INFECTIOUS MODULE MICROBIOLOGY SUMMARY

(Reference- Levinson Microbiology)

The list of organsims taught in infectious module is given at the end of this doc.

PARASITES:

Intestinal Parasites:
NAME CHARACTERSTICS TRANSMISSION PATHOGENESIS CLINICAL SYMPTOMS DIAGNOSIS TREATMENT PREVENTION OTHER
IMPORTAN
T POINTS
Entamoeba histolytica • Present as cyst • Cyst contaminated • Cysts colonize • Acute= dysentery • O&P=can be false negative • Metronidaz Filtration and Wet
(intestine) and water in caecum and (bloody, mucous • Cysts in normal stools ole or boiling prevent mount= a
trophozoite • Fecal oral route colon containing (carriers) trophozoites in tinidazole cysts while drop of
(after • Male homosexuals • Invade diarrhea),lower diarrhea (symptomatic • Iodoquinol, chlorination water is
intestinal (anal-oral route) epithelium and abdominal patients) paramomyci doesn’t placed b/w
invasion) • NO animal cause ulcers pain,tenesmus,flatu • Cyst with 4 nuclei n for the slides
• chromatin. reservoir (flask-shaped) lence. • Cyst has 4 nuclei= 8 patients with
• Trophozoites • Chronic= occasional with specimen
invade portal diarrhea, weight intestinal to observe
circulation=righ loss, fatigue. disease only under
t liver lobe • Amebic abscess= trophozoites. (cysts) microscope
abcess right upper • Trophozoite nucleus= central . It is done
• Intestinal quadrant pain, nucleolus with even lining of for those
abcess= ulcers+ weight loss, fever, peripheral organisms
bloody diarhea tender enlarged • PCR= For antigen that live in
liver • Indirect hematoglutination watery
test are +ve in invasive environme
disease nt.
• Trophozoite with To watch
endocytosed RBCs intestinal
protozoa
iodine
’ stained,
trichrome
stained
and normal
saline wet
mount is
used.
Gardnere
lla= clue
cells

Figure 1 Clue
cells

Candida=
pseudohyp
hae with
budding
yeast.

Figure 2
Vaginal
candidiasis
saline wet
mount.
Giardia lamblia • Cyst and • Cyst contaminated • In duodenum • Watery (non- • O&P • Metronidaz Boil, filter, iodine PCR= To
trophozoite water • Doesnot invade bloody), foul • PCR? ole or treated water detect
• In Hikers • Fecal oral route mucosa (no smelling diarrhea • String test tinidazole antigen
• Oral anal route bloody • Nausea, anorexia, • Trophozoite= pear shaped, 2 ELISA=To
diarrhea) nuclei, 4 pair of flagella and detect the
flatulence,
• Doesnot enter abdominal cramps suction disk presence
blood stream of
for week or
• Cause excessive months.
antibodies.
mucous
secretion= fat
• No fever Figure 3 Giardia lamblia trophozoite

malabsorption • Cyst= thick walled, 4 nuclei,

several internal fibres

Figure 4 Giardia lamblia cyst iodine stained

Cryptosporidium hominis Causes • oocyst • In jejunum • Watery non bloody • Only protozoan that stain DOC=Nitazox Filtration Chlorinatio
cryptosporoidosis= contaminated • No invasion diarrhea, more acid-fast. Kinyoun acid fast onide for n is
diarrhea in water • No toxin sever in stain is used. Looks like ineffective
immunocmpromise • Fecal oral route immunocompromis
immunocomp against
d patients and most • Humans and ed etent cysts.
severe in HIV animals are emerald gems Paramomycin
patients. reservoir Figure 5 Cryptosporidium hominis for
Oocysts, • PCR immunocomp
sporozoites,trophoz
oites, schizonts, romised
merozoites,micro
and macrogametes
Trichomonas vaginalis • Causes • STI Vaginitis, cervicitis • Watery, foul • Strawberry cervix • Metro • No
trichmoniasis smelling • Vaginal pH more than nidaz prophylaxis
greenish 4.5
ole or
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
• Only • Only present in vaginal • Trophozoites=pear tinida • Treat the
trophozoites humans, no discharge shaped with jerky zole partner
and no cycts animal reservoir • Itching and motion. Have central • Condoms
• In vagina and burning nucleus, 4 anterior • Maint
prostate sensation flagella, undulationg ainen
• Men are mostly membrane extending ece of
asmyptomatic 2/3rd of length. vagin
al pH

Blood Parasite:
Plasmodium: • P.falciparum= • Via Anopheles • P. vivax and • Fever,chills,night • Blood smear+Giemsa-stain: • DOC for • Chemoprop Plasmodiu
• P. Malariae most aedes mosquito, P.ovale form time sweats, o Thick=presence of uncomplicat hylaxis m species
• P. vivax dangerous placenta, blood hypnozoites( nausea, vomiting, , organism ed malaria= before produces
• P.ovale • P Vivax=most transfusion, IV dormant stage) abdominal pain, o Thin= identification Chloroquine travelling to hemozoin
• P. falciparum prevalent drug abuse. in the liver= anemia, of species (kill endemic pigment by
• P.falciparum= • Human=schizogon relapse splenomegaly, merozoite, area breakdown
chloroquine y (asexual stage) • Periodic release hyperplasia no effect on • Non of
resistance • Mosquito= of merozoites macrophages and hypnozoites chloroquine hemoglobi
(areas:) sporogony (sexual causes fever lymphocytes = ) resistant P. n while
stage) symptoms= headache myalgia Figure 6: P.falciparum • Primaquine falciparum Babesia
• Sporozoites chills, fever, arthralgia. (Trophozoite)=Signet ring shaped, = kills or other species
present in the sweat. • Fever is continuous Mutiple trophozoites in 1 RBC is hypnozoites Plasmodium donot.
saliva of mosquito • Sporozoites, in the start but unique to P.falciparum. (causes species
and enters in the merozoite, later intermittent in severe endemic
liver from the trophozoite (in nature. hemolysis in areas=
blood within 30 rbcs), male and • P.malariae= G6PD chloroquine
mintues. female Quartan fever deficiency= • Chloroquine
gametocytes (in (after every 72 contraindica resistant
RBCs, ingested hrs=every 4th day) Figure 7: P.vivax (Trophozoites)=1 ted) P.falciparum
by mosquito) • P.vivax,P.ovale, trophozoite per RBC. RBC larger • Uncomplicat =
P.falciparum=tertia than normal RBCs. 1.5x ed mefloquine
n fever (after every P.falciparum or
48 hrs=every 3rd malaria= doxycycline
day) Coartem OR
• P.falciparum= (artemether atovaquone
malignant malaria, +lumafantri +proguanil.
extensive Figure 8: P.malaria (trophozoite)= ne) or • Primaquine
hemolysis, cerebral same as P.ovale but normal sized Malarone in P.vivax
malaria, kidney RBC (atovaquon and P.ovale
damage=hemoglobi e+ endemic
nuria (black water proguanil) areas.
fever). • Complicated • Netting,
• P.vivax and P.falciparum water
P.ovale= benign = IV drainage,
malaria. Figure 9: P. falciparum artesunate insect
• Sicle cell (Gametocyte)= crescent/ banana or repellent,
anemia=safe from shaped quinidine. inseticide,
malaria DDT.
• G6PD Deficiency= • No vaccine
save from
P.falciparum
• Duffy blood
homozygous Figure 10: P. malaria
(Gametocyte)=granular, round,
recessive (no duffy
have the size of normal RBC
blood group)= save
from P.vivax

Figure 11: P. ovale (Gametocyte)=

round, granular, schuffner's dots,
gametocyte is larger than normal
RBC

Figure 12: P. malaria

(Schizont)=granular, 6-12
merozoites

Figure 13: P.vivax (schizont)=16-

24 merozoites, granular, larger
than normal RBC.

Figure 14: Schuffner's dots=

P.vivax and P.ovale
• Schuffner dots= red stain
(Romanvsky stain)
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
Leishmania • Visceral • Use sand fly • Promasti • L.donovani=hy • L.donovani:Biopsy or DOC=sodium Netting, •
• L.donovani leishmani as gotes=sa perpigmented touch preparation (bone Stibogluconate. insecticide,
• L. tropica asis(kala- vectors.Many lesions, marrow, spleen, lymph However,
ndfly insect
• L. mexicana azar)= vertebrates pancytopenia,f nodes)= amastigotes in liposomal
• L. brazilliensis L.donova are • Amastig ever,weakness macrophages, High IgG, amphotericin B is repellent,
ni reservoirs. otes= ,hepatospleno Indirect ELISA,Skin also used for protective
• Cutaneou human megaly. test=negative in active L.donovani. clothing
s disease but +ve after
macroph
leishmani
asis= ages
L.tropica • L.
and donovani Figure 15: Visceral
L.mexican =Infects leishmaniasis recovery
a • L.braziliensis=i Figure 18: amastigotes in the
reticuloe
• Mucocuta nitially papule macrophages. L.donovani
neous ndotheli • For all other
at the bite site
leishmani al system then at leishmania=
asis= (liver,spl mucocutaneo antimastigotes in smear
L.brazillie een and us junction at taken from the lesion.
nesis nose and Leshmanian skin test is
bone +ve
mouth.
marrow) Disfigurating
• L.brazilli granulomatou
ensis=inf s lesions at
ects thenasal
cartilage but
mucous not the
memebr adjacent bone.
anes,
cartilage
and skin.
• L. tropica
and Figure 16:
L.mexica Mucocutaneous
na= skin leishmaniasis
only • L.mexicana
and L.tropica=
red papule at
the bite site
enlarges
slowly into
multiple
satellite
nodules that
coalsce and
ulcerate

Figure 17: Cutaneous

leishmanisis.
Trypanosoma • T.cruzi • T. cruzi life T.cruzi is transmitted • Bites • Trypomastigotes=blood, • Nifurti • Insect •
• T.cruzi causes cycle: via reduviid bug, preferentially amastigotes=cells(mycar mox(D control
• T.gambiensa Chagas’di reduviid bug blood transfusion, arround the dial, glial, OC) or ,
• T.rhodesiense sease ingests organ eyes and lips. reticuloendothelial cells. benzid housin
(America trypomastigo transplantation, Effect i.e: bone marrow, liver, azole g
n tes from across myocardial spleen. for improv
typanoso reservoir or placenta.Host= cells(endocard • Bone marrow aspirates trypan ement,
miasis) host. In the humans and animals itis), glial cells or muscle biopsy show omasti using
• T. insect they (fox, (megacolon, amastigotes, culture in gotes. insect
gambiens multiply and racoons,armadillo, megaesophag special medium, • No repelle
a and differentiate rat),Reduviid bugs us), cardiac Xenogiagnosis (An u such nt.
T.rhodesi into lives in the walls of arrythmias. ninfected laboratory very Blood
ense epimastigote village houses. • Acute: lips raised reduviid bug is effectiv screeni
causes s. Insect • T.gambien (facial edema, allowed to feed on the e drug ng.
sleeping inject the sa and nodule patient and after several against • No
sickness trypomastigo T.rhodesie (chagoma) weeks its gut contents amasti prophy
(African tes in the nse near bite site, are analyzed for gotes. lactic
trypanoso host and transmitte fever, organism, Indirect ELISA, • Sumari or
miasis) reservoir and d via tsetse lymphadenopa indirect n vaccine
form non- fly. thy, hemagglutination test, (Canno availble
flagellated Humans hepatospleno complement fixation t cross yet.
amastigotes are megaly), eyes test. BBB),
which effect reservoirs (Romana’s Penta
every cell for sign= midine.
mainly glial, T.gambien unilateral When
myocardial sa and palpaberal CSF is
and animals swelling). 2 infecte
reticulaendot (domestic months. d give
helial. .i.e. cattle • Chronic: melars
Figure 20: T.cruzi
Amastigotes and wild) myocarditis, oprol.
trypomastigotes. Acute
divide into are constipation,
trpomastigot reservoir cardiac
es, enter in for arrythmia or
blood, T.rhodesie congestive
ingested by nse. heart failure
reduviid bug. • T.gambien (most
• T.gambiensa sa and common
and T.rhodesie cause of
T.rhodesiens nse: death). Figure 21: T.cruzi amastigotes in
e life cycle is trypomasti • Tgambiense heart tissue biopsy. Chronic
same as gotes and
T.cruzi except injected in
T.gambiense and
T.rhodesiense:
amastigotes skin then skin ulcer at T.rhodesiense= 1)
are not blood then bite site, aspiration biopsy of the
formed. Both cervical inermitent chancre and enlarged
have 3 week lyphadeno weekly fever cervical lymph nodes also
life cycle. pathy and and
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
Both have brain enlargement shows trypanosomes. 2)
antigenic (encaphiliti of posterior Trypanosomes present in
variation that s) causing cervical lymph
changes solmnolen node CSF with elevated protein
every 10th ce and (Winterbotto and pleocytosis. 3) ELISA for
day coma. m’s sign), IgM.
conitnuously encephalitis
invading host (headache,
immune insomnia,
system. mood
changes,
muscle
tremors,
slurred
Figure 22: difference between
speech,
T.cruzi and T.brucei gambiense
solmnolence
and T.brucei rhodesiense
and
coma).fatal
due to
pneumonia

Figure 19:
Trypanosomal chancre
(African sleeping
sickness)
Intestinal cestodes: • • • • • • •
Taenia • Taenia is • Taenia • Teania • Taeniasis: • O&P stool test= • Praziqu • Adequ •
• Teania solium (causes the solium: solium:Tae diarhea and proglostids are more antel ately
cystecercosis and largest transmitted nisis= malabsorption commonly seen than • Albend cooked
taeniasis) tapewor via caused by • Cysticercosis: eggs. Eggs have same azole meat.
• Taenia saginata m. Maybe undercooked ingestion Skin nodular morphology but (for • Proper
(causes taeniasis only) upto 5 m. pork in which of adult lesion proglotids have neuroc sewage
cystecerci form or conataining different. ysticerc drainag
(larvae) are larvae.divi cycts, brain= osis). e
present and des in neurocyscerco system.
water small sis: seizures,
contaminate intestine hydrocephalus
d with human for 3 , eyes= uveitis,
feces (eggs). months to retinitis.
• Teania adult form.
saginata: Causes
transmitted diarhea
via and
undercooked malabsorpt Figure 24: Taenia solium; scolex
Figure 23: Cutaneous
beef ion. has 4 sucker and circle of hooks.
cysticercosis
conatining Cystecerco
cystecerci or sis= the
human feces adult form
containing proglottide
eggs. burst with
• The cow and eggs
pig don’t release
shed eggs. It which Figure 25: Taenia saginata scolex
is only unique differentiat with 4 suckers but no hooks.
to humans e into
instead the embryo
pig and cow (oncospher
have cycterci e) that
in their buries in
muscles the
which infects intestine
humans. to blood
vessels and
Figure 26: Taenia solliun
effects
proglotid has 5-10 primary
every
uterine branches while Taenia
tissue but
saginata has 15-25.
mainly
skin, eyes • C.T. Scan
and brain. • ELISA (maybe
• Taenia negative in
saginata: neurocysticercosis)
Taeniasis=
caused by
ingestion
of
cyctecerci
(larvae ) in
uncooked
beef and
water
contamina
ted with
human
feces
(eggs)
Diphyllobothrium latum • Longest • Transmitted • Effects • Abdominal • O&P: adult=No hooks, • Praziqu • Adequ •
(fish- tapeworm): causes tapewro via small discomfort, have only 2 elongated antel ate fish
diphyllobothriasis. inadequately intestine, diarhea, sucking grooves.
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
m:upto cooked fish uptakes magaloblastic Proglotids are wider cookin
13m or water vit-B12- anemia. than long. Egg= yellow- g
contaminate mgaeloblas brown with no hooks • Propal
d with human tic anemia. and operculum at one disposa
feces. end. l of
• Pleocercoids human
(larvae) in feces.
the muscles
of the fish.

Figure 27: Diphyllobothrium

latum scolex

Figure 28: Diphyllobothrium

latum egg
Echinococcus granulosus • • Eggs • Unilocular • Maybe Biopsy: • Albezd • Don’t •
(Dog-tapeworn); causes transmitted hydatid asymotmoatic azole feed
echinococcosis via dog feces, cyst= one but may have • May the dog
ingested by large fluid liver hydatid need with
Figure 29: Echinococcus
humans and filled cyst. cyst (liver surgical slaught
granulosus; unilocular hydatid
sheep (eggs Outer layer dysfunction), excisio ered
cyst show brood capsules
mature and is thick and cerebral cyst n. A sheep
showing multiple protoscoleces.
embryo fibrous. (headache, protosc meat
burries in the Inner side focal Indirect hemagglutination olicidal or
intestine has neurological test. agent organs.
specially thousand deficit), Cyts in should •
liver, lungs, of cysts in lung can erode be
bones and fluid called into bronchus used
brain forming scoleces (bloody i.e.
hydatid cysts. and sputum). hypert
Dog eats daughter • If cyst onic
sheep liver cysts called rupture= saline
with hydatid protoscole anaphylactic to
cyst. ces within shock preven
them. t
Scoleces acciden
settle in tal
the bottom dissemi
of hydatid nation.
cyst called
hydatid
sand.
Echinococcus • • Eggs • Cyst has no • Jaundice and Biopsy: • Albend • •
multilocularis transmitted fibrous weight loss azole
via fox feces. capsule so • Surgica
Consumed by it spreads l
rodents and in the liver remova
humans like honey l
(hunters and comb
trappers).
Eggs ,ature,
embryo Figure 30: Echincoccus
burries in multilocularis; multilocular
intestine and hydatid cyst show no fibrous
gets to the capsule
liver, forms
multilocular
hydatid cyst.
INTESTINAL TREMATODES: • • Fresh water • Infect liver, • May be O&P test: eggs • Praziqu • Proper •
larvae spleen, gut asypmtomatic antel disposa
Schistisoma (blood-flukes) (cercariae) wall and • Moderate l of
• S. mansoni and S. penetrate bladder eosinphilia human
japonicum skin and (S.hemato • Acute: feces
effects GIT differentiate bium). swimmer • Eradica
• S. haematobium into larvae • Liver= itching tion of
effect urinary which enters granuloma (dermatitis),af snail
tract veins and s (fibrosis), ter 2-3 weeks host
Figure 31: S.mansoni; left lateral
move against heaptosple fever, chills, • Avoid
spine
portal nomegaly, diarhea, swimm
circualtion, portal lymphadenopa ing in
reach arterial HTN, thy, endemi
circulation undamage hepatospleno c areas.
and liver. d megaly.
• Larva hepatocyte • Chronic: GI
matures in s and haemorhage,
adult form in normal hepatospleno
the liver, lay LFTs. megaly, death
eggs that by ruptured
pass in stool esophageal Figure 32: S.japonicum; very
and urine. In varices. small or absent spine
fresh water • S.haematobiu
eggs release m=
miracidia that haematuria,
penetrate bladde cancer.
snails., in
snails divide Figure 33: S.haematobium; lagre
and terminal spine.
differentiate Serologic test are not useful.
in cercariae. Because they cover themselves
with host antigen.
Moderate eosinophilia.
INTESTINAL • • • • • • •
NEMATODES:
Enterobius vermicularis; • Ingestion • Present only • Eggs • Perianal Scotch tape technique • Alband • Washin •
pin worms (causes of egg, in humans; causes pruritis and Eggs are not present in stool so no azole, g
enterobiasis) egg hatch no animal allergic in superimposed O and P test. meben hands
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
in small host and perianal bacterial No serology test. dazole, when
intestine, reservoir. skin. infection on Worms are found near the anus pyrant prepari
larvae • Eggs are not scratching. and on stool in diapered children. el ng food
differenti excreted in pamoa and
ate into stool so no te. bed
adult transmission • Drugs sheet,
male and via fecal oral don’t clothin
female In route kill the g etc.
the colon, eggs so
adult retreat
male and in 2
female weeks
live in the
colon,
female
comes to
anus in
night to
lay eggs,
these
eggs are
transmitt
ed by nail
via
scratching
.
Trichuris trichiuria • Eggs • Via humans, • Attach to • Mild anemia, Oand P stools= oval eggs with • albend • proper •
(whipworm)= trichuriasis ingested fecal-oral intestinal diarrhea, plugs at both ends. azole disposa
by route. Eggs mucosa rectal l of
humans, contaminate prolapsed feces.
eggs water or (children)
hatch in food.
small
intestine,
larvae
differenti
ate to
adult,
adult lives
in colon,
eggs
come in
feces,
deposit in
soil.
Ascaris lumbricoides; giant • Human • Present only • Do not • Ascaris Oand P: stools; oval eggs with • Alben • Proper •
roundwrom (causes ingest in humans. attach to pneumonia: irregular surface. disposa
dazol
ascariasis) eggs, Transmitted intestinal fever, cough, l of
hatch in via fecal-oral walls eosinophilia. e, feces.
small route. • Intestinal mebe
intestine, obstruction ndazo
larva and abdominal le and
migrate pain due to iverm
from worms
small • Malnutirtion ectin.
intestine (In children)
to
bloodstre
am, lungs,
alveoli,
bronchi,
trachea,
swallowe
d again
reach
small
intestine,
become
adults, lay
thousand
of eggs
every day
that come
in feces.
Ancylostoma duodenale • Eggs • Only in • Worms • Ground itch= a OandP stool: • Albend • Disposi •
(old world hookworm) excreted humans, via releases pruritic papule Occult blood in stool azole, ng
Necator americanus (New in human eggs in moist anticoagul at the site of Eosinalphilia meben sewage
world hookworms). Also feces soil ant and entry of worm dazole, , avoid
called hookworms differenti penetrating feed on • Major pyrant walking
ate into skin of hands blood, microcytic el barefo
moist soil and feet. blood loss anemia pamoa oted in
in 2 and oozing • Pneumonia te. soil.
forms. 1) from the with
Rhabditif intestine. eosinophilia.
orm
larvae (
feeding;
non
infectious
),
Filariform
(non-
feeding;
infectious
)
• Filariform
larvae
penetrate
the skin
through
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
hands
and feet,
blood,
lung,
alveoli,
bronchiol
es,
trachea,
swallowe
d,
become
adult in
small
intestine
and
attach its
wall (via
teeth=anc
ylostama
and
cutting
plates=
necator),
feed on
blood
capillaries
of
intestinal
villi, eggs
are
excreted
in feces.
strongiloides stercoralis; • Life cycle • Present only • • Maybe Oand P (stools): larvae is detected • Albend • Proper •
small round worms can occur in humans asymptomatic. Major eosinophilia azole, disposa
(causes strongyloidiasis) independ • Watery ELISA iverme l of
ently in diarrhea, ctin sewage
soil or in ground itch= ,
humans. pruritic papule wearin
• Filariform at the site of g
larvae can entry of proper
penetrate larvae, shoes.
through pneumonia, • Don’t
the skin causes give
in the cutaneous immun
blood larva migrans. osuppr
stream, • Autoinfection; esive
lungs, chronic= drugs
alveoli, abdominal (I.e,
bronchi, pain, cortico
trachea fluctuating steroid
and rashes, s, TNF-
swallowe moderate inhibito
d, adult eosinophillia. rs) to
enter • Damage of these
intestinal intestinal patient
mucosa mucosa= s.
and sepsis caused
produces by enteric
eggs that bacteria i.e;
differenti E.coli and
ate in to Bacteriodes
rhabditifo fragalis
rm larvae
that pass
in feces
and also
filarifrom
larva that
either
pass in
feces aur
penetrate
the
mucosa
or
perianal
skin to
reach
lungs
(autoinfec
tion;
specially
seen in
immunoc
ompromis
ed
patients).
• Also the
rhabbditf
orm
larvae
mature in
soil, mate
and
become
adult, life
cycle
complete
s
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
independ
ently
Trichinella spiralis (trichina • Present in pig • Eating • • Few days after Muscle biopsy= larvae within • Properl • •
worm; causes trichinosis) (mainly) and rat undercooked eating striated muscles. y
flesh containing pork undercooked Serologic tests= bentonite cookin
larvae, human pork patient flocculation test is +ve after 3 g pork.
ingest it, larvae experiences weeks of infection.
mature into diarrhea
adult form, lay followed 1 to
eggs, eggs form 2 weeks later
larvae, larvae by fever,
released in muscle pain,
bloodstream, PERIORBITAL
reach and EDEMA and
develop in eosinophilia,
striated muscle SUB-
cells (nurse CONJUCTICAL
cells), encyst in HEMORRHAGE
a fibrous S (imp
capsule, remain diagnostic
viable for criterion).
several years Larvae migrate
and then calcify. to cardiac and
CNS tissues as
well.
TISSUE NEMATODES: • • • • • • •
Wuchereria bancrofti; • Female • Host=Human • Adult • Early Thick smear taken at night shows • Diehytl • •
filarial worms (causes Anophele s worms infection= microfilariae carbam
filariasis) s and • Vector=Mosq obstruct asymptomatic. No serology test azine
Culex uito lymphatic Later, fever, (only
mosquito (Anopheles vessels; lymphangitis for
bites and Culex). edema, and cellulitis. microfil
humans elephantia Then edema ariae)
and sis. and fibrosis • No
deposits • legs of legs drug
larvae on and genitilia. availabl
the skin, Elephentaisis e for
larvae occurs only in adult
penetrate repeated worm
s the skin, infections. • Doxycy
enter • Pulmonary cline
lymph eosinophilia; kill
node, coughing, Wolbac
microfilari wheezing hia
ae are specially at which
produced night. ultimat
after 1 ely kills
year, wucher
circulate eria.
in blood,
again
ingested
by
mosquito.

BACTERIA:
NAME CHARACTERSTIC TRANSMISSION PATHOGENESIS CLINICAL SYMPTOMS DIAGNOSIS TREATMENT PREVENTION OTHER IMPORTANT
POINTS
Staphylococcus: Cell wall S. aureus: Humans: S.aureus S.aureus: S.aureus: golden Beta lactamase Staphylococci
• S.aureus components: nose, skin (hospital produce both 1 Pyogenic: colonies, beta hemolytic, resistant penicillin produce catalase
• S.epidermidis • Protein A: workers and patients), endotoxin and • abcess, furuncles, coagulase =ve, mannitol (nafcillin, while streptococci
• S.saprophyticus it binds to vagina, shedding from exotoxins. carbuncles salt agar is used doxacillin), some donot. [Mnemonic:
Fc portion the lesions. Risk Endotoxin: it impetigo, cellulitis, 9ferments mannitol → cephalosporin or CAT (catalase) loves
of IgG and factors: Diabetes, IV stimulates folliculitis, turn yellow. vancomycin. grapes
prevent drug abuse and macrophages to conjuctivitis, Staph epidermis and Beta lactamse (styaphylococcus)]
activation Chronic produce blepharitis and staph saprophyticus: inhibitor: clavulanic Catalase degrades
of granulomatous cytokines and hordeolum coagulase negative. S. acid. H2O2 into H2O and
compleme disease (CGD). can activate • Septicemia (sepsis) epidermis is sensitive to Timethoprim and O2; protecting
nt, i.e, no S.epidermis: normally compliment and • Endocarditis novobiocin while S. sulfa-methoxazo against neutrophil.
C3b on human skin; enter coagulation • Osteomyelitis and saprophyticus is not. Coagulase is only
produced. bloodstream at site of cascade). septic arthritis produced by
Only injection. Exotoxin: 3 • Post op staphylococcus
coagulase S.saprophyticus: types pneumonia aureus while staph
positive normally on mucosa 1) Enterotoxin: 2) Toxin mediated: food epidermis and
S.aureus on genital tract of stimulates poisoning (gastroenteritis), Staph.
produce young women; ascend release of IL- Toxic shock syndrome saprophyticus are
protein A. urinary bladder. 1 and IL-2 (fever, hypotension, diffuse coagulase negative.
• Techoic from macular sunburn like rash. (activate
acid: macrophage Involve 3 or more organs: prothrombin to
causes s and helper liver, kidiney, GIT, CNS, form thrombin,
adherence T cells; food muscle and blood etc. thrombin catalyzes
to mucosa. poisoning, 3) scalded skin syndrome: activation of
Lipotechoic vomiting, Fever, erythematous fibrinogen to form
acid causes watery non macular rash, large bullae. fibrin clot and
septic bloody Hair and nails loss. causes coagulation).
shock by diarheae. Recovery in 7-10 days. Staphylococcus
inducing IL- 2) Toxic shock 4) Kawasaki disease: in aureus produces
1 and TNF syndrome children, vasculitis of small pigment called
from toxin (TSST): and medium sized arteries. staphyloxanthin
macrophag supra For ex. Coronary artery. (golden colonies)
es. antigen; IL-1, There is high fever, which inactivates
• Polysaccha IL-1 and TNF. bilateral non purulent the antimicrobial
ride 3) Exfoliatin: conjuctivits, lesions of lips effect of
capsule xcauses and oral mucosa, cervical neutrophils while
• Surface “scalded skin lymphadenopathy, a streptococci donot
receptors: syndrome”; diffuse edematous macula- produce it and
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
helps in acts as papular rash, erythema and produce white
“phage protease edema of hands and feet. colonies.
typing” of that cleaves Also arrhythmia, S aureus ferments
strains. desmoglein myocarditis, regurgitation, mannitol while
• Peptidogyl in aneurysm of coronary s.aureus and
can: desmosomes artery. s.saprophyticus
endotoxin leading to s. saprophyticus: UTI donot.
(activate separation of S.epidermis: endocarditis, S.aureus produces
macrophag epidermis at arthritis and osteomyelitis. hemolysins; causing
es to the granular hemolysis.
produce cell layer.
cytokines 4) also
and can produces PV
activate leukocidin
compleme (pore
nt and forming; kill
coagulation WBC) and
cascade). alpha toxin
(necrosis of
skin and
hemolysis).
5) Enzymes:
coagulase,
hyaluronidas
e, proteases,
nucleases
and lipases.
S. epidermis and
S.saprophyticus
donot produce
exotoxin, don’t
cause food
poisoning and
toxic shock
syndrome.
S.epidermis
causes pyogenic
infections.
S.saprophyticus
causes urinary
tract infections.

Gram –ve cocci: (Neisseria

meningitidis and Nisseria
Gonorrhea)
Neisseria Meningitidis: present only in • Meningococcocemia • Gram –ve bacteria Penicillin Vaccine More than 80% of
humans. Transient (bacteria in blood, can and Increased no. of ceftriaxone bacterial meningitis
flora of nasopharynx. embed in any organ) polymorphonuclear in infants after 2
Transmits via air • Meningitis. Signs: leukocytes in CSF. months of age is:
borne droplets. fever headache, stiff • Oxidase +ve S.pneumonia,
neck. colonies. N.meningitidis.
• Water-house • Ferment maltose
Friderichsen (gonococci can’t
syndrome: severe fermetn;
form of distinguishing
meningococcocemia. point)
Signs: high fever, • Immunoflouresence
shock, widespread .
purpura, DIC, • Latex agglutinition
thrombocytopenia, test= for short hand
adrenal insufficiency diagnosis; detect
(due to adrenal capsular
heamorrhage). polysaccharide in
spinal fluid
Niesseria Gonorrhea: Present only in Have porin A 1. Genital tract infections: 1. Men- smear of Ceftriaxone, Condoms
humans, sexually protein in cell women: asymtomatic or urethral Azithromycin,
transmitted or at the wall→ urethritis (dysuria), discharge→ gram – ciprofloxacin.
time of birth. inactivated C3b purulent vaginal ve diplococci;
complement. dischage, cervicitis, Women- smear of
salpingitis (PID); Men: cervix an culture
urethritis, dysuria, (because gram –ve
purulent discharge, diplococci are
proctitis. present in normal
2. Disemminated infection: flora too).
a. septic arthritis 2. Cultured in Thayer-
b. Tenosonyvitis Martin Medium
c. Pustules. {chocolate
3. Anorectal infection: agar+antibiotic
women or (vanvomycin,
homosexuals colistn,
4. Pharyngitis. trimethoprim,
5. Conjuctivitis: in nystatin)}.
neonates after birth; 3. Oxidase +ve colony.
treatment- 4. Ferment glucose
erythromycin drops. but not lactose
5. NAAT ( nucleic acid
amplification test)
Gram +ve rods: (Bacillus,
clostridium)
Bacillus anthracis: Spores present in soil 2 exotxins: 1. Cutaneous anthrax: 1. Microscopy: gram – Ciprofloxacin Vaccine (but
and animal products 1. Edema cutaneous ulcer with ve rods weak )
(wools,bristles and factor: it is black crust, malignant 2. Non-hemolytic
hides); inhaled, eaten adenylate pustules, bacteremia colony on blood
(contaminated meat), cyclase and death aagr.
wound entry causes 2. Pulmonary anthrax 3. PCR
increase in (wool sooter’s 4. ELISA
cyclic disease): influenza,
AMP→outpo sub-sternal pressure,
uring of fluid heamorrhagic
from ECF. mediastinitis, bloody
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
2. Lethal factor: pleural effusion,
it is a shock, death.
protease; Mediastinal widening
cleaves on chest X-ray.
phophokinas 3. Gastrointestinal
e that anthrax:vomiting,
activates abdominal pain and
mitogen bloody diarhea.
activated
prtein kinase
(MAPK)
signal
transduction
pathway→
inhibit cell
growth.
Bacillus cereus Spores on grains(rice), Exotoxin works Food poisoning: watery non symptomatic Labs usually done.
germinate on same as bloody diarrhea.
reheated rice. cholerae
Ingested. toxin.i.e. it adds
aadenosine
diphosphate
ribose to a G-
protein which
stimulated
adenylate
cyclase and lead
to increase
concentration of
cAMP within
enterocyte.
Clostridium tetani: Spores present in soil; Tetanus toxin Tetanus → spastic paralysis. 6. No microbiologic or 1. Tetanus 1. Vaccination: Tetanus toxoid and
enter by wound, IV (Tetanospasmin 1. Lock jaw (trismus) serologic testing. immunoglobulin Tetanus anti-toxin gives
drug abuse and ): 2. Grim smile (risus 7. Organsim rarely (tetanus anti- toxoid. passive-active
contaminated Exotoxin, sardonicus) isolated from wound toxin) (formaldeyde immunity.
umblicus (in produced by 3. Arching back site. 2. Metronidazole or treated toxin) Tetanus causes
neonates). vegetative cells (opisthotonos) 8. Under microscope- penicillin G 2. Tetanus spastic paralysis
arround wound 4. Exagerrated reflex tetanus appears as 3. Respiaratory toxoid is while botulism
site, carried 5. Respiratory failure “tennis racket”- support (patent usually given causes flaccid
intra axonally because it has a airway to children in paralysis.
(retrograde) to terminal spore. maintainance) combination
CNS→ binds to 4. Benzodiazipines with diptheria
ganglioside (diazepam, toxoid and
receptor and valium) acellular
blocks release of pertussis
glycine and vaccine
GABA at spinal (DtaP).
synapses. 3. Little wound-
give only
tetanus toxoid
4. Grossly
contaminated
wounds- give
tetanus
toxoid+
tetanus anti-
toxin+
penicillin.
• Half
immunoglobu
lin at wound
site and half
via IM.
Clostridium botulinum Spores present in soil, Botulinum toxin Descending paralysis: 1. Toxin separated 1. Heptavalent Proper Botulinum toxin in
contaminate is absorbed in • Flaccid paralysis from uneaten food toxin (contain sterilization and minute amount is
vegetables and meat, gut and • Diplopia 2. ELISA all 7 serotypes vacuum packed used to treat
IV drug abuse. transported to • Dysphagia 3. PCR A-G) canned food. torticollis, writer’s
Spores can survive and peripheral nerve • Respiratory 4. Mouse protection Discard swollen cramps,
germinate in synapses via muscle failure test: mice are cans (clostridial blepharospasm.
anaerobic blood→ blocks • NO FEVER inoculated with proteolytic
environment. Ach release. sample of specimen anzymes forms
Germinate in canned and will die unless gas, which
food. Preformed toxin protected by swells cans).
is infested. antitoxin (and that’s
High risk foods: cruel )
vegetables (green
beans, peppers and
mushrooms) and
smoked fish.
Clostridium prefringens: 1. Spores present in 1. Gas Gas gangrene: Gas gangrene: Gas gangrene: Wound should
soil; enter by gangrene: • pain 1. Smears of tissue and penicillin G be cleaned and
ingestion and war organism • edema exudates= gram –ve debrided,
wounds. grows in • cellulitis rods. Spores are not Food poisoning: penicillin as
2. Vegetative cells traumatized • gangrene seen (forms only in symptomatic prophylaxis
(cells that donot tissue→ • crepitus felt in nutritional deficient Food is cooked
form spores) are produce palpation in wound conditions) adequately.
present in normal alpha toxin tissue- gas 2. Ferment sugar
flora of colon and (lecithinase) • hemolysis 3. Culture- colonies
vagina-NO → damages • jaundice form double zones of
SPORES SO NO cell • shock hemolysis on blood
TRANSMISSION. membranes • death agar.
3. Gas gangrene= including Food poisoning: 4. Produce precipitates
road accident, RBCs causing in egg yolk (by the
• 8-16 hour incubation
war wounds and hemolysis. action of lecithinase).
period
septic abortions Degradative
• Watery diarrhea
4. Food poisoning= enzymes Food poisoning:
• Cramps
contaminated produces not usually done
• Little vomiting
food, reheated gas. no serologic assay
• Self limiting (in 24
food with spores. 2. Food organism can be isolated
poisoning: it hours) from uneaten food.
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
is normal
flora of
colon but in
small bowel
enterotoxin
causes
diarrhea. It
works same
as
staphylococc
al
enterotoxin.i
.e. works as
superantigen
)
Clostridium difficile • Normal flora of • Antibiotics Pseudomembranous colitis: 1. Sigmoidoscopy= 1. Stop antibiotic No vaccine
(pseudo membranous colitis, colon (3% general (specially 1. Non-bloody pseudomembranes. 2. Metronidazole Saccharomyces
MOST COMMON CAUSE OF population, 30% clindamycin) diarrhea 2. Neutrophils in stools 3. Vancomycin (yeast)-
NOSOCOMIAL (HOSPITAL hospital patients). suppress the 2. Fever 3. Exotoxin in stool- via (used instead of prophylaxis.
ACQUIRED) CAUSE OF • Via fecal oral-route drug sensitive 3. Abdominal pain ELISA metronidazole in
DIARRHEA. members of 4. Toxic megacolon 4. Genes encoding emergency)
normal flora (complication) exotxin- PCR 4. IV hydration
of colon, Pseudomembranes are Culture is useless 5. Fecal
causing called by this name because because some people transplantation:
c.difficile to they are not like other have it in normal flora. via enema or
multiply. membranes of body and nasoduodenal
• Exotoxin A have thick, adherent, grayish tube
and B- or yellowish exudates are
glucosyltranfe present on these
rase, adds membranes. Such embranes
glucose to are present in oropharynx in
Rho-GTPase. cases of diphtheria too.
• Exotoxin B
causes
depolymerizat
ion of actin,
loss of
cytoskeletal
integrity,
apoptosis and
death of
enterocytes.
ENTEROBACTERIACEAE: Characterstics: 5. 6. 5.
Family of gram –ve rods 1. All are facultative
found in colon of humans anaerobes
and other animals as part of 2. Ferment glucose
normal flora. It includes: 3. Don’t have
1. Escherchia cytochrome
2. Salmonella oxidase.i.e. they
3. Shigella are oxidase
4. Vibrio negative.
5. Campylobacter 4. Reduce nitrites to
6. Helicobacter nitrates.
Labs:
1. Culture medium:
a. Blood agar
b. Mac Conkey’s
agar
c. Eosin
Methylene
Blue agar
(EMB)
2. Non lactose
fermenters
(colourless
colonies)=
salmonella,
shigella.
3. Lactose
fermenters
(coloured
colonies)=
Escherichia,
enterobacter,
E.coli, klebsiella.
E.coli colonies
have
characterstic
green sheen.
4. Triple Sugar Iron
(TSI)
5. Urea agar
Escherichia coli • Present in colon • Systemic 1. Traveller’s diarrhea: 1. Culture: green sheen 1. Cystitis: 1. No vaccine
(most common cause of of both humans disease is • Caused by colonies trimethoprim 2. Prophylactic
urinary tract infection and and animals. causd by enterotoxigenic E.coli 2. Ferment lactose- pink sulfamethoxazole use of
gram negative sepsis). • Transmits via capsule and (ETEC) colonies or nitrofurantoin. trimethoprim
Also causes neonatal ingestion of endotoxin • Watery diarrhea 3. Produce indole from 2. Pyelonephritis: sulfamethoxa
meningitis, traveler’s faeces • UTI caused by (non-bloody) tryptophan ciprofloxacin, zole,
diarheae. • However pilli. • Self limiting (1-3 4. Decarboxylates lysine ceftriaxone. ciprofloxacin,s
E.coli (O157:H7) causes HUS enterohemorrhag • Exotoxin are days) 5. Uses acetate as only 3. Sepsis: oxycycline
(Hemolytic Uremic ic strain (E. coli of 3 types: 2. Bloody diarrhea: source of carbon ceftriaxone (IV) etc.
Syndrome) O157:H7) 1. Heat labile • Caused by 6. Motile and gentamycin 3. Avoid
transmits via toxin (LT): enteroheamorrhagic These characterstics (aminoglycoside). uncooked
undercooked stimulate E.coli (EHEC) helps to distinguish E.coli 4. Diarrhea: food and
beef (animals). adenylate • Bloody diarheae from other lactose symptomatic, unpurified
• Neonates gets cyclase • Abdominal cramps fermenters. sometimes use water.
infected during irreversibly • Fever 7. E.coli O157:H7 Trimethoprim
birth-meningitis → increase 3. Bloody diarrhea and doesnot ferment Sulfamethoxazole
and sepsis. intracellular HUS: sorbitol or lopermaide
cAMP→stim • E.coli O157:H7 (STEC) (Imodium)
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
ulate cAMP • Bloody diarrhea (distinguishing
dependent • Hemolytic uremic feature)
protein syndrome (HUS):
kinase→pho kidney failure,
sphorylates hemolytic anemia,
ion thrombocytopenia,
transporters schistocytes (due to
→ export K+ DIC)
and Cl- in 4. UTI:
lumen of • Cystitis: no fever,
gut. dysuria, increased
2. Heat stable frequency.
toxin: • Pyelonephritis: fever,
stimulates flank pain,
guanylate costovertebral
cyclase tenderness, dysuria,
3. Shiga toxin: frequency (may or
produced by maynot).
E.coli 5. Neonatal meningitis
O156:H7; and sepsis
removes
adenine
from (28s)
RNA
stopping
protein
synthesis.
• Pilli: has
adehsin
protein
which attach
urinary tract
epithelium.
Canberry
juice has
flavinoids
that inhibits
binding of
pilli to
urinary tract
epithelium.
Salmonella • Present on • Vi antigens- 1. Enterocolitis: nausea, 1. Enterocolitis: stool 1. Symptomatic Weak vaccines
Enterocolitis, enteric fever normal flora of capsular vomiting, abdominal pain sample treatment; self against S.typhi
(typhoid fever), septicemia human and antigens that and diarrheae. With or 2. Enteric fever: blood limited disease Proper sewage
(osteomyelitis etc) animals increase without blood. Most culture, bone arrow 2. Enterocolitis= disposal and
virulence of commonly caused by culture, stool cuture. fluid and food cooking.
salmonella S.typhimurium. 3. Non lactose electrolytes.
typhi 2. Typhoid fever: initially fermenters (colorless 3. Typhoid fever,
• Enterocolitis: fever and constipation colonies) septicemia and
bacyeria later diarrhea and 4. TSI+ acidic, yellow metastatic
invades into vomiting. Bacteremia sland and red butt. infection=
lamina (high fever, delirium, 5. Vidal test: rise in ceftriaxone,
propria, tender abdomen, enlarge antibody titer in ciprofloxacin.
inflammation spleen, rose spots on patients serum.
• Typhoid fever: abdomen), leucopenia 6. It produces H2S.
bacteria and neutropenia,
invade and complication is intestinal
multiply in heamorrhage.
mononuclear 3. Septicemia: most
phagocytes in commonly by S.
peyer’s chloraesuis; fver, no
patches, liver, enterocolitis, may
gall bladder involve meninges, bone
and spleen. or lung.
Survives
inside
phagocytes.
Stays in gall
bladder for
long- carrier
state.
Shigella • Present only in • Some strains 1. Incubation period 1-4 1. Non lactose Mild: fluid and • No vaccine
(enterocolitis- dysentery) humans produce days. fermenter-colorless electrolyte • Proper
• Transmits via enterotoxin- 2. Fver, abdominal colonies’TSI; replacement only sewage
fecal oral route (4 shiga toxin cramps, watery alkaline slant, acid Severe: fluid and disposal,
Fs: fingers, flies, • Some strains diarheae, later with butt. No H2S electrolyte water
food and feces) invades blood and mucous produced replacement + chlorination,
mucosa (dysentery) 2. Neutrophils in flouroquinolone personal
stools- via methlene (ciprofloxacin) or hygiene.
blue stain. Indicated trimethoprin
presence of invasive sulfamethoxazole.
organism (i.e.
shigella, salmonella
and campylobacter)
are present rather
than toxin
producing
organsisms (i.e.
E.coli, V.cholerae,
Clostridium
prefringens).
Vibrio cholerae • O is a cell wall • Transmits via • Sensitive to • Rice water stools 1. Stool culture 1. Water and • Water water
antigen. fecal-oral route stomach acid; • There is no RBC or 2. Lactose fermenters electrolyte and food
• O1- epidemic • In Humans- colonize in WBCin stool 3. Oxidase +ve colony replacement. supply
disease asymptomatic small • NO ABDOMINAL PAIN (distinguishes it 2. Glucose • Vaccines:
• Non-O1 sporadic carriers. intestine, • Marked dehydration from other 3. Tetracyclines Dukarol,
disease or non • In marine shell ingestion in • Acidosis and enterobacteriaceae (not necessary; Shanchol.
pathogens. fish (shrimp, large no is hypokalemia (due to ) but reduce the • Prophylaxis:
oysters) - required. lass bicarbonate and 4. TSI= acid slant, acid duration) tetracyclines
potassium in stool). butt. .
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
inadequately • Patients with 5. H2S maybe seen (by Self resolving
cooked. low stomach sucrose disease. Within 7
acid or taking fermentation). days.
acid
suppressing
medines or
gastrectomy
are more at
risk!
• Reach small
intestine,
secrete
enzyme
mucinase
which
dissolves the
glycoprotein
cover over
intestinal
cells, adheres,
multiplies,
produce
enterotoxin
(chloragen)
• Cholaragen
has 2
subunits:
1. A subunit
(active):
inserts in
cytosol, add
ADP-ribose
to Gs protein
(stimualtooo
ery G
protein),
stimulation
of Gs
protein,
persistent
stimulation
of adenylate
cyclase,
overproducti
of cyclic
AMP
dependent
kinase
causing
phophrylatio
n of ion
transporters,
opened, loss
of ions and
water from
the cell.

Vibrio parahaemolyticus • Ingestion of raw or • Enterotoxin- • Watery diarrhea It can grow in 8% NaCl Symptomatic • proper
undercooked works like • Abdominal cramps solution while V.cholerae treatment; self refrigeration
seafood. chloragen • Nausea and vomiting doesnot. resolving (within 3 and cooking
• Fever days) seafood.
Vibrio vulnificus • seafoods like • 1. Cellulitis (shell fish Doxycycline. •
shellfish handlers who already have
skin wounds)
2. Septicemia
(immunocompromised who
eat raw fish)
3. Hemorrhagic bullae over
the skin of patients with
sepsis.
Compylobacter jejuni Comma or s shaped • Present on cattle, • Inflammation 1. Enterocolitis: initially • Stool culture C.jejuni= • No vaccine
Complylobacter chickens, dogs. of intestinal watery foul smelling • Oxidase +ve colonies erythromycin and • Proper
jejuni is the leading • Transmits via mucosa. diarrhea, later bloody and failure to gorw at ciprofloxacin sewage
cause of diarrhea fecal-oral route. diarrheae, fever 25 degree Celsius and C.intestinalis= disposal
with drinking of • Also via poultry, abdominal pain. sensitivity to nalidixic aminoglycosides. and
unpasteurized milk. meat and 2. Guillain-Barre acid is diagnostic. personal
unpasteurized syndrome: Grows well at 42 hygiene.
milk. • Associated with degree Celsius.
enteric infection • C.intestnalis cannot
• Autoimmne; gorw at 42 degree
antibodies against Celsius but grows well
C.jejuni and cross at 25 gegree Celsius
react with antigens on and is resistant
neurons. nalidixic acid.
• Also associated with
other autoimmiune
diseases: reactive
arthritis and Reiter’s
syndrome.
3. Bacteremia- mainly
caused by
C.intestinalis; fever
and malaise.
Helicobacter pylori • Fecal-oral route. • Attaches to Peptic ulcer disease and • Stool culture Triple therapy: PPI+ No vaccine H.pylori causes
mucus- gastritis causes upper • H.pylori is urease +ve Penicillin (or Proper hygiene gastritis, gastric
secreting cells abdomen pain, bleeding of (C.jejuni is not)- metronidazole for ulcer, gastric
of gastric GI tract sometimes. assessed via urea penicillin allergic carcinoma and are
mucosa. NO SEPTICEMIA OCCURS breath test patients)+ associated with
• Produce (rodiolabelled urea is clrithromycin. MALToma
urease- ingested, if organism is lymphoma.
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
converts urea present, urease will Quadruple therapy:
into ammonia cleave it into PPI+ bismuth
which radiolabelled CO2 salicylate+
neutralizes which is exhaled and metronidazole+tetr
gastic acid. radioactivity is acycline.
• Inflammation detected in Quadruple therapy
of mucosa breath)endoscopic is given in case of
• Mucosal biopsy clarithromycin
damage leads • IgG antibodies. resistance.
to peptic ulcer
and gastritis.
• MALToma:
H.pylori is
found in the
lesion.
Chronic
infection with
H.pylori leads
to stimulation
of B cell
proliferation
and B cell
lymphoma.
MYCOBACTERIA: 1. Acid fast
1. Mycobacterium a. Don’t absorb
tuberculosis (cuase gram stain.i.e.
tuberculosis) not gram –ve
2. Mycobacterium leprae or +ve.
(cause leprosy) b. Only bacteria
3. Atypical mycobacteria that are acid
(Cause tuberculosis like fast (however
disease in Nocardia
immunocompromised asteroides is
and whom in which also acid fast)
prosthetic devices are c. Acid fast refers
implanted; includes to organisms
mycobacterium avium ability to retain
intercellulare and carbolfuchsin
mycobacterium stain despite
chelonae) subsequnt
treatment with
an ethanol
hydrochloric
acid mixture.
This high lipid
content (60%)
makes
mycobacteria
cell wall acid
fast.
Mycobacterium tuberculosis • Normally most • Human are natural Primary TB: ▪ Fever, fatigue, night 1. Acid fast staining • Depends on • Contact • Worldwide
bacteria has and main • Ghon sweats and weight loss. Auramine stain- via resistance pattern prevention mycobacterium
doubling time of 1 reservoirs for TB Complex-in ▪ Scrofula- cervical fluorescence microscopy • DOC= isoniazid with TB tuberculosis
hour but M. but some animals lower lobbe of lymphadenitis: swollen, (rapid screening test) • Pulmonary TB= patients-use causes more
tuberculosis might also be lung. non tender lymph nodes, 2. Treat with NaOH, then isoniazid, respirators deaths than any
doubles in 18 involved (like • can progress usally unilateral. culture in Lowenstein- rifampin, when close to other single
hours. cattle) to: Lymphadenitis is the jensen agar for 8 pyrazinamide and them microbial agent.
• Therefore cultures • Via repiratory 1. Heals by most common extra weeks. It willlnot grow ethambutol for 2 • BCG vaccine- • Aprrox. 1/3rd of
should be held for aerosoles- fibrosis: pulmonary on blood agar months. Then give partial world’spopulatio
6-8 weeks before coughing. delayed manifestation of TB. 3. BATEC liquid medium isoniazid and prevention for n is infected with
considering • Mycobacterium hypersensitivi ▪ Erythema nodosum: has radioactive rifampin for 4 M.bovis M.tuberculosis.
negative. bovis- present in ty, tuberculin tender nodules on nutrients- +ve in TB, months. • Pasteurized • Primary
• M. leprae connot unpasteurized test +ve. extensor surfaces of tibia when radioactive CO2 • For milk tuberculosis-
be cultured cow’s milk; can 2. Progressive and ulna. is produced in 2 immunosupprese lungs lower lobe
• Culture media= cause intestinal ling disease: ▪ Military TB: multiple weeks. d, disseminated • Secondary
Lowenstein-Jensen tuberculosis. in HIV and disseminated lesion, like 4. M.TB produce niacin infection and tuberculosis:
medium (egg yolk malnourished millet seeds. while all other lIsoniazid lungs upper lobe
+ dyes.i.e patients- ▪ Tuberculous meningitis mycobacteria donot. resistant TUBERCULIN TEST
malachite green) death ▪ Tuberculous 5. It produces catalase. patients= give (PPD):
• Obligate aerobe- 3. Severe osteomyelitis- in 6. NAAT drugs for 9-12 • Positive in people
likes to grow in bacteremia: vertebrae (Pott’s To check up drug months. with previous TB
high oxygen. i.e. military TB- disease). resistance: • Patients sputum infection but
upper lob of lung death. ▪ GI TB: abdominal pain, 7. Molecular tests that becomes non mpostly not
and kidney. Secondary TB: diarheae, fever, weight detects chrnosomal infectious in 2-3 positive in active
• Acid fast- due to 4. Lymphatic or loss, may cuase intestinal mutations: i.e.catalase weeks of disease.
mycolic acid (C78- hematogenou obstruction, gene→ isoniazid treatment. • It is a delayed
C90) fatty acid s haemorrhage. Mostly at resistance and RNA • Treatment will hypersensitivity
chain. dissemination ileocaecal junction. (also polymerase gene→ not eradicate reaction.+ve 4-6
• Virulent strain : latent caused by M.bovis) rifampin resistance. metabolically weeeks after
grown in tuberculosis ( ▪ Renal TB: dysuria, 8. Luciferase assay: inactive bacteria infection.
“serpentine” cord (dormant hematuria, flank pain, luciferase enzyme is which are latent Becomes
like pattern in tubercle sterile pyuria taken from fireflies and can • Mediated by
culture while bacilli in (characterstic finding). that produces flashes reactivate. CD+4 cells (helper
avirulent strains several ▪ Oropharyngeal TB: of light in the presence • Tx. for latent t cells).
donot. organs)- painless ulcers, local of ATP. Antibiotic (asymptomatic) • There is also
• Purified protein reactivation in adenopathy. sensitive bacteria infections: circulating
derivative (PPD) adult life. when treated with Isoniazid for 6-9 antibodies in
skin test OR Cavitary antibiotic will produce months or with serum but they
tuberculin test= lesion in lung less amount of ATP, rifapentine for 3 are useless and
+ve. is usually in hence less light is months. For the play no role in
• Pthiocerol upper lobe: produced, resistant ones whose PPD tuberculin test
dimycoserosate- Extrapulmona one will produce test recently too.
lipid in cell wall, ry normal light. converted to +ve. • The diameter of
helps in tuberculosis: Tests for TB previous • DOT(vdirectly induration
pathogenesis of 1. CNS infection: observed (thickening) is
(parenchymal 9. PPD (tuberculin test) therapy: health
lung. measured.
tuberculoma 10.  interferon release
• Resistant to acid care workers • Equal to or
or meningitis). assay (IGRA): two observe the
and alkalis. (NaOH greater than 15
is used to 2. Vertebral types. Quantiferon TB patient taking the mm=assumed as
concentrate body and T-spot TB. The medications. infected with TB
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
clinical specimen; osteomyelitis lood cells of patient virus even if they
it destroys mucous (pott’s are exposed to TB have taken BCG
membranes and disease) antigens and the vaccine
other bacterias but 3.lymphadenit amount of interferon • Equal to or more
not TB virus. is released by them is than 10mm=
• Resistant to 4. Renal measured. Don’t give people with high
dehydration.i.e. 5.GI +ve results after BCG risk factori.e.
spores can survive 6. Adrenals. vaccine. hoeless, iv drug
in dried abuser, nursing
expectorated • Doesnot home residents.
sputum. produce toxin • Equal to more
(endo or exo) than 5 mm=
• Live in immunosuppress
macrophages- ed (AIDS), people
inside in close contact
phagosome, with active TB
produce patient.
“exported • BCG vaccine also
repetitive causes +ve test
protein” that • Predesposition to
prevents TB is more in -
phagosome interferon and
from fusing Nramp gene
with mutation.
lysosome. • Drugs
• Lesions are of predisposing to
2 types: TB relapse:
Exudative- infliximab
acute (antibody),
inflammation, Remicade
in lungs at
initial site of
lesion. i.e.
ghon
complex=
exudative
lesion+drainin
g lymph
nodes.
• Granulomato
us lesions:
contains
central area
of giant cells
(called
Langhan’s
giant cells)
containing
tubercle
bacilli
surrounded
by epitheloid
cells. A
tubercle is a
granuloma
surrounded
by fibrous
tissue and has
central
casseating
necrosis. It
heals by
fibrosis and
calcification.
▪
▪
Mycobacterium Laprae • Can’t grow in any • Humans are natural • Grows • Gradual in onset; 1. Acid fast stain in skin Tuberculoid • Isolation of
(causes Hensen’s disease) culture media. reservoirs, aniamals intracellularly incubation period of lesion and nasal leprosy: lepromatous
Grows only in can be hosts like in skin several years. scrapping- dapsone+rifampin leprosy
human and animals. armidallo. histiocytes, Tuberculoid leprosy: lepromatous leprosy for 6-12 months patients
• Optimal growth • Transmits via nasal endothelial 1. hypopigmented only Lepromatous • Dapsone as
temperature is 30 secretion or cells and macular or plaque like 2. Foam cells- lipid laden leprosy: prophylaxis to
degree celsius. discharge from skin schwann cells. skin lesions macrophages seen in dapsone+rifampin+ children
• Grows preferably lesion of infected • Nerve 2. thickened superficial skin- under clofazimine for 12- • No vaccine
over skin and people. damage is nerves microscpoe— 24 months.
superficial nerves • Most cases reported caused by: 3. significant anesthesia of lepromatous leprosy Alternative is
• Doubling time 14 in tropical regions direst contact skin. only oxyflacin+clarithro
days of asia and africa. of bacteria Lepromatous leprosy: 3. Cutures= -ve mycin.
and cell 1. multipple nodular skin 4. IgM again phenolic
mediated lesion glycolipid (+ve in
immunity 2. leonine (loin like) facies lepromatous but –ve
attack. 3. erythema nodusum in tuberculoid).
2 forms of leprosum (ENL): 5. PCR
leprosy: painful nodule on
• Tuberculoid extensor surfaces of
leprosy ( tibia and ula, neuritis
paucibacillary and uveitis.
leprosy): CMI 4. Skin anesthesia
(CD-4, TH-1 5. Loss of nose and finger
cells, tips (due to bone
interferon  resorption)
and IL-2, IL- 6. Thickineing and folding
12) rsponse is of skin (due to
strong, very infiltration in akin and
few acid fast nerves).
bacilli,
granuloma
contains giant
cells, nerve
damage is due
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
to CMI,
lepromin test
+ve
• Lepromatous
leprosy
(multibacillar
y): CMI
response is
weak, skin
and mucous
membrane
have foamy
histiocytes
rather than
granulomas,
nerve damage
by direct
contact with
bacteria,
lepromin skin
test –ve.
Spirochetes: • • • • •
Treponema pallidum • Can’t grow in • Infected humans are • Produces no Already covered in 1. Dark field mircoscopy • Penicllin G- for all • Condoms
(causes syphilis) cultural medium reservoir only; no toxin (exo or pathogenesis column ☺ or direct flourescent stages of syphillis. • Antibiotic
(same as animal reservoir. endo) antibody (DFA) test: • Benzathine intake afer
mycobactera case) • Transmits via • Infects Can show spirochetes penicillin suspected
spirochete endothelium from lesions of primary • Doxycycline (in exposureserol
containing lesions of of blood and sec syphilis. Not penicillin allergy) ogic follow up
skin and mucous vessels in all seen in gram stained • Neurosyphillis- of infected
membranes (i.e. stages but smear. high doses of individuals
mouth, genitals and specially in 2. Treponemal antigens aqueous pen G. • No vaccine.
anus) of an infected brain and 3. Reagin antibodies Jarisch-Herxheimer
person with cardiovascular (IgM+IgG) present in reaction: due to
intimate contact. lesion in patients serum- lysis of treponemes
• via blood tertiary detected by reacting and the release of
transfusion (but syphilis. them with with endotoxin like
only in primary Primary cardiolipin from beef substances;
syphilis case). syphilis: non heart-cheap cost, for symptoms of fever,
tender ulcer screening chills, myalgias-
(chancre) forms 4. Flocculation tests influenza like
in 2-10 weeks, (VDRL) and Rapid symtoms. Lasts
resolve plasma reagin (RPR) upto24 hours. (also
spontaneously, detects antibodies. occurs in treatment
but spirochetes 5. Antibodies titer of other
get into blood decreases with effective spirochetes.i.e.
and spread to treatment (unlike lyme disease,
many organs. ordinary antibodies) leptospirosis and
Secndary 6. Prozone phenomenon: relapsing fever)
syphillis: when antibody titer is
• 1-2 months too high, flocculation
after test is negative. when
resolution of serum is diluted, on
pri. Syphillis diluton of serum, test
• maculopapula becomes +ve.
r rash on 7. Congenital syphilis:
palms and VDRL test- newborn is
soles and found high antibody
moist papules titer than mother.
on mucous 8. (as antibody crosses
membranes placenta- neonnate has
and skin anitbodies but in
(mucous normal neonate-
patches) antibody titer is
• mosit lesions declined with time in
on genitals uninfected infant but
(condyloma remains high in infected
lata)- self one.
resolving 9. Immunoflourescence
• patchy 10. Hemagglutination.
alopecia 11. Antibodies arise after
• fever, 2-3 weeks of infections
malaise, and remains in blood
anorexia, for lifetime.
weight loss,
headache,
myalgia,
generalized
lymphadenop
athy.
• Pharyngitis,
meningitis,
nephritis may
occur.
• 1/3rd pts of
pri. Ad sec.
syphillis gets
cured without
treatment but
2/3rd remains
latent.i.e.
without
symptoms but
+ve serology.
• Latent period
has 2 types:
early latent
period:1-2
years after sec
syphilis stage.
Late latent
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
period: for
many years.
Tertiary
syphillis:
• Granuloma
(gumma)-
specially skin
and bones
• Neurosyphilli
s- tabes paresis
• CVS-aortitis,
aneurysm of
ascending
aorta.
• In tertiary
syphillis
lesions,
treponemes
are rarely seen.
Congenital
syphilis:
• transmits
across
placenta
• after 3rd
month of
pregnancy
• infected
neonates
have:
Hutchinsons’s
teeth
(pointed
incisors),
mulberry
molar, saber
shins, saddle
nose,
rhagades,
snuffles,
frontal
bossing. May
also cause
hepatospplen
omegaly,
interstitial
keratitis and
8th nerve
deafness.
• Fetal
infections can
lead to
stillbirth.
CHLAMYDIAE:
Chlamydiae trichomatis • Obligate • Infects only humans • There are 15 Already covered in 1. Immunoflourescence- 1. Tetracyclines • No vaccine
intracelluar • Transmits via sexual immunogenot pathogenesis ☺ cytoplasmic inclusions (doxycycline) • Condoms
• Most common contact or passage ypes (A-L) by Giemsa stain. 2. Macrolides • Oral
bacterial cause of through birth canal. Trochoma: 2. Gram stain is not (erythromycin erythromycin
sexually • Via finger to eye or • Genotype useful; however in and azithromycin) in newborns
transmitted fomite to eye A,B,C urethritis, a gram stain 3. Azithromycin- of infected
disease. contact. • Chrnoic shows increased DOC mother.
• Frequently food in conjuctivits neutrophils and No 4. Neonal
developing, dry, hot • Endemic in gram –ve diplococci conjuctivits=
countries like Africa and resembling erythromycin
northern africa and Asia N.gonorrheae is
is leading cause of • May rcur over presumptive evidence
blindness there. many years. of C.trichomatis.
• May lead to 3. NAAT- via patients
blindness but urine
no systemic 4. ELISA
illness. 5. Flourescent antibody
Genital tract staining or
infections: hybridization with a
• Genotypes D- DNA probe- exudative
K. discharge having
• In men, epithelial cells too.
gonnococcal 6. Cell cultures- treat
urethritis with cycloheximide
(because it that inhibits normal
mostly co- flora and enhance
infects with trichomatis
gonorrheae)- replication.
dysuria, 7. Inclusions contain
watery non- glycogen- iodine
purulent staining to view.
urethral
discharge
(slight,
detectable in
underwear
overnight
only), lead to
didymitis,
proctitis.
• In women-
cervicits,
salpingitis,
PID. Lead to
infertility or
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
ectopic
pregnancy.
• Infants: born
from infected
mother,
mucopurulent
conjuctivitis
(neonatal
inclusion
conjuctivits)
after 7-12
days of
delivery.
Autoimmune:
reactive
arthritis and
REITER’s
SYNDROME
(urethritis,
arthritis and
uveitis)

Viruses:

NAME CHARACTERSTIC TRANSMISSION PATHOGENESIS CLINICAL SYMPTOMS DIAGNOSIS TREATMENT PREVENTION OTHER
IMPORTANT
POINTS
Herpes DNA enveloped HSV-1=SALIVA. Replicates in skin Maculopapular Cell culture, ELISA. Acyclovir; NO VACCINE Erythema
simplex virus Bind to receptor LATENCY:retrogra and mucosal cells lesions in both HSV-1 The HSV-1 is encephalitis and C-SECTION multiforme
heparin sulfate de axonal flow, and travel to and 2. dintinguished by systemic disease by Suppresive caused by:
and nectin. stay on sensory sensory ganglia HSV-1=fever, HSV-2 by HSV-1. Treat lesions chemoprophylax HSV-1 and 2,
Replicate with ganglia of via sensory gingivostomatitis, monoclonalantibo of HSV-1 and 2, is with Sulfonamides,
the help of trigimenal nerve. neurons. heal sponateously in dy against prevents shedding valcyclovir and Mycoplasma
enzymes DNA HSV-2=SEXUAL 2-3 weeks., herpes glycoprotein G in in asymptomatic famciclovir (for pneumonia,
polymerase and CONTACT, labialis, ELISA. carriers but doesnot patients in hep. B and
Thymidine kinase LATENCY: keratoconjuctivitis, Microscopy with cure the latent frequent hep. C.
(both are targets retrograde axonal Enephalitis TZANCK SMEAR state. recurrence) Erythema
of drug acyclovir) flow, stay in (temporal lobe; and Giemsa stain Foscarnet is used in multiforme
sensory ganglia of fever, headache, show case of acyclovir major (steven
lumbar and sacral vomiting, seizures, MULTINUCLEATE resistance. johnson
nerves. alterd mental status) GIANT CELLS. Trifluridine syndrome;
Latent virus CSF analysis shows PCR (detects HSV (Viroptic)= for HSV-1 fever, erosive
becomes active by moderate increase in DNA in CSF) eye infection. oral lesions
inducers.i.e: lymphocytes and NEUTRALIZATION Penciclovir or and extensive
sunlight, hormonal protein. Glucose TEST show a rise in docosonal= for desquamating
change, trauma, level is normal. antibody titer in herpes labialis skin lesions)
stress and fever. Herpetic whitlow: primary infection. Valacyclovir or caused by
lesion on the palms famciclovir= for MYCOPLASMA
and hands of persons genittal herpes and PNEUMONIA.
in contact. supress reccurence.
Herpes gladiatorum: NO DRUG CURE
in wrestlers: lesion LATENT PHASE BUT
on the head, neck CAN SUPPRESS
and trunk. RECURRENCE.
Disseminated
infection in
immunocompromise
d; esophagitis and
pneumonia.

HSV-2:
Painful
maculopapular
lesion on male and
female genital
regions with fever
and inguinal
lymphadenopathy.
Asymptomatic
shedding in both
men and women.
Neonatal herpes;
disseminated
infection or
encephalitis, skin,eye
and mouth lesions.
Maybe
asymptomatic
ASEPTIC MENINGITIS
BY HSV-2
Erythema multiform
occurs in both HSV-1
and 2; target sign or
bull’s eye on then
trunk, hands and
feet.
Varicella Varicella=chicken Via repiratory Infects upper Varicella: fever, TZANCK SMEAR No therapy needed. Vaccination: REYE’S
Zoster Virus pox droplets and direct respriatory tract, malaise followed by shows Immunocompromis VARIVAX (1-12 SYNDROME:
Zoster=shingles contact with skin enters in blood maculopapular rash, MULTINUCLEATE ed adults or years old Encephalopath
lesions. and reach skin, then vesicles, GIANT CELLS, Cell chilldren with children) y and liver
Incubation rash. pustules and crusts. culture, rise in complicated ZOSTAVAX (older degeneration;
period=14-21 days START FROM TRUNK antibody titer. disseminated than 60 years occurs in
AND SPREADS TO infection should be old patients) children who
HEAD AND treated with VZIG (Varicella are given
EXTREMITIES. acyclovir. Foscarnet Zoster ASPIRIN and
Complications is used in case of Immunoglobin) having VZV or
encepahlitis and acyclovir resistance. is used for HEPATITIS B.
pneumonia Famciclovir and prophylaxis.
valciclovir can also
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
Zoster: recurrence be used for zoster
case; painful vesicle lesions to accelerate
along the course of cure.
sensory nerve root
of head and trunk.
Adenovirus Serology type Via fecal-oral Infects mucosa Fever, sore throat, No Tx needed Cell culture Vaccine available
3,4,7,21 cause route, respiratory (e.e upper and coryza (runny nose), Rise in antibody titer but for military
respiratory droplets, direct lower respiratory keratoconjuctivitis, Complement personals only.
disease. 8 and 19 innoculation in tract, GIT, brochiolistis and fixation test Live attenuated,
cause conjuctiva by conjuctiva) ATYPICAL Hemagglutination for serology
keratoconjuctiviti fingers or Latent phase: PNEUMONIA. test. types 4,7 and 21.
s. tonometers. adenoids and HAEMORHAGIC Hand washing
11 and 12= tonsillar tissue. CYSTITIS before working
heamorhagic (haematuria) with eye lens
cystitis GASTROENTERITIS
40 and 41= WITH NON BLOODY
infantile DIARHEA IN
gastroenteritis. CHILDREN YOUNGER
THAN 2 YEARS OF
AGE
Human Causes Via skin to skin Viral genes E6 and Genital warts Microscopy= Podophyllin, alpha Vaccines:
Papillomaviru papillomas contact; E7 inactivate (condyloma KOILOCYTES interferon for Gardasil 9,
s (HPV) (benign tumors microabbaration proteins encoded accuminata)- HPV 6 PCR rise in genital warts Cervarix.
of squamous Virus first infects by p53 gene and and 11. Also causes antibody (but not Liquid nitrogen= skin
cells;warts) the basal alyer of RB laryngeal papilloma diagnostic) warts
HPV 1-4= skin skin and then (retinoblastoma) in young children. Salicylic acid for
warts replicate and gene causing Skin and plantar plantar warts
HPV 6 and 11= infect the cancer. warts- HPV-1-HPV-4. Cidofovir
genital warts uppermost layer of Carcinoma of penis,
skin. anus and cervix=
HPV 16 AND 18.
Ocult premalignant
lesions are visible by
applying acetic acid.
Parvovirus Infects cells in S Infects Slapped cheek IgM antibodies; No Tx. needed No vaccine
B19 phase only.i.e. erythroblasts, IgG throat swab Pooled
onfects red blood or IgM complex (Also called PCR analysis aof immunoglobulins=
cell precursors. causes erythema amniotic fluid chronic state
Transmit via endothelial infectiosum or fifth
repiratoy, damage (rash) disease)
transplacental, and arthritis. Aplastic anemia. Also
blood transfusion Severe hemolysis aplastic cisi with
of fetus red cells sickle vell anemia or
then congestive thallesemia or
heart failure, heriditary
Hydrops fetalis spherocytosis.
In pregnancy+ 1st
trimester; fetal
death, 2nd trimester;
hydrops fetalis; 3rd
trimester no
significant effect.
Arthritis: bilateral;
small joints of hands
and feet.
Measles virus Transmits via Infect upper Fever, cough, Rise in antibody No antiviral therapy Vaccine (live,
repiratroy droplets respiratory tract conjuctivitis titer available. attenuated)
lining then infect (photophobia), PCR
reticuloendothelia coryza (runny nose)
l cells and KOPLIK SPOTS ON
replicate their. BUCCAL MUCOSA.
Spreads via blood RASH APPERS ON
to the skin and THE FACE AND NECK
causes AND THEN SPREADS
maculopapular LOWER DOWN THE
rash TRUNK TO PALM
AND SOLES
ATYPICAL MEASLES:
occurs when a
person already
infected with
measles virus get
measles vaccine. So
the symptoms
appear without
koplik spots.
MUMPS Via respiratory Infects upper Fever, malaise, Cell culture frpom No Tx needed. Vaccine; live, ASEPTIC
droplets respiratory tract anorexia,PAROTID saliva, CSF and attenuated- MENINGITIS=
and then spread GLAND SWELLING urine. MMR mumps,
in blood and AND PAIN IS PCR Coxsackie
infect salivary INCREASED ON Increase in virus,
glands (especially DRINKING CITRUS antibody titer echovirus.
parotid), testes, JUICE; RESOLVE IN 1 CF= S antigen;
ovaries , pancreas WEEK. current infection. V
and meninges. orchitis (unilateral antigen; shows
Virus may ascend or bilateral); bilateral that pateint has
from buccal orchitis leads to had mumps in the
mucosa to parotid sterility. past
gland via stenen’s Postpubertal
duct orchtis:tunica
albugenia becomes
fibrous and fails to
expand therefore
pressure necrosis of
the sperms occurs.
Rubella virus Via respiratory Infects Fever, malaise, Cell culture No Tx. needed MMR
droplets and nasopharynx and followed by PCR
transplacentally lymph nodes, maculopapular rash ELISA
then enter into on the face and
the blood and progresses
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
other organs and downwards to the
skin. extremities.
Posterior auricular
lymph nodes
swelling.
Teratogen; specailly
in the 1st trimester of
pregnancy. Effects
heart(PDA), eyes
(cataracts) and brain
(deafness and
mental retardation).
Rabies Attaches Ach Bite of an animal Virus multiply at Fever, anorexia, Brain tissue biopsy No Tx. Needed. Vaccine: HDCVA
receptor on cell already having the bite site then sensory changes ta of animal or supportive and RIG
surface viral encephalitis go in retrograde bite sote human shows
due to this virus. axonal flow from (parasthesia), pateint NEGRI BODIES in
Rodents, rocoons, the bite site into maybe furious the cytoplasm of
dogs and bats the CNS. Virus (encephalitic; hippocampal
Non bite multiply in CNS common; agitation, neurons. Negri
rabies=via aerosols and travels to delirium, seizures, bodies are also
of bats waste salivary glands HYDROPHOBIA- due found in corneal
and other organs to spasm of scrappings.
pharyngeal muscles) PCR
or dumb (paralytic; Biospy sample
rare. Spinal cord is taken from the
involved in skin between neck
ascending paraysis). and hairline by
flourescent
antibody to rabies
Cell culture; saliva,
spinal cord, brain
tissue.
Norovirus Most common Via fecal oral route Infects mucosal Sudden onset of Stool PCR No Tx. Needed, Personal hygiene
cause of viral cells of intestine. vomiting, diarheae, supportive, and sewage
gastroenteritis in Watery diarhae low grade fever, rehydration disposal.
adults. without red cell or abdominal cramping.
white cell VOMIT OR DIARHEA
DON’T CONTAIN
BLOOD. Illness
typically lasts for 2-3
days.
Immuncompormised
patients may have
meningitis
Rotavirus Masot common Fecal-oral rouote Replicates in the Nausea, vomiting, Stool ELISA No Tx. needed Vaccines:
cause of viral mucosal cells of watery non bloody Rise in antibody Rotarix, Rotateq
gastroenteritis in small intestine diarheae. titer
young children causing secretions
Attaches to Beta of the fluid and
adrenergic electrolyte in
receptor. bowel lumen. NO
INFLAMMATION
AND DIARHEA IS
NON-BLOODY.
Hepatits B Hepadna virus, Transmits via After it enters Maybe HbsAg= present in No antiviral therapy VACCINES: Hepadna virus
virus Partially double blood transfusion, blood, it reaches asymptomatic acute illness and is used normally. RECOMBIVAX= are the only
stranded circular during labor and hepatocytes. Viral Incuabtion prodrome period. Entecavir and for persons viruses that
DNA. sexual contact. antigens appear period=10-12 weeks Presence for more tenofovir (both of exposed produce
Genome consists NOT VIA on cell Fever, anusea, than 6 months them are nucleoside frequently to genome DNA
of 4 genes: s BREASTFEEDING. surface.Cytotoxic vomiting, anorexia indicates= carrier analogues that block blood (e.g. med with reverse
gene=surface t cells attack the and jaundice.dark state, maybe transcription)=DOC students, transcription
antigen, c gene= cells and cause urine, pale stool, hepatic carcinoma for chronic carriers. dentisits, IV drug with viral RNA
core antigen, p necrolysis. elevated HbsAb= not Peginterferon alpha abusers, as template.
gene= Formation of transaminase level. detectable in 2 a, lemivudine, multiple
polymerase, x antigen-antibody Chronic active chronic carrier adefovir, transfusion,
gene= C protein complex= hepatitis= cirrhosis state telbivudine. dialysis.
(HBX, it is arthralgias, and death. Window phase= THESE DRUGS ONLY TWINRIX=
involved in viral arthritis, urticaria when HbsAG and REDUCE protect againnts
RNA transcription etc. HbsAb is not INFLAMMATION both HEP A and
and suppression Complications of detectable but AND VIRAL LOAD HEP B.
of p53 chronic hepatitis= HbcAb is present BUT DOESNOT CURE HBIG (Hepatits B
genea=cancer). glumerulonephriti (at time of acute THE HEP.B immunoglobin)=
Use REVERSE s, infection, 6 passive
TRANSCIPTASE cryoglobulinemia, months after protection,
enzyme for vasculitis. infection); test not needle prick
replication Chronic carrier: readily avialable injury.
Viruses release patient who has HbeAg present in C- section
via budding HbsAg persisting prodrome, acute delivery
through the cell in their blood for and chronic
membrane. 6 months or infections.
longer; mostly
newbron because
their immunity is
weak, leads to
hepatocellular
carcinoma.
E antigen positive
chronic carriers
(those who make
e antigen)= cause
disease
transmissions,
make virions
mostly.
E antigen negative
chronic carriers
(those who don’t
make e antigen)=
less likely to
transfer the
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
disease, low
chances of amking
virions.
Yellow fever arbovirus Jungle yellow Sudden onset of Isolation of virus Vaccine: live,
fever: Transmits fever, headache, Rise in antibody attenuated
via mosquito of myalgia, titer
Haemogoggus PHOTOPHOBIA,
species, infects juandice. UPPER GI
monkey, humans HEMORRHAGE WITH
are accidental host HEMATEMESIS
(tree cutters etc) (BLACK VOMIT).

Urban yellow
fever: Transmits
via Aedes aegypti
mosquito which
breeds in stagnant
water.
Dengue virus arbovirus Via Aedes aegypti Hemorrhagic Classic dengue fever Cell culture No Tx. available No vaccine
mosquito shock syndrome: (break bone fever)= Rise in antibody Draining
2 hypothesis fever, malaise, retro- titer stagnant water
1) virus-antibody orbital pain, PCR (it a mosquito
complex activate headache, myalgia, breeding place)
complement arthralgia, enlarged
causing increase lymph nodes, facial
vascular flushing,
permeability and maculopapular rash,
thrombocytopeni leukopenia.
a
2) The anitbodies Dengue hemorrhagic
increase the entry fever= same
of virus itno symptoms as classic
monocytes and dengue fever but
macrophages with there is shock and
the consequent hemorrhage
liberation of (specially GIT and
cytokines. skin).
Ebola Virus Filovirus Via fruit bat, body Its Incubation period=5- EISA NO. Tx. Available. No vaccine
(Causes EHF; RNA virus fluids, blood gylcorproteintkills 7 days PCR Supportive
Ebola transusion endothelial cells= Fever, headache, treatment via IV
Hemorrhagic hemorrhage. sore throat, myalgia, fluids and
Fever) Kills arthralgia, epigastric electrolytes
lymphocyctes, pain, vomiting,
macrophages and diarrhea. Later
dendritic cells and bleeding into skin
hepatocyctes and GIT followed by
shcok and DIC.

Post Ebola
syndrome: eye pain,
blurred vision,
hearing loss,
headache, joint pain,
fatigue, insomnia,
uveitis.
Marburg Virus Filovirus Same as ebola Same as ebola Same as ebola PCR No Tx. available No vaccine Both Ebola
(Causes Rise in antibody available and Marburg
Hemorrhagic titer viruses just
fever). differ in their
antigens
otherwise they
are same.
Hantavirus Bunyavirus family Via rodents KOREAN PCR No. drug avialable. No vaccine
(KOREAN HEMORRHAGIC ELISA Ribavarin is used but
HEMORRHAGI FEVER: Headache, ineffective.
C FEVER) petachial
hemorrhages, shock
and renal failure.

HANTAVIRUS
PULMONARY
SYNDROME: inluenza
like symptoms, leads
to acute repiratory
failure.
Lassa fever Arenavirus family Via rodents, Fever, headache, PCR No drug available. No vaccine
virus (causes contamination of vomiting, diarhea Rise in antibody Ribavarin can available.
hemorrhagic food and water with involvement of titer. decrease mortality
fever with with animal urine. lungs,heart, kidney rate
multiorgan and brain.
involvement) Petechial rash, GI
hemorrhage.
Death by vascular
collapse.

AIDS

REGARDS: AREEBA QURESHI D’22

These organsims are taught in infectious module.

Ch: 15
1.Staphylococcus Aureus
2.Streptococcus Pneumoniae
 INFECTIOUS MODULE MICROBIOLOGY SUMMARY
Ch:16
3.Nisseria Meningitidis
4.Nisseria Gonorrhoaeae
Ch: 17
5.Bacillus Cereus
6.All 4 types of Clostridium

Ch: 18
8.Enterobacteriaceae
9.Escheria
10.Salmonella
11.Shigella
12.Vibrio Cholerae
13.Campylobacter
14.Helicobacter

Ch:21
16.Mycobacterium Tuberculosis
17.Mycobacterium Leprae

Ch:24
19.Treponema Pallidu
Ch:25
20.Chlamydia Trachomatis

Ch:37
22.Herpes Simplex Virus
23.Vaicella-Zooster Virus
Ch:38
24.Adenovirus
25.Papillomavirus
Ch:39
26.Measles Virus
27.Mumps Virus
28.Rabies Virus
Ch:40
29.Norwalk Virus
30.Rotavirus
Ch:41
31.Hepatitus B Virus
Ch:42
32.Dengue Virus
yellow fever
Ch:45
33.HIV
Ch:51
34.Entamoeba
35.Giardia
36.Cryptosporidium
37.Trichomonas
Ch:52
38.Plasmodium
39. types of Leishmania

Ch:54
41.Taenia Solium
42.Taenia Saginata
43.Echinococcus

Ch:55
45.Schistosoma
Ch:56
46.Enterobius
47.Trichuris
48.Ascaris Lumbricoides
49.Ancylostoma & Necator
50.strongyloides
51.Trichinella
52.Wuchereria
53. Rubella virus.

Best of luck!!!