What is Mumpsant pancreatitis?
Mumps pancreatitis – an infectious lesion of the pancreas, caused by the causative agent of epidemic parotiditis.
Mumps pancreatitis can be both isolated and can be combined with the defeat of other glands. The frequency of involvement in the process of the pancreas varies from 3 to 2%.
Causes of Mumps Pancreatitis
The causative agent of parotid pancreatitis 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 Mumpsant Pancreatitis
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 immune mechanisms play a role in the lesions of the central nervous system, peripheral nervous system and pancreas: 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 Mumpsant pancreatitis:
A typical clinical picture of pancreatitis is expressed in the form of severe abdominal pain mainly in the epigastric region or left hypochondrium. Pain is often shingles. Sometimes pain syndrome is so pronounced that it creates a clinical picture of “acute abdomen.” In addition to pain, nausea, vomiting, loss of appetite, and loose stools may occur. The above symptoms are observed against the background of fever, headache, and feeling unwell. Language overlaid, dryish. In severe forms, repeated vomiting is noted; pulse is speeded up, arterial pressure is lowered, a collaptoid state may develop.
Symptoms of Mumps Pancreatitis
A typical clinical picture of pancreatitis is expressed in the form of severe abdominal pain mainly in the epigastric region or left hypochondrium. Pain is often shingles. Sometimes pain syndrome is so pronounced that it creates a clinical picture of “acute abdomen.” In addition to pain, nausea, vomiting, loss of appetite, and loose stools may occur. The above symptoms are observed against the background of fever, headache, and feeling unwell. Language overlaid, dryish. In severe forms, repeated vomiting is noted; pulse is speeded up, arterial pressure is lowered, a collaptoid state may develop.
For parotid pancreatitis favorable. Typically, after 10-12 days, the clinical symptoms subside: the pain syndrome disappears, the patient’s overall condition improves. The function of the pancreas is restored more slowly for 3-4 weeks of illness.
Diagnosis of Mumps Pancreatitis
A pancreas lesion is a potentially serious manifestation of mumps, which in rare cases can be complicated by shock or the formation of a pseudocyst. It should be suspected in patients who, at the same time as the clinical or epidemiological signs of mumps, experience abdominal pain and tension in the abdominal wall.
It is very difficult to diagnose this complication, since hyperaemilasemia, a classic symptom of pancreatitis, is also common in parotitis. In many cases, the patient exhibits symptoms resembling gastroenteritis. Despite the fact that diabetes or pancreatic insufficiency rarely complicates parotitis pancreatitis, in some children 2-3 weeks after the mumps, development of fragile diabetes was noted.
In the blood at the height of the clinical manifestations, the essence of amylase, lipase, trypsin significantly increases. At the same time increases the activity of diastase in the urine. Coprological examination of feces often reveals a significant increase in the number of unchanged muscle fibers, fatty acids, and extracellular starch. Changes in peripheral blood are not characteristic.
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 Pancreatitis
In acute pancreatitis, a liquid sparing diet is prescribed, atropine, papaverine, cold on the stomach, vomiting – aminazine, as well as drugs that inhibit enzymes, in particular, contrical (trasilol), which is administered intramuscularly (slowly) in a glucose solution, on the first day 50,000 AU, then 3 days for 25,000 IU / day and another 5 days for 15,000 IU / day. Local warming compresses.
Prevention of Mumps pancreatitis
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).