Infectious diseases pathology - PowerPoint Presentation

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Infectious diseases pathology Lecture 1 

Mays Ibrahim, Arab board of pathology, CABPUniversity of Al-Mustansiriyah, college of medicine

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Learning objectives

You should:Know what infectious diseases are and identify infectious agents.Understand

host barriers to infection and causes of failure of these barriers

.

Able to explain

types of inflammatory responses

to infection.

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Infectious diseases are disorders in which tissue damage or dysfunction is produced by microorganisms.

Despite the availability and use of effective vaccines and antibiotics, infectious diseases remain an important health problem worldwide.The cooperation between humans and microorganisms is the rule; and disease is the exception.

The relationships between human and microorganisms are:

Symbiotic:

benefit of both partner

Commensal

: the microorganism shares the host’s food without causing harm

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Infectious agents:

Prions: which are modified host proteins lacking genetic molecules.Viruses

: obligate intracellular organism which only replicate intracellularly (requiring host cell metabolism for replication.

Bacteria

: prokaryotes (lacking nucleic acid and endoplasmic reticulum) but have cell walls.

Fungi

Protozoa

: motile, single-celled eukaryotes.

Helminthes:

multicellular parasites with complicated life cycles often involving several hosts.

Ectoparasites:

bedbugs, fleas

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Host barrier to infection

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Host barrier to infection Skin

: normal defense in skin include epidermal barrier:Dense keratinized outer skin layer

Low PH of skin (5.5)

Presence of fatty acids within the layer of skin also inhibit microbial growth

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Failure of local defense in skin occurs when there is:Mechanical defects (puncture, burn, ulcer)

Needle sticks (e.g. may transmit hepatitis B or C).Arthropods and animal bites.Direct penetration (e.g.

Schistosomiasis

).

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Respiratory system: Normal defenses including

Hair of the nose and sneezingThe mucous layer secreted by the goblet cells in the nose and upper respiratory tract.

The

mucocilliary

clearance of the respiratory epithelium.

Mucosal immunoglobulin (IgA).

Alveolar macrophages and neutrophils recruited to the lungs by cytokines.

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Note: large particles are trapped in the mucociliary

blanket that lines the nose and the upper respiratory tract, while particles smaller than 5 microns are carried into the alveoli, where they are phagocytized by alveolar macrophages or by neutrophils .Failure of local defense in respiratory system occurs when there is;

Mucociliary

clearance mechanism is disrupted (e.g., by smoking that cause metaplasia) or

hyperviscosus

mucus in cystic fibrosis

Host macrophage clearance is ineffective (e.g., in tuberculosis)

Attachment and local proliferation of microbes.

 

 

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GIT:

Normal defenses against infected pathogens are:Epithelial barriers.Acidic gastric secretions.

Mucous secretions.

Bile and pancreatic enzymes.

Immunoglobulin A (IgA) antibodies, secreted by B cells located in the mucosa associated lymphoid tissues.

The normal protective gut flora.

Most gastrointestinal pathogens are transmitted by food or drink contaminated with

fecal material

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Failure of local defense in GIT system occurs when there is;Attachment and local proliferation and invasion of microbes.

Acid-resistant cysts and eggs.Resistant microbial external coats.

Broad spectrum antibiotic use that affect the normal flora.

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Urogenital tract:

Normal defenses against infected pathogens areFrequent bladder flushing with urine.Normal vaginal flora, catabolism of glycogen by normal commensal lactobacilli lowers the pH and reduces fungal growth.

Intact epithelial barrier.

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Failure of local defense in urogenital system occurs when there is:

Bladder atonia, flow obstruction, or reflux.Antibiotics kill the lactobacilli and render the vagina susceptible to candidal infection.

Microbial attachment and local proliferation.

Direct infection/local invasion.

Local trauma (e.g. sexually transmitted diseases).

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The transmission can beFrom person-to-person: via respiratory e.g

, T.B, fecal-oral e.g. HAV, sexual e.g. AIDS, or transplacental routes e.g. congenital Syphilis or through sharing neeedles. Animal-to-human trans- mission can occur through direct contact or ingestion (zoonotic infections).Insect or arthropod vectors may passively spread infection e.g., leishmaniasis

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Immune evasion by microbes:After bypassing host tissue barriers, infectious microorganisms need to evade host immunity

Strategies include:Remaining inaccessible to host defense either in areas not reachable by antibodies or mononuclear cells (e.g GIT lumen or epidermis).

Antigenic variation

Inactivating antibodies or complement.

Resisting phagocytosis

, e.g. by producing a

capsule

Suppressing the host adaptive immune response, e.g. by interfering with cytokines or inhibiting MHC expression and antigen presentation.

Establishing

latency

, during which viruses survive in a silent state in infected cells.

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How can the microorganism cause a disease?

Infectious disease results from the interaction of microbial virulence characteristics and host immune responses.

Infectious agents cause damage by:

• Entering cells and

directly causing cell death

.

• Releasing

toxins

that kill cells (microbial products including endotoxin, exotoxins or

superantigens

).

• Releasing

enzymes

that degrade tissue components

•

Damaging blood vessels

, causing ischemic necrosis

• Inducing

host inflammatory cell responses

that directly or indirectly injure tissues.

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Spectrum of Inflammatory Responses to Infection:

Microbes produce 5 types of tissue reactions:Suppurative

(Purulent) Inflammation

Mononuclear & granulomatous inflammation

Cytopathic-cytoproliferative

response

Necrotizing inflammation

Chronic inflammation and scarring

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Suppurative (Purulent) Inflammation:

Is an acute tissue reaction to damage usually caused by pyogenic bacteria.

Pyogenic bacteria : is bacteria cause pus formation.

These elicit increased vascular permeability and

neutrophil

recruitment through

bacterial

chemoattractants

.

Massing of neutrophils and liquefactive necrosis of the tissue form

pus

.

E.g. consolidation of entire lung lobes in pneumonia; these may resolve without sequelae (pneumococcal pneumonia) or may scar (Klebsiella).

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The alveolar architecture is still maintained, which is why even an extensive pneumonia often resolves with minimal residual destruction or damage to the pulmonary parenchyma

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Mononuclear & granulomatous inflammationDiffuse, predominantly

mononuclear, interstitial infiltrates are a common feature of all chronic inflammatory processesBut when they develop acutely

, they often are response to

viruses.

For example:

plasma cells are abundant in syphilis

lymphocytes predominate in HBV infection.

 

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Granulomatous inflammation

is a distinctive form of mononuclear inflammation characterized by accumulation of activated macrophages called “epithelioid” cells, which may fuse to form giant cells. In some cases there is a central area of caseous necrosis.

Cause:

Usually evoked by

infectious agents that resist eradication and are capable of stimulating strong T cell–mediated immunity

.

e.g., M. tuberculosis,

Histoplasma

capsulatum

,

schistosome

eggs.

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DDX of chronic granulaomatous infections

T.BLeprosy (tuberculoid leprosy).

Schistosome eggs.

Histoplasma

capsulatum

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Cytopathic-cytoproliferative response

These reactions are characteristic of viral mediated damage to the host cell & these include:Virus may replicate inside the cell 

formation of viral aggregate which may be visible as inclusion bodies

e.g

Cytomegalovirus.

Virus may induce cells to fuse and form multinucleated cells (e.g., measles virus or herpes-viruses).

May cause focal cell damage



discohesion

of the epithelial cells



blister formation.

May cause proliferation of the epithelial cells,

e.g

warts that are caused by HPV.

May cause dysplastic changes and cancer formation.

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nuclei contain large, eosinophilic inclusions surrounded by a clear halo, classic owel eye inclusion of CMV

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Koilocytic changes in HPVproliferation of the epithelial cells

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Necrotizing inflammationMicrobes that secrete

powerful toxins cause rapid and severe tissue necrosis often in the absence of inflammation. Examples:Clostridium perfringins that cause severe cell death just like (

coagulative

necrosis)

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Chronic inflammation and scarring:

Many infections may end in chronic inflammation which can lead to either:

Complete healing, or:

Extensive scarring

e.g

chronic HBV infection may cause cirrhosis of the liver

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Bacterial infection Staphylococcal S

treptococcal Tubeculosis Leprosy Syphilis

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gram-positive cocci that cause acute diseases due to direct infection or due to the production of toxins. It is pyogenic infection. Commonly colonize the nares, and skin.Staph aureus infections can cause :Skin infections Boil or furuncle : the most common staph infection, a pocket of pus around the hair follicle.

Carbuncle: it is a more extensive lesion. As a cluster of boils that are connected to each other under skinCellulitis: infection of deep skin layers Impetigo: is a highly contagious painful rash that mainly affects children caused by staph.after a week of formation it bursts and develop honey colored crusts Or streptococcal infection) Toxin mediated disease

toxic shock syndrome, scalded skin syndrome, rapid onset food poisoning .

MRSA

(methicillin resistant S aureus) infection.

Bacteremia

Staphylococcal infection

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Streptococcal infection:Are gram positive coccus grow in pairs or chain. They are classified according to the pattern of hemolysis on blood agarBeta hemolyticstrept:group A-s. pyogen(cause pharyngitis, scarlet fever,

erysepilas, impetigo, R.F.) and group B-S. agalactiae(colonize female genital tract).Alfa hemolytic: S. pneumonia(cause of community acquired pn.)Gamma hemolytic: normal oral flora but common cause of endocarditis.

Streptococcal infection

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Cellulites:Acute painful suppurative spreading infection of deeper dermis and subcutaneous tissues. Often starts with a break in skin.Usually

from strept pyogens or staph aureusThe infection spread through the lymphatic leads to L.N swelling and tenderness of these L.N.Clinically:The affected area will be red, edematous, indurated with NO well defined margin.

Erysipelas:

infection involving upper dermis and superficial

lymphatics

, usually

from

strept

pyogens

NO suppuration unless deeply infected. Clinically:

The affected area has red, The rash has a sharp, well-demarcated border.

Types of streptococcal infection

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Erysipelas

cellulitis

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