Q fever outbreak during the Czech Army deployment in Bosnia

Military Medicine, Oct 2003 by Splino, Miroslav, Beran, Jiri, Chlibek, Roman

An epidemic of Q fever was identified among soldiers from the Czech Republic serving in the U.N. Stabilization Force in Bosnia and Herzogovina in 1997. There were 26 serologically confirmed infections, or 4.6% of those exposed. There were 14 cases of febrile illness and 12 subclinical infections. Prodromal symptoms of malaise, headache, backache, and fatigue were followed by fever > or =39[degrees]C with an intermittent course. Physical findings were unremarkable except in five cases with radiographically confirmed pneumonia. Cases were treated with doxycycline, trimethoprim-sulfamethoxazole, or ceftriaxone and supportive care. Q fever occurred at four U.N. Stabilization Force bases with the highest incidence at Dolna Ljubija (attack rate 9.4% vs. 2.3% at other locations (risk ratio = 4.0; 95% confidence interval [CI] = 2.7-5.9; p

Introduction

Coxiella burnetii, the etiologic agent of Q fever, is an obligate intracellular pathogen inducing acute or chronic disease.1-4 The respiratory tract is the usual portal of entry. Q fever usually presents in three major clinical pictures: as an undifferentiated febrile illness (flu-like illness); as an atypical pneumonia; or hepatic involvement.5-8 Infection is very often subclinical. Serologie confirmation is limited to the identification of specific antibodies.8-11

An important property of C. bumetii is its ability to cause epidemics in humans.3,10 The reservoirs of C. burnetii include goats, sheep, cattle, and, less frequently, other mammals.2,3,12,13 C. burnetii persists in the soil over a wide temperature range. Infectious environmental aerosols containing viable C. bumetii may spread over considerable distances (up to several kilometers), transmitting both sporadic and epidemic Q fever. The geographic distribution of cases is influenced by the number of breeding animals in farms, their infection rate, the generation of environmental aerosols, and the prevailing wind direction.2,13,14 Infection can also be transmitted by ingesting unpasteurized milk from infected animals. Q fever occurs globally and with varied incidence in European countries.11,14

An epidemic of Q fever occurred among soldiers of the Czech Army 6th Rifle Mechanized Battalion deployed within the framework of Stabilization Forces (SFOR) in Bosnia and Herzegovina in May and June 1997. The 6th Battalion consisted of four units: Headquarters (located at Dolna Ljubija); 1st Company (stationed at Stary Majdan); 2nd Company (stationed at Blatna Japra); and 3rd Company (stationed at Bosenska Krupa).

The goal of this investigation was to identify the source of infection and the route of transmission of Q fever.

Design and Methods

All affected soldiers underwent medical examinations in the battalion infirmary, including assessment of subjective complaints, medical history, and objective physical findings.

Public Health Assessment

The conditions of lodging, catering, and sanitation were assessed in the sites of deployment at the four bases.

Various data have been taken into consideration, including the local disease endemicity in the area of deployment, the epidemic course, and the geographic distribution of cases at the four bases. The goal of this investigation was to identify the source of infection and route of transmission of Q fever.

Serologic Examination

Sera were obtained from all 610 deployed soldiers. The 14 serum samples of clinically ill soldiers were transported to the Czech Republic on dry ice and stored in the laboratory at -2O0C. Next, 596 subclinical soldiers were examined and serum samples were obtained after their repatriation in the Czech Republic. All serum samples were examined in a military laboratory by two different methods.

IFAT (indirect immunofluorescence method) was the first method used, which is more specific and a faster test in the early detection of Q fever.15 The C. burnetii antigen was used (Spot IF, second phase IgM and IgG [Bio-Merieux, France]). Serodiagnosis of Q fever relies on the demonstration of rising titers of antibodies against phase II antigens. Serum specimens were placed on a C. burneti-Spot IF substrate slide. Antibodies fixed to this antigen are revealed by a fluorescein-labeled anti-human IgM and IgG globulin. A positive reaction is indicated by fluorescence of C. burneti on the slide, visible under an ultraviolet microscope. Sera can only be considered positive if fluorescence occurs at the 1:80 dilution upward. Reciprocal of the highest dilution still showed a positive reaction. In acute infection, IgM can be demonstrated 2 weeks after the onset of symptoms.16 These antibodies can persist for up to 14 weeks. High IgG antibodies and borderline IgM are typical for chronic Q fever.

The next method used was complement fixation reaction (CFT) with C. bametii second phase antigen. All the serum samples were examined by a standard method specified by the manufacturer.

Results

The first case in the outbreak was a British soldier from the Dolna Ljubija base (International Multinational SFOR Division) on May 15, 1997 in Banja Luka. He presented with signs of upper respiratory tract infection initially thought to be influenza.

Subsequently, pneumonia was diagnosed in three Czech soldiers and two British servicemen at the end of May (May 24, 1997). These patients were transferred to two different SFOR military hospitals (Sipovo and Sarajevo) with radiographically confirmed "atypical (nonlobar) pneumonia." Finally, an additional 12 soldiers (11 Czech and 1 British) presented between May 26 and May 28 with a flu-like respiratory syndrome featuring severe headaches, lethargy, weakness of the lower extremities, backache, nonproductive cough, and fever of 39[degrees]C. Physical findings were unremarkable, except for abnormal pulmonary auscultory findings in five patients with radiographically confirmed pneumonia. Cases were treated with doxycycline, trimethoprim-sulfamethoxazole, or ceftriaxone in addition to supportive care. Although fever initially responded poorly to antipyretic therapy, all patients made a complete clinical recovery within 10 to 20 days.