Secondary immunodeficiency in infections

June 27, 2018 08:30 | Symptoms And Treatment
Secondary immunodeficiencies are largely expressed in parasitic infections( protozoa, helminths).Oppression of humoral immunity is possible with infections caused by plasmodia and trypanosomes, a violation of cellular immunity in schistosomiasis. The question arises about the causes of these processes, about the mechanisms that underlie immune disorders. In all likelihood, the answer can not be unambiguous. The following reasons are known:

- oppression of macrophage function( for example, with malaria);

- impaired immunoregulation( in particular, the global activity of suppressor cells in mice infected with trypanosomes);

is the mitogenic effect of parasite products( polyclonal hypergammaglobulinemia in malaria and trypanosomiasis with primary response failure);

- production of lymphocytotoxins( Fasciola hepatica, Trichinella spiralis) or suppressive factors.

In developing countries, infection plays a special role in the development of immunodeficiency.

Bacterial infections only in exceptional cases lead to secondary immunodeficiency. A detailed analysis of these disorders was performed with leprosy. A part of patients with generalized form of tuberculosis received negative results of skin tests. They reduce the proliferative activity of lymphocytes stimulated by the mitogen of PHA.With syphilis, such violations of the response of lymphocytes to mitogens can be the result of the action of circulating inhibitors. In infections caused by pneumo- and meningococci, a decrease in the response of lymphocytes to antigens and mitogens is also noted, which is associated with frequent recurrences of herpes infection. Both in the clinic and in the experimental models, the inhibition of the reaction to tuberculin in infections such as whooping cough, typhoid, scarlet fever, brucellosis and others was suppressed. Lipopolysaccharides or elements of the cytoplasm( streptococci) or enterotoxins( staphylococci) probably play a special role. Mechanisms for the development of immunodeficiency are still unclear( dysfunction of the thymus gland, suppression of the function of the monocyte-macrophage system, changes in cellular kinetics or intracellular cAMP level.) Experimental studies have shown that many endo- and exotoxins suppress the immune response if they are administered prior to antigenic stimulation and display adjuvanteffect if they are injected after the injection of the antigen

The most active effect on the immune system is caused by viral infections. Anergy to test antigens in patients in the acute period of measles, rubella, influenza, mumps, acute hepatitis is reduced. The decrease in the reactions of cellular immunity in viral infections can be the cause of recurrence of bacterial infections. In addition, measles and flu have been found to have a violation of neutrophil function.viral infections( hepatitis B, subacute sclerosing panencephalitis), researchers are trying to answer the question of whether a violation of the immune response is the cause or result of the persistence of the virus. The facts of serious consequences of intrauterine infection caused by the rubella virus( combined immunodeficiencies) are known, to a lesser extent it refers to the action of cytomegalovirus. In other cases with cytomegalovirus infection, a persistent imbalance of immunoregulatory cells was observed. Secondary immunodeficiency in AIDS is also caused by the action of the virus. The use of viral rubella, chickenpox, ECHO and herpes, poliomyelitis and smallpox viruses in the culture of lymphocytes led to inhibition of the immune response to PHA mitogen.

Mechanisms responsible for immunodeficiency in viral infections are quite diverse. We can name the most important of them:

- direct infection with the virus of lymphocytes or macrophages( for example, AIDS, EBV);

- immunosuppression mediated by virus-induced T-suppressor cells;

is a modification of lymphocyte membranes caused by a virus;blocking factors( immune complexes), lymphocytotoxic antibodies, the effect of interferon;

- interference of viral infection and differentiation( IgA deficiency due to rubella virus infection in the prenatal period.)