Download Parasitology: (Protozoa and Helminthes)

Musculoskeletal system infection
 Infection of skin ( Cellulitis, Subcutaneous layer infection).
 Infection of skeletal muscles ( Infectious Myositis).
( Infectious Pyomyositis).
 Infection of Tendon (Tendonitis, Infectious Tenosynovitis).
 Infection of Bursa (Bursitis)
 Septic arthritis.
 Infection of bone (osteomyelitis).
Infection of skin
Infection of skin:
Cellulitis and subcutaneous layer infection:
Cellulitis is a diffuse inflammation of connective tissue with severe inflammation
of dermal and subcutaneous layers of the skin.
Cellulitis can be caused by normal skin flora or by exogenous bacteria.
It often occurs where the skin has previously been broken: cracks in the skin,
cuts, burns, insect bites, surgical wounds, intravenous drug injection or sites of
intravenous catheter insertion.
Cellulitis
Bacterial causes of cellulitis:
Group A Streptococcus and Staphylococcus are the most common cause of
cellulitis.
Predisposing conditions for cellulitis include:
Insect or spider bite, animal bite, tattoos, itchy skin rash, recent surgery, athlete's
foot, dry skin, eczema, and drugs injections.
Signs and symptoms:
Erythema, edema, with necrosis and inflamed margins.
Pus formation mainly associated with the pyogenic infection.
Cellulitis
The reddened skin or rash may considered as a signal of deeper, more
serious infection of the inner layers of skin. Once below the skin, the bacteria
can spread rapidly, entering the lymph nodes and the blood stream and
spreading throughout the body. This can result in influenza- like symptoms
with a high temperature and sweating or feeling very cold.
Cellulitis
Bacterial infection of dermis could extend to hypodermis(the subcutaneous layer of
skin) causing:
- Hair follicle root infection (folliculitis)
- Sweat gland infection
- Bursae infection (Bursitis)
-Fibrous bands infection
Leading to deep fascia infection and necrotizing fasciitis.
Folliculitis could extend in the hypodermis layer to form:
Furuncles: large, painful, raised nodules with an underlying collection of dead and necrotic
tissue.
Carbuncles result from the untreated furuncles. Multiple sinus tracts are usually present.
Chills and fevers are associated with carbuncles and indicate systemic spread of the
pathogenic bacteria.
Bacteremia with secondary spread to other tissues is common with carbuncles.
Bursitis
Bursitis:
The most common pathogen is Staphylococcus aureus.
Ultrasonography (US) will not differentiate an infected bursa
and post-traumatic bursitis.
So, accumulated fluid should be collected for laboratory
investigations.
Erythema, edema and inflammation of Bursae
Infectious Tenosynovitis and Tendonitis
Infectious Tenosynovitis and Tendonitis:
Tenosynovitis is the inflammation of the fluid-filled sheath ( the synovium) that
surrounds a tendon.
Symptoms of tenosynovitis include pain, swelling and difficulty moving the
particular joint where the inflammation occurs.
Acute tenosynovitis is caused predominantly by Staphylococcus aureus or
Streptococcus pyogenes and most frequently involves the tendon sheaths of the
flexor muscles .
It is usually the result of a penetrating injury ( animal bite, puncture wound) and may be
complicated by the presence of foreign bodies.
Pus accumulated within the tendon sheath should be extracted for microbiology
laboratory tests (by US help).
Tenosynovitis and Tendonitis
Necrotizing Fasciitis
Necrotizing fasciitis (NF):
Commonly known as flesh-eating disease is a rare infection of the deeper layers of
skin and subcutaneous tissues, easily spreading across the fascial plane within the
subcutaneous tissue.
Type I describes a polymicrobial infection, whereas Type II describes a
monomicrobial infection.
Many types of bacteria can cause necrotizing fasciitis : Group A Streptococcus
(Streptococcus pyogenes), Staphylococcus aureus, Vibrio vulnificus, Clostridium
perfringens, and Bacteroides fragilis.
Necrotizing fasciitis
 Group A Streptococcus made up most cases of Type II infections.
However, since as early as 2001, another serious form of
monomicrobial necrotizing fasciitis has been observed with increasing
frequency.
 In these cases, the bacterium causing it is methicillinresistant Staphylococcus aureus (MRSA).
 The infection begins locally at a site of trauma, which may be
severe (such as the result of surgery), or minor.
 Over 70% of cases are recorded in patients with one of the following
clinical situations: immunosuppression, diabetes, alcoholism/drug
abuse, malignancies, and chronic systemic diseases.
Bacterial cellulitis & Necrotizing fasciitis
Staphylococcal cellulitis
Caucasian male with necrotizing fasciitis. The left leg shows extensive redness and
necrosis.
Necrotizing Fasciitis
Pathophysiology:
"Flesh-eating bacteria" cause the destruction of skin and muscle by releasing
toxins (virulence factors), which include Streptococcal pyogenic exotoxins.
Streptococcus pyogenes produces an exotoxin known as a superantigen. This
toxin is capable of activating T-cells non-specifically, which causes the
overproduction of cytokines and severe systemic illness (Toxic shock syndrome).
Streptococcus
pyogenes
cellulitis
Necrotizing Fasciitis
The Streptococcus Cellulitis
Streptococcus pyogenes infection: Erythema, edema, and pus formation.
Bacterial cellulitis & Necrotizing fasciitis
Laboratory diagnosis:
Clinical specimen: Pus exudate, wound swab.
Culture:
Clinical specimens should be cultivated on blood agar, chocolate agar, and lactose
differential medium by four quadrant streaking method.
Identification of Staphylococcus aureus : Gram+ve Cocci in clusters.
Bacterial cellulitis & Necrotizing fasciitis
Identification of Streptococcus pyogenes
Gram +ve Cocci arranged in chains or in pairs.
Beta Hemolytic due to its phospholipase C activity.
Bacitracin sensitive.
Subcutaneous Mycosis
Subcutaneous Mycosis:
SPOROTRICHOSIS:
Chronic infection involving cutaneous, subcutaneous and lymphatic tissue.
Frequently encountered in gardeners.
May develop in otherwise healthy individuals.
Most common in Mexico, endemic in Brazil, Uruguay, South Africa.
Etiology: Sporothrix schenkii, thermally dimorphic fungus naturally present in
soil. At 37°C: Round/cigar-shaped yeast cells, at 25°C: Septate hyphae, rosettelike clusters of conidia at the tips of the conidiophores.
SPOROTRICHOSIS
SPOROTRICHOSIS: Pathogenesis and Clinical findings:
Skin: lesions usually follows minor trauma, appear in the form of nodules that ulcerate
ulcer necrosis.
Skin/subcutaneous tissue lymphatic vessels lymph nodes
Systemic dissemination: Skeletal muscles, bones, joints.
Diagnosis:
Samples: aspiration fluid, pus, biopsy
Microscopy: direct microscopic examination (KOH) and histopathological
examination (methenamine silver stain) reveal yeast cells and asteroid body.
Culture: on Sabouraud dextrose agar for 4-6 weeks at 25°C (Moulds). At 37°C (yeast)
Serology: Yeast agglutination test, sporotrichin skin test.
CHROMOBLASTOMYCOSIS
CHROMOBLASTOMYCOSIS:
Post-traumatic chronic infection of subcutaneous tissue.
Papules verrucous flower-like lesions on lower extremities.
Necrosis and subcutaneous inflammation.
Etiology: Fonsecaea and Phialophor species.
Pigmented (dematiaceous) fungi in soil.
Diagnosis:
Direct microscopic examination of lesion scrapings (KOH): sclerotic body.
Skin scrapings from a
patient showing
characteristic brown
pigmented, planate-dividing,
rounded sclerotic bodies.
MYCETOMA
MYCETOMA:
Post-traumatic chronic infection of subcutaneous tissue
Common in tropical climates.
Etiology:
Saprophytic fungi (Eumycetoma) and Actinomyces (Actinomycetoma): Madurella mycetomatis, and
Exophiala jeanselmei.
Clinical findings:
Site: feet, lower extremities, hands
Findings: abscess formation, draining sinuses containing granules and deformities.
Dissemination: muscles and bones.
Treatment:
Eumycetoma: surgery and antifungal therapy (Potassium iodide (Topical/oral),
And Amphotericin B.
Actinomycetoma: antibiotic combinations
Chromoblastomycosis & Mycetoma
Chromomycosis of the foot caused
by Fonsecaea pedrosoi
Mycetoma of foot: Madurella mycetomatis
Protozoan infection of skin
Protozoan infection of skin:
Leishmania genera: The Blood and Tissue Mastigophora.
1- L. donovani:
The causative organism of Visceral leishmaniasis (Kala-azar)
2- L. tropica:
The causative organism of Cutaneous leishmaniasis of old world (Oriental sore)
3- L. mexicana:
The causative organism of Cutaneous leishmaniasis of new world (Chiclero ulcer)
4-L. braziliense:
The causative organism of Mucocutaneous leishmaniasis of new world.
LEISHMANIA DONOVANI
LEISHMANIA DONOVANI:
(Visceral leishmaniasis, Kala-azar, Dum-Dum fever)
Distribution: India, (1. d donovani), Mediterranean Coast, China (L d infantum),
Central Africa (1. d. archibaldi), South America (1. d chagasi).
Habitat: Reticuloendothelial system (blood, spleen, liver, bone marrow, lymph node,
skin).
Morphology: Leishmania exist in two forms:
1-Leishmania form (amastigote): in tissues of man.
2- Leptomonad form (promasigote): in the gut of vector LB. (Sand fly) or in culture.
D.H.: Man, Dog and Rodents (Dog and Rodents act as a reservoir host in certain areas
as Mediterranean Coast, Central Africa and South America).
LEISHMANIA DONOVANI
Vector: Female sand fly of the genus Phlebotomus.
Life cycle in vector:
(Cyc1opropagative transmission):
When the sand fly takes an infected meal, the amastigotes go to mid gut where they
multiply and by the end of the 2nd day, it will be converted into promastigotes which
elongate, Multiply and increase in number forming rosettes filling the lumen of the
mid gut (fifth day).
Promastigotes return back to pharynx, buccal cavity and proboscis, now they are
ready to infect another person, where they change into amastigotes (promastigotes do
not invade salivary gland of the vector).
LEISHMANIA DONOVANI
Life cycle of Leishmania:
LEISHMANIA DONOVANI
Pathogenesis:
- The promastigote engulfed by skin macrophages, converted into the
amastigote stage.
- The skin macrophage carry the microbe to viscera via blood stream, where it
infects the R.E.S.
- Skin, liver, spleen, bone marrow, kidney, and lymph nodes will be colonized
by infected macrophage.
LEISHMANIA DONOVANI
Clinical picture:
-Onset: usually gradual with high or low grade fever.
-Toxaemia, anorexia, loss of weight.
-Splenomegaly, Hepatomegaly, jaundice, disturbed liver function,
↑globulin and ↓ albumin, reversed A/G ratio.
-Anaemia, leucopaenia with monocytosis.
- Lymphadenopathy.
-Glomerulonephritis and dysentery with leishmania bodies in urine and stool.
-Nasal and pharyngeal granulomata
LEISHMANIA DONOVANI