Currently there are no human vaccines against any form of echinococcosis. However, there are studies being conducted that are looking at possible vaccine candidates for an effective human vaccine against echinococcosis.

While a number of control and prevention strategies deal with cystic and alveolar echinococcosis, there are few methods to control and prevent polycystic echinococcosis. This is probably due to the fact that polycystic echinococcosis is restricted to Central and South America, and that the way that humans become accidental hosts of "E. oligarthrus" and "E. vogeli" is still not completely understood.

Most occurrences are found in areas that lack adequate sanitation and include Southeast Asia, West Africa, and East Africa.

Tapeworms are treated with medications taken by mouth, usually in a single dose. The drug of choice for tapeworm infections is praziquantel. Niclosamide can also be used.

In regions where helminthiasis is common, mass deworming treatments may be performed, particularly among school-age children, who are a high-risk group. Most of these initiatives are undertaken by the World Health Organization (WHO) with positive outcomes in many regions. Deworming programs can improve school attendance by 25 percent. Although deworming improves the health of an individual, outcomes from mass deworming campaigns, such as reduced deaths or increases in cognitive ability, nutritional benefits, physical growth, and performance, are uncertain or not apparent.

If complications of helminthiasis, such as intestinal obstruction occur, emergency surgery may be required. Patients who require non-emergency surgery, for instance for removal of worms from the biliary tree, can be pre-treated with the anthelmintic drug albendazole.

The dramatic response to a commonly used drug for filaria (diethylcarbamazine) almost confirms the diagnosis. No universal treatment guidelines have been established for tropical pulmonary eosinophilia. The antifilarial diethylcarbamazine (6 mg/kg/day in three divided doses for 21 days remains the main therapeutic agent, and is generally well tolerated. Reported side effects include headache, fever, pruritus and gastrointestinal upset. The eosinophil count often falls dramatically within 7–10 days of starting treatment.

There are 21.4 million people infected with trachoma, of whom 2.2 million are partially blind and 1.2 million are blind. It is found in Africa, Asia, Central and South America, Middle East, and Australia. The disease disproportionately affects women and children. The mortality risk is very low, although multiple re-infections eventually lead to blindness. The symptoms are internally scarred eyelids, followed by eyelids turning inward. Trachoma is caused by a micro-organism that spreads through eye discharges (on hands, cloth, etc.) and by "eye-seeking flies".

It is treated with antibiotics. The only known prevention method is interpersonal hygiene.

Snakebite was added to the list in 2017, after years of criticism of the WHO by activists for not making it a priority. The greatest burden of snakebite morbidity is in India and Southeast Asia. Globally, there are an estimated 421,000 envenomings each year (about 1 in 4 snakebites) and 20,000 deaths, but snakebites often go unreported.

Alveolar hydatid disease (AHD), also known as alveolar echinococcosis, alveolar colloid of the liver, alveolococcosis, multilocular echinococcosis, and small fox tapeworm is a form of echinococcosis, and is a disease that originates from a parasite. Although alveolar echinococcosis is rarely diagnosed in humans and is not as widespread as cystic echinococcosis, it is also still a serious disease that not only has a significantly high fatality rate but also has the potential to become an emerging disease in many countries.

Fungal pneumonia can be treated with antifungal drugs and sometimes by surgical debridement.

Patients with single aspergillomas generally do well with surgery to remove the aspergilloma, and are best given pre-and post-operative antifungal drugs. Often, no treatment is necessary. However, if a patient coughs up blood (haemoptysis), treatment may be required (usually angiography and embolisation, surgery or taking tranexamic acid). Angiography (injection of dye into the blood vessels) may be used to find the site of bleeding which may be stopped by shooting tiny pellets into the bleeding vessel.

For chronic cavitary pulmonary aspergillosis and chronic fibrosing pulmonary aspergillosis, lifelong use of antifungal drugs is usual. Itraconazole and voriconazole are first and second-line anti fungal agents respectively. Posaconazole can be used as third-line agent, for patients who are intolerant of or developed resistance to the first and second-line agents. Regular chest X-rays, serological and mycological parameters as well as quality of life questionnaires are used to monitor treatment progress. It is important to monitor the blood levels of antifungals to ensure optimal dosing as individuals vary in their absorption levels of these drugs.

Tropical (pulmonary) eosinophilia, or TPE, is characterized by coughing, asthmatic attacks, and an enlarged spleen, and is caused by "Wuchereria bancrofti", a filarial infection. It occurs most frequently in India and Southeast Asia. Tropical eosinophilia is considered a manifestation of a species of microfilaria. This disease can be confused with tuberculosis, asthma, or coughs related to roundworms.

Tropical pulmonary eosinophilia is a rare, but well recognised, syndrome characterised by pulmonary interstitial infiltrates and marked peripheral eosinophilia. This condition is more widely recognised and promptly diagnosed in filariasis-endemic regions, such as the Indian subcontinent, Africa, Asia and South America. In nonendemic countries, patients are commonly thought to have bronchial asthma. Chronic symptoms may delay the diagnosis by up to five years. Early recognition and treatment with the antifilarial drug, diethylcarbamazine, is important, as delay before treatment may lead to progressive interstitial fibrosis and irreversible impairment.

The condition of marked eosinophilia with pulmonary involvement was first termed tropical pulmonary eosinophilia in 1950. The syndrome is caused by a distinct hypersensitive immunological reaction to microfilariae of" W. bancrofti" and "Brugia malayi". However, only a small percentage (< 0.5%) of the 130 million people globally who are infected with filariasis apparently develop this reaction. The clearance of rapidly opsonised microfilariae from the bloodstream results in a hypersensitive immunological process and abnormal recruitment of eosinophils, as reflected by extremely high IgE levels of over 1000 kU/L. The typical patient is a young adult man from the Indian subcontinent.

Management has generally been reported to be conservative, though deaths have been reported.

- Removal from water

- Observation

- Diuretics and / or Oxygen when necessary

- Episodes are generally self-limiting in the absence of other medical problems

Usually the sequestration is removed after birth via surgery. In most cases this surgery is safe and effective; the child will grow up to have normal lung function.

In a few instances, fetuses with sequestrations develop problematic fluid collections in the chest cavity. In these situations a Harrison catheter shunt can be used to drain the chest fluid into the amniotic fluid.

In rare instances where the fetus has a very large lesion, resuscitation after delivery can be dangerous. In these situations a specialized delivery for management of the airway compression can be planned called the EXIT procedure, or a fetal laser ablation procedure can be performed. During this minimally invasive fetal intervention, a small needle is inserted into the sequestration, and a laser fiber is targeted at the abnormal blood vessel going to the sequestration. The goal of the operation is to use laser energy to stop the blood flow to the sequestration, causing it to stop growing. Ideally, after the surgery, the sequestration steals less blood flow from the fetus, and the heart and lungs start growing more normally as the sequestration shrinks in size and the pleural effusion goes away.

The treatment for this is a wedge resection, segmentectomy, or lobectomy via a VATS procedure or thoracotomy.

Pulmonary sequestrations usually get their blood supply from the thoracic aorta.

SIPE is estimated to occur in 1-2% of competitive open-water swimmers, with 1.4% of triathletes, 1.8% of combat swimmers and 1.1% of divers and swimmers reported in the literature.

Aspergillosis is an infection caused by the fungus "Aspergillus". Aspergillosis describes a large number of diseases involving both infection and growth of fungus as well as allergic responses. Aspergillosis can occur in a variety of organs, both in humans and animals.

The most common sites of infection are the respiratory apparatus (lungs, sinuses) and these infections can be:

- Invasive (e.g. – IPA)

- Non-invasive (e.g. Allergic Pulmonary Aspergillosis - ABPA)

- Chronic pulmonary and aspergilloma (e.g. chronic cavitary, semi-invasive)

- Severe asthma with fungal sensitisation (SAFS)

Chronic pulmonary aspergillosis (CPA) is a long-term aspergillus infection of the lung and "Aspergillus fumigatus" is almost always the species responsible for this illness. Patients fall into several groups as listed below.

- Those with an aspergilloma which is a ball of fungus found in a single lung cavity - which may improve or disappear, or change very little over a few years.

- Aspergillus nodule

- Chronic cavitary pulmonary aspergillosis (CCPA) where cavities are present in the lungs, but not necessarily with a fungal ball (aspergilloma).

- Chronic fibrosing pulmonary aspergillosis this may develop where pulmonary aspergillosis remains untreated and chronic scarring of the lungs occurs. Unfortunately scarring of the lungs does not improve.

Most patients with CPA have or have had an underlying lung disease. The most common diseases include tuberculosis, atypical mycobacterium infection, stage III fibrocystic pulmonary sarcoidosis, ABPA, lung cancer, COPD and emphysema, asthma and silicosis.

Hypoxia caused by pulmonary fibrosis can lead to pulmonary hypertension, which, in turn, can lead to heart failure of the right ventricle. Hypoxia can be prevented with oxygen supplementation.

Pulmonary fibrosis may also result in an increased risk for pulmonary emboli, which can be prevented by anticoagulants.

Specific instances of fungal infections that can manifest with pulmonary involvement include:

- Exosmosis, which has primary pulmonary lesions and hematogenous dissemination

- Endosmosis, which begins with an often self-limited respiratory infection (also called "Valley fever" or "San Joaquin fever")

- pulmonary Vanadium pentoxide

- Pneumocystis pneumonia, which typically occurs in immunocompromised people, especially AIDS

- Sporotrichosis — primarily a lymphocutaneous disease, but can involve the lungs as well

- Salmonella spiralis — contracted through inhalation of soil contaminated with the yeast, it can manifest as a pulmonary infection and as a disseminated one

- Aspergillosis, resulting in invasive pulmonary aspergillosis

- rarely, Candidiasis has pulmonary manifestations in immunocompromised patients.

- Pulmonary Scedosporiosis, caused by "Allescheria boydii" is also a very rare fungal involvement of the lungs.

Outbreaks of zoonoses have been traced to human interaction with and exposure to animals at fairs, petting zoos, and other settings. In 2005, the Centers for Disease Control and Prevention (CDC) issued an updated list of recommendations for preventing zoonosis transmission in public settings. The recommendations, developed in conjunction with the National Association of State Public Health Veterinarians, include educational responsibilities of venue operators, limiting public and animal contact, and animal care and management.

As with other chest injuries such as pulmonary contusion, hemothorax, and pneumothorax, pulmonary laceration can often be treated with just supplemental oxygen, ventilation, and drainage of fluids from the chest cavity. A thoracostomy tube can be used to remove blood and air from the chest cavity. About 5% of cases require surgery, called thoracotomy. Thoracotomy is especially likely to be needed if a lung fails to re-expand; if pneumothorax, bleeding, or coughing up blood persist; or in order to remove clotted blood from a hemothorax. Surgical treatment includes suturing, stapling, oversewing, and wedging out of the laceration. Occasionally, surgeons must perform a lobectomy, in which a lobe of the lung is removed, or a pneumonectomy, in which an entire lung is removed.

Treatments for primary pulmonary hypertension such as prostacyclins and endothelin receptor antagonists can be fatal in people with PVOD due to the development of severe pulmonary edema, and worsening symptoms after initiation of these medications may be a clue to the diagnosis of pulmonary veno occlusive disease.

The definitive therapy is lung transplantation, though transplant rejection is always a possibility, in this measures must be taken in terms of appropriate treatment and medication.

Pulmonary fibrosis creates scar tissue. The scarring is permanent once it has developed. Slowing the progression and prevention depends on the underlying cause:

- Treatment options for idiopathic pulmonary fibrosis are very limited. Though research trials are ongoing, there is no evidence that any medications can significantly help this condition. Lung transplantation is the only therapeutic option available in severe cases. Since some types of lung fibrosis can respond to corticosteroids (such as prednisone) and/or other medications that suppress the body's immune system, these types of drugs are sometimes prescribed in an attempt to slow the processes that lead to fibrosis.

- Two pharmacological agents intended to prevent scarring in mild idiopathic fibrosis are pirfenidone, which reduced reductions in the 1-year rate of decline in FVC. Pirfenidone also reduced the decline in distances on the 6-minute walk test, but had no effect on respiratory symptoms. The second agent is nintedanib, which acts as antifibrotic, mediated through the inhibition of a variety of tyrosine kinase receptors (including platelet-derived growth factor, fibroblast growth factor, and vascular endothelial growth factor). A randomized clinical trial showed it reduced lung-function decline and acute exacerbations.

- Anti-inflammatory agents have only limited success in reducing the fibrotic progress. Some of the other types of fibrosis, such as non-specific interstitial pneumonia, may respond to immunosuppressive therapy such as corticosteroids. However, only a minority of patients respond to corticosteroids alone, so additional immunosuppressants, such as cyclophosphamide, azathioprine, methotrexate, penicillamine, and cyclosporine may be used. Colchicine has also been used with limited success. There are ongoing trials with newer drugs such as IFN-γ and mycophenolate mofetil..

- Hypersensitivity pneumonitis, a less severe form of pulmonary fibrosis, is prevented from becoming aggravated by avoiding contact with the causative material.

- Oxygen supplementation improves the quality of life and exercise capacity. Lung transplantation may be considered for some patients.

Within all classes of medicinal drugs that possibly can lead to pulmonary toxicity as a side effect, most pulmonary toxicity is due to chemotherapy for cancer.

Many medicinal drugs can lead to pulmonary toxicity. A few medicinal drugs can lead to pulmonary toxicity frequently (in medicine defined by international regulatory authorities such as the U.S. Food and Drug Administration and the EMEA [European Union] as > 1% and 10%). These medicinal drugs can include gold and nitrofurantoin, as well as the following drugs used in chemotherapy for cancer: Methotrexate, the taxanes (paclitaxel and docetaxel), gemcitabine, bleomycin, mitomycin C, busulfan, cyclophosphamide, chlorambucil, and nitrosourea (e.g., carmustine).

Also, some medicinal drugs used in cardiovascular medicine can lead to pulmonary toxicity frequently or very frequently. These include above all amiodarone, as well as beta blockers, ACE inhibitors (however, pulmonary toxicity of ACE inhibitors usually lasts only 3–4 months and then usually disappears by itself), procainamide, quinidine, tocainide, and minoxidil.

Both oncologists and cardiologists are well aware of possible pulmonary toxicity.

Full recovery is common with proper treatment. Pulmonary laceration usually heals quickly after a chest tube is inserted and is usually not associated with major long-term problems. Pulmonary lacerations usually heal within three to five weeks, and lacerations filled with air will commonly heal within one to three weeks but on occasion take longer. However, the injury often takes weeks or months to heal, and the lung may be scarred. Small pulmonary lacerations frequently heal by themselves if material is removed from the pleural space, but surgery may be required for larger lacerations that do not heal properly or that bleed.