RABIES = Major viral disease of the tropics causing fatal encephalomyelitis
Epi
• Dogs accounts for >96% of reported cases
• Canids (dogs,foxes wolves,jackals), Skunks, Farm animals, Cats, Bats, Mongoose
• Young males 1-14 years
• Commoner in urban populations
Mortality
• India > China> Bangla > Sri Lanka
Reservoir
• Tropical areas = Dog
• America = Skunks, raccoons, foxes and bats
• Artic = fox
• Caribbean = Mongoose and vampire bats
• Europe = Foxes Wolves, raccoons dogs and bats
• Africa and Asia = Wolves, jackals and small carnivores
Transmissi
• Animal bites and licks
on
• Human to human
• Inhalation
• penetrate broken skin and intact mucous membranes
Virus
• Enveloped single stranded RNA virus
• Distinctive bullet shape
• Duvenhage, Makolo, European bat Lyssavius
Pathogene
• Inoculation via bite
sis
• Primary replication in muscle cells
• Progress via axoplasm to CNS where rapid spread occurs – onset of symptoms
• Finally centrifugal spread via nerves to most organs
• No detectable response until symptoms develop
• Neutralising antibodies develop 7 days after onset of illness
Clinical fea • Incubation period -7 days to years
• Prodromal phase = vague symptoms (fever, malaise etc) + intense itch at wound site
• Furious rabies
• Paralytic or “dumb” rabies
• Characterised by hydrophobia
• Rapid onset progresses to coma and diffuse
Furious
•
Aerophobia
flaccid paralysis
rabies
• Intermittent periods of general arousal
• All parts of CNS affected
• Lucid intervals
• Survival usually about 7 days
•
Less
common
in
humans
>
furious
rabies
• Paraesthesiae + flaccid ascending paralysis
Paralytic
• Particular feature of vampire bat rabies
• Duration can be 2-3 weeks
rabies
DX
• Immunofluorescent testing = Usually skin biopsy (neck) or corneal impressions
• Virus detection (Saliva, throat swabs and tracheal aspirations, + PCR)
• Antibody testing days 5-8
• Post mortem diagnosis- Negri bodies are not pathognomonic for rabies
• Management is aimed at
Treatment
o Relieving suffering
o Managing complications (Cardiac arrhythmias, Pneumothorax, Cerebral oedema,
Convulsions, Fluid + electrolyte d/o, Hyperpyrexia, Stress ulceration
• Admission, sedation and analgesia
• suspect rabies when pt develops neurological symptoms after being bitten by a mammal in
Differential
a rabies endemic area. Hydrophobia is pathognomonic
diagnosis
• Tetanus: also can follow a bite but: Shorter incubation period, Persistence of muscle rigidity
between spasm, Absence of Meningoencephalitis
• Encephalitides: no hydrophobia and behaviour in furious rabies is typical
• Poliomyelitis: no sensory symptoms and fever does not persist into the paralytic phase
Prevention
• Regular vaccination of pets
• Keep pets away from wild animals + seek veterinary advice if pet is bitten by wild animal
• Avoid direct contact with wild animals
Rabies
vaccination
Rabies
treatment –
first aid
Animal
bites – post
exposure
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Death
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Prevent bats from taking up residence where there are humans
Reporting strays or animals that are acting strangely to relevant authorities
Avoid contact with dogs in developing countries
Nervous tissue vaccines
Human diploid cell vaccine (HDVC)
Purified Vero cell vaccine (PVRV)
Purified chick embryo vaccine (PCEC)
Prophylactic regimes possible with cell culture vaccines 3 vaccines on day 0, 7 and 21 or
28 days. Malaria prophylaxis can interfere with ID dosing.
Scrub wound with soap and water and rinse with copious amounts of water for 5 minutes
Remove foreign material
Swab thoroughly with viricidal agent
Seek medical help immediately
Minor exposure: lick of
Major exposure
Explore, debride +
skin,scratches and abrasions, minor
including licks of
irrigate deep wounds
bites
on
covered
areas
arm,
trunk
mucosa or major bites –
Avoid suturing and
and legs
multiple on face, head,
occlusive dressing
• if animal available + not vaccinate
fingers or neck.
Tx for tetanus +
• Vaccine
• Serum and vaccine
potential bact infection
• Stop tx if animal healthy 10 days
• Stop tx if domestic
Give rabies post
• Stop tx if FA animal brain negative
cat or dog remains
exposure tx if relevant
• If animal unavailable for for
healthy for 10 days
(either serum + vaccine
observation = Give serum
• Stop tx if FA brain is
or vaccine alone)
+vaccine
–ve
Inadequate wound toilet
Delay in starting vaccine
Injections into the buttock
Lack of RIG
Failure to infiltrate around wound
Impaired immune response
DENGUE FEVER (DF)
Epi
 Emerging pandemic which has spread globally during the past 30 years as a result of
changes in human ecology.
 Around 2.5 billion people in >100 tropical & subtropical countries are exposed.
 Mainly in Asia and the Pacific then Americas, Middle East, Africa, Queensland (Aus). In
endemic areas over 50% of the population is seropositive.
 Seasonality = all yr around in the tropics and in the wet seasons in sub tropical regions.
 Travellers at risk = most initial cases are asymptomatic. Returned travelers from Asia
have clinical dz + seropositive for DV
Dengue virus  Dengue Virus = single stranded RNA w 4 serologic types = D1, D2, D3 and D4. each
serotype provide spec lifetime immunity + short term cross-immunity (6mths)
 It is a flavivirus. (In addition to DF, flaviviruses can cause yellow fever (YF), WNF, JE,
Tick Borne Encephalitis (TBE), and Zika Fever.
 Arboviruses = arthropod-borne virus. arboviral dz eg: DF and YF. Both are carried by
mosquitoes but DF is unusual in that humans are the natural host.
 Arthropods = largest and most diverse phylum in the animal kingdom and include
crustaceans, insects, centipedes, and millipedes. They are characterized by a
segmented body, a disposable exoskeleton and jointed appendages. Most arboviral
diseases are carried by insects e.g. mosquitoes, ticks, sandfiles, midges.
Mosq vector Aedes (stegomyia)
Aedes (stegomyia) albopicta
Mansonia species
aegypti
 Asian tiger mosquito (albopictus
 Female mansonia
(male) and albopicta (female)
 commonest
mosq eg Ma titilans, Ma
dives, and Ma uniformis
 peridomestic =
 Aggressive daytime biter, carries
= major vectors of
breeds in and
at least 24 types of virus eg DenV.
brugian filariasis in
around houses
 Lives +bites outdoors + prefer
India/SEA
particularly in clean
biting towards dusk.
water.
 can also transmit
 Easily distinguished = white
dengue.
 Rests in dark areas
stripes on its back.
within houses, bites  When it enters a new area A
 mainly swamp breeders
at dawn + early
and thrive in outside
albopictus mates with the local
morning.
pools of water, blocked
mosq causing them 2b infertile so
drains and neglected
 One mosquito can
that only its own type multiplies.
rivers and canals.
infect many ppl
 resembles genocide!
living in the same

nocturnal biters (bite at
 Enter USA thru importation of
house causing a
night) and are
tyres, in which the mosq was
mini epidemic of
especially active
breeding, into Houston in 1985.
dengue in a
around 0300h.
 Able to survive in cold
particular family.

They are predominantly
environment. This means that it
rural mosquitoes and
can take up winter quarters in a
live outdoors. Although
suitably insulated spot + emerge
found in Central
to transmit dz in Spring.
America e.g. Panama
Transmission Mosquito to human to mosquito (NO human to human transmission)
Disease
 Dengue is classified as a Viral Hemorrhagic Fever (VHF) = capable of producing
severe hemorrhage and capillary leakage in any part of the body just like
 Flaviviruses: Yellow Fever YF, Crimean-Congo Hemorrhagic Fever CCHF
 Bunyaviruses: Rift Valley Fever RVF, Hantaan Fever
 Arenavirus: Lassa Fever
 Filoviruses: Ebola, Marburg Fever
 any sign of bleeding, bruising, petechiae or +ve tourniquet test = viewed with alarm.
 VHF = Dengue commonly presents w fever, arthralgia + rash = FAR syndrome.
Clinical
presentation
DX
TX
The Riddle
of DHF








usually asymptomatic @ transient flu-like illness
Short incubation period. Normally about 2 – 5 days but may be up to 15 days
Acute high Fever (‘saddle back fever’)
Arthralgia (Not as pronounced as in Chikungunya)
Myalgia ( non specific but very common)
Severe headache
Retro-orbital pain is often very prominent
Rash which is usually confined to the trunk. May blanch under pressure. The rash type
varies but is often maculopapular and often very itchy.
 Photophobia
 Lymphadenopathy
Recovery in a few days is the rule. There is no specific treatment.
1. History of travel or residence in dengue endemic area
2. Constellation of clinical symptoms and signs above
3. Viremia only lasts 5 days so unlikely to grow virus from blood
4. Leukopenia (greater than that of malaria)
5. Thrombocytopenia (marked. Usually < 150,000)
6. Eosinophilia ( > 500 this is not found in malaria or rickettsia)
7. ALT ( more elevated than in malaria)
8. IgM and IgG usually unhelpful in early cases. Higher in convalescent serum. False +ve
common because of cross reactions with other flaviviruses.
9. Positive tourniquet test (>20 petechiae in 22.5cm2 area of forearm after inflating BP
cuff midway between systolic and diastolic pressure for 5 minutes)
10. A negative malaria slide in the presence of dengue like symptoms
11. Travellers: consider dengue in anyone w long stay in an endemic area, is a first time
traveller, has a thrombocytopenia and whose symptoms (fever etc ) have begun a
short time after return.
There is no specific vaccine or treatement.
Treat symptom and maintain the circulation.
Avoid aspirin because of the bleeding tendency and the possibility of an associated Reyelike syndrome
1. Immune Enhancement Hypothesis or Antibody Dependent Enhancement (ADE).
Each serotype provides specific life-long immunity + short-term cross immunity for 6 mths.
After 6 mths, non protective. if get attacked by other serotype after 6 mths, they will cover
the virus – will be ansorbed in macrophage – allow new virus of other serotype to multiply)
Aka: the first attack by a serotype of a virus give non protective immune response that
allow other serotypes of the same virus multiply in the host.
2. Geneticically different dengue virus
3. Racial genetic resistance
DYSENTERY
Diarrhoea with bloody mucous + abdominal pain + tenesmus (severe pain when straining to pass stool)
Shigella
Amebiasis
Epi
All over world, esc impoverished areas Worldwide, common in tropic/ subtrophic
4types: pathogenic (E.histolytica), non pathogenic
(E.dispar, E.coli, E. hatmannii)
Transmissi Foecal oral
Faecal oral, direct contact (dirty hands), sex contact
on
Host factor
Stress, malnutrition alcoholism, corticosteroid,
immunodeficiency, alteration of bact flora.
Clinical
• Mild: 2-3 days = diarrhoea + blood
• mostly asymptomatic
features
• Severe: 2-3 wks = fever, malaise,
• Clinically = self limited (90%), local invasive
colicky abd pain, red current jelly ,
(10%), extra intestinal –liver, brain (1%)
odourless
Complicati • dehydration
• fulminant amoebic colitis w perforation
ons
• Hyponatraemia
• liver abscess (w/o jaundice)
• perforation
• massive haemorrhage (due to vasculitis)
• toxic megacolon
• amoebomas (grauloma)
• protein losing enteropathy
• amoebic stricture (fibrosis of intestinal wall)
DX
• clinical
• stool microscopy (identify trophozoites/cyst)
• blood + pus in stool
• serology (IHA, ELISA etc)
• culture (Mc Conkey)
• stool ag detection
• colonoscopy
Tx
• hydration
• oral metronidazole (10 days)
• Ampicillin + cotrimoxazole
• liver abscess = dysentery (surgical drainage)
• nalidixic acid, quinolone
TYPHOID = Enteric fever
Aetiology
• Salmonella thypi (human)
Transmis Carrier: gall bladder
• Salmonella paratyphi A,B,C
sion
Foecal oral
• GNB
Incubation period: 7-14 days
• Facultative anerobe
Pathoge
1. Penetrate ileal mucosa
Clinical
• 1st week: step ladder T rise, headache, abd
nesis
2. Multiply in mesenteric LN
features
pain, constipation
3. Invade BS via thoracic duct
• 2nd week: mild hepatosplenomegaly,
4. Infect liver, GB, spleen, kidney,
bradycardia, rose spot
BM
• 3rd week: typhoid state (apathy, toxaemia,
nd
5. 2 blood invasion – heavier
delirium, disorientation, coma) – untreated =
bacteraemia
intestinal haemorrhage, perforation
DX
- culture
Tx
- chloramphenicol
- typhoid test (presence of IgM,
- amoxicillin
IgG)
- ampicillin
- serology – detect ab against O
- ciprofloxacin
+ H ag
- resistant = azythromycin
Control reservoir • detect + treat
Immunization: 3 types
• isolation
1. Heat killed whole
• disinfection of stools/urine
2. Oral live attenuated
• detection + tx carrier
3. Vi capsular polysacccharide
Route
• water, food sanitation
Indications for vaccination:
• excrete disposal
1. travel to endemic area
• fly control
2. intimate exposure to S. typhi carrier
3. microbiology lab woker
Suscepti • immunoprophylaxis
4. Immigrant,
5. military
ble
• health education
LEPROSY - MYCOBACTERIUM LEPRAE
Epi
Angola, Brazil, Central African Republic, India, Congo, Madagascar etc
Manifest
Affect skin, nerves, mucosa membrane
tation
1. Anesthetic skin lesion
2. Peripheral neuropathy
3. Peripheral nerve thickening
Types +
1. Indeterminate
clinical
 Start = painless hypo[igmnted / erythematous area of skin
2. Tuberculoid (high CMI w elimination of leprosy bacilli) = PAUCIBACILLARY
 Asymmetrical anular plaque/ macules w flat centre + nerve thickening
 Tuberciloid lesion – well defined border + hairless
3. Borderline (common)
 multiple, asymmetrical even band like lesion
 raised dome-like centre
 nerve involvement early + widespread
4. Lepromatous (poor/ no CMI) = MULTIBACILLARY
 symmetrical, stable, widespread, hypo/hyperpigmented macules all over., skin thickened
mucosa involvement eg eyes, nose
 thinning eyebrow + ear, leonine facies
 nerves
WHO
Paucibacillary Hansen’s dz
Multibacillary Hansen’s dz
class
- Tuberculoid leprosy
- Lepromatous leprosy
- Few skin lesion, Milder
- > 5 skin lesions, most severe
- 1 or more hypopigmented skin - a/w nodules, plaques, thickened dermis, involvmt nasal
macules
mucosa → epistaxis (nose bleed)
- only 1 nerve trunk affected
- eye lesion: cataract, iritis, madorosis (missing eyebrow)
Pathology Intracellular organism induces cell mediated response – some ppl very susceptible
Ab appears but useless.
Granuloma formation results from mycobacterium persistence w continue cytokine release
- long incubation period (2-5 yr)
- only occurs in man
- not very contagious
DX
1. Clinical – examine pt – look for peripheral nerve thickening (hand = ulnae, median, radial,
knee = peroneal, ankle = sural) + skin macules + papules
2. Bacteriological – GPB, acid + alcohol +ve, hard to grow, uniform stain
3. Histological
4. Lepromin Test TX
1. Triple therapy = Dapsone, Rifampicin, Clofazamine
2. BCG (TB, Leishmania + leprosy)
common tropical dermatomes
 leprosies, mycobacterium leprae
 cutaneous myasis, Diptera fly larvae of tumbu and botfly
 tungiasis, female sand flea
 cutaneous larva migrans, nematode larvae
 strongyloides, nematode larvae larva currens
 cutaneous leishmaniasis, sandfly
HELMINTHS – TREMATODES (FLUKES)
- unsegmented, flat leaf-like (except schistosomes)
- hermaphrodite (except schistosomes- hv 2 sexes)
- produce iperculated eggs, dev in water (except schistosomes)
- intermediate host- snail
- definitive host - human
Schistosomiasis (bilharzia)
Type
Life
cycle
General
DX
TX
Preventi
on
Fasciola hepatica.
(liver fluke)
Metacercariae
ingested on
aquatic plants
Metacercariae
excyst in
duodenum.
Immature penetrate
liver.
mature in bile
ducts.
Eggs produced &
passed in faeces.
Eggs hatch
miracidia.
Miracidia enter
snail, develop to
cercariae.
Cercariae encyst
on plant
Mansoni, Japanicum, Haematobium, Mekongi, Intercalatum
•
Cercarial larvae → penetrate skin → (via BS) lung, liver →become
schistosomulae → mature in portal vein → migrates to intestine
(Mansoni) / bladder (haematobium) → eggs excreted in stool (mansoni) / •
urine (haematobium) → contact w water, egg release miracidium
(immature larvae) → intermediate host (snail) → become cercarial larvae
•
 Cercariae = allergic dermatitis (Swimmer’s itch)
 Schistosomulae = cough + fever
•
 Adult worm = rarely pathogenic
 Eggs = Katayama fever (immune complex formation)
•
S. Mansoni
S. haematobium (Urinary) S. Japanicum
(Intestinal)
•
• Asymptomatic
• Asymptomatic
• Katayama fever
• Hepatoslenomeg • Urinary: haematuria,
(hypersensitivity
•
aly
dysuria, freq, recurrent
rxn, fever,
• Pseudopolyposis,
UTI, nephrotic, bladder
myalgia,
• Intestinal
carcinoma
arthralgia,
schistosomiasis
• Neuro: epilepsy,
lymphadenopathy, •
• liver fibrosis
granuloma in SC, lower
faeces –ve for
• portal HTN
muscle weakness
egg)
• lung: cor pulmonale,
Light: asymptomatic.
pulm HTN
Heavy: acute dz with
Lateral spine
Terminal spine
Small,
inconspicuous spine serious liver damage
1. Travel hx
2. Microscopy : eggs in faeces (Mansoni) / urine (Haematobium)
3. Urine dipstick
4. Blood eosinophilia
5. Serological markers
6. antibody assay = look for schistosomal ab
7. antigen detection
8. rectal biopsy (S. mansoni)
1. Praziquantel
2. Oxamniquine (S. Mansoni)
3. Metrifonate (S. Haematobium)
1. Reduce water contamination – health education, mass chemotherapy, provision of
sanitation, reduce egg excretion by drugs, prevent access to transmission sites
2. attack on snails: chemical + naturally occurring plant pdt
3. reduce contack with infection
HELMINTH – CESTODES (TAPEWORMS)
• Segmented & tape-like body.
• Head (scolex), many segments (proglottids).
• Hermaphrodite.
• Eggs released when gravid segment becomes detached and ruptures.
• definitive host = human
1. CYSTICERCOSIS / TAENIASIS
Life cycle
• Larvae cyst (cysticercus) ingested in undercooked meat → human (definite host) →
faeces contaminated w eggs → consumed by pig (intermediate host)
• BUT, human can also be IH if they ingest egg (Cysticercosis)
T. saginata
T. solium
Diphyllobothrium latum
Taeniasis
Cysticercosis
Diphyllobothriasis
Transmission Undercooked beef Undercooked pork
Faecal oral
Undercooked fish
IH
Cattle
Pig / Human
Human
DH
Human (upper
Human (travel in
jejunum)
lymphatics + vessels)
Clinical
GI: Nausea, loss appetite, abd pain,
Muscle pain,
Abd pain, diarrhoea
vomiting, diarrhoea
weakness, ocular
alternated by
Other: cyst formation in brain, eye, lung,
(blurred/blind),
constipation, vomiting,
liver
neural, cerebral,
wt loss, vit B12 def
cardiac
DX
Hx of eating undercooked meat
• CT, MRI,
Eggs in stool
Microscopy of proglottids / eggs in stool
• CSF (↑protein, ↓
glucose)
• muscle, brain bx
• Ab detection
TX
Praziquantel
Praziquantel
Praziquantel
Albendazole
2. HYMENOLEPIASIS Intestinal
Hyemenolepis nana (dwarf tapeworm)
- only cestodes that parasitizes human w/o requiring an intermediate host
Clinical
Light: abd disturbance
Heavy: enteritis
DX
Rodent infestation ova in faeces
TX
Praziquantel + rodent population control
3. HYADATID – cyst rupture → problem!!
Echinococcus multilocularis
Transmission Ingestion of infective ova
DH
Fox, dog, cat, coyote, wolf
IH
Mammal (human + herbivourous)
Epi
Northern hemisphere
Cyst
alveolar/ multilocular cyst
Clinical
symptoms mimic cirrhosis/ HCC
DX
TX
More resistant to chemo
Poor px
Echinococcus granulosus
Ingestion of infective ova
Dog + other carnivore
Small rodents, rarely human
Worldwide (frequent in rural, shhep raising area)
Single, big (daughter cyst)
- Abd: distension, ascites
- Liver: obstructive jaundice
- Lung: pulm, abscess, cough, chest pain
- CNS: Jacksonian epilepsy, fever, pruritus
Clinical, XR, serology, US
Surgery, percutaneous aspiration + albendazole
NEMATODES
- Cylindrical worms. Separate sexes.
- Most are geohelminths, spread by faecal contamination of the soil.
- Infection by swallowing infective eggs or larvae penetrating skin.
- Heavy infections in children 3-8 years.
1. SOIL TRANSMITTED – caused by eggs
Ascaris lumbricoides Trichuriasis
(whipworm)
Life cycle
Ingest egg → larvae Ingest egg →
→ liver, heart, lung,
larvae →crypts of
alveoli
lieberkhun
→bronchioles,
(intestinal) →
bronchi, trachea,
migrates within
epiglottis → swallow mucosa→ large
→small intestine→
bowel→ adult
adult
(mature)
Pathogenesis
Loeffler’s syndrome
complication
Appendicitis,
cholecystitis,
pancreatitis
Microscopy =
Sputum, faeces,
vomit
DX
TX
Mebendazole,
albendazole,
levamizole
Rectal prolapse
Lab: eosinophilia,
↑ serum
creatinine, lactate
dehydrogenase
Eggs in stools
Mebendazole,
albendazole,
steroid
(inflammatory)
Strongyloides stercolaris Hookworm
Ingest egg @ larvae
penetrate skin → larvae
– (thru BS) lungs +
intestine → infective
larvae in soil
AUTOINFECTION –
reinfect host –
persistence of infection
for >40yrs
Larva curren
Hyperinfection in
immunosupressed
except HIV
CXR
Stool microscopy
sputum
Ivermectin, albendazole
Ancylostoma
duodenale
Nector Americana
Ingest egg @ larvae
penetrate skin →
larvae →lung→
cough up → swallow
→small intestine→
adult
Anemia / stunt
growth
Stool microscopy
Correct anaemia –
ferrous sulphate, folic
acid
mebendazole
2. FILIRIASIS: elephantosis – caused by worms
Adult worm live and damage the lymphatic system
Transmitted by mosq
Clinical:
• Early:Lymphadenopathy, oedema, pulmonary eosinophilia (nocturnal wheezing)
• Late: lymphatic obstruction, varicose lymphatic rupture into liver, kidney, peritoneum (ascites),
joints, elephantiasis
• chronic: grade severity = 1 (reversible pitting eodema by elevating the leg), 2 (non pitting
oedema), 3 (severe swelling + sclerosis + skin change)
Wuchereria bancrofti
Brugia malayi
Brugia timori
DH
Human
Human
Human
No known reservoir
Found in macaques, leaf monkeys,
cats, civet cats
IH
Culex, Aedes, Anopheles sp
Anopheles, Mansonia
DX
Giemsa stain
Serology – increase IgE + IgG
TX
Diethylcarbamazine
Albendazole – kill adult worm
Ivermectin