The patient is a pediatric and is likely to be suffering from chickenpox, erythema infectiosum, or measles infection. According to Grossman (2013), chickenpox starts as a small non-palpable lesion on the face that makes the child feel uncomfortable. The lesion is reddish and very itchy. Initially, the lesion looks like an insect bite that later develops into blisters and scabs. The lesion spreads to the whole body including the mouth, eyes and genitals within a span of two to four days. Fever accompanies the patient leading to loss of appetite, development of sore throat and headaches (Mysore, 2007).
Erythema infectiosum is a potential infection on the four-year-old patient. The condition starts with a rash that has a slapped cheek appearance. The rash progresses into three phases (Mysore, 2007). The slapped-cheek rash occurs during the first phase and fades after two to four days. The second phase involves the appearance of maculopapular rash that fades into lace-reticular pattern. The third phase involves recurrent appearance of red lesions that are itchy and cause severe irritation on the skin. The patient’s temperature elevates, experiences abdominal pain, headache, and sore throat (Grossman, 2013).
Measles appears in children as skin vesicles filled with fluids. The vesicles are reddish-brown and they first show on the face. The lesions have a blotchy appearance similar to that of an insect bite (Grossman, 2013). Upon close examination, the lesions have blue-white centers, which is an indispensable sign of measles. The measles lesion starts from the forehead, and then spreads downwards to the other parts of the body. The disease is highly contagious due to the oozing droplets from an infected patient. The symptoms of measles start to appear from day one and up to day four after infection (Mysore, 2007).
Chickenpox is caused by the varicella-zoster virus that initiates the production of antibodies. During chickenpox infection, the immunoglobulins G, M, and A provides a cell-mediated immune response that is lifelong protection. In some situations, the pediatric patient may develop low immunity resulting in reactivation of the varicella-zoster virus (Mysore, 2007). The varicella-zoster virus diffuses cutaneous rash by infecting the lymphocytes. The skin lesions develop due to varicella-zoster virus that appear after the virus has reached the cutaneous sites of replication. The T-cells migrate to the skin sites of replication without triggering the latent viremia hence causing viral transmission to the skin profile (Grossman, 2013).
Parvovirus B19 has an association with erythema infectiosum. The virus decreases the activity of immunoglobulin M and G through the use of erythrocyte P antigen as its receptor. Additionally, the virus causes the fall of hemoglobin level due to decreasing in the survival time of the erythrocytes leading to weakening of the patient (Grossman, 2013). The inhibition of colony formation results for prolonged periods of virus incubation. Extensive virus incubation increases viremia that causes changes on the extensor surfaces causing the appearance of the skin lesions (Mysore, 2007).
Measles is caused by measles virus that infects the alveolar macrophages and lymphoid tissues. Increase in viremia results in the systemic dissemination of infected lymphocytes, resulting in damage to epithelial cells. The measles virus uses the nectin-4 receptor to transmit to the infected CD150+ lymphocytes to the submucosa cells. The measles virus replicates on the reticuloendothelial and epithelial tissues for two to three days before extending to lymph nodes. Mysore (2007) argues that the skin rashes, fever, and malaise are manifestations of secondary viremia that ceases after development of cellular mediated antibodies (Grossman, 2013).
Grossman, S. (2013). Porth’s Pathophysiology: Concepts of Altered Health States (9th Ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
Mysore, V. (2007). Dermatalogical Diseases: A Practical Approach. New Delhi: BI Publications Pvt Ltd.