In adult animals, immunodeficiencies often result from virus infections, malnutrition, stress, old age, 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 suppressing the immune system of their host. 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. Feline panleukopenia, caused by a parvovirus, is characterized by a drastic and acute loss of leukocytes, as demonstrated in blood smears of infected cats. 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 infection is associated with an increased susceptibility to secondary and opportunistic infections. Acquired immunodeficiency in FeLV infection is multifactorial. Infected cats can have neutropenia, decreased synthesis of antibodies (especially to bacterial antigens), decreased cellular immunity, and reduced complement levels. FeLV also appears to suppress immunity to the feline infectious peritonitis (FIP) coronavirus and may lead to reactivation of quiescent FIP.
Simian type D retrovirus 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 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; or they may become lifelong asymptomatic carriers; or they sometimes recover fully.
Simian immunodeficiency virus is a lentivirus closely related to human immunodeficiency virus. Many species/strains of SIV exist. Their 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, and it rarely causes disease in the host African species. If infected animals are under 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 also frequent consequences of SIV infection in macaques.
Feline immunodeficiency virus 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 the 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. The virus targets lymphocytes, leading to a gradual loss of CD4+ helper T cells, which causes the widespread immunodeficiency. 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 is a lentivirus that has been isolated from cattle with persistent lymphocytosis, hemolymphadenopathy, and bovine lymphosarcoma virus-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.