Infectious Myositis: Infectious myositis is an uncommon acute, or chronic infection of skeletal muscle.

Most often seen in young adults.

The most common infectious agent is the bacterium, Staphylococcus aureus (77-90% of Myositis cases)(prevalent in tropical countries).

Viruses, other bacteria (including Mycobacteria), fungi, and parasites can cause myositis.

It consists of a primary abscess, edema, and hypoechoic inflammatory Mass.

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Viral etiologies typically cause diffuse myositis, whereas

bacteria and fungi usually lead to a local myositis which may

be associated with sites compromised by trauma or surgery

and are more common among immuno-compromised

patients.

Localized collections within the muscles are referred to as

pyomyositis.

Other pyogenic causes of myositis include gas gangrene,

group A Streptococcal myonecrosis, and other types of non-

Clostridial myonecrosis.

Bacterial pyomyositis: Pyomyositis consists of a primary muscle abscess and is prevalent in tropical countries.It is associated mainly with immunocompromised patients, and intravenous drug abusers who traumatically contaminate their muscles with foreign material.

The clinical presentation is often nonspecific with muscle aches and a deep induration. This may at first suggest an intramuscular neoplasm. The causative agent is Staphylococcus aureus in over 90% of cases.

Streptococcus Myonecrosis: -Streptococcal myositis is a rare, often fatal, acute infection of the muscle, caused by an invasive group A beta-haemolytic Streptococcus. -It is characterized by muscle necrosis without abscess formation, and, in contrast to necrotizing fasciitis, does not primarily affect the subcutaneous tissue or skin.-It is a predisposing factor or septic shock. -Management:- high-dose intravenous antibiotics. - intensive fluid and nutritional support. Streptococcal toxic shock syndrome.

Clostridium Myonecrosis: (Gas gangrene): Clostridial Myonecrosis is a bacterial infection that produces gas (tissues) in gangrene (necrotic damage of tissue specifically muscles). It is a deadly form of gangrene usually caused byClostridium perfringens bacteria.

This bacterium causes Myonecrosis via specific exotoxins . -In general, different clostridium species are opportunistic and enter the body via significant skin breakage.

The exotoxin is commonly found in C. perfringens type A strain and is known as alpha toxin.

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The alpha toxin is a phospholipase requiring zinc for

activation.

First, The C-terminal domain binds calcium and allows the

toxin to bind to the phospholipid head-groups on the cell

surface.

The N-terminal domain has phospholipase activity.

This property allows hydrolysis of phospholipids such as

phosphatidyl choline to diacylglycerol.

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The end result includes activation of arachidonic

acid pathway and production of thromboxane A2

(vasoconstrictor), production of IL-8, platelet-

activating factor, and several intercellular adhesion

molecules. These actions combine to cause edema

due to increased vascular permeability.

Clinical presentation of Clostridium perfringens infection : a

Tetanus ( lockjaw disease):

It is a medical condition characterized by a prolonged

contraction of skeletal muscle fibers.

The primary symptoms are caused by tetanospasmin (A-

light chain, B-heavy chain), a neurotoxin produced by the

Clostridium tetani.

Infection occurs through wound contamination and often

involves a cut or deep puncture wound.

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- As the infection progresses, muscle spasms develop in the jaw and elsewhere in the body.- Mortality rates reported vary from 48% to 73%. - In recent years, approximately 11% of reported tetanus cases have been fatal.

Pathophysiology: - Tetanus begins when endospores of Clostridium tetani enter damaged tissue. - The spores transform into rod-shaped bacteria and produce the neurotoxin tetanospasmin. - This toxin is inactive inside the bacteria.

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When the toxin is released , it will be activated by

proteases.

Active tetanospasmin enters at neuromuscular junctions of

motor neurons, B-chain (heavy) binds to neuronal

membrane sphingolipid.

The light- A chain carried by axonal transport of

peripheral nerve terminals to cell bodies in the spinal cord

and brain stem where it binds to receptors at these sites.

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-The A-chain, a zinc endopeptidase, attacks the vesicle-associated membrane protein ( synaptobrevin ) of central nervous system neurons.

-The action of the A-chain stops the affected neurons (inhibitory synapses) from releasing the inhibitory neurotransmitters GABA (gamma-aminobutyric acid) and glycine. -Consequence dangerous overactivity in the muscles from the smallest stimulus.

Clostridium tetani also produces an oxygen-labile hemolysin called tetanolysin that destroy the muscle protein.

Forms of tetanus:

Generalized tetanus :

It is the most common type of tetanus, representing about

80% of cases.

The generalized form usually presents with a descending

pattern. The first sign is lockjaw, and the facial spasms

called risus sardonicus ( Sardonic smile), followed by

stiffness of the neck, difficulty in swallowing, and rigidity

of pectoral and calf muscles.

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Other symptoms include elevated temperature, sweating,

elevated blood pressure, and cardiac arrhythmias.

Other forms: Neonatal , localized and cephalic tetanus.

Clinical presentation of Clostridium tetani:

Muscle spasms in a patient suffering from tetanus. Neonatal Tetanus. Painting by Sir Charles Bell, 1809.

Facial spasms called Risus Sardonicus- First Symptom of Generalized Tetanus.

Laboratory diagnosis :Clinical specimens: Pus swab, exudate (thioglycolate media).

C. perfringens: Beta surrounded Beta hemolytic filamentous by Alpha hemolysis. C. tetani.

Parasitic Myositis:

Trypanosoma cruzi : Transmission : when the Winged bug  of the genus Triatoma deposits feces on the skin surface and subsequently bites; the human host. Late ( chronic) stage infection: affects the nervous system, digestive system and cardiac muscle. The protozoa will infect Skeletal muscleby its Amastigote stage.

Amastigote stage in skeletal muscle.

Trichinella spiralis : It is a nematode parasite, occurring in rats, pigs, and humans, and is responsible for the disease trichinosis.Humans typically become infected when they eat improperly cooked pork (Trichinella infected) meat.Female Trichinella worms stay for about six weeks, in small intestine, and in that time can produce up to 1,500 larvae. Larvae will migrate with blood to striated muscles causing myositis. The muscles invaded mainly are: pectoral muscles, tongue, and the gastrocnemius.

Cysticercosis:

Cysticercosis involves infection of individuals with the larval stage of Taenia solium, the cysticerci, which normally infects pigs. Autoinfection may occur due to fecal-oral transmission. The oncosphere ( hexacantho-embryo) penetrates the intestinal wall and migrates in the circulation to the tissue ( skeletal muscles).

Rabies: Virology: The rabies virus is the type species of the Lyssavirus genus, in the family Rhabdoviridae.Lyssaviruses have helical symmetry, with a length of about 180 nm and a cross-sectional diameter of about 75 nm. These viruses are enveloped and have a single-stranded RNA genome

Electron microscopy Show the helical Enveloped single strandedRNA virus.

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Rabies is a viral disease that causes acute encephalitis

(inflammation of the brain) in warm-blooded animals.

The virus is usually present in the nerves and saliva of

a symptomatic rabid animal. The route of infection

usually, but not always, is the animal bite.

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The infection is initiated by inoculation of virus into

skeletal muscles, virus will be replicated in muscle and

transferred to peripheral nervous system.

The rabies virus travels to the brain by following the

peripheral nerves.

Rabies kills around 55,000 people a year, mostly in Asia

and Africa (2010).

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Osteomyelitis:

Osteomyelitis is the infection of the bone or bone marrow. It can

be classified on the basis of the causative organism (pyogenic

bacteria or mycobacteria), the route, duration and anatomic

location of the infection.Pathogenesis:

Microorganisms may infect bone through one or more of three

basic methods: via the bloodstream, from local areas of infection

(as in cellulitis), penetrating trauma, joint replacements or

internal fixation of fractures or root-canaled teeth.

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Once the bone is infected, leukocytes enter the infected

area, and engulf the infectious organisms, release

enzymes that are associated with bone lyses.

Pus spreads into the bone's blood vessels, impairing their

flow, and cause necrotic dead area of the bone called

sequestra , form the basis of a chronic infection.

Often, the body will try to create new bone around the

area of necrosis. The resulting new bone is often called an

involucrum .

Causes of Osteomyelitis: a

Most common organisms Age group:

S. aureus, Enterobacter species, and group A and B Streptococcus species

Newborns (younger than 4 mo)

S. aureus, group A Streptococcus species, Haemophilus influenzae, and Enterobacter species

Children (aged 4 mo to 4 y)

S. aureus and occasionally Enterobacter or Streptococcus species

Adult

Staphylococci (50%), and Tuberculosis (50%).

Vertebral osteomyelitis

Osteomyelitis : clinical picture:a

Septic arthritis:

Septic arthritis is the invasion of a joint by an infectious

agent which produces arthritis.

People with artificial joints are more at risk than others. Septic

arthritis is considered a medical emergency.

If untreated, it may destroy the joint

in a period of days. The infection

may also spread to other parts

of the body.

Prevalence, and pathogenesis:

The incidence of septic arthritis has been estimated at 2 to 10 cases per 100,000 in the general population, and as high as 30 to 70 cases per 100,000 in patients with rheumatoid arthritis.

Pathogenesis:-Routes of Entry: 1- Dissemination of pathogens via the blood. hematogenous2- From contaminated needle.3- Dissemination from soft tissue infection, entry via penetrating trauma.

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-Primary infection: -The Synovial A cell (APC) engulfs the microbe. - Production of TNF, IL-8, and PLAF. - Chemotaxis, cellular infiltration, and edematous edema. - Toxic free radicals production. - Proteoglycan and collagen destruction, cartilage destruction. - Direct pressure necrosis, more cartilage destruction. - Specific T-cell response, and Polyclonal B cell activation. Secondary: Osteomyelitis.

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Bacteria that are commonly found to cause septic arthritis are:1-Staphylococcus aureus - the most common cause in adults; (40-50% of cases).

Others: 10-20%: 2-Streptococci - the second most common cause 3-Haemophilus influenzae - was the most common cause in children but is now uncommon in areas where Haemophilus vaccination is applied.4-Neisseria gonorrhoea - in young adults5-Escherichia coli - in the elderly, IV drug users and the seriously ill.

Signs and Symptoms of Septic arthritis:

Patients with septic arthritis usually present with :1-Joint pain. 2-Redness over the joint. 3-Joint inflammation and swelling. 4-Synovial fluid accumulation.

Synovial fluid analysis: 1- Physical examination: The normal appearance of a sample of synovial fluid is usually: A-Straw colored. B-Clear. C-Moderately Viscous.

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Changes in the physical characteristics may provide clues

to the disease present such as:

A-Less viscous fluid may be seen with inflammation.

B-Cloudy synovial fluid may indicate the presence of

microbes, white blood cells, or crystals.

C-Reddish synovial fluid may indicate the presence of

blood.

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2-Chemical examination:A-Glucose: typically lower than blood glucose levels. -Could be significantly decreased with joint inflammation and infection.

B-Protein: increased with bacterial infection.

C- Lactate dehydrogenase: -increased LD (LDH) level may be seen in rheumatoid arthritis, infectious arthritis.

D-Uric acid—increased with gout.

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3-Microscopic examination :

Normal synovial fluid has small numbers of white blood

cells (WBCs) and red blood cells (RBCs) but no

microorganisms or crystals present.

Specimens should be concentrated by centrifugation for:

A-Total WBCs count: could be elevated.

B-Differential count:

Neutrophils increased with bacterial infection.

Eosinophils elevated in Lyme disease.

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C-Gram’s stain: for detection of Gram-positive and negative bacteria.D-AFB (Z.N stain) smear: for Mycobacterium tuberculosis.

4-Culture and sensitivity test:

specimens should be cultured on blood and chocolate

agar and incubated at aerobic and anaerobic (10%CO2)

conditions respectively.

Neisseria and Haemophilus species grow only on

chocolate agar.