Other countries, such as Germany, had reported 16,183 cases, while Australia and China had a reported number of 12,114 and 10,390 pertussis cases. US outbreaks
In 2010, 10 babies in California died and health authorities declared an epidemic with 5,978 confirmed, probable and suspected cases. They found that doctors had failed to correctly diagnose the babies condition during several visits. Statistical analysis identified significant overlap in communities with a cluster of nonmedical child exemptions and cases. The number of exemptions varied widely among communities, but tended to be highly clustered. In some schools, more than 75 % of parents filed for vaccination exemptions. The data suggest vaccine refusal based on nonmedical reasons and personal belief exacerbated the outbreak. Other factors included reduced duration of immunity following the acellular vaccine and most vaccinated adults and older children not receiving a booster shot.In April and May 2012, pertussis was declared to be at epidemic levels in Washington, with 3,308 cases. In December 2012 Vermont declared an epidemic of 522 cases. Wisconsin had the highest incidence rate, with 3,877 cases, although it did not make an official epidemic declaration. History
Discovery
B. pertussis was discovered in 1906 by Jules Bordet and Octave Gengou, who also developed the first serology and vaccine. Efforts to develop an inactivated whole-cell vaccine began soon after B. pertussis was cultured that year. In the 1920s, Louis W. Sauer developed a weak vaccine for whooping cough at Evanston Hospital (Evanston, IL).
Desquamative interstitial pneumonia (DIP) is a form of idiopathic interstitial pneumonia featuring elevated numbers of macrophages within the alveoli (air sacs) of the lung. The alveolar macrophages have a characteristic light brown pigmentation and accumulate in the alveolar lumen and septa regions of the lower lobes of the lungs. The typical effects of the macrophage accumulation are inflammation and later fibrosis (thickening and stiffness) of the lung tissue.The term DIP is a misnomer. Its name is derived from the former belief that these macrophages were pneumocytes that had desquamated.It is associated with patients with a history of smoking. Since more than 80% of cases occur in smokers, it has been suggested that the term DIP should be discarded and the subset occurring in smokers should be replaced with more accurate terms such as smoking-related interstitial fibrosis (SRIF). Although smoking is the most common cause, studies have shown a relationship between occupational exposures and the development of DIP, including occupational dust, fire-extinguisher powder, diesel fumes, nylon filaments and beryllium and copper dust. Additionally, DIP has been observed in children where it typically presents as a result of surfactant protein gene mutations, indicating that the disease is not always acquired in adulthood.Smoking cessation and avoidance of secondhand smoke exposure are both crucial to preventing disease progression, however, treatment with corticosteroids and immunosuppressive therapy has been reported to be effective pharmacologic intervention. Treatment with methylprednisolone has been reported. References


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