Atypical Measles Syndrome Research Articles

Pertinence of immune waning in measles virus infection – a short review

A striking occurrence will mark an acute infection with the measles virus. The patient soon acquires a lifelong specific immunity to the virus. But, unexpectedly, a transient cellular immune deficiency takes place as well, for several months. The causes of this paradox have not been entirely elucidated. An atypical measles syndrome was scrutinized in order to evaluate the immune status of patients who developed this disorder, subsequently to the administration of the formalin inactivated measles virus vaccine. Although considered not to occur in classic measles, an immune waning develops, at least, in atypical measles syndrome.

A Forty- Four Year - Old Immunized Woman with Maculopapular and Petechial Rash, Diagnosed as Measles: An Extremely Rare Presentation

Introduction: Measles is a highly contagious viral disease, which affects mostly children and rarely adults, which results in a more severe presentation. After a prodromal phase (malaise, anorexia, and the classic triad of conjunctivitis, cough, and coryza and a high fever), enanthem (Koplik spot) appears at buccal mucosa and then, typical erythematous maculopapular rash happens. There are several reports of atypical measles in the adults who have been immunized by killed type vaccine, therefore, prior history of vaccination with the original killed - virus among individuals who present with maculopapular rash and fever do not rule out measles. Case Presentation: Here we report a 44 - year - old woman with fever, chills, myalgia, odynophagia, exudative pharyngitis, bilateral parotitis, anterior cervical lymphadenopathy, tender splenomegaly, conjunctival suffusion and disseminated pruritic erythematous maculopapular, as well as a petechial rash all over her body. She was evaluated mainly for infectious mononucleosis, acute human immunodeficiency virus infection, and acute viral hepatitis, when all investigations were negative for possible diagnoses, although she mentioned immunization against measles, evaluations for measles were done and she had positive IgM antibody with high titer and also positive measles virus RT - PCR. Conclusions: The aim of this report is to emphasize that physicians should be aware of the atypical measles syndrome and entertain the diagnosis of measles in adults with a febrile illness and rash in order to make the most accurate diagnosis and prevent complications.

Relevance of the Measles Virus Expression in Cancer - an Update.

Evidence of an association between classical Hodgkin lymphoma and the measles virus has previously been presented by our group. Arguments held against our thesis were reevaluated. Substantiation of a relationship between the measles virus and additional solid tumors was submitted. Moreover, a pathogenic pathway was suggested to support a possible contribution of the measles virus to the development of classical Hodgkin lymphoma. We have chosen to exclude a discussion of measles virotherapy, since this carries distinct implications. We now add new evidence regarding the expression of the measles virus phosphoprotein in a few cancers. We also suggest a role in this context for atypical measles syndrome in malignant tumors. Last, we propose a collaboration which may make the best, on the one hand of our cohort of classical Hodgkin lymphoma, half of which carry the measles virus expression in their tumor cells. The planned study will also look into the patients vaccination records and into a previous history of the measles disease. On the other hand, cohorts of patients diagnosed with late onset measles will be assessed for the eventual diagnosis of atypical measles syndrome and will be followed up for the subsequent development of a malignant tumor.

The Measles Virus Expression Correlates with Classical Hodgkin Lymphoma and Other Malignancies. A Short Commentary

We have suggested, several years ago, an association between the measles virus and classical Hodgkin lymphoma. However, this relationship was not accepted by the isolated research groups which dealt with the issue. In this short commentary, we recall the traits of the virus which were suggestive of a familiarity with Hodgkin lymphoma. We mention, in addition, older articles which highlight these similarities. As the impact of apoptosis in Hodgkin lymphoma is controversial, a chapter is saved for it. Atypical measles syndrome has long been forgotten. It is mentioned in the present context. The consensus agrees that immunity waning is not a significant factor regarding the measles virus. Is it indeed?

Measles

Measles is a distinct exanthematous and enanthematous disease of viral etiology characterized by respiratory tract involvement and fever. The central nervous system is affected in the acute disease to a minor degree, but occasionally major encephalitis may follow an acute infection. Measles is spread via the respiratory route and tends to exhibit seasonal variation in endemic areas. The incubation period of measles is 9–11 days from the time of contact to the first onset of symptoms, and rash appears 2–3 days later. This is followed by 5–10 days of illness, after which a lifelong immunity is afforded in the immunocompetent host. The mortality of measles is quite low in the industrialized nations, but worldwide measles accounted for 1% of all deaths in the prevaccine era. The development of effective killed and live virus vaccines in the past 25 years has greatly diminished the incidence of measles in the United States but also has resulted in the appearance of an atypical measles syndrome, primarily in recipients of killed measles virus vaccine.

Atypical Measles Syndrome: Pathologic and Serologic Findings

The clinical course of measles occurring in 17 adolescents who had previously received killed measles vaccine is described. All adolescents had a peripheral dermatitis. Fifteen had characteristic pulmonary infiltrates. Serologic study in six adolescents using immunoprecipitation of 35S-methionine-labeled measles virus antigens revealed that 5/6 acute sera lacked antibody to the hemolysin antigen whereas 5/6 sera contained antibody to hemagglutinin antigen. Skin biopsies, obtained from three patients, demonstrate a combination of an Arthus reaction and delayed hypersensitivity. The typical measles histologic complex was absent. Measles virions were seen in the deep dermal blood vessels. The serologic and histopathologic presentation of this disease indicates that killed vaccine does not adequately induce antibody to the hemolysin (F) which is necessary to prevent cell-to-cell spread of paramyxoviruses. Killed vaccine does, however, produce hemagglutinin antibody and simultaneously incites later hypersensitivity to wild virus infection, producing the unusual dermatopathologic reaction seen.

Acute Hepatitis in an Adult With Rubeola

MEASLES (rubeola) is a contagious, acute, febrile illness that predominately affects children, although it may occur in any age group. Data in the United States indicate a recent shift to a greater proportion of rubeola cases in older age groups, undoubtedly a result of past and current immunization efforts. 1 Typically, the symptoms and signs include cough, coryza, conjunctivitis, abdominal pain, fever, lymphadenopathy, Koplik's spots, and a diffuse, erythematous maculopapular rash. Serious complications most often occur in compromised hosts, especially malnourished children. Reported complications associated with measles include upper and lower respiratory tract infection, otitis media, encephalitis (including subacute sclerosing panencephalitis), ileocolitis, myocarditis, thrombocytopenic purpura, and complications due to bacterial superinfections. The atypical measles syndrome was first recognized in the 1960s and is seen primarily in young adults exposed to the wild measles virus many years after immunization with the killed measles vaccine. The atypical measle syndrome is distinguished by

Live Measles Vaccine Not a Cause of Atypical Measles Syndrome

In the August issue of PIR (3:55, 1981)1 there is an abstract regarding atypical measles which we believe is misleading and may deter vaccination of a group of adolescents for whom live measles vaccine is indicated. We have received calls from a number of concerned pediatricians and believe the abstract should be corrected. The author states that the atypical measles syndrome is a possible consequence of administering live measles vaccine to former recipients of killed measles vaccine. Although severe local reactions and occasionally systemic reactions do occur following administration of live measles vaccine to former recipients of killed measles vaccine, there is no evidence that the live vaccine causes classic atypical measles syndrome. Three patients, referred to as having severe systemic reactions by Krause et al,2 experienced fever to 103 F (39.4 C), malaise, marked local pain, swelling and erythema seven days following vaccination; these reactions lasted an average of eight days. However, the abstract was incorrect because these patients did not develop the atypical measles syndrome. Although the reactions were more severe than reactions that might be observed in persons who had never received killed measles vaccine, they were substantially less severe than the atypical measles syndrome. Atypical measles is characterized by high fever, pneumonitis (often with pulmonary consolidation and pleural effusion), pedal and hand edema, and an unusual rash which may be maculopapular, petechial, vesicular or urticarial. The rash is often most concentrated on the extremities.3 Revaccination with live measles vaccine is indicated for former recipients of killed measles vaccine to induce permanent immunity to measles, so that the atypical measles syndrome does not develop when the vaccinee is exposed to natural measles. Revaccination will not cause the syndrome. Atypical measles has occasionally been reported in individuals exposed to natural measles who had previously received live measles virus vaccine within a few months of receiving inactivated measles vaccine.4-6 This raises the possibility that the temporary immunity conferred by the killed vaccine precluded an adequate immunologic response to the live measles virus vaccine. Therefore, persons who received live measles vaccine within three months of receiving inactivated measles vaccine should also be revaccinated with live measles vaccine. Killed measles vaccine was used in the United States between 1963 and 1967 when an estimated 1,836,000 doses were distributed. Persons vaccinated with an unknown type of measles vaccine during that period should also be revaccinated with live measles vaccine as the unknown vaccine may have been killed measles vaccine.

Live Measles Vaccine Not a Cause of Atypical Measles Syndrome

In the August issue of PIR (3:55, 1981)1 there is an abstract regarding atypical measles which we believe is misleading and may deter vaccination of a group of adolescents for whom live measles vaccine is indicated. We have received calls from a number of concerned pediatricians and believe the abstract should be corrected. The author states that the atypical measles syndrome is a possible consequence of administering live measles vaccine to former recipients of killed measles vaccine. Although severe local reactions and occasionally systemic reactions do occur following administration of live measles vaccine to former recipients of killed measles vaccine, there is no evidence that the live vaccine causes classic atypical measles syndrome.Three patients, referred to as having severe systemic reactions by Krause et al,2 experienced fever to 103 F (39.4 C), malaise, marked local pain, swelling and erythema seven days following vaccination; these reactions lasted an average of eight days. However, the abstract was incorrect because these patients did not develop the atypical measles syndrome. Although the reactions were more severe than reactions that might be observed in persons who had never received killed measles vaccine, they were substantially less severe than the atypical measles syndrome. Atypical measles is characterized by high fever, pneumonitis (often with pulmonary consolidation and pleural effusion), pedal and hand edema, and an unusual rash which may be maculopapular, petechial, vesicular or urticarial. The rash is often most concentrated on the extremities.3 Revaccination with live measles vaccine is indicated for former recipients of killed measles vaccine to induce permanent immunity to measles, so that the atypical measles syndrome does not develop when the vaccinee is exposed to natural measles. Revaccination will not cause the syndrome. Atypical measles has occasionally been reported in individuals exposed to natural measles who had previously received live measles virus vaccine within a few months of receiving inactivated measles vaccine.4-6 This raises the possibility that the temporary immunity conferred by the killed vaccine precluded an adequate immunologic response to the live measles virus vaccine. Therefore, persons who received live measles vaccine within three months of receiving inactivated measles vaccine should also be revaccinated with live measles vaccine. Killed measles vaccine was used in the United States between 1963 and 1967 when an estimated 1,836,000 doses were distributed. Persons vaccinated with an unknown type of measles vaccine during that period should also be revaccinated with live measles vaccine as the unknown vaccine may have been killed measles vaccine.

Public health policy toward atypical measles syndrome in the United States.

Public health policy toward atypical measles syndrome in the United States.

Atypical measles syndrome: a continuing problem.

Atypical measles syndrome: a continuing problem.

Atypical Measles Syndrome Identified in 56 Patients

Atypical Measles Syndrome Identified in 56 Patients

Additional evidence that the cell-associated immune system is the primary host defense against measles (rubeola)

Indirect evidence, such as the ability of agammaglobulinemic children to respond normally to measles and the inability of thymic-deficient children to survive measles led Burnet to postulate that the cell-associated immune system is the primary host defense against measles. Using a classical leukocyte culture system, which measures 3 H-thymidine incorporation as its endpoint, we have recently described an in vitro assay for lymphocyte responsiveness to measles complement fixation antigen (CFA) that has allowed us to study this question directly. Two pediatric residents who had negative HIA titers against measles and who had frequent exposure to measles were tested using this assay. Neither resident has had clinical measles or atypical measles syndrome. Both subjects displayed strong cellular responsiveness to measles in this system. We feel that the lymphocyte responsiveness to measles CFA seen in these residents is the in vitro correlate of their clinical protection against measles and offers additional evidence for the fundamental role of cell-associated immunity in the host's response to common viral infections.

A clinical and serologic study of 103 children with measles vaccine failure

During the spring of 1971, 103 children with measles vaccine failure were studied. Seventy-six children had typical measles, 15 had mild modified measles, and 12 had an illness resembling the atypical measles syndrome; 6 of these latter 12 patients had previously received only live measles vaccine. Eighty-seven patients had serologic evidence of recent measles infection; 2-mercaptoethanol (2-ME) treatment of the acute-phase sera from these children revealed different antibody patterns by clinical category. The majority of sera from typical measles cases had ≥4-fold reduction in titer with 2-ME treatment, whereas the majority of sera from modified and atypical cases had no reduction in titer with 2-ME treatment. The acute-phase sera of 15 patients with vaccine failure were found to contain only gamma-G measles antibody when separated by sucrose gradient centrifugation. Thirteen of these sera were from children with modified or atypical illnesses. These findings suggest that some vaccine failures occur in patients who were antigenically simulated previously by measles virus and that illness in these children is likely to be less severe. During the spring of 1971, 103 children with measles vaccine failure were studied. Seventy-six children had typical measles, 15 had mild modified measles, and 12 had an illness resembling the atypical measles syndrome; 6 of these latter 12 patients had previously received only live measles vaccine. Eighty-seven patients had serologic evidence of recent measles infection; 2-mercaptoethanol (2-ME) treatment of the acute-phase sera from these children revealed different antibody patterns by clinical category. The majority of sera from typical measles cases had ≥4-fold reduction in titer with 2-ME treatment, whereas the majority of sera from modified and atypical cases had no reduction in titer with 2-ME treatment. The acute-phase sera of 15 patients with vaccine failure were found to contain only gamma-G measles antibody when separated by sucrose gradient centrifugation. Thirteen of these sera were from children with modified or atypical illnesses. These findings suggest that some vaccine failures occur in patients who were antigenically simulated previously by measles virus and that illness in these children is likely to be less severe.