Anti-HAV 196 - pasting/recovery - > Provide lifelong immunity

Hepatitis A virus (HAV): Picorna virus IgM - Auteing

(short-lifed)
- Anti Har
01-hepatitis (gulden)
.

• Transmission: fecal-oral
• Naked + stable - > resistant to detergents

• Inactivated by: chlorine treatment of drinking water

• Pathogenesis: virus shed in large quantity 10 days before symptoms of jaundice
• Antibody protection against reimfection is lifelong
• Can’t initiate chronic infection + not associated with hepatic cancer
• May be asymptomatic ( in children may be asymptomatic) symptoms accurdue to injury : immune-med
hepatocyte
• Adults: abrupt onset hepatitis
to

• Preg women: serious, hospitalized

• Means of contro: 1) good hygiene
2) passive antibody protection for contacts (killed vaccine)
• Clinical syndrome: 1) dark urine + pale stool + jaundice
2) symptoms may occur abruptly 15-50 days after exposure
• Diagnosis: anti-HAV igM by ELISA → positive means immune
• Treatment: 1)proper handwashing,
2)chlorine treatment of drinking water
3)prophylaxis with immune serum globulin (before/ea;ry incubation period after 2 weeks of exposure)
4) killed HAV vaccine administer on 2 doses 6 months apart , can be administered with HBV vaccine
• More contagious before jaundice
replicate thru MNA intermediate

>
DdsDNA circular
↑ ·
not sensitive
Hepatitis B virus (HBV): ·
chronic inf ↓ with Age

• enveloped DNA virus -

• It encodes reverse transcriptase

• Structure: 1)Encodes several proteins: HBsAg (released into serum of infected person, outnumber actual virion+
Dane practicle whole HBV
- virion immunogenic)
HBcAg
HBeAg
2)virion also called Dane practical
3) resist treatment with: ether, low PH, freezing, moderate heating
• Source: blood
• Found in: semen, saliva, milk, vaginal + menstrual secretion, amniotic fluid
• Common but less infection route: sexual contact + birth
• Transmission: needle sharing, acupuncture, ear piercing, tattooing
• Household contact - highest risk HBIG Administered to them -

• High risk group: babies with HBV mothers, drug abusers, multiple sex partners, health care personal with blood
contact, hemodialysis patient…..
• Determination of acute + chronic: # arte
Chronic occurs 5-10%
hepatocellular cancer

Cirrhosis

fulmilant hepatatis
-
Chronic
dertz
jaundice
release a
benzyme

• Spread in body: insubation : 1-6 months

Virus in
>
-

blood stream

• For HBV if we have the antigen that means you have the virus
• HBC antigen which is core, is found in nucleus of hepatocyte of the
• Symptoms: infected, then HBeAg: this shows potential infectivity only when
HBsAg is present (means your re infected)
• Anti- HBS: means you have protection + resolution of disease,
+marks past infection or vaccination
• Anti HBC igM: you have acute infection because its M
• Anti HBC igG: you have past/chronic infection
• Can contribute to PHC, but is vaccine preventable human cancer Persistant over Chrani
t

[
HBsAg-D Surf Antigen excel in serum-
• Diagnosis: clinical symptoms+ presence of liver enzymes on blood * G months

disease (marker past inflvaccine

• Vaccinations: 3 injections, 2nd and 3rd being 1 and 6 months after 1st Anti-HBs - protection/resolution against
indicates immunity
• Anti HBS should be detected 1 month after last injection >=10 IU/ml →no rappel needed HBCAg ofinf hepatocyte

v
-1 in nucleus
• Disinfected with: 10% bleach solution, not inactivated by detergents Anti-HBcIgM s Acute int

Anti-HBs IgG Absence of HBsAg Anti-HB = -

Recovery In Anti-HBS ,
inf
& Anti-HBC
,

Igo part/chronic
-
-

↑ infectivity
replication +
inefectivity - HBeAg + HBV DNA
HBeAg-D potential infectivity (shown when HBsAg is present too) - n Active viral

Anti-HBE -
Antibody to HBeAg
Hepatitis C virus (HCV): >
- linear SS-RNA ,
+sens-novaccine -
>
multiply rapidly + multiple genotypes Detects early infection
• flaviviridae fam Viremia: presence of virus in bloodstream HCV antigen -

/part/present) 02-hepatitis 2 (gulden)

to Detects expacume to HsV
anti-her
• Major cause of post transfusion hepatitis before routine screening of blood supply for HCV L this is basically anti-HIV
1g6
load
monitor viral
• Transmission: similar to HBV → in infected blood + sexually blood borne (common) confirmActiveinfection
- +
>
-

HCV RNA-D
s
• Leads to cirrhosis and potentially hepatocellualr carcinoma Diag +
follow-up

• Enveloped detection for choosing antiviral therapy

>
-
imp
genotype
• At last 7 genotypes: generates antigentic variability → makes vaccine dev difficulty → persistent infection ↑
predict resp
• Genotype 1: most prevalent worldwide -
Klantibody to reep
• Cell-mediated response resp for both resolution + tissue damage IgM : ·

Hand B Anti-HAVIgM thow infection

in hepatatic
• Causes 3 types of diseases: 1) acute hepatitis
·

Anti-HBVIgM
HIV Doesn't trigger strong
2) chronic president infection: possible rohesrion to a disease for 70% of patients
·

its useless
resp-
3) severe rapid progression to cirrhosis
• Diagnosis: 1) ELISA recognition of anti-HCV antibody (now 4th gen ELISA →antigen +antibody present)
2) genome detection. + quantitative by RT-PCR → for success of antiviral drug therapy
• Anti-HCV + HCV RNA → 4th gen ELISA After HIV infection HCURNA Appears --

• Antibiotic test/ELISA/rapid test: 1)positive: indicates current infection (acute/chronic) or past resolved inf
Test orderi
-

ELISA
2) if antibody test → positive → sequential HCV RNA testing to
1) Anti-HCV Antibody -Davening
2) ACURNA PCR-a confir
-
confirm HCV viraemia
3) Western bolt- >
Alt conti 3)HCV RNA test →unavailable → HCV core antigen test (ELISA)
• Treatment: Pan-genotyping HCV drug regimens + identify certain genotypes before starting 1st-line thaerapy
is useful DAA - targets Her replication

• Screening challenges: many ppl are unaware of the infection -to know if

• Recon for 1-time HCV testing: for ppl 1945-1965, other ppl should be screened for risk factors it's active infection
>
-

• Blood Door Screening: in turkey it started in 1997 ancogenic risk no

↓ no carrier+

HCV diagnostic markers : HSV

= no vaccine
HAV only Acute + naked a

• HCV RNA (RT-PCR) HDV

> can use
- HisV vaccine rarely chronic
• HCV antigen

HAVIDALIRNA
• Anti HCV ABVEDNA
• Genotype detection HDV
HEV

Hepatitis D virus (HDV):

• HDV RNA is very small + HBsAg contains envelope
• Similar to HBV spread by → blood, semen , vaginal secretions, can replicate and cause disease only in ppl
with HBV infection → person co-infected with HBV + delta agent HBVHDV severe fulminant hepatatis
& =

• Superinfection of a person alr with HBV (carriers) cause more rapid, severe progression than co-infection
• As,me groups are at risk of infection as HBV
• Clinical syndrome: fulminant hepatitis →more likely to dev in ppl infected with delta agent than those inf
-

with other hepatitis virus

• Diagnosis: detect RNA genome, delta antigen, Anti-HDV antibodies
• Treatment: no known treatment + but immunization with HBV vaccine protects against subsequent delta
virus infection
LAB methods -
1 Anti-ADV ELISA

Hepatitis E virus (HEV):

• spread: fecal-oral route esp in contaminated water
• Unique but resembles caliciviruses
• Symptoms + course similar to HAV: it caissons only acute disease, but symptoms occur later than HAV
• Severe mortality for preg women
Acute + self limited -> in
healthy
Adults

Chronic inf >

- immunocompromised
patients

not in immunocompetent patients

&
 Leishmania Spp:
03-common parasites (sibel) • Definitive host: female sandfly (Phlebotomus) → vector
• 2 types: 1)old world → cutaneous + visceral
2)new world → cutaneous+ mucocutaneous + visceral
• Infective form: promastigote → in saliva of sandfly
• Diagnostic form: amastigote →intracellular in macrophage in humans (seen in smear)
• Types of leishmania: 1) cutaneous leishmania: localized skin ulcer (“oriental sore”)
2) mucocutaneous leishmania: nose ,mouth, throat (“Espundia”)
X
3) visceral leishmania: sever systemic disease → fever, weight loss, hepatosplenomegaly
• Infects human + dogs
Trichomonasvaginalis Echino
-

·
nocyst form
gravoa case
• Transmission: bite of sandflies
Visceral leishmania:
• Clinical features: enlarged liver + spleen
• Main reservoirs: dogs
• Affected esp young children + malnourished individuals
Entamoeba histolytia • Usually benign and subclinical
Protozoa: -
• Sympt: irregularly recurring fever, anorexia, malaise, diarrhea, weight loss, abdominal pain, opportunistic inf in
• Unicellular eukaryotic organisms -
moves by pseudopodia
HIV, death occurs after month-years
• Free-living/ parasitic
• Test done: rK39 dipstick test
• Live in soil, water, inside hosts
Cutaneous leishmania:
• No cell wall, but have nucleus and cytoplasmic organelles
• Oriental sore: 1)dry type: [Link], urban type, ulcer remains dry, , Chronic course with late ulceration, inc
• 2 stages: 1)trophozite: motile, feeding, active form
period: 1 year
2)cyst: nonmotile, infective, resistant stage (survive outside host)
2)wet type: [Link], rural type, acute course with eartly, ulceration + exudation, incu period: 2-3
• Transmission: mostly fecal oral, vector bites, sexual contact
months
• In turkey [Link] resp for most cases
• Lab diagnosis: 1)direct microscopy: blood, bone marrow, lymph node
a
2) culture
infestation :presence of arthopods
on
in pat 3)serology
• Treatment: pentavalent antimonial drugs, sodium stibogluconate, and meglumine antimoniate → most used
Intra-lesionary antimonials → in CL cases, systemic antimonials → in VL
—————————————————
• Affected liver, spleen, bone marrow
Sibel-Style Exam Focus (matching her past question tone)
Plasmodium Spp: 1) infective form in mosquito, gametocyte 1. “Which form of Leishmania is transmitted to humans by the sandfly?” Promastigote ✅
2. “Which of the following is the diagnostic form of Leishmania donovani in humans?” Amastigote (Leishman–Donovan body) ✅
• Causes: malaria 3.
4.
“Which of the following organs are affected in visceral leishmaniasis?” Liver, spleen, bone marrow ✅
“What is the vector of Leishmania donovani?” Female Phlebotomus sandfly ✅
• Malaria is caused by: bite of infected female mosquito (Anophels) ① sporozite (mosquito-shuman) 5.
6.
“Which of the following Leishmania species causes mucocutaneous leishmaniasis?” L. braziliensis ✅
“Which of the following test detects amastigotes within macrophages?” Microscopic examination of tissue or bone marrow aspirate ✅
• Definitive host: female anophels mosquito (sexual reproduction) ② liver (pre-erythrocytis/EX0-erythrocytic
stage) 7.
8.
“Which of the following is not a feature of Kala-azar?” (E.g. Localized skin lesion) ❌
“What is the infective form of Leishmania for the vector?” Amastigote ✅
merozite
• Intermediate host: human (sexual reproduction/schizogony) schizants-prupture-preleas 9.
10.
“Which host is the definitive host in the life cycle of Leishmania?” Sandfly ✅
“Which test is used for field diagnosis of visceral leishmaniasis?” rK39 dipstick test ✅
③ inside RBC)
• Infective form: sporozite (in mosquito saliva)
TrophieSee 3 rupture
mu
releas malaria -

symptoms
• Diagnostic form: trophozite, schizont, gametocyte → in human blood merczite .
3
Giarda Lambila:
1. Plasmodium Vivax: Giarda intestinalis: Attaches by Ventral sucking · Diss

• 48 hr cycle • Intestinal C
flagellated protozoan Affects Dudoneum (the most ·
:

• Infect young cells • Motility organ: flagella

• Enlarged RBCs • Definitive host: human
• Schuffner’s dots • Reservoir host: beavers, dogs, cats, rodents
• Ameboid trophozite2 • Infective form: cyst → 4 nuclei (ingested via fecal-oral)
2. Plasmodium malariae: • Diagnostic form: cyst + trophozite (ingested stool sample)
• 72 hr cycle • Transmission: 1) fecal-oral route → contaminated food, water, hand-to-mouth environment
• Infect old cells 2)resistant cyst can survive weeks in moist environments
• Normal size RBCs 3)outbreaks common in campers, daycare centers, travelers
• Ziemann dots
• Trophozite tend to form ‘bands’ across cell
• Daisy forms (shizonts)
3. Plasmodium falciparum: Cerebral >
- causes

• 36-48 hr cycle malaria

• Infect any cell, any age

• Maurer dots • Less common symptoms: itchy skin, rash, swelling of eye+joints, weight loss, failure to absorb fat+lactose+Vit
• Multiple rings/cell A +Vit B12, in children it causes malnutrition
• Only young rings, gametocyte seen in peripheral blood • Lab Diagnosis: 1)stool microscopy: detect cyst/trophozite using saline/iodone
• Crescent shaped gametocyte 2)antigen detection
—————————————————————— 3) duodenal aspiration/biopsy
• Symptoms in uncomplicated malriae: fever, chills, sweats, headaches, nausea, vomit, 4)string test(entero-test): detect trophozite from duodenal fluid
body aches, general malaise • Treatment: metronidazole (1st line), tinidazole + nitazoxanide (alternative)
• Diagnosis: blood microscopy using giemsa stain • Prevention: boil/filter water, hygiene, proper sewage disposal, avoid consuming unwashed food
• Treatment: 1)chloroquine → for intraerythrocytic phase → be careful about resistance
2)primaquine → for hypnozoites + radical cure Sibel-Style Exam Focus (based on her question structure)
1. “Which form of Giardia lamblia is transmitted to humans by ingestion of contaminated water or food?” Cyst ✅
Sibel-Style Exam Focus (based on her previous question structure) 2. “Which of the following is the diagnostic form of Giardia lamblia?” Cyst and trophozoite ✅
1. “Which form of Plasmodium in the saliva of Anopheles mosquito is responsible for transmission to humans?” Sporozoite ✅ 3. “What is the infective form of Giardia lamblia?” Cyst ✅
2. “Which of the following is the definitive host for Plasmodium?” Female Anopheles mosquito ✅ 4. “Which intestinal protozoon attaches to the intestinal mucosa with a sucking disc?” Giardia lamblia ✅
3. “Which of the following cells are primarily affected during the erythrocytic phase?” Red blood cells ✅ 5. “Which part of the GI tract is affected by Giardia lamblia?” Duodenum ↑ and jejunum ✅
4. “Which Plasmodium species causes malignant tertian malaria?” P. falciparum ✅ 6. - -
“Which of the following clinical findings is typical for giardiasis?” Foul-smelling, fatty stool (steatorrhea) ✅
5. “Which species of Plasmodium can relapse due to hypnozoites in the liver?” P. vivax / P. ovale ✅ 7. “Which of the following statements about Giardia lamblia is false?” “It invades intestinal mucosa.” ❌
6. “What is the infective form of Plasmodium for humans?” Sporozoite ✅ 8. 6 in stool?” ELISA
“Which of the following tests can detect Giardia lamblia antigen ✅
-

7. “What is the diagnostic method used for malaria?” Microscopic examination of blood smear ✅ 9. “Which of the following is a flagellated intestinal protozoa?” Giardia lamblia ✅
8. “Which Plasmodium form is taken by mosquito during a blood meal?” Gametocyte ✅ 10. “What is the shape of Giardia lamblia trophozoite?” Pear-shaped with two nuclei ✅
9. “Which organ is involved in the pre-erythrocytic stage?” Liver ✅
10. “Which of the following can cause cerebral malaria?” P. falciparum ✅
Cestodes:
• Tapeworms → flat, ribbon-like, set worms, no digestive system
• Definitive host: human (harbors adult worms)
03-common parasites (sibel)
• Intermediate host: anima (harbors larval stage)

# Taenia saginata (Beef tapeworm)

• Definitive host: Human
• Intermediate host: Cattle
• Infective stage: Cysticercus bovis (in undercooked beef)
• Site: Small intestine
• Features: 4 suckers, no hooks on scolex (“unarmed”)
• Disease: Taeniasis → mild abdominal discomfort
• Diagnosis: Eggs or proglottids in stool
• Prevention: Cook beef thoroughly; sanitation

$ Taenia solium (Pork tapeworm)

• Definitive host: Human
• Intermediate host: Pig (also human in cysticercosis)
• Infective stage: Cysticercus cellulosae (in pork)
• Scolex: 4 suckers + hooks (“armed”)
• Diseases:
• Taeniasis: adult worm in intestine (mild GI symptoms)
• Cysticercosis: when human ingests eggs → larvae form cysts in brain, eyes, muscles → neurocysticercosis
(seizures, hydrocephalus)
• Diagnosis: Stool exam (eggs/proglottids); imaging for cysticercosis
• Prevention: Avoid raw pork; hygiene (prevent fecal-oral transmission)

⸻
All of this not included
% Diphyllobothrium latum (Fish tapeworm)
• Longest tapeworm in humans (up to 10 m)
• Intermediate hosts: 1st = Copepod, 2nd = Freshwater fish
• Infective stage: Plerocercoid larva in fish
• Disease: Diphyllobothriasis → Vitamin B12 deficiency megaloblastic anemia
• Diagnosis: Eggs or proglottids in stool
• Prevention: Cook or freeze freshwater fish

& Echinococcus granulosus (Hydatid tapeworm)

• Definitive host: Dog and other canines
• Intermediate host: Sheep, goat, human (accidental host)
• Infective form: Egg (from dog feces)
• Larval stage: Hydatid cyst in liver, lungs, brain, etc.
• Disease: Hydatid cyst disease → pressure symptoms, anaphylaxis if cyst ruptures
• Diagnosis: Imaging (CT/US), serology, surgical observation
• Prevention: Control stray dogs, avoid contact with infected animals, hygiene
———
Laboratory Diagnosis (General)
• Stool microscopy: Eggs or proglottids
• Serology: Useful for Echinococcus
• Imaging (CT/US): Detect cystic lesions (Echinococcus)

' Treatment
• Praziquantel → Taenia and Diphyllobothrium infections
• Albendazole or mebendazole → Echinococcus and cysticercosis
• Surgical removal of large cysts (Echinococcus)
Sibel-Style Exam Focus (like her MCQs)
⸻ 1. “Which of the following is the infective form of Taenia saginata for humans?” Cysticercus bovis ✅
2. “What is the intermediate host of Taenia solium?” Pig ✅
' Prevention (General)
• Proper cooking of beef, pork, fish 3. “Which of the following species has hooks on its scolex?” Taenia solium ✅
• Sanitary disposal of human feces 4. “Which cestode infection may cause cysts in the brain and eyes?” Taenia solium (Cysticercosis) ✅
• Deworm dogs regularly 5. “Which of the following tapeworms is transmitted by ingestion of raw freshwater fish?” Diphyllobothrium latum ✅
• Control livestock feeding 6. “Which cestode infection causes vitamin B12 deficiency anemia?” Diphyllobothrium latum ✅
7. “Which cestode causes hydatid cyst disease in humans?” Echinococcus granulosus ✅
8. “Which of the following is the definitive host of Echinococcus granulosus?” Dog ✅
9. “Which of the following is the infective stage of Echinococcus granulosus for humans?” Egg ✅
10. “Which Taenia species is unarmed (no hooks)?” Taenia saginata ✅
 Endocarditis:
• inf of inner lining of heart (endocardium), mostly inv heart valves
04-cardiovascular
subacute mitral value

(gulden)
,

• Main pathogens: 1) alpha-hemolytic streptococcus (streptococcus viridans) -usually After dental procedure
2) [Link], CNS
> Acute tricupsid
-
value no petechiae , ,

• Pathogeneis: 1) valvular endotel changes

2) bacteremia (transient +common)
3) bacterial adherence
• Symptoms: due to alpha-streptococci they show slowly over months
Subacute: viridanc Acute:

3
S .
S Aureus .

exam

=>

Bacteremia:
• common and transient
• mouth → [Link] S viridians
O D Acute
.

• Skin → [Link] • Peripheral manifestation: splinter hemorrhage, janeway lesions, conjunctival petechiae -
• Urinary tract → [Link], enterocossus • Complications: new stroke with fever → endocarditis, complications: mycotoxins aneurysm,
meningitis, intracranial hemorrhage &

&
Septicemia: & • Diagnosis: 2 separate positive blood culture with typical organism → blood culture most valuable
• systemic inf →microorganisms multiply in blood + release parameter, positive in 85-90% at initial phase, systolic murmur
toxins -> t BiP • Blood culture negativety: slowly growing bacteroa HACEK/funhgal endocardit must be in
• Clinical pic: ill appearance, chills, low BP, GI symptoms + consideration, brucella endocarditis → needs prolonged incubation than normal (as 14 days)
high breathing rate → respiratory alkalosis • Treatment: therapy must be microbial;, antibiotics gives at maximal doses, additional given for
• Caused by: bacteria/fungi long time
• Virulence factor: cell wall/membrane comp • Prognosis: viral → resolved spontaneously, bacterial → can be severe, result in death
• Diagnosis: blood culture O
• Treatment: broad spectrum antibiotic until identification + &
susceptibility tested
byitself m
Naviral
- resolves -

imp
Pericarditis: -D very
-

• infl of pericardium (outer sac of heart)

• Types: 1)Infectious: viral (most common), TB, bacterial = =

2)Non-infectious: trauma, uremia (renal failure),

radiation,autoimmune (SLE) =>
3) acute/chronic T
• Main pathogens: 1) HIV 2) Enteroviruses(coxsackievirus, echovirus)
3) [Link]. [Link] (bacteria). 4) [Link] - > bacterial
⑧ After Dental
procedure
E -

3
value
staph epidermic usually prosthetic - grampositive
&
I

• Treatment: anti-inflammatory drugs, monitor for dev of pericardial effusion/tamponade, bacteria

-

-
Dental
Usually After
FE ,
Viridans streptococci-+ subacute
inf requires specific antibiotic therapy Procedure -> Dev Slowly coag neg staphylococci
• Prognosis: viral → resolved spontaneously, bacterial
-
→ can be severe, result in death E . coli + pseudomonal - I rare , usually
in immuno camp /health care 9210(
Catheter-related infections: >
- most common pathogens

• CDC defines central line as: catheter whose tip terminates in great vessel
-

• Common organism: 1)children → coag neg staphylococci (CNS)(34%) followed by [Link](25%)

Myocarditis: 2)neonates →CNS(51%), followed by candida, enterococci, and gram-neg bacilli
complications
3)infants → with short gut syndrome are more likely to have CRBSI secondary to gram-neg bacilli
KeCriter
#
is
• infl of myocardium (heart muscle)
-

mycotic aneurysm
• Pathogenesis: colonization from skin/hands of worker, intraluminal/hub contamination,2nd seeding of infusate/additives
-

-
• Types: 1)Infectious: viral (Enterovirus → coxackie B), bacterial - intracranial hemorrhagi
3 mini
-

2)Non-infectious: allergy, toxic, autoimmune

-
pulmonary embalism -
1 +
such as heparin flush, risk → repeated cathterization
ocardial infraction Smihr -
my • Diagnosis: only done when bloodstream inf is suspected, blood sample obtained protein to antibiotic therapy, skin prep
- -

3) acute/chronic -

congestive
~
heart failure

• Most associated with viral inf in heart + infiltration of cardiac muscle by T-lymphocytes most common

• Symptoms: chest pain, arrhythmia, sudden death

• Treatment: for heart failure
• Prognosis: early resolution for com recovery(<2 weeks), prolonged symptoms (>2 weeks-
months) worsens heart failure → death/cardiac transplant • Treatment:

&

•
O E
Most isolated pathogen from catheter related infections: [Link]

Brucella:
•
•
•
Zoonotic
pasta Y
Transmission: raw milk + dairy products(unpasteurized white cheese)
Ondulent fever
Infection of central nervous system:
• Diagnosis: achieved by laboratory examination
Lab diagnosis of CSF: 05-CNS infection (gulden)
Gram Stain:
• Serious + potentially life-threatening
• [Link] → EZN stain
• Caused by: bacteria, viruses, fungi, spirochetes, parasites
• Cytocentrifuge prep of CSF in case of aspecting meningitis: lymphocytes
• Diagnosis based on: 1) age 2)symptoms+clinical signs 3)CSF analysis
present, background bloody, no organmsims
4)imaging (CT/MRI). 5)laboratory test (culture, PCR..)
• Resulting from tularemia: reactive lymphocytes with monocytoid feature (not
viral) no organisms seen, culture positive → Wright Stain
neontal period /postpartum >
- E Coli
-
Culture:
very early
Meningitis: most common sympti headache • [Link]: at least 3 tubes of lowenstein-Jensen medium, best grown using
• infl of meninges multiple large vol of CSF sample, at lest 15 ml (40-50 mL), positive (56% on
Bacterial: most severe + life-threatening 1st time)
• Age groups: 1)Neonates (<1month): [Link], streptococcus agalactiae (group B), Listeria monocytogenes
-
• [Link]: sus from India ink/clinical ground, sediment should ne
2)infants (1-23 months): [Link]. streptococcus agalactiae (group B), [Link], inculcated on 2 tubes of sabouraud dextrose away at 35-37 C for 1 month,
streptococcus pneumoniae, [Link] fungal cultures →positive 95% of [Link], 66% →candidal meningitis
3)children (>2 years): streptococcus pneumoniae, [Link] Blood culture:
4) older adults (>65 years): streptococcus pneumoniae, [Link], Listeria monocytogenes
-
• Bacterial meningitis is often with bacteremia and causative organism is
sometimes isolated from blood when CSF culture is neg
All ages -> H influenza-N-meningitis J pasQ
• Group B strep and [Link] dominate early life
• [Link] and [Link] dominate later Latex agglutination:
neonates - E coli Butrept
• Listeria in elderly+ immunocompromised
.
-
group • Allows rapid detection of bacterial antigens in CSF
Viral: milder + self limiting Adults
- Nimeningitis S
+ Pneumonial
.

• Sensitivity varies btw bacteria

• HSV-1→ causes encephalitis&+ HSV-2 → resurrect aseptic meningitis
Elderly
- Listeria • For [Link] sensitivity is 60-100%, Lower for other bacteria
• In CSF → high lymphocytes, protein N/slightly high, glucose N PCR:
• Outcome → full recovery > mostcommon- enterovirus (COX Eno)
viral -
• High sensitivity + specificity, can be done with small volumes of CSF
• Diagnostic tool →PCR
,
• Multiplex PCR by CSF
fastest for
sensitive
CSF shunt infections:
+

meningitis
Viral

• Some,tomes patients need CSF shunt, tube that diverts fluid, when bacteria colonize → infection
• Incidence: 5-41%, occur within few months of surgery, caused by skin flora
• Agent: highest incidence →staphylococci
• Diagnosis; direct culture of CSF/shunt fluid → definitive diagnosis
neutrophil predominance
↓ glucose i protein
,
,

Spreumonial
lamcet-shape
gram Dos
,

Diplocacci

Encephalitis:
• Caused by: Herpesvirus (HSV-1) + Enterovirus
• Diagnosis: MRI + PCR (fpr HSV)
• Treatment: acyclovir (empiric), supportive care
• Prognosis: depends on cause, HSV untreated → fatal
Brain Abscesses:
• localized area of infection in brain →leads to collection of pus
• contains: organism and infl cells
• Diagnosis: contrast CT/MRI + surgery (aspirated material and specimens)+ when results are
given empirical anti microbial therapy should be initiated according to patient’s condition
• LAB diagnosis: examine CSF Sample (insert sterile hollow needle into spinal subarachnoid
space)+Blood Culture
Macroscopic appearance/lab diagnosis:
bein
1) normal CSF → crystal + colorless lowens
2)pathological process → cloudy, turbid, bloody, viscous,clotted - jensen
3) Xanthochromia → yellow color from old RBC break down bilirubin →in [Link]
4) turbid CSF →pus-like in bacterial meningitis
 Primary immunodeficiency: *
• C inherited/occurs by exposure to utero to environmental factors 06-infection in immunocompromised
• Rare patients (gulden)
• Factors affecting innate system: complement deficiencies, phagocyte cell
deficiency
• Chronic granulomatous disease: inherited
• Factors affecting adaptive system:T-cell defect, B-cell deficiencies, severe
combined immunodeficiency CMV , HSV , VzV

mycobacterium Listeria
Toxoplasma
Secondary/acquired immunodeficiency:
• underlying disease state → occurs as result of treatment for a disease
• Increasing
• Factors affecting innate system: burns, trauma, major surgery, catheterization,
foreign bodies, obstruction
• Factors affecting adaptive system: malnutrition, infectious diseases, neoplasia,
chemotherapy, transplantation, and splenectomy
Burn Wound Infections:
• damage body mechanics barrier
• Imp pathogens: 1)[Link]. 2)other gram neg rods 3)[Link]
-

4)[Link] 5) Enterococci
• [Link] → most imp cause of → surgical wounds
-

• [Link] → most common cause of → prosthetic valve + joint inf → highly

-

resistant to antibiotics
• Exam tip: burn wounds often inv mixed flora (gram-neg rods + gram-pos cocci
+fungi)

Compromised patients:
• can be inefcted with any pathogen that infect immunocompromised patients
• Effective antimicrobial therapy: 1) difficult to achieve in absence of functional immune
response even when pathigen is susceptible to the drug
in vitro

Important opportunistic pathogens:

G
• Candida → most common fungal pathogen in compromised patients
• [Link] → most common in ppl with impaired-cell mediated immunity
• [Link] → may occur after years of exposure
• Invasive aspergillosis → high mortality in compromised patients
• [Link] → cause systemic disease only in ppl with deficient cellular immmunity
• Cryptosporidium + cystoisospora bellli infections → severe diarrhea inG AIDS
• Immunosuppression may lead to reactivating of → strongyloides stercoralis

Agents most likely to cause nosocomial infections:

• [Link]
•
•
[Link]
[Link] S paste
Pre-transplantation baseline serology:
• Carried out to determine both donor + recipient status for amulet of virus infections:
1. HIV, HTLV,
2. CMV
3. hepatitis B + C: in transplant recipients
4. Adenovirus: high mortality rate
5. EBV: can lead to tumor dev
6. HSV reactivation
>
- seen in
patient
immunocom

7. Polymaviruses(Bk and JC): can cause haemorrhagic cystitis + progressive multifocal

leukoencephalopathy

Amavirusjc
-
Brain
is
at
a
-
AIDs
patientsmost
pheroonia

No cardia Asteroides
mem
immunocomprimised
pulmonary inf
in
 Primary SSTIs:
Skin defense: 07-skin soft TIs (gulden)
• Single bacterial pathogen directly invades intact healthy skin
• Natural barrier
• Thru: mini truma, insect bite, microscopic break
• Main factors: 1) limited moisture 4) salty sweat
• Acute localized → responds well to antibiotic therapy
2) acidic PH. 5) sebum, fatty acids, urea
• Majority: [Link] + [Link] (most freq isolated from primary skin inf)
3) low surf temp 6)comp from normal flora
• Community associated → methicillin-resistant [Link] (CA-MRSA) has emerged
• Infection occurs: when skin barrier broken/local condition favors Burn wound inf:
• Empirical therapy starts before lab confirmation
growth • Secondary polymicrobila inf occurs in skin damaged by thermal/chemical/electric
• Diagnosis: CRP, white blood cell count (WBC), culture BUT blood culture is not recommended
Diseases: burns
Predisposing factors for SSTI: Erysipelas: • Skin barrier is destroyed allowing bacteria from patient skin, GI tract, hospitals env
• Although skin has protection certain local + systemic factors can • Inf of superf layer of skin sutaneous lymphatics
- to invade
weaken it • Caused by: beta-hemolytic streptococcus Pyogene (usually) • Infected by [Link]
1. High concentration of bacteria → large bacteria of surf • Treatment: Penchillin G (for moderate and serious) • Treatment based on: AST with these nosocimial resistant pathogens
2. Excessive moisture → sweat, humid environments Impetigo: silver sulfadiazine
producing blue-green P Aeruginosa
pus fruity
ador -

3. Inadequate blood supply → reduce oxygen + immune cell • Superf skin inf of epidermis
· ,

>
-

honey colored crusted region

delivery localized impetigo treatment Tropical mupirocin

• Highly contagious, by contact -
-

4. Presence of bacterial nutrients → accumulation of serum, pus, • Caused by: [Link], but [Link] either alone or in combo with [Link] Bite wound inf:
tissue debris • Treatment:dicloxacillin Bullars impetigo -D Arreus
S. • After anima/human bite due to microorganisms from flora of mouth
5. Damage to corneal layer (epidermis) → cuts, abrasions, insect Cellulitis: • Secondary polymicrobial infection
bites, burns • Acute spreading inf of dermis and subcutaneous 1. Dog Bite → localized cellulitis +pain → pasteurella multocida
• Ch by: disuse, ill defined erythema, swelling, warmth, tenderness 2. Cat Bite → 20% inf →pasteurella multocida
Microbial invasion “lines of attack”: • By: [Link] or [Link] 3. Human Bite → aerobic (30% Eikenella corrodens) + anaerobic ([Link] +
Direct entry thru skin: • Streptococcal cellulitis and staphylococcal cellulitis are indistinguishable so we give →semisynthetic streptococci)
• Enters thru breaks/truma to epidermis penicillin (dicloxacillin) or 1st-gen cephalosporin (cephalzolin) is recommended until def diagnosis by • All wound should be be irrigated with sterile saline solution to reduce bacterial
• Local skin infection culture in 5-10 days count of bite
• Ex: [Link], [Link], anaerobic bacteria, fungi • Possible side effects of penicillin: irritation of mouth/throat, severe all aerobic reaction (hospital) • Treatment: amoxicillin-clavulanic acid for oral outpatient therapy
(dermatophyte) • Approach to dog bites: 1)tetanus/diphtheria toxoids administered
Spread from systemic (hematogenous) inf: Secondary SSTIs: 2)if exposed to rabies →irrigation of bite wound +wash with
• Spread from primary internal focus Diabetic foot infection: soap, tetanus prophylaxis, antibiotics prophylaxis (if
• Via bloodstream to skim, producing secondary cutaneous lesions • Chronic poly microbial infection that dev with diabetes mellitus due to neuropathy, ischemia, impaired indicated), start rabies immunization scheme
• Reflects systemic disease wound healing 3)post-exposure prophylaxis → passsive antibiotic + vaccine
• Ex:[Link], [Link], [Link] pseudomonas • Early/mild → [Link] , streptococci administration
Skin manifestation of mucocutaneous viral inf: aeruginosa • Chronic/deep/necrotic → polymicrobial (mix)
• Viruses replicate in epith cells of skin causing →vesicular/wart- - • Foul smelling discharge + necrosis
like lesion • Osteomyelitis: 30-40% of it occurring
• May shed infectious viruses • Occurs on preexisting ulcer/ischemic tissue
• Viruses found in vesicular fluid
• Crusted/dry lesion no longer shed viruses
Infected pressure ulcers:
• Transmission: direct contact with active lesions
• Predisposing factors: prolonged immobility, poor nutrition, dehydration, diabetes mellitus, vascular
• Ex:HPV, HSV, VZV, monkey pox
disease, fecal/urinary incontinence, elderly/debilitated - Bedridden (immobile patients
• Causative agent: polymicrobial
Decubitus ulcer
• Aerobic gram-pos, gram-neg and anaerobes are frequently isolated
• Treatment:at least 2 weeks trial of topical antibiotic (silver sulfadiazine/ triple antibiotic) recom for clean
ulcer

foul-smelling discharge from Anaerobic bacteria

Chronic ulcer indicates
 far
Kolt Keratinized specimen
-
pre-treatment on

fungal microscopic examination

Superficial mycoses:
1)colonize the keratinized outer layers of the skin, hair,
and nails

2)Infections caused by these organisms elicit little or no

host immune response + nondestructive + asymptomatic

3)They are usually of cosmetic concern only

Causative
Disease Affected Area Key Features. . Treatment
Organism

Versicolor
Tinea Hypo- or hyperpigmented scaly patches (“spaghetti. Topical azoles or selenium sulfide shampoo
Pityriasis Malassezia Skin (trunk, and meatballs” on KOH prep),wood’s lamp; yellow-green For widespread infection oral ketoconazole or itraconazole
versicolor. furfur (yeast) shoulders) fluorescence, asymptomatic. Culture; olive oil as lipoid
source+ yeastlike colonies in5-7 days

Hortaea Brown or black macules (looks like a stain), not Topical therapy, whitefield ointment, anole creams, and
Tinea nigra Palms or soles
werneckii contagious, septate hyphae, irregular edges terbinafine

Hard black nodules on hair, related to poor Haircut+ proper regular washing
Black piedra Piedraia hortae Hair shaft (scalp)
hygiene

Soft white nodules on hair, related to poor Topical azoles, improved hygiene, shave infected hair
Trichosporon Hair shaft (beard, hygiene
White piedra
species pubic hair)
Pityriasis (Tinea) Versicolor:
• caused by; Malassezia furfur (yeast)
• Infection type: superficial mycosis
• Skin lesions: hypo/hyper pigmented scaly patches often on trunk/shoulders
• Diagnosis: G KOH shows “Spaghetti
-
and meatballs”
• Wood’s Lamp: lesions fluorescence = yellow-green under wood lamp
• Geography: world-wide
• Immune testing: clinical + microscopy
• Olive oil source of lipid for culture
• Yeast like colonies at 30 C for 5-7 days
•

Mucocutaneous:
• causes virus shedding from lesion → Papillomavirus
Cutaneous mycoses:
1)fungal infections that involve the keratinized layers of the skin, hair, and
nails.
2)infections go deeper than superficial mycoses but do not invade living
tissues.
3)They cause more inflammation and are often itchy, scaly, or disfiguring.

Dye used:
Macroconidia + microconidia Lactophenol cotton blue (LPCB) stain
1)Dermatophytoses:

All 3 of them produce macroconidia in culture tinea infections, these are cutaneous mycoses caused
specifically by dermatophytes — fungi that digest
keratin.
Arthraconidia
hyaline septate hyphae
-
Appear As:

Causative agents:
Has macro
[Link]
+microconidia [Link]
[Link]

2)Non-dermatophytoses:

fungal infections of the skin, nails, or hair caused by

only macroconidia non-dermatophyte fungi, including yeasts and molds.

Laboratory diagnosis: L
causes cutaneous my
coris
Causative agents:
• SDA agar
• Colonies in 7-28 days [Link] - moist skin folds, oral, genital
• Colonies before 3 days are saprophytic molds [Link] versicolor - superficial skin
Direct microscopy+
culture
Caborrad dextrose
Agar [Link] onychomycosis - nail infections by
Treatment:
• topical agents (cuz they are localized) Scopulariopsis or Fusarium
• Oral anti-fungal agents
Subcutaneous mycoses;
1)chronic fungal infections that occur beneath the skin, usually after traumatic implantation
of fungal spores (e.g., via thorns, splinters, or soil-contaminated wounds).

2)These infections extend into deeper tissues like the dermis, subcutaneous tissue, and
even bone, but rarely become systemic.

Route of entry: Traumatic implantation (e.g., walking barefoot)

Progression: Slow, chronic, and often localized infections
Immune response: Granulomatous inflammation, abscesses, sinus tracts
Geography: More common in tropical and subtropical regions
Occupational risk: Farmers, gardeners, laborers

Disease Causative Organism(s) Clinical Features Clinical manifestation Treatment

Able to synthesize melanin present in Chain of subcutaneous Oral potassium iodide (3-4
Sporotrichosis Sporothrix schenckii (dimorphic fungus) dark cell walls of conidia, Nodules along nodules along the lymphatic weeks)
lymphatics (“rose gardener’s disease”), sporadic drainage

Warty, cauliflower-like lesions; black sclerotic Chronic fungal infection Itraconazole +terbinafine in
Chromoblastomycosis Fonsecaea, Cladosporium, Phialophora
bodies (“copper pennies”), forms Medlar bodies affecting skin and refractory cases cuts
subcutaneous tissue combined with flucytosine

Swelling, sinus tracts, draining granules Chronic, painless, soft tissue Requires combined ,edical +
Mycetoma Fungal: Madurella spp. Bacterial: Actinomadura, (black or white) swelling, surgical therapy, oral azole
Nocardia (actinomycetoma)
(6-24 months)
Cystic or nodular lesions; usually in
Phaeohyphomycosis Pigmented fungi (e.g., Exophiala) immunocompromised Itraconazole; oral potassium
in saturated solution

Facial swelling or subcutaneous masses;

Entomophthoromycosis Basidiobolus & Conidiobolus species Itraconazole; oral potassium
mostly in children (Africa, India)
in saturated solution
Eumycotic Mycetoma:
• chronic granulomatous fingal infection of the skin, subcutaneous tissue, and sometimes bones
• CH BY; dwelling, draining sinuses, and grains (aggregated of infecting organisms)
• lab diagnosis; microscopic examination (phialides), culture (brown diffusable pigment in agar),
radiographic techniques
• treatment; combined medical and surgical therapy, antifungal drugs for 6-24 months
• Caused by fungi like madurella mycetomatis