Molecular Characterization of a Catalase-Negative Staphylococcus aureus subsp. aureus Strain Collected from a Patient with Mitral Valve Endocarditis and Pericarditis Revealed a Novel Nonsense Mutation in the katA Gene

Abstract

We report a case of endocarditis and pericarditis caused by catalase-negative Staphylococcus aureus. Molecular characterization revealed a novel nonsense mutation in the katA gene, leading to a loss of 238 amino acids (47% of the wild-type catalase protein), including the heme-binding site, NADPH-binding region, and Tyr-337, essential for catalysis. CASE REPORTA 15-year-old boy presented to the Accident and Emergency Department with a 2-day history of fever, rhinorrhea, vomiting, and colicky abdominal pain. His past health was good except for a repaired cleft lip. His body temperature was 37.7°C, with blood pressure of 98/37, a pulse rate of 122 beats per minute, and oxygen saturation of 98% while breathing ambient air. With a clinical diagnosis of upper respiratory tract infection, the patient was not admitted to the hospital. One day later, he presented to the Accident and Emergency Department again for left-side chest pain and generalized bone pain. Electrocardiography showed ST segment elevation in leads I, II, III, and V2 to V6. The level of troponin was 0.03 g/liter, and the level of creatinine kinase was 135 IU/liter. Chest radiography was normal. After admission, he complained of neck pain and stiffness and was found to be confused. Physical examination revealed vesicles on the palms and feet and oral ulcers. Computed tomography of the brain was unremarkable. Lumbar puncture was performed, and analysis of the cerebrospinal fluid revealed a white cell count of 2 per mm 3 , with glucose and protein within their normal ranges. Bacterial culture of the cerebrospinal fluid was negative. Further questioning revealed that one of the patient's classmates had recently been diagnosed to have hand, foot, and mouth disease. Due to the clinical suspicion of severe hand, foot, and mouth disease, intravenous immunoglobulin was given on the day of admission. Paired sera, collected 14 days apart, revealed a rise in the titer of antibody to coxsackievirus B virus type 4 from Ͻ10 to 40, compatible with acute infection. Viral culture and reverse transcriptase PCR for enterovirus/coxsackievirus on the nasopharyngeal aspirate, throat swab, rectal swab, and cerebrospinal fluid were all negative. However, blood culture taken on days 1, 3, 6, and 7 of admission grew Gram-positive cocci in clusters (Bactec 9240 blood culture system; Becton, Dickinson, MD). After incubation at 37°C in 5% CO 2 for 24 h, 2-mm creamy white colonies were seen. The bacterium was negative for catalase, but both the slide and tube coagulase tests using rabbit plasma were positive. It was also positive with Slidex Staph Plus (bioMérieux). A BD Phoenix PID panel (Becton, Dickinson and Company, Sparks, MD) identified the bacterium as Staphylococcus aureus, while the Vitek system Grampositive identification (GPI) test (bioMérieux, Durham, NC) could not identify the organism. According to the 2010 Clinical and Laboratory Standards Institute interpretive criteria, the isolate was susceptible to cloxacillin, cotrimoxazole, minocycline, and gentamicin but resist...

Catalase-Negative Staphylococcus lugdunensis Strain with a Novel Point Mutation in the Catalase Gene Isolated from a Patient with Chronic Suppurative Otitis Media

“…In this study, we detected a nonsense mutation at position C1180T, which caused a codon change from CAA to TAA (stop codon). We therefore hypothesize that a single codon mutation is responsible for the loss of catalase activity in this bacterium, similar to what has been previously described (21). Sequence analysis showed that the N-terminal arm of the catalase gene in our isolate was conserved, whereas the rest of the gene was either disrupted or lost due to the premature termination of the translation process.…”

“…Grüner et al reported a frameshift mutation due to a 5-base deletion upstream of the initiation codon of the catalase gene (16), whereas a T172C substitution, leading to a histidine 58-to-tyrosine change, and a G636A substitution, leading to an arginine 212-to histidine change, have been reported by Piau et al (11). To et al (21) identified 15 silent mutations; a critical nonsense mutation at position 802, leading to a change from codon GAA to TAA (stop codon); and 4 additional mutations downstream of the nonsense mutation. In this study, we detected a nonsense mutation at position C1180T, which caused a codon change from CAA to TAA (stop codon).…”

Molecular Characterization of a Catalase-Negative Staphylococcus aureus Blood Culture Isolate

“…Some researchers have observed a correlation between virulence and catalase activity (8,22,23), and yet others have not found any evidence of such a correlation (24,25). Nevertheless, clinical isolates of catalase-negative S. aureus appear to have a role in human infections (11)(12)(13)(14)(15)26). Clonal outbreaks of catalase-negative S. aureus infections have been reported, suggesting that such strains are as virulent as wild-type strains (27,28).…”

Molecular Characterization of a Catalase-Negative Methicillin-Susceptible Staphylococcus aureus subsp. aureus Strain Collected from a Patient with Cutaneous Abscess

“…While infections caused by catalase-negative S. aureus have been reported, these reports are rare. Furthermore, few studies have used robust molecular testing to definitively identify the organism or to determine the mutation responsible for catalase deficiency (7)(8)(9). Therefore, we sought to further characterize the catalase-negative infecting strain.…”