Viruses Bacteria Fungi Parasites

1.Acellular Prokaryotes Eukaryotes Eukaryotes

2.No nucleus Nucleiod region Nucleus with Nucleus with
but nuclear nuclear membrane nuclear membrane
membrane absent
3.Can be DNA & DNA & RNA DNA & RNA DNA & RNA
RNA
4.Replicates only in
host cell
6.No Ribosomes 70s Ribosomes 80 ribosomes 80 ribosomes
(50s+30s) (60s+40s)
7.Few viruses are Cell membrane Cell membrane Cell membrane
enveloped does not have contains have cholesterol
sterols. ergosterol

8.Do not have cell Bacteria cell wall is Cell wall made up No cell wall in
wall made of of chitin parasites & human
peptidoglan cells

Viruses exists in 2 forms

Virions - have naked nuclear material without protein coat.

Prions - only protein without nucleic acid.

Carrier: person having a pathogen without presence of disease.

Bacteremia: presence of bacteria in blood without clinical signs & symptoms.

Septicemia: bacteria in blood with clinical signs & symptoms.

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Normal flora in body

 On Skin - Staph epidermidis

 In Nose – Staph Aureus
 Oropharynx -Strep Viridens like strep mutans
 In Stomach – No bacteria
 In Blood – No bacteria
 Colon – In babies - Bifido bacterium
o In adult - Bacteroids, Ecoli
 Vagina: Lacto bacillus

Major pathogenic mechanisms of bacteria:

 Adherence to cell surface

o Pili /Fimbriae are seen in most Gram –ve
o Techoic acid is seen in most Gram +ve bacteria
 Strep Pneumonia, Neisseria, and H.Influenza produce IgA proteases
 Biofilm produced by Strep mutans, Staph epidermidis

Anti-phagocytic Nature of bacteria:

 Capsule / Slime layer inhibits phagocytic uptake

 Strep pyogens has M-proteins that act as anti phagocyte component
 Pili of Neisseria gonorrhea inhibits phagocytosis
 Protein A of Staph Aureus inhibits phagocytosis by binding to FC fragment
of Ig prevents phagocytosis.
 Intracellular bacteria like Mycobacterium Tuberculosis inhibit phagosome &
lysosome fusion.
 Listeria escapes from phagosome before phagosome & lysosome fusion.

Capsulated Organisms:

Strep pneumonia
Klebsiella pneumonia
Haemophilus influenza

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 Pseudomonas aeroginosa
Pasturella
Neisseria meningitides
Cryptococcus neoformans
Bordetella pertussis
 Most capsules are made of polysaccharides.
 Capsule of Bacillus anthracis is made up of d-glutamate.

Toxins:
Exotoxin Endotoxin
1.Exotoxin are protein toxin Lipopolysaccharides (LPS)
2. Secreted by gram –ve & +ve Secreted by gram –ve bacteria only
[Gram +ve bacteria- Listeria]
3. Secreted outside cell wall 3. Endotoxin are structural components
of outermember of cell wall, released
only when cell is dead or during lysis.
[Neisseria Meningitidis overproduces
endotoxin and can secrete it]
4. Heat labile 4. Heat stable
5. Immunogenic 5. Not Immunogenic
6. Toxic component are 6. Active component is lipid A
A- active component
B- Component helps to bind to
receptors

Mechanism of Action of Toxins:

Protein synthesis inhibitors
 Diptheria Toxin has ADP ribosyl transferase activity and inactivates
elongation factor ii Major targets heart, nerves, epithelium
 Pseudomonas Aeroginosa also acts by ADP ribosyl transferase activity and
inhibits EF ii
o Primary target is Liver.

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  Shiga toxin produced by shigella dysentery interferes with 60s ribosomal
subunit and inhibits protein synthesis.
 EHEC [Entero haemorrhagic E.coli] produce verotoxin called as “ shiga like
toxin” & interferes with 60s ribosome.
Neurotoxins
 Clostridium botulinum produces Botulinum toxin that inhibit release of Ach.
 Clostridium tetani produce tetanus toxin that block or inhibit the release of
inhibitory neurotransmitters.
C-AMP inducers
 C - vibrio cholera produces cholera toxin, acts by stimulating Gs, increases
activity of adenylate cyclase that stimulate cyclic AMP
 A - Bacillus Anthracis produces anthrax toxic that makes adenylate cyclase
& increases C-AMP causes Edema
 M – ETEC [Entero Toxic E.coli] causes traveller’s diarrhoea, its heat labile
toxin stimulate Gs, increases activity of adenylate cyclase that stimulate
cyclic AMP
 P- Pertussis toxin acts by inhibiting Gi prtn & C-AMP
Cyto toxins
 Clostridium Perfringens produces (alpha) toxins, which has lecithinase
activity that causes myonecrosis.
 Staph Aureus produces (alpha) toxins, which damages the cells
Super antigens
 Toxic shock syndrome toxin of Staph Aureus (TSST1)
 Erythrogenic toxin Strep pyogenes
 They act as superantigens producing prolonged stimulation of T cells &
decrease endotoxin clearance by the liver & cause profound endotoxin
shock so also called as Endotoxin enhancers.
Gram Staining
1.Crystal violet is reagent used that stains gram+ve and gram –ve into purple or
blue colour.

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2.Grams iodine acts as a fixative giving purple or blue colour to both gram +ve and
gram –ve.
3. De-colourising agent used is alcohol or acetone.
Gram +ve remains same, gram –ve becomes colourless.
4. Countor stain used is safranin.
Gram +ve remain same purple or blue colour but gram –ve becomes or turns
red/pink colour.

Acid fast staining

1.Regent used is carbol fuchsin
2. Heat as a fixative
3.Decolourising agent used is acid alcohol.
4. Counter stain used is methylene blue.
Acid fast stains red or pink
Non-acid fast stains blue or purple.
At the end of gram staining gram +ve is purple or blue, gram –ve is red or pink.
At the end of acid fast staining acid fast pink, non-acid fast blue.
Acid-fast bacilli:
1. Mycobacterium tuberculosis
2. Mycobacterium leprae
3. Legionella
4. Oocyst of cryptosporidium
5. Oocyst of isospora
Nocardia is partially acid fast.
Organism not staining with gram stain:
1. Treponema pallidum
2. Rickettsia
3. Chlamydia
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4. Mycobacterium
5. Mycoplasma

Special Stains:
1. Giemsa stain for Chlamydia, Plasmodium, Borellia
2. Zeihl neelsen staining for Mycobacteria tuberculosis
3. India ink staining for Cryptococcus neoformans.
4. Silver staining used for Legionella, Pneumocystis jerovosi

Gram +ve Gram –ve

Cocci Cocci

 Staphylococcus Neisseria meningitidis/gonorrhoea

 Streptococcus Moraxella

Gram +ve Bacilli Gram -ve Bacilli

 Actinomyces E.coil
 Bacillus Shigella
 Corynebacterium Haemophilus
 Clostridium Salmonella
 Listeria Chlamydia
 Mycobacterium Klebsiella
 Nocardia Spirochetes
Rickettsia

Bacterial growth curve:

Log phase: there is high metabolic activity without cell division

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No of cells before log phase = no of cells after end of log phase
Log phase/Exponential phase: rapid cell growth & rapid cell division.
Stationary phase: No of new cells= no of dying cells
Nutrients start getting used up & spore formation begins in stationary phase.
Death phase: its due to depletion of nutrients & build up of waste products.

Organisms Culture medium

Haemophilus influenza Chocolate agar with factor V (NAD)

factor X (Haematin)
Neisseria Gonorrhoea Thayermartin medium or VPN medium
Nesseria from sterile site Chocolate agar
Corynebacterium diptheria Tellurite agar & loffler’s serum
Mycoplasma pneumonia Eatons agar (requires cholestrol)
Legionella Charcoal yeast extract & cystein
Fungus Sabouroud’s dextrose agar with 10%
KOH
Enteric bacteria Eosin methyleve blue and mac conkeys
agar
Enteric pathogens Xylose lysine deoxychocolate agar
Vibrio cholera TCBS
Mycobacterium tuberculosis Lowenstein Jenson medium, Bactec
medium.

Clostridium Robertson’s cooked meat broth

 Mac-conkeys differentiates lactose fermenters from lactose non-

fermenters
Lactose fermenters converts mac-conkeys agar into pink.
Lactose non-fermenters converts mac-conkeys agar colourless.
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 Cholesterol used in the culture of Mycoplasma.
Cystein is used in culture of Legionella, Brucella, Pasturella, Francisella
Protoporphyrin is used in culture of Haemophillus

Obligate aerobes:
 Bacillus Anthracis
 Mycobacterium Tuberculosis
 Pseudomonas Aeroginosa
Obligate anaerobes:
 Actinomyces
 Bacteroides
 Clostridium
Obligate Intracellular bacteria:
Rickettsia, Chlamydia
Micro Aerophilic Bacteria:
 Helicobacter Pylori
 Campylobacter jejuni
Requires low O2 tension
Quellung Reaction:
Swelling up of capsule when specific anti serum is added, seen with all capsulated
bacteria.
Urease +ve bacteria:
 Proteus
 Ureoplasma
 Klebsiella
 H.pylori

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  Cryptococus neoformans
 Nocardia
Spore forming bacteria:
 Bacillus Anthracis
 Clostridium
 Coxiella burnetii
Pigment Producing Bacteria:

1. Staph Aureus produces golden yellowish pigment.

2. Pseudomouas Aerugiuosa produces pyocyanin & fluorescin.
3. Serratia prod red pigment.
4. Actinomyces Israeli produces yellow sulphur granules.
Types of Molility:
 Tumbling motility: Listeria [culture medium]
 Actinogenic motility: Listeria in the cells
 Swaming motility: Proteus
 Dartiling motility: Vibrio cholera, Campylobacter jejuni
 Shooting star motility: Vibrio cholera
 Cork- screw motility: Treponema pallidum
 Falling leaf motility: Giardia
Catalase +ve organisms:
Produces infection in patients with chronic granulomatous disease (CGD)
 Staph Aureus
 Pseudomonas aeroginosa
 Aspergillus
 Candida
 E.coli
Phage coded toxins:
 ShigA like toxin
 Botulinum
 Cholera

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  Diphtheria
 Erythrogenic toxin of Strep Pyogenes

Bacteriology
Gram +ve cocci.
Catalase (+) Catalase (–)

Steaphylococus Streptococcus

Coagulase (+) Coagulase (-)

Staph Aureus Novobiocin test

Novobiocin Novobiocin

Sensitive Resistance

Staph Epidermidis Staph Saprophyticus

Staphylococcus Aureus:
 Catalase (+), coagulase (+)
 It ferments mannitol, produces Beta-hemolysis.
 It produced yellow color colonies in blood agar.
 Its normal flora in the nasal mucosa.
 M/C route of infection is case or carrier.
 M/C route of infection is skin.
 It is the M/C cause of acute endocarditis
 It is the M/C cause of acute osteomyelitis
 It is the M/C cause of Nosocomial pneumonia
 It is the M/C cause of Surgical wound infection
 It is the M/C cause of Paronychia
 It is the M/C cause of Spiral epidural abscess

It also causes Botryomycosis and Mastitis.

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Transmission of Staph Aureus:

1. By hands 2. Sneezing 3. Surgical wounds 4. Canned foods

Virulence:

Protein A of Staph Aureus binds to Fc component of IgG and inhibits phagocytosis.

Extracellular enzymes:

1. Coagulase converts to fibrinogen to fibrin

2. Hyaluronidase
3. Heat stable Nuclease or DNAase

Toxins:

1. Cytotoxins: S.Aureus produces alpha Toxins which damages cells

2. Exterotoxin: Produced by them are heat stable and fast acting. Causes
Gastroenteritis within 2-5 hrs after consuming salted canned foods and
custards.
3. Toxic shock syndrome toxin (TSST1)
1. Super antigen
2. Common in female using tampons presents with
 Hypotension
 Fever
 Erythematous rash
 Multi organ failure
 TSST1 enchances the endotoxin shock by decreasing the clearance of
lipopolysacchasides.

4.Exfoliative toxin: responsible for staphylococcal-scalded skin Syndrome [SSSS]

Neonates: Ritter’s Disease

Elders: Toxic Epidermal necrosis [TEN]
Milder forms: Pemphigus neonatorum
Bullous impetigo

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Botryomycosis is a skin infection of staph aurcus:

Rx of Staph Aureus:

 Methicillin
 Naphicillin
 Oxacillin

Methicillin resistance Staph Aureus [MRSA]

 Vancomycin
 Teicoplanin

Vancomycin Resistance Staph Aureus [VRSA]

 Linezolid
 Quinpristine
 Dalphopristine

Staph Aureus diseases:

 Skin: Surgical wound infection, Spiral epidural abscess, Paronychia, Bullous

impetigo, Botryomycosis, Folliculitis, Furuncle, Cellulitis, Hordeolum.
 Musculoskeletal: Osteomyelitis
 Respiratory: Nosocominal Pneumonia
 CNS: Meningitis
 Endovascular: Endorcarditis [Acute]

Staphylococcus Epidermidis:
 Normal Flora: skin
 Coagulase –ve, Novobiocin Sensitive.
 It has predilection on growth and implanted foreign bodies like skin grafts,
cathelers, and prosthetic valves.

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  It produces a biofilm and is M/C pathogen producing endocarditis,
complicating patients of i.v catheters and exogenous implants.
 It produces stitch abcess

Staphylococcus Saprophyticus:

 It novobiocin resistance, Coagulase –ve

 It produces honeymoon cystitis [infection of urinary blader] in sexually
active young women

Streptococcus [catalase –Ve] on blood agar:

Alpha α -hemolysis [partial] (green color due to biliverdin):

Optochin sensitive Optochin resistant

Strep Pneumonia/pneumococcus Strep viridans

Beta β -hemolysis (complete):

Bacitracin sensitive Bacitracin resistant

Strep pyogenes (Group A Streptococcus) Strep Agalactiae

(group B Step)

Gamma γ-hemolysis (no hemolysis):

6.5% Nacl sensitive 6.5% Nacl resistant

Strep bovis Enterococcus

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Streptococcus Pneumoniae/Pneumococcus:
 Diplococci [they occur in pairs] lancet shaped, bile soluble.
 Alpha hemolytic, Optochin sensitive.
 Transmitted by resp droplets and is responsible for community acquired
pneumonia & produces typical Pneumonia with rusty brown sputum.
 M/C cause of adult meningitis.
 M/C cause of otitis media & sinusitis in children.
 Predisposing factors asplenia [Splenectomy]
 Influenza
 Measles
 Alcoholism
 Sickle cell anemia
 COPD
 CHF
 It’s a capsulated organism, produces IgA proteases
 Quellung’s reaction +ve
 Produces lobar Pneumonia with productive cough.

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  M/C complication of pneumococcal pneumonia is Empyema.
Rx: Macrolides for bacteria pneumonia
Ceftriaxone for adult meningitis
Amoxicillin in adults – otitis media, sinusitis
Erythromycin in children

Prevention:

 Done by antibodies in capsule.

 Paediatric vaccine consists of seven serotypes.
 Adult pneumococcal vaccine consists of 23 serotypes and is recommended
for all adults > 65 years and high risk individuals like Asplenia, Sickle cell
anemia, DM, HIV, Chronic lung, renal, heart diseases.
 Latex agglutination particle test produces pneumococcal capsule antigen in
CSF.

Streptococcus Viridens:
 Catalase –ve, alpha hemolytic, optochin resistant, bile insoluble
Eg: Strep mutans, Strep sanguis.
 They are nomal flora of oropharynx.
 Strep mutans is responsible for dental plague, dental caries & produces
biofilm.
 Strep viridens grows on damaged heart valves & is the m/c cause of sub–
acute bacterial endocarditis after dental extraction/procedures.
 Infective endocarditis presents with malaise, weight loss, splinter h’ages,
night sweats, fever, heart murmurs, and Janeway’s lesion.

Rx: Pencillin G with aminoglycosides for endocarditis

Always give prophylactic antibiotic before dental produces for individuals with
damaged heat valves.

B-hemolytics:

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Streptococcus Pyogenes:
 Also called as group-A streptococci.
 It is Beta-hemolytic, bacitrian sensitive, PYR+ve.
 They are divided into groups based on carbohydrate antigen of cell wall
 It is divided into 20 lance field groups A-V (w/o I-J)
 Most pathogenic streptococci is group A streptococci
 Group A-strep are further divided into different types based on M-proteins
[80 griffithe types]

Pathogenesis:

 Produces hyaluronidase, which is non-immunogenic. M-protein is

antiphagocytic.
 Streptolysin O:
o Immunogenic
o Hemolysis/cytolysin
o O2 labile
o Cardiotoxic
o Poor prognostic factor
 Streptolysin S:
o Non-immunogenic
o O2 stable
o Causes hemolysis on surface only
 Streptokinase is produced that breaks down fibrin clots.
 They produce DNA are NADase
 Strep pyogenes also produces exotoxin [A-C] also called pyrogenic toxin or
erythrogenic toxin that acts as super antigen, which is responsible for
scarlet fever.
 They inhibit clearance of endotoxin by liver, thus acting as endotoxin
enchancers.

Diseases caused:

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Scarlet fever:

 It is caused by erythrogenic/pyrogenic toxin

 Type A is most common causative agent.
 M/c infection caused is sore throat.
 Streptococcal pharygitis accompanied by sandpaper rash, strawberry
tongue, circum-oral pallor.

Skin involvement in the form of:

o Impetigo
o Cellulititis
o Erysipelas
o Necrotising fasciitis

Acute Rheumatic fever:

 It develops only after throat infection by Strep pyogenes.

 ASO titres are always raised.
 Antibody produces against heart tissue.
 It is type II hypersensitivity.
 Jones criteria is used for diagnosis
 Penicillin prophylaxis is indicated.

Acute glomerulo nephritis [PSGN]:

 Occurs after streptococcal pharygitis & streptococcal skin infection.

 M/c its due M12 proteins.
 ASO titre may or may not be raised.
 Pencillin prophylaxis is not indicated.
 Immune complex deposition producing smoky cocoa coloured urine.
 Type III hypersensitivity.

Dx:

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  Throat swab culture, Pike’s medium [transport medium for strep pyogenes]
 ASO titre >200 indicate prior streptococcal infection mainly useful for
rheumatic fever.
 Aso titre may be low after skin infection.

Rx:
 Pharyngitis, Impetigo, Cellulitis - Penicillin
 Necrotising fasciitis - surgical debridement, penicillin, clindamycin
 Endocarditis - Pencillin G+ Aminoglycosides.

Clindamycin reduces toxin synthesis & is used in toxic shock syndrome & Scarlet
fever.

Streptococcus Agalactiae:
 It is group B, Beta hemolytic, Bacitracin resistant, CAMP +ve.
 Hydrolyes hippurate.
 Reservoir is vagina.
 Risk factor is preterm rupture of membranes.
 Its M/C cause of neonatal septecemia worldwide.
 Neonatal GBS infection is acquired in utero.
 Rx:
 Pencillin
 Treat the mother prophylactically intrapartum if vaginal cultures are +ve for
GBS.

γ -Hemolytic streptococci:
Group D Streptococci: 1) Enterococcus

2) Non-entercoccal Group D Streptococci

Enterococcus
 Important species are enterococcus faecalis, Enterococcus faecium.

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  Enterococcus grows in 40% bile, hydrolyzes aesculin in bile, grows in 6.5%
Nacl, PYR +ve.
 Reservoir: human intestines
 Usually survive in bowel & gall bladder.
 It causes urinary & biliary tract infection and also associated with
endocarditis.

Rx:
 Enterococci are resistance to Penicillin, so treated by Vancomycin.
 In vancomycin Resistance Linezolid is used against all entercocci.
 Quinupristin, Dalfopristin are effective against Vancomycin resistant
enterococcus faecium.
 E-Faecium all 3 drugs are used 1. Linezolid, Quinupristin, Dalfopristin
 E.Faecalis only linezolid

Mechanism of resistance:

 Vancomycin resistance is due to change of D-ala, D-ala of cell wall NAM (N-
acetyl muramic acid) with D-ala, D-lactate.

Non Enterococcal Group D Streptococcus

 Grow in bile, do not grow in 6.5% Nacl, PYR –ve
Eg: Streptococcus Bovis
 Strep Bovis associated c endocarditis after bowel surgeries/GI/GU
surgeries.

GRAM +ve Bacilli

 Most bacillus are motile except Bacillus Anthracis
 Branching bacilli are Actinomyces & Nocardia
 Spore producing bacilli are Bacillus & Clostridium
 Nocardia is partially Acid fast
 Mycobacterium is acid fast

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  Gram +ve anaerobes are Actinomyces & Clostridium.

Bacillus Anthracis:

 It’s a large gram +ve, spore forming aerobic bacillus.

 Capsule is made of polypeptide [D-glutamate].
 It’s a potential warfare agent.
 On microscopy it has Medusa head appearance on agar plates.
 On gelatin stab it produces inverted fur tree appearance.
 Bacillus Anthracis shows “ string of Pearls” appearance when grow on solid
medium which differentiates it form B cereus.
 On staining with polychrome methyline blue it produces Mac Fadyean‘s
reaction
 Toxin of Bacillus Anthracis has 3 factors:
o Edema factor that acts by cyclic-AMP
o Lethal factor causes cell death
o Protective antigen

Clinical features:

Anthrax is a zoontic disease effecting herbivores. Humans became infected, when

spores are inhaled from infected animals or with contact with infected animals.

Anthrax types:

1. Cutaneous Anthrax
2. Pulmonary Anthrax
3. Gastrointestinal Anthrax

1.Cutaneous Anthrax:

 It is also called as “ Hide porter’s disease”

 M/c type of anthrax. There is a central necrotic lesion, which is covered by
a black eschar. This lesion is called a “Malignant Pustule”
 Resolves spontaneously. Fatal septicemia occurs in 10-20% of patients

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  Patient may have painful regional lymphadenopathy.

2. Pulmonary Anthrax:

 It is also called as “ wool sorter’s disease”

 Its life threatening pneumonia with cough, fever, facial edema & cyanosis.
 There is characteristic mediastinal haemorrhagic lymphadenitis &
mediastinal widening on X-ray.
 Most of the times it’s fatal.

3. Gastointestinal Anthrax:

 It is the rare form with primary lesion in tonsils causing edema, bloody
diarrhoea, & high mortality.
Rx:
 Doc is penicillin
 In penicillin allergy, Erythromycin is used.
 Vaccine for B.Anthracis is Acellular vaccine Adsorbed [AVA]

Bacillus Cereus:
 It’s similar to bacillus anthracis, but does not show “ String of Pearls”
appearance & is motile, non-capsulated.
 Its usually food borne.
 1st type is associated with fried rice [reheat foods] in Chinese restaurants.
 2nd type is associated with improper cooked meat & vegetables.
 Food poisoning due to B.cereus is also fast onset i.e within 6-8 hrs.
2 types of toxins:
 Diarrhoeal type resemble heat labile toxin of ETEC
 Emetic type resembles heat stable toxin of Staph Aureus.

Clostridium:
 It’s a Gram +ve, anaerobic, spore forming bacill.
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  Culture medium: Robertson’s cooked meat broth
 C.perfringen’s & C.tetani are non-motile.

Clostridum tetani:
 Produces Tennis racket/drumsticks shaped terminal spores.
 Common Reservoir is mud.
 Transmission is by puncture wounds and trauma.
 They require low O2 tension, strict anaerobes.

Toxins:

2 types: Tetanolysin, Tetanospasmin

Tetanospasmin:
 It’s the toxin responsible for tetanus.
 It’s transported retrograde in the axon.
 It inhibits the release of inhibitory neurotransmitters causing muscle
spasms and rigidity.
 Tetanospasmin affects spinal cord mainly.
 Strychnine poisoning also show similar muscle spasms appearance.

Clinical features:

 Average time of onset after injury is 7 days.

 Trismus/Lock jaw.
 Risus sardonicus
 Opisthotonos
 In tetanus deep tendon reflexes are exaggerated (UMN)
 C.Tetani doesn’t invade tissues but the toxin is transported retrograde in
the axons.
 Tetanus patient are not infectious & there is no person to person
transmission

Rx:

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  By giving antitoxin i.e, Human tetanus immunoglobulin.
 Antibiotics used are Penicillin & Metronidazole
Alternative is Clindamycin.
 Spasmolytic drugs like Diazepam.
 Proper wound debridement.
 Delayed wound closure.
 Hyperbarric oxygen.
 Prevention is done by active immunization using active toxoid. It’s a
formaldehyde-inactivated toxin. Usually 2 doses of TT are given 1 month
apart.
 1st booster dose after 1 year, 2nd booster dose after 5 years.
 Passive immunization is done by given human hyper immunoglobin.
 Combined active & passive immunization with TT in one arm & Tetanus
23mmunoglobulin in other arm is usually given in patients of dirty wound,
with no history of vaccination.
 Tetanus spores are resistant to disinfectants.

Clostridium Botulinum:
 It’s an anaerobic, Gram +ve, spore forming bacilli.
 Botulinum toxin is most potent bacterial toxic known.
 Spores survive in soil.
 Transmission is food borne or traumatic.
 Botulinum toxin acts by inhibiting the release of Ach.
 Botulinum toxin is coded by a prophage [viral DNA gets incorporated into
bacterial chromosome in lysogenic cycle]
 Botulinum toxin is heat labile i.e.boiling food removes the bacteria.

Type of Botulism:

Adult food borne botulism:

 It’s due to the preformed toxin present in canned food, green beans,
and peas.

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  Symptoms usually arise 1-2 days later with weakness, blurred vision,
symmetric descending flaccid paralysis, severe constipation, nausea ,
vomiting ,diplopia,dysphagia & death is due to respiratory failure
commonly.
 Rx:
 Resp support & trivalent antitoxin.
 Prevention: Is by proper canning of foods & heating all canned foods.
 No antibiotics are required.

Wound botulism:

 It is due to traumatic implantation of spores.

 Resemble food poisoning without GI symptoms.
 Diplopia, Paralysis & respiratory weakness.
Rx:
 Wound debridement.
 Delayed closure.
 Amoxicillin
 Antitoxin & respiratory support.

Infant botulism:

 It’s the most common type.

 It’s due to ingestion of botulimum spores, usually spores seen in honey.
 The toxin is produced in the gut. There is constipation flaccid paralysis,
diplopia weak crying, and respiratory arrest.
 Toxin can be demonstrated in stool & serum.

Rx:
 Respiratory support.
 Hyperimmune serum [Botulinum immunoglobulin]
 Antibiotics generally not used
 Prevention- avoid honey in the 1st year of life

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  Botox injections [toxins] are used to treat strabismus [crossed eyes],
blepherospasms (eye twitching) and cervical dystonia/spasmodic torticollis.

Clostridum Perfringens:
 It’s a Gram +ve, spore forming, and anaerobic bacilli.
 It causes gas gangrene, myonecrosis.
 It shows stormy fernentation in milk media.
 It shows double zone of B-hemolysis.
 It produces Alpha-toxin, which has lecithinase activity, which disrupts the
membrane of RBC’s platelets, endothetial cells produces massive
hemolysis.
 It also shows Nagler’s reaction on egg yolk agar. A zone of opacity is formed
are the egg yolk agar plate with no antitoxin.
 Enterotoxin product can cause food poisoning, watery diarrhoea similar to
E.coli.

Gas Gangrene:

 Its myonecrosis due to contamination of wound with soil & feaces

especially battle field wounds.
 There is edema, gas production, and dense tissue pain.
 C. Perfringens doesn’t produce spores in artificial medium.
 Crepitus is present
 Systemic symptoms: fever, disproportionate tachycardia.
 There is rapid & high mortality due to circulatory failure

Rx:
 Surgery in main stray of treatment.
 Penicillin & Clindamycin
 Hyperbarric oxygen.

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Clostridium difficile:
 Its responsible for antibiotic associated diarrhoea also called
“pseudomembranous colitis “.
 M/c diarroheal infection acquired in hospital.
 Clindamycin, Ampicillin, Cephalosporin, Amoxicillin are associated
antibiotics
 Formation of whitish yellow plaques over colon is called as
pseudomembrane
 It can lead to toxic megacolon / sepsis
 C.difficile is normal flora is Gut, so culture is not diagnostic
 Demostration of toxin in the feaces is the gold standard
 Rx: Doc is Metronidazole alternate is Vancomycin

Corynebacterium diptheriae:
 Its gram +ve rod that produces black colored colonies or Tellurite agar &
Loeffler’s serum slope.
 It produces metachromatin granules called Volutin granules/Babes-Ernst
granules on Albert’s stain.
 Bacteria are club shaped arranged in Chinese letter pattern.
 Diptheria toxin is coded by a prophage and acts by inhibiting protein
synthesis by inhibiting EF–II

Pathogenesis:

 It spreads via respiratory droplets.

 It is not invasive it colonizes on pharynx producing a dirty
pseudomembrane that can extend onto the trachea & larynx causing
mechanical obstruction.
 Systemic effects are due to the toxin mainly damage heart, nerves &
epithelium.

Respiratory Diptheria:

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Clinical features:

 M/C type is Tonsilo pharyngeal [Faucial type]

 Fever
 Sore throat
 Weakness
 Bull neck appearance
 Asphyxia
 Myocarditis
 Cardiac dysfunction
 Recurrent laryngeal nerve palsy
 Peripheral polyneuropathies
 Dysphagia
 The 1st muscle effected is palato-pharyngeus
 Cause of death is circulatory failure.
Dx:
 It is usually clinical.
 Demonstration of org by gram staining of throat swab & culture in specific
media are useful investigations.

Cutaneous Diphtheria:

 It causes punched out ulcers in the skin & is caused by non-toxogenic

strains of C.diptheriae.
 Elek’s test: it’s done to demonstrate toxin production in vitro. Toxin
produced by toxin producing strains reacts with the anti-toxin diffusing
from the filter producing a precipitation line.
 Schick test: a test used to determine whether or not a person is susceptible
to diphtheria.

Rx:
 Penicillin G, alternative is erythromycin.

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  Prevention: by active immunization by diphtheria toxoid combined DPT is
used. Pertussis increases the potency of diphtheria toxoid.

Listeria:
 It’s a gram +ve bacillus that shows tumbling motility at 20-25o C & non
motile at 37o C [body temp] of 98o F
 It’s a facultative intracellular non spore-forming bacillus.
 Listeria monocytogenes is Beta-hemolytic. It shows tumbling motility in
Broth & Actin jet motility in the cells.
 Its characteristically shows cold growth.
 Reservoir: Unpasteurized milk products
 Stored cheese, cabbages
 GI, GU, tracts of animals.
 Transmission: food borne, also spreads vertically across placenta.
 It produces listeriolysion O or LLO that that disrupts the phagosome
membrane & allow it to escape before phagosome lysosome fusion with
actin jet motility.

Diseases caused:

Listeriosis:

 It is seen in pregnant women in 3rd trimester.

 It causes fever, myalgia, choreoamnionitis, abortions, and stillbirths.
 Healthy adults & children have mild symptoms of diarrhoea.

Neonatal listeriosis:

 It due to in-utero transfusion.

 There is profound sepsis, disseminated granulomas with central necrosis &
high mortality.
 Late onset disease can be associated with meningitis, septicemia
 Neonatal listeriosis is also called as “Granulomatosis infantisepticum”
 Listeria is the m/c cause of meningits in kidney transplant patient.

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  Listeriosis not associated with pregnant presents, as meninigitsis &
septicemia in immunocompromised patients like renal transplant patient,
chronic gluco-corticoid therapy, malignancy & AIDS.
 Prevention: Pregnant women should not eat cold stored foods.

Actinomyces:
 It’s an anaerobic, gram +ve, and filamentous branching bacilli.
 Normal flora: gingival cervices, female genital tract.
 Transmission: endogenous due to tooth pick injuries.
 M/c Actinomyces Israeli prod indurated swelling & draining sinus tract that
contains yellow sulphur granules the drains out on skin
 M/c site is lower jaw
 M/c type of actinomycosis is Cervico-facial produces “Lumpy-jaw” that
occurs due to dental trauma & poor oral hygiene.
 Pelvic actionomycosis is associated with use of IUD’s.
 In CNS, it produces solitary brain abcess.
 It also causes actinomycetoma.
 On microscopy the Gram +ve filamentous bacteria have sunray appearance.
 Culture on solid media prod colonies resembles molar tooth
Rx:
 Actinomycetoma by Streptomycin + Dapsone.
 Doc is penicillin.

Nocardia:
 Its aerobic, gram +ve, partially acid fast, branching filmentous by bacteria.
 Transmission is air borne & traumatic transplantation [mainly by inhalation]
 It usually produces pulmonary infection in immune compromised or cancer
patient.
 Norcardiosis is mostly caused by Nocardia asteroides that produces
bronchopulmonary pneumonia with cavitations causing cough, fever
dyspnoea, and cavitations in Lungs.

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  Haematogenous spread to brain produces multiple brain abscesses.

Cutaneous nocardiosis:

 It is caused by Nocardia Brasiliensis.

 It presents with draining granules & cellulitis.

Rx:
 Doc for Nocardia is Cotrimoxazole.

Actinomyces Nocardia

 Anaerobic Aerobic.
 Non-acid fast Partially acid fast
 Normal flora of Gingiva In soil dust /vegetative matter.
 Produces solitary brain abcess. Produces multiple brain abcesses
 Infection is endogenous Exogenous
 Doc penicillin Doc- cotrimoxazole

Mycobacterium tuberculosis:
 Acid fast, obligate aerobe.
 Cell wall of mycobacteria has concentration of lipid especially mycolic acid
which is responsible for its acid fastness.
 Mycobacterium is highly sensitive to disinfectants like NaOH & dessication.
 M.tuberculosis produces niacin & heat sensitive catalase.

Virulence factors:

 KAT-G gene encodes for Oxidase & Catalase

Mutations in KAT-G gene leads to resistance to Isoniazid.
 Sulfatides produced inhibits phagosome, lysosome fusion & allows
intracellular survival
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  CORD factor: main virulence factor [Trihelose Dimycolate] that causes
serpentine growth in vitro & inhibits leukocyte migration & also disrupts
mitochondrial phosphorylation.
 Tuberculin protein: Responsible for delayed hypersensitivity reaction.

Pathogenesis:

Primary pulmonary Tuberculosis:

 Localised in the sub pleural regiow, near the obique fissure in the middle
lobe and upper part of lower lobes.
 Ghon’s focus is the lesion in the lung that is due to inflammation &
consolidation.
 Ghon’s complex consists of a calcified focus of infection & an associated
lymph node.
 Depending on host immunity the primary Ghon’s complex can undergo
healing, fibrosis or calcification (Ranke’s complex) or could progress to
Secondary Tuberculosis in the form of cavitation, consolidation or miliary
T.B.
Secondary T.B or Reactivational T.B:
 Usually develops in apical & posterior segment of upper lobe due to high
oxygen concentration in these areas.

C/F:

 Productive Cough
 Hemoptysis
 Cavitations
 Pleural effusion
 Low grade fever especial during the evenings
 Weight loss
 Night sweats
 Anorexia
It can spread by hematogenous route & become miliary TB with wide
spread organ involvement.

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 Extra pulmonary Tuberculosis:
 M/c site is lymph nodes mainly in cervical & supra clavicular region k/a
Scrofula.
 Skeleton T.B m/c involves the spine called as Potts spine.
 M/c site of GI T.B is ileocecal junction.
 It can involve the pericardium producing constrictive pericarditis and also
involve meninges and Genito urinary tract.

Dx:
 TB is stained by Zeihl-Neelsen staining or by Auramine-rhodamine
fluorescent dye.
 Auramine-Rhodamine fluorescent dye is highly sensitive & rapid procedure
is used for screenings of sputum but is not specific.
 Sputum is best collected in the mornings before any meal.
 3 sputum samples are taken.
 Positive samples for auramine-rhodamine are confirmed by acid fast
staining.

Culture:

 Lowenstein Jenson medium- it is a standard solid medium used but slow

growing & -ve reports is given only after 8-12 weeks.
There is production of niacin +ve acid-fast bacilli in the LJ medium from +ve
sputum.
 Bactec- it’s a liquid medium and gives results within 2 weeks.
 Broth with palmatic acis
 PCR & ligase chain reaction are fastest.

Mantoux’s/tuberculin test:

 It is done to demonstrate hypersensitivity to tuberculin protein.

 It’s an intra dermal test using purified proteinn derivative PPD
 The test is read after 72 hrs.
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  The area of in duration is looked at and is said to be +ve if its >10mm & -ve
if <5mm
 Its considered doubtful b/w 5-10mm
 This test indicates only exposure to bacilli with or without clinical illness. Its
not a confirmatory test for active infection
 False –ve mantoux is seen in Sarcoidosis, Malnutrition, Miliary T.B, and
Immune suppression, impaired cell mediated immunity.
 False +ve mantoux is seen in infection by atypical mycobacterium infection,
BCG vaccine
 Catalase produced by mycobacterium is heat sensitive, so under standard
catalase testing [68o C] its catalase –ve
 Rx - Multiple drug treatment is given as ATT. Minimum 6 months of
treatment is required for uncomplicated patients.
 HRZE is given for 2 months followed by HR for next 4 months
 H- Isoniaxid [INH]
 R- Rifampician
 Z- Pyranxinamide
 E- Ethambutol

Streptomycin is given in relapse/failure cases or defaulters

BCG (Bacillus calmette Guerin) vaccine:

 It is live attenuated vaccine, derived from attenuated Bovine strains. Its

used to prevent disseminated disease & given by a intradermal injection.
 It’s also used to treat Bladder cancer by folle’s catheter.

Mycobacterium Leprae:
 They are acid fast bacilli, obligate intracellular rods, that grows in
macrophages in the form of cigar shaped bundles appearance called
“Globi”
 Reservior: human mucosa, skin, nerves.

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  Transmission: nasal discharge from an affected untreated patient or
close contact with infected part for long period of time is required for
infection.
 Skin to skin contact is not an important route of infection.
 Grows in cooler parts of body like ear lobes, skin, mucous membrane &
peripheral nerves.
 The disease caused by leprosy is also called as Hansen’s disease
 Morphological index is total no of live bacilli in tissues that stains
uniformly.
 Bacteriological index is total no of live & dead bacilli in tissue.
 Incubation period for leprosy is 5-7 yrs.

Leprosy is divided into 5 clinical types:

1. Tuberculoid
2. Border line tuberculoid
3. Border line
4. Border line lepromatous
5. Lepromatous
 Symptoms of leprosy are confined to skin & nerves.
 M/c nerve involved is Ulnar nerve & Posterior auricular nerve.
 Medial popliteal nerve is never involved in leprosy
 Invasion & destruction of nerve by TH, cells is pathognomic of
“tuberculoid reprosy”
 Presence of bacilli in blood & other organs is a feature of “ lepromatous
leprosy”
 Lung & CNS are not involved in leprosy.

Diagnosis:

 Punch biopsy from advancing edge of lesion or nasar scrapings shows

acid-fast bacilli

Rx:

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 Dapsone & Rifampicin

Clofazamine is added for Rx of lepromatous leprosy.

Tuberculoid Leprosy Lepromatous leprosy

Strong cell mediated immunity Weak cell mediated immunity

No of bacilli in tissue are low No of bacilli in tissue are medium

Nerve & tissue damage is due to immune sys Due to bacteria.

Few lesions present multiple lesions

Lepramine test +ve Lepramine test –ve

Skin lesion upto 3 in no, sharply defined. Nodular,multiple, poor margins.

Hypopigmented, asymmetric. Symmetric, leonine faces.

Langerhan Giant cells, macrophages, T cells Langerhan Giant cells & T cells
are more are reduced.

Granulomas are seen Granulomas are absent

Type I lepra reaction (or) reversal reaction:

 It’s a type IV hyper sensitivity reaction

 Seen in border line leprosy
 There is tissue edema, pain after starting treatment.
 Rx- Glucocorticoids + Clofazamine
 M/c nerve involument in type I real is Ulnar Nerve

Type II Lepra Reaction:

 Also called Erythema Nodosum Leprosum (ENL).

 It’s a type III hypersensitivity reaction.
 Seen in borderline lepromalous & lepromatous leprosy.
 Usually follows dapsone therapy for lepromatous leprosy patient
 Numerous painful, erythematous papules are seen.
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  M/c feature is TNF plays central role in this type II lepra reaction
 Rx- Anti-pyretics & NSAID’s in mild cases.
 Gluco corticoids are used in moderate to severe cases.
 Doc for moderate to severe in type II lepra reaction is “ Thalidomide”
o Single lesion pauci bacillary leprosy can be treated by giving ROM
therapy
 Rifampicin
 Oflaxacin
 Minocyclin

Lepramine Test:

 Its type IV hypersensitivity

 Early reaction of Fernandez is similar to tuberculin reaction & is read in 24-
48 hrs.
 Late reaction of Mitsuda is more meaningful reaction read after 4 weeks.
o Mycobacterium leprae can grow in “armadillos”.
 It can’t be grown in artificial medium, but can multiply in footpad of mice.
Bacterial generation time is 12-13 days.

Atypical Mycobacterium:
 Further divided into 4 groups, based on pigment product
 Group I photochromogen: They produce pigment only in the presence of
light.
Eg: M.kansasii causes chronic pulmonary disease in old people.
M.marinum causes warty skin lesions called swimming pool granuloma/fish
tank granulomas.
 Group II is scotochromogen: Can produce pigment even in presence or
absence of light.
Eg: M.scrofulacium causes scrofula i.e. cervical lymphadenitis is produced
 Group III/Non-photo chromogens: do not produce pigment
Eg: M.Avium complex (MAC) disseminated pulmonary disease especially
AIDS patients

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 Rx-clarithromycin for patients MAC infection
Mycobacterium intraellularae
 Group IV is rapid growers. Their colonies appear within 7 days.
Ex: - M.chelonie alos k/a title tubercle bacilli
M.fortitium also k/a frog tubercle bacilli
M.ulcerens prod buruli ulcer.

GRAM –ve Cocci:

 Neisseria meningitides.
 Neisseria gonorrhoea
 Moraxella

Neisseria:

Grow –ve diplocci that are oxidase +ve

They grow on chocolate agar

Neisseria Meningitidis Neisseria Gonorrhoea

 Lens shaped Kidney shaped

 Capsulated Non-capsulated
 Resp droplets STD
 Ferments both glucose & maltose Only glucose
 Have a vaccine YWCA No vaccine
 B-laclamase prod not seen B-laclamase production is seen

Neisseria Meningitidis:
 Gram –ve capsulated, diplococcic grows on chocolate agar with 5% CO2
 It ferments mannitol & is oxidase +ve

Virulence factors:

 Capsular polysaccharide
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  Outer membrane protein endotoxin
 Produces IgA proteases.

Its divided into 5 groups based on capsular polysaccharide into Group A, B, C, W,

Y.

 Reservoir: Human Nasopharynx

 Transmission: Respiratory droplets.
 Neisseria meningitids, M/C cause Adult Meningitis.
 It has over prod of endotoxin & it secretes endotoxin
 Complement deficiency esp in C5-C9 factors [MAC deficiencies leads to
infections with Neisseria].

Diseases Caused:

Meningitis:

 Its due to blood borne dissemination to meninges & presents with abrupt
onset of
o Fevers
o Chills
o Gen petechial rash with haemorrhagic lesion.
 Rash is m/c distinctive feature
 In fulminate cases, there is
o Rapid septic shock, DIC , Ecchymosis, Bilateral adrenal haemorrhages
(Waterhouse friedrichsen syndrome),Death

Lab diagnosis:

Done by gram staining of CSF

 PCR amplification of DNA of CSF is most sensitive method

 Latex agglutination test identifies capsuals of N.meningitidis.
 Growth med is muiler-Hinton or chocolate agar with 5% CO2.

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  Thayer Martin med is a sclective media for culture.
 Nasopharyngeal & throat specimen.

Rx: Ceftriaxone is Doc

Rifampicin is Doc for meningo-coccal prophylaxis.

Prevention: is done by YWCA vaccine. There is no vaccine against group B

Neisseria Gonorrhoea:
 Gram –ve, kidney shaped, non-capsulated, B-lactamase producing
diplococci
 Reservoir: human genital tract
 Transmission: is by sexual contact & during birth

Pathogenesis:

 Pili are important for all attachment to mucosal surface. They inhibit
phagocytic uptake & is responsible for antigenic variation.
 It also produces IgA proteases.
 Most abundant gonococcal surface protein is Sporin.

Disease Caused:

 Urethritis
 Proctitis
 Endocervicitis [female]
 Pelvic inflammatory disease
 Its m/c cause of Septic arthritis
 Its infants it causes Opthalmia neonatorum.

Dx:
 Gram staining of urethral exudates with presence of Gram –ve
diplococci in neutrophils is suggestive of Gonorrhoea.
 Selective medium is Thayer martin medium.
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  Diagnosis is common done by genetic probes in western countries.
 Gonorrhoea is B-lactamase producing, so most are penicillin Resistant.

Rx:
 Cefriaxone is Doc for Gonorrhoea
 Ciprofloxacin 500mg
 Ofloxacin 400mg
 Doxycycline (or) erythromycin

Prevention:

 No vaccine for Gonorrhoea.

 Use of condoms is best for prevention.
 Incubation period for N. Gonorhea is 7 days
 Giving erythromycin ointment in eyes after birth prevents neonatal
Opthamia neonatorum.

Moraxella:
 Gram –ve diplococci similar to Neisseria that causes otitis media, sinusitis,
Bronchopneumonia in elderly patient with COPD.
 Causes Angular conjunctivitis.

Rx: Zinc sulphate

GRAM –ve Bacilli
Pseudomonas Aeroginosa:
 Gram –ve aerobic, oxidase +ve rod shaped bacillus.
 It produces a blue green pigment called as “pyocyanine” and ‘ fluroscein’.
 It has a capsule that produce slime layer.
 It produces non-lactose fermenting colonies on Mac-conkey’s agar.
 It’s present in fresh waters, water aerosols and also in raw vegetables and
flowers.
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 It produces an endotoxin that causes septicemic shock.
 Pseudomonas exotoxin A acts by inhibiting elongation factor EF II &
inhibition of protein synthesis. The primary organ involved is liver.

Diseases Caused:

 It causes Gastroenteritis, hot tub folliculitis, and corneal ulcers in contact

lens users.
 It causes cellulitis with production of blue green pus & causes septicemia in
‘burn patients’
 It’s an important source of pneumonia & septicemias in neutropenic
patient.
 Its catalse +ve & can cause infection in chronic Granulomatous disease
(CGD).
 Skin lesion is in form of Ecthyma Gongrenosum with black necrotic area
associated with fever & shock.
 It’s also causes UTI’s in catheterised patient & is an important source of
pneumonia in patients of cystic fibrosis.

Rx- Piperacillin, carbenicillin, Ticarcillin & Aminoglycoside.

Legionella:
 Its gram –ve fastidious bacteria, cultured in charcoal agar & requires
cysteine & iron for its growth.
 It’s stained by silver.

Reservoir: water tanks, air conditioners, streams.

 Causes “pneumonia in smokers” with a high alcohol intake and in

immunosupressed patient, like kidney transplant patient.
 It’s a facultative intra cellular pathogen.
 There is no human-to-human transmission.

Mode of transmission: is an aerosol from contaminated Air conditioners.

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 Diseased Caused:

Legionaires disease: it’s an atypical pneumonia associated with Diarrhoea,

mental confusion, hyponatremia.
Pontiac fever: its acute febrile self-limiting disease with malaise & myalgia.
Legionella haemophilli: m/c legionella affecting human.
Legionella micdadei is partially acid fast like nocardia.

Diagnosis: it’s done bye direct fluorescent antibody testing.

Rx: Azithromycin, fluroquinolones.

Francisella tularensis:
 Its gram –ve, intra cellular facultative pathogen.
 Reserviors: Rabbits, Deers, rodents.
 Spread: through Tick Bite.
 Its important zoonosis.
 Spreads through tick bite [dermacentor] produces “ Ulcero glandular
disease” Characterized by ulcer at bite site with lymphadenitis, fever during
skinning of rabbits.
 Aerosols during skinning can produce pneumonia (commonly seen in
U.S.A).
 “Tularemia” is a disease caused by francisella.
o “Tularemia’ is also called as ulceroglandular disease.
 Usually it is diagnosed by serological methods.

Rx- DOC is Streptomycin.

Ingestion of under cooked rabbit meat can prod gastro intestinal tularemia.

Bordetella Pertussis:
 It produces whooping cough with inspiratory whoop.
 It’s an encapsulated organism.

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  Reservoir: are vaccinated human beings.
 Transmission: Respiratory droplets, it attaches to nasal mucosa by its
heam agglutinins.
 It produces a pertussis toxin that acts by CAMP by causing inhibition (Gi)
of –ve regulator of adenylate cyclase. [ADP ribosylase Gi protein]
 Characteristic feature are lymphocytosis, hypoglycemia & increased
histamine sensitivity.

Whooping Cough:

 Its highly contagious disease with incubation period of 7-10 days.

 Initially there is rhinorrhoea
 Sneezing
 Fever
 Malaise followed by peroxims of cough and whoof.
 The frenulum is swollen & there could be capillary ruptures due to
intense cough.
 Complications like Pneumonia, Seizures & Encephalopathy can occur.
 Pertussis vaccine is “ acellular Pertussis toxoid given as DTaP.
 The immunogens used for vaccine are pertussis toxoid, haem agglutinin
& outer membrane protein like pertactin.
 Cough with sub conjunctival haemorrhages.

Rx:

 Hospitalization & Erythromycin is DOC.

 Erythromycin should be given to all household contacts.
 Maximum infectivity of bordetella is during catarrhal stage.
 Culture on Bordet-genjou or potato agar produces aluminium paint
appearance.
 Culture films have thumbprint appearance.
 Best specimen for diagnosis is naso-pharyngeal aspiration.
 The immunization due to pertussis vaccine that’s wanes of in 5-10 years.
 The immunity is mainly of IgA.

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Brucella:
 It’s zoonoses.
 Reservoir is domestic live cattle
 Spread by unpasteurised dairy products & by direct contact by animal or
animal placenta as in slaughterhouses.
 It produces undulent fever called as brucellosis that presents as:
Acute septicemia
High-grade fever with myalgia
Arthralgias
Profuse sweating & hepatomegaly.
 Diagnosis is usually made by serological examination.
 Culture is hazardious.

Rx:

 Rifampacin + Doxycyclin
 Prevention: is by pasteurisation of milk, vaccination of cattle & vaccination
of high-risk humans.
 Brucella produces granulomatous response with the parasite multiplying in
reticulo endothelial cells & causing septiciemia.

Campylobacter Jejuni:
 It’s a curved rod with polar flagella in the form of gull’s wings.
 Its micro aerophilic.
 Transmission: poultry.
 It can cause infection even after low infectious dose producing
inflammatory diarrhoea with blood & pus in stools.
 Its an important cause of infectious diarrhoea that is self limiting
 Ten or more bloody stools per day.
 Imp complication is Guillain Barre Syndrome & Reactive arthritis .

Culture: done on schirro agar at 42 degrees.

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 Rx: mostly supportive.

Helicobacter Pylori:
 It gram –ve spiral bacilli.
 It’s micro aerophilic.
 It grows in campy or schirro agar.
 Its urease +ve, oxidase +ve.
 Transmitted by feco – oral route.
 It’s motile with flagella.
 It produces mucinase that destroys mucous layer of stomach.
 Its imp cause for chronic gastritis & duodenal ulcers.
 It’s a type 1 carcinogen associated with gastric adenocarcinoma and
maltoma [B cell lymphoma].
 Diagnosis is done biopsy and culture.
 Stained by giemsa staining.
 Urea breath test is usually used in diagnosis of H.pylori.
 Its oxidase +ve, urease +ve.

Rx:

Triple regimens like

 Omeprazole +Amoxicillin + Clarithromycin.

Entero bacteraciae
 They are gram –ve oxidase -ve, reduce nitrate to nitrites.
 Catalase +ve.

Entero Bactericae

Lactose fermenters Non- Lactose fermenters

[Pink colories on mac conkey’s agar] [Colorless colonies on mac conkey’s agar]
Ex: Citrobacter Non-motile Motile H2s

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 Enterobacter [Non H2s producing] producing
Escherichia Ex: Shigella Ex:Proteus
Klebsiella Yersenia Salmonella
[CEEK] [ShY] [PS]

E. Coli:
 They are gram –ve capsulated facultative anerobes
 Oxidase –ve, lactose fermenters.
 Biochemical test of E.coli IMVC ++-- [indole +, mythelene –ve, vogs roskou –
ve, citrate –ve]
 Reservoir: human colon.
 Transmission: Endogenous.
 They prod pink colour colonies on eosin methylene blue. They prodouce
greenish shine.
 Enterohaemorrhagic E.coli usually prodouces colourless colonies.
 Spread through bovine fecal contamination.

Antigenic structure of E.coli:

 Capsular antigen ‘K’ is heat labile & is associated with virulence.

 Somatic antigen ‘O ‘ is heat stable.
 Flageller antigen ‘H’.
 Normal colorn stains belong to group ‘o’.

Different types of E.coli:

1. Entero pathogenic E coli [EPEC].

2. Entero invasive E.coli [EIEC]
3. Enterotoxigenic E.coli [ETEC]
4. Enterohaemorrhagic E.coli [EHEC]
5. Entero aggrevative E.coli [EAEC]

EPEC:

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  Enteropathogenic e.coli causes prolonged water diarrhoea in infants &
children [paediatric group].
 There is effacement of brush border microvilli.
 Its non-toxigenic & non invasive.

EIEC:
 It invades large bowel, similar to shigellosis produces watery diarrhoea
with excess of leukocytes, fever and abdominal pain. It causes
inflammatory diarrhoea.

Rx: Fluroquinolones

 It penetrates cells. Penetration of HELA /HEP-2 cell culture is diagnostic.

 Sereny test is used in diagnosis of EIEC.

ETEC:
 Its m/c cause of traveller’s diarrhea.
 ETEC labile toxin acts by inducing C-AMP.
 It produces dianhoea.
 ETEC stable toxin acts rapidly by stimulating guanylate cyclase.
 Capsule impedes phagocytosis.
Rx: Rehydration.

EHEC:
 Also called as verotoxigenic E.coli.
 O157 H7 is MC serotype.
 Transmitted through contaminated bovine feces.
 It prodouces diarrhea, haemorrhagic colitis & haemolytic uremic syndrome
[HUS]
 Virotoxin is shiga like toxin. It acts by inhibiting protein synthesis by binding
to 60s ribosome.

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  It does not ferment sorbitol. Its non-invasive no inflammatory response &
no fever.
 Bloody diarrhoea in absence of fecal leukocytes is an indicator of EHEC.
 It produces colourless colories on mac conkey’s agar.
 Antibiotics are not given as they increase risk of hemolytic uremic
syndrome [HUS]

EAEC:
 Imp cause of persistant diarrhea.
 Produces stalk brick appearance,
 Produces yeast toxin Entero aggregative heat stable toxin [EAST].

Diseases caused by E.coli.

 M/c cause of UTI’s by endogenous contamination.

 Pyelonephritis associated pili allows adherens to urothelium.
 Gram –ve bacilli > 105 /ml of urine in asymptomatic patient in a urine
sample is said to be having UTI.
 Any bacteria in supra pubic aspirate indicated UTI.
 E. Coli is the m/c cause of Neonatal meningitis in India.Its mainly due to
maternal fecal contamination during parturition.
 E.Coli is the M/C cause of intra abdominal abscess, peritonitis, and
cholangitis.
 E.Coli is the 2nd M/C cause of Nosocomial pneumonia.

Rx: Fluroquinolones are DOC for UTI.

Klebsiella:
 Klebsiella pneumonia is gram –ve, enterobactereciae.
 It’s a Lactose fermenters, has a large polysaccharide capsule producing
mucoid lactose fermenting colonies on Mac Conkey’s agar.
 Klebsiella is also called as Friedlander’s bacillus.

Diseases Caused:
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  It’s an imp cause of pneumonia in alcoholics, diabetics and patient of
chronic lung disease.
 It produces frequent abcesses in the lung.
 Sputum is thick and bloody called current jelly sputum.
 Klebsiella pneumoniae produces bulging fissure sign of the lung lobes.
 Its an imp source of catheter associated UTI’s.

Rx: Cabipenem is the most active antibiotic against klebsiella.

Shigella:
 They are gram –ve, oxidase –ve rods.
 They are non-lactose fermenters, non-motile, non-H2S producing.
 Classified on basis of somatic O antigen.
 M/C Shigellosis worldwide is by Shigella sonnei.
 M/C Shigellosis in India is Shigella Flexneri.
 Most Severe Shigellosis is caused by Shigella Dysentery type 1.
 Selective media for shigellosis is Deoxycholate citrate agar.
 Hektoen enteric agar is used for growth of Shigella and Salmonella.
 Triple sugar Iron agar differentiates Salmonella and Shigella from other
gram –ve rods in the stool.
 Reservoir of shigella is colon. No animal carriers.
 Transmission is by feco oral route.

Pathogenesis:

 Endotoxin triggers inflammation and irritation of bowel.

 It has no H antigen (flagellar antigen).
 It invades M cells, polymerises acting jet trails. Produces very shallow
ulcers.
 Shiga toxin is produced by Shigela Dysentery type 1. It acts by proten
synthersis inhibition by binding to 60s ribosome.
 Shiga toxin is neurotoxic, cytotoxic, and enterotoxic.

Clinical Features:
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  It causes bacillary dysentery.
 A very low infective dose is enough to start infection.
 It’s highy acid resistant with an incubation period of 1-4 days.
 It produces bloody diarrhea, abdominal cramps, fever, tenismus, and
progresses to septicemia.

Complications:

 Haemolytic Uremic Syndrome (HUS), toxic dilatation and colonic

perforations.
 Majority of lesions are in the distal colon.

Rx:

 It’s a self-limiting disease requiring electrolytic fluid and electrolyte

replacement.
 Antibiotics are used only in severe infections.

Yersinia:
 It causes plague.
 Its gram –ve enterbactereciae.
 It has bipolar staining.
 Coagulase +ve, zoonosis.
 It’s a potential biowarfare agent.
 It has a safety pin appearance.
 It shows stalactile growth in ghee broth.
 Reservoir: Rodents, squirrels.
 Spread by fleabite Xenopsylla Cheopis.
 Transmission: human – human by respiratory droplets.
 The plaque spread by wild rodents, fleabites are called sylvatic plague.

Bubonic Plaque:

 Characterized by regional bubos, high-grade fever, conjunctivitis, after

fleabite.
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  It leads to septicemia & death if untreated.
 It’s most common plague.
 Bubos are commonly seen in femoral axillary, cervical, inguinal region.

Pneumonic Plaque:

 It is by septic embolic from a bubos or by inhalation of organism from

infected person.
 Its highly contagious & most fatal type of plague.
 The bacteria produce evelope antigen F1 that inhibit phagocytosis & has
type III secretion system that suppresses cytotoxine production.

Rx:

 Doc for plaque streptomycin.

 Prophylaxis of choice – tetracyclin.
 Culture: hazardious.
 Diagnosis: sero diagnosis & direct immunofluroroscence.

Type III secretion system:

 Protein appendage produced by gram –ve bacteria. It has needle like
structure & help the bacteria to secrete protein into eukaryotic cells or the
host cells.
 Bacteria showing type III secretion system:
o Shigella
o Pseudomonas
o Salmonella
o E.coli
o Yersenia
o Chlamydia.

Salmonella:
 Its gram –ve, non lactose fermenters, motile, H2S producers.
 Its sensitive to gastric acid, high infective dose required.

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  Culture characterstics: salmonella typhi produces jet black colonies on
Wilson Blair media due to production of H2S.
 The enrichment media is Selenite F Broth.
 Salmonella is classified on the basis of somatic antigen ‘o’, flagellar antigen
H & Virulence antigen Vi.
 H- antigen is responsible for immunogenecity producing fluffy clumps with
anti sera.
 O antigen produces chalky granular clumps when mixed with anti sera.
 Vi antigen is associated with virulence.

Pathogenicity:

 Transmission is by feco oral route by human carriers through contaminated

food and water.
 Stomach acid kills Salmonella bacilli. Decrease in gastric acid production
and sickle cell disease predisposes the patient to Salmonella infection.

Thyphoid fever [enteric fever]

 Typical feature: step – ladder pyrexia with relative bradycardia.

 Rose spots located on chest usually appear in 1st week of infections.
 A large infective dose is required if gastric acid secretion is normal.
 Infection usually begins in ileo – coecal region.
 Salmonella reaches mesenteric lymph nodes & then the blood producing
bacteremia.
 The infection is mainly caused S typhi [Typhoid] and S.paratyphi A, B, C
(milder infection).
 Blood reports are +ve in 80% of patients by 1st week.
 Liver & spleen get infected with additional release of bacteria into the
blood.
 Patient complains of constipation & abdominal pain.

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 S.paratyphi survives intracellularly being resistant to macrophage killing
with reduced fusion of lysosome and phagosome.
 Gall bladder & biliary tract is infected & excrete the bacilli in bile.
 Stool cultures become +ve by 3rd week.

Complications:

 Necrosis of peyer’s patches can lead to perforation.

 Cholecystitis [biliary tract].
 Thromboflebitis.
 Abscess formation.
 3% of patients become carriers.
 Those who excrete bacilli for more than a year is k/a chronic carrier.
 Fecal carriers are more common.

Diagnosis:

 Blood culture is diagnostic -Gold standard, +ve in 1st week.

 Widal test is +ve only after 1st week, peaks at 3rd week and declines.
 Stool cultures are +ve from 3rd week & are useful in a patient on
antibiotics.
 Diagnosis is made by isolation of organism from blood, bone marrow,
urine & tissue biopsy.
 Widal test has no value in detection of carriers. Demonstration of Vi
agglutinin indicates carrier state and is used for screening of cariers.
 Widal test measures H & O agglutinins for typhoid & para typhoid bacilli.
 ‘O’ agglutinin has a better diagnostic value and is common in Typhi &
para typhi.
 ‘H’ agglutinins are different for Typhi & para typhi & can differentiate
the infection.
 Widal test is never confirmatory. False +ve widal is seen in cases of prior
infection or immunization.
 Widal test +ve: if titre > 1:60

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 Rx: DOC for typhi ciprofloxalin.

DOC for typhi in children is Ceftriaxone.

Prevention: against typhoid is done by proper sanitation.

 Ty21A is a live attenuated oral vaccine available for typhoid.

 Other vaccines are VIR-EPA.

Note:

 Salmonella enteridis, salmonella Typhimurium are responsible for

gastroenteritiswhich presents with nausea, vomiting & diarrhea usually
after ingestion poultry products.
 They can lead to septicemia, osteomyelitis especially in sickle cell
anemia patient.
 Widal could be +ve but gastroenteritis is never caused by S.typhi.
 Gastroenteritis is self-limiting and antibiotics are avoided.

Proteus vulgaris:
 They are gram –ve, enterobacteracia, and non-lactose fermenters, H2S
producing.
 Has peritrichous flagella and shows swarming motility.
 Its urease +ve.
 Proteus vulgaris also called Proteus Mirablis.
 Proteus differs from other enterobacteracia by presence of enzyme
phenyalanine- D- aminase.
 Urease production makes the urine alkaline [↑ Urinary PH ] and ↑risk
of triple stones [NH4,Mg.Phosphate] also called as struvite or staghorn
calculi.
 Proteus is a common cause of UTI with alkaline urine.
 Ox strain of P.Vulgaris cross react with rickettsial organanisms & is the
basis of Weil-Felix reaction.

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Gardnarella:
 It causes bacterial vaginosis.
 Its Gram –ve, pleomorphic rod.
 Its oxidase –ve, similar to Entero bactercia.
 It’s responsible for vaginal discharge in a female patient, post antibiotic
therapy or menses.
 The number of lacto bacillus is reduced which increases the vaginal PH
due to antibiotic use and predisposes to gardnerella infection.

Pathogenesis:

 Bacterial vaginosis is thin grey fluid discharge from the vagina with vaginal
odour.
 Diagnosis is made when vaginal PH is >4.5 with the presence of clue cells
that are epithelial cells covered by bacteria on vaginal smear or sample.
 Whiff Test: Is addition of KOH to vaginal sample producing fishy amine
odour.
 Gardnerella is gram variable [i.e sometimes +ve and -ve]

Vibrio Cholera:
 It’s a gram –ve curved rod with polar flagella.
 It is oxidase +ve and grows well on alkaline medium.
 Culture medium: TCBS [Thiosulphate Citrate Bile salt Sucrose].
 Reservoir: Human colon.
 Vibrio cholera O1 is divided into 2 sub types: ELTOR and Classical
cholera.
 V.Cholera has fish in stream appearance and shows darting motility.
 It catalase +ve, oxidase +ve indole +ve, sucrose fermentor & converts
nitrates to nitrites.
 Ogawa serotype of ELTOR is M/C strain causing cholera.
 O139 strain is called as Bengal vibrio cholera.

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  It differs from ELTOR in production of O139 lipopolysaccharide (LPS)
toxin and a capsule.

Cholera:

 Spreads by feco oral route.

 Bacilli are sensitive to gastric acid and high infective dose of atleast 10*7
bacilli is required.
 Incubation period is of 1-2 days .
 Patient presents with painless rice watery stools, a non –inflammatory
diarrhea.
 Achlorhydria (absence of gastric Hcl) predisposes to cholera &
salmonella infections.
 ‘O’ blood group individuals are more susceptible for cholera.
 Cholera enterotoxin acts by ADP ribosylating Gs protein & increasing
Cyclic AMP causing efflux of chloride & water.
 Vibrio cholera is non-invasive. Major problem is tremendous fluid loss
and hypovolemia.

Diagnosis:

 Stool examination and culture on TCBS.

 Stool collected from rectum is best sample.
 It shows darting motility or shooting star motility, which is inhibited by
adding antisera under dark field microscopy.

Rx:

 TOC is rehydration with proper fluid and electrolyte replacement.

 ORS for moderate to mild dehydration.
 For severe dehydration ringer- lactate i.v fluid is best.
 Doc for adults Tetracyclin (doxycyclin).
 Doc for children <8yrs is Furazolidone.

Halophilic vibrio:

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 1. Vibrio para hemolyticus: is a capsulated vibrio showing bi polar staining .It
exhibits kanagawa phenomen causing gastroenteritis after consumption of
under cooked sea food(shell fish).
2. Vibrio vulnificus: is highly salt tolerant causing infection of eye, ear &
wounds producing cellulitis after exposure to sea water.It also causes
gastroenteritis after consumption of sea food.

Pasturella:
 P.multocida causes` cat bite fever’.
 Rservoir is mouths of cats and dogs.
 Transmission is by cat bite.
 It produces cellulitis, lymphadenitis after cat bite.
 It’s capsulated and produces endotoxin.

Rx: most bites are treated with Amoxicillin + Cluvulanic acid (augmentin) and
proper wound cleaning.

Eikennella Corrodens:
 Prod cellulitis after human bites and fist fight injuries.
 It corrodes agar and has bleach like odour.

Rx: Amoxilcillin+Clavulanic acid.

Bartonella Henslea:
 It produces `cat scratch fever’ and bacillary angiomatosis in AIDS patients.

Hacek Group:

 They are gram –ve organism resp for 10% cases of infective endocarditis.

H -Haemophillus

A – Actino bacillus

C- Cardio bacterium

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 E- Eikennella

K –Kingella.

Haemophilus:
 Gram –ve bacilli requiring factor V and factor X-hematin for its growth on
blood agar.
 Its shows satellite phenomenon i. e growth near staph aureus on blood agar.
 Chocolate agar contains both factor V and X.
 Spread: respiratory droplets.
 Its capsulated organism, which is most important virulence factor.
 It’s a polysaccharide capsule.
 Haemphillus type B has polyribitol phosphate capsule.
 It produces IgA protease & helps in colonizing in the mucosa.
 Quelleng reaction is +ve.
 Latex particle agglutination test is used to detect capsule antigens in the
CSF.

Disease caused:

 It’s an important cause of meningitis in children between three months to 2

yrs.
 It produces pneumonia, bronchitis and otitis media.
 It’s an imp cause of bronchitis in COPD patient.
 It’s an imp cause of epidemic epiglottitis.

Rx:

 Ceftriaxone.
 Nasal and oropharyngeal carriers are also treated.
 Rifampacin for meningococcal prophylaxis given to close contacts.

Prevention:

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  Capsular polysaccharides protein vaccine. The polyrubitol capsule is bound
to protein to make it‘T’ cell dependent.
 Polysaccharides moiety is combined with outermembrane protein to make
it more immunogenic.
 Vacination also prevents Haemophillus Influenza Type B also.

H. Ducreyi:
 It produces chancroids, which is a soft genital ulcer that is extremely
painful transmitted by STD.

Rx: Ceftriaxone.

Bacteroides:
 They are gram –ve anerobic, commonly present in colon.[mostly]
 Its an endogenous infection occurring due to bowel defects, trauma,
surgery, cancer.
 It produces septicemia, mixed peritonitis & abominal abscess after
abdominal surgeries.
Rx: Metronidazole is Doc [for all anerobes]
 Abscesses should be drained surgically.
 Antibiotic resistance is common with bacteroids.
 Giving prophylactic antibiotics before GI and biliary tract surgeries does
prevention.
 Bacteroids Melanogenica is melanin producing also k/a Prevotella.
 It produces gingival abscess & can grow in mouth.
 Fuso bacterium is fusiform oral flora. Grows with spirochetes in the mouth
& is responsible for Vincent’s angina.

Treponema Pallidum:

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  It’s a spirochete, that can’t be grown in artificial media, grown in rabitts
testis. It has an endoflagellum called axial flament.
 Its thin spirochete not properly stained by gram staining.
 It’s transmitted by sexual contact or across the placenta.

Primary syphilis:

 It has an incubation period upto 10 to 90 days.

 It produces non-tender indurated chancer that is highly contagious.
 It heals spontaneously in 3-6 weeks.
 Organism can be visualized by dark field microscopy or fluroscent
microscopy of the lesion.
 1-3 months later the patient develop secondary syphilis.

Secondary syphilis:

 There is a maculo papular rash [copper colored rash] with involvement of

palms & soles.
 There is patchy aloplecia, condylomata lata, which are multiple warty lesions
in genital & perianal region that are highly infectious.

Tertiary Syphilis:

 It occurs years later in an untreated patient.

 It’s characterized by syphilitic granulomas called `gummas’.
 CNS & CVS involved, causes aortitis.

Congenital syphilis:

 It can cause still births, keratitis, 8th nerve damage [auditory N] & notched
teeth [ Hutchinson’s teeth].
 Most babies are asymptomatic with major complaint being Rhinitis
[Snuftles] at birth.
 Later on there is saddle nose & a desquamating rash.

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 Diagnosis: The organisms are visualized by inmuno fluroscence or dark field
microscopy.

Serological diagnosis:

 Done by non-treponemal antibody screening test. The antibody here binds

to cardiolipin, which is an antigen, found in cow’s heart.
 Cardiolipin antigen is used in screening tests like VDRL, rapid plasma reagent
test [RPR].
 These test are very sensitive to diagnose primary and secondary syphilis but
are not specific.
 The diagnosis is usually confirmed by FTA-ABS.

Specific tests for treponemal antibody are:

 These bind to spirochetes and are more specific but are more expensive.
1. Fluroscent treponemal antibody absorption test [FTA-ABS]
2. Treponema pallidum heam agglutination test (MHATP).
 These are confirmatory test.

Rx:

 Benzathine Penicillin. Long acting form of penicillin G for primary &

secondary syphilis.
 Penicillin G for neuro & congenital syphilis.
 Jarish – Heximer reaction occurs 24 hrs after antibiotic Rx with increase in
temperature, rigor & occurs due to death of spirochetes.

Borellia:
 It’s a spirochete.
 Borellia burgdoferi causes Lyme’s disease.
 Reservoir, are white footed mile & white tailed deers.
 Ixodes Tick does transmission.
 Borellia burgdoferi invades skin after tick bite & spreads via blood stram to
involve heart, joints & CNS.

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  Arthritis is due to immune complex deposition.

Lyme’s disease:

 Initial symp is erythema migrans, which is annular bull’s eye skin lesion.
 There is fever, headache, myalgias & lymphoadenopathy.
 Several weeks later there could be involvement of facial nerve leading to
Bells Palsy, meningitis.
 Cardiac defects like arrythmias, myocarditis.
 Very late in the disease patients develop arthralgias & migratory arthritis.

Diagnosis:

 Sero diagnosis by immunofluroscence & ELISA.

 DNA probes & western blotting techniques are also used.

Rx: Doxycyclin & Ceftriaxone.

Leptospira:
 Is a thin sphirochete with terminal hooks.
 Can be seen on dark field microscopy.
 Reservoir: wild & domestic animals [zoonosis].
 Transmission: contact with animal urine, sewer workers, contaminated
recreational water (contaminated with rat urine).
 Leptospirosis is also k/a swineherd’s disease or swamp or mud fever.
 It presents with influenza like disease with GI symptoms [weil’s disease]
 There is hepatitis & rental failure [Hepatorenal syndrome]

Rx: penicillin G or Doxycyclin.

Characteristic Chlamydia Rickettsia Mycoplasma

1. Obligate intra Yes Yes No
cellularity
2. Production of No Limited Normal
ATP
3. Peptidoglycan in Modified Normal No

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 cell wall

Rickettsia:
 It’s an aerobic gram –ve bacilli that are obligate intra cellular parasite.

Bacteria Diseases Vector

R. Rickettsia Rocky mountain Ticks
spotted fever
R. Atari Rickettsial pox Mite
R. Prowazaki Epidemic typhus Human louse
R. typhi Endemic typhus Fleas
R.tsutsugamushi Scrub typhus Mites
Coxiella burnetti Q-fever Air borne
Rochalimara Trench fever Louse
Ehrlichiar Ehrlichiosis Tick
R. Conorri Indian tick typhus Ticks

 R.ricketsii produces Rocky Mountain spotted fever.

 R.akari produces Rickettsial pox.
 R.ricketsii is spread by Dermacentor a hard tick.
 It also shows transovarian transmission.
 It damages endothelial lining of capillaries producing vasculitis in many
organs incluin skin, lungs, brain and kidneys.
 It causes Rocky Mountain spotted fever characterized by high-grade fever,
headache, petechial rash on ankles and wrist then spreading to trunk and
face (centripetal rash).

Diagnosis:

 Is done by clinical symptoms and history of tick bite.

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  Start Rx without laboratory confirmation.
 Serological immunofluroscent assay is most widely used.
 Weil-Felix reaction is a heterophile agglutination test using OX strains of
Proteus.
 Ox 19 strains are used in endemic & epidemic typhi.
 Ox-k strain is used in scrub typhus.
 Ox 19 & Ox -2 are used in Rocky Mountain spotted fever.
 Weil-felix reaction is of no value or –ve in a fever Q-fever, trench fever &
Rickettsial pox.

Rx: Doxycyclin.

Note:

 Weils Disease- Leptospirosis.

 Weil-Felix reaction- to diagnose Rickettsia.

Coxiella Burnetti [Q-fever]:

 It’s an obligate intracellular bacteria.
 Reservoir: domestic stalk.
 Pregnant animal have high titres.
 Transmission: inhalation of aerosols from amniotic fluid or placental tissue.
 It survives drying and producing spores.
 Q fever: presents with fever, pneumonia & granulomatous hepatitis.
 Diagnosis is by serology.
 Weil– Felix test –ve.

Rx: Doxycyclin [ no vector & no rash in Q fever]

Chlamydia:
 Its obligate intracellular bacteria, cannot be stained by gram stain.
 Can’t produce its own ATP.
 It has modified peptidog lycan layer lacking muramic acid.

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  Chlamydia occurs in 2 forms.
Elementary body: Extracellular, infective form.
Reticulate body: Intracellular, replicating form.
 It’s seen in human genital tracts & eyes.
 Its m/c bacterial STD.
 STD’s are due to chlamydial serotypes D to K.
 It causes non – gonococeal cervicitis, urethritis, pelvic inflammatory disease.
 Chlamydia trachomatis:
 Produces inclusion conjunctivitis & pneumonia in neonates & infants.
Children have staccato cough.
 Chlamydia serotypes L1, L2, L3 produce lymphogranuloma venerum [LGV]
characterised by swollen lymph nodes & genital elephentiasis.
 Chlamydia Trachomatis serotypes A, B; Ba & C is leading cause of
preventable infectious blindness [Trachoma].
 Tachoma is characterised by Follicular conjunctivitis, Entropion [inversion of
eye lids], corneal scarring & blindness.

Diagnosis:

 It can’t be cultured on inert medium.

 So requires tissue culture or embryonated eggs.
 DNA probes are used and PCR is helpful in diagnosis.
 Cytoplasmic inclusion bodies can be seen on Giemsa staining.

Rx: Doxycyclin.

 SAFE stratergy is used for trachoma.

Chlamydia psittaci:

 Produce atypical pneumonia on exposure to parrots.

 Chlamydia pneumophylli also called Chlamydia pneumonia.
 Has a potential association with Atherosclerosis.

Mycoplasma:

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 It’s the smallest free-living bacteria.
 It does not have cell wall.
 Has sterol in its membrane.
 It requires cholesterol for its growth.
 Produces fried egg colonies on Eaton’s agar.
 Mycoplasma pneumonia is m/c cause of atypical pneumonia. There is dry
cough without production of sputum.
 Transmission- Respiratory droplets.

Diagnosis:

 Primarily clinical diagnosis is done.

 ELISA & immunofluorescence can be used.
 Mulberry shaped colonies on stool containing media.
 Mycoplasma shows cold agglutinins.

Rx: Azithromycin, clarithromycin or Erythromycin.

Zoonotic infections:

1. Bacillus Anthracis
2. Listeria
3. Francisella tularensis
4. Brucella
5. Campylobacter jejuni
6. Q-fever [Coxiella burnetti)
7. Chlamydia
8. Salmonella
9. Brucellosis
10. Yersina pestis [plague}

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Mycology
 Study of fungi is k/a mycology.
 All fungal spores are reproductive.
 Fungi are eukaryotes with 80s ribosomes.
 Cell wall consists of Chitin, mannan & other polysaccharides.
 Cell membrane contains ergosterol.
 Cytoplasmic membrane contains sterols.
 Some fungi are useful to man such as edible mushrooms. Certain yeasts are
used in fermentation and some fungi in elaborating antibiotics
(Penicillium).
 Imidozole, antifungal agents act by inhibiting the synthesis of ergosterol.
 Polyene antifungal like Amphoteracin B acts by binding to ergosterol

Classification of fungi:
Based on morphology:

 Yeast is single celled. Ex: Cryptococcus neoformans, Saccharomyces.

 Yeast like contains pseudohyphae. Ex: Candida albicans.
 Moulds have branching filaments called hyphae. Ex: Dermatophytes,
Aspergillus, Rhizopus, Mucor, and Penicillium.
 Dimorphic fungi exist in 2 forms. Yeast like in tissues [i.e at 37® C] &
Filamentous forms in soil & culture [i.e at 25®C]
Ex: Histoplasma capsulatum, Sporothrix schenckii, Blastomyces
dermatitidis, Coccidiodis immitis, Paracoccidiodis brasiliensis.

Based on sex spores:

 Zygomycetes- zygospores & oospores.

 Ascomycetes- ascospores.
 Basidiomycetes- basidiospores.
 Deuteromycetes/ Fungi imperfecti.

Asexual spores can be vegetative spores or aerial spores.

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  Vegetative spores- Blastospores, Arthrospores, Chlamydospores
 Aerial spores- Conidiospores, Microconidia, Macroconidia,
Sporangiospores.

Dx:
 Direct examination:
 10% KOH wet mount.
 KOH with Calcofluor white
 Gram stain
 India Ink preparation
 Wood’s lamp exam
 Culture:
 Sabouraud’s dextrose Agar (SDA)
 Brain heart infusion (BHI)
 Tissue sections:
 Methamine silver stain
 Periodic acid Schiff (PAS) stain.

Fungal Infections
 Superficial Fungal Infections
Pityriasis versicolor/Tinea Versicolor:

 Caused by Malassezia furfur (Pityrosporum oribiculare)

 Presents with hypogigmented spots on back, chest, abdomen & neck.
 KOH staining shows characteristic sphegetti & meat balls/ banana &
grape appearance.
 Diagnosis is done by fluroscence under wood lamp
 It involves only dead layers of skin (keratinized layer) and is an
endogenous infection.

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 Rx: Topical Selinum sulphide
 In pre-mature infants on IV lipid supplement, it can produce fungiemia.

 Cutaneous fungal infections

 It can be in the form of dermatophytes or cutaneous candidiasis.

Dermatophytes:
 Dermatophytoses are also k/a Tinea or Ring Worm.
 Itching is the m/c symptom of Tinea infection.
 They are of 3 types –Trichophyton, Microsporum, Epidermophyton.

Epidermophyton Trichophyton Microsporum

Tissue inv: Skin & Nails. Skin, Hair, Nails. Skin & Hair.

On SDA: No microconidia Micro > Macro Micro < Macro

Shape (macroconidia): Pear shaped Pencil shape Spindle shape

Tinea capitis is the ringworm infection of scalp. Most serious form of infection is
called Favus [causes permanent hair loss]

Tinea barbae/barber’s itch is seen in beard area.

Tinea corporis is the infection of the non-hairy skin of the body

Tinea cruis/Jock itch involves perineum or inguinal region

Tinea pedis is infection around foot.

Tinea unguam is infection around nail.

 Transmission occurs from infected person by towels, combs, public places
etc.
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  Tinea produces arthrospores in the lesion.
Ectothrix- arthrospores found on surface of hair shaft
Endothrix- arthrospores found within the hair shaft.
Dermathophytid reaction is allergic reaction to circulating fungal antigen.

Dx:
 Wood lamp examination with UV light of infected hair shows fluorescence.
 KOH mounting shows hyphae & arthroconidia.
 Culture is by Sabouraud’s Dextrose Agar
Rx:
Topical Terbinfine Ointment
Oral Griseofluvin is the DOC for dermatophytes.

 Sub-Cutaneous Infections
Sporotrichosis:
 Sporothrix schenckii is the only dimorphic fungus causing subcutaneous
infection.
 Sporotrichosis is also called as Rose Garden’s Disease.
 Usually transmitted by thorn prick of rose and other parts of trees.
 Produces subcutaneous swelling with lymph nodes enlargement.
 There is a painless papule at the site of infection, which often ulcerates.
 M/c site of infection is extremities.
Dx:
 Yeast phase appears as Cigar shaped cells (in tissues)
 Filamentous form is seen on SDA.
 Asteroid bodies can be seen with in the tissue, it is due to antigen
antibody reaction.
Rx:
 Intraconazole [cutaneous sporotrichosis]

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  i.v Amphoteracin B [extra cutaneous ]
 KI

Mycetoma:

 It is a chronic granulomatous infection of the subcutaneous tissue, usually

affects foot and rarely the other parts of body.
 It is of 2 types- Bacterial & Fungal.
 This disease begins as a subcutaneous swelling usually of foot that
produces characteristic abscess. The abscess bursts forming multiple
sinuses discharge pus that contains granules.
 A condition resembling mycetoma is k/a botryomycosis.
D x:
 Diagnosis is made from examination of granules.
 Granules are washed & examined with naked eye & under microscope.
 Under naked eye they can be yellow or black/brown in nature.
 However, staining and microscopy do confirmation.
 If fungal, then septate hyphae are seen.
 If bacterial, gram +ve bacteria are seen.
Rx:
 Actinomycotic mycetoma- Streptomycin & Dapsone
 Mycotic mycetoma- may require amputation.

Chromoblastomycosis:
 It is the disease confined to the subcutaneous tissue of the feet and
lower legs.
 It’s caused by black mould that belong to the family Dematiaceae.
 It causes warty nodules/ cauliflower lesions on skin.

Dx:

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  On H&E staining, yeast like bodies appears that shows copper penny
appearance. They are also known as muriform cells/ sclerotic bodies.

Rx:
 Itraconazole with or w/o 5-fluorocytosine.
 Amphoteracin B.

Rhinosporidiosis:
 It is caused by Rhinosporidium seeberi.
 It is a chronic granulomatous disease characterized by formation of friable
polpys on the nose k/a strawberry polyps.
 These polyps are also seen on mouth and eye and are rich in blood supply
that bleeds on touching.
 The infection is seen mainly seen on coastal areas of India & Sri Lanka and
is acquired by swimming or frequent contact with stagnant water or
aquatic life.

Dx:
 The fungus has not been cultivated.
 Diagnosis depends on the demonstration of sporangia.
 Biopsy sample typically shows Sporangium filled with endospores.

Rx:
 Surgical removal of polyps.

 Deep Fungal Infections

Produces systemic pulmonary disseminated disease.

Histoplasmosis:
 It is caused by Histoplasma capsulatum.
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  It is a dimorphic fungus.
 Primarily it involves reticuloendothelial system and also produces acute
pulmonary symptoms.
 Infection is acquired from inhalation of spores coming from soil/dust
contaminated with birds/bats droppings.
 Disseminated histoplasmosis infection in immunocompromised patient
presents with fever & hepatosplenomegaly.

Dx:
 Tissue samples shows yeast forms that typically shows figure of 8
appearance.
 When cultured on SDA shows thick walled spherical spores with tubercles.
 Histoplasmin skin test

Rx:
 Intraconazole
 Amphoteracin B

Coccidiomycosis:
 It is caused by Coccidiodes immitis.
 It is a dimorphic fungus.
 It occurs as primary infection of the lung in endemic areas of South-West
USA & Nothern Mexico.
 It’s highly pathogenic & infection is acquired by inhalation of barrel shaped
arthro-spores from the environment.
 Disseminated disease presents as Respiratory infection, Arthritis,
Rheumatism.
 It’s also called as Valley fever or Desert dump.
Dx:
 Biopsy or culture on SDA shows yeast form, which is a thick double walled
spherule, filled with endospores.

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  Coccidiodin skin test.
Rx:
Amphoteracin B

Blastomycosis:
 It is caused by Blastomyces dermatitidis.
 It is a dimorphic fungus, with septate hyphae & single globose conidia.
 Source of infection is inhalation of conidia from soil & wet rotten wood.
 Produces pulmonary symptoms that can be chronic and spread to skin,
bone & GU tract.
 It’s also known as North American Blastomycosis.

Dx:
 In tissues it appears as budding yeast.
 10% KOH shows broad base, budding yeast with thick double contoured
walls.

Rx:
Amphoteracin B

Paracoccidiodomycosis:
 It is caused by Paracoccidiodes brasiliensis.
 It is a dimorphic fungus.
 It produces pulmonary infection that spreads by haematogenous route to
mucous membranes of mouth, nose, lymph nodes & adjacent skin,
producing chronic granulomatous reaction.
 It is also k/a South American Blastomycosis.
Dx:
 It produces budding yeast with capitain’s wheel formation.
Rx:
Amphoteracin B.
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  Oppurtunistic infections:

Candidiasis:
 M/c agent responsible is candida albicans.
 Candida albicans forms pseudo-hyphae both in culture & tissues.
 Its normal inhabitant of skin, GI tract, oral & vaginal cavities.
 Predisposing factors: Diabetes, AIDS, Pregnancy, OCP’s, Infants & elderly,
prolonged administration of antibiotics, patients on immunosuppressive
drugs & i.v catheters.
Mucocutaneous lesions: Oral thrush, Vulvovaginitis, Balanitis,
Conjunctivitis, Keratitis.
 Oral thrush is adherent white plaque seen on oral mucosa common in AIDS
patient.
 Vulvo-vaginal candidiasis is seen in 3rd trimester of preg, common in
diabetics, with intense use of antibiotics.
 Esophageal candidiasis is seen in AIDS & immunocompromised patient.
Systemic candidiasis: UTI, Intestinal candidiasis, pulmonary candidiasis,
endocarditis, meningitits, septicaemia.
 Candida can cause endocarditis, septicemia, disseminated infection can
occur in neutropenic & immunocompromised patient.
Dx:
 On KOH mount shows pseudohyphae & budding yeast.
 Gram staining- shows oval cells with pseudohyphae.
 Tests to differentiate C.albicans from other species are:
o Germ tube test/Reynold’s Braude phenomenon: formation of germ
tubes when incubated in human serum [at 37®C]
o Chlamydospore formation.
o Carbohydrate assimilation tests.

Rx:
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  Amphoteracin B with 5-fluorocytosine in systemic infections.
 Nystatin for superficial infection.

Cryptococcosis:
 It is caused by Cryptococcus neoformans.
 It is a capsulated fungus.
 It is urease +ve yeast.
 Infection is acquired by inhalation of dust from pigeon droppings.
 Produces meningitis commonly in AIDS patients, Hodgkin’s lymphoma.
 It produces soap bubble lesion in brain.
Dx:
 India ink staining stains the capsule.
 Gram staining.
 Niger seed agar is the selective agar.
 Latex particle agglutination test detects polysaccharide capsular antigen in
CSF
 Cryptococcus are best seen in tissues with methenamine silver & periodic
and shift [PAS]
Rx:
Amphoteracin B + Flucytosin

Pneumocystis jirovesi [Pneumocystis carinii pneumonia]:

 It was previously classified as protozoa.
 Molecular studies (ribotyping) proved it as a fungus, an ascomycete.
 It lacks ergosterol.
Imp Risk Factor HIV infections
Immunosuppressive therapy like glucocorticoids
Cancer therapy
Pathogenesis
 It is an air borne disease.
 Transmission: Person to Person

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  Most infections are asymptomatic, but damage type1 pneumocytes &
causes hypertrophy of type 2 pneumocytes.
 It produces Interstitial Pneumonia.

Symptoms:

o Dyspnoea
o Fever
o Non-productive cough
o Tachypnea
o Tachycardia
o Cyanosis

Dx:
 Mainstray of diagnosis is Broncho-alveolar lavage using fiber optic
bronchoscopy.
 Lung biopsy is done, when diagnosis can’t be made by Broncho alveolar
lavage.
 Most sensitive method of diagnosis is DNA amplification by PCR

Stains used are - methenamine silver & toluidine blue, giemsa stain.

Rx:
DOC for prevention & treatment is Cotrimoxazole.
Start prophylaxis for PCP with CD4 count =/> 200 in HIV patient.

Aspergillosis:
 Aspergillus fumigatus is the main opportunistic pathogen.
 It is caused by inhalation of Aspergillus conidia present in soil/air.
 It is an opportunistic fungus that is filamentous with dichotomous
branching.
 The branching is usually at 45® angle (acute angle)
 Aspergillus is a septate fungus.

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Types of Aspergillus

 M/c cause of otomycosis – A.niger.

 M/c cause of aflatoxin production – A.flavus (produces hepatoma)
 M/c cause of fungal keratitis – A.fumigatus.
 Resp disease like Allergic Broncho pulmonary aspergillosis [ABPA] is seen in
Asthma patients.
 Fungus ball/Aspergilloma is seen in cavities of TB or other lung cavities
presenting with cough & hemoptysis.
 Sometimes, pulmonary aspergillosis is angioinvasive.
 Invasive Aspergillosis occurs only in immunocompromised patients with
granulocyte count < 500.
 Patients of acute Leukemia & tissue transplant recipients (especially near
construction site) are at  risk.
 It can also lead to meningitis, pneumonia & cellulitis.
 It is also m/c cause for fungal corneal ulcer after injury with vegetative
matter and animal tail.
Dx:

 Earliest CT findings include pulmonary nodules with halo sign.

 Sputum examination is done & on direct microsopy septate hyphae are
seen.
 Selective media used for A.niger is Czapek dox agar.
Rx:
 Lobe-ectomy for fungus ball.
 Gluco corticoids for ABPA
 Amphoteracin B & Itraconazole for Invasive Aspergillosis.

Zygomycosis:
 They are non-septate, filamentous fungi.
 Zygomycetes, Rhizopus, Mucor, and Absidia cause it.
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 Zygomycosis includes mucormycosis & entomophthoramycosis.
 Predisposing conditions are Diabetic ketoacidosis [DKA] & Leukemia.
 Rhizopus causes zygomycosis & otomycosis
 M/c presentation is Rhinocerebral zygomycosis.
 Pulmonary zygomycosis is angioinvasive.
Dx:
 On SDA medium Rhizopus has rhizoids, & sporangiophores arise in groups
directly above the rhizoids.
 Absidia also has rhizoids but sporangiphores arise from the aerial mycelium
in between the rhizoids.
 In Mucor, sporangiophores are present but rhizoids are absent.

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