[From scrophula to mycobacterial lymphadenitis]. / De la escrófula a la linfoadenitis micobacteriana.

In the 19th century it was widely believed that both tuberculosis and cervical lymph node swelling, known as scrophula, affected individuals predisposed to an inherited "diathetic constitution". In 1882 Robert Koch proved that human tuberculosis and scrophulous lesions were caused by the bacillus Mycobacterium tuberculosis. In the early twentieth century it was stated that Mycobacterium bovis, the bacillus of cattle tuberculosis, could also cause cervical lymphoadenitis in humans, especially in children, by the intake of milk from sick cows. The incidence of this condition decreased after the infection was controlled in cattle and pasteurization of the milk was introduced. A type of granulomatous necrotizing and suppurative cervico-facial lymphadenitis associated to non-tuberculous mycobacteria was described in 1956. It mainly affects children younger than 5 years old, particularly those born in countries with non-endemic tuberculosis. Tuberculous cervical lymphadenitis is prevalent in young adults from tuberculosis-endemic countries and in HIV-infected subjects. Infectious etiology displaced the importance of a personal disposition in the development of scrophula. Nevertheless, mutations that confer susceptibility to mycobacterial infection are currently investigated.

De la escrófula a la linfoadenitis micobacteriana / From scrophula to mycobacterial lymphadenitis

Resumen En el siglo XIX se pensaba que la tuberculosis y la tumefacción ganglionar cervical llamada escrófula afectaban a individuos predispuestos por una "constitución diatésica" heredada. En 1882 Robert Koch demostró que lesiones tuberculosas y escrofulosas humanas eran causadas por el bacilo Mycobacterium tuberculosis. A principios del siglo XX se estableció que Mycobacterium bovis, bacilo de la tuberculosis del ganado, podía también causar linfoadenitis cervical en humanos, especialmente en niños, por la ingestión de leche de vacas enfermas. La condición disminuyó después que se controló la infección en el ganado y se introdujo la pasteurización de la leche. En 1956 se describió la linfoadenitis cervicofacial granulomatosa necrosante y supurada causada por micobacterias no tuberculosas. Afecta principalmente a niños bajo los cinco años, especialmente en países sin endemia de tuberculosis. Las linfoadenitis cervicales tuberculosas predominan en adultos jóvenes en países con tuberculosis endémica y en individuos infectados por VIH.

In the 19th century it was widely believed that both tuberculosis and cervical lymph node swelling, known as scrophula, affected individuals predisposed to an inherited "diathetic constitution". In 1882 Robert Koch proved that human tuberculosis and scrophulous lesions were caused by the bacillus Mycobacterium tuberculosis. In the early twentieth century it was stated that Mycobacterium bovis, the bacillus of cattle tuberculosis, could also cause cervical lymphoadenitis in humans, especially in children, by the intake of milk from sick cows. The incidence of this condition decreased after the infection was controlled in cattle and pasteurization of the milk was introduced. A type of granulomatous necrotizing and suppurative cervico-facial lymphadenitis associated to non-tuberculous mycobacteria was described in 1956. It mainly affects children younger than 5 years old, particularly those born in countries with non-endemic tuberculosis. Tuberculous cervical lymphadenitis is prevalent in young adults from tuberculosis-endemic countries and in HIV-infected subjects. Infectious etiology displaced the importance of a personal disposition in the development of scrophula. Nevertheless, mutations that confer susceptibility to mycobacterial infection are currently investigated.

The role of nerve growth factor in modulating herpes simplex virus reactivation in vivo.

The role of nerve growth factor (NGF) in the modulation of herpes simplex virus (HSV) latency and reactivation was investigated in a mouse model. To determine whether NGF depletion would reactivate latent virus, concentrated anti-NGF serum antibodies were administered intraperitoneally to latently infected mice for 9 consecutive days. To determine whether NGF given prophylactically could suppress UV-B-induced viral reactivation, mice were irradiated with UV-B while being treated with NGF using diverse regimes over a 4-day period. Following intraperitoneal administration of anti-NGF antibodies, viral shedding was detected in a small number (10%) of mice, but it was not possible to pharmacologically suppress UV-B-induced viral reactivation with NGF. It would appear, therefore, that HSV latency in neurons innervating the cornea can be sustained and disrupted by physiological factors independent of NGF levels.