Pertussis encephalopathy …

Ravindra Kumar Garg DM FRCP

Infectious Disorders

Updated 07.03.2024
Released 05.12.2006
Expires For CME 07.03.2027

Pertussis encephalopathy

Author: Ravindra Kumar Garg DM FRCP

See Contributor Disclosures

Editor: Christina M Marra MD

Pertussis encephalopathy

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Introduction

Overview

Pertussis or whooping cough is an important cause of infant death worldwide. Pertussis is caused by the organism Bordetella pertussis, a gram-negative bacillus. In 2019, the World Health Organization estimated 132,754 cases of pertussis globally, 95% of which were in developing countries. Whooping cough cases have surged globally since December 2023, with the United Kingdom reporting 4793 cases and eight infant deaths by April 2024. Declining vaccination rates, especially maternal, are major contributing factors. Severe complications of pertussis include pneumonia, encephalopathy, and meningoencephalitis. Central hypoventilation secondary to pertussis encephalopathy occurring during childhood has been described in an isolated case. An increased risk of epilepsy was noted in children with hospital-diagnosed pertussis compared with the general population. Infants who survive critical pertussis illness often have poor neurocognitive development. In the past, several neurologic complications were identified in infants immunized with the whole-cell pertussis vaccine, including acute encephalopathy, seizures, hypotonic-hyporeactive episodes, inconsolable crying, and anaphylactic reactions. Experts now believe that there is no convincing evidence proving an association between the pertussis vaccine and persistent brain damage. Vaccine encephalopathy is, in fact, an inherited genetic defect of the SCN1A gene that codes for the voltage-gated neuronal sodium channel. In fact, children who presented with earlier diagnoses of alleged vaccine encephalopathy in infancy were diagnosed years later with Dravet syndrome. The prenatal maternal tetanus, diphtheria, and acellular pertussis vaccination is safe, and the vaccine is not associated with an increased risk of autism spectrum disorder in offspring. That vaccine triggers autoimmune encephalitis remains unconfirmed. In regions with complete switch over to acellular vaccine, a resurgence of pertussis has been witnessed, along with some new cases of pertussis encephalopathy. Genetic variants linked to seizures post-diphtheria, tetanus, and whole-cell pertussis vaccination in India were identified, suggesting a genetic influence in vaccine-associated seizures. Based on a review of current literature, the author presents an overview focusing on pertussis encephalopathy and vaccine encephalopathy; in addition, he also discusses the epidemiology, pathogenesis, pathology, diagnosis, and treatment of pertussis.

Key points

	• Encephalopathy is a rare complication of pertussis.
	• Several neurologic complications have been described with the pertussis vaccines, particularly with whole-cell vaccines.
	• There is no convincing evidence proving an association between vaccine and persistent brain damage.
	• Vaccine encephalopathy is, in fact, caused by an inherited genetic defect of the voltage-gated neuronal sodium-channel gene.

Historical note and terminology

In 1640, Guillaume de Baillou provided the first detailed description of whooping cough as a distinct entity when he described an epidemic in 1578 (38). Kohn suggests that the description of the Perinthus cough by Hippocrates (around 400 BC) might possibly be whooping cough or a mix with other diseases, such as viral respiratory infections. In 1682, Thomas Willis was the first person to recognize the epidemic nature of pertussis. Bordet was credited with first describing the bacteria Bordetella pertussis. In 1900, he observed numerous coccobacilli in respiratory secretions collected from his own daughter who was suffering from pertussis. In 1906 Bordet and Gengou cultured Bordetella pertussis. Encephalopathy was first described as a complication of pertussis infection in 1877. Sydenham first used the term “infantum pertussis” in 1679.

Following the widespread use of whole-cell pertussis vaccines containing diphtheria and tetanus toxoids in the 1940s, the mean incidence rates of pertussis in United States of America decreased from 150 of 100,000 to approximately 1 of 100,000 by 1980. Vaccine encephalopathy was first identified in a report by Byers and Moll in 1948. Eight efficacy trials evaluating acellular pertussis vaccines were conducted in the early 1990s; the results were reported in publications from 1995 to 1998. In 1996, less immuno-reactogenic diphtheria, tetanus, and acellular pertussis vaccines were licensed and recommended for routine use in infants and young children, replacing whole-cell pertussis and diphtheria and tetanus toxoid vaccines completely in the United States. Acellular pertussis vaccines were not associated with enhanced risk of neurologic complications (10).

The British National Childhood Encephalopathy Study was established in 1976 as an independent scientific enquiry into severe acute neurologic illnesses associated with whole-cell pertussis vaccine. The study concluded that there was no significant association between vaccination and brain disease in most instances of encephalopathy, unexplained coma, convulsions lasting more than 30 minutes or associated with persistent complications, infantile spasms, or Reye syndrome in previously normal children within 7 days of immunization (27; 38).

Clinical manifestations

Presentation and course

Pertussis, a highly communicable disease, is recognized by paroxysmal spasms of severe cough, without fever, followed by characteristic episodes of inspiratory whoop and posttussive vomiting. Encephalopathy is a rare complication of pertussis. As with other complications of pertussis, encephalopathy is more common in females, and a familial predisposition is observed. Most cases of pertussis encephalopathy are clinically apparent between the second and fourth weeks of paroxysmal cough. In an old review of 148 cases, 9% of cases of encephalopathy occurred during the first week of pertussis, 76% during weeks 2 to 4, and 16% during weeks 5 to 7 of the illness. There were two types of encephalopathy, one in which convulsions were the major manifestation in absence of other signs of cerebral dysfunction, and another variety with more insidious onset progressing to coma (45; 14). It was earlier alleged that vaccination, particularly whole-cell pertussis vaccines, cause vaccine encephalopathy in children with SCN1A mutations (05).

Pertussis encephalopathy is usually associated with fever; seizures; alteration of consciousness; and focal neurologic signs, most notably acute visual loss in the presence of normal optic discs. It has been suggested that pertussis encephalopathy is secondary to retinal changes induced by cough paroxysms. Computed tomography studies in pertussis encephalopathy are normal. Autoimmune encephalitis is an acute brain disorder; clinical manifestations range from psychiatric manifestations, movement disorders, cognitive decline, and autonomic dysfunction. It is still speculative to consider that tetanus, diphtheria, and pertussis vaccine may trigger the occurrence of autoimmune encephalitis (11; 41).

With reemergence of pertussis, new cases of pertussis encephalopathy in infants are reported. The more recent acellular vaccines have demonstrated efficacy against severe disease and a lower incidence of serious adverse events. However, they do have certain limitations, including their inability to prevent nasal colonization by the bacterium and the fact that their protective effects diminish relatively quickly over time (19). Anh Tuan and colleagues reported three such cases from Vietnam. Patients initially presented with whooping cough and then developed lethargy, encephalopathy, and seizures (01). In all three cases, Bordetella pertussis DNA was detected by polymerase chain reaction (PCR) in CSF. After treatment, two patients survived with normal neurologic examination on subsequent follow ups. One patient succumbed to her illness.

Neurologic complications are observed in neonatal pertussis. These include seizures, subarachnoid hemorrhage, and encephalopathy. Severe episodes of intractable hypoglycemia are reported by several authors. Feeding difficulties are common. Repeated vomiting may lead to derangement of the serum electrolytes and the acid-base balance, dehydration, and weight loss in some patients (09; 08; 39). An increased risk of epilepsy is noted in children with hospital-diagnosed pertussis infections compared with the general population. Investigators assessed 4700 patients with pertussis (from population-based medical registries covering all Danish hospitals), 90 of whom developed epilepsy during follow-up. The cumulative incidence of epilepsy at age 10 years was 1.7% for patients with pertussis and 0.9% for the matched comparison group (26). A prospective cohort study assessed cognitive development in infants with critical pertussis 1 year after PICU discharge (03). Conducted across 26 U.S. hospitals, it involved 111 of 196 eligible patients who completed the Mullen Scales of Early Learning. Results showed significantly lower scores in visual reception, receptive language, and expressive language compared to norms. Abnormal scores in at least one domain were found in 37% of patients, with 9% scoring 2 or more standard deviations below norms. Older age and Hispanic ethnicity were linked to lower scores.

In typical cases, a diagnosis of whooping cough can be made on the basis of clinical presentation. A variety of viral and bacterial pathogens other than Bordetella pertussis can cause paroxysmal cough. Therefore, laboratory tests are used to confirm a diagnosis of Bordetella infection. Mild increases in the leukocyte count and marked lymphocytosis are classic markers of pertussis and have been shown to be useful in making an early diagnosis (Table 1).

Table 1. Diagnostic Criteria for Whooping Cough

A cough illness lasting 2 weeks or longer
One or more of the following:
	• Paroxysms of cough • An inspiratory whoop • Posttussive vomiting • No other obvious cause of cough
Cases are considered confirmed by:
	• Positive culture in respiratory secretions • Positive polymerase chain reaction test in respiratory secretions • Positive paired serology (ie, at least a 4-fold increase) • First testing should ideally be done within the first 2 weeks of symptom onset
(12)

Prognosis and complications

The most frequent complication of pertussis is pneumonia, which occurs in 6% of cases. Other complications include sinusitis, otitis media, viral and bacterial superinfections, and nutritional deficiencies resulting from repeated vomiting. Lumbar disc herniation and rectal prolapses can occur because of increased intra-abdominal pressure as a consequence of frequent vomiting and coughing. Increased venous pressure at times produces subconjunctival hemorrhages.

Pertussis mortality in the United States is two to three in 1000 cases; seizures occur in 1.9% and encephalopathy in 0.3%. Neurologic sequelae, such as learning disabilities, were seen in one third of the survivors; the remainder of survivors were normal (23; 40). A single case of central hypoventilation secondary to pertussis encephalopathy occurring during childhood has been described. The patient was successfully managed by negative pressure ventilation. In adult age, the patient was found to be asymptomatic (13).

Biological basis

Etiology and pathogenesis

Pertussis or whooping cough is caused by the organism Bordetella pertussis, a gram-negative coccobacillus, which is an obligate human pathogen. It is a strictly aerobic bacterium. Bordetella pertussis is encapsulated and does not produce spores. Bordetella pertussis is transmitted person to person by close contact with aerosolized droplets. The incubation period of pertussis averages 7 to 10 days (range: 5 to 21 days) and may be as long as 6 weeks. Bordetella pertussis has a strong affinity for the mucosal layers of the human respiratory system. Bordetella pertussis bacteria are not invasive, and they remain attached to the cilia of the respiratory epithelium. Bacteria damage the epithelium of the airway and the alveoli through the combined action of several virulence factors. These virulence factors include pertussis toxin, adenylate cyclase toxin, filamentous hemagglutinin, fimbriae, tracheal cytotoxin, pertactin, and dermonecrotic toxin. Bacteria attach to and multiply on the respiratory epithelium, starting in the nasopharynx and ending primarily in the bronchi and bronchioles (16; 21).

The exact etiology of the pertussis encephalopathy is debated. Suggested mechanisms include central nervous system hemorrhage, hypoxia, or vascular occlusions; loss of cerebral vascular autoregulation; secondary bacterial or viral infection; an unrecognized preexisting neurologic condition; or the effects of toxin(s) produced by Bordetella pertussis on the brain. Pertussis toxin has been postulated to act either directly on the central nervous system or indirectly by causing hypoglycemia or other metabolic disturbances (28; 34; 14). It was suggested that hypoxia might result in a breakdown of the blood-brain barrier, allowing the bacterial toxins to enter the central nervous system (23; 30). In some autopsied patients, the pathology was consistent with severe anoxic changes, possibly as a result of prolonged apnea during paroxysms of cough. Venous congestion, petechial hemorrhages, and thromboses were other changes that were observed (23).

In a murine model, respiratory infection with Bordetella pertussis resulted in persistent expression of mRNA transcripts for interleukin-1-beta and tissue necrosis factor-alpha and transient expression of interleukin-6 in the hippocampus and hypothalamus (20). These changes correlated with elevated levels of cytokine protein in the same brain areas. The results demonstrate that infection at a mucosal surface can result in the induction of proinflammatory cytokine production in the brain and suggest that these locally synthesized mediators may contribute to the pathogenesis of pertussis encephalopathy. The timing of the encephalopathy suggests that it results from increased lysis of bacteria and release of endotoxin (23).

Several investigations show that infants with vaccine encephalopathy have severe myoclonic epilepsy of infancy, which is a rare early childhood encephalopathy associated with unilateral and generalized convulsions that are often triggered by fever (18). SCN1A is the most important epilepsy gene, and mutations within the gene are seen in patients with severe myoclonic epilepsy of infancy (including generalized epilepsy with febrile seizure plus and Dravet syndrome). The generalized epilepsy with febrile seizures plus syndrome spectrum comprises a range of mild to severe phenotypes varying from classical febrile seizures to Dravet syndrome, which is a severe infantile-onset epilepsy syndrome with multiple seizure types, developmental slowing, and poor outcome (31). Genetic studies suggest that sodium channel mutations, rather than vaccines, are the cause of vaccine encephalopathy in most patients (33). Reyes and colleagues described five children who presented with presumed earlier diagnoses of alleged vaccine encephalopathy caused by pertussis vaccinations in infancy (29). All of the patients were diagnosed with Dravet syndrome years later with the help of genetic testing.

Berkovic and colleagues studied 14 patients with vaccine encephalopathy for whom the first seizure occurred within 72 hours of vaccination (04). Neuronal sodium channel alpha1 subunit (SCN1A) gene mutations were identified in 11 of 14, and a diagnosis of a specific epilepsy syndrome was made in all 14 individuals. Five mutations predicted truncation of the protein, and six were missense in conserved regions of the molecule (04). A report suggests that pertussis vaccination might trigger earlier onset of Dravet syndrome in children who, because of an SCN1A mutation, are destined to develop the disease (22). In a retrospective study of 70 patients with Dravet syndrome and SCN1A mutations, seizures following vaccinations were reported in 27% of patients (36). In 58% of these patients, vaccination-related seizures represented the first clinical manifestation of the syndrome. Most seizures occurred after diphtheria, pertussis, and tetanus (DPT) vaccinations and within 72 hours after vaccination. Two-thirds of events occurred in relation to fever.

A study investigated the genetic basis for seizures associated with the diphtheria, tetanus, and whole-cell pertussis vaccine in India, which is a major cause of vaccine hesitancy. Of the 54 children studied who had experienced these seizures, 33 showed pathogenic variants of 12 genes. The most commonly found variant was in the SCN1A gene. The study found significant predictors for a genetic diagnosis were five or more seizures, drug-resistant epilepsy, and neurodevelopmental impairment (25).

Management

The Centers for Disease Control and Prevention recommend macrolides erythromycin (40 to 50 mg/kg per day for 14 days), clarithromycin (15 mg/kg per day for 7 days), and azithromycin (10 mg/kg per day for 5 days) as treatments of choice for pertussis infection. Antibiotics should be started no later than 21 days after the onset of cough. Antibiotics (erythromycin 40 to 50 mg/kg per day for 14 days) will eliminate viable Bordetella pertussis organisms from the respiratory tract within two days (02; 17; 12). Currently, shorter courses (3 to 5 days) of azithromycin or clarithromycin or erythromycin for a week is considered sufficient. A longer 14-day antibiotic treatment is now not required (12). Azithromycin and clarithromycin are easier to use than erythromycin as they need to be given fewer times a day and have shorter regimens. Erythromycin and azithromycin are associated with an enhanced risk of infantile hypertrophic pyloric stenosis that needs to be carefully monitored. Oral trimethoprim-sulfamethoxazole can be used as an alternative treatment for patients who do not tolerate erythromycin (02; 35; 07). Antibiotics in patients with encephalopathy may be administered through a nasogastric tube. Infants with encephalopathy should be carefully observed for apnea, cyanosis, or hypoxia. General supportive measures (eg, oxygenation, breathing treatments, and mechanical ventilation) should be administered as needed (17). It has been suggested that children receiving pertussis vaccination should not receive prophylactic antipyretics, as antipyretics do not decrease chance of febrile convulsions. In fact, prophylactic antipyretic use potentially decreases the immune response to these vaccines (24).

Outcomes

Pertussis related prognosis can be influenced by several factors. In a retrospective study involving 213 children with pertussis-like coughing, factors associated with a poor prognosis were the presence of Bordetella pertussis, a white blood cell count exceeding 20 × 10^9/L, and a lymphocyte ratio above 60%. Thus, these could serve as vital risk factors in assessing the likely outcomes for patients (06).

Between 1999 to 2004, a study examining U.S. infant mortality rates linked to pertussis found 91 deaths, all aged 7 months or younger. The average yearly infant mortality rate due to pertussis was 3.8 per 1 million live births, and 13.1 for infants aged less than two months. Factors significantly associated with pertussis deaths included low birth weight, female gender, low Apgar score, and maternal education of less than 12 years. Pertussis-related mortality rate was 2.6 times higher among Hispanic infants aged less than two months. To prevent pertussis transmission, adults and adolescents in close contact with infants should receive booster vaccinations, especially in higher-risk settings (15).

A Chinese study assessed medical records of 144 hospitalized children with severe pertussis, aiming to identify mortality risk factors. Patients' median age was two months, with the majority being less than 6 months of age. The mortality rate was 34.2%, with 76.9% of deaths occurring in patients under 6 weeks. Independent risk factors identified for death were a white blood cell count greater than 70.0 × 10^9/L and pulmonary hypertension (32).

References

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04: Berkovic SF, Harkin L, McMahon JM, et al. De-novo mutations of the sodium channel gene SCN1A in alleged vaccine encephalopathy: a retrospective study. Lancet Neurol 2006;5(6):488-92. PMID 16713920
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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Ravindra Kumar Garg DM FRCP

Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.
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Editor

Christina M Marra MD

Dr. Marra of the University of Washington School of Medicine has no relevant financial relationships to disclose.
See Profile

Patient Profile

Age range of presentation: 0 month to 44 years
Sex preponderance: female>male, >1:1
Heredity: none
Population groups selectively affected: none
Occupation groups selectively affected: none

ICD & OMIM codes

ICD-10: Whooping cough due to Bordetella pertussis: A37.0

Encephalopathy, unspecified: G93.4
ICD-11: Encephalopathy, not elsewhere classified: 8E47

Whooping cough due to Bordetella parapertussis: 1C12.1

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Pertussis encephalopathy

Differential Diagnosis

other viral and bacterial pathogens
other encephalopathies

Also Relevant

Cough syncope
Diphtheritic neuropathy
Drug-induced seizures
Febrile seizures
Neurologic complications of vaccination
- West syndrome

Clinical Categories

Infectious Disorders

Pertussis encephalopathy …

Pertussis encephalopathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Diagnostic Criteria for Whooping Cough

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Outcomes

References

Contributors

Author

Editor

Patient Profile

ICD & OMIM codes

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to access the full version.

Questions or Comment?

Also in This Category

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Genital herpes: neurologic complications

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Pneumococcal meningitis

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Japanese encephalitis

Pertussis encephalopathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Diagnostic Criteria for Whooping Cough

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Outcomes

References

Contributors

Author

Editor

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Neuropathies associated with cytomegalovirus infection

Genital herpes: neurologic complications

Zika virus: neurologic complications

Gram-negative bacillary meningitis

Pneumococcal meningitis

HTLV-1 associated myelopathy

Infective endocarditis

Japanese encephalitis

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