"Streptococcus pneumoniae" — amoxicillin (or erythromycin in patients allergic to penicillin); cefuroxime and erythromycin in severe cases.

"Staphylococcus aureus" — flucloxacillin (to counteract the organism's β-lactamase).

People who have difficulty breathing due to pneumonia may require extra oxygen. An extremely sick individual may require artificial ventilation and intensive care as life-saving measures while his or her immune system fights off the infectious cause with the help of antibiotics and other drugs.

Antibiotics improve outcomes in those with bacterial pneumonia. Antibiotic choice depends initially on the characteristics of the person affected, such as age, underlying health, and the location the infection was acquired. In the UK, treatment before culture results with amoxicillin is recommended as the first line for community-acquired pneumonia, with doxycycline or clarithromycin as alternatives. In North America, where the "atypical" forms of community-acquired pneumonia are more common, macrolides (such as azithromycin or erythromycin), and doxycycline have displaced amoxicillin as first-line outpatient treatment in adults. In children with mild or moderate symptoms, amoxicillin remains the first line. The use of fluoroquinolones in uncomplicated cases is discouraged due to concerns about side-effects and generating resistance in light of there being no greater clinical benefit.

For those who require hospitalization and caught their pneumonia in the community the use of a β-lactam such as cephazolin plus macrolide such as azithromycin or a fluoroquinolones is recommended. The addition of corticosteroids also appears to improve outcomes.

The duration of treatment has traditionally been seven to ten days, but increasing evidence suggests that shorter courses (three to five days) are similarly effective. Recommendations for hospital-acquired pneumonia include third- and fourth-generation cephalosporins, carbapenems, fluoroquinolones, aminoglycosides, and vancomycin. These antibiotics are often given intravenously and used in combination. In those treated in hospital, more than 90% improve with the initial antibiotics.

Treatment for "Klebsiella" pneumonia is by antibiotics such as aminoglycosides and cephalosporins, the choice depending upon the person’s health condition, medical history and severity of the disease.

"Klebsiella" possesses beta-lactamase giving it resistance to ampicillin, many strains have acquired an extended-spectrum beta-lactamase with additional resistance to carbenicillin, amoxicillin, and ceftazidime. The bacteria remain susceptible to aminoglycosides and cephalosporins, varying degrees of inhibition of the beta-lactamase with clavulanic acid have been reported. Infections due to multidrug-resistant gram-negative pathogens in the ICU have invoked the re-emergence of colistin. However, colistin-resistant strains of "K. pneumoniae" have been reported in ICUs. In 2009, strains of "K. pneumoniae" with gene called New Delhi metallo-beta-lactamase ( NDM-1) that even gives resistance against intravenous antibiotic carbapenem, were discovered in India and Pakistan."Klebsiella" cases in Taiwan have shown abnormal toxicity, causing liver abscesses in people with diabetes mellitus (DM), treatment consists of third generation cephalosporins.

Neuraminidase inhibitors may be used to treat viral pneumonia caused by influenza viruses (influenza A and influenza B). No specific antiviral medications are recommended for other types of community acquired viral pneumonias including SARS coronavirus, adenovirus, hantavirus, and parainfluenza virus. Influenza A may be treated with rimantadine or amantadine, while influenza A or B may be treated with oseltamivir, zanamivir or peramivir. These are of most benefit if they are started within 48 hours of the onset of symptoms. Many strains of H5N1 influenza A, also known as avian influenza or "bird flu", have shown resistance to rimantadine and amantadine. The use of antibiotics in viral pneumonia is recommended by some experts, as it is impossible to rule out a complicating bacterial infection. The British Thoracic Society recommends that antibiotics be withheld in those with mild disease. The use of corticosteroids is controversial.

Patients with HCAP are more likely than those with community-acquired pneumonia to receive inappropriate antibiotics that do not target the bacteria causing their disease.

In 2002, an expert panel made recommendations about the evaluation and treatment of probable nursing home-acquired pneumonia. They defined probably pneumonia, emphasized expedite antibiotic treatment (which is known to improve survival) and drafted criteria for the hospitalization of willing patients.

For initial treatment in the nursing home, a fluoroquinolone antibiotic suitable for respiratory infections (moxifloxacin, for example), or amoxicillin with clavulanic acid plus a macrolide has been suggested. In a hospital setting, injected (parenteral) fluoroquinolones or a second- or third-generation cephalosporin plus a macrolide could be used. Other factors that need to be taken into account are recent antibiotic therapy (because of possible resistance caused by recent exposure), known carrier state or risk factors for resistant organisms (for example, known carrier of MRSA or presence of bronchiectasis predisposing to Pseudomonas aeruginosa), or suspicion of possible Legionella pneumophila infection (legionnaires disease).

In 2005, the American Thoracic Society and Infectious Diseases Society of America have published guidelines suggesting antibiotics specifically for HCAP. The guidelines recommend combination therapy with an agent from each of the following groups to cover for both "Pseudomonas aeruginosa" and MRSA. This is based on studies using sputum samples and intensive care patients, in whom these bacteria were commonly found.

- cefepime, ceftazidime, imipenem, meropenem or piperacillin–tazobactam; plus

- ciprofloxacin, levofloxacin, amikacin, gentamicin, or tobramycin; plus

- linezolid or vancomycin

In one observational study, empirical antibiotic treatment that was not according to international treatment guidelines was an independent predictor of worse outcome among HCAP patients.

Guidelines from Canada suggest that HCAP can be treated like community-acquired pneumonia with antibiotics targeting Streptococcus pneumoniae, based on studies using blood cultures in different settings which have not found high rates of MRSA or Pseudomonas.

Besides prompt antibiotic treatment, supportive measure for organ failure (such as cardiac decompensation) are also important. Another consideration goes to hospital referral; although more severe pneumonia requires admission to an acute care facility, this also predisposes to hazards of hospitalization such as delirium, urinary incontinence, depression, falls, restraint use, functional decline, adverse drug effects and hospital infections. Therefore, mild pneumonia might be better dealt with inside the long term care facility. In patients with a limited life expectancy (for example, those with advanced dementia), end-of-life pneumonia also requires recognition and appropriate, palliative care.

Most newborn infants with CAP are hospitalized, receiving IV ampicillin and gentamicin for at least ten days to treat the common causative agents "streptococcus agalactiae", "listeria monocytogenes" and "escherichia coli". To treat the herpes simplex virus, IV acyclovir is administered for 21 days.

In 2001 the American Thoracic Society, drawing on the work of the British and Canadian Thoracic Societies, established guidelines for the management of adult CAP dividing patients into four categories based on common organisms:

- Healthy outpatients without risk factors: This group (the largest) is composed of otherwise-healthy patients without risk factors for DRSP, enteric gram-negative bacteria, "pseudomonas" or other, less-common, causes of CAP. Primary microoganisms are viruses, atypical bacteria, penicillin-sensitive "streptococcus pneumoniae" and "haemophilus influenzae". Recommended drugs are macrolide antibiotics, such as azithromycin or clarithromycin, for seven to ten days.

- Outpatients with underlying illness or risk factors: Although this group does not require hospitalization, patients have underlying health problems (such as emphysema or heart failure) or are at risk for DRSP or enteric gram-negative bacteria. They are treated with a quinolone active against "streptococcus pneumoniae" (such as levofloxacin) or a β-lactam antibiotic (such as cefpodoxime, cefuroxime, amoxicillin or amoxicillin/clavulanic acid) and a macrolide antibiotic, such as azithromycin or clarithromycin, for seven to ten days.

- Hospitalized patients without risk for "pseudomonas": This group requires intravenous antibiotics, with a quinolone active against "streptococcus pneumoniae" (such as levofloxacin), a β-lactam antibiotic (such as cefotaxime, ceftriaxone, ampicillin/sulbactam or high-dose ampicillin plus a macrolide antibiotic (such as azithromycin or clarithromycin) for seven to ten days.

- Intensive-care patients at risk for "pseudomonas aeruginosa": These patients require antibiotics targeting this difficult-to-eradicate bacterium. One regimen is an intravenous antipseudomonal beta-lactam such as cefepime, imipenem, meropenem or piperacillin/tazobactam, plus an IV antipseudomonal fluoroquinolone such as levofloxacin. Another is an IV antipseudomonal beta-lactam such as cefepime, imipenem, meropenem or piperacillin/tazobactam, plus an aminoglycoside such as gentamicin or tobramycin, plus a macrolide (such as azithromycin) or a nonpseudomonal fluoroquinolone such as ciprofloxacin.

For mild-to-moderate CAP, shorter courses of antibiotics (3–7 days) seem to be sufficient.

Some patients with CAP will be at increased risk of death despite antimicrobial treatment. A key reason for this is the host's exaggerated inflammatory response. On one hand it is required to control the infection but on the other, it leads to bystander tissue damage. As a consequence of this recent research focuses on immunomodulatory therapy that can modulate the immune response to reduce injury to the lung and other affected organs such as the heart. Although the evidence for these agents has not resulted in their routine use, there potential benefits are highly promising.

Usually initial therapy is empirical. If sufficient reason to suspect influenza, one might consider oseltamivir. In case of legionellosis, erythromycin or fluoroquinolone.

A third generation cephalosporin (ceftazidime) + carbapenems (imipenem) + beta lactam & beta lactamase inhibitors (piperacillin/tazobactam)

"Klebsiella" resistant strains have been recorded in USA with a roughly threefold increase in Chicago cases, quarantined individuals in Israel, United Kingdom and parts of Europe, possible ground zero, or location of emergence, is the India-Pakistan border.

A strain known as Carbapenem-Resistant Klebsiella pneumonia (CRKP) was estimated to be involved in 350 cases in Los Angeles county between June and December 2010.

When comparing the bacterial-caused atypical pneumonias with these caused by real viruses (excluding bacteria that were wrongly considered as viruses), the term "atypical pneumonia" almost always implies a bacterial cause and is contrasted with viral pneumonia.

Known viral causes of atypical pneumonia include respiratory syncytial virus (RSV), influenza A and B, parainfluenza, adenovirus, severe acute respiratory syndrome (SARS)

and measles.

The most common causative organisms are (often intracellular living) bacteria:

- "Chlamydophila pneumoniae": Mild form of pneumonia with relatively mild symptoms.

- "Chlamydophila psittaci": Causes psittacosis.

- "Coxiella burnetii": Causes Q fever.

- "Francisella tularensis": Causes tularemia.

- "Legionella pneumophila": Causes a severe form of pneumonia with a relatively high mortality rate, known as legionellosis or Legionnaires' disease.

- "Mycoplasma pneumoniae": Usually occurs in younger age groups and may be associated with neurological and systemic (e.g. rashes) symptoms.

Atypical pneumonia can also have a fungal, protozoan or viral cause.In the past, most organisms were difficult to culture. However, newer techniques aid in the definitive identification of the pathogen, which may lead to more individualized treatment plans.

Since the start of the AIDS epidemic, PCP has been closely associated with AIDS. Because it only occurs in an immunocompromised host, it may be the first clue to a new AIDS diagnosis if the patient has no other reason to be immunocompromised (e.g. taking immunosuppressive drugs for organ transplant). An unusual rise in the number of PCP cases in North America, noticed when physicians began requesting large quantities of the rarely used antibiotic pentamidine, was the first clue to the existence of AIDS in the early 1980s.

Prior to the development of more effective treatments, PCP was a common and rapid cause of death in persons living with AIDS. Much of the incidence of PCP has been reduced by instituting a standard practice of using oral co-trimoxazole (Bactrim / Septra) to prevent the disease in people with CD4 counts less than 200/μL. In populations that do not have access to preventive treatment, PCP continues to be a major cause of death in AIDS.

There is low or very-low quality evidence that probiotics may be better than placebo in preventing acute URTIs. Vaccination against influenza viruses, adenoviruses, measles, rubella, "Streptococcus pneumoniae", "Haemophilus influenzae", diphtheria, "Bacillus anthracis", and "Bordetella pertussis" may prevent them from infecting the URT or reduce the severity of the infection.

In immunocompromised patients, prophylaxis with co-trimoxazole (trimethoprim/sulfamethoxazole), atovaquone, or regular pentamidine inhalations may help prevent PCP.

Antipneumocystic medication is used with concomitant steroids in order to avoid inflammation, which causes an exacerbation of symptoms about four days after treatment begins if steroids are not used. By far the most commonly used medication is trimethoprim/sulfamethoxazole, but some patients are unable to tolerate this treatment due to allergies. Other medications that are used, alone or in combination, include pentamidine, trimetrexate, dapsone, atovaquone, primaquine, pafuramidine maleate (under investigation), and clindamycin. Treatment is usually for a period of about 21 days.

Pentamidine is less often used as its major limitation is the high frequency of side effects. These include acute pancreatic inflammation, kidney failure, liver toxicity, decreased white blood cell count, rash, fever, and low blood sugar.

Pneumococcal pneumonia is a type of bacterial pneumonia that is specifically caused by Streptococcus pneumoniae. "S. pneumoniae" is also called pneumococcus. It is the most common bacterial pneumonia found in adults. The estimated number of Americans with pneumococcal pneumonia is 900,000 annually, with almost 400,000 cases hospitalized and fatalities accounting for 5-7% of these cases.

The symptoms of pneumococcal pneumonia can occur suddenly, typically presenting as a severe chill, later including a severe fever, cough, shortness of breath, rapid breathing, and chest pains. Other symptoms like nausea, vomiting, headache, fatigue, and muscle aches could also accompany the original symptoms. Sometimes the coughing can produce rusty or blood-streaked sputum. In 25% of cases, a parapneumonic effusion may occur. Chest X-rays will typically show lobar consolidation or patchy infiltrates.

In most cases, once pneumococcal pneumonia has been identified, doctors will prescribe antibiotics. These antibiotic usually help alleviate and eliminate symptoms between 12 and 36 hours after being taken. Despite most antibiotics' effectiveness in treating the disease, sometimes the bacteria can resist the antibiotics, causing symptoms to worsen. Additionally, age and health of the infected patient can contribute to the effectiveness of the antibiotics. A vaccine has also been developed for the prevention of pneumococcal pneumonia, recommended to children under age five as well as adults over the age of 65.

While it has been commonly known that the influenza virus increases one's chances of contracting pneumonia or meningitis caused by the streptococcus pneumonaie bacteria, new medical research in mice indicates that the flu is actually a necessary component for the transmission of the disease. Researcher Dimitri Diavatopoulo from the Radboud University Nijmegen Medical Centre in the Netherlands describes his observations in mice, stating that in these animals, the spread of the bacteria only occurs between animals already infected with the influenza virus, not between those without it. He says that these findings have only been inclusive in mice, however, he believes that the same could be true for humans.

The best prevention against viral pneumonia is vaccination against influenza, adenovirus, chickenpox, herpes zoster, measles, and rubella.

In cases of viral pneumonia where influenza A or B are thought to be causative agents, patients who are seen within 48 hours of symptom onset may benefit from treatment with oseltamivir or zanamivir. Respiratory syncytial virus (RSV) has no direct acting treatments, but ribavirin in indicated for severe cases. Herpes simplex virus and varicella-zoster virus infections are usually treated with aciclovir, whilst ganciclovir is used to treat cytomegalovirus. There is no known efficacious treatment for pneumonia caused by SARS coronavirus, MERS coronavirus, adenovirus, hantavirus, or parainfluenza. Care is largely supportive.

Both intramuscular and intranasal vaccines are available. Isolation of new horses for 4 to 6 weeks, immediate isolation of infected horses, and disinfection of stalls, water buckets, feed troughs, and other equipment will help prevent the spread of strangles. As with any contagious disease, handwashing is a simple and effective tool.

The Centers for Disease Control describe protocol for treating sinusitis while at the same time discouraging overuse of antibiotics:

- Target likely organisms with first-line drugs: Amoxicillin, Amoxicillin/Clavulanate

- Use shortest effective course: Should see improvement in 2–3 days. Continue treatment for 7 days after symptoms improve or resolve (usually a 10–14 day course).

- Consider imaging studies in recurrent or unclear cases: some sinus involvement is frequent early in the course of uncomplicated viral URI

Treatment comprises symptomatic support usually via analgesics for headache, sore throat and muscle aches. Moderate exercise in sedentary subjects with naturally acquired URTI probably does not alter the overall severity and duration of the illness. No randomized trials have been conducted to ascertain benefits of increasing fluid intake.

Possible complications include the horse becoming a chronic carrier of the disease, asphyxia due to enlarged lymph nodes compressing the larynx or windpipe, bastard strangles (spreading to other areas of the body), pneumonia, guttural pouch filled with pus, abscesses, purpura haemorrhagica, and heart disease. The average length for the course of this disease is 23 days.

The Hib vaccine is very effective at preventing the disease.

In household contacts of any unvaccinated child infected with H. influenzae, rifampicin is used as prophylaxis.

The incidence of pleural empyema and the prevalence of specific causative microorganisms varies depending on the source of infection (community acquired vs. hospital acquired pneumonia), the age of the patient and host immune status. Risk factors include alcoholism, drug use, HIV infection, neoplasm and pre-existent pulmonary disease. Pleural empyema was found in 0.7% of 3675 patients needing hospitalization for a community acquired pneumonia in a recent Canadian single-center prospective study. A multi-center study from the UK including 430 adult patients with community acquired pleural empyema found negative pleural-fluid cultures in 54% of patients, Streptococcus milleri group in 16%, Staphylococcus aureus in 12%, Streptococcus pneumoniae in 8%, other Streptococci in 7% and anaerobic bacteria in 8%. Given the difficulties in culturing anaerobic bacteria the frequency of the latter (including mixed infections) might be underestimated.

The risk of empyema in children seems to be comparable to adults. Using the United States Kids’ Inpatient Database the incidence is calculated to be around 1.5% in children hospitalized for community acquired pneumonia, although percentages up to 30% have been reported in individual hospitals, a difference which may be explained by an transient endemic of highly invasive serotype or overdiagnosis of small parapneumonic effusions. The distribution of causative organisms does differ greatly from that in adults: in an analysis of 78 children with community acquired pleural empyema, no micro-organism was found in 27% of patients, Streptococcus pneumoniae in 51%, Streptococcus pyogenes in 9% and Staphylococcus aureus in 8%.

Although pneumococcal vaccination dramatically decreased the incidence of pneumonia in children, it did not have this effect on the incidence of complicated pneumonia. It has been shown that the incidence of empyema in children was already on the rise at the end of the 20th century, and that the widespread use of pneumococcal vaccination did not slow down this trend. This might in part be explained by a change in prevalence of (more invasive) pneumococcal serotypes, some of which are not covered by the vaccine, as well a rise in incidence of pneumonia caused by other streptococci and staphylococci. The incidence of empyema seems to be rising in the adult population as well, albeit at a slower rate.

There is no readily available evidence on the route of administration and duration of antibiotics in patients with pleural empyema. Experts agree that all patients should be hospitalized and treated with antibiotics intravenously. The specific antimicrobial agent should be chosen based on Gram stain and culture, or on local epidemiologic data when these are not available. Anaerobic coverage must be included in all adults, and in children if aspiration is likely. Good pleural fluid and empyema penetration has been reported in adults for penicillins, ceftriaxone, metronidazole, clindamycin, vancomycin, gentamycin and ciprofloxacin. Aminoglycosides should typically be avoided as they have poor penetration into the pleural space. There is no clear consensus on duration of intravenous and oral therapy. Switching to oral antibiotics can be considered upon clinical and objective improvement (adequate drainage and removal of chest tube, declining CRP, temperature normalization). Oral antibiotic treatment should then be continued for another 1–4 weeks, again based on clinical, biochemical and radiological response.

Some patients may develop pneumonia, lymphadenopathy, or septic arthritis.