Anger
Cholera is an acute or chronic intestinal infectious-contagious disease, caused by serotypes O1 and O139 of the bacterium Vibrio cholerae, which produces secretory diarrhea characterized by Copious, pale, milky watery stools, similar to rice wash water, high in sodium, bicarbonate, and potassium, and low in protein.
It is transmitted primarily by undrinkable water and food contaminated with human fecal matter containing the bacteria. Undercooked seafood is a common source of transmission. Humans are the only living beings affected.
Some of the risk factors for the disease are lack of access to sanitation infrastructure, lack of drinking water, and poverty. It is estimated that climate change and rising sea levels will increase the presence of this disease.
In its severe form, it is characterized by large-volume watery diarrhea that rapidly leads to dehydration of the body.
Etymology
The disease has been called by various names throughout history, such as "blue sickness", "black sickness", "severe high fever", "angry passion", "choleric diarrhea", "cholera morbus", " cholera gravis" and simply "cholera".
The origin of the term is debated. It may come from the Greek χολή cholé, 'bile' or 'bile', and ῥέω reo, 'current', that is, 'current or flow of bile'; or from the Greek χολέρα cholera, derived from χολή, which means 'bile'.
Heinrich Häser and Aulus Cornelius Celsus believed that cholera was derived from bile (hence it was called cholera morbus, disease of the bile ); Alejandro de Trales, who came from the intestines; while Rudolf Kraus and Alexis Littré were in favor of its transmission through the water of streams.
History
The earliest descriptions of the disease can be seen in the writings of Hippocrates (460-377 BC), Galen (129-216), and Wang Shuhe (180-270). In the history of ancient India there are writings that describe the disease in populations settled on the banks of the Ganges River. However, it is not demonstrable that these descriptions are produced specifically by V. cholerae, nor is it clear that it has occurred in the currently known epidemic form of the disease.
The first reference in Western documented history to the existence of cholera in India is found shortly after Vasco da Gama's arrival in Calicut in 1498. It was in 1503 when an epidemic of Asiatic cholera was described in the Calicut Sovereign's Army; and later in the year 1543 in the population of the city.
The first documented reference to a cholera outbreak outside India is from 1629, and it occurred in Jakarta, on the island of Java.
From that time to 1817, there are sixty-four reports of relatively isolated outbreaks of cholera, first in the Goa region, the first territory known to Europeans in India; and later in other towns on the west coast of that country, moving progressively to the east and north. Epidemics of the disease are described on the Coromandel Coast between 1772 and 1782. In Ganjam cholera was prevalent in 1781. In Uttar Pradesh an epidemic broke out in April 1783. Between 1781 and 1782 the disease had spread to Sri Lanka and Burma. Other outbreaks in India occurred during 1787 and 1794 at Arcot and Vellore; in the year 1790 again in Ganjam; and in the year 1814 in Bengal. Outside of India, outbreaks stand out in the islands of Mauritius and Réunion in 1775, and in Sri Lanka in 1804. After a period of recession in the outbreaks, the first cholera pandemic began in 1817.
In 1854 the Italian physician Filippo Pacini described the bacillus vibrio cholerae, which in the same year was also described by the Spanish Joaquín Balcells y Pascual and in 1856 probably by the Portuguese António Augusto da Costa Simões and José Ferreira de Macedo Pinto. Also in 1854, John Snow, a British doctor, demonstrated that cholera was caused by the consumption of water contaminated with fecal matter, when verifying that the cases of this disease were grouped into areas where drinking water was contaminated with feces. In 1884, Robert Koch, unaware of the work of Filippo Pacini, isolated and identified the vibrio bacterium that causes cholera. Given its great prominence, the discovery was widely reported.
After this discovery, in 1885, the cholera vaccine was prepared and administered for the first time to thousands of people thanks to Dr. Jaime Ferrán y Clúa.
Throughout the 19th century, cholera spread around the world from its original reservoir in the Ganges delta, in India. Six pandemics in succession killed millions of people on every continent. The current pandemic (the seventh) began in South Asia in 1961 and reached Africa in 1971 and the Americas in 1991. Cholera is now endemic in many countries.
Pandemics
Although other studies refer to between four and six cholera pandemics in the 19th century, Pollizter, commissioned by the World Health Organization to write a monograph on the subject in 1959, refers to six: 1817, 1829, 1852, 1863, 1881-1896 and 1899-1923.
First pandemic (1817)
In August 1817 the disease appeared in Calcutta with greater virulence than is usually described. From there it spread rapidly through all of Bengal, then to all of India, in the northeast, passing through Vindhya Pradesh, Uttar Pradesh, Delhi, Punjab, reaching Surat and Bombay; to the south, passing through Hyderabad, Bangalore, Srirangapatna; and by Ganjam and Chennai. From there, he reached the island of Madura. In December 1818, the pandemic reached Sri Lanka, beginning in Trincomalee, and then joining the ports of Jaffna and Colombo in 1819, from where the disease spread throughout the island.
The pandemic reached Burma and the former kingdom of Siam in 1819. Bangkok was reached by sea route in 1820, and from there the devastating disease spread throughout the region. That same year he reached Malacca, Penang and Singapore. The islands of Indonesia, Borneo and the Philippines were also hit this year. In 1822, from Java, the disease reached Japan.
China was affected early (1817) by land, but the disease spread with great intensity after 1820, when it entered through the ports of Canton, Wenzhou and Ningbo. The north of China was affected in 1821, highlighting Beijing, and between 1822 and 1824 the disease reached the territories of central China.
The Middle East and the countries of the Persian Gulf were affected since 1819, appearing in the city of Aleppo, in Syria; then, in 1821, it entered Oman through Muscat, and then Iraq through Basra, also affecting the island of Bahrain. In Baghdad it produced a great casualty among the Syrian army, which was attacking the city at the time. The subsequent northward advance of this army brought the disease to Tbilisi (in present-day Georgia) and Astrakhan in Russia between the years 1822 and 1823. It reached Turkey through the city of Alexandretta in 1823.
Finally, the most remote places that were affected by this pandemic were Mauritius through its Port Louis port, coming from Sri Lanka; and the island of Zanzibar in Tanzania.
Second Pandemic (1829)
The second pandemic began in 1829 in Persia, Afghanistan, Bukhara (Uzbekistan) and Orenburg (Russia). It then reached Rasht (Iran) and Baku (Azerbaijan). From there it spread throughout the area known as the Middle East. The Russian authorities made great efforts, with cordons and quarantines, to stop the advance of the epidemic to the north, however, in the fall of 1830, cholera reached Moscow. In the year 1831, the disease continued to advance north and west, reaching Saint Petersburg and Archangel, and from there to Finland; it came to Poland by Polish soldiers who were at the time in an uprising against the Russian Empire, which continued with a war until 1831. The emigration of Polish soldiers to the west spread the disease to the rest of Europe. Due to the arrival of sick soldiers, he entered Galicia (current sector of Ukraine) and from there to Austria, arriving in Vienna in August 1831. In June of that year he had also arrived in Hungary. Despite the efforts of the authorities to prevent its arrival in Prussia, the disease entered that country from Riga (of present-day Latvia) to the port of Gdansk from where it spread rapidly, affecting Berlin and Hamburg in 1832.
Given the important commercial contact between the European ports and the island, cholera arrived in England in June 1831, in Medway, southwest of London, from patients who were on quarantined ships coming from Riga. In October he arrived in Sunderland and then cases appeared in Newcastle, Gateshead, Edinburgh, and, in February 1832, in London. Then, it continued to spread to various cities on the island. That year, 14,796 cases of cholera were recorded with 5,432 deaths.
Other European countries joined the pandemic: It arrived in Ireland in March 1832 through Dublin; to France in March 1832, through Calais and then in Paris; to Belgium in the spring, through the neighboring towns of France; to the Netherlands in June, via Scheveningen; to Norway in the fall, via Drammen, Moss, and Oslo; to Portugal, in December, through the Duero and then, in April of the following year, he arrives in Lisbon; It arrived in Spain in August 1833. From the port of Ceuta, in Spain, the disease crossed into North Africa. In 1834 the disease reached Sweden.
In America, it first affected Canada, through the port of Quebec in June 1832, from where it spread rapidly through the Saint Lawrence River and its tributaries; in the United States it was presented on June 23 in New York, and on July 5 in Philadelphia. From there, he traveled the country past the Rocky Mountains until he reached the west coast of the northern continent. It is believed that he arrived in Peru and Chile in 1832; he arrived in Mexico and Cuba in 1833; to the Guianas, Nicaragua and Guatemala in 1837.
The second pandemic showed a decrease in the year 1834 in Europe. However, in 1835, there were outbreaks of resurgence in France (Marseille, Toulon and other cities in the south of the country), from the south of France it reached Italy, where it spread, arriving in Malta in 1837. In 1836, from northern Italy, the disease passed to Switzerland through the Canton of Ticino and spread through Tyrol. From there he went to Bavaria (and then to Munich in October 1836). In the summer of 1837, the disease flared up again in Prussia, Hamburg and Poland, the last attacks of the first wave of this pandemic in Europe.
French troops in Algeria spread the disease throughout that country. Between 1835 and 1837, it spread through Egypt, then west to Libya (via Tripolitania) and Tunisia; and to the south to Sudan and Ethiopia. Between 1836 and 1837 it reappeared in Somalia and Zanzibar.
To the east of India, (a country where the disease remained relatively inactive), outbreaks were reported in Indonesia and the Philippines until 1830; in Japan it reappeared in 1831; in Australia it was introduced in 1832; in China, there was an outbreak in Canton in 1835; In Bengal, it reappeared in 1837, from where it spread eastward, reaching Afghanistan in 1839. In 1840, troops were moved from Bengal to China and the Straits Settlements, spreading the disease to those territories. From Canton, the disease moved up the Irawadi River into Burma, reaching Rangoon in 1842; from China the disease returned to its pandemic beginnings, spreading along its trade routes from Kasgar and Yarkand, to Kokand and Bukhara in 1844. On the other hand, from Afghanistan, where the disease reached Kabul in 1844, it spread to Pakistan, through Punjab and then Karachi in 1845. Toward India, due to being en route, he arrived in Delhi that same year. The disease returned to Russia via Iran, through the Mashhad-Tehran-Tabriz-Derbent route.
In Bengal, cholera flared between 1845 and 1846, advancing along the sea route to India, Madras in the east and then Bombay in the west, passing through Sri Lanka. In May 1846, he came from India to Aden and Moca (in Yemen), and Jeddah in Saudi Arabia. It then spread to Oman. From Arabia, it spread throughout Persia, and advanced northwards becoming a new wave of the disease towards Russia, adding to the focus that was still latent in Derbent, in April 1847. The wave spread along the coasts of the sea Caspian, affecting Astrakhan, then going up the Volga River. To the west it reached Tiflis (Georgia), and continued to spread in that direction along the shores of the Black Sea; to the northwest, it advanced through the Caucasus into the interior of Russia. Through the Ural River basin, the disease reached Orenburg, and from there it spread through Siberia until it reached Tobolsk in July 1847. In the summer, the disease covered practically all of Russia, reaching Moscow in September. This last wave of the pandemic in Europe culminated in the arrival from the north to Riga in 1848, from where it reached Norway.
Thus, in 1848, the disease was present in Europe from Norway in the north to the Balkan Peninsula in the south; it encompassed England, Scotland, and Ireland to the north-west; and to Spain to the west. That same year, the disease reached the United States. On the other hand, it worsened in Anatolia, Syria, Palestine and Persia. It also affected North Africa.
Third Pandemic (1852)
The third pandemic, unlike the first two, did not follow a linear course, but rather responded to the sum of local resurgences in various areas, added to successive migrations and imports.
Starting with outbreaks in India in 1852, it flared up in Persia and Mesopotamia; in parallel, an extensive wave affected all of northern Europe, North America, Mexico and the East Indies.
In the year 1854, it remained in these areas, and advanced through Europe, through the French troops that participated in the Crimean War, to Greece and Turkey; in America, the disease reached South America through Colombia.
In 1855, without leaving the previously affected areas, he advanced from India to Syria and Asia Minor by way of Arabia. In Africa, it appeared in Egypt and from there it advanced to Sudan, Morocco, and, for the first time, affected Cape Verde. In Europe, he advanced to Italy, Austria, and Switzerland. In America, he stopped in the United States, but appeared in Venezuela and Brazil.
Between 1856 and 1858, the disease receded in Europe, with the exception of outbreaks in Spain and Portugal (including Madeira).
Between the years 1857 and 1859, the disease, which had already arrived early (1852) in Indonesia, worsened in China and Japan. In 1858 he reappeared in the Philippines and in 1859 he appeared in Korea.
Characterization of the disease
The disease was discovered by Filippo Pacini in 1854, and later Jaime Ferrán y Clúa developed the first vaccine. The infection is usually benign or asymptomatic, but can sometimes be serious. Approximately one in 20 infected people may have severe disease, characterized by profuse watery diarrhea, vomiting, and numbness in the legs. In these people, the rapid loss of body fluids leads to dehydration and prostration. Without proper treatment, death can occur within a few hours.
Epidemiology
Cholera is endemic in more than 50 countries and has produced several worldwide epidemics. Since 1817, seven cholera pandemics have spread from Asia to the rest of the world. The last of these occurred in 1961 and affected between 3 and 5 million people per year, killing around 120,000 people.
In January 1991, a cholera epidemic broke out in several countries in northern South America and spread rapidly. The cholera outbreak in Haiti in 2010 followed the earthquake in January 2010.
Cholera has been rare in industrialized countries for the past 100 years; however, this disease is still common in other parts of the world, including the Indian subcontinent, Southeast Asia, Central America, and sub-Saharan Africa.
It is presented as an epidemic where there are deficient sanitary conditions, overcrowding, war and starvation. Endemic areas are: Asia, Africa, the Mediterranean and more recently, Central America and northern South America. One type of Vibrio has been associated with shellfish, especially raw oysters. Residing in or traveling to endemic areas, as well as drinking contaminated or untreated water, are also risk factors.
Etiology
There are two types of serotypes, O1 and O139, and they are those that cause epidemic outbreaks. O1 causes most outbreaks, while O139, which was first identified in Bangladesh in 1992, is confined to Southeast Asia. Strains other than O1 and O139 can cause mild diarrhea but do not cause epidemics.
The main reservoirs of V. cholerae are humans and brackish water sources and estuaries; there is often a relationship with algae multiplication. Recent studies indicate that global warming creates a favorable environment for vibrios.
A person can get cholera by drinking liquids or eating food contaminated with cholera bacteria. During an epidemic, the source of contamination is usually the feces of an infected person. The disease can spread rapidly in areas with inadequate drinking water and wastewater treatment. The cholera bacterium can also live in brackish rivers and coastal waters.
Transmitting cholera directly from person to person is rare; therefore, casual contact with an infected person does not constitute a risk for contracting the disease.
Pathogenesis
V.cholerae produces a potent toxin that, in cells of the intestinal mucosa, blocks the GTPase of the alpha subunit of a G protein, preventing this protein from being inactivated. By remaining active, it also keeps adenylyl cyclase active, which continues to produce cAMP (cyclic adenosine monophosphate) in a sustained manner, which binds to the Cl- channels. These channels open and the ion comes out of the intestine in a massive way, dragging other ions with it and causing excessive intestinal secretion of water with sodium, bicarbonate and potassium, which exceeds its absorption capacity.
Clinical picture
It has a short incubation period that fluctuates between two hours and five days. The main symptoms are:
- Abdominal pain from mucosa irritation.
- Aquatic diarrhea with a high number of depositions (up to 30 or 40 in 24 hours). This data guides the diagnosis of this painting.
- Depositions have a whitish tone with small granules. They are called "rice water". This is due to the release of decamation products, fragments of fibrin and destroyed cells. Moreover, due to the secreted ions are isotonic, that is, with a osmolarity similar to that of plasma (this occurs in the most serious forms). It should be noted that this diarrhea has a slight smell of fish, or a scent.
- Diarrhea is accompanied by vomiting, which causes rapid loss of water and electrolytes (potassium, sodium, magnesium, chloride, phosphate hydrogen, bicarbonate), causing rapid dehydration.
- It does not cause fever (or this is moderate) because the picture is produced by enterotoxin and not by germ.
For all of the above, we are dealing with a patient who could present one or more of the following:
- Apathy, decay.
- Sexual dysfunction.
- Memory loss.
- Diarrhea, defects in the intestinal flora.
- Friality and cyanosis.
- Muscle cramps.
- manifest hypotension (for the great loss of fluids), weak pulse (the irrigation is difficult in peripheral tissues), tachycardia.
- Wrinkled hands, by subcutaneous dehydration.
- Increased blood viscosity due to fluid loss. This, in predisposed subjects, can lead to complications such as ictus, infarts, intermittent claudication, ischemia, among others.
- Storm dehydration.
Except in its most advanced forms, the state of consciousness is maintained unscathed. When electrolyte loss is severe, vomiting may occur as a result of acidosis and severe muscle cramps as a result of hypokalemia. In these severe cases, severe signs of dehydration, hypotension, and oliguria appear.
Diagnosis
Cholera is suspected in the face of very watery diarrhea, in large volume and high frequency in endemic areas. It is a picture with little inflammation.
- Hemogram: presence of leucopenia although salmonelosis toxin can also cause it.
- Feces test: there are no leukocytes in the feces.
There are other examinations that, although important in the diagnosis of epidemics, have no clinical relevance for a specific case:
- Direct examination of the vibrion in feces. Relatively aseptic diarrhea.
- Antisueros to detect the antigen of the vibrion.
- Immunofluorescence.
Treatment
Aggressive rehydration is the most important measure, lowering mortality from more than 50% to less than 0.2%.
Serums
Saline solution. You have to give a large amount of serum, the routes of administration are:
- Oral: serum dripping in the mouth, which although slow at the end of the day can provide an important amount.
- Intravenous: ideal to replenish high volumes of liquids, especially in patients with moderate or severe dehydration or in hypovolemic shock, or if it is impossible to hydrate the patient by mouth.
These serums should contain sodium, chlorine, potassium and bicarbonate depending on what you need at any given time (it is calculated based on losses). As a prepared oral serum formula we have alkaline lemonade, but if you don't have that on hand you will have to give it whatever (lemon water, isotonic drinks and even carbonated drinks).
WHO: 1 L (litre) of water, 2.6 g of NaCl, 1.5 g (grams) of KCl, 2.9 g of trisodium citrate and 13.5 g of glucose.
Antibiotics
The use of antibiotics reduces the duration of diarrhea by 50% and is recommended for patients with moderate and severe diarrhea. They are indicated to eradicate the bacteria, but the initial management of the patient is based on vigorous fluid replacement, since dehydration is what can lead to the death of the patient.
They reduce the duration of diarrhea, fluid requirements and the period of vibrio excretion. The use of tetracyclines (such as oxytetracycline; 500 mg every 6 hours for 3 days),[citation needed] quinolones (such as ciprofloxacin) and trimethoprim and sulfamethoxazole (cotrimoxazole; 320 mg every 12 hours for 3 days).[citation needed] Another alternative would be nitrofurans such as furazolidone (because it is like the previous bactericidal and bacteriostatic antibiotics).[citation needed]