overt clinical signs of CHV occur almost exclusively in puppies from 3 weeks before birth until 3 weeks after birth. This is manifested as a reproductive failure in infected bitches or a highly fatal systemic disease in newborn puppies.



Fetal Infection



• Reproductive failure in infected bitches results from early fetal resorption, late-term abortion, or stillbirth associated with in utero CHV infection.


Neonatal Systemic Infection



• Infection at birth until 2 to 3 weeks of age leads to viremia and virus dissemination to all tissues, resulting in a fatal generalized form of disease. The incubation period is 3 to 6 days.

• The susceptibility to this form of CHV is related to the narrow temperature range of 35°C to 36°C needed for optimal growth of CHV, which coincides with the low body temperatures and lack of febrile responsiveness found in neonates in the first week of life.

• Neonatal infection causes multifocal lesions of necrosis and hemorrhage (DIC) in many organs, including the kidneys, adrenal glands, liver, spleen, gastrointestinal tract, lungs, and CNS.

• Signs include depression, refusal to nurse, incessant crying, subnormal body temperature, yellow-green diarrhea, abdominal pain, nasal discharge, petechial hemorrhages on mucosal surfaces, skin papules, and CNS signs (coma, opisthotonus, and seizures). Nursing ceases and death usually occurs within 24 to 72 hours.

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Miscellaneous Viral Diseases

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