What is Glomerulonephritis?

Definition: Glomerulonephritis (GN) is an inflammatory condition affecting the glomeruli, the tiny filtering units within the kidneys. These filters are essential for removing waste products, excess fluids, and electrolytes from the blood to produce urine. When the glomeruli become inflamed and scarred, their ability to perform this function deteriorates, leading to a buildup of waste and fluid in the body.

What are the Causes of glomerulonephritis?

1. Infections:
   • Viral Infections: Certain viruses can trigger GN. Notable examples include HIV, hepatitis B, and hepatitis C.
   • Bacterial Infections: Bacteria that cause common throat and skin infections, such as Streptococcus spp or Staphylococcus spp
2. Autoimmune Diseases:
   • Lupus: Systemic lupus erythematosus (SLE) can lead to kidney inflammation as part of a broader autoimmune response.
   • IgA Nephropathy (Berger Disease): This condition involves the buildup of immunoglobulin A (IgA) in the glomeruli, causing inflammation and damage.
3. Genetic Conditions:
   • Alport Syndrome: An inherited disorder that not only causes kidney disease but also affects hearing and vision.
4. Toxins and Medications:
   • Certain drugs or exposure to toxins can damage the glomeruli and trigger GN.

What are the symptoms of glomerulonephtitis?

• Early Symptoms: Often, the kidneys may be significantly damaged before symptoms become apparent. Common early symptoms include:
  • Fatigue: Persistent tiredness that can be a sign of kidney dysfunction.
  • High Blood Pressure: Elevated blood pressure often accompanies GN.
  • Swelling: Accumulation of fluid leading to swelling in the face, hands, feet, and abdomen.
  • Blood and Protein in Urine: Known as hematuria and proteinuria, respectively. These indicators can be detected through urine tests.
• Progressive Symptoms:
  • Decreased Urine Output: Reduced production of urine may signal worsening kidney function.
  • Nausea and Vomiting: These symptoms can occur due to toxin buildup in the body.
  • Fever and Flu-like Symptoms: Systemic inflammation can cause these general symptoms.

How to diagnosis glomerulonephritis?

1. Medical History and Physical Exam: Initial assessment to understand symptoms and possible underlying conditions.
2. Urinalysis: Examines urine for the presence of red and white blood cells, protein, and signs of infection.
3. Blood Tests: Measures levels of waste products like creatinine and urea to evaluate how well the kidneys are filtering blood.
4. Ultrasound: Uses high-frequency sound waves to create images of the kidneys. It helps to assess kidney size, shape, and blood flow, and to identify any abnormalities or blockages.
5. Kidney Biopsy: A definitive diagnostic procedure where a small tissue sample is removed from the kidney and examined under a microscope to detect inflammation, scarring, and other pathological changes.

How to treat glomerulonephritis?

1. Management of Mild Cases:
   • Monitoring: Regular follow-ups to track kidney function and symptoms.
   • Lifestyle Adjustments: Includes dietary changes to reduce salt, protein, and potassium intake.
2. Treatment for Severe Cases:
   • Medications:
     • Blood Pressure Medicines: ACE (angiotensin-converting enzyme) inhibitors help protect kidney function by managing blood pressure.
     • Corticosteroids: These drugs reduce inflammation and prevent scarring of the glomeruli.
     • Diuretics: Help to manage fluid retention by increasing urine production.
   • Dietary Modifications: Limiting protein, sodium, and potassium to reduce kidney strain.
   • Advanced Treatments:
     • Dialysis: An external process that filters blood when the kidneys can no longer perform this function.
     • Kidney Transplant: Replaces the diseased kidney with a healthy kidney from a donor, often considered when kidney function declines to end-stage renal disease (ESRD).

What are the main complications of glomerulonephritis?

• Kidney Failure: Progressive GN can lead to kidney failure, requiring dialysis or a transplant.
• High Blood Pressure: Persistent elevated blood pressure may develop or worsen.
• High Cholesterol: Elevated cholesterol levels are common in chronic kidney conditions.
• Blood Clots: Increased risk of clots such as deep vein thrombosis (DVT) or pulmonary embolism.
• Damage to Other Organs: Prolonged GN can affect other body systems.

When to Contact a Healthcare Provider:

• Seek medical advice if symptoms worsen, new symptoms develop, or if there are concerns about kidney function.

Key Points:

Glomerulonephritis is an inflammatory disease of the kidneys’ filtering units, leading to impaired waste removal and potential complications. Early diagnosis and treatment are crucial for managing symptoms, preventing progression, and addressing potential kidney failure. Regular monitoring and treatment adjustments can significantly impact the management of this condition.

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• Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia resulting from impaired insulin secretion

Classification of Diabetes

I. Type 1 Diabetes

1. Insulin- dependent diabetes mellitus
2. Juvenile- onset diabetes

Characteristics of Type I Diabetes

• Hypoinsulinemia
• 10% of diabetes case
• Patient require insulin
• Age onset is childhood
• Ketoacidosis

Etiology of Type I Diabetes

• Autoimmune disease
• Selective destruction of beta cells by T cells
• Several circulating antibodies against beta cells
• Cause of autoimmune attack
• Both genetic and environmental factor are important

II. Type 2 Diabetes

• Non- insulin- dependent diabetes mellitus
  Adult- onset diabetes

Characteristics of Type 2 Diabetes

• Impaired insulin action
• Insulin secretion is normal or increased
• 90% 0f diabetes cases
• Age of onset is adulthood
• Associated with obesity
• Ketoacidosis but rare
• Most cases don’t require insulin

Etiology of Type 2 Diabetes

• Response to insulin is decreased
• The mechanism of insulin resistance is unclear
• Both genetic and environmental factor are responsible
• Post insulin receptor defect

Mechanism of hyperglycemia in diabetes

1. Increase in hepatic glucose output

• Decrease insulin secretion in Liver
• Decrease homeostatic effect on glucagon secretion resulting in increased glucagon
• Gluconeogenesis and glycogenolysis occurs in Liver
• Results in increased plasma glucose

2. Decrease in uptake of glucose in Muscles

• Decrease in insulin in muscles
• Decreased uptake of glucose and amino-acids in muscles
• Increased breakdown of proteins
• Results in increased plasma glucose and plasma amino acids

3. Decrease in uptake of glucose in adipose tissue

• Decrease in insulin
• Increased lipolysis and decreased lipogenesis
• Results in increased plasma fatty acids

Sign and symptoms of Diabetes

• thirst and frequent drinking
• most frequent urination particularly at night
• unexplained weight loss
• fatigue
• blurred vision
• frequent infection of skin, genital

Diagnostic evaluation of Diabetes

• history taking
• physical examination
• symptoms + random plasma glucose > 11.1 Mm (200mg/ dl )
• fasting plasma glucose >7Mm (126mg/dl)
• oral glucose tolerance test (OGTT) 2 hour plasma glucose >11.1Mm (200mg/dl)

Management of Diabetes mellitus

1. Medical management of Diabetes

Type 1 Diabets

• insulin injection should be given as per needed by analyzing blood sugar level
• frequent blood sugar check
• carbohydrate counting should be done

Type 2 Diabetes

• 7,5 % monotherapy ( metformin unless contraindicated)
• 5 – 9,0% dual therapy ( metformin + other medication)
• If the patient have diabetic complication then we must go for insulin therapy
• As Metformin is contraindicated in-case of renal failure, liver, or lung disease

2. Surgical management of Diabetes

• Gastric bypass and biliopancreatic diversion
• Pancreatic transplantation
• Islet cell transplantation

3. Nursing management of Diabetes

1. Nursing assessment of Diabetes A

• History taking, history of family and past medical history
• Past surgical history and other treatment
• Information about medication and insulin therapy
• Assessment of nutritional status
• Assess the blood sugar level
• Assess for sign and symptoms

2. Nursing diagnosis of Diabetes

• Imbalanced nutrition less than body requirement related to reduction of carbohydrate metabolism due to insulin deficiency
• Fluid volume deficit related to polyuria, decreased fluid intake
• Impaired skin integrity related to decreased sensory sensation, impaired circulation
• Risk for infection related to high glucose level reduction in leukocyte function
• Deficit knowledge about the disease the process related to lack of information

3. Nursing intervention of Diabetes

• Monitor vitals sign of the patient
• Provide medication as per cardex , administer insulin or an oral anti diabetic drug
• Analysis blood glucose level
• Maintain fluid and electrolyte balance
• Increase knowledge about diabetes management
• Monitoring and managing potential cmplications
• Provide skin care especially to the feet and legs
• Assist the client for coping mechanism
• Teach patient self- care and about disease condition

Complications of Diabetes mellitus

1. Acute complications of Diabetes

• Glucosuria ( glucose appear in urine)
• Polyuria( frequent urination)
• Polydipsia( excessive thirst)
• Polyphagia(excessive food intake)
• Ketoacidosis

2. Chronic complications of Diabetes

• Neuropathy ( loss of sensation due to damage of nerve fibres )
• Retinopathy ( damage of retina)
• Cataract ( damage of lens)
• In cardiovascular there may be atherosclerosis, hypertension, myocardial infraction
• In nephropathy there may be severe kidney failure and follow- up proteinuria

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What is Bronchitis?

• Bronchitis is defined as persistent cough with sputum production for atleast 3 month in 2 consecutive years

There are three types of bronchitis:

1. simple chronic bronchitis: it Is a kind of bronchitis in which cough is present with no physiologic evidence of airflow obstruction.
2. chronic asthmatic bronchitis: it is kind of bronchitis in which hyper reactive airways is present with intermittent bronchospasm and wheezing
3. obstructive chronic bronchitis: it is a kind of bronchitis in which there is development of chronic airflow obstruction_ emphysema in a heavy smokers

What are the causes of Bronchitis?

• Chronic irritation by inhaled substances
• Microbial infection
• Middle age
• Cigarette smoking
• Other pollutants like sulfur dioxide, nitrogen dioxide,
• Hyper secretion of mucus in large airways- hallmark of chronic bronchitis
• Hypertrophy of the submucosal glands of trachea and bronchioles
• Marked increased in goblet cells of small airways

What is the Pathophysiology of Bronchitis?

• Hypermeia, swelling of mucus membrane
• Increased number of goblet cells
• Bronchial wall become thickened, bronchial lumen is narrowed
• Mucus may plug airwayAlveoli adjacent to bronchioles may damaged and fibrosed
• Respiratory infection
• Bronchitis

What are the clinical features of Bronchitis?

• Persistent productive cough with copious sputum
• Dyspnea on exertion
• Hypercapnia, hypoxemia, and mild cyanosis
• Cor-pulmonale with cardiac failure
• Chest pressure, headache, shortness of breath, sleeping difficulty,or sore throat
• Fatigue or malaise
• death

What are the diagnostic evaluation for Bronchitis?

• history taking: take the history of the patient like personal history, history of smoking, history of bronchitis in family member, allergy history, history of infection, any past medical and surgical history

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Central nervous system infections including Meningitis

• The first step in the diagnosis of a patient with suspected CNS infection is a lumbar puncture (spinal tap).

Specimen: Cerebrospinal fluid (CSF)

Collection and Transport of CSF:

• Aseptically CSF is collected.
• A needle is inserted into the subarachnoid space (lumbar puncture), at the lumbar spine region between L3, L4, or L5.
• In the sterile collection tubes, three or four tubes of CSF should be collected. It should not contain additives.
• Tube 1 is used for:
  • chemistry studies
  • glucose and protein count
  • immunology studies
• Tube 2 is used for culture.
• Tubes 3 and 4 are used for cell count and differential count.
• The amount of volume to be collected depends on the volume available in the patient which may differ between the adults and the neonates.
• When the needle first punctures the subarachnoid space, the opening pressure of the CSF is observed.
• In the high opening pressure, CSF should be collected slowly to prevent the collection of a larger volume of fluid.
• For the detection of mycobacteria and fungi, a minimum of 5 to 10 mL is recommended.
• Centrifugation and subsequent culture are done.
• The false-negative result may be seen if the sample is inadequate.
• CSF should be sent to the laboratory as soon as possible.
• In the case of delay after an hour or longer, agents such as Streptococcus pneumoniae, may not be detectable.
• CSF should not be refrigerated for microbiological studies.
• In the case of delay, it should be left at room temperature or incubated at the 35°C.
• For the viral study, CSF may be refrigerated, for as long as 23 hours after collection or frozen at −70°C.
• For hematology studies, CSF specimens can be refrigerated,
• For chemistry and serology, CSF can be frozen (−20° C).

Initial processing of CSF:

• All the CSF specimens for the bacterial, fungal, or parasitic studies should be centrifuged.
• Volume greater than 1 ml should be used.
• Centrifugation should be done at 1500× g for 15 minutes.
• Suspected specimens for cryptococci or mycobacteria should be handled carefully.
• When CSF fewer than 1 mL is available, Gram stain should be done and plated directly to the blood and chocolate agar plates.
• The supernatant is removed to a sterile tube, leaving approximately 0.5 mL of fluid.
• For visual examination and culture, the remaining fluid is used to suspend the sediment.
• The supernatant can be used:
• To test the presence of antigens
• rapid diagnostic test (vertical flow immunochromatography)
• for meningitidis
• For chemistry evaluations (e.g., protein, glucose, lactate, C-reactive protein).

Laboratory diagnosis:

• Communication between the physician and the microbiology laboratory is essential for the proper diagnosis and treatment of the patient.
• The diagnosis of acute bacterial meningitis can be excluded in patients with normal fluid parameters in almost all cases.
• Similar criteria have been used to exclude the performance of smear and culture for tuberculosis, as well as syphilis serology, on CSF specimens.

1. Visual Detection of Etiologic Agents in CSF:

• CSF sediment is examined for the presence of cells and organisms.

i) Stained Smear of Sediment:

• Gram staining should be performed on all the CSF sediments.
• The use of contaminated slides may give false-positive smears.
• The sediment should be thoroughly mixed and a heaped drop should be placed in the slide.
• The slide should be sterile or alcohol-cleaned.
• The sediment should never be spread out on the slide surface.
• It is because of the difficulty to find small numbers of microorganisms.
• The drop of sediment is allowed to air dry.
• Then it is heated or methanol fixed.
• Then it is stained by either Gram or acridine orange.
• A faster examination of the slide under high-power magnification (400×) can be done by the acridine orange fluorochrome stain.
• The brightly fluorescing bacteria can be visualized easily.
• Confirmation of the presence and the morphology of the organism can be done, using the Gram stain (directly over the acridine orange.
• The use of a cytospin centrifuge is an excellent alternative method for the preparation of slides for staining.
• It concentrates cellular material and bacterial cells up to 1000-fold.
• Centrifugation is done then the CSF is concentrated onto a circular area of a microscopic slide.
• It is then fixed, stained, and examined.
• Reporting should be done for the presence or absence of bacteria, inflammatory cells, and erythrocytes.

ii) Wet Preparation:

• Amoebas are best observed by this method.
• Sediment can be examined as wet preparation under phase-contrast microscopy.
• The light microscope can be used as an alternative, by slightly closing the condenser.
• Amoebas must be distinguished from motile macrophages, which occasionally occur in CSF.
• A trichrome stain can be used in the differentiation of amoebas from somatic cells.
• On the lawn of Klebsiella pneumoniae or Escherichia coli, the pathogenic amoebas can be cultured. Lawn.

iii) India Ink Stain:

• Cryptococcus neoformans consists of the large polysaccharide capsule which could be visualized by the India ink stain.
• For capsular antigen, latex agglutination testing is more sensitive and extremely specific.
• Antigen test is recommended than the India ink stain.
• Culture is essential in case of the AIDS patients because detectable capsules of neoformans may be absent.
• A drop of CSF sediment is mixed with one-third volume of India ink, for the India ink preparation.
• By the addition of 0.05 mL thimerosal, India ink can be protected from contamination.
• Smooth suspension is made by mixing the CSF and ink.
• Then a coverslip is applied to the drop.
• Then it is examined under high-power magnification (400×) for characteristic encapsulated yeast cells.
• Examination can be done under oil immersion.
• White blood cells must not be confused with yeasts.
• The presence of encapsulated buds, smaller than the mother cell, is diagnostic.

2. Direct Detection of Etiologic Agents:

Antigen detection:

• For the rapid detection of antigen in the CSF, commercial reagents and kits are available.
• By latex agglutination, rapid antigen detection can be done from CSF.
• An antibody-coated particle binds to a specific antigen which results in macroscopically visible agglutination.
• The soluble capsular polysaccharide, including the group B streptococcal polysaccharide, is well suited to serve as bridging antigens.
• Polyclonal or monoclonal antibody or an antigen from an infectious agent is present in the agglutination assay.
• Different commercial systems have been developed.
• Soluble antigens may concentrate in the urine from Streptococcus agalactiae and Haemophilus influenza.
• For the performance of antigen detection test systems, the manufacturers’ directions must be followed
• Some systems may also require the pretreatment of samples which is usually for 5 minutes.
• The pretreatment, called rapid extraction of antigen procedure (REAP), is recommended for laboratories that use commercial body fluid antigen detection kits.
• Only a limited number of clinically useful situations warrant bacterial antigen testing (BAT).
• Practice guidelines for the diagnosis and management of bacterial meningitis do not recommend routine use of BAT.

Bacteria involved in meningitis:

Cryptococcus neoformans:

• For the detection of polysaccharide capsular antigen of Cryptococcus neoformans, the reagents are available commercially.
• When the positive result for cryptococcal antigen is obtained in CSF specimens, a second latex agglutination test for rheumatoid factor should be done.
• Both latex agglutination assays (numerous commercial manufacturers) and enzyme immunoassays are available for the detection of Cryptococcus antigen.
• The false-negative reaction may be seen in the undiluted specimens which contain large amounts of capsular antigens.
• False-negative reaction is caused by a prozone phenomenon.
• Patients with AIDS may have an antigen titer over 100,000.
• It requires many dilutions to reach an endpoint.
• Parasites and Viruses are also involved in meningitis

  Conditions for the culture of free-living amoebae and viral agents should be maintained to detect viruses and parasites.

3. Molecular methods:

• PCR (Polymerase Chain Reaction )
• Real-time PCR

4. Other Tests

• the Limulus lysate test
• CSF lactate determinations,
• C-reactive protein
• mass spectrometry
• gas-liquid chromatography

5. Culture:

• Routine bacteriologic media: chocolate agar plate, 5% sheep blood agar plate, and an enrichment broth, usually thioglycolate without indicator.
• Blood agar plates help in the recognization of pneumoniae.
• For the isolation of influenzae and N.meningitidis, a chocolate agar plate is used.
• Plates should be incubated at 37° C in 5% to 10% carbon dioxide (CO2) for at least 72 hours.
• Candle jar can be used, if a CO2 incubator is not available.
• The broth should be incubated in the air at 37° C for at least 5-10 days.
• Anaerobic blood agar plate may also be inoculated, when Gram stain shows the morphologically resembling anaerobic bacteria.
• If a brain abscess is suspected then also anaerobic blood agar plate is used.
• For CSF fungal cultures, two drops of the well-mixed sediment should be inoculated onto:
• Sabouraud dextrose agar
• other non-blood containing medium
• brain-heart infusion with 5% sheep blood.
• Incubation of Fungal media should be done at 30° C for 4 weeks.
• If possible, two sets of media should be inoculated.
• One set should be incubated at 30° C and the other at 35° C.

Specimen: Brain Abscess/Biopsies samples

Collection, Transport, and Processing of brain absscess and biopsies

• Under anaerobic conditions, biopsy specimens or aspirates from brain abscesses should be submitted.
• Devices are commercially available too for transportation.
• Swabs are not considered an optimum specimen.
• If swabs are used to collect abscess material, during transportation, they should be maintained in an anaerobic environment.
• Before plating and smear preparation, biopsy specimens should be homogenized in sterile saline.
• processing should be kept to a minimum to reduce oxygenation.
• Inoculation should be done onto 5% sheep blood and chocolate agar plates, for the abscess and biopsy specimens.
• Incubation should be done in 5% to 10% CO2 for 72 hours at 35° C.
• In addition, an anaerobic agar plate and broth with an anaerobic indicator, vitamin K, and hemin should be inoculated and incubated in an anaerobic environment at 35° C.
• Incubation of the anaerobic culture plate is done at a minimum of 72 hours.
• It is examined after 48 hours of incubation.
• Anaerobic broths should be incubated for a minimum of 5 days.
• When fungi are suspected, fungal media, such as brain-heart infusion with blood and antibiotics or inhibitory mold agar, should be inoculated.

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• Different infectious agents may get entrance to the eye either through the external or endogenous source.
• Superficial structures like the conjunctiva and the cornea are affected during external infections.
• Microorganisms present in the blood (e.g., endocarditis )may cause infection endogenously
• Endogeneous infection may be caused by the reactivation of latent viruses or parasites (e.g., cytomegalovirus or toxoplasmosis).

Different types of eye infections

1. Blepharitis:

• It is the inflammation of the margins(edges) of the eyelids; (eyelids, eye lashes, or associated pilosebaceous glands or meibomian glands).
• Symptoms include irritation, redness, burning sensation, and occasional itching. Condition is typically bilateral.
• Causative agents:
  • Bacteria: Staphylococcus aureus
  • Virus: Herpes simplex virus
  • Fungi; Malassezia furfur
  • Parasites: Phthirus pulis

2. Conjunctivitis:

• Inflammation (conjunctivitis) produces redness (pink eye), itching, and a discharge, which may be mucous or purulent.
• In this case, eyelids may stick together because of the exudation in bacterial infections which are thick, sticky, and encrusted.
• In patients having seasonal allergies, acute noninfectious inflammation may also occur.
• Conjunctivitis is highly contagious and can be transferred easily to the other eye or other individuals by contact (e.g., rubbing the infected eye and then the normal eye).
• Causative agents:
• Bacteria
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Staphylococcus aureus
  • Haemophilus spp.
  • Pseudomonas aeruginosa
  • Chlamydia trachomatis
  • Neisseria gonorrhoeae
  • Streptococcus pyogenes
  • Moraxella spp.
  • Corynebacterium spp.

• Viruses
  • Adenoviruses
  • Herpes simplex (HSV)
  • Varicella-zoster
  • Epstein-Barr virus (EBV)
  • Influenza virus
  • Paramyxovirus
  • Rubella
  • HIV
  • Enterovirus
  • Coxsackie A

3.Keratitis:

• Keratitis, inflammation of the cornea, is a much more serious infection than conjunctivitis.
• Although there are no specific clinical signs to confirm infection, most patients complain of pain.
• Usually decrease in vision may occur, with or without discharge from the eye.
• Keratitis can result in scarring and blindness.
• Causative agents:
• Bacteria
  • S. aureus
  • S. pneumoniae,
  • Pseudomonas, aeruginosa
  • Moraxella lacunata
  • Bacillus spp.
• Virus
  • Herpes Simplex Virus
  • adenoviruses,
  • varicella-zoster

• Fungi
  • Fusarium solani,
  • Aspergillus spp.
  • Candida spp.
  • Acremonium,
  • Curvularia

• Parasites
  • Acanthamoeba spp
• A different non-infectious injury like trauma and ultraviolet radiation can cause keratitis.

4. Keratoconjunctivitis:

• It is an infection that involves both the conjunctiva and cornea.
• Ophthalmia neonatorum is acute conjunctivitis or keratoconjunctivitis of the newborn which is caused by either gonorrhoeae or C. trachomatis.
• Causative agents:
• Bacteria
• It includes the agents for keratitis/ conjunctivitis.
  • Streptococcus pneumoniae,
  • Haemophilus influenzae,
  • Staphylococcus aureus,
  • Haemophilus spp.
  • Pseudomonas aeruginosa
  • Chlamydia trachomatis,
  •  Neisseria gonorrhoeae,
  • Streptococcus pyogenes,
  • Moraxella spp.,
  • Corynebacterium spp.
  • Bacillus spp
• Virus
  • It includes the agents for keratitis/ conjunctivitis
  • Adenoviruses,
  • Herpes simplex (HSV),
  • Varicella-zoster.
  • Epstein-Barr virus (EBV)
  • Influenza virus,
  • Paramyxovirus,
  • Rubella,
  • HIV
  • Enterovirus,
  • Coxsackie A

• Fungi
• It includes the agents for Keratitis
  • Fusarium solani,
  • Aspergillus spp.,
  • Candida spp.,
  • Acremonium,
  • Curvularia
• Parasites
  • Toxoplasma gondii,
  • Toxocara

5. Chorioretinitis and uveitis:

• It is the inflammation of the retina and underlying choroid or the uvea.
• The infection can result in loss of vision.
• Causatiive agents:
•  Bacteria:
  • Mycobacterium tuberculosis
  • Treponema pallidum,
  • Borrelia burgdorferi
• Virus
  • Cytomegalovirus
  • HSV

• Fungi
  • Candida spp.

• Parasites
  • Toxoplasma gondii,
  • Toxocara
  • Treponema pallidum

6. Endophthalmitis

• It is the infection of the aqueous or vitreous humor.
• This infection is usually caused by bacteria or fungi. It is rare, develops suddenly, and progresses rapidly, often leading to blindness.
• During the movement of the eye, there is pain. Vision is decreased.
• Causative agent:
• Bacteria:
  • S. aureus,
  • S. epidermidis,
  • pneumoniae,
  • Streptococcal spp.
  • P. aeruginosa,
  • Gram-negative organisms,
  • Nocardia spp

• Virus
  • HSV
  • Varicella zoster

• Fungi
  • Candida spp.,
  • Aspergillus spp.,
  • Volutella spp.,
  • Acremonium spp

• Parasite
  • Toxocara
  • Onchocerca volvulus

7. Lacrimal infections, canaliculitis:

• It is a rare, chronic inflammation of the lacrimal canals in which the eyelid swells and there is a thick, mucopurulent discharge.
• Causative agent:
• Bacteria:
  • Actinomyces,
  • Propionibacterium
  • Propionicum

8. Dacryocystis:

• It is the inflammation of the lacrimal sac that is accompanied by pain, swelling, and tenderness of the soft tissue in the medial canthal region.
• Causative agents:
• Bacteria:
  • S. pneumoniae
  • S. aureus,
  • S. pyogenes,
  • Haemophilus influenza

• Fungi:
  • C. albicans,
  • Aspergillus spp.

9. Dacryoadenitis

• It is an acute infection of the lacrimal gland.
• These infections are rare and can be accompanied by pain, redness, and swelling of the upper eyelid, conjunctiva discharge.
• Causative agents:
• Bacteria:
• S. pneumoniae,
• S. aureus
• S. pyogenes

Laboratory Diagnosis of eye infection:

Specimen Collection and Transport

• A sterile swab should be taken for sample collection.
• From the lower conjunctiva sac and inner canthus (angle) of the eye, purulent material is collected on the sterile swab.
• Both eyes need to be cultured separately.
• For the Chlamydial culture, a dry calcium alginate swab should be taken.
• Then it should be placed in a 2-SP (2-sucrose phosphate) transport medium.
• If for the detection, Direct Fluorescent antibody (DFA) are to be used, then in such case additional slide also should be prepared.
• In that slide, the swab should be rolled across its surface which needs to be fixed with methanol.
• In the case of keratitis, scrapings of the cornea should be taken with a heat-sterilized platinum spatula.
• Multiple inoculations with the spatula are made to blood agar, chocolate agar, an agar for the isolation of fungi, thioglycollate broth, and an anaerobic blood agar plate.
• Other special media may be used if indicated.
• Corneal specimens for the detection of HSV and adenovirus should be cultured. They should be placed in viral transport media.
• Recently, the collection of two corneal scrapes (one used for Gram stain and the other transported in brain heart infusion medium and used for culture) was determined to provide a simple method for diagnosis of bacterial keratitis.
• From the anterior and posterior chambers of the eye, wound abscesses, and wound dehiscence (splitting open) specimens are collected for the culture of endophthalmitis.
• Lid infection material is collected on a swab conventionally.
• Under anaerobic conditions, transportation of the material should be done from the lacrimal canal in the case of canaliculitis.
• Aspiration of fluid from the orbit is contraindicated in patients with orbital cellulitis.

Direct Visual Examination:

• The smear should be prepared and a Gram stain should be performed.
• If there are other appropriate microscopic techniques, it should be performed.
• In bacterial conjunctivitis, polymorphonuclear leukocytes predominate; in viral infection, the host cells are primarily lymphocytes and monocytes.
• For the detection of Chlamydia, elementary body or inclusions should be checked.
• For this, it should be stained immediately with a monoclonal antibody conjugated to fluorescein.
• Using histologic stains, basophilic intracytoplasmic inclusion bodies are seen in epithelial cells.
• To detect herpes group infection in the conjunctivitis specimens, a Tzanck smear can be made. It shows the multinucleated epithelial cells.
• For the rapid diagnosis of the virus infection, DFA stains available for both HSV and VZV
• For the keratitis, the examination can be done using:
  • Gram stain
  • Giemsa stain
  • periodic acid-Schiff (PAS)
  • methenamine silver stains.
• Motile trophozoites should be observed by using the direct wet preparation in case of Acanthamoeba or other amebae and a trichrome stain should be added to the regimen.
• Culture is the most sensitive detection method for the diagnosis.
• In the case of endophthalmitis, the specimen needs to be examined by:
  • Gram
  • Giemsa
  • Periodic Acid-schiff (PAS)
  • Methenamine silver stains.
• Centrifugation should be done if the specimen is fluid and is in large volume.

Culture for eye infection:

• The number of organisms recovered from culture is low due to the washing action of tears.
• If the specimen is not purulent, large inoculums in a variety of media should be used to find out the etiological agent.
• The best result can be obtained when the conjunctival scrapings are placed directly onto the media.
• At a minimum, blood and chocolate agar plates should be inoculated and incubated under increased carbon dioxide tension (5% to 10% CO2).
• Sample from Both eyes should be cultured.
• Potential pathogens also may be present in an eye without causing infection.
• If the organism is isolated from both the infected and non-infected eye, it may not responsible for causing infection.
• If an organism only grows in culture from an infected eye, it might be the causative agent.
• Loeffler’s medium can be used when Moraxella lacunata is suspected.
• In this case, the growth of the medium causes the proteolysis and pitting of the medium.
• Loeffler’s or cystine-tellurite medium should be used if diphtheritic conjunctivitis is suspected.
• For the isolation of the organism from the keratitis, endophthalmitis, and orbital cellulitis, a reduced anaerobic blood agar plate, a medium for the isolation of fungi, and a liquid medium such as thioglycolate broth should be used.
• A reduced anaerobic blood agar plate should be used for the more serious eye infections.
• Blood culture also should be done in severe infections.
• From the transport broth, Chlamydia and virus should be inoculated inappropriate media.
• Cycloheximide-treated McCoy cells should be used for the Chlamydia
• For viral isolation, human embryonic kidney, primary monkey kidney, and Hep-2 cell lines can be used.

Molecular diagnosis for eye infection:

• Enzyme-linked immunosorbent assay (ELISA) tests and DFA staining are available for the detection of Chlamydia trachomatis.
• An ELISA test of aqueous humor is available for the diagnosis of Toxocara
• Single and multiplex polymerase chain reaction (PCR) assays

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Resident Microbial Flora of Ear

• Pneumococci
• Streptococcus pneumonia
• Propionibacterium acnes
• Staphylococcus aureus,
• More frequently Enterobacteriaceae are encountered.
• Occasionally Pseudomonas aeruginosa is found.
• Candida (non-C. albicans) is also common.

1. External Ear Infections: Otitis externa

• Otitis externa is similar to skin and soft tissue infection.
• Two major types of external otitis exist:
  • Acute
  • chronic

a) Acute external otitis:

• It may be localized or diffuse.

i. Acute localized disease:

• It occurs in the form of a pustule or furuncle.
• It is typically is caused by Staphylococcus aureus.
• Group A Streptococci causes Erysipelas.
• The soft tissue of the ear and external ear canal may be involved.

ii. Acute diffuse otitis externa (swimmer’s ear):

• It is related to softening of tissue(maceration) of the ear.
• It results from swimming or hot, humid weather.
• Pseudomonas aeruginosa, play an important role.
• aeruginosa also causes external otitis which can be severe and hemorrhagic.
• Occasionally it is found to be related to hot tub use which is also difficult to treat.

b)Chronic otitis externa:

• In the patients with chronic, suppurative otitis and the persons having perforated eardrums, the irritation of drainage from the middle ear results in chronic otitis externa.
• Malignant otitis externa is a necrotizing infection.
• It spreads to adjacent areas of soft tissue, cartilage, and bone.
• It may result in a life-threatening condition when the infection spreads to the central nervous system or vascular channel.
• It is caused by P. aeruginosa and anaerobes.
• In the diabetic patient having blood vessel disease, Malignant otitis media is seen.
• Occasionally, external otitis can spread to the cartilage of the ear.

Different parts of the ears like an external auditory canal, the soft tissue of the ear, or the tympanic membrane may be infected with the virus.

• Though it’s not established suspicion is made to the influenza A virus.
• Within the soft tissue of the ear and the ear canal. VZV causes painful vesicles.
• Viral agents such as influenza are the bacterial agents typically associated with acute otitis media:
  • pneumonia
  • influenza
  • catarrhalis
• Mycoplasma pneumoniae is rarely associated with this condition.

2. Middle Ear Infections: Otitis media

• It is the most common infection in children.
• Causative agents are:
  • Pneumococci
  • Haemophilus influenza
  • Group A streptococci (Streptococcus pyogenes)
  • Moraxella catarrhalis
  •  Staphylococcus aureus,
  • gram-negative enteric bacilli
  • anaerobes
  • Respiratory syncytial virus (RSV)
  • Influenza virus
• Otitis media with effusion (fluid) is considered a chronic sequela of acute otitis media.
• From the patients with otitis media with effusion, Alloiococcus otitis has been isolated.
• Pathogens of Chronic otitis media:
  • Peptostreptococcus
  • Bacteroides fragilis group,
  • Prevotella melaninogenica
  • Porphyromonas
  • Prevotella
  • Fusobacterium nucleatum a less
• The complication of chronic otitis media is mastoiditis.

Pathogenesis of otitis media:

• External ear infection (otitis media) can be caused due to many reasons such as:
  • Local trauma
  • the presence of foreign bodies
  • excessive moisture can lead to otitis externa
• Infection can progress up to the external ear by the purulent drainage from the middle ear.
• Otitis media also can be developed by anatomic or physiologic abnormalities.
• Infection may occur when the fluid develops in the middle ear.
• The auditory tube plays a major role in the protection of the middle ear:
  • protects from the nasopharyngeal secretion.
  • drains the secretions which are produced in the middle ear into the nasopharynx
  • Ventilates the middle ear
  • Maintains the air pressure in the equilibrium state with the external ear canal
• When there occurs any malfunctioning of these conditions, the infection may occur.
• Example: There is inflammation and swelling of the auditory canal when there is a viral upper respiratory infection. It hampers the ventilating function in the middle ear. These alternations in the pressure allow the potentially pathogenic bacteria present in the nasopharynx to get the entrance into the middle ear.

Laboratory Diagnosis of otitis media:

Specimen Collection and Transport

• Generally, culture is not done for the diagnosis of middle ear infection or otitis media.
• Diagnosis of external otitis is done by culture.
• Using mild germicide such as 1:1000 aqueous solution of benzalkonium chloride, the external ear should be cleansed.
• It helps to reduce the number of contaminating skin flora.
• Materials are obtained by spontaneous perforation of the eardrum or by the needle aspiration of the middle ear fluid (tympanocentesis) using sterile equipment.
• Specimens from the mastoid are generally taken on swabs during surgery, although actual bone is preferred.
• Specimens should be transported anaerobically.

Direct Visual Examination:

• Aspiration is done from the middle ear or mastoid, the direct examination is done for bacteria and fungi.
• Fungal elements can be revealed from the calcofluor white or PAS stains.
• Bacterial, fungal, and several parasitic species can be stained efficiently by the use of Methenamine silver stains.

Culture and Nonculture Methods:

• Inoculation of the ear specimens should be done in blood agar, MacConkey agar, and Chocolate agar.
• On the specimens obtained by tympanocentesis or those obtained from patients with chronic otitis media or mastoiditis, anaerobic culture also should be done.
• To detect the common middle ear pathogens, conventional and real-time PCR can be done because, in only 20% to 30% of patients, cultures are positive.

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• Any event or condition, characteristics or combination of these factor which plays an important role in producing the disease cause may not be a single factor and often comprises several components.
• For e.g., in case of food poisoning due to Salmonella. The presence of Salmonella is necessary cause. Contaminated food (salad) is the sufficient cause.
• Necessary cause is the component of sufficient cause.

Factors involved in disease causation:

• Four types of factors that play important role in disease causation.
  • Predisposing factor
  • Enabling
  • Precipitating
  • Re-enforcing factor

1. Predisposing factor may create a state of susceptibility of disease to host. E.g., age, sex, previous illness.
2. Enabling factor favours the development of disease. E.g., poor housing, poor sanitation, poor nutrition, low economy.
3. Precipitating factor is most important for disease causation. It is associated with onset of disease. E.g., exposure to specific infectious agents or toxins.
4. Re-enforcing factor may aggravate and establish disease. E.g, repeated exposure, hardwork.

Establishing cause of disease:

Causal inference:

• It is the term used for the process of determining whether observed association are likely to be causal for establishing disease.
• Guidelines for causal inference:
  • Temporal relationship:
    • Most crucial factor cause must proceed the effect (disease). This type of relation is called temporal relationship.
    • In case of case control and cross-sectional study, confusion may arise but in case of longitudinal study or experimental study it can be determined.
  • Plausibility:
    • Association should be possible (plausible).
    • Is the association consistent with the knowledge or not?
  • Consistency:
  • Different studies should lead the same result.
  • Strength:
    • Strength should be higher. It can be determined by odds ratio.
  • Dose-response relationships:
    • Should be applicable to the cause and effect.
  • Reversibility:
    • If exposure is present, effect is seen and on removal of exposure causes absence of effect.
  • Study design:
  • Judging the evidence:
    • There is no completely reliable criteria for guiding the result.
    • It is tentative and uncertainty remain must important guideline is temporal relation, plausibility, study design, consistency etc.

Natural history of disease:

• Co-interrupted pathway of disease. It refers to the description of uninterrupted progression of disease in an individual from the moment of exposure to causal agent until death, recovery or disability.
• Deletion and treatment of any stage of disease can alter the natural history.
• It comprises various stages:
  • Pre-pathogenesis phage: Interaction between agent, host and environment.
  • Pathogenesis phage: Entry of pathogen, incubation period and appearance of sign and symptoms of disease. This phage is called pathogenesis phage.
  • Late pathogenesis phage: recovery, disability or death
  • Prognosis: Prediction of the course of particular event of disease that will occur in future.
  • Based on defined group of patients and can be done by clear understanding of natural history of disease.

Interaction of agent, host and environment

• Can be bi-directional or triangular
  • Agent – environment interaction
  • Host – environment interaction
  • Host-agent interaction
  • Agent-host-environment interaction

Management of disease:

• Prevent, control, elimination, eradication

Prevention:

• Can be done in four level corresponding to the phases of disease development. They are:
  • Primordial prevention (most recent concern)
  • Primary prevention
  • Secondary prevention
  • Tertiary prevention
• Primordial:
  • It was identified as increase in knowledge of epidemiology of cardiovascular disease.
  • The base underlying cause of coronary heart diseases have identified as diet high in saturated fatty acid.
  • Aim of primordial prevention is to avoid the emergence and establishment of social, economic, and cultural pattern of living to host contributed to elevated risk of disease, primordial prevention helps in declining the mortality from infectious diseases and reducing un-intentional injuries and diseases such as cancer coronary heart disease by avoiding high risk behavior.
  • Effective primordial prevention requires strong government, regulatory and fiscal action to stop the promotions of the items that increase the risk.
• Primary prevention:
  • The aim of prevention is to limit the incidence of disease by controlling causes and risk factor.
  • Primary prevention involves two strategy:
  • Population strategy
  • High risk individual strategy
• Secondary prevention:
  • The aim is to cure patient and reduce the more serious consequences of disease through early diagnosis and treatment.
  • It comprises the measure available to individuals and population for early detection and prevent the effective interventions.
  • It Is directed at the period between onset of disease and normal time of diagnosis and aims to reduce prevalence of disease.
  • Main requirement of useful secondary prevention program are:
  • Safe and accurate methods of disease detection, preferably of preclinical state.
  • Effective method of intervention.
• Tertiary prevention:
  • The aim is to reduce the progress or compilation of established disease.
  • It reduces impairment and disability and minimize suffering due to disease.

Concept of Disease causation in epidemiology and management of disease

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• Prions are unusual proteinaceous infectious particles that cause a group of universally fatal neurodegenerative disease called the spongiform encephalopathies by an entirely unique mechanism.
• The word ‘prion’ was coined by Stanley B. Prusiner in 1982.
• Prion is derived from the word protein and infection.
• Prions, like viruses, are not actually active, although both can reproduce by hijacking the functions of living cells.
• Prions are small protein-containing infectious particles with no detectable nucleic acids.
• They are abnormal proteins with an abnormal folding structure (β‐pleated sheets), that have an equivalent protein with the same primary structure within the host, that folds normally (2 α‐helices).
• The function of this protein, whose gene is located on chromosome 20, is unknown.
• The misfolded protein molecules form aggregates (“amyloid”) that interfere with cellular function.
• The normal protein is called PrPc (for prion protein cellular), and the abnormal protein is called PrPsc (for scrapie, a transmissable infectious spongiform encephalopathy of sheep and goats).
• The abnormal proteins transmit their information to the normal proteins, causing them to fold abnormally. The abnormal aggregates lead to tissue damage, which affects primarily the brain, leading to a slowly progressive encephalopathy and death.

Structural features of infectious prions:

• Different hypotheses have been suggested for the makeup of proteins.
• However, the widely accepted hypothesis is the ‘protein only hypothesis’ first suggested by Griffith (1965) and re-established subsequently by Prusiner.
• Prions show following features:
  • They do not contain nucleic acids.
  • They contain an aggregated of hydrophobic glycoprotein resistant to protease.
  • The protein present in humans and other animals is called cellular prion protein. It is similar to glycoprotein in scrapie; also known as scrapie prion protein (molecular wt. is 27,000-30,000 Da) in sequence but differs from it in being sensitive to protease and being present in plasma membrane.

Mode of transmission of prion disease:

• The disease is transmitted either orally or transcutaneously by direct contact through body fluids such as saliva, blood, urine of infected animals
• The other possible route is by the blood circulation.

Pathogenesis of prion disease:

• PrPsc (scrapic protein) is generated endogenously or enter inside the body through exogenous sources from infected animals or human. But, how the prions reach the CNS, their target is yet unknown. However, It is convinced that the prions may reach the CNS via splanchnic nerves at the level of the thoracic spinal cord and via parasympathetic fibers connecting with the brain.
• PrPsc (Scrapic protein) binds to the normal cellular protein (PrPc) of the host found in most tissues but abundantly in the CNS particularly the neurons.
• PrPsc is ingested by neurons and phagocytic cells but continues to remain intact without being degraded.
• This may support to vacuolation of the neuron, a key pathological alteration seen in encephalitis caused by prions.
• In addition, accumulation of prions in high concentration causes damage is the brain tissue.
• These include the formation of amyloid containing plagues and fibrils, a proliferation and hypertrophy of astrocytes, and fusion of neurons and adjacent glial cells.

Clinical symptoms caused by prion:

• Prions cause neurodegenerative disease by aggregating extracellularly within the CNS to form plagues also known as amyloid which disrupt the normal tissue structure.
• The neurogenerative symptoms can include compulsions, dementia, ataxia and behavioral or personality changes.
• In all species, it is characterized by spongy appearance of the cerebral gray matter, very long incubation period, slow course, fatal termination, predilection for involvement of CNS, absence of immune response and genetic predisposition.
• Prion cause the following diseases in humans:
  • Kuru
  • Crutzfelt-Jacob disease
  • Variant CJD
  • Gerstmann-Straussler-Scheinker (GSS) syndrome
  • Fatal familial insomnia
  • Sporadic fatal insomnia
• Prion cause the following diseases in animals:
  • Scrapic
  • Bovine sporyiform encephalopathy (BSE) also known as mad cow disease
  • Transmissible mink encephalopathy
  • Chronic washing disease of deer, mule and elk.

Laboratory diagnosis of prion disease:

• The diagnosis of prion disease is always critical.
• It is usually confirmed by the histopathology of the brain tissue showing characteristic biological changes.
• No serological tests are available.
• Detection of protein 14-3-3 in the CSF by Western blot in a sensitive and specific method in the cases of sporadic CJD and in rCJD.
• A specific reduction in uric acid level in the CSF have been shown in VCTD but not in sporadic CJD, thus facilitating in the differential diagnosis of VCJD.

Treatment of prion disease:

• No specific treatment is available.
• All known prion diseases are untreatable and fatal.

Prevention and control of prion disease:

• Special care while handling materials from patients with CJD or VCJD.
• Special disinfection protocols have been developed by WHO for prevention of these diseases.
• Autoclaving at 15lbs for 1hr before handling infectious products
• Treatment with 0.1M NaOH and 5% hypochlorite solution before handling infectious products.

Prion disease (an infectious protein)

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Steps in outbreak investigation:

• Considered 6 headings:
  • Preliminary enquiry
  • Management of incidence
  • Identification of cases and collection and analysis of data
  • Control
  • Communication
  • Further epidemiological and lab studies

Outbreak (epidemic) investigation

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Characteristics of epidemiological marker:

• Typeability
• Reproducibility
• Descriminatory power
• Ease of performance
• Ease of interpretation

Phenotypic method:

• Phenotyping method is based on the expressed characteristics.
• Characteristics of organism that is used for typing is marker.
• Organism of same source origin or source- type/strain.
• Phenotyping includes;
  • Biotyping
  • Serotyping
  • Phage typing
  • Antibiogram typing
  • Bacteriocin typing
• Biotyping:
  • Classified on the basis of physiological or bio-chemical tests.
  • Commonly used characters are morphology, cultural characteristics, biochemical reactions (nitrate reduction test, indole test, pigment production, H₂S production, carbohydrate fermentation)
• Serotyping:
  • Typing method done by the use of hyper-immune anti-sera or purified immunoglobulin to detect specific antigen.
  • Serotyping is generally done for Salmonella, Klebsiella, etc. for detection of O-antigen, H-antigen, R-antigen, K-antigen, etc.
• Phage typing:
  • Bacteriophage typing identify strains by the pattern of specific set of phages.
  • Generally used for Staphylococcus aureus and for Salmonella Typhi.
• Antibiogram typing:
  • Typing method on the basis of antibiotic susceptibility or resistance pattern.
• Bacteriocin typing:
  • On the basis of bacteriocin production.

Genotyping method:

• Genotyping includes;
  • Plasmid profiling
  • G+C ratio
  • Ribotyping
  • Restriction endonuclease
  • RPLP
  • PFGE
  • PCR amplification
• Plasmid profiling:
  • On the basis of no. of plasmid, size of plasmid in the organism.
• G+C ratio:
  • Same strains have similar G+C ratio.
• Ribotyping:
  • 16sRNA is highly specific for organism.
• Restriction endonuclease enzyme:
  • Whole genome is fragmented using same set of restriction endonuclease enzyme and analyzed.
• RFLP (Restriction fragment length polymorphism):
  • Particular enzyme is used to fragment whole genome.
• PFGE (Pulse field gel electrophoresis):
  • Electric field is applied diagonally in two field.
  • The electric field is applied and then pulsed and re-applied perpendicularly.

Epidemiological marker-(Phenotype and Genotype)

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