I've just done some googling, found this on Medscape, not something I've looked at before, I suppose I'll have to check its credentials. Maybe it's why the death rate has gone up, maybe the worst cases are the parapertussis strain which the vaccinedoesn't protectagain.
B parapertussis has been reported to cause whooping cough either as a single infective agent or with coinfection with B pertussis in almost 40% of laboratory-confirmed cases.[1]
Parapertussis afflicts very young infants as well as adults. The clinical presentation of B parapertussis infection is variable: 40% of infected persons may be asymptomatic, but most patients have paroxysmal cough that lasts for less than a week, with the entire illness lasting for less than 3 to 4 weeks.[4] Whoop has been reported in almost 60% of patients with parapertussis, but usually its persistence is of shorter duration than that seen in patients with pertussis. Post-tussive emesis as well as nocturnal cough are less frequent in those with parapertussis than in those with pertussis.[5]
Lymphocytosis observed in patients with pertussis is caused by PT, and because B parapertussis does not produce PT, lymphocytosis is not observed in patients with parapertussis.[6]Severe cases of whooping cough are associated with dual infection with B pertussis and B parapertussis.[7] Parapertussis confers long-lasting immunity, but there is no cross-immunity between pertussis and parapertussis.[8,9] Therefore, vaccination against pertussis does not protect against parapertussis.[10]
The diagnosis of parapertussis can be made in a number of ways. B parapertussis is less fastidious than B pertussis and can be grown from nasopharyngeal secretions in 2 to 3 days on the same culture medium (Bordet-Gengou agar) used to isolate B pertussis. The direct fluorescent an tibody test performed on nasopharyngeal specimens provides rapid diagnosis, but the test has low sensitivity and specificity and therefore needs to be performed simultaneously with culture.[11] Recently, PCR assays performed on nasopharyngeal specimens have been shown to provide rapid diagnosis with high specificity and sensitivity.[3]
To date, no studies have been conducted on the management of parapertussis. Because many persons infected with B parapertussis are asymptomatic and the majority have a mild course, many infections remain undetected. These persons can act as carriers of infection, however, and may transmit the disease to young infants, who may have a severe course. In fact, fatality from parapertussis has been reported.[7] Thus, it may be important to treat all patients who have B parapertussis infections.
In vitro studies have shown that in general, B parapertussis is more resistant to antibiotics than B pertussis, and the minimal inhibitory concentration (MIC) of most antibiotics is higher for B parapertussis than for B pertussis, except for TMP-SMX and fluoroquinolones. Erythromycin may not be effective in eradicating B parapertussis, because the peak concentration it achieves in respiratory secretions is only 2-fold higher than the MIC90 for B parapertussis. In addition, the concentration of erythromycin in bronchial secretions may vary considerably.[13,14] Because the MICs for TMP-SMX and fluoroquinolones are low and also because the newer fluoroquinolones achieve higher concentrations in respiratory secretions, these drugs may be more effective in eradicating B parapertussis. The role of macrolides (azithromycin and clarithromycin) in the management of parapertussis is not clear.
Because there have been no treatment studies, it is not surprising that there are no data available on the prophylaxis of B parapertussis infection. In the case of our day-care center, we do not know whether prophylactic agents administered to day-care attendees and their parents prevented further spread of parapertussis, because the majority of the day-care attendees were infants and maternal antibodies could have protected at least some of them.