1. Myositis

2. Myositis: inflammation in one or more muscles. Symptoms:
weakness (may be detectable with testing and affects large muscle groups in the neck, shoulders, hips, and back), weakness can lead to falls or make it difficult to get up from a chair.
swelling
pain (myalgia),
dermatomyositis,
polymyositis.
Other symptoms include: Rash, fatigue, thickening of the skin on the hands, difficulty swallowing, difficulty breathing.
Dermatomyositis

3. Diagnosis of Myositis:
Magnetic resonance imaging (MRI scan).
Electromyography (EMG).
Muscle biopsy.
Blood tests: culture and serology.

4. Causes include:
Infection.
Injury.
autoimmune conditions.
drug side effects.
Infectious myositis may consists of abscess, edema, or hypoechoic inflammatory mass.
Localized collection of pus within the muscles are referred to as pyomyositis.

5. Infectious myositis
Infectious myositis is an uncommon acute, or chronic infection of skeletal muscle. Most often seen in young adults.
Pathogens include:
Viral:
HIV (one of the most common causes of myositis)
Coxsackie B virus (epidemic myalgia)*,
Influenza virus.
HTLV-1,
Cytomegalovirus,
Rabies virus.
*Attacks of severe pain in the lower chest, often on one side. Transmitted by fecal oral rout and can cause outbreaks.

6. Spirochetes: Borrelia burgdorferi *.
Bacterial:
S. aureus (77-90% of Myositis cases), Clostridium perfringens (gas gangrene), Streptococcus pyogenes (myonecrosis), Salmonella enteriditis; Neisseria species , Yersinia species.
Spirochetes: Borrelia burgdorferi *.
Mycobacterial: Mycobacterium avium.
Parasitic: Echinococcus granulosus, Taenia solium, T. cruzi, Trichinella spiralis.
Fungal: Cryptococcus neoformans, Candida species, Histoplasma capsulatum, Aspergillus species.
*post-treatment Lyme disease syndrome

7. 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.

8. Bacterial pyomyositis
Primary muscle abscess and is prevalent in tropical countries.
Risk factors: immunodeficiency, and intravenous drug abuse.
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.
Diagnosis: MRI, CT scan, ultra sound, & culture.
Treatment: Guided aspiration and antibiotics.

10. Streptococcus Myonecrosis
Streptococcal myositis is a rare but often fatal, caused by an invasive group A beta hemolytic 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 for septic shock (streptococcal toxic shock syndrome).
Management:
Intravenous antibiotics.
intensive fluid and nutritional support.

11. streptococcal toxic shock syndrome

12. Clostridium Myonecrosis: (Gas gangrene):
Gas gangrene: production of gas in gangrene tissue (necrotic damage of the muscles).
Causative organism: Clostridium perfringens bacteria.
Source of infection: C. Perfringens type A is a gut normal flora of animals and human that can contaminate wounds in bad hygiene conditions from soil and air contaminated by the spores (opportunistic infection).

13. Virulence factors and pathogenesis:
Exotoxins alpha toxin is a zinc activated phospholipase.
First, The C-terminal domain binds calcium and allows the toxin to bind to the phospholipids on the cell membrane.
The N-terminal domain has phospholipase activity
hydrolyze phosphatidyl choline to diacylglycerol leading to cell death.
Activation of arachidonic acid pathway and production of thromboxane A2 (vasoconstrictor).
Production of IL-8, platelet-activating factor cause edema by increased vascular permeability.

15. Dry gangrene caused by poor blood supply (no infection)

16. 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.
C. tetani spores are found in the gut of human and animals and the soil.
Mortality rates vary from 48% to 73% and in recent years, approximately 11%.

17. Endospores of Clostridium tetani enter damaged tissues.
Pathophysiology:
Endospores of Clostridium tetani enter damaged tissues.
The spores transform into rod-shaped bacteria and produce an oxygen-labile hemolysin called tetanolysin that destroy the muscle protein.
the Clostridium tetani also produce a neurotoxin tetanospasmin.
This toxin is inactive when released, it will be activated by proteases.
B-chain of tetanospasmin binds to neuronal membrane sphingolipid at the neuromuscular junction.

18. 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.
The action of the A-chain stops the release of inhibitory neurotransmitters glycine and GABA (gamma-aminobutyric acid).
This results in dangerous over activity in the muscles from the minor stimulus.
As the infection progresses, muscle spasms develop in the jaw and then elsewhere in the body. a

19. The muscle

20. Clinical forms of tetanus:
- Generalized tetanus : The most common type of tetanus (80% of cases).
The generalized form usually presents with a descending pattern. The first sign is lockjaw, and facial spasms called risus sardonicus (sardonic smile), followed by stiffness of the neck, difficulty in swallowing, and then pectoral and calf muscles.
Other symptoms include elevated temperature, sweating, elevated blood pressure, and cardiac arrhythmias.
- Other forms: Neonatal , localized* and cephalic tetanus**.
*in people with partial immunity and is usually mild, progression to generalized tetanus can occur.
**associated with lesions of the head or face and with ear infections. Unlike generalized and localized tetanus, results in flaccid cranial nerve palsies.

21. Clinical presentation of Clostridium tetani:
Muscle spasms in a patient suffering from tetanus Neonatal Tetanus.
Painting by Sir Charles Bell, 1809.
risus sardonicus

22. Laboratory diagnosis:
Clinical specimens: Pus swab, exudate (thioglycolate media).
C. perfringens: Beta surrounded Beta hemolytic filamentous
by Alpha hemolysis C. tetani.

23. Rabies
Virology:
family Rhabdoviridae Genus: Lyssavirus.
Lyssaviruses have helical symmetry, enveloped and have a Ss RNA genome.
Rabies is a viral disease that causes acute encephalitis (inflammation of the brain) in warm-blooded animals.
Rabies kills around 55,000 people a year, mostly in Asia and Africa (2010).

24. Pathogenesis:
Rout of transmission: usually, but not always, is the animal bite (the virus is present in the nerves and saliva of symptomatic rabid animals).
The infection is initiated by inoculation* of virus into skeletal muscles, virus will replicate in the muscle and transferred the to peripheral nerves.
The rabies virus travels to the spinal cord and the brain by following the peripheral nerves. And then descend (eyes, salivary glands, kidneys…...).
Symptoms start with difficulty in swallowing and hydrophobia and proceed to coma and death (mortality rate ≈ 100%) N
* Incubation period can last up to 12 months depending on the inoculum and the site of bite.

25. a a

26. Parasitic Myositis: Protozoa: Trypanosoma cruzi. Helminths:
Trichinella spiralis (nematode)
Taenia solium (flat worm, cestodes).

27. Trypanosoma cruzi :
Transmission : By 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 and skeletal muscle by the amastigote stage.

28. Trichinella spiralis :
It is a nematode of rats, pigs, and humans.
Transmission: Eat undercooked pork infected meat.
Female Trichinella worms stay about six weeks, in small intestine, and in that time can produce up to 1,500 larvae. Larvae migrate with blood to striated muscles causing myositis (trichinosis) The muscles invaded mainly are: pectoral muscles, tongue, and the gastrocnemius.

29. Cysticercosis:
Transmission:
Eating undercooked pork meat containing the larval stage (cysticerci) of Taenia solium.
fecal-oral transmission by autoinfection (ingestion of the egg stage).
The oncosphere (hexacanth-embryo) hatch and penetrates the intestinal wall and migrates in the circulation to the tissue ( skeletal muscles, brain and eyes).