- Trimethoprim-sulfamethoxazole (TMP-SMX) : First-line prophylaxis for both PCP and toxoplasmic encephalitis, especially when CD4 count <200 cells/μL or <100 ce
- Trimethoprim-sulfamethoxazole (TMP-SMX) : First-line prophylaxis for both PCP and toxoplasmic encephalitis, especially when CD4 count 12–30 lateral branches . - T. solium : <13 branches . - Scolex Recovery (Rare) Post-treatment, recovery of the scolex (unarmed in T. saginata ) may help confirm species. - Serological Tests (Not routine) Used occasionally to detect circulating antigens or antibodies, especially in unclear cases. B. Treatment (7 marks) - First-Line Therapy Praziquantel : Single dose of 5–10 mg/kg orally . - Causes spastic paralysis and detachment of the worm. - Alternative Therapy Niclosamide : 2 g orally (adults); chewable tablet followed by laxative to expel worm. - Supportive Measures Laxatives may be used to aid in worm expulsion. - Patient education on hygiene and proper cooking of beef to prevent reinfection. - Public Health Note Meat inspection, proper cooking (≥57°C), and sanitation are essential to control transmission. A. Pathogenesis of Severe Malaria (8 marks) - Causative Agent Most commonly Plasmodium falciparum . - Cytoadherence and Sequestration Infected RBCs adhere to endothelium via PfEMP1 , causing microvascular obstruction and tissue hypoxia (e.g., cerebral malaria). - RBC Destruction and Anemia Hemolysis of infected and non-infected RBCs leads to severe anemia and hemoglobinuria ("blackwater fever"). - Immune Activation and Cytokine Storm TNF-α, IL-1 release contributes to fever, inflammation, and endothelial damage. - Metabolic Derangements Hypoglycemia , acidosis , hyperlactatemia , and renal failure due to parasite metabolism and host response. - Cerebral Malaria Neurological symptoms due to sequestration in cerebral microvasculature (confusion, seizures, coma). B. Treatment of Severe Malaria (7 marks) - Antimalarial Therapy (Parenteral) Artesunate IV (preferred): 2.4 mg/kg at 0, 12, 24 hrs, then daily. - Quinine dihydrochloride IV if artesunate unavailable. - Follow-up Oral Therapy Complete course with ACT (artemisinin-based combination therapy) once oral therapy is tolerated. - Supportive Treatment IV fluids, correction of hypoglycemia, antipyretics, anticonvulsants (for seizures), dialysis if needed. - Monitoring Frequent monitoring of parasitemia, renal function, blood glucose, and neurological status. A. Life Cycle Stages (7 marks) - Vector Transmitted by tsetse fly ( Glossina spp). - Infective Stage Metacyclic trypomastigote injected into human host during fly bite. - Bloodstream Stage Parasite transforms into bloodstream trypomastigotes , multiplying by binary fission in blood, lymph, and cerebrospinal fluid. - Lymphatic and CNS Invasion Progression leads to sleeping sickness with neurological involvement (late stage). - Transmission to Vector Tsetse fly ingests trypomastigotes during blood meal. - Procyclic Stage in Fly Midgut Transform into procyclic trypomastigotes , multiply, then migrate to salivary glands. - Epimastigote to Metacyclic Forms Develop into epimastigotes , then into infective metacyclic trypomastigotes . B. Treatment (8 marks) - Stage I (Hemolymphatic stage) Pentamidine : 4 mg/kg IM/IV daily for 7 days. - Effective with minimal CNS penetration. - Stage II (CNS involvement) NECT regimen : Nifurtimox-Eflornithine Combination Therapy .Eflornithine IV + Nifurtimox orally for 10 days. - Alternative: Melarsoprol (older, more toxic). - Supportive Care Treat neurological symptoms, monitor fluid/electrolyte status. - Prevention and Control Tsetse fly control, surveillance, early detection, and treatment are key public health strategies. A. Introduction to Viral Receptors (3 marks) - Viral receptors are specific molecules (usually glycoproteins or glycolipids) on host cell surfaces that viruses bind to in order to gain entry into cells . - The nature and distribution of these receptors determine host specificity , tissue tropism , and transmission dynamics , all of which influence whether an infection remains localized or escalates into an epidemic/pandemic. B. Roles of Viral Receptors in Epidemic and Pandemic Infections (10 marks) - Host Range Expansion Mutation or recombination in viruses can allow binding to receptors of new species , facilitating zoonotic spillover (e.g., SARS-CoV, SARS-CoV-2 via ACE2). - This jump can spark new outbreaks in immunologically naïve populations. - Tissue Tropism and Severity Receptors like DC-SIGN or CD4 guide viruses to specific tissues (e.g., HIV to T-helper cells), affecting disease progression and clinical outcome. - Severe outcomes can increase viral shedding and community transmission. - Viral Fitness and Transmission High-affinity binding (e.g., HA of influenza virus to sialic acid ) increases viral entry efficiency and replication, contributing to higher viral loads and greater transmission potential . - Genetic Variation in Host Populations Polymorphisms in receptors (e.g., CCR5-Δ32 mutation confers HIV resistance) influence susceptibility, shaping outbreak dynamics and geographic spread. - Antigenic Shift and Receptor Usage Change Influenza A virus can acquire genes from animal strains via reassortment , changing receptor preferences (e.g., from α-2,3-linked to α-2,6-linked sialic acids), promoting human-to-human transmission . - Immune Evasion Some viruses bind to complement receptors or use decoy receptors to modulate immune detection, allowing wider spread before containment. C. Conclusion (2 marks) - Viral receptors play a central role in determining transmission patterns, host adaptation, and outbreak severity. - Understanding receptor biology is crucial for predicting epidemics , vaccine design , and antiviral drug development . A. Introduction (2 marks) - Antimicrobial resistance (AMR) results from genetic and biochemical adaptations in bacteria that allow them to survive drug exposure. - Resistance can arise via mutation or horizontal gene transfer , and involves various biochemical mechanisms . B. Key Biochemical Mechanisms of Drug Resistance (12 marks) - Enzymatic Drug Inactivation Bacteria produce enzymes that chemically modify or degrade antibiotics.Example: β-lactamases hydrolyze β-lactam rings of penicillins and cephalosporins. - Aminoglycoside-modifying enzymes (acetyltransferases, adenyltransferases). - Target Modification Mutations or enzymatic alterations of antibiotic targets reduce drug binding.Example: Altered PBPs (penicillin-binding proteins) in MRSA. - Methylation of 23S rRNA in macrolide resistance (via erm genes). - Reduced Permeability Decreased expression or mutation of porins reduces drug entry, especially in Gram-negative bacteria.Example: Pseudomonas aeruginosa limiting carbapenem uptake. - Efflux Pumps Active expulsion of antibiotics via efflux proteins lowers intracellular drug concentration.Example: Tet(A) efflux pump for tetracycline resistance. - Bypass of Metabolic Pathways Alternative enzymes or pathways reduce dependence on the drug-inhibited target.Example: Resistance to sulfonamides via a plasmid-encoded dihydropteroate synthase with lower affinity for the drug. - Biofilm Formation Biofilms protect bacteria from antibiotics and host defenses.Reduced drug penetration, altered pH, and presence of dormant cells contribute to resistance. - Quorum Sensing and Persistence Communication via quorum sensing can trigger resistance gene expression or induce a persister state . C. Conclusion (1 mark) - These biochemical adaptations reflect the plasticity of bacterial physiology under selective pressure, and pose a major challenge to effective antimicrobial therapy. a) Etiology (2 marks) - Paragonimiasis is caused by lung flukes of the genus Paragonimus . - The most common species affecting humans is Paragonimus westermani , found mainly in East Asia. Other species (e.g., P. africanus , P. mexicanus ) occur in other regions. b) Transmission and Control (3 marks) - Transmission : Humans acquire infection by consuming undercooked or raw freshwater crabs or crayfish harboring metacercariae . - Control Measures :Proper cooking