YOU ARE NOW CONNECTED TO THE TOXLINE (1981 FORWARD, NON-ROYALTY) FILE. ==PERTUSSIS SYMPTOMS== 2 AUTHOR WIRSING VON KOENIG CH AUTHOR FINGER H TITLE Role of pertussis toxin in causing symptoms of Bordetella parapertussis infection. SOURCE EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES; 13 (6). 1994. 455-458. ABSTRACT BIOSIS COPYRIGHT: BIOL ABS. Whooping cough can be caused by either Bordetella pertussis or Bordetella parapertussis. Although the two species share an almost complete DNA identity, Bordetella parapertussis does not produce pertussis toxin, which is thought to be the main virulence factor of Bordetella pertussis. In order to elucidate the role of pertussis toxin in causing the typical symptoms of whooping cough, clinical information from 33 patients with culture-positive Bordetella parapertussis infection was collected and compared to that from 331 patients with infection caused by Bordetella pertussis. Isolated strains of Bordetella parapertussis lacked pertussis toxin expression, as was demonstrated by negative tests for histamine sensitization. This was further substantiated in vivo by a significantly lower leukocyte count in the parapertussis group as compared to the pertussis group. Frequencies of typical symptoms of whooping cough, such as paroxysmal coughing, whooping and vomiting, were almost identical in the two groups. Nocturnal coughing and contact anamnesis were noted more often in the Bordetella pertussis group. Children in the parapertussis group were significantly more often vaccinated with whole-cell pertussis vaccine than children infected with Bordetella pertussis. The results indicate that pertussis toxin may not play a decisive role in causing the typical symptoms of whooping cough, such as paroxysmal coughing, whooping and vomiting. 3 AUTHOR LONG SS AUTHOR WELKON CJ AUTHOR CLARK JL TITLE Widespread silent transmission of pertussis in families: Antibody correlates of infection and symptomatology. SOURCE J INFECT DIS; 161 (3). 1990. 480-486. ABSTRACT BIOSIS COPYRIGHT: BIOL ABS. Four children with pertussis and theirs 18 family members were subjects of a 1-year study to detect infection and antibody responses to Bordetella pertussis. Attack rate for pertussis infection in contacts was 83%. Two-thirds of cases in these immunized contacts were subclinical. All infected family contacts had diagnostically elevated serologic tests for pertussis at the time the index case was diagnosed. Culture identified only 20% of infected contacts. Infected individuals had a mean of 5.5 of 10 antibody tests diagnostic for recent infection. ELISA assay for IgG to pertussis toxin and assay for IgA to filamentous hemagglutinin on serum and nasal secretions were the most discriminating diagnostic tests. Indexes cases and immunized contacts had different type and timing of antibody responses, making a single assay or sampling unable to identify all infected individuals. Symptomatic infection was characterized by higher magnitude of pertussis toxin antibody response and asymptomatic infection by filamentous hemagglutinin. After pertussis immunization, immunity to disease is greater than is protection from infection. 1 AUTHOR Pittman M TITLE Neurotoxicity of Bordetella pertussis. SOURCE Neurotoxicology; VOL 7, ISS 2, 1986, P53-67 (REF: 50) ABSTRACT Pertussis is a unique disease in which the harmful effects are mediated by an exotoxin that effects stimulation of the adrenergic system which is neuronally controlled. The interdependence of the growth of bacteria and toxin production, and the local colonization of the bacteria that precedes the clinical symptom of the disease reflect the nature of the disease. Pertussis toxin enzymatically alters the function of numerous regulatory cells that is demonstrable, after an interval of time, by a specific stimulus. The toxin also may act rapidly and effect action at a target tissue. The latter appears to be associated with the rapid adverse events after vaccination whereas both may occur in the disease. The pathophysiologic responses associated with specific clinical symptoms have not been clearly defined. Responses to be evaluated relative to encephalopathy are increased vascular permeability, hypoglycemia and enhanced activity of neuronal glutamate and aspartate. The intensity of responses is related to the amount of pertussis toxin available, genetic susceptibility, ethnic and allotype, and external factors. The reason for the non-linear dose response shown by the critical level between the sublethal and the lethal infection in mice is unclear. Bacterial adenylate cyclase may be a candidate. Much remains to be elucidated about the enzymatic pathways that effect the many disparate events, the identity of the neurons that effect the clinical symptoms and their CNS location, the identity of the neuronal transmitters and the pathoneuronal pharmacodynamics.