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Typhus fever

  • Typhus refers to a group of zoonotic diseases caused by bacteria that are spread to humans by fleas, lice, and chiggers.
  • Typhus fevers include scrub typhus, murine typhus, and epidemic typhus.
  • The most common symptoms are fever, headaches, and sometimes rash.

Historical perspective

  • In 1083, Typhus was first identified as a disease in Spain.
  • In 1489, during the Spanish siege of Moorish Granada, the first reliable description of the disease was made.
  • In 1546, Fracastoro extensively described the disease and distinguished it from plague in his book Contagione.
  • In 1676, Von Zavorziz wrote a book on typhus called The Infection of Military Camps.
  • In 1739, Huxham stated typhus and typhoid as two different entities, later in the same year Boissier de Sauvages confirmed this and called it exanthematic typhus.
  • In 1829, Louis, French clinician clearly differentiated Typhus Fever from Typhoid Fever.
  • In 1836, Gerhard(United States) clearly distinguished the two diseases from each other based on pathologic findings.
  • In 1909, Charles Nicolle for the first time described the role of lice bite in transmission of typhus. In 1928, he was awarded the Nobel Prize for his discovery.
  • In 1916, Weil and Felix reported the isolation of a Proteus that was agglutinated by the sera of patients with typhus, which was the basis for the first serological test for the disease.
  • In 1916, DaRocha-Lima isolated and identified Rickettsia prowazeki.
  • In 1926, Maxcy described the various forms of typhus.
  • In 1938, Starzyk demonstrated that patients are infected by the feces and not the bite of the louse.
  • In 1922, Wolbach described the human histopathology of R prowazekii infection.[1]
  • In 1938, Cox was successful in growing cell cultures of R prowazekii in embryonated eggs.[2]
  • In 1940, Cox and Bell prepared an Epidemic Typhus vaccine based upon the use of tissue culture.
  • In 1943–1944, during World war II DDT (a pesticide) was employed to control lice and typhus.
  • In 1998, Andersson et al, sequenced the entire genome after much study of the fundamental mechanisms of R prowazekii's intracellular life and its effects on host cells.[3]

Pathophysiology

Typhus fever is a zoonotic disease, Humans could be infected by bites from ticks, lice, inhalation of the bacteria, and direct contact of bacteria with skin wounds or mucous membranes. Following transmission, white blood cells phagocyte the pathogen and transports it via hematologic or lymphatic route to different organs, specially to those of the reticuloendothelial system. The pathophysiology of typhus fever can be described in the following steps.

Transmission

  • Rickettsial pathogens are harboured by parasites such as fleas, lice, mites, and ticks.
  • Organisms are transmitted by the bites from these parasites or by the inoculation of infectious fluids or feces from the parasites into the skin.
class="wikitable"
Disease Etiological agent Vector
Epidemic typhus  Rickettsia prowazekii Human body louse
Murine typhus Rickettsia typhi Infected fleas
Scrub typhus Orientia tsutsugamushi  Larval mites

Dissemination

  • Scratching a louse-bite site allows the rickettsia-laden excrement to be inoculated into the bite wound.
  • Following transmission, rickettsia are ingested by macrophages and polymorphonuclear cells. On ingestion, they replicate intracellularly inside the lysed cells and disseminate systemically.

Incubation

Incubation period of Typhus fever varies from one to two weeks.

Pathogensis

  • On transmission, Rickettsia is actively phagocytosed by the endothelial cells of the small venous, arterial, and capillary vessels.
  • It is followed by systemic hematogenous spread resulting in multiple localizing vasculitis. The major pathology is caused by vasculitis and its complications.
  • This process of inflammatory response (aggregation of leukocytes, macrophages, and platelets) along with occlusion of small blood vessels results in formation of nodules.
  • Occlusion of supplying blood vessels also causes gangrene of the distal portions of the extremities, nose, ear lobes, and genitalia.
  • This vasculitic process also results destruction of the endothelial cells and leakage of the blood leading to volume depletion and subsequent decreased tissue perfusion and, possibly, organ failure.
  • Endotheleal damage lead to activation of clotting system

Natural history

fatal in 20%–60% of untreated cases

History

  • History of travel to endemic areas
  • History of tick bite

Symptoms

Most common symptoms

  • Fever
  • Headache
  • Malaise
  • Maculopapular, vesicular, or petechial rash
  • Eschar
  • Nausea and vomiting.

Less common symptoms

  • Abdominal pain
  • Cough
  • Prostration
  • Confusion
  • Photophobia
  1. Woodward TE (1971). "Typhus verdict in American history". Trans. Am. Clin. Climatol. Assoc. 82: 1–8. PMC 2441062. PMID 4997497.
  2. Cox, Herald R. (1938). "Use of Yolk Sac of Developing Chick Embryo as Medium for Growing Rickettsiae of Rocky Mountain Spotted Fever and Typhus Groups". Public Health Reports (1896-1970). 53 (51): 2241. doi:10.2307/4582741. ISSN 0094-6214.
  3. Andersson SG, Zomorodipour A, Andersson JO, Sicheritz-Pontén T, Alsmark UC, Podowski RM, Näslund AK, Eriksson AS, Winkler HH, Kurland CG (1998). "The genome sequence of Rickettsia prowazekii and the origin of mitochondria". Nature. 396 (6707): 133–40. doi:10.1038/24094. PMID 9823893.