Nervous system: from adaptation to exhaustion
Upon pathogen invasion, the nervous system responds with a stress reaction aimed at mobilizing resources.
- Adaptation: the body attempts to localize the infection and normalize functions.
- Intoxication: with massive toxin exposure, the activation phase is replaced by profound CNS depression.
- Neurotrophic disorders: specific lesions (e.g., in botulism) lead to organ dysfunction.
Central mechanisms also affect the respiratory center, suppressing its activity, which, combined with peripheral lung damage, worsens the patient's condition.
Immune system: surveillance failure
Normally, immunity aims at pathogen elimination, but pathological conditions frequently arise during infection:
- Allergy: most commonly type III (immune complex), occurring when antigens are in excess.
- Immune autoaggression: develops due to the modification of self-antigens, their mimicry of microbial antigens, or the integration of viral DNA into the genome.
- Immunodeficiencies: usually transitory in nature, but become persistent in HIV infection, blocking the immune response and promoting the development of pathological tolerance.
Systemic consequences
The infectious process is not limited to the lesion site. Toxins and metabolic disorders cause:
| System | Typical disorders |
|---|---|
| Cardiovascular | Arrhythmias, heart failure, microcirculation disorders |
| Excretory | Renal dysfunction |
| Digestive | Gastrointestinal and hepatic dysfunction |
Briefly: answers to topical questions
What are the mechanisms underlying the development of pathological immunological tolerance in infections?
The mechanisms of pathological immunological tolerance include hyporegenerative processes and impaired recognition of foreign antigens.
- Hyporegenerative mechanism — inhibition of the proliferation of hematopoietic stem cells and multipotent cells.
- Immunodeficient states — general insufficiency of immune system function.
- Masking of antigenic determinants — shielding of foreign cells by antibodies, which hinders their recognition by T-killers.
- Insufficiency of T-lymphocyte costimulation — the absence of a second activation signal leads to anergy.
- Increased T-suppressor activity — excessive suppression of the immune response.
- Antigenic overload of the immune system — antigen excess depletes resources or blocks receptors.
Which pathogens are capable of integrating viral DNA into the host cell genome?
The ability to integrate viral DNA into the host cell genome is possessed by:
- DNA viruses — in the presence of circular double-stranded DNA, the viral genome attaches to the cell DNA at homology regions and integrates into a specific chromosomal locus; the process is facilitated by restrictases, endonucleases, and ligases.
- Retroviruses (e.g., HIV) — DNA is synthesized on a viral RNA template using reverse transcriptase, which is then integrated into the cell chromosome to form a provirus.
Which bacterial toxins, besides botulinum toxin, cause specific neurotrophic disorders?
In addition to botulinum toxin, nervous system damage is caused by the exotoxin of Clostridium tetani. It induces attacks of generalized tonic and tetanic seizures against the background of marked muscular hypertonus.
S-A-I-D: Stress — Adaptation — Intoxication — Depression.
Class and exam questions
Why do autoimmune reactions occur during infection?
They arise due to antigenic mimicry (similarity between microbial and host antigens), modification of self-proteins by toxins, or the integration of viral DNA into the cell genome.
Which types of allergic reactions are most characteristic of infections?
Type III hypersensitivity reactions (Gell and Coombs classification) associated with immune complex formation are most frequently observed.
Are immunodeficiencies permanent during infections?
In most cases, they are transient. The exception is diseases with direct destruction of immune cells, such as HIV/AIDS.
What else to study on this topic
- Mechanisms of immune complex glomerulonephritis formation.
- The effect of microbial toxins on ion and water metabolism.
- Specifics of local immunity disorders in intestinal infections.
- Pathophysiological differences between the prodromal period and the peak period.
- The role of hemostasis and blood rheology in the development of cardiovascular complications.
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