Fever Q

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Q fever
Other names	Query fever, coxiellosis
File:Immunohistochemical detection of Coxiella burnetii in resected cardiac valve of a 60-year-old man with Q fever endocarditis.jpg
Immunohistochemical detection of C. burnetii in a resected cardiac valve from a 60-year-old infected man from Cayenne, French Guiana, using monoclonal antibodies against C. burnetii and hematoxylin for staining. (Shown at 50x magnification)
Symptoms	fever chills profuse perspiration malaise severe headache muscle pain joint pain loss of appetite upper respiratory tract issues dry cough pleuritic pain confusion nausea gastroenteritis
Usual onset	2–3 weeks
Duration	Approx. 3 days when treated early, 2 weeks if left untreated
Types	acute chronic
Causes	Contact with infected livestock or other domestic mammals, their milk, urine, feces, vaginal mucus or semen
Diagnostic method	Indirect fluorescent antibody test (ref. standard) or PCR assay for more rapid results
Differential diagnosis	pneumonia influenza brucellosis leptospirosis meningitis viral hepatitis dengue fever malaria other rickettsial infections
Treatment	two-week course of oral antibiotics
Medication	doxycycline tetracycline chloramphenicol ciprofloxacin ofloxacin hydroxychloroquine
Prognosis	Acute:  full recovery Chronic: 10% mortality when treated, otherwise fatal

Q fever or query fever is a disease caused by infection with the obligate intracellular pathogenic parasite Coxiella burnetii, a Gram-negative bacterium that affects humans and other animals. This organism is uncommon, but may be found in cattle, sheep, goats and other domestic mammals—including cats and dogs. The infection results from inhalation of a spore-like small-cell variant of the pathogen or from direct contact with the milk, urine, feces, vaginal mucus or semen of infected animals, with an incubation period of 9–40 days. Rarely, the disease is tick-borne.

Signs and symptoms

The typical incubation period is between two to three weeks. Common presentations include flu-like symptoms with an abrupt onset of fever, chills, profuse perspiration, malaise, severe headache, muscle and joint pain, loss of appetite, upper respiratory tract problems, a dry cough, pleuritic pain, confusion, nausea and gastroenteritis. However, roughly half of infected individuals are asymptomatic.

During its course, the disease can progress to an atypical, or "walking," pneumonia which can result in life-threatening acute respiratory distress syndrome (ARDS), with such symptoms usually occurring during the first four to five days of infection.

Less often, Q fever causes granulomatous (chronic) hepatitis, which may be asymptomatic or becomes symptomatic with malaise, fever, liver enlargement and abdominal right upper quadrant pain. Elevated transaminase (liver enzymes) values are common, however jaundice is not. Retinal vasculitis is also a known symptom, though rare.

The chronic form of Q fever is virtually identical to endocarditis (inflammation of the inner lining of the heart, often involving the heart valves, as well) and can occur months or decades following the initial infection. It is usually fatal if left untreated, but with appropriate treatment the mortality rate falls to roughly 10%.

Diagnosis

File:Q fever management algorithm.gif

Q fever management algorithm from the CDC.

Several aspects of the disease make diagnosis of Q fever a difficult and lengthy process, usually relying on serology, after the onset of symptoms. The reference standard is an indirect fluorescent antibody (IFA) test to look for an immunoglobulin G (IgG) response to the infection, performed on paired serum samples taken at least two weeks apart. A fourfold or greater rise in antibody titers is needed for a positive result, with accuracy increasing commensurate to the interval between when the samples are taken, three to six weeks being optimal. Antibodies to C. burnetii tend to remain elevated for many months and sometimes even years after the disease has resolved. Statistical sampling suggests that approximately 3% of healthy adults in the U.S. and up to 20% of people in high-risk professions—veterinarians, ranchers, etc.—have elevated titers from past Q fever infections, though the large majority of those prior infections will have been asymptomatic, and thus, untreated.

If a more rapid determination of Q fever infection is needed during the acute phase of the illness (such as when a differential diagnosis cannot exclude other, more serious potential causes), a polymerase chain reaction (PCR) assay can be performed on a sample of whole blood—or serum, at some laboratories—to detect the presence of C. burnetii DNA sequences at the molecular level. This method is most sensitive in the first week of illness, before the appearance of detectable levels of organism-specific antibodies, and is quickly rendered mostly ineffective following the start of standard treatment regimens. While a positive PCR result can be a key element in diagnosis, particularly for patients suffering an extreme course of symptoms, a negative result does not rule out the infection and a serological result should be determined afterwards for greater certainty.

Diagnosis of the chronic form of the infection relies on the two distinct antigenic phases (I and II, corresponding to the more and less virulent forms of the pathogen, respectively) of human antibody responses. In acute infections, the phase II antigen will be predominant, due to a combination of natural immune response as well as the necessary delay between patient samples for the test comparison. However, the reverse is true for chronic infections, which are associated with a rising phase I IgG titer (≥1:2¹⁰)—potentially higher than even phase II—showing the failure of the immune system to arrest the progression of the disease as expected.

Looking for the bacteria themselves in blood via culture isolation is both technically difficult and time consuming, and only available at specialized microbiology laboratories, making it ill-suited for routine diagnoses; common hospital blood cultures are unable to detect the organism.

When Q fever causes endocarditis, transesophageal echocardiography may be required to properly diagnose it. Q fever hepatitis manifests as an elevation of alanine transaminase and aspartate transaminase, but a definitive diagnosis is only possible on liver biopsy, which shows the characteristic fibrin ring granulomas.

Prevention

Prophylactic protection is possible with the use of Q-Vax: a whole-cell, inactivated vaccine developed by Australian vaccine manufacturer CSL Limited. The intradermal vaccination is composed of killed C. burnetii organisms. Skin and blood tests should be done before vaccination to identify pre-existing immunity, because vaccinating people who already have an immunity can result in a severe local reaction. After a single dose of vaccine, protective immunity lasts for many years. Revaccination is not generally required. Annual screening is typically recommended.

In 2001, Australia introduced a national Q fever vaccination program for people working in “at risk” occupations. Vaccinated or previously exposed people may have their status recorded on the Australian Q Fever Register, which may be a condition of employment in the meat processing industry or in veterinary research. An earlier killed vaccine had been developed in the Soviet Union, but its side effects prevented its licensing abroad.

Preliminary results suggest vaccination of animals may be a method of control. Published trials proved that use of a registered phase vaccine (Coxevac) on infected farms is a tool of major interest to manage or prevent early or late abortion, repeat breeding, anoestrus, silent oestrus, metritis, and decreases in milk yield when C. burnetii is the major cause of these problems.

Treatment

Treatment of acute Q fever with antibiotics is very effective and should be given in consultation with an infectious diseases specialist. Commonly used antibiotics include doxycycline, tetracycline, chloramphenicol, ciprofloxacin, ofloxacin, and hydroxychloroquine. Chronic Q fever is more difficult to treat and can require up to four years of treatment with doxycycline and quinolones or doxycycline with hydroxychloroquine.Q fever in pregnancy is especially difficult to treat because doxycycline and ciprofloxacin are contraindicated in pregnancy. The preferred treatment is five weeks of co-trimoxazole.

Epidemiology

File:Coxiella burnetii 01.JPG

C. burnetii, the Q fever-causing agent

The pathogenic agent is found worldwide, with the exception of New Zealand. The bacterium is extremely sustainable and virulent: a single organism is able to cause an infection. The common source of infection is inhalation of contaminated dust, contact with contaminated milk, meat, or wool, and particularly birthing products. Ticks can transfer the pathogenic agent to other animals. Transfer between humans seems extremely rare and has so far been described in very few cases.

Some studies have shown more men to be affected than women, which may be attributed to different employment rates in typical professions.

“At risk” occupations include:

• Veterinary personnel
• Stockyard workers
• Farmers
• Sheep shearers
• Animal transporters
• Laboratory workers handling potentially infected veterinary samples or visiting abattoirs
• People who cull and process kangaroos
• Hide (tannery) workers

History

File:Pneumonia x-ray.jpg

Image A: A normal chest X-ray Image B: Q fever pneumonia

Q fever was first described in 1935 by Edward Holbrook Derrick in slaughterhouse workers in Brisbane, Queensland. The "Q" stands for "query" and was applied at a time when the causative agent was unknown; it was chosen over suggestions of abattoir fever and Queensland rickettsial fever, to avoid directing negative connotations at either the cattle industry or the state of Queensland.

The pathogen of Q fever was discovered in 1937, when Frank Macfarlane Burnet and Mavis Freeman isolated the bacterium from one of Derrick's patients. It was originally identified as a species of Rickettsia. H.R. Cox and Gordon Davis elucidated the transmission when they isolated it from ticks found in the US state of Montana in 1938. It is a zoonotic disease whose most common animal reservoirs are cattle, sheep, and goats. Coxiella burnetii – named for Cox and Burnet – is no longer regarded as closely related to the Rickettsiae, but as similar to Legionella and Francisella, and is a proteobacterium.

Society and culture

An early mention of Q fever was important in one of the early Dr. Kildare films (1939, Calling Dr. Kildare). Kildare's mentor Dr. Gillespie (Lionel Barrymore) tires of his protégé working fruitlessly on "exotic diagnoses" ("I think it's Q fever!") and sends him to work in a neighborhood clinic, instead.

Q fever was also highlighted in an episode of the U.S. television medical drama House ("The Dig", season seven, episode 18).

Biological warfare

C  burnetii has been developed as a biological weapon.

The United States investigated it as a potential biological warfare agent in the 1950s, with eventual standardization as agent OU. At Fort Detrick and Dugway Proving Ground, human trials were conducted on Whitecoat volunteers to determine the median infective dose (18 MICLD₅₀/person i.h.) and course of infection. The Deseret Test Center dispensed biological Agent OU with ships and aircraft, during Project 112 and Project SHAD. As a standardized biological, it was manufactured in large quantities at Pine Bluff Arsenal, with 5,098 gallons in the arsenal in bulk at the time of demilitarization in 1970.

C. burnetii is currently ranked as a "category B" bioterrorism agent by the CDC. It can be contagious, and is very stable in aerosols in a wide range of temperatures. Q fever microorganisms may survive on surfaces up to 60 days. It is considered a good agent in part because its ID₅₀ (number of bacilli needed to infect 50% of individuals) is considered to be one, making it the lowest known.

Other animals

Cattle, goats, and sheep are most commonly infected, and can serve as a reservoir for the bacteria. Q fever is a well-recognized cause of abortions in ruminants and pets. C. burnetii infection in dairy cattle has been well documented and its association with reproductive problems in these animals has been reported in Canada, the US, Cyprus, France, Hungary, Japan, Switzerland, and Germany. For instance, in a study published in 2008, a significant association has been shown between the seropositivity of herds and the appearance of typical clinical signs of Q fever, such as abortion, stillbirth, weak calves, and repeat breeding. Moreover, experimental inoculation of C. burnetii in cattle induced not only respiratory disorders and cardiac failures (myocarditis), but also frequent abortions and irregular repeat breedings.