VIBRIO CHOLERAE: CHARACTERISTICS, MORPHOLOGY, HABITAT - BIOLOGY - 2024

Vibrio cholerae is a facultative, flagellate, gram-negative anaerobic bacterium. The species is the cause of cholera disease in humans. This intestinal disease causes severe diarrhea and can cause death if not properly cared for. It causes more than 100,000 deaths a year, the majority in children.

Cholera is transmitted through contaminated food and water or through person-to-person contact. Treatment includes rehydration therapy and specific antibiotics. There are relatively successful oral vaccines.

Vibrio cholerae seen under a transmission electron microscope. By Tom Kirn, Ron Taylor, Louisa Howard - Dartmouth Electron Microscope Facility (http://remf.dartmouth.edu/imagesindex.html), via Wikimedia Commons

General characteristics

Vibrio cholerae is a unicellular organism with a cell wall. The cell wall is thin, composed of peptidoglycan between two phospholipid membranes. It lives in aquatic environments, especially estuaries and ponds, associated with plankton, algae and animals. Two biotypes and several serotypes are known.

Biofilms

The bacterium is part of the bacterioplankton in bodies of water, both in free form (vibrios) and in thin films (biofilms) on organic surfaces.

These biofilms are made up of groups of bacteria surrounded by water channels. The adhesion of the biofilm is possible thanks to the production of polysaccharides from the outer membrane.

Genes

Vibrio cholerae has two chromosomes in the form of plasmids. Pathogenic breeds carry genes that code for the production of cholera toxin (CT).

Additionally they include genes for the so-called colonization factor. The pilus is co-regulated by toxin (TCP) and a regulatory protein (ToxR). This protein co-regulates the expression of CT and TCP. Part of the genetic information that encodes these pathogenicity factors is provided by bacteriophages.

Genome

Its genome is composed of 4.03 Mb distributed in two chromosomes of unequal size. The DNA sequence of the entire genome of V. cholerae O1 strain N16961 is known.

The organized sequences on chromosome 1 appear to be responsible for various processes. Among these, DNA multiplication, cell division, gene transcription, protein translation, and cell wall biosynthesis.

On chromosome 2 ribosomal proteins are synthesized, which are responsible for the transport of sugars, ions and anions, the metabolism of sugars and the repair of DNA.

Within this bacterium, at least seven bacteriophages or filamentous phages have been detected. Phages are parasitic viruses of bacteria. Phage CTX contributes part of the sequence that codes for the synthesis of cholera toxin (CT). This is due to lysogenic conversion, In short, the pathogenicity of certain strains of Vibrio cholerae depends on a complex genetic system of pathogenic factors. Among them the pilus colonization factor co-regulated by toxin (TCP) and a regulatory protein (ToxR) that co-regulates the expression of CT and TCP.

Contagion

When humans consume contaminated food or water, the bacteria enter their digestive system. Upon reaching the small intestine, it adheres en masse to the epithelium.

Once there, it secretes the toxin, causing the biochemical processes that cause diarrhea. In this environment, the bacteria feed and reproduce, being released back into the environment through the feces. Its reproduction is by bipartition.

Phylogeny and taxonomy

The genus Vibrio includes more than 100 described species. Of these, 12 cause disease in humans. It belongs to the Bacteria domain, Proteobacteria phylum (gamma group), Vibrionales order, Vibrionaceae family.

Vibrio cholerae is a species well defined by biochemical and DNA tests. It tests positive for catalase and oxidase; and does not ferment lactose.

The Italian physician Filippo Pacini was the first to isolate the cholera bacteria in 1854. Pacini gave it a scientific name and identified it as the causal agent of the disease.

More than 200 serogroups of Vibrio cholerae are known, but to date only 01 and 0139 are toxic. Each serogroup can be divided into different antigenic forms or serotypes. Among these are the Ogawa and Inaba, or different biotypes such as the classical and the Tor.

Morphology

Vibrio cholerae is a bacillus (rod or rod-shaped bacteria) 1.5-2 μm long and 0.5 μm wide. It has a single flagellum located at one of its poles. It has a cytoplasmic membrane surrounded by a thin wall of peptidoglycan.

The outer membrane has a more complex structure made up of phospholipids, lipoproteins, lipopolysaccharides, and polysaccharide chains.

The outer membrane projects towards polysaccharide chains that are responsible for the adhesion capacity of bacteria and form biofilms.

In addition, together with the cell wall, it protects the cytoplasm from bile salts and hydrolytic enzymes produced by the human intestinal tract.

Habitat

It occupies two very different habitats: aquatic environments and the human intestines. In its free phase, Vibrio cholerae thrives in warm, low-salinity waters.

It can live in rivers, lakes, ponds, estuaries or in the sea. It is endemic in Africa, Asia, South America and Central America. Then as a parasite it lives in the small intestine of human beings.

The bacterium is even found in tropical beach areas, in waters with 35% salinity and temperatures of 25 ° C.

The presence of pathogenic Vibrio cholerae has been reported in arid zones and inland in Africa. This indicates that the species can survive in a much greater range of habitat variation than previously thought.

Some studies show that Vibrio cholerae is a wild bacterium in freshwater bodies in tropical rainforests.

Reproduction and life cycle

Being a bacterium, it reproduces by binary fission or bipartition. Vibrio cholerae persists in water as free planktonic vibrios or aggregates of vibrios.

Aggregates of vibrios form biofilms in phytoplankton, zooplankton, insect egg masses, exoskeletons, detritus, and even on aquatic plants. They use chitin as a source of carbon and nitrogen.

Biofilms consist of stacked bacteria surrounded by water channels, adhered to each other and to the substrate by external polysaccharide production. It is a thin, gelatinous layer of bacteria.

Environmental vibrios are ingested through consumption of contaminated food or water. Once inside the digestive system, the bacteria colonize the epithelium of the small intestine.

Subsequently the vibrio binds to the mucosa by pilis and specialized proteins. Then, it begins its multiplication and the secretion of the cholera toxin. This toxin promotes diarrhea whereby the bacteria re-enter the external environment.

Nutrition

This bacterium has a metabolism based on the fermentation of glucose. In the free state, it obtains its food in the form of carbon and nitrogen from various organic sources. Some of these are chitin or carbon exuded by algae from phytoplankton.

For the assimilation of iron, the species produces the siderophore vibriobactin. Vibriobactin is an iron chelating compound that dissolves this mineral allowing it to be absorbed by active transport.

In aquatic environments, it fulfills important functions related to its nutrition in the ecosystem. Contributes to the remineralization of organic carbon and mineral nutrients.

On the other hand, it is bacterivorous. All this assigns it a relevant role as part of the bacterioplankton in the microbial loops or microbial food webs in aquatic ecosystems.

Vibrio cholerae carries out the fundamental processes to digest its food outside, through the substances it secretes. This mechanism is similar to that of other bacteria.

The species acts on the substrate causing the dissolution of the essential mineral elements for its nutrition, which are subsequently absorbed. Also, in the search and processing of food they attack other bacteria. They can attack the same species, but not their own strain.

To kill other bacteria, V. cholerae uses a mechanism called the Type VI Secretion System (T6SS). This system is similar to a harpoon that penetrates the cell wall of other Gram negative bacteria, causing them to die.

Thus, the nutritional compounds of these bacteria are available. T6SS is similar to the system used by bacteriophages to inoculate their genetic information into bacterial cells. This system is possibly also used by Vibrio cholerae to inoculate its toxin in epithelial cells.

Pathogeny

Transmission

The bacteria is transmitted by the fecal-oral route, either person to person, through contaminated water, objects or food. Cholera is explosive when it occurs in a population without prior immunity.

For years it was thought that the main route of transmission of the disease was the intake of contaminated water. Today it is known that there are foods that can be vehicles for the transmission of Vibrio cholerae. Some of these foods include: clams, oysters, mussels, shrimp, and crabs.

A high dose of inoculum is required to make a healthy individual sick, about 10 ⁵ - 10 ⁸ bacteria. However, in weakened or malnourished individuals a much smaller amount of inoculum is sufficient. The incubation period for the disease ranges from 6 hours to 5 days.

epidemiology

Although there is information on cholera epidemics since the 14th century, the first documented pandemics date from the early 19th century. Between 1817 and 1923, at least six known cholera pandemics occurred, caused by the classical biotype of Vibrio cholerae.

This series of pandemics started from India, mainly from the Ganges River Delta. Once it reached the Middle East, it expanded from there to Europe. Another route of entry to Europe was the Mediterranean, through caravans from Arabia. From Europe it came to America.

From 1923 to 1961 there was a pandemic-free period for this disease and only local cases of cholera were known. Starting in 1961, it resurfaces with a new biotype called Tor that caused the seventh pandemic.

Since the 1990s, more than 200 serogroups and atypical forms of Tor have been identified. In 1991 the eighth cholera pandemic occurred. Currently, cholera cases are mainly restricted to regions of sub-Saharan Africa, India, Southeast Asia and some areas of the Caribbean. In these regions it has become endemic.

Form of action

The bacteria produce several toxins, but the classic dehydrating diarrheal symptoms of the disease are caused by cholera enterotoxin (TC).

It is made up of a non-toxic B subunit and an enzymatically active A subunit. The B subunit acts on the receptors of the epithelial cells of the small intestine. Subunit A activates adenylate cyclase.

Enterotoxin binds to the cells of the intestinal mucosa through bacterial pili and causes diarrhea and dehydration by activating the enzyme adenylate cyclase.

This leads to increased production of intracellular cyclic adenosine monophosphate, which causes the mucosal cells to pump large amounts of water and electrolytes.

Vibrio cholerae releases other toxins such as ZOT and ACE. They act by neutralizing cells of the immune system that are capable of eliminating vibrios (IgG case). They can also neutralize cholera enterotoxin (IgA case).

Symptoms and Treatment

Symptoms include: hypovolemic shock, vomiting, diarrhea, acidosis, muscle cramps, dry skin, glassy or sunken eyes, high heart rate, lethargy, and drowsiness.

In endemic areas, the presence of the bacteria has been detected in people close to people with cholera. Patients do not present visible symptoms of the disease, indicating the existence of asymptomatic individuals.

Cholera is preventable and there are oral vaccines that are effective against the disease up to 60-66%. However, outbreaks can be caused by natural events or caused by humans. This occurs by contaminating water or compromising access to safe water and sanitation.

Adequate and timely rehydration therapy can reduce mortality to less than 1%. Antibiotic treatment can decrease vibrio shedding. However, none of these treatment measures have significantly altered the spread of the disease.

Antibiotics commonly used in adults are those of the group of Doxycycline and Tetracycline. Nitrofuran Furazolidone is used in pregnant women. Sulfamethoxazole and trimethoprim (SMZ + TMP) are recommended in children.

A fundamental element for the control of epidemics is the adequate sanitary management of sewage and sanitary conditions in general. In this sense, cholera is a disease associated with conditions of poverty.

The presence of Vibrio cholerae in the body is detected with laboratory tests such as PCR, ELISA test or the use of selective culture media.

References

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