Superficial Mycoses:

1-Pityriasis Versicolor (Tinea versicolor): caused by Malassezia spp, Hyper-, or hypopigmented macules
or patches occur on the skin mostly on the back,no symptoms,treated by selenium sulfide, KOH 10%
Spaghett(filaments)i and meatball (yeasts)appearance is seen, fluorescent microscope ( Light with
wavelength 365nm)

2-Tinea Nigra: caused by Hortaea werneckii,asymptomatic, lesions appear as a dark (brown to black)
discoloration,found in soil,not transmitted by contact,often on the palm,treated by antifungals.

3-Piedra: black one is caused by Piedraia hortae,infects the hair.White one is caused by Trichosporon
spp.Treatment: removing hair +topical antifungal.

Cutaneous mycoses

Tinea Pedis (athlete’s foot) Tinea Unguium Tinea corporis Tinea capitis Tinea cruris (jock itch)
(Onychomycosis) (ringworm) (scalp ringworm)

Trichophyton rubrum Trichophyton Trichophyton rubrum Epidermophyton

mentagrophytes, Epidermophyton Trichophyton floccosum, several
floccosum mentagrophytes, species Trichophyton Epidermophyton floccosum
cause
Epidermophyton ofTrichophyton, tonsurans and Trichophyton rubrum
floccosum Microsporum

peeling and cracking of the skin,pain yellowing of the nail, Advancing annular small, scaling smilar to ringworm,
due to inflammation and it beomes brittle, rings with scaly patches to
Symptoms pruritus.inflammation is more if thickened and centres,usually involvement of the
transmitted from animal to human than crumbly. inflamed and entire scalp with
and signs
from human to human vesiculated extensive hair loss..

Between the toes Nails of the feet Anywhere but they scalp. Moist groin area
location
most commonly
grow on the trunk
(torso, back)
 scraping of the culturing of the sample,
lesion and scraping of the lesion and
diagnosis SDA media, Obtainind nail observing the observing the sample
clipping. sample underthe under the microscope, and
microscope,or we use 10% KOH to
culturing sample dissolve the keratin.

. thorough removal of
infected and dead
It can be cured by topical or oral epithelial cells ,topical
treatment
treatment but if it antifungals,azoles antfungal like miconazole.
was left untreated it and amphotericin
will remain chronic B(this one in
(not latent!!) severe cases)

Exam questions:
*Histoplasmosis:Histoplasma capsulatum >> An important feature is that it is the only fungus that
exhibits intracellular parasitism, So the main site of infection is the RES, The yeast cells of this fungus are
engulfed by macrophages but they survive there.

*HBV,HCV,HDV >> enveloped viruses so they are acid sensitive(cannot withstand acidity of the stomach
unlike HEV and HAV.

*Hepatitis viruses they have the same clinical manifestations and they are histopathologically the same
so we use lab tests to distinguish between them.

*DANGEROUS PERIOD IN HAV is incubation period(shedding of the virus in feces without knowing)

*the HBV has a higher level of genetic variability than the DNA viruses but still has a lower level of
genetic variability than the RNA viruses, why??? Because the overlapping nature of its gene.

*first marker is viral DNA that appears within the first few days and then HBsAg (present on the
envelop ).

*THE only effective marker in window period is hepatitis B core AB of IgM type(present on the capsid)

*Group M in HIV-1 :The most common subtype globally is subtype C (50%), while in western Europe,
Northern America, Middle east and North Africa subtype B is the most common.

*most common mode of transmission of HIV-1in the world is heterosexual contact.

 *homozygous CCR5 delta32 resistant to HIV-1

Oral cases:
Paracocidomycosis:- The most common secondary site of infection is the mucosa of the mouth.Has a
marine wheel appearance.

Diseases caused by Candida:- Thrush:-oral cavity lesions may be patchy or confluent (making a whitish
pseudomembrane). These lesions are composed of epithelial cells, yeast and pseudohyphae.May occur
any place on the oral cavity (tongue, lips, gums).

Mucormycosis:- Caused by Mucor or Rhizopus genera, the infection Associated with diabetes and

cause destructive nasal disease and oral disease.

HCV can be caused due to dental procedures.

HIV -1 can occur due to needle stick injury.(low percentage but may happen)

AIDS issues:
-Significant overgrowth of Candida is seen AIDS patients who are not properly managed.

- esophageal candidiasis is one of the AIDS defining conditions, even if CD4 T cell count is more than 200.

-cryptoccosis caused by Cryptococcus neformans >>Mostly associated with AIDS patient causing fatal
meningitis(cryptococcal meningitis), so if AIDS patient has meningitis it is the first thing to doubt of.

- lower viral set point >>longer AIDS development and vice versa.

HEPATITIS VIRUSES
viru genome family Seroty genotype People infected Route of receptor Vaccine and treatment
s pe tran
And diagnosis

HA +ssRNA picornavirida one seven Developed Feco-oral. TIM- Formaldehyde

V nonsegment e ..adults(symptom 1(HAVcr-
ed, naked atic) 1) inactivated vaccine,

Developing..child supportive treatment.

ren(a
symptomatic)
HEV +ssRNA , hepeviridae one 5 only Dangerous when Feco-oral No vaccine yet but
naked 1,2,3,4 it infects
associate pregnant candidate recombinant
d with women(20% trials
humans mortality)
Supportive treatment

(self limiting disease)

HBV Partially Hepadnavirid Eight, Found worldwide Vertical,sex NTCP IFN,several nucleotide and
dsDNA ae but highly ual,drug
(peculiar Most endemic in abuse,needl Nucleoside analogs sych
circular Only human common Southeast e stick Ribavirin and lamivudine.
genome), virus that in Jordan Asia(mother to injury,blood
negative beolongs to is (D). child) transfusion( Vaccine(recombinant
this
complete Common rarely
family,others 90%Sever acute HBsAg)
strand and sub- nowadays)
partial cause infection in
hepatitis in genotype adults(symptoma
strand.it is is D1.
enveloped animals and tic), 90%chronic
birds. infection in
children(asympto
matic)

HDV -ssRNA unclassified *non-endemic Same as NTCP Tests for the presence
circular, areas (injection HBV
enveloped. drug users) and of HDV RNA(imp for
miditerranean(en ongoing HDV replication)
demic mainly by
non-
percutaneous
means)

HCV +ssRNA Flaviviridae Seven(m Egypt ,Pakistan Mainly:Expo CD81(mos HCV RNA testing(to look
ost and Cameroon sing to t imp)
common highest contaminat For ongoing infections
globally 1 prevalence 10% ed blood Claudin
,serologic secreening(past
then 3 through Occludin
).in Injecton infection )
Jordan 1 drug use. Scavenger
receptoe and chemilumininesecnt
and 4(rj3
hka Sexual calss b Immunoassays.
bsheet behavior,ver type 1
 tanyeh tically,healt INF and DAA(this one
enu bs 4) h care
,in Egypt associated Has less side effects and
4 infections,in Short duration of therapy
framilial
spread,tatto Like sofosbuvir(nucleotide
oinf,piercing
Inhibitor that inhibit
and
acupuncture NS5B).

NO EFFECTIVE VACCINE

Only trials.

RETROVIRUSES: (diploid,ssRNA) enveloped with RNA dependent DNA

polymerase.

Nam transmissi location Diagnosis,treat features diseases

e on ment and
prevention
HTLV Vertically in Southwestern ELISA(diagnosis genetically and 1-Adult T cells
high endemic part of Japan, biologically similar by 65- leukemia
-1 areas. sun-Saharan ) 70%, 2. Cutaneous
Sexually((They Africa and tax gene(oncogene)>>so T cells
are considered South For prevention: stimulating mitosis and lymphoma
one of the American a) Screening of blood immortalize T 3-HTLV-
STDs) units lymphocytes>>chromoso associated
Blood products b) Experimental mal myelopathy
vaccines aberrations>malignant “tropical
phenotype spastic
*most are paraparesis”
asymptomatic. Characterized
*latency could stay more by loss of
than 40 years. myelin
Vertically in native For prevention: genetically and 1-Hairy cells
HTLV Americans and
high endemic a) Screening of blood biologically similar by 65- leukemia(affe
-2 areas. some Central units 70%, tax cts spleen)
African
Sexually((They b) Experimental gene(oncogene)>>so 2-HTLV-
tribes,common
are considered vaccines stimulating mitosis and associated
in IV drug users
one of the and their sexual immortalize T myelopathy
STDs)) partners in lymphocytes>>chromoso “tropical
Blood products Euoroe and mal spastic
North America aberrations>malignant paraparesis”
phenotype Characterized
*most are by loss of
 asymptomatic. myelin
*latency could stay more
than 40 years.

HIV1 Sexual,vertic WORLD HAART, Groups M and N came AIDS

al,blood WIDE(global from Chimpanzees
pandemic) (SIVcpz) while the other
transfusion Most in sub Diagnosis: groups (O
,IDU,needle Saharan Africa Enzyme immune and P) came from Gorilla
stick injury. assay followed by (SIVgor).
western blot(look Regulatory gene is Vpu,
-virus starts to establish
for proteins) or the infection 10 days
detection of HIV-1 locally before systemic
RNA. spread.
Prevention: Latency>>average 8-10
*Consideration of years
PEP and
PrEp,*counseling
and
education,initiation
of ART among HIV-1
infected
individuals,condoms
NO VACCINE.
HIV2 WEST HAART -more time to develop to AIDS
AFRICA(mostly AIDS.
endemic) Regulatory gene is Vpx,
HIV-2 came from SIV that
infect sooty mangabey
monkeys (SIVsmm).

Per-act risk for each mode of transmission

1 Blood transfusion
2 Vertical without treatment
3 Vertical with treatment
4 Receptive anal intercourse
5 Needle sharing
6 Percutaneous needle stick injury
7 Insertive anal intercourse
8 Receptive vaginal intercourse
9 Insertive vaginal intercourse
Pathogenisis of HIV-1

Acute retrovial syndrome(primary infection)(it has the same as

mononucleosis like symptoms,systemic symptoms)(0-6
months)(macrophages,monocytes,dendritic cells then to the lymph nodes(T cells) and the
release of cytokines.
Immune system starts working
Drop in the viral count
(HIV set point is a prognostic marker for assessment of disease progression)
Blood CD4 restore to almost its normal number
GALT is yet severly impacted,not returning to its normal
number>> chronic infection
Virus establishes latency and the imuune system is tired(loss of
memory cells)
Severe decline in CD4 cells and incline in the viral load
AIDS PATIENT( CD4 cells <200mg/microL)

Imp notes:

Viral load testing (to know if there is active replication or not,enter AIDS stage
or not)

CD4 and CD8 ratio will infrom us if the patient enters AIDS stage or not.

Antiviral drugs :NRTI(MOST IMP TENOFOVIR),NNRTI,PI,Integrase

inhibitors,Fusion inhibitors,CCR5 anatgonists.