The secondary stage most often occurs 10–30 days later, but can present up to six months later. The infection spreads to the lymph nodes through lymphatic drainage pathways. The most frequent presenting clinical manifestation of LGV among males whose primary exposure was genital is unilateral (in 2/3 of cases) lymphadenitis and lymphangitis, often with tender inguinal and/or femoral lymphadenopathy because of the drainage pathway for their likely infected areas. Lymphangitis of the dorsal penis may also occur and resembles a string or cord. If the route was anal sex the infected person may experience lymphadenitis and lymphangitis noted above. They may instead develop proctitis, inflammation limited to the rectum (the distal 10–12 cm) that may be associated with anorectal pain, tenesmus, and rectal discharge, or proctocolitis, inflammation of the colonic mucosa extending to 12 cm above the anus and associated with symptoms of proctitis plus diarrhea or abdominal cramps.

In addition, symptoms may include inflammatory involvement of the perirectal or perianal lymphatic tissues. In females, cervicitis, perimetritis, or salpingitis may occur as well as lymphangitis and lymphadenitis in deeper nodes. Because of lymphatic drainage pathways, some patients develop an abdominal mass which seldom suppurates, and 20–30% develop inguinal lymphadenopathy. Systemic signs which can appear include fever, decreased appetite, and malaise. Diagnosis is more difficult in women and men who have sex with men (MSM) who may not have the inguinal symptoms.

Over the course of the disease, lymph nodes enlarge, as may occur in any infection of the same areas as well. Enlarged nodes are called buboes. Buboes are commonly painful. Nodes commonly become inflamed, thinning and fixation of the overlying skin. These changes may progress to necrosis, fluctuant and suppurative lymph nodes, abscesses, fistulas, strictures, and sinus tracts. During the infection and when it subsides and healing takes place, fibrosis may occur. This can result in varying degrees of lymphatic obstruction, chronic edema, and strictures. These late stages characterised by fibrosis and edema are also known as the third stage of LGV and are mainly permanent.

LGV may begin as a self-limited painless genital ulcer that occurs at the contact site 3–12 days after infection. Women rarely notice a primary infection because the initial ulceration where the organism penetrates the mucosal layer is often located out of sight, in the vaginal wall. In men fewer than 1/3 of those infected notice the first signs of LGV. This primary stage heals in a few days. Erythema nodosum occurs in 10% of cases.

These are only local and no systemic manifestations are present.

The ulcer characteristically:

- Ranges in size dramatically from 3 to 50 mm (1/8 inch to two inches) across

- Is painful

- Has sharply defined, undermined borders

- Has irregular or ragged borders

- Has a base that is covered with a gray or yellowish-gray material

- Has a base that bleeds easily if traumatized or scraped

- painful swollen lymph nodes occurs in 30 to 60% of patients.

- dysuria (pain with urination) and dyspareunia (pain with intercourse) in females

About half of infected men have only a single ulcer. Women frequently have four or more ulcers, with fewer symptoms.

The initial ulcer may be mistaken as a "hard" chancre, the typical sore of primary syphilis, as opposed to the "soft chancre" of chancroid.

Approximately one-third of the infected individuals will develop enlargements of the inguinal lymph nodes, the nodes located in the fold between the leg and the lower abdomen.

Half of those who develop swelling of the inguinal lymph nodes will progress to a point where the nodes rupture through the skin, producing draining abscesses. The swollen lymph nodes and abscesses are often referred to as buboes.

Chancroid ( ) (also known as soft chancre and ulcus molle) is a bacterial sexually transmitted infection characterized by painful sores on the genitalia. Chancroid is known to spread from one individual to another solely through sexual contact.

Rhinoscleroma has been divided into 3 stages: catarrhal/atrophic, granulomatous, and sclerotic stages. The catarrhal stage begins with a nonspecific rhinitis, which progresses into purulent, fetid rhinorrhea, and crusting, which can last for weeks or even months. The granulomatous stage results in the development of a bluish red nasal mucosa and the development of intranasal rubbery nodules or polyps. Nose bleeds, nasal deformity, and destruction of the nasal cartilage are also noted (Hebra nose). The damage may result in anesthesia of the soft palate, enlargement of the uvula, dysphonia, and various degrees of airway obstruction. The fibrotic stage is characterized by sclerosis and fibrosis. Lymphadenitis is absent.

Rhinoscleroma, or simply scleroma, is a chronic granulomatous bacterial disease of the nose that can sometimes infect the upper respiratory tract. It most commonly affects the nasal cavity—the nose is involved in 95–100 per cent of cases—however, it can also affect the nasopharynx, larynx, trachea, and bronchi. Slightly more females than males are affected and patients are usually 10 to 30 years of age. Rhinoscleroma is considered a tropical disease and is mostly endemic to Africa and Central America, less common in the United States.

The most common finding on ear examination is the presence of greyish white thick debris and heaviness in the ear.

Otomycosis is a fungal ear infection, a superficial mycotic infection of the outer ear canal. It is more common in the tropical countries. The infection may be either subacute or acute and is characterized by malodorous discharge, inflammation, pruritus, scaling, and severe discomfort. Suppuration can occur due to superimposed bacterial infection commonly due to pseudomonas species and proteus species. The mycosis results in inflammation, superficial epithelial exfoliation, masses of debris containing hyphae, suppuration, and pain.

The abscesses within the muscle must be drained surgically (not all patient require surgery if there is no abscess). Antibiotics are given for a minimum of three weeks to clear the infection.

The infection in most instances presents as a painless lump just under the skin. In southern Australia, the presentation is more often as a pimple in the skin (dermis) rather than under it. The infection is mostly in the limbs, most often in exposed areas, but not on the hands or feet. In children, all areas may be involved, including the face or abdomen. A more severe form of infection produces diffuse swelling of a limb, which, unlike the papule or nodule, can be painful and accompanied by fever. Infection may frequently follow physical trauma, often minor trauma such as a small scratch.

Pyomyositis, also known as tropical pyomyositis or myositis tropicans, is a bacterial infection of the skeletal muscles which results in a pus-filled abscess. Pyomyositis is most common in tropical areas but can also occur in temperate zones.

The initial lesion is a small subcutaneous swelling following minor trauma. Later, sinuses that discharge purulent and seropurulent exudates containing grains which are fungal colonies are formed. Destruction of deeper tissues, and deformity and loss of function in the affected limbs may occur in later stages.

Eumycetoma is a chronic granulomatous fungal disease of humans, affecting mainly the limbs, and sometimes the abdominal and chest walls or the head. "Mycetoma pedis" (mycetoma of the foot), the most common form of mycetoma, is known widely as the Madura foot. The infection is endemic in Africa, India and Central and South America.

Buruli ulcer is an infectious disease caused by "Mycobacterium ulcerans". The early stage of the infection is characterised by a painless nodule or area of swelling. This nodule can turn into an ulcer. The ulcer may be larger inside than at the surface of the skin, and can be surrounded by swelling. As the disease worsens, bone can be infected. Buruli ulcers most commonly affect the arms or legs; fever is uncommon.

"M. ulcerans" releases a toxin known as mycolactone, which decreases immune system function and results in tissue death. Bacteria from the same family also cause tuberculosis and leprosy ("M. tuberculosis" and "M. leprae", respectively). How the disease is spread is not known. Sources of water may be involved in the spread. As of 2013 there is no effective vaccine.

If people are treated early, antibiotics for eight weeks are effective in 80%. The treatment often includes the medications rifampicin and streptomycin. Clarithromycin or moxifloxacin are sometimes used instead of streptomycin. Other treatments may include cutting out the ulcer. After the infection heals, the area typically has a scar.

In 2015 about 2,000 cases were reported. Buruli ulcers occur most commonly in rural sub-Saharan Africa especially Cote d'Ivoire, but can also occur in Asia, the Western Pacific and the Americas. Children are most commonly infected. Cases have occurred in more than 32 countries. The disease also occurs in a number of animals other than humans. Albert Ruskin Cook was the first to describe buruli ulcers in 1897. It is classified as a neglected tropical disease.

Within 90 days (but usually less than a month) of infection a painless but distinctive "mother yaw" nodule appears, which enlarges and becomes warty in appearance. Nearby "daughter yaws" may also appear simultaneously.

This primary stage resolves completely within six months. The secondary stage occurs months to years later, with typically widespread skin lesions that vary in appearance, including "crab yaws" on the palms of the hands and soles of the feet with desquamation. These secondary lesions frequently ulcerate and are then highly infectious, but heal after six months or more. About 10% of people then go on to develop tertiary disease within five to ten years (during which further secondary lesions may come and go), with widespread bone, joint and soft tissue destruction, which may include extensive destruction of the bone and cartilage of the nose (Rhinopharyngitis mutilans or "gangosa").

Yaws is a tropical infection of the skin, bones and joints caused by the spirochete bacterium "Treponema pallidum pertenue". The disease begins with a round, hard swelling of the skin, 2 to 5 centimeters in diameter. The center may break open and form an ulcer. This initial skin lesion typically heals after three to six months. After weeks to years, joints and bones may become painful, fatigue may develop, and new skin lesions may appear. The skin of the palms of the hands and the soles of the feet may become thick and break open. The bones (especially those of the nose) may become misshapen. After five years or more large areas of skin may die, leaving a scar.

Yaws is spread by direct contact with the fluid from a lesion of an infected person. The contact is usually of a non-sexual nature. The disease is most common among children, who spread it by playing together. Other related treponemal diseases are bejel ("Treponema pallidum endemicum"), pinta ("Treponema pallidum carateum"), and syphilis ("Treponema pallidum pallidum"). Yaws is often diagnosed by the appearance of the lesions. Blood antibody tests may be useful but cannot separate previous from current infections. Polymerase chain reaction (PCR) is the most accurate method of diagnosis.

Prevention is, in part, by curing those who have the disease thereby decreasing the risk of transmission. Where the disease is common, treating the entire community is effective. Improving cleanliness and sanitation will also decrease spread. Treatment is typically with antibiotics including: azithromycin by mouth or benzathine penicillin by injection. Without treatment, physical deformities occur in 10% of cases.

Yaws is common in at least 14 tropical countries as of 2012. The disease only infects humans. In the 1950s and 1960s the World Health Organization (WHO) nearly eradicated yaws. Since then the number of cases has increased and there are renewed efforts to globally eradicate the disease by 2020. The last estimate of the number of people infected was more than 500,000 in 1995. Although one of the first descriptions of the disease was made in 1679 by Willem Piso, archaeological evidence suggests that yaws may have been present among humans as far back as 1.6 million years ago.

Frequently asymptomatic. Gastrointestinal system symptoms include abdominal pain and diarrhea. Pulmonary symptoms (including Löffler's syndrome) can occur during pulmonary migration of the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and waist areas as well as larva currens. Eosinophilia is generally present.

Strongyloidiasis can become chronic and then become completely asymptomatic.

Pyoderma means any skin disease that is pyogenic (has pus). These include superficial bacterial infections such as impetigo, impetigo contagiosa, ecthyma, folliculitis, Bockhart's impetigo, furuncle, carbuncle, tropical ulcer, etc. Autoimmune conditions include pyoderma gangrenosum. Pyoderma affects more than 111 million children worldwide, making it one of the three most common skin disorders in children along with scabies and tinea.

The primary symptom of podoconiosis is swelling and disfigurement of the lower extremities. The swelling can either be soft and fluid or hard and fibrotic. Multiple firm nodules may develop over time, as well as hyperkeratotic papillomata that resemble moss, which has led to the disease's alternate name of Mossy Foot. The edema of podoconiosis is usually bilateral and asymmetric. Prior to the development of lymphatic failure and frank lymphedema, a prodrome consisting of itching, burning, hyperkeratosis, plantar edema, and rigid digits may occur. As with other forms of tropical lymphedema, chronic disease can lead to fusion of the toes, ulceration, and bacterial superinfection. The disease has an acute component, and sufferers may experience recurrent episodes of lower extremity warmth, firmness, and pain.

Disseminated strongyloidiasis occurs when patients with chronic strongyloidiasis become immunosuppressed. It presents with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal. The worms enter the bloodstream from the bowel wall, simultaneously allowing entry of bowel bacteria such as "Escherichia coli". This may cause symptoms such as sepsis (bloodstream infection), and the bacteria may spread to other organs where they may cause localized infection such as meningitis.

Dissemination can occur many decades after the initial infection and has been associated with high dose corticosteroids, organ transplant, HIV, lepromatous leprosy, tertiary syphilis, aplastic anemia, malnutrition, advanced tuberculosis and radiation poisoning. It is often recommended that patients being started on immunosuppression be screened for chronic strongyloidiasis; however, this is often impractical (screen tests are often unavailable) and in developed countries, the prevalence of chronic strongyloidiasis is very small, so screening is usually not cost-effective, except in endemic areas.

It is important to note that there is not necessarily any eosinophilia in the disseminated disease. Absence of eosinophilia may indicate poor prognosis.

Toxoplasma chorioretinitis, more simply known as ocular toxoplasmosis, is probably the most common cause of infections in the back of the eye (posterior segment) worldwide. The causitive agent is "Toxoplasma gondii", and in the United States, most cases are acquired congenitally. The most common symptom is decreased visual acuity in one eye. The diagnosis is made by examination of the eye, using ophthalmoscopy. Sometimes serologic testing is used to rule out the disease, but due to high rates of false positives, serologies are not diagnostic of toxoplasmic retinitis.

If vision is not compromised, treatment may not be necessary. When vision is affected or threatened, treatment consists of pyrimethamine, sulfadiazine, and folinic acid for 4–6 weeks. Prednisone is sometimes used to decrease inflammation.

A unilateral decrease in visual acuity is the most common symptom of toxoplasmic retinitis.

Under ophthalmic examination, toxoplasmic chorioretinitis classically appears as a focal, white retinitis with overlying moderate inflammation of the vitreous humour. A unifocal area of acute-onset inflammation adjacent to an old chorioretinal scar is virtually pathognomonic for toxoplasmic chorioretinitis. Focal condensation of vitreous and inflammatory cells may be seen overlying the pale yellow or gray-white raised lesion in the posterior pole.

Podoconiosis, also known as nonfilarial elephantiasis, is a disease of the lymph vessels of the lower extremities that is caused by chronic exposure to irritant soils. It is the second most common cause of tropical lymphedema after filariasis, and it is characterized by prominent swelling of the lower extremities, which leads to disfigurement and disability.

Totally drug-resistant tuberculosis (TDR-TB) is a generic term for tuberculosis strains that are resistant to a wider range of drugs than strains classified as extensively drug-resistant tuberculosis. TDR-TB has been identified in three countries; India, Iran, and Italy. The emergence of TDR-TB has been documented in four major publications. However, it is not yet recognised by the World Health Organization.

TDR-TB has resulted from further mutations within the bacterial genome to confer resistance, beyond those seen in XDR- and MDR-TB. Development of resistance is associated with poor management of cases. Drug resistance testing occurs in only 9% of TB cases worldwide. Without testing to determine drug resistance profiles, MDR- or XDR-TB patients may develop resistance to additional drugs. TDR-TB is relatively poorly documented, as many countries do not test patient samples against a broad enough range of drugs to diagnose such a comprehensive array of resistance. The United Nations' Special Programme for Research and Training in Tropical Diseases has set up a TDR Tuberculosis Specimen Bank to archive specimens of TDR-TB.

In the initial phase of the disease, the mucosa feels leathery with palpable fibrotic bands. In the advanced stage the oral mucosa loses its resiliency and becomes blanched and stiff. The disease is believed to begin in the posterior part of the oral cavity and gradually spread outward.

Other features of the disease include:

- Xerostomia

- Recurrent ulceration

- Pain in the ear or deafness

- Nasal intonation of voice

- Restriction of the movement of the soft palate

- A budlike shrunken uvula

- Thinning and stiffening of the lips

- Pigmentation of the oral mucosa

- Dryness of the mouth and burning sensation

- Decreased mouth opening and tongue protrusion