- Email: [email protected]
Pertussis in an infant
TheJournal of Emergency Medicine, Vol. 7, pp. 345-348, 1989
Printed in the USA ??Copyright 0 1989 Maxwell Pergamon Macmillan plc
PERTUSSIS
IN AN INFANT
Joseph J. Bocka,
MD
Department of Emergency Medicine, William Beaumont Hospital, Royal Oak, Michigan Reprinf address: Joseph J. Bocka, MD, William Beaumont Hospital, Department of Emergency Medicine, 3601 West 13 Mile Road, Royal Oak, Ml 48072
0 Abstract -This paper reports a one-month-old female with a one-week history of low grade fever and rhinorrhea, and one day of intermittent cough and cyanosis. The signs and symptoms are typical for pertussis in an infant less than six months old. The incidence of pertussis in the neonate and infant appears to be increasing. The disease still carries significant morbidity and mortality, especially in this age group. Pertussis should be included in the differential diagnosis of protracted cough with cyanosis or vomiting, persistent rhinorrhea, and marked lymphocytosis in children under six months of age.
ing poorly all day. No vomiting or diarrhea was noted. The child appeared lethargic, 5 % to 10% dehydrated, and in mild respiratory distress. Her vital signs were temperature 37.9”C (100.2”F); respirations 30 per minute; pulse 156 beats per minute; blood pressure palpable at 78 mm Hg systolic; and weight 4.84 kg (birth weight=4.6 kg). Smpanic membranes and pharynx were normal, and there were crusts about the nares. On chest examination, there were no retractions, coarse transmitted upper airway breath sounds were heard on auscultation, and there was no cardiac murmur. The child moved all four extremities equally well and had symmetrical reflexes. The rest of the physical examination was normal. An intravenous infusion of DY0.45 % NS was administered. A 5-minute bout of coughing was then witnessed, during which the infant became persistently cyanotic. She was bag-ventilated briefly before being easily intubated. No seizure activity was noted. Copious amounts of thick, rust-colored sputum were suctioned from the endotracheal tube. Ceftriaxone (100 mg) was given intravenously for possible sepsis. Laboratory studies revealed a white blood count of 55,000 cells/mm2, with 95% lymphocytes; hemoglobin, 13.5 gram%. The sodium was 144 mEq/L; chloride, 100 mEq/L; potassium, 4.1 mEq/L; CO,, 15 mEq/L; BUN, 20 mg/dL; creatinine, 0.8 mg/dL; glucose, 88 mg/dL. The ammonia was 12 units/L (normal=up to 50); SGGT, 29 pg/dL (normal =up to 40). Arterial blood gases obtained (prior to intubation) on simple mask at 10 L/minute were pH, 7.54; pCO,, 44 torr; PO,, 60 torr; and O2 saturation of 89%. Chest x-
0 Keywords- pertussis; whooping cough; infants
INTRODUCTION
In the prevaccination era, pertussis (whooping cough) was a leading cause of infant deaths (1). Though the number of cases reported had dropped by more than 99% from the 1930s (2), an alarming increase has been seen (especially in those less than 2 years of age) in the United States, England, and Sweden during the 1980s (l-8). CASE REPORT
A 28-day-old female was brought to the emergency department because of a cough and fever. The infant had been healthy until approximately 3 weeks of age, when she developed rhinorrhea with intermittent fever to 37.8”C (100°F). On the night of presentation, the infant was noted by her parents to have “coughing fits” lasting 2 to 5 minutes, accompanied by cyanosis. Because of these, she had been feed-
Clinical Communications: Pediatrics features articles on the assessment v
ties. Clinical Communications: Colorado.
Pediatrics
is coordinated
RECEIVED: 10 May 1988; FINAL SUBMISSIONRECEIVED:20 ACCEPTED: 13 December 1988
and management of childhood emergenby Roger Burkin, MD of the Rose Medical Center, Denver,
November 1988;
345
0736-4679/89 $3.00 + .OO
Joseph J. Bocka
346
ray studies demonstrated bilateral upper lobe atelectasis. The cerebrospinal fluid had no cells. Direct fluorescent antibody (FA) testing performed from nasopharyngeal swabs was positive for Bordetella pertussis. Per recommendation from the infectious disease department, the patient was treated with intravenous erythromycin 50 mg and chloramphenico1 100 mg every 6 hours. Nasopharyneal cultures (including Bordet-Gengou platings) from the patient and her family were negative, as were blood, urine, CSF, viral, and chlamydial cultures from the patient. The atelectasis cleared after aggressive pulmonary toilet, and she was easily extubated 36 hours after admission. A residual cough resolved in 5 days, and the patient was discharged after 7 days.
DISCUSSION Epidemiology Bacterial transmission is from human to human via aerosol droplets. The disease is highly contagious, with 80% to 90% of those exposed developing the disease. Most cases occur between June and September (our case was in June) (5). In the prevaccination era, pertussis was a leading cause of death in infants (1). In 1930, there were 265,000 cases reported in the United States, with 7,000 deaths (3). In 1985, there were 3589 cases with 19 deaths (5). Of those deaths, 18 were less than six months old. This is an increase from 1982, when there were 1895 cases with only 4 deaths (4). Moreover, only 5% to 10% of pertussis cases are believed to be recognized and reported to the CDC (9). More than 50% of all cases occur in infants less than 3 months of age, and more than 90% of all deaths occur in those less than 6 months old. While recovery from the disease provides lifelong immunity, 3 injections of the vaccine provide only about 12 years of protection (1,2,4,10,11). This accounts for the lo-fold increase from 1982 to 1985 reported in those over 18 years of age (4). The mother of our patient had a 2-week history of a slowly remitting bronchitis for which she had been started on erythromycin. In retrospect, this was believed to have been Pertussis . In England, the proportion of population vaccinated over the last two decades has dropped to 30%. This has resulted in more than 50,000 cases being reported from 1977-1980, with more than 100 deaths and 5,000 “prolonged hospitalizations” (12). This approaches the prevaccination era incidence (12). Recent similar epidemic outbreaks have occurred in
Oklahoma, Wisconsin, Washington, Colorado, as, and Sweden (l-8).
Tex-
Pathogenesis Bordetella pertussis is an aerobic nonmotile gramnegative coccobacillus that attaches to and multiplies on the respiratory epithelium, starting initially in the nasopharynx and ending up primarily in the bronchi and brochioles. This accounts for the various stages of the disease. The lung parenchyma and blood vessels are not invaded. Thus, blood cultures are negative. B. Pertussis grows poorly in blood agar. Incubation with Bordet-Gengou or Regan-Lowe medium for 7 days is required for identification (13). Because of this fastidiousness, sputum cultures are usually negative and immediately plated nasopharyngeal swabbings (as were used in our cases) are the most reliable. A mucopurulosanguinous exudate is formed in the respiratory tract. This compromises the small airways, especially of infants, and predisposes to atelectasis, cough, and cyanosis (as in our patient) as well as pneumonia.
Clinical Classically, pertussis consists of three stages: incubation, catarrhal, and paroxysmal. The incubation period of 7 to 10 days is followed by the catarrhal stage of 2 to 7 days of minimal or no fever, rhinorrhea, anorexia, and a mild, but increasing cough. The paroxysmal stage follows, lasting about 1 to 8 weeks. It is characterized by paroxysms of coughing, provoked by feeding and exertion. These are less spontaneous than in typical respiratory infections. The inspiratory gasp/whoop eventually develops in those between 6 months and 18 years of age, but usually is absent in those under the age of 6 months and most adults. We saw two other patients who were diagnosed with pertussis during this same month of June. Both (an 8 year old and a 4 year old) presented with the classic whoop and were DFA positive. Infants less than 6 months old often vomit in association with the cough, becoming dehydrated. Hypoxia tends to be more severe than the clinical appearance of the child suggests. A significant number will present with cyanosis and apneic spells. Adults usually only develop a prolonged bronchitis (as the mother of this child had) without a whoop. Mortality was formerly greater than 50% in hospi-
Pertussis
talized patients. Most died from dehydration, hypoxia, secondary bacterial pneumonia, or cerebral hemorrhage. Today, about 25% of those under age 4 and 12% overall will secondarily develop a bacterial pneumonia. Two percent will develop seizures, most of these patients being less than 6 months old (4). These are believed to be a result of hypoxia or cerebral hemorrhage from the prolonged coughing spells.
Diagnosis A knowledge of the epidemiology and clinical presentation of pertussis and a careful history are the best guides to early diagnosis in the infant. In one study, pertussis was considered in the differential of only 35% of patients found to have the disease (14). Recognition in the catarrhal stage is unlikely unless one is alert to the history of contact. In infants less than 6 months old, the history of a gradually increasing cough provoked by feeding or exertion, and associated with cyanosis or vomiting should suggest the diagnosis. Fevers, if any, should be below 38.4”C (101 “F). The classic “whoop” is not usually seen in those under 6 months of age. Lymphocytosis is profound (greater than 70% of the total white blood cell count) with the WBC usually rising to 20-40,000 cells/mm2, and often up to 100,000. Definitive culture diagnosis is not always possible. Blood cultures are uniformly negative, for reasons mentioned earlier. Immediately plated deep nasopharyngeal swabs grown for one week in BordetGengou agar are considered to be the gold standard of diagnosis, but are positive in only 15% to 40% and give results too late for clinical usefulness. Direct fluorescent antibody studies performed immediately from nasopharyngeal samples are positive in 40% to 80%) and now provide the majority of case confirmations along with a consistent history. Results are available within minutes. Diagnosis is best for both of these methods if specimens are obtained within the first 3 weeks of the disease (that is, in incubation, catarrhal, or early paroxysmal stages (5,15,16). Serologic testing using ELISA techniques are promising in an adjunctive role (17,18).
Differential In infants, pertussis is often misdiagnosed as viral gastroenteritis. The initial catarrhal phase, with increasing nonspontaneous cough producing vomiting (especially with feeding), and profound lymphocytosis should be recognized. RSV/bronchiolitis usually
347
presents with a more rapid onset, greater respiratory distress, higher temperature, and less profound cough and lymphocytosis. Members of the genus Chlamydia will present as an interstitial pneumonia with a spontaneous deep productive cough and conjunctivitis in those less than 4 months old. Reye’s syndrome may be considered if there is an antecedent viral illness and aspirin use followed by persistent vomiting. The patient with pertussis should have normal liver function testing and a more profound lymphocytosis. Foreign bodies should be distinguishable by obtaining a catarrhal stage history. Adenoviruses can produce a clinically similar disease, but usually have less coughing and should be FA negative and viral-testing positive. Pyloric stenosis should be differentiated by the lack of a catarrhal stage or coughing and by the presence of an epigastric mass. Likewise, reflux should have a paucity of upper respiratory symptoms and a relation of vomiting to feeding, but rarely to exertion. Coughing should be present only if aspiration has occurred.
Treatment Erythromycin estolate is the antibiotic of choice to prevent interpersonal transfer. The oral dosage is 30 to 50 mg/kg/day QID for 14 days (12,19,20). The effectiveness of prophylaxis for exposed susceptible persons has not been determined, but is recommended for household and close contacts (erythromycin 40 to 50 mg/kg/day BID to QID) (21). Erythromycin is effective in reducing symptoms and the course if initiated within the first 10 to 14 days, but is not proven beyond this period (12,20). Hyperimmune globulin and steroids are not proven in efficacy and may even be counterproductive once the disease has progressed to the paroxysmal stage (5,15). Hyperimmune globulin is no longer commercially available in the United States.
Vaccine The vaccine used in the United States since the 1940s consists of a whole cell with endotoxin. It is given at 2, 4, and 6 months of age. Over 80% will acquire effective protection with this regimen. Two doses may provide some portal immunity, while one dose alone is of little benefit (2,10,11). Because of this, infants will continue to experience the majority of the cases, morbidity, and mortality. Full immunity persists for 3 years and rapidly falls to providing essentially no protection after 12 years. This is in contrast to recovery
Joseph J. Bocka
348
from the natural disease, which appears to provide lifelong protection. Thus, the number of cases in adults is also rising dramatically and will continue to do so, especially since the vaccine is not recommended after age 7 (2,6). A local reaction is observed in 50% and severe neurologic sequelae in 1 : 310,000 (11,22). Concern over CNS side effects is a major reason for many choosing not to be vaccinated. A new killed cell-free vaccine has been given experimentally in Japan since 1981 and in Sweden since 1984, and is under extensive field study in the United States. Summary
elect not to be vaccinated and as those who have been vaccinated lose their immunity after 12 years. Infants under 6 months of age do not gain maternal immunity, nor can they become effectively vaccinated. They also have fragile narrow airways and are easily dehydrated. Thus, this high-risk group will continue to be particularly susceptible and have the greatest morbidity and mortality. A detailed history, recognition of the presentation in infants (including lack of the classic “whoop”), lymphocytosis, and a protracted nonspontaneous cough associated with vomiting or cyanosis are important in the diagnosis. Immediate nasopharyngeal cultures are recommended. Treatment is with erythromycin for 14 days. Acknowledgment-Special thanks
Pertussis is an underdiagnosed disease, and may become an increasingly important entity as more people
to Judith for her help and encouragement this manuscript. MD, FACEP,
E. Tintinalli, in preparing
REFERENCES 1. Centers for Disease Control. Pertussis-United States, 198283. MMWR. 1984;33:573-5. 2. Bass, JW, Stephenson S. The return of pertussis. Ped Infect Dis J. 1987;6:141. 3. Centers for Disease Control. Annual Summary- 1980. MMWR. 1981;29:17. 4. Centers for Disease Control. Pertussis surveillance-United States, 1984 & 1985. MMWR. 1987;36:168-71. 5. Centers for Disease Control. Pertussis-Maryland. MMWR. 1983;32:297-305. 6. Nkowane BM, Wassilak SG, McKee A, et al. Pertussis epidemic in Oklahoma. AJDC. 1986;140:433. 7. Cherry JD. The pertussis epidemic in Oklahoma-A Warning for the Future. AJDC. 1986;140:417-18. 8. Romanus V, Jonsell R, Bergquist SO. Pertussis in Sweden after the cessation of general immunization. Ped Infect J. 1987;6(4): 364-71. 9. Hinman AR, Koplan JP. Pertussis and pertussis vaccine: reanalysis of benefits, risks and costs. JAMA. 1984;251:3109. 10. Begg RC. Pertussis. NZ Med J. 1984;11:408-11. 11. Immunization Practice Advisory Committee. Guidelines for vaccine prophylaxis. MMWR. 1985;34:405-26. 12. Bass JW. Pertussis: current status of prevention & treatment. Ped Infect Dis J. 1985:4:614-19.
13. Parker CD, Payne BJ. Bordetella. In: Manual for clinical microbiology. 4th ed. Edited by EH Lennette, Washington, DC: American Society for Microbiology; 1985:394-9. 14. Sotomayer J, Weiner LB, McMillan JA. Inaccurate diagnosis in infants with pertussis. Am J Dis Child. 1985;139:724-7. 15. Onorato IM, Wassilak SG. Laboratory diagnosis of pertussis: state of the art. Ped Infect Dis J. 1987;6:145-51. 16. Marcon M. Comparison of nasopharyngeal and throat swab specimens for diagnosis of pertussis infection. J Clin Microbiol. 1987;25:1109-10. 17. Mertsola J, Ruuskanen 0, Kuronen T, Viljanen MK. Serologic diagnosis of pertussis. J Infect Dis. 1983;147:252-7. 18. Skeketee R. A comparison of laboratory and clinical methods for diagnosing pertussis. J Infect Dis. 1983;147:252-7. 19. Bass JW. Use of erythromycin in pertussis outbreaks. Pediatrics. 1983;72:748-9. 20. Berquist SO. Erythromycin in the treatment of pertussis. Ped Infect Dis J. 1987;6:458-61. 21. Report of the Committee on Infectious Disease (Red Book). Pub AAP. 1986;268-9. 22. Miller DL, Ross EM, Alderslade R, Bellman MH, Rawson NSB. Pertussis immunization and serious acute neurologic illness in children. Brit Med J. 1981;282:1595-7.
Printed in the USA ??Copyright 0 1989 Maxwell Pergamon Macmillan plc
PERTUSSIS
IN AN INFANT
Joseph J. Bocka,
MD
Department of Emergency Medicine, William Beaumont Hospital, Royal Oak, Michigan Reprinf address: Joseph J. Bocka, MD, William Beaumont Hospital, Department of Emergency Medicine, 3601 West 13 Mile Road, Royal Oak, Ml 48072
0 Abstract -This paper reports a one-month-old female with a one-week history of low grade fever and rhinorrhea, and one day of intermittent cough and cyanosis. The signs and symptoms are typical for pertussis in an infant less than six months old. The incidence of pertussis in the neonate and infant appears to be increasing. The disease still carries significant morbidity and mortality, especially in this age group. Pertussis should be included in the differential diagnosis of protracted cough with cyanosis or vomiting, persistent rhinorrhea, and marked lymphocytosis in children under six months of age.
ing poorly all day. No vomiting or diarrhea was noted. The child appeared lethargic, 5 % to 10% dehydrated, and in mild respiratory distress. Her vital signs were temperature 37.9”C (100.2”F); respirations 30 per minute; pulse 156 beats per minute; blood pressure palpable at 78 mm Hg systolic; and weight 4.84 kg (birth weight=4.6 kg). Smpanic membranes and pharynx were normal, and there were crusts about the nares. On chest examination, there were no retractions, coarse transmitted upper airway breath sounds were heard on auscultation, and there was no cardiac murmur. The child moved all four extremities equally well and had symmetrical reflexes. The rest of the physical examination was normal. An intravenous infusion of DY0.45 % NS was administered. A 5-minute bout of coughing was then witnessed, during which the infant became persistently cyanotic. She was bag-ventilated briefly before being easily intubated. No seizure activity was noted. Copious amounts of thick, rust-colored sputum were suctioned from the endotracheal tube. Ceftriaxone (100 mg) was given intravenously for possible sepsis. Laboratory studies revealed a white blood count of 55,000 cells/mm2, with 95% lymphocytes; hemoglobin, 13.5 gram%. The sodium was 144 mEq/L; chloride, 100 mEq/L; potassium, 4.1 mEq/L; CO,, 15 mEq/L; BUN, 20 mg/dL; creatinine, 0.8 mg/dL; glucose, 88 mg/dL. The ammonia was 12 units/L (normal=up to 50); SGGT, 29 pg/dL (normal =up to 40). Arterial blood gases obtained (prior to intubation) on simple mask at 10 L/minute were pH, 7.54; pCO,, 44 torr; PO,, 60 torr; and O2 saturation of 89%. Chest x-
0 Keywords- pertussis; whooping cough; infants
INTRODUCTION
In the prevaccination era, pertussis (whooping cough) was a leading cause of infant deaths (1). Though the number of cases reported had dropped by more than 99% from the 1930s (2), an alarming increase has been seen (especially in those less than 2 years of age) in the United States, England, and Sweden during the 1980s (l-8). CASE REPORT
A 28-day-old female was brought to the emergency department because of a cough and fever. The infant had been healthy until approximately 3 weeks of age, when she developed rhinorrhea with intermittent fever to 37.8”C (100°F). On the night of presentation, the infant was noted by her parents to have “coughing fits” lasting 2 to 5 minutes, accompanied by cyanosis. Because of these, she had been feed-
Clinical Communications: Pediatrics features articles on the assessment v
ties. Clinical Communications: Colorado.
Pediatrics
is coordinated
RECEIVED: 10 May 1988; FINAL SUBMISSIONRECEIVED:20 ACCEPTED: 13 December 1988
and management of childhood emergenby Roger Burkin, MD of the Rose Medical Center, Denver,
November 1988;
345
0736-4679/89 $3.00 + .OO
Joseph J. Bocka
346
ray studies demonstrated bilateral upper lobe atelectasis. The cerebrospinal fluid had no cells. Direct fluorescent antibody (FA) testing performed from nasopharyngeal swabs was positive for Bordetella pertussis. Per recommendation from the infectious disease department, the patient was treated with intravenous erythromycin 50 mg and chloramphenico1 100 mg every 6 hours. Nasopharyneal cultures (including Bordet-Gengou platings) from the patient and her family were negative, as were blood, urine, CSF, viral, and chlamydial cultures from the patient. The atelectasis cleared after aggressive pulmonary toilet, and she was easily extubated 36 hours after admission. A residual cough resolved in 5 days, and the patient was discharged after 7 days.
DISCUSSION Epidemiology Bacterial transmission is from human to human via aerosol droplets. The disease is highly contagious, with 80% to 90% of those exposed developing the disease. Most cases occur between June and September (our case was in June) (5). In the prevaccination era, pertussis was a leading cause of death in infants (1). In 1930, there were 265,000 cases reported in the United States, with 7,000 deaths (3). In 1985, there were 3589 cases with 19 deaths (5). Of those deaths, 18 were less than six months old. This is an increase from 1982, when there were 1895 cases with only 4 deaths (4). Moreover, only 5% to 10% of pertussis cases are believed to be recognized and reported to the CDC (9). More than 50% of all cases occur in infants less than 3 months of age, and more than 90% of all deaths occur in those less than 6 months old. While recovery from the disease provides lifelong immunity, 3 injections of the vaccine provide only about 12 years of protection (1,2,4,10,11). This accounts for the lo-fold increase from 1982 to 1985 reported in those over 18 years of age (4). The mother of our patient had a 2-week history of a slowly remitting bronchitis for which she had been started on erythromycin. In retrospect, this was believed to have been Pertussis . In England, the proportion of population vaccinated over the last two decades has dropped to 30%. This has resulted in more than 50,000 cases being reported from 1977-1980, with more than 100 deaths and 5,000 “prolonged hospitalizations” (12). This approaches the prevaccination era incidence (12). Recent similar epidemic outbreaks have occurred in
Oklahoma, Wisconsin, Washington, Colorado, as, and Sweden (l-8).
Tex-
Pathogenesis Bordetella pertussis is an aerobic nonmotile gramnegative coccobacillus that attaches to and multiplies on the respiratory epithelium, starting initially in the nasopharynx and ending up primarily in the bronchi and brochioles. This accounts for the various stages of the disease. The lung parenchyma and blood vessels are not invaded. Thus, blood cultures are negative. B. Pertussis grows poorly in blood agar. Incubation with Bordet-Gengou or Regan-Lowe medium for 7 days is required for identification (13). Because of this fastidiousness, sputum cultures are usually negative and immediately plated nasopharyngeal swabbings (as were used in our cases) are the most reliable. A mucopurulosanguinous exudate is formed in the respiratory tract. This compromises the small airways, especially of infants, and predisposes to atelectasis, cough, and cyanosis (as in our patient) as well as pneumonia.
Clinical Classically, pertussis consists of three stages: incubation, catarrhal, and paroxysmal. The incubation period of 7 to 10 days is followed by the catarrhal stage of 2 to 7 days of minimal or no fever, rhinorrhea, anorexia, and a mild, but increasing cough. The paroxysmal stage follows, lasting about 1 to 8 weeks. It is characterized by paroxysms of coughing, provoked by feeding and exertion. These are less spontaneous than in typical respiratory infections. The inspiratory gasp/whoop eventually develops in those between 6 months and 18 years of age, but usually is absent in those under the age of 6 months and most adults. We saw two other patients who were diagnosed with pertussis during this same month of June. Both (an 8 year old and a 4 year old) presented with the classic whoop and were DFA positive. Infants less than 6 months old often vomit in association with the cough, becoming dehydrated. Hypoxia tends to be more severe than the clinical appearance of the child suggests. A significant number will present with cyanosis and apneic spells. Adults usually only develop a prolonged bronchitis (as the mother of this child had) without a whoop. Mortality was formerly greater than 50% in hospi-
Pertussis
talized patients. Most died from dehydration, hypoxia, secondary bacterial pneumonia, or cerebral hemorrhage. Today, about 25% of those under age 4 and 12% overall will secondarily develop a bacterial pneumonia. Two percent will develop seizures, most of these patients being less than 6 months old (4). These are believed to be a result of hypoxia or cerebral hemorrhage from the prolonged coughing spells.
Diagnosis A knowledge of the epidemiology and clinical presentation of pertussis and a careful history are the best guides to early diagnosis in the infant. In one study, pertussis was considered in the differential of only 35% of patients found to have the disease (14). Recognition in the catarrhal stage is unlikely unless one is alert to the history of contact. In infants less than 6 months old, the history of a gradually increasing cough provoked by feeding or exertion, and associated with cyanosis or vomiting should suggest the diagnosis. Fevers, if any, should be below 38.4”C (101 “F). The classic “whoop” is not usually seen in those under 6 months of age. Lymphocytosis is profound (greater than 70% of the total white blood cell count) with the WBC usually rising to 20-40,000 cells/mm2, and often up to 100,000. Definitive culture diagnosis is not always possible. Blood cultures are uniformly negative, for reasons mentioned earlier. Immediately plated deep nasopharyngeal swabs grown for one week in BordetGengou agar are considered to be the gold standard of diagnosis, but are positive in only 15% to 40% and give results too late for clinical usefulness. Direct fluorescent antibody studies performed immediately from nasopharyngeal samples are positive in 40% to 80%) and now provide the majority of case confirmations along with a consistent history. Results are available within minutes. Diagnosis is best for both of these methods if specimens are obtained within the first 3 weeks of the disease (that is, in incubation, catarrhal, or early paroxysmal stages (5,15,16). Serologic testing using ELISA techniques are promising in an adjunctive role (17,18).
Differential In infants, pertussis is often misdiagnosed as viral gastroenteritis. The initial catarrhal phase, with increasing nonspontaneous cough producing vomiting (especially with feeding), and profound lymphocytosis should be recognized. RSV/bronchiolitis usually
347
presents with a more rapid onset, greater respiratory distress, higher temperature, and less profound cough and lymphocytosis. Members of the genus Chlamydia will present as an interstitial pneumonia with a spontaneous deep productive cough and conjunctivitis in those less than 4 months old. Reye’s syndrome may be considered if there is an antecedent viral illness and aspirin use followed by persistent vomiting. The patient with pertussis should have normal liver function testing and a more profound lymphocytosis. Foreign bodies should be distinguishable by obtaining a catarrhal stage history. Adenoviruses can produce a clinically similar disease, but usually have less coughing and should be FA negative and viral-testing positive. Pyloric stenosis should be differentiated by the lack of a catarrhal stage or coughing and by the presence of an epigastric mass. Likewise, reflux should have a paucity of upper respiratory symptoms and a relation of vomiting to feeding, but rarely to exertion. Coughing should be present only if aspiration has occurred.
Treatment Erythromycin estolate is the antibiotic of choice to prevent interpersonal transfer. The oral dosage is 30 to 50 mg/kg/day QID for 14 days (12,19,20). The effectiveness of prophylaxis for exposed susceptible persons has not been determined, but is recommended for household and close contacts (erythromycin 40 to 50 mg/kg/day BID to QID) (21). Erythromycin is effective in reducing symptoms and the course if initiated within the first 10 to 14 days, but is not proven beyond this period (12,20). Hyperimmune globulin and steroids are not proven in efficacy and may even be counterproductive once the disease has progressed to the paroxysmal stage (5,15). Hyperimmune globulin is no longer commercially available in the United States.
Vaccine The vaccine used in the United States since the 1940s consists of a whole cell with endotoxin. It is given at 2, 4, and 6 months of age. Over 80% will acquire effective protection with this regimen. Two doses may provide some portal immunity, while one dose alone is of little benefit (2,10,11). Because of this, infants will continue to experience the majority of the cases, morbidity, and mortality. Full immunity persists for 3 years and rapidly falls to providing essentially no protection after 12 years. This is in contrast to recovery
Joseph J. Bocka
348
from the natural disease, which appears to provide lifelong protection. Thus, the number of cases in adults is also rising dramatically and will continue to do so, especially since the vaccine is not recommended after age 7 (2,6). A local reaction is observed in 50% and severe neurologic sequelae in 1 : 310,000 (11,22). Concern over CNS side effects is a major reason for many choosing not to be vaccinated. A new killed cell-free vaccine has been given experimentally in Japan since 1981 and in Sweden since 1984, and is under extensive field study in the United States. Summary
elect not to be vaccinated and as those who have been vaccinated lose their immunity after 12 years. Infants under 6 months of age do not gain maternal immunity, nor can they become effectively vaccinated. They also have fragile narrow airways and are easily dehydrated. Thus, this high-risk group will continue to be particularly susceptible and have the greatest morbidity and mortality. A detailed history, recognition of the presentation in infants (including lack of the classic “whoop”), lymphocytosis, and a protracted nonspontaneous cough associated with vomiting or cyanosis are important in the diagnosis. Immediate nasopharyngeal cultures are recommended. Treatment is with erythromycin for 14 days. Acknowledgment-Special thanks
Pertussis is an underdiagnosed disease, and may become an increasingly important entity as more people
to Judith for her help and encouragement this manuscript. MD, FACEP,
E. Tintinalli, in preparing
REFERENCES 1. Centers for Disease Control. Pertussis-United States, 198283. MMWR. 1984;33:573-5. 2. Bass, JW, Stephenson S. The return of pertussis. Ped Infect Dis J. 1987;6:141. 3. Centers for Disease Control. Annual Summary- 1980. MMWR. 1981;29:17. 4. Centers for Disease Control. Pertussis surveillance-United States, 1984 & 1985. MMWR. 1987;36:168-71. 5. Centers for Disease Control. Pertussis-Maryland. MMWR. 1983;32:297-305. 6. Nkowane BM, Wassilak SG, McKee A, et al. Pertussis epidemic in Oklahoma. AJDC. 1986;140:433. 7. Cherry JD. The pertussis epidemic in Oklahoma-A Warning for the Future. AJDC. 1986;140:417-18. 8. Romanus V, Jonsell R, Bergquist SO. Pertussis in Sweden after the cessation of general immunization. Ped Infect J. 1987;6(4): 364-71. 9. Hinman AR, Koplan JP. Pertussis and pertussis vaccine: reanalysis of benefits, risks and costs. JAMA. 1984;251:3109. 10. Begg RC. Pertussis. NZ Med J. 1984;11:408-11. 11. Immunization Practice Advisory Committee. Guidelines for vaccine prophylaxis. MMWR. 1985;34:405-26. 12. Bass JW. Pertussis: current status of prevention & treatment. Ped Infect Dis J. 1985:4:614-19.
13. Parker CD, Payne BJ. Bordetella. In: Manual for clinical microbiology. 4th ed. Edited by EH Lennette, Washington, DC: American Society for Microbiology; 1985:394-9. 14. Sotomayer J, Weiner LB, McMillan JA. Inaccurate diagnosis in infants with pertussis. Am J Dis Child. 1985;139:724-7. 15. Onorato IM, Wassilak SG. Laboratory diagnosis of pertussis: state of the art. Ped Infect Dis J. 1987;6:145-51. 16. Marcon M. Comparison of nasopharyngeal and throat swab specimens for diagnosis of pertussis infection. J Clin Microbiol. 1987;25:1109-10. 17. Mertsola J, Ruuskanen 0, Kuronen T, Viljanen MK. Serologic diagnosis of pertussis. J Infect Dis. 1983;147:252-7. 18. Skeketee R. A comparison of laboratory and clinical methods for diagnosing pertussis. J Infect Dis. 1983;147:252-7. 19. Bass JW. Use of erythromycin in pertussis outbreaks. Pediatrics. 1983;72:748-9. 20. Berquist SO. Erythromycin in the treatment of pertussis. Ped Infect Dis J. 1987;6:458-61. 21. Report of the Committee on Infectious Disease (Red Book). Pub AAP. 1986;268-9. 22. Miller DL, Ross EM, Alderslade R, Bellman MH, Rawson NSB. Pertussis immunization and serious acute neurologic illness in children. Brit Med J. 1981;282:1595-7.