PATHOBIOLOGY MICROBIOLOGY SUMMARY

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 Bacteria
Yersinia pestis Yersinia Bacillus anthracis C. tetani C.perfringens Neisseria
{plague} enterocolitica Anthrax meningitidis
{diarrhea}
Morphology  Gm-ve bacilli  Gm-ve bacilli - Gram+ve bacilli , - Slender, motile, - Large, Gm+ve - Gm-ve
 Capsulated at 37oC(at  Non-spore Non-motile arranged Gm+\ve rods bacilli non diplococcic
tissue) and non- forming in chains - Spores placed at motile. - flattened &
capsulated at flea bacilli - Has polypeptide one end giving - Spores are oval concave at sides
temperature  Motile at 25 capsule a drumstick &The bacilli are “bean-shaped”
 Bipolar staining with and non- Spores are oval and appearance often capsulated - Intra PMNLs
Wayson stain pin like motile at 37 central in position in tissues
appearance degrees
 Non motile, non-spore
forming
Culture - Facultative anaerobe - Aerobe and - Strict anaerobe  Anaerobe & - Anaerobe
- Grow better at 25 than 37 degrees facultative anaerobe. - They grow on Grows best on - Grow at 37o
- NLF on McCoy's agar - Grows on ordinary ordinary media CHO containing - needs (5-10%)
- Definitive identification by immunoflurecent media at 37 C. & on blood agar media. CO2
- On agar  grayish, swarming  On horse blood - grows better on
granular, circular &haemolysis. agar,  double blood
discs resembling a - The organism zone of hemolysis; containing
grows readily - a zone of complete media
hair lock (Medusa
hemolysis
head appearance) on cooked meat - selective media
broth - a darker zone of  Thayer-
incomplete
Martin
hemolysis
**Grow rapidly on blood
and fluid medium and
slowly on solid medium =48
hrs.

BACTERIA 2
Biochemical I CO U (- + - -)NLF
tests  Indole –ve
 Catalase +ve
 Oxidase –ve
 Urease –ve
 NLF on McCoy's agar
Virulence PLC
factors 1- Plasminogen-activating
proteaseit is temp.
dependent :
**coagulase at: 20-28 D.
flea temp.( Blocking)
**fibrinolytic at: 35-37 D.
Host temp.
(Dissemination)
2- Lipopolysaccharides
endotoxin
3- Capsuleanti-
phagocytic activity
BACTERIA
CO U (+ - +)NLF 1. Ferment sugar with  asaccharolytic  (Saccharolytic).  Oxidase +ve
 Catalase +ve the production of slowly liquefy  In cooked meat  acid production
 Oxidase –ve acid only gelatin broth medium is from glucose &
 Urease +ve saccharolytic reddened with sour maltose
 NLF on 2. Catalase +ve smell.
McCoy's agar Liquefy gelatin giving  Grows in litmus
the “inverted fir-tree” milk medium
appearance producing acid and
gas “stormy clot”
reaction.
 Grows on egg-
yolk medium
producing zones of
opacity due to
lecithinase activity
(Nagler’s
reaction)
1. An extracellular ** Toxins produced **There are 5 types 1- pilli 
toxin {protective by C. tetani: of C. perfringens (A- adherence
antigen, lethal Tetanospasmin: E) 2- polysaccharide
factor, and edema is a very potent  Alphatoxin capsule  anti-
factor}cytolytic toxin, extremely (lecithinase)destr phagocytic
to macrophages small amounts  oy cell membranes. 3- outer membrane
causing edema and lethal for humans. Hyaluronidase, protein 
shock biologic  Tetanolysin: is collagenase adhesion
warfare. an oxygen-labile spread of infection. 4- lipo-
2. Capsular hemolysin.  Enterotoxin by polysaccharide
polypeptideinhib C.perfringens which  antitoxin
its opsonization and cause food poisoning 5- IgA protease
phagocytosis (type Aalters the
permeability of the
enterocyte
3
 Pathogenesis

Yersinia pestis Yersinia enterocolitica

Neisseria Meningitidis
{plague}: {diarrhea}

- Ingestion of contaminated food and - Droplet from patient / carrier …

drinks with y. enterocolitica which is
present in the intestine of animals: cattle,
sheep's…
- Man become infected
- Suffer from acute enterocolitis
- Man become infected
- the organism attaches itself to cells of
nasopharynx
- It may enter blood stream

Bacillus anthracis
*Factors which help spore
“Anthrax” C. tetani C.perfringens germination are:
1. Traumatic wounds with
1. Gas gangrene deep devitalized tissue.
(clostridia myonecrosis) 2. Foreign bodies.
3. Impaired blood supply
4. Mixed pyogenic
infections

*Plague is an infection of rodent 2. Endometritis

2. Endometritis
transmitted between them and to man by
fleas' bites Infection of a post-partum uterus
**C. tetani is non invasive necrosis of uterine tissue
Cause millions fatalities  Black Death
*Death usually results from interference intravascular hemolysis  septicemia
with the mechanics of respiration.
BACTERIA 4
 Clinical Picture
Yersinia pestis Yersinia Bacillus anthracis C. tetani C.perfringens Neisseria
enterocolitica meningitidis
Bubonic Pneumonic Septicemic **Acute Cutaneous Inhalation 1. Muscular Gas gangrene 1. Bacteremia:
plague plague plague enterocolitis anthrax anthrax spasms at Occurs in small
(malignant (Woolsorters' site of Endometritis percentage of
pustule) disease): infection patients
2. jaw lock
- lymphatic Primary - High 1. Fever Spores enters Haemorrhagic food poisoning
3. interferenc
gland of (direct level of 2. Abdominal through pneumonia 2. Meningitis:
e with
groin inhalation) , bacterem pain  at abrasions in the Organisms reach
mechanism
swell, severe ia before right lower skin  Gastrointestin through blood 
s of
The spores al anthrax meninges
V.painfull respiratory buboes quadrant as respiration
germinate
- mortality distress& - Symptom appendiciti  multiply
multiply
rate 50- mortality s very s  Injection  acute inf.
70% rate 100% sever& 3. Diarrhea(w At the site of anthrax response
- Secondary poor atery) entry a papule (↑↑ PMNLs)
(metastatic prognosis 4. Heat stable vesicle  purulent
from bubonic) - Mortality enterotoxin pustule meningitis
rates invade necrotic
100% blood& LN black crusty 3. Joint symptoms &
ulcer petechial rash
**characteristic “PATHOGNOMONIC OF
central black MENINGOCOCCAL
eschar  Death MENINGITIS”

 Headache – vomiting
– fever – stiff neck -
coma

Lab diagnosis
1) Specimen 1) Specimen: 1) Specimen 1. Specimen  Specimen Specimen A. Clinical A. Clinical Specimen CSF, blood,
aspiration patients Blood aspiratio fluid from Sputum or (Mainly) (mainly ) aspirate from
from the sputum n from the vesicle. pleural fluid once as B. Laboratory: nasopharyngeal swab
enlarged LN. **2, 3,4 as enlarged  Smear are obtained tetanus, - Specimen: wound
**2, 3,4 as the  LN.  large gm+ve 2, 3,4 as the treatment with exudates Smear  neisseria
2) EM the  Bubonic 2. Cold bacilli spores  malignant antitoxin particularly from inside PMNLs
film shows Bubonic plague enrichment are not present pustule should start at
the deeper parts
short Gm-ve where the
plague film once
bacilli infection seems to
BACTERIA 5
3) Culture shows  Culture B. Lab be most Culture 
 blood agar, short Gm- *Colonies Diagnosis pronounced. Oxidase +ve
maCconky's ve bacilli medusa -Specimen: - Direct Gram- Gm film
then 3. Culture  head {Nutrient wound stained smear: Acid production
biochemical& The presence of
maCconky agar}. exudates Serotyping 
immunoflurece Gram-stained large Gram
'sNLF *Colonies  positive rods is
agglutination
nt. smear: drum
non-hemolytic suggestive
4) Serology
4. Biochemic on{blood stick Culture : Non - Culture 
In un- appearance.
al tests: agar}. On blood agar PCR
vacinated -Culture
CO U (+ - incubated Latex agglutination
patient titre Into cooked
+)NLF  Definitive anaerobically.
16 meat: growth - Identification: BY
identifi-
suggestive& leads to *Morphology
cation
Rising titre blackening of *Biochemical
*Detection
diagnostic the medium. tests as mentioned
capsule by
Onto blood before.
fluorescent
agar, incubated *MALDI-TOF
antibody
anaerobically, it MS: is a rapid and
*Identification
shows a sensitive method
of toxin genes
swarming for identification
by (PCR)
growth and of invasive
haemolysis Clostridium
(due to species recovered
tetanolysin). in culture
Identification
A) Biochemical
tests
b)Animal
pathogenicity
test: The
unprotected
animal dies of
tetanus while
the protected
control
remains alive

BACTERIA 6
 Prevention
Yersinia pestis Bacillus anthracis C. tetani C.perfringens Neisseria meningitidis
1. Vaccination : 1. Disposal of animal (1) active immunization with 1. Administration of 1. Detection of carriers:
killed whole-cell bodies toxoids; antibiotics early nasopharyngeal swab 
vaccine was used, 2. Decontamination - “DPT”{ tetanus toxoid, 2. cleaning of wounds culture on Thayer-Martin
others are under 3. The use of gloves pertussis vaccine & diphtheria 3. Removal of foreign medium
when handling toxoid}3 IM injections at bodies  if +ve  Rifampin
development
2,4 and 6 months with a 4. Surgical debridement
Chemoprophylaxis: infected material.  Ciprofloxacin  adults
booster dose is given a year 5. Antitoxin for prophylaxis
Doxycycline 4. Immunization of later and another upon entry is unreliable. X  Ceftriaxone  children
domestic animals. into school. 6. Toxoids are not available 2. Avoid overcrowded areas
5. Vaccination of people - A booster dose of (TD) is for active immunization. X 3. Vaccines:
working with animals recommended every 10 years  Trivalent
with toxoid - Booster doses are given to polysaccharide vaccine
military personnel & for  Trivalent conjugate
pregnant women. vaccine
(2) prophylactic use of antitoxin  2 new serogroup B
IV; vaccines
 antitetanic serum (ATS) after
skin test, obtained by immunizing
horses with toxoid
Human tetanus immunoglobulin
(HTIG
(3) Proper care of wounds
contaminated with soil.
(4) Administration of penicillin.

BACTERIA 7
 Treatment
Yersinia pestis Yersinia Bacillus anthracis C. tetani C.perfringens Neisseria meningitidis
enterocolitica
** combination - 3rd generation - Penicillin G ( early) - Patients with symptoms - Surgical  Penicillin G
streptomycin+ cephalosporin in - Ciprofloxacin of tetanus  nonspecific debridement,  Chloramphenicol
doxycycline for 10 severe cases+ - Recombinant human supportive measures Amputation may be  3rd generation
days aminoglycosides monoclonal antibody {dark environment, needed. cephalosporin
*Ciprofloxacin muscle relaxants}. - Penicillin in large
Inhalational anthrax
may be used - A very large doses of doses.
antitoxin (HTIG IV if not - Hyperbaric oxygen
available, AST is given in therapy 
bigger doses ½ IV and ½ oxygenates tissues
IM} which are hypoxic.
- Antitoxic sera +/-

Clostridium difficile Bacteroides

BACTERIA 8
 Superficial & Opportunistic Mycosis
1) Dermatophytes
1. Geophilic dermatophytes: contact with soil.
2. Zoophilic dermatophytes: contact with infected animals.
3. Anthropophilic dermatophytes: contact with infected humans.

Microsporum Trichophyton Epidermophyton

Species 14 20 1
Macro- Multiseptate, variable Thick wall, clavate Thick wall, smooth
candida in forms, big sized, to fusiform in shape surface, clavate, oval
thick wall & irregular or pyriform in shape
surface
Micro- Present Spherical, pyriform, Absent
candida irregular in shape &
size
Affected Skin – hair Skin – nail – hair Skin – nail
organs
Examples M. Canis T. Rubrum E. Floccosum
M. Audouinii T. Violaceum
M. Gypseum T. Mentagrophytes

Dermatophytid: formation of sterile itching lesions on body sites distant from point of infection.

MYCOSIS (FUNGI) 9
 2) Pityriasis Versicolor
(Tinea Versicolor)
- lesions in epidermis which are non-contagious, non-inflammatory with branny scales.
- causative fungus: pityrosporum orbiculare = malassezia furfur
- It’s a lipophilic fungus

* Difference between onychomycosis & Tinea unguinum:

Onychomycosis: Tinea unguinum:
Infection of nail – nail beds Caused exclusively by
Mostly caused by dermatophytes, dermatophytes
but can be also caused by other
fungi.

Opportunistic fungal infections

1) Aspergillosis
- Fungal infection caused mainly by genus aspergillus.
- The clinical picture is dominated mainly by respiratory manifestations

Causative agents: FnFn

- A. Fumigatus  90%
- A. nigra  5%
- A. Flavis  4%
- A. nidulans  1%

MYCOSIS (FUNGI) 10
 2) Candidiasis
* It results in superficial and disseminated mycosis
* Candida albicans is the most common frequent etiologic agent
* It is common in micro flora of the atmosphere – saprophyte in the alimentary tract and vagina of 10-50% of healthy
people.

Predisposing factors to candidiasis:

A- Internal factors:
I- Physiological: II- Pathological:
- Pregnancy - Debilitation
- Infancy & old age - Neoplasms (especially lymphoid ones)
- Obesity - Endocrinopathy (DM)
- Autoimmune disease
“chronic mucocutaneous candidiasis”
B- External factors:
- radiotherapy - surgery
- drugs: antibiotics & cytotoxic - peritoneal dialysis
drugs - drug addiction (IV ingection)

MYCOSIS (FUNGI) 11
 3) Cryptococcosis “Cryptococcus neoformans”
* It causes pulmonary and meningeal infections, it’s present mainly in pigeon excreta.
Morphology:
Spherical yeast, reproducing by budding, surrounded by large mucoid polysaccharide capsule.
Epidemiology:
Occurs frequently in males,
Exposure to pigeon excreta is the most common cause.
Immunity:
- Capsule is a very important virulence factor, “inhibits phagocytosis”
- Cell-mediated immunity is important to resist infection
Humoral immunity has no role against the infection

4) Zygomycosis “Zygomycetes”
* They are primitive, fast growing saprophytic fungi.
They include 2 genera:
a- Mucor
b- Rhizopus

MYCOSIS (FUNGI) 12
 Dermatophytosis Pityriasis Aspergillosis Candidiasis Cryptococcosis zygomycosis
Versicolor
Clinical Infections of Hair and  Interference with A- Pulmonary GIT Candidiasis:-  Involvement of CNS is  The most acute
Presentation Hair Follicles: the normal aspergillosis -oral more frequent than fulminant fungal
1-Tinea Favosa:- pigmentation of -Esophageal lung involvement. infection known
Caused by T.Shoenleinii the skin B- Disseminated -Enteric  After pulmonary .
 Infection of Hair aspergillosis: (less commonly affection
Follicles  Ocular Spread : by blood diagnosed ante- ,hematogenous spread  Rhino-facial-
 Crusty lesion made of May be Diagnosis : mortem) occurs to various cranial area is
dead epithelial cells -primary as cerebral 1-serological tests organs affected
and Fungal mycelia aspergillosis. 2-Histo- 2-Bronchial
"Scutula" pathological Pulmonary Predisposing factors It has many
 Permanent hair loss -Secondary due to examination -AIDS predisposing
and scar tissue abuse of antibiotics. 3-Candida - Reticulo-endothelial factors
formation. Corneal ulcer C- localized endocarditis malignancy
2-Gray patch ring worm aspergillosis: very common -Diabetes
caused by M.audouinii  Onychomycosis 1-Endocarditis -Starvation
and M. canis Very common -after open heart 4-Renal candidiasis -severe burns
 Infection of Hair disease surgery . -candiuria benign -IV addiction
Follicles then Shafts -diagnosed by :- colonization. -Leukemia
from inside " Electro- -True infection -Lymphoma
Ectothrix" cardiography Can lead to
 Mainly in Childhood Serological tests. pyelonephritis and
3-Black dot ring worm 2-cerebral abscess:' cortical renal
caused by T.Tansurans -Metastasis by infection.
T. Violecia blood
 Infection -surgical operation 5-Vaginal and vulvo
of Hair Follicles then -direct infection vaginal candidiasis
Shafts from inside " From nasal sinus During pregnancy in
Ectothrix" diabetic patients.
MYCOSIS (FUNGI) 13
  Breaking of hair 3- Bone abscess: 6-Candida
shafts beneath the Direct extension septicemia.
scalp from maxillary
Infection of Nail-Nail sinus 7-Candida meningitis
bed: -invasion by blood )Newborn infants)
Caused by - infiltration by
T.Tansurans corticosteroids 8-Candida
T.rubrum intertrigo:-
T.mentagrophytes 4-Cutaneous Due to exposure to
infections heat and humidity
Athlete's Foot AIDS patients and to tropical
T.rubrum Invasion by blood moisture.
T.interdigitale stream
9-Onychia-
5-Sinusitis Paronychia:
Very common in Chronic infection
Sudan due to immersion of
A.Flavus hands in water.
Mainly affect
maxillary sinus may 10-chronic
lead to proptosis. mucocutaneous
6-otomycosis candidiasis
A.Niger Children under 6 ys
Very common in due to congenital
Egypt cellular
immunodeficiency.

MYCOSIS (FUNGI) 14
 Lab Specimen Specimen Specimen Specimen Specimen Specimen
Skin Scales-Hairs-Pieces of Adhesive tape is According to the According to the CSF-sputum-serum-urine. Sputum-nasal
Diagnosis
nail. applied on the infected lesions examined. lesions examined. dicharges-scrapings.
skin then to the slide Direct Microscopy Direct Microscopy
Direct Microscopy or collect scales with Direct Microscopy Budding yeasts and -Round or oval organisms Direct Microscopy
-Add KOH(10-30%)to soften blunt scalpel. Appear as septate pseudomyceluim budding. Broad non septate
and clear the specimen. hyphae with angular Culture -India ink will reveal the thin walled hyphae
-Branching hyphae and Direct Microscopy dichotomous Yeast like colonies capsule. with focal bulbous
chains of arthrospores are Hyphae are short branching. Culture dilations
Antigen assays
seen . ,curved are rarely On SDA Shiny mucoid And irregular
-In case of hair you have to branching with Culture colonies. branching.
Identification of C
see if it is outside the hair spherical cells. Conidial morphology Under microscopy Culture
albicans
shaft or inside. and color on SDA Appear as spherical yeasts On SDA
-Germ Test tube
Culture with buds (white
-Rice agar tween test
Culture Budding yeast like cells Serology -can assimilates glucose, to grey
-Fermentation and
On SDA with Ag detection maltose, sucrose but not cottony
assimilation test
chloroamphenicol Ab detection lactose colonie
+Actidione to kill Histopathological -Urease + s
saprophytes. Molecular Technique examination serolog
Serology
Grow at room temp.for 3 PCR Blastospores and y
Detection of antigen
weeks pseudohyphae can be
Histo-pathological
demonstrated
examination
Serology
Appear as pale blue often
Detection of antibodies
thin walled spherical or oval
Molecular Technique
bodies with a clear halo
PCR and probes
around.
Treatment 1-Keratinolytic agents 1-Keratinolytic agents 1-Itraconazole Polyene group Combined drug therapy AmphotericinB
2-Local Ontiments: 2-Loca:l Clotrimazole, 2-voriconazole Imidazole derivatives 1-Flucytosine Newer drugs
Clotrimazole,Miconazole Econazole 3- AmphotericinB +amphotericin B Posaconazole
3-Oral drugs: 3-Oral drugs: (nephrotoxic) 2-Fluconazole
-Griseofulvin fluconazole +amphotericin B
- fluconazole
-Itraconazole
-terbinafine
MYCOSIS (FUNGI) 15
 Rabies, Parvovireses, Arbo & Robo viruses
Rabies virus Parvoviruses JC virus & BK virus
Family Rhabdoviridae Parvoviridae Polymavirus family
Properties - Bullet shape, SS RNA virus - They are the smallest DNA animal - Small non enveloped viruses
- Enveloped with glycoprotein spikes viruses - Cubic symmetry.
- Has ribonucleocapsid - Icosahedral, non-enveloped particles, - The genome is circular, DS DNA
SS RNA virus.
- Viral replication is dependent by
coinfecting helper virus.
Pathology  it multiplies in muscle  peripheral  The only recognized human pathogen 1) BK and JC viruses' infection usually occurs early
&mode of nerves multiply CNS {Encephalitis} in this group of viruses is the childhood.
infection Spread to the salivary gland and other Parvovirus B19 2) Both viruses may persist in the kidneys &
tissues (cornea, kidney…  Infection is common in childhood lymphoid tissues of healthy individuals after
 highest titre submaxillary salivary gland  Mode of infection: primary infection
cannot be isolated from blood of the infected 1) Respiratory route. 3) may reactivate when the hosts immune response
person 2) The virus can be transmitted is impaired
 incubation period depends on: parentally by blood transfusions the
- Virus conc. & severity of wound principal target for B19
- Distance from entry to CNS 3) vertically from mother to fetus
- Host age and immune system
Clinical  In human( incubation period 1-3 months)  Erythema infectiosum (fifth disease): —  *(BK)
picture 3 phases : children 1) Nephropathy usually happens in 5% of kidney
 short incubation phase: - The most common of B19 & recipients
- Lasts 2-10 days with no specific associated with a faint rash the face 2) BK hemorrhagic cystitis in patients with bone
symptoms: has a “slapped cheek” appearance. morrow transplantation.
(headache, anorexia, N, V, photophobia - Joint involvement is a prominent  JC virus
&abnormal sensation at the site of the bite) feature in adult cases. 1) (PML) occurs in some immunocompromised
acute neurologic phase:  Transient aplastic crisis: patients
- Lasts 2-7 days with neurological - may complicate chronic haemolytic 2) JC virus has been recently associated with
dysfunction anaemias e.g. sickle cell anemia, human brain tumors
(hallucination, over-activity, papillary
VIRUSES 16
 dilatation, increased salivation, hydrophobia thalassemia decrease red cell synthesis
& painful spasm of throat muscle in the bone marrow
 coma phase:  chronic suppression of the bone
Convulsion , coma, death D.t cardiorespiratory marrow
arrest Called pure cell aplasia  in
 in dogs( incubation period 3-8 Weeks) immunodeficient host
Divided into 3 phases as in man  during pregnancy may result in
hydrops fetalis and fetal death in due to
severe fetal anemia abortion occur
Lab  In human: - Virus is difficult to glow = cannot be 1) Cytopathology
diagnosis  cytopathology: isolated Urine samples can reveal the presence of JC & BK
- The presence of Negri bodies specific - The most sensitive tests are DNA viruses  showing enlarged cells with intra-nuclear
eosinophilic intracytoplasmic inclusions with detection by PCR, NA probes inclusions.
viral nucleocapsid
- Serology to measure ab: 2) Polyoma antigens may be demonstrated in
 detection of rabies Ag or NA:
*B19 IgM recent infection persist for infected cells by IF.
- Using immunofluorescence by monoclonal Ab
- RT-PCR: amplify part of the genome 2-3 months 3) PCR& N.A. probes can detect viral N.A.
 viral isolation: *B19 IgG recovery  persist for years 4) E.M. can be used to visualize VIRUSES particles
- Brain examination after encephalitis death of *** not detectable in in brain tissue in case of PML
mice for rabies ag and Negri bodies immunocompromised person
- Mouse culture cell line with rapid growth of - Ag detection assay
rabies virus which is identified by fluorescent - In fetal infection  PCR analysis of
antibodies amniotic fluid
serology:
Serum ab (immuno- CSF ab
fluorescence)
- Slowly developed - Detected in
in infected person rabies infected
- Quickly detected person
in vaccinated - Not detected in
person vaccinated
person
 in dogs:
- Should be sacrificed for lab examination
- Others are hold for 10 days if encephalitis
occur they should be killed for examination

VIRUSES 17
Prevention  SEE THE DIAGRAM BELOW  1) Immunoglobulin for ………
** This depends on decrease the chance for immunocompromised patient with
viral replication and CNS invasion. chronic B19 infection
 Frist Protective measure: 2) There is no vaccine.
- Wound cleaning with soap and water 3) Good hygiene as hand washing can
- Stitching should be avoided prevent B19 spread through respiratory
- Instillation of Rabies immunoglobulin the secretions
wound
(HRGH passively till respond to HDCD,
PCEC actively to produce ab).
 vaccination and doses:
 immunocompetant: 4 doses at day 0,3, 7, 14
immunocompromised: 5 doses at day 0,3, 7,
14, 28
Treatment  No specific treatment only symptomatic  Fifth disease treated …………..
 Interferon, ribavirin has no beneficial symptomatically
effects  Severe anemia  transfusion therapy

VIRUSES 18
 Slow virus infection & prion disease (transmissible spongiform encephalitis)
Definition &  Chronic degenerative disease caused by slow, chronic
persistent infection by classic viruses
pathogenesis  "slow" is the rate of progression and not the rate of
replication
 Characterized by: "long" incubation period, "gradual"
onset& "fetal" progress
Clinical picture
In animal Visna :
- Chronic progressive neurological disease of sheep
- Caused by: retrovirus
- Characterized by: All organ are affected specially : brain,
lungs& RES
"long" incubation period, "SLOW OR RAPID" progression
In human Subacute sclerosing panencephalitis (SSPE):
- Slow progressive CNS demyelination in patient early
infected by measles
- Characterized by: Progressive mental depression ,
involuntary movement, muscle rigidity
 measles ab in CSF, SERUM & measles particles in brain
tissue
 Progressive multifocal leukoencephalopathy (PML):
Fetal demyelination of white matter of the brain in multiple sites
Occurs mainly in immunocompromised patients AIDS
Caused by: JC virus & BK virus
Characterized by: visual defect, mental change, blindness coma
VIRUSES
 Degenerative CNS diseases
 The causative agent is not a conventional virus but proteinaceous material with no
DNA or RNAPrion which is only composed by single glycoprotein that
encoded by the host cell
 Conformational change to the disease form (PrPSc)  causing neural cell death
 PrPSc has the ability to interact with PrPC converting it to the disease form
(PrPSc)
Features:
- Neural degeneration and vacuolation
- Amyloid accumulation
Characteristics : 4 NO
 "long" incubation period followed by no remission& no recovery
 No inflammatory response & no immune response
Scrapie:
 Disease of sheep
 Characterized by: tremors , ataxia &itching  the sheep scrape off their wool
against wall
Bovine spongiform encephalopathy( BSE): ( mad cow disease)
- Acquired by: eating cattle feed supplemented with organs as brain obtained from
sheep infected with Scrapie prions
Kuru:
- Fetal disease with progressive tremors and ataxia
- Spread by cannibalism of dead relative and has disappeared
Creutzfeldt-jakob disease:
 Associated with: dementia &myogenic jerking and progress into death
 Sporadic mainly with 15% hereditary
Transmission by:
- GH from cadaver pituitary
- Corneal transplantation & dura matter graft
- Contaminated Surgical instruments & ECG electrodes
Variant Creutzfeldt-jakob disease: occur in younger people
 It is a new variant of CJD & BSE caused by a common agent
 The pathological characteristic similar to BSE
 human infected through consumption of BSE contaminated beef
19
 Arboviruses Arboviruses
Definition Arthropods born viruses they are transmitted by blood sucking Persistent infection in rodent transmitted between rodents without
arthropods with lifelong infection with no damage to arthropod vector
themselves
Cycle and Triad : vector, vertebrate host & viruses Transmission by
biological ** when female mosquito feeds on blood  mid gut  - Direct contact with body fluid or rodent excreta
multiply {1ry viremia} - Inhalation of dust containing rodent excreta
transmission&
** tissue invasion (salivary gland) multiply 2ndry viremia
Pathogenesis Most  subclinical
 Rash, pharyngitis or encephalitis & hemorrhagic fever
With biphasic course
- Primary viremia followed by remission
- Recrudescence of pyrexia  2ndry viremia + encephalitis
Fever + haemorrhage =haemorrhagic fever
General - have biological method for transmission …….
characters - RNA viruses
- Ether sensitive
Examples of 1- Encephalitis - Most of them produce haemorrhagic fever:
infection 2- Specific fevers:  Hantavirus : -
* haemorrhagic fever& renal syndrome (renal failure) in Korea
*pulmonary syndrome in USA
 Lassa fever virus
South America haemorrhagic fever
Ebola virus Africa haemorrhagic fever
lymphocytic choriomeningitis virus:
Roboviral infection not cause haemorrhagic fever

Treatment …………. Supportive with IV ribavirin

VIRUSES 20
 Zika virus Ebola virus
Characters Arboviruses & Highly Arboviruses
aggressive spread
Reservoir ….. Rodents & fruit bats
Virulence …… 1- Secretory glycoprotein bind with neutrophils and inhibit their activation
factors and so rapid dissemination of the virus
2- Two other proteins suppress the interferon response
Incubation 3-12 days 2-21 days
period
Pathogenesis ………….

C/P  Most cases with no symptoms  Early: fever , headache

 Mild resemble dengue fever  Followed by: abdominal pain V, D and bleeding {internal& external}
 Symptoms:  Late: shock& death
Fever, rash, conjunctivitis… *** No specific treatment only supportive
Transmission - Mosquito bites 1. Person to person
- From pregnant women to fetus: 2. Nosocomial
** congenital abnormalities, 3. Laboratory infection
microcephaly, trigger Guillain-Barre
syndrome
- Sexual contact
- Blood transfusion
VIRUSES 21
 HIV
Morphology: Pathogenesis:
 Enveloped single stranded RNA virus 1- Virus affects CD4+ve cells
(t4 lymphocytes – macrophages – monocytes )
 The nucleocapsid is formed of :- and also some CD4-ve cells
a- 2 identical strands of RNA cerry genes (renal –GI epithelial cells – brain –astrocytes )
-Gag gene 2- Macrophages → qualitatively affected
-Pol gene t4 lymphocytes → qualitatively – quantital
-pro gene affected
-Env gene
b- Enzymes ( RT-P-I)
c- Structural protein : p24 Clinical picture:
1- Primary infection ( acute retroviral infection )
 On the envelop , these are gp 120-40  ↑viremia
(gp120) surface .. (40)transmembrane  The patient is highly infections
Look at the book  Virus is widely disseminated acute
mononucleosis like syndrome .

2- Asymptomatic chronic infections ( clinical latency )

:
 Patient is asymptomatic
virus is replicating – infecting other cells

VIRUSES 22
Transmission: Treatment:
1- Horizontal transmission : 1- Reverse transcriptase inhibitors :
A. sexual transmission - Nucleoside RTI (NRTI )
“especially if there is genital lesion ,ulcesrs “ - Nucleotide RTI (NtRTI )
B. blood and blood products ozidothymidine –tenofovir
2- vertical transmission : - NONnucleoside RTI :
A. congenital →transplacental nevirapine (NNRTI )
B. intranatal → during passage along the birth canal 2- Protease inhibitor (PI ) :
C. breast feeding - Saquinavir – ritonavir
3- Integrase inhibitor :
Diagnosis: - Elvitegrevir (INSTI )
1- immunologic features : 4- Receptor CCR5 antagonist :
great reduction in number of CD4 lymphocytes , low ratio of t-helper - Maravoric
→ it drops ( 50-100 cells/mm3) 5- Fusion inhibitor
→ ›500 ( clinical year latency ) - Fuzeon
→200-500 ( first degree of immunodeficiency )
→ ‹ 200 (frank AIDs ) HAART
2- viral antigen of N.A : Highly active antiretroviral rheraby
-ELISA - Compination theraby
-PCR→most sensitive especially in newborn . 2 drug of NRTIs
3- viral isolation : 1 drug of NNRTIs , PIs, INSTIS .
only in research centres .
4- Antibody essay :
 EILISA is used in routine screening → if+ve test is repeated
 To conferm →western blot technique ( WB )
Immunoflourescent assay

VIRUSES 23
 Herpes Viruses
Varicella zoster EBV
Important  DS DNA, icosahedral
properties  Enveloped,
 Single serotype
Transmission  Direct contact with lesion  Saliva
&  Respiratory droplets
epidemiology
Pathology & 1. Infect mucosa of the upper respiratory tract 1. Infect oropharynx
immunity 2. Initial replication in the regional LN then 2. Infect B cells and spread the infection through the body
spread via blood to the skin 3. T-cell react against infected B-cell and for atypical
3. Swelling, ballooning and degeneration of lymphocytes
epithelial cells of the skin and 4. Heterophile antibodies also appear which can agglutinate
accumulation of tissue fluid vesicles sheep and hours RBCs
formation
4. During immunosuppression periods
replication in the ganglia occurs, virus
travel down to the nerve to the skin &
induce vesicles formation
Clinical 1. Varicella: 1. In children:
finding - Symptoms of fever, malaise& Papular rash - Usually silent and asymptomatic
**In immunocompromised children: 2. In adolescent:
- Encephalitis & pneumonia - Fever, sore throat
2. Zoster: - Lymphadenopathy, splenomegaly & hepatitis
- Rash limited to the area innervated by that 3. Reactivation is usually silent
single nerve
- Sever pain
VIRUSES 24
 Diagnosis - Cytopathology - Blood smears atypical lymphocytes
- Viral immunology - Serologyspecific EBV antibodies
- DNA detection - DNA detection
Treatment &  No treatment  No treatment
prophylaxis  LAV for varicella  No vaccines
 Herpes zoster vaccine: frequency& severity

VIRUSES 25