Bordetella parapertussis Bacteremia: Two Case Reports : The Pediatric Infectious Disease Journal

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Bordetella parapertussis Bacteremia

Two Case Reports

Wallihan, Rebecca MD*†; Selvarangan, Rangaraj BVSc, PhD‡§; Marcon, Mario PhD†¶; Koranyi, Katalin MD*†; Spicer, Kevin MD, PhD, MPH*†; Jackson, Mary Anne MD§**

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The Pediatric Infectious Disease Journal: July 2013 - Volume 32 - Issue 7 - p 796-798
doi: 10.1097/INF.0b013e31828d2ca4
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Since its initial description by Eldering and Kendrick1 in 1937, Bordetella parapertussis has become well-recognized as a significant agent of pertussis-like illness in Europe and the United States.2–4 It can cause respiratory infection similar to B. pertussis, although reportedly less severe,4–6 and comprises 2–22% of Bordetella species recovered from individuals with suspected pertussis.3–5,7 Although Bordetella holmesii and Bordetella bronchiseptica have both been reported to cause bacteremia in immunocompromised hosts,2,8,9 reports of invasive illness or death due to B. parapertussis are rare.10,11 We describe 2 cases of B. parapertussis bacteremia and the laboratory identification techniques and treatment strategies used.


A 6-year-old white boy with history of asthma and obstructive sleep apnea presented to the emergency department (ED) with a 3-year history of dyspnea, chest pain with exertion and exercise intolerance. His symptoms had been slowly progressing over the preceding 6 months, with the additional development of fatigue and nonproductive cough 2–3 months before presentation, both of which had worsened in the past 2 weeks. He sought medical care on multiple occasions during this period and was diagnosed with asthma and prescribed inhaled bronchodilator therapy and multiple short courses of corticosteroid therapy. A chest radiograph 1 day before presentation revealed mild cardiomegaly, gradually increasing when compared with previous studies, and outpatient cardiology follow-up was to be arranged. His medical history was significant only for asthma and obstructive sleep apnea for which he underwent adenoidectomy 6 months earlier. He had no known sick contacts, and his only animal exposures were to 2 cats and 2 dogs, which lived in the home.

His vital signs on presentation to the ED were remarkable for fever to 38.9°C, respiratory rate 60 breaths per minute, pulse 152 beats per minute, blood pressure 125/80 mmHg and oxygen saturation of 92% in ambient air. Initial physical examination revealed an overweight child in moderate respiratory distress with nasal flaring, prolonged expiratory phase of breathing and scattered wheezes. The heart was without murmur, although there was an intermittent gallop rhythm. An electrocardiogram showed right ventricular hypertrophy, right atrial enlargement and T-wave inversions in the inferolateral leads, and echocardiogram was significant for severe pulmonary hypertension. He was admitted to the cardiac intensive care unit for further monitoring and evaluation and for initiation of milrinone.

Because of fever on presentation, a blood culture was obtained. Additional studies were unremarkable, with the exception of detection of rhinovirus by polymerase chain reaction (PCR) performed on a nasopharyngeal (NP) specimen. The white blood cell count was 12.6 k/mm3 with 67% segmented neutrophils, 18% band forms and 11% lymphocytes. Chest radiograph did not show any acute pulmonary abnormalities, but ceftriaxone and azithromycin were started because of concern for lower respiratory tract infection. Computed tomography (CT) of the chest showed patchy bilateral airspace disease suggestive of atypical or viral pneumonia.

On the fifth day of incubation, the blood culture became positive with short, Gram-negative coccobacilli. The organism grew slowly on subculture to blood and chocolate agars but not on MacConkey agar, gave positive tests for catalase and urease activity, but was negative for oxidase activity and motility. Identification by traditional biochemical methods was unsuccessful. Antibiotic susceptibility testing performed by the E-test method on Mueller Hinton agar at 35°C for 72 hours showed minimal inhibitory concentration to ceftriaxone (16 μg/mL) but relatively low minimal inhibitory concentrations to azithromycin, ciprofloxacin, gentamicin, meropenem and trimethoprim/sulfamethoxazole, suggesting susceptibility to these agents. Serotyping by slide agglutination and PCR performed on the culture isolate were both positive for B. parapertussis (pIS1001 insertion sequence). Partial sequencing of the 16S rRNA gene was consistent with an organism in the B. pertussis/B. parapertussis/B. bronchiseptica group. An NP swab submitted at the time of admission for PCR testing for respiratory viruses was tested retrospectively by PCR and was also positive for B. parapertussis. The patient completed a 7-day course of ciprofloxacin and had no further infectious issues during the hospitalization. A repeat blood culture and repeat B. parapertussis PCR from an NP specimen were both negative. His pulmonary hypertension remained severe, despite antimicrobial therapy, and he was eventually discharged on day 27 to continue epoprostenol and bosentan as an outpatient.

Given the recovery of this organism from the blood, an immunological evaluation was performed. This included quantitative immunoglobulins (IgG, IgA, IgM and IgE), T-/B-cell immunophenotype, pneumococcal antibody response and antibodies against diphtheria and tetanus toxoids, all of which were normal. Ultrasound of the left upper quadrant confirmed the presence of a spleen, and there were no Howell-Jolly bodies seen on microscopic examination of a peripheral blood smear.


A 6-year-old boy with T-cell acute lymphoblastic leukemia, initially diagnosed 7 months prior, was admitted to the hospital for evaluation of fever and pneumonia. Cough, rhinorrhea, abdominal pain and nonbloody diarrhea had been present for several days, and he complained of leg and back pain on the day of admission. He had completed delayed intensification chemotherapy with vincristine, doxorubicin, intrathecal methotrexate, dexamethasone and intramuscular Erwinia 10 days prior. On admission, the absolute neutrophil count was 800 cells/mm3. A blood culture was obtained, and he received cefepime 50 mg/kg/dose every 8 hours. A chest radiograph revealed a left medial basilar opacity.

Fever, cough and watery diarrhea persisted, but the absolute neutrophil count became normal and then elevated by day 5 of his illness. CT scan with contrast of the chest at that time revealed bilateral airspace disease, worsening in the right lower lobe and new disease in the left lower lobe. Concurrently, the blood culture obtained at admission was positive for Gram-negative rods on the third day of incubation. The organism grew in aerobic blood culture bottle and failed to grow in the anaerobic blood culture bottle. On subculture, bacterial growth was evident on blood and chocolate agar after 48 hours of incubation and growth was absent on MacConkey agar. The isolate tested oxidase negative and catalase positive. Automated and rapid identification systems failed to provide acceptable identification of the organism. Reference laboratory identified the organism as B. parapertussis, and susceptibility testing was unable to be performed due to poor growth. The organism was sent to Centers for Disease Control and Prevention where the identification was confirmed by latex agglutination with B. parapertussis antibody and susceptibility testing revealed susceptibility to erythromycin and azithromycin. Twelve subsequent blood cultures were negative.

He required oxygen supplementation by mask and intermittent biphasic positive airway pressure; daily fevers of >39°C persisted. On day 9 of his course, toxigenic Clostridium difficile was identified from stool. Therapy at that time was modified to include cefepime and metronidazole; voriconazole that had been initiated a week into his clinical course was continued. A repeat chest CT demonstrated cavitary disease in both lower lobes.

Levofloxacin was initiated on hospital day 13 after definitive organism identification and continued for 2 weeks. Fever abated within 24 hours of instituting levofloxacin, and he was weaned off oxygen within 72 hours. While his respiratory symptoms continued to improve, an intercurrent fever elevation prompted further evaluation by bronchoalveolar lavage (BAL) and lung biopsy on day 17; B. parapertussis was confirmed by real-time PCR from lung, pleural fluid and BAL at a reference laboratory. However, the organism failed to grow from aerobic subcultures of the pleural fluid and BAL specimens. Lung biopsy revealed focal neutrophil infiltration of bronchioles and neutrophils. His chemotherapy was reinstituted on day 25, and he was discharged on day 39 of his course.


B. parapertussis is 1 of the 9 species of Bordetella and well-recognized as a cause of pertussis syndrome in humans. While documented B. parapertussis cases in the United States were uncommon between 1975 and 2005,2 data from 9 states between 2008 and 2010 suggest that it may represent a significant proportion of whooping cough cases.3

Invasive infection caused by Bordetella species has been most often noted in immunocompromised hosts or those with chronic respiratory disease. Among these patients, the respiratory tract has most frequently been involved, with a range of clinical manifestations noted, such as sinusitis, tracheobronchitis, classical whooping cough and pneumonia. Cavitary disease has been described but usually in association with B. bronchiseptica, the organism traditionally associated with canine kennel cough, and most often implicated in cases of bacteremia. Besides Bordetella bronchiseptica, B. pertussis and B. holmesii have been reported as causes of bacteremia in immunocompromised hosts, but reports of B. parapertussis bacteremia are rare.10

Our first case occurred in a seemingly immunocompetent child with pulmonary hypertension. To our knowledge, there is no known association between B. parapertussis and pulmonary hypertension, although it is a known complication of B. pertussis infection. Given the prolonged nature of his symptoms, it is unlikely that this was the cause of his cardiac disease. Instead, we postulate that this infection likely exacerbated his underlying condition, and the abnormalities on chest CT raise the possibility of direct entry from a lower respiratory tract infection. In addition, although evaluation of his immune system did not reveal any abnormalities, it is possible that the multiple courses of systemic steroids for presumed asthma may have caused a temporary immunologic dysfunction. In case 2, the clinical course, positive blood isolate and detection by PCR in lung, pleural fluid and BAL fluid provided good evidence of bacteremic pneumonia in an immunocompromised host.

Here, we report the second and third cases of B. parapertussis bacteremia in the literature and describe the laboratory identification techniques used and antibiotic therapies given. Although previously thought to cause only minor respiratory illness, the cases described demonstrate that B. parapertussis can cause invasive disease in both immunocompromised and immunocompetent hosts.


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Bordetella parapertussis; bacteremia

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