Documenting The History Of Infection

A major goal in questioning the patient and reviewing the medical records is to develop a firm impression of the types of infections that the patient has suffered so that subsequent laboratory tests can be targeted to analyze specifically those components of the immune system whose defects would most likely explain the patient's symptoms. This will be best served by keeping in mind general patterns of infection that might be caused by defects in specific immunologic defense mechanisms. Thus, infections with encapsulated extracellular bacterial pathogens, particularly of the respiratory tract, are suggestive of defects in antibody production ( 19,20), which constitute the majority of all immune deficiencies (1). Superficial mucosal infections may particularly suggest isolated IgA deficiency ( 21). Infections with opportunistic pathogens, including protozoans and fungi, and recurrent episodes of chickenpox or chronic herpetic lesions, may suggest problems in cell-mediated immunity (20). Failure to clear bacteria promptly from the blood stream, resulting in bacteremia, sepsis, or hematogenously disseminated infections such as osteomyelitis, may be seen in deficiencies of C3 or early-acting components of the complement system (22), but may also indicate asplenia or poor reticuloendothelial system function, as in sickle cell disease. Problems with recurrent or disseminated neisserial infections may suggest deficiency of the later-acting complement components that form the membrane attack complex (22). Abscesses and infections with unusual bacteria or fungi may suggest neutropenia or defects in neutrophil function (19,20,23,24). Enteroviral meningoencephalitis may suggest X-linked agammaglobulinemia.

The number and types of infections and their individual and cumulative morbidity should be assessed. It is necessary to exclude carefully other causes of nonspecific symptoms; for example, is sniffling or congestion due to recurrent upper respiratory infection, allergy, or other types of rhinitis? If cough is a major complaint, it is important to determine whether this is due to sputum production, irritation, or other causes. Could it represent cough-equivalent asthma? If failure to thrive and cough are both present, could the patient have cystic fibrosis? Inflammatory bowel disease may mimic hypogammaglobulinemia in children with poor weight gain who also have recurrent rhinitis due to multiple mucosal viral infections, which by themselves would not be considered significant.

Isolation and identification of responsible organisms is clearly the gold standard for rigorous diagnosis of infection. Documentation of fever, white blood count with differential, and sensitive but nonspecific measures such as the erythrocyte sedimentation rate and C-reactive protein, can help distinguish between chronic, recurrent sinusitis and headaches due to other causes and can help with the differential diagnosis of recurrent cough or other chest symptoms. The importance of culture and examination of smears of nasal secretions for bacteria and neutrophils versus eosinophils cannot be overemphasized in distinguishing infectious from allergic and other noninfectious etiologies, particularly in small children. In some cases, the most appropriate step in the workup is to send the patient back to the primary care physician with instructions to have appropriate cultures and those simple laboratory tests performed every time an infection is suspected or the symptoms recur. Sometimes, the culture result points to the diagnosis, as in the case of Pseudomonas aeruginosa suggesting cystic fibrosis, invasive aspergilli suggesting neutropenia or chronic granulomatous disease (CGD) (24) or Streptococcus pneumoniae or Haemophilus influenzae suggesting an antibody deficiency (19,20).

Clues to the severity and overall morbidity resulting from infection may be obtained by asking whether hospitalization or intravenous antibiotics have been required to treat infections or whether oral antibiotics have generally been sufficient. The response to therapy should be evaluated carefully. Continued high fever or other symptoms suggesting a lack of response of culture-confirmed bacterial infection to antibiotics is more likely indicative of a significant immune deficiency than is the frequently seen pattern in which the fever and symptoms resolve promptly when antibiotic therapy is started (e.g., for otitis media) only to recur again shortly after the prescribed course of therapy is concluded. In many situations, the latter may actually represent a distinct new infection. This pattern is quite commonly seen in children in day care and in adults with frequent exposure to small children. Similarly, it is also important to distinguish inadequate or inappropriate therapy from failure to respond, and it is important to differentiate chronic infections from recurrent episodes. Absence from school or work should be quantitated if possible, and any long-term sequelae or disability should be documented.

The family history should include questions about siblings and preceding generations. Family trees with premature deaths of male infants should raise suspicion of X-linked immune deficiencies (T.aMe.2.2). Questions should also be asked about the family history of asthma and allergy as well as other genetic diseases that may present with recurrent infection such as cystic fibrosis. In evaluating a child, it may be important to determine whether the parents have died prematurely or have known risk factors for HIV infection.

The age at onset of infections of unusual frequency or severity may yield important insights into possible underlying immune deficiencies. It must be kept in mind that term newborns have IgG levels equivalent to those of their mothers, from whom most of their IgG has been transferred across the placenta ( 25). Thus, babies who have problems with infections before the age of 6 months may have T-cell or phagocyte problems but are unlikely to have agammaglobulinemia or other isolated problems in antibody production. In contrast, disorders of antibody production are more likely to present after the age of 6 months. The history of exposure must be carefully considered in evaluating this issue because the frequency of common types of infections often increases after a child's exposure to infectious agents is increased after attending day care or preschool, particularly if there are no siblings in the home. Although patients with severe antibody deficiency such as that seen in Bruton agammaglobulinemia generally present between 6 months and 2 years of age (6,26), the diagnosis of the X-linked hyper-IgM syndrome is frequently delayed until later in childhood (27,28), and those with common variable immunodeficiency disease (CVID) may present at any age (5,29). It may not be clear whether this represents an early-onset deficiency that has not been previously recognized or a newly acquired problem. Just as some infants may have delayed development of the full range of immune responses (30), it seems likely that some adults may undergo premature senescence of immune responsiveness (31) and may present with recurrent bacterial infections in their 40s or 50s.

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