How do rickettsia reproduce

Such invaders include Microorganisms commonly called germs, such as bacteria, viruses, and fungi Parasites A sore covered by a black scab eschar may form at the site of the bite.

Because the rash often does not appear for several days, early rickettsial infection is often mistaken for a common viral infection, such as influenza. People may have swollen lymph nodes. As the infection progresses, people typically experience confusion and severe weakness—often with cough, difficulty breathing, and sometimes vomiting.

In scrub typhus tsutsugamushi disease , a black scab eschar forms at the site of a chigger bite top. A rash develops later bottom. When the infection is advanced, gangrene may develop, the liver or spleen may enlarge, the kidneys may malfunction, and blood pressure may fall dangerously low causing shock Shock Shock is a life-threatening condition in which blood flow to the organs is low, decreasing delivery of oxygen and thus causing organ damage and sometimes death.

Blood pressure is usually low Death can result. Because rickettsiae and rickettsia-like bacteria are transmitted by ticks, mites, fleas, and lice, doctors ask people. Being bitten is a helpful clue—particularly in geographic areas where rickettsial or a related infection is common.

However, many people do not recall such a bite. If doctors suspect Q fever, they may also ask whether people were at or near a farm because cattle, sheep, and goats are the host for the bacteria that cause this infection. A physical examination is done to determine which parts of the body are affected and what the rash looks like. Doctors also look for an eschar that people may not have noticed and for swollen lymph nodes.

Testing is usually needed to confirm the diagnosis. Often, doctors cannot confirm an infection with rickettsiae or rickettsia-like bacteria quickly because these bacteria cannot be identified using commonly available laboratory tests. Special blood tests for these bacteria are not routinely available and take so long to process that people usually need to be treated before test results are available.

Doctors base their decision to treat on the person's symptoms and the likelihood of possible exposure. In immunofluorescence assays, foreign substances produced by the bacteria antigens are labeled with a fluorescent dye. The polymerase chain reaction PCR technique is used to increase the amount of the bacteria's DNA, so that the bacteria can be detected more rapidly.

Antibiotics are usually started without waiting to get the results of tests. Early treatment of rickettsial infections can prevent complications from developing, reduce the risk of dying, and shorten the recovery time. Rickettsial infections respond promptly to early treatment with the antibiotics doxycycline preferred or chloramphenicol. These antibiotics are given by mouth unless people are very sick. In such cases, antibiotics are given intravenously.

After treatment, most people with a mild infection noticeably improve in 1 or 2 days, and fever usually disappears in 2 to 3 days. People take the antibiotic for a minimum of 1 week—longer if the fever persists. When treatment begins late, improvement is slower and the fever lasts longer.

The bacteria spread through the bloodstream and infect the endothelium. Adherence to the host cell is the first step of rickettsial pathogenesis. The adhesins are presumed to be outer membrane proteins. The outer membrane protein OmpA has been implicated in adherence of R. The host cell receptor for any Rickettsia has yet to be identified. Although the main target cells of Rickettsia in vivo are endothelial cells, rickettsiae can infect virtually every cell line in vitro.

Thus, either the receptor for Rickettsia is ubiquitous among cells, or rickettsiae can bind to different receptors. Invasion of Host Cells Upon attaching to the host cell membrane, rickettsiae are phagocytosed by the host cell. The rickettsiae are believed to induce host cell phagocytosis because they can enter cells that normally do not phagocytose particles.

Once phagocytosed by the host cell, rickettsiae are observed to quickly escape from the phagosome membrane and enter the cytoplasm. The mechanism of escape from the phagosome membrane is not well understood, but it is thought to be mediated by a rickettsial enzyme, phospholipase A2. Movement within and Release from the Host Cell Observations in cell culture systems suggest that the mechanisms of intracellular movement and destruction of the host cells differ among the spotted fever group and typhus group rickettsiae.

Typhus group rickettsiae are released from host cells by lysis of the cells. After infection with R. Phospholipase A2 may be involved in cell lysis. Typhus group rickettsia-infected host cells have a normal ultrastructural appearance.

Spotted fever group rickettsiae seldom accumulate in large numbers and do not lyse the host cells. They escape from the cell by stimulating polymerization of host cell-derived actin tails, which propel them through the cytoplasm and into tips of membranous extrusions, from which they emerge.

Infected cells exhibit signs of membrane damage associated with an influx of water, but the means by which rickettsiae damage host cell membranes is uncertain. There is evidence to suggest a role for free radicals of oxygen, phospholipase, and a protease. The protein responsible for the actin-based movement in spotted fever group rickettsiae has yet to be identified, but it is apparently different than the proteins responsible for actin polymerization by Listeria monocytogenes and Shigella flexneri.

Rickettsial diseases vary in clinical severity according to the virulence of the Rickettsia and host factors, such as age, male gender, alcoholism, and other underlying diseases.

The most virulent rickettsiae are R. All rickettsial infections begin with introduction of the organisms into the skin, either through a tick bite or cutaneous abrasions contaminated by flea or louse feces.

In this environment, rickettsiae are provided with a rich source of biosynthetic precursors not normally encountered by free-living bacteria and have evolved a number of unique mechanisms to transport such metabolites as nucleotides and nucleotide sugars.

Other than the obvious property of replicating inside eukaryotic cells, the molecular mechanisms of cellular damage are ill defined. The typhus-group rickettsiae multiply within host cells to great numbers without profound damage until lysis occurs. In contrast, the spotted fever-group rickettsiae spread rapidly from cell to cell by an actin-based motility.