MEDICAL MICRO EXAM INFOR

Aspect Details
Name of Disease Measles (also known as rubeola)
Causative Agent Measles virus (MeV)
Classification Family: Paramyxoviridae, Genus: Morbillivirus, Species: Measles virus
Morphological: Measles virus is enveloped, pleomorphic, and contains single-stranded RNA as its genetic material. Biological: The virus can be cultured in
Type of Organism Vero or other susceptible cell lines.
Vectors Measles is highly contagious and spreads through respiratory droplets. There is no known vector other than human-to-human transmission.
Recognize Disease Symptoms include high fever, cough, runny nose, conjunctivitis, and the characteristic rash starting on the face and spreading downwards.
Compared to rubella, measles tends to cause more severe symptoms and complications. It affects both genders equally. Immunocompromised individuals
Comparison are at higher risk of severe complications.
Measles outbreaks occur mainly in areas with low vaccination rates. Calculations involve assessing herd immunity levels. Control involves vaccination
Epidemiology campaigns and isolation of infected individuals.
Anatomical Location Measles virus primarily infects the respiratory epithelium and then spreads systemically to various organs, including lymphoid tissues.
Measles virus initially infects respiratory epithelial cells, then spreads via lymphatics and bloodstream. It targets immune cells, leading to immune
Pathogenesis suppression.
Virulence Factors MeV evades the immune system by inhibiting interferon production and modulating host immune responses.
Life Cycle Measles virus enters cells via receptor-mediated endocytosis, replicates in the cytoplasm, and buds from the cell membrane.
Signs and Symptoms Early symptoms include fever, cough, and runny nose. Later, the characteristic rash appears. Complications can include pneumonia, encephalitis, and death.
Transmission Measles spreads from respiratory secretions of infected individuals, through coughing and sneezing. It is highly contagious and can survive in the air for hours.
Vaccination with the measles, mumps, and rubella (MMR) vaccine is the most effective prevention. Isolation of infected individuals and post-exposure
Prevention prophylaxis are also crucial.
There is no specific antiviral treatment for measles. Supportive care includes hydration, antipyretics, and vitamin A supplementation. Antibiotics may be used
Treatment for secondary bacterial infections.
Antibiotics Antibiotics such as amoxicillin or azithromycin may be prescribed for bacterial complications like pneumonia or otitis media.
Laboratory Diagnosis Samples for diagnosis include throat swabs, nasal swabs, and blood. Laboratory tests include PCR for viral RNA or serology for IgM antibodies.
Measles progresses through an incubation period (10-14 days), prodromal phase (fever, cough, runny nose), exanthem phase (rash), and convalescent phase
Phases of Disease (recovery).

Aspect Rubella (German Measles)

Causative Agent Rubella virus (RV)
Classification Genus: Rubivirus, Family: Togaviridae
Type of Organism Enveloped, single-stranded RNA virus
Vectors Humans (respiratory droplets)
Anatomical Location Respiratory epithelium
Pathogenesis 1. Inhalation of virus particles
2. Virus infects respiratory mucosa
Virulence Factors E1 glycoprotein, E2 glycoprotein
Signs and Symptoms Mild fever, rash (maculopapular), lymphadenopathy
Transmission Respiratory droplets
Prevention/Prophylaxis MMR vaccine
Treatment Supportive care (e.g., hydration, antipyretics)
Antibiotics Used Trimethoprim-sulfamethoxazole, Azithromycin, Erythromycin
Susceptibility Testing Not applicable for viruses
Laboratory Diagnosis RT-PCR, IgM serology
Phases of Disease Incubation, prodromal, exanthematous

Aspect Respiratory Syncytial Virus (RSV)

Causative Agent Respiratory syncytial virus (RSV)
Classification Genus: Orthopneumovirus, Family: Pneumoviridae
Type of Organism Enveloped, single-stranded RNA virus
Vectors Humans (respiratory droplets)
Anatomical Location Respiratory epithelium
Pathogenesis 1. Inhalation of virus particles
 Aspect Respiratory Syncytial Virus (RSV)
2. Virus infects respiratory mucosa
3. Causes inflammation, necrosis, and formation of syncytia
Virulence Factors F (fusion) protein, G (attachment) protein
Signs and Symptoms Cough, wheezing, difficulty breathing, cyanosis in severe cases
Transmission Respiratory droplets
Prevention/Prophylaxis Palivizumab (monoclonal antibody), Hand hygiene, isolation precautions, especially in healthcare settings
Treatment Supportive care (e.g., oxygen therapy, bronchodilators), Ribavirin (in severe cases)
Antibiotics Used Antibiotics are not effective against viruses
Susceptibility Testing Not applicable for viruses
Laboratory Diagnosis Rapid antigen detection test, RT-PCR
Phases of Disease Incubation, prodromal, acute, convalescent

Aspect Details
Name Influenza
Causative Agent Influenza viruses (Orthomyxoviridae family)
Classification Virus: Orthomyxoviridae family, Influenza virus genus
Influenza viruses are enveloped RNA viruses with segmented genomes. Morphologically, they are spherical or filamentous particles, approximately 80-120
Type of Organism nm in diameter. Biological tests include viral culture, PCR, and antigen detection assays such as rapid influenza diagnostic tests (RIDTs).
Vectors Influenza viruses primarily spread through respiratory droplets from coughing and sneezing of infected individuals.
Influenza is characterized by sudden onset of fever, chills, cough, sore throat, runny or stuffy nose, muscle or body aches, headaches, fatigue, and
Disease Recognition occasionally gastrointestinal symptoms. Scientific Name: Influenza virus infection.
Influenza outbreaks occur seasonally, with peaks during colder months. Control measures include vaccination, antiviral medications, and public health
campaigns promoting hygiene and respiratory etiquette. Recognition of outbreaks involves monitoring of influenza-like illness (ILI) and laboratory
Epidemiology confirmation.
Anatomical Location Influenza viruses primarily target respiratory epithelial cells, infecting the upper and lower respiratory tract.
Following respiratory transmission, influenza viruses attach to respiratory epithelial cells via viral hemagglutinin, replicate within the host cells, and spread
Pathogenesis locally and systemically, leading to inflammation and tissue damage. The host immune response contributes to symptoms and disease severity.
Influenza viruses possess surface glycoproteins hemagglutinin and neuraminidase, which facilitate viral attachment and release. Antigenic variation,
Virulence Factors particularly in hemagglutinin and neuraminidase, contributes to the virus’s ability to evade preexisting immunity.
Influenza viruses enter the host through the respiratory tract, attach to host cells, and enter via receptor-mediated endocytosis. Viral RNA is released into the
Life Cycle host cell, where replication and assembly of new virions occur. Newly formed virions are released from the host cell to infect neighboring cells.
Fever, chills, cough, sore throat, runny or stuffy nose, muscle or body aches, headaches, fatigue, occasionally gastrointestinal symptoms such as nausea,
Signs and Symptoms vomiting, or diarrhea.
Transmission Source: Respiratory secretions of infected individuals. Transmission occurs through close contact, airborne droplets, or cont act with contaminated surfaces.
Influenza vaccination, annual vaccination is recommended to prevent infection and reduce the severity of illness. Antiviral medications such as
Prevention/Prophylaxis neuraminidase inhibitors (oseltamivir, zanamivir) are used for prophylaxis in high-risk individuals or during outbreaks.
Antiviral medications (oseltamivir, zanamivir) can reduce the duration and severity of illness if initiated early. Supportive care includes rest, hydration, and
Treatment over-the-counter medications to alleviate symptoms. Antibiotics may be prescribed for secondary bacterial infections.
Influenza viruses are tested for susceptibility to antiviral medications through viral culture or molecular methods. Antiviral susceptibility testing can guide
Susceptibility Testing treatment decisions, especially in cases of severe or prolonged illness.
Control measures include vaccination, antiviral prophylaxis in high-risk individuals, promotion of respiratory hygiene, and outbreak management strategies
Control such as isolation and quarantine.
Sample collection involves respiratory specimens (nasopharyngeal swabs, nasal aspirates) for viral detection. Laboratory diagnosis includes rapid antigen
Laboratory Diagnosis tests, PCR, viral culture, and serological assays to detect antibodies.
Disease
Phases/Stages Incubation period (1-4 days), prodromal phase (symptoms onset), acute phase (peak symptoms), convalescent phase (resolution of symptoms).

Aspect Details
Name Rabies
Causative Agent Rabies virus (Rabies lyssavirus)
Classification Virus: Rhabdoviridae family, Lyssavirus genus
Rabies virus is a bullet-shaped, single-stranded RNA virus with a helical nucleocapsid. Morphologically, it appears as bullet-shaped virions, approximately
Type of Organism 180 nm in length and 75 nm in diameter. Biological tests include direct fluorescent antibody (DFA) test and PCR for detection.
Vectors Rabies virus is primarily transmitted through the bite of an infected animal, typically a rabid mammal such as a dog, bat, raccoon, or fox.
Rabies presents with flu-like symptoms initially, followed by neurological symptoms such as agitation, confusion, hallucinations, hydrophobia (fear of water),
Disease Recognition and aerophobia (fear of drafts of air or of fresh air). Scientific Name: Rabies virus infection.
 Aspect Details
Rabies is endemic in many parts of the world, particularly in regions with high populations of stray dogs. Control measures include vaccination of domestic
animals, post-exposure prophylaxis for humans, and wildlife management strategies. Recognition of cases involves clinical suspicion and laboratory
Epidemiology confirmation.
Rabies virus initially replicates at the site of the bite, then spreads along peripheral nerves to the central nervous system (CNS), including the brain and spinal
Anatomical Location cord.
Following transmission through a bite, rabies virus replicates at the site of entry, then enters peripheral nerves, traveling to the CNS. Once in the CNS, the
Pathogenesis virus spreads to other tissues, leading to encephalitis and eventually fatal neurological dysfunction.
Rabies virus evades the immune system by infecting neurons, which limits immune surveillance. The virus also produces neurotropic factors that enhance its
Virulence Factors ability to spread within the nervous system.
Rabies virus enters the host through the bite wound, replicates locally, and then travels along peripheral nerves to the CNS. Within neurons, viral replication
Life Cycle occurs, leading to widespread infection of the CNS and eventual dissemination to other tissues.
Signs and Symptoms Initially, flu-like symptoms, followed by neurological symptoms such as agitation, confusion, hallucinations, hydrophobia, aerophobia, paralysis, and coma.
Transmission Source: Saliva of infected animals, usually through a bite. Transmission occurs through contact with mucous membranes or broken skin.
Prevention involves vaccination of domestic animals, especially dogs, to prevent transmission to humans. Post-exposure prophylaxis (PEP) with rabies
Prevention/Prophylaxis vaccine and rabies immune globulin (RIG) is recommended immediately following exposure to a potentially rabid animal.
There is no cure for rabies once symptoms appear. Treatment involves supportive care to manage symptoms, including sedation for agitation, pain
Treatment management, and palliative care. Post-exposure prophylaxis (PEP) can prevent the onset of rabies if administered promptly after exposure.
Susceptibility Testing Not applicable for viruses like rabies.
Control measures include vaccination of domestic animals, surveillance of wildlife populations, education on rabies prevention, and prompt administration of
Control post-exposure prophylaxis for individuals exposed to potentially rabid animals.
Sample collection involves skin biopsy from the site of the bite, saliva, cerebrospinal fluid (CSF), or brain tissue post-mortem. Laboratory diagnosis includes
Laboratory Diagnosis direct fluorescent antibody (DFA) test, PCR, and virus isolation from tissue samples.
Disease Incubation period (typically several weeks to months), prodromal phase (flu-like symptoms), acute phase (neurological symptoms), and fatal outcome
Phases/Stages without treatment.

Aspect Details
Name Cholera
Causative Agent Vibrio cholerae
Classification Bacteria: Vibrio cholerae species, family Vibrionaceae, order Vibrionales
Vibrio cholerae is a Gram-negative, curved rod-shaped bacterium with a single polar flagellum. Morphologically, it appears as comma-shaped cells,
Type of Organism approximately 1-3 μm in length. Biological tests include culture on selective media, biochemical tests, and serological assays.
Vectors Cholera is primarily transmitted through the ingestion of contaminated water or food, particularly under conditions of poor sanitation and hygiene.
Cholera presents with sudden onset of profuse watery diarrhea, often described as “rice-water stool,” vomiting, and dehydration. Severe cases can lead to
Disease Recognition rapid dehydration, electrolyte imbalance, and shock. Scientific Name: Vibrio cholerae infection.
Cholera outbreaks occur in areas with inadequate sanitation and access to clean water. Control measures include improvement of water and sanitation
infrastructure, promotion of hygiene practices, and mass vaccination campaigns in high-risk areas. Recognition of outbreaks involves surveillance and
Epidemiology laboratory confirmation.
Vibrio cholerae primarily colonizes the small intestine, where it adheres to and colonizes the intestinal mucosa, leading to toxin production and fluid
Anatomical Location secretion.
Following ingestion, Vibrio cholerae colonizes the small intestine and produces cholera toxin, which binds to intestinal epithelial cells, leading to activation of
Pathogenesis adenylate cyclase and increased cyclic AMP (cAMP) levels, resulting in secretion of electrolytes and water into the intestinal lumen.
Cholera toxin is the main virulence factor of Vibrio cholerae, responsible for the characteristic watery diarrhea. Other virulence factors include adhesins that
Virulence Factors facilitate colonization of the intestinal mucosa and toxins that disrupt host cell function.
Vibrio cholerae is ingested via contaminated water or food. In the small intestine, the bacterium colonizes the mucosa and produces cholera toxin. The toxin
Life Cycle induces secretion of electrolytes and water into the intestinal lumen, leading to profuse diarrhea. The bacterium is shed in feces, perpetuating transmission.
Profuse watery diarrhea, vomiting, dehydration, electrolyte imbalance, muscle cramps, rapid heart rate, low blood pressure, shock, and in severe cases,
Signs and Symptoms death.
Source: Fecal matter of infected individuals. Transmission occurs through ingestion of contaminated water or food, or through direct contact with
Transmission contaminated surfaces.
Prevention involves improvements in sanitation, access to clean water, and hygiene practices such as handwashing and food safety measures. Oral cholera
Prevention/Prophylaxis vaccines are also available for high-risk populations and travelers to endemic areas.
Treatment involves rehydration therapy with oral or intravenous fluids to replace lost fluids and electrolytes. Antibiotics such as doxycycline or azithromycin
Treatment may be used to shorten the duration and severity of symptoms, particularly in severe cases.
Susceptibility testing of Vibrio cholerae isolates involves culture-based methods followed by antibiotic susceptibility testing using agar diffusion or broth
Susceptibility Testing microdilution methods.
Control measures include surveillance, case management, outbreak response, provision of safe water and sanitation, hygiene promotion, and vaccination in
Control high-risk areas.
Sample collection involves stool specimens from suspected cases. Laboratory diagnosis includes culture on selective media, biochemical tests, and
Laboratory Diagnosis serological assays for detection of cholera toxin or molecular methods such as PCR for detection of Vibrio cholerae DNA.
Disease Incubation period (a few hours to five days), prodromal phase (asymptomatic or mild symptoms), acute phase (profuse watery diarrhea), and recovery phase
Phases/Stages with appropriate treatment.
 Aspect Details
Name Plague
Causative Agent Yersinia pestis
Classification Bacteria: Yersinia pestis species, family Enterobacteriaceae, order Enterobacterales
Yersinia pestis is a Gram-negative, rod-shaped bacterium. Morphologically, it appears as coccobacilli, approximately 0.5-0.8 μm in width and 0.5-3 μm in
Type of Organism length. Biological tests include culture on selective media, biochemical tests, serological assays, and molecular detection methods.
Vectors Plague is primarily transmitted through the bite of infected fleas, particularly Xenopsylla cheopis (the Oriental rat flea), which commonly infests rodents.
Plague presents in several forms: Bubonic plague (characterized by swollen, tender lymph nodes called buboes), Septicemic plague (resulting from the
spread of Y. pestis in the bloodstream), and Pneumonic plague (infection of the lungs, leading to severe respiratory symptoms). Scientific Name: Yersinia
Disease Recognition pestis infection.
Plague occurs in endemic foci, particularly in rodent populations. Control measures include surveillance and control of rodent populations, flea control,
antibiotic treatment of cases and contacts, and vaccination in high-risk areas. Recognition of outbreaks involves epidemiological investigation and laboratory
Epidemiology confirmation.
Yersinia pestis initially infects the lymph nodes, leading to lymphadenitis in bubonic plague. In septicemic plague, the bacterium disseminates via the
Anatomical Location bloodstream, affecting multiple organs. In pneumonic plague, the lungs are the primary site of infection.
Following transmission, Yersinia pestis infects host cells and evades host immune responses, leading to systemic infection. The bacterium produces
Pathogenesis virulence factors such as the type III secretion system and toxins, contributing to tissue damage and disease progression.
Yersinia pestis produces various virulence factors, including the type III secretion system (injectisome), which delivers effector proteins into host cells to
Virulence Factors modulate immune responses and promote bacterial survival. Toxins such as Yersinia outer proteins (Yops) and the Pla protease contribute to pathogenesis.
Yersinia pestis cycles between fleas and mammalian hosts, particularly rodents. Infected fleas transmit the bacterium to humans through bites. In humans,
Life Cycle the bacterium causes disease, leading to transmission to other hosts through respiratory droplets (in pneumonic plague) or blood (in septicemic plague).
Bubonic plague: Fever, chills, headache, muscle aches, and the development of painful, swollen lymph nodes (buboes). Septicemic plague: Fever, chills,
Signs and Symptoms weakness, abdominal pain, and shock. Pneumonic plague: Fever, cough, chest pain, difficulty breathing, and coughing up blood.
Source: Fleas (infected with Yersinia pestis) and rodents. Transmission occurs through the bite of infected fleas, inhalation of respiratory droplets from
Transmission infected individuals (in pneumonic plague), or contact with contaminated materials or body fluids.
Prevention involves controlling rodent populations, flea control measures, and early detection and treatment of cases. Antibiotic prophylaxis may be
Prevention/Prophylaxis recommended for individuals exposed to confirmed cases. A vaccine is available for high-risk populations, although its efficacy is limited.
Antibiotic treatment with drugs such as streptomycin, gentamicin, doxycycline, or ciprofloxacin is effective in treating plague. Supportive care to manage
Treatment symptoms and complications may also be necessary, particularly in severe cases.
Susceptibility testing of Yersinia pestis isolates involves culture-based methods followed by antibiotic susceptibility testing using agar diffusion or broth
Susceptibility Testing microdilution methods.
Control measures include surveillance, vector control, prompt diagnosis and treatment of cases, implementation of quarantine measures in outbreaks, and
Control public health education on prevention strategies.
Sample collection involves blood, sputum, or lymph node aspirates from suspected cases. Laboratory diagnosis includes culture on selective media,
Laboratory Diagnosis biochemical tests, serological assays, and molecular methods such as PCR for detection of Yersinia pestis DNA.
Disease Incubation period (typically 2-6 days), prodromal phase (non-specific symptoms), acute phase (development of characteristic symptoms), and convalescent
Phases/Stages phase with appropriate treatment.

Aspect Details
Name Streptococcal Pharyngitis
Causative Agent Streptococcus pyogenes (Group A Streptococcus)
Classification Bacteria: Streptococcus pyogenes species, family Streptococcaceae, order Lactobacillales
Streptococcus pyogenes is a Gram-positive, cocci-shaped bacterium, arranged in chains or pairs. Morphologically, it appears as spherical cells,
Type of Organism approximately 0.5-1.5 μm in diameter. Biological tests include culture on blood agar, serological assays, and molecular detection methods such as PCR.
Vectors Streptococcal pharyngitis is primarily transmitted through respiratory droplets from coughing or sneezing of infected individuals.
Streptococcal pharyngitis presents with sore throat, fever, difficulty swallowing, swollen lymph nodes in the neck, and sometimes headache and abdominal
Disease Recognition pain. Symptoms may be accompanied by tonsillar exudates and petechiae. Scientific Name: Streptococcus pyogenes infection.
Streptococcal pharyngitis is common, particularly in children aged 5-15 years. Transmission occurs through close contact with infected individuals or
exposure to respiratory secretions. Control measures include prompt diagnosis and treatment, as well as measures to prevent transmission in crowded
Epidemiology settings.
Anatomical Location Streptococcus pyogenes colonizes the mucous membranes of the throat and tonsils, leading to infection and inflammation of the pharynx (pharyngitis).
Following transmission, Streptococcus pyogenes adheres to and colonizes the pharyngeal mucosa, producing toxins and enzymes that contribute to tissue
Pathogenesis damage and inflammation. The bacterium may also produce exotoxins such as streptococcal pyrogenic exotoxins, which can lead to scarlet fever.
Streptococcus pyogenes produces various virulence factors, including streptolysins (hemolysins), streptokinase, hyaluronidase, and exotoxins such as
Virulence Factors streptococcal pyrogenic exotoxins (SPEs). These factors contribute to tissue damage, inflammation, and systemic complications.
Streptococcus pyogenes is transmitted through respiratory droplets and enters the host through the respiratory tract. In the pharynx, the bacterium adheres
Life Cycle to and colonizes the mucous membranes, leading to infection and inflammation.
Signs and Symptoms Sore throat, fever, difficulty swallowing, swollen lymph nodes in the neck, headache, abdominal pain, tonsillar exudates, and petechiae on the soft palate.
Source: Respiratory secretions of infected individuals. Transmission occurs through close contact with infected individuals or exposure to respiratory
Transmission droplets.
Prevention involves measures to reduce transmission, including proper hand hygiene, covering coughs and sneezes, and avoiding close contact with
Prevention/Prophylaxis individuals who have respiratory infections. Antibiotic treatment of confirmed cases can reduce the duration of symptoms and prevent complications.
Antibiotic treatment with penicillin or amoxicillin is effective in treating streptococcal pharyngitis and preventing complications. Supportive care includes rest,
Treatment hydration, and over-the-counter medications to alleviate symptoms such as fever and throat pain.
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Susceptibility testing of Streptococcus pyogenes isolates involves culture-based methods followed by antibiotic susceptibility testing using agar diffusion or
Susceptibility Testing broth microdilution methods.
Control measures include prompt diagnosis and treatment of cases, proper hand hygiene, respiratory etiquette, and avoiding close contact with infected
Control individuals. School and workplace policies may also help prevent transmission in community settings.
Sample collection involves throat swabs for culture or molecular testing. Laboratory diagnosis includes culture on blood agar, identification of Group A
Laboratory Diagnosis Streptococcus, and antimicrobial susceptibility testing. Rapid antigen tests may also be used for rapid diagnosis.
Disease
Phases/Stages Incubation period (1-3 days), acute phase (onset of symptoms), and recovery phase with appropriate treatment.

Aspect Details
Name Trichomoniasis
Causative Agent Trichomonas vaginalis
Classification Protist: Trichomonas vaginalis species
Trichomonas vaginalis is a flagellated protozoan parasite. Morphologically, it appears as pear-shaped with four anterior flagella and one recurrent flagellum,
Type of Organism approximately 10-20 μm in size. Biological tests include microscopic examination of vaginal secretions.
Vectors Trichomoniasis is primarily transmitted through sexual contact with an infected individual.
Trichomoniasis in women typically presents with vaginal itching, burning, redness, and a frothy, malodorous vaginal discharge. Men may experience urethral
Disease Recognition discharge or irritation. Scientific Name: Trichomonas vaginalis infection.
Trichomoniasis is one of the most common sexually transmitted infections worldwide. Control measures include condom use during sexual activity,
screening and treatment of infected individuals, and partner notification and treatment to prevent reinfection. Recognition involves testing of symptomatic
Epidemiology individuals or those at risk.
Anatomical Location Trichomonas vaginalis primarily colonizes the urogenital tract, including the vagina and urethra in women and men, respectively.
Following transmission through sexual contact, Trichomonas vaginalis adheres to and colonizes the urogenital epithelium. The parasite disrupts host cell
Pathogenesis membranes, leading to inflammation and tissue damage. Trichomonas vaginalis also produces proteases and other virulence factors.
Trichomonas vaginalis produces various virulence factors, including proteases, adhesins, and cytoadherence factors, which facilitate attachment to host
Virulence Factors cells and tissue invasion. The parasite’s ability to evade host immune responses also contributes to its pathogenicity.
Trichomonas vaginalis has a direct life cycle, with transmission occurring through sexual contact. Upon infection, the parasite colonizes the urogenital tract,
Life Cycle where it undergoes binary fission to multiply. The trophozoites are responsible for colonization and pathogenesis.
Women: Vaginal itching, burning, redness, frothy, malodorous vaginal discharge, pain during urination or sexual intercourse. Men: Urethral discharge or
Signs and Symptoms irritation, discomfort during urination or ejaculation.
Transmission Source: Infected individuals. Transmission occurs through sexual contact, including vaginal, anal, or oral sex.
Prevention involves practicing safe sex, including the consistent and correct use of condoms during sexual activity. Screening and treatment of infected
Prevention/Prophylaxis individuals and their partners are essential to prevent transmission and reinfection.
Treatment Trichomoniasis is typically treated with oral metronidazole or tinidazole. Sexual partners should also be treated simultaneously to prevent reinfection.
Susceptibility testing of Trichomonas vaginalis isolates involves in vitro culture-based methods followed by drug susceptibility testing using broth
Susceptibility Testing microdilution or agar dilution methods.
Control measures include education on safe sex practices, routine screening for sexually active individuals, prompt treatment of infected individuals, and
Control partner notification and treatment.
Sample collection involves vaginal or urethral swabs for microscopic examination or culture. Laboratory diagnosis includes microscopic visualization of
motile trichomonads in wet mounts or culture-based methods for detection of Trichomonas vaginalis. Rapid antigen tests may also be available for point-of-
Laboratory Diagnosis care diagnosis.
Disease
Phases/Stages Incubation period (variable), acute phase (onset of symptoms), and resolution phase with appropriate treatment.

Aspect Details
Name Trypanosomiasis (Sleeping Sickness)
Causative Agent Trypanosoma brucei gambiense (West African sleeping sickness) and Trypanosoma brucei rhodesiense (East African sleeping sickness)
Classification Protist: Trypanosoma brucei species
Trypanosoma brucei is a flagellated protozoan parasite. Morphologically, it appears as elongated, spindle-shaped cells with a single flagellum, approximately
Type of Organism 20-30 μm in length. Biological tests include microscopic examination of blood, cerebrospinal fluid (CSF), or lymph node aspirates.
Vectors Trypanosomiasis is primarily transmitted through the bite of infected tsetse flies (Glossina spp.).
Trypanosomiasis presents in two stages: Early stage (hemolymphatic phase) with nonspecific symptoms such as fever, headache, joint pain, and itching; Late
stage (meningoencephalitic phase) with neurological symptoms including confusion, sleep disturbances, tremors, and coma. Scientific Name: Trypanosoma
Disease Recognition brucei infection.
Trypanosomiasis occurs in sub-Saharan Africa, where tsetse flies are endemic. Two forms of the disease exist: West African sleeping sickness caused by T.
brucei gambiense and East African sleeping sickness caused by T. brucei rhodesiense. Control measures include vector control, surveillance, and treatment
Epidemiology of infected individuals.
Trypanosoma brucei primarily resides in the blood and lymphatic system during the early stage of infection. In the late stage, the parasite crosses the blood-
Anatomical Location brain barrier and infects the central nervous system (CNS), leading to meningoencephalitis.
Following transmission by tsetse flies, Trypanosoma brucei multiplies in the bloodstream and lymphatics, leading to systemic infection. In the late stage, the
Pathogenesis parasite crosses the blood-brain barrier and infects the CNS, leading to meningoencephalitis and neurological symptoms.
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Trypanosoma brucei produces various surface proteins (variant surface glycoproteins, VSGs) that allow it to evade the host immune system by antigenic
Virulence Factors variation. The parasite also produces factors that disrupt the blood-brain barrier, facilitating invasion of the CNS.
Trypanosoma brucei has a complex life cycle involving transmission between mammalian hosts and tsetse flies. In humans, the bloodstream form
Life Cycle (trypanomastigotes) circulates, while the insect form (procyclic trypomastigotes) develops in the midgut of tsetse flies.
Early stage: Fever, headache, joint pain, itching, enlarged lymph nodes; Late stage: Confusion, sleep disturbances, tremors, coordination problems, seizures,
Signs and Symptoms coma.
Transmission Source: Infected individuals and animals. Transmission occurs through the bite of infected tsetse flies, which inject trypanosomes while feeding on blood.
Prevention involves vector control measures such as insecticide-treated traps, insecticide spraying, and personal protective measures to avoid tsetse fly
Prevention/Prophylaxis bites. Prompt diagnosis and treatment of infected individuals are essential to prevent the spread of the disease.
Treatment depends on the stage and form of the disease. Drugs such as suramin and pentamidine are used for early-stage infection, while melarsoprol and
Treatment eflornithine are used for late-stage disease. Combination therapies may be necessary due to drug resistance.
Susceptibility testing of Trypanosoma brucei isolates involves in vitro culture-based methods followed by drug susceptibility testing using broth microdilution
Susceptibility Testing or agar dilution methods.
Control measures include vector control, surveillance, early diagnosis, and treatment of infected individuals. Public health education and community
Control engagement are also crucial for prevention and control efforts.
Laboratory Diagnosis Sample collection involves blood, lymph node aspirates, or cerebrospinal fluid (CSF) for microscopic examination or molecular testing.

Aspect Details
Name Chagas Disease (American Trypanosomiasis)
Causative Agent Trypanosoma cruzi
Classification Protist: Trypanosoma cruzi species, family Trypanosomatidae, order Kinetoplastida
Trypanosoma cruzi is a flagellated protozoan parasite. Morphologically, it appears as elongated, spindle-shaped cells with a single flagellum, approximately
Type of Organism 15-30 μm in length. Biological tests include microscopic examination of blood, xenodiagnosis, and serological assays.
Vectors Chagas disease is primarily transmitted through the bite of infected triatomine bugs (commonly known as “kissing bugs” or “assassin bugs”).
Chagas disease has acute and chronic phases. Acute phase: Often asymptomatic or presents with mild flu-like symptoms. Chronic phase: May lead to
severe complications such as heart disease (cardiomyopathy) or digestive system disorders (megacolon, megaesophagus). Scientific Name: Trypanosoma
Disease Recognition cruzi infection.
Chagas disease is endemic in Latin America, where triatomine bugs are prevalent. Control measures include vector control, blood screening, and treatment
Epidemiology of infected individuals. Recognition involves screening of blood donors, testing of at-risk populations, and diagnosis of symptomatic individuals.
Anatomical Location Trypanosoma cruzi primarily infects cardiac and smooth muscle cells, as well as cells of the digestive tract, during the chronic phase of infection.
Following transmission by triatomine bugs, Trypanosoma cruzi enters the bloodstream and invades various tissues, where it multiplies. Chronic infection can
Pathogenesis lead to tissue damage and inflammation, particularly in the heart and digestive system.
Trypanosoma cruzi produces various virulence factors, including enzymes that facilitate invasion of host cells, immune evasion mechanisms, and factors that
Virulence Factors contribute to tissue damage and inflammation. The parasite can also undergo antigenic variation to evade host immune responses.
Trypanosoma cruzi has a complex life cycle involving transmission between mammalian hosts and triatomine bugs. Infection occurs when the bugs deposit
Life Cycle feces containing parasites near the site of the bite wound. Parasites enter the bloodstream through mucous membranes or breaks in the skin.
Acute phase: Fever, headache, fatigue, rash, swelling at the site of the bite (chagoma), swollen lymph nodes, hepatosplenomegaly. Chronic phase: Cardiac
Signs and Symptoms symptoms (palpitations, chest pain), digestive symptoms (difficulty swallowing, constipation), neurological symptoms, sudden death due to heart failure.
Source: Infected triatomine bugs. Transmission occurs through the bite of infected bugs, or through contact with feces or urine of infected bugs entering
Transmission mucous membranes or breaks in the skin.
Prevention involves vector control measures to reduce triatomine bug infestation, screening of blood donors, and early diagnosis and treatment of infected
Prevention/Prophylaxis individuals. Personal protective measures, such as using insecticide-treated bed nets, can also help prevent transmission.
Treatment depends on the stage of infection. Antiparasitic drugs such as benznidazole and nifurtimox are used to treat acute and early chronic infections.
Treatment Symptomatic treatment may be necessary for complications in the chronic phase, such as heart failure or digestive disorders.
Susceptibility testing of Trypanosoma cruzi isolates involves in vitro culture-based methods followed by drug susceptibility testing using broth microdilution
Susceptibility Testing or agar dilution methods.
Control measures include vector control, screening of blood donors, early diagnosis and treatment of infected individuals, public health education, and
Control research on new treatment options and vaccines.
Sample collection involves blood for microscopic examination or molecular testing, as well as serological assays for detection of antibodies against
Laboratory Diagnosis Trypanosoma cruzi.
Disease Acute phase (1-2 months post-infection): Often asymptomatic or mild symptoms; Chronic phase (years to decades post-infection): Development of severe
Phases/Stages complications affecting the heart, digestive system, and nervous system.

Aspect Details
Name Cryptococcosis
Causative Agent Cryptococcus neoformans (most common) or Cryptococcus gattii
Classification Fungi: Cryptococcus neoformans and Cryptococcus gattii species, family Tremellaceae, order Tremellales
Cryptococcus species are encapsulated yeasts. Morphologically, they appear as round to oval-shaped cells, approximately 5-10 μm in diameter, with a
Type of Organism prominent polysaccharide capsule. Biological tests include culture on Sabouraud agar and molecular detection methods.
Vectors Cryptococcosis is not transmitted through vectors. It is acquired through inhalation of airborne fungal spores.
 Aspect Details
Cryptococcosis can present as pulmonary cryptococcosis (lung infection), cryptococcal meningitis (infection of the brain and spinal cord), or disseminated
Disease Recognition cryptococcosis (infection spread to other organs). Scientific Name: Cryptococcus neoformans or Cryptococcus gattii infection.
Cryptococcosis is found worldwide and is commonly associated with immunocompromised individuals, such as those with HIV/AIDS or organ transplant
Epidemiology recipients. Environmental sources include bird droppings (for C. neoformans) and trees (for C. gattii).
Cryptococcus species primarily infect the lungs upon inhalation of spores. In immunocompromised individuals, the fungus can disseminate to other organs,
Anatomical Location including the brain, spinal cord, skin, and bones.
Following inhalation, Cryptococcus spores reach the alveoli of the lungs, where they are phagocytosed by alveolar macrophages. The fungus can evade host
Pathogenesis immune responses and disseminate hematogenously, particularly in immunocompromised individuals, leading to systemic infection.
Cryptococcus species produce various virulence factors, including the polysaccharide capsule, which helps the fungus evade phagocytosis and modulate
Virulence Factors host immune responses. Other factors include melanin production, urease activity, and the ability to grow at body temperature.
Cryptococcus species have a saprophytic life cycle in the environment, particularly in soil contaminated with bird droppings (C. neoformans) or certain trees
Life Cycle (C. gattii). In the host, the fungus can cause localized or disseminated infection, depending on host immune status and other factors.
Pulmonary cryptococcosis: Asymptomatic or mild respiratory symptoms (cough, shortness of breath); Cryptococcal meningitis: Headache, fever, neck
Signs and Symptoms stiffness, confusion, blurred vision; Disseminated cryptococcosis: Variable symptoms depending on organs involved (skin lesions, bone pain, etc.).
Source: Environmental sources contaminated with Cryptococcus spores (soil, bird droppings, trees). Transmission occurs through inhalation of airborne
Transmission spores. Cryptococcosis is not transmitted from person to person.
Prevention involves avoiding exposure to environmental sources of Cryptococcus spores, particularly for individuals with weakened immune systems.
Prevention/Prophylaxis Antifungal prophylaxis may be considered for high-risk individuals, such as those with advanced HIV/AIDS.
Treatment of cryptococcosis typically involves antifungal medications, such as amphotericin B and flucytosine for induction therapy, followed by fluconazole
Treatment for consolidation and maintenance therapy. Duration and choice of therapy depend on the severity of infection and host factors.
Susceptibility testing of Cryptococcus isolates involves culture-based methods followed by antifungal susceptibility testing using broth microdilution or agar
Susceptibility Testing dilution methods.
Control measures include education on risk factors and prevention strategies, early diagnosis and treatment of infections, and minimizing exposure to
Control environmental sources of Cryptococcus spores, particularly for high-risk individuals.
Sample collection involves respiratory specimens (sputum, bronchoalveolar lavage), cerebrospinal fluid (CSF), or other body fluids or tissues for microscopic
Laboratory Diagnosis examination, culture, or molecular testing. Laboratory diagnosis includes India ink staining, fungal culture, antigen detection, and molecular methods.
Disease Cryptococcosis can present in various stages, including asymptomatic colonization, localized infection (e.g., pulmonary cryptococcosis), and disseminated
Phases/Stages infection (e.g., cryptococcal meningitis or disseminated cryptococcosis).

Microorganism Antibiotic(s)
Measles None (Measles is a viral infection)
Rubella None (Rubella is a viral infection)
Respiratory Syncytial Virus
(RSV) None (RSV is a viral infection)
Influenza Oseltamivir, Zanamivir
Rabies None (Rabies is usually prevented through vaccination after exposure)
Cholera Doxycycline, Azithromycin, Ciprofloxacin
Plague (all forms) Streptomycin, Doxycycline, Gentamicin
Streptococcal Pharyngitis Penicillin, Amoxicillin, Cephalexin
Trichomoniasis Metronidazole
Trypanosomiasis Suramin, Pentamidine, Eflornithine, Melarsoprol
Chagas’ Disease Benznidazole, Nifurtimox
Cryptococcosis Amphotericin B, Fluconazole