Module 4

Microbiology and Diseases

Common Diseases Caused by Microbes:
Diseases caused by Bacteria
1) TB
2) Cholera
3) Typhoid
4) Pneumonia
5) Plague
6) Diphtheria
7) E. coli infections

1. TB
 Tuberculosis (TB) is a potentially fatal contagious disease that can affect almost any part of
the body but is mainly an infection of the lungs.

 Neo-Latin word: “Tubercle”- Round nodule/Swelling and “Osis”- Condition

Causative Organisms
 Human -Mycobacterium tuberculosis
 Animals- Mycobacterium Bovis
Other causative organisms
 Mycobacterium africanum
 Mycobacterium microti
 Non-Mycobacterium Genus
 Mycobacterium leprae
 Mycobacterium avium
 Mycobacterium asiaticum
 M. tuberculosis complex- M.africanum, M. Bovis, M. Canetti, M. Microti
Mycobacterium tuberculosis characteristics
 Gram positive
 Obligate aerobe
 Non spore forming
 Non motile rod
 Mesophile
 0.2 ¿ 0.6 ×2−4 μ m
2

 Slow generation time: 15-20 hours

- may contribute to virulence

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  Lipid rich cell wall contains mycolic acid- 50% of the cell wall dry weight
- Responsible for many of this bacterium’s characteristic properties
- Acid fast- retains acidic stains
- Confers resistance to detergents, antibacterials
Classification
Extra pulmonary
 Lymph node TB
 Pleural TB
 TB of upper airways
 Skeletal TB
 Genitourinary TB
 Miliary TB
 Pericardial TB
 Gastrointestinal TB
 Tuberculous Meningitis
 Less common forms

Epidemiology

In 2011, there were an estimated 8.7million incidence cases of TB globally.

Its equivalent to 125 cases in 1,00,000 population.
Asian 59%
African 26%
Eastern Mediterranean Region 7.7%
The European Region 4.3%
Region of the America 3%

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 Incidence of tuberculosis

Spread of tuberculosis

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 Severe symptoms
 Persistent cough
 Chest pain
 Coughing with bloody sputum
 Shortness of breath
 Urine discoloration
 Cloudy & reddish urine
 Fever with chills.
 Fatigue
Based on types of tuberculosis

Types
A. Pulmonary TB
1. Primary Tuberculosis
 The infection of an individual who has not been previously infected or immunised is called
Primary tuberculosis or Ghon’s complex or childhood tuberculosis.
 Lesions forming after infection is peripheral and accompanied by hilar which may not be
detectable on chest radiography.
2. Secondary Tuberculosis
 The infection that individual who has been previously infected or sensitized is called
secondary or post primary or reinfection or chronic tuberculosis.

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 B. Extra pulmonary TB
 20% of patients of TB Patient
 Affected sites in body are: -
1. Lymph node TB (Tuberculuous lymphadenitis)
 Seen frequently in HIV infected patients.
 Symptoms: Painless swelling of lymph nodes most commonly at
 cervical and Supraclavical (Scrofula)
 Systemic systems are limited to HIV infected patients.
2. Pleural TB:
 Involvement of pleura is common in Primary TB
 and results from penetration of tubercle bacilli into pleural space.
3. TB of Upper airways
 Involvement of larynx, pharynx and epiglottis.
 Symptoms: Dysphagia, chronic productive cough
4. Genitourinary TB
 15% of all Extra pulmonary cases.
 Any part of the genitourinary tract gets infected.
 Symptoms: Urinary frequency, Dysuria, Haematuria.
5. Skeletal TB
 Involvement of weight bearing parts like spine, hip, knee.
 Symptoms: Pain in hip joints n knees, swelling of knees, trauma.
6. Gastrointestinal TB
 Involvement of any part of GI Tract.
 Symptoms: Abdominal pain, diarrhoea, weight loss
7. TB Meningitis & Tuberculoma
 5% of All Extra pulmonary TB
 Results from Hematogenous spead of 10 & 20 TB.
8. TB Pericarditis
 8% of All Extra pulmonary TB cases.
 Spreads mainly in mediastinal or hilar nodes or from lungs.
9. Miliary or disseminated TB
 Results from Hematogenous spread of Tubercle Bacilli.
 Spread is due to entry of infection into pulmonary vein producing lesions in different extra
pulmonary sites.
10. Less common Extra Pulmonary TB
 uveitis,
 pan ophthalmitis,
 painful Hypersensitivity related phlyctenule conjuctivis.

Pathogenesis

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 Diagnosis
1. Bacteriological test:
 Zeihl-Nelsen stain
 Auramine stain (fluorescence microscopy)
2. Sputum culture test:
 Lowenstein –Jensen (LJ) solid medium: 4-18 weeks
 Liquid medium: 8-14 days
 Agar medium: 7 to 14 days
3. Radiography: Chest X-Ray (CXR)
4. Nucleic acid amplification
 Species identification; several hours
 Low sensitivity, high cost
 Most useful for the rapid confirmation of tuberculosis in persons with AFB-positive sputa
 Utility
 AFB-negative pulmonary tuberculosis
 Extra pulmonary tuberculosis
5. Tuberculin skin test (PPD)
 Injection of fluid into the skin of the lower arm.
 48-72 hours later – checked for a reaction.
 Diagnosis is based on the size of the wheal.
One dose = 0.1 ml contains 0.04µg Tuberculin PPD.
6. Other biological examinations
 Cell count(lymphocytes)
 Protein (Pandy and Rivalta tests) – Ascites, pleural effusion and meningitis

Tuberculin test interpretation

Diameter of induration Interpretation Action
Less than 6mm Negative Previously unvaccinated
individuals may be given BCG
provided there are no
contraindications

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6mm or greater but less than Hypersensitive to tuberculin Should not be given BCG
15mm protein. May be due to
previous TB infection, BCG or
exposure to atypical
mycobacterium
>= 15mm Strongly hypersensitive to Should not be given BCG.
tuberculin protein. Suggestive Refer for further investigation
of TB infection or disease and supervision which may
include chemotherapy.

Pathogenesis of Tuberculin Test

Preventive measures
1. Mask
2. BCG vaccine
3. Regular medical follow up
4. Isolation of Patient
5. Ventilation
6. Natural sunlight
7. UV germicidal irradiation
BCG Vaccine
 Bacille Calmette Guerin (BCG).
 First used in 1921.
 Only vaccine available today for protection against tuberculosis.
 It is most effective in protecting children from the disease.
 Given 0.1 ml intradermally.
 Duration of Protection 15 to 20 years
 Efficacy 0 to 80%.
 Should be given to all healthy infants as soon as possible after birth unless the child presented
with symptomatic HIV infection.
Management

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 Drugs MOA
Isoniazid Inhibits mycolic acid synthesis
Rifampicin Blocks RNA synthesis by blocking DNA dependent RNA polymerase
Pyrazinamide Bactericidal-slowly metabolizing organism within acidic
environment of Phagocyte or caseous granuloma.

Ethambutol  Bacteriostatic
 Inhibition of Arabino Syl Transferase

Streptomycin Inhibition of Protein synthesis by disruption of ribosomal function

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 ARDs and it’s management

Dosage regimen
 Intensive phase + Ccontinuation phase
 HREZ (2 months) + HRE (4 months)

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 Treatment regimen according to WHO
Isoniazid (H), Rifampicin (R),Pyrazinamide (Z), Ethambutol (E), Streptomycin (S)

DOTS
DOTS - Directly observed treatment, short-course
DOT means that a trained health care worker or other designated individual provides the prescribed TB drugs
and watches the patient swallow every dose.

Multi-Drug Resistance TB
 TB caused by strains of Mycobacterium tuberculosis that are resistant to at least isoniazid and
rifampicin, the most effective anti- TB drug.
 Globally, 3.6% are estimated to have MDR-TB.
 Almost 50% of MDR-TB cases worldwide are estimated to occur in China and India.

Extensively Drug Resistance TB

Extensively drug-resistant TB (XDR-TB) is a form of TB caused by bacteria that are resistant to isoniazid and
rifampicin (i.e. MDR-TB) as well as any fluoroquinolone and any of the second-line anti-TB injectable drugs
(amikacin, kanamycin or capreomycin).

Epidemiological Impact
 Reactivation of latent infection- People who are infected with both HIV and TB are 25 to 30 times
more likely to develop TB again than people only infected with TB.
 Primary Infection- New tubercular infection in people with HIV can progress to active disease very
quickly.
 Recurring infection- in people who were cured of TB.

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 Diagnosis of TB
Common Sites of TB Disease
 Lungs
 Pleura
 Central nervous system
 Lymphatic system
 Genitourinary systems
 Bones and joints
 Disseminated (miliary TB)
Systemic Symptoms of TB
 Fever
 Chills
 Night sweats
 Appetite loss
 Weight loss
 Fatigue
Evaluation for TB
1. HIV test
2. Medical history
3. Physical examination
4. Bacteriologic or histologic exam (Chest radiograph if indicated)
Medical history
 HIV status
 Symptoms of disease
 History of TB exposure, infection, or disease
 Past TB treatment
 Demographic risk factors for TB
 Other medical conditions that increase risk for TB disease (e.g., diabetes)
Symptoms of Pulmonary TB
 Productive, prolonged cough (duration of 2-3 weeks)
 Chest pain
 Hemoptysis (bloody sputum)
 Signs may vary based on HIV status.
Specimen Collection Procedure
 Obtain 3 sputum specimens for smear examination and culture
 Spot, first morning, spot
 Follow infection control precautions during specimen collection
Sputum Smear Examination
 Specimens should be sent to the lab immediately to preserve the quality of the specimens
 Always aim for three specimens at each exam
 Always store at a cool temperature and away from sunlight to preserve the quality of
specimens
 3 respiratory specimens will detect 90% of smear-positive cases

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  AFB smear-microscopy: Acid-fast bacilli (AFB) (shown in red) are tubercle bacilli

Smear-positive PTB vs. Smear-negative PTB-

A. PTB+ (Pulmonary TB smear-positive): One AFB-positive smear; i.e. any patient with at least
one positive smear result (irrespective of quantity of AFBs seen on microscopy)
B. PTB- (smear-negative): Any pulmonary TB case that does not meet the definition of being
smear-positive. This includes:
1. Patients with three negative smear results and radiological findings and doctor’s decision to
treat for TB
2. Patients with negative smear results and a positive culture result for M. tuberculosis
3. Patients who are unable to produce sputum and with highly suspicious radiological and
clinical findings and doctor's decision to treat for TB
Other Acid-Fast Bacilli
 Mycobacteria other than those comprising the M. tuberculosis complex are called Non-
Tuberculous Mycobacteria (“NTM”) or Mycobacteria Other Than Tuberculosis (“MOTT”).
 These mycobacteria may cause pulmonary disease resembling TB. Increasingly, cases from
these organisms are being reported in patients with weakened immune systems, especially
due to HIV.
 It is important to note that infection with MOTT also may produce AFB-positive sputum
smear results and positive Mantoux skin test readings mimicking M. tuberculosis. Culture can
distinguish between M. tuberculosis and MOTT. Disease due to MOTT is usually
unresponsive to first-line anti-TB drugs.
Chest Radiograph

• Diagnosis of PTB solely on basis of CXR not encouraged

• May have unusual appearance in
• HIV-positive persons
• CXR is helpful in HIV+, smear- negative patients
• Cannot confirm diagnosis of TB
• Arrow points to cavity in patient's right upper lobe

Cultures
 Should be requested for ALL retreatment patients
o Relapse
o Failure
o Return after default
 Culture is indicated for
o New and retreatment PTB cases still smear- positive at end of intensive phase
o Symptomatic contacts of known MDR cases
Diagnosis in Children
1. Patient history
 Contact to PTB+

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  Symptoms consistent with TB
 HIV test
2. Clinical Exam
3. TST
4. Bacteriological confirmation
5. Investigations for PTB and EPTB
Key Risk Factors in Children
 Household contact with a newly diagnosed smear-positive case
 Age less than 5 years
 HIV infection
 Severe malnutrition.
Key Features of TB in Children
 Chronic symptoms suggestive of TB
 Physical signs highly of suggestive of TB
 A positive tuberculin skin test
 Chest X-ray suggestive of TB
(The presentation in infants may be more acute, resembling acute severe pneumonia and should be
suspected when there is a poor response to antibiotics. In such situations, there is often an
identifiable source case, usually the mother)

2. Cholera
Cholera is an acute diarrheal illness caused by infection of the intestine with the bacteria Vibrio
cholerae.
Pathophysiology
 V cholerae is
- comma-shaped,
- gram-negative aerobic or facultative anaerobic bacillus
- bacillus that varies in size from 1-3 µm in length by 0.5-0.8 µm in diameter
 Its antigenic structure consists of
- flagellar H antigen
- somatic O antigen.

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 Virulence and pathogenicity

Host factors
1. Age: Children: 10x more susceptible than adults, and Elderly also higher susceptible.
2. Sex: Equal in both male and female.
3. Immunity: Less immune higher risk.
4. People with low gastric acid levels
5. Blood types: O>> B > A > AB
Risk factors
Poor sanitary conditions  Rare in developed countries
 Common in Asia, Africa, & Latin
America
Raw or undercooked food  Contaminated seafood, even in
developed countries.
 Especially shellfish.
Hypochlorhydria  People with low levels of stomach acid

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  Such as children, older adults, and some
medications.
Type O blood  Reasons aren't entirely clear
 Twice more likely

Transmission
 Humans only reservoirs
 Contaminated food or water
- Inadequate sewage treatment
- Lack of water treatment
- Improperly cooked shellfish
- Transmission by casual contact unlikely
Period of communicability
 During acute stage
 A few days after recovery
 By end of week, 70% of patients non-infectious
 By end of third week, 98% non-infectious
Incubation
 Ranges from a few hours to 5 days
 Average is 1-3 days
 Shorter incubation period:
- High gastric pH (from use of antacids)
- Consumption of high dosage of cholera
Infectious dose
 water, the infectious dose is 103-106 organisms.
 ingested with food, fewer organisms (102 -104)
Symptoms
 Usually mild, or no symptoms at all
- 75% asymptomatic
- 20% mild disease
- 2-5% severe
 Vomiting
 Cramps
 profuse, painless diarrhoea and vomiting of clear fluid. "Rice water" (1L/hour) >20 mL/kg
during a 4-hour observation period
 Without treatment, death in 18 hours-several days
Cholera Gravis
 More severe symptoms
 Rapid loss of body fluids
- produce 10 to 20 litres
- 107 vibrio/mL
 Rapidly lose more than 10% of body weight
 Dehydration and shock

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  patient's skin turning a bluish-grey hue from extreme loss of fluids.
 Death within 12 hours or less
 Death can occur within 2-3 hours
Cholera sicca
 Cholera sicca is an old term describing a rare, severe form of cholera that occurs in epidemic
cholera.
 This form of cholera manifests as ileus and abdominal distention from massive outpouring of
fluid and electrolytes into dilated intestinal loops.
 Mortality is high, with death resulting from toxaemia before the onset of diarrhoea and
vomiting.
 The mortality in this condition is high.
- Because of the unusual presentation, failure to recognize the condition as a form of
cholera is common.
Cholera in children
 Breast-fed infants are protected.
 Symptoms are severe & fever is frequent. Shock, drowsiness & coma are common.
 Hypoglycaemia is a recognized complication, which may lead to convulsions.
 Rotavirus infection may give similar picture & need to be excluded.
Consequences of severe dehydration
1. Intravascular volume depletion
2. Severe metabolic acidosis
3. Hypokalaemia → cardiac arrest
4. Low blood sugar (hypoglycaemia)
a. Seizures
b. coma, especially in the young
5. Cardiac and renal failure
6. Sunken eyes, decreased skin turgor
7. Almost no urine production
Diagnosis
Clinical diagnosis Differential diagnosis
Cholera should be considered in all cases with Enterotoxigenic e. Coli
severe watery diarrhoea and vomiting.
Traveling to affected areas and Bacterial food poisoning
eating shellfish
No distinguishing clinical manifestations for Viral gastroenteritis (Rotavirus)
cholera
Other ways of diagnosis:
 Stool culture
 Confirm presence of cholera toxin
 Cholera Rapid Test Dipsticks
Other lab findings
 Dehydration leads to high blood urea & serum creatinine.
 Haematocrit & WBC will also be high due to haemoconcentration.

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  Dehydration & bicarbonate loss in stool leads to metabolic acidosis with wide-anion gap.
 Total body potassium is depleted, but serum level may be normal due to effect of acidosis.
Treatment
1. Rehydration
 Oral
 Intravenous
2. Antimicrobial theory
WHO guidelines for cholera management
Steps in the treatment of a patient with suspected cholera are as follows:
1. Assess for dehydration (see Table 1)
2. Rehydrate the patient and monitor frequently, then reassess hydration status
3. Maintain hydration; replace ongoing fluid losses until diarrhoea stops
4. Administer an oral antibiotic to the patient with severe dehydration
5. Feed the patient
More detailed guidelines for the treatment of cholera are as follows:
 Evaluate the degree of dehydration upon arrival
 Rehydrate the patient in 2 phases; these include rehydration (for 2-4 h) and maintenance
(until diarrhoea abates)
 Register output and intake volumes on predesigned charts and periodically review these data
 Use the intravenous route only (1) during the rehydration phase for severely dehydrated
patients for whom an infusion rate of 50-100 mL/kg/h is advised, (2) for moderately
dehydrated patients who do not tolerate the oral route, and (3) during the maintenance phase
in patients considered high stool purgers (ie,>10 mL/kg/h)
 During the maintenance phase, use oral rehydration solution at a rate of 800-1000 mL/h;
match ongoing losses with ORS administration
 Discharge patients to the treatment centre if oral tolerance is greater than or equal to 1000
mL/h, urine volume is greater than or equal to 40 mL/h, and stool volume is less than or equal
to 400 mL/h.
Assessment of the Patient with Diarrhoea for Dehydration (based on WHO classification)
Clinical features Predicted degree of dehydration
None (<5 percent) Some dehydration (5- Severe dehydration
10 percent) (>10 percent)
General appearance Well, alert restless, irritable Abnormally sleepy or
lethargic
Eyes Normal Sunken sunken
Thirst Drinks normally, not Thirsty, drinks eagerly Drinks poorly or
thirsty unable to drink
Skin pinch Goes back quickly Goes back slowly (<2 Goes back very slowly
sec) (>2 sec)
Estimated fluid deficit <50 mL/kg 50-100 mL/kg >100 mL/kg
Decision Patient has no Patient has no If the patient has 2 or
dehydration dehydration more of these signs,
severe dehydration is

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 present
Treatment of cholera
1. Rehydration is accomplished in 2 phases:
a. Rehydration
 The goal of the rehydration phase is to restore normal hydration status, which should take no
more than 4 hours.
 Set the rate of intravenous infusion in severely dehydrated patients at 50-100 mL/kg/hr.
 Lactated Ringer solution is preferred over isotonic sodium chloride solution because saline
does not correct metabolic acidosis
b. Maintenance.
 The goal of the maintenance phase is to maintain normal hydration status by replacing
ongoing losses.
 The oral route is preferred, and the use of oral rehydration solution (ORS) at a rate of 500-
1000 mL/hr is recommended
 Fluids should never be restricted
2. Antibiotic treatment
Antimicrobial therapy is useful for
 prompt eradication of the vibrio
 diminish the duration of diarrhoea
 decrease the fluid loss.
 Antibiotics should be administered to moderate or severe cases

Prevention
 Comprehensive Multidisciplinary Approach: water, sanitation, education, and communication
 Basic health education and hygiene
 Mass chemoprophylaxis
 Provision of safe water and sanitation

3. Typhoid
 Typhoid fever, also known simply as typhoid, is a bacterial infection due to a specific type
of Salmonella that causes symptoms.

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  Symptoms may vary from mild to severe, and usually begin 6 to 30 days after
exposure. Often there is a gradual onset of a high fever over several days.
 This is commonly accompanied by weakness, abdominal pain, constipation, headaches, and
mild vomiting. Typhoid fever is a type of enteric fever, along with paratyphoid fever.
 Causative Organism: Typhoid fever is caused by virulent bacteria called Salmonella typhi.
 Morphological features: Gram positive bacilli, 1-3µm X0.5µm, motile, possess peritrichate
flagella.
 Cultural characteristics:
a. Aerobic/facultative anaerobe
b. pH 6.0 -8.0
c. Temperature :150 C - 410 C (optimum 370C)
d. Colony: 2-3mm diameter, circular, convex, smooth
e. Media:
- MacConkey - colorless
- Wilson & Blair Bismuth sulphite media-Black colony with metallic sheen(H2S)
Classification
 Domain: Bacteria - As bacteria, Salmonella are prokaryotes with a simple cell structure that
lacks membrane bound organelles.
 Order: enterobacteriales - Gram-negative rods (Bacillus) that typically move by using
flagella and do not form endospores/microcysts
 Family: Enterobacteriaceae - This is the only family in Order enterobacteriales and is
composed of rod-shaped gram-negative bacteria.
 Genus: Salmonella
 Species: S. bongori and S. enterica
 Subspecies: S. bongori has a single subspecies referred to as Subspecies V.
The following are subspecies of Salmonella enterica:
a. enterica I
b. salamae II
c. arizonae IIIa
d. diarizonae IIIb
e. houtenae IV
f. indica VI
 In addition to the subspecies, there are also various serotyes of Salmonella that have been
suggested to range from 2,200 to about 4,400 serotypes/serovar.
Serotype grouping is based on cell surface antigens.
Serotypes (Kauffman Classification):With regards to Salmonella serotypes, the bacteria has
been shown to possess three types of antigen. These include:
- Antigen H (flagella antigen),
- Antigen O (somatic antigen) and
- Vi (capsular).
These antigens play an important role when it comes to grouping or serotyping the organisms.

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 Symptoms
Signs and symptoms are likely to develop gradually — often appearing one to three weeks after
exposure to the disease.
1. Early illness
• Once signs and symptoms do appear, you're likely to experience:
• Fever that starts low and increases daily, possibly reaching as high as 104.9 F (40.5 C)
• Headache
• Weakness and fatigue
• Muscle aches
• Sweating
• Dry cough
• Loss of appetite and weight loss
• Abdominal pain
• Diarrhea or constipation
• Rash
• Extremely swollen abdomen
2. Later illness
• If you don't receive treatment, you may:
• Become delirious
• Lie motionless and exhausted with your eyes half-closed in what's known as the typhoid state
• In addition, life-threatening complications often develop at this time.
• In some people, signs and symptoms may return up to two weeks after the fever has subsided.
3. Fecal-oral transmission route
• The bacteria that cause typhoid fever spread through contaminated food or water and
occasionally through direct contact with someone who is infected.
4. Typhoid carriers
• Even after treatment with antibiotics, a small number of people who recover from typhoid
fever continue to harbor the bacteria in their intestinal tracts or gallbladders, often for years.
These people, called chronic carriers, shed the bacteria in their feces and are capable of
infecting others, although they no longer have signs or symptoms of the disease themselves.
Diagnosis
 Blood culture: 5-10ml blood + 0.5%bile broth/ MacConkey agar (37oC), biochemical tests
(indole, urease), motility test
 Isolation of bacilli: staining & detection
 Agglutination reaction: detection of titer value (2-3 serum sample), repeat after 1 week.
 Widal test: Widal test is a serological method to diagnose enteric or typhoid fever that is
cause by the infection with pathogenic microorganisms like Salmonella typhi, Salmonella
paratyphi a, b and c.
 The method of diagnostic test is based upon a visible to the naked eye agglutination (clumps)
reaction between antibodies of patient serum and antigens specifically prepared from
Salmonella sp.
 Salmonella possesses the following 3 antigens:
1. Flagellar antigen or H antigen
2. Somatic antigen or O antigen
3. Surface antigen or Vi antigen

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  The tests measure agglutinating antibodies directed against a Salmonella O somatic surface
antigen and/or
 A Salmonella H flagella antigen of the suspected organism.
 The Widal test detects antibodies against O and H antigens.
 Type of techniques is using direct agglutination.
 Widal test, firstly descried by Fernand Widal in 1896

4. Pneumonia
What is pneumonia?
Pneumonia is an infection in your lungs caused by bacteria, viruses or fungi. Pneumonia causes your
lung tissue to swell (inflammation) and can cause fluid or pus in your lungs. Bacterial pneumonia is
usually more severe than viral pneumonia, which often resolves on its own.
Pneumonia can affect one or both lungs. Pneumonia in both of your lungs is called bilateral or
double pneumonia.
Pneumonia causes your lung tissue to swell. It can cause fluid or pus in your lungs.

What’s the difference between viral and bacterial pneumonia?

 While all pneumonia is inflammation caused by an infection in your lungs, you may have
different symptoms depending on whether the root cause is a virus, bacteria or fungi.
 Bacterial pneumonia tends to be more common and more severe than viral pneumonia. It’s
more likely to require a hospital stay. Providers treat bacterial pneumonia with antibiotics.
Viral pneumonia causes flu-like symptoms and is more likely to resolve on its own. You
usually don’t need specific treatment for viral pneumonia.
What are the types of pneumonia?
 We categorize pneumonia by which pathogen (virus, bacteria or fungi) caused it and how you
got it — community-acquired, hospital-acquired or ventilator-associated pneumonia.
1. Community-acquired pneumonia (CAP): When you get pneumonia outside of a healthcare
facility, it’s called community-acquired pneumonia.
Causes include:

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 i. Bacteria: Infection with Streptococcus pneumoniae bacteria, also called pneumococcal
disease, is the most common cause of CAP. Pneumococcal disease can also cause ear
infections, sinus infections and meningitis. Mycoplasma pneumoniae bacteria causes atypical
pneumonia, which usually has milder symptoms. Other bacteria that cause CAP
include Haemophilus influenza, Chlamydia pneumoniae and Legionella (Legionnaires’
disease).
ii. Viruses: Viruses that cause the common cold, the flu (influenza), COVID-19 and respiratory
syncytial virus (RSV) can sometimes lead to pneumonia.
iii. Fungi (molds): Fungi, like Cryptococcus, Pneumocystis jirovecii and Coccidioides, are
uncommon causes of pneumonia. People with compromised immune systems are most at risk
of getting pneumonia from a fungus.
iv. Protozoa: Rarely, protozoa like Toxoplasma cause pneumonia.
2. Hospital-acquired pneumonia (HAP): You can get hospital-acquired pneumonia (HAP)
while in a hospital or healthcare facility for another illness or procedure. HAP is usually more
serious than community-acquired pneumonia because it’s often caused by antibiotic-resistant
bacteria, like methicillin-resistant Staphylococcus aureus (MRSA). This means HAP can
make you sicker and be harder to treat.
3. Healthcare-associated pneumonia (HCAP): You can get HCAP while in a long-term care
facility (such as a nursing home) or outpatient, extended-stay clinics. Like hospital-acquired
pneumonia, it’s usually caused by antibiotic-resistant bacteria.
4. Ventilator-associated pneumonia (VAP): If you need to be on a respirator or breathing
machine to help you breathe in the hospital (usually in the ICU), you’re at risk for ventilator-
associated pneumonia (VAP). The same types of bacteria as community-acquired pneumonia,
as well as the drug-resistant kinds that cause hospital-acquired pneumonia, cause VAP.
5. Aspiration pneumonia: Aspiration is when solid food, liquids, spit or vomit go down your
trachea (windpipe) and into your lungs. If you can’t cough these up, your lungs can get
infected.
Symptoms of bacterial pneumonia
 Symptoms of bacterial pneumonia can develop gradually or suddenly. Symptoms include:
 High fever (up to 105 F or 40.55 C).
 Cough with yellow, green or bloody mucus
 Tiredness (fatigue).
 Rapid breathing.
 Shortness of breath.
 Rapid heart rate.
 Sweating or chills.
 Chest pain and/or abdominal pain, especially with coughing or deep breathing.
 Loss of appetite.
 Bluish skin, lips or nails (cyanosis).
 Confusion or altered mental state.
Symptoms of viral pneumonia
Symptoms of viral pneumonia usually develop over several days. You might have symptoms similar
to bacterial pneumonia or you might additionally have:
 Dry cough.
 Headache.

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  Muscle pain.
 Extreme tiredness or weakness.
What tests will be done to diagnose pneumonia?
Your provider may perform tests that look at your lungs for signs of infection, measure how well
your lungs are working and examine blood or other body fluids to try to determine the cause of your
pneumonia. These include:
 Imaging: Your provider can use chest X-ray or CT scan to take pictures of your lungs to look
for signs of infection.
 Blood tests: Your provider can use a blood test to help determine what kind of infection is
causing your pneumonia.
 Sputum test: You’re asked to cough and then spit into a container to collect a sample for a
lab to examine. The lab will look for signs of an infection and try to determine what’s causing
it.
 Pulse oximetry: A sensor measures the amount of oxygen in your blood to give your
provider an idea of how well your lungs are working.
 Pleural fluid culture: Your provider uses a thin needle to take a sample of fluid from around
your lungs. The sample is sent to a lab to help determine what’s causing the infection.
 Arterial blood gas test: Your provider takes a blood sample from your wrist, arm or groin to
measure oxygen levels in your blood to know how well your lungs are working.
 Bronchoscopy: In some cases, your provider may use a thin, lighted tube called a
bronchoscope to look at the inside of your lungs. They may also take tissue or fluid samples
to be tested in a lab
How is pneumonia treated?
 Antibiotics: antibiotics treat bacterial pneumonia. They can’t treat a virus but a provider may
prescribe them if you have a bacterial infection at the same time as a virus.
 Antifungal medications: Antifungals can treat pneumonia caused by a fungal infection.
 Antiviral medications: Viral pneumonia usually isn’t treated with medication and can go
away on its own. A provider may prescribe antivirals such
as oseltamivir (Tamiflu®), zanamivir (Relenza®) or peramivir (Rapivab®) to reduce how
long you’re sick and how sick you get from a virus.
 Oxygen therapy: If you’re not getting enough oxygen, a provider may give you extra
oxygen through a tube in your nose or a mask on your face.
 IV fluids: Fluids delivered directly to your vein (IV) treat or prevent dehydration.
 Draining of fluids: If you have a lot of fluid between your lungs and chest wall (pleural
effusion), a provider may drain it. This is done with a catheter or surgery.
How do I manage the symptoms of pneumonia?
Over-the-counter medications and other at-home treatments can help you feel better and manage the
symptoms of pneumonia, including:
 Pain relievers and fever reducers: Your provider may recommend medicines like ibuprofen
(Advil®) and acetaminophen (Tylenol®) to help with body aches and fever.

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  Cough suppressants: Check with your healthcare provider before taking cough suppressants
for pneumonia. Coughing is important to help clear your lungs.
 Breathing treatments and exercises: Your provider may prescribe these treatments to help
loosen mucus and help you to breathe.
 Using a humidifier: Your provider may recommend keeping a small humidifier running by
your bed or taking a steamy shower or bath to make it easier to breathe.
 Drinking plenty of fluids.
Vaccines for pneumonia
 There are two types of vaccines (shots) that prevent pneumonia caused by pneumococcal
bacteria. Similar to a flu shot, these vaccines won’t protect against all types of pneumonia,
but if you do get sick, it’s less likely to be severe.
 Pneumococcal vaccines: Pneumovax23® and Prevnar13® protect against pneumonia
bacteria. They’re each recommended for certain age groups or those with increased risk for
pneumonia. Ask your healthcare provider which vaccine would be appropriate for you or
your loved ones.
 Vaccinations against viruses: As certain viruses can lead to pneumonia, getting vaccinated
against COVID-19 and the flu can help reduce your risk of getting pneumonia.
 Childhood vaccinations: If you have children, ask their healthcare provider about other
vaccines they should get. Several childhood vaccines help prevent infections caused by the
bacteria and viruses that can lead to pneumonia.

5. Pneumonia
1. Plague:
A. Causative Organism: Yersinia pestis
 It is an infectious disease caused by bacteria & typified as bubo nil plague, septicemic plague,
pneumonic plague.
 Bubonic & septicemic plague is generally spread by flea bites or handling infected animals.
B. Morphology: Yersinia pestis (formerly Pasteurella pestis) is a gram-negative, non-
motile, rod-shaped, coccobacillus bacterium, without spores. It is a facultative anaerobic
organism that can infect humans via the Oriental rat flea (Xenopsylla cheopis).
C. Symptoms:
 Y.pestis can reproduce inside cells, so even if phagocytosed they can still survive. Once in
body the bacteria can enter lymphatic system & drain interstitial fluid.
 Fever, weakness, headache & pneumonia
D. Cause/Occurrence:
1. Droplet contact: - coughing or sneezing,
2. Direct physical contact
3. Indirect contact: -usually by touching soil contamination.
4. Airborne transmission
5. Fecal-oral transmission
6. Vector borne transmission: -carried by insects
E. Diagnostic Method: - detection of bacterium in lymph node, blood sputum.
F. Treatment:
 If diagnosed in time, the various forms of plague are responsive to antibiotic therapy.
 Antibiotic used are streptomycin, chloramphenicol & tetracycline.
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  Amongst the new generation of antibiotics, gentamycin &doxycycline have proven effective
in mono-therapeutic treatment.

6. Diphtheria
Edwin Klebs In 1883, Klebs demonstrated that Corynebacterium diphtheriae was the agent of
diphtheria
Alexandre Yersin, Pierre Paul Émile Roux
By 1888, Roux and Yersin showed that animals injected with sterile filtrates of C diphtheriae
developed symptoms similar to that of human diphtheria: this demonstrated that a potent exotoxin
was the major virulence factor.
General characteristics
 It is also known as the Klebs-Löffler bacillus
 Gram-positive, highly pleomorphic organisms with no particular arrangement
 Special stains like Albert’s stain and Ponder's stain are used to demonstrate the
metachromatic granules formed in the polar regions
 It is also known as the Klebs-Löffler bacillus
 Gram-positive, highly pleomorphic organisms with no particular arrangement
 Special stains like Albert’s stain and Ponder's stain are used to demonstrate the
metachromatic granules formed in the polar regions
 Corynebacterium diphtheriae is a nonmotile, non-capsulated, club-shaped, gram-positive
bacillus
 Toxigenic strains are lysogenic for one of a family of corynebacteriophages that carry the
structural gene for diphtheria toxin, tox
 Corynebacterium diphtheriae is classified into biotypes (mitis, intermedius, and gravis)
according to colony morphology on tellurite containing media, as well as into lysotypes
based upon corynebacteriophage sensitivity
Classification

Mitis Gravis Intermedius

Long rods Short rods Long- barred forms, clubbed
end
Curved shaped Uniform Poor granulation
Pleomorphic Few or no granules Very pleomorphic
Prominent granules May be pleomorphic Gray, opaque glossy, smooth
surface, poached egg colonies
Greyish black, opaque colonies Grey colony, dark centre Obstructive and endemic
shining
Glycogen and starch Non- haemolytic

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 fermentation
Paralytic and epidemic Haemorrhagic and epidemic

Diphtheria
Diphtheria is most commonly an infection of the upper respiratory tract and causes
 Fever
 sore throat
 malaise
A thick, grey-green fibrin membrane, the pseudo membrane, often forms over the site(s) of
infection as a result of the combined effects of
 bacterial growth
 toxin production
 necrosis of underlying tissue
 host immune response
There are two types of clinical diphtheria: nasopharyngeal and cutaneous.
 Symptoms of pharyngeal diphtheria vary from mild pharyngitis to hypoxia due to airway
obstruction by the pseudo membrane
 The involvement of cervical lymph nodes may cause swelling of the neck (bull neck
diphtheria), and the patient may have a fever (≥ 103°F)
 The skin lesions in cutaneous diphtheria are usually covered by a grey-brown pseudo
membrane
 Life-threatening systemic complications, principally loss of motor function (e.g., difficulty in
swallowing) and congestive heart failure, may develop as a result of the action of diphtheria
toxin on peripheral motor neurons and the myocardium.
Pathogenesis
The pathogenesis of diphtheria is based upon two primary determinants:
1. The ability of a given strain of C diphtheriae to colonize in the nasopharyngeal cavity
and/or on the skin
2. It’s ability to produce diphtheria toxin
3. The structural gene for diphtheria toxin, tox, is carried by a family of closely related
corynebacteriophages
4. The regulation of diphtheria tox expression is mediated by an iron-activated repressor,
DtxR, which is encoded on the C diphtheriae genome
5. When iron become the growth limiting diphtheria toxin is synthesized and secreted at
maximal rates

• Diphtheria toxin is extraordinarily

potent: as little as 100 to 150 ng/kg
of body weight is lethal
• Diphtheria toxin is composed of a
single polypeptide chain of 535
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• Intoxication of a single eukaryotic
cell by diphtheria toxin can lead to
 Diagnosis
 Laboratory confirmation of toxigenic C diphtheriae in throat or lesion cultures
 Sterile cotton-tipped applicators are used to swab the pharyngeal tonsils or their beds.
 Swabs may be inserted through both nares to collect nasopharyngeal samples for culture.
Since diphtheritic lesions are often covered with a pseudo membrane, the surface of the
lesion may have to be carefully exposed before swabbing
 The most common in vitro assay for toxigenicity is the Elek immunodiffusion test
 This test is based on the double diffusion of diphtheria toxin and antitoxin in an agar medium.
 A sterile, antitoxin-saturated filter paper strip is embedded in the culture medium, and C
diphtheriae isolates are streak-inoculated at a 90° angle to the filter paper
 The production of diphtheria toxin can be detected within 18 to 48 hours by the formation of
a toxin-antitoxin precipitin band in the agar.
Elek immunodiffusion test
Sterile filter paper impregnated with diphtheria antitoxin
is imbedded in agar culture medium.
Isolates of C diphtheriae are then streaked across the plate
at an angle of 90° to the antitoxin strip.
Toxigenic C diphtheriae is detected because secreted toxin
diffuses from the area of growth and reacts with antitoxin to
form lines of precipitin.
Signs and Symptoms
 The symptoms of diphtheria usually begin two to seven days after infection
 Fever of 38 °C (100.4 °F) or above, chills, fatigue, bluish skin coloration (cyanosis), sore
throat, hoarseness, cough, headache, difficulty swallowing, painful swallowing, difficulty
breathing, rapid breathing, foul-smelling and bloodstained nasal discharge, and
lymphadenopathy
 Within two to three days, diphtheria may destroy healthy tissues in the respiratory system
 Dead tissue forms a thick, grey coating that can build up in the throat or nose. This thick grey
coating is called a “pseudo membrane.”

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  It can cover tissues in the nose, tonsils, voice box, and throat, making it very hard to breathe
and swallow.
 Symptoms can also include cardiac arrhythmias, myocarditis, and cranial and peripheral
nerve palsies
 Diphtheria can cause a swollen neck, sometimes referred to as a bull neck
 An adherent, dense, grey pseudo membrane covering the tonsils is classically seen in
diphtheria
 A diphtheria skin lesion on the leg.
Control
 Although antibiotics (e.g., penicillin and erythromycin) are used as part of the treatment of
patients who present with diphtheria, prompt passive immunization with diphtherial antitoxin
is most effective in reducing the fatality rate
 The long half-life of specific antitoxin in the circulation is an important factor in ensuring
effective neutralization of diphtheria toxin; however, to be effective, the antitoxin must react
with the toxin before it becomes internalized into the cell.
 Metronidazole, Erythromycin, Procaine penicillin G, rifampin or clindamycin diphtheria
toxin spreads through the blood and can lead to potentially life-threatening complications that
affect other organs, such as the heart and kidneys. Damage to the heart caused by the toxin
affects the heart's ability to pump blood or the kidneys' ability to clear wastes. It can also
cause nerve damage, eventually leading to paralysis
Immunization coverage

How did they make diphtheria vaccine?

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 7. E. coli infection
What is E. coli?
 Escherichia coli (E. coli) is a group of bacteria that normally lives in the gut
(gastrointestinal/GI tract) of healthy people and animals.
 The type that lives in our GI tract usually doesn’t hurt us — it even helps us digest our food.
But under certain circumstances, many strains (types) of E. coli can make us sick. Many of
the strains that cause infection can adhere (stick) to our cells and release toxins.
What is an E. coli infection?
 An E. coli infection is any illness you get from strains of E. coli bacteria. For instance, there
are harmful strains of E. coli that cause watery diarrhea, stomach pain and other digestive
symptoms (gastroenteritis) if we accidentally ingest them. These are sometimes called
diarrheagenic E. coli, and they’re often what people mean when they talk about E.
coli infections. But the E. coli that usually live in our gut can also get in places they’re not
supposed to be (like our urinary tract). This causes an E. coli infection there.
 Many strains of E. coli cause mild infections. But some strains, like those that produce Shiga
toxin, can cause serious illness, including kidney damage.
Types of E. coli infection
 Common types of E. coli infection include gastrointestinal and urinary tract
infections (UTIs). Other types of E. coli infections include:
 Bloodstream infections.
 Prostatitis (prostate infection).
 Pelvic inflammatory disease (PID).
 Gallbladder infection (cholecystitis).
 Wound infections.
 Pneumonia (rare).
 Meningitis (rare).
How common are E. coli infections?

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There are about 265,000 Shiga toxin-producing E. coli (STEC) infections each year in the U.S.
STEC is the most common cause of E. coli outbreaks and serious illness from E. coli in the U.S.
Symptoms and Causes
What are the symptoms of an E. coli infection?
 Symptoms of E. coli gastroenteritis include:
 Diarrhea. This is often watery and sometimes bloody.
 Stomach pains and cramps.
 Loss of appetite.
 Low fever.
 Watery diarrhea is usually the first symptom of an E. coli infection in our GI tract. We can
also have different symptoms depending on where in our body we’re infected.
How soon do symptoms of an E. coli infection start?
We usually develop symptoms of an STEC infection within three to five days after drinking or eating
foods contaminated with this E. coli bacteria. Other strains can make us sick within hours.
Sometimes, symptoms start up to 10 days after exposure.
What kind of E. coli causes traveler’s diarrhea?
Enterotoxigenic E. coli (ETEC) is a type of E. coli that causes infections known as traveler’s
diarrhea. Symptoms start quickly after exposure — sometimes within just a few hours. ETEC is
common in warm climates.
What causes E. coli infections?
Many strains of E. coli can cause diarrheagenic infections in your GI tract. Most cause similar
symptoms, like watery diarrhea, but some are more serious than others. Scientists categorize them by
how they attach to our cells and the types of toxins they release.
Types of diarrheagenic E. coli include:
 Shiga toxin-producing E. coli (STEC).
 Enterotoxigenic E. coli (ETEC).
 Enteropathogenic E. coli (EPEC).
 Enteroaggregative E. coli (EAEC).
 Enteroinvasive E. coli (EIEC).
 Diffusely adherent E. coli (DAEC).
 Other notable types of E. coli include uropathogenic E. coli (UPEC), which can cause UTIs,
and E. coli K1, which can cause meningitis in newborns.
What is Shiga toxin-producing E. coli (STEC)?
 STEC is a strain of E. coli that releases a toxin (Shiga toxin) that damages our cells. These
are the same toxins released by Shigella bacteria. STEC is known for causing severe
outbreaks of E. coli (where many people get sick), often from contaminated food.
 STEC is also called enterohemorrhagic E. coli (EHEC) because it can lead to bleeding in
your intestines, causing bloody diarrhea (hemorrhagic colitis). About 5% to 10% of people
with STEC develop hemolytic uremic syndrome (HUS), a condition that causes blood clots
and damages our kidneys. The subtype E. coli O157:H7 is the most likely to cause severe
illness.
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 How do we get E. coli?
1. Eating contaminated foods. This includes undercooked meat and raw fruits and veggies that
aren’t washed well enough.
2. Drinking unpasteurized beverages. This includes milk, cider or juice (and foods made from
them, like cheese or ice cream).
3. Drinking contaminated water (or getting it in our mouth). E. coli in poop from animals
and people can contaminate natural water sources (like lakes, streams and rivers), swimming
pools and drinking water that isn’t sanitized.
4. Touching poop or contaminated surfaces. We can get poop on our hands from changing
diapers, wiping after a bowel movement, touching petting zoo or farm animals, or sharing
objects or surfaces with someone with an E. coli infection. We can swallow E. coli when it
transfers from our hands to our mouth.
5. Not wiping properly after going to the bathroom. This can move E. coli from your poop to
your urinary tract, causing a UTI.
6. Babies sometimes get E. coli infections during birth.
Who’s at risk for E. coli?
 Anyone who comes into contact with a disease-causing strain of E. coli can get infected.
People who are at greatest risk include:
 Newborns and young children.
 People over the age of 65.
 People who have weakened immune systems (for example, those with HIV or cancer or who
take immunosuppressive medications).
 People with diabetes.
 People with ulcerative colitis
Management and Treatment
How are E. coli infections treated?
 We often don’t need to treat E. coli infections that cause digestive symptoms. Healthcare
providers specifically don’t treat STEC with antibiotics or antidiarrheal medicines. These
medications can increase our risk of HUS if we have STEC. Instead, they’ll monitor our
condition and give us fluids to prevent dehydration if needed.
 But if we have another type of E. coli infection — like a UTI, meningitis or sepsis — or if
our symptoms are severe, our provider will treat you with antibiotics.
Antibiotics for E. coli infections
 Some antibiotics providers use to treat E. coli infections include:
 Trimethoprim/sulfamethoxazole (TMP/SMX).
 Ciprofloxacin.
 Rifaximin.
 Trimethoprim/sulfamethoxazole (TMP/SMX).
 Nitrofurantoin.
Prevention
Can we prevent E. coli infections?
 The most important thing we can do to protect against E. coli infections is to wash our hands.
It’s particularly important to wash them thoroughly with warm water and soap:

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  Before and after cooking and after handling raw meat or poultry.
 After using the restroom, changing diapers or contact with animals.
 We can also reduce our risk of an E. coli infection by following safe food preparation
procedures:
 Don’t drink unpasteurized milk or ciders.
 Rinse all raw fruits and vegetables under running water before eating them.
 Don’t defrost frozen meat unwrapped on the counter. Keep frozen meat in a separate plastic
bag when thawing.
 Don’t rinse meat before cooking. Washing the meat could spread bacteria to nearby surfaces,
utensils and other food.
 Use a plastic, silicone or ceramic cutting board to cut raw meat. Wooden cutting boards are
harder to clean completely, leaving bacteria behind.
 Use different surfaces for prepping different types of food. Surfaces like cutting boards can
spread bacteria. If we don’t have different cutting boards, wash surfaces thoroughly with soap
and hot water after we’ve worked with raw meat and before putting another type of food
(such as a raw vegetables) on it.
 Cook all meat to a safe temperature before eating. Don’t put cooked meat on a plate that had
raw meat on it.
 Refrigerate leftovers right away.

Diseases caused by virus

1. Polio
2. H1N1
3. SARS
4. Covid-19
5. HIV
6. Hepatitis

1. Polio/poliomyelitis
 Poliomyelitis, commonly shortened to Polio, is an infectious disease caused by
the Poliovirus. In about 0.5 percent of cases, it moves from the gut to affect the central
nervous system and there is muscle weakness resulting in a flaccid paralysis. This can occur
over a few hours to a few days.
 Causative organism – polio virus
 Morphology – spherical, 27nm in diameter, 60subunits, 4 viral proteins (VP1-VP4),
icosahedral symmetry
 Genetic material – ss+RNA-uses host ribosomes-11 different proteins.
 Resistance – chloroform, bile, enzymes of intestine, detergent
 pH- 3.0, temperature – 4oC up to months & -20oC for years.
 Inactivated by heat - 55oC within 30minutes.

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  Host range – Humans, chimps, monkeys, rodents, embryos
Symptoms
It’s estimated that 95 to 99 percent of people who contract poliovirus are asymptomatic. This is
known as subclinical polio. Even without symptoms, people infected with poliovirus can still spread
the virus and cause infection in others.
Non-paralytic Polio: Signs and symptoms of non-paralytic polio can last from one to 10 days. These
signs and symptoms can be flu-like and can include
 fever
 sore throat
 headache
 vomiting
 fatigue
 meningitis
Non-paralytic polio is also known as abortive polio.
Paralytic Polio
 About 1 percent of polio cases can develop into paralytic polio. Paralytic polio leads to
paralysis in the spinal cord (spinal polio), brainstem (bulbar polio), or both (bulbospinal
polio).
 Initial symptoms are similar to non-paralytic polio. But after a week, more severe symptoms
will appear. These symptoms include:
 loss of reflexes
 severe spasms and muscle pain
 loose and floppy limbs, sometimes on just one side of the body
 sudden paralysis, temporary or permanent
 deformed limbs, especially the hips, ankles, and feet
 It’s rare for full paralysis to develop. Less than 1 % Trusted Source of all polio cases will
result in permanent paralysis. In 5–10 percent of the polio paralysis cases, the virus will
attack the muscles that help you breathe and cause death.
Post-Polio Syndrome

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It’s possible for polio to return even after recovery. This can occur after 15 to 40 years. Common
symptoms of post-polio syndrome (PPS) are:
 continuing muscle and joint weakness
 muscle pain that gets worse
 becoming easily exhausted or fatigued
 muscle wasting, also called muscle atrophy
 trouble breathing and swallowing
 sleep apnea, or sleep-related breathing problems
 low tolerance of cold temperatures
 new onset of weakness in previously uninvolved muscles
 depression
 trouble with concentration and memory
Diagnosis
 Doctors often recognize polio by symptoms, such as neck and back stiffness, abnormal
reflexes, and difficulty swallowing and breathing. To confirm the diagnosis, a sample of
throat secretions, stool or a colorless fluid that surrounds your brain and spinal cord
(cerebrospinal fluid) is checked for poliovirus.
Vaccination
 Inactivated polio vaccine (IPV) is the only polio vaccine that has been given in the United
States since 2000. It is given by shot in the arm or leg, depending on the person’s age. Oral
polio vaccine (OPV) is used in other countries.
 CDC recommends that children get four doses of polio vaccine. They should get one dose at
each of the following ages:
- 2 months old
- 4 months old
- 6 through 18 months old
- 4 through 6 years old
- Almost all children (99 out of 100) who get all the recommended doses of polio vaccine will
be protected from polio.

2. SARS
 Severe Acute Respiratory Syndrome (SARS) is a serious form of viral pneumonia caused by
the SARS virus. The virus that causes SARS was first identified in 2003.
 The World Health Organization has designated SARS a global health threat. In 2003, an
epidemic killed approximately 774 people.
 The 2002-2003 outbreak of SARS spread to several countries, but through aggressive public
health measures, including quarantine and isolation of cases, the outbreak was eventually
contained.
 International cooperation and surveillance played a crucial role in preventing further
transmission.
 Since 2004, there have not been any known cases of SARS reported anywhere in the world.
Are SARS and COVID the same?

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There are many similarities between COVID-19 and SARS. However, there are also important
differences. COVID-19 cases can range from mild to severe, while SARS cases, in general, were
more severe. But SARS-CoV-2, the virus that causes COVID-19, is transmitted more easily.
Symptoms of SARS
 SARS symptoms are similar to those of the flu, including:
 Fever over 100.4°f
 Dry cough
 Sore throat
 Problems breathing, including shortness of breath
 Headache
 Body aches
 Loss of appetite
 Malaise
 Night sweats and chills
 Confusion
 Rash
 Diarrhea
Causes
 SARS can spread when an infected person sneezes, coughs, or comes into face-to-face
contact with someone else. Face-to-face contact refers to:
 Caring for someone with SARS
 Having contact with the bodily fluids of a person with SARS
 Kissing, hugging, touching, or sharing eating or drinking utensils with an infected person
 You can also contract SARS by touching a surface contaminated with respiratory droplets
from an infected person and then touching your eyes, mouth, or nose. The disease may also
be spread through the air, but researchers have not confirmed this.
How is SARS diagnosed?
 Various lab tests have been developed to detect the SARS virus.
 During the first outbreak of SARS, there were no laboratory tests for the disease. Diagnosis
was made primarily through symptoms and medical history.
 Now, laboratory tests can be performed on nasal and throat swabs or blood samples.
 A chest X-ray or CT scan may also reveal signs of pneumonia characteristic of SARS.
Complication associated with SARS
 Most of the fatalities associated with SARS result from respiratory failure.
 SARS can also lead to heart and liver failure.
 group most at risk of developing complications is people over 60 who have been diagnosed
with another chronic condition.
Treatment
 There is no confirmed treatment that works for every person who has SARS.
 Antiviral medications and steroids are sometimes given to reduce lung swelling, but aren’t
effective for everyone.
 Antibiotics are ineffective against it
 Treatment is mainly supportive with antipyretics.

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 Prevention/prophylaxis
 It’s important to take as many preventive measures as possible.
 Here are some of the best ways to prevent transmission of SARS if you’re in close contact
with someone who’s been diagnosed with the disease:
 Wash your hands frequently.
 Wear disposable gloves if touching any infected bodily fluids.
 Wear a surgical mask when in the same room with a person with SARS.
 Disinfect surfaces that may have been contaminated with the virus.
 Wash all personal items, including bedding and utensils, used by a person with SARS.

3. H1N1- swine flu

 Swine flu is also known as H1N1.
 Epidemics of swine flu Were in: 1918 and 1968
 The swine flu pandemic was in 2009.
 Total swine flu deaths from 2009 pandemic:14,286.
 Epidemic meaning: An outbreak of a contagious disease that spreads rapidly and widely.
 Pandemic meaning: Epidemic over a wide geographic area and affecting a large proportion
of the population.
What is swine flu (H1N1)?
Swine Influenza (swine flu) is a respiratory disease of pigs caused by Type A influenza viruses that
causes regular outbreaks in pigs.
Swine flu viruses have been reported to spread from person-to- person, but in the past, this
transmission was limited and not sustained beyond three people
What does H1N1 mean?
 The “H1” (Hemagglutinin) and “N1” (Neuraminidases).
 Influenza viruses are split up into three broad groups known as influenza A, B and C.
 Influenza A is the most common type, and H1N1 is a type of influenza A.
 The designation “H1N1” indicates unique traits, which exhibit characteristics that identify the
virus to the immune system and allows for attachment and replication of the virus.
a. Hemagglutinin‐ protein the virus uses to attach to the host cells.
b. Neuraminidase‐ enables the virus to be released from the host cell.
c. M2 Ion Channel‐ Allows protons to move through the viral envelope and is essential for the
virus replication process.
d. RNP‐ Ribonucleoprotein containing the virus RNA genome.

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 Swine flu differs from human flu
The H1N1 swine flu viruses are antigenically very different from human H1N1 viruses and,
therefore, vaccines for human seasonal flu would not provide protection from H1N1 swine flu
viruses.
How it spreads?
 Spread of this swine influenza A (H1N1) virus is thought to be happening in the same way
that seasonal flu spreads.
 Flu viruses are spread mainly from person to person through coughing or sneezing of people
with influenza.
 Sometimes people may become infected by touching something with live flu viruses on it and
then touching their mouth or nose.
Is the current swine flu virus contagious?
 Various international agencies (US Centres for Disease Control & Prevention, World Health
Organization) have determined that this swine influenza A (H1N1) virus is contagious and is
spreading from human to human.
 WHO has escalated the world Pandemic Phase from Phase 3 to Phase 4 (in a 6-scale Phase),
indicating that a worldwide pandemic due to swine flu H1N1 is possible.
Symptoms
Fever, sore throat, vomiting, diarrhoea, runny nose, coughing and nausea are all symptoms of swine
flu in humans.
Diarrhoea, coughing, sore throat, lack of appetite, fever, sneezing and weight loss are the main
symptoms of swine flu in pigs.
Sources of contamination
 The virus can be spread when a person touches something that is contaminated with the virus
and then touches his or her eyes, nose, or mouth.
 Droplets from a cough or sneeze of an infected person move through the air. The virus can
then be spread when a person touches respiratory droplets from another person on a surface
like a desk, doorknob, child’s toy or phone handset and then touches their own eyes, mouth or
nose before washing their hands.
In children emergency warning signs
 Fast breathing or trouble breathing.
 Bluish skin colour.
 Not drinking enough fluids.
 Not waking up or not interacting.
 Being so irritable that the child does not want to be held.
 Flu-like symptoms improve but then return with fever and worse cough.
 Fever with a rash.
In adult emergency warning signs
 Difficulty breathing or shortness of breath.
 Pain or pressure in the chest or abdomen.
 Sudden dizziness.
 Confusion.

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  Severe or persistent vomiting

Diagnosis
 To diagnose swine influenza A infection, a respiratory specimen would generally need to be
collected within the first 4 to 5 days of illness (when an infected person is most likely to be
shedding virus).
 However, some persons, especially children, may shed virus for 10 days or longer.
 Identification as a swine flu influenza A virus requires sending the specimen to a hospital
laboratory for testing.
Vaccine
 Because the virus is new, there will be no vaccine ready to protect against pandemic flu.
 Vaccine against Swine Flu virus H1N1 needs at least 6-12 months to be produced.
 Seasonal flu vaccine or past flu immunization will not provide protection
Medicines to treat
 The US CDC recommends the use of oseltamivir (Tamiflu®) or zanamivir (Relenza®) for the
treatment and/or prevention of infection with these swine influenza viruses.
 Antiviral drugs are prescription medicines (pills, liquid or an inhaler) that fight against the flu
by keeping flu viruses from reproducing in your body.
 For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of
symptoms).
Prevention of swine flu
 Farmers should wear face masks and gloves when dealing with infected animals to prevent
swine flu.
 Cover your nose and mouth with a tissue when you cough or sneeze. Throw the tissue in the
trash after you use it.
 Wash your hands often with soap and water, especially after you cough or sneeze. Alcohol-
based hand cleaners are also effective.

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  Try to avoid close contact with sick people.
 If you get sick with influenza, stay home from work or school and limit contact with others to
keep from infecting them.

4. Covid-19
 The coronavirus disease 2019 (COVID-19) pandemic, caused by a novel severe acute
respiratory syndrome coronavirus-2 (SARS-CoV-2), emerged at the end of 2019 in China and
affected the entire world population, either by infection and its health consequences, or by
restrictions in daily life as a consequence of hygiene measures and containment strategies.
 As of September 2021, more than 231,000.000 infections and 4,740.000 deaths due to
COVID-19 have been reported.
 The infections present with varied clinical symptoms and severity, ranging from
asymptomatic course to fatal outcome.
 Several risk factors for a severe course of the disease have been identified, the most important
being age, gender, comorbidities, lifestyle, and genetics.
 While most patients recover within several weeks, some report persistent symptoms
restricting their daily lives and activities, termed as post-COVID.
 At the end of 2019, many people in Wuhan, China, developed signs of a hitherto unknown
infection. Hospitalized individuals presented primarily with fever, cough, and muscle pains,
many of them showed abnormalities in the chest computed tomography (CT) and 29%
developed acute respiratory distress syndrome (ARDS; Huang et al., 2020).
 A novel coronavirus was identified as the causal agent and dubbed as severe acute respiratory
syndrome coronavirus 2 (SARS-CoV-2). The disease itself was called coronavirus disease
2019 (COVID-19).
 The infection then spread throughout the entire world and was declared a pandemic by the
WHO on March 11, 2020.
 Due to the contagiousness of the virus, many nations attempted to flatten the epidemiological
curve and avoid overburdening of the healthcare systems by enforcing specific hygiene
measures, social distancing, mask wearing, travel restrictions, closing of borders, national
lockdowns, and mandatory quarantine for the infected and their contact persons.
 During the course of the pandemic, extensive studies analyzed the virus, the epidemiology,
immunology, and pathophysiology of COVID-19 and tried to establish optimized diagnostic
and prevention strategies.
 In addition, major efforts were undertaken to identify targeted therapies by re-purposing
existing drugs or by applying existing knowledge from best clinical practice of other
respiratory infectious diseases to the treatment of COVID-19.
 Finally, by using different and even novel strategies, numerous effective vaccines have been
developed within a surprisingly short period of time.
Epidemiology
 The viruses classified as coronaviridae, first discovered at the beginning of the twentieth
century, are single-strand RNA viruses that have their primary animal reservoir in bats and
birds.
 The reservoir animal, while carrying the virus, seldom develops a life-threatening,
symptomatic infection.
 The virus may, however, replicate inside the host when its immune response is diminished,
leading to a large number of random mutations which may generate variants capable of

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 infecting other species including humans. This event is referred to as a cross-species spillover
event.
 The spillover event for SARS-CoV-2 is believed to have happened sometime in 2019,
although the definitive animal origin, whether snake or bats, remains elusive thus far.
Virology
 The SARS-CoV-2, reportedly first isolated at the beginning of 2020 in China, is one of the
coronaviridae, a family of positive-sense single-strand RNA viruses first associated with
avian respiratory infections in the 1930s.
 Coronaviridae are made up of four distinct genera (alpha, beta, gamma, and delta), with
SARS-CoV-2 belonging to the genus of beta-coronaviridae.
 Severe acute respiratory syndrome coronavirus-2 is believed to have evolved into its present
state in bats, the original animal reservoir, and may have passed through an intermediate host
before being finally transmitted to humans.
Virus Structure and Classification
 SARS-CoV-2 is a member of the coronavirus family, which includes viruses that can cause
respiratory illnesses in humans and animals.
 It is an enveloped virus with a single-stranded RNA genome.
Transmission
 COVID-19 primarily spreads through respiratory droplets produced when an infected person
talks, coughs, or sneezes.
 Fomites (contaminated surfaces) can also contribute to transmission when people touch
surfaces and then their face.
Pathogenesis
 The virus enters the body through the respiratory tract and uses its spike (S) protein to bind to
angiotensin-converting enzyme 2 (ACE2) receptors on human cells, particularly in the lungs.
 The infection can lead to a range of symptoms, from mild respiratory issues to severe
pneumonia, acute respiratory distress syndrome (ARDS), and other complications.
Symptoms
 Common symptoms include fever, cough, and difficulty breathing.
 Other symptoms may include fatigue, body aches, loss of taste or smell, sore throat, and
gastrointestinal symptoms.
Severity
 Severity can range from mild or asymptomatic cases to severe respiratory distress,
pneumonia, and organ failure.
 Certain populations, such as the elderly and those with underlying health conditions, are at a
higher risk of severe outcomes.
Immune Response
 The immune system plays a crucial role in clearing the virus. T cells, B cells, and antibodies
are involved in the adaptive immune response.
 Severe cases of COVID-19 are often associated with an exaggerated immune response,
sometimes leading to a cytokine storm.

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 Diagnosis
 Microbiological techniques, such as reverse transcription-polymerase chain reaction (RT-
PCR), are commonly used to detect the presence of viral RNA in respiratory samples.
 Serological tests detect antibodies against the virus, indicating a past infection.
Treatment and Vaccines
 Antiviral drugs, such as remdesivir, have been used to treat severe cases.
 Vaccines, developed using various technologies like mRNA and viral vector platforms, have
been crucial in preventing infection and reducing the severity of the disease.
Variants
 SARS-CoV-2 has undergone genetic mutations, leading to the emergence of variants with
different characteristics.
 Monitoring and understanding these variants are essential for vaccine development and
public health strategies.
Prevention and Control
 Public health measures, such as social distancing, mask-wearing, and hand hygiene, are
crucial in preventing the spread of the virus.
 Vaccination campaigns have been instrumental in reducing the impact of the disease.
 Microbiological research continues to be vital for understanding the dynamics of COVID-19,
developing new treatments, and improving public health strategies to control the pandemic.

5. HIV
Human Immunodeficiency Virus (HIV) is a virus that attacks the immune system, specifically the
CD4 cells (T cells), which help the immune system fight off infections. If left untreated, HIV can
lead to the disease acquired immunodeficiency syndrome (AIDS). The acquired immune deficiency
syndrome AIDS was first recognized in 1981 in US.
Centers for Disease Control and Prevention reported the unexplained occurrence of Pneumocystis
jiroveci pneumonia in five previously healthy homosexual men in Los Angeles and of Kaposi's
sarcoma with or without P. jiroveci pneumonia in 26 previously healthy homosexual men in New
York and Los Angeles.

Etiology
 AIDS is caused by HIV, a human retrovirus.
 Two types-mHIV I and HIV II which are genetically different but has related forms.
 HIV I is most common type associated with AIDS in US, Europe and Central Africa.
 HIV II causes similar disease in West Africa and India.
 HIV-II is transmitted less efficiently than HIV-I.
Structure
 HIV is a typical retrovirus with a small RNA genome of 9300 base pairs.
 Is a spherical and contains nucleocapsid core surrounded by a lipid bilayer or envelop derived
from host cell membrane.
 The viral genome encodes 3 major open reading frames-
1. gag encodes a polyprotein that is processed to release major structural proteins of virus.

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 2. pol encodes 3 important enzymes are RNA dependent DNA polymerase or reverse
transcriptase with RNAse H, Protease and integrase.
3. env encodes for large transmembrane envelop proteins responsible for cell binding and entry.
 Several small genes encode regulatory proteins that enhances virion production or combat
host defence.

Pathogenesis
 HIV can infect many tissues, there are 2 major targets
- Immune system
- Central nervous system.
 Primarily affect cell mediated immunity.
 Results in severe loss of CD4+ T cells and impairment in the function of helper T cells.
 Macrophages and dendritic cells also infected.
Life cycle of HIV
STEP’S INVOLED
1. INVASION
a) Attachment
b) Fusion
2. MATURATION
a) Reverse transcriptase
b) Integration
3. RELEASE
a) Budding
b) Exit from cell

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 Role of enzymes
1. Reverse Transcriptase (RT)
 Multifunctional enzymes having RNA dependent DNA polymerase activity
 Also having RNase H (helicase) activity
 Catalyses formation of double stranded proviral DNA from signal stranded RNA genome
 Due to its central role in the viral replication RT is prime target for anti-aids therapy
 Inhibitors of RT can be classified as
1. Nucleoside RT inhibitor (NRTI)
2. Non-Nucleoside RT inhibitor (NNRTI)
 NRTI are competative in nature while NNRTI are non competative
2. Protease
 Protease essential for production of mature, infectious virions
 HIV protease is responsible for post-translational processing of poly proteins & proteolytic
activity
 Inhibition of these protease enzyme is also attractive target for anti-aids therapy
3. Integrase
 Catalyses the integration of double stranded DNA copy of their RNA genome into
chromosome of a host cell
 Inhibition of integrase enzyme is prime target for anti-aids therapy
Common signs symptoms
 Severe impairment or suppression of immune system.
 Pneumocystis carinii pneumonia (pcp) is mostly seen.
 Opportunistic infection
 CD4+T- cells count falls below 200 cells/mm3 of blood.
 In healthy adult its value is 600-1500 cells/mm3 of blood.
 Weight loss
 Pharyngitis
 Neurological symptoms.
 Rash
 Headache
 Fever
 Lymphadenopathy
Modes of transmission of HIV/AIDS
1. Through Body Fluids
 Semen
 Vaginal fluids
 Breast Milk
2. HIV enters the bloodstream through
 Open Cuts

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  Breaks in the skin
 Mucous membranes
 Direct injection
 Sharing Needles- Without sterilization
3. Through Sex
 Intercourse
 Oral
 Anal
4. Mother-to-Baby
 During pregnancy transplacental transmitted.
 During post-partum period through contamination with maternal blood, infected amniotic
fluid or breast milk
Diagnosis
1. Blood detection test
 Enzyme-Linked Immunosorbent Assay/Enzyme Immunoassay (ELISA/EIA)
 Radio Immunoprecipitation Assay/Indirect Fluorescent Antibody Assay (RIP/IFA)
 Polymerase Chain Reaction (PCR)
 Western Blot Confirmatory test
2. Urine test
 Urine Western Blot
 As sensitive as testing blood
 Safe way to screen for HIV
 Can cause false positives in certain people at high risk for HIV
3. Orasure
 The only FDA approved HIV antibody.
 As accurate as blood testing
 Involves collecting secretions between the cheek and gum and evaluating them for HIV
antibodies.
Antiretroviral agents
1. Nucleoside/Nucleotide Analogues: Abacavir Didanosine Emtricitabine Lamivudine
Stavudine Tenofovir Zalcitabine
2. Non-nucleoside Reverse Transcriptase Inhibitors: Delavirdine, Efavirenz, Etravirine,
Nevirapine
3. Protease Inhibitors: Amprenavir,Atazanavir ,Darunavir Fosamprenavir, Indinavir,
Lopinavir/Ritonavir Nelfinavir ,Ritonavir, quinavir
4. Fusion Inhibitors: Enfuvirtide
5. Chemokine Coreceptor Antagonists: Maraviroc
6. Integrase Inhibitors: Raltegravir
I. Nucleoside/Nucleotide Analogues
 Nucleoside and nucleotide reverse transcriptase inhibitors prevent infection of susceptible
cells but have no impact on cells that already harbour HIV.
 Nucleosides that must be Tri phosphorylated at the 5’-hydroxyl to exert activity.
 tenofovir, is a nucleotide monophosphate analog that requires two additional phosphates to
acquire full activity.
A. Zidovudine:

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  3’ azido- 3’ deoxythymidine.
 Synthetic thymidine analogue with potent broad-spectrum activity.
Mechanism of Action:
Due to similar structure, it incorporates in to growing DNA strand and terminate synthesis due to
lack of OH group.

Untoward Effects
 They are mainly due to partial inhibiton of cellular DNA polymarase.
 Fatigue, malaise, myalgia, nausea, anorexia, headache, and insomnia.
 Bone marrow suppression, mainly anemia and granulocytopenia.
 Gastrointestinal disturbances
 Abnormal liver functions
 Hyperlipidemia
Therapeutic Uses:
 Zidovudine is FDA approved for the treatment of adults and children with HIV infection and
for preventing mother-to-child transmission of HIV infection.
 It is also recommended for postexposure prophylaxis in HIV-exposed healthcare workers,
also in combination with other antiretroviral agents.
II. Non-nucleoside reverse transcriptase inhibitors
 Nonnucleoside reverse transcriptase inhibitors (NNRTIs) include a variety of chemical
substrates that bind to the HIV-1 reverse transcriptase.
 These compounds induce a conformational change in the three-dimensional structure of the
enzyme that greatly reduces its activity, and thus they act as noncompetitive inhibitors
A. Nevirapine:
 Is a dipyridodiazepinone NNRTI with potent activity against HIV-1.
 nevirapine does not have significant activity against HIV-2 or other retroviruses.
Mechanism of Action:

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  Nevirapine is a noncompetitive inhibitor that binds to a site on the HIV-1 reverse
transcriptase that is distant from the active site, inducing a conformational change that
disrupts catalytic activity.

Untoward Effects
 Hepatotoxicity
 Stevens-Johnson syndrome
 Rash
 Pruritus
 Fever, fatigue, headache, somnolence, and nausea.
Uses:
 Pregnant women
 Used to prevent mother to infant HIV infection
 HIV-1 infection in adults and children in combination with other antiretroviral agents.
III. Protease inhibitors
 HIV protease inhibitors are peptide like chemicals that competitively inhibit the action of the
virus aspartyl protease.
 This protease is a homodimer consisting of two 99-amino-acid monomers; each monomer
contributes an aspartic acid residue that is essential for catalysis.
A. Saquinavir:
 A peptidomimetic hydroxyethyl amine HIV protease inhibitor.
 Inhibits both HIV-1 and HIV-2 replication.
Mechanisms of Action
 Reversibly binds to the active site of HIV protease, preventing polypeptide processing and
subsequent virus maturation.
 Potently inhibiting the HIV-encoded protease but not host-encoded aspartyl proteases.

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Untoward Effects:
 Nausea, vomiting, diarrhoea, and abdominal discomfort.
 Lipodystrophy.
Therapeutic Use:
 Reduction of viral load with other nucleotide analogues.
IV. Fusion inhibitors
 Enfuvirtide is the only available HIV entry inhibitor.
 Enfuvirtide is a 36-amino-acid synthetic peptide whose sequence is derived from a part of the
transmembrane gp41 region of HIV-1.
 Not active against HIV-2.
 The peptide blocks the interaction between the N36 and C34 sequences of the gp41
glycoprotein by binding to a hydrophobic groove in the N36 coil
 This prevents formation of a six-helix bundle critical for membrane fusion and viral entry
into the host cell.
 Treatment-experienced adults who have evidence of HIV replication despite ongoing
antiretroviral therapy.
V. CCR5 antagonists
 In order to enter a human cell, HIV must first attach itself to proteins on the cell’s surface.
 The next stage involves proteins called co- receptors, two main types: CCR5 and CXCR4.
Some strains of HIV use CCR5, others use CXCR4.
 CCR5 antagonists are drugs that bind to the CCR5 co-receptor so that HIV cannot exploit it
to gain entry to a cell.
 The main drawback of these drugs is that they don’t work against all strains of HIV.
 Maraviroc is an example for this class
A. Raltegravir:
 First in class HIV integrase inhibitor
 The integration of HIV-1 proviral DNA into the host cell genome
 Integrase mainly involved in integration of viral DNA in to host DNA.
 Inhibition of this enzyme prevents integration.
 Impressive antiviral potency in heavily treatment-experienced patients.
Recent therapy for AIDS
Drug class Recently approved Phase III Phase II
Entry inhibitor (CCR5) Maraviroc (Aug. Vicriviroc PRO 140
2007)
Entry inhibitor (CD4) TNX-355
Integrase inhibitor Raltegravir (Oct. Elvitegravir
2007)
Maturation inhibitor Bevirimat
NNRTI Etravirine (Jan. 2008) Rilpivirine
NRTI Apricitabine KP-1461
Racivir
Elvucitabine

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 Gene therapy
 RNA-interference is damage to a certain RNA sequence with participation of a different,
“defending" RNA molecule.
 This system prevents viral infection, unless viruses had learned to cut it off in the course of
evolution.
 Researchers from countries including Russia are developing the artificial RNA-interference
system.
 It is non-injurious to the patient and, due to high specificity of action, does not damage its
own RNA in cells infected by the virus.
 To fight HIV, Russian biologists have created three genetic structures.
 These structures contain short nucleotide against sequences that find the most conservative
molecules among all RNA molecules, that is, sequences that do not change quickly and are
important to the virus.
 These sequences are then "damaged".
 Genetic structures significantly suppress viral reproduction.
Vaccine
Difficulties in developing an HIV vaccine
 Classic vaccines mimic natural immunity against reinfection generally seen in individuals
recovered from infection; there are almost no recovered AIDS patients.
 Most vaccines protect against disease, not against infection; HIV infection may remain latent
for long periods before causing AIDS.
 Most effective vaccines are whole-killed or live- attenuated organisms; killed HIV-1 does not
retain antigenicity and the use of a live retrovirus vaccine raises safety issues.
 Most vaccines protect against infections through mucosal surfaces of the respiratory or
gastrointestinal tract; the great majority of HIV infection is through the genital tract.
Phase I
 Most initial approaches have focused on the HIV envelope protein.
 Thirteen different gp120 and gp160 envelope candidates have been evaluated.
 Most research focused on gp120 rather than gp41/gp160.
Phase III
 AIDSVAX vaccine.
 This is the first successful HIV vaccine trial in history.
 The percentage rate reduced to 26% compared with those who had been given a placebo.
Planned Clinical Trials
 Novel approaches, including modified vaccinia Ankara (MVA), adeno-associated virus,
Venezuelan equine encephalitis (VEE).
Monoclonal antibodies
 Monoclonal antibodies, produced after immunizing mice, have binding characteristics that
look similar to two well-known broadly neutralizing human monoclonal antibodies, known as
2F5 and 4E10, which also bind to HIV-1 protein and lipid.
 That might be useful in an effective HIV-1 vaccine.

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 6. Hepatitis
 Hepatitis is an inflammation of the liver. It is commonly the result of a viral infection, but
there are other possible causes of hepatitis.
 The five main viral classifications of hepatitis are hepatitis A, B, C, D, and E. A different
virus is responsible for each type of viral hepatitis.
 The World Health Organization (WHO) estimates that 354 million Trusted Source people
currently live with chronic hepatitis B and C globally.
1. Hepatitis A
 Hepatitis A is the result of an infection with the hepatitis A virus (HAV). This type of
hepatitis is an acute, short-term disease.
2. Hepatitis B
 The hepatitis B virus (HBV) causes hepatitis B. This is often an ongoing, chronic condition.
The Centers for Disease Control and Prevention (CDC) estimates that around 826,000Trusted
Source people are living with chronic hepatitis B in the United States and around 257 million
people worldwide.
3. Hepatitis C: Hepatitis C comes from the hepatitis C virus (HCV). HCV is among the most
common bloodborne viral infections in the United States and typically presents as a long-
term condition.
 According to the CDC, approximately 2.4 million AmericansTrusted Source are currently
living with a chronic form of this infection.
4. Hepatitis D
 This is a rare form of hepatitis that only occurs in conjunction with hepatitis B infection.
The hepatitis D virus (HDV) causes liver inflammation like other strains, but a person cannot
contract HDV without an existing hepatitis B infection.
 Globally, HDV affects almost 5 percent Trusted Source of people with chronic hepatitis B.
5. Hepatitis E
 Hepatitis E is a waterborne disease that results from exposure to the hepatitis E virus (HEV).
Hepatitis E is mainly found in areas with poor sanitation and typically results from ingesting
fecal matter that contaminates the water supply.
 This disease is uncommon Trusted Source in the United States, according to the CDC.
 Hepatitis E is usually acute but can be particularly dangerous in pregnant women.
Causes of Hepatitis

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 Common Symptoms of Hepatitis
If you are living with a chronic form of hepatitis, like hepatitis B and C, you may not show
symptoms until the damage affects liver function. By contrast, people with acute hepatitis may
present with symptoms shortly after contracting a hepatitis virus.
Common Symptoms of Infectious Hepatitis include:
 fatigue
 flu-like symptoms
 dark urine
 pale stool
 abdominal pain
 loss of appetite
 unexplained weight loss
 yellow skin and eyes, which may be signs of jaundice
How Hepatitis is Diagnosed
It is crucial to understand what is causing hepatitis in order to treat it correctly. Doctors will progress
through a series of tests to accurately diagnose your condition.
1. History and physical exam
2. Liver function tests
 Liver function tests use blood samples to determine how efficiently your liver works.
 Abnormal results of these tests may be the first indication that there is a problem, especially
if you don’t show any signs on a physical exam of liver disease. High liver enzyme levels
may indicate that your liver is stressed, damaged, or not functioning correctly.
3. Other blood tests

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 4. Liver biopsy: When diagnosing hepatitis, doctors will also assess your liver for potential
damage Trusted Source. A liver biopsy is a procedure that involves taking a sample of tissue
from your liver.
5. Ultrasound: An abdominal ultrasound uses ultrasound waves to create an image of the
organs within your abdomen. This test allows your doctor to take a close look at your liver
and nearby organs. It can reveal:
 fluid in abdomen
 liver damage or enlargement
 liver tumors
 abnormalities of your gallbladder
 Sometimes the pancreas shows up on ultrasound images as well. This can be a useful test in
determining the cause of your abnormal liver function.
Hepatitis treatment
Treatment options will vary by the type of hepatitis you have and whether the infection is acute or
chronic.
1. Hepatitis A: Hepatitis A is a short-term illness and may not require treatment. However, if
symptoms cause a great deal of discomfort, bed rest may be necessary. In addition, if you
experience vomiting or diarrhea, doctor may recommend a dietary program to maintain your
hydration and nutrition.
2. Hepatitis B
 There is no specific treatment program for acute hepatitis B.
 However, if you have chronic hepatitis B, you will require antiviral medications. This form
of treatment can be costly, as you may have to continue it for several months or years.
 Treatment for chronic hepatitis B also requires regular medical evaluations and monitoring to
determine if the virus is responding to treatment.
3. Hepatitis C
 Antiviral medications can treat both acute and chronic forms of hepatitis C.
 Typically, people who develop chronic hepatitis C will use a combination of antiviral drug
therapies. They may also need further testing to determine the best form of treatment.
People who develop cirrhosis or liver disease due to chronic hepatitis C may be candidates for
a liver transplant.
4. Hepatitis D: The WHO lists pegylated interferon alpha as a treatment for hepatitis D.
However, this medication can have severe side effects. As a result, it’s not recommended for
people with cirrhosis liver damage, those with psychiatric conditions, and people with
autoimmune diseases.
5. Hepatitis E
 Currently, no specific medical therapies are available to treat hepatitis E. Because the
infection is often acute, it typically resolves on its own.
 Doctors will typically advise people with this infection to get adequate rest, drink plenty of
fluids, get enough nutrients, and avoid alcohol. However, pregnant women who develop this
infection require close monitoring and care.

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 Vaccines
 A vaccine for hepatitis A is available and can help prevent the contraction of HAV. The
hepatitis A vaccine is a series of two doses and most children begin vaccination at age 12 to
23 months. This is also available for adults and can also include the hepatitis B vaccine.
 The CDC recommends hepatitis B vaccinations for all newborns. Doctors typically
administer the series of three vaccines over the first 6 months of childhood.
 The CDC also recommends the vaccine for all healthcare and medical personnel. Vaccination
against hepatitis B can also prevent hepatitis D.
 There are currently no vaccines for hepatitis C or E.
Complications of Hepatitis
Chronic hepatitis B or C can lead to more severe health problems. Because the virus affects the liver,
people with chronic hepatitis B or C are at risk of:
 chronic liver disease
 cirrhosis
 liver cancer
When your liver stops functioning normally, liver failure can occur. Complications of liver failure
include:
 bleeding disorders
 a buildup of fluid in your abdomen, known as ascites
 increased blood pressure in portal veins that enter your liver, known as portal hypertension
 kidney failure
 hepatic encephalopathy, which can involve fatigue, memory loss, and diminished mental
abilities
 hepatocellular carcinoma, which is a form of liver cancer
 Death
People with chronic hepatitis B and C should avoid alcohol as it can accelerate liver disease and
failure. Certain supplements and medications can also affect liver function. If you have chronic
hepatitis B or C, check with your doctor before taking any new medications.

Common Types of Fungal Infections

1. Ringworm
2. Yeast Infection

1. Ringworm
Dermatophytes
 Ringworm
 Tinea
 Dermatomycosis
Taxonomy
 Fungi
1. Microsporum, Trichophyton-Animal pathogens
2. Epidermophyton- Human pathogen
 Classification

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 - Zoophilic
- Anthropophilic
- Geophilic
Dermatophytes: skin plants
 Etiological agents are called dermatophytes - "skin plants". Three important anamorphic
genera, (i.e., Microsporum, Trichophyton, and Epidermophyton), are involved in ringworm.
 Dermatophytes are keratinophilic - "keratin loving". Keratin is a major protein found in
horns, hooves, nails, hair, and skin.
 Ringworm - disease called ‘herpes' by the Greeks, and by the Romans ‘tinea' (which means
small insect larvae).
Dermatophytes
 Microsporum - infections on skin and hair (M-N-No Nails)
 Epidermophyton - infections on skin and nails (not the cause of TINEA CAPITIS)
 Trichophyton - infections on skin, hair, and nails.
Zoophilic Organisms
 Epidermophyton- E. floccosum
 Microsporum- M.canis, M. gypseum
 Trichophyton- T. rubrum, T. mentagrophytes, T. verrucosum, T.violaceum
History
 30 A.D.: First historical reference
 Terminology
- Tinea
- Ringworm
 19th century: Mycotic etiology described
 Dermatophytes most common fungal pathogens in the U.S.
(Dermatophytes have likely existed for millions of years; however, the first historical reference did
not come unto 30 A.D., when Roman encyclopedist Aulus Cornelius Celsus described a “suppurative
infection of the scalp” that was attributed to a dermatophyte. In that era, dermatophytes were
described as “tineas.” The term “ringworm” emerged later, probably around the 16th century. In the
19th century, the mycotic etiology of these skin infections was finally described. Dermatophytes
remain the most common fungal pathogens (except finger onychomycosis due to Candida) in the
U.S. Sources: Libero A. Natural history of the dermatophytes and related fungi. Mycopathologia.
1974;53(1-4): 93-110. Seebacher C., Bouchara J.P., Mignon B. Updates on the epidemiology of
dermatophyte infections. Mycopathologia. 2008;166(5-6): 335-352.)
Geographic Distribution
 Optimal conditions
- Tropics/subtropics
- Warm, humid environment
 Some worldwide
- M. canis, M. nanum,
- T. mentagrophytes,
T. verrucosum, T. equinum
 Some regionally limited

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 Transmission
 Contact with:
1. Arthrospores: Asexual spores formed in the hyphae of the parasitic stage
2. Conidia: Sexual or asexual spores formed in the “free-living” environmental stage
3. Growing hairs or skin are infected: contains essential nutrients
4. Modes of transmission
- Contact with infected animals/humans
- Airborne hairs/scales
- Fomites
- Soil
5. Warm damp areas (e.g., tropics, moisture accumulation in clothing and shoes).
6. Schools, military camps, prisons.
7. Animals (e.g., dogs, cats, cattle, poultry, etc.).
(Infection usually begins in a growing hair or the stratum corneum of the skin. Dermatophytes do not generally invade resting hairs, since the essential
nutrients they need for growth are absent or limited. Hyphae spread in the hairs and keratinized skin, eventually developing infectious arthrospores.
Transmission between hosts usually occurs by direct contact with a symptomatic or asymptomatic host, or direct or airborne contact with its hairs or
skin scales. Infective spores in hair and dermal scales can remain viable for several months to years in the environment. Fomites such as brushes and
clippers can be important in transmission. Geophilic dermatophytes are usually acquired directly from the soil rather than from another host.)

Clinical manifestations of ringworm infections are called by different names on basis of

location of infection sites
• Tinea capitis - ringworm infection of the head, scalp, eyebrows, eyelashes
• Tinea favosa - ringworm infection of the scalp (crusty hair)
• Tinea corporis - ringworm infection of the body (smooth skin)
• Tinea cruris - ringworm infection of the groin (jock itch)
• Tinea unguium - ringworm infection of the nails
• Tinea barbae - ringworm infection of the beard
• Tinea manuum - ringworm infection of the hand
• Tinea pedis - ringworm infection of the foot (athlete's foot)
Clinical manifestations of ringworm
Tinea pedis - Athletes' foot infection
 between toes or toe webs (releasing of clear fluid) - 4th and 5th toes are most common.
 Soreness and itching of any part of the foot.
 Fungi probably transmitted host to host through infected squames; flat, keratinised, dead cells
shed from the outermost layer of a stratified squamous epithelium.
 Three causal agents, T. rubrum, T. mentagrophytes, and Epidermophyton floccosum
Clinical manifestations of ringworm Symptoms and treatment
Three Grades of Infection
a. Grade I - Subclinical
 An itching between toes, skin may be soft and macerated, blistering my occur.
 Treatment - keeping feet dry and clean, drying between the toes lightly each time you bathe
to remove some skin. Application of fungicidal powders or ointments containing
1) salicylic acids to promote peeling of the skin and/or
2) tonaftate or other topical fungicides.
b. Grade II

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  Host is conscious of a burning sensation while walking and standing.
 Soaks are recommended (paints or liquids) such as 1:4000 KMnO4 (stains the skin purple) or
topical fungicides.
 Remove clear liquid from blisters by having a doctor puncture near the base or unroofing the
blister.
 Dusting powder in morning to help keep feet dry.
c. Grade III
 A secondary bacterial infection sets in.
 Patient should go to bed.
 Use systemic antibiotics to fight bacterial infection.
 Use of soaks and compresses.
 After infection subsidies, go to treatments as for Grade I or II infections.
 For persistent cases, (T. rubrum is usually the culprit), resort to systemic griseofulvin therapy
or other antifungal systemic drugs (i.e., Lamisil trademark or terbinafine HCl)
o Griseofulvin is fungistatic, so it won't kill the fungus, just inhibit its growth.
- Improvement occurs in 2-6 weeks as long as 6 months.
- Sometime griseofulvin treatment is ineffective.
o Some patients may not tolerate terbinafine HCL depending on sensitivity to drug.
Clinical manifestation of ringworm
Tinea corporis - body ringworm
 Generally restricted to stratum corneum of the smooth skin.
 Produces concentric or ring-like lesions on skin
 Severe cases -raised and inflamed.
 All forms of tinea corporis caused by T. rubrum, T. mentagrophytes, T. tonsurans, M. canis,
and M. audouinii...
Transmission:
- infected scales hyphae or arthroconidia on the skin.
- direct contact between infected humans or animals, by fomites
 Normally resolves itself in several months.
Symptoms result from fungi metabolites such as toxin/allergens. Disease found throughout the world are treatable with topical agent containing
tolnaftate, ketoconazole, miconazole, etc (any agent such a bedding or clothing capable of retaining a pathogen and transmitting to a new host).
Transfer form on area to the body to another (from tinea pedis to tinea corporis). T. verrucosum and T. violaceum infections require more vigorous
treatment including cleaning of area to remove of scales and older fungicidal topical applications of ammoniated mercury ointment, 3 % salicylic and
sulfuric acid, or tincture of iodine for several weeks. Widespread tinea corporis and more severe types (lesions) require systemic griseofulvin treatment
(about 6 weeks for effective treatment).

Clinical manifestations of ringworm Symptoms and treatment

Tinea cruris - ringworm of the groin and surrounding region
 More common in men
 Infection seen on scrotum and inner thigh; the penis is usually not infected.
 Epidemics associated with grouping of people into tight quarters - athletic teams, troops, ship
crews, inmates of institutions.
 Several causes of tinea cruris include T. rubrum (does not normally survive long periods
outside of host), E. flocossum (usually associate with epidemics because resistant
arthroconidia in skin scales can survive for years on rugs, shower stalls, locker room floors),
T. mentagrophytes

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 Clinical manifestation of ringworm
Tinea unguium - ringworm of the nails
 Tinea unguium or onchomycosis can take two forms:
- Leukonychia mycotica - superficial white onychomycosis, invasion of fungus restricted to
patches or pits on surface of the toenail.
- Invasive subungual dermatophytosis - Invasion of nail plates by dermatophytes.
 Most commonly caused by T. rubrum, then E. floccosum or other Trichophyton species.
 Resistant to treatment, rarely resolves spontaneously
lateral or distal edges first involved, followed by establishment of the infection beneath the nail plate. Topical treatments - poor record
of cure. Ablation - surgical or chemical removal of nail. Onychomycosis (infection of nails caused by non-dermatophytic fungi and
yeasts Systemic griseofulvin therapy can lead to remission (usually a year or more of treatment required - results vary about 29 % cure
rate). Use of another systemic antifungal (i.e., Lamisiltrademark or terbinafine HCl). Filing down the nail to paper thin consistency and
soaking or painting with KMnO4 (1:4000), phenol, 10 % salicylic acid, or 1% iodine is useful adjunct to systemic griseofulvin
treatment.

Tinea capitis - ringworm of the scalp, eyebrows and eyelashes

 Cause- Microsporum and Trichophyton.
 Fungus grows into hair follicle.
 Ectothrix infection - fragmentation of mycelium into conidia (called arthroconidia) around
the hair shaft or just beneath the cuticle with destruction of the cuticle. Caused by M.
audounii, M. canis
 Endothrix infection - arthroconidia formation occurs by fragmentation of hyphae with the
hair shaft with destruction of the cuticle. T. tonsurans (most common cause).
 "Id" reaction may occur.
Using a Wood's lamp, on hair Microsporum species tend to fluoresce green while Trichophyton species generally do not fluoresce. "Gray patch
ringworm” ectothrix common disease in children usually not associated with inflammation. Lack of fluorescence does not mean it isn't Microsporum.
Subculture any strands of hair that fluoresce to help identify the causal agent. Zoophilic and geophilic dermatophytes infections on man associate with
inflammation. Microsporum canis, T. verrucosum, and T. mentagrophytes (zoophilic); M. gypseum and M. fulvum (geophilic species). Ecto-M.
ferrugineum, T. mentagrophytes, T. verrucosum and T. megninii. Endo-T. violaceum, T. rubrum, and T. gourvillii. All these pathogen species are
anthropophilic

Treatment of Tinea Capitis

 Ectothrix infections often resolve on their own.
 Endothrix infections my become chronic and may continue into adulthood.
 Topical treatments are ineffective (don't use tonaftate or topical griseofulvin)
 Fungistatic agents are somewhat effective (miconazole, clotrimazole) in combination to
systemic administration of griseofulvin.
 Vigorous daily scrubs of scalp help removal of infectious debris. Do not use this treatment
on patients with porphyria (an accumulation of blood pigment called porphyrins in blood
stream and urine) or is hypersensitive to griseofulvin.
a. Favus
b. Kerion
c. Grey Patch
Lab Diagnosis
 Note the Symptoms.
 Woods Lamp Examination
 Sample- skin & nail scrapping (edge), plucked hair

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  Direct Microscopic examination of slides of skin scrapings, nail scrapings, and hair with10 %
KOH
 Branching hyaline septate hyphae
Culture
 SDA (with chloramphenicol & cycloheximide)
 25, 300, 370 CX21 days
 DTM=25oC- red
 Hair Perforation test
 Urease test

2. Yeast infection
Yeast infection
What is a yeast infection?
 Yeast is a fungus normally found on your skin. It’s also found in your digestive system.
 When too much yeast grows on your skin or other areas, it can cause an infection. This
infection is also called candidiasis.
 A yeast infection, also known as candidiasis, is a common fungal infection that can affect
various parts of the body.
 The most common type of yeast infection is caused by the fungus Candida albicans.
 While it commonly occurs in the genital area, it can also affect the mouth, throat, esophagus,
and other areas.
What causes a yeast infection?
 A yeast infection can happen if your skin gets damaged.
 Yeast can also “overgrow” in warm or humid conditions.
 An infection can also happen if you have a weak immune system.
 Taking antibiotics can also cause an overgrowth of yeast. That’s because antibiotics kill the
healthy bacteria in your body that normally keep the yeast in balance.
What are the risk factors for yeast infection?
 Anyone can get a yeast infection. Those at higher risk for it include:
 Infants
 People who wear dentures
 People taking antibiotics
 People getting cancer treatment
 People with other health conditions, such as HIV or diabetes
What are the symptoms of a yeast infection?
The symptoms of a yeast infection depend on where it is located in the body. The chart below shows
the most common symptoms of a yeast infection.
1) Skin folds or navel
 Rash with redness and skin breakdown
 Patches that ooze clear fluid
 Pimples
 Itching or burning

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 2) Corners of the mouth (angular cheilitis): Cracks and/or tiny cuts at the corners of the
mouth
3) Nail beds
 Swelling
 Pain
 Pus
 White or yellow nail that separates from the nail bed
4) Oral Thrush: In the mouth, a yeast infection is known as oral thrush. Symptoms include:
 White patches on the tongue, inner cheeks, gums, or throat
 Soreness or difficulty swallowing
 Redness or discomfort in the mouth
5) Genital Yeast Infection (Vaginal Candidiasis): Symptoms of a vaginal yeast infection may
include:
 Itching and irritation in the vaginal area
 Redness and swelling of the vulva
 White, cottage cheese-like discharge
 Burning sensation during urination
How is yeast infection treated?
 Your healthcare provider will consider your age, overall health, how widespread the infection
is and other factors to determine your treatment.
 Yeast infections can be easily treated with ointments or other anti-yeast (antifungal) creams.
 Yeast infections of the vagina or penis can be treated with creams or medicated suppositories.
Sometimes an oral anti-yeast medicine is used.
 Yeast infection in the mouth (thrush) may be treated with a medicated mouthwash. Or it may
be treated with lozenges that dissolve in the mouth.
 If you have a severe infection and have a weak immune system, you may need to take an oral
anti-yeast medicine.
 Esophageal yeast infections are usually treated with oral or intravenous anti-yeast medicines.
 Yeast infections of the nails are treated with an oral anti-yeast medicine.
 Yeast infections in the skin folds can be treated with anti-yeast powders.
Can a yeast infection be prevented?
 You can prevent some yeast infections by doing these things:
 Use good oral hygiene to help prevent yeast infection in your mouth (thrush). This includes
brushing and flossing your teeth every day and using mouthwash as needed.
 Wear cotton underwear to help to prevent a vaginal or genital yeast infection. If you are a
woman and get vaginal yeast infections often, you may want to take probiotics.
 Keep areas where skin rubs up against skin dry and try to reduce friction.
 Limit antibiotic use: Use antibiotics only when prescribed by a healthcare professional.
 Manage diabetes: If you have diabetes, keep your blood sugar levels under control.
Key points about yeast infection
 Yeast infection is caused by yeast on the skin or mucous membranes.
 The symptoms of a yeast infection depend on where it happens on your body. Common
symptoms are a rash, white discharge, or itching.

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  Yeast infections are treated with medicated ointments or other anti-yeast (antifungal)
preparations.

Common diseases caused by protozoans

1. Malaria
2. Leishmaniasis
3. Amebiasis

1. Malaria
Name is derived from Italian word Mal’ aria or bad air
Human malaria is caused by one of protozoan parasites:
 Plasmodium falciparum
 Plasmodium vivax
 Plasmodium ovale
 Plasmodium malariae
 Plasmodium knowlesi- forested regions of south east Asia
Malaria is transmitted through the bite of an infected
Malaria remains the world's most devastating human parasitic infection. Malaria affects over 40% of
the world's population. WHO, estimates that there are 350 - 500 million cases of malaria worldwide.
In India 2 million cases and 1000 deaths annually
Malaria is transmitted by blood, so it can also be transmitted through:
 an organ transplants
 a transfusion
 use of shared needles or syringes
The malaria life cycle is a complex system with both sexual and asexual aspects. cycle of all species
that infect humans is basically the same. There is an exogenous sexual phase in the mosquito
called sporogony during which the parasite multiplies. There is also an endogenous asexual phase
that takes place in the vertebrate or human host that is called schizogony

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60 | P a g e
A complex Life cycles

Human Cycle
1. Pre erythrocytic schizogony
2. Erythrocytic Schizogony
3. Gametogony
4. Exoerythrocytic schizogony

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 Events in Humans Start with Bite of Mosquito
1. Man – Intermediate host.
2. Mosquito – Definitive host
– Sporozoites are infective forms
 Present in the salivary gland of
female anopheles’ mosquito
 After bite of infected mosquito
sporozoites are introduced into
blood circulation.

Pre Erythrocytic-Cycle

 Sporozoites undergo developmental

phase in the liver cell
 Multiple nuclear divisions develop
to Schizonts
 A Schizont contains
20,000 – 50,000 merozoites.

Period of Pre Erythrocytic-Cycle

1. P. vivax 8 days
2. P. falciparum – 6 days
3. P. malariae-13 – 16 days,
4. P. ovale - 9 days
On maturation Liver cells rupture liberate Merozoites into blood stream
Erythrocyte Cycle
 Merozoites released invade red cells
 P. vivax infects young erythrocytes
 P. malariae Infects old erythrocytes
 P. falciparum infects RBC of all ages
 The Merozoites are pear shaped 1-5 microns in length
 The receptors for Merozoites are on red cells in the glycoprotein

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 Erythrocytic Schizogony
 Liberated Merozoites
penetrate RBC
 Three stages occur
1. Trophozoites
2. Schizont
3. Merozoite

Exo-erythrocytic (tissue) Phase

 P. malariae or P. falciparum sporozoites do not form hypnotizes, develop directly into
pre-erythrocytic schizonts in the liver
 Schizonts rupture, releasing merozoites which invade red blood cells (RBC) in liver
Gametogony
 Merozoites differentiate into Male and female gametocytes
 They develop in the red cells
 Found in the peripheral blood smears
 Microgametocyte of all species are similar in size
 Macro gametocytes are larger in size.
Mosquito cycle Sexual cycle
 Sexual cycle will be initiated in the Humans by the formation of Gametocytes
 Develop further in the female Anopheles Mosquito
 Fertilization occurs when a Microgametocyte penetrate into Macrogametocyte
 ZYGOTE is formed matures into OOKINETE
 OOKINETE to OOCYST
 OOCYST matures with large number of Sporozoites (A few hundred to thousands)
Malaria the disease, what causes it?
 Malaria is a life-threatening disease. It’s typically transmitted through the bite of an
infected Anopheles mosquito. Infected mosquitoes carry the Plasmodium parasite. When this
mosquito bites you, the parasite is released into your bloodstream.
 Once the parasites are inside your body, they travel to the liver, where they mature. After
several days, the mature parasites enter the bloodstream and begin to infect red blood cells.
 Within 48 to 72 hours, the parasites inside the red blood cells multiply, causing the infected
cells to burst open.
 The parasites continue to infect red blood cells, resulting in symptoms that occur in cycles
that last two to three days at a time.

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 Symptoms
Early symptoms: The common first symptoms – fever, headache, chills and vomiting – usually
appear 10 to 15 days after a person is infected. If not treated promptly with effective medicines,
malaria can cause severe illness and is often fatal.
How Malaria present Clinically
1. Stage 1(cold stage)
 Chills for 15 minutes to 1 hour
 Caused due to rupture from the host red cells escape into Blood
 Preset with nausea, vomitting, headache
2. Stage 2(hotstage): Fever may reach upto 400c may last for several hours starts invading
newer red cells.
3. Stage 3(sweating stage)
 Patent starts sweating, concludes the episode
 Cycles are frequently Asynchronous Paroxysms occur every 48 – 72 hours
 In P. malariae pyrexia may last for 8 hours or more and temperature my exceed 410c
More commonly, the patient presents with a combination of the following symptoms
 Fever
 Chills
 Sweats
 Headaches
 Nausea and vomiting
 Body aches
 General malaise.
Severe complicated malaria
Confusion, or drowsiness with extreme weakness (prostration). In addition, the following may
develop:
 Alteration in the level of consciousness (ranging from drowsiness to deep coma)
 Cerebral malaria (unrousable coma not attributable to any other cause in a patient with
falciparum malaria)
 Respiratory distress (metabolic acidosis bicarb less than 15 meq/l)
 Multiple generalized convulsions (2 or more episodes within a 24-hour period)
 Shock (circulatory collapse, septicaemia)
 Pulmonary oedema
 Abnormal bleeding (Disseminated Intravascular coagulopathy)
 Jaundice
 Haemoglobinuria (black water fever)
 Acute renal failure - presenting as oliguria or anuria
 Severe anaemia (Haemoglobin < 5g/dl or Haematocrit < 15%)
 High fever
 Hypoglycaemia (blood glucose level < 2.2. mmol/l) defined as the detection of P. falciparum
in the peripheral blood

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 Why Falciparum Infections are Dangerous
Can produce fatal complications,
1. Cerebral malaria
2. Malarial hyperpyrexia
3. Gastrointestinal disorders.
4. Algid malaria(SHOCK)
5. Black water fever can lead to death
Pernicious Malaria
 Is a life-threatening complication in acute falciparum malaria
 It is due to heavy parasitisation
 Manifest with
1. Cerebral malaria – it presents with hyperpyrexia, coma and paralysis. Brain is congested
2. Algid malaria – presents with clammy skin leading to peripheral circulatory failure.
Cerebral Malaria
 Malignant malaria can affect the brain and the rest of the central nervous system. It is
characterized by changes in the level of consciousness, convulsions and paralysis.
 Present with Hyperpyrexia
 Can lead to Coma
 Paralysis and other complications.
 Brain appears congested
Black Water Fever
 In malignant malaria a large number of the red blood corpuscles are destroyed.
 Haemoglobin from the blood corpuscles is excreted in the urine, which therefore is dark and
almost the colour of cola.
How long Malaria infection can last in humans?

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  Without treatment P. falciparum will terminate in less than 1 year.
 But in P. vivax and P. ovale persist as hypnozoites after the parasites have disappeared from
blood.
 Can produce periodic relapses up to 5 years
 In P.malariae may last for 40 years (Called as recrudescence X relapse) Parasites survive in
erythrocytes Liver ?
Diagnosis
 Blood film examination (Microscopy)
 QBC system
 Rapid Diagnostic Tests" (RDTs)
 PCR
Microscopy
Malaria parasites can be identified by examining under the microscope a drop of the patient’s blood,
spread out as a "blood smear” on a microscope slide. Prior to examination, the specimen is stained
(most often with the Giemsa stain) to give to the parasites a distinctive appearance. This technique
remains the gold standard for laboratory confirmation of malaria.

QBC system has evolved as rapid and precise method in Diagnosis

The QBC Malaria method is the simplest and most sensitive method for diagnosing the following
diseases.
 Malaria
 Babesiosis
 Trypanosomiasis (Chagas disease, Sleeping Sickness)
 Filariasis (Elephantiasis, Loa-Loa)
 Relapsing Fever (Borreliosis)
Appearance of Malarial parasite in QBC system

Antigen Detection Methods are Rapid and Precise

Antigen Detection
 Various test kits are available to detect antigens derived from malaria parasites and provide
results in 2-15 minutes. These "Rapid Diagnostic Tests” (RDTs). Rapid diagnostic tests

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 (RDTs) are immunochromatographic tests based on detection of specific parasite antigens.
Tests which detect histidine-rich protein 2 (HRP2) are specific for P.falciparum while
those that detect parasite lactate dehydrogenase (pLDH)-OptiMAL
 or aldolase have the ability to differentiate between P. falciparum and non-P. falciparum
malaria
Newer Diagnostic Methods
Molecular Diagnosis
Parasite nucleic acids are detected using polymerase chain reaction (PCR). This technique is more
accurate than microscopy. However, it is expensive, and requires a specialized laboratory (even
though technical advances will likely result in field-operated PCR machines).
Malaria Relapses
In P. vivax and P. ovale infections, patients having recovered from the first episode of illness may
suffer several additional attacks ("relapses") after months or even years without symptoms. Relapses
occur because P. vivax and P. ovale have dormant liver stage parasites ("hypnozoites") that may
reactivate.

Treatment of Uncomplicated P. Falciparum Infection

 The treatment of choice for uncomplicated falciparum malaria is a combination of two or
more antimalarial medicines with different mechanisms of action.
 ACTs are the recommended treatments for uncomplicated falciparum malaria.
 The artemisinin derivative components of the combination must be given for at least three
days for an optimum effect
2nd line antimalarial treatment
 Alternative ACT known to be effective in the region
 Artesunate + tetracycline/doxycycline/clindamycin, any of these combinations should be
given for 7 days
 Quinine (10mg/kg 3 times daily) + tetracycline (250mg qid)/doxycyline (100mg
bd)/clindamycin (450mg tds), any of these combinations should be given for 7 days
Treatment of P. vivax and P. ovale Infection
 Chloroquine 25 mg base/kg body weight divided over 3 days, combined with primaquine
0.25 mg base/kg body weight, taken with food once daily for 14 days is the treatment of

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 choice for chloroquine-sensitive infections. in oceania and south-east asia, the dose of
primaquine should be 0.5 mg/kg body weight.
 ACTS combined with primaquine for chloroquine-resistant vivax malaria.

Monitoring & Follow-up

 Blood smear should be repeated daily (twice daily in severe infection). Within 48-72 hr after
start of treatment, patients usually become afebrile and improve clinically except in
complicated cases.
 All patients should be investigated with repeated blood film of malarial parasite one month
upon recovery of malarial infection, to ensure no recrudescence.
Prevention
 Avoid mosquito bites:
 Wearing long sleeves, trousers.
 Insecticide Treated Bed nets
 Repellent creams or sprays.

2. Leishmaniasis
 Leishmaniasis is a parasitic disease caused by the protozoa belonging to the genus,
Leishmania
 Human leishmaniasis is not a disease, but a group of diseases.
 While several ways to classify leishmaniasis (eg, by geography or taxonomy) are available,
clinically, it can present itself in various ways, and is more easily classified as cutaneous,
mucocutaneous, and visceral leishmaniasis
Classification
Eukaryota (organisms with nucleated cells),
 Kingdom Protista,
 Phylum Protozoa,
 Class Flagellates,
 Genus Leishmania

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 Species, Reservoirs, and Clinical Diseases

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  During blood meal, infected sandflies inject the infective stage, the so-called promastigote
parasite, into the human host.
 Injected promastigotes are first phagocytized by macrophages and transform into so-called
amastigote parasites.
 These multiply in the infected cells and also affect different tissues, depending on the
Leishmania species, which causes the corresponding clinical manifestation of the disease.
 When sandflies take blood meals from an infected host, they take up parasitized
macrophages.
 In the vector fly's midgut, these parasites differentiate into the so-called promastigote form,
which multiplies and finally migrates to the fly's proboscis.
Clinical forms: cutaneous, mucocutaneous, visceral

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 Visceral Leishmaniasis
(Kala-azar)
Etiology
The L. donovani species complex includes several species:
 L. infantum and
 L. chagasi
Epidemiology
 The species of visceral leishmaniasis are endemic in areas of India, China, Central and South
America, East and West Africa, and the countries surrounding the Mediterranean.
 In India, no extrahuman reservoirs are known, but in other regions, infection may involve
several mammalian species, including dogs, foxes, and wild rodents.
 Sandflies of the genus Phlebotomus are the insect vectors that spread L. donovani.
Pathogenesis
 The flagellated promastigotes of L. donovani are introduced by an insect bite.
 After entering macrophages of the reticuloendothelial system, these forms change into
amastigotes, which multiply in phagocytic cells.
 Released amastigotes disseminate hematogenously and invade reticuloendothelial cells in the
spleen, liver, lymph nodes, bone marrow, and skin.
Incubation and Clinical Symptoms
Incubation period is 6-8 months.
Symptoms:
 weakness, dizziness, weight loss, diarrhea, and constipation.
 Fever, may spike twice daily;
 chills and sweating.
 hepatosplenomegaly
 anemia and leukopenia.
 bleeding from the gingivae, nose, or GI tract,
 ecchymoses and petechiae on the skin.
Cutaneous and Mucocutaneous Leishmaniasis
Etiology and Epidemiology
Old World cutaneous leishmaniasis is caused by three species of Leishmania that belong to the L.
tropica complex:
 L. tropica is present in the Middle East and the Mediterranean littoral;
 L. major is found in the Middle East, Arabia, India, and sub-Saharan Africa;
 L. aethiopica is found principally in Ethiopia and Kenya.
 Phlebotomus sandflies are the principal vectors.
 Infections that are caused by Leishmania can be acquired by travelers, as well as by military
and other personnel residing in endemic areas.

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  Military personnel in the Middle East have acquired cutaneous leishmaniasis with L. major
and viscerotropic infections with L. tropica.
 New World cutaneous leishmaniasis arises from infection with parasites belonging to the L.
mexicana group or the L. braziliensis (Viannia subgenus) group.
 The patterns of illness vary with the nature of the infecting leishmanial organisms, which are
found in different regions of North, Central, and South America.
 Infections with strains of L. viannia, which are endemic in various areas of South America,
cause cutaneous leishmaniasis and, in a small percentage of those infected, result in the later
development of mucocutaneous leishmaniasis. Such mucocutaneous disease (espundia)
involves the nasal or oropharyngeal mucosa, or both, and may prove fatal.
 All of these New World leishmanial parasites are transmitted principally by sandfly vectors,
although direct human contact may also bring about infection.
 Various mammals are naturally infected reservoirs of the organisms.
Pathogenesis
 Both Old World and New World forms of leishmaniasis are initiated when the bite of an
infected sandfly injects promastigotes into the human host.
 The organisms enter tissue macrophages and capillary endothelial cells, become amastigotes,
and multiply.
 A granulomatous inflammatory response develops at the bite site.
 With local ischemia, the lesion ulcerates; a bacterial infection of the necrotic area may extend
the ulceration.
Incubation and Clinical Symptoms
Incubation period is from 2-8 months to 1,5 years and more.
In Old World symptoms of cutaneous leishmaniasis:
 a papule (at the inoculation site).
 papule ulcerates and a shallow circular lesion appears that is several centimeters in diameter
and has a raised margin.
 lymphadenopathy.
 Healing of the lesions is slow, sometimes requiring more than a year.
Clinical Symptoms of New World leishmaniasis
Incubation period is 2-3 weeks to 1-3 months.
L. mexicana
 single lesion or a few lesions on exposed surfaces of the body such as the face and ear, which
heals spontaneously over 6 months.
 extensive destruction of the pinna.
L. viannia
 lesions on the skin or mucous membranes.
 progressive ulcerations of lymphatic nodes and mucous membranes.
 the infection metastasizes to the nasal or oral mucosa.
 Metastatic lesions can erode the nasal septum or the hard palate or soft palate.

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  Some patients die of malnutrition or bacterial infection.
Immunity
 In visceral leishmaniasis (Kala-Azar) cellular immunity is responsible for resolving mild
disease. High levels of antibodies are found.
 In cutaneous and mucocutaneous leishmaniasis host defense relies on cell-mediated
immunity; antibody titers are low. The response ranges from a local granuloma with few
parasites to a histiocytoma with many parasites.
Laboratory Diagnostics of visceral leishmaniasis
 Demonstration of the organism in host tissues cultured on a Novy-MacNeal-Nicolle (NNN)
or other medium or detection of Leishman-Donovan bodies (amastigotes) in stained tissue
samples.
 PCR can be performed using genus- or species-specific oligonucleotides.
 Established by examining bone marrow aspirates.
 Splenic aspirates have the highest yields but may be risky.
 Liver biopsy or aspiration of enlarged lymph nodes can also provide diagnostic material.
Laboratory Diagnostics of cutaneous and mucocutaneous leishmaniasis
 Demonstrating amastigotes on stained smears of a biopsy or of scrapings from the border of
an ulcer.
 Culturing amastigotes on NNN medium inoculated with lesion material.
 PCR targeting parasite kinetoplast DNA has allowed detection of organisms that might be
missed on histologic section or culturing.
 Except in diffuse cutaneous leishmaniasis, the leishmanin skin test is usually positive
Treatment
 There are two common therapies containing antimony, meglumine antimoniate (Glucantim®)
and sodium stibogluconate (Pentostam®). Unfortunately, in many parts of the world, the
parasite has become resistant to antimony and for visceral or mucocutaneous leishmaniasis,
amphotericin is now the treatment of choice.
 Miltefosine (Impavido®), is a new drug for visceral, mucocutaneous and cutaneous
leishmaniasis.
 Drug-resistant leishmaniasis may respond to immunotherapy (inoculation with parasite
antigens plus an adjuvant) which aims to stimulate the body's own immune system to kill the
parasite.
Prevention
 Preventing sandfly bites is the most immediate form of protection. Insect repellent,
appropriate clothing, screening of windows, and fine mesh netting around the bed (in
endemic areas) will reduce exposure.
 Public health measures to reduce the sandfly population and animal reservoirs are important.
There are no preventive vaccines or drugs for leishmaniasis.

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 3. Amoebiasis
 Amoebiasis is a parasitic protozoan disease that affects the gut mucosa and liver, resulting in
dysentery, colitis and liver abscess.
 The causative agent, Entamoeba histolytica, is a potent pathogen that is spread via ingestion
of contaminated food and water. Globally, amoebiasis is highly prevalent, and is the second
leading cause of death to parasitic disease.
Causative Organism
 The causative organism is parasitic protozoan, called Entamoeba histolytica.
 What was once thought to be a single entity, is now recognised as two morphologically
identical but genetically distinct forms; E. histolytica (pathogen) and E. dispar (commensal).
 This has affected our understanding of amoeba distribution. Many suspected cases of E.
histolytica carrier, may simply have been E. dispar colonisation
 The WHO recommends that E. histolytica colonisation should be treated, however, treatment
is unnecessary for E. dispar colonisation
Life cycle and Transmission – 1
Entammoeba histolytica has a biphasic life cycle, existing in two forms; as an infectious cyst and an
amoeboid trophozoite

Mouth - Cyst ingested

Excyst to trophozoite
Passed in stool

Amoebic disease

Cyst Trophozoite

Invades gut mucosa – cyst formation

Life cycle and Transmission – 2
 Cysts (10-15μm) are ingested via contaminated food or water. A refractile wall containing
chitin, allows the cyst to survive stomach acid.
 In the terminal ileum or colon, the parasite excysts and begins the trophozoite stage.
 Trophozoites (10-50μm) are highly motile and pleomorphic. They are unable to survive
outside the human gut.
 Energy is derived from the ingestion of bacteria and food particles. No mitochondria are
present in trophozoites. Respiration enzymes are prokaryotic in origin and are anaerobic,
converting:
o glucose + pyruvate ethanol

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  Trophozoites reproduce by binary fission and encyst in the colonic wall. Cysts are passed in
the stool where they become infectious.
 The signal for encystation is thought to be via epithelial galactose/N-acetylgalactosamine
specific lectin (gal-lectin) binding protein.
Pathogenesis 1
Amoebic trophozoites invade the colon causing colitis. They may also invade the portal circulation
and travel to the liver, causing liver abscess.
Gastrointestinal Pathology
 The spectrum of colitis in amoebiasis ranges from mucosal thickening, to multiple cyst
formation, to diffuse Inflammation / oedema, to necrosis and perforation of colonic wall.
 Binding of E. histolytica to epithelial cells via gal-lectin. This molecule shows homologous to
human CD59, conferring resistance to complement. A change in the epithelial permeability is
induced, probably via the inter-cellular tight junctions.
 Cell lysis and apoptosis of mucosa are thought to be mediated by amoeba pores, peptides
capable of forming pores in lipid bi-layers.
 Trophozoites invade through to the submucosa causing flask shaped cysts.
 Cysteine proteases released by trophozoites digest extracellular matrix in liver and colon, and
induce interleukin-1 mediated inflammation. Proteases also cleave IgA and IgG antibodies.
 Neutrophils and macrophages are drawn to invasion sites. E. histolytica can lyse neutrophils
leading to further tissue damage, and contributing towards the induction of diarrhoea.
 Inflammation is a significant cause of tissue damage; however, innate immunity may be the
main combatant against the disease.
Pathogenesis 2
Hepatic Pathology
 Trophozoites invading the colonic mucosa may enter the hepatic circulation and reach the
liver
 Well circumscribed abscesses are formed in the liver containing liquefied cells surrounded by
inflammatory cells and trophozoites
 Adjacent parenchyma is usually unaffected
Epidemiology
 Amoebiasis is found primarily in developing tropical and subtropical countries where
sanitation is poor, leading to a direct link between faeces and ingestion. Occasionally cases
are reported in non-endemic areas e.g. UK and USA. Usually due to travel and immigration
from endemic areas.
 There are an estimated 40,000-100,000 deaths due to amoebiasis worldwide each year.
Box-1. Amoebiasis rates/figures in endemic regions
 Egypt: accounts for 38% of patients presenting with acute diarrhoea in outpatient clinic.
 Mexico:1.3 million cases reported in 1996.
 Hue, Vietnam: 1500 of a 1million population over 5 years

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 Susceptibility
 Generally considered to affect children and adults, of both sexes equally. However, some data
and anecdotal evidence suggests a male predominance.
 Amoebic liver abscesses are most common in males, 18-55.
 Susceptibility to liver abscess conferred by HLA-DR3 and complotype SC01 in the Mexican
populations
 Other risk factors include oral and anal sex, and contact with contaminated enema apparatus.
Diagnosis
 Clinical history is important. In low resource settings this may be the means of diagnosis. A
good travel history is important as disease may develop years after a visit to an endemic area.
 Demonstration of E. histolytica in stool by microscopy (old), or ELISA assay for antigen
detection. Trophozoites only survive for short periods of time, therefore, fresh stool samples
should be used
 Colonoscopy to confirm colitis and tissue biopsy for amoeba
 Liver abscess; space occupying lesion on CT with positive amoebic serology
Treatment and management
 Amoebiasis, in particular with liver involvement, can be fatal if not treated. Chemotherapy
can effectively cure ameobiasis.
 Nitroimidazole (e.g.metronidazole) is used to treat the invasive pathogens – 800mg t.d.s for
10 days.
 This is followed by a luminal agent (e.g.diloxanide furoate) to eliminate colonisation –
500mg t.d.s for 10 days. This is also suitable for asymptomatic individuals.
 Complicated liver abscesses should be drained surgically.
Prevention
 Boiling water for at least ten minutes kills amoebic cysts effectively. Chlorine and iodine
tablets are not thought to be 100% effective.

Microbiome and gut health

 The microbiome refers to the diverse community of microorganisms, including bacteria,
viruses, fungi, and other microbes, that inhabit a particular environment.
 The human microbiome is the collection of trillions of microbes living in and on the human
body.
 The gut microbiome specifically refers to the microorganisms residing in the gastrointestinal
tract, particularly the colon.
 Gut health is closely tied to the balance and diversity of the gut microbiome.
 The gut microbiome plays a crucial role in various physiological functions, including
digestion, nutrient absorption, and the development and function of the immune system.

What is the gut microbiome?

 A biome is a distinct ecosystem characterized by its environment and its inhabitants.
 Our gut — inside our intestines — is in fact a miniature biome, populated by trillions of
microscopic organisms. These microorganisms include over a thousand species of bacteria, as
well as viruses, fungi and parasites.
 Our gut microbiome is unique to us. Infants inherit their first gut microbes during vaginal
delivery or breastfeeding.

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  Later, our diet and other environmental exposures introduce new microbes to our biome.
Some of these exposures can also harm and diminish our gut microbiota

Gut Microbiota Predominance.

Why is the gut microbiome important?

 Most of the microorganisms in our guts have a symbiotic relationship with us, their hosts.
That means we both benefit from the relationship. We provide them with food and shelter,
and they provide important services for our bodies. These helpful microbes also help to
keep potentially harmful ones in check.
 We can think of our gut microbiome as a diverse native garden that we rely on for nutritious
foods and medicines. When our garden is healthy and thriving, we thrive, too. But if the soil
is depleted or polluted, or if pests or weeds are overrunning the helpful plants, it can upset
our whole ecosystem

Function
What does our gut microbiome do?
Our gut microbiome interacts with many of our body systems and assists with many body functions.
It plays such an active role in our body that some healthcare providers have described it as being
almost like an organ itself.
1) Digestive system: Bacteria in our gut help break down certain complex carbohydrates and
dietary fibers that we can’t break down on our own. They produce short-chain fatty acids —
an important nutrient — as byproducts. They also provide the enzymes necessary to
synthesize certain vitamins, including B1, B9, B12 and K.
2) Immune system:
 Beneficial microbes in our gut help to train your immune system to tell them apart from the
unhelpful, pathogenic types.

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  Our gut is our largest immune system organ, containing up to 80% of our body’s immune
cells.
 These cells help to clear out the many pathogens that pass through it every day.
 Some of the chronic bacterial infections that can affect our GI tract, including C.
difficile and H. pylori, are directly related to having a diminished gut microbiome.
3) Nervous system: Gut microbes can affect our nervous system through the gut-brain axis —
the network of nerves, neurons and neurotransmitters that runs through our GI tract. Certain
bacteria actually produce or stimulate the production of neurotransmitters (like serotonin).
4) Endocrine system: Gut microbes and their products also interact with endocrine cells in our
gut lining. These cells (enteroendocrine cells) make our gut the largest endocrine
system organ in our body. They secrete hormones that regulate aspects of our metabolism,
including blood sugar, hunger and satiety and send chemical signals to our brain.

Anatomy
Where is our gut microbiome?
 Our “gut” roughly refers to our gastrointestinal (GI) tract. Most people use it to mean our
intestines. We have some gut microbiota in our stomach and small intestine, but most of them
are in our large intestine (colon). They float around inside or attach to the mucous lining on
the inner walls (mucosa).
 The types of gut bacteria that live in our colon are different from the types that live
elsewhere. They’re mostly anaerobic bacteria that require a low-oxygen environment to
survive. The higher oxygen, faster movement and strong digestive juices in our upper GI tract
prevent them from colonizing there.

Conditions and Disorders

What is dysbiosis?
 Healthcare providers use the term “dysbiosis” to refer to an unbalanced or unhealthy gut
microbiome.
 Dysbiosis means:
 A loss or deficit of beneficial bacteria.
 Overgrowth of potentially pathogenic (bad) bacteria.
 Loss of overall bacterial diversity.
 Dysbiosis may start with one of these three factors, but the others tend to soon follow. A loss
of beneficial bacteria leaves our gut vulnerable to more disease-causing or invasive types.
These types can overrun the other microorganisms living there, diminishing the overall
diversity in our microbiome.
What environmental factors affect our gut microbiome?
Just like a garden, our gut microbiome is affected by the nutrients and pollutants, pests and weeds it’s
exposed to. The diversity of plants and their different seasons or life cycles also affect it. In our gut,
this means our diet, chemical exposures, disease-causing organisms and bowel movement regularity.
What are common signs or symptoms of a problem with my gut microbiome?
Typical symptoms of gut dysbiosis include:
 Gas and gas pain.
 Bloated stomach.
 Poor digestion.

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  Lower abdominal pain.
 Diarrhea.
 Constipation.

Factors known to impact the Gut Microbiome

Can I take a test to check the health of my gut microbiome?

 Many commercial labs offer gut microbiome testing kits to consumers. We can send a poop
sample to a lab, and they’ll send us back a report telling us a little bit about the composition
of our gut microbiome. Clinical healthcare providers generally don’t use or recommend these
tests, though.
 The reason is that we still don’t know enough about the different types of gut microbiota or
how they affect our health to make a report like this useful. There’s a lot of exciting research
in progress, but it has some ways to go before a gut microbiome test can give you practical,
personalized healthcare advice.

How do healthcare providers test for gut dysbiosis?

Healthcare providers don’t check for dysbiosis, per se, but they can check for specific conditions,
like infections and bacterial overgrowth. They may use blood tests, stool tests or breath tests. A
breath test can measure different gases in our breath that are the byproducts of certain bacteria in our
gut.

How do healthcare providers treat gut microbiome conditions?

1) Elimination diet. An elimination diet is a short-term diet designed to isolate the foods
causing our gastrointestinal symptoms. These are often foods that our gut microbes like to
eat. When too many microbes are eating too many of these foods, they produce too many
byproducts, causing intestinal gas, diarrhea and other symptoms. Starving them is one way to
reduce them.
2) Antibiotics. If we have an infection or overgrowth of a certain gut bacteria, the standard
treatment is a course of antibiotics. When that’s done, a healthy gut microbiome can recover.
But some people’s guts will need a little help recovering. Healthcare providers might suggest
following with supplements like prebiotics and probiotics to help restore our microbiome.

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 3) Fecal transplant. One treatment for restoring a severely diminished gut microbiome is fecal
transplantation, which means transferring a sampling of gut microbiota from a healthy gut to
a diseased one. So far, it’s only been approved to treat recurrent C. diff infections that are
resistant to antibiotics. But researchers are looking into it as a treatment for other conditions.

What can I do to take care of my gut microbiome?

A healthy diet and lifestyle encourage a healthy gut microbiome. For example:
1) Improve your gut health naturally with a diverse and plant-rich diet. Aim for a variety of
whole foods like whole grains, vegetables and fruits. These offer plenty of dietary fiber for
your gut microbes as well as micronutrients for you. These foods also reduce inflammation in
your gut, which affects the environment inside. Processed and convenience foods do the
opposite.
2) Try probiotics and prebiotics. You can get probiotics and prebiotics in supplement form, or
from foods. Probiotics are helpful microbes that you can ingest, through supplements or
fermented foods, that’ll take up residence in your colon. Your healthcare provider can help
you pick the best probiotic for you. Prebiotics are the dietary fibers that feed your helpful gut
bacteria.
3) Use antibiotics with care. There are times when you need to take antibiotics, but other times
when you really don’t. Overuse of antibiotics in the general population leads to antibiotic
resistance. In the individual, it can kill your good bacteria along with the bad. Sometimes this
disrupts the balance in your gut microbiome, leading the wrong kind to come back stronger.
4) Maintaining a healthy gut microbiome involves factors such as a balanced diet rich in fiber,
prebiotics, and probiotics, as well as avoiding unnecessary antibiotic use and managing
stress.
5) Research in the field of the microbiome is ongoing, and scientists continue to uncover the
intricate connections between the gut microbiome and overall health.

A Healthy, Whole Foods Diet Is Key to A Healthy Gut.

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