Rabies is a zoonotic disease of warm-blooded animals is caused by a Rhabdovirus belonging to Lyssavirus. It is a bullet-shaped virus.

Mode of transmission-

Bites and licks on abrasions or intact mucus membrane by infected animals. Saliva is the vehicle of transmission. Bites,Licks,corneal graft,salivary aerosol can cause transmission.

Common sources of infection-

Rabid dogs, Monkey, Cat, Mice, Vampire bats.

Worldwide- Dogs,cats,canines,cattles, even Humans. Skunks,raccoons,vampire bats, cave dwelling bats in North and Latin America.

Inoculation period – 9 days to months . In general its 4-8 weeks.

CNS and Salivary glands are the target organs of rabies virus. They travel from axons to the Brain.

Stages

I.            Prodormal stage 1-10 days

II.            Acute Neurological phase

III.            Coma/Death

Clinical Features-

Not all people bitten by a rabid animal develop disease, but once it manifests it is almost always fatal.

• Fever
• Parasthesia at the bitten site.
• Anxiety
• Hydrophobia-50%, Photophobia, Aerophobia
• Delusion and Hallucinations
• Spitting, Biting, Mania
• Neurological abnormalities- descending paralysis
• Hyperpyrexia
• Death within a week.

On Examination-

• High fever
• Exaggerated jerks
• Spasticity
• Sympathetic overactivity- dilation of pupil
• Cause of death- Respiratory paralysis, cardiac arrhythmias.

Diagnosis-

History of bite, Examination of wound.

Immunofluroscent Study- Fluroscent Ab used to detect Ag. In Corneal impression and salivary secretion.

Classic Negri bodies detected in brain in Post-mortem examination. (99% cases). Negri bodies are eosionophilic cytoplasmic ovoid bodies 2-10 mm in diameter. Seenusually in cells of hippocampus and cerebellum.

Treatment-

Only symptomatic. Once the disease has started death is almost inevitable.

Patient should be kept in quite, dark room avoiding any stimuli.

Respiratory and Cardiovascular support may be necessary.

Nutritional Support.

Drugs- Morphine,Diazepam, Cholorpromazine.

All patient should receive post-exposure prophylaxis.

Tetanus toxoids and Antibiotics.

Care of wound after Bite by Animal-

• Immediately wash the wound with soap water for 5 minutes.
• Adequate cleansing of the wound.
• Virucidal agents- Alcohol, Tincture Iodine,Povidine Iodine can be used for cleaning.
• Do not suture the wound immediately, remove any necrotic debris if present.
• Tetanus toxoid.
• Watch for the symptoms in animal if traceable.
• Go for post-exposure Prophylaxis.

Guidelines for Post-exposure Prophylaxis.

• Category I- touching or feeding of animals, licks on intact skin
• Category II- Nibbling of uncovered skin, minor scratches,licks on broken skin.
• Category III- Single or multiple transdermal bites or scratches, contamination of mucus membrane with saliva.

Management-

• Category I- nothing needed
• Category II- Vaccine immediately.local treatment of the wound
• Category III- Rabies Ig + Vaccine immediately.local treatment of the wound

Vaccine- Human Diploid Cell-culture vaccine 1.0ml IM total 5 doses on 0,3,5,7,14,21 days.

Human Rabies Immunoglobulin- HRIg- 20 IU/kg  ½ dose IM and other ½ injected around the wound.

Pre-exposure Prophylaxis-

Indicated for-

• Lab workers.
• Animal handlers.
• Vetenarians.

2 doses of HDCV 1.0ml deep Subcutaneous or IM. Re-enforcing dose after 12 months and then after every 1-3 years.

SOME FACTS on RABIES by WHO ( September 2010)

• Rabies affects  more than 150 countries worldwide.
• Worldwide, > 55 000  die of rabies each yr.
• Dogs are the source of 99% of the rabies related deaths in Human.
• Wound cleansing and immunization within a few hours of contact can prevent the onset of rabies and death.
• Every year, more than 15 million people worldwide receive a post-exposure preventive regimen to avert the disease – this is estimated to prevent 327 000 rabies deaths annually.

Rabies Vaccines from CDC

Giardiasis is the Infection of the upper small intestine caused by a Flagellate Protozoan , Giardia lamblia ( aka G. intestinalis or G. duodenalis).

Epidemiology-

• Occurs Worldwide, most abundantly in areas with poor sanitation.
• Persons of all ages area affected, but is particularly high among children.

Life Cycle and Pathogenesis-

Organism occurs in faeces. Only the cyst is infectious, trophozoites are destroyed by gastric acidity. Cyst remains viable in water upto 3 months and are transmitted as a result of fecal contamination of water, food and from person to person.

Man is the only reservoir of infection.

Ingestion of as few as 10 cysts is sufficient to cause infection in the humans.  After the cysts are ingested trophozoites emerge in the Duodenum and Jejunum.

Trophozoites cause-

• Epithelial damage
• Atrophy of villi
• Hypertrophic crypts
• Cellular infiltration of lamina propria
• Rarely, mucosal invasion.

Risk factors for infection- Hypogammaglobulinemia,  IgA deficiency,  Achlorhydria,  Malnutrition.

Clinical Features-

• Incubation period= 1-3 days
• Large proportion of infected person remain asymptomatic cyst carriers and their infections clear spontaneously
• Prolonged diarrhea  specially froathy diarrhea with mucus.
• With high episode of evacuation the stool becomes more watery, mucus . Blood may be seen.
• Copious, froathy, malodorous and greasy
• Less commonly anorexia, nausea, vomiting, mild epigastric discomfort, cramps, belching, flatulence, borborgymi, abdominal distension.
• Marked weightloss, impaired growth and development is children.

Forms of Giardiasis-

1. Acute diarrhea
2. Chronic Diarrhea
3. Malabsorption syndrome- marked weightloss, protein losing enteropathy, Vit A,B12 and dissacharide deficiency.

Investigations-

Stool RME- Samples obtained at 2-3 days interval on 3 separate occasions.Examine for the cyst

Duodenal fluid aspirate

Jejunla biopsy- Endoscopic.

Management-

Treatment options include-

• Tinidazole Single dse 2 Gm
• Metronidazole 2 Gm  daily for 3 days
• Albendazole 400mg daily for 5 days

During Pregnancy-

• Paromomycin 25-35mg/kg in 3 divided doses for 7 days

Reference- Harrison, Davidson, Lecture note

are the most popularly used antibiotics. They are  any antibiotic agent that contains a β-lactam chain in the molecular structure. Penicillin is the prototype drug and once was a cure for almost anything. Sir Alexander Fleming discovered Penicillin. It was a miracle discovery in history of Mankind.

Sir Alexander Fleming Discovered Penicillin

Mechanism of Action:

-          Interfere with the synthesis of bacterial cell wall

-          Inhibit transpeptidases so that cross linking does not take place

-          When susceptible bacteria divide in the presence of it- cell wall deficient forms are produced resulting in the lysis of bacterial cell

-          Peptidoglycan cell wall is unique to bacteria and it is non toxic to man

-          Gram positive bacteria have higher susceptibility to PnG

Penicillin G (Benzyl Penicillin):

-          Narrow spectrum; gram positive

-          Majority of gram negative bacilli, M.tuberculosis, ricketsiae, chlamydiae, virus insensitive

-          Resistance:

1. Inherent: PBPs located deeper under lipoprotein where PnG is unable to penetrate
2. Penicillinase: opens the beta lactam ring
3. Penicillin tolerant but not penicillin destroying like pneumococci

-          Pharmacokinetics:

1. Acid labile: gastric acid
2. Low oral absorption and rapid and complete absorption from i.m site
3. Plasma t1/2  30 minutes
4. Poor CSF  and serous cavity penetration but increased in inflammation
5. Rapid renal excretion (GFR-10 % and rest tubular secretion)
6. Tubular secretion blocked by Probenecid: higher and longer lasting plasma concentration

-          Preparation and Dose:

1. Sodium Penicillin G injection
2. Repository Penicillin G injection
   1. Procaine Penicillin G
   2. Benzathine Penicillin G

-          Adverse Effects:

1. Local irritancy and direct toxicity: pain at im site, nausea, thrombophlebitis, mental confusion, muscular twitchings, convulsions, bleeding, hallucinations, CNS stimulation
2. Hypersensitivity: Urticaria, fever, wheezing, edema, serum sickness
3. Superinfections
4. Jarisch Herxheimer reaction

Semisynthetic Penicillins:

1. Acid resistant alternative: Phenoxymethyl penicillin (Penicillin V)
2. Penicillinase Resistant: Methicillin, Cloxacillin
3. Extended Spectrum:
   1. Aminopenicillin: Amoxycillin, Ampicillin, Bacampicillin
   2. Carboxypenicillin: Carbenicillin, Tircarcillin
   3. Ureidopenicillin: Poperacillin, Mezlocillin
   4. Beta- lactamase inhibitor: Clavulanic acid, Sulbactam, Tazobactam

How prepared are we?

Smallpox is believed to have emerged in human populations about 10,000 BC. The disease killed an estimated 400,000 Europeans each year during the 18th century (including five monarchs), and was responsible for a third of all blindness. Of all those infected, 20–60%—and over 80% of infected children—died from the disease.

During the 20th century, it is estimated that smallpox was responsible for 300–500 million deaths. In the early 1950s an estimated 50 million cases of smallpox occurred in the world each year. As recently as 1967, the World Health Organization (WHO) estimated that 15 million people contracted the disease and that two million died in that year.

After successful vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the eradication of smallpox in December 1979. To this day, smallpox is the only human infectious disease to have been completely eradicated.

The last cases of smallpox in the world occurred in an outbreak of two cases (one of which was fatal) in Birmingham, England in 1978. A medical photographer, Janet Parker, contracted the disease at the University of Birmingham Medical School and died on 11 September 1978,after which the scientist responsible for smallpox research at the university, Professor Henry Bedson, committed suicide. In light of this accident, all known stocks of smallpox were destroyed or transferred to one of two WHO reference laboratories; the Centers for Disease Control and PreventionState Research Center of Virology and Biotechnology VECTOR in Koltsovo, Russia. In 1986, the World Health Organization recommended destruction of the virus, and later set the date of destruction to be 30 December 1993. This was postponed to 30 June 1995. In 2002 the policy of the WHO changed to be against its final destruction. Destroying existing stocks would reduce the risk involved with ongoing smallpox research; the stocks are not needed to respond to a smallpox outbreak. However, the stocks may be useful in developing new vaccines, antiviral drugs, and diagnostic tests.

In March 2004 smallpox scabs were found tucked inside an envelope in a book on Civil War medicine in Santa Fe, New Mexico. The envelope was labeled as containing scabs from a vaccination and gave scientists at the Centers for Disease Control and Prevention an opportunity to study the history of smallpox vaccination in the US.

Now the fear is

What if the Outbreak Occurs again?

Only for Learning Purpose

Fact sheet: Derieved from Wikipedia

Read more on what and latest activities on Small pox.

http://www.bt.cdc.gov/agent/smallpox/index.asp