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The laughter epidemic began on January 30, 1962, at a mission-run boarding school for girls in Kashasha. The laughter started with three girls and spread haphazardly throughout the school, affecting 95 of the 159 pupils, aged 12–18. Symptoms lasted from a few hours to 16 days in those affected. The teaching staff were not affected but reported that students were unable to concentrate on their lessons. The school was forced to close down on March 18, 1962.
After the school was closed and the students were sent home, the epidemic spread to Nshamba, a village that was home to several of the girls. In April and May, 217 people had laughing attacks in the village, most of them being school children and young adults. The Kashasha school was reopened on May 21, only to be closed again at the end of June. In June, the laughing epidemic spread to Ramashenye girls’ middle school, near Bukoba, affecting 48 girls.
The school from which the epidemic sprang was sued; the children and parents transmitted it to the surrounding area. Other schools, Kashasha itself, and another village, comprising thousands of people, were all affected to some degree. Six to eighteen months after it started, the phenomenon died off. The following symptoms were reported on an equally massive scale as the reports of the laughter itself: pain, fainting, flatulence, respiratory problems, rashes, attacks of crying, and random screaming. In total 14 schools were shut down and 1000 people were affected.
The Tanganyika laughter epidemic of 1962 was an outbreak of mass hysteriaor mass psychogenic illness (MPI)rumored to have occurred in or near the village of Kashasha on the western coast of Lake Victoria in the modern nation of Tanzania (formerly Tanganyika) near the border of Uganda.
Mass psychogenic illness (MPI), also called mass sociogenic illness or just sociogenic illness, is "the rapid spread of illness signs and symptoms affecting members of a cohesive group, originating from a nervous system disturbance involving excitation, loss, or alteration of function, whereby physical complaints that are exhibited unconsciously have no corresponding organic" cause. MPI is distinct from other collective delusions, also included under the blanket terms of mass hysteria, in that MPI causes symptoms of disease, though there is no organic cause.
There is a clear preponderance of female victims. The DSM-IV-TR does not have specific diagnosis for this condition but the text describing conversion disorder states that "In 'epidemic hysteria', shared symptoms develop in a circumscribed group of people following 'exposure' to a common precipitant."
The hypothesis that those prone to extroversion or neuroticism, or those with low IQ scores, are more likely to be affected in an outbreak of hysterical epidemic has not been consistently supported by research. Bartholomew and Wesseley state that it “seems clear that there is no particular predisposition to mass sociogenic illness and it is a behavioural reaction that anyone can show in the right circumstances.”
Females are affected with mass psychogenic illness at greater rates than males. Adolescents and children are frequently affected in cases of MPI.
The virus is thought to have been introduced into Eritrea in 1887 by Indian cattle brought by the Italians for their campaign against Somalia. It spread throughout the Horn of Africa, and crossed the Zambezi in March of 1896.
When the Malays were asked why they thought that women were more likely to suffer from latah, they responded with the cultural explanation that women have less 'semangat' or soul substance. They also said women are simply easier to tease than men, and coupling these two together: latah becomes more readily observable and developed throughout recurrent provocation in women than in men. This also accounts for the higher prevalence of latah in lower status persons, as they are more vulnerable to abuse than others. The Malay also believe women are more susceptible because they lose more blood than men, through menstruation. Some Malay believe that excess tickling of a child will predispose them to latah later in life.
The onset of Latah is often associated with stress. In a study done by Tanner and Chamberland in 2001, a significant number of research participants had experienced a life stressor (such as a child or husband dying) just before becoming latah. Additionally, a large number of participants from many research studies have reported strange dreams occurring just before the onset of latah. These dreams usually had a sexual element to them, often involving penises or enlarged penises. According to Tanner and Chamberland, perhaps the dreams, although with variation, indicate some sort of dysfunction in a specific anatomical area. Exploring this further might lead to more insights as to the cause and/or cure of latah.
Osborne (2001) states that latah is a possible emotional outlet in a stifling culture. Winzeler’s believes that latah is less demeaning for women than it is for men, and that women actually have more freedom in society because they are not held to as strict of standards as men are. He argues that as men age, they become more concerned with personal dignity and poise while women become less so. Because of this, women feel more freedom to engage in latah behavior, while men do not.
In the 1890s, an epizootic of the rinderpest virus struck Africa, considered to be "the most devastating epidemic to hit southern Africa in the late nineteenth century". It killed more than 5.2 million cattle south of the Zambezi, as well as domestic oxen, sheep, and goats, and wild populations of buffalo, giraffe, and wildebeest. This led to starvation resulting in the death of an estimated third of the human population of Ethiopia and two-thirds of the Maasai people of Tanzania.
Psychosexual conflicts, personality factors, and cultural beliefs are considered as being of etiological
significance to koro. Sexual adjustment histories of non-Chinese victims are often significant, such as premorbid sex inadequacy, sexual promiscuity, guilt over masturbation, and impotence.
When considering the biological mechanisms and evolutionary history of koro, it is important to look at it in the larger framework of mass hysteria. While the underlying mechanisms are still poorly understood, it has been suggested that the mirror neurons play a major role in mass hysteria outbreaks. Mirror neurons, which have been found in both human and non-human primates, are neurons that fire when one performs an action and when they observe another individual performing the same action. It is hypothesized that we evolved these mechanisms to learn from observation of others, as well as to facilitate imitation. However, within mirror neurons, there is some form of inhibitory process, which prevents us from blindly mimicking every action we observe others perform. New research into this area suggests that in mass hysteria outbreaks something goes amiss in this inhibitory process.
Epidemic typhus is a form of typhus so named because the disease often causes epidemics following wars and natural disasters. The causative organism is "Rickettsia prowazekii", transmitted by the human body louse ("Pediculus humanus humanus").
have been proposed among "possible causes" of the disease. For instance, the above-mentioned declaration produced by the April 2013 International Conference which took place in San Salvador said that:
The nature of multifactorial problems is, that the observed disease can be caused from regionally different sets of risk factors, e.g. agrochemicals and heavy metals are ubiquitous in endemic and non-endemic areas, feature proteinuria, or have not been related previously to CKD but only to acute kidney injury. Mesoamerican volcanic soils, for instance, are rich in arsenic and cadmium (e.g. CKDu miners).
Coxsackie B virus is spread by contact and epidemics usually occur during warm weather in temperate regions and at any time in the tropics.
In Central America, it is a cultural pattern that men do the field work while women stay home to perform domestic chores; since the disease is mainly seen in men/workers, it has been speculated it may be related to occupation, heat-stress or agrochemicals (particularly pesticides). Any widespread-environmental or community well water contamination cannot explain this particular gender/labor pattern; agrochemicals traditionally have been widely used in these and other farming areas where the disease is not prevalent, so a specific product – or products combination – not used elsewhere but only in the coastlands should be brought into consideration by the pesticides hypothesis to offer a plausible explanation as the main culprit.
As of 2017 there is no commercially available vaccine. A vaccine has been in development for scrub typhus known as the scrub typhus vaccine.
Feeding on a human who carries the bacterium infects the louse. "R. prowazekii" grows in the louse's gut and is excreted in its feces. The disease is then transmitted to an uninfected human who scratches the louse bite (which itches) and rubs the feces into the wound. The incubation period is one to two weeks. "R. prowazekii" can remain viable and virulent in the dried louse feces for many days. Typhus will eventually kill the louse, though the disease will remain viable for many weeks in the dead louse.
Epidemic typhus has historically occurred during times of war and deprivation. For example, typhus killed hundreds of thousands of prisoners in Nazi concentration camps during World War II. The deteriorating quality of hygiene in camps such as Auschwitz, Theresienstadt, and Bergen-Belsen created conditions where diseases such as typhus flourished. Situations in the twenty-first century with potential for a typhus epidemic would include refugee camps during a major famine or natural disaster. In the periods between outbreaks, when human to human transmission occurs less often, the flying squirrel serves as a zoonotic reservoir for the "Rickettsia prowazekii" bacterium.
Henrique da Rocha Lima in 1916 then proved that the bacterium "Rickettsia prowazekii" was the agent responsible for typhus; he named it after H. T. Ricketts and Stanislaus von Prowazek, two zoologists who had died from typhus while investigating epidemics. Once these crucial facts were recognized, Rudolf Weigl in 1930 was able to fashion a practical and effective vaccine production method by grinding up the insides of infected lice that had been drinking blood. It was, however, very dangerous to produce, and carried a high likelihood of infection to those who were working on it.
A safer mass-production-ready method using egg yolks was developed by Herald R. Cox in 1938. This vaccine was widely available and used extensively by 1943.
Katagelasticism is a psychological condition in which a person excessively enjoys laughing at others (coined by Christian F. Hempelmann and Sean Harrigan from ("katagelastēs"), Ancient Greek for “mocker”). Katagelasticists actively seek and establish situations in which they can laugh at others (at the expense of these people). There is a broad variety of things that katagelasticists would do—starting from harmless pranks or word plays to truly embarrassing and even harmful, mean-spirited jokes. They would be of the opinion that laughing at others is part of the daily life and if others do not like being laughed at, they should just fight back. For the katagelasticists it is fun laughing at others and there is almost nothing that might hinder them from doing so. For them, some people even might provoke getting laughed at (and surely deserve being laughed at). This condition often makes it difficult for sufferers to gain and maintain acquaintances and romantic partners.
As is typical with this virus family, it is shed in large amounts in the feces of infected persons. The disease can be spread by sharing drink containers, and has been contracted by laboratory personnel working with the virus.
The first academic paper to investigate this phenomenon was published in 2009. Along with gelotophobia and gelotophilia it can be measured through a questionnaire that consists of 45 questions (the PhoPhiKat-45; the PhoPhiKat-30 is a short form that consists of 30 items). This is a reliable and valid instrument that has been used in a variety of studies. The questionnaire is also online for a free self-assessment in an English form at gelotophobia.org and in a German form here.
Gelotophobia, gelotophilia, and katagelasticism describe three different stances towards laughter and laughing at. Empirical studies with the PhoPhiKat-45 show that, of course, people can not at the same time fear and like being laughed at (i.e., be gelotophobes and gelotophiles at the same time). However, there is at least a subgroup of gelotophobes that enjoys laughing at others, despite knowing how harmful this can be. Finally, gelotophilia and katagelasticism are positively related; i.e., those who enjoy being laughed at might also enjoy laughing at others.
Encephalitis lethargica or Nellysa disease is an atypical form of encephalitis. Also known as "sleeping sickness" or "sleepy sickness" (distinct from tsetse fly-transmitted sleeping sickness), it was first described in 1917 by the neurologist Constantin von Economo and the pathologist Jean-René Cruchet.
The disease attacks the brain, leaving some victims in a statue-like condition, speechless and motionless. Between 1915 and 1926, an epidemic of encephalitis lethargica spread around the world. Nearly five million people were affected, a third of whom died in the acute stages. Many of those who survived never returned to their pre-existing "aliveness".They would be conscious and aware – yet not fully awake; they would sit motionless and speechless all day in their chairs, totally lacking energy, impetus, initiative, motive, appetite, affect or desire; they registered what went on about them without active attention, and with profound indifference. They neither conveyed nor felt the feeling of life; they were as insubstantial as ghosts, and as passive as zombies.No recurrence of the epidemic has since been reported, though isolated cases continue to occur.
The causes of encephalitis lethargica (EL) are uncertain.
Veins of modern research have explored its origins in an autoimmune response, and, separately or in relation to an immune response, links to pathologies of infectious disease (viral and bacterial, e.g., in the case of influenza, where a link with encephalitis is clear). Postencephalic Parkinsonism was clearly documented to have followed an outbreak of EL following 1918 influenza pandemic; evidence for viral causation of the Parkinson's symptoms is circumstantial (epidemiologic, and finding influenza antigens in EL patients), while evidence arguing against this cause is of the negative sort (e.g., lack of viral RNA in postencephalic parkinsonian brain material).
In reviewing the relationship between influenza and EL, McCall and coworkers conclude, as of 2008, that while "the case against influenza [is] less decisive than currently perceived… there is little direct evidence supporting influenza in the etiology of EL," and that "[a]lmost 100 years after the EL epidemic, its etiology remains enigmatic." Hence, while opinions on the relationship of EL to influenza remain divided, the preponderance of literature appears skeptical.
In 2010, in a substantial Oxford University Press compendium reviewing the historic and contemporary views on EL, its editor, Joel VIlensky of the Indiana University School of Medicine, quotes Pool, writing in 1930, who states, "we must confess that etiology is still obscure, the causative agent still unknown, the pathological riddle still unsolved…", and goes on to offer the following conclusion, as of that publication date:Subsequent to publication of this compendium, an enterovirus was discovered in EL cases from the epidemic.
Diplococcus has been implicated as a cause of EL.
The American Public Health Association recommends treatment based upon clinical findings and before culturing confirms the diagnosis. Without treatment, death may occur in 10 to 60 percent of patients with epidemic typhus, with patients over age 60 having the highest risk of death. In the antibiotic era, death is uncommon if doxycycline is given. In one study of 60 hospitalized patients with epidemic typhus, no patient died when given doxycycline or chloramphenicol. Some patients also may need oxygen and intravenous (IV) fluids.
The earliest known report of "bakanae" is from 1828; it was first described scientifically in 1898 by Japanese researcher Shotaro Hori, who showed that the causative agent was fungal.
The fungus affects rice crops in Asia, Africa, and North America. In epidemic cases yield losses may reach up to 20% or more. A 2003 publication from the International Rice Research Institute estimated that outbreaks of bakanae caused crop losses that were 20% to 50% in Japan, 15% in Thailand and 3.7% in India.
Human-to-human transmission of diphtheria typically occurs through the air when an infected individual coughs or sneezes. Breathing in particles released from the infected individual leads to infection Contact with any lesions on the skin can also lead to transmission of diphtheria, but this is uncommon. Indirect infections can occur, as well. If an infected individual touches a surface or object, the bacteria can be left behind and remain viable. Also, some evidence indicates diphtheria has the potential to be zoonotic, but this has yet to be confirmed. "Corynebacterium ulcerans" has been found in some animals, which would suggest zoonotic potential
There is no vaccine for SARS to date. Isolation and quarantine remain the most effective means to prevent the spread of SARS. Other preventative measures include:
- Handwashing
- Disinfection of surfaces for fomites
- Wearing a surgical mask
- Avoiding contact with bodily fluids
- Washing the personal items of someone with SARS in hot, soapy water (eating utensils, dishes, bedding, etc.)
- Keeping children with symptoms home from school
Many public health interventions were taken to help control the spread of the disease; which is mainly spread through respiratory droplets in the air. These interventions included earlier detection of the disease, isolation of people who are infected, droplet and contact precautions, and the use of personal protective equipment (PPE); including masks and isolation gowns. A screening process was also put in place at airports to monitor air travel to and from affected countries. Although no cases have been identified since 2004, the CDC is still working to make federal and local rapid response guidelines and recommendations in the event of a reappearance of the virus.