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Tick-Borne Diseases, Q Fever
Updated: Dec 9, 2008
Introduction
Background
First described in 1935 by Derrick, Q fever is an acute infectious disease. Derrick investigated a cluster of febrile illnesses of unknown etiology in Australian abattoir workers and subsequently named the malady Q (for query) fever. Most commonly spread by means of inhalation or ingestion, Q fever can also be tick-borne. Q fever usually presents as an undifferentiated febrile illness with predominant respiratory or hepatic manifestations.
Pathophysiology
The causative organism is Coxiella burnetii. Classically grouped with the rickettsial organisms, C burnetii differs from the other organisms in that group; in fact, its genetic makeup is more closely related to Legionella and Francisella species than to the other Rickettsia species.
C burnetii is a small gram-negative organism that lives inside acidic lysosomes, a point that has therapeutic implications. The organism exists in 2 forms, phase I and phase II, which are analogous to the lipopolysaccharide rough and smooth phase of Enterobacteriaceae organisms. The phase I form is isolated from animals and is the infectious form. In mammals, the macrophage, which is unable to kill C burnetii, is the usual host cell. The organism is remarkably resistant to environmental extremes. A spore form also exists.
The reservoir in nature includes mammals, birds, and ticks; the last is an important vector in infecting mammals. A strong association between the disease and exposure to farm animals exists. Furthermore, because the organism is reactivated in pregnant animals, a strong association between the disease and contact with parturient animals (especially cows, sheep, goats, dogs, cats, rabbits) also exists. Aerosol from newborn animals and their placentas can spread Q fever. Other modes of transmission include aerosol from contaminated wool, hides, and dust; ingestion of raw milk or goat cheese; blood transfusions; and tick bites.
Even wind patterns may make a difference by spreading aerosolized organisms downwind. Outbreaks of Q fever have occurred in an industrial setting from straw board that had been drilled open during part of the construction process.
Recent studies in patients with chronic Q fever in which polymerase chain reaction (PCR) was used to detect C burnetii DNA revealed evidence that the organism persists in human liver, blood monocytes, and most commonly, bone marrow.
Most humans who are infected with C burnetii experience asymptomatic infections. HIV-infected patients may be at greater risk for more severe disease, and infected pregnant women are at risk for spontaneous abortion or premature labor.
Frequency
United States
Q fever is present throughout the United States. The precise incidence is unknown. Although the actual frequency is likely low, the Centers for Disease Control and Prevention still regularly report cases that occur in the United States.
International
Q fever exists worldwide. A seroprevalence study of blood donors in Marseille, France, showed that 4% of donors had antibodies to C burnetii. Similar studies in other European countries have shown figures of 5-30%, with lower figures seen in urban areas and higher figures in rural zones.
Mortality/Morbidity
- Acute Q fever generally is self-limited. In fact, about one half of the cases in one study had asymptomatic seroconversion. Of symptomatic patients, fewer than 5% require hospitalization.
- Chronic Q fever, which often presents as culture-negative endocarditis, is difficult to treat and can be fatal.
- Mortality is uncommon, even in hospitalized patients, and tends to occur in older patients.
Age
Patients of all ages can contract Q fever, but it seems to be more prevalent in men between the ages of 30 and 70 years. After exposure, women and children are more commonly asymptomatic than men and adults. The incidence, as determined by the age at which seroconversion of blood donors occurs, can be deceptive because children, elderly persons, and sick persons do not donate blood.
Clinical
History
Q fever can manifest various signs; no one classic presentation exists. The major clue is the epidemiologic circumstance, exposure to parturient mammals or their newborn, and tick bites. The most common presentation of Q fever may vary with geography. For example, in the Basque region of northern Spain, pneumonia is a common finding, whereas in southern Spain, hepatitis predominates.
Findings with acute and chronic Q fever may include the following:
- Acute Q fever
- Fever and systemic symptoms: Abrupt onset of high fever with or without a flulike illness is common. The incubation period ranges from 14-39 days but averages 20 days. Arthralgias can occur.
- Respiratory symptoms: While some patients with respiratory involvement have a (usually dry) cough, shortness of breath, and chest pain, others with pneumonia have no respiratory symptoms. Respiratory involvement is discovered only when a chest radiograph is obtained during the evaluation of fever.
- Skin symptoms: Q fever often is assumed not to be associated with a rash. However, one French study of acute Q fever revealed that roughly 20% of patients have a nonspecific exanthem, most commonly a maculopapular rash on the trunk.
- Cardiovascular symptoms: Some patients with acute Q fever pericarditis report chest pain. Patients with myocarditis also may experience palpitations, chest pain, or dyspnea. Q fever myocarditis can be fatal.
- GI symptoms: Hepatitis is a common manifestation and usually is associated with elevated hepatic transaminase levels, since Q fever rarely causes jaundice or acute GI symptoms.
- Neurologic symptoms: Some patients have headache, confusion, and neck stiffness. The 3 major neurologic syndromes of Q fever are meningoencephalitis or encephalitis, meningitis, and myelitis and peripheral neuropathy.
- Chronic Q fever: Endocarditis with negative culture findings is, by far, the most common manifestation of chronic Q fever. It can occur months to years after the acute infection. Symptoms include fever, fatigue, dyspnea, and rash from septic thromboembolism.
Physical
Physical findings vary with the presenting clinical syndrome. No pathognomonic findings exist.
- During the acute phase, fever can be high or low grade.
- Tachypnea, rales, rhonchi, and wheezing can be present in patients with pneumonia. Signs of pleural effusion may exist.
- A pericardial rub can be observed in pericarditis. Patients with myocarditis can have tachycardia, an irregular pulse, and a gallop rhythm.
- Jaundice rarely is observed in patients with hepatitis.
- In endocarditis with chronic Q fever, cardiac murmurs, purpuric rash, and hepatomegaly can be present.
Causes
The cause of Q fever is infection with the bacteria C burnetii.
In this age of concern for terrorism with biological agents, Q fever is on the list of possible agents. It is highly infectious and spread by aerosol. Although the mortality rate is low, it could provoke considerable disability and disorganization. Initial diagnosis might be delayed by the fact that it is so uncommon in most locations.
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References
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Further Reading
Keywords
Q fever, tick-borne disease, Coxiella burnetii, C burnetii, fever, vector-borne disease, tick bite, acute Q fever, chronic Q fever, febrile illness
