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Infectious Disease
disorder in which tissue damage or dysfunction is produced by a MO
Virulence
capacity of an MO to achieve infection
To establish infection the MO must:
  1. gain access to the body
  2. avoid host defenses
  3. accomodate to grow in the human
  4. parasitize human resources: Tissue damage (not a commensalism anymore)
Tissue damage by MOs
  1. contact/enter host cells & directly cause cell death
  2. release toxins that kill @ a distance; or release enzymes that degrade tissues or damage blood vessels
  3. induced host cellular response that cause addtnl tissue damage (immune-mediated mechanisms)
Viral Injury
virus = small obligate intracellular parasites

directly damage host cells by entering & replicating (by using host metabolic components) w/in them

Tissue Tropism
viral predilection to infect certain cell types

determined by
  • binding to a specific cell surface protein: (Ex. HIV binds CD4 & CXCR4 on T cells)
  • cell type specific transcription factors (Ex. JC virus can only proliferate in oligodendroglia)
Virus host cell killing
Viruses kill host cells by:
  • inhibiting host DNA/RNA, protein synthesis: Polio virus
  • damaging the plasma membrane: HIV
  • lysing cells: Rhino & Influenza viruses
  • Inducing an immune response against host infected cells
Alteration of fxn & morphology in host infected cells
  1. Vacuolation/Condensation of nucleus & cytoplasm/Rapid or slow
  2. Viral induced neoplastic transformation: proliferation of infected epithelial cells (Ex. Pox viruses & HPV)
  3. Viral infected cells formation of inclusions: inclusion bodies are formed during synthesis in the cytoplasm or nucleus (Ex. HSV, Rabies, Pox group, measles, adenovirus)
  4. Variable viral alteration of cellular morphology-cytoskeleton: Giant cells formed (Ex. HSV, Measles= Warthin-Finkeldey cells, Parainfluenza, RSV)
Giant cell formation
Division of the nucleus WITHOUT division of the cytoplasm or fusion of cytoplasmic membranes
Host immune response generates tissue injury
  • Granulomatous response: aims to sequester the pathogen but can --> tissue damage & fibrosis
  • Ex. Immune response against HBV infected liver cells-->liver damage
  • Ex. Poststreptococcal glomerulonephritis: Anti-sprept antibodies:antigen complexes deposit in glomerular basement membrane, activate complement & produce nephritis
Histologic patterns of tissue reaction in infections
  1. Supperative (PMN) inflam.
  2. Mononuclear & Granulomatous inflam.
  3. Cytopathic-cytoproliferative inflam.
  4. Necrotizing inflam.
  5. Chronic inflam. & scarring
Suppurative (Polymorphonuclear) Inflammation
  • Histologic patterns
PMNs are attracted to site by chemo-attractants from pyogenic bacteria (extracellular Gm +/- cocci & Gm. - rods)

PMNs (alive/dead) + cell debris = pus
Mononuclear & Granulomatous Inflammation
  • Histologic Patterns
  • Acute inflam. response to viruses, intracellular bacteria/parasites
  • Chronic inflam. response to shirochetes & helminths
  • Reflects cell-mediated immune responses
  • Granulomatous inflammation: epithelioid cells can fuse to form giant cells
  • Possible central area of caseous necrosis
Granulomatous Inflammation
usually evoked by agents that resist eradication
  • M. tuberculosis
  • Histoplasma capsulatum
  • Shistosoma eggs
Characterized by accum. of activated MΦ (epithelioid cells) that may fuse to form giant cells
Cytopathic-Cytoproliferative Inflammation
  • Histologic patterns
  • usually produced by viruses
  • lesions characterized by cell necrosis or cellular proliferation
  • few inflammatory cells
  • focal cell damage in skin--> detached epithelial cells--> blister
Necrotizing Inflammation
  • Histologic Patterns
  • powerful toxins--> gangrenous necrosis (rapid, severe)
  • Tissue damage = domininant feature
  • Few inflammatory cells present
  • Lesions resemble infarcts
Clostridia: gets into muscle tissue by trauma or infection of the bowel in a neutropenic host

Entamoeba histolytica: causes colonic ulcers
Viral Necrotizing Inflammation
Viruses (different mechanisms)--> necrosis of host cells--> destruction of the liver by acute HBV infx (w/ inflammation), or of the temporal lobes by herpes virus
Chronic Inflammation & Scarring
  • Histologic Patterns
Exuberant scarring --> organ dysfunction
  • Ex. Schistosoma--> fibrosis of the bladder wall (caused by Schistosome eggs), Mycobacterium tuberculosis--> constrictive fibrous pericarditis
Chronic HBV infx.--> cirhosis of the liver--> dense fibrous septae around nodules of regenerating hepatocytes
Different Types of Infection: Viral
  1. Transient infections
  2. Chronic latent infections (HSV)
  3. Chronic productive infections
  4. Transforming infections
Transient Infections
Produced by structurally heterogenous viruses

Elicit a succesful immune response that eliminates the virus

Does NOT mean lifelong immunity

Some affect skin & produce a specific erythema
Transient Infections: Serotype
ONE serotype = infx. only once (Ex. Measles)

Antigenic variation = repeated infxs in same individual (Ex. Influenza)

Immune response lessens over time = same serotype can repeatedly infect (Ex. RSV)

Viral Portal Entry
respiratory, GI/GU, skin
Viral Spread
bloodstream, lymphatics, nerves
Viremia
virus in circulating blood
Transient infections
  1. Measles
  2. German Measles
  3. Small pox
  4. Mumps
  5. Poliovirus
  6. Arboviral diseases: St. Louis, Colorado tick fever, West nile
  7. Hemorrhagic fevers: Arenaviruses, Filoviruses, Bunyaviruses, Flaviviruses (Yellow fever, Dengue)
  8. Parainfluenza Virus PNA
  9. Respiratory Syncytial Virus
  10. Coronavirus-SARS
Measles aka Rubeola
  • Clinical
Usually kids (BAD if malnourished)

Transmission: DROPLET

Clinical: prodromal fever, tracheo-bronchitis, coryza, conjunctivitis interstitial PNA
If malnourished: kerratitis w/ scarring & blindness, diarrhea w/ protein-losing enteropathy, encephalitis, hemorrhagic rashes = "black measles"
SSPE = rare, late complication


Measles
  • Skin
Blotchy reddish brown rash-behind ears, trunk, face, extremities

Vascular congestion & pervascular mononuclear infiltrate
Koplik Spot
  • Measles
buccal mucosa ulceration near opening of Stensen salivary duct: necrosis, neutrophil exudate, neo-vascularization
Warthin-Finkeldey (W-F) Cells
  • Measles
In lymphoid organs, germinal follicle hyperplasia, giant cells w/ eosinophilic inclusions in nucleus & cytoplasm
German Measles aka Rubella
caused by Togavirus
Usually in kids

Highly contagious, but mild: swollen tender lymph nodes (posterior cervical, auricular & epitrochlear) regions

2nd-3rd day: measles-like rash appears, starts on face & spreads downward as it clears on the face
Congenital Rubella
Placental Transmission

Severe congenital malformations in fetus: Microphtalmia & Cataract & Cardiac
Small Pox (Variola Virus)
eradicated through vaccination

high mortality

widespread vesicular & pustular skin lesions
Mumps (Contagious parotitis)
Transmission: inhalation of droplets--> viremia --> general infection

Virus develops in salivary glands --> parotitis & submaxilitis

Microscopy: exudation & interstitial mononuclear infiltrate

May infect CNS (meningitis & encephalitis) & pancreas, possible post mumps diabetes

Common complication: orchitis-->male sterility
Complications of Mumps
Pancreatitis (fat necrosis & PMN rich inflammation)--> post mumps diabetes

Orchitis: inflammation of testicle: usually unilateral, painful, hemorrhage, parenchymal swelling may compromise the blood supply & cause infarction of tunica albuginuea--> scarring & male sterility
**
most freq. inflam in GU of males = epididymitis (NOT orchitis)
Poliovirus infections (Enteroviruses)
Transmission: Fecal-oral route-->oro-pharynx-->saliva secretion & swallowing of virus--> multiplucation in intestinal mucosa & lymph nodes-->transient viremia & fever

Most
infx = asymptomatic (bc antiviral antibodies usually clear, not known why they don't sometimes)
Symptomatic Polio
  • Poliovirus infections
1/100 infected, invasion of CNS: replicating in motor neurons (spinal poliomyelitis) or brain stem (bulbar poliomyelitis)

Morphology: mononuclear cell perivascular cuffs & neuronophagia of Anterior Motor Neurons
Spread may be: secondary to viremia or by retrograde transport along axons of motor neurons
Polio Vaccination
10% of toddlers (<3yoa) in USA,  not vaccinated in poor areas (CDC)

Sabin vaccine: Live Attenuated
No longer used in US bc virus in vaccine has mutated & rarely caused poliomyelitis
Arboviral Diseases (USA)
Arthropod-borne viruses = transmission through blood sucking ticks & insects
  • St. Louis encephalitis virus
  • Colorado tick fever virus
  • West nile virus
St. Louis Encephalitis Virus
animal host, reservoir=birds; vector=mosquitoes
Colorado Tick Fever Virus
  • high fever
  • chills
  • joint & muscle pains
  • severe HA
  • ocular pain
  • coagulopathy
  • GI bleeding
  • encephlalitis
Children: may have hemorrhagic manifestations-->GI bleeding or encephalitis
West Nile Virus
arthropod borne: transmitted by mosquitos to wild birds (reservoir) & mammals (incidental host)

can be transmitted by transplanted organs

Outbreaks: Agrica, Middle east, europe, SE asia, Australia, 1999 NYC:(62 cases, 7 deaths)
West Nile Virus
  • Clinical
Greatest risk= IC ppl. & elderly

Usually asymptomatic (20% mild, febrile illness, HA, myalgia, rash)
Complications: 1/150 clinically apparent infx--> CNS (meningitis, encephalitis), acute flaccid paralysis (clinically indistinguishable from polio)
Rare: hepatitis, myocarditis, pancreatitis (Mortality 10%)



West Nile Virus
  • Morphology
mononuclear cell perivascular & leptomeningeal chronic inflammation, microglial nodules, neuronophagia in temporal lobes & brain stem
Viral Hemorrhagic Fevers (VHF)
systemic infx. characterized by fever & hemorrhage

viruses are restricted to areas where insect host resides

potential biologic weapons

humans are NOT natural reservoir for ANY the VHFs, cases are sporadic & unpredictable

Human-to-human transmission

Virus enters by: bite, inhalation, mucous membrane
Types of VHF
  • Arenaviruses (Lassa, etc.)
  • Filoviruses (Marburg & Ebola)
  • Bunyaviruses (Congo-Crimean hemorrhagic fever virus & hantavirus)
  • Flaviviruses (Yellow fever, Dengue)
Clinical aspects of VHF
Mild acute: fever, HA, myalgia, rash, neutropenia, thrombocytopenia, hemorrhage
Severe disease: hemorrhage, sudden hemodynamic & shock

Infection of endothelial cells & immune complex formation--> increased vascular perm, thrombocytopenia, necrosis & hemorrhage in organs (liver), MINIMAL INFILTRATE, disseminated intravascular coagulation (DIC)

no cures or therapies
Yellow Fever
  • Flavivirus
  • Africa, Central & South America
  • Mammal host: monkeys
  • Vector: mosquitoes
  • Clinical: bleeding from GI tract--> hemorrhage resembling coffee grounds=hematemesis, Liver damage--> jaundice, renal damage
Morphology: hepatocyte necrosis w/ fatty degeneration & eosinophilic intra-nuclear inclusions (Councilman bodies)
Hemorrhagic Dengue Fever
  • Flavivirus
Vector = mosquitoes
SE asia, Indonesia, Pakistan, Caribbean epidemics

Cutaneous & intestinal hemorrhage; thromobocytopenia; shock

Clinical: severe, rash (capillary vasodilation), blanching @ pressure, scleral hemorrhages, ecchymoses & subcutaneous hemorrhage-->fatal outcome
VIRAL respiratory disorders
  • transient infections
  • Common cold: URT infx.
  • Viral PNA: LRT infx
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