What is Mumps Encephalitis?
Mumps encephalitis (encephalitis with mumps) is an infectious lesion of a brain substance caused by a causative agent of mumps.
Mumps encephalitis is a rare manifestation of mumps (less than two cases per 100 thousand) (K. L. Davison et al., 2003).
Causes of Mumps Encephalitis
The causative agent of parotitis encephalitis belongs to paramyxoviruses (family Paramyxoviridae, genus Paramyxovirus). The mumps pathogen was first isolated and studied in 1934 by E. Goodpascher and K. Johnson.
Virions are polymorphic, rounded virions have a diameter of 120-300 nm. The virus contains RNA, has hemagglutinating, neuraminidase and hemolytic activity. The virus agglutinates the erythrocytes of chickens, ducks, guinea pigs, dogs, etc. In vitro, the virus is cultivated on 7-8-day-old chicken embryos and cell cultures. Primarily trypsinized cultures of kidney cells of the guinea pig, monkeys, Syrian hamster, chick embryo fibroblasts are sensitive to the virus. Laboratory animals are not sensitive to the mumps virus, only in monkeys it is possible to reproduce a disease similar to human parotiditis. The virus is unstable, inactivated when heated, with ultraviolet irradiation, when in contact with lipid solvents, 2% formalin solution, 1% lysol solution. Attenuated virus strain (L-3) is used as a live vaccine. Antigenic structure of the virus is stable. It contains antigens that can cause the formation of neutralizing and complement-binding antibodies, as well as an allergen, which can be used to form an intracutaneous test.
The source of infection is only human (patients with manifest and inapparent forms of parotitis). The patient becomes infectious 1-2 days before the onset of clinical symptoms and in the first 5 days of the disease. After the disappearance of the symptoms of the disease, the patient is not contagious. The virus is transmitted by airborne droplets, although the possibility of transmission through contaminated objects (such as toys) cannot be completely ruled out.
The susceptibility to infection is high. More often sick children. Males suffer from parotiditis 1.5 times more often than women. The incidence is characterized by pronounced seasonality (seasonality index 10). The maximum incidence occurs in March-April, the minimum – in August-September. After 1-2 years, there are periodic increases in incidence. It is found in the form of sporadic diseases and in the form of epidemic outbreaks. In institutions, outbreaks last from 70 to 10 days, giving separate waves (4–5) with intervals between them equal to the incubation period. In 80-90% of the adult population, anti-parotid antibodies can be found in the blood, which indicates a wide spread of this infection (in 25% of infected people, the infection proceeds inapparently). After the introduction of live vaccine immunization, the incidence of mumps has decreased significantly.
Pathogenesis during Mumps Encephalitis
The gateway of the infection is the mucous membrane of the upper respiratory tract (possibly the tonsils). The pathogen enters the salivary glands not through the parotid (stenon) duct, but by the hematogenous route. Viremia is an important link in the pathogenesis of mumps, which is proved by the possibility of isolating the virus from the blood already in the early stages of the disease. The virus spreads throughout the body and finds favorable conditions for reproduction (reproduction) in the glandular organs. The defeat of the nervous system and other glandular organs can occur not only after the defeat of the salivary glands, but also at the same time, earlier and even without damaging them (very rarely).
It has been established that in the lesions of the CNS, peripheral nervous system and pancreas, immune mechanisms play a certain role: a decrease in the number of T-cells, a weak primary immune response with a low IgM titer, a decrease in the content of IgA and IgG.
When parotitis in the body produces specific antibodies (neutralizing, complement-binding, etc.), detectable for several years, and develops an allergic restructuring of the body, continuing for a very long time (perhaps throughout life).
Symptoms of Mumps Encephalitis
Encephalitis with mumps can develop in parallel with the defeat of the salivary glands, and after one or two weeks from the onset of the disease, indicating a different mechanism of its development. The clinical picture is characterized by high fever, severe condition of patients, lethargy, impaired consciousness, agitation, clonic-tonic convulsions, focal symptoms. Despite the severity of the lesion, mortality in parotid encephalitis is from 0.5 to 2.3%.
In some patients after suffering encephalitis, long-term asthenic syndrome and neurological disorders can persist.
Mumps encephalitis is the most common cause of changes in the central nervous system, including behavioral disorders, headaches, convulsions, hearing impairment (most often it is unilateral deafness) and vision. At least seven cases of stenosis of the cerebral aqueduct were reported, followed by the formation of hydrocephalus, which appeared to be a late complication of mumps encephalitis. However, this relationship has remained unproven.
In children under 3 years of age, the consequence of severe parotitic encephalitis is mental retardation, at an older age – pathocharacterological reactions and psychopathic behavior.
Diagnosis of Mumps Encephalitis
Diagnosis of parotitis encephalitis is based on clinical and epidemiological data and in typical cases does not present great difficulties.
Of the laboratory methods for confirming the diagnosis, the most evidential is the isolation of the mumps virus from the blood, swabs from the pharynx, secretion of the parotid salivary gland, cerebrospinal fluid and urine. Immunofluorescent methods can detect viruses on cell culture after 2-3 days (with a standard study method – only after 6 days). Immunofluorescence method allows to detect viral antigen directly in the cells of the nasopharynx, which makes it possible to get the answer most quickly. Serological methods allow to detect an increase in antibody titer only after 1-3 weeks from the onset of the disease, for which various methods are used.
The most informative is the enzyme-linked immunosorbent assay, later results are obtained using more simple reactions (RSK and RTGA). Examine paired sera; the first is taken at the beginning of the disease, the second – after 2-4 weeks. Diagnostic is the increase in titer 4 times or more. An intradermal test with an antigen (allergen) can be used. Diagnostic is the transition from negative to positive. If the skin test is positive already in the first days of the disease, then this indicates that the person has previously suffered a parotitis.
Treatment of Mumps Encephalitis
With encephalitis apply a course of treatment with corticosteroids. Some importance is moderate dehydration therapy.
Prevention of Mumps Encephalitis
For specific prophylaxis, live mumps vaccine from the attenuated Leningrad-3 (L-3) strain is used. Children aged from 15 months to 7 years who have not previously had mumps have been scheduled for prophylactic vaccination against mumps. If the medical history is unreliable, the child must be vaccinated. Vaccination is carried out once, subcutaneous or intradermal method. In the subcutaneous method, 0.5 ml of the diluted vaccine is administered (one vaccination dose is dissolved in 0.5 ml of the solvent applied to the preparation). With the intradermal method, the vaccine is injected in a volume of 0.1 ml with a needleless injector; in this case, one vaccination dose is diluted in 0.1 ml of solvent. Children who have been in contact with a sick parotitis who have not been ill and have not previously been vaccinated, can immediately be vaccinated with parotitis vaccine (in the absence of clinical contraindications).