Clinically, neonates with omphalitis present within the first two weeks of life with signs and symptoms of a skin infection (cellulitis) around the umbilical stump (redness, warmth, swelling, pain), pus from the umbilical stump, fever, fast heart rate (tachycardia), low blood pressure (hypotension), somnolence, poor feeding, and yellow skin (jaundice). Omphalitis can quickly progress to sepsis and presents a potentially life-threatening infection. In fact, even in cases of omphalitis without evidence of more serious infection such as necrotizing fasciitis, mortality is high (in the 10% range).

Omphalitis of newborn is the medical term for inflammation of the umbilical cord stump in the neonatal newborn period, most commonly attributed to a bacterial infection. Typically immediately after an infant is born, the umbilical cord is cut with a small remnant (often referred to as the stump) left behind. Normally the stump separates from the skin within 3–45 days after birth. A small amount of pus-like material is commonly seen at the base of the stump and can be controlled by keeping the stump open to air to dry. Certain bacteria can grow and infect the stump during this process and as a result significant redness and swelling may develop, and in some cases the infection can then spread through the umbilical vessels to the rest of the body. While currently an uncommon anatomical location for infection in the newborn in the United States, it has caused significant morbidity and mortality both historically and in areas where health care is less readily available. In general, when this type of infection is suspected or diagnosed, antibiotic treatment is given, and in cases of serious complications surgical management may be appropriate.

Anaerobes can be isolated from most types of upper respiratory tract and head and neck and infection and are especially common in chronic ones. These include tonsillar, peritonsillar and retropharyngeal abscesses, chronic otitis media, sinusitis and mastoiditis, eye ocular) infections, all deep neck space infections, parotitis, sialadenitis, thyroiditis, odontogenic infections, and postsurgical and nonsurgical head and neck wounds and abscesses., The predominant organisms are of oropharyngeal flora origin and include AGNB, "Fusobacterium" and Peptostreptococcus spp.

Anaerobes involve almost all dental infections. These include dental abscesses, endodontal pulpitis and periodontal (gingivitis and periodontitis) infections, and perimandibular space infection. Pulpitis can lead to abscess formation and eventually spread to the mandible and other neck spaces. In addition to strict anaerobic bacteria, microaerophilic streptococci and "Streptococcus salivarius" can also be present.

"Fusobacterium" spp. and anaerobic spirochetes are often the cause of acute necrotizing ulcerative gingivitis (or Vincent's angina) which is a distinct form of ulcerative gingivitis.

Deep neck infections that develop as a consequence of oral, dental and pharyngeal infections are generally polymicrobial in nature. These include extension of retropharyngeal cellulitis or abscess, mediastinitis following esophagus perforation, and dental or periodontal abscess.

Secondary peritonitis and intra-abdominal abscesses including splenic and hepatic abscesses generally occur because of the entry of enteric micro-organisms into the peritoneal cavity through a defect in the wall of the intestine or other viscus as a result of obstruction, infarction or direct trauma. Perforated appendicitis, diverticulitis, inflammatory bowel disease with perforation and gastrointestinal surgery are often associated with polymicrobial infections caused by aerobic and anaerobic bacteria, where the number of isolates can average 12 (two-thirds are generally anaerobes). The most common aerobic and facultative bacteria are "Escherichia coli", "Streptococcus" spp. (including Enterococcus spp.), and the most frequently isolated anaerobic bacteria are the "B. fragilis" group, "Peptostreptococcus" spp., and "Clostridium" spp.

Abdominal infections are characteristically biphasic: an initial stages of generalized peritonitis associated with "Escherichia coli" sepsis, and a later stages, in which intra abdominal abscesses harboring anaerobic bacteria ( including "B. fragilis" group ) emerge.

The clinical manifestations of secondary peritonitis are a reflection of the underlying disease process. Fever, diffuse abdominal pain, nausea and vomiting are common. Physical examination generally show signs of peritoneal inflammation, isuch as rebound tenderness, abdominal wall rigidity and decrease in bowel sounds. These early findings may be followed by signs and symptoms of shock.

Biliary tract infection is usually caused by "E. coli, Klebsiella" and "Enterococcus" spp. Anaerobes (mostly "B. fragilis" group, and rarely "C. perfringens") can be recovered in complicated infections associated with carcinoma, recurrent infection, obstruction, bile tract surgery or manipulation.

Laboratory studies show elevated blood leukocyte count and predominance of polymorphonuclear forms. Radiographs studies may show free air in the peritoneal cavity, evidence of ileus or obstruction and obliteration of the psoas shadow. Diagnostic ultrasound, gallium and CT scanning may detect appendiceal or other intra-abdominal abscesses. Polymicrobial postoperative wound infections can occur.

Treatment of mixed aerobic and anaerobic abdominal infections requires the utilization of antimicrobials effective against both components of the infection as well as surgical correction and drainage of pus. Single and easily accessible abscesses can be drained percutaneously.

The main sign of the disease is life-threatening, recurrent bacterial or fungal soft tissue infections. These infections are often apparent at birth and may spread throughout the body. Omphalitis (infection of the umbilical cord stump) is common shortly after birth. Other signs include delayed separation of the umbilical cord, periodontal disease, elevated neutrophils, and impaired wound healing, but not increased vulnerability to viral infections or cancer. Such patients have fever as the manifestation of infection, inflammatory responses are indolent.

LAD was first recognized as a distinct clinical entity in the 1970s. The classic descriptions of LAD included recurrent bacterial infections, defects in neutrophil adhesion, and a delay in umbilical cord sloughing. The adhesion defects result in poor leukocyte chemotaxis, particularly neutrophil, inability to form pus and neutrophilia.

Individuals with LAD suffer from bacterial infections beginning in the neonatal period. Infections such as omphalitis, pneumonia, gingivitis, and peritonitis are common and often life-threatening due to the infant's inability to properly destroy the invading pathogens. These individuals do not form abscesses because granulocytes cannot migrate to the sites of infection.

Leukocyte adhesion deficiency (LAD), is a rare autosomal recessive disorder characterized by immunodeficiency resulting in recurrent infections. LAD is currently divided into three subtypes: LAD1, LAD2, and the recently described LAD3, also known as LAD-1/variant. In LAD3, the immune defects are supplemented by a Glanzmann thrombasthenia-like bleeding tendency.

Leukocyte adhesion deficiency-1 (LAD1) is a rare and often fatal genetic disorder in humans.