Pediatric Brucellosis 

The first clinical case compatible with brucellosis was credited to JA Maston, an assistant surgeon in the Royal Army Medical Corps. Brucellosis in an alphaproteobacteria that was discovered in 1887 by David Bruce, an English doctor working with British soldiers in Malta, by microscopic examination of a spleen from a fatal case. An example of Brucella species is shown in the image below.

Brucellosis is primarily a zoonotic infectious disease found in both domestic and wild animals. Humans are accidental hosts, but brucellosis continues to be a major public health concern worldwide and is the most common zoonotic infection. Brucellosis has been known by various names, including Mediterranean fever, Malta fever, gastric remittent fever, and undulant fever.

Brucellosis can be acquired via exposure to infected animals or infected food. The primary means of prevention is the pasteurization of dairy products, but slaughter campaigns of infected cattle have also been used to control the infection at its source in some countries.

Brucella species are facultative intracellular pathogens that are capable of surviving and replicating within phagocytic cells of the host. Shortly after gaining entry to the body, brucellae are ingested by polymorphonuclear leukocytes (PMLs), which are attracted to the site of inoculation. The principal virulence factor is cell wall lipopolysaccharide (LPS). Normal serum factors, including complement, are involved in opsonization of the organisms to allow phagocytosis, but PMLs have limited ability to kill bacteria within phagocytes. A copper-zinc superoxide dismutase, o- polysaccharide, and nucleotidelike substances are among the factors that protect brucellae from being killed by PMLs.

Brucellae that are not killed by PMLs are ingested by macrophages, where they become localized within organs of the reticuloendothelial system (ie, liver, spleen, bone marrow) and multiply in macrophages and monocytes. However, any organ system can be involved in brucellosis (ie, CNS, heart, joints, genitourinary system, pulmonary system, and skin), and localization of the process may cause focal symptoms or findings.

Shortly after infection, humoral antibodies directed against LPS and other cell wall antigens are produced. However, development of cell-mediated immunity is the principle mechanism of recovery. The host response to infection with Brucella abortus is characterized by the development of tissue granulomas indistinguishable from those of sarcoidosis. In contrast, infection with the more virulent species (Brucella melitensis, Brucella suis) more commonly results in visceral microabscesses.

Frequency

United States

Brucellosis is still a reportable disease in the United States, although the Centers for Disease Control and Prevention (CDC) has received reports of only 100-200 cases annually (a rate of 0.4 per one million population) in the last several years. Texas has the highest incidence of cases (1.38 per one million population). Nationally, the infection is due to 2 main sources: importation of disease (from infected food products or international travel) and cross-border spread^[1] (mostly B melitensis) from Mexico into neighboring states (mostly affecting Hispanics).

International

The geographic distribution of brucellosis is limited by effective public and animal health programs, and prevalence of the disease widely varies from country to country.^[2] Brucellosis is still endemic in the Mediterranean countries, the Arabian Peninsula, Western Asia, Eastern Europe, and parts of Africa and Latin America. Control campaigns have effectively removed it from countries like the United Kingdom and Ireland. Early vaccination attempts were problematic; the vaccine controlled symptoms of the disease but did not actually prevent infection.

A clear (although nonlinear) association between gross domestic product (GDP) and rates of brucellosis is evident according to European Union (EU) data. No countries with a GDP above 90% of the mean had an incidence above 10 annual cases per million population.

In very resource-poor countries (such as some African countries) in which brucellosis is endemic, control through animal slaughter is a poor option because of the fragile nature of the food supply.

Mortality/Morbidity

Duration of symptoms for more than 30 days before diagnosis is the major risk factor for developing focal disease. Mortality is low (< 2%) and is most frequently found in those with endocarditis due to brucellosis.

• The most common focal complications are as follows:

  • Osteoarticular complications - Especially, sacroiliitis (20-30% - but rarer in children)
  • Genitourinary tract complications - Especially, epididymoorchitis in males (2-49%)
  • Neurobrucellosis^[3] - Meningitis^[4] (1-2%) and, less commonly, papilledema, optic neuropathy, radiculopathy, stroke, and intracranial hemorrhage
  • Endocarditis (1%) - Responsible for most mortality associated with the disease
  • Hepatic abscess (1%)
• Other less common complications include the following:

  • Splenic abscess
  • Thyroid abscess
  • Epidural abscess
  • Pneumonitis
  • Pleural empyema
  • Uveitis
  • Aneurysm of the aorta
  • Aneurysm of the cerebral vessels
  • Peritonitis

Race

No racial predilection is known (however, see United States for information about cross-border cases).

Sex

Food-borne brucellosis is not limited according to age or sex and is found in women and men in equal numbers.

Age

Farmers, ranchers, veterinarians, and meat inspectors have the highest risk; however, people of all ages are susceptible. Childhood brucellosis is more common in countries where B melitensis is the prevalent species; in the United States, only about 10% of cases occur in people younger than 19 years.