Two potentially serious bacterial diseases are Rocky Mountain Spotted Fever (RMS

Question

Two potentially serious bacterial diseases are Rocky Mountain Spotted Fever (RMSF) and cholera.
(a) What is the causative agent of RMSF? In your own words, give a description of the causative agent and the disease. Be sure to include general characteristics of the microbe, how the disease is transmitted, a general description of the disease, and some ways you can avoid being infected. (10 pts.)
(b) What is the causative agent of cholera? In your own words, give a description of the causative agent and the disease. Be sure to include general characteristics of the microbe, how the disease is transmitted, a general description of the disease, and some ways you can avoid being infected. (10 pts.)
(c) Why do you think it would be more difficult to rid a community of RMSF than cholera?

Explanation / Answer

(a)Rocky mountain spotted fever/blue fever is a lethal and a ricketsial disease.

Rocky Mountain spotted fever, like all rickettsial infections, is classified as a zoonosis. Zoonoses are diseases of animals that can be transmitted to humans. Some zoonotic diseases require a vector (e.g., a mosquito, tick, or mite) to be transmitted from the animal host to the human host. In the case of Rocky Mountain spotted fever, ticks are the natural hosts, serving as both reservoirs and vectors of R. rickettsii. Ticks transmit the organism to vertebrates primarily by their bites. Less commonly, infections may occur following exposure to crushed tick tissues, fluids, or tick feces.

A female tick can transmit R. rickettsii to her eggs in a process called transovarial transmission. Ticks can also become infected with R. rickettsii while feeding on blood from the host in either the larval or nymphal stage. After the tick develops into the next stage, the R. rickettsii may be transmitted to the second host during the feeding process. Furthermore, male ticks may transfer R. rickettsii to female ticks through body fluids or spermatozoa during the mating process. These types of transmission represent how generations or life stages of infected ticks are maintained. Once infected, the tick can carry the pathogen for life.

Rickettsiae are transmitted to a vertebrate host through saliva while a tick is feeding. It usually takes about 24 hours of attachment and feeding before the rickettsiae are transmitted to the host. In general, about one to three percent of the tick population carries R. rickettsii, even in areas where the majority of human cases are reported. Therefore the risk of exposure to a tick carrying R. rickettsii is low.

Vectors include the American dog tick Dermacentor variabilis, Dermacentor andersoni, Rhipicephalus sanguineus, and Amblyomma cajennense. Not all of these are of equal importance, and most are restricted to certain geographic areas.

The two major vectors of R. rickettsii in the United States are the American dog tick and the Rocky Mountain wood tick. American dog ticks are widely distributed east of the Rocky Mountains and they also occur in limited areas along the Pacific Coast. Dogs and medium-sized mammals are the preferred hosts of an adult American dog ticks, although it feeds readily on other large mammals, including human beings. This tick is the most commonly identified species responsible for transmitting R. rickettsii to humans. Rocky Mountain wood ticks (Dermacentor andersoni) are found in the Rocky Mountain states and in southwestern Canada. The life cycle of this tick may require up to three years for its completion. The adult ticks feed primarily on large mammals. The larvae and nymphs feed on small rodents.

Other tick species have been shown to be naturally infected with R. rickettsii or serve as experimental vectors in the laboratory. These species are likely to play only a minor role in the ecology of R. rickettsii.

You can decrease your chances of contracting Rocky Mountain spotted fever by taking some simple precautions:

Remove a tick with tweezers. Gently grasp the tick near its head or mouth. Don't squeeze or crush the tick, but pull carefully and steadily. Once you have the entire tick removed, apply antiseptic to the bite area.

Though there are many purportedly effective methods for helping to remove a tick, such as petroleum jelly, alcohol or even applying a hot match to the tick's body, none is a good method for tick removal.

(b)The causative agent of cholera is a baceria called Vibrio cholerae.

Vibrio cholerae is a Gram-negative, comma-shaped bacterium. Initial isolates are slightly curved, whereas they can appear as straight rods upon laboratory culturing. The bacterium's natural habitat is brackish or saltwater. Some strains of V. cholerae cause the diseasecholera. V. cholerae is a facultative anaerobic organism and has a polar flagellum at one cell pole as well as pili. V. cholerae can undergo respiratory and fermentative metabolism. It is one of the most devastating human diseases, with a rapid onset of diarrhea and vomiting within several hours to 2-3 days of ingestion. Due to massive fluid losses (15-20 liters/day), the untreated mortality rate is in excess of sixty percent. However, rehydration therapy brings the mortality rate to below one percent. V. cholerae was first isolated as the cause of cholera by Italian anatomist Filippo Pacini in 1854, but his discovery was not widely known until Robert Koch, working independently 30 years later, publicized the knowledge and the means of fighting the disease.

Transmission

Cholera has been found in two animal populations: shellfish and plankton.

Cholera is typically transmitted to humans by either contaminated food or water. Most cholera cases in developed countries are a result of transmission by food, while in the developing world it is more often water. Food transmission occurs when people harvest seafood such as oysters in waters infected with sewage, as Vibrio cholerae accumulates in zooplankton and the oysters eat the zooplankton.

People infected with cholera often have diarrhea, and disease transmission may occur if this highly liquid stool, colloquially referred to as "rice-water", contaminates water used by others. The source of the contamination is typically other cholera sufferers when their untreated diarrheal discharge is allowed to get into waterways, groundwater or drinking water supplies. Drinking any infected water and eating any foods washed in the water, as well as shellfish living in the affected waterway, can cause a person to contract an infection. Cholera is rarely spread directly from person to person.

Both toxic and nontoxic strains exist. Nontoxic strains can acquire toxicity through a temperate bacteriophage. Coastal cholera outbreaks typically follow zooplankton blooms, thus making cholera a zoonotic disease.

Mechanism

When consumed, most bacteria do not survive the acidic conditions of the human stomach.[21] The few surviving bacteria conserve theirenergy and stored nutrients during the passage through the stomach by shutting down much protein production. When the surviving bacteria exit the stomach and reach the small intestine, they must propel themselves through the thick mucus that lines the small intestine to reach the intestinal walls where they can attach and thrive.

Once the cholera bacteria reach the intestinal wall they no longer need the flagella to move. The bacteria stop producing the protein flagellin to conserve energy and nutrients by changing the mix of proteins which they express in response to the changed chemical surroundings. On reaching the intestinal wall, V. cholerae start producing the toxic proteins that give the infected person a watery diarrhea. This carries the multiplying new generations of V. cholerae bacteria out into the drinking water of the next host if proper sanitation measures are not in place.

The cholera toxin (CTX or CT) is an oligomeric complex made up of six protein subunits: a single copy of the A subunit (part A), and five copies of the B subunit (part B), connected by a disulfide bond. The five B subunits form a five-membered ring that binds to GM1gangliosides on the surface of the intestinal epithelium cells. The A1 portion of the A subunit is an enzyme that ADP-ribosylates G proteins, while the A2 chain fits into the central pore of the B subunit ring. Upon binding, the complex is taken into the cell via receptor-mediated endocytosis. Once inside the cell, the disulfide bond is reduced, and the A1 subunit is freed to bind with a human partner protein called ADP-ribosylation factor 6 (Arf6). Binding exposes its active site, allowing it to permanently ribosylate the Gs alpha subunit of theheterotrimeric G protein. This results in constitutive cAMP production, which in turn leads to secretion of H2O, Na+, K+, Cl, and HCO3into the lumen of the small intestine and rapid dehydration. The gene encoding the cholera toxin was introduced into V. cholerae by horizontal gene transfer. Virulent strains of V. cholerae carry a variant of temperate bacteriophage called CTXf or CTX.

Microbiologists have studied the genetic mechanisms by which the V. cholerae bacteria turn off the production of some proteins and turn on the production of other proteins as they respond to the series of chemical environments they encounter, passing through the stomach, through the mucous layer of the small intestine, and on to the intestinal wall. Of particular interest have been the genetic mechanisms by which cholera bacteria turn on the protein production of the toxins that interact with host cell mechanisms to pump chloride ions into the small intestine, creating an ionic pressure which prevents sodium ions from entering the cell. The chloride and sodium ions create a salt-water environment in the small intestines, which through osmosis can pull up to six litres of water per day through the intestinal cells, creating the massive amounts of diarrhea. The host can become rapidly dehydrated if an appropriate mixture of dilute salt water and sugar is not taken to replace the blood's water and salts lost in the diarrhea.

By inserting separate, successive sections of V. cholerae DNA into the DNA of other bacteria, such as E. coli that would not naturally produce the protein toxins, researchers have investigated the mechanisms by which V. cholerae responds to the changing chemical environments of the stomach, mucous layers, and intestinal wall. Researchers have discovered a complex cascade of regulatory proteins controls expression of V. choleraevirulence determinants. In responding to the chemical environment at the intestinal wall, the V. cholerae bacteria produce the TcpP/TcpH proteins, which, together with the ToxR/ToxS proteins, activate the expression of the ToxT regulatory protein. ToxT then directly activates expression of virulence genes that produce the toxins, causing diarrhea in the infected person and allowing the bacteria to colonize the intestine. Current research aims at discovering "the signal that makes the cholera bacteria stop swimming and start to colonize (that is, adhere to the cells of) the small intestine."

Prevention

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