Nocardia

Definitions & Key takeaways

Nocardia is a gram-positive rod, filamentous, branching bacteria commonly found in soil. It is known to cause nocardiosis, a nocardia infection that can affect different parts of the body, including the skin, respiratory tract, and central nervous system

Nocardia infections are more common in people with weakened immune systems, such as those who have HIV/AIDS, organ transplants, or certain types of cancer. People with conditions that cause a deficiency in their immune system, such as diabetes, are also at an increased risk for Nocardia infections.

Symptoms vary depending on the location of the infection but commonly include fever, cough, chest pain, difficulty breathing, redness, swelling, and pain at the site of the infection. Nocardiosis of the central nervous system can cause symptoms such as headache, fever, seizures, and changes in mental function.

Diagnosis is done by identifying bacteria in a smear or a culture from respiratory secretions, skin biopsy samples, aspirates from abscesses or CSF and blood in case of disseminated disease and treatment is with antibiotics, preferably trimethoprim-sulfamethoxazole.

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Nocardia is a genus of Gram-positive branching filamentous rods that are often found in soil. There are over 80 species of Nocardia and around 30 of them causes disease in humans, and the most notable ones are Nocardia asteroides, Nocardia brasiliensis, Nocardia cyriacigeorgica, Nocardia farcinica and Nocardia nova.
Nocardia causes a disease called nocardiosis which has three major forms - pulmonary, cutaneous and disseminated.OK, Nocardia is a rod-shaped Gram-positive bacteria, we’ve got that part down, and this means it goes purple when Gram-stained.
When there’s many of them, they arrange themselves in the shape of purple branching filaments. They are obligate aerobes, meaning they need oxygen to grow, they are also non-motile, and don’t form spores.
But wait… that sounds exactly like Actinomyces israelii, another group of rod shaped, gram-positive, filamentous bacteria with a lot of other similar features.
To distinguish them, an acid-fast stain, also called Ziehl-Neelsen stain is done. With this test, a red dye called carbon fuchsin, binds to lipids in the cell wall, coloring them red.
Then alcohol is applied to wash out any dye that hasn’t colored bacteria, and a second dye, methylene blue, is applied. Now, Nocardia is a weak acid-fast bacteria which means that a less concentrated solution of alcohol is needed during staining and that’s because the mycolic acids in its cell wall have intermediate-length.
So, because it has plenty of lipids in its cell wall, it retains the carbon fuchsin, and it looks red under the microscope, making it an acid-fast bacteria.
On the other hand, in bacteria who don’t have a lot of lipids in their cell wall, like A. Israelii, all the red dye is washed off by alcohol, so it looks blue under the microscope, making it a non-acid-fast bacteria.
Also, Nocardia can be visualized with auramine-rhodamine stain using fluorescence microscopy, which can show a reddish-yellow fluorescence.
This stain is not as specific as Ziehl-Neelsen stain, so it has more false-positive results, but it’s more sensitive, so it has less false-negative results, and it’s also inexpensive.
So the auramine-rhodamine stain is often used for screening.Another difference is that Nocardia is catalase positive, so it makes an enzyme called catalase which converts hydrogen peroxide to water and oxygen, and also urease positive which means that it produces an enzyme called urease that can break urea into ammonia and carbon dioxide, whereas A.
israelii is catalase and urease negative.Finally, Nocardia species grows on routine media, like blood agar or chocolate agar, on selective media, such as modified Thayer-Martin agar or BCYE agar, on mycobacterial media, like Lowenstein Jensen agar and on fungi media, like Sabouraud dextrose agar.
Nocardia forms white, yellow or orange long branching filamentous colonies with a powdered aspect, which usually takes 3 to 5 days to grow, but sometimes it may take as long as 2 to 3 weeks.
Now, Nocardia has a low virulence and therefore nocardiosis occurs more often as an opportunistic infection in immunocompromised people.
It enters the body through inhalation or skin trauma and once inside, it’s ingested by macrophages. Inside macrophages, it gets wrapped in a vesicle called a phagosome, which normally merges with lysosomes, to form a phagolysosome inside which bacteria are killed by lysosomal enzymes.
However, the cell wall of Nocardia contains a cord factor, or trehalose dimycolate, which is a glycolipid that inhibits phagolysosomal fusion.
Ok, now, another immune system weapon is that neutrophils and macrophages destroy invading bacteria by generating a bunch of toxic oxygen radicals, such as superoxide, which results from oxidative metabolic burst.
But, Nocardia makes two enzymes that break these toxic oxygen radicals. First, there’s superoxide dismutase which breaks superoxide radicals into oxygen and hydrogen peroxide.
And since hydrogen peroxide is still harmful, Nocardia also makes catalase, which breaks hydrogen peroxide into water. Now, in pulmonary nocardiosis, the presence of Nocardia triggers an inflammatory response that calls more macrophages to the site of battle.
As more of them make their way there, they surround the bacteria from all sides, and form a granuloma, which prevents it from spreading.
In the center of the granuloma, there’s caseous necrosis, which literally means cheese-like necrosis, because the tissue in the center dies off, and it’s soft, white and looks a bit like cheese.
Ok, now, pulmonary nocardiosis is the most common type of nocardiosis and it’s usually caused when a species called Nocardia asteroides enters the body through inhalation.
Pulmonary nocardiosis can be seen in immunocompromised people, such as those with HIV infection, malignancy, chronic granulomatous disease, which are associated with low numbers of granulocytes, or in people with underlying lung disease, such as chronic obstructive pulmonary disease, cystic fibrosis or bronchiectasis.
Pulmonary nocardiosis can progress to pneumonia with cavitary lesions, pleural effusion, or fluid in the pleural cavity, and empyema, when there’s pus in the pleural cavity.
Disseminated nocardiosis is usually a complication of pulmonary nocardiosis, and the bacteria most often spreads to the central nervous system causing meningitis or brain abscesses, or to the heart causing endocarditisCutaneous nocardiosis, on the other hand, is caused by Nocardia brasiliensis, and usually affects immunocompetent people after the bacteria enters the body through skin lesions.
Cutaneous nocardiosis has three clinical types: superficial skin infection, which can progress to cellulitis, or inflammation of the subcutaneous tissue, and skin abscesses; deep skin infections, specifically mycetomas, which are chronic, and progressively destructive infections that affect the skin, subcutaneous tissues, muscles and may even reach the bone; and finally, there’s lymphocutaneous infection, when the bacteria spreads to lymphatic vessels and may form lymphatic abscesses.
When regional lymph nodes are affected, lymphocutaneous nocardiosis is called sporotrichoid nocardiosis because of its resemblance with a fungal disease caused by Sporothrix schenckii.
Now, symptoms depend on the type of disease. So, with pulmonary nocardiosis, there’s fever, cough with sputum production, shortness of breath and hemoptysis, or blood in the sputum, if there are cavities in the lungs.
With disseminated disease, there can be symptoms of meningitis and brain abscesses, like fever, headache, a stiff neck, and altered mental status, or endocarditis, like fever and new heart murmurs.
Finally, skin infections. With cellulitis, there’s erythema, or redness, tenderness and purulent drainage and with abscesses, there may be local redness, heat, swelling and pain.
With lymphocutaneous infections, lesions progress along the path of dermal and subcutaneous lymphatics, and with mycetomas, there’s swelling, deformation of the affected area and multiple drainage orifices that ooze pus.
That sure doesn’t sound like fun… Diagnosis is done by identifying Nocardia in a smear or a culture from respiratory secretions, skin biopsy samples, aspirates from abscesses or CSF and blood in case of disseminated disease.
When pulmonary nocardiosis is suspected, A PPD test should be done to rule out tuberculosis, since the symptoms are quite similar.
A chest X-ray can be done, which shows irregular nodules, cavities, pulmonary infiltrates, lung abscess formation or pleural effusions.
Also, a brain MRI can be done to diagnose brain abscesses, and an echocardiogram can show bacterial vegetations on the heart to confirm endocarditis.
Treatment of Nocardia infections is done with sulfonamides, and the drug of choice is usually trimethoprim-sulfamethoxazole.
Alternatives include imipenem, amikacin, and linezolid, which are usually given in severe cases.##SummaryAlright, as a quick recap.
Nocardia is a Gram-positive, branching, filamentous, rod bacteria that is often found in soil. It’s a non-motile, non-spore forming, obligate aerobe, catalase and urease positive, weak acid-fast bacillus that can be visualized with Ziehl-Neelsen and auramine-rhodamine stain and it can grow on multiple medias into white, yellow or orange filamentous colonies with a powdery appearance.
It has few virulence factors such as cord factor, catalase and superoxide dismutase and uses them to avoid immune system.
It causes a disease called nocardiosis which has three forms - cutaneous, pulmonary and disseminated. Diagnosis is done by identifying bacteria in a smear or a culture from respiratory secretions, skin biopsy samples, aspirates from abscesses or CSF and blood in case of disseminated disease and treatment is done using trimethoprim-sulfamethoxazole as the first drug of choice.
from respiratory secretions Skin biopsy samples aspirates from abscesses or and blood in case of disseminated disease And treatment is done using trimethoprim sulfa mezo as the first drug