Hand-foot-and-mouth disease pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]

Overview

HFMD usually affects infants and children, and is quite common. It is highly contagious and is spread through direct contact with the mucus or feces of an infected person. It typically occurs in small epidemics in nursery schools or kindergartens, usually during the summer and autumn months.

Pathophysiology

• HFMD outbreaks typically occur during summer and autumn months in the United states.

Mode of transmission

• HFMD is a contagious disease that is spread from person to person by:

• Close personal contact
• Nasopharyngeal secretions
• Contact with feces (fecal-oral transmission)
• Contact with contaminated objects and surfaces
• Contaminated water (Swimming pools not properly treated with chlorine)

• The virus can be isolated from the following sources:

• Nose and throat secretions (such as saliva, sputum, or nasal mucus)
• Blister fluid
• Feces (stool)

• Following the disease, the infected person (symptomatic or asymptomatic) is most contagious during the first week of illness but can spread disease for days or weeks after symptoms go away.
• Hand foot and mouth disease is not transmitted to or from pets or other animals.
• Factors affecting the transmission:

• Level of hygiene
• Water quality
• Extent of crowding
• Seasonal variations
  • Tropical and subtropical: Circulation of virus tends to be year long, with more outbreaks in rainy season
  • Temperate regions: Autumn and spring

Pathogenesis

The exact pathogenesis of HFMD is not fully understood.The pathogenesis of HFMD caused by EV71 includes:

• EV71 replicates in the lymphoid tissues of the oropharyngeal cavity(tonsils), small bowel(payer's patches) and regional lymph nodes(deep cervical and mesenteric nodes) leading to a mild viremia.
• Most of the viruses are destroyed in these lymphatic tissues and the patients remain asymptomatic.
• Patients present with clinical symptoms when the virus disseminates to other organs like reticuloendothelial system(liver, spleen, bone marrow, lymph node), heart, lung, pancreas, skin, mucous membranes and CNS.
• The virus is typically shed for between two and four weeks, and sometimes for as long as 12 weeks post-infection.
• Replication also occurs in the upper respiratory tract and the virus has been recovered from throat swabs for up to two weeks post-infection.
• The relationship between pathogenesis and distribution of viral entry receptors (scavenger receptor B2, P-selectin glycoprotein ligand-1 and sialic acid-linked glycans) and host factors, such as gender and age group, is unknown.
• The pathogenesis of EV71 depends on following factors:

Viral factors Viral virulence factors are still unknown. Host factors

• Inflammatory factors: High levels of following factors are seen in pulmonary edema.

• Interleukin 6 (IL-6)
• Tumor necrosis factor alpha
• Interleukin-1 beta (IL-12)
• Interleukin-10(IL-10)
• Monocyte chemo attractant protein (MCP-1)
• Monokine induced by interferon gamma (MIG)

• Cell mediated immunity

• Reduction in T-lymphocytes and NK cells

• Human Leukocyte antigen(HLA)

• HLA-A33: Associated with increased susceptibility of EV71 in Asian population
• HLA-A2: Increased risk of cardiopulmonary complications

Microscopic pathology

• Microscopic examination of the vesicular lesions will demonstrate loose strands of fibrin, lymphocytes and neutrophils in the vesicular fluid. The presence of acantholysis in the epidermis and perivascular infiltration of leukocytes is seen in hand foot and mouth disease. The absence of intracelluar inclusion bodies differentiates it from the herpes simplex infection.