Orientia tsutsugamushi
"O. tsutsugamushi" causes a complex and dangerous infection scrub typhus. Infection starts when chiggers bite on the skin during their feeding. The bacteria are deposited at the site of feeding (inoculation), where they multiply. They cause progressive tissue damage (necrosis). Necrosis progresses to inflammation of the blood vessels called vasculitis. This in turn causes inflammation of the lymph nodes, called lymphadenopathy. Within a few days, vasculitis extends to various organs including liver, brain, kidney, meninges and the lung. The disease is responsible for nearly a quarter of all the febrile (high fever) illness in endemic areas. Mortality in severe case or due to improper treatment or misdiagnosis may be as high as 30-70%. About 6% of infected people die untreated, and 1.4% of the patients die even with medical treatment. Moreover, death rate can be as high as 13% where medical treatment is not properly handled. In cases of misdiagnosis and failure of treatment, systemic complications rapidly develop including acute respiratory distress syndrome, acute kidney failure, encephalitis, gastrointestinal bleeding, hepatitis, meningitis, myocarditis, pancreatitis, pneumonia, septic shock, sub-acute thyroiditis, and multi-organ dysfunctions. Harmful symptoms involving multiple organ failure and neurological impairment are difficult to treat, and can be lifelong debilitation or directly fatal. The central nervous system is often affected and result in various complications including cerebellitis, cranial nerve palsies, meningoencephalitis, plexopathy, transverse myelitis, neuroleptic malignant syndrome, and Guillan-Barré syndrome. Death rates due to complications can be up to 14% in brain infections, and 24% with multiple organ failure. It is the major cause of acute encephalitis syndrome in India, where viral infection Japanese encephalitis has been regarded as the main factor.
Orientia tsutsugamushi
The bacterium is enclosed by a cell wall on the outside and cell membrane on the inside. The cell covering take up stains such as Giemsa and Gimenez stains. Although its cell wall has a classic bacterial double layer, its outer leaflet is much thicker than the inner one, which is just the opposite in "Rickettsia" species. A capsule layer that forms a spherical halo in other bacteria is missing. The cell wall is soft and tender due to the absence of peptidoglycan, which is otherwise characteristic of the rigid cell walls of other bacteria. Classic bacterial lipophosphoglycans such as muramic acid, glucosamine, hydroxy fatty acids, heptose, and 2-keto-3-deoxyoctonic acid are also absent in the cell wall. Due to the absence of peptidoglycan, the bacterium is naturally resistant to all β-lactam antibiotics (such as penicillin), while "Rickettsia" species are normally sensitive to such drugs. Its genome totally lacks the genes for lipophosphoglycan synthesis, but does contain those for peptidoglycan. In fact, peptidoglycan is synthesised in very small quantity that can hardly be detected and plays minor or no role in the cell wall. There are unique genes such as "PBP1", "alr", "dapF", and "murl", which are not known in other bacteria. The cell membrane is also chemically different in its protein composition, and this difference gives rise to strain variations within the species itself. The cytoplasm is clear and shows distinct DNA and ribosomes.
The bacterium is highly virulent such that its isolation and cell culture are done only in a laboratory with biosafety level 3 facility. Unlike other bacteria which can easily grow on different culture media, it can be grown only in the yolk sacs of developing chicken embryos and in cultured cell lines such as HeLa, BHK, Vero, and L929 cell lines. In contrast to "Rickettsia" species which reside in the nucleus of the host cell, it mostly grow within the cytoplasm of the host cell. Genetically, it differs from other "Rickettsia" by only 9%. Even though adaptation to obligate intracellular parasitism among bacteria generally results in reduced genome, it has a genome size of about 2.0–2.7 Mb depending on the strains, which is comparatively larger than those of other rickettsiales – two times larger than that of "R. prowazekii", the most well-known member. The entire genome is distributed in a single chromosome. Whole genome sequences are available only for Ikeda and Boryong strains, both from the Republic of Korea. The genome of Ikeda strain is 2,008,987 base pairs (bp) long, and contains 1,967 protein-coding genes. The Boryong strain is larger with 2,127,051 bp and 2,179 protein-coding genes.