Dates
Geographical reaches
Public health measures and particular events
1817–1825
Asia and East Africa, spreading to Russia and Europe in 1823
1826–1841
Spreading from Mecca to Egypt, Europe and Algeria
1846–1861
Spreading from China to Maghreb, crossed the Atlantic to Latin America
The 1851 International Health Conference edited hygiene measures that allowed to spare the United States and England
1863–1876
Starting from India and China, invading Europe via the French troops coming back from Indochina, and reaching the United States, Latin America, Russia and Poland (1866), and North Africa
Helped by the opening of the Suez Canal (1863), by the Secession War and by population displacements in Eastern Europe
1883–1896
Starting from India
Bouchet observes the bacteria. Koch describes its characteristics. Ferran proposes the first vaccine
1899–1923
Spread from Asia to Russia, and Central and Eastern Europe
1961 on
Starting from Indonesia, generalized to Asia (1962), India (1964), Middle East (1966) and Eastern Europe (1970), and Latin America (1991). The epidemics reached sub-Saharan Africa (1970), extended to the Great Lakes region (1973) and generalized to the whole continent (1979)
The new extension to Latin America came after almost a century free of the disease. It has been attributed to climatic disasters
The seventh epidemic hit sub-Saharan Africa in 1971. Since initial reports, several epidemic outbreaks were reported. The recent Congo–Brazzaville (2009–2013) epidemic is illustrated in Table 19.2. The epidemic spread widely in the Likouala region—an area where forestry alternates with marshes drained by large rivers (Likouala aux herbes, Sangha, Likouala Mossaka, Oubangui). It affected populations living in scattered villages and campsites. The epidemic was less active in the Cuvette and Plateaux regions. The outbreak concentrated in the large cities of Brazzaville (in 2009 and 2012) and Pointe-Noire (2012–2013). The number of casualties was greater in Brazzaville than in other cities, despite modern hospital facilities. This paradox may be linked to the degraded environment created by poor water supply and sanitation.
Table 19.2
Epidemiological situation during the Congo outbreaks (2009-2013)
Region | Population | Cholera cases | Incidence per 100,000 | Casualties | Proportion of casualties (% of cholera cases) |
|---|---|---|---|---|---|
Likouala | 154,115 | 739 | 479.5 | 22 | 3.0 |
Cuvette | 156,044 | 60 | 38.5 | 1 | 1.7 |
Plateaux | 174,591 | 87 | 49.8 | 4 | 4.6 |
Brazzaville | 1,373,382 | 180 | 13.1 | 9 | 5.0 |
Pointe-Noire | 715,334 | 240 | 33.6 | 8 | 3.3 |
Total | 2,573,466 | 1306 | 50.7 | 44 | 3.4 |
Vibrio cholerae and Pathogenicity
Vibrio cholerae was discovered by Filippo Pacini in 1854 [3, 4], but the bacterium microscopic structure was only specified by Robert Koch in 1884 [3] in Calcutta, India. Koch linked his Bacillus komma to cholera . In 1885, Ferran proposed the concept of cholera vaccine for humans [5]. In 1894, Pfeiffer initiated the concept of “endotoxin” released by the Vibrio cholerae membrane. The choleragen toxin was identified in the 1950s in India and was purified and crystallized by Finkelstein in 1969 [4, 6, 7]. The bactericidal action of the waters of the Ganges River was described in 1896, especially on Vibrio cholerae [8]. The El Tor biotype was discovered in 1905 from pilgrim corpses in the Sinai. Between 1907 and 1920 in Indela, Sir Leonard Rogers rehydrated the patients with intravenous hypertonic saline, which significantly changed the death toll of patients from 60–70 % to 3–0 %. In 1911, a cholera epidemic was stopped in Marseille by water chlorination. In 1931, Hérelle and Eliava marketed the first anticholera Tbilisi phages [1, 8, 9].
Descriptive Epidemiology
Incidence (OMS [10])
Nearly all developing countries are dealing with a cholera outbreak or threat of an epidemic. According to the World Health Organization (WHO) [10], in 2003, 45 countries reported a total of 111,575 cases and 1984 deaths (CFR 1.7 %). African cases amounted to 108,067, representing 96 % of the world incidence. In 2004, 56 countries reported 101,389 cases and 2,345 deaths (CFR 2.31 %). Although the number of cases had decreased by 9 % compared to 2003, the number of deaths had increased by 24 %. In contrast, the number of cases remained low in America (36 cases, with 5 cases in the USA, and 3 cases in Canada), and 7 European countries reported only 21 imported cases (13 in UK).
The number of reported cases increased to 230,000 in 2006 with approximately 6000 deaths [11]. However, the true incidence is probably higher.
Factors Favoring Outbreaks (OMS [24])
Cholera outbreaks are favored by degraded environments. Natural climatic disasters have been followed by epidemics , such as in Haiti after the 2010 earthquake [11], in Central America after Hurricane Mitch (1998), and in Mozambique after large floods in 2000. The El Nino phenomenon may have been at the origin of the Horn of Africa outbreaks in 1997–1998 [11].
Civil war or political unrest may also favor cholera outbreaks. A massive outbreak (58,000 cases and 4200 deaths) hit Rwandan refugee camps in Goma, Democratic Republic of Congo in 1994. Wars favored the appearance of cholera in Darfur, worsened the 1997 and 1998 outbreaks in the Horn of Africa, and caused outbreaks in Kabul (Afghanistan).
Degraded environments, favored by the anarchic development of metropolitan cities, where water supply and treatment are often deficient, contribute to cholera outbreaks.
Analytical Epidemiology [10, 12, 13, 14]
The pathogen is a slightly curved, mobile, 2–3-µm-long, Gram-negative bacterium. It favors a pH 8 milieu at 37 °C and dislikes heat, cold, and acidity. It is sensitive to antiseptics and many antibiotics (including cyclins). It may survive for weeks in shaded fecal matters and 10–15 days in the host. The El Tor biotype of Vibrio cholerae, the agent of current outbreaks, has the greatest vitality compared to conventional cholerae and albensis biotypes.
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