In adult animals, immunodeficiencies often occur as a consequence of virus infections, malnutrition, stress, or toxins. These are called secondary immunodeficiencies. Virus-induced secondary immunodeficiencies are the most important of these.
One way in which viruses survive in infected animals is by immunosuppression. For example, canine distemper virus infects and kills lymphocytes, causing a profound combined immunodeficiency in affected puppies. The infection is associated with a progressive decline in immunoglobulin levels and increased susceptibility to agents normally controlled by cellular immunity such as Pneumocystis, and Toxoplasma. Parvoviral infection in both dogs and cats also causes a profound depression in the resistance to fungal infections such as aspergillosis, mucormycosis or candidiasis in the immediate post-recovery period.
Feline Leukemia Virus (FeLV)
This infection is associated with acquired immunodeficiency and increased prevalence of secondary and opportunistic infections. Acquired immunodeficiency in FeLV infection is multifactorial. Infected cats can have deficiencies of neutrophils, decreased synthesis of antibodies (especially to bacterial antigens), decreased cellular immunity, and variable levels of complement. Immune responses to FeLV infection also appear to suppress immunity to the feline infectious peritonitis (FIP) coronavirus and so lead to reactivation of quiescent FIP. (see Feline Leukemia Virus and Related Diseases.)
Simian Type D Retrovirus
This viral infection of macaques has a similar pathogenesis to that of FeLV infection of cats but can induce even more severe immunodeficiency. Type D retrovirus infection of macaques can cause severe disease in adolescent animals in collections with large breeding groups. Affected macaques either die within several months with fever, lymphadenopathy, and opportunistic infections of the CNS, respiratory tract and intestines; become lifelong asymptomatic carriers; or recover fully.
Simian Immunodeficiency Virus (SIV)
This lentivirus is related to human immunodeficiency virus. Many strains of SIV exist in nature. The common hosts are African primates such as African green monkeys, sooty mangabeys, mandrills, baboons, and other guenons. Transmission between infected and noninfected monkeys is probably by bites and in utero exposure. SIV is not present in native populations of Asian primates. It rarely causes disease in the host African species. If infected animals are under heavy stress, as in captivity, some may develop AIDS-like disease. SIV, especially of sooty mangabey origin, causes severe disease in macaques (rhesus, stump-tail, pig-tail, bonnet, etc). The immunosuppression associated with SIV can last for weeks or years. Encephalitis (usually asymptomatic except for wasting) and lymphomas are frequent consequences of SIV infection in macaques.
Feline Immunodeficiency Virus (FIV)
FIV has been identified in domestic and wild felids. The infection is endemic in cats throughout the world. Virus is shed in the saliva, and the principal mode of transmission is through bites. Free-roaming, male, and aged cats are at the greatest risk of infection. FIV infection is uncommon in closed purebred catteries. After infection, there is a transient period of fever, lymph-adenopathy, and neutropenia. Most cats recover and appear normal for many months or years before progressive immunodeficiency develops. Cats with acquired immunodeficiency induced by FIV then develop chronic secondary and opportunistic infections of the respiratory, GI (including mouth), and urinary tracts, as well as the skin. FIV-infected cats have a higher than expected incidence of FeLV-negative lymphomas, usually of the B-cell type, and myeloproliferative disorders (neoplasia and dysplasias).
Bovine Immunodeficiency-like Virus
This lentivirus is isolated from cattle with persistent lymphocytosis and hemolymphadenopathy. It also has been isolated from cattle with BLV-negative lymphosarcomas. The overall incidence in cattle appears to be ~1%, although in some herds it may be as much as 15%. Evidence indicates that the virus is not pathogenic.
Last full review/revision July 2011 by Ian Tizard, BVMS, PhD, DACVM