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Mycobacterium leprae

Leprosy is also known as Hansen’s disease, after the scientist who discovered M. leprae in 1873.

Taxonomy
Family: Mycobacteriaceae

History
Leprosy has been around since ancient times, often surrounded by terrifying, negative stigmas and tales of leprosy patients being shunned as outcasts.

Outbreaks of leprosy have affected, and panicked, people on every continent.

The oldest civilizations of China and Egypt, and India feared leprosy was an incurable, mutilating, and contagious disease.

Natural habitats
This bacteria is believed to live in the soil.

Scientists think that the reservoir for this bacteria is the new world armadillos and African primates.

At the beginning the idea that the habitat of this bacteria was in soil was just an hypothesis but some research were done and DNA of the M. leprae was found in soil close to where people were infected with leprosy.

Its ideal temperature is about 30-33oC

Clinical significance
Leprosy
Is an infectious disease that causes severe, disfiguring skin sores and nerve damage in the arms and legs.

Leprosy is actually not that contagious.

You can catch it only if you come into close and repeated contact with nose and mouth droplets from someone with untreated leprosy.

Children are more likely to get leprosy than adults.

Symptoms
Leprosy primarily affects the skin and the nerves outside the brain and spinal cord, called the peripheral nerves.

It may also strike the eyes and the thin tissue lining the inside of the nose.

The main symptom of leprosy is disfiguring skin sores, lumps, or bumps that do not go away after several weeks or months.
The skin sores are pale-colored.

It usually takes about 3 to 5 years for symptoms to appear after coming into contact with the leprosy-causing bacteria. Some people do not develop symptoms until 20 years later.

There are three forms of the disease, with lepromatous being the most severe, tuberculoid, and borderline leprosy.
The precise mode of transmission is not fully understood.

The bacteria are likely spread by direct contact and through air dispersement, from coughing or sneezing.

Manifestations
Infected individuals will notice skin lesions in early stages, leader to paralysis or loss of sensation in those areas, and eventually loss of extremities.
Blindness can occur as the disease advances.

Mycobacterium fortuitum (Mycobacteroides fortuitum)

M. fortuitum belongs to the family of nontuberculous mycobacteria (NTM) classified in the rapidly growing mycobacteria (RGM)

Taxonomy
Family: Mycobacteriaceae
Genus: Mycobacteroides fortuitum
Formely: Mycobacterium fortuitum

M. fortuitum group
M. fortuitum
M. bonickei, M. houstonense, M. mageritense, M. mucogenicum, M. peregrinum, M. senegalense, M. septicum

Natural habitats / RGM
They are generally considered to be environmental saprophytes which are widely distributed in nature; they have been isolated from soil, dust, natural surface and municipal water, wild and domestic animals, and fish

Contaminated ice machines are a relatively important hospital reservoir for the RGM, especially M. fortuitum

Clinical significance
The most frequently recognized clinical diseases.
Localized post-traumatic wound infections. Surgical wound infections, especially following augmentation mammoplasty, cardiac surgery and catheter infections.

Localized infection in sporadic community-acquired disease usually occurs after a traumatic injury followed by potential soil or water contamination. Such injuries as stepping on a nail, motor vehicle accidents, compound fractures, etc., are typical of the clinical histories seen in patients with RGM disease.

Disseminated infections with M. fortuitum are rare.

The first case report appeared in 1990, when Sack described a patient with a history of intravenous IV drug abuse and AIDS, who had cutaneous lesions from which M. fortuitum was isolated. Cultures of specimens from lymph nodes, urine, pleural effusions, and feces all yielded M. fortuitum.

Mycobacterium chelonae (Mycobacteroides chelonae)

M. chelonae belongs to the family of nontuberculous mycobacteria (NTM) classified in the rapidly growing mycobacteria (RGM)

Taxonomy
Family: Mycobacteriaceae
Genus: Mycobacteroides chelonae
Formely: Mycobacterium chelonae

M. chelonae is further grouped in the M. chelonae-abscessus group
M. chelonae
M. abscessus
M. immunogenum

Natural habitats / RGM
They are generally considered to be environmental saprophytes which are widely distributed in nature; they have been isolated from soil, dust, natural surface and municipal water, wild and domestic animals, and fish.

They resist the activity of disinfectants and biocides such as organomercurials, chlorine, and alkaline glutaraldehyde

Clinical significance
The most frequently recognized clinical diseases.
M. chelonae in normal hosts, localized post-traumatic wound infections and post-traumatic or post-surgical corneal infections and catheter infections
M. chelonae in immunosuppressed persons.

Disseminated skin infections in patients receiving corticosteroids and in organ transplant recipients and catheter infections.

M. abscessus in normal hosts, chronic lung infections, localized post-traumatic wound infections and surgical wound infections and chronic otitis media.

M. abscessus in immunosuppressed persons.
Disseminated skin infections in patients receiving corticosteroids and in organ transplant recipients

Localized infection in sporadic community-acquired disease usually occurs after a traumatic injury followed by potential soil or water contamination.
Such injuries as stepping on a nail, motor vehicle accidents, compound fractures, etc., are typical of the clinical histories seen in patients with RGM disease.

Pulmonary disease with M .chelonae is uncommon, and other atypical mycobacteria such as M. avium complex, M. kansasii, and M. abscessus are the more likely lung pathogens.
Confirmation of the presence or absence of mycobacteria in clinical specimens has traditionally required culture, because of the relative insensitivity of direct microscopy.

In general, clinical specimens that are normally sterile, such as blood, cerebrospinal fluid, or serous fluids, can be inoculated directly onto media.

In comparison, nonsterile specimens, such as sputum or pus, must be chemically decontaminated first in order to eliminate common bacteria and fungi that would overwhelm the culture.

However, decontamination procedures may inhibit the growth of mycobacteria, especially NTM, as well.

Corynebacterium diphtheriae

Diphtheriae is an acute, toxin-mediated disease caused by the bacterium C. diphtheria.

The name of the disease is derived from the Greek diphtheria, meaning ”leather hide”, because of the leathery layer that grows on the tonsils, throat, and nasal passage.

Taxonomy
Family: Corynebacteriaceae
- C. diphtheria biotype gravis
- C. diphtheria biotype mitis
- C. diphtheria biotype belfanti
- C. diphtheria biotype intermedius (lipophyl)

Natural habitats
Human carriers are the reservoir for C. diphteriae and are usually asymptomatic.

C. diphtheria can be isolated from the nasopharynx as well as from skin lesions, which actually represent a reservoir for the spread of diphtheria.

Transmission
Transmission is most often person-to-person contact or contact with items that have the bacteria on them, such as an infected person’s cup or used tissue.

Rarely, transmission may occur from skin lesions.

Clinical significance
C. diphtheria infects the nasopharynx or skin.

Toxigenic strains secrete a potent exotoxin which cause diphtheria.

Toxin production (toxigenicity) occurs only when the bacteria itself infected (lysogenized) by a specific virus (bacteriophage) carrying the genetic information for the toxin (tox gene). Only toxigenic strains can cause severe disease.

The symptoms of diphtheria include pharyngitis, fever, swelling of the neck or area surrounding the skin lesion.

Diphtheritic lesions are covered by an adherent pseudomembrane. (characteristic)

The toxin is distributed to distant organs by the circulatory system and may paralysis and congestive heart failure.

C. diphtheria may also cause cutaneous diphtheria.

Some people with poor hygienic standards (e.g., drugs or alcohol abusers) are prone to colonization on the skin, (more often than in the pharynx ) by C. diphtheria strains, which are often nontoxigenic.

Diphtheria spread easily, but can be prevented through the use of vaccines.

If left untreated, diphtheria can cause severe damage to kidneys, nervous system, heart and can be fatal.

Mycobacterium tuberculosis

History
M. tuberculosis (MTB) was the cause of the "White Plague" of the 17th and 18th centuries in Europe. During this period nearly 100 percent of the European population was infected with MTB, and 25 percent of all adult deaths were caused by MTB

M. tuberculosis, then known as the "tubercle bacillus", was first described on 24 March 1882 by Robert Koch who subsequently received the Nobel Prize in physiology or medicine for this discovery in 1905; the bacterium is also known as "Koch's bacillus".

Tuberculosis has existed throughout history, but the name has changed frequently over time, consumption, phtisis, white plague

General information
MTB is an obligate aerobe.

For this reason, in the classic case of tuberculosis, are always found in the well-aerated upper lobes of the lungs.

The bacterium is a facultative intracellular parasite, usually of macrophages, and has a slow generation time, 15-20 hours, (a physiological characteristic that may contribute to its virulence), compared to other bacteria, which tend to have division times measured in minutes (Escherichia coli can divide roughly every 20 minutes).

It is a small bacillus that can withstand weak desinfectants and can survive in a dry state for weeks.

Its unusual cell wall, rich in lipids (e.g. mycolic acid), is likely responsible for this resistance and is a key virulence factor

Taxonomy
Family: Mycobacteriaceae

Natural habitats
MTB is the etiologic agent of tuberculosis in humans.

Humans are the only reservoir for the bacterium.

Clinical significance
Tuberculosis (TB) is the leading cause of death in the world from a bacterial infectious disease.

The disease affects 1.8 billion people/year which is equal to one-third of the entire world population.

Tuberculosis (TB)
Tuberculosis is caused by a bacterium called Mycobacterium tuberculosis. The bacteria usually attack the lungs, but TB bacteria can attack any part of the body such as the kidney, spine, and brain.

If not treated properly, TB can be fatal.

TB is spread through the air from one person to another.

The TB bacteria are put into the air when a person with TB of the lungs or throat coughs, sneezes, speaks, or sings. People nearby may breathe in these bacteria and become infected.

TB is NOT spread by
- shaking someone’s hand
- sharing food or drink
- touching bed linens or toilet seats
- sharing toothbrushes
- kissing

Not everyone infected with TB becomes sick.

As a result, two TB-related conditions exist: latent Tuberculosis and Tuberculosis

Latent Tuberculosis Infection
TB bacteria can live in the body without making you sick.
This is called latent TB infection.
In most people who breathe in TB bacteria and become infected, the body is able to fight the bacteria to stop them from growing.
People with latent TB infection do not feel sick and do not have any symptoms.
People with latent TB infection are not infectious and cannot spread TB bacteria to others.
However, if TB bacteria become active in the body and multiply, the person will go from having latent TB infection to being sick with TB disease. source: CDC

Tuberculosis
TB bacteria become active if the immune system can't stop them from growing.

When TB bacteria are active (multiplying in your body), this is called tuberculosis.

People with tuberculosis are sick. They may also be able to spread the bacteria to people they spend time with every day.

Many people who have latent TB infection never develop TB.
Some people develop TB soon after becoming infected (within weeks) before their immune system can fight the TB bacteria.

Other people may get sick years later when their immune system becomes weak for another reason. For people whose immune systems are weak, especially those with HIV infection, the risk of developing TB is much higher than for people with normal immune systems M. tuberculosis contain complex waxes & cord factor they prevent destruction by lysosomes and macrophages source: CDC

Bacillus anthracis

Taxonomy
Family: Bacillaceae

Bacillus cereus group: B. anthracis, B. cereus, B. mycoides, B. thuringiensis

Natural habitats
Soil inhabitant in sporulated form. Anthrax spores in soil can remain infectious for decades.

They are obligate pathogens.

Isolated from blood of animals and human with anthrax, animal carcasses and products and soil contaminated with spores

Clinical significance / ANTHRAX

- cutaneous anthrax
Infection occurs through a break in the skin. Following the incubation period of usually 2 to 3 days, a small papule appears, progressing over the next 24h to a ring of vesicles, with subsequent ulceration and formation of a characteristic blackened eschar.
Subsequent eschar formation may become thick and surrounded by extensive edema.
Fever and pus and pain at the side are normally absent; their presence probably indicate a secondary bacterial infection.

- gastrointestinal anthrax
The symptoms are the result of ulcerations developing primarily in the cecal and terminal ileal mucosae: vomiting, nausea and abdominal pain, accompanied by fever.

This can rapidly progress to bloody diarrhea and systemic infection

- inhalation anthrax / bioterrorism
The inhaled spores are ingested by macrophages and carried from the lungs to the lymphatic system, where the infection progresses.
During transit to lymph nodes, spores germinate into vegetative cells, begin to replicate and produce the capsule and toxins that lead to bacteremia and associated hemorrhage and necrosis.

Anthrax is high on the list of agents that could be used in biological warfare or bioterrorism.

aerobic Gram positive rods