Also see

Some strains now produce poisonous hydrogen sulfide (H2S) gas and Necrotizing ulcerative gingivitis

Actinobacillosis was first described by Lignieres & Spitz (1902) in cattle in Argentina, and was
subsequently reported in sheep (Davis & Stiles 1939, Marsh & Wilkins 1939, Taylor 1954,
Laws 1969) and in the dog (Carb 1969). The appearance of multiple nodules in the
subcutaneous tissue is a common feature in infected animals. The mouth, tongue, pharynx,
internal organs and regional lymph nodes are frequently involved. The nodules become
necrotic and ulcerated, discharging a yellow-green viscoid purulent content. Contrary to
actinomycetes which demonstrate a predilection for the skeletal system, the actinobacillus has
a tendency to invade the soft tissue and organs like the lungs, abdominal and pelvic viscera,
and lymph nodes (Custis et al. 1944).

Human infection is extremely rare. A review of the literature reveals only eight cases of
proven Actinobacillus lignieresii infection in man, three of them fatal. Ravault & Pinoy (1911)
reported actinobacillar meningitis complicating otitis and mastoiditis. Additional reports
include: fatal meningitis in a newborn infected by cow's milk (Gerdine & Pease 1926); sepsis
developing in a butcher with a traumatic abdominal wound probably produced by a
contaminated knife (Thompson & Willius 1932); fulminating suppurative bronchopneumonia
with metastatic abscesses in the liver, kidneys and spleen (Beaver & Thompson 1933); fatal
mitral endocarditis with focal embolic nephritis and embolic disturbances in the spleen, the
meninges and the skin (Custis et al. 1944); ileocaecal lymph node involvement in a girl
operated with a diagnosis of acute appendicitis (Flamm & Jonas 1956); conjunctivitis (Flamm
& Wiedermann 1962); and pneumonia (Pavckova et al. 1973).
Journal ofthe Royal Society ofMedicine Volume 73 April 1980

Human epithelial cell death caused by Actinobacillus actinomycetemcomitans infection
The gingival sulcus is the shallow crevice around the tooth, and its epithelium is a gateway for initial
bacterial infection in periodontal disease. Recent studies have shown that Actinobacillus
actinomycetemcomitans invades an epithelial cell line, KB cells, in vitro. The aim of the present study
was to clarify the changes in KB cells after A. actinomycetemcomitans infection. The cytotoxic effects of
A. actinomycetemcomitans on KB cells were determined at 72, 96 and 120 h after infection by an MTT
assay. Nuclear morphological changes were observed by staining with Hoechst 33258. Cytoplasmic
histone-associated DNA fragmentation in the infected KB cells was determined by ELISA. A.
actinomycetemcomitans was cytotoxic on KB cells, and condensation and degradation of the nuclei were
observed. DNA fragmentation was increased after the infection. In addition, A. actinomycetemcomitans
showed similar cytotoxic effects on human gingival epithelial cells. The present study demonstrated that
A. actinomycetemcomitans induces apoptotic cell death of oral epithelial cells in an in-vitro culture
system. This induced apoptosis might be involved in the initiation and progression of periodontitis
J. Med. Microbiol. -- Vol. 49 (2000), 739-745

Dynamics of infection by leukotoxic strains of actinobacillus actinomycetemcomitans in juvenile
Abstract. Juvenile periodontitis is associated with a high incidence of infection by Actinobacillus
aclinomycetemcomilans (Aa). The data presented indicate that the ability of Aa to destroy human PMNs is
altered during the course of infection. Leukotoxic strains of Aa are characteristically found in isolates
obtained from younger patients (6–12 years of age) but not in older subjects (13–25 years old). This
suggests that the leukotoxin may be more important during early as opposed to more advanced phases
of juvenile periodontitis.
Journal of Clinical Periodontology, Volume 13 Issue 4 Page 330-331, April 1986

Actinobacillus equuli Septicemia: an Unusual Zoonotic Infection
We describe the isolation of Actinobacillus equuli from the blood of a 53-year-old butcher with
septicemia. This species of the genus Actinobacillus is primarily associated with animals and animal
diseases, especially septicemia in foals. This is the first report of the isolation of A. equuli from a human
with septicemia.
Journal of Clinical Microbiology, September 1998, p. 2789-2790, Vol. 36, No. 9

Identification of Actinobacillus actinomycetemcomitans antigens for use in the diagnosis, treatment, and
monitoring of periodontal diseases
Actinobacillus actinomycetemcomitans (Aa) is the principal etiologic agent of early-onset periodontitis
including localized and generalized prepubertal periodontis, localized and generalized juvenile
periodontis, and rapidly progressive or refractory adult periodontitis. Currently, diagnosis of these
diseases is made by X-ray analysis usually long after the onset of the disease and after considerable
damage to the supporting bone and tissue has occurred. Tooth loss is the ultimate detrimental effect of
destructive periodontal disease. A national survey of the United States revealed a prevalence of
localized juvenile periodontitis of 0.53% and of generalized juvenile periodontitis of 0.13%. Loe & Brown,
J. Periodontol. 62:608–616 (1991). Findings from a number of studies corroborate the conclusion that
early-onset disease is similar in other industrialized countries and is more frequent in developing
countries. Loe & Brown, J. Periodontol. 62:608–616 (1991). Therefore, methods of early diagnosis of early-
onset periodontitis, localized and generalized juvenile periodontis, and rapidly progressive or refractory
adult periodontitis are needed in the art. In addition, certain types of adult periodontitis, which in
general is a very common condition affecting over half the adult population, are likely to be caused by
Aa. Furthermore, Aa can cause extra-oral diseases such as endocarditis, thyroid gland abscesses,
urinary tract infections, brain abscesses, and vertebral osteomyelitis.