Q fever
Q fever is a zoonosis caused by the bacterium Coxiella burnetii (small, gram-negative, exists in three forms - phase I and phase II). This organism is not common but can be found in cattle, cattle, sheep, goats, and other domestic mammals. It does not produce symptoms in animals (eventually sporadic abortion could occur) but it is contained in milk as well as in body fluids.
The disease was initially described in 1937 in Australia as a fever of unknown cause, hence its name Q (query).
History
In August 1935, Edward Holbrook Derrick, medical director of the Microbiology and Pathology Laboratory at the Queensland Department of Health in Brisbane, Australia, was commissioned to investigate an outbreak of febrile illness among slaughterhouse workers in Brisbane. The disease was given the name "Q" by "query" (in consultation). Derrick inoculated guinea pigs with the blood and urine of sick patients, generating the disease in them. However, Derreck was unable to isolate the agent in the guinea pigs, and decided to send the emulsate from the livers of the infected animals to Macfarlane Burnet in Melbourne. Burnet together with Mavis Freeman, managed to reproduce the disease in guinea pigs, rats and monkeys, being able to observe in the spleen cells of mice, vacuoles with numerous rod-shaped microorganisms similar to Rickettsias.
In parallel and independently, Gordon Davis, a physician at the Rocky Mountain Laboratory in Montana, United States, was working on possible vectors of Rocky Mountain fever and tularemia. Davis had collected ticks from Nine Mile Creek, a tributary of the Clark Fork River, which were presumed to contain the agent for these diseases, and fed them to guinea pigs, which became ill. However, the illness they presented did not resemble Rocky Mountain fever. In 1936, Herald Rea Cox joined Davis's work to characterize the disease they named "Nine Mile Fever". Davis and Cox, as well as Burnet and Freeman, demonstrated that the etiologic agent had both viral and rickettsial properties. In May 1938, Rolla Eugene Dyer, director of the National Institute of Health, visited Cox in Montana to test Cox's report indicating the spread of this agent in large numbers of embryonated eggs. Ten days after his visit, Dyer fell ill with a febrile picture equal to Q fever, allowing at that time to relate this picture to the disease described in Australia. Inoculation of Dyer's blood into guinea pigs developed the disease and the Nine Mile agent was found in their spleens. In April 1938, Burnet sent Dyer spleens from mice infected with Q fever, the agent of which turned out to be identical to Agent Nine Mile.
Cox named the Nine Mile agent as Rickettsia diaporica (diaporic refers to the property of these microorganisms to pass through filters). On the other hand, Derrick proposed the name Rickettsia burnetti, in honor of Burnet. In 1948 Cornelius B. Philip, a researcher at the Rocky Mountain Laboratory, proposed the name Coxiela burnetii, since it is a unique microorganism among the Rickettsiae, and at the same time allowed its two discoverers to be recognized. Both Cox and Burnet died in 1986.
Epidemiology
Goats, sheep and cattle are the primary natural reservoir of C. burnetii. However, infection has been demonstrated in multiple other vertebrate species including wild animals, marine mammals, domestic mammals, birds, and reptiles.
The disease is known worldwide and occurs mainly in people who handle parturient goats, sheep, cows, or cats. It has drawn attention due to outbreaks in medical and veterinary centers where large numbers of people are exposed to animals that shed Coxiella. Transmission occurs by inhalation of dust contaminated with spores from placenta, feces, urine, or dried milk, or from aerosols in traces. Humans are highly susceptible to the disease, but about half of those affected are asymptomatic and it is rarely transmitted from person to person. Q fever is also transmitted by ticks.
Cause
Q fever is caused by Coxiella burnetii, an obligate intracellular gram-negative bacterium. It enters the cell by a passive mechanism, surviving inside the phagolysosomes.
Clinical picture
When there are symptoms, it occurs after an incubation period of 10 to 40 days. The most classic form of presentation corresponds to a flu syndrome with high fever (lasting between one and two weeks), intense headache, myalgia, arthralgia, confusion, nausea, vomiting and diarrhea, as well as respiratory symptoms such as pleuritic pain and dry cough..
During the course of infection, the disease can progress to atypical pneumonia, which can trigger acute respiratory distress syndrome, such symptoms usually occurring during the first 4-5 days of infection.
Less commonly, Q fever causes granulomatous hepatitis, which may be asymptomatic or become symptomatic with fever, hepatomegaly, and right upper quadrant pain. In the laboratory, an increase in transaminases can be observed, however, jaundice is very rare. Retinal vasculitis is another rare manifestation of Q fever.
Diagnosis
Diagnosis relies primarily on serology testing to find antibodies against the bacterial antigen rather than looking for it. Molecular detection of bacterial DNA is increasingly used. Culture is technically difficult and not routinely available in most microbiology laboratories. Q fever can cause endocarditis (infection of the heart valves) which may require transesophageal echocardiography to diagnose. Q fever hepatitis manifests as elevated Alanine aminotransferase and Aspartate aminotransferase, but definitive diagnosis is only possible with a liver biopsy, which shows the characteristic fibrin ring granuloma.
Treatment
Tetracyclines and chloramphenicol if treatment is started early in the disease, in Phase 1. Tetracycline or chloramphenicol are given orally daily and continued 3 to 4 days after defervescence. In seriously ill patients, the initial dose may be administered intravenously. Continued tetracycline therapy for many months—sometimes with valve replacement—may prolong survival. Sulfonamides aggravate the disease and are contraindicated. Some fluoroquinolones (eg, ciprofloxacin) are effective in spotted fevers. Antibiotics do not kill coccyellae from the body, but they do suppress their growth (bacteriostatic). Recovery depends in part on the patient's immune mechanisms.