pulmonary anthrax



Overview

Pulmonary anthrax is an acute infectious disease caused by Bacillus anthracis. It is originally an infectious disease of herbivores and can be transmitted directly from person to person. The disease has a high mortality rate, acute onset, chills, high fever and other symptoms of poisoning. Coughing and chest pain, dyspnea, hemoptysis, can be due to respiratory and circulatory failure within 24 hours of death, rare occurrence of anthrax meningitis.

People are infected by contact with diseased animals and their products or by eating meat from diseased animals. The incubation period is usually 1 to 5 days.

Pulmonary anthrax is mostly primary, but can also be secondary to cutaneous anthrax. Initially, it is a mild upper respiratory tract infection with low fever, dry cough and myalgia. After a few days, the condition worsens rapidly, characterized by high fever, chills, shortness of breath, wheezing, cyanosis, hemoptysis, profuse sweating and increased heart rate, and subcutaneous edema of the neck and chest.

Scattered fine wet rales and twanging sounds can be heard in the lungs, and there may be a large amount of pleural effusion. Signs are not proportional to the severity of the disease, and there may be signs of lung inflammation and pleural effusion on X-ray or CT.

The patient’s condition is mostly critical, often complicated by sepsis and infectious shock, but also secondary to meningitis, manifested by severe headache, vomiting, convulsions, coma, with obvious meningeal irritation. Bacillus anthracis can be detected in the bloody cerebrospinal fluid.

Questions you may be concerned about

What does pulmonary anthrax mean

Pulmonary anthrax is a clinical type of anthrax, an acute pulmonary infection caused by Bacillus anthracis, which can be contracted through the respiratory tract.

The pathology of pulmonary anthrax is characterized by hemorrhagic lobular pneumonia with enlarged bronchial and mediastinal lymph nodes. The disease has an acute onset, with nonspecific flu-like manifestations such as low-grade fever and fatigue most often occurring 2 to 5 days after exposure.

After 2 to 3 days, the symptoms worsen, with mild cases showing chest tightness, chest pain, fever, cough, and hemoptysis with bloody mucus sputum. In severe cases, chills, high fever and severe respiratory distress occur.

Most patients with pulmonary anthrax are in critical condition, often complicated by sepsis and infectious shock, etc., with high mortality rate. Patients should go to specialized infectious disease hospitals as early as possible for timely treatment and proper isolation.

What is the incubation period of pulmonary anthrax?

The incubation period of pulmonary anthrax refers to the period from the entry of Bacillus anthracis cells into the lungs through the respiratory tract to the earliest appearance of clinical symptoms in patients.

Generally, the incubation period of pulmonary anthrax is about one to five days, followed by low-grade fever, chest tightness and other symptoms.

Pulmonary anthrax is highly contagious, and the onset of the disease is very sudden and urgent, and the probability of death is relatively high. Symptoms such as respiratory distress or coughing up blood may occur, and a small percentage of people may get anthrax meningitis.

Pneumoconiosis can be contracted through direct contact with diseased livestock or by eating meat or products made from diseased livestock, so it is important to take precautions, especially for those at high risk.

Causes

Anthrax is caused by infection with Bacillus anthracis, and there are three basic conditions that lead to epidemics.

1. Source of infection

The main source of infection is animals suffering from anthrax, mostly herbivores such as cattle, horses, sheep, camels, donkeys, mules, etc., followed by pigs and dogs.

Patients with pulmonary anthrax are contagious and can cause the disease to spread.

2. Transmission routes

Respiratory transmission: inhalation of dust and droplets with Bacillus anthracis spores can cause pulmonary anthrax.

Other ways: blood-sucking insects biting anthrax-affected animals and then biting people can occasionally cause anthrax, but it is very rare.

3. Susceptible people

People are generally susceptible.

It is common in herders, farmers, workers in slaughterhouses, meat and fur processing plants, veterinarians and laboratory personnel.

Symptoms

Sharp onset, chills, high fever, cough, chest pain, shortness of breath, cyanosis, coughing mucus and blood sputum, generally conscious. In severe cases, cyanosis, drop in blood pressure, thin pulse, and shock. Respiratory failure, loss of consciousness and death follow rapidly.

1. Cutaneous anthrax

It is the most common, accounting for about 95% of anthrax cases. It is divided into anthrax carbuncle and malignant edema. Anthrax carbuncle: mostly seen in face, neck, shoulder, hands and feet and other exposed parts of the skin, the initial papule or patchy rash, gradually forming blisters, ulcers, and eventually forming a black coal-like dry scab, with granulation tissue under the scab, surrounded by non-sunken oedema, firmness, unremarkable pain, and ulceration without pus as its characteristics. Fever, headache, and localized lymph node enlargement appear 1 to 2 days after the onset of the disease.

Malignant edema: the involved parts are mostly lax eyelids, neck, thighs and other parts, without black scab formation but large edema, spreading rapidly, which can lead to large necrosis. Local numbness and mild swelling and pain, systemic toxic symptoms are obvious, if the treatment is not timely, can cause sepsis, pneumonia and meningitis and other complications. In the absence of antibiotics, the mortality rate of cutaneous anthrax is 20%-30%.

2. Pulmonary anthrax

It is caused by inhalation of Bacillus anthracis spores and mostly occurs in fur processors. Initial cold symptoms, then develop into severe bronchopneumonia and systemic symptoms of poisoning, die of toxic shock within 2-3 days.

3. Intestinal anthrax

It is caused by eating uncooked meat products of diseased animals, such as beef and mutton skewers. There is continuous vomiting, blood in the stool and intestinal paralysis, and death from toxemia in 2~3 days.

Pulmonary anthrax and intestinal anthrax may develop into sepsis, often causing acute hemorrhagic meningitis and death.

Examination

1. Laboratory examination

(1) Peripheral blood picture: the number of white blood cells increases, (10~25)×109/L. It can even be as high as (60~80)×109/L. Neutrophils increase significantly, platelets may decrease, and there may be leukemia-like reaction.

(2) Pathologic examination

(1) Bacterial smear and culture According to the clinical manifestations, secretion, sputum, stool, blood and cerebrospinal fluid can be taken for direct smear staining and microscopic examination, which can see coarse gram-positive bacilli; culture can show the growth of Bacillus anthracis.

(2) Animal inoculation Inoculate the above specimens into rabbits, guinea pigs and mice subcutaneously, after 24 hours, there are typical local swelling, bleeding and other positive reactions. Most of the inoculated animals die within 48 hours, and B. anthracis can be detected and cultured in their blood and tissues.

(3) Serum immunological examination There are indirect hemagglutination test, complement binding test, immunofluorescence method and ELISA method to detect anti-podocarpine antibodies in blood. Anthrax patients start to produce this antibody 3 days after the onset of the disease, and most of them are positive after 1 week. In the recovery period, the serum antibody increases more than 4 times compared with the acute period, which is positive.EⅡSA, immunofluorescence method has higher sensitivity and specificity, and the positive rate reaches 80%~100%.Ascoli precipitation test is mainly used to test whether the animal’s hair and organs are contaminated with germs or not.

4) Anthrax skin test Subcutaneous injection with chemical extracts of attenuated strains, 2~3 days after symptoms appear, 82% of patients show positive results, and 99% after 4 weeks.

2. Other auxiliary examinations

X-ray or CT examination may show signs of lung inflammation and pleural effusion.

Diagnosis

Diagnosis is generally not difficult based on the life history of exposure to diseased animals and products, occupational history and typical clinical manifestations. Confirmation of the diagnosis depends on the detection of the pathogen and serologic examination. Symptoms of toxicity in pulmonary anthrax are much more severe than in lobar pneumonia, and X-rays help to differentiate. Diagnostic criteria:

1. History of exposure

History of close contact with diseased animals or their hides.

2. Clinical manifestations

Scorched ulcers in cutaneous anthrax, hemorrhagic pneumonia in pulmonary anthrax, hemorrhagic enteritis in intestinal anthrax, and severe systemic toxemia with hemorrhagic tendency in sepsis.

3. Confirmation of diagnosis requires bacterial smear staining examination, bacterial culture and animal inoculation.

Differential diagnosis

Cutaneous anthrax should be differentiated from carbuncle, cellulitis, dengue, scrub typhus, rabbit fever, etc. Pulmonary anthrax should be differentiated from lobar pneumonia, pneumonic plague, leptospirosis, etc. Intestinal anthrax should be differentiated from Salmonella enterocolitis, hemorrhagic necrotizing enterocolitis, and other acute peritonitis, etc. Sepsis should be differentiated from sepsis caused by other bacteria.

Treatment

1. General treatment

Bed rest and isolation of patients, attention to drink more water. Penicillin is the most effective antibiotic. Sulfa drugs are also often effective.

2.Pathogen treatment

Penicillin G is the drug of choice and no resistance has been found. For pulmonary anthrax and concomitant meningitis sepsis, penicillin is incrementally administered intravenously, and streptomycin is added as a daily divided intramuscular injection, or amikacin for more than 2 weeks. Lung anthrax treatment drugs: hormone, effective in controlling the development of local edema and reducing toxemia, hydrocortisone or dexamethasone can be used intravenously, such as edema leading to airway obstruction must be used to keep the airway open measures.

3.Symptomatic treatment

Intravenous rehydration and volume expansion. If the bleeding is serious, appropriate amount of blood transfusion should be given. If there is circulatory failure, anti-shock treatment should be given and adrenocorticotropic hormone should be applied.