SlideShare a Scribd company logo
1 of 77
Download to read offline
INFECTIOUS DISEASE OF
PATHOLOGY
(Part-1)
Dr.Naila Awal
(Postgraduate student)
Categories of infectious agents
•
•
•
•
•
•
•

Prion
Viruses
Bacteria
Fungi
Protozoa
Helminths
Ectoparasites
PRION
• Definition- Infectious particle composed of protein
Definition
(prp)

• DiseasesHuman
1) kuru
2)Creutzfeldt- Jackob Disease (CJD)
3)Variant CJD
AnimalBovine spongiform encephalopathy

TransmissionIartogenically
Surgery

Organ transplantation
Blood transfusion
Pathogenesis- Prp normally found in neuron. Disease
occur when prp conformational change protease
resistant prp
I
Normal Protease I Abnormal
Sensitive prp ------ prp
---Neuronal damage

Inactivation- By protein and lipid disrupting agent such
as Phenol
Ether

NaOH
Hypochlorite
New and Emerging infectious
diseases
• DefinitionNewly identified & previously unknown
agent that appeared in human population
& causes public health problem is known
as emerging infectious disease.
These includes1) Disease caused by newly developed strains/
microorganismEx- MDR-TB
XDR-TB

MRSA
Chloroquine resistant malaria

2) Disease caused by pathogens, endemic in other
species (birds) that recently entered into human populationEx-HIV, SARS

3) Disease caused by pathogens that have been present in
human population but show recent incidence
Ex-Dengue fever
Factors contributing to emergence—
1)Enviornment–
Climate & changing ecosystem
Urbanization & deforestation
2)International travel
3)Breakdown of public health measures
(war, overcrowding)
Bioterrorism
• Definition- Intentional release of viable
bacteria, virus & toxin in order to harm
people, animal/plant.
• Category A
-->Highest risk
-->Easily disseminated/
transmitted from person
to person
-->High mortality

• Anthrax- Bacillus
anthracis

• Botulism- Clostridium
botulinum

• Plague- Yersinia pestis
• Small pox- Variola
major virus

• Viral hemorrhagic
fever- Filovirus
• Category B
Moderately easy to
disseminated
Moderate morbidity but low
mortality

• Brucellosis- Brucella
• Melioidosis- Burkholderia
pseudomallei

• Glanders- Mallei
• Staphylococcal
enterotoxin B
• Epsilon toxin of Clost.
perfringes
• Food safety threats
Salmonella, Shigella, E.coli

• Water safety threatsV.cholerae, Cryptosporidium
pavum
• Category C

• Emerging pathogensNipah virus
Hanta virus
Transmission & dissemination of
microbes
• ROUTE OF ENTRY
• SKINNatural barrier1)Dense keratinized layer of skin
2)Low pH
3)Fatty acid- the growth of micro organism
• Unbroken skin-

• Penetrate through broken
skin

• I/V catheter

• Schistosoma larva
Release collagenase, elastase
dissolve ECM penetrate
swimmers skin
• Superficial prick-Fungus
• Wound-Staph
• Burn-Pseudomonas
• Bacteremia
• Needle stick
• Insect bite

• Animal bite

• HBV,HCV,HIV
• Tick transmitRickettsiae-RMSF
Brucella-Lyme disease
• Flea--Y.pestis- plague
• Mosquito-Malaria, Filaria
• Sand fly- L.donavanileishmaniasis
• Dog-Rabies
• GIT
• Natural defense1)Mucosal covering of intestinal epithelium
2) Mucosal antimicrobial agent-defensin
3)Lytic pancreatic enzyme & bile detergent
4)Normal flora
5)Secretory IgA
1)Enteropathogenic bacteria1)Staphgrow in contaminated food release
enterotoxin food poisoning without multiplication in the
gut.

2)V. cholerae, ETEC multiply inside the mucus layer
covering gut epithelium exotoxin release watery
diarrhea.

3)Salmoella,Shigella,Champylobacterinvade &
damage intestinal mucosa & lamina propria ulceration,
inflammation & hemorrhage dysentery.

4)S.typhisystemic infection.
• FungusCandidal infection- mainly in immunocompromised
person.

• Intestinal protozoaGiardia lamblia
Entamoeba histolytica
Cryptosporidia
• Intestinal helminthsAscaris lumbricoides gut obstruction/invade &
damage the bile duct

Hookworm IDA
Diphyllobothrium latum vit B12 depletionmegaloblastic anemia

T.Solium larva- encyst in muscle
E. Granulosus larva-encyst in lung, liver
• Respiratory tract• Natural defense1)Mucocilliary apparatus large particles are trapped.
2)Alveolar macrophage & neutrophil particle<5micro
meter alveoli phagocytosed by alveolar macrophage
& neutrophil.
Mechanism1)Micro organism attached to lower respiratory
tract & laryngeal epithelium
ExampleInfluenza virus-has 2 cell surface proteins-

– Hemagglutinin (function at the beginning of the
infection)

-Neuraminidase-(function at the end of the infection.
They degrade the protective layer of mucus in
respiratory tract)
Influenza virus
Hemagglutinin

Neuraminidase

Bind with epithelial surface receptor 1)Cleave the sialic acid allow
the virus to release from host cell
Host cell engulf the virus

Replicate within the cell

2) the viscosity of mucus
facilitate viral transit within
respiratory tract
2) Impaired ciliary activityExample• H. Influenzae & B. pertussis- release toxin ciliary
paralysis.

• Mycoplasma pneumoniae- produce ciliostatic
substances

• Smoker/people with cystic fibrosis-chronic
damage to mucociliary apparatus
3)Some respiratory pathogen avoid
phagocytosis/destruction after phagocytosis
Example• M tuberculosis- escape killing within phagolysosome
of macrophage

4)Opportunistic fungus- infect when CMI /when
leukocyte are in number.
ExamplePneumocystis jirovechi in AIDS
Aspergillus followed by chemotherapy.
• Urinary tract
• Natural defense
Regular flushing of urinary tract by urine
Spread & dissemination of
microbes
Some micro-organism proliferate locally at the site
of infection & others spread to distant site vialymphatic's, blood & nerve.

•

Local-

a) Confined to lumen of hollow visceraV. cholerae.

b) Adhere /proliferate in/on epithelial cell-

HPV/dermatophytes.
Invasive• LymphaticsEx- Staphylococcus-localized abscess/furuncle through
lymphatic  drain into regional lymph node
sometimes bacteremia & colonize to distant organ.
• Blood-Most of bacteria & fungus,
Virus- HBV, Polio
Protozoa- African trypanosoma
All helminths.
WBC- MTB,LD, Toxoplasma, HIV, Herpes
RBC- Plasmodium, Babesia
• Nerve- Polio virus
Placental-fetal route• BacteriaMycoplasma placentitis premature delivery/still birth.
T.Pallidum2nd trimester osteochondritis, periostitis
leads to multiple bony lesion.
• VirusRubella1st trimester-Congenital heart disease,
Cataract,
Deafness.
3rd trimester-Little damage
• Infection during passage of birth canalRickettsia/Chlamydia-Conjuctivitis
• Milk- CMV,HBV,HTLV-1
Release of microbes from the
body
It depends on the location of infection.

Transmission from person-person• Respiratory route- Virus & bacteria.
• Saliva- EBV, CMV, Mumps
• Feco-oral route- HAV, HEV , Rota virus,
Hookworm, Schistosomes

• Blood & blood product- HBV, HCV,HIV
• Sexual transmission
•

Transmission from animal-human1) Direct contact / Consumption of animal
fat
Ex- Bacillus anthracis.
2) Indirectly via invertebrate host.
Ex- Malaria – by mosquito.
Sexually Transmitted Infection
• Definition- Infection that are transmitted
through sexual route.

• High risk group1)Adolescent
2)Homosexual men
3)Illegal drug abuser

• Site- Initial siteVagina
Rectum

Urethra
Oropharynx
General featuresInfection with 1 STI associate organism the risk
for additional STI
Ex-

N. Gonorrhea/ Chlamydia trachomatis epithelial
injury local tissue damage chance of co-infection
with the other & also the risk of HIV infection. .

STI can spread by vertical transmission & causes
severe damage to fetus/ child
Ex- Chlamydia trachomatis Conjunctivitis
Syphilis Miscarriage
Examples of STI
• Bacteria
•
•
•
•
•

Neisseria gonorrhoeae
Treponema pallidum
Haemophilus ducreyi
Klebsiella granulomatis
Chlamydia trachomatis

• Ureaplasma urealyticum

•
•
•
•
•

Gonorrhea
Syphilis
Chancroid
Granuloma inguinale
Lymphogranuloma
venereum
• Urethritis
• Virus
•
•
•
•
•
•

HSV
HBV
HPV
HIV
Protozoa
Trichomonas vaginalis

•
•
•
•

Herpes
Hepatitis
Condyloma acuminatum
AIDS

• Urethritis
• Vaginitis
Nosocomial Infection
• Definition
These are hospital acquired infection which
develops 48hrs after hospitalization /within 48
hrs after release from hospital.
Source
1)Hands of health worker
2)Contaminated surface
3)Used equipment & instrument

4)Blood transfusion
5)Organ transplantation
Organism causing Nosocomial Infection
• Bacteria• Gram positive

•
•
•
•
•

• Gram negative

• Pseudomonas
• Proteus
• E coli

Staph aureus
MRSA,VRSA
Staph epidermidis
Strep pneumoniae
Clostridium tetani
• Virus

• Fungi
• Parasite

• HBV,HCV,HDV
• HIV, HSV,CMV

• Candida
• Pneumocystis jiroveci
• Toxoplasma
Risk factor•
•
•
•
•
•

Long time hospital stay
Mechanical ventilation
I/V catheter
Use of indwelling catheter
Overdose of antibiotic
Failure of health care worker to wash hand.
• Prevention
1) Frequent hand washing can transmission of MRSA &
VRE.
2) Proper sterilization & disinfection of inanimate object of
the hospital.
3) Proper disposal of hospital waste.
4) Rational use of antibiotics.
5)Personal hygiene of patient, attendants, doctor & medical
stuff.
6) Detection of proper carrier & proper diagnosis.
Host defense against infection
• 1) Innate immunitya) Intact skinSebaceous gland--> contain fatty acid antibacterial
& antifungal
Low pH- antimicrobial.

b) Mucous membraneMucociliary apparatus- prevent the entry of microbes
through URT
Lysozyme in tear & mucus- degrade peptidoglycan
layer of bacterial cell wall protect from infection.
c) Cellular componentMacrophage, neutrophil phagocytose the microbes.
N-K cellproduce toxic substances perforin destroy
microbes.

d) Soluble componentComplement activation-->formation of MAC

destroy cellular Ag.
IFNα, IFNβ –released by virus infected cell this
IFN replication of viruses. (that’s why viral infection are
self limiting)
• 2) Acquired immunity- develops after exposure to
microbes.
They are B & T lymphocyte.
Ex- Measles virus enters into the body
Ab production
Ab binds with measles virus
Virus eliminated

Provides specific immunity
How micro-organism causes
diseaes
• By 3 mechanisms1)They can directly enter into host cell causes cell
death.

2)They may-release toxins kill the cell
3)They may-release enzymes degrade tissue
components/damage blood vessel ischemic necrosis.

4)They induce host cell responses causes
additional damage.
Mechanism of viral injury
Virus can directly damage the host cell by entering
& replicating within it.
• Virus has a affinity for specific body tissue which is
determined by –

1)Presence of receptor on host cellExgp120 of HIV binds with CD4 on Tcell
CXC R4(T cell)
CCR5(macrophage)
gp350 of EBV binds with CR2/CD21 on B cell
2) Cellular transcription factor that recognize
viral enhancer & promoter sequence
Ex- JC virus causes leuko encephalopathy, replicate
specially in oligodendroglia in CNS. (B/c enhancer &
promoter sequence regulating viral genes are active in
glial cell).

3) Physical barrierEx- Entero virus replicate in intestine b/c they can resist
inactivation by acid, bile & digestive enzyme.

4)TemparatureEx- Rhinovirus infect only within URT b/c they replicate at
lower temperature of URT.
Virus can damage the host cell by a number
of mechanism• 1) Direct cytopathic effect- Virus can kill the cell

directly bya) Prevent the synthesis of host macromolecules
(DNA,RNA/protein)
Ex-Polio virus- inactivate cap binding protein which is
essential for translation of host cell mRNA.
b) Producing degradative enzyme & toxic proteins
Ex- HSV-Produce protein that synthesis of cellular DNA &
mRNA & other proteins that degrade host DNA.
c) Inducing apoptosis by producing pro-apoptic protein
Ex- HIV vrp protein.
2)Anti viral immune response• Viral protein on the surface of host cell may be
recognized by immune system & lymphocyte may
attack the virus infected cell.
Ex- In HBV infection, acute liver failure is caused by cytotoxic T cell
mediated destruction of infected hepatocytes.

3)Transformation of infected cells--> benign/

malignant neoplasm
• Oncogenic virus stimulate cell growth & survival by
following M/AExpression of virus encoded oncogene
Anti-apoptic strategies
Insertional mutagenesis
Mechanism of bacterial injury
• 1) Adherence to the host cell surfacea) Adhesin - is present in bacterial cell surface. Through

this they bind to host cell/ECM.
Ex- Strep. pyogens adhere to host tissue by protein F &
teichoic acid.

b) Pili Ex- E.Coli through P pili bind with gal-gal moiety of
uroepithelium.
c) Glycocalyx Ex-Stap. epidermidis/ Strep. viridians bind with heart
valve.
• 2)Virulence of intracellular bacteria• Facultative intracellular bacteria infect 
-->Epithelial cell (Shigella, ETEC)
-->Macrophage (MTB,ML)
-->Both (S. typhi)

• Growth of bacteria in cell may allow the bacteria
to escape the immune system /facilitate the
spread.
Ex- MTB macrophage lung to other site.
Bacteria have a number of mechanism
to enter into the cella) Bacteria is coated with Ab/ complement 
phagocytosed by macrophage.
• Ex-MTB activate alternative pathway of complement
opsonization with C3b C3b coated MTB bind with CR3
on macrophage endocytosis into macrophage.

b) Gm- bacteria use complex secretion system to
enter into epithelial cell.

• This system consists of needle like structure form pore
inside host cell membrane inject protein
rearrangement of cell cytoskeleton bacteria entry.
• Ex- L. monocytogenes.
c) Effect of bacteria inside the host cella)
b)

Shigella, E. coli- host protein synthesis within 6
hours host cell lysis.
Within macrophage most bacteria killed when
phagosome fuse with lysosome & form
phagolysosome. But certain bacteria evade this
defense.

Ex- MTB- block the fusion of phagosome with lysosome unchecked
MTB
proliferation within macrophage.
L. Monocytogenes- produce pore forming protein-listeriolysin O & 2
phospholipase degrade phagosome membrane bacteria
escape into cytoplasm.
3) Toxin production• A) Endotoxin- is a LPS, component of Gm- bacterial cell wall.
It is both beneficial & harmful.

BeneficialActivate protective immunity.
 Induction of cytokine & chemokine
 expression of co-stimulatory molecules enhance T cell
activation.

Harmful-

High level of LPS induction of excessive level of
cytokines TNF, IL-1,IL-12Septic shock, DIC, ARDS.
• B) Exotoxin- secreted from bacteria & causes celluar
injury.

1)Enzymes- bacteria secret protease, coagulase,
hyaluronidase, fibrinolysin
Ex• Stap. aureus produce protease degrade protein that
hold keratin together detachment of epidermis from
deeper skin.
2)Toxin that alter intercellular signaling &
regulating pathway—
• Most of the toxins have
A sub unit- enzymatic activity
B sub unit- binds with the receptor on cell surface &
delivers the A subunit into cell cytoplasm.
Ex- Bacillus anthracis, V. cholerae.
3) Neurotoxin• Clostridium botulinum, Clostridium tetani
•
release of neurotransmitters paralysis respiratory
failure death.

• 4) Super Ag• Stimulate T lymphocyte massive Tcell proliferation &
release of cytokines high level of cytokines Capillary
leakage & shock.
Injurious effects of host
immunity
1) Immune response to microbes
sometimes causes tissue injury.
• a) MTB- causes granulomatous inflammation--delayed
hypersensitivity prevents the spread of bacilli but also
causes tissue damage & fibrosis.

• b) HBV,HCV- causes liver damage due to immune
response to infected hepatocyte, not to cytopathic effect .
.
2)Humoral immune response to microbes has
also pathological consequence
• S. pyogenes- Ab produce against streptococcal M
protein cross react with cardiac protein damage
heart valve RHD.

• S. pyogenes- anti streptococcal Ab cross react with
glomerular basement membrane  form Ag-Ab
complexes deposit in renal glomeruli Post
streptococcal GN.
• 3)Infection may be associated with chronic
inflammatory disorder as well as cancer.

Ex• HBV/HCV Hepatitis HCC
• H.Pylori Gastritis gastric adenocarcinoma
• Schistosomia Chronic cystitis bladder carcinoma.
Immune evasion by microbes
Micro organism develops many M/A to evade host immune
system.

1) Growth in niches that are inaccessible to host
immune response
a)

Microbes are multiply in the lumen of the intestine (C.
difficili) / gall bladder (S. typhi)

b) Some organism are rapidly invade host cell before
humoral immune response become effective.
Ex•
•

Malarial parasite--sporozoite enters into hepatocyte.
Trichinella/T. cruzei-enters into skeletal/cardiac muscle.
c) Some Parasite form cyst in host cell.
Ex- Tapeworm
d) During viral latency, viral genes are not expressed.
Ex- Herpes virus
2)Antigenic variationVirus can escape immune attack by changing their Ag.

Mechanism
• High mutation rate
• Genetic ressortment
• Genetic rearrangement

•
•
•
•
•
•
•
•

HIV
Influenza virus
Influenza virus
Rota virus
N. gonorrhoeae
Borrelia
Trypanosoma
Plasmodium
3) Resistance to innate immune response

• Resistance to antimicrobial peptide
(defensin, cathelicidins& thrombocidin)prevents killing of microbes by neutrophil
& macrophage.
• Carbohydrate capsule -present on the
surface of the micro organism prevent
phagocytosis by neutrophil.
• Ex- Pneumococci, meningococci, H.influenza
• Bacteria by covering with host protein -evade
immune defense.
Ex- Staphylococcus aureus covered by protein A that bind
with Fc portion of Ab phagocytosis.

• Some bacteria secret protease degrade Ab.
Ex- Niesseria, Haemophilus, Streptococcus
• Some organisms replicate within phagocytic cell.
Ex- MTB, Liesteria, Leishmania, Trypanosoma,
Toxoplasma, Cryptococcus neoformans.
• Virus can produce molecules that innate
immunity.
Ex- Herpes virus, Pox virus produce protein block
complement activation.

• Some virus produce homologous of
IFNα ΙFΝβ /IFN R which the action of IFN.
4) Recognition of infected cell by CD4 TH cell/
CD8 cytotoxic T cell.
Ex- HSV,CMV,EBV bind/ alter the localization of MHC-1
impair the peptide presentation to CD8 T cell.
Infection in immunosuppressed
hosts
• Inherited• 1)Patient with Ab deficiencyEx- X-linked aγglobulinaemia•
•
•
•

Severe bacterial infectionStrep . pneumoniae
Haemophilus influenzae
Stap. Aureus

• 2)T cell defect- susceptible to infection with
intracellular pathogens, virus, some parasite.
• 3) Complement deficiency• Strep . pneumoniae
• Haemophilus influenzae
• Neisseria menigitidis

• 4) Defect in neutrophilic function• Stap. Aureus
• Gm- bacteria
• Fungi
Acquired• 1) AIDS
• 2) Impaired production of leukocyte leukemia fills the bone
marrow with cancerous cell & vulnerable to infection.

• 3)Iartogenic cause of immunosuppression•

Ex-Immunosuppressive drug.

• Disease of organ systems other than immune
system• Cystic fibrosis---- RTI with P. aeruginosa
•

S. aureus

• Sickle cell disease----Strep. pneumoniae
• Burn---- P. aeruginosa.
Spectum of inflammatory responses
to infection
• 5 major histological patterns of tissue
reaction in infections are1) Suppurative inflammation2)Mononuclear & granulomatous
inflammation
3)Cytopathic- cytoproliferative reaction4)Tissue necrosis5) Chronic inflammation & scarring-
1) Suppurative inflammationCharacterized by production of large amount
pus/purulent exudates consisting of neutrophil,
liquefactive necrosis & edema fluid.
• Sometimes the lesion are destructive.

Ex- Pneumococci spare alveolar wall lobar
pneumonia.
Staphylococci & Klebsiella destroy alveolar wall
form abscess fibrosis.
Suppurative inflammation
2)Mononuclear & granulomatous inflammation
Granulomatous inflammation- is a distinctive
pattern of chronic inflammation characterized by
accumulation of activated macrophagesepithelioid cells which may fuse to form giant
cells. In some cases there is a central area of
caseous necrosis.
• Ex- TB
Mononuclear cell predominate• Plasma cell abundant Primary & secondary
syphilis.

• Lymphocyte predominate HBV infection/viral
infection of brain.
Infectious disease of pathology
3) Cytopathic- cytoproliferative reactionIt is characterized by cell necrosis/cellular
proliferation, usually with scattered
inflammatory cell.
a) Some virus replicate within cytoplasm/nucleus
& visible as inclusion body.
• Ex-Herpes virus, Adeno virus.
b) Some virus induce cell to fuse & form
multinucleated giant cell.
• Ex- Warthin- Finkeldy cells in measles.
Herpes virus.

c) Some virus causes epithelial cell to detach &
form blister
• Ex- Herpes virus.

d) Some virus causes epithelial cell to proliferate &
form wart.
• Ex- HPV, Pox virus.
e) Finally they contribute to develop malignant
neoplasm.
4)Tissue necrosisEx-

• Clostridium perfringes- secret toxin gangrenous
necrosis.

• E. histolytica- liquefactive necrosis.
• Herpes virus (brain)/ HBV (Temporal lobe)-severe
necrosis.

• 5) Chronic inflammation & scarringEx-

• Chronic HBV cirrhosis
• Schistosoma egg Pipe-stem fibrosis of liver
• TB Constrictive fibrous pericarditis.
Infectious disease of pathology

More Related Content

What's hot (20)

Genetics pathology revision notes
Genetics pathology revision notes Genetics pathology revision notes
Genetics pathology revision notes
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 
6 infarction
6 infarction6 infarction
6 infarction
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 
Morphology of-acute-inflammation
Morphology of-acute-inflammationMorphology of-acute-inflammation
Morphology of-acute-inflammation
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 
Inflammation
InflammationInflammation
Inflammation
 
Hemodynamic disorders
Hemodynamic disorders Hemodynamic disorders
Hemodynamic disorders
 
Ch 6 diseases of the immune system part 1
Ch 6 diseases of the immune system part 1Ch 6 diseases of the immune system part 1
Ch 6 diseases of the immune system part 1
 
Pathology cptr5-genetics
Pathology   cptr5-geneticsPathology   cptr5-genetics
Pathology cptr5-genetics
 
Acute and chronic inflammation
Acute and chronic inflammationAcute and chronic inflammation
Acute and chronic inflammation
 
Infarction
InfarctionInfarction
Infarction
 
AMYLOIDOSIS
AMYLOIDOSISAMYLOIDOSIS
AMYLOIDOSIS
 
Inflammation part 1
Inflammation part 1Inflammation part 1
Inflammation part 1
 
Neoplasia Robbin's path
Neoplasia Robbin's pathNeoplasia Robbin's path
Neoplasia Robbin's path
 
2 hyperemia-congestion
2 hyperemia-congestion2 hyperemia-congestion
2 hyperemia-congestion
 
Inflammation....
Inflammation....Inflammation....
Inflammation....
 
Pathologies of the gastrointestinal tract
Pathologies of the gastrointestinal tractPathologies of the gastrointestinal tract
Pathologies of the gastrointestinal tract
 
Chronic inflammation
Chronic inflammation Chronic inflammation
Chronic inflammation
 
Chronic inflammation
Chronic inflammationChronic inflammation
Chronic inflammation
 

Similar to Infectious disease of pathology

laboratory Rat diseases &control measures
laboratory Rat diseases &control measureslaboratory Rat diseases &control measures
laboratory Rat diseases &control measuresPlavan Majunder
 
Zoonotic infections.ppt
Zoonotic infections.pptZoonotic infections.ppt
Zoonotic infections.pptFatima Fasih
 
infectious diseases
infectious diseasesinfectious diseases
infectious diseasesAndrea B.
 
06 infectious disease gram negative
06 infectious disease gram negative06 infectious disease gram negative
06 infectious disease gram negativemed_students0
 
Infection control concepts
Infection control conceptsInfection control concepts
Infection control conceptsAnupam Niraula
 
Infectious diseases: an introduction
Infectious diseases: an introductionInfectious diseases: an introduction
Infectious diseases: an introductionGuvera Vasireddy
 
Herpesviridae.pptx
Herpesviridae.pptxHerpesviridae.pptx
Herpesviridae.pptxNMdcat2021
 
Human herpesviruses.pdf
Human herpesviruses.pdfHuman herpesviruses.pdf
Human herpesviruses.pdfÖmer Aslankan
 
PICORNA VIRUS POLIO dr. someshwaran may 2015
PICORNA VIRUS POLIO dr. someshwaran may 2015 PICORNA VIRUS POLIO dr. someshwaran may 2015
PICORNA VIRUS POLIO dr. someshwaran may 2015 SOMESHWARAN R
 
OHH Unit 3 Biological and ergonomical hazards 1.ppt
OHH Unit 3 Biological and ergonomical hazards 1.pptOHH Unit 3 Biological and ergonomical hazards 1.ppt
OHH Unit 3 Biological and ergonomical hazards 1.pptABHINANDHKA1
 
Pediatric communicable Diseases
Pediatric communicable DiseasesPediatric communicable Diseases
Pediatric communicable DiseasesAparna Harshan
 
DNA Viruses - Microbiology
DNA Viruses - MicrobiologyDNA Viruses - Microbiology
DNA Viruses - MicrobiologySijo A
 
Reduviid bug,T. cruzi & Chagas disease
Reduviid bug,T. cruzi & Chagas diseaseReduviid bug,T. cruzi & Chagas disease
Reduviid bug,T. cruzi & Chagas diseaseKapil Sharma Neupane
 

Similar to Infectious disease of pathology (20)

laboratory Rat diseases &control measures
laboratory Rat diseases &control measureslaboratory Rat diseases &control measures
laboratory Rat diseases &control measures
 
Zoonotic infections.ppt
Zoonotic infections.pptZoonotic infections.ppt
Zoonotic infections.ppt
 
Viral lesions in children
Viral lesions in childrenViral lesions in children
Viral lesions in children
 
infectious diseases
infectious diseasesinfectious diseases
infectious diseases
 
HIV/AIDS
HIV/AIDSHIV/AIDS
HIV/AIDS
 
Chlamydia
ChlamydiaChlamydia
Chlamydia
 
06 infectious disease gram negative
06 infectious disease gram negative06 infectious disease gram negative
06 infectious disease gram negative
 
13.Herpesviridae.ppt
13.Herpesviridae.ppt13.Herpesviridae.ppt
13.Herpesviridae.ppt
 
Infection control concepts
Infection control conceptsInfection control concepts
Infection control concepts
 
Chlamydia
Chlamydia Chlamydia
Chlamydia
 
Infectious diseases: an introduction
Infectious diseases: an introductionInfectious diseases: an introduction
Infectious diseases: an introduction
 
Herpesviridae.pptx
Herpesviridae.pptxHerpesviridae.pptx
Herpesviridae.pptx
 
Human herpesviruses.pdf
Human herpesviruses.pdfHuman herpesviruses.pdf
Human herpesviruses.pdf
 
Opportunistic infections (oi) deepa
Opportunistic infections (oi) deepaOpportunistic infections (oi) deepa
Opportunistic infections (oi) deepa
 
PICORNA VIRUS POLIO dr. someshwaran may 2015
PICORNA VIRUS POLIO dr. someshwaran may 2015 PICORNA VIRUS POLIO dr. someshwaran may 2015
PICORNA VIRUS POLIO dr. someshwaran may 2015
 
OHH Unit 3 Biological and ergonomical hazards 1.ppt
OHH Unit 3 Biological and ergonomical hazards 1.pptOHH Unit 3 Biological and ergonomical hazards 1.ppt
OHH Unit 3 Biological and ergonomical hazards 1.ppt
 
Pediatric communicable Diseases
Pediatric communicable DiseasesPediatric communicable Diseases
Pediatric communicable Diseases
 
chn.pptx
chn.pptxchn.pptx
chn.pptx
 
DNA Viruses - Microbiology
DNA Viruses - MicrobiologyDNA Viruses - Microbiology
DNA Viruses - Microbiology
 
Reduviid bug,T. cruzi & Chagas disease
Reduviid bug,T. cruzi & Chagas diseaseReduviid bug,T. cruzi & Chagas disease
Reduviid bug,T. cruzi & Chagas disease
 

More from Nailaawal

Planning, sturcturing and Preparing small group teaching in Medical education...
Planning, sturcturing and Preparing small group teaching in Medical education...Planning, sturcturing and Preparing small group teaching in Medical education...
Planning, sturcturing and Preparing small group teaching in Medical education...Nailaawal
 
How to evaluation of breast lump
How to evaluation of breast lump How to evaluation of breast lump
How to evaluation of breast lump Nailaawal
 
Cellular adaptation
Cellular adaptation Cellular adaptation
Cellular adaptation Nailaawal
 
Neoplasia [part 1]
Neoplasia [part 1]Neoplasia [part 1]
Neoplasia [part 1]Nailaawal
 
Introduction of pathology
Introduction of pathologyIntroduction of pathology
Introduction of pathologyNailaawal
 
Pathology of cns
Pathology of cnsPathology of cns
Pathology of cnsNailaawal
 
Cns tumor rest (2)
Cns tumor rest (2)Cns tumor rest (2)
Cns tumor rest (2)Nailaawal
 
Cns tumor, gliomas
Cns tumor, gliomasCns tumor, gliomas
Cns tumor, gliomasNailaawal
 
Gynaecomastia
GynaecomastiaGynaecomastia
GynaecomastiaNailaawal
 

More from Nailaawal (14)

Planning, sturcturing and Preparing small group teaching in Medical education...
Planning, sturcturing and Preparing small group teaching in Medical education...Planning, sturcturing and Preparing small group teaching in Medical education...
Planning, sturcturing and Preparing small group teaching in Medical education...
 
How to evaluation of breast lump
How to evaluation of breast lump How to evaluation of breast lump
How to evaluation of breast lump
 
Cellular adaptation
Cellular adaptation Cellular adaptation
Cellular adaptation
 
Neoplasia [part 1]
Neoplasia [part 1]Neoplasia [part 1]
Neoplasia [part 1]
 
Introduction of pathology
Introduction of pathologyIntroduction of pathology
Introduction of pathology
 
Pathology of cns
Pathology of cnsPathology of cns
Pathology of cns
 
Meningioma
MeningiomaMeningioma
Meningioma
 
Cns tumor rest (2)
Cns tumor rest (2)Cns tumor rest (2)
Cns tumor rest (2)
 
Cns tumor, gliomas
Cns tumor, gliomasCns tumor, gliomas
Cns tumor, gliomas
 
Gynaecomastia
GynaecomastiaGynaecomastia
Gynaecomastia
 
Toxoplasma
ToxoplasmaToxoplasma
Toxoplasma
 
Neisseria
NeisseriaNeisseria
Neisseria
 
Fungus
FungusFungus
Fungus
 
Spirochetes
SpirochetesSpirochetes
Spirochetes
 

Recently uploaded

Quality Assurance_GOOD LABORATORY PRACTICE
Quality Assurance_GOOD LABORATORY PRACTICEQuality Assurance_GOOD LABORATORY PRACTICE
Quality Assurance_GOOD LABORATORY PRACTICESayali Powar
 
HED Office Sohayok Exam Question Solution 2023.pdf
HED Office Sohayok Exam Question Solution 2023.pdfHED Office Sohayok Exam Question Solution 2023.pdf
HED Office Sohayok Exam Question Solution 2023.pdfMohonDas
 
The basics of sentences session 10pptx.pptx
The basics of sentences session 10pptx.pptxThe basics of sentences session 10pptx.pptx
The basics of sentences session 10pptx.pptxheathfieldcps1
 
Philosophy of Education and Educational Philosophy
Philosophy of Education  and Educational PhilosophyPhilosophy of Education  and Educational Philosophy
Philosophy of Education and Educational PhilosophyShuvankar Madhu
 
How to Manage Cross-Selling in Odoo 17 Sales
How to Manage Cross-Selling in Odoo 17 SalesHow to Manage Cross-Selling in Odoo 17 Sales
How to Manage Cross-Selling in Odoo 17 SalesCeline George
 
Easter in the USA presentation by Chloe.
Easter in the USA presentation by Chloe.Easter in the USA presentation by Chloe.
Easter in the USA presentation by Chloe.EnglishCEIPdeSigeiro
 
Diploma in Nursing Admission Test Question Solution 2023.pdf
Diploma in Nursing Admission Test Question Solution 2023.pdfDiploma in Nursing Admission Test Question Solution 2023.pdf
Diploma in Nursing Admission Test Question Solution 2023.pdfMohonDas
 
How to Add Existing Field in One2Many Tree View in Odoo 17
How to Add Existing Field in One2Many Tree View in Odoo 17How to Add Existing Field in One2Many Tree View in Odoo 17
How to Add Existing Field in One2Many Tree View in Odoo 17Celine George
 
What is the Future of QuickBooks DeskTop?
What is the Future of QuickBooks DeskTop?What is the Future of QuickBooks DeskTop?
What is the Future of QuickBooks DeskTop?TechSoup
 
How to Add a New Field in Existing Kanban View in Odoo 17
How to Add a New Field in Existing Kanban View in Odoo 17How to Add a New Field in Existing Kanban View in Odoo 17
How to Add a New Field in Existing Kanban View in Odoo 17Celine George
 
2024.03.23 What do successful readers do - Sandy Millin for PARK.pptx
2024.03.23 What do successful readers do - Sandy Millin for PARK.pptx2024.03.23 What do successful readers do - Sandy Millin for PARK.pptx
2024.03.23 What do successful readers do - Sandy Millin for PARK.pptxSandy Millin
 
5 charts on South Africa as a source country for international student recrui...
5 charts on South Africa as a source country for international student recrui...5 charts on South Africa as a source country for international student recrui...
5 charts on South Africa as a source country for international student recrui...CaraSkikne1
 
Education and training program in the hospital APR.pptx
Education and training program in the hospital APR.pptxEducation and training program in the hospital APR.pptx
Education and training program in the hospital APR.pptxraviapr7
 
How to Solve Singleton Error in the Odoo 17
How to Solve Singleton Error in the  Odoo 17How to Solve Singleton Error in the  Odoo 17
How to Solve Singleton Error in the Odoo 17Celine George
 
Ultra structure and life cycle of Plasmodium.pptx
Ultra structure and life cycle of Plasmodium.pptxUltra structure and life cycle of Plasmodium.pptx
Ultra structure and life cycle of Plasmodium.pptxDr. Asif Anas
 
UKCGE Parental Leave Discussion March 2024
UKCGE Parental Leave Discussion March 2024UKCGE Parental Leave Discussion March 2024
UKCGE Parental Leave Discussion March 2024UKCGE
 
How to Use api.constrains ( ) in Odoo 17
How to Use api.constrains ( ) in Odoo 17How to Use api.constrains ( ) in Odoo 17
How to Use api.constrains ( ) in Odoo 17Celine George
 
CHUYÊN ĐỀ DẠY THÊM TIẾNG ANH LỚP 11 - GLOBAL SUCCESS - NĂM HỌC 2023-2024 - HK...
CHUYÊN ĐỀ DẠY THÊM TIẾNG ANH LỚP 11 - GLOBAL SUCCESS - NĂM HỌC 2023-2024 - HK...CHUYÊN ĐỀ DẠY THÊM TIẾNG ANH LỚP 11 - GLOBAL SUCCESS - NĂM HỌC 2023-2024 - HK...
CHUYÊN ĐỀ DẠY THÊM TIẾNG ANH LỚP 11 - GLOBAL SUCCESS - NĂM HỌC 2023-2024 - HK...Nguyen Thanh Tu Collection
 
M-2- General Reactions of amino acids.pptx
M-2- General Reactions of amino acids.pptxM-2- General Reactions of amino acids.pptx
M-2- General Reactions of amino acids.pptxDr. Santhosh Kumar. N
 

Recently uploaded (20)

Quality Assurance_GOOD LABORATORY PRACTICE
Quality Assurance_GOOD LABORATORY PRACTICEQuality Assurance_GOOD LABORATORY PRACTICE
Quality Assurance_GOOD LABORATORY PRACTICE
 
Prelims of Kant get Marx 2.0: a general politics quiz
Prelims of Kant get Marx 2.0: a general politics quizPrelims of Kant get Marx 2.0: a general politics quiz
Prelims of Kant get Marx 2.0: a general politics quiz
 
HED Office Sohayok Exam Question Solution 2023.pdf
HED Office Sohayok Exam Question Solution 2023.pdfHED Office Sohayok Exam Question Solution 2023.pdf
HED Office Sohayok Exam Question Solution 2023.pdf
 
The basics of sentences session 10pptx.pptx
The basics of sentences session 10pptx.pptxThe basics of sentences session 10pptx.pptx
The basics of sentences session 10pptx.pptx
 
Philosophy of Education and Educational Philosophy
Philosophy of Education  and Educational PhilosophyPhilosophy of Education  and Educational Philosophy
Philosophy of Education and Educational Philosophy
 
How to Manage Cross-Selling in Odoo 17 Sales
How to Manage Cross-Selling in Odoo 17 SalesHow to Manage Cross-Selling in Odoo 17 Sales
How to Manage Cross-Selling in Odoo 17 Sales
 
Easter in the USA presentation by Chloe.
Easter in the USA presentation by Chloe.Easter in the USA presentation by Chloe.
Easter in the USA presentation by Chloe.
 
Diploma in Nursing Admission Test Question Solution 2023.pdf
Diploma in Nursing Admission Test Question Solution 2023.pdfDiploma in Nursing Admission Test Question Solution 2023.pdf
Diploma in Nursing Admission Test Question Solution 2023.pdf
 
How to Add Existing Field in One2Many Tree View in Odoo 17
How to Add Existing Field in One2Many Tree View in Odoo 17How to Add Existing Field in One2Many Tree View in Odoo 17
How to Add Existing Field in One2Many Tree View in Odoo 17
 
What is the Future of QuickBooks DeskTop?
What is the Future of QuickBooks DeskTop?What is the Future of QuickBooks DeskTop?
What is the Future of QuickBooks DeskTop?
 
How to Add a New Field in Existing Kanban View in Odoo 17
How to Add a New Field in Existing Kanban View in Odoo 17How to Add a New Field in Existing Kanban View in Odoo 17
How to Add a New Field in Existing Kanban View in Odoo 17
 
2024.03.23 What do successful readers do - Sandy Millin for PARK.pptx
2024.03.23 What do successful readers do - Sandy Millin for PARK.pptx2024.03.23 What do successful readers do - Sandy Millin for PARK.pptx
2024.03.23 What do successful readers do - Sandy Millin for PARK.pptx
 
5 charts on South Africa as a source country for international student recrui...
5 charts on South Africa as a source country for international student recrui...5 charts on South Africa as a source country for international student recrui...
5 charts on South Africa as a source country for international student recrui...
 
Education and training program in the hospital APR.pptx
Education and training program in the hospital APR.pptxEducation and training program in the hospital APR.pptx
Education and training program in the hospital APR.pptx
 
How to Solve Singleton Error in the Odoo 17
How to Solve Singleton Error in the  Odoo 17How to Solve Singleton Error in the  Odoo 17
How to Solve Singleton Error in the Odoo 17
 
Ultra structure and life cycle of Plasmodium.pptx
Ultra structure and life cycle of Plasmodium.pptxUltra structure and life cycle of Plasmodium.pptx
Ultra structure and life cycle of Plasmodium.pptx
 
UKCGE Parental Leave Discussion March 2024
UKCGE Parental Leave Discussion March 2024UKCGE Parental Leave Discussion March 2024
UKCGE Parental Leave Discussion March 2024
 
How to Use api.constrains ( ) in Odoo 17
How to Use api.constrains ( ) in Odoo 17How to Use api.constrains ( ) in Odoo 17
How to Use api.constrains ( ) in Odoo 17
 
CHUYÊN ĐỀ DẠY THÊM TIẾNG ANH LỚP 11 - GLOBAL SUCCESS - NĂM HỌC 2023-2024 - HK...
CHUYÊN ĐỀ DẠY THÊM TIẾNG ANH LỚP 11 - GLOBAL SUCCESS - NĂM HỌC 2023-2024 - HK...CHUYÊN ĐỀ DẠY THÊM TIẾNG ANH LỚP 11 - GLOBAL SUCCESS - NĂM HỌC 2023-2024 - HK...
CHUYÊN ĐỀ DẠY THÊM TIẾNG ANH LỚP 11 - GLOBAL SUCCESS - NĂM HỌC 2023-2024 - HK...
 
M-2- General Reactions of amino acids.pptx
M-2- General Reactions of amino acids.pptxM-2- General Reactions of amino acids.pptx
M-2- General Reactions of amino acids.pptx
 

Infectious disease of pathology

  • 2. Categories of infectious agents • • • • • • • Prion Viruses Bacteria Fungi Protozoa Helminths Ectoparasites
  • 3. PRION • Definition- Infectious particle composed of protein Definition (prp) • DiseasesHuman 1) kuru 2)Creutzfeldt- Jackob Disease (CJD) 3)Variant CJD AnimalBovine spongiform encephalopathy TransmissionIartogenically Surgery Organ transplantation Blood transfusion
  • 4. Pathogenesis- Prp normally found in neuron. Disease occur when prp conformational change protease resistant prp I Normal Protease I Abnormal Sensitive prp ------ prp ---Neuronal damage Inactivation- By protein and lipid disrupting agent such as Phenol Ether NaOH Hypochlorite
  • 5. New and Emerging infectious diseases • DefinitionNewly identified & previously unknown agent that appeared in human population & causes public health problem is known as emerging infectious disease.
  • 6. These includes1) Disease caused by newly developed strains/ microorganismEx- MDR-TB XDR-TB MRSA Chloroquine resistant malaria 2) Disease caused by pathogens, endemic in other species (birds) that recently entered into human populationEx-HIV, SARS 3) Disease caused by pathogens that have been present in human population but show recent incidence Ex-Dengue fever
  • 7. Factors contributing to emergence— 1)Enviornment– Climate & changing ecosystem Urbanization & deforestation 2)International travel 3)Breakdown of public health measures (war, overcrowding)
  • 8. Bioterrorism • Definition- Intentional release of viable bacteria, virus & toxin in order to harm people, animal/plant.
  • 9. • Category A -->Highest risk -->Easily disseminated/ transmitted from person to person -->High mortality • Anthrax- Bacillus anthracis • Botulism- Clostridium botulinum • Plague- Yersinia pestis • Small pox- Variola major virus • Viral hemorrhagic fever- Filovirus
  • 10. • Category B Moderately easy to disseminated Moderate morbidity but low mortality • Brucellosis- Brucella • Melioidosis- Burkholderia pseudomallei • Glanders- Mallei • Staphylococcal enterotoxin B • Epsilon toxin of Clost. perfringes • Food safety threats Salmonella, Shigella, E.coli • Water safety threatsV.cholerae, Cryptosporidium pavum
  • 11. • Category C • Emerging pathogensNipah virus Hanta virus
  • 12. Transmission & dissemination of microbes • ROUTE OF ENTRY • SKINNatural barrier1)Dense keratinized layer of skin 2)Low pH 3)Fatty acid- the growth of micro organism
  • 13. • Unbroken skin- • Penetrate through broken skin • I/V catheter • Schistosoma larva Release collagenase, elastase dissolve ECM penetrate swimmers skin • Superficial prick-Fungus • Wound-Staph • Burn-Pseudomonas • Bacteremia
  • 14. • Needle stick • Insect bite • Animal bite • HBV,HCV,HIV • Tick transmitRickettsiae-RMSF Brucella-Lyme disease • Flea--Y.pestis- plague • Mosquito-Malaria, Filaria • Sand fly- L.donavanileishmaniasis • Dog-Rabies
  • 15. • GIT • Natural defense1)Mucosal covering of intestinal epithelium 2) Mucosal antimicrobial agent-defensin 3)Lytic pancreatic enzyme & bile detergent 4)Normal flora 5)Secretory IgA
  • 16. 1)Enteropathogenic bacteria1)Staphgrow in contaminated food release enterotoxin food poisoning without multiplication in the gut. 2)V. cholerae, ETEC multiply inside the mucus layer covering gut epithelium exotoxin release watery diarrhea. 3)Salmoella,Shigella,Champylobacterinvade & damage intestinal mucosa & lamina propria ulceration, inflammation & hemorrhage dysentery. 4)S.typhisystemic infection.
  • 17. • FungusCandidal infection- mainly in immunocompromised person. • Intestinal protozoaGiardia lamblia Entamoeba histolytica Cryptosporidia
  • 18. • Intestinal helminthsAscaris lumbricoides gut obstruction/invade & damage the bile duct Hookworm IDA Diphyllobothrium latum vit B12 depletionmegaloblastic anemia T.Solium larva- encyst in muscle E. Granulosus larva-encyst in lung, liver
  • 19. • Respiratory tract• Natural defense1)Mucocilliary apparatus large particles are trapped. 2)Alveolar macrophage & neutrophil particle<5micro meter alveoli phagocytosed by alveolar macrophage & neutrophil.
  • 20. Mechanism1)Micro organism attached to lower respiratory tract & laryngeal epithelium ExampleInfluenza virus-has 2 cell surface proteins- – Hemagglutinin (function at the beginning of the infection) -Neuraminidase-(function at the end of the infection. They degrade the protective layer of mucus in respiratory tract)
  • 21. Influenza virus Hemagglutinin Neuraminidase Bind with epithelial surface receptor 1)Cleave the sialic acid allow the virus to release from host cell Host cell engulf the virus Replicate within the cell 2) the viscosity of mucus facilitate viral transit within respiratory tract
  • 22. 2) Impaired ciliary activityExample• H. Influenzae & B. pertussis- release toxin ciliary paralysis. • Mycoplasma pneumoniae- produce ciliostatic substances • Smoker/people with cystic fibrosis-chronic damage to mucociliary apparatus
  • 23. 3)Some respiratory pathogen avoid phagocytosis/destruction after phagocytosis Example• M tuberculosis- escape killing within phagolysosome of macrophage 4)Opportunistic fungus- infect when CMI /when leukocyte are in number. ExamplePneumocystis jirovechi in AIDS Aspergillus followed by chemotherapy.
  • 24. • Urinary tract • Natural defense Regular flushing of urinary tract by urine
  • 25. Spread & dissemination of microbes Some micro-organism proliferate locally at the site of infection & others spread to distant site vialymphatic's, blood & nerve. • Local- a) Confined to lumen of hollow visceraV. cholerae. b) Adhere /proliferate in/on epithelial cell- HPV/dermatophytes.
  • 26. Invasive• LymphaticsEx- Staphylococcus-localized abscess/furuncle through lymphatic  drain into regional lymph node sometimes bacteremia & colonize to distant organ. • Blood-Most of bacteria & fungus, Virus- HBV, Polio Protozoa- African trypanosoma All helminths. WBC- MTB,LD, Toxoplasma, HIV, Herpes RBC- Plasmodium, Babesia • Nerve- Polio virus
  • 27. Placental-fetal route• BacteriaMycoplasma placentitis premature delivery/still birth. T.Pallidum2nd trimester osteochondritis, periostitis leads to multiple bony lesion. • VirusRubella1st trimester-Congenital heart disease, Cataract, Deafness. 3rd trimester-Little damage
  • 28. • Infection during passage of birth canalRickettsia/Chlamydia-Conjuctivitis • Milk- CMV,HBV,HTLV-1
  • 29. Release of microbes from the body It depends on the location of infection. Transmission from person-person• Respiratory route- Virus & bacteria. • Saliva- EBV, CMV, Mumps • Feco-oral route- HAV, HEV , Rota virus, Hookworm, Schistosomes • Blood & blood product- HBV, HCV,HIV • Sexual transmission
  • 30. • Transmission from animal-human1) Direct contact / Consumption of animal fat Ex- Bacillus anthracis. 2) Indirectly via invertebrate host. Ex- Malaria – by mosquito.
  • 31. Sexually Transmitted Infection • Definition- Infection that are transmitted through sexual route. • High risk group1)Adolescent 2)Homosexual men 3)Illegal drug abuser • Site- Initial siteVagina Rectum Urethra Oropharynx
  • 32. General featuresInfection with 1 STI associate organism the risk for additional STI Ex- N. Gonorrhea/ Chlamydia trachomatis epithelial injury local tissue damage chance of co-infection with the other & also the risk of HIV infection. . STI can spread by vertical transmission & causes severe damage to fetus/ child Ex- Chlamydia trachomatis Conjunctivitis Syphilis Miscarriage
  • 33. Examples of STI • Bacteria • • • • • Neisseria gonorrhoeae Treponema pallidum Haemophilus ducreyi Klebsiella granulomatis Chlamydia trachomatis • Ureaplasma urealyticum • • • • • Gonorrhea Syphilis Chancroid Granuloma inguinale Lymphogranuloma venereum • Urethritis
  • 35. Nosocomial Infection • Definition These are hospital acquired infection which develops 48hrs after hospitalization /within 48 hrs after release from hospital. Source 1)Hands of health worker 2)Contaminated surface 3)Used equipment & instrument 4)Blood transfusion 5)Organ transplantation
  • 36. Organism causing Nosocomial Infection • Bacteria• Gram positive • • • • • • Gram negative • Pseudomonas • Proteus • E coli Staph aureus MRSA,VRSA Staph epidermidis Strep pneumoniae Clostridium tetani
  • 37. • Virus • Fungi • Parasite • HBV,HCV,HDV • HIV, HSV,CMV • Candida • Pneumocystis jiroveci • Toxoplasma
  • 38. Risk factor• • • • • • Long time hospital stay Mechanical ventilation I/V catheter Use of indwelling catheter Overdose of antibiotic Failure of health care worker to wash hand.
  • 39. • Prevention 1) Frequent hand washing can transmission of MRSA & VRE. 2) Proper sterilization & disinfection of inanimate object of the hospital. 3) Proper disposal of hospital waste. 4) Rational use of antibiotics. 5)Personal hygiene of patient, attendants, doctor & medical stuff. 6) Detection of proper carrier & proper diagnosis.
  • 40. Host defense against infection • 1) Innate immunitya) Intact skinSebaceous gland--> contain fatty acid antibacterial & antifungal Low pH- antimicrobial. b) Mucous membraneMucociliary apparatus- prevent the entry of microbes through URT Lysozyme in tear & mucus- degrade peptidoglycan layer of bacterial cell wall protect from infection.
  • 41. c) Cellular componentMacrophage, neutrophil phagocytose the microbes. N-K cellproduce toxic substances perforin destroy microbes. d) Soluble componentComplement activation-->formation of MAC destroy cellular Ag. IFNα, IFNβ –released by virus infected cell this IFN replication of viruses. (that’s why viral infection are self limiting)
  • 42. • 2) Acquired immunity- develops after exposure to microbes. They are B & T lymphocyte. Ex- Measles virus enters into the body Ab production Ab binds with measles virus Virus eliminated Provides specific immunity
  • 43. How micro-organism causes diseaes • By 3 mechanisms1)They can directly enter into host cell causes cell death. 2)They may-release toxins kill the cell 3)They may-release enzymes degrade tissue components/damage blood vessel ischemic necrosis. 4)They induce host cell responses causes additional damage.
  • 44. Mechanism of viral injury Virus can directly damage the host cell by entering & replicating within it. • Virus has a affinity for specific body tissue which is determined by – 1)Presence of receptor on host cellExgp120 of HIV binds with CD4 on Tcell CXC R4(T cell) CCR5(macrophage) gp350 of EBV binds with CR2/CD21 on B cell
  • 45. 2) Cellular transcription factor that recognize viral enhancer & promoter sequence Ex- JC virus causes leuko encephalopathy, replicate specially in oligodendroglia in CNS. (B/c enhancer & promoter sequence regulating viral genes are active in glial cell). 3) Physical barrierEx- Entero virus replicate in intestine b/c they can resist inactivation by acid, bile & digestive enzyme. 4)TemparatureEx- Rhinovirus infect only within URT b/c they replicate at lower temperature of URT.
  • 46. Virus can damage the host cell by a number of mechanism• 1) Direct cytopathic effect- Virus can kill the cell directly bya) Prevent the synthesis of host macromolecules (DNA,RNA/protein) Ex-Polio virus- inactivate cap binding protein which is essential for translation of host cell mRNA. b) Producing degradative enzyme & toxic proteins Ex- HSV-Produce protein that synthesis of cellular DNA & mRNA & other proteins that degrade host DNA. c) Inducing apoptosis by producing pro-apoptic protein Ex- HIV vrp protein.
  • 47. 2)Anti viral immune response• Viral protein on the surface of host cell may be recognized by immune system & lymphocyte may attack the virus infected cell. Ex- In HBV infection, acute liver failure is caused by cytotoxic T cell mediated destruction of infected hepatocytes. 3)Transformation of infected cells--> benign/ malignant neoplasm • Oncogenic virus stimulate cell growth & survival by following M/AExpression of virus encoded oncogene Anti-apoptic strategies Insertional mutagenesis
  • 48. Mechanism of bacterial injury • 1) Adherence to the host cell surfacea) Adhesin - is present in bacterial cell surface. Through this they bind to host cell/ECM. Ex- Strep. pyogens adhere to host tissue by protein F & teichoic acid. b) Pili Ex- E.Coli through P pili bind with gal-gal moiety of uroepithelium. c) Glycocalyx Ex-Stap. epidermidis/ Strep. viridians bind with heart valve.
  • 49. • 2)Virulence of intracellular bacteria• Facultative intracellular bacteria infect  -->Epithelial cell (Shigella, ETEC) -->Macrophage (MTB,ML) -->Both (S. typhi) • Growth of bacteria in cell may allow the bacteria to escape the immune system /facilitate the spread. Ex- MTB macrophage lung to other site.
  • 50. Bacteria have a number of mechanism to enter into the cella) Bacteria is coated with Ab/ complement  phagocytosed by macrophage. • Ex-MTB activate alternative pathway of complement opsonization with C3b C3b coated MTB bind with CR3 on macrophage endocytosis into macrophage. b) Gm- bacteria use complex secretion system to enter into epithelial cell. • This system consists of needle like structure form pore inside host cell membrane inject protein rearrangement of cell cytoskeleton bacteria entry. • Ex- L. monocytogenes.
  • 51. c) Effect of bacteria inside the host cella) b) Shigella, E. coli- host protein synthesis within 6 hours host cell lysis. Within macrophage most bacteria killed when phagosome fuse with lysosome & form phagolysosome. But certain bacteria evade this defense. Ex- MTB- block the fusion of phagosome with lysosome unchecked MTB proliferation within macrophage. L. Monocytogenes- produce pore forming protein-listeriolysin O & 2 phospholipase degrade phagosome membrane bacteria escape into cytoplasm.
  • 52. 3) Toxin production• A) Endotoxin- is a LPS, component of Gm- bacterial cell wall. It is both beneficial & harmful. BeneficialActivate protective immunity.  Induction of cytokine & chemokine  expression of co-stimulatory molecules enhance T cell activation. Harmful- High level of LPS induction of excessive level of cytokines TNF, IL-1,IL-12Septic shock, DIC, ARDS.
  • 53. • B) Exotoxin- secreted from bacteria & causes celluar injury. 1)Enzymes- bacteria secret protease, coagulase, hyaluronidase, fibrinolysin Ex• Stap. aureus produce protease degrade protein that hold keratin together detachment of epidermis from deeper skin.
  • 54. 2)Toxin that alter intercellular signaling & regulating pathway— • Most of the toxins have A sub unit- enzymatic activity B sub unit- binds with the receptor on cell surface & delivers the A subunit into cell cytoplasm. Ex- Bacillus anthracis, V. cholerae.
  • 55. 3) Neurotoxin• Clostridium botulinum, Clostridium tetani • release of neurotransmitters paralysis respiratory failure death. • 4) Super Ag• Stimulate T lymphocyte massive Tcell proliferation & release of cytokines high level of cytokines Capillary leakage & shock.
  • 56. Injurious effects of host immunity 1) Immune response to microbes sometimes causes tissue injury. • a) MTB- causes granulomatous inflammation--delayed hypersensitivity prevents the spread of bacilli but also causes tissue damage & fibrosis. • b) HBV,HCV- causes liver damage due to immune response to infected hepatocyte, not to cytopathic effect .
  • 57. . 2)Humoral immune response to microbes has also pathological consequence • S. pyogenes- Ab produce against streptococcal M protein cross react with cardiac protein damage heart valve RHD. • S. pyogenes- anti streptococcal Ab cross react with glomerular basement membrane  form Ag-Ab complexes deposit in renal glomeruli Post streptococcal GN.
  • 58. • 3)Infection may be associated with chronic inflammatory disorder as well as cancer. Ex• HBV/HCV Hepatitis HCC • H.Pylori Gastritis gastric adenocarcinoma • Schistosomia Chronic cystitis bladder carcinoma.
  • 59. Immune evasion by microbes Micro organism develops many M/A to evade host immune system. 1) Growth in niches that are inaccessible to host immune response a) Microbes are multiply in the lumen of the intestine (C. difficili) / gall bladder (S. typhi) b) Some organism are rapidly invade host cell before humoral immune response become effective. Ex• • Malarial parasite--sporozoite enters into hepatocyte. Trichinella/T. cruzei-enters into skeletal/cardiac muscle.
  • 60. c) Some Parasite form cyst in host cell. Ex- Tapeworm d) During viral latency, viral genes are not expressed. Ex- Herpes virus
  • 61. 2)Antigenic variationVirus can escape immune attack by changing their Ag. Mechanism • High mutation rate • Genetic ressortment • Genetic rearrangement • • • • • • • • HIV Influenza virus Influenza virus Rota virus N. gonorrhoeae Borrelia Trypanosoma Plasmodium
  • 62. 3) Resistance to innate immune response • Resistance to antimicrobial peptide (defensin, cathelicidins& thrombocidin)prevents killing of microbes by neutrophil & macrophage. • Carbohydrate capsule -present on the surface of the micro organism prevent phagocytosis by neutrophil. • Ex- Pneumococci, meningococci, H.influenza
  • 63. • Bacteria by covering with host protein -evade immune defense. Ex- Staphylococcus aureus covered by protein A that bind with Fc portion of Ab phagocytosis. • Some bacteria secret protease degrade Ab. Ex- Niesseria, Haemophilus, Streptococcus • Some organisms replicate within phagocytic cell. Ex- MTB, Liesteria, Leishmania, Trypanosoma, Toxoplasma, Cryptococcus neoformans.
  • 64. • Virus can produce molecules that innate immunity. Ex- Herpes virus, Pox virus produce protein block complement activation. • Some virus produce homologous of IFNα ΙFΝβ /IFN R which the action of IFN. 4) Recognition of infected cell by CD4 TH cell/ CD8 cytotoxic T cell. Ex- HSV,CMV,EBV bind/ alter the localization of MHC-1 impair the peptide presentation to CD8 T cell.
  • 65. Infection in immunosuppressed hosts • Inherited• 1)Patient with Ab deficiencyEx- X-linked aγglobulinaemia• • • • Severe bacterial infectionStrep . pneumoniae Haemophilus influenzae Stap. Aureus • 2)T cell defect- susceptible to infection with intracellular pathogens, virus, some parasite.
  • 66. • 3) Complement deficiency• Strep . pneumoniae • Haemophilus influenzae • Neisseria menigitidis • 4) Defect in neutrophilic function• Stap. Aureus • Gm- bacteria • Fungi
  • 67. Acquired• 1) AIDS • 2) Impaired production of leukocyte leukemia fills the bone marrow with cancerous cell & vulnerable to infection. • 3)Iartogenic cause of immunosuppression• Ex-Immunosuppressive drug. • Disease of organ systems other than immune system• Cystic fibrosis---- RTI with P. aeruginosa • S. aureus • Sickle cell disease----Strep. pneumoniae • Burn---- P. aeruginosa.
  • 68. Spectum of inflammatory responses to infection • 5 major histological patterns of tissue reaction in infections are1) Suppurative inflammation2)Mononuclear & granulomatous inflammation 3)Cytopathic- cytoproliferative reaction4)Tissue necrosis5) Chronic inflammation & scarring-
  • 69. 1) Suppurative inflammationCharacterized by production of large amount pus/purulent exudates consisting of neutrophil, liquefactive necrosis & edema fluid. • Sometimes the lesion are destructive. Ex- Pneumococci spare alveolar wall lobar pneumonia. Staphylococci & Klebsiella destroy alveolar wall form abscess fibrosis.
  • 71. 2)Mononuclear & granulomatous inflammation Granulomatous inflammation- is a distinctive pattern of chronic inflammation characterized by accumulation of activated macrophagesepithelioid cells which may fuse to form giant cells. In some cases there is a central area of caseous necrosis. • Ex- TB
  • 72. Mononuclear cell predominate• Plasma cell abundant Primary & secondary syphilis. • Lymphocyte predominate HBV infection/viral infection of brain.
  • 74. 3) Cytopathic- cytoproliferative reactionIt is characterized by cell necrosis/cellular proliferation, usually with scattered inflammatory cell. a) Some virus replicate within cytoplasm/nucleus & visible as inclusion body. • Ex-Herpes virus, Adeno virus.
  • 75. b) Some virus induce cell to fuse & form multinucleated giant cell. • Ex- Warthin- Finkeldy cells in measles. Herpes virus. c) Some virus causes epithelial cell to detach & form blister • Ex- Herpes virus. d) Some virus causes epithelial cell to proliferate & form wart. • Ex- HPV, Pox virus. e) Finally they contribute to develop malignant neoplasm.
  • 76. 4)Tissue necrosisEx- • Clostridium perfringes- secret toxin gangrenous necrosis. • E. histolytica- liquefactive necrosis. • Herpes virus (brain)/ HBV (Temporal lobe)-severe necrosis. • 5) Chronic inflammation & scarringEx- • Chronic HBV cirrhosis • Schistosoma egg Pipe-stem fibrosis of liver • TB Constrictive fibrous pericarditis.