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The investigation of a recurrence of an AHC virus epidemic at Lucknow: a serosurvey for AHC virus antibodies before and after the epidemic.

An epidemic of acute haemorrhagic conjunctivitis (AHC) recurred at Lucknow during July to September 1975, after a gap of 4 years. Out of the 35 cases investigated thoroughly, 20 Entero-70-like cytopathogenic agents were isolated from the conjunctiva which were neutralized by antisera against AHC virus J670/71 of Japan. Seroconversion was seen in 7 out of 11 paired sera from patients. Serological study was also done on 100 sera collected before the AHC epidemic of 1971, 100 sera after 1971 and 100 sera after 1975 epidemic. There were no neutralizing antibodies in the pre-epidemic period, while 18% of sera after the first epidemic and 32% after the second epidemic showed antibodies. The incidence of antibodies was highest (43%) in children aged below 10 years. Of the children born after the first epidemic, 44% had antibodies. Thus our findings show that the AHC virus appeared for the firt time at Lucknow in 1971 and the almost complete absence of disease in children, and its mildness during second epidemic, may be due to immunity.

Adult

[Characteristics of the course of the last epidemic of epidemic cerebrospinal meningitis (ECSM) in the city of Bucharest].

Active survey of the epidemiologic potential of cerebrospinal meningitis, in Bucharest, starting in 1967, made it possible to carry out a complex study of the last epidemic wave in 1968-1972. Details are given concerning the results of the complex epidemiologic, clinical and laboratory investigations, which revealed the particularities of this epidemic episode, including the frequency and gravity of the cases, territorial distribution, prevalent affection of certain age groups and children's communities, the prevalence of certain clinical forms, antigenic structure of the pathogenic agent and its sensitivity to antibiotics, comparative efficiency of the different methods of laboratory diagnosis, real and apparent contagiousness, etc. The authors discuss the efficiency of present methods applied in the prevention and control of meningococcal infections in general and of epidemic cerebrospinal meningitis in particular.

Adolescent

A comparative study of meningoencephalitis epidemics caused by echovirus type 7 and coxsackievirus type B5. Clinical and virological observations during two epidemics in northern Sweden.

Two epidemics of meningoencephalitis caused by echovirus type 7 and coxsackievirus type B 5 in the summer and autumn of 1973 in Umeå in Northern Sweden were compared. Most patients with echovirus 7 meningoencephalitis were neck stiff and 50% had a polymorphonuclear pleocytosis in the cerebrospinal fluid (CSF). The illness was usually mild. It appears to be the first time that an epidemic caused by this virus is described from Scandinavia. On the other hand most patients with coxsackievirus B 5 meningoencephalitis showed a more profound involvement of the central nervous system, with abnormal electroencephalograms in 70% and a long convalescence period. The number of cells in CSF was normal in 70% of these patients.

Adolescent

Epidemiological approaches to 'epidemic neuromyasthenia': syndromes of unknown aetiology (epidemic myalgic encephalopathies).

The study of future outbreaks of 'epidemic neuromyasthenia' syndromes would be easier if there were a standing advisory arrangement for the co-ordination of basic standart studies, diagnostic tests and long term survey of patients. It is proposed that this might be achieved by establishing an 'EN Outbreaks Panel' at Colindale which, in addition to epidemiologists and virologists might include specialists in infectious diseases, neurology and psychiatry and other fields. The approach to such a panel would be through the Communicable Diseases Surveillance Centre (CDSC) when outbreak is suspected. Arrangements could then be made by the CDSC with the Epidemiological Research Laboratory and the Virus Reference Laboratory to assist immediate investigations and for a follow-up to ascertain the incidence of sequelae, as well as for long storage of sera and other specimens.

Disease Outbreaks

[Epidemic keratoconjunctivitis: a report on a clinical epidemic (author's transl)].

After description of the clinical and serological features of an epidemic keratoconjunctivitis caused by adeno-virus (Type 8) the author compares results of 4 methods of treatment. The schedule consisted of "Okuzell-Coldan" eye drops as placebo, eye drops of corticosteroid content, intramuscular inoculation with Interferonogen and a combined treatment with 0.3 percent "Neutralrot" eye drops and radiation with daylight lamp HPR 125 W produced by Philips Co. Ltd. The transition from the conjunctival form to the keratic form could be best prevented through the last named therapy.

Adenoviridae Infections

Epidemic Venezuelan equine encephalitis in North America in 1971: vector studies.

A major epidemic of Venezuelan equine encephalitis occurred in south Texas in the summer of 1971. More than 1500 equines died of VEE in Texas, and 110 human cases with no deaths were reported. Vector studies in south Texas and northern Tamaulipas revealed that the overall mosquito infection rates during the peak of the epidemic were about 1:100, one of the highest rates observed for a major epidemic. Mosquito infection rates of this magnitude could easily explain the intensity of VEE outbreaks in both equines and man. A total of 943 VEE virus isolations were made from mosquitoes. Eight of the 12 mosquito species found infected were implicated in the epidemic cycle of VEE for the first time. Sufficient laboratory and field evidence is available to prove that Psorophora confinnis was one of the primary vectors of VEE. The lack of laboratory evidence necessitates the use of the term "probable" primary vectors for other species apparently equally as involved on the basis of field infections; these include Aedes sollicitans, Aedes thelcter and Psorophora discolor. Eight other species from which less than 10 VEE virus isolations were made were considered auxiliary vectors. Mosquitoes of some species were tested individually; such tests showed 2-4% of the probable primary vectors to be infected. The first isolation of VEE virus of the epidemic was made from P. confinnis on June 28, 1971. Highest mosquito infection rates occurred during the week of July 5. Mosquito infection rates declined precipitously in the last 3 weeks of July 1971, signaling the end of the epidemic in the study area. One explanation for the decline was that equines, the principal epidemic hosts, were eliminated as a source of virus by death or by acquisition of natural or induced immunity. Mosquito control appeared to be effective in reducing the infected mosquito population while the immunization of equines with TC 83 VEE vaccine was accomplished. Quarantines appeared to be effective in restricting the VEE virus activity to south Texas. Undoubtedly all of the control measures contributed to stopping the epidemic. Continued VEE surveillance by various government and other agencies failed to reveal any further epidemic VEE activity in the US in 1972. Other arboviruses isolated during the VEE studies in south Texas included St. Louis encephalitis virus, and San Angelo subtype of the California Group. A virus of the Bunyamwera Group was also isolated from Palo Blanco, Tamaulipas.

Animals

The 2026 Bundibugyo Ebola Outbreak: A Warning for Global Preparedness for Future Epidemics.

Dear Editor, The 2026 Bundibugyo Ebolavirus (BDBV) outbreak has once again demonstrated that the threat of emerging diseases remains a major global health challenge. The outbreak, first detected in the Democratic Republic of Congo (DRC) and spread to Uganda, is not only a regional crisis but also a test of the world's preparedness for pathogens with epidemic potential. Unlike Zaire Ebolavirus (EBOV), which has benefited from effective vaccines and treatments in recent years, BDBV still lacks a licensed vaccine or specific treatment[1]. As of June 6, a total of 515 laboratory-confirmed cases and 91 deaths have been reported in DRC, while Uganda has reported 19 laboratory-confirmed cases and two deaths. The occurrence of unexplained deaths among both the community and healthcare workers, along with prior reports of an unidentified hemorrhagic fever, suggest that the outbreak has been likely originated in March 2026 or even earlier. Accordingly, the virus is believed to have spread unnoticed for several weeks before being identified through genomic sequencing in mid-May 2026[2]. The resurgence of Ebola in Africa results from a complex interaction of environmental, social, and political factors. Deforestation, the development of mining activities, the expansion of agriculture, and increased human contact with wildlife have elevated the likelihood of spillovers from wildlife reservoirs, particularly fruit bats, which are considered the most likely natural hosts of ebolaviruses. Moreover, weak disease surveillance systems and limited access to health services have delayed the identification of early cases. The similarity of the initial symptoms of Ebola to other endemic diseases in the region, such as malaria, makes early diagnosis difficult and provides ample opportunity for transmission to spread. Insecurity, misinformation, attacks on healthcare facilities, and armed conflict in the region have also posed serious challenges to the implementation of contact tracing programs and rapid response to the epidemic[3,4]. One of the most critical challenges highlighted by this outbreak is the weakness of diagnostic capacities in the affected areas. The initial 2007 outbreak of BDBV proved that delayed lab confirmation paralyzes public health responses[5]. Now, dealing with a much larger outbreak in 2026, the persistence of this challenge highlights a dangerous failure to invest in diagnostic infrastructure over the last 19 years. Many health facilities do not have access to molecular laboratories, rapid sample transport systems, and biosafety infrastructure[6]. These limitations delay the diagnosis and isolation of patients, thus perpetuating disease transmission. Investment in the development of mobile laboratories, rapid point-of-care diagnostic tests, and digital reporting systems can dramatically reduce the time to diagnosis and response to an outbreak. The BDBV outbreak shows that laboratory preparedness must be considered an essential part of global health security. Furthermore, the early detection of emerging pathogens depends not only on diagnostic technologies but also on the expertise of local scientists who are able to recognize unusual epidemiological and laboratory patterns. During the current outbreak, suspected Ebola cases initially tested negative using common diagnostic tests (designed for Zaire Ebola Virus), which delayed the identification of the BDBV. Specifically, field-based diagnostics in Bunia were calibrated exclusively to detect the EBOV responsible for recent Congolese outbreaks. Consequently, patient samples collected throughout late April and early May yielded negative results, requiring cross-country transport to Kinshasa for genomic confirmation[2]. This experience revealed a major vulnerability in outbreak preparedness: diagnostic tools designed for known threats may be ineffective in detecting less common or unexpected pathogens. Therefore, strengthening local scientific capacities, developing genomic surveillance, and expanding access to flexible and adaptable diagnostic platforms should be considered as a top priority for global health security. The lack of a licensed vaccine for BDBV was one of the most significant challenges of this epidemic. While the rVSV-ZEBOV vaccine has played a significant role in controlling Zaire ebolavirus, there is no licensed vaccine for BDBV. In response to this outbreak, efforts to develop mRNA-based vaccines, adenoviral vectors, rVSV-based vaccines, and multipotent vaccines have been accelerated[7]. However, the experience of this epidemic has shown that the development of medical products for rare diseases continues to face financial and investment constraints. This challenge highlights the need for sustained support from governments and international institutions for research and development of pathogens with epidemic potential. The 2026 Bundibugyo outbreak provides several key lessons for the global community. First, early detection and rapid diagnosis are the most important factors in containing the epidemic. The 19-year interval between the 2007 BDBV outbreak and the 2026 outbreak underscores persistent shortcomings in investment toward decentralized, pan-ebolavirus diagnostic infrastructure, with diagnostic delays hindering timely outbreak identification in both instances. Second, the trust and active participation of local communities are as important as medical interventions. Additionally, the rapid cross-border transmission dynamics between the DRC and Uganda demonstrate that blanket travel restrictions and border closures are impractical. As communities in the Great Lakes region routinely cross national borders for trade and healthcare, coordinated regional surveillance and timely information sharing are likely to be more effective than broad border closures in mitigating disease transmission[8]. Third, the protection of health workers must be a priority in preparedness plans. Fourth, a "One Health" approach is essential for simultaneous monitoring of humans, animals, and the environment. Although BDBV is not a new pathogen, the lack of licensed medical interventions and limited investment in research reflect many of the vulnerabilities associated with the concept of "Disease X."[9]. Unlike Zaire Ebola Virus, for which licensed vaccines and monoclonal antibody therapies are available, BDBV forces public health responses to rely almost entirely on non-pharmaceutical interventions such as isolation and infection control[10]. This gap reflects the structural inequity in global health research and development funding, with pathogens affecting resource-limited regions receiving insufficient attention until they spark an international emergency[2]. The BDBV outbreak proves that global epidemic preparedness cannot be pathogen-selective; it requires proactive investment in broad-spectrum countermeasures and resilient frontline health systems[8]. In conclusion, the 2026 BDBV outbreak is a serious wake-up call for the global health system. The epidemic revealed that gaps in surveillance systems, diagnostic capacities, vaccine development, and preparedness for emerging diseases persist. Investing in health infrastructure, developing Pan-Ebolavirus vaccines, strengthening laboratories, expanding the One-Health approach, and supporting research on emerging zoonotic pathogens must be at the top of global health security priorities. Otherwise, the BDBV outbreak may be just a prelude to larger crises to come.

Ebolavirus

Japanese encephalitis in Sri Lanka--the study of an epidemic: vector incrimination, porcine infection and human disease.

A prospective study of mosquito vectors, porcine infection and human disease was carried out during a Japanese encephalitis (JE) epidemic in the North Central province of Sri Lanka (November-December 1987) and a subsequent non-epidemic year (1988). The epidemic involved 361 cases of human encephalitis, virologically confirmed by immunoglobulin M enzyme-linked immunosorbent assay (ELISA), and was preceded 2-3 weeks earlier by sentinel porcine seroconversion. Virus isolation and viral antigen detection (ELISA) in field-caught mosquitoes incriminated Culex tritaeniorhynchus (Giles) and Cx gelidus Theobald as the major vectors of virus transmission during the porcine amplification and human 'spill-over' phases of the epidemic. Virus was also demonstrated in Cx fuscocephala Theobald, Cx whitmorei (Giles) and Mansonia uniformis (Theobald) during the epidemic. The major difference between the epidemic (1987) and non-epidemic (1988) years was a lower vector biomass and lower rates of virus carriage in the mosquito population.

Animals

Epidemic poliomyelitis in The Gambia following the control of poliomyelitis as an endemic disease. I. Descriptive findings.

An epidemic of type 1 poliomyelitis involving 305 cases occurred in The Gambia (estimated 1986 population, 768,995) from May through November 1986, following a 6-year period when only five cases were reported. Cases were identified by physician reporting during the epidemic and by a national village-to-village search conducted after the epidemic. The national attack rate was 40 cases per 100,000 people. Cases lived in all parts of the country except the capital, Banjul. The peak month of the epidemic was August (139 cases). The highest attack rate by year of age was in 1-year-old children (394 cases per 100,000 persons), and 75% of cases were 3 years of age or less. A vaccination coverage survey showed that 64% (95% confidence interval 60-68) of 1- to 2-year-old children were vaccinated with at least three doses of trivalent oral polio vaccine at the beginning of the epidemic. Fifty-seven cases became paralyzed more than 2 weeks after a national mass campaign in which 95% of children 1-7 years old were reported to have received a dose of trivalent oral polio vaccine. Experience in The Gambia shows that a several-year period of excellent control of endemic poliomyelitis by a vaccination program can be followed by a major epidemic and that a mass vaccination campaign may be only partially successful in ending the epidemic.

Age Factors

Results of virological and serological studies of three influenza A Hong-Kong epidemics in Leningrad.

An analysis of morbidity of the population in the course of 3 influenza A/Hong-Kong epidemics showed a pronounced decrease in influenza affection of adult population in the last epidemic in 1971--1972. Comparative studies of the diagnostic value of CFR and HIT demonstrated identical sensitivity of CFR as a method of influenza diagnostics in both the epidemic and interepidemic periods. HIT was suitable for the detection of influenza only in the epidemic period. In the interepidemic period, the percentage of influenza infection diagnosed by means of HIT ammounted to only 23--24 of all serologically confirmed cases of influenza. The highest percentage of virus isolation was observed when material from patients with serologically confirmed influenza was used. All strains of influenza A virus isolated in 1969 and 1970 were similar in their sensitivity to inhibitors of animal sera. During the last influenza epidemic, 2 of the 136 isolated strains were found to be resistant to gamma inhibitors and highly sensitive to the inhibitors showed their close relationship to gamma inhibitors. Antigenic analysis of the influenza A strains isolated during the 3 influenza epidemics revealed changes in the antigenic structure of the agents of the influenza epidemic in Leningrad in comparison with the standard strain A/Hong-Kong/I/68 (H3N2).

Adolescent

Antigenic variation of influenza viruses isolated from the recent epidemics.

In the winters of 1975-76 and 1976-77 there were fairly heavy epidemics of influenza in Japan, and on those occasions considerable discussions were held on the efficacy of influenza vaccine in connection with the variability of antigenic structure of the influenza virus. The type of the virus which prevailed in the winter of 1975-76 belonged to type A, but detailed antigenic analysis revealed that there had been two main antigenic types somewhat but definitely distinguishable from each other, the one is the well-known A/Victoria/75 type while the other is A/Tokyo/75 type. This epidemic seems to have started with the latter type, but soon the two types of virus prevailed hand in hand until the late part of the epidemic when the type A/Victoria/75 became overwhelming. The virus for the vaccine was however A/Tokyo/6/73 for that season, which is antigenically considerably different from both of these two strains. In the beginning of 1976, namely at the end of the epidemic season of type A, a few scattered epidemics due to type B influenza were reported from some parts of Japan. The result of antigenic analysis found that the virus belonged to B/Hong Kong/72 type, though showing some degree of antigenic schift. The same type of virus caused the epidemic of the winter 1976-77, which was considerably wide-spread and developed unexpectedly large number of cases. There were active discussion on the effectiveness of vaccine, of which B type was B/Gifu/1/73, recovered from the fairly large epidemic in 1973, and belonging to B/Hong Kong/72.

Antibodies, Viral

Results of virological and serological studies of three influenza A Hong-Kong epidemics in Leningrad.

An analysis of morbidity of the population in the course of 3 influenza A/Hong-Kong epidemics showed a pronounced decrease in influenza affection of adult population in the last epidemic in 1971--1972. Comparative studies of the diagnostic value of CFR and HIT demonstrated identical sensitivity of CFR as a method of influenza diagnostics in both the epidemic and interepidemic periods. HIT was suitable for the detection of influenza only in the epidemic period. In the interepidemic period, the percentage of influenza infection diagnosed by means of HIT amounted to only 23--24 of all serologically confirmed cases of influenza. The highest percentage of virus isolation was observed when material from patients with serologically confirmed influenza was used. All strains of influenza A virus isolated in 1969 and 1970 were similar in their sensitivity to inhibitors of animal sera. Suring the last influenza epidemic, 2 of the 136 isolated strains were found to be resistant to gamma inhibitors and highly sensitive to the inhibitors showed their close relationship to gamma inhibitors. Antigenic analysis of the influenza A strains isolated during the 3 influenza epidemics revealed changes in the antigenic structure of the agents of the influenza epidemic in Leningrad in comparison with the standard strain A/Hong-Kong/I/68 (H3N2).

Adolescent