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Special Feature |

Pathological Case of the Month FREE

[+] Author Affiliations

Section Editor: Enid Gilbert-barness, MD

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Arch Pediatr Adolesc Med. 1998;152(9):926. doi:.
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Published online

Figure 1. A, The lungs appear unremarkable on day 3 of illness. B, An infiltrate in the right upper lobe was present on day 6 of illness. C, Complete "whiteout" of the right lung field with incipient infiltration on the left along the oblique fissure was present on day 7.

Figure 2. At autopsy the right lung shows complete consolidation with focal involvement along the left oblique fissure, exactly mirroring the chest x-ray film.

Figure 3. A bronchiole (left upper corner) contains desquamated respiratory epithelium and exudate. There is no surrounding lymphocytic infiltrate. The interstitium is congested while the alveoli are filled with macrophages, proteinaceous debris, and necrotic cells (hematoxylin-eosin, original magnification ×40).

Figure 4. Immunohistochemical staining for pertactin demonstrates the organisms localized to the ciliated border on the surface of the bronchiole mucosal epithelium. No organisms were detected in the alveoli (alkaline phosphatase fast red with Harris hematoxylin counterstain, original magnification ×40).

A polymerase chain reaction amplification assay1 confirmed Bordetella pertussis in both premortem and postmortem specimens. Detection of B pertussis using standard microbiologic culture or direct fluorescent antibody detection may be unreliable. Polymerase chain reaction–based assays, while not widely available, have demonstrated increased sensitivity relative to traditional methods2 and have the advantage of remaining positive even after therapy has started.3 In addition, immunohistochemical staining with a monoclonal antibody for pertactin antigen4 demonstrated that the organisms attached to the cilia were B pertussis (Figure 4). Special stains did not show other organisms; no viral inclusions were noted. These findings suggest that B pertussis was the sole infecting agent.

A remarkable feature of this case is the rapid progression of B pertussis pneumonia. Premortem clues to the diagnosis include the absolute lymphocytosis noted on day 3 of illness and the paroxysms of cough interspersed with periods of apparent well-being. In retrospect, earlier administration of erythromycin might have altered the outcome. Suspicion of pertussis on clinical grounds should dictate initiation of treatment until diagnostic testing for the organism is completed.

Pertussis mortality, typically due to pneumonia, is associated with median maternal age of 20 years, gestational age of 36 weeks or less, and age younger than 1 year.5,6 There may be an increased incidence of mortality in Hispanics, presumably as a result of difficulties with communication or genetic or socioeconomic factors. While the mechanism of death is uncertain, perfusion through the consolidated lung may lead to pulmonary hypertension with subsequent right-sided heart failure ending in cardiac arrhythmia.7

Accepted for publication May 1, 1997.

Corresponding author: Mark A. Lovell, MD, Box 168, University of Virginia Health Sciences Center, Charlottesville, VA 22908 (e-mail: mal3u@virginia.edu).

McLafferty  MHaricus  DHewlett  E Nucleotide sequence and characterization of a repetitive DNA element from the genome of Bordetella pertussis with characteristics of an insertion sequence. J Gen Microbiol. 1988;1342297- 2306
Glare  EMPaton  JCPremier  RRLawrence  AJNisbet  IT Analysis of a repetitive DNA sequence from Bordetella pertussis and its application to the diagnosis of pertussis using the polymerase chain reaction. J Clin Microbiol. 1990;281982- 1987
Edelman  KNikkari  SRuuskanen  OHe  QViljanen  MMertsola  J Detection of Bordetella pertussis by polymerase chain reaction and culture in the nasopharynx of erythromycin-treated infants with pertussis. Pediatr Infect Dis J. 1996;1554- 57
Link to Article
Blom  JHeron  IHendley  JO Immunoelectron microscopy of antigens of Bordetella pertussis using monoclonal antibodies to agglutinogens 2 and 3, filamentous haemagglutinin, pertussis toxin, pertactin, and adenylate cyclase toxin. APMIS. 1994;102681- 689
Link to Article
Hackman  RPerrin  DGKarmali  MCutz  E Fatal Bordetella pertussis infection. Pediatr Pathol Lab Med. 1996;16643- 653
Link to Article
Wartis  NStrebel  PMWharton  MBardenheier  BHardy  IRB Pertussis deaths. Pediatrics. 1996;97607- 612
Goulin  GDKaya  KMBradley  JS Severe pulmonary hypertension associated with shock and death in infants infected with Bordetella pertussisCrit Care Med. 1993;211791- 1794
Link to Article

Tables

References

McLafferty  MHaricus  DHewlett  E Nucleotide sequence and characterization of a repetitive DNA element from the genome of Bordetella pertussis with characteristics of an insertion sequence. J Gen Microbiol. 1988;1342297- 2306
Glare  EMPaton  JCPremier  RRLawrence  AJNisbet  IT Analysis of a repetitive DNA sequence from Bordetella pertussis and its application to the diagnosis of pertussis using the polymerase chain reaction. J Clin Microbiol. 1990;281982- 1987
Edelman  KNikkari  SRuuskanen  OHe  QViljanen  MMertsola  J Detection of Bordetella pertussis by polymerase chain reaction and culture in the nasopharynx of erythromycin-treated infants with pertussis. Pediatr Infect Dis J. 1996;1554- 57
Link to Article
Blom  JHeron  IHendley  JO Immunoelectron microscopy of antigens of Bordetella pertussis using monoclonal antibodies to agglutinogens 2 and 3, filamentous haemagglutinin, pertussis toxin, pertactin, and adenylate cyclase toxin. APMIS. 1994;102681- 689
Link to Article
Hackman  RPerrin  DGKarmali  MCutz  E Fatal Bordetella pertussis infection. Pediatr Pathol Lab Med. 1996;16643- 653
Link to Article
Wartis  NStrebel  PMWharton  MBardenheier  BHardy  IRB Pertussis deaths. Pediatrics. 1996;97607- 612
Goulin  GDKaya  KMBradley  JS Severe pulmonary hypertension associated with shock and death in infants infected with Bordetella pertussisCrit Care Med. 1993;211791- 1794
Link to Article

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