Friday, January 25, 2008

dPBL Package 2

Problem Statement

There are outbreaks of viral, fungal and protozoa diseases among platoons of army soldiers in Indonesia. Soldiers reported sick after 2 weeks of jungle warfare training. It is of concern to the ministry that there are also sporadic reports of avian flu in the nearby villages. In view of these outbreaks, you have been tasked to conduct a pre-mission briefing with blogs and poster to educate future batches of soldiers.
Your group needs to keep a blog containing information about a variety of pathogens that cause problems during jungle training so that the soldiers are made aware of the dangers and could take the necessary precautions.

Indonesia -

located in South East Asia

experience tropical climates year-long (warm and humid + rainy seasons)

Army conditions -

jungle (may be warm and humid or damp pending weather changes)

warfare (exposed to soil, air, water - living conditions for pathogens)

soldiers (army of soldiers: many people; cluster)

exposure to wildlife animals including birds (avian)

harsh living conditions with improper sanitation

shortage of food/water (may lead to consumption of contaminated food/water)

Thursday, January 24, 2008

Possible Protozoa Agents


Ingestion of cysts that are transmitted primarily by the fecal-oral route in contaminated food or water.

The ingested cysts differentiate into trophozoites in the ileum but tend to colonize the cecum and colon. Trophozoites invade the colonic epithelium and secrete enzymes that cause localized necrosis. Little inflammation occurs at the site. As the lesion reaches the muscularis layer, a typical flasked-shaped ulcer forms that can undermine and destroy large areas of the intestinal epithelium. Progression into the submucosa leads to invasion of the portal circulation by the trophozoites.

Clinical Syndrome
Lower abdominal discomfort
Weight loss
Amebic abscess of liver
Asymptomatic infections

Laboratory Diagnosis
Detecting trophozoites in diarrheal stools or cysts formed in stools.

Infection occurs worldwide but occurs most frequently in tropical countires, especially in areas with poor sanitation. It is widely prevalent in male homosexuals.

Metronidazole or tinidazole

Prevention and Control
Avoiding fecal contamination of food and water and observing good personal hygiene. Purification of water and avoid using human waste to fertilize crops.


Ingestion of cysts that are transmitted primarily by the fecal-oral route in contaminated food or water.

Encystation takes place in the duodenum, where the trophozoites attaches to the gut wall but does not invade. The trophozoites causes inflammation of the duodenal mucosa, leading to malabsorption of protein and fat.

Clinical Syndrome
Watery, foul-smelling diarrhea
Abdominal cramps (week to months)

Laboratory Diagnosis
Detecting trophozoites or cysts in diarrheal stools or cysts formed in stools. ELISA test detects a Giardia cyst wall antigen.

It occurs worldwide. Half of those infected excrete cysts in the stool, which then contaminates water sources. Giardia infection is common in homosexual males, children in day-care centres and patients in mental hospitals.

Metronidazole or quinacrine hydrochloride.

Prevention and Control
Drinking boiled, filtered or iodine-treated water in endemic areas and while hiking. No prophylactic drug or vaccine is available.


Acquired by fecal-oral transmission of oocysts from either human or animal sources.

The oocysts excyst in the small intestine, where the trophozoites attach to the gut wall. Invasion does not occur. The jejunum is the site most heavily infested. The pathogenesis of diarrhea is unknown.

Clinical Syndrome
Watery, nonbloody diarrhea causing large fluid loss and malnutrition

Laboratory Diagnosis
Finding oocysts in fecal smears when using a modified Kiyoun acid-fast stain.

Cryptosporidia cause diarrhea worldwide. Large outbreaks of diarrhea caused by cryptosporidia in several cities in the United States are attributed to inadequate purification of drinking water.

Paromomycin, Nitazoxanide for children aged 1 to 11 years old.

Prevention and Control
Purification of the water supply, including filtration to remove the cysts, which are resistant to the chlorine used for disinfection, can prevent cryptosporidiosis.


Anopheles mosquito

Red blood cells are destroyed by the release of merozoites and by the action of the spleen to first sequester the infected red cells and then to lyse them.

Clinical Syndrome
Sudden fever
Abdominal pain
Hepatomegaly in 1/3 of infections

Laboratory Diagnosis
Microscopic examination of thick and thin Giemsa-stained smears. PCR test for Plasmodium nucleic acids. ELISA test for a protein specific P. Falciparium.

More than 200 million people worldwide have malaria, and more than 1 million die of it each year, making it the most common lethal infectious diseas. IT occurs primarily in tropical subtropical areas, especially in Asia, Africa and Central and South America. Malaria in the United States is seen in Americans who travel to areas of endemic infection without adequate chemoprophylaxis and in immigrants from areas of endemic infection. It is not endemic in the United States. Certain regions in SEA, South America, and east Africa are particularly affect by chloroquine-resistant strains of P. falciparium. People who have lived or traveled in areas where malaria occurs should seek medical attention for febrile illnesses up to 3 years after leaving the malarious area.

Chloroquine, Malarone and Mefloquine.

Prevention and Control
Chemoprophylaxis consisting of mefloquine or doxycyline for travelers going to areas where chloroquine-resistant P. falciparium is endemic. Choloroquine used for travelers to areas where other plasmodia are found.


 > Images > entamoeba

 > Images > Giardia

 > Images > Cryptosporidium > Images > Plasmodium

Desmond Heng



Possible Viral Agents Part 3

1) Adenoviruses- Serotypes 3, 4, 7
What are adenoviruses?
Adenoviruses can replicate and produce disease in the respiratory, gastrointestinal and urinary tracts and in the eye. Many adenovirus infections are subclinical and may persist in the host for months.

Mode of transmission:

  • Direct contac
  • Respiratory droplet
  • Fecal-oral route
Pathogenesis: Adenoviruses infect and replicate in epithelial cells of the respiratory and gastrointestinal tracts, urinary bladder and liver. They usually do not spread beyond the regional lymph nodes.

Clinical syndrome:
  • Respiratory diseases: cough, nasal congestion, fever and sore throat
  • Eye infections: acute conjunctivitis
  • Gastrointestinal disease: gastroenteritis
Laboratory diagnosis:
Polymerase Chain Reaction (PCR) assays in which primers from a conserved viral sequence can detect all serotypes of adenovirus infections in tissue samples or body fluids.
Serological methods such as the Complement Fixation (CF) test can be used to detect complement-fixing antibodies to adenovirus group antigens.

Epidemiology: Adenoviruses exist in all parts of the world. They are present year-round and usually do not cause community outbreaks of disease. Respiratory disease due to types 3, 4 and 7 is common among military recruits.

Treatment: No specific treatment

Prevention and control:
  • Careful hand washing
  • Disinfect environment surfaces with sodium hypochlorite
  • Use of paper towels
2) Hepatitis viruses- Hepatitis A virus (HAV)
What are HAV?

HAV is a distinct member of the picornavirus family.

Mode of transmission:
  • Fecal-oral route
  • Close contact
Pathogenesis: The virus replicates in the hepatocytes and interferes with normal liver function. The individual’s immune system is then activated to produce a specific reaction to combat the infectious agent. As a result, the liver becomes inflamed.

Clinical syndrome:
  • Jaundice
  • Fever
  • Fatigue
  • Gastrointestinal symptoms: abdominal pain, loss of appetite, nausea, vomiting and vomiting
Laboratory diagnosis:
Immune electron microscopy is used for the detection of HAV in stool and liver preparations.
Sensitive serological assays such as ELISA and PCR methods are used to measure specific HAV antibodies.

Epidemiology: HAV is widespread throughout the world. Outbreaks of type A hepatitis are common in families, institutions, summer camps, day care center, neonatal intensive care units and among military troops.

Treatment: Viral vaccines and protective immune globulin preparations against HAV

Prevention and control:
  • Hands washing after using the bathroom, changing a diaper, and before preparing and eating food.
  • Use own personal products
3) Poxviruses- Monkeypox virus
What is monkey virus?
Monkeypox virus is a species of Orthopoxvirus. The disease was first recognized in captive monkeys in 1958.

Mode of transmission: Direct contact with primary hosts (eg. rodents. Monkeys)

Pathogenesis:Monkeypox virus replicates in lymphoid tissue and localizes in mononuclear phagocytic cells. It is then release into the bloodstream, and then localizes again in skin cells.

Clinical syndrome: Similar to that of smallpox with the exception of enlargement of the cervical and inguina lymph nodes.

Laboratory diagnosis:
Direct examination of clinical materials under electron microscope is used for rapid identification of virus particles.
Antibody assays such as ELISA or RIA can be used as confirmatory tests.

Epidemiology: The disease is a rare zoonosis that has been detected only in remote villages in tropical rain forests.

Treatment: Vaccination with vaccinia

Prevention and control: Vaccinia vaccination is recommended for laboratory workers who directly handle cultures or animals infected with monkeypox virus.

4) Paramyxoviruses- Mumps virus
What is Mumps virus?
Mumps virus mostly causes a mild childhood disease, but in adults complications including meningitis and orchitis are fairly common. More than one-third of all mumps infections are asymptomatic.

Mode of transmission:
  • Direct contact
  • Air-borne droplets
Pathogenesis: Primary replication occurs in nasal or upper respiratory tract epithelial cells. Viremia then disseminates the virus to the salivary glands and other major organ systems.

Clinical syndrome:
  • Swell and pain of the paratid glands
  • Fever
  • Headache
  • Loss of appetite

Laboratory diagnosis:
Immunofluorescence using mumps-specific antiserum can detect mumps virus antigens as early as 2-3 days after inoculation of cell cultures in shell vials.
ELISA is useful because it can detect mumps-specific IgM antibody or mumps-specific IgG antibody.

Epidemiology: Cases appear throughout the year in hot climates. Epidemics may occur in army camps.

Treatment: No specific therapy

Prevention and control: Immunization with attenuated live mumps virus vaccine

5) Herpes Simplex Viruses- Epstein-Barr Virus (EBV)
What is EBV?
EBV is the causative agent of acute infections mononucleosis and lymphoproliferative disorders in immunodeficient individuals.

Mode of transmission:

  • Respiratory secretions
  • Infected saliva
Pathogenesis: Viral replication occurs in epithelial cells of the pharynx and salivary glands. Infected B cells spread the infection from the oropharynx throughout the body. Following primary infections, the virus persists in a latent form in the B lymphocytes of the host. Periodic reactivation of the virus is associated with shedding of virus in saliva.

Clinical syndrome:
  • Infectious mononucleosis: headache, fever, malaise, fatigue and sore throat
  • Oral hairy leukemia: wart like growth on the tongue
  • Lymphoma
Laboratory diagnosis:
Nucleic acid hybridization is the most sensitive means of detecting EBV in patient materials.
Common serologic procedures for detection of EBV antibodies include ELISA tests, immunnoblot assays and indirect immunofluorescence tests using EBV-positive lymphoid cells.

Epidemiology: EBV is common in all parts of the world. In industrialized nations, more than 50% of EBV infections are delayed until late adolescence and young adulthood.

Acycloir reduces EBV shedding from the oropharynx during the period of drug administration.
Adoptive transfer of EBV-reactive T cells shows results of acceptable treatment for EBV-related lymphoproliferative disease.

Prevention and control: No EBV vaccine available

1) Adenovirus- under ELectron Microscopy> image search> adenovirus

2) Hepatitis A virus (HAV)- under Electron Mircoscopy> image search> hepatitis A virus

3) Monkeypox virus> image search> monkeypox virus

4) Mumps virus> image search> mumps virus

5) Epstein-Barr virus (EBV)- in the nucleus of a mammalian cell> image search> epstein-barr virus

1) Geo.F.Brooks, Janet S.Butel, Stephen A.Morse. (2004). Medical Microbiology. Asia: The McGraw-hill Companies.

2) Centers for Disease Control and Prevention. Viral Hepatitis A. (2007). Retrieved 22nd January 2008, from

3) Stanford Education Group. Monkeypox virus. (2000). Retrieved 22nd January 2008, from

4) Medicine Net. Mumps. (2007). Retrieved 22nd January 2006, from

Tham Wan Jin June

Possible Fungal Agents

1. Dermatophytes (Epidermophyton, Microsporum, and Trichophyton species)
Transmission: Direct contact with the skin scale
Pathogenesis: Fungi only grow in the superficial keratinized layer of the skin. Presences of lesions are due to the inflammatory response to the fungi. Frequency of infection is enhanced by moisture and warm.
Clinical Symptoms: May present as asymptomatic, usually mild itching lesion with a scaling, inflammation usually manifest as a vesicular or bullous disease.
Laboratory Diagnosis: Skin scale is examined microscopically in a KOH preparation for the presence of hyphae. It is identified by the appearance of its mycelium and it asexual spore on SDA plates.
Treatment: Topical anti-fungal agents such as miconazole, clotrimazole or tolnaftate are used
Prevention: Practise personal hygiene such as chamging sock frequently, wiping area between toes to keep it dry.

2. Histoplasma capsulatum
Transmission: Inhalation of airborne sexual spores. Mould grows preferentially in soil enriched with bird dropping. It also grows well in a warm and moist environment, prevalent in Americas, India and southeastern Asia.
Pathogenesis: Microcondia (spores) enter the lungs and differentiate into yeast cells. The yeast cells are ingested by the alveolar macrophages and multiply within them.
Clinical Symptoms: Non-specific respiratory symptoms such as cough and flu. Enlargement in spleen, adrenal can be seen in severe infection.
Laboratory Diagnosis: Sputum can be examined microscopically and cultured on SDA plate. Presence of tuberculate chylamydospores in culture at 25 degree Celsius is diagnostic.
Treatment: Amphotericin B for disseminated disease; itraconazole for pulmonary disease
Prevention: No vaccine is available

3. Coccidioides Immitis
Transmission: Inhalation of airborne arthrospores. It grows well in the soil of arid regions.
Pathogenesis: Arthrospores differentiate into spherules in the lungs. Spherules rupture, releasing endospores that form new spherules, spreading the infection within the body.
Clinical Symptoms: Fever, mild respiratory distress, rashes
Laboratory Diagnosis: Sputum should be examined microscopically for spherules and cultured on SDA plate.
Treatment: Amphotericin B or itraconazole for disseminated disease
Prevention: No vaccine is available

4. Crytococcus neoformans
Transmission: Inhalation of airborne yeast cells. This heavily encapsulated yeast grows well in soil enriched by bird dropping (especially pigeon droppings).
Pathogenesis: Yeast cells spread via the bloodstream to the meninges. Reduced cell-mediated immunity pre-disposes to severe disease, cryptococcal meningitis occur in immunocompetent people.
Clinical Symptoms: May present as asymptomatic, usually pneumonia-like symptoms such as flu and fever, unusual sweating at night, skin rash, chest pain, confusion, nausea
Laboratory Diagnosis: Gram stain is not preferred due to reliable result. Stain such as methenamine-silver, periodic acid-Schiff will allow the organism to be visualized. Colonies are presented as mucoid due to presence of large amount of capsular polysaccharide. Serologic test such as cryptococcal antigen test can be used to determined organism presence.
Treatment: Combined treatment with amphotericin B and flucytosine is used in disseminated disease and meningitis.
Prevention: No known specific mean of prevention.

5. Aspergillus fumigatus
Transmission: Inhalation of airborne spore (conidia)
Pathogenesis: It exists as an opportunistic pathogen, invasive in immunocompetent patient. The organism invades the blood vessels, causing thrombosis and infarction. “Fungal ball” may be developed in tuberculosis patient and allergic brochopulomonary asperigillosis may developed in allergic patient.
Clinical Symptoms: Fever, weakness, chest pain, aches, blood in urine.
Laboratory Diagnosis: Examined microscopically for invasive septate hyphae. Form characteristic mycelium when cultured on SDA plate.
Treatment: Amphotericin B for invasive asperigillosis. Lesion such as fungal ball can be surgically removed. Steroid therapy is recommended for allergic brochopulomonary asperigillosis
Prevention: No vaccine or prophylactic drug is available

1) WARREN LEVINSON, MD, PhD (2006) REVIEW OF Medical Microbiology and Immunology. NINTH EDITION; McGraw-Hill company
2)> search> organism name
3) MMIC lectures notes

Yeo Ching Wei

Possible Viral Agents Part 2


Poliomyelitis Viruses

A microscopic image shows poliomyelitis viruses, which enter the body through the nose and mouth and destroy nerve cells by multiplying rapidly inside of them. It can cause permanent paralysis. An effective vaccine have developed and poliomyelitis has been nearly eliminated in developed countries.

Taken from

Hepatitis A

Hepatitis A magnified 225,000 times

Hepatitis E
Hepatitis E
Taken from

Yellow Fever Virus
An electron micrograph of Yellow Fever Virus virions. Virions are spheroidal, uniform in shape and are 40-60nm in diameter. The name "Yellow Fever" is due to the ensuing jaundice that affects some patients. The vector is the Aedes aegypti or Haemagogus spp. mosquito

Schematic illustration of the relation between climate and the transmission of tick-borne diseases in humans. In this study, the different direct and indirect climate-dependent interactions, here shown within the yellow field, have been treated as a black box.

Taken from


1) Geo, F.B., Janet, S.B., Stephen, A.M. (2001). Medical Microbiology, Twenty Third Edition: The McGraw-Hill Companies
2)>search>virus name
3) lecture notes from medical microbiology

Lin Juexiu

Wednesday, January 23, 2008

Possible Viral Agents Part 1

Please click to enlarge image


Rabies virus>image search>Rabies virus


Influenza virus >image search>influenza virus

Dengue virus> image search> Dengue virus

Chikungunya virus>image search>Chikungunya virus


Arbovirus> image search>Arbovirus


1) Geo, F.B., Janet, S.B., Stephen, A.M. (2001). Medical Microbiology, Twenty Third Edition: The McGraw-Hill Companies.

2) Medical Microbiology Lecture Notes

Done by Sim kai lin (0503211E)

Possible Protozoa Agents

1. Entamoeba histolytica
Transmission: Contaminated food/water, person to person, fecal exposure during sexual contact, rodents (vectors for transmitting E. histolytica cysts)
Pathogenesis: Following ingestion, the cysts pass through the stomach, where exposure to gastric acid stimulates release of the pathogenic trophozoite in the duodenum. The trophozoites divide and produce extensive local necrosis in the large intestine. The basis of tissue destruction may be attributed to the production of a cytotoxin. Necrosis requires direct contact with the amoeba, so lysosomal enzymes (phospholipase A2) may be important.
Epidemiology: Worldwide distribution. Its incidence is highest in tropical and subtropical regions that have poor sanitation and contaminated water.
Clinical syndromes: Intestinal or extraintestinal amebiasis (symptoms: abdominal pain, cramping, colitis with diarrhea, bloody stools, hepatomegaly)
Lab diagnosis: Identification of E. histolytica trophozoites and cysts in stools and trophozoites in tissue under microscope, specific serologic tests, immunological tests for detection of fecal antigen and DNA-probe assays for E. histolytica nucleic acids.
Treatment: Treated with metronidazole followed by iodoquinol
Prevention and control: Introduction of adequate sanitation measures and education about the routes of transmission, water should be boiled and fruits/vegetables should be thoroughly cleaned before consumption

Picture of Entamoeba histolytica and its life cycle ( > image > Entamoeba histolytica)

2. Giardia lamblia
Transmission: Contaminated food/water, person to person, fecal-oral or oral-anal routes
Pathogenesis: Infection with G. lamblia is initiated by ingestion of cysts. Gastric acid stimulates excystation with release of trophozoites in the duodenum and jejunum, where organisms multiply by binary fission. Trophozoites can attach to intestinal villi by a prominent ventral sucking disk.
Epidemiology: Worldwide distribution
Clinical syndromes: Result in either asymptomatic carriage or symptomatic disease, ranging from mild diarrhea to a severe malabsorption syndrome (symptoms: watery diarrhea, abdominal cramps, flatulence)
Lab diagnosis: Stool specimens should be examined for cysts and trophozoites under microscopy, specific serologic and immunological tests.
Treatment: Quinacrine, metronidazole
Prevention and control: Avoidance of contaminated food/water and high-risk sexual behaviour, public health efforts to identify reservoir of infection and proper functioning filtration systems in water supplies
Picture of Giardia lamblia ( > image > Giardia lamblia)

3. Balantidium coli
Transmission: Swine and monkeys, fecal-oral route, contaminated water, person to person
Pathogenesis: Similar to amebiasis as organisms elaborate proteolytic and cytotoxic substances that mediate tissue invasion and intestinal ulceration
Epidemiology: Worldwide distribution
Clinical syndromes: Result in either asymptomatic carriage or symptomatic disease (symptoms: abdominal pain and tenderness, tenesmus, nausea, anorexia, watery stools with blood and pus, ulceration of intestinal mucosa)
Lab diagnosis: Microscopic examination of feces for trophozoites and cysts
Treatment: Tetracycline, iodoquinol and metronidazole
Prevention and control: Appropriate personal hygiene, maintenance of sanitary condtions and careful monitoring of pig feces

Picture of Balantidium coli ( > image > Balantidium coli)
4. Isospora belli
Transmission: Contaminated food/water, oral-anal sexual contact
Pathogenesis: Both sexual (gametogony) and asexual (schizogony) reproduction in the intestinal epithelium can occur. The end product of gametogenesis is the oocyst.
Epidemiology: Worldwide distribution
Clinical syndromes: May be asymptomatic carriers or gastrointestinal disease ranging from mild to severe. Disease most commonly mimics giardiasis, with a malabsorption syndrome characterized by loose, foul-smelling stools.
Lab diagnosis: Careful examination of concentrated stool sediment and special staining with either iodine or a modified acid-fast procedure will reveal the parasite.
Treatment: Trimethoprim sulfamethoxazole, combined pyrimethamine-sulfadiazine
Prevention and control: Maintain personal hygiene, high sanitary conditions and avoidance of oral-anal sexual contact

Picture of Isospora belli ( > image > Isospora belli)

5. Cryptosporidium parvum
Transmission: Zoonotic spread from animal reservoirs to humans, person to person, fecal-oral and oral-anal routes
Pathogenesis: Typical of coccidians. In contrast to Isospora, Cryptosporidium is found within the brush border of the intestinal epithelium. The coccidian attach to the surface of the cells and replicate by a process that involves schizogony.
Epidemiology: Worldwide distribution
Clinical syndromes: May be asymptomatic carriers or mild self-limiting enterocolitis characterized by watery diarrhea without blood
Lab diagnosis: Stool examination, modified zinc sulfate centrifugal flotation technique or by Sheather’s sugar flotation procedure, specimens may be stained with modified acid-fast method or by an indirect immunofluorescence assay
Treatment: No broadly effective therapy
Prevention and control: Due to the widespread distribution of organism in humans and animals, preventing infection is difficult. Maintain personal hygiene, high sanitary conditions and avoidance of oral-anal sexual contact.
Picture of life cycle of Cryptosporidium parvum ( > image > Cryptosporidium parvum)

6. Plasmodium species (P. vivax, P. falciparum, P. ovale, P. malariae)
Transmission: Via bite of female Anopheles mosquito vector
Pathogenesis: Infectious plasmodia sporozoites are introduced after a bite through the saliva of the Anopheles mosquito. The sporozoites are carried to the hepatocytes where asexual reproduction occurs. Some species (P. vivax and P. ovale) can establish a dormant hepatic phase in which hypnozoites do not divide. The hepatocytes eventually rupture, liberating merozoites which attach to specific RBC receptors and invade them, initiating the erythrocytic cycle. Asexual replication progresses through a series of stages (ring, trophozoite, schizont) that culminates in the rupture of the RBC, releasing more merozoites. Some merozoites also develop within RBCs into male and female gametocytes.
Epidemiology: Worldwide distribution depending on the type of species
Clinical syndromes: Fever, chills, rigors, muscle and joint pains, anaemia and convulsions. Severe malaria (usually caused by P. falciparum) may cause cerebral malaria, blackwater fever which could lead to coma, death.
Lab diagnosis: Thick and thin blood smears stained with Giemsa stain and observed under microscopy, rapid diagnostic kits
Treatment: Chloroquine, primaquine, mefloquine, quinine, doxycyline (however, there are increasing multidrug-resistant P. falciparum strains)
Prevention and control: Chemoprophylaxis and prompt eradication of infections, control of mosquito breeding and protection of individuals by screening, netting, protective clothing and insect repellents.

Picture of life cycle of Plasmodium species ( > image > Plasmodium)

7. Toxoplasma gondii
Transmission: Ingestion of improperly cooked meat from animals serving as intermediate hosts or infective oocysts from cat fecal contamination, transplacental infection
Pathogenesis: Organisms develop in the intestinal cells of the cat, as well as during an extraintestinal cycle with passage to the tissues via bloodstream. The organisms from the intestinal cycle are passed in cat feces and mature in the external environment within 3 to 4 days into infective oocysts. These oocysts can be ingested by mice and other animals (including huamsn) and produce acute and chronic infection of various tissues.
Clinical syndromes: May be asymptomatic carriers or symptomatic disease (symptoms: chills, fever, headaches, myalgia, lymphadenitis)
Lab diagnosis: Serologic tests, ELISA test for detecting IgM antibodies, biopsy specimens
Treatment: Depends on the nature of both the infectious process and the immunocompetence of the host
Prevention and control: Avoidance of consumption and handling of raw or undercooked meat and exposure to cat feces

Picture of Toxoplasma gondii ( > image > Toxoplasma gondii)

8. Leishmania species
Transmission: Via sandflies (Phlebotomus or Lutzomyia)
Pathogenesis: The hemoflagellates are flagellated insect-transmitted protozoa that infect blood and tissues. The diseases are distinguished by the ability of the organism to infect deep tissues (visceral leishmaniasis) or replicate only in cooler superficial tissues (cutaneous or mucocutaneous leishmaniasis). The reservoir hosts and geographical distribution differ for the 3 species. There are two morphological forms in the cells: promastigote (with an anterior flagellum) in the insect host, and amastigote (without flagella) in the vertebrate host.
Clinical syndromes: Visceral (fever, swelling of spleen and liver, anaemia), cutaneous/mucocutaneous (skin reactions)
Lab diagnosis: Amastigote stafe can be demonstrated in tissue biopsy, bone marrow examination, lymph node aspiration and through examination of properly strained smears. Culture of blood, bone marrow and other tissues often demonstrates the promastigote stage. Specific serologic testing is also available.
Treatment: Stibogluconate
Prevention and control: Protection from sandflies by screening and use of insect repellents

Picture of Leishmania species ( > image > Leishmania)

9. Wuchereria bancrofti and Brugia malayi
Transmission: Via bite of Anopheles, Aedes and Culex mosquitoes
Pathogenesis: The infective larvae migrate from the location of bite to the lymphatics, where growth to adulthood occurs. For 3 to 12 months after the initial infection, the adult male worm fertilizes the female, who in turn produces the sheathed larval microfilariae that find their way into the circulation. Both species have a periodicity in production of microfilariae (nocturnal periodicity) which results in greater numbers of microfilariae in blood at night.
Epidemiology: W. bancrofti occurs in both tropical and subtropical areas and is endemic in central Africa and many parts of Asia with no animal reservoir identified. B. malayi is found primarily in parts of Asia, while cats and monkeys are recognized as animal reservoirs.
Clinical syndromes: Fever, lymphanigitis, filarial elephantiasis of extremities
Lab diagnosis: Eosinophilia present, thick and thin blood smears stained with Giemsa stained under microscopy, anticoagulated blood and urine specimens, specific serological testing
Blood specimens are recommended to be taken between 10pm – 4am.
Treatment: Diethylcarbamazine
Prevention and control: Education regarding filarial infections, mosquito control, use of protective clothing and insect repellents, treatment of infections to prevent further transmission

Picture of microfilariae ( > image > microfilariae)

- Murray, P.R., Kobayashi, G.S., Pfaller, M.A., Rosenthal, K.S. (1994). Medical Microbiology Second Edition. London: Mosby-Year Book, Inc
- Medical Microbiology Notes
- > search

Researched by: Alex Tan 0503222B

Monday, December 10, 2007

Biochemical tests for bacteria indentification-Group post 2

Biochemical tests for gram negative bacteria identification


-measure the ability to hydrolyse and deaminate tryptophan

-Klesiella-enterobacter-salmonella-serratia are mostly negative

-positive-red colour

2)Methyl red

-methyl red, a pH indicator with a range between 4.4(red) and 6.0(yellow)

-only species that produce suffiicient acids can maintian the pH at below4.4 against the buffer system of the test medium

-most species of Enterobacteriaceae produce strong acids. Enterobacter-serratia do not produce enough acids

-positive-stable red colour in the surface layer of the medium

3)Voges-proskauer reaction test

-this test is based on the conversion of acetoin to a red coloured complex through the action of KOH, atmospheric 02 and alpha napthol

-Klesiella-enterobacter-serratia is able to perform this pathway

-red colour at the surface of the medium after 15 mins following the addition of reagents

4)Citrate utilisation test

-some bacteria have the ability to utilize citrate as the sole carbon sourc and turn the medium allkaline due to production of ammonia

-Escherichia-Edwardisella-shigella-salmonella cannot utilise citrate as the sole source of carbon

-positive-from colour green to blue

5)Urease test

-some species posses the enzyme urease and able to hydrolyze urea with the release of ammonia and carbon dioxide

-this is used mainly to differentiate urease positive Proteus species from other member of Enterobacteriaceae

-positive-yellowish orange to pink

Biochemical tests for gram positive bacteria

1)Oxidase test

-this is to differentiate those that possess the enzyme cytochrome oxidase c from those that lack of the enzyme

-useful in screening for bacteria species which belong to the Enterobacteriaceae or the Pseudomonas genus

-positive-development of purple colour

2)Coagulase test

-the coagulase test is used to differentiate staphylcoccus aures from other staphylcoccus species

-positive-clot forms

Particulars of patient

Name:Khong Fay Seah
Clinical Diagnosis
Complaints: fever,chills,dysuria
Diagnosis:urinary tract infection
Antibiotic treatment: if any (nil)

Possible Microorganisms



Escherichia coli(Most common cause of UTI)

-Belongs to family of Enterobacteriaceae(Escherichia)

-Clinical findings: UTI (Pyelonephritis and Cystitis), diarrhea disease

-Is a member of normal intestinal flora

-Microscopy and gram staining: Gram negative rod

-Culture: Haemolyic colonies on blood agar, lactose fermenting colonies (Red/Pink) on MacConkey agar, green metallic sheen on EMB agar

-Biochemical tests:
-Indole positive
-Methyl red positive
- Voges-Proskauer (VP) negative
-Urease negative
-Citrate negative
-Catalase positive
-Oxidase negative
-TSI: acidic slant/acidic deep/no H2S

-Susceptibility testing: ampicillin, cephalosporin, aminoglycosides, sulfonamides

Staphylococcus saprophyticus(Second most common cause of UTI)

-Belongs to family of staphylococci

-Clinical findings: Urinary tract infection

-Present in the urinary tract and bladder of sexually active females

-Microscopy and gram staining: Gram positive cocci in clusters

-Culture: Pale colonies on blood agar

-Biochemical tests:
-Catalase positive
-Coagulase negative

-Susceptibility testing:Quinilone

Klebsielle Pneumoniae

- Belongs to family of Enterobacteriaceae(Klesbsiella)

- Clinical findings: urinary tract infection

-Present in the respiratory tract and feces of about 5% normal individuals

-Microscopy and gram staining: Gram negative rod

-Culture: Pink, mucoid colonies on MacConkey agar

-Biochemical tests:
-Indole negative
- Methyl red negative
-Voges-Proskauer reaction positive
- Urease negative
-Citrate positive
- TSI: acidic slant/acidic deep/no H2S

-Susceptibility testing:Cephalosporin

Enterobacter aerogenes

- Belongs to family of Enterobacteriaceae(Enterobacter)

- Clinical findings: urinary tract infections and sepsis

- Present in the intestinal tract-

-Microscopy and gram staining: Gram negative rod

-Culture:Pink to purple colonies on EMB agar

-Biochemical tests:
-Indole negative
-methyl red negative
-VP positive
-urease negative
- Citrate positive
-TSI: acidic slant/acidic deep/no H2S

Susceptibility testing: cephalosporin

Proteus mirabilis

- Belongs to family of Enterobacteriaceae(Proteus)

- Clinical findings: urinary tract infections and produce bacteremia, pneumonia

-Microscopy and gram staining: Gram negative rod
-Culture: Pale colonies on MacConkey agar, swarming growth on blood agar

-Biochemical testing:
-Indole negative
-Methyl red positive
-VP positive/negative
-Urease positive
- Citrate positive
-Oxidase negative
-TSI: alkaline slant/acidic deep/H2S

-Susceptibility testing: penicillin, cephalosporins, quinolones

Enterococcus faecalis

- Belongs to family of Streptococci

-Clinical findings: abdominal abscess, urinary tract infection ((bladder infection, Pyelonephritis)

-Present in colon

-Microscopy and gram staining: Gram positive cocci in chains

-Culture: Red dot colonies on MacConkey agar

-Biochemical testing:
-Decolourise the litmus milk,
-Indole negative
-Catalase negative

-Susceptibility testing: Vancomycin,ampicillin

Pseudonomas aeruginosa

- Belongs to family of Pseudomonads

-Clinical findings: Typically infects the pulmonary tract, urinary tract(Pyelonephritis)

-Distributed in nature and is commonly present in moist environments in hospital

-Microscopy and gram staining: Gram positive spherical

-Culture: Greenish pyocyanin pigment on MacConkey agar

-Biochemical testing:
-Indole negative
-Urease negative
-Oxidase positive,
-TSI: allaline slant/alkaline deep

-Susceptibility testing: Ciprofloxacin,imipenam


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E Coli ( red dot colonies on Mac agar)

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K. Pneumonia (red/pink colonies on Mac)

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Staphyloccocus Saprophyticus
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Pseudomonas aeruginosa
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Enterococcus faecalis
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Enterobacter aerogenes
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Proteus mirabillis
References>image search> Proteus mirabilis>image search> Enterobacter Aerogenes>image search>Enterococcus faecalis>image search>Pseudomonas aeruginosa>image search>Staphyloccocus Saprophyticus>image search>K. Pneumonia>image search> E Coli>EMB agar> MacConkey Agar> blood agar
Tony Hart, Paul Shears (2004).Color Atlas of Medical Microbiology: Elsevier’s Health Sciences Department

kai lin

Sunday, December 9, 2007

MMIC dPBL Case 3 (Maisy Hong - 2nd posting cont)

Pictures of possible causative agents of case 3

Pseudomonas aeruginosa growing on XLD agar Acinetobacter baumanii as seen under microscopy
Serratia marcescens growing on XLD agar
Candida albicans as seen under microscopy

Staphylococcus saprophyticus growing on nutrient agar Enterococcus faecalis as seen under scanning electron microscopy
Escherichia coli as seen under microscopy
Proteus mirabilis growing on XLD agar

Klebsiella pneumoniae as seen under microscopy
All images are credited to
1) > image search > "microorganism name"
2) > "microorganism name" > search
Information are credited to
3) Murray, P.R., Kobayashi, G.S., Pfaller, M.A., Rosenthal, K.S. (1994). Medical Microbiology Second Edition. London: Mosby-Year Book, Inc
4) Medical Microbiology Notes
5) > "microorganism name"
6) > "microorganism name"
Tan Yi Wei Alex Tg02 0503222B