Rinoplastia secundaria: infección nasal en el postoperatorio / Secondary rhinoplasty: postoperative nasal infection

La rinoplastia es una de las intervenciones más comunes en cirugía plástica. Se opera aquí una rinoplastia secundaria por vía abierta injertando los alares y la punta con cartílagos auriculares, mientras el tabique cartilaginoso fue usado para los spreader grafts. Se describe aquí una infección posoperatoria de su punta nasal. Al 9no día de su posoperatorio comienza con la punta nasal congestiva y levemente inflamada. Se medica con una crema con antibióticos, pero el día 14 aparece con la punta nasal muy inflamada y con colección. Cuando en el consultorio el cirujano la ve, como cualquier absceso, decide realizarle drenaje con un trocar 18G, 3 miniincisiones en la piel debajo de la punta nasal, de la que drena un líquido amarronado. Luego con el mismo trocar se realiza un lavado dentro de la cavidad con rifampicina solución. Se medica con trimetoprima-sulfametoxazol (Bactrimforte®) 2 comp/día. Al otro día se observa una notable mejoría. Se continuó con lavado diario durante 4 días con el mismo antibiótico evolucionando rápidamente bien. El Bactrim se lo continúa por 20 días. Al mes la punta nasal está muy bien, deshinchada con cicatrices apenas visibles. A los cuatro meses, la punta está muy blanda, las alas nasales y las narinas normales, la punta con buena proyección igual que el dorso con los spreader graft.

Rhinoplasty is one of the most common interventions in plastic surgery. A secondary open rhinoplasty was carried out grafting the allae and the tip of the nose with conchae cartilage, while the septum was used for spreader grafts. We are here describing this post operatory with a tip of the nose infection.In the control, at the 9th postoperative day, the nasal tip began to be congested and at the 14th post op day the patient showed a clear inflammatory collection. In the office, the surgeon decided to evacuate it with three punctureslike little incisions at the inferior part of the skin tip with a trocar 18G. Through them, drained brownish purulent secretion. With the same trocar, rifampicin solution was injected through these little incisions, like washing the subdermal area. It was medicated with trimethoprim-sulfamethoxazole (Bactrim forte®) 2 tablets/day. The following day, there was a clear improvement in the congestion and erythema of the nose. This procedure of washing was repeated for four days. There was a quick evolution of the inflammatory process and 20 more days, there was no sign of the infection. Four months later, the tip of the nose was soft and the result was considered optimal by the patient and doctors.

Coxiella burnetii, the agent of Q fever in Brazil: its hidden role in seronegative arthritis and the importance of molecular diagnosis based on the repetitive element IS1111 associated with the transposase gene

Coxiella burnetii is the agent of Q fever , an emergent worldwide zoonosis of wide clinical spectrum. Although C. burnetii infection is typically associated with acute infection, atypical pneumonia and flu-like symptoms, endocarditis, osteoarticular manifestations and severe disease are possible, especially when the patient has a suppressed immune system; however, these severe complications are typically neglected. This study reports the sequencing of the repetitive element IS1111 of the transposase gene of C. burnetii from blood and bronchoalveolar lavage (BAL) samples from a patient with severe pneumonia following methotrexate therapy, resulting in the molecular diagnosis of Q fever in a patient who had been diagnosed with active seronegative polyarthritis two years earlier. To the best of our knowledge, this represents the first documented case of the isolation of C. burnetii DNA from a BAL sample.

Dinâmica da infecção de Babesia bovis (Babés, 1888, Starcovici, 1893) em fêmeas ingurgitadas e ovos de Boophilus microplus (Canestrini, 1887) / Dynamic of infection of Babesia bovis (Babés, 1888, Starcovici, 1893) in engorged females and eggs of Boophilus microplus (Canestrini, 1887)

A dinâmica da infecção de B. bovis no carrapato-vetor B. microplus foi estudada em condições laboratoriais na Universidade Federal Rural do Rio de Janeiro no Laboratório de Protozoologia. Para tanto, foram examinadas 100 fêmeas ingurgitadas que se desprenderam naturalmente do hospedeiro vertebrado, sendo que 84 fêmeas apresentaram-se infectadas com esporocinetos de B. bovis, com a seguinte distribuição: 39 por cento, 33 por cento, e 12 por cento nos dias 3, 4 e 5 de incubação, respectivamente. Foram obtidas amostras de ovos provenientes das fêmeas positivas para B. bovis, 100 por cento das amostras de ovos estavam infectadas, apresentado a seguinte distribuição: 46,4 por cento, 34,5 por cento, 16,7 por cento e 2,4 por cento nos dias 4, 5, 6 e 7 de incubação, respectivamente. As freqüências acumuladas, tanto de fêmeas infectadas (84 por cento) quanto de ovos infectados (100 por cento) mantiveram-se até o 17° dia de incubação. De acordo com as freqüências acumuladas e o aumento do grau de infecção, conclui-se que amostras coletadas a partir do 5° e 7° dia de incubação, são ideais para o diagnóstico de B. bovis, em hemolinfa e ovos, respectivamente.

Long-term exacerbation by interleukin 13 of IgE-mediated eosinophilia in rats.

Recent work shows that at least two cycles of antigen challenge applied in a 7-day interval are required to yield tissue eosinophil accumulation in IgE-passively sensitized rats. Since interleukin (IL)-13 is widely regarded as a key mediator in eosinophilic responses associated with mast cells and IgE, we investigated whether this cytokine could replace the first cycle of sensitization and challenge in its proeosinophilic role. We found that IL-13 (25 and 50 ng/cavity) injected into the rat pleural space led to eotaxin generation and a dose-dependent accumulation of eosinophils following IgE-passive sensitization and challenge 7 days later. IL-13 failed to cause eosinophil chemotaxis in vitro but induced eosinophil accumulation into the pleural cavity of naïve rats, which peaked 1 day and faded 72 h post-challenge. No changes were found 1 week after intrapleural injection of IL-13, except an approximately 40-50% increase in the number of adhered and non-adhered pleural mast cells. As recovered from the pleural effluent 1 week after IL-13, mast cells expressed the same amount of IgE bound on their surface as compared to controls. However, they generated 3-fold more LTC(4) following IgE-sensitization and challenge in vitro, keeping intact the amount of histamine released. Finally, pretreatment with zileuton (50 microg/cavity) 1 h before allergen challenge prevented eosinophil accumulation in those animals injected with IL-13 1 week before. In conclusion, our findings show that IL-13 causes a long-term exacerbation of the IgE-mediated eosinophilic response in a mechanism associated with heightened cysteinyl-leukotriene (cys-LT) production by resident mast cells.