[Seroepidemiology of chickenpox, measles and parotitis in the Republic of Mexico, V. Parotitis].
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The immunoepidemiological survey of 54 foci of epidemic parotitis showed that the epidemiological effectiveness index at preschool institutions, equal to 2.7, was essentially higher than at schools (2.1). The significant difference (t = 3.35) in the epidemiological effectiveness indices was due to the presence of a large number of persons having had inapparent and faintly pronounced forms of epidemic parotitis among school children, as well as due to more close contacts of children with the foci of infection at preschool institutions. The study showed that among children immunized with some lots of parotitis vaccine elevated morbidity in epidemic parotitis was registered. In the foci of infection children, immunized in the presence of low initial titers of specific hemagglutinins in their sera, responded by a booster effect with different duration of stimulation of antibody formation. The hemagglutinin titer of 1:20 was shown to protect children from epidemic parotitis.
By means of acrylamidgelectrophoresis parotid secretions of patients with acute and chronic parotitis were examined. Thereby significant changes in protein patterns of electrophoretic separation were found. Especially two bands are described in detail. One in the cathodal near gel region, the isoamylases, and the otherone in the anodal part of the gel, identified as albumin. In rest and under stimulation these bands show signficant changes compared to normal secretions. Furthermore information about the capacity of the parotid gland parenchyma is won by observing the changes of amylase bands in rest and under stimulation in chronic parotitis without actute exacerbations. The amylase shows a remarked decreased secretion in chronic parotitis under stimulation corresponding to parenchymalteration. The same happens with the albuminexcretion as parameter for ductlesions. In chronic parotitis albmuninexcretion goes parallel to duct changes in sialography. Therefore by discelectrophoretic separation of native parotid saliva a helpful mean for diagnostic use is given, besides sialography and scintigraphy.
Clinical stomatologic and cytologic studies were carried out in 31 patients with Sjogren's disease, 12 ones with chronic parotitis, and 5 normal subjects. Patients with Sjogren's disease, in contrast to those with chronic parotitis, develop clinically manifest signs of dry exfoliative cheilitis, xerostomia, atrophic changes in the buccal mucosa; this condition is associated with a very high caries intensity and no clinical manifestations of periodontitis or tartar. Elevated leukocyte levels in oral washings and oral fluid of patients with Sjogren's disease and chronic parotitis point to inflammations in the salivary glands, buccal mucosa, and periodontal tissues. Assessment of the leukocyte levels may be used for monitoring the disease course and treatment efficacy. A 3-5-fold enlargement of the deep-layer epitheliocytes, seen on the cytogram of oral washings, is characteristic of patients with Sjogren's disease, in contrast to those with chronic parotitis or normal subjects. A differentiated estimation of the epitheliocyte types in the cytogram of oral washings may be used in the diagnosis of Sjogren's disease along with the criteria suggested before.
Chronic, recurrent parotitis was classified as a disease of the salivary glands of bacterial and inflammatory origin. Forty biopsy specimens of the parotoid gland taken from patients with chronic, recurrent parotitis were examined via light and electron microscopy; virus or bacteria could not be identified. The pathomorphologic findings with chronic, recurrent parotitis correspond basically with those of an experimental ligature of the ganglia. The pathogenesis was discussed. The results of the investigation indicated that, in terms of the pathogenesis, chronic, recurrent parotitis represents a special form of electrolytic and/or obstructive sialadenitis.
Staphylococcus aureus is the predominant pathogen in acute suppurative parotitis. Although anaerobic bacteria are prevalent in the normal oral and upper respiratory tract flora and frequently are involved in oral and facial infections, they have seldom been isolated from patients with suppurative parotitis. It may be that a role for anaerobes in parotitis has not been documented because of inadequate specimen transport or anaerobic culture techniques. We describe two cases of acute suppurative parotitis in which cultures yielded anaerobic bacteria. In one case, no aerobes were isolated; in the other, the anaerobe was the predominant organism numerically.
Mumps is presumed to confer permanent immunity. Three patients previously known to possess mumps serum antibodies subsequently developed clinical parotitis and showed a diagnostic fourfold rise in mumps V antibody. A review of the literature disclosed several cases of parotitis, either recurrent or postimmunization, but the preparotitis immune status of the patient was unknown or the cause of the mumps was not verified. Case reports of parotitis due to parainfluenza 3 and coxsackie viruses A and the heterotypic serological responses among the myxoviruses are reviewed. Parotitis, especially after prior immunization, requires definitive diagnosis by viral isolation and/or serology before it can be attributed to mumps virus.
Of all the salivary glands, the parotid gland is most commonly affected by an inflammatory process. Infections of the parotid gland range from acute to severe. Assessment of the disease process should differentiate local primary parotid infection from systemic infection when this gland is also involved as part of a generalized inflammatory condition. Viral parotitis can be caused by paramyxovirus (mumps), Epstein-Barr virus, coxsackievirus, and influenza A and parainfluenza viruses. Acute suppurative parotitis is generally caused by Staphylococcus aureus, Streptococcus species, and rarely, gram-negative bacteria. Anaerobic bacteria, mostly Peptostreptococcus species and Bacteroides species, and pigmented Porphyromonas species and Prevotella species have been recently recognized as an important cause of this infection. beta-Lactamase-producing organisms can be isolated in almost three fourths of the patients. Predisposing factors to suppurative infections are dehydration, malnutrition, oral neoplasms, immunosuppuration, sialolithiasis, and medications that diminish salivation. Pus, aspirated from a suppurative parotic abscess, should be plated on media that are supportive for the growth of aerobic and anaerobic bacteria, mycobacteria, and fungi. Early and proper antimicrobial therapy may prevent suppuration. Initial empiric therapy that is directed against both aerobic and anaerobic bacteria may be required until a specific causal diagnosis is available. Surgical drainage may be indicated when pus has formed. This may prevent complications and facilitate recovery.
During a prospective clinical study of melioidosis in northeast Thailand, suppurative parotitis was observed as a characteristic presentation in children. Parotitis constituted 6.3% of all culture-positive melioidosis and 38% of melioidosis in children. Nine cases are described. None had apparent predisposition to infection, although two patients developed rising mumps virus antibody titers, suggesting a possible relation between these conditions. Complications included abscess formation (nine), spontaneous rupture into the auditory canal (five), facial nerve palsy (two), and septicemia and osteomyelitis with septic arthritis (one each). All children initially responded to surgical drainage and appropriate antibiotic therapy. Pseudomonas pseudomallei parotitis should be considered in children from endemic areas with fever and facial swelling. It has a good prognosis with appropriate treatment. It may also prove to be a sensitive clinical indicator of the presence of melioidosis within a particular geographic area.
Elevated vascular tone, lengthened time of intraglandular arterial bed filling, fibrinogenemia, elevated plasma tolerance to heparin were detected in 32 patients with chronic interstitial parotitis (CIP) during exacerbation and in a number of CIP patients with the remission of the disease. Correction of microcirculation disturbances is advisable during CIP exacerbation; in remission it may be effective in patients with the late stage of parotitis, in those with parotitis coursing along with diabetes mellitus, essential hypertension, or against the background of prolonged oral drug therapy (e. g. clofelin). Drugs correcting the microcirculatory disorders are conducive to a sooner alleviation of the inflammation and better and longer preservation of the function of the parotid glands.
A unique case of fatal necrotizing mediastinitis secondary to acute suppurative parotitis is reported. The infection was the result of synergistic necrotizing cellulitis caused by mixed aerobic and anaerobic bacteria. To the best of the authors' knowledge, this is the first reported case of necrotizing mediastinitis resulting from a descending acute suppurative parotitis. Acute parotitis should be included in the broad spectrum of infections resulting from synergism between aerobic and anaerobic bacteria in which anaerobes indigenous to the oral cavity predominate.
Time course of the process was examined in 16 patients with chronic parenchymatous parotitis. The follow-up started in children and was proceeded in adults, thus permitting an answer to the problem of parenchymatous parotitis outcome. Dynamic sialographic studies have shown that the process in the gland may develop in three directions, i.e. improvement, deterioration, or stabilization. Positive changes were the most manifest in the initial stage of the disease and not manifest in the late one. The authors' findings help predict the course of parotitis and outcome of the changes in the parotid gland in children.
Excessive release of glandular kallikrein into the interstitial space around the salivary gland ducts plays a significant role in chronic recurrent parotitis. In the present study 26 patients suffering from acute exacerbated chronic recurrent parotitis were subjected to treatment with the kallikrein inhibitor aprotinin (Trasylol, Bayer AG). During the first hour of treatment 1 mio KIU Aprotinin were infused intravenously, followed by 250 000 KIU/h for another 35 h. Within 12 h after initiation of therapy in all patients we observed remission of pain. Salivary gland function which had been seriously impaired prior to therapy was found to be largely normalized within 48 h in most patients treated in this way. The success of this therapy schedule underlines the suggestion that glandular kallikrein is a trigger enzyme in the pathogenesis of chronic recurrent parotitis.
Infectious parotitis as a complication of the sicca syndrome has rarely been reported. A patient with bilateral parotitis due to H. influenza in reported and the literature regarding this rare complication of the sicca syndrome is reviewed. The host defense mechanisms which ordinarily protect normal individuals or patients with Sjögren's syndrome against purulent parotitis are discussed.
Specific prophylaxis against epidemic parotitis is considered to be necessary. It is epidemiologically justifyable at first to conduct selective immunization with the monovaccine of children aged over one year (in creches and kindergartens) and schoolchildren (and 10-year-olds inclusively) who had had no epidemic parotitis, and later to vaccinate children over one year newly-admitted to the creches, kindergartens and schools. In order to bring to the minimum the risk of supervention of the living parotitis vaccine on the asymptomatic infectious process it is necessary to conduct the vaccination at the period between the end and the beginning of the stable seasonal rise, which in Leningrad falls on the period between the second decades of August and October.
Paralysis of the facial nerve in association with suppurative parotitis is rare, with only ten previously reported cases. In some situations, inflammation surrounding a benign neoplasm accounted for the observed paralysis. In this article, three new cases of parotitis with associated facial nerve dysfunction are described, none of which was associated with a neoplasm. In one, an occult abscess was present and in another an aggressive necrotizing process was seen. The treatment of this disease should initially be conservative management with high doses of wide-spectrum antibiotics. In the majority of cases, resolution of the facial paralysis should follow. However, persistence of a parotid mass with continued facial palsy mandates surgical exploration to exclude the presence of an underlying neoplasm.
The release of glandular kallikrein into the interstitium of the parotid gland appears to play an important role in the occurrence of the inflammatory interstitial edema in chronic recurrent parotitis. This provides fresh impetus for the treatment of this parotid disease with a kallikrein inhibitor. In our present study, seven patients with acute exacerbated chronic recurrent parotitis were treated with the kallikrein inhibitor aprotinin (Trasylol, Bayer AG, Leverkusen). With this therapy all patients were free of pain 12 h after the start of the therapy and most salivary gland function had returned to normal by 48 h after beginning treatment. Within this period of time, concomitant swelling of the affected parotid gland disappeared completely in five patients and resolved in the other two patients after 1 week.