Rickettsia burneti is an intracellular parasitic gram-negative bacterium, can cause human acute Q fever. Human infection occurs due to inhalation of dust contaminated by infected animal fluids, consumption of unpasteurized dairy products and contact with milk, urine, faeces, vaginal mucus or semen of infected animals[7] .People at highest risk for this infection are farmers, laboratory workers, sheep and dairy workers, and veterinarians[8]. Q fever sufferers may have high fever, chills, severe headache and muscle aches all over the body. Sore throat, nausea, vomiting, diarrhea, abdominal pain and delirium may be present in few patients. The clinical manifestations of Q fever were non-specific and 60% showed no symptoms, with serious misdiagnosis and missed diagnosis. Hepatitis, endocarditis or meningitis are among complications observed in the rare chronic course of the disease, with a mortality rate of up to 65%, if untreated, in confront of 1–2% in the acute form[9]. Q fever is effective in the early treatment of the disease with antibiotics. If the treatment is delayed, it is easy to lead to chronic Q fever, which has a long treatment cycle, easy recurrence and high mortality rate. Therefore, early and accurate diagnosis of Q fever is extremely important. At present, the diagnosis of Q fever mainly relies on serological and molecular biological methods. But Rickettsia infection is often ignored by people, the bacteremia period is very short, coupled with Rickettsia is intracellular parasitic bacteria, the content of bacteria in clinical samples is very low, which brings difficulties to the detection. In our case, the patient developed symptoms such as high fever, excessive sweating, weakness, loss of appetite and headache, but no rash was found. WBC, platelet (PLT), ALT, AST showed no significant changes, but PCT and CRP increase significantly (Table1).Chest CT showed no obvious abnormality (Fig. 1.A). However, Rickettsia Burneti IgM was positive in the patient's serum by IFA test (Fig. 1.B). Although the patient's clinical symptoms were atypical and there was no significant abnormality in laboratory examination or CT, taking the epidemiological history (contact with sheep) into account, Q-fever were suspected.
Brucellosis is one of the neglected bacterial zoonoses, disease in humans can be severely debilitating, often with longterm adverse consequences for health [2]. Brucellosis is caused by bacteria of the genus Brucella; species considered important agents for human disease are B. Melitensis, B. Abortus and B.Suis[10, 11]. Brucella is more common in cattle, sheep, pigs and other domestic animals, patients are mainly infected by contact with infected sheep or by drinking infected goat milk ,Brucella can also be transmitted from person to person, the most common vertical transmission between mother and child [12].The incubation period is usually 5–60 days[13].After infection, the symptoms of Brucellosis are atypical and the clinical manifestations are varied, including fever, bone and arthropathy, sweating, fatigue, etc., which can be combined with other diseases. Because of its characteristics, it is easy to cause clinical missed examination and misdiagnosis, so that the disease delay, and even cause arthritis, myocarditis, liver and spleen involvement and other complications[14–16].Lots of studies have shown that CRP and PCT are sensitive indicators for the diagnosis of Brucellosis [17, 18].The cure rate of infection in the acute stage of brucellosis is 90–95%, and the chronic infection caused by brucellosis has not been cured, so early diagnosis, early treatment of brucellosis is very important. After 72 hours of blood culture, the culture system reported positive results. The culture medium was extracted for Gram staining, and Gram-negative spherical bacilli were found (Fig. 1.C). After 24 hours of pure bacteria culture, tiny colonies grew on the plate, after 48 hours of culture, typical colony morphology of Brucella appears on the plate (Fig. 1.D). The colony was identified as Brucella melitensis by mass spectrometry, so we thought that the patient was also infected with Brucella. On laboratory tests, we noticed that the patient's PCT and CRP were significantly elevated (Table1).
Brucellosis and Q fever are both zoonotic infectious diseases that have attracted worldwide attention. They share the same infection source, host, transmission route and have similar clinical manifestations. The frequency of interstitial pneumonitis and bronchopneumonia is low in brucella infections [19, 20], however, pneumonia occurs in almost half of the patients with acute Rickettsia burneti infection [21]. The incidence of Q fever is lower, organ damage is more severe, and mortality is higher. If the two diseases enter the chronic phase, it is difficult to cure, so early diagnosis, symptomatic treatment is crucial. Rickettsia burneti and Brucella melitensis coinfection is fairly rarely reported in clinical. To our knowledge, this is the first case report in China. In PubMed, we only found one similar case report [6]. Although it is rare for patients to be infected with Brucella and Rickettsia at the same time, we should not ignore this situation. For potentially infected people, we should use a variety of tests to improve the detection rate of the pathogen. Since brucellosis and Q-fever have the same sensitive drugs [24, 25], the patient was treated with doxycycline and rifampicin. Three days later, the patient's temperature returned to normal. The treatment regimen was continued after the patient was discharged from hospital. Ten days later, the patient's liver function became abnormal (Table1), as doxycycline and rifampicin may cause liver damage, so we added liver protection drugs, and in the latest follow-up, the patient's liver function returned to normal (Table1). Therefore, we should pay attention to the detection of changes in liver function when treating co-infection.