Cells, tissues and organs of the immune system

•       Cells of the immune system
• tissues of the immune system
• organs of the immune system

  Cells of the immune system

        leukocytes

Mast cells

Granulocytes

Basophils,

Eosinophils,

        Neutrophils

Monocytes

Macrophages

Dendritic cells

Lymphocytes

T- Lymphocytes

        B- Lymphocytes

NK cell

Lymphocytes. T cells, B cells, and natural killer, or NK, cells.

 

Lymphocytes

• Lymphocytes are the major cells of the adaptive immune system.
• Lymphocytes can be divided into three populations:

                     1) T cells,

                     2) B cells, and

                     3) natural killer, or NK, cells.

• B and T lymphocytes differentiate from their respective

lymphoid precursor cells and

• leave the bone marrow in a kind of cellular stasis-not

actively replicating like other somatic cells .

• These cells are said to be naive.

 T- lymphocytes or T cells

• Lymphocytes destined to become T lymphocytes or T cells leave the bone marrow and

mature in the thymus gland.

• They can remain in the thymus, circulate in the blood, or reside in lymphoid organs such as the lymph nodes and spleen.
• Naïve T cells require a specific antigen to bind to a specific, membrane bound receptor (the T-cell receptor) to signal the continuation of replication.
• The now "activated" T cells differentiate into effector cells and memory cells.

     1. EffectorT cells include the

• T-helper cells (TH) ,
• cytotoxic lymphocytes (CTLs),
• natural killer T cells, or
• T-regulatory cells,
• that respond to a myriad of antigens by producing and secreting cytokines .
• The cytokines secreted from effector T cells control specific responses directing theactions of other host cells.

     2. Memory cells are quiescent, only to become activated T cells upon a subsequentexposure to the antigen.

• They provide a faster, heightened response.

B lymphocytes or B cells

• After B lymphocytes or B cells reach maturity within the bone marrow,
• they also circulate in the blood and
• disperse into various lymphoid organs where they await to become activated.
• The activated B cell becomes more ovoid.
• Its nuclear chromatin condenses, and numerous folds of endoplasmic reticulum become more visible.
• A mature, activated B cell is called a plasma cell.
• Plasma cells secrete large quantities of antibodies .
• Activated B cells also produce memory cells that are primed to act upon subsequent exposure to antigen

Natural killer (NK) cells

• Natural killer (NK) cells are a small population of large,

non phagocytic granular lymphocytes that play an important role in innate immunity.

• The major NK cell function is to attack and destroy
• malignant cells and
• cells infected with microorganisms, such as viruses and intracellular bacteria;
• however, NK cells do not recognize antigen.
• They recognize their targets in one of two ways
• First, NK cells survey somatic cells for a specific membrane-bound protein,known as the class I major histocompatibility complex (MHC) protein.

• Normal healthy host cells express class I MHC proteins on the cell surface, andNK cells bear a receptor that recognizes MHC class I.

• When NK cells encounter host cells with altered or missing class I MHC proteins, as sometimes happens during intracellular infection and oncogenesis, the aberrant cells are destroyed.
• NK cells also recognize and eliminate infected and malignant cells, expressing what are called stress, or shock, proteins on their surface.

• Finally, because NK cells have receptors for antibodies, they can also attack cells that are opsonized by antibodies. This process is called antibody dependent cell-mediated cytotoxicity (ADCC) and causes the death of the target cell.

• In all cases, attack by the NK cell results in the release of

pore-forming, perforin proteins and enzymes called granzymes.

• Together the perforins and granzymes induce target cell to commit suicide (apoptosis) .

• Unlike T and B cells, NK cells do not exhibit memory responses to target cells, thus they are considered part of the innate immune response.

GRANULOCYTES,types of granulocytes

 

  granulocytes

• Granulocytes have irregularly shaped nuclei with two to five lobes.
• Their cytoplasm has granules that contain reactive substances that kill microorganisms and enhance inflammation.

  Three types of granulocytes exist:   1. Basophils                                                                                   

                                                            2.Eosinophil

                        

                                                            3. Neutrophils 

1. Basophils  

•        Basophils (Greek basis, base, and philein, to love) have irregularly shaped nuclei with two lobes.
• The granules contain histamine and other substances similar to those in mast cells.
• However, basophils arise from a different cellular lineage
• basophils tend to infiltrate specific tissue sites rather than circulate through the bloodstream.
• Basophils are also important in the development of allergies and hypersensitivities

 2.Eosinophil

• Eosinophils have a two lobed nucleus connected by a slender thread of chromatin.
• Eosinophil granules contain hydrolytic enzymes (nucleases,

glucuronidases, and peroxidases), and major basic protein.

• It circulate in low numbers and migrate from the bloodstream into tissue spaces, especially mucous membranes, when recruited by soluble chemotactic mediators.
• They are important in the defense against protozoan and helminth parasites, mainly by releasing enzymes, cationic peptides and reactive oxygen species into the extracellular fluid.
• These molecules damage the parasite's plasma membrane, killing it.
• Eosinophils also play a role in allergic reactions, as they have granules that contain histaminase and aryl sulphatase, down regulators of the inflammatory mediators histamine and leukotrienes, respectively.
• Thus their numbers circulating in the bloodstream often increase during

allergic reactions, especially type l hypersensitivities

 3.Neutrophils 

• Neutrophils are highly PHAgocytic cells with a nucleus that has

three to five lobes connected by slender threads of chromatin .

• Because of the irregularly shaped nuclei, neutrophils are also called

polymorphonuclear neutrophils, or PMNs.

• Neutrophils have inconspicuous organelles known as primary and secondary granules.
• Primary granules contain peroxidase, lysozyme, defensins, and various hydrolytic
• enzymes
• secondary granules have collagenase, lactoferrin, cathelicidins, and lysozyme. 
• These enzymes and other molecules help digest foreign material after it is phagocytosed.
• Neutrophils also use oxygen-dependent and oxygen-independent Pathways that generate additional antimicrobial substances to kill ingested microorganisms.
• Mature neutrophils leave the bone marrow and circulate in blood so they can rapidly migrate to a site of tissue damage and infection, where they become the principal phagocytic and microbicidal responders.
• Neutrophils have toll-like pattern recognition receptors (PRRs), as well as receptors for antibodies and complement proteins, so that PAMPs and opsonize particles,respectively, can be more readily phagocytosed.
• PRRs bind to specific patterns that characterize microbial macromolecules and that their binding upregulates transcription pathways for phagocytosis
• Neutrophils have a limited life span that shotens upon activation of the phagocytic
• processes.

Physical and chemical barrier .Defence of innate resistance

     - potential microbial pathogen invading a human host immediately confronts a vast array of innate defense mechanisms.

     -  Although the effectiveness of an individual mechanism may not be great, collectively they are formidable.

         Many direct factors (age, nutrition, physiology, fever, genetics) and indirect factors (personal hygiene, socioeconomic status, living condition) contribute in some degree to all host-microbe relationships.

- At times, they favor the establishment of the microorganism; at other times, they provide the host some measure of general defense.

 Physical and mechanical barriers along with host secretions are the host's first line of defense against pathogens. e.g.,

1. Skin

2. Mucous membranes

3. Epithelia of the respiratory

4. Gastrointestinal, and

5. Genitourinary systems

1. SKIN

- Intact skin contributes greatly to innate host resistance because it is a

very effective mechanical barrier to microbial invasion.

- Its outer LAyer consists of thick, closely packed cells called Keratinocytes, which produce Keratins- Scleraproteins (insoluble proteins) that are the main components of hair, nails, and the outer skin cells.

- These outer skin cells shed continuously, removing microorganisms that manage to adhere to their surface.

- The skin is slightly acidic (around pH 5 to 6) due to sebum, secretions from sweat glands, and organic acids produced by commensal staphylococci & high concentration of sodium chloride and is subject toperiodic drying.

2. MUCOUS MEMBRANES

- The mucous membranes of the eye (conjunctiva) and the respiratory, digestive, and urogenital systems withstand microbial invasion because the intact stratified epithelium and mucus form a protective covering that resists penetration and traps microorganisms.

- Many mucosal surfaces are bathed in specific antimicrobial secretions. For example, cervical mucus, prostatic fluid, and tears are toxic to many bacteria.

- The conjunctiva that lines the interior surface of each eyelid and the expose surface of the eyeball is a good example of how a mucous membrane functions to provide chemical as well as physical protection from microorganisms.

- It is kept moist by the continuous flushing action of tears from the lacrimal glands.

- Tears contain large amounts of lysozyme, lactoferrin, and other antimicrobial chemicals.

Lysozyme:

lyses bacteria by hydrolyzing the β(1-4) bond connecting N-acetylmuramic acid(NAG) and N-acetylglucosamine

(NAM) of the bacterial cell wall peptidoglycan especially inGram-positive bacteria.

Lactoferrin:

- Tears and other mucous secretions also contain significant amounts of the iron-binding protein lactoferrin.

- Lactoferrin is released by activated phagocytic cells called macrophages and polymorphonuclearleukocytes (PMNs).

- It sequesters iron from the blood plasma, reducing the amount of iron available to invading microbial pathogens thereby limiting their ability to multiply.

Lactoperoxidase:

- mucous membranes produce lactoperoxidase,

- catalyzes the production of superoxide radicals, a reactive oxygen species that is toxic to many microorganisms.

3. Respiratory System

- The average person inhales at least eight microorganisms a minute, or 10,000 each day.

- Once inhaled, microorganism must first survive and penetrate the air- filtration system of the upper and lower respiratory tracts.

- Airflow in these tracts is very turbulent, microorganisms are deposited on the moist, sticky mucosal surfaces. Microbes lArger tHAn 10 µm usually are trapped by hairs and cilia lining the nasal cavity.

- The cilia in the nasal cavity beat toward the pharynx, so that mucus with its trapped microorganisms is moved toward the mouth to be expelled

 - Humidification of the air within the nasal cavity causes many microorganisms to swell, and this aids phagocytosis.

- Microbes sMAller THAn 10 µm (i.e., most bacterial cells) pass through nasal cavity and trapped by the mucociliary blanket that coats the mucosal surfaces of lower respiratory system.

- The trapped microbes are transported by ciliary action the

mucociliary escalator-that moves them away from the lungs.

- Coughing and sneezing reflexes clear the respiratory system of microorganisms by expelling air forcefully from the lungs through the mouth and nose, respectively.

- SAlivAtion also washes microorganisms from the mouth and nasopharyngeal areas into the stomach.

- Microorganisms that succeed in reaching the alveoli of the lungs encounter a population of specialized cells called alveolar macrophages that ingest and kill most inhaled microorganisms by phagocytosis.

4. Gastrointestinal Tract

- Most microorganisms that reach the stomach are killed by the acidic gastric juice (pH 2-3): mixture of

hydrochloric acid + proteolytic enzymes + mucus.

- However, some microorganisms and their products

(e.g., protozoan cysts, HeliCOBACTER pylori, Clostridium spp., and staphylococcal toxins) can survive the stomach acidity.

- Organisms embedded in food particles may be protected from gastric juice and reach the small intestine and damaged by pancreatic enzymes, bile, enzymes in intestinal secretions, and the GALT( Gut associated lymphoid tissue) system.

  Peristalsis and the normal shedding of columnar epithelial cells act in concert to purge intestinal microorganisms.

- In addition, the normal micro biota of large intestine is extremely important in preventing the establishment of pathogenic organisms.

- E.g., metabolic products (e.g., fatty acids) of many normal microbiota in the intestinal tract prevent unwanted microorganisms from becoming established.

- Other normal microbiota outcompete potential pathogens for attachment sites and nutrients.

-       The mucous membranes of the intestinal tract contain cells called Paneth cells - produce lysozyme , peptides called cryptidins- are toxic for some bacteria, as they form membrane channels that result in cell lysis.

5. Genitourinary Tract

- Kidneys, ureters, and urinary bladder of mammals are sterile in normal condition.

- Urine within the urinary bladder also is sterile.

- However, in both males and females, a few bacteria are usually

present in the distal portion of the urethra.

- The factors responsible for this sterility are complex. In addition to removing microbes by flushing action, urine kills some bacteria due to its low pH and the presence of urea and other metabolic end products (e.g., uric acid, fatty acids, mucin, enzymes).

- Portions of the kidney are so hypertonic that few organisms can

survive there.

- In males, the anatomical length of the urethra (20 cm) provides distance barrier that excludes microorganisms from the urinary bladder.

- In females, short urethra (5 cm) is more readily traversed by

microorganisms;

- This explains why urinary tract infections are 14 times more

common in females than in males.

- The vagina has another unique defense.

- Under the influence of ESTROGENS,

- Vaginal epithelium produces increased amounts of glycogen that is degrade to form lactic acid by acid- tolerant LACTOBACIllus ACIdophilus bacteria.

- Normal vaginal secretions contain up to 108 of these bacteria per ml.

- Thus an acidic environment (pH 3-5) unfavorable to most other organisms for establishment.

- Cervical mucus also has some antibacterial activity.

Innate resistance overview & immunity,immunity meaning,what is immunity,humoral immunity,herd immunity

       To establish an infection, an invading microorganism must first overcome many surface barriers, such as

 - skin, degradative enzymes, and mucus,

 - that have either direct antimicrobial activity or 

 - inhibit attachment of the microorganism to the host.

 - Because neither the surface of the skin nor the mucus- lined body cavities are ideal environments for the vast majority of microorganisms, 

 -  Most pathogens, or disease-causing microorganisms, must breach these barriers and reach underlying tissues to cause disease.

         However, any microorganism that penetrates these barriers encounters two levels of host defenses:

1. Innate resistance mechanisms and
2. Adaptive immune response.

- Animals (including humans) are continuously exposed to microorganisms that can cause disease.

- Fortunately animals are equipped with an immune system that usually protects against adverse consequences of this exposure.

- The immune system is composed of widely distributed proteins, cells, tissues, and organs that recognize foreign substances, including microorganisms.

- Together they act to neutralize or destroy them, maintaining host integrity.

            

                 immunity

           Immunity: (Latin immunis, free of burden) refers to the general ability of a host to resist infection or disease.

- Immunology is the science focused on immune responses to foreign substances and how these responses are used to resist infection.

- It includes the distinction between "self" and "nonself" and all the biological, chemical, physiological, metabolic, and physical aspects of the immune response.

- There are two fundamentally different yet complementary components of the mammalian immune response.

1. The first component arises by virtue of being a vertebrate animal.Vertebrates have evolved to express unique features that inherently protect against invasion by foreign substances. Some of these features are physical and act as barriers.

2. chemical in nature and directly kill or inhibit invaders.

- Still other features result when specialized cells recognize generic yet highly conserved chemical motifs (expressed on bacteria, fungi, and viruses) and initiate processes to engulf and degrade the foreign substance.

- These features are collectively called the innate resistance

mechanisms.

- The second component of the mammalian immune response is much more sophisticated, being directed by highly specialized cells that can respond to specific invaders through

- receptor-mediated capture events,

- be programmed to "remember" their encounters with foreign substances,

- amplify individual responses, recruiting other components of the host immune system to eliminate or reduce the threat posed by the invader.

Innate resistance mechanisms, also known as

- nonspecific resistance and

- innate, nonspecific, or

- natural immunity,

- is the first line of defense against any foreign material, including microorganisms, encountered by the host.

- It includes general mechanisms inherited as part of the innate structure and function of each animal (such as skin, mucus, and constitutively produced antimicrobial chemicals such as lysozyme).

- Innate resistance mechanisms defend against foreign invaders equally and to the same maximal extent each time a foreign invader is encountered.

Adaptive immune response, also known as

- Acquired or

- Specific immunity, defends against a particular foreign agent.

- The effectiveness of adaptive immune responses increases on repeated exposure to foreign agents such as viruses, bacteria, or toxins; that is to say, adaptive responses have "MEMORY.

- ANTIGEN: Substances recognized as foreign that provoke immune responses

Also known as immunogens (immunity generators).

- The presence of foreign antigens causes specific cells to replicate and manufacture a variety of proteins that function to protect the host. One such cell, the B cell, produces and secretes glycoproteins called ANTIBODIES.

- Antibodies bind to specific antigens and inactivate them or contribute to their

elimination.

- Other immune cells become activated to destroy host cells harboring intracellular  destroy host cells harboring intracellular pathogens, such as viruses.

- Innate resistance mechanisms and the adaptive immune responses work

together to eliminate pathogenic microorganisms and other foreign materials.

 -innate systems react immediately upon initial exposure to foreign

substances,

- multiple bridges occur between the two immune system components .

- variety of cells function in both innate and adaptive immunity, These cells are known as the white blood cells, or leukocytes.

- White Blood cell development occurs in the bone marrow of mammals during the process of hematopoiesis.

- Leukocytes function in the innate system, whereas others are part of a specific immune response.

- Some are important because they link the innate arm of the immune system to the adaptive.

- The leukocytes form the basis for immune responses to invading microbes and foreign substances. Many of these cells reside in specialized tissues and organs. Some tissues and organs provide supportive functions in nurturing the cells so that they can mature and respond correctly to antigens.

 

 

SYPHILIS,syphilis symptoms,what is syphilis,syphilis test

 SYPHILIS IS : a sexual transmitted disease caused by spirochetal bacterium Treponema pallidum a motile anaerobic.

• Transmission : is almost always through sexual contact or congenitally through the placenta to a foetus or at birth from an infected mother.

• Different manifestations occur depending on the stage of the disease

                       Primary Syphilis

• It’s the first stage after infection.

• Painless & localized ulcer with rolled edge (chancres)

• Single or multiple

• Appear 2-3 weeks after contact

• Most common site are cervix, vagina, vulva, anus and mouth

• Regional lymphatic node become enlarged

Incubation period 9-90 days, usually <21 days Develops at site of contact/inoculation

Classically : single, painless, clean-based, indurated ulcer (increasing fibrous material), with firm, raised borders. Atypical presentations may occur.

Mostly anogenital (related to anus and genitals), but may occur at any site (tongue, pharynx, lips, finger, nipples, etc)

Non-tender regional adenopathy Very infectious

May be darkfield positive but serologically negative

Untreated, heals in several weeks, leaving a faint scar.

                               Secondary Syphilis

   

• The skin rash : Diffuse; often with a superficial scale (papulosquamous); may leave residual pigmentation or depigmentation

• Condylomata Lata : formed by coalescene of large, pale, flat-topped papules; occur in warm, moist areas such as the perineum (the area between the anus & scrotum); Highly infectious.

• Mucosal lesions : 30% of secondary syphilis patients develop mucous patch (slightly raised, oval area covered by a greyish white membrane, with a pink base that does not bleed). Highly infectious.

• Systemic : 1-6 months after contact; fever, malaise, general adenopathy and non-itchy maculopapular skin rash “money spot”; involve the palms of the hands and the soles of the feet; mucous patches and linear (snail track) ulcers are seen on the mucosal surfaces.

Seen 6 weeks to 6 months after primary chancre

• Usually diffuse non-pruritic, indurated rash, including palms & soles.

• May also cause : fever, malaise, headache, sore throat, myalgia (pain in a muscle), arthralgia (related to joint pain), generalized lymphadenopathy; hepatitis (10%)

• Renal : an immune complex type of nephropathy with transient nephrotic syndrome (kidney disease); iritis (an inflammation of middle layer of eye) or an anterior uveitis

• Bone : periostitis (inflammation of the membrane enveloping a bone)

• CSF pleocytosis (large number of lymphocytes) in 10-30% (but, symptomatic meningitis is seen in <1%)

Differential diagnosis of Secondary Syphilis

• The rash may be confused with pityriasis rosea (a skin rash begins as a large spot on the chest); drug eruptions; acute febrile exanthems (skin rash) ; psoriasis (a condition in which skin cells build up & form scales and itchy, dry patches) ; lichen planus (an inflammatory condition of the skin and mucous membranes); scabies (a contagious, intensely itchy skin condition caused by a tiny burrowing mite)

• The mucous patch may be confused with oral thrush ( fungal infection of mouth).

• Malaise, sore throat; generalized adenopathy, hepatitis & rash may be confused with infectious mononucleosis (extreme fatigue). accuracy is 99%.

 

Latent Syphilis

• Positive syphilis serology without clinical signs of syphilis (& has normal CSF).

• It begins with the end of secondary syphilis and may last for a lifetime.

• Pt may or may not have a primary or secondary syphilis

• Diseases known to cause occasional false-positive nontreponemal test reactions for syphilis, such as systemic lupus erythematosus (autoimmune disease in which body’s immune system mistakenly attacks healthy tissue in many parts of the body) (SLE), and congenital syphilis must be excluded before the diagnosis of latent syphilis can be made.

• It is divided into early and late latency.

(1) Early latent :

• The first year after the resolution of primary or secondary lesions, or

• A reactive serologic test for syphilis in an asymptomatic individual who has had a negative serologic test within the preceding year.

• infectious

(2)Late latent :

Usually not infectious, except for the pregnant woman, who transmit infection to her foetus

Latent Syphilis / Tertiary Syphilis

• It is the destructive stage of the disease.

• Lesions develop in skin, bone, & visceral organs (deep down of organ) (any organ).

• The main types are : late benign (gummatous/ non-cancerous tissues formed during late stage of syphilis); cardiovascular; neurosyphilis

• It can be crippling and life threatening.

• Blindness, deafness, deformity, lack of coordination, paralysis, dementia (memory loss) may occur.

• It is usually very slowly progressive, barring certain neurologic syndromes which may develop suddenly due to endarteritis (an inflammation of the inner lining of an artery) and thrombosis (local coagulation or clotting of the blood in a part of the circulatory system) in the CNS.

• Late syphilis is non-infectious

• Positive syphilis serology without clinical signs of syphilis (has normal CSF)

• It begins with the end of secondary syphilis and may last for a lifetime

• Pt may or may not have a primary or secondary syphilis.

• Disease known to cause occasional false-positive nontreponemal test reactions for syphilis, such as systemic lupus erythematosus (SLE), and congenital syphilis must be excluded before the diagnosis of latent syphilis can be mode.

• It is again divided into early and late latency

• Latent syphilis :

       Absent of symptoms or physical finding.

    • I/3 proceed to tertiary

 

• Tertiary syphilis :

• Occur :1-10 years after infection

• Gummas : ulcerative nodule in the skin, bone and nervous system as a result of heper-sensitivity reactions

• Systemic manifestation: CVS, CNS and bone

Conenital Syphilis :

• Mode of transmission :

• Trans placental passage from infected mother

• At birth

• Congenital infection is associated with several adverse outcome including :

• Low birth weight

• Premature birth

• Congenital abnormalities

• Miscarriages or death of baby

Early

• Skin lesions, maculopapular tissue

• Lymphadenopathy

• Hepatosplenomegaly

• Failure to thrive

• Jaundice, anaemia

• osteochondritis

 

Late :

gummites ulcers

bony prominence of forehead saddle nose

short maxilla (jaw bone)

keratitis (inflammation of the cornea of the eye) nerve deafness and dental deformities

Diagnostic Evaluation of Syphilis


• Direct detection of Treponema pallidum
• Nontreponemal Serological Tests
• Treponemal Serological Tests

TESTS FOR DIRECT DETECTION OF T. pallidum

• Animal Inoculation

• Dark Field microscopy

• Direct fluorescent antibody testNONTROPONEMAL SEROLOGICAL TESTS

Serological nontreponemal tests

• VDRL (Venereal disease research laboratory test)

    • USR (Unheated of serum regain Test)  

• Macroscopic nontreponemal tests

• RPR (Rapid plasma regain test)

• TRUST ( Toluidine red unheated serum test)

• Direct tests for T. pallidum in tissue sections

• Nucleic acid amplification methods

TREPONEMAL SEROLOGICAL TESTS

• FTA-ABS (Fluorescent treponemal antibody absorption test)

• FTA-ABS double staining (Fluorescent treponemal antibody absorption double staining test)

• TP-PA test (Treponema pallidum particle agglutination test)

• Western blots

• ElAs (Enzyme immunoassays) / Rapid tests

Animal Inoculation

• Oldest method for detecting infection

• Most sensitive method for detecting infectious treponemes and is used as the gold standard for measuring the sensitivity of methods such as the PCR

• Rabbit is most commonly used

• Any source of specimen can be used as long as the material is less than 1 h old or was frozen immediately after collection

• Inoculation of sample : intra-testicular or intradermal

• Incubation period : inversely proportional to the size of inoculum

• Sensitivity of RIT approaches 100% if the number of organisms exceeds 23 and patient has not received antibiotic treatment.

Dark Field Microscopy

• One simplest and most reliable for the direct detection of T. pallidum

• exudates and fluids from lesions are examined as a wet mount

• Examination should be done immediately

• Most productive during 1*, 2*, early relapsing, and early congenital syphilis when lesions contains large numbers of treponemes (chancres, condylomata latum, or mucous patches)

dengue, dengue fever

 ALTERNATIVE NAMES :

▪ Haemorrhagic dengue

▪ Dengue shock syndrome

▪ Philippine haemorrhagic fever

▪ Thai haemorrhagic fever

▪ Singapore haemorrhagic fever

Dengue Haemorrhagic fever is an acute infectious viral disease usually affecting infants and young children. This disease used to be called break-bone fever because it sometimes causes severe joint and muscle pain that feels like bones are breaking.

▪ It is a severe, potentially deadly infection spread by certain species of mosquitoes (Aedes aegypti)

▪ Philippine haemorrhagic fever was first reported in 1953. in 1958 haemorrhagic fever became a notifiable disease in the country and was later reclassified as Dengue haemorrhagic fever.

SIGNS AND SYPTOMS :

▪ An acute febrile infection of sudden onset with clinical manifestation of 3 stages :

▪ First 4 days – Febrile or Invasive stage : high fever; abdominal pain and headache; later flushing which may accompanied by vomiting, conjunctival infection and epistaxis (bleeding from the nose).

▪ 4th – 7th days – Toxic or Haemorrhagic stage : lowering of temperature; severe abdominal pain; vomiting and frequent bleeding from gastrointestinal tract in the form of haematemesis (vomiting of stomach contents mixed with blood) or melena; unstable blood pressure; narrow pulse pressure; shock

▪ 7th – 10th day – Convalescent / recovery stage : generalized flushing with intervening areas of blanching appetite (digestion becoming regular) regained; blood pressure becoming stable.

Classification :

▪ Severe, frank type : with flushing, sudden high fever, severe haemorrhage, followed by sudden drop of temperature, shock and terminating in recovery or death.

▪ Moderate : with high fever, but less haemorrhage, no shock.

▪ Mild : with slight fever, with or without petenchial (red / purple spot) haemorrhage but epidemiologically related to typical cases usually discovered in the course of investigation of typical cases.

ETIOLOGIC AGENT :

▪ Flavivirus, dengue virus type 1,2,3, & 4

▪ Chikungunya virus

SOURCE OF INFECTION :

▪ Vector mosquito : Aedis aegypti; Aedis albopictus

▪ The infected person

▪ INCUBATION PERIOD :

▪ Uncertain : from 6 days to 7 days

▪ PERIOD FOR COMMUNICABILITY :

▪ Unknown. Presumed to be an the first week of illness when virus is still present in the blood.

EXAMS AND TESTS :

▪ Physical examination may reveal the following : low blood pressure; a weak & rapid pulse; rashes; red eyes; red throat; swollen glands; enlarged liver (haepatomegaly)

▪ Tests include : haematocrit (ratio of the volume of rbc to the total volume of blood); platelet count; electolytes; coagulation studies; liver enzymes; blood gases; tourniquet(device for stopping the flow of blood through a vein/artery) test ( causes petechiae below the tourniquet); x-ray of the chest; serologic studies; serum studies from samples taken during acute illness and convalescence (high in titre to dengue antigen)

METHODS OF PREVENTION AND CONTROL :

▪ The infected individual, contacts and environment :

▪ Recognition of the disease; isolation of patient; epidemiological investigation; case finding and reporting; health education.

Control Measures :

▪ Eliminate the vector by : changing water and scrubbing sides of lower vases once a week; destroy breeding places of mosquito by cleaning surroundings; proper disposal of rubber tyres, empty bottles, & cans.

▪ Avoid too many hanging clothes inside the house

▪ Residual spraying with insecticides

    

Video by Ravi Kant from Pexels