Typhus Clinical Presentation

  • Author: Jason F Okulicz, MD; Chief Editor: Michael Stuart Bronze, MD   more...
 
Updated: Nov 22, 2011
 

History

Patients with typhus may have a history that includes the following:

  • Patients may have had exposure to an endemic area
  • Occupational exposure: Medical and military personnel are potentially at higher risk for typhus than the general population in endemic areas.
  • Overcrowding leads to close personal contact and spread of arthropod vectors (particularly lice) among individuals.
  • Lack of personal hygiene: Infrequent bathing and changing of clothes provides a hospitable environment for body lice.
  • Appropriate season: Cold weather may lead to overcrowding indoors and infrequent bathing and changing of clothes, which are advantageous for lice. Flea vectors are more abundant in warmer weather, when their hosts are more plentiful.
  • Abrupt onset of fever, headache, and rash are common symptoms in rickettsial infections.
  • Patients may have a history of flea bite.
  • History may include exposure to natural disaster or war.
  • Other less common symptoms of typhus include nonproductive cough and deafness/tinnitus.
  • The duration of most clinical symptoms and signs in untreated typhus is approximately 2 weeks. Several months may pass before complete recovery from fatigue and malaise.
  • Epidemic typhus is the prototypical infection of the typhus group. As described in the Pathophysiology section, typhus is a multisystem vasculitis and may cause a wide array of clinical manifestations.
    • Fever is characterized by abrupt onset.
    • Headache is characterized by abrupt onset and is unremitting.
    • A maculopapular/petechial rash occurs on days 4-7 and may begin on the axilla and trunk and spread peripherally. The rash of Rocky Mountain spotted fever (RMSF) typically begins on the extremities and spreads centrally.
    • Other symptoms of typhus may include rigors, myalgias, malaise, and CNS symptoms (ranging from mental dullness to coma).
  • Scrub typhus may be difficult to recognize and diagnose because the symptoms and signs of the illness are often nonspecific.
    • A painless papule develops at the site of the chigger bite and subsequently undergoes central necrosis with formation of an eschar.
    • Regional lymphadenopathy, with development of large and tender lymph nodes, occurs at the site of the bite and may lead to generalized lymphadenopathy.
    • The nonspecific presentation and lack of the characteristic eschar in 40% of patients leads to many undiagnosed cases of scrub typhus.
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Physical

  • Fever
    • Fever rises to 39-41ºC and is persistent in patients with untreated typhus.
    • Patients with typhus have relative bradycardia with the fever.
    • Fever may persist for 24-72 hours after initiation of antibiotic therapy.
  • Tachypnea and cough: This is most common in scrub typhus because of frequent pulmonary involvement.
  • Rash
    • The macular, maculopapular, or petechial rash initially occurs on the trunk and axilla and spreads to involve the rest of the body except for the face, palms, and soles.
    • Rash may be petechial in patients with epidemic or murine typhus.
  • Regional lymphadenopathy
    • This occurs in scrub typhus in the region of the arthropod bite and inoculation. Generalized lymphadenopathy may follow.
    • Lymph nodes are often tender and enlarged.
  • Generalized lymphadenopathy
  • Eschar
    • This is found in the scrub form of typhus and is essential in confirming a clinical diagnosis. It occurs in up to 60% of cases.
    • Eschar occurs at the site of the arthropod bite. It starts as a painless papule, and the lesion becomes indurated and enlarged. The center of the lesion becomes necrotic and develops into a black scab.
  • Other features
    • Mild splenomegaly may occur.
    • Mild hepatomegaly may occur.
    • Conjunctival suffusion may occur in scrub typhus.
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Causes

Typhus is an acute febrile illness caused by rickettsial organisms. Rickettsia are pleomorphic bacteria that may appear as cocci or bacilli and are obligate intracellular parasites.

  • Epidemic typhus is caused by the bacterium R prowazekii, and the vector is the body louse.
    • P corporis is the most common louse vector; however, Pediculus capitis and Phthirus pubis also transmit epidemic typhus.
    • Humans are the host in epidemic typhus, but the flying squirrel has also been linked with the disease in several cases in the United States.[1]
    • The louse becomes infected with R prowazekii after feeding on a rickettsemic person with a primary case of typhus or during a recrudescent case (Brill-Zinsser disease).
    • Of all the typhus vectors, the louse is the only arthropod that dies of this infection. Rickettsia live in the alimentary tract and cause obstruction and subsequent death of the louse after 2-3 weeks of infection.
    • All arthropod vectors cause inoculation of Rickettsia into the host by the same mechanism described above (see Pathophysiology).
  • Murine typhus is caused by R typhi, and the vector is the rat or cat flea (Xenopsylla cheopis, Ctenocephalides felis).
    • Rats (Rattus rattus), mice, and cats are the usual hosts; human infection is accidental.
    • Fleas become infected after engaging in a blood meal of a rickettsemic host; however, the fleas are not affected by the bacteria as are the lice in epidemic typhus.
    • Infected fleas may subsequently cause disease by direct inoculation or by indirect inoculation of the infected feces into the site of the bite wound.
    • Aerosolization of the feces and inoculation into the respiratory tract or into a mucous membrane are other possible routes of infection.
  • Scrub typhus is caused by O tsutsugamushi (formerly Rickettsia tsutsugamushi) via the mite Leptotrombidium akamushi and possibly Leptotrombidium deliense.
    • The life cycle of the mite involves 4 stages of development, but only the larval stage (chigger) requires a blood meal and is infectious to humans and other mammals.
    • Once the mite is infected, it acts as a reservoir for Rickettsia.
    • The infection is maintained in mites from generation to generation by transovarial transmission.
    • Humans are accidental hosts in scrub typhus; rats, mice, and larger mammals are the usual hosts.
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Contributor Information and Disclosures
Author

Jason F Okulicz, MD  Assistant Professor of Medicine, Uniformed Services University of the Health Sciences; Staff, Infectious Disease Service, Brooke Army Medical Center

Jason F Okulicz, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Mark S Rasnake, MD, FACP  Assistant Professor of Medicine, Program Director, Internal Medicine Residency, University of Tennessee Graduate School of Medicine; Consulting Staff, Department of Infectious Diseases, University of Tennessee Medical Center at Knoxville

Mark S Rasnake, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Eric A Hansen, DO  Fellow, Clinical Instructor, Department of Internal Medicine, Division of Infectious Diseases, Winthrop-University Hospital, State University of New York at Stony Brook

Eric A Hansen, DO is a member of the following medical societies: American Medical Association, American Osteopathic Association, Infectious Diseases Society of America, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

John M Leedom, MD  Professor Emeritus of Medicine, Keck School of Medicine of the University of Southern California

John M Leedom, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Thomas M Kerkering, MD  Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD  Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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