Biological Sciences
Typhus
Typhus is a group of infectious diseases caused by bacteria transmitted by lice, fleas, or mites. Symptoms include fever, headache, and rash, and severe cases can lead to organ failure and death. Historically, typhus has been associated with crowded and unsanitary living conditions, and outbreaks have occurred during wars and natural disasters.
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10 Key excerpts on "Typhus"
eBook - PDF- Michael R. Conover, Rosanna M. Vail(Authors)
- 2014(Publication Date)
- CRC Press(Publisher)
257 17 Epidemic Typhus and Murine Typhus After World War I, 20–30 million people died in Eastern Europe from this dis-ease [epidemic Typhus], and an additional several million died during and after World War II. Crowding, the scarcity of clean clothes, and dirt were the principal factors enabling the spread of Typhus. Gross (1996) 17.1 INTRODUCTION AND HISTORY The Typhus group of rickettsiae includes two diseases—epidemic Typhus and murine Typhus—which are produced by Rickettsia prowazekii and R. typhi , respectively. Both pathogens are small (0.3–2.0 µm), Gram-negative coccobacilli (Figure 17.1). Neither disease should be confused with typhoid fever, which is a disease caused by Salmonella bacteria. Epidemic Typhus is also known as louse-borne Typhus, camp fever, hospital fever, and ship fever. It is a contagious disease and is spread among humans by the human body louse ( Pediculus humanus corporis ; Figure 17.2). Dr. Charles Nicolle discov-ered in 1909 that lice spread epidemic Typhus from one person to another; he later admitted that his discovery was made quite by accident. While a physician in Tunis (Tunisia’s largest city) during an epidemic, he observed that people waiting to be admitted to the hospital often spread Typhus to others, including workers in the hos-pital’s laundry room, but that once patients were admitted to the hospital, received a hot bath, and dressed in hospital clothing, the patients ceased to be infectious. Nicolle realized that the infection was spread by the patients’ clothing and hypoth-esized that lice in the clothing were the vector responsible for transmitting the patho-gen from one person to another. His discovery earned him the Nobel Prize in 1928 (Gross 1996). The origins of epidemic Typhus are unclear. Some believe that it originated in the Old World and was an ancient scourge of humans.
eBook - PDF- David Mabey, Geoffrey Gill, Eldryd Parry, Martin W. Weber, Christopher J. M. Whitty(Authors)
- 2013(Publication Date)
- Cambridge University Press(Publisher)
Rickettsioses sensu stricto Louse-borne rickettsiosis: epidemic Typhus Epidemic Typhus may have been responsible for the plague described in Athens in the fifth century BC. The term was first used in the eighteenth century and it derived from the Greek word typhos, meaning ‘smoky’ or ‘hazy’, emphasizing the often stuporous and slumberous state of its victims. The disease was certainly recognized by the mid-nineteenth century, when Typhus was differentiated from typhoid and a number of other fevers, although in the sixteenth century G. Fracastoro had already described typical exanthems. In 1909–1910 Nicolle demonstrated it was transmitted by the body louse and, for this discovery, he was awarded the Nobel Prize (Bechah et al., 2008). The problem in Africa Body lice thrive during times of war, conflict, famine and natural catastrophes and high prevalence of pediculosis is indispensable for Typhus epidemics. As Zinsser stated in 1935, epidemic Typhus probably caused more deaths than all the wars in human history. During World War II, Typhus was prevalent in northern Africa and in southern, central and eastern Europe. Foci remained in the cooler mountainous countries in northern, north-eastern and cen- tral Africa. Only a few cases were recorded from these sites, how- ever, and in the 1980s the WHO ceased monitoring the disease in most countries. In 1995 it was suspected to be endemic only in Ethiopia, but it dramatically re-emerged in 1997, with more than 100 000 cases during the civil war in Burundi. Morbidity still continues to register in Rwanda and the disease is probably emerging in DRC. A case was recently reported in North Africa. Epidemic Typhus remains a potential major health risk in Africa, particularly in refugee camps in the cooler mountainous areas (Bechah et al., 2008). Epidemiology Epidemic Typhus is caused by Rickettsia prowazekii, which belongs to the Typhus group of the genus Rickettsia.
eBook - PDF- Alfonso J. Rodriguez-Morales(Author)
- 2012(Publication Date)
- IntechOpen(Publisher)
Table 1. Rickettsia spp. causing medical diseases, vectors and distribution Rickettsiosis as Threat for the Traveller 7 2. Typhus syndrome Typhus syndrome refers to a febrile syndrome with mental status impairment and rash. It is caused by Rickettsia prowazekii (epidemic Typhus) and Rickettsia typhi (formerly, R. mooseri ). Rickettsia felis may also produce a Typhus syndrome named flea-borne spotted fever, which is similar to R. typhi infection (perhaps less severe) (Walker & Raoult, 2010; Dumler & Walker 2010; Oteo et al., 2006). Nowadays epidemic Typhus is only present in some regions of Africa, Russia and in Peru. It is associated with bad hygienic conditions that are necessary for body lice parasitization. Sporadic cases associated with contact with flying squirrels and their parasite arthropods, which have been involved as new reservoirs of the infection, have also been reported in USA. A possible source of R. prowazekii infection may be a recrudescent case (Brill-Zinsser disease) of R. prowazekii infection. If hygienic conditions are altered and an epidemic of body lice appears may be an epidemic of Typhus, as occurred in Burundi with hundreds of affected people (Raoult et al., 1998). Some cases of louse-borne Typhus in travellers have been published (Zanetti et al., 1998; Kelly et al., 2002). Endemic Typhus or murine Typhus is associated with the presence of fleas. The main vector is the rat flea ( Xenopsylla cheopis ) associated with dirt and poor hygienic conditions. Flea-borne spotted fever is associated with the cat flea, and in this case bad hygienic conditions are not necessary. Murine Typhus and flea-borne spotted fever are distributed all over the world. Although they are more frequent in tropical and subtropical areas, cases have also been reported in the Mediterranean area (Greece, Italy, Spain, France and Portugal) (Bernabeu-Wittel et al., 1999; Angel-Moreno et al., 2006; Gikas et al,. 2009; Pérez-Arellano et al., 2005; Oteo et al., 2006).
eBook - PDF- Stephen A. Morse(Author)
- 2012(Publication Date)
- IntechOpen(Publisher)
It killed millions of people through this period. Although worldwide epidemics of Typhus may not occur again, the threat of louse-borne Typhus is still real as small scale epidemics or large scale epidemics in settings of extreme poverty and natural and manmade disasters. Louse-borne Typhus occurs in epidemics when social, economic, or political systems are disrupted exposing a large population such as refugees to louse infestation due to lack of hygiene. This situation has been observed in recent outbreaks of Typhus in Burundi, Algeria, Peru, and Russia. In 1997, it was estimated that as many as 100,000 cases of Typhus occurred in the refugee camps of Burundi during a civil war (Raoult et al., 2004). RMSF originated as an emerging infectious disease on the western frontier in the Rocky Mountains. Now the disease is found all over the United States, and over half of the cases occur in the southeastern and south-central regions of the United States and in South America (Center for Disease Control and prevention[CDC], 2010). Bioterrorism 180 2. Etiologic agents Rickettsia are small (0.3 – 0.5 x 0.8 – 1.0 μm) gram-negative obligately intracellular bacterial parasites of eukaryotic cells. The genus is subdivided into the Typhus group (TG) and spotted fever group (SFG) based on lipopolysaccharide (LPS) antigens. The TG rickettsiae include louse-borne R. prowazekii that causes epidemic Typhus and flea-borne R. typhi that causes murine Typhus. The SFG rickettsiae consist of more than 20 named species, which are transmitted by tick bite except for R. akari (mite-borne) and R. felis (flea-borne). Antibodies to LPS antigens cross-react among organisms within the same biogroup, but do not cross-react between the two groups (Vishwanath, 1991). There are two major outer membrane proteins in Rickettsia OmpA (Sca 0) and OmpB (Sca5). OmpB exists in all Rickettsia and OmpA exists only in SFG rickettsiae.
eBook - PDF- Edward Bittar(Author)
- 1998(Publication Date)
- Elsevier Science(Publisher)
The classical transmission cycle for murine Typhus is rat-flea-rat and accidentally rat-flea-man. The rats display no evidence of infec- tion and have a normal life span. Fleas do not appear to be harmed by their infection. Once infected, fleas remain infected for life. The disease can be year round if climatic conditions in these foci are favorable for survival of rats and their ectoparasites. The majority of cases occur during the late spring and early autumn or whenever warm and humid climates prevail. R. typhi is spread to man by contamination of the wound with infected feces, which are deposited on the skin of the host at the time of feeding, by contamination of the respiratory tract, or conjunctivae of the host with infected flea feces. Rubbing the rickettsia into the skin promotes entry into the host. R. typhi are hardy organisms and may remain viable in fecal matter for years provided that the humidity and temperature are appropriate. Beside the classical rat-flea cycle, recent studies suggest the involvement of an opossum-flea cycle. Endemic areas include South West United States, Mexico and Central America, the Balkans, West Africa, and southeast Asia. Bacterium The Typhus fever bacterium resembles the spotted fever bacterium in morphology. The G + C content of DNA is 28.5 - 29.7 mol.% and the genome size is 1.1 • 10 9 daltons. Typhus group rickettsiae grow in the cytoplasm of eukaryotic cells (Figure 2). During the exponential growth very few bacteria exit from the infected cell to set up secondary infections in neighboring cells. Instead they grow and fill the cytoplasm until, presumably, the host can no longer support the growth of the parasite. The host cell then bursts and hundreds of bacteria are released to initiate infections in many new host cells. It appears that phospholipase A stimulates the
- James H.S. Gear(Author)
- 2019(Publication Date)
- CRC Press(Publisher)
Louse-borne Typhus fever ranks among the top epidemic diseases causing suffering and death. The greatest recorded epidemics occurred in Russia and eastern Poland during 1915 to 1922, when Typhus afflicted 30 million inhabitants and caused an estimated 3 million deaths. Now the scourge is under control, largely through better hygienic methods and improvement in socioeconomic standards. Yet, it occurs in underdeveloped countries in Asia, in Africa (e.g., Ethiopia and Burundi), and in the highlands of Central and South America (e.g., Mexico, Peru, and Columbia), where it is endemic. It occurs during the cold winter months when lousiness is more prevalent.Epidemic Typhus now occurs in the U.S. as a flying squirrel-(Glaucomys volans ) related illness. For the years 1977 to 1982, in excess of 30 human squirrel-related Typhus cases were reported by the Center for Disease Control in various eastern states. The disease is milder than the classic form and is nonfatal.14The clinical differentiation between Typhus and typhoid fever was established by Gerhard in 1836, based on clinical observations and post-mortem findings.15 Murchison gave the classic description of the illness in 1884.16 Following Ricketts’ description of R. rickettsii 8in 1906, Nicolle, working in Tunisia, reproduced Typhus fever in monkeys and demonstrated transmission by the body louse.17 Brill, in New York, recognized a febrile disease which resembled Typhus and was unassociated with lousiness18 , now known as recurrent Typhus or Brill-Zinsser disease.19
eBook - ePub- Irwin W. Sherman(Author)
- 2017(Publication Date)
- ASM Press(Publisher)
Nicolle also solved another mystery: he noticed that Typhus tended to occur in individuals who were unable to clean themselves of their body lice and lice-infested clothing—in particular criminals lodged in the filthy jails—and that “prison fever” could spread from felon to judge, not by foul-smelling air but through infected lice. In September 1909 he wrote that it was obvious that Typhus was transmitted by lice. Nicolle received the 1928 Nobel Prize for his work on the transmission of Typhus; the discovery of the causative agent of Typhus, however, was left to others.Typhus is not the same as typhoid fever, which is a waterborne disease caused by a bacillus, Salmonella. Today we know the causative agent of the disease Typhus to be a bacteria-like organism, Rickettsia prowazekii, related to the organisms that produce Rocky Mountain spotted fever, Rickettsia rickettsii, described by H. T. Ricketts in 1906, with a tick vector and a fatality rate of 20%. Rickettsias are small, oblong, Gram-negative bacteria-like organisms (Fig. 6.5 ) that are intracellular parasites. Rickettsias range in size from 0.3 to 0.6 µm and therefore are of intermediate size between viruses and bacteria.Howard Ricketts (1871-1910) described the infectious agents responsible for both Rocky Mountain spotted fever and Typhus. Ricketts graduated from Northwestern University Medical School, and before taking up a position as an assistant professor of pathology at the University of Chicago, he traveled to the Pasteur Institute in Paris. There he became a bona fide microbe hunter. In the spring of 1906, Ricketts went to Montana to study “spotted fever,” and while examining stained specimens of blood from infected monkeys and guinea pigs, he found “a bipolar bacillus.” He saw the same bacillus in humans suffering from the disease; however, despite his training in standard techniques of bacteriology, such as culturing in nutrient broth and on blood agar, all attempts on his part to grow these bacilli failed. Ricketts did note that “spotted fever” was associated with people who had tick bites, and upon examining the salivary glands and gut of ticks that had fed on infected guinea pigs, he found the telltale microbe. But when ticks were fed on uninfected guinea pigs, no such microbes were seen. He concluded that this “spotted fever” of the Rocky Mountains was transmitted by the bite of ticks that carried the “bipolar bacilli.”
- Pratibha Singhi, Diane E Griffin, Charles R Newton(Authors)
- 2014(Publication Date)
- Mac Keith Press(Publisher)
20 RICKETTSIAL DISEASE Timothy D Minniear and Steven C Buckingham Rickettsiae are arthropod-borne gram-negative coccobacilli that can cause a broad range of human diseases. The agents of spotted fevers, Typhus and ehrlichiosis are included within the class Alphaproteobacteria , all members of which are incapable of prolonged survival outside of a host cell. Coxiella burnetii , the causative agent of Q fever, belongs to the class Gammaproteobacteria and is capable of surviving in the environment. Rickettsia: spotted fever group E PIDEMIOLOGY The vectors and natural hosts for the spotted fever group (SFG) rickettsiae are arachnids: ticks and mites. These rickettsiae can be found across the globe (Table 20.1). Ticks are cap-able of passing these organisms to other ticks through copulation, by transovarian passage, and by feeding in close proximity to other ticks. Humans are dead-end hosts for all SFG rickettsiae. P ATHOGENESIS AND C LINICAL M ANIFESTATIONS The vector primarily transmits infection via contaminated saliva during a blood meal; it takes several hours of feeding before infection is established. Once inside the host, the primary targets for all SFG rickettsiae are vascular endothelial cells, which they infect directly near the site of tick attachment or by transportation to distant endothelial cells through lymphatics or blood vessels. The ensuing endothelial necrosis and inflammatory response produce a widespread vasculitis that results in vascular leakage and intravascular coagulation and is responsible for the bulk of the manifestations in spotted fever disease (Walker et al. 2003). The rickettsia responsible for the most severe disease is R. rickettsii ; other pathogenic rickettsiae cause similar though less severe clinical diseases. Rickettsia rickettsii (Rocky Mountain spotted fever) The range of clinical disease in Rocky Mountain spotted fever (RMSF) is broad.
eBook - PDFTropical Medicine
A Clinical Text, 8th Edition, Revised and Expanded
- Kevin M. Cahill(Author)
- 2013(Publication Date)
- Fordham University Press(Publisher)
Bacterial and Rickettsial Diseases Typhoid Fever Typhoid occurs worldwide but is much more prevalent in the tropics and subtropics. Typhoid and malaria are the two most common causes of fever in persons recently returned from a visit abroad. More than 90% of patients with typhoid in developed countries are infections imported from the tropics. The Organism Salmonella typhi is a gram negative, motile, rod-shaped bacteria with a flagellum. Unlike E. coli, which has a similar appearance, it does not ferment lactose. Tryptic broth or 10% Oxgall are used for culturing the organism from the blood, and selective Salmonella-Shigella medium (SS) is employed in culturing feces. After infection, antibodies are raised against three antigens: a somatic 0 lipopolysaccharide antigen, a flagel- lar H protein antigen, and a capsular Vi polysaccharide antigen. Pathology Infection is acquired by the ingestion of an adequate number of S. typhi, the chance of acquiring clinical typhoid being directly related to the number of organisms. Common vehicles of infection are contaminated water, milk, and food. Hypochlorhydric persons are at greater risk. The organisms penetrate small intestinal mucosal cells (the micro- fold or M cells), which overlie lymphatic aggregations (Peyer’s patches). They then multiply within the mononuclear cells of these aggregates and in related mesenteric lymph nodes. At a critical point, sufficient organisms are released into the blood to cause a bacteremia, and this 70 bacterial and rickettsial diseases coincides with the end of the incubation period. S. typhi are then car- ried to various tissues, especially of the liver, spleen, and lymph nodes, where they further multiply in macrophages. The gall bladder is invaded, and S. typhi reappear in the intestine and penetrate the mucosa. Hyperplasia within Peyer’s patches of the ileum may be fol- lowed by necrosis and sloughing.
- Dongyou Liu(Author)
- 2014(Publication Date)
- CRC Press(Publisher)
367 32 32.1 INTRODUCTION Zoonotic rickettsial infections occur naturally in both urban and rural communities worldwide. Transmitted via vectors such as ticks, fleas, mites, and lice, rickettsial infections are often viewed as mild or are misdiagnosed as common ail-ments such as the common cold and flu. Through lack of understanding of the actual cause of disease, complications leading to organ failure and possibly even death. The genus Rickettsia was first described by Howard Ricketts in 1906 and 1907, where he investigated an outbreak of Rocky Mountain spotted fever (RMSF). 1 His work was instrumental in paving the way for modern rickettsiology. Most significant were the roles that ectoparasites were found to play as vectors of rickettsial infection and reservoirs of rickettsial organisms in an endemic area. 1 Today, we know that the rickettsial life cycle involves both vertebrate and invertebrate hosts. Not only do hematophagous arthropods play an important role as vectors, they are also a primary res-ervoir and amplifying host. In some instances, small mam-mals such as rats and opossums also act as hosts. 2 Rickettsiae are obligate intracellular Gram-negative para-sitic bacteria. Their ability to grow within the cytoplasm and nucleus of the eukaryotic host cell differentiates them from other obligate intracellular bacteria of the genera Coxiella , Ehrlichia , and Chlamydia . Rickettsial entry into host cells is by induced phagocytosis. 3 32.2 TAXONOMY The original classification of species within the genus Rickettsia into the spotted fever group (SFG) and Typhus group (TG) depended on a variety of characteristics including intracellular localization, optimal growth tempera-ture, and the cross-reaction of sera from an infected patient with somatic antigens of three strains of Proteus (Weil–Felix test).
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