Updated: Sep 21, 2023
Author: Raymond D Pitetti, MD, MPH; Chief Editor: Russell W Steele, MD 


Practice Essentials

Lymphangitis is defined as an inflammation of the lymphatic channels that occurs as a result of infection at a site distal to the channel. (See Etiology.)

The lymphatic system encompasses a network of vessels, glands, and organs located throughout the body. Functioning as part of the immune system, it also transports fluids, fats, proteins, and other substances in the body. Lymph nodes, or glands, filter the lymph fluid. Foreign bodies such as bacteria and viruses are processed in the lymph nodes to generate an immune response to fight infection.

However, when pathogenic organisms enter the lymphatic channels, invading directly through an abrasion or wound or as a complication of infection, local inflammation and subsequent infection ensue, manifesting as red streaks on the skin. The inflammation or infection then extends proximally toward regional lymph nodes. Bacteria can grow rapidly in the lymphatic system (see the image below). (See Etiology and Prognosis.)

Trypanosomal chancre on shoulder with lymphangitis Trypanosomal chancre on shoulder with lymphangitis toward axilla.

Although no specific data regarding sex-related demographics are available for lymphangitis, two thirds of patients with cellulitis (a complication of lymphangitis occurring in the absence of appropriate antimicrobial therapy) are reported to be male. (See Presentation and Workup.)

Nodular lymphangitis is a distinct clinical entity, separate from lymphangitis. This disorder is characterized by inflammatory nodules along the lymphatics draining a primary skin infection. (See Etiology and Treatment.)


In individuals with normal host defenses, species of group A beta-hemolytic streptococci (GABHS) are the most common causes of lymphangitis. These organisms elaborate fibrinolysins and hyaluronidase, which aid their invasion of lymphatic channels. Lymphangitis caused by GABHS can rapidly progress and has been associated with serious complications.

Staphylococcus aureus can also cause lymphangitis, although the disorder is more likely to occur in patients with cellulitis due to GABHS than in those with cellulitis resulting from S aureus.

Other organisms that can cause lymphangitis include the following:

  • Pseudomonas species

  • Streptococcus pneumoniae - A relatively uncommon cause of lymphangitis

  • Pasteurella multocida - Associated with dog and cat bites; can cause cellulitis and lymphangitis

  • Gram-negative rods, gram-negative bacilli, and fungi - May cause cellulitis and resultant lymphangitis in immunocompromised hosts

  • Aeromonas hydrophila - Can contaminate wounds that occur in freshwater

  • Wuchereria bancrofti - This filarial nematode is a major cause of acute lymphangitis worldwide; signs and symptoms of lymphangitis caused by W bancrofti are indistinguishable from those of bacterial lymphangitis[1, 2]

In addition, individuals with diabetes, immunodeficiency, varicella, chronic steroid use, or other systemic illnesses have increased risk of developing serious or rapidly spreading lymphangitis.

A literature review by Cohen et al indicated that nonbacterial etiologies of lymphangitis with lymphangitic streaking include viral and fungal infections, insect and spider bites, and noninfectious, iatrogenic causes, with the latter reportedly including treatment with bacillus Calmette-GuĂ©rin vaccine, purified protein derivative placement, and topical treatment of verrucae vulgaris with cantharidin.[3]  Lieberman et al reported a case of viral lymphangitis associated with palmar herpetic whitlow in a child.[4]

Nodular lymphangitis

Nodular lymphangitis commonly follows superficial inoculation with one of the following organisms:

  • Sporothrix schenckii

  • Nocardia brasiliensis

  • Mycobacterium marinum

  • Leishmania panamensis

  • L guyanensis

  • Francisella tularensis

​Trepanowski et al described a rare case of nodular lymphangitis caused by methicillin-resistant Staphylococcus aureus.[5]


The prognosis for patients with uncomplicated lymphangitis is good. Antimicrobial regimens are effective in more than 90% of cases. Without appropriate antimicrobial therapy, however, cellulitis may develop or extend along the channels; necrosis and ulceration may occur.

Morbidity and mortality

Lymphangitis may spread within hours. The morbidity and mortality associated with the disease is related to the underlying infection. Although no specific data are available regarding complications and mortality associated with lymphangitis alone, lymphangitis caused by GABHS can lead to bacteremia, sepsis, and death.




A history of minor trauma to an area of skin distal to the site of infection is often elicited in patients with lymphangitis.[6, 7, 8]

Children with lymphangitis often have fever, chills, and malaise, and some children may report a headache, loss of appetite, and muscle aches.

Patients often have a history of a recent cut or abrasion or of an area of skin that appears infected and spreading.

Lymphangitis can progress rapidly to bacteremia and disseminated infection and sepsis, particularly when caused by group A streptococci.

Physical Examination

Upon clinical examination, erythematous and irregular linear streaks extend from the primary infection site toward draining regional nodes. These streaks may be tender and warm. Other characteristics can include the following:

  • The primary site may be an abscess, an infected wound, or an area of cellulitis

  • Blistering of the affected skin may occur

  • Lymph nodes associated with the infected lymphatic channels are often swollen and tender

  • Patients may be febrile and tachycardic



Diagnostic Considerations

Conditions to consider in the differential diagnosis of lymphangitis include the following:

  • Contact dermatitis

  • Cellulitis

  • Septic thrombophlebitis

  • Superficial thrombophlebitis

  • Necrotizing fasciitis

  • Myositis

  • Sporotrichosis



Approach Considerations

In any individual who presents with lymphangitis, a complete blood cell (CBC) count and blood culture should be obtained. In addition, a leading-edge culture or aspiration of pus should be considered. The CBC count and differential often reveal marked leukocytosis.

Incision and drainage

Abscessed areas may require incision and drainage. Cultures and Gram staining of fluid may help in the identification of the causative organism and the selection of appropriate antimicrobial agents.


Plain radiography is unnecessary in routine cases.

Cultures and Gram Staining

Blood cultures may reveal that infection has spread to the bloodstream; however, results are rarely positive.

Culture and Gram staining of aspirate from the primary site of infection may help in identifying the infectious organism and in choosing antimicrobials. Some authors recommend aspiration of the leading edge of the infection; others prefer sampling the area of maximum inflammation.

Aspiration is relatively insensitive for diagnosing causative organisms. The low density of pathogens present in the infected tissue results in the low sensitivity of aspiration. Published data from a small, comparative study appear to suggest that aspiration of the area of maximal inflammation may increase the yield of positive cultures.

The threshold sensitivity of Gram staining is approximately 100,000 microorganisms per milliliter, a concentration rarely found in cellulitis or lymphangitis.

Aspiration of the leading edge of maximal inflammation is not thought to be helpful in the acute management of cases of acute lymphangitis but may be helpful with treatment-resistant cases. Aspiration may identify antibiotic-resistant organisms or unsuspected organisms.

Imaging Studies

A study found that multidetector computed tomography (MDCT) imaging was very useful in determining the morphology (cellulitis with a few small subcutaneous nodules and channels) and the extension of the lesion in a case of nodular lymphangitis caused by Mycobacterium marinum.[9]




Approach Considerations

Patients with lymphangitis should be treated with an appropriate antimicrobial agent.[10] Children in stable social situations who appear nontoxemic and who are older than 3 years, afebrile, and well hydrated may be treated initially with oral antibiotics in an outpatient setting. Adult patients who appear nontoxemic, are afebrile, and well hydrated may also be treated initially with oral antibiotics in an outpatient setting. Ensure close follow-up.

Parenteral antibiotics may be required for patients with signs of systemic illness (eg, fever, chills and myalgia, lymphangitis).

Aggressively treat patients who are suspected of having group A beta-hemolytic streptococcus infection; these cases can progress rapidly and have been associated with serious complications.

Analgesics can be used to control pain, and anti-inflammatory medications can help to reduce inflammation and swelling. Hot, moist compresses also help to reduce inflammation and pain.

If possible, elevate and immobilize affected areas to reduce swelling, pain, and the spread of infection. An abscess may require surgical drainage.


Guidelines to prevent transmission of methicillin-resistant S aureus have been established.[11]

Nodular lymphangitis

Treatment of nodular lymphangitis is determined by identifying the underlying cause. Sporotrichosis is most often identified in this disease and is commonly found among gardeners.

Inpatient Care

Some patients with lymphangitis may require admission for intravenous (IV) antimicrobial therapy. Most authors recommend that children younger than 3 years or children who are febrile and who appear toxic initially be treated with IV antibiotics.

Children who have not improved clinically after 48 hours of appropriate oral antimicrobial therapy should receive IV antistaphylococcal and antistreptococcal therapy. When erythema, warmth, and edema are markedly reduced, oral antibiotics can be used.

Adults who are febrile and appear toxic should be initially treated with IV antibiotics.



Medication Summary

Analgesics can help to control pain in patients with lymphangitis, and anti-inflammatory medications can help to reduce inflammation and swelling.

Antibiotics, including the following, can be used in the treatment of group A beta-hemolytic streptococci (GABHS) and S aureus infections:

  • Dicloxacillin

  • Cephalexin

  • Cefazolin

  • Cefuroxime

  • Ceftriaxone

  • Clindamycin

  • Nafcillin

  • Trimethoprim and sulfamethoxazole (TMP/SMZ)


Class Summary

Antibiotics provide empiric coverage for group A streptococcal species and S aureus. Acceptable outpatient regimens include penicillinase-resistant synthetic penicillin or a first-generation cephalosporin. Acceptable inpatient regimens include a second- or third-generation cephalosporin (eg, cefuroxime, ceftriaxone) or a penicillinase-resistant synthetic penicillin. In certain geographic areas of the country with high rates of methicillin-resistant S aureus (MRSA), alternative antimicrobial agents, such as clindamycin or TMP-SMZ, should be considered.


Dicloxacillin binds to 1 or more penicillin-binding proteins, inhibiting synthesis of bacterial cell walls.

Cephalexin (Keflex)

Cephalexin, a first-generation cephalosporin, arrests bacterial growth by inhibiting bacterial cell-wall synthesis. It provides bactericidal activity against rapidly growing organisms.


This agent is a first-generation, semi-synthetic cephalosporin that arrests bacterial cell-wall synthesis, inhibiting bacterial growth.

Cefuroxime (Zinacef, Ceftin)

Cefuroxime is a second-generation cephalosporin that arrests bacterial cell-wall synthesis, inhibiting bacterial growth.

Ceftriaxone (Rocephin)

Ceftriaxone, a third-generation cephalosporin, arrests bacterial growth by binding to 1 or more penicillin-binding proteins.

Clindamycin (Cleocin)

This agent is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of the 7(R)-hydroxyl group of the parent compound, lincomycin. Clindamycin inhibits bacterial growth, possibly by blocking the dissociation of peptidyl transfer ribonucleic acid (tRNA) from ribosomes, causing RNA-dependent protein synthesis to arrest. Clindamycin widely distributes in the body without penetration of the central nervous system (CNS). The drug is protein bound and excreted by the liver and kidneys.

Clindamycin is used to treat serious skin and soft-tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci but not against enterococci.


Nafcillin binds to 1 or more penicillin-binding proteins, inhibiting synthesis of bacterial cell walls. Because of thrombophlebitis, administer this agent parenterally for only 1-2 days; change to oral antibiotic therapy as clinically indicated.

Trimethoprim and sulfamethoxazole (TMP/SMZ, Bactrim, Bactrim DS, Septra DS)

TMP/SMZ inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Its antibacterial activity includes common urinary-tract pathogens, except Pseudomonas aeruginosa.


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