Hubbry Logo
Pneumonic plaguePneumonic plagueMain
Open search
Pneumonic plague
Community hub
Pneumonic plague
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Pneumonic plague
Pneumonic plague
Pneumonic plague
View on Wikipedia
from Wikipedia

Pneumonic plague
A scanning electron micrograph depicting a mass of Yersinia pestis bacteria
SpecialtyInfectious disease
SymptomsFever, headache, shortness of breath, cough, coughing up blood[1]
Usual onset3 to 7 days[2]
CausesYersinia pestis[3]
Risk factorsRodents[3]
Diagnostic methodSputum testing[1]
TreatmentAntibiotics[1]
PrognosisNearly 100% fatal if untreated[4]
Frequency3% of all Plague cases (CDC MMWR 2015) [5]

Pneumonic plague is a severe lung infection caused by the bacterium Yersinia pestis.[3] Symptoms include fever, headache, shortness of breath, chest pain, coughing, and coughing up blood.[1] They typically start about three to seven days after exposure.[2] It is one of three forms of plague, the other two being septicemic plague and bubonic plague.[3]

The pneumonic form may occur following an initial bubonic or septicemic plague infection.[3] It may also result from breathing in airborne droplets from another person or animal infected with pneumonic plague.[1] The difference between the forms of plague is the location of infection; in pneumonic plague the infection is in the lungs, in bubonic plague the lymph nodes, and in septicemic plague within the blood.[3] Diagnosis is by testing the blood, sputum, or fluid from a lymph node.[1]

While vaccines are being developed, in most countries they are not yet commercially available.[1][3] Prevention is by avoiding contact with infected rodents, people, or cats.[1][3] It is recommended that those infected be isolated from others.[2] Treatment of pneumonic plague consists of antibiotics.[1]

Plague is present among rodents in Africa, the Americas, and Asia.[3] Pneumonic plague is more serious and less common than bubonic plague.[1] The total reported number of cases of all types of plague in 2013 was 783.[2] Left untreated, pneumonic plague is almost always fatal.[6] Some hypothesize that the pneumonic version of the plague was mainly responsible for the Black Death that resulted in approximately 25 million deaths in the 1300s.[2][7]

Signs and symptoms

[edit]

The most apparent symptom of pneumonic plague is coughing, often with hemoptysis (coughing up blood). With pneumonic plague, the first signs of illness are fever, headache, weakness and rapidly developing pneumonia with shortness of breath, chest pain, cough and sometimes bloody or watery sputum.[8]

The pneumonia progresses for two to four days and may cause respiratory failure and shock. Patients will die without early treatment, some within 36 hours.[citation needed]

Initial pneumonic plague symptoms can often include the following:[citation needed]

Rapidly developing pneumonia with:[citation needed]

Causes

[edit]

Pneumonic plague can be caused in two ways: primary, which results from the inhalation of aerosolized plague bacteria, or secondary, when septicemic plague spreads into lung tissue from the bloodstream. Pneumonic plague is not exclusively vector-borne like bubonic plague; instead, it can be spread from person to person. There have been cases of pneumonic plague resulting from the dissection or handling of contaminated animal tissue. This is one of the types of plague formerly known as the Black Death.[9]

Treatment

[edit]

Pneumonic plague is a very aggressive infection requiring early treatment, which must be given within 24 hours of first symptoms to reduce the risk of death.[8] Streptomycin, gentamicin, tetracyclines and chloramphenicol are all able to kill the causative bacterium.[citation needed]

Antibiotic treatment for seven days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.[8]

The mortality rate from untreated pneumonic plague approaches 100% although victims of the Black Death who vomited blood occasionally survived, such as the chronicler Marcha di Marco Battagli.[10][11]

Modern outbreaks

[edit]

Since 2002, the World Health Organization (WHO) has reported seven plague outbreaks, though some may go unreported because they often happen in remote areas. Between 1998 and 2009, nearly 24,000 cases were reported, including about 2,000 deaths, in Africa, Asia, the Americas, and Eastern Europe. Ninety-eight percent of the world's cases occur in Africa.

Democratic Republic of the Congo

[edit]

Two outbreaks occurred in the Democratic Republic of the Congo in 2005 and 2006.[12] The outbreak in 2005 was only detected by looking back at blood samples.[12] The total death toll was 111.

India

[edit]

In September 1994, India experienced an outbreak of plague that killed 50 and caused travel to New Delhi by air to be suspended until the outbreak was brought under control.[13] The outbreak was feared to be much worse because the plague superficially resembles other common diseases such as influenza and bronchitis; over 200 people who had been quarantined were released when they did not test positive for the plague.[14] All but three of the deaths occurred around the city of Surat.[15]

China

[edit]

A major outbreak of the pneumonic plague occurred in Manchuria from 1910 to 1911, in what became known as the Manchurian plague, killing around 60,000 people.[16] The Qing court dispatched Wu Lien-teh, a doctor educated at Cambridge University, to oversee disease control and treatment efforts. He made the novel observation that the disease was transmitted by air, and developed prototypical respirators to help prevent its spread.[17] A second, less deadly outbreak occurred in 1920–21, killing approximately 9,300 people.[16]

The People's Republic of China has eradicated pneumonic plague from most parts of the country, but still reports occasional cases in remote western areas, where the disease is carried by rats and the marmots that live across the Himalayan plateau. Outbreaks can be caused when a person eats an infected marmot or comes into contact with fleas carried by rats. A 2006 WHO report from an international meeting on plague cited a Chinese government disease expert as saying that most cases of the plague in China's northwest occur when hunters are contaminated while skinning infected animals.[18]

The expert said at the time that, due to the region's remoteness, the disease killed more than half the infected people. The report also said that since the 1990s, there was a rise in plague cases in humans, from fewer than 10 in the 1980s to nearly 100 cases in 1996 and 254 in 2000.[19] In September 2008, two people in East Tibet died of pneumonic plague.[20]

An outbreak of the disease in China began in August 2009 in Ziketan Town located in Qinghai Province. The town was sealed off, and several people died as a result of the disease.[18][21] According to spokesperson Vivian Tan of the WHO office in Beijing, "In cases like this [in August 2009], we encourage the authorities to identify cases, to investigate any suspicious symptoms among close contacts, and to treat confirmed cases as soon as possible. So far, they have done exactly that. There have been sporadic cases reported around the country in the last few years so the authorities do have the experience to deal with this."[22]

In September 2010, five cases of pneumonic plague were reported in Tibet.[23]

In July 2014, Chinese media reported one case found in Gansu.[24]

On 12 November 2019, it was announced that two people from the Chinese province of Inner Mongolia were diagnosed with pneumonic plague. They received treatment in Chaoyang District, Beijing, and authorities implemented preventative control measures.[25] Later in November, a third case of plague was confirmed. A 55-year-old man was diagnosed with bubonic plague after eating wild rabbit in Inner Mongolia. The region's health commission says it has no evidence to suggest that this case is linked to the previous two.[26] By the end of November, a fourth case was confirmed. Chinese health authorities reported a fresh case of bubonic plague in the country's northern Inner Mongolia region, bringing the total number of reported plague cases originating from Inner Mongolia to four.[27]

Peru

[edit]

In August 2010, Peru's health minister, Oscar Ugarte, announced that an outbreak of plague had killed a 14-year-old boy and had infected at least 31 people in a northern coastal province. The boy died of bubonic plague on 26 July 2010. Ugarte stated that authorities were screening sugar and fish meal exports from Ascope Province, located about 325 miles (520 km) northwest of Lima, not far from the popular Chicama beach. Most of the infections in Peru were bubonic plague, with four cases of pneumonic plague.[28]

The first recorded plague outbreak in Peru was in 1903. Before the above case, the last known outbreak was in 1994, killing 35 people.[29]

Madagascar

[edit]
Medical team working together during a plague outbreak in Madagascar (October 2017).

In November 2013, an outbreak of plague occurred in the African island nation of Madagascar.[30] As of 16 December, at least 89 people were infected, with 39 deaths[31] with at least two cases involving pneumonic plague. However, as many as 90% of cases were later reported to have involved pneumonic plague.[32]

From 23 August to 30 September 2017, a total of 73 suspected, probable, and confirmed cases of pneumonic plague, including 17 deaths, were reported in Madagascar.[33] The diagnosis was confirmed by the Institut Pasteur de Madagascar by a polymerase chain reaction test, while field health workers used a Rapid Diagnostic Test. The WHO and Institut Pasteur de Madagascar were both involved in administering antibiotic compounds and attempting to stop the spread of the disease. By mid-October, there were an estimated 684 confirmed cases of plague with 474 pneumonic, 156 bubonic and one septicemic. The remainder were not classified. At least 74 deaths have been ascribed to pneumonic plague.[34]

The outbreak officially ended on 26 November 2017 with 2,348 cases and 202 deaths officially reported.[35]

United States

[edit]

In the fall of 1924, an outbreak occurred in Los Angeles[36] that killed 30 people.

On 2 November 2007, wildlife biologist Eric York died of pneumonic plague in Grand Canyon National Park. York was exposed to the bacteria while conducting a necropsy on a cougar carcass.[37]

In 2014, the Colorado Department of Public Health and Environment confirmed that a Colorado man had been diagnosed with pneumonic plague, the first confirmed human case in Colorado in more than 10 years, and one of only 60 cases since 1957. The man was found to have the disease after the family dog died unexpectedly, and a necropsy revealed that the disease was the cause.[38][39] Three additional pneumonic plague cases were confirmed in Colorado before the outbreak ended.[40]

A person near Flagstaff, Arizona died of pneumonic plague in July 2025.[41]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Pneumonic plague

View on Grokipedia
from Grokipedia
Pneumonic plague is the most severe and highly contagious form of plague, a bacterial that primarily affects the lungs and is caused by the bacterium . It can occur as a primary through of respiratory droplets from an infected person or animal, or as a secondary complication when the bacteria spread from untreated bubonic or to the lungs. This form of plague is distinguished by its potential for rapid person-to-person transmission via airborne droplets, making it a significant threat if not promptly identified and contained. Transmission of pneumonic plague occurs through close contact with infected individuals who cough out bacteria-laden droplets, or less commonly through exposure to infected animals like or cats that develop . Symptoms typically emerge suddenly after an of 1 to 3 days, including high fever, chills, , weakness, rapid progression to , shortness of breath, chest pain, and a that may produce bloody or watery . Unlike , which is flea-borne and causes swollen lymph nodes, or septicemic plague, which leads to bloodstream and tissue damage, pneumonic plague directly targets the and can be fatal within 18 to 24 hours without treatment. Effective treatment relies on immediate administration of antibiotics such as , gentamicin, or , which can cure the infection if started early, though delays increase the risk of death to nearly 100%. Prevention strategies include avoiding contact with potentially infected animals and fleas in endemic areas, using protective measures like masks during outbreaks, isolating patients, and providing prophylactic antibiotics to close contacts. Historically, pneumonic plague has fueled devastating pandemics, including the 14th-century that killed over 50 million people in , and it remains endemic in regions such as parts of , , and the , with rare but ongoing cases reported, including a fatal primary pneumonic plague case in in July 2025.

Overview and Classification

Definition and Key Features

Pneumonic plague is a severe and highly contagious caused by the bacterium , representing the most virulent form of plague with the potential for rapid person-to-person spread via respiratory droplets. As a pulmonary manifestation, it directly targets the , distinguishing it from other plague variants in its capacity for airborne transmission among humans. Key features of pneumonic plague include an typically lasting 1 to 3 days, which can shorten to as little as 24 hours after exposure, allowing for swift disease progression. Untreated cases exhibit a fatality rate approaching 100%, making prompt intervention critical to survival. Additionally, due to its high transmissibility, dissemination potential, and lethality, Y. pestis is designated a Category A agent by the Centers for Disease Control and Prevention, emphasizing the public health risks associated with intentional release. The nomenclature "pneumonic" originates from the Greek term pneumōn, denoting the , which underscores the disease's primary involvement of pulmonary tissues. Plague itself is a zoonotic illness, originating in animal reservoirs before occasionally spilling over to populations.

Distinction from Other Forms of Plague

Pneumonic plague is distinguished from other forms of plague primarily by its involvement of the s and potential for direct , whereas is characterized by of the s following a bite, leading to painful swelling known as buboes, and involves a primary bloodstream without focal or involvement. , the most common form accounting for 80-95% of cases, is typically -borne with low person-to-person transmissibility, while arises from systemic dissemination via bites or contact with infected tissues and manifests without buboes but with widespread vascular effects. Within pneumonic plague itself, a key distinction exists between primary and secondary forms: primary pneumonic plague results directly from of respiratory droplets containing Yersinia pestis, bypassing other sites and producing no buboes, whereas secondary pneumonic plague develops as a complication when the spread from untreated bubonic or to the lungs. This primary form is particularly rare outside outbreaks but highly dangerous due to its rapid onset. The most critical differentiator of pneumonic plague from bubonic and septicemic forms is its capacity for person-to-person spread through airborne respiratory droplets, making it the only highly contagious variant among the plagues and a significant threat in close-contact settings. In contrast, bubonic and septicemic plagues are not transmitted directly between humans and require vector or direct contact exposure.

Etiology and Transmission

Causative Organism

is a Gram-negative, non-motile, rod-shaped or coccobacillary bacterium that exhibits bipolar staining, giving it a characteristic "safety-pin" appearance under microscopic examination. As a member of the family, it is a facultative anaerobe capable of growth in both aerobic and anaerobic conditions, though it grows slowly and does not form spores. This bacterium is the etiological agent of plague, including its pneumonic form, and its non-motile nature distinguishes it from related species like . Key virulence factors enable Y. pestis to evade host defenses and facilitate infection. The F1 antigen forms a capsule that is anti-phagocytic, preventing uptake by immune cells such as macrophages. Yops (Yersinia outer proteins), a family of effector proteins injected via the , inhibit immune responses by disrupting , signaling, and dynamics in host cells. Additionally, the Pla plasminogen activator is a surface that promotes bacterial dissemination by degrading clots and activating plasminogen to , enhancing tissue invasion and spread. Y. pestis demonstrates remarkable environmental adaptability, forming biofilms in the of that block feeding and promote transmission to new hosts. These biofilms, dependent on the hms gene locus for production, allow the bacterium to thrive in nutrient-poor conditions within the vector. In nature, Y. pestis persists in reservoirs, where it cycles enzootically among wild rodents and their fleas, occasionally spilling over to cause epizootics. Evolutionarily, Y. pestis emerged as a clonal derivative of the enteric Yersinia pseudotuberculosis approximately 1,500 to 20,000 years ago through key genetic acquisitions, including enhancements to its transmission capability.

Transmission Routes

Pneumonic plague primarily spreads through the of aerosolized respiratory droplets containing , expelled by coughing individuals or animals infected with the pneumonic form of the disease. This direct person-to-person transmission occurs when droplets from an infected person's cough are inhaled by someone in close proximity, making it highly contagious in crowded or enclosed settings. Animals such as domestic cats, which are particularly susceptible to plague after consuming infected , can also transmit the bacteria via respiratory droplets when symptomatic, posing a risk to humans through close contact like petting or handling. For example, a fatal case of primary pneumonic plague in in July 2025 was linked to inhalation exposure from handling an infected animal. Secondary transmission routes include the progression of untreated to the pneumonic form in the same individual, where bacteria from swollen lymph nodes spread to the lungs, enabling respiratory expulsion of infectious droplets. Additionally, rare cases involve handling infected human corpses or animal carcasses, where intensive manipulation can aerosolize respiratory droplets from decomposition processes, as documented in a 2021 study analyzing outbreaks in . In the zoonotic cycle, Y. pestis maintains reservoirs in wild rodents such as rats and prairie dogs, primarily transmitted among them via bites from infected fleas like Xenopsylla cheopis. However, unlike , which relies heavily on flea vectors for human infection, pneumonic plague is less dependent on fleas and more commonly arises from respiratory spread or secondary dissemination within the host. Key risk factors for transmission include prolonged close contact with infected individuals or animals in endemic regions, such as parts of , , and the , where populations sustain the bacterial cycle. Furthermore, pneumonic plague has significant potential due to the ease of aerosolizing Y. pestis for widespread exposure, classifying it as a Category A agent.

Pathophysiology and Clinical Manifestations

Pathogenic Mechanisms

Pneumonic plague is initiated when bacteria are inhaled as aerosolized droplets, depositing primarily in the alveoli of the lungs. Upon entry, the bacteria are rapidly taken up by alveolar macrophages, where they exploit the (T3SS) to inject Yop effector proteins, such as YopE, YopH, and YopT, directly into the host cell cytoplasm. These effectors disrupt actin cytoskeleton dynamics and dephosphorylate key signaling proteins, effectively blocking and allowing intracellular survival without triggering immediate immune activation. Following evasion, Y. pestis undergoes intracellular replication within lung tissue macrophages during a pre-inflammatory phase, multiplying silently for the first 24 hours post-inhalation. This growth transitions to extracellular proliferation as bacteria exit host cells, leading to rapid dissemination within the pulmonary and alveoli. Bacteremia emerges within 24 to 48 hours, as bacteria invade the bloodstream via lymphatic drainage, disseminating systemically and overwhelming host defenses. The release of (LPS) endotoxin from replicating bacteria activates (TLR4), contributing to through excessive proinflammatory signaling in later stages. Lung-specific pathology arises from unchecked bacterial proliferation, culminating in characterized by alveolar destruction and fibrinous exudates. This process is exacerbated by a dysregulated inflammatory response, including a driven by elevated levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which promote massive influx and tissue . Hemorrhagic pneumonia develops as increases, leading to bloody effusions and further compromise of gas exchange. In contrast to , where Y. pestis primarily targets lymphatic tissues following bites, pneumonic plague establishes a direct pulmonary focus with accelerated replication due to the bacteria's pre-adaptation to mammalian temperatures during transmission. This bypasses the slower colonization seen in bubonic forms, enabling faster progression to .

Signs, Symptoms, and Progression

Pneumonic plague typically has an of 1 to 3 days following of Yersinia pestis-containing droplets. Early symptoms emerge suddenly and include high fever often exceeding 38°C, chills, severe , , , and a productive that may initially lack blood. These nonspecific flu-like signs reflect the initial bacterial replication in the lungs, leading to inflammation. As the disease advances within the first 24 hours, patients develop respiratory distress characterized by dyspnea, , and . A hallmark feature is the production of bloody (), which becomes increasingly prominent and frothy, often accompanied by due to . The condition progresses rapidly, with untreated cases deteriorating to and multi-organ failure within 24 to 48 hours of symptom onset, resulting in near-100% mortality. Recent cases, such as a fatal infection in in 2025, underscore the rapid progression to death without prompt treatment. Common complications include (ARDS) from overwhelming pneumonia and (DIC) from systemic sepsis. Prompt administration significantly improves survival, with reported mortality rates of 10–50% depending on timeliness; untreated cases approach 100% mortality. Atypical presentations, particularly in children or immunocompromised individuals, may include prominent gastrointestinal symptoms such as , , , and , potentially preceding or overshadowing respiratory features.

Diagnosis

Clinical Assessment

Clinical assessment of suspected pneumonic plague relies on a detailed patient and targeted to facilitate early recognition and isolation, given the disease's rapid progression and high transmissibility. History taking should prioritize inquiries into recent travel or residence in endemic regions, such as Madagascar or the Democratic Republic of the Congo (DRC), where Yersinia pestis circulates among rodent populations. Key exposures include contact with infected animals, rodents, or fleas, as well as close interaction with individuals displaying respiratory illness in outbreak settings, which heighten the risk of primary pneumonic acquisition. The emphasizes and pulmonary evaluation to identify systemic and localized involvement. Patients often exhibit high fever, , and signaling early , alongside respiratory distress. of the lungs may disclose rales or areas of consolidation indicative of alveolar infiltration, while the notable absence of tender, enlarged lymph nodes (buboes) helps differentiate pneumonic plague from bubonic forms. Rapid triage incorporates sepsis criteria, such as the quick Sequential Organ Failure Assessment (qSOFA) score, which evaluates altered mentation, ≥22 breaths/min, and systolic ≤100 mmHg to stratify risk in suspected cases; scores ≥2 warrant heightened urgency. A high index of suspicion is crucial during known outbreaks, prompting immediate airborne isolation to mitigate spread. Diagnostic challenges arise as pneumonic plague closely resembles other acute pneumonias, such as , due to overlapping features like and fever, underscoring the need for vigilant assessment in at-risk individuals.

Laboratory Confirmation

Laboratory confirmation of pneumonic plague relies on microbiological identification of from respiratory specimens, such as , alongside supportive imaging findings. Direct microscopic examination of sputum smears using Gram, Wright-Giemsa, or Wayson stains reveals small, Gram-negative coccobacilli with a characteristic bipolar "safety pin" appearance, providing rapid presumptive evidence. Culture remains the gold standard for definitive diagnosis, with Y. pestis isolated from or on blood agar plates, where it forms small, gray-white, translucent colonies after 48-72 hours of incubation at 28-37°C due to its slow growth. Handling and culturing Y. pestis requires biosafety level 3 (BSL-3) facilities and practices to mitigate aerosol transmission risks. Molecular methods, particularly (PCR) assays targeting Y. pestis-specific genes such as ypo2088, caf1, or pla, offer rapid and highly sensitive detection of bacterial DNA in or blood, often within hours and even after initiation when cultures fail. Serological tests, such as (ELISA) for the fraction 1 (F1) capsular or antibodies, can support diagnosis but are less useful in the acute phase due to delayed , typically requiring paired acute and convalescent sera for a fourfold rise. detection via rapid immunochromatographic dipstick tests for F1 provides presumptive diagnosis at the bedside, with high sensitivity (up to 100%) but moderate specificity (67-71%), particularly beneficial in outbreak settings. Imaging supports laboratory findings but is not specific to pneumonic plague. Chest X-rays typically show bilateral patchy infiltrates, lobar consolidation, or cavitation, reflecting hemorrhagic and . Computed tomography (CT) scans may reveal multiple nodules, central consolidations, or bilateral infiltrates with cavitation, aiding in differentiating from other . According to CDC and WHO guidelines, presumptive diagnosis can be made via tests or while awaiting confirmatory PCR or culture, with immediate notification to authorities essential; however, challenges in resource-poor settings, such as limited access to BSL-3 labs, delayed specimen transport, and poor infrastructure, often hinder timely confirmation and increase reliance on clinical suspicion.

Treatment

Antimicrobial Therapy

Antimicrobial therapy is the cornerstone of treating pneumonic plague, caused by , and must be initiated empirically upon suspicion of the disease to improve survival rates. In the United States, first-line treatments include gentamicin at a dose of 5 mg/kg administered intramuscularly or intravenously once daily, or at 1 g intramuscularly twice daily, both for a total duration of 10 to 14 days. These aminoglycosides are preferred due to their bactericidal activity against Y. pestis and demonstrated efficacy in reducing mortality when started early. Alternative regimens, suitable when first-line agents are unavailable or contraindicated, consist of tetracyclines or fluoroquinolones, such as 100 mg orally or intravenously twice daily, 400 mg intravenously twice daily or 500 mg orally twice daily, or levofloxacin 750 mg orally or intravenously once daily, also for 10 to 14 days. A 2025 confirmed the efficacy of oral ciprofloxacin for plague treatment, supporting its use as an alternative to aminoglycosides. For severe cases, intravenous administration is recommended initially, with a switch to oral once the patient stabilizes clinically. with two antibiotics from different classes may be considered in critically ill patients to enhance efficacy and mitigate potential resistance risks. Prompt initiation of therapy is critical, as untreated pneumonic plague progresses rapidly and can be fatal within 18 to 24 hours of symptom onset; treatment started within this window achieves survival rates exceeding 80%. The full course should be completed even if symptoms resolve early, with extension beyond 14 days if fever persists or complications arise. Special considerations apply for vulnerable populations: in , gentamicin is preferred over due to the latter's risk of fetal . For pediatric patients, is acceptable if the child is over 8 years old, while younger children may receive adjusted doses of gentamicin or based on weight and renal function. Antibiotic resistance in Y. pestis remains rare in natural isolates but is actively monitored globally, with 2025 research identifying multidrug-resistant plasmids as an emerging threat, alongside occasional reports of resistant strains in outbreak settings. The World Health Organization's 2021 recommendations emphasize early use and include levofloxacin as a key alternative, particularly in outbreak scenarios where facilitates mass treatment.

Supportive Care

Supportive care plays a critical role in managing complications of pneumonic plague, complementing to improve outcomes in hospitalized patients. Patients often require intensive care due to rapid progression involving , , and multiorgan dysfunction. Respiratory support is essential for addressing hypoxemia and acute respiratory distress syndrome (ARDS), common in severe cases. Oxygen therapy is administered to maintain adequate saturation, and mechanical ventilation is indicated for patients with respiratory failure or ARDS, using lung-protective strategies to minimize ventilator-induced injury. To prevent transmission via respiratory droplets, patients are isolated under droplet precautions, typically in single rooms, for at least 48-72 hours after initiating effective therapy or until clinical improvement and negative sputum cultures are confirmed. Fluid and hemodynamic management focuses on treating , a frequent complication. Intravenous fluids are provided aggressively to restore volume and perfusion, with vasopressors such as norepinephrine added if persists despite resuscitation. Close monitoring for (DIC) is necessary, as it can arise from gram-negative sepsis. Ongoing monitoring includes serial laboratory assessments of coagulation parameters, renal function (to detect ), and other markers of , alongside and clinical status. Pain control is managed with analgesics to alleviate chest discomfort from , and nutritional support via enteral or parenteral routes is provided for patients unable to eat adequately due to illness severity. Post-treatment follow-up involves evaluating for residual effects such as persistent respiratory compromise. Hospital discharge criteria generally include clinical stability (e.g., normalized , ability to maintain oxygenation without support, and negative infectious workup), typically after 48-72 hours of isolation precautions are lifted with documented improvement. Long-term monitoring may be needed for any lingering sequelae from ARDS or .

Prevention and Control

Prophylaxis Strategies

(PEP) is a critical intervention to prevent the development of pneumonic plague in individuals at high risk following potential exposure to . It is recommended for those with close, sustained contact (within 6 feet) with a confirmed or suspected pneumonic plague without adequate , laboratory personnel exposed to infectious materials, or individuals with direct contact with infected animals. Prophylaxis should be initiated immediately upon identification of exposure risk, ideally within 24 hours, and is particularly urgent in outbreak or scenarios where via respiratory droplets poses a threat. The preferred antimicrobial regimens for PEP in adults include oral at 100 mg twice daily or at 500 mg twice daily, each administered for a duration of 7 days following the last known exposure. Alternative options, such as levofloxacin (500 mg once daily) or (400 mg once daily), may be used based on patient factors like allergies or local resistance patterns. For pediatric patients, dosing is weight-based, such as at 2.2 mg/kg twice daily (maximum 100 mg per dose) or at 15 mg/kg twice daily (maximum 500 mg per dose). The full course must be completed even in the absence of symptoms, with close monitoring for adherence and potential adverse effects; for instance, commonly causes , necessitating sun avoidance. No licensed plague vaccine is currently available for use in the United States or globally to prevent pneumonic plague. Experimental vaccines, such as the recombinant F1-V candidate, have shown promise in preclinical and early-phase trials for eliciting protective immunity against aerosolized Y. pestis but remain unlicensed and unavailable outside settings as of 2024; development continues into 2025, including U.S. Department of Defense funding for an adjuvanted rF1V version and emerging mRNA and other candidates in preclinical stages. Historically, the Haffkine —an inactivated whole-cell preparation developed in the late —was used to mitigate outbreaks but was discontinued due to limited efficacy against pneumonic forms and safety concerns.

Public Health Measures

Public health measures for pneumonic plague emphasize integrated strategies to interrupt transmission at the level, targeting the rodent-flea-human cycle and rapid outbreak containment. These efforts are guided by international standards that prioritize , environmental interventions, and coordinated responses to minimize spread, particularly in endemic regions like parts of and the . Vector control forms the cornerstone of prevention by reducing vectors and reservoirs that sustain Yersinia pestis circulation. In endemic areas, rodenticides are deployed to lower populations, while insecticides such as dust (applied at 0.05% concentration to burrows) effectively suppress numbers and interrupt plague transmission for up to 12-24 months. Additional measures include modification, such as clearing brush, rock piles, and food sources around human settlements to deter , and treating pets with control products to prevent spillover. Surveillance of animal reservoirs, including monitoring epizootics in , enables proactive interventions before human cases emerge. Outbreak response protocols focus on swift to prevent secondary person-to-person transmission, which is a hallmark of pneumonic plague. Contact tracing identifies individuals exposed within 6 feet of cases, followed by and monitoring for symptoms; mass prophylaxis with antibiotics, such as or for 7 days, is administered to close contacts to avert further spread. Suspected, probable, or confirmed cases are isolated under droplet precautions for at least 48 hours after starting antimicrobials or until clinical improvement, with cohorting in alternative facilities during large-scale events. The World Health Organization's standardized case definitions—categorizing cases as suspected, probable, or confirmed—facilitate uniform reporting and trigger alerts. Education and initiatives build capacity in high-risk regions to enhance detection and response. Healthcare workers receive on plague recognition, safe handling of specimens, and implementation of infection control, while national plans address scenarios through stockpiling antibiotics and coordinating with emergency response networks like the U.S. . Community education promotes behaviors such as using insect repellents (e.g., on skin and on clothing) during outdoor activities in endemic zones and reporting dead animals to authorities. International efforts coordinate and control across borders, with the and providing updated guidelines for regions like and the . The PAHO Disease Elimination Initiative identifies cost-effective "best buys," including integrated vector management and community-based , to accelerate plague reduction toward elimination thresholds. These frameworks, revised as recently as 2024, support resource allocation, monitoring, and advocacy in affected countries.

Epidemiology

Historical Outbreaks

The , which ravaged from 1347 to 1351, marked one of the most devastating pandemics in human history, with the pneumonic form playing a crucial role in its rapid dissemination across Asia and . Originating likely in , the outbreak was exacerbated during the Mongol siege of the Genoese trading post at Caffa (modern-day , ) in 1346, where Mongol forces catapulted plague-infected corpses over the city walls, facilitating the disease's transmission to fleeing merchants who carried it westward via trade routes. The pneumonic variant, transmitted directly from person to person through respiratory droplets, thrived in the colder, drier conditions of winter, enabling explosive outbreaks in densely populated urban centers with poor sanitation and high mobility along caravans and Mediterranean shipping lanes. Overall mortality was catastrophic, claiming an estimated 25 to 50 million lives in alone, representing 30 to 50 percent of the continent's population, with untreated pneumonic cases exhibiting near-100 percent fatality rates. The Third Plague Pandemic, spanning 1894 to 1922, originated in China's province and spread globally through colonial networks, with pneumonic outbreaks underscoring the disease's adaptability to varied climates. first emerged in in 1894, where the bacterium was isolated by bacteriologist amid an epidemic that killed thousands, but the pandemic's pneumonic form gained prominence in , where it caused over 12 million deaths between 1898 and 1918, fueled by , overcrowded slums, and inadequate in ports like Bombay. A particularly lethal pneumonic wave struck in 1910–1911, originating from infected marmots hunted by fur traders; this winter-dominant epidemic, characterized by in cold, arid conditions, resulted in approximately 60,000 deaths across northeastern , highlighting how in and accelerated interstate spread despite international efforts. In the early , pneumonic plague reached the via global shipping, as seen in the 1924 Los Angeles outbreak, the last major urban epidemic in the United States. Triggered by rodent infestations in the city's expanding amid poor sanitation and high population density from and , the incident involved 33 confirmed cases of pneumonic and bubonic forms, resulting in 33 deaths and prompting aggressive responses like and . These historical outbreaks illustrate pneumonic plague's pandemic potential through factors like seasonal transmission in winter, when low and indoor crowding enhanced spread, compounded by poor , proliferation in hubs, and mobility via . The advent of antibiotics in the mid-20th century shifted control paradigms, reducing fatality rates from near-certain death to treatable outcomes with prompt intervention, though early epidemics underscored the need for rapid isolation and to curb airborne contagion.

Modern Outbreaks

In , experienced a major outbreak of pneumonic plague from August to November 2017, with 2,417 confirmed cases and 209 deaths, of which approximately 77% were classified as pneumonic plague. This urban surge, centered in , marked the largest pneumonic plague epidemic in the , driven by factors such as poor and high . In the (DRC), plague has been endemic since 2005, particularly in , with 100–500 suspected cases reported annually, including both bubonic and pneumonic forms. Between 2004 and 2014 alone, the DRC recorded over 4,630 suspected cases and 349 deaths, accounting for more than half of global plague reports during that period. In , the 1994 Surat outbreak in involved 693 suspected cases of bubonic and pneumonic plague, resulting in 56 deaths, primarily from pneumonic complications in an urban setting exacerbated by overcrowding and flooding. reported a pneumonic plague cluster in 2009 in Ziketan, Province, with 12 cases and 3 deaths linked to consumption of infected meat, prompting a town-wide to contain . In the Americas, Peru documented a small pneumonic plague outbreak in 2010 in Ascope Province, La Libertad Department, with 17 cases including 4 pneumonic forms, highlighting persistent sylvatic foci in rural areas. In the United States, rare human cases occur sporadically; a 2014 pneumonic plague outbreak in involved 4 cases and 1 death, transmitted from an infected to its owner and veterinary staff via respiratory droplets. Oregon reported a bubonic plague case in 2015 from flea exposure during , with no deaths, underscoring ongoing zoonotic risks in western states. More recently, a fatal pneumonic plague case occurred in , in July 2025, marking the first such death in the county since 2007. Globally, pneumonic plague incidence remains low at 1,000–2,000 cases per year, predominantly in , though case-fatality rates can reach 10–50% even with treatment due to diagnostic delays. is contributing to increased populations and vector activity, potentially elevating outbreak risks in endemic regions.

Global Distribution and Surveillance

Pneumonic plague, the most severe and contagious form of plague caused by , maintains endemic foci in approximately 10-20 countries worldwide, primarily in rural and semi-rural areas where reservoirs and flea vectors persist. These foci are concentrated in , with the (DRC), , and reporting the highest burdens, accounting for over 90% of global cases since the 1990s. In , endemic transmission occurs in regions of , , , , , and , often linked to sylvatic cycles in populations. The host smaller but persistent foci, including Peru's Andean highlands, , and the , where plague cycles in prairie dogs and other mammals sustain low-level human risk. Global incidence of plague, including pneumonic cases, remains low but underreported, with the (WHO) receiving notifications of 1,000 to 2,000 human cases annually as of 2025, though estimates suggest the true figure could reach several thousand due to diagnostic limitations in remote endemic areas. Pneumonic plague constitutes approximately 10-15% of reported cases globally, though this proportion rises significantly during urban outbreaks, as seen in where secondary pneumonic transmission amplifies spread. Underreporting is particularly acute in conflict-affected or impoverished regions, where access to confirmation is limited, masking the disease's ongoing presence. Surveillance for pneumonic plague relies on integrated zoonotic monitoring systems that track human, , and environmental indicators to detect outbreaks early. The WHO's Global Alert and Response Network coordinates international reporting, while national programs like the U.S. National Notifiable Diseases System (NNDSS) monitor plague cases through serosurveys and collections, focusing on high-risk areas such as the Southwest. In endemic countries, enhanced includes active case-finding in hotspots and rapid diagnostic networks, as outlined in WHO's 2024 manual for plague , diagnosis, prevention, and control. Genomic tracking has advanced strain monitoring, particularly in , where whole-genome sequencing identifies lineages like the 4.ANT1 , revealing multiple introductions during urban pneumonic outbreaks and informing transmission dynamics. Key risk factors exacerbating pneumonic plague distribution include socioeconomic vulnerabilities such as and conflict, which disrupt and healthcare access in endemic zones. Climate variability, including El Niño events, influences outbreak timing by altering rainfall patterns that boost and populations; for instance, anomalous weather in 2017 contributed to Madagascar's urban pneumonic epidemic by facilitating spillover from rural reservoirs. Additionally, systems maintain vigilance against , as Y. pestis is classified as a Category A agent due to its potential for aerosolized dissemination and high lethality.

References

  1. https://www.who.int/news-room/fact-sheets/detail/plague
  2. https://www.cdc.gov/plague/about/index.html
  3. https://www.cdc.gov/plague/signs-symptoms/index.html
  4. https://www.cdc.gov/plague/causes/index.html
  5. https://www.cidrap.umn.edu/plague/arizona-reports-pneumonic-plague-death-coconino-county
  6. https://www.cdc.gov/plague/hcp/diagnosis-testing/index.html
  7. https://wwwnc.cdc.gov/eid/article/26/10/pdfs/19-1270-combined.pdf
  8. https://www.cdc.gov/mmwr/volumes/70/rr/rr7003a1.htm
  9. https://www.merriam-webster.com/dictionary/pneumonia
  10. https://www.ncbi.nlm.nih.gov/books/NBK549855/
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC3417512/
  12. https://www.epa.gov/sites/default/files/2015-07/documents/asm-ypestis.pdf
  13. https://www.abcdcatsvets.org/guideline-for-plague-due-to-yersinia-pestis/
  14. https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2013.00106/full
  15. https://www.nature.com/articles/s41435-019-0065-0
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC3727414/
  17. https://journals.asm.org/doi/10.1128/jb.01187-13
  18. https://www.pnas.org/doi/10.1073/pnas.0404012101
  19. https://news.northeastern.edu/2025/07/16/bubonic-plague-arizona-death/
  20. https://wwwnc.cdc.gov/eid/article/23/3/16-1406_article.htm
  21. https://wwwnc.cdc.gov/eid/article/27/8/20-0136_article
  22. https://www.cdc.gov/plague/bioterrorism/index.html
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC3871965/
  24. https://doi.org/10.1111/j.1462-5822.2010.01448.x
  25. https://doi.org/10.1016/j.mib.2008.01.005
  26. https://pmc.ncbi.nlm.nih.gov/articles/PMC1606397/
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC3492934/
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC7920731/
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC6652753/
  30. https://www.ncbi.nlm.nih.gov/books/NBK7798/
  31. https://wwwnc.cdc.gov/eid/article/26/10/19-1270_article
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC10185452/
  33. https://www.cdc.gov/plague/hcp/clinical-care/index.html
  34. https://www.mdcalc.com/calc/2654/qsofa-quick-sofa-score-sepsis
  35. https://emedicine.medscape.com/article/235627-workup
  36. https://www.health.ny.gov/guidance/oph/wadsworth/yersinia_pestis.pdf
  37. https://www.cdc.gov/labs/pdf/SF__19_308133-A_BMBL6_00-BOOK-WEB-final-3.pdf
  38. https://pmc.ncbi.nlm.nih.gov/articles/PMC7568250/
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC7387759/
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC11295852/
  41. https://www.ncbi.nlm.nih.gov/books/NBK571125/
  42. https://www.nejm.org/doi/full/10.1056/NEJMoa2413772
  43. https://netec.org/2022/08/08/plague-symptoms-treatment-and-infection-prevention/
  44. https://emedicine.medscape.com/article/235627-guidelines
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC8907612/
  46. https://journals.asm.org/doi/10.1128/aac.01497-24
  47. https://www.who.int/publications/i/item/9789240015579
  48. https://oeps.wv.gov/plague/documents/lhd/plague_protocol.pdf
  49. https://emedicine.medscape.com/article/235627-treatment
  50. https://pmc.ncbi.nlm.nih.gov/articles/PMC5744195/
  51. https://www.cdc.gov/plague/prevention/index.html
  52. https://www.nature.com/articles/s41541-019-0105-9
  53. https://www.vax-before-travel.com/2025/02/21/30-million-continues-fund-dod-plague-vaccine-candidate
  54. https://www.passporthealthusa.com/2025/09/new-plague-vaccine-offers-powerful-protection-across-deadly-strains/
  55. https://nypost.com/2025/07/15/health/scientists-crack-the-code-on-new-vaccine/
  56. https://www.who.int/publications/i/item/9789240090422
  57. https://pubmed.ncbi.nlm.nih.gov/31124240/
  58. https://www.cdc.gov/plague/hcp/emergency-guidance/index.html
  59. https://www.paho.org/en/documents/best-buys-accelerate-disease-elimination-americas-plague
  60. https://pmc.ncbi.nlm.nih.gov/articles/PMC2732530/
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC7513766/
  62. https://pmc.ncbi.nlm.nih.gov/articles/PMC4013036/
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC8072022/
  64. https://pmc.ncbi.nlm.nih.gov/articles/PMC7341932/
  65. https://www.sciencedirect.com/science/article/pii/S1201971215000508
  66. https://pubmed.ncbi.nlm.nih.gov/16684896/
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC2595158/
  68. https://pmc.ncbi.nlm.nih.gov/articles/PMC8277479/
  69. https://pmc.ncbi.nlm.nih.gov/articles/PMC7152251/
  70. https://www.who.int/emergencies/disease-outbreak-news/item/15-november-2017-plague-madagascar-en
  71. https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(17)30730-8/fulltext
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC5782875/
  73. https://www.who.int/emergencies/disease-outbreak-news/item/plague-democratic-republic-of-the-congo
  74. https://www.cdc.gov/mmwr/preview/mmwrhtml/00032992.htm
  75. https://pubmed.ncbi.nlm.nih.gov/21288842/
  76. https://www.who.int/emergencies/disease-outbreak-news/item/2010_08_10-en
  77. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6416a1.htm
  78. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6433a6.htm
  79. https://www.coconino.az.gov/3465/Plague
  80. https://www.nature.com/articles/s41558-022-01426-1
  81. https://www.cdc.gov/plague/maps-statistics/index.html
  82. https://pmc.ncbi.nlm.nih.gov/articles/PMC10622459/
  83. https://www.mdpi.com/2673-947X/2/1/2
  84. https://wwwnc.cdc.gov/eid/article/31/13/24-1227_article
  85. https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=2100&context=icwdm_usdanwrc
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC11210753/
  87. https://wwwnc.cdc.gov/eid/article/30/2/23-0759_article
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC7733672/
  89. https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2023.1215929/full
Add your contribution
Related Hubs
User Avatar
No comments yet.