Trench Fever Clinical Presentation

  • Author: Alfred Scott Lea, MD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Jan 12, 2012
 

History

Trench fever was recognized and precisely described as a distinct syndrome by several physicians during World War I.[10, 1, 2, 3, 4] The clinical incubation period seemed to be 3-48 days.[38] Associated infestation with lice was common. Young soldiers with trench fever would experience headache, relapsing fevers, shin pain, truncal rash, and splenomegaly. Most patients could remember vividly the specific time of symptom onset.

The differential diagnoses of the initial symptoms associated with trench fever included typhoid fever, epidemic typhus, influenza, and meningitis. While there was no recognized mortality, the disability it caused was prolonged and total.

Headaches were sudden in onset and were described as frontal or retroorbital. They were often associated with a stiff neck and photophobia, raising the possibility of meningitis. Other neurologic symptoms included weakness, depression, restlessness, giddiness, and insomnia. Many patients with trench fever would experience severe prostration that resulted in disability and the inability to get out of bed.

The onset of fever was also dramatic and coincided with the onset of headaches. Temperatures were often as high as 104ºF and were associated with malaise, chills, rigors, and sweats. Fever occurred in three distinct patterns. Abortive fever was described as a temperature elevation lasting several days, after which the fever abated and disappeared. Relapsing fever was the most commonly observed pattern and occurred at 5-day intervals (range, 4-8 d), leading to the names quintan fever and five-day fever. The fever would progressively increase during the first episode and then progressively improve during subsequent paroxysms. The third pattern was continuous fever, which lasted for the duration of the disease. Fever occurring months to years after the original defervescence were occasionally reported.

Bone pain, particularly involving the shins, progressively worsened throughout the duration of the illness. The pain worsened dramatically with exercise and was so severe that prostrate patients did not move in their beds because of the pain. Another similar symptom was loin pain, which radiated to the lower extremities or up into the back.

Gastrointestinal symptoms of trench fever would begin with diffuse abdominal pain, often associated with anorexia, nausea, vomiting, weight loss, diarrhea, and constipation. Conjunctivitis was another common initial symptom. An erythematous truncal rash and tachycardia would develop during the febrile episodes. The rapid heart rate worsened with exercise. Dyspnea was associated with the fever and tachycardia.

More recently, urban trench fever has been characterized by one or more of the described symptoms described above, but with less uniformity.[6, 39, 31, 13, 15, 36] Urban trench fever occurs in homeless and alcoholic persons who exhibit poor personal hygiene. The presence of lice and other external parasites is less prevalent in these individuals. Headaches, conjunctivitis, relapsing fever, and shin pain have been documented, while abdominal and neurologic symptoms appear to be uncommon.

The descriptions of other syndromes associated with B quintana infection over the last thirty years were unknown to physicians during World War I. A large percentage of persons with B quintana infection may be totally asymptomatic, and those with any of the identified syndromes may have negative blood culture results. Chronic lymphadenopathy typically manifests as enlarged cervical lymph nodes and no fever or other associated symptoms.[6] Individuals with bacillary angiomatosis are asymptomatic and exhibit only the characteristic skin lesions, with or without regional lymphadenopathy.[15] B quintana endocarditis manifests as fever, new murmurs, and heart failure and causes embolic phenomena in at least 20% of patients.[37] Chronic B quintana bacteremia is occasionally accompanied by all of the syndromes described above and may last for years.[24]

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Physical

The physical findings of trench fever during World War I were fairly consistent. Infected persons experienced an abrupt onset of fever (up to 104ºF), associated with shivering, rigors, and diaphoresis. Patients would initially exhibit a toxic appearance associated with prostration. A furred or coated tongue was common. Some patients were able to continue with their daily activities and recover after a short fastigium, but most would develop a chronically ill appearance with obvious depression and significant disability for months. The fever patterns are described above (see History).

Patients with trench fever exhibited a characteristic blanching, erythematous, macular rash that typically started on the trunk and extend as far as the abdomen, neck, and proximal extremities. The rash accompanied fever and would recur with each febrile paroxysm. It was not pruritic, but coexisting body louse and scabies infestations frequently resulted in itching and excoriations.

The vast majority of patients with trench fever developed conjunctivitis at the illness onset. Photophobia was common. Paroxysmal tachycardia generally paralleled the fever and could be exacerbated with exercise. Splenomegaly was common in those with the more prolonged courses of illness. Bone and muscle tenderness accompanied the shin pain and became progressively more severe and debilitating as the disease progressed. Loss of the Achilles reflex was common.

The characteristic physical findings of urban trench fever are less typical. Rash, fever, conjunctivitis, bone tenderness, splenomegaly, and neurologic signs (eg, absent Achilles reflexes) have been documented, but their appearance seems to be variable and less prevalent than in the initial descriptions from World War I. Nonspecific findings such as weight loss and weakness have also been reported. Many patients with microbiologic or serologic evidence of B quintana infection are totally asymptomatic.

Patients with B quintana endocarditis present with fever and murmur. Lesions typically involve the left side of the heart, resulting in the systolic murmur of mitral insufficiency, the diastolic murmur of aortic insufficiency, or both. Right-sided cardiac involvement is unusual. Heart failure may occur, and embolic lesions develop in up to 20% of patients.[37]

Patients with chronic lymphadenopathy usually have lymphatic involvement of the cervical and mediastinal lymph nodes. They do not experience fever and are otherwise asymptomatic.

Immunocompetent individuals with bacillary angiomatosis typically exhibit one or more papules that progress to nodules that may be confined to one or more anatomical regions. They may also be disseminated. The lesions are red, purple, or nonpigmented and can be superficial or subcutaneous. They may be mobile or fixed to underlying structures, such as bone, and bleed profusely when punctured or incised. Associated regional adenopathy is common. Patients are typically afebrile. The same lesions occurring in immunocompromised patients are generally more widespread and are more likely to involve visceral organs such as the liver, spleen, and GI tract.

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Causes

B quintana causes both trench fever and urban trench fever.[6, 9] Humans are the predominant reservoir of the pathogen, although infection has been shown in some subhuman primates and cats.[40, 38, 41, 42] In infected persons, the organisms can be found in human blood, tissues (particularly skin), and urine.[6]

Predisposing factors for B quintana infection have included war, famine, malnutrition, homelessness, alcoholism, intravenous drug abuse, and poor hygiene.

Since B quintana bacteremia may be intermittent or prolonged for years, ingestion of organisms infecting human erythrocytes suggests that blood-sucking arthropods are efficient transmitters of B quintana infection.[17, 15] External parasitic infestations are also associated with conditions of squalor. The body louse P humanus is the major vector for both trench fever and urban trench fever, but its presence is not always demonstrated in patients with urban trench fever.[9, 14, 43]

Breaks in the skin contaminated by louse feces and arthropod bites are documented portals of entry. Other possible vectors include mites, ticks, and fleas.[6] Contamination of mucous membranes, transfusion, transplantation, and intravenous drug abuse are also potential portals of entry. Human-to-human transmission of trench fever has not been well-described.

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Contributor Information and Disclosures
Author

Alfred Scott Lea, MD  Associate Professor of Internal Medicine and Infectious Diseases, University of Texas Medical Branch School of Medicine

Alfred Scott Lea, MD is a member of the following medical societies: American Academy of Wound Management, American College of Physicians, American Medical Association, Harris County Medical Society, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Jeffrey M Zaks, MD  Clinical Associate Professor of Medicine, Wayne State University School of Medicine; Vice President, Medical Affairs, Chief Medical Officer, Department of Internal Medicine, Providence Hospital

Jeffrey M Zaks, MD is a member of the following medical societies: American College of Cardiology, American College of Healthcare Executives, American College of Physician Executives, and American Medical Association

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

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.

Additional Contributors

The author would like to thank A. Clinton White, MD, for his encouragement and suggestions during the composition of this article.

The authors and editors of eMedicine also gratefully acknowledge the contributions of previous author Eleftherios Mylonakis, MD, and previous coauthor Michael Forgione, MD, to the development and writing of this article.

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This illustration depicts a dorsal view of a female body louse, Pediculus humanus var. corporis. The human body louse P humanus var. corporis is a known vector responsible for the transmission of epidemic typhus, trench fever, and Asiatic relapsing fever. It also causes a dermatitic condition known as pediculosis. Courtesy of the CDC.
 
 
 
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