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. This 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 postrecovery period.
Feline Leukemia Virus (FeLV)
FeLV is associated with an increased susceptibility to 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 reduced complement levels. Immune responses to FeLV infection also appear to suppress immunity to the feline infectious peritonitis (FIP) coronavirus and may lead to reactivation of quiescent FIP. (Also 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. Affected macaques may either die within several months with fever, lymphadenopathy, and opportunistic infections of the CNS, respiratory tract, and intestines; become lifelong asymptomatic carriers; or sometimes recover fully.
Simian Immunodeficiency Virus (SIV)
This lentivirus is closely 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 a result of bites or 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 biting is the principal mode of transmission. As a result, free-roaming, male, and aged cats are at greatest risk of infection. FIV infection is uncommon in closed purebred catteries. After infection, there is a transient fever, lymphadenopathy, and neutropenia. Most cats then recover and appear to be clinically 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 has been isolated from cattle with persistent lymphocytosis, hemolymphadenopathy, and BLV-negative lymphosarcomas. The overall prevalence in North American cattle appears to be ~1%, although in some herds it may be as much as 15%. The virus does not appear to be pathogenic.
Last full review/revision September 2013 by Ian Tizard, BVMS, PhD, DACVM