A central spot of bleeding may also occur due to the release of blood thinning substances in the bugs saliva.Symptoms may not appear until some days after the bites have occurred. Reactions often become brisker after multiple bites due to possible sensitization to the salivary proteins of the bed bug. Numerous bites may lead to a red rash or hives. Psychological
Serious infestations and chronic attacks can cause anxiety, stress, and sleep difficulties. Development of refractory delusional parasitosis is possible, as a person develops an overwhelming obsession with bed bugs. Other
A number of other symptoms may occur from either the bite of the bed bugs or from their exposure. Serious allergic reactions including anaphylaxis from the injection of serum and other nonspecific proteins have been rarely documented. Due to each bite taking a tiny amount of blood, the chronic or severe infestation may lead to anemia. Bacterial skin infection may occur due to skin breakdown from scratching. Systemic poisoning may occur if the bites are numerous. Exposure to bed bugs may trigger an asthma attack via the effects of airborne allergens although evidence of this association is limited. There is no evidence that bed bugs transmit infectious diseases even though they appear physically capable of carrying pathogens and this possibility has been investigated. The bite itself may be painful thus resulting in poor sleep and worse work performance.Bed bugs can feed on warm-blooded animals other than humans, such as pets.
C3a and C5a, proteins produced from the complement system, attract neutrophils to the vessels. Once activated, neutrophils then release preformed substances, including enzymes causing damage to vessel tissue. Evidence of this process can be seen with a sample of removed skin tissue, or biopsy, viewed under a microscope. Neutrophils are seen surrounding blood vessels and their debris within vessel walls, causing fibrinoid necrosis. This finding on histological examination is termed "leukocytoclastic vasculitis".Considering the wide range of potential causes leading to cutaneous small vessel vasculitis, there are subtle variations in the underlying pathophysiology for each cause. For example, medications are metabolized to smaller molecules that can attach to proteins in the blood or vessel walls. The immune system senses these altered proteins as foreign and produces antibodies in efforts to eliminate them from the body. A similar process occurs with infectious agents, such as bacteria, in which antibodies target microbial components. Diagnosis
The diagnostic testing for vasculitis should be guided by the patients history and physical exam. The clinician should ask about the duration, onset, and presence any associated symptoms such as weight loss or fatigue (that would indicate a systemic cause). It is important to distinguish between IgA and non-IgA vasculitis. IgA vasculitis is more likely to present with abdominal pain, bloody urine, and joint pain. In the case that the cause is not obvious, a reasonable initial workup would include a complete blood count, urinalysis, basic metabolic panel, fecal occult blood testing, erythrocyte sedimentation rate (ESR), and C-reactive protein level.